a review of the marine biotoxin monitoring

Transcription

A REVIEW OF THE MARINE BIOTOXIN
MONITORING PROGRAMME FOR
NON-COMMERCIALLY HARVESTED
SHELLFISH
PART 1: TECHNICAL REPORT
A Report for the NZ Ministry of Health
Brenda E. Hay
Coral M. Grant
Dorothy-Jean McCoubrey
AquaBio Consultants Ltd
P. O. Box 560
Shortland St P.O.
Auckland 1
New Zealand
Hay@AquaBio.co.nz
December
2000
DISCLAIMER
This technical resources document was prepared under contract to the New Zealand
Ministry of Health. The copyright in the report is owned by the Crown and
administered by the Ministry. The views of the author do not necessarily represent
the views or policy of the New Zealand Ministry of Health. The Ministry makes no
warranty, express or implied, nor assumes any liability or responsibility for the use of
or reliance on the contents of this report.
Neither AquaBio Consultants Limited, nor any of its employees makes any warranty,
express or implied, or assumes any liability or responsibility for use of the technical
resource document or its contents by any other person or organisation.
For bibliographic purposes, this document should be cited as follows:
Hay, B. E., Grant, C. M. & McCoubrey, D-J. (2000) A Review of the marine biotoxin
monitoring programme for non-commercially harvested shellfish. Part 1: Technical
Report. A report prepared for the NZ Ministry of Health by AquaBio Consultants
Ltd. NZ Ministry of Health.
This document is available on the NZ Ministry of Health’s Web site:
http://www.moh.govt.nz
ISBN (Book) 0-478-24348-0
ISBN (Internet) 0-478-24349-9
i
ACKNOWLEDGEMENTS
We wish to thank all those people, scientists and regulators, who have provided
invaluable assistance in the form of information and discussion in the preparation of
this report. Special thanks to Penny Truman and Yvonne Galloway from ESR,
Kirsten Todd, Lesley Rhodes, Lincoln Mackenzie, and Alison Haywood from
Cawthron Institute, Hoe Chang from NIWA, Paul Roberts (Ministry of Health) and
the local Health Protection Officers in each area. We are very grateful to Beatriz
Reguera (Instituto Español de Oceanografia), Paul Anderson (University of Maine)
and Don Richard (Canadian Food Inspection Agency), who spent what must have
been many hours reviewing our first draft. Particular thanks to Phil Busby (MAF),
who, in addition to commenting on our drafts, provided us with access to many papers
and books, and waited patiently for us to return them. Lastly, thanks to Janet Young,
of the Ministry of Health, who efficiently provided us with information and feedback,
and smoothed the process of this review throughout its course.
ii
FOREWORD
Any review of an on-going monitoring programme runs the risk of being superseded
by events subsequent to the period for which data analysis has been undertaken. This
review is based on analysis of phytoplankton and shellfish data up to the end of June
1999. Since that time, there has been a major bloom of Gymnodinium catenatum off
the western coast of the North Island. In addition, David Stirling of the Institute of
Environmental and Scientific Research (ESR), is currently undertaking analysis of
archived shellfish samples using LC-MS, which may throw some light on the identity
of some of the unexplained acetone screen positive test results. The implications of
these additional sets of data have not been considered in this review.
Brenda Hay
December 2000
iii
EXECUTIVE SUMMARY
Prior to a major biotoxins event in the summer of 1992-93, New Zealand had no
recorded incidence of marine biotoxins of public health significance. A marine
biotoxin monitoring programme, covering both commercial and non-commercial
shellfish harvesting, has been operating since 1993. The current non-commercial
marine biotoxin monitoring programme involves regular sampling at 30
phytoplankton sampling sites and 57 shellfish sampling sites. Data from the
commercial biotoxin monitoring programme are also purchased. The programme is
designed to monitor for potentially toxic phytoplankton, and for the presence of
Neurotoxic Shellfish Poisoning (NSP), Paralytic Shellfish Poisoning (PSP), Amnesic
Shellfish Poisoning (ASP) and Diarrhetic Shellfish Poisoning (DSP) (Okadaic acid
and dinophysistoxins) toxins at levels that present a risk to human health.
Internationally, New Zealand is unusual in having detected a wide range of different
biotoxins. In addition to those producing PSP, ASP, NSP and “classic” DSP,
pectenotoxin and yessotoxin have been detected in shellfish, and palytoxin in
phytoplankton. A range of non-toxic compounds, or compounds of unknown toxicity,
have also been found, including gymnodimine, and “Wellington Harbour toxin” (oral
toxicity unknown). Compounds that are inferred to have caused Respiratory Irritation
Syndrome (RIS) in New Zealand include brevetoxin and the “Wellington Harbour
toxin”.
The data collected in the marine biotoxin monitoring programme since 1993 presents
some challenges to analysis: the data are not independent, and are stratified both
spatially and temporally over several different scales. Analysis is further complicated
by changes in toxin test methods, and differences in biotoxin accumulation and
retention between different shellfish species. Effectively only a small proportion of
the data can be used for meaningful quantitative analysis.
In very broad overview, the situation in New Zealand with respect to marine biotoxins
is characterised by:
•
•
•
•
•
Wide distribution of potentially toxin-producing phytoplankton throughout New
Zealand.
Periods of low frequency of biotoxin occurrence followed by periods of higher
biotoxin occurrence, generally in relatively localised areas. Biotoxins may then
persist in a localised area for a period of time, sometimes in one shellfish
species/at one location.
Possible seasonal patterns in the occurrence of some biotoxins in shellfish (for
example, NSP and ASP), and not in others.
In periods of low biotoxin activity, some toxins are present very rarely (e.g. NSP
toxins) and others are common at low levels in some areas (e.g. Domoic acid).
Possible differences in the accumulation and retention of biotoxins by different
New Zealand shellfish species. These differences are potentially significant in
terms of the risk of Toxic Shellfish Poisoning (TSP) to consumers.
Currently there is a poor understanding, both here and internationally, of the factors
influencing the occurrence of toxic phytoplankton blooms. There is insufficient
iv
information to be able to predict the future occurrence of marine biotoxins in New
Zealand with confidence.
The potential risks presented by marine biotoxins in New Zealand are not distributed
evenly across the population. There is a disproportionate potential impact on sectors
of the population that consume more non-commercially harvested shellfish (for
example, Maori, and possibly Pacific and Asian peoples), on older people or people in
poor health, and on asthmatics. The potential risks of TSP are distributed
geographically with availability of desirable shellfish for harvest. There have been
few studies undertaken on non-commercial shellfish harvesting in New Zealand, and
there are significant discrepancies between the results of the studies. There are
limited good quality epidemiological data for TSP in New Zealand: although 457
cases potentially related to TSP have been reported between January 1993 and June
1999, only 9 (1.97%) have been classed as probable cases of TSP. There are no
confirmed cases under the current case definitions.
The oral toxicity of some of the marine biotoxins found in New Zealand, including the
effect of long-term ingestion of low levels of toxin, are still unknown. The current
outcome surveillance may not detect these impacts.
Lack of robust data severely limits quantitative assessment of the risks associated with
biotoxins in New Zealand. There are sufficient data to suggest that in the absence of a
non-commercial biotoxin monitoring programme, a significant number of people
could become ill as a result of TSP in some years. Some of these people would be
severely ill, with the risk of death. For example, one scenario suggests that 50% of
the PSP cases (amounting to nearly 2000 people in a scenario relating to the Bay of
Plenty) would have moderate to severe symptoms. The long-term effects of ingestion
of “DSP” toxins, including Okadaic acid, dinophysistoxins, yessotoxin and
pectenotoxin, are unknown, but potentially present a risk. The incidences of these
two latter toxins are unknown because they are not currently included in the
monitoring programme. The levels of Domoic acid detected in shellfish to date would
only produce relatively mild symptoms of ASP in adults (although one scenario
suggests that up to 750 people could be affected). The potential impact of NSP
remains somewhat unknown due to a lack of robust data on shellfish toxicity levels
from the 1993 event, but has been very low in subsequent years. RIS events have
occurred in two of the last six years, and depending on wind strength and direction,
affect anyone within a few kilometres of the coast. Asthmatic people are the most
seriously affected, and data suggest that approximately 9.8% of people exposed to
RIS toxins in New Zealand could potentially suffer an asthma attack as a result.
Within the strategic framework for public health, and the global context of
developments relating to marine biotoxins, a range of broad issues relating to the
management of marine biotoxins in New Zealand require consideration. These
encompass both strategic and technical issues.
It is suggested that a more proactive, strategic approach to the collection and use of
data would result in substantial improvements in cost effectiveness in the future. This
would involve:
v
•
•
•
Improved management of the data collected in the marine biotoxin monitoring
programme.
A sampling strategy to ensure that robust, long-term data are available to
detect patterns in the geographic and temporal distribution of biotoxins.
A co-ordinated management strategy that ensures that sampling and analytical
techniques used in the monitoring programme are scientifically validated, and
that changes in the programme are consistent with the results of risk analysis
and long-term strategies to increase cost-effectiveness.
An increased emphasis on advocacy and facilitation of relevant research utilising
strategic alliances with organisations with common interests, is suggested to increase
the cost-effectiveness of the marine biotoxin monitoring programme in the future.
Research is required to:
•
•
•
•
•
•
Determine inter-specific differences between shellfish with respect to biotoxin
uptake, accumulation and detoxification processes.
Determine the oral toxicity, including the impacts of long-term ingestion of low
levels of toxin, for those compounds currently known to be toxic to mice by IP
injection, but for which oral toxicity is unknown.
Relate environmental parameters and processes to the occurrence of toxic
phytoplankton, and toxin levels within species.
Validate new toxin testing methods for biotoxins found in New Zealand (such as
the PSP MISTTM Alert Kit).
Rigorously determine non-commercial shellfish harvest patterns.
Evaluate the effectiveness of education and communication strategies with respect
to the management of the risk of marine biotoxins in New Zealand.
A variety of changes to the marine biotoxin monitoring programme are discussed in
response to both the results of data analysis, and to interest expressed by the Ministry
of Health:
•
Consideration is given as to whether costs could be reduced by broad
reduction in temporal or spatial components of the monitoring programme in
the light of a re-evaluation of risk arising from analysis of historical data.
Based on consideration of risks to public health in the absence on monitoring,
the value of the available historical data in the prediction of future events, and
the lack of definitive data on non-commercial harvesting patterns, it is
concluded that broad reductions in monitoring could not be recommended
unless an increased level of risk to the public were acceptable under the
current strategy for public health.
•
It is suggested that species-specific public warnings be considered in areas
where consumption of non-commercially harvested shellfish is very important
culturally or economically, and that are subject to public warnings for a long
period of time due to biotoxin persistence in one shellfish species only. This
would help to maintain the credibility of the marine biotoxin monitoring
programme, which is compromised when people consistently harvest shellfish
when a public health warning is in place but do not become ill. A telephone
vi
“hotline” with regularly up-dated recorded messages containing information
about the biotoxin status of each area, is suggested as a useful method of
conveying more complex information that the public may not remember from
media messages.
•
It is noted that there is currently no specific surveillance or management of
risk with respect to RIS, although this does occur informally to some extent.
Formalisation of protocols for RIS, based on utilisation of the current
phytoplankton monitoring programme, is suggested as an option.
•
The development of new biotoxin test methods, changing social attitudes
toward the use of animals in testing, and moves by the shellfish industry to
adopt new test methods, provide opportunities and impetus for consideration
of new test methods. Testing that focuses more specifically on identifying
particular toxins, or, in the case of functional assays, specific modes of toxic
activity, has advantages in the reduction of “false positive” toxicity results that
may occur in mouse bioassays. However, a move to testing for specific
biotoxins or types of toxin activity would remove the hazard surveillance for
new biotoxins currently provided by the mouse bioassays. In this situation,
robust outcome surveillance would be of increased importance. In some
instances, new biotoxin test methods may provide cost advantages over the
current mouse bioassays. Specific options with respect to the potential use of
new test methods are discussed in Part 2 of this report under separate cover.
•
Further data are required to confirm the robustness of the current
phytoplankton monitoring programme in predicting shellfish toxicity. With
respect to some phytoplankton species, the impact of the low level of precision
in the phytoplankton methods currently used, and whether any additional
assurance gained by improving this precision justifies additional cost, needs to
be considered. In addition, the impact of succession of Pseudo-nitzschia
species within a Pseudo-nitzschia bloom on the protocols for use of gene
probes within the monitoring programme, requires further investigation before
being formally incorporated into the marine biotoxin monitoring programme.
Many of the technical issues that require consideration in marine biotoxin monitoring
are complex and specialised. It is suggested that an increased level of advice, from
appropriately qualified technical specialists independent of organisations that may
provide monitoring services, should be sought to peer review technical proposals
when considering major changes to the marine biotoxin monitoring programme.
vii
TABLE OF CONTENTS
FOREWORD
iii
EXECUTIVE SUMMARY
iv
TABLE OF CONTENTS
viii
LIST OF FIGURES
xiii
LIST OF TABLES
xv
SECTION 1:
INTRODUCTION
1.1
BACKGROUND
1.2
THE CURRENT MONITORING PROGRAMME
1.3
BIOTOXINS IN NEW ZEALAND
1.3.1 Paralytic Shellfish Poisoning (PSP)
1.3.2 Amnesic Shellfish Poisoning (ASP)
1.3.3 Diarrhetic Shellfish Poisoning (DSP)
1.3.4 Neurotoxic Shellfish Poisoning (NSP)
1.3.5 Respiratory Irritation Syndrome
1.3.6 Other Marine Biotoxins in New Zealand
1.4
THE STRATEGIC FRAMEWORK AND SCOPE OF THIS
REVIEW
1
1
4
7
7
9
10
11
12
12
SECTION 2:
ANALYSIS OF BIOTOXIN MONITORING DATA
2.1
INTRODUCTION
18
18
2.2
13
GENERAL METHODOLOGY
2.2.1 Identification of a Valid Dataset
2.2.2 Determination of Areas for Analysis
2.2.3 Analysis of Phytoplankton Occurrence
a) Geographical Distribution
b) Temporal Distribution
2.2.4 Reliability of Phytoplankton Monitoring as a
Predictor of Biotoxins in Shellfish
2.2.5 Differences in Biotoxin Accumulation between
Shellfish Species
2.2.6 Summary of Cumulative Monitoring ResultsShellfish and Phytoplankton
2.2.7 Analysis of Occurrence of Biotoxins in Shellfish
a) Geographical Distribution
b) Temporal Distribution
26
2.3
CUMULATIVE MONITORING RESULTS
30
2.4
RESULTS OF ANALYSIS – PSP
2.4.1 Geographic Distribution
2.4.2 Temporal Distribution
2.4.3 Phytoplankton as a Predictor of PSP in Shellfish
2.4.4 Conclusions
32
32
41
44
46
viii
19
20
21
24
24
25
26
26
27
27
28
2.5
RESULTS OF ANALYSIS – ASP
48
48
59
2.5.3 Phytoplankton as a Predictor of ASP in Shellfish
62
2.5.4 The use of Whole Cell DNA Probes for Pseudo-nitzschia
Species as a Predictor of Risk of Shellfish Toxicity
63
2.5.5 Conclusions
66
2.6
RESULTS OF ANALYSIS – DSP
2.6.3 Reliability of Acetone Screen
2.6.4 Phytoplankton as a Predictor of DSP in Shellfish
2.6.5 Conclusions
68
68
79
81
84
85
2.7
RESULTS OF ANALYSIS – NSP AND RESPIRATORY
IRRITATION SYNDROME
2.7.1 Introduction
2.7.4 Conclusions
86
86
86
96
97
3.1
NON-COMMERCIAL SHELLFISH GATHERING
AND CONSUMPTION IN NEW ZEALAND
INTRODUCTION
98
98
3.2
DISTRIBUTION OF SHELLFISH IN NEW ZEALAND
98
3.3
SHELLFISH GATHERING
104
3.4
POPULATION STRUCTURE AND SHELLFISH
CONSUMPTION
109
3.5
TEMPORAL PATTERNS
112
3.6
CONCLUSION
112
SECTION 3:
SECTION 4:
ANALYSIS OF EPIDEMIOLOGICAL DATA
4.1
INTRODUCTION
113
113
4.2
METHODOLOGY AND ASSUMPTIONS IN ANALYSIS
114
4.3
RESULTS
116
4.4
DISCUSSION
122
SECTION 5:
RISK ASSESSMENT
5.1
INTRODUCTION
125
125
5.2
PARALYTIC SHELLFISH POISONING
5.2.1 Hazard Identification
ix
125
125
5.2.2 Dose-Response Assessment
5.2.3 Exposure Assessment
5.2.4 Risk Characterisation
127
127
128
5.3
AMNESIC SHELLFISH POISONING
130
130
131
131
132
5.4
DIARRHETIC SHELLFISH POISONING
134
134
136
136
137
5.5
NEUROTOXIC SHELLFISH POISONING
139
139
139
140
141
5.6
RESPIRATORY IRRITATION SYNDROME
142
142
143
143
144
SECTION 6:
6.1
6.2
6.3
6.4
6.5
6.6
6.7
6.8
6.9
6.10
6.11
SUMMARY BY AREA
ZONE A
ZONE B
ZONE C
ZONE D
ZONE E
ZONE F
ZONE G
ZONE H
ZONE I
ZONE J
ZONE K
146
146
148
149
150
151
152
153
155
156
157
158
SECTION 7:
BIOTOXIN MANAGEMENT IN NEW ZEALAND
AND OVERSEAS
EDUCATION AND COMMUNICATION STRATEGIES
161
161
OVERSEAS BIOTOXIN MONITORING PROGRAMMES
AND TECHNOLOGY DEVELOPMENTS
164
7.1
7.2
7.3 NEW ZEALAND BIOTOXIN MANAGEMENT IN A
GLOBAL CONTEXT
SECTION 8:
DISCUSSION AND CONCLUSION
x
168
170
LITERATURE CITED
178
APPENDICES
193
APPENDIX I(A)
PHYTOPLANKTON TRIGGER LEVELS
194
APPENDIX I(B)
THE COMMERCIAL AND NON-COMMERCIAL
MONITORING PROGRAMME SAMPLING
REGIMES
195
APPENDIX I(C)
FLOW DIAGRAM ILLUSTRATING SHELLFISH TISSUE
TESTING FOR NSP AND DSP
202
APPENDIX I(D)
MAP SHOWING LOCATION OF BIOTOXIN
ZONES
203
APPENDIX II
PHYTOPLANKON SITES INCLUDED IN ANALYSIS
OVER THE “IDENTIFIED TIME INTERVAL”
204
APPENDIX III
TEMPORAL PERIODICITY OF EL NINO/LA NINA
WEATHER CONDITIONS
206
APPENDIX IV(A)
MAP SHOWING THE LOCATION OF SAMPLING
SITES IN THE MARLBOROUGH SOUNDS
(ZONE G)
207
SITE COMPARISONS OF PSEUDO-NITZSCHIA
OCCURRENCE IN THE HAURAKI GULF AND
MARLBOROUGH SOUNDS/COLLINGWOOD
209
APPENDIX IV(B)
APPENDIX IV(C)
SITE COMPARISONS OF DINOPHYSIS OCCURRENCE
IN THE HAURAKI GULF AND MARLBOROUGH
SOUNDS/COLLINGWOOD
212
APPENDIX IV(D)
SITE COMPARISONS OF GYMNODINIUM c.f.
MIKIMOTOI OCCURRENCE IN THE HAURAKI
GULF AND MARLBOROUGH SOUNDS
/COLLINGWOOD
215
APPENDIX V
RESULTS FROM WHOLE CELL DNA PROBES FOR
PSEUDO-NITZSCHIA SPECIES
218
APPENDIX VI
PSEUDO-NITZSCHIA SPECIES COMPOSITION AT THE
SAME SITE OVER CONSECUTIVE WEEKS,
DETERMINED BY WHOLE CELL GENE
PROBES
223
xi
LIST OF FIGURES
SECTION 1:
Figure 1.1
SECTION 2:
Figure 2.1
Figure 2.2
Figure 2.3
Figure 2.4
Figure 2.5
Figure 2.6
Figure 2.7
Figure 2.8
Figure 2.9
Figure 2.10
Figure 2.11
Figure 2.12
Figure 2.13
Figure 2.14
Figure 2.15
Figure 2.16
Figure 2.17
Figure 2.18
Figure 2.19
INTRODUCTION
1
Current Phytoplankton Monitoring Sites
6
18
Distribution of Biotoxin Zones and relevant
hydrographical features associated with the
New Zealand coastline
Distribution of potentially toxic species of
Alexandrium throughout New Zealand
Distribution of PSP at shellfish sample sites
throughout New Zealand
Box and whisker plots showing the frequency
distribution of potentially toxic Alexandrium sp.
above the regulatory levels
Comparison of levels of PSP in Greenshell™ mussels
and tuatua from Ohope Beach
Comparison of levels of PSP in mussels, tuatua, and
scallops from Waihi Beach
Comparison of levels of PSP in mussels and scallops
from Rangaunu Bay
Cumulative incidence of PSP toxins above the
detectable level within each zone by month
Distribution of detectable levels of PSP toxin in
shellfish from consistently monitored sites
Distribution of Pseudo-nitzschia sp. in
New Zealand
Distribution of ASP at shellfish sampling sites
distribution of Pseudo-nitzschia sp. above
the regulatory levels
Comparison of levels of ASP in Greenshell™ mussels
and scallops from Takaka River
Comparison of levels of ASP in Greenshell™ mussels,
scallops and cockles from Four Fatham Bay
Cumulative incidence of ASP toxins above the
detectable level within each zone by month
Distribution of detectable levels of ASP toxin in
Distribution of potentially toxic species of
Dinophysis throughout New Zealand
Distribution of potentially toxic Prorocentrum
lima throughout New Zealand
Distribution of DSP at shellfish sample sites
xii
23
33
34
36
39
39
40
42
42
49
50
52
57
58
61
61
69
70
71
Figure 2.20
Figure 2.21
Figure 2.22
Figure 2.23
Figure 2.24
Figure 2.25
SECTION 3:
Figure 3.1
SECTION 4:
Figure 4.1
Figure 4.2
distribution of Dinophysis acuminata
above the regulatory levels
distribution of Dinophysis acuta above the
regulatory levels
Cumulative incidence of DSP toxins above the
detectable level within each zone
Distribution of detectable levels of DSP toxin in
Distribution of potentially toxic Gymnodinium
species throughout New Zealand
distribution of potentially toxic Gymnodinium
c.f. mikimotoi above the regulatory levels
73
75
80
81
88
91
98
Population distribution by ethnic origin for each regional
authority within New Zealand
110
113
Distribution of suspected and confirmed cases of TSP
arising from non-commercially harvested shellfish
120
Number of suspected and confirmed cases of TSP from
consumption of different seafood species
121
xiii
LIST OF TABLES
SECTION 1:
Table 1.1
Table 1.2
SECTION 2:
Table 2.1
Table 2.2
Table 2.3
Table 2.4
Table 2.5
Table 2.6
Table 2.7
Table 2.8
Table 2.9
Table 2.10
Table 2.11
Table 2.12
Table 2.13
Table 2.14
INTRODUCTION
1
Specific toxicity of species of Alexandrium found
in New Zealand waters.
Maximum level of Domoic Acid found in New
Zealand isolates of Pseudo-nitzschia.
10
18
Summary of the cumulative results of the
monitoring for PSP, ASP, DSP and NSP toxins
in shellfish (Jan 1993-Jun 1999). Current regulatory
levels for each toxin group are also given
Cumulative results of phytoplankton monitoring
for all Biotoxin Zones
Percentage occurrence of potentially toxic
Alexandrium sp. and percentage above the
regulatory levels
Summary by zone of the total occurrence of PSP
toxins detected in shellfish and PSP toxins above the
regulatory levels
Summary by zone of the occurrence of PSP toxins
in Greenshell™ mussels from consistently monitored
sites
Summary of the occurrence of PSP toxins in the
major shellfish species sampled
Percentage occurrence of Pseudo-nitzschia sp.
and percentage occurrence above the regulatory
levels
Summary by zone of the total occurrence of ASP
toxins detected in shellfish and ASP toxins above the
regulatory level
Results of analysis for ASP in whole, and portions, of
scallops sampled concurrently
Summary by zone of the occurrence of ASP toxins in
Greenshell™ mussels from consistently monitored
sites
Summary by zone of the occurrence of ASP toxins in
scallops from consistently monitored sites
Summary of the occurrence of ASP toxins in the major
shellfish species sampled
Comparison of Domoic Acid levels in scallops and
mussels sampled concurrently
Risk assessment guidelines for toxin flesh testing in
shellfish for various Pseudo-nitzschia sp.
xiv
8
30
31
35
37
38
38
51
53
54
55
55
56
58
64
Table 2.15
Table 2.16
Table 2.17
Table 2.18
Table 2.19
Table 2.20
Table 2.21
Table.2.22
Table 2.23
Table 2.24
SECTION 3:
Table 3.1
Table 3.2
Table 3.3
Table 3.4
Table 3.5
SECTION 4:
Table 4.1
Table 4.2
Table 4.3
Percentage occurrence of Dinophysis acuminata
and percentage above the regulatory levels
Percentage occurrence of Dinophysis acuta
Percentage occurrence of Prorocentrum lima
Summary by zone of the occurrence of DSP toxins in
shellfish samples
Summary by zone of the occurrence of DSP toxins in
Greenshell™ mussels from consistently monitored
sites
Summary of the occurrence of DSP toxins in
the major shellfish species
The corrected results for samples recorded in FoodNet
as having negative Acetone Screen Results, but positive
DSP ELISA results
Percentage occurrence of potentially toxic
Gymnodinium c.f. breve and percentage above the
regulatory levels
Percentage occurrence of Gymnodinium c.f. mikimotoi
Summary of the occurrence of lipid soluble toxins in
shellfish samples
Number of trips by survey respondents targeting the
main shellfish species in each Biotoxin Zone
Comparison of the percentage of trips targeting each
bivalve species within each zone
The number of each species taken from each Biotoxin
Zone by respondents from the survey
Estimated percentage of non-commercial shellfish
harvesting by ethnicity, per year, throughout
New Zealand
Numbers and percentages of total weight of cockles
harvested, and harvesting population structure by
ethnic group at Lews Bay, Whangateau
72
74
76
77
78
78
83
89
90
93
98
106
106
108
109
111
113
Summary of reported cases of TSP by year as assessed
with respect to the causative agents
116
Comparison of the number of cases and rates per
100, 000 people in New Zealand between TSP, and
illness caused by Campylobacter and Vibro
parahaemolyticus
117
Age distribution of the “suspected” and “probable”
cases of TSP
118
xv
Table 4.4
Table 4.5
Table 4.6
Analysis of “suspected” and “probable” cases of
TSP from non-commercially and commercially
harvested seafood by ethnic origin
118
Analysis of source of seafood, by ethnic origin, for
“suspected” and “probable” cases of TSP
119
Geographical distribution of sites from which shellfish
were gathered in “suspected” and “probable” cases
of TSP
119
xvi
SECTION 1:
1.1
INTRODUCTION
BACKGROUND
Awareness of marine biotoxins with respect to public health in New Zealand is
relatively short: prior to a major biotoxin event in the summer of 1992-1993, New
Zealand had no recorded incidence of shellfish biotoxins of public health significance.
Preceding this, most concern focussed on the effects of harmful algal blooms with
respect to potential impacts on fish farming, shellfish farming and wild marine species
(e.g. Taylor et al., 1988; Chang et al., 1990; Mackenzie, 1992; Mackenzie et al., 1992;
Rhodes et al., 1993). A basic monitoring programme for Paralytic Shellfish
Poisoning (PSP) had been established in April 1992, based on monthly mouse
bioassays from shellfish sampled from four sites: Bay of Islands, Coromandel,
Marlborough Sounds, and Southland (Till, 1993). Although it was known that
phytoplankton potentially able to produce Diarrhetic Shellfish Poisoning (DSP) toxins
were present in New Zealand waters (e.g. Burns & Mitchell, 1982), there was no
routine monitoring for these toxins. However, a limited number of commercial
samples of mussels from Coromandel and Marlborough destined for the Japanese
market had been tested for PSP and DSP since July 1989. No toxins had been
detected in any of these samples (Till, 1993).
In January 1993, authorities became aware of the presence of biotoxins in shellfish
when a veterinarian in Northland reported poisoning in cats that had been fed with
shellfish. Owners of the animals were also found to have experienced toxic
symptoms after eating shellfish (Bates et al., 1993). Publicity led to further
notifications of human illness following shellfish consumption and the coastline was
progressively closed for shellfish harvesting. Consequently, by January 23rd the entire
coastline was closed.
About 186 people were affected with symptoms that resembled a case definition that
had been used in an outbreak of Neurotoxic Shellfish Poisoning (NSP) in North
Carolina (Bates et al., 1993). This case definition was sufficiently broad not to
exclude other known shellfish toxins and narrow enough to exclude most
gastrointestinal illnesses associated with infectious agents (Bates et al., 1993).
In addition to symptoms related to consumption of shellfish, the NZ Communicable
Disease Centre (CDC) also received reports of dry cough and eye irritation affecting
large numbers of people visiting or working near the beach at Orewa, north of
Auckland. These symptoms were consistent with reports of “respiratory irritation
syndrome” (RIS) associated with blooms of Gymnodinium breve in Florida caused by
brevetoxin aerosols (Bates et al., 1993; Steidinger & Joyce, 1973; Pierce, 1986).
An epidemiological investigation, which included consideration of data regarding
phytoplankton species present at coastal sites, subsequently suggested that:
“The major toxicity involved in the shellfish poisoning outbreak was Neurotoxic
Shellfish Poisoning (NSP), which affected mainly the north-eastern coastline of the
North Island from the Bay of Islands to the Bay of Plenty. It is likely that some cases
were of Diarrhetic Shellfish Poisoning (DSP). It is likely that Paralytic Shellfish
1
Poisoning (PSP) played no more than a minor role at the most in the outbreak, and
that Amnesic Shellfish Poisoning (ASP) probably played no role at all” (Bates et al.,
1993).
However, while only NSP and possibly DSP, played a role in the epidemiological
events, a range of shellfish toxins was detected in shellfish testing (Hannah et al.,
1993). These included a minimum of toxins related to ASP, DSP, NSP, PSP, and
non-specific 24-hour mouse toxicity.
While the toxin event of 1992-93 caught everyone somewhat by surprise, biotoxin
management structures were quickly brought into place to provide a coordinated
response. By February 1993, the Ministry of Agriculture and Fisheries (MAF) had
formulated a National Management Plan for Marine Biotoxin Control. A National
Marine Biotoxin Coordination Committee comprised of representatives from
regulatory bodies (Ministry of Agriculture & Fisheries, Ministry of Health, Public
Health Commission), research organisations, and the Fishing Industry Board was
established (Ministry of Agriculture & Fisheries, 1993a). The plan outlined the
guidelines for reporting and shared decision-making, the objectives for the
management programme, an overview of a multi-tiered management plan, operation
standards, and the responsibilities of regional agencies.
A comprehensive “National Management Plan for Marine Biotoxin Control in New
Zealand” was completed in March 1993 (Ministry of Agriculture & Fisheries, 1993b).
This included a Marine Biotoxin Management Plan for each regional area.
Management within the National Management Plan was based on:
•
•
•
•
•
“Assay and analytical results demonstrating the presence of marine biotoxins in
shellfish; and
Reports of marine biotoxins being involved in food-borne illness; and
Phytoplankton analysis; and
General environmental information including aerosol-borne illness and evidence
from bathing, kills or other evidence of the possible detrimental effects of toxin
producing algae on sea-birds, fish or other marine life; and
The flexibility to review and modify the programme as the database develops.”
The operational standards in the Plan specified 106 shellfish sampling sites (reduced
from the initial 244 sites) sampled weekly. These sites included 60 sites within
commercial shellfish farming/harvesting areas, and 46 sites where there was no
commercial shellfish activity (recreational areas). In practice however, sampling
continued at approximately 165 sites.
In November 1993 the Toxic Shellfish Coordination Committee was replaced by a
Marine Biotoxin Management Board, comprised of senior representatives from MAF,
Ministry of Health (now restructured to incorporate the functions of the Public Health
Commission) and NZ Fishing Industry Board. The Marine Biotoxin Management
Board established a Marine Biotoxin Surveillance Unit in January 1994 to manage the
operation of the biotoxin and phytoplankton monitoring programmes. Several
committees reported to the Board: a Financial Committee, which prepared advice on
contracts for sampling and analysis, a Technical Committee, which set standards and
specifications, and a Communications Committee, which handled media coordination,
2
press releases, Board communications and publications. Each committee comprised
representatives from each of the three member organisations (NZ Marine Biotoxin
Management Board, 1995). The Marine Biotoxin Surveillance Unit was comprised of
a Technical Coordinator from MAF, and two National Advisors, one from MAF with
expertise in marine science, and one from Ministry of Health with expertise in public
health protection (Trusewich et al., 1996). Health Protection Officers in each of the
21 Crown Health Enterprises were responsible for shellfish sampling, and decisions
on closure and re-opening of areas were made jointly between the Surveillance Unit
and the local Health Protection Officer. The programme was jointly funded by
industry (23%) through a Fishing Industry Board levy, and vote Health (77%).
Following a review of data collected, including the correlation of data between sites,
and the patterns of accumulation of toxins in different species, the number of sample
sites was reduced down to 120 sites per week in the 1994-95 year (Trusewich et al.,
1996). The cost-effectiveness of this monitoring was of some concern both to the
shellfish industry and the Ministry of Health. This prompted reviews of the
programme by both parties (NZ Fishing Industry Board, 1995; Wilson, 1996; Wilson
& Sim, 1996).
The moves for change resulted in the establishment of weekly phytoplankton
monitoring in 1995 in a few areas where biotoxin activity had occurred. The purpose
of this was to gather the data necessary to establish a robust phytoplankton monitoring
programme. A major restructuring of the marine biotoxin monitoring programme
followed in 1997. This restructuring involved changes to the monitoring programme
itself, and to the funding and administration of the programme.
The commercial marine biotoxin monitoring programme is now managed by MAF
and administered at a local level by Health Protection Officers from the local Hospital
and Health Services as part of a Shellfish Quality Assurance Programme. Each
commercial shellfish farming/harvesting area is now responsible for the funding of the
monitoring programme in its area. Based on the 1993-97 data on biotoxins in each
area, the monitoring programmes were modified in consultation with the Marine
Biotoxin Technical Committee. In most areas these modifications included the
introduction of weekly phytoplankton monitoring as an early warning system
(undertaken by trained personnel), and a reduction in the frequency of shellfish
samples tested. Specified numbers of potentially toxin-producing phytoplankton in
the water trigger shellfish flesh testing, or at a higher number, closure to harvest
pending the results of shellfish flesh testing. The frequency of routine shellfish
testing for each of the four toxins (PSP, NSP, DSP, and ASP) is related to the toxin
activity in each area.
The Ministry of Health manages routine monitoring in non-commercial sites, through
Health Protection Officers in each Hospital & Health Services organisation. The
Ministry of Health also purchases information from commercial biotoxin programmes
to supplement their own monitoring programme. The non-commercial marine
biotoxin monitoring programme was revised to include phytoplankton monitoring
where environmental conditions allow, with a reduction of shellfish testing in areas of
low biotoxin activity.
3
With the restructuring of the marine biotoxin monitoring programme in 1997, the
Marine Biotoxin Management Board, and the Marine Biotoxin Surveillance Unit were
disbanded, and their functions decentralised. However, the Marine Biotoxin
Technical Committee has continued to function in an informal capacity, and is an
example of the continuing cooperation in marine biotoxin issues between MAF (now
the Ministry of Agriculture & Forestry), Ministry of Health, and the shellfish industry.
Awareness of the potential problems of marine biotoxins in shellfish has resulted in
the establishment of significant research capability in the field of marine biotoxins in
New Zealand. Research has focussed primarily on identification of biotoxins and
their sources, and the development of new test methods. Every six months
researchers, regulators, public health officials and shellfish industry representatives
meet at a “Marine Biotoxin Science Workshop”, facilitated by MAF. These
workshops provide an opportunity for the presentation of research results in the field
of marine biotoxins, and for discussion about issues of concern. A Marine Biotoxin
Science Strategy is being developed through this group, to ensure that adequate
research funding is directed to marine biotoxin research from the Foundation for
Research, Science and Technology.
1.2
THE CURRENT MONITORING PROGRAMME
The Health Act (1956) provides the legislative framework for the management of
public health with respect to marine biotoxins in New Zealand. Section 3A defines
the function of the Ministry in relation to public health: “Without limiting any other
enactment or rule of law, and without limiting any other functions of the Ministry or
of any other person or body, the Ministry shall have the function of improving,
promoting and protecting public health”. Section 117 of the Act provides for the
ability of the Director General to make such regulations as necessary to conserve
public health. In addition, Section 37 of the Food Act (1980) provides for statements
to be issued by the Director General of Health, and this provision is used occasionally
to issue national press statements from the Director General warning the public not to
eat shellfish from defined areas.
The management of public health with respect to marine biotoxins is set out in the
Ministry of Health’s Food Administration Manual: Section 27: Marine Biotoxin
Control (Ministry of Health, 1997a). Health Protection staff in Hospital and Health
Services are responsible for the public health management of marine biotoxins in
commercial and non-commercial shellfish harvesting areas. This includes sample
collection, opening and closing commercial growing areas, domestic market product
recall, and warning the public when non-commercial growing areas should not be
harvested for shellfish. Generally, sample collection is contracted out to locally based
private individuals.
Each Hospital and Health Services Public Health Unit is responsible for maintaining a
local marine biotoxin management plan. The local marine biotoxin management
plans cover both non-commercial and commercial harvesting of shellfish. This is
because in some areas non-commercial sample sites may be used to close commercial
growing areas, and vice versa.
4
The non-commercial marine biotoxin monitoring programme is designed to match the
levels of biotoxin activity and shellfish availability in each area, and utilizes
phytoplankton monitoring where possible. In areas where testing of shellfish samples
has shown persistent or recurrent PSP, ASP, NSP or DSP toxins, weekly sampling
and testing of shellfish for the specific biotoxins is undertaken. In areas where
shellfish testing has shown a low risk of toxin accumulation, and that are not suitable
for phytoplankton monitoring, fortnightly shellfish samples are taken for analysis of
all toxins. In areas of low risk where phytoplankton testing is possible, weekly
phytoplankton samples are taken, and monthly shellfish samples for analysis for all
four toxins. Phytoplankton results are used to trigger shellfish testing and closure at
the same levels as in the commercial programme. Details of these levels are provided
in Appendix I(A).
There are currently 61 routine phytoplankton sampling sites throughout New Zealand.
Thirty of these sites are either non-commercial sites, or sampled under the noncommercial marine biotoxin monitoring programme when the shellfish industry is not
sampling there. All phytoplankton sites are sampled weekly. The distribution of
phytoplankton sampling sites is illustrated in Figure 1.1 on the following page. (Note
that where sites are too close together, only one site is marked due to the limitations of
scale).
At sites where phytoplankton monitoring occurs, phytoplankton numbers provide an
early warning of toxicity in shellfish. For each type of potentially toxic
phytoplankton, there are trigger levels at which shellfish monitoring is instigated, and
closures to harvest implemented (Refer to Appendix I(A)).
The non-commercial marine biotoxin monitoring programme includes 57 sites from
which shellfish samples are taken. Some of these sites are monitored as part of the
commercial monitoring programme and only monitored as part of the non-commercial
monitoring programme when the shellfish industry is not sampling there. Details of
the monitoring regime for both the commercial and non-commercial programmes,
including frequency of sampling and testing for each type of toxin, are provided in
Appendix I(B).
Shellfish samples are tested for PSP, ASP, NSP and DSP. Samples are tested for PSP
using acid extraction techniques followed by mouse bioassay (Delaney, 1985). HPLC
techniques are used for the detection of ASP (Wright et al., 1989; Lawrence &
Menard, 1991; Lawrence et al., 1991). Detection of NSP and DSP is a two-step
procedure (a flow diagram to illustrate this process is provided in Appendix I(C)).
Initially shellfish samples are screened using an acetone extraction technique and
mouse bioassay (Hannah et al., 1995; Yasumoto et al., 1978). If the results of the
screening step are positive, this is followed by a DSP ELISA (DSP-Check Kit,
Panapharm Laboratories) for DSP, and a mouse bioassay using ether extraction
techniques for NSP (Delaney, 1985; Yasumoto et al., 1978).
5
2 non-commercial sites and 1
shared site
Current Phytoplankton
Monitoring Sites
2 commercial
sites at
Coromandel
1 non-commercial site and 1
shared site (Tamaki Strait and
Waimangu Point)
2 non-commercial and 24
commercial sites in the
Marlborough Sounds
Non-Commercial site
Commercial site
Shared site
Figure 1.1:
Current phytoplankton monitoring sites along the New Zealand
coastline.
6
1.3
BIOTOXINS IN NEW ZEALAND
New Zealand is unusual in having four of the five biotoxin groups, i.e. PSP, ASP,
NSP and DSP. No AZP (Azaspiracid Poisoning, now recognised as a separate toxin
group) has been found in New Zealand to date. Several additional lipophilic
compounds, some of them toxic, are also present, and these complicate the detection
of NSP. Few other countries have such a range of toxins present in one place
(Andersen, 1996). The major marine biotoxin groups found accumulated in New
Zealand shellfish are discussed below.
1.3.1
Paralytic Shellfish Poisoning (PSP)
Paralytic Shellfish Poisoning (PSP) may be caused by several species of
phytoplankton, including a range of species of the genus Alexandrium (Halim),
Gymnodinium catenatum, and most commonly in tropical areas, Pyrodinium
bahamense (Hallegraeff, 1995). Several Alexandrium species have been found in
New Zealand, with varying levels of toxicity. These include Alexandrium
angustitabulatum, A. catenella, A. minutum, A. ostenfeldii, A. tamarense, A.
margalefii, A. pseudogonyaulax, A. concavum, A. c.f. fraterculus, and an isolate from
Marsden Point (Northland) tentatively ascribed to A. cohorticula or A. tamiyavanichi
(Mackenzie et al., 1994; Mackenzie et al., 1996a; Mackenzie et al., 1997; Mackenzie
et al., 1998a). (Note that subsequent to the preparation of this report, Gymnodinium
catenatum has also been found in New Zealand waters).
The toxins that cause PSP comprise a suite of at least 24 naturally occurring
neurotoxic tetrahydropurine analogues. They act as sodium channel blocking agents
in vertebrate nervous systems. The PSP toxin analogues can be classified according
to their chemical structure and specific potency in mammals: The carbamate toxins
(GTX1-GTX4, Neo, STX) are the most potent, whereas the N-sulfocarbamoyl
derivatives (B1, B2, C1-C4) have much lower specific toxicity. The decarbamoyl
(dc-) analogues are of intermediate toxicity (Cembella et al., 1993).
In the absence of environmental stress and in the exponential growth phase, different
strains of Alexandrium have characteristic toxin profiles (Cembella et al., 1987).
Since different toxin derivatives have different toxicity, the toxin profile impacts on
the overall toxicity of the strain. The detoxification processes within different species
of shellfish also alters the toxin profile of PSP toxins within the shellfish, and this
may vary from species to species (Cembella et al., 1993; Chang et al., 1997).
The toxicity of New Zealand Alexandrium species is summarized in Table 1.1
(summarized from Chang et al., 1997; Mackenzie et al., 1998a).
7
Species
A. angustitabulatum (Bream Bay)
A. catenella (Bay of Plenty)
A. minutum (Anakoha A)
A. minutum (Anakoha B)
A. minutum (Croiselles 1)
A. minutum (Bay of Plenty)
A. minutum (Bay of Plenty)
A. minutum (Whangarei)
A. ostenfeldii (Kaitaia)
A. ostenfeldii (Taharoa)
A. ostenfeldii (Wellington)
A. ostenfeldii (Timaru)
A. tamarense (Tasman Bay)
A. margalefii (Bream Bay)
A. pseudogonyaulax (Hauraki Gulf)
A. concavum (Northland/Hauraki Gulf)
A. c.f. fraterculus (Coromandel/Hauraki Gulf)
A. sp. (Marsden Point)
Table 1.1:
Specific Toxicity
(pg STX eq./cell)
1.1
3.4
2.2
1.9
1.8
11.6
6.0
0.9
217.0
21.4
0
13.4
Unknown
0
0
0
0
3.2
Specific toxicity of species of Alexandrium found in New Zealand
waters. STX eq./cell= Saxitoxin equivalent per cell.
It can be seen from Table 1.1 that there is some variation in specific toxicity within
the same species, most notably in A. ostenfeldii, in which specific toxicity of isolates
ranges from 0 to 217 pg STX eq./cell.
The phytoplankton monitoring that occurs as part of the marine biotoxin monitoring
programme is based on the detection of significant numbers of potentially toxic
species using morphological features (size and shape) visible under a light
microscope. In the case of Alexandrium species, Calcofluor stain may be used to
assist in identification. However, distinguishing between toxic and non-toxic species
using these methods is not always possible. For example, A. c.f. fraterculus (which
has so far exhibited no toxicity in New Zealand, although it has been associated with
toxicity in shellfish in Uruguay (Balech, 1995)), has been found to exist in three
morphophytes in culture: in chains, and in large and small morphophytes as single
cells. The general size and form of chains of A. c.f. fraterculus is superficially like A.
catenella, a toxic species found in the Bay of Plenty. In its single cell form, the
smaller morphophytes resemble the toxic Alexandrium species isolated from Marsden
Point (possibly A. cohorticula or A. tamiyavanichi), while the larger morphophytes
closely resemble A. concavum (also non-toxic) (Mackenzie et al., 1998a). The
difficulties in distinguishing between toxic and non-toxic species on a routine basis in
the monitoring programme are overcome by the initiation of toxicity testing in
shellfish whenever significant numbers of apparent A. c.f. fraterculus occur in the
plankton. Molecular probes are being developed to distinguish between toxic and
non-toxic species (Rhodes et al., 1998a).
Like some other dinoflagellates, Alexandrium species produce resting cysts. Research
on toxic Alexandrium blooms overseas suggests that the cyclical development of
8
blooms can be dependent upon the presence of seedbeds of cysts (Anderson & Wall,
1978). High numbers (up to 70,000 cysts per square meter) of Alexandrium
ostenfeldii have been found in sediments around New Zealand, but cysts of other
species are less evident (L. Mackenzie, Cawthron Institute, pers. comm.).
The number of Alexandrium present in the plankton in order to trigger toxicity testing
in shellfish is relatively low: 100 cells/L of species known to be toxic (including
Alexandrium c.f. fraterculus because of gross morphological similarities to toxic
species). This is set at the level of detection for the phytoplankton methodology used.
An immediate public health warning is issued if numbers in the phytoplankton reach
5,000 cells/L.
1.3.2
Amnesic Shellfish Poisoning (ASP)
Amnesic Shellfish Poisoning (ASP) is caused by Domoic acid (Wright et al., 1989).
Species within the genus Pseudo-nitzschia produce Domoic acid. This toxin is
unusual in being produced by diatoms rather than dinoflagellates.
A range of Pseudo-nitzschia species occur in New Zealand. Domoic acid has been
confirmed in some but not all New Zealand isolates of Pseudo-nitzschia australis, P.
pungens, P. turgidula (Rhodes et al., 1996), P. delicatissima, and P.
pseudodelicatissima (Rhodes et al., 1998b). Two other species are frequent
components of Pseudo-nitzschia blooms: P. heimii and P. multistriata (L. Rhodes,
Cawthron Institute, pers. comm.), but to date neither of these species have been found
to be toxic.
Discrimination between some species of Pseudo-nitzschia is virtually impossible
under a light microscope because of morphological similarity between species – some
species differ in details that can only be detected under an electron microscope.
However, whole cell DNA probes have been developed to distinguish between
species (Rhodes et al., 1997), and these are utilised by industry in risk management
when deciding whether to implement voluntary closures to harvesting, pending the
results of shellfish toxicity testing. Although not part of the formal biotoxin
management plan, they also appear to be used at non-commercial monitoring sites in
the event of a Pseudo-nitzschia bloom, as a means of deciding whether shellfish
samples should be taken for toxicity testing. (This is discussed in more detail in
Section 2.5.4).
Pseudo-nitzschia blooms differ from blooms of most other toxic phytoplankton in that
high numbers of cells (50,000-100,000 cells/L) are required to reach a significant
toxin level in shellfish. The toxicity of Pseudo-nitzschia species varies widely
between and within species, and temporally. Table 1.2 summarises the maximum
level of Domoic acid per cell found in New Zealand isolates.
9
Species
Domoic Acid Maximum Level (pg/cell)
P. australis
35.0
P. pungens
0.47
P. fraudulenta
0.03
*
P. delicatissima
0.12
*
P. turgidula
0.03
P. pseudodelicatissima
0.12
P. heimii
0
P. multistriata
0
*
There is some evidence to suggest that P. delicatissima and P. turgidula are
the same species (L. Rhodes et al., 1998b).
Table 1.2:
Maximum level of Domoic acid found in New Zealand isolates of
Pseudo-nitzschia. (Summarised from Rhodes et al., 1998b).
It should be noted that some species are not always toxic (for example, P. pungens),
so an accurate measure of the risk of ASP cannot be gained by identification of the
phytoplankton species alone.
Domoic acid production varies with the stage of the Pseudo-nitzschia bloom, with
maximum production in the stationary or senescent phase (Bates et al., 1996; Bates et
al., 1998). Consistent with this is the appearance of toxins in shellfish several days
after the peak of a bloom of toxic Pseudo-nitzschia. Because of this, the monitoring
of phytoplankton levels can provide an effective early warning system for Domoic
acid in shellfish.
It appears that different species of shellfish may accumulate Domoic acid at different
rates, although few controlled experiments have been undertaken on New Zealand
species. It is thus difficult to distinguish environmental factors from differences
between species. However, feeding experiments have shown that Domoic acid is very
rapidly eliminated from the GreenshellTM mussel, Perna canaliculus – under some
conditions the rate of excretion is equivalent to the rate of ingestion, and accumulation
within the tissue does not take place (Mackenzie et al., 1993).
1.3.3
Diarrhetic Shellfish Poisoning (DSP)
Diarrhetic Shellfish Poisoning (DSP) is produced by dinoflagellates in the genera
Dinophysis, and Prorocentrum (Murakami et al., 1982; Lee et al., 1989; Jackson et
al., 1993). Species that are potentially toxic include Dinophysis acuminata, D. acuta,
D. fortii, D. mitra, D. norvegica, D. rotundata, D. tripos, Prorocentrum lima, and P.
concavum. The species in New Zealand that have been found to contain DSP toxins
include Dinophysis acuta and Prorocentrum lima (Rhodes & Syhre, 1995). Low
levels of DSP toxins have also been found associated with Dinophysis acuminata (L.
Mackenzie, Cawthron Institute, pers. comm.). Prorocentrum lima is an epibenthic
dinoflagellate, and thus is not commonly found in plankton samples from the water
column.
DSP toxins are lipophilic. There are several toxins in the “DSP group”. They are
sub-divided into three groups: Okadaic acid (OA) and the closely related
10
dinophysistoxins (DTX); the pectenotoxins, which are polyether lactones consisting
of three compounds with known structure (PTX 1-3) and at least two additional
compounds with presumed slightly modified skeletons; and thirdly, yessotoxin
(YTX), with two sulphate esters, which resemble the brevetoxins from Gymnodinium
breve (Aune & Yndestad, 1993). Of these toxins, only Okadaic acid, DTX1 and
DTX3 are generally associated with diarrhoea. However because they are frequently
found together and are all extracted by the acetone extraction method, they tend to be
grouped together as the “DSP group”.
The pectenotoxins and yessotoxin are acutely toxic to mice. Both these toxins are
present in New Zealand: the causative agent of yessotoxin in the Marlborough Sounds
was identified as Protoceratium reticulatum (Satake et al., 1997; Mackenzie et al.,
1998b), and new analogues of pectenotoxin have been found in Dinophysis acuta
(Daiguji et al., 1998).
1.3.4
Neurotoxic Shellfish Poisoning (NSP)
Neurotoxic Shellfish Poisoning (NSP) is caused by toxins produced predominantly by
Gymnodinium species. Several species of phytoplankton in New Zealand have been
found to produce NSP toxins. These include: Gymnodinium c.f. breve, Gymnodinium
c.f. mikimotoi (which may include three separate species), Gyrodinium galatheanum
and a species of Heterosigma (Mackenzie et al., 1995a; Haywood, 1998). The
identity of the causative agent in the 1993 NSP event in Northland is uncertain: both
Gymnodinium c.f. breve and Gymnodinium c.f. mikimotoi were present in elevated
numbers at the time (Chang, 1996; Mackenzie et al., 1995b).
Recently, further work on elucidating the New Zealand species of Gymnodinium has
been undertaken by Alison Haywood of Cawthron Institute. This has resulted in the
proposal of two new species: Gymnodinium papilonaceum (recorded as Gymnodinium
c.f. breve in the biotoxin monitoring data) and Gymnodinium selliforme (recorded as
Gymnodinium c.f. mikimotoi in the biotoxin monitoring data). Gymnodinium
mikimotoi is also present in New Zealand waters (A. Haywood, Cawthron Institute,
pers. comm.).
Lipophilic, polycyclic ether compounds, known as brevetoxins, cause NSP. The
brevetoxins have been classified under several nomenclatures since toxicity was first
detected in the causative organism, and this is somewhat confusing (Baden, 1989).
According to the structure of the backbone skeleton, they can be classified into three
categories: brevetoxin A (BTX-A), brevetoxin B (BTX-B) and hemi-brevetoxin
(HemiBTX). Within each category, several analogues are known.
Brevetoxins act as sodium channel activators. Different analogues of the toxins have
different potencies (Baden, 1989). The toxin profiles of brevetoxin-producing
dinoflagellates vary between species, and with the growth stage of the algae (Roszell
et al., 1990).
NSP ELISA has detected brevetoxins in cultures of Gymnodinium papilonaceum, G.
selliforme, G. mikimotoi and Gyrodinium galatheanum from New Zealand waters (Ian
Garthwaite, AgResearch, pers. comm.). Several known brevetoxin analogues were
isolated from shellfish collected during the 1992-93 biotoxin event in New Zealand.
11
These included brevetoxins PbTX-2 and PbTX-3 from oysters in the Coromandel area
(Ishida et al., 1994). Several new brevetoxin analogues were also isolated: Brevetoxin
B1 (Ishida et al., 1995), Brevetoxin B2 (Murata et al., 1998) and Brevetoxin B3
(Morohashi et al., 1995). As a result of this work, it was suggested that the
detoxification mechanism for brevetoxin differed between cockles (Austrovenus
stutchburyi) and green-lipped (GreenshellTM) mussels (Perna canaliculus).
1.3.5
Respiratory Irritation Syndrome
Two Respiratory Irritation Syndrome (RIS) events have occurred in New Zealand –
one that was associated with the 1993 biotoxin event, in which residents of Orewa, a
coastal settlement north of Auckland, complained of sore throats, eye and nose
irritation and dry coughing (Bates et al., 1993). The second event occurred in the
summer of 1998, and affected residents and visitors of Hawkes Bay and the
Wairarapa coast. The symptoms reported during this event were very similar to those
in the earlier event (Chang et al., 1998a).
Similar symptoms have been reported for some years in association with the Florida
(USA) “red tides” that are caused by blooms of Gymnodinium breve (Pierce, 1986).
The respiratory irritation reported in Florida has been attributed to aerosolised
brevetoxins produced by Gymnodinium breve. The mechanism by which the toxins
become aerosolised follows the process of bursting bubbles caused primarily by windgenerated whitecaps and breaking waves (Pierce, 1986).
The 1998 respiratory irritation event in New Zealand was associated with a dense
bloom of Gymnodinium c.f. mikimotoi that was also responsible for fish kills off
Wairarapa, Kaikoura, and in Wellington Harbour (Chang et al., 1998b). While the
respiratory symptoms were very similar to those caused by brevetoxin, analysis by
neuroblastoma assay indicated that the toxin was not brevetoxin (F. H. Chang, NIWA,
pers. comm.). Chemical analysis is currently being undertaken to determine the
structure of the new toxin. The Gymnodinium species responsible for the toxin has
been identified as a new species, and named Gymnodinium brevisulcatum (F. H.
Chang, NIWA, pers. comm.).
1.3.6
Other Marine Biotoxins in New Zealand
Several other marine biotoxins have been identified in New Zealand since 1993. In
1994 a new toxic imine (named Gymnodimine) was isolated from Foveaux Strait
oysters and a Gymnodinium species similar in appearance to Gymnodinium mikimotoi
(Mackenzie, 1994; Seki et al., 1995; Seki et al., 1996; Mackenzie et al., 1996b) was
identified as the causative agent. (This has subsequently been named Gymnodinium
selliforme (A. Haywood, Cawthron Institute, pers. comm.)). A limited short-term rat
feeding trial was undertaken to ascertain the oral toxicity of gymnodimine (Towers,
1994). The results of this trial and epidemiological evidence indicated that
gymnodimine does not produce Toxic Shellfish Poisoning when consumed in
contaminated shellfish. Long-term feeding trials are currently being undertaken by
AgResearch, using gymnodimine extracted from Gymnodinium species cultured by
Cawthron Institute. This will determine whether the consumption of gymnodimine
over a long period of time has any impact on health (I. Garthwaite, AgResearch, pers.
comm.). In the meantime, the lack of any epidemiological evidence to suggest that
12
gymnodimine is a threat to public health resulted in its exclusion from the regulatory
marine biotoxin monitoring programme.
The morphological similarities between the species grouped together as Gymnodinium
c.f. mikimotoi, and the variations within one species, mean that these species/strains
are difficult to separate under the light microscope. However, they may produce a
variety of toxins (brevetoxins, gymnodimine, “Wellington Harbour toxin”), or no
toxin at all. This means that the results of phytoplankton monitoring do not provide a
clear indication of the risk of Toxic Shellfish Poisoning. As a result, phytoplankton
trigger levels are set on the assumption that the species contain brevetoxins.
Other toxins identified in New Zealand include a novel neurotoxin isolated from
cockles (from the Bay of Plenty) following the 1993 biotoxin event ((4methoxycarbonyl butyl) trimethylammonium chloride) (Ishida et al., 1994), a novel
polyether compound from Coolia monotis from Rangaunu Harbour (Rhodes &
Thomas, 1997), and palytoxin in Ostreopsis siamensis (also from the Rangaunu
Harbour) (Briggs et al., 1998). Palytoxin is a sodium channel activator and potent
tumour producer (Redondo et al., 1996; Yasumoto & Satake, 1998).
1.4
THE STRATEGIC FRAMEWORK AND SCOPE OF THIS REVIEW
Options for the management of the risk of Toxic Shellfish Poisoning and Respiratory
Irritation Syndrome can only be formulated and recommended if there are clear
objectives to be achieved. The goal and objective of this review of the noncommercial marine biotoxin monitoring programme were stated in the project scope
as follows:
•
To ensure a social and physical environment which improves, promotes and
protects public health and whanau public health.
•
To optimise the safety of all food available for consumption in New
Zealand.
This goal and objective are contained within a broader strategic framework for public
health in New Zealand. This public health strategy is outlined in a paper produced by
the Ministry of Health’s Public Health Group, entitled Strengthening Public Health
Action: The strategic direction to improve, promote and protect public health
(Ministry of Health, 1997b). This strategy sets out a vision for public health action,
values to guide public health action, goals, objectives and targets, and criteria for
determining priorities for action. The vision for public health action outlined in the
strategy is:
We see New Zealand as a country in which Maori and non-Maori enjoy
equitable health outcomes. Everyone lives longer in good health, disease is
progressively reduced and people with disabilities are able to achieve
independence. We see people empowered to realise their full potential
through effective healthy public policy, supportive social, cultural and
physical environments, strong communities, well-developed personal skills
and a health system focused on health gain. We see fully informed and
13
resourced people able to make healthy choices in the context of a healthy and
sustainable environment.
The values to guide public health action include:
•
•
•
•
•
•
•
•
Appropriateness
Effectiveness
Efficiency
Empowerment
Equity
Partnership
Safety
Sustainability
All these values are defined in more detail in the strategy document.
The goal and objective outlined in the project scope (see above) are those from the
strategy that primarily relate to the non-commercial marine biotoxin monitoring
programme. There were no specific targets set for this particular objective in the
Ministry of Health’s strategic document. There are several other potentially relevant
objectives outlined in the strategy. These include the goals and relevant objectives
relating to Maori and Pacific peoples’ health, the global environment, and sustainable
management of natural and physical resources:
•
To improve, promote and protect Maori heath status so in the future Maori will
have the opportunity to enjoy at least the same level of health as non-Maori.
• To ensure that all services funded are culturally appropriate and
compatible with gains in Maori health.
• To show an understanding of, and commitment to the Treaty of Waitangi.
•
To improve, promote and protect the health of Pacific people.
• To ensure that all services are culturally appropriate and relevant to
Pacific people in structures, settings and languages that Pacific
communities can identify with and use.
• To provide Pacific people with the opportunity to play a major role in the
design, development, implementation and evaluation of public health
services which affect their communities.
•
To improve, promote and protect the health of children.
• To reduce disability and death rates from asthma.
•
To reduce the adverse health effects and optimise the positive health effects of the
global environment, including climate change, import control, international
travel, ozone depletion, and vector control.
•
To ensure public health issues are identified and addressed in decisions made on
sustainable management of natural and physical resources.
14
(These are goals and objectives potentially relevant to the management of the risk of
marine biotoxins in New Zealand. The full set of goals and objectives is provided in
“Strengthening Public Health Action: The strategic direction to improve, promote and
protect public health” (Ministry of Health, 1997b).
The essential criteria outlined for use in determining public health priorities are:
•
•
Does the health issue have a significant impact on the current and future health
status of the total population or priority groups in terms of morbidity, mortality,
quality of life, and/or potential years of life lost?
Are there effective means, using population-based methods, to improve, promote
or protect health, or prevent disease, in respect of the particular health issue? If
not, are there potential innovative means that could be evaluated?
The criteria given high weighting are:
•
•
If the health issue is tackled, will this contribute to reducing inequalities in health
status, including reducing the inequalities between Maori and non-Maori?
Will tackling this issue provide the best health gain for the resources required?
The criteria given medium weighting are:
•
•
•
Is there public support for tackling the issue?
If programmes are developed to address an issue, are they sustainable over time
and across sectors?
Is it possible to engage other sectors of government and the community, including
Maori and iwi, in efforts to address the issue?
Cross-cutting themes identified as underpinning all public health goals, objectives and
targets include (Ministry of Health, 1997b):
•
•
•
•
Focusing on the determinants of health.
Building strategic alliances.
Implementing comprehensive programmes.
Strengthening public health infrastructure.
This broad strategic framework is utilised in the evaluation of management options
arising from our review of the marine biotoxin monitoring programme.
The Ministry of Health has defined the scope of this review in their project proposal.
The purpose of this review is to:
Analyse all shellfish flesh and phytoplankton data collected in the New Zealand
marine biotoxin monitoring programme since January 1993, both non-commercial
and commercial, assess the risk to the New Zealand public from consumption of toxic
shellfish, and recommend options for cost effective management and mitigation.
15
The scope of the review is summarised as follows:
•
Review and report on the data collected in the Ministry of Health database (and
other data sources if necessary) from shellfish flesh analysis by the marine
biotoxin monitoring programme (non-commercial and commercial) for NSP,
DSP, PSP and ASP for the period January 1993 to March 1999.
•
Review the data collected in the Ministry of Health database from phytoplankton
analyses by the marine biotoxin monitoring programme on algae that can
produce biotoxins capable of causing NSP, DSP, PSP, and ASP, and on algae
which cause respiratory irritation syndrome for the period November 1996 to
March 1999.
•
Gather local information including environmental, climatic and oceanographic
variables that may influence development and demise of toxic algal blooms.
•
Review the epidemiological data on cases of Toxic Shellfish Poisoning and
respiratory irritation syndrome in New Zealand since January 1993.
•
Analyse, interpret and summarise all data on an area by area basis; relate this
information to shellfish gathering and consumption patterns in New Zealand.
•
Assess whether there is any relationship between toxic phytoplankton
concentrations and concentration of toxins in shellfish that could be used to
predict the likelihood of risk to the consumer.
•
Using the results of analysis and consultation:
• Assess the risk of Toxic Shellfish Poisoning to consumers of non-commercially
gathered shellfish, in New Zealand as a whole, and on an area by area basis;
• Assess the risk of respiratory irritation syndrome to the public.
•
Examine environmental factors and educational strategies that already exist or
could be implemented to contribute towards effective management or mitigation of
Toxic Shellfish Poisoning and toxic algae in New Zealand.
•
Identify cost-effective options available to protect the New Zealand public from
Toxic Shellfish Poisoning from non-commercially gathered shellfish and from
respiratory distress syndrome.
The analyses in this report are based on up to six years of epidemiological and
shellfish toxin data, and, depending upon the area, up to two or three years of
phytoplankton data. This is a comparatively short time period from which to gain
some understanding of the risk of TSP in the future. While convening a session at the
“Harmful Algal Bloom 2000” conference in Hobart in February 2000, Don Anderson
commented that “even after 20 years of intensive study to determine the
environmental factors impacting on the blooms of PSP-causing phytoplankton off the
coast of Maine, prediction of blooms is still not possible”. The structure of this report
reflects consideration of these limitations, with an emphasis being placed on broad
trends across New Zealand rather than working with a possibly ill-founded initial
16
assumption that there are distinct differences in the risk of biotoxin occurrence in
different geographical areas.
The results of our review of the marine biotoxin monitoring programme for noncommercially harvested shellfish are reported in two parts, in separate documents.
This report (Part 1), contains the results of analysis of available data, risk analysis,
and a general discussion of the resulting conclusions with respect to management of
marine biotoxins in non-commercially harvested shellfish in New Zealand. The
second report (Part 2) provides a more specific discussion of the options and
recommendations to the Ministry of Health for the cost effective management and
mitigation of marine biotoxins in New Zealand.
17
SECTION 2:
2.1
INTRODUCTION
Since 1993, much has been learnt about the types of biotoxins present in
phytoplankton in New Zealand waters. The marine biotoxin monitoring programme
has evolved with the development of new, more precise methods to cope with the
range of toxins present. This evolution has improved the quality of the data collected
as part of the monitoring programme.
Since the initiation of the marine biotoxin monitoring programme in 1993, a
substantial amount of data has been collected. This includes the results of tests for
biotoxins in shellfish, results of monitoring for toxic phytoplankton, some
environmental data recorded at the time the shellfish or phytoplankton samples were
collected, and epidemiological data. This section of the review covers the analysis of
shellfish test results and phytoplankton monitoring results. The analysis of the
epidemiological data is undertaken in Section 4 of this report.
The collection of the shellfish toxin analysis data and phytoplankton data within the
monitoring programme has not been planned with a view to facilitating meaningful
data analysis in the long term. Rather, its primary function has been the immediate
determination of the biotoxin status at specific sites. Consequently, a number of
challenges are faced in the analysis of the monitoring data. These include the
following factors:
•
Missing or incomplete data, and data that are incorrectly reported in the database.
•
Variations in the interpretation and reporting of results.
•
Changes in test methods for biotoxin detection, including changes in toxin
extraction procedures, and in overall testing procedures for biotoxins in shellfish.
•
Difficulties with and improvements made in the identification of toxin-producing
phytoplankton.
•
Changes in the number of sample sites and the frequency of sampling over time
(seasonally, and from year to year).
•
Clumping of sample sites both within and between zones (i.e. the sample sites are
not distributed evenly around the coastline).
•
Variations in sampling position within one “sample site”.
•
The relationship between the occurrence of positive results, and the frequency of
sampling and number of sites sampled (for example, under the current
programme, shellfish sampling frequency may increase if positive results are
returned, and in some places this also triggers sampling at additional sites).
18
•
Differences in species of shellfish sampled within and between sample sites,
coupled with the possible variation in the uptake and retention of toxins in
different shellfish species.
Basically the data are not independent, and are stratified both spatially and temporally
over several different scales. This suggests that meaningful quantitative analysis is
extremely difficult. Extreme care must therefore be taken to avoid misleading
conclusions or unfounded extrapolation from this data set.
Some of the initial analysis of data undertaken in this review was designed to provide
a framework for further analysis.
Overseas research and observations from the natural environment have indicated that
different shellfish species may accumulate biotoxins to different levels and detoxify at
different rates (e.g. Shumway et al., 1988; Gainey & Shumway, 1988; Shumway et
al., 1990; Cembella et al., 1993; Bricelj et al., 1996). Similar observations have been
made in New Zealand (Marsden, 1993; Chang et al., 1997; Mackenzie et al., 1998b),
but comparatively little research has been undertaken here. These potential
interspecific differences are significant in determining how the analysis of patterns of
biotoxins is undertaken. If the differences are significant, then the composition of
sample species needs to be taken into consideration when making comparisons both
between and within sites. Species-specific differences are also of potential
importance in assessing the risk of TSP to shellfish consumers.
2.2
GENERAL METHODOLOGY
Shellfish test results from January 1993 to June 1999, and phytoplankton monitoring
results from 1997 to June 1999 from the FoodNet database were downloaded into
Microsoft Access. Analysis of data was undertaken using Microsoft Excel.
Phytoplankton monitoring began in 1994 in the Marlborough Sounds, and in January
1995 in the Hauraki Gulf, and also occurred sporadically in some other areas prior to
1997. There are a number of problems associated with the analysis of phytoplankton
data prior to 1997 on the FoodNet database: the naming of sites is extremely
inconsistent (some sites are identified by up to four different names, and site codes are
generally not used), and the data appears incomplete. The most comprehensive
phytoplankton data from this time period were collected in the Hauraki Gulf and the
Marlborough Sounds. Because of the difficulties associated with the data in FoodNet,
phytoplankton data for these areas were sourced from elsewhere. A complete set of
data from phytoplankton monitoring at the Marlborough Sounds was kindly provided
to us for analysis by the Marlborough Sounds Shellfish Quality Assurance
Programme, who keep their own database. Data relating to Pseudo-nitzschia,
Dinophysis and Gymnodinium mikimotoi for the Hauraki Gulf phytoplankton sites
was obtained from an AquaBio Consultants database. The Hauraki Gulf data were
originally compiled from hard-copy monitoring results supplied to shellfish farmers in
the area by Cawthron Institute.
Before discussing methods for specific analyses, the generic assumptions in this data
analysis are outlined.
19
2.2.1
Identification of a Valid Data Set
The analysis of data presented in this report is based on data collected using
appropriate test methods and from which valid conclusions can be drawn.
Changes in test methods were in general not implemented simultaneously over
samples received from all sample sites. When changes were made, it was usually
necessary for the testing laboratory to phase in the new method over a period of
several weeks, to allow time to train staff in the new methods. Where these changes
are significant in terms of data analysis, the data set has been selected to ensure that
all samples were analyzed using the same methods by the laboratory.
The data sets used for each of the four toxins are thus as follows:
•
For PSP, only results of toxicity testing in shellfish after June 1993 are used in
data analysis. Prior to this, the method of extracting PSP toxins from shellfish
tissue involved a modification of the standard APHA acid extraction method.
This modification, which was recommended by the US FDA at the time, used a
concentration of hydrochloric acid ten times above the standard method (Hall,
1991). Several test results above the regulatory level for PSP were an artifact of
this modified method. Our analysis therefore only considers data produced from
tests using the current extraction method (Delaney, 1985). All samples were
being analyzed by the current extraction method by the end of June 1993 (Penny
Truman, ESR, pers. comm.)
•
Routine analysis for ASP toxins by HPLC was introduced in mid-May 1993, and
was being undertaken at all sites by the beginning of July 1993. Data from July
1993-June 1999 are thus included in our analysis.
•
Testing for lipid soluble toxins has been somewhat problematical over the course
of the marine biotoxin monitoring programme. Initially, all lipid soluble toxins in
shellfish samples were detected by mouse bioassay, using an acetone extraction
method (Hannah et al., 1995). This method was developed early in 1993 to
replace the standard APHA ether extraction method for detection of NSP toxins,
since the testing laboratory was processing very large numbers of samples, and the
volatility of diethyl ether was a hazard to laboratory workers. This acetone
extraction method detected all lipid soluble compounds that can cause mouse
deaths, including NSP toxins, DSP toxins, gymnodimine and possibly free fatty
acids. However, all the toxin levels were calculated from the mouse bioassay
results as if they were NSP toxins. These toxin levels (from January 1993 to
September 1994) have thus been excluded from our data analysis.
•
The dataset for NSP toxins includes the results of toxicity tests in shellfish using a
mouse bioassay following an extraction of the toxins using diethyl ether (Delaney,
1985; Yasumoto et al., 1978). This was introduced in conjunction with a DSP
ELISA test for DSP toxins along with the introduction of a prior screening step
using an acetone extraction method in September 1994. It is acknowledged that
this test is not necessarily specific to NSP toxins (i.e. brevetoxins), but this is the
test on which regulation is based. It is likely that some of the NSP positive results
could be confounded by the presence of other lipid soluble toxins (such as
20
pectenotoxin, yessotoxin) and free fatty acids. Where possible these data are thus
used in conjunction with data from the phytoplankton monitoring programme.
•
Analysis for DSP using the DSP ELISA (DSP Check-Kit, Panapharm
Laboratories) began in September 1994 when the revised protocols for detection
of lipid soluble toxins were introduced. All these data are included in our
analysis. The DSP Check-Kit does not detect the presence of DTX-3 or Okadaic
acid diol esters. Thus it is possible that the incidence of DSP toxins in shellfish
tissue is under-reported in the biotoxin monitoring results.
With respect to the dataset for phytoplankton analysis, increasing knowledge of the
phytoplankton species that cause shellfish toxicity has meant an increase in the
number of species specifically identified in the phytoplankton counts. In our analysis,
a species has only been assumed absent in a sample when it was noted as a zero count
in the data. Where it is apparent that data may be missing, as distinct from species not
present in the sample counts, these instances were noted.
2.2.2
Determination of Areas for Analysis
Part of our brief was analysis of monitoring data on an “area by area” basis. From the
beginning of the marine biotoxin monitoring programme in 1993, there has been a
division of the coastline into eleven areas, known as Biotoxin Zones A-K (see
Appendix I (D)). Initially in 1993 all the sites within each Zone were opened and
closed for harvesting shellfish collectively. However, this quickly changed so that
areas within each zone were regulated separately. Nonetheless, the naming of sample
sites according to the zone in which they are located has persisted.
Figure 2.1 illustrates the Biotoxin Zones in relation to basic hydrographic influences
around the coastline.
It has been assumed that the sizes of the areas required for analysis were similar in
scale to the regulatory zones, and that the analysis should be designed to investigate
broad differences comparing risk to shellfish consumers. The benefits of redefining
the areas for the purpose of analysis were considered. The two very broad influences
on the coastal marine environment in New Zealand are the surface circulation patterns
(the currents shown in Figure 2.1) and prevailing south-westerly swells that arise in
the storm belt between 40o-60o South. The differentiation of coastal areas between
existing biotoxin zones is consistent with these very broad patterns.
It is recognized that within these areas there may be significant variation between
individual sites, due to differences in environmental conditions related to geography,
wave exposure, flushing action, nutrient availability due to run-off from the land, etc.
Variation in the same environmental conditions may also occur as a result of smallscale patches, such as differences in phytoplankton abundance at different depths, and
horizontal differences due to small-scale concentration of phytoplankton, such as that
caused by Langmuir cells. It thus seemed that a redistribution of existing biotoxin
zones into areas considering more detailed environmental factors would achieve little.
Conversely, consolidation of zones into larger areas (for example, merging Zones A
and B into one area) would result in a loss of detail from which we have benefited in
21
previous analysis. Since the existing biotoxin zones are well recognised in the public
health arena and in the shellfish industry, it seemed expedient to retain these as areas
for comparison, while noting significant differences within zones.
Our analysis of the monitoring data on a broad area by area basis does not presume to
investigate causative relationships for any differences between areas, but merely
provides a description of relative risk to shellfish consumers in each area. In this
analysis an underlying assumption is made that the distribution of sample sites is
representative of shellfish harvesting patterns. This appears a reasonable assumption
given that the monitoring programme has been designed in this way.
The methods and assumptions related to specific analyses undertaken are described in
the following sections.
22
TASMAN FRONT
NORTH CAPE EDDY
EAST AUCKLAND
CURRENT
WEST AUCKLAND
CURRENT
Zone B : Cape Brett to
Zone A : Tauroa Point to Cape Brett
Cape Rodney
Zone C : Cape Rodney to
EAST
CAPE
EDDY
Cape Colville
Zone D : Cape Colville to
Cape Runaway
Zone F : Tauroa Point to Cape Egmont
Zone E : Cape
Runaway to Cape
Palliser
Zone H : Cape Egmont to Cape
Palliser
EAST
CAPE
CURRENT
D’URVILLE CURRENT
WESTLAND CURRENT
Zone G : Cape
Farewell to Cape
Campbell
WAIRARAPA
EDDY
Zone K : Chatham
Prevailing SouthWesterly Storm
Swells.
Islands
Zone I: Cape Campbell to Bluff
SOUTHLAND
CURRENT
Zone J : Cape
Farewell to Bluff
Figure 2.1:
Distribution of Biotoxin Zones and relevant hydrographical
features associated with the New Zealand coastline.
Hydrographical features summarised from Carter et al. 1998.
23
2.2.3
Analysis of Phytoplankton Occurrence
a)
Geographical Distribution
To provide an indication of the extent of the geographic distribution of potentially
toxic phytoplankton species, the occurrence of potentially toxic phytoplankton species
was mapped for species related to all four toxin groups (PSP, ASP, NSP and DSP) as
follows:
Regularly monitored phytoplankton sample sites were mapped, and those where
potentially toxic phytoplankton species had been detected were identified from the
FoodNet database. Causative agents for PSP, ASP, NSP and DSP were included in
this analysis. There were several limiting factors in this analysis:
•
Much of the phytoplankton data on the FoodNet database does not distinguish
between toxic and non-toxic species, since often this distinction cannot be made
under the light microscope (for example, Pseudo-nitzschia species). In some
cases, gene probes have been used to further distinguish toxic from non-toxic
species, but unfortunately these results have not been recorded on the database.
•
Knowledge of the phytoplankton causing toxicity in shellfish has grown over the
period the monitoring programme has been in operation. Thus in samples taken
early in the phytoplankton monitoring programme some species may not have
been specifically identified in the recorded data.
This analysis is not quantitative, but merely provides a visual representation of the
areas in New Zealand in which potentially toxic phytoplankton have been detected.
The occurrence of potentially toxic phytoplankton and the percentage of samples at
elevated levels in each zone were analysed as follows:
The occurrence of potentially toxic phytoplankton relating to each of the four toxin
groups (PSP, ASP, NSP and DSP) was analysed. Analysis was undertaken using both
the entire number of phytoplankton samples from each zone (=Total Samples Taken),
and also for an “Identified Time Interval” (from the week of 19/12/97 to 25/5/99) to
standardize for the different temporal sampling lengths at different sites. No
phytoplankton samples were available from Zones F or K (there are no phytoplankton
monitoring sites in these zones), and Zones B, H, and J were represented by one
phytoplankton monitoring site only. In the analysis using the “Identified Time
Interval”, some sites were not used because they started after the initial date
(19/12/97) or because large amounts of data were missing or incomplete. Thus out of
a possible 61 sites, only 48 sites were used for the “Identified Time Interval” analysis.
A list of these sites is provided in Appendix II.
Analysis included the following species: Pseudo-nitzschia species (all species were
included, since individual species are not identified on the database), Dinophysis
acuta, D. acuminata, Prorocentrum lima, Gymnodinium c.f. breve, Gymnodinium
mikimotoi, Alexandrium species including Alexandrium minutum, A. ostenfeldii, A.
angustitabulatum, A. catenella, A. tamarense, and A. cohorticula/tamiyavanichi.
24
For each species, the percentage occurrence in total samples, the percentage of
samples above the level to trigger flesh testing, the percentage above the level to
trigger voluntary industry closure, and (where they occurred) the percentage above the
level to trigger a public health warning, were analysed. Analysis was by zone for both
the “Total Samples” taken, and the samples in the “Identified Time Interval”. These
results were recorded in tabular form. Where five or more data points exist, data
above the levels to trigger flesh testing or voluntary closure by industry were
represented graphically as “Box and Whisker Plots”. Where there were less than five
data points, the numbers were simply stated. This analysis provided information on
the distribution of potentially toxic phytoplankton by zone, including relative
abundance by zone.
“Box and Whisker Plots” are a simple graphical way of representing the range of a
data set. Interpretation of the “Box and Whisker Plots” is as follows:
5% of the data lies below the bottom whisker line, and 25% of the data lies below the
bottom of the box. The median (middle value) dissects the box, and 75% of the data
lies below the top of the box. 95% of the data lies below the top whisker. Any
outlying points are marked as single points.
Median
b)
Temporal Distribution
The phytoplankton monitoring data available on the FoodNet database represents an
insufficient time period for meaningful analysis of temporal patterns. However, some
analysis of temporal patterns of potentially toxic phytoplankton was possible for Zone
G using data from the database supplied by the Marlborough Sounds Shellfish Quality
Assurance Programme, and for Zone C using data from AquaBio Consultants Ltd.
database.
For some toxins, seasonal patterns in the occurrence of potentially toxic
phytoplankton were investigated by determining the percentage of the total samples
for each season (summed over five years, i.e. 1994-1999), that were above the level to
trigger flesh testing. The seasons analysed were spring (September-November),
summer (December-February), autumn (March-May), and winter (June-August). In
addition, the phytoplankton counts of potentially toxic species for selected sites with
continuous data from 1995 to 1999 were graphed to investigate seasonality of
occurrence. For each selected site, the phytoplankton counts for each week of the
year were plotted on the same graph to determine whether consistent seasonal patterns
occurred. This also allowed qualitative comparison of seasonal distribution patterns
between sites.
25
2.2.4
Reliability of Phytoplankton Monitoring as a Predictor of Biotoxins in
Shellfish
Analysis was undertaken to investigate the probability that phytoplankton monitoring
at all phytoplankton monitoring sites might fail to predict the occurrence of significant
levels of toxin in shellfish at the same site. All phytoplankton monitoring sites with
associated shellfish monitoring sites were used in this analysis. Analysis was
undertaken for each of the four major toxin groups. For each toxin, the biotoxin
events at each shellfish site were identified from the FoodNet database. An event was
defined as a single or consecutive series of shellfish samples with toxin levels above
the regulatory level. In some instances where there were no samples above the
regulatory level, a lower detectable level was used to investigate this relationship. For
each event, the number of cells of the relevant potentially toxic phytoplankton in the
concurrent, and previous water samples (1-3 weeks earlier, depending on the species)
were identified from the database.
The percentage of shellfish samples above the regulatory levels for closure due to
biotoxin that were not associated with levels of the appropriate potentially toxic
phytoplankton was calculated. Similarly, in cases where there were no shellfish
samples with toxins above the regulatory level, the percentage of shellfish samples
with biotoxin above the detectable level but no corresponding occurrence of toxic
phytoplankton was calculated.
2.2.5
Differences in Biotoxin Accumulation between Shellfish Species
For each of the four toxins (PSP, ASP, NSP and DSP), the number of samples with
detectable levels of biotoxin, and the number of samples with biotoxin levels above
the regulatory level, were determined for each of the major shellfish species sampled.
The percentage of the total tests for each species was then calculated for each toxin
level. It is recognized that this analysis has major limitations: there is no account
taken of the impact of seasonal sampling (for example, scallops), clumping of sites
with respect to shellfish species, or the increase in frequency of shellfish sampling,
and in some cases, the number of sample sites, in the event of positive biotoxin
results. However, as a small part of a larger picture, it was decided that this analysis
could still be useful if viewed cautiously and in conjunction with other data.
The shellfish monitoring data in the FoodNet database was examined to determine
where possible, the differences in accumulation and depuration of biotoxins between
New Zealand species of shellfish. Instances in which different shellfish species had
been sampled concurrently from the same site were identified, and graphed. Where
there were more than 30 data points, differences in biotoxin levels were analysed
using a single factor ANOVA, and in some instances, two sample t-tests. Our ability
to rigorously investigate these relationships was greatly limited by lack of good data.
2.2.6
Summary of Cumulative
Phytoplankton
Monitoring
Results
–
Shellfish
and
A summary of the cumulative results of the monitoring for PSP, ASP, NSP and DSP
was developed using all valid results recorded on the FoodNet database from shellfish
toxicity testing (see Section 2.2.1 for criteria in selection of datasets). This summary
26
provides a description of the scale of the marine biotoxin monitoring programme in
comparison to the detection of biotoxins in shellfish over the last six years. The total
number of samples using valid testing techniques, the number of these samples in
which toxins were detected, the number of samples exceeding the relevant regulatory
level for that toxin, and the percentage of the total samples that this represents, were
calculated. The maximum toxin level for any sample over the same time period was
also recorded.
Similarly, a summary of the cumulative results of the phytoplankton associated with
PSP, ASP, NSP and DSP toxins was developed using all the phytoplankton results
recorded on the FoodNet database, plus data from the Marlborough Sounds Quality
Assurance Programme. The data were analysed to determine the percentage of total
samples in which toxic phytoplankton were detected, and the percentages of total
samples that were above the level to trigger shellfish sampling, above the level to
trigger voluntary closure by industry, and above the level to trigger a public health
warning.
2.2.7
Analysis of Occurrence of Biotoxins in Shellfish
A comparison of the occurrence of biotoxins in shellfish by zone and through time
was undertaken using data from shellfish monitoring on FoodNet. This analysis was
made difficult by differences in toxin accumulation characteristics between shellfish
species, the clumping of sample sites, changes in test methods, and the variations in
sampling regimes both through time and between sample sites. By using only
regularly monitored sites over the same time period subsequent to the introduction of
valid toxin test methods, and accounting for changes in sampling frequency, it was
possible to identify a data set that could be used to analyze the occurrence of biotoxins
through time. However, data able to be used in this analysis represented a small
proportion of the total data, and thus significant information with respect to the
geographical distribution of biotoxins was lost. For this reason, some analysis of the
total data set was also included.
a)
Geographical Distribution
To provide an indication of the extent of the geographic distribution of biotoxins in
shellfish throughout New Zealand, the occurrence of PSP, ASP, NSP and DSP in
shellfish samples was mapped.
Using all valid results from shellfish toxicity tests for each toxin group recorded on
the FoodNet database, all sample sites at which levels of toxin above the regulatory
level were recorded were marked on a map of New Zealand in red. Similarly, sites at
which detectable levels of toxin were recorded were mapped in yellow. From the
remaining sites, only those sites that had been frequently monitored over the 1993-99
period were selected, and these were mapped in blue. Where sample sites were too
close together to mark separately, the area in which the sites are situated was marked
with the colour representing the highest level of toxin found in the area.
This analysis is not quantitative, but merely provides a visual representation of the
areas in New Zealand in which biotoxins have been detected in shellfish.
27
Using the complete data set for each of the four biotoxin groups (PSP, ASP, DSP and
NSP), a summary by zone of the occurrence of biotoxins was undertaken. The
percentage of samples containing biotoxins above the level of detection, and
percentage of samples containing biotoxin above the regulatory level, were calculated.
The maximum toxin levels were also noted by zone for the samples with biotoxin
levels above the regulatory level.
For all four toxins (PSP, ASP, NSP and DSP), a set of sample sites that had been
regularly and consistently monitored since the initiation of valid toxin test method
was identified. The species of shellfish sampled at each site was identified, and
single-species sites were chosen (i.e. sites where the shellfish species sampled had
been consistent). Using the sites for the most widely sampled shellfish species (and in
some cases, shellfish species in which biotoxins had been frequently recorded), the
percentages of biotoxin levels above the regulatory level, and above the level of
detection, were calculated by zone.
Several assumptions were made in this analysis in order to standardize the data to
cope with changes in shellfish sampling since the introduction of phytoplankton
sampling:
•
Since 1997, the frequency of shellfish sampling has been reduced to fortnightly or
monthly samples at many sites. In order to accommodate differences in the
frequencies of sampling between different sites, it was assumed that
phytoplankton monitoring would reliably trigger shellfish sampling (i.e. that
between fortnightly or monthly shellfish samples that were recorded as having an
undetectable level of toxin, any intervening weekly shellfish samples, had they
been taken, would have had no detectable levels of toxin). Sites that were not
monitored weekly following detectable levels of toxin were not used in this
analysis.
•
At sites where there was only fortnightly shellfish sampling (except when toxins
were detected, at which time the frequency of sampling increased to weekly) it
was assumed that toxin levels in shellfish in the intervening weeks between
samples with no detectable toxin levels would have been zero had they been
tested.
b)
The seasonal distribution of biotoxins in shellfish was investigated for all four toxins
(PSP, ASP, NSP and DSP), using a set of sample sites that had been regularly and
consistently monitored since the initiation of a valid toxin test method. The species of
shellfish sampled at each site were identified, and single-species sites were chosen.
Several assumptions were made in this analysis in order to standardize the data to
cope with changes in shellfish sampling since the introduction of phytoplankton
sampling:
•
Since 1997, the frequency of shellfish sampling has been reduced to fortnightly or
monthly samples at many sites. In order to accommodate differences in the
frequencies of sampling between different sites, it was assumed that
phytoplankton monitoring would reliably trigger shellfish sampling (i.e. that
28
between fortnightly or monthly shellfish samples that were recorded as having an
undetectable level of toxin, any intervening weekly shellfish samples, had they
been taken, would have had no detectable levels of toxin).
•
At sites where there was only fortnightly shellfish sampling (except when toxins
were detected, at which time the frequency of sampling increased to weekly) it
was assumed that toxin levels in shellfish in the intervening weeks between
samples with no detectable toxin levels would have been zero had they been
tested.
Within each zone, the number of samples above the detectable level for each month
were determined, and summed for each month across years (i.e. the number for June
1994 plus the number for June 1995 etc.). To account for differing numbers of sites
per zone, the data were standardized, by dividing the total for each zone by the
number of sites in the zone. The results were graphed cumulatively for each month,
to obtain the distribution of detectable levels of toxin by month.
The same data set was used to examine the temporal distribution of biotoxin
occurrence between years. The toxin level for each sample was graphed as a point in
time, by zone, on a scatter plot. This showed the comparative frequency of toxin
occurrence year by year. It should be noted that the relative frequency of toxin
occurrence between zones within one year is influenced by the number of sites within
each zone included in the data set, so comparisons between zones cannot be made
from the data presented in this particular analysis.
29
2.3
CUMULATIVE MONITORING RESULTS
The following table presents an overall summary of the cumulative results of the
monitoring for PSP, ASP, NSP and DSP toxins in shellfish from January 1993 until
the end of June 1999 for Biotoxin Zones A-J.
Table 2.1:
Samples exceeding
regulatory levels
% of
No.
total
samples
Maximum
toxin level
(per 100g
shellfish
tissue from
whole
shellfish)
Regulatory
levels
-
20 mu/100g
18,326(a)
117
26
0.14
44 mu
–
20 µg/100g
18,572(b)
229
82
0.44
96 µg
–
80 µg/100g
29,367
1,002
94
0.32
1,007 µg
-
20 µg/g
18,814
933
36
0.19
210 µg
Biotoxin
(time period)
NSP toxins
(Sept 1994
June 1999)
DSP toxins
(Sept 1994
June 1999)
PSP
(May 1993
June 1999)
ASP
(Jan 1993
June 1999)
No. of
samples
with
positive
toxin
results
Total No.
of samples
taken
Summary of the cumulative results of the monitoring for PSP,
ASP, NSP and DSP toxins in shellfish from January 1993 until the
end of June 1999. Current regulatory levels for each toxin group
are also given. (a) Total samples = total number of acetone screen
tests, plus the ether extraction assays that were undertaken without
prior acetone screen tests. (b) Total samples = total number of
acetone screen tests, plus ELISA tests that were undertaken
without prior acetone screen tests.
Table 2.1 shows the magnitude of the number of shellfish samples tested for each
toxin over the duration of the monitoring programme in comparison to the relatively
low number of samples that represent a potential health hazard to shellfish consumers.
The cumulative results of phytoplankton monitoring in all biotoxin zones are
presented in Table 2.2. These data are drawn both from the FoodNet database (late
1997 to June 1999), and the data for the Marlborough Sounds area supplied from the
Marlborough Sounds Shellfish Quality Assurance Programme (1994-June 1999). The
data are therefore biased toward the results of Zone G, both because of differences in
temporal length (sampling data collected over a longer period of time) and because
there are comparatively more phytoplankton sampling sites in Zone G than in other
zones. Note also that there is no distinction made in the phytoplankton monitoring
results on the database between toxic and non-toxic species/strains of Pseudonitzschia. These data cannot therefore be used as an accurate indication of the
occurrence of potentially toxic phytoplankton in New Zealand overall. However, it is
pertinent in providing an indication of the occurrence of potentially toxic
30
phytoplankton with respect to the scale of the marine biotoxin monitoring programme
thus far.
Total
No. of
samples
Percentage
of samples
in which
species were
present (%)
Percentage
at level to
trigger
shellfish
testing (%)
Percentage
at level to
trigger
voluntary
industry
closure (%)
Percentage
at level to
issue public
health
warning
(%)
Alexandrium sp.
9124
4.67
4.11
0.53
0.03
Pseudo-nitzschia sp.
9134
65.40
6.95
2.38
n/a
Gymnodinium breve
9126
0.28
0.02
0.01
0.01
Dinophysis acuta
9116
4.31
0.31
0.33
n/a
Dinophysis
acuminata
9120
4.93
0.76
0.50
n/a
Species
Table 2.2:
Cumulative results of phytoplankton monitoring for all Biotoxin
Zones by potentially toxic species using all of the available data.
Data for Zone G is the period 1994-1999, and for all other zones
from 1997-1999. Pseudo-nitzschia species data includes both nontoxic and potentially toxic species, as no differentiation is made in
the database, or in the regulatory trigger levels. Trigger levels for
Pseudo-nitzschia species assume that Pseudo-nitzschia cells
comprise more than 50% of the total biomass of the sample.
It can be seen from both of the preceding tables that the percentages of samples taken
that resulted in regulatory closure to harvesting or a public health warning, due either
to biotoxin or phytoplankton levels, was comparatively low. However, these figures
represent the cumulative dynamics of the monitoring programme over the last six
years, during which time the monitoring regime has changed considerably. As will be
seen in the following sections, biotoxin occurrence can also vary significantly from
year to year. Care therefore needs to be taken in the use of these data in a predictive
sense. However, if it can be assumed that the marine biotoxin monitoring programme
has been somewhat representative of shellfish harvesting patterns over the last six
years, then these data suggest that the incidence of biotoxin levels that represented a
risk to shellfish consumers was relatively low.
31
2.4
RESULTS OF ANALYSIS - PSP
2.4.1
Geographic Distribution
The distribution of potentially toxic Alexandrium species in New Zealand is shown in
Figure 2.2. These data are drawn from the phytoplankton monitoring data on
FoodNet, as described in Section 2.2.3. Species included in the analysis were those
for which regulatory levels exist in the marine biotoxin monitoring programme:
Alexandrium minutum, A. ostenfeldii, A. catenella, A. tamarense, and A. c.f.
tamiyavanichi.
Figure 2.3 shows the sites throughout New Zealand where PSP toxins above the
regulatory level, and above the level of detection have been found in shellfish tested
in the marine biotoxin monitoring programme (Refer to Section 2.2.7 for details of the
method of analysis used).
Neither of these figures provides quantitative information about the frequency of
occurrence of potentially toxic phytoplankton or PSP in shellfish samples. Figure 2.2
indicates that the distribution of potentially toxic Alexandrium species is widespread
around New Zealand. Their distribution does not appear to be limited by latitude, nor
by biogeographic region. This is not surprising, since strains of Alexandrium species
may be found in a variety of environments: for example, Alexandrium tamarense can
be found in sub-Arctic and temperate areas (e.g. Taylor, 1984; Cembella et al., 1988),
as well as tropical regions (Reyes-Vasquez et al., 1979).
The occurrence of PSP toxins in shellfish is similarly widespread (Figure 2.3). There
were variations in toxin presence between adjacent sites. While there are many sites
at which PSP has not been detected in shellfish, the sites where it has occurred include
both the north and south of the country, and the western and eastern coasts. The
widespread distribution of PSP-producing phytoplankton suggests that there is
potential for the occurrence of PSP in shellfish anywhere around the coastline should
the right conditions for an increase in the population of Alexandrium species occur.
Table 2.3 shows the occurrence, and levels above the regulatory limits of potentially
toxic Alexandrium species by Biotoxin Zone in New Zealand as described in Section
2.2.3. (Note there are no phytoplankton monitoring sites in Zones F or K.). This table
summarizes the results of analysis of two sets of data: the first (“Total Samples”) is
the data set of all the phytoplankton samples recorded on the FoodNet and
Marlborough Sounds Shellfish Quality Assurance Programme databases. The second
set of data includes all the samples recorded on these databases within an “Identified
Time Interval” (i.e. 19/12/97-25/5/99).
The data relating to the occurrence of PSP-producing Alexandrium species using the
total number of samples on the database is the best information that we have on an
individual zone basis. The quantity of data varies considerably from zone to zone –
for example, thanks to the Marlborough Sounds Shellfish Quality Assurance
Programme, a full set of phytoplankton data from the beginning of 1994 through to
June 1999 has been included for most sites in Zone G. However, in order to compare
32
the relative occurrence of Alexandrium between zones, the data relating to the
identified time interval must be used.
Figure 2.2:
Distribution of potentially toxic species of Alexandrium throughout
New Zealand (to June 1999).
Distribution of Potentially
Toxic Alexandrium species in
New Zealand
Potentially toxic Alexandrium
species detected at 22 of the 26
sites in the Marlborough Sounds
Potentially toxic
Alexandrium species detected
No potentially toxic
Alexandrium species detected
33
Figure 2.3:
Distribution of PSP at shellfish sample sites at two levels (above the
level of detection, and above the regulatory level of 80 µg PSP/100g
shellfish tissue) throughout New Zealand (to June 1999).
Distribution of PSP in
New Zealand
There are 18 regularly monitored
sites in the Marlborough Sounds
area. PSP above the regulatory
level has occurred in shellfish at
one site. PSP above the level of
detection has occurred in
shellfish at a further three sites.
Sites with samples above regulatory level for
PSP
Sites at which PSP has been detected
Frequently sampled sites where PSP has not
been detected
34
From analysis of the “Identified Time Interval” data set, the zones can be ranked in
descending order of frequency of occurrence as follows: A, E, H, D, B, I, J, G, C.
However, it must be remembered that this analysis is based on only 17 months of
recorded data, which is a comparatively short time interval.
Zone
Percentage occurrence in
Total samples (%).
N=
Percentage of Total
samples with 100-400
cells/L (%)
Percentage of Total
samples with 500 to 4900
cells/L (%)
Percentage of Total
samples with 5,000
cells/L or more (%)
the identified time
interval (%)
N=
Percentage of samples in
the identified time
interval with100-400
cells/L (%)
the identified time
interval with 500-4900
cells/L (%)
the identified time
interval with 5,000 cells/L
or more (%)
A
B
C
D
E
G
H
I
J
9.7
7.5
1.9
10.1
7.1
3.9
8.5
4.5
3.8
432
107
583
622
240
6486
82
468
104
6.9
7.5
1.7
6.3
5.8
3.7
8.5
4.5
2.9
2.8
0.0
0.2
3.4
1.3
0.2
0.0
0.0
1.0
0.0
0.0
0.0
0.5
0.0
0.0
0.0
0.0
0.0
13.4
7.9
2.2
8.9
10.6
3.1
9.2
5.3
5.2
456
532
152
1941
76
304
304
76
76
9.5
7.9
2.2
5.3
8.6
3.0
9.2
5.3
3.9
3.9
0.0
0.0
3.4
2.0
0.1
0.0
0.0
1.3
0.0
0.0
0.0
0.2
0.0
0.0
0.0
0.0
0.0
Table 2.3:
Percentage occurrence of potentially toxic Alexandrium species,
and percentage occurrence above the regulatory levels (100 - 400
cells/L, 500 – 4,900 cells/L and ≥ 5,000 cells/L) in total samples and
in samples from 19/12/97 to 25/5/99 (the “Identified Time
Interval”) by zone.
To show the spread of the data in the “Identified Time Interval” data set, the same
ranges of data (100-400 cells/L; 500-4,900 cells/L) have been represented graphically
as “Box and Whisker Plots” (where five or more data points exist) or, where there are
less than five data points, numbers are simply stated. This summary is presented in
Figure 2.4.
Zone D is the only Zone where there has been a level of potentially toxic Alexandrium
species in excess of the level requiring a Public Health Warning ( ≥ 5,000 cells/L),
with a maximum level of 6,500 cells/L (of A. catenella from Te Kaha on 20/12/98).
The next highest level was in Zone E, where 4,700 cells/L were recorded (A. minutum
35
Alexandrium spp.
500
N=6
N=28
N=16
N=58
400
300
200
100
N=29
N=10
N=13
N=7
0
A
B
C
D
E
Zone
G
H
I
Range of data above the Industry Voluntary
Closure Level (500-4900 cells/Litre)
Range of data above the Flesh Testing
Trigger Level (100-400 cells/Litre)
from Tolaga Bay on 18/1/99). In both Zones A and D, 75% of the samples that were
in the range to trigger a voluntary industry closure were less than 1,500 cells/L, and
95% were less than 3,000 cells/L. Samples recorded in the range to trigger flesh
testing were predominantly in the lower half of the range – in Zones A, C, D, E, G,
and I, 75% of the samples were 200 cells/L or less. Zones A, E, H, and I had median
values of 100 cells/L. These median values were not visible on the Box and Whisker
Plot since they were the same as the 25th percentile in the distribution of cell counts in
this range. Zone C and G had a median value of 200 cells/L. These values were the
same as the 75th percentile.
3500
Alexandrium spp.
3000
2500
2000
1500
1000
500
N=12
N=18
A
D
0
Zone
Zone D:
Above Public Health Warning Level (5000 cells/L): 6 500
Zone E:
Above Industry Voluntary Closure Level (500 cells/L): 500, 800,
4 700
Zone G:
Above Industry Voluntary Closure Level (500 cells/L): 600, 600
Zone J:
Above Flesh Testing Trigger Level (100 cells/L): 100, 100, 100
Above Industry Voluntary Closure Level (500 cells/L): 800
Figure 2.4:
Box and whisker plots showing the frequency distribution of (a)
potentially toxic Alexandrium species above the level to trigger
flesh testing (100 cells/L) by zone, and (b) potentially toxic
Alexandrium species above the level to trigger a voluntary closure
to commercial harvesting (500 cells/L) in the two zones (A & D)
where these levels occur. Data are also given for levels above the
Public Health Warning limit (i.e. ≥ 5,000 cells/L).
36
Zone
Total No.
of
Samples
A
B
C
D
E
F
G
H
I
J
K
3127
1902
3172
4262
1226
1897
6320
1127
2184
1269
374
Table 2.4:
Number of
samples in
which PSP
was
detected
157
48
6
743
9
2
23
3
1
10
0
Percentage
of samples
in which
PSP was
detected
5.02
2.52
0.19
17.43
0.73
0.11
0.36
0.27
0.05
0.79
0
No. of
samples
above
regulatory
level
1
0
0
91
0
0
2
0
0
0
0
Percentage
of samples
above
regulatory
level
0.03
0.00
0.00
2.14
0.00
0.00
0.03
0.00
0.00
0.00
0.00
Maximum
toxin level
(µg/100g)
83
1007
127
Summary by zone of the total occurrence of PSP toxins detected in
shellfish samples, and PSP toxins above the regulatory level of
80µg/100g detected in shellfish samples from 1/7/93 to 30/6/99.
A summary of PSP toxin occurrence in shellfish for all sites in all zones from July
1993 to end of June 1999 is provided in Table 2.4. It can be seen that PSP was
detected in a much higher percentage of samples in Zone D than in other zones, and
that only Zones A, D and G had levels of PSP above the level for closure to
harvesting (i.e. 80 µg/100g). The 1,007 µg/100g maximum toxin level in Zone D (at
Tokata on 21/4/97) was also considerably higher than those in Zones A or G (Zone A
was only just above the level for closure).
Examination of the data where there were high numbers of samples in which PSP was
detected, revealed that many of the “detects" in Zone A and D related to long-running
levels of PSP toxins in tuatua (specifically at Tokerau Ramp in Northland (Zone A),
and Ohope Beach, Bay of Plenty (Zone D)). This potentially suggests two things:
one, that the occurrence of PSP in particular areas might be related to the presence of
“seed beds” of toxic Alexandrium cysts, causing repeated toxicity in that area.
Secondly, that the variation in occurrence of PSP toxins is not geographical but
related to the species of shellfish being sampled in each area. There have been no
surveys undertaken to determine the presence of Alexandrium cysts in the sediments
in either of these areas (L. Mackenzie, Cawthron Institute, pers. comm.). However,
some investigation of the comparative differences in levels of PSP in different species
of shellfish was possible using the available data.
It should be noted that the analysis presented in Table 2.4 did not use standardized
data, and that potential differences in toxin accumulation characteristics between
shellfish species, the clumping of sample sites, and variations in sampling regimes,
both through time and between sample sites has been ignored. In an attempt to reduce
some of this bias, a similar analysis was carried out using data from a single species,
from sites that had been consistently monitored over the whole time period, as
described in Section 2.2.7. Because they were the most widely sampled species,
Greenshell™ mussels were chosen as the sample species. The data were standardized
to account for the changes in the shellfish sampling programme since the introduction
of phytoplankton sampling, as described in Section 2.2.7.
37
Table 2.5 provides a summary of the PSP toxin occurrence in Greenshell™ mussels
by zone from July 1993 to the end of June 1999. The scope of the data is less than
that in the previous table as Greenshell™ mussels had only been consistently
monitored at sites in Zones C, D, G, H, and I over that time period. No data were
available from the other zones. However, these data suggest that the occurrence of
PSP toxins in Greenshell™ mussels in Zone D was higher than that in the other zones.
Zone
Total No. of
Samples
C
D
G
H
I
1192
743
3709
599
307
Table 2.5:
Percentage of
Samples with PSP
above Detectable
Levels (%)
0.0
5.7
0.5
0.5
0.0
Percentage of Samples
with PSP above the
Regulatory Level (%)
0.0
1.3
0.05
0.0
0.0
Summary by zone of the occurrence of PSP toxins in Greenshell™
mussels from consistently monitored sample sites from 1/7/93 to
30/6/99.
Given that there is potential for the accumulation of PSP to differ between species,
these differences were investigated within the limits of the available data. Table 2.6
provides a summary of the occurrence of PSP in the major shellfish species sampled
in the marine biotoxin monitoring programme.
Species
Total
No. with
detectable
levels of
PSP
Percentage
of samples
above
detectable
level (%)
No. of
samples
above the
regulatory
level
Percentage
above the
regulatory
level (%)
10587
1616
3293
623
2848
2189
2023
1696
485
121
6
22
9
88
738
13
0
2
1.14
0.37
0.67
1.44
3.09
33.71
0.64
0.00
0.41
15
0
0
0
0
78
0
0
0
0.14
0.00
0.00
0.00
0.00
3.56
0.00
0.00
0.00
TM
Greenshell
mussel
Blue mussel
Pacific oyster
Dredge oyster
Scallop
Tuatua
Pipi
Cockle
Paua
Table 2.6:
Summary of the occurrence of PSP toxins in the major shellfish
species sampled at all sites in the marine biotoxin monitoring
programme from 1/7/93 to 30/6/99.
These data indicate that a higher percentage of tuatua samples contained a detectable
level of PSP than other shellfish species sampled, and that tuatua samples had a
greater percentage of PSP levels above the regulatory level of 80 µg/100g. However,
these data are not sufficient to indicate species differences with respect to biotoxin
accumulation and retention, since the toxin accumulation might be site specific rather
than species specific.
38
While the data are scarce, there are a few occasions on which several species of
shellfish from the same site have been monitored concurrently and tested for PSP.
The most comprehensive data are summarized in Figures 2.5 to 2.7. Note that in
these figures, sample results below the level of detection are portrayed as zero.
PSP Level (µg/100g)
350
300
250
200
Greenshell
mussels
150
Tuatua
100
50
0
98 98 98 98 98 98 98 98 98 98 99
3/ 04/ 05/ 06/ 07/ 08/ 09/ 10/ 11/ 12/ 01/
0
1/ 1/
1/ 1/
1/
1/
1/
1/
1/ 1/
1/
Time
Figure 2.5:
Comparison of levels of PSP in GreenshellTM mussels (Perna
canaliculus) and tuatua (Paphies subtriangulata) at Ohope Beach
from March 1998 to January 1999.
250
200
Mussel
150
Tuatua
100
Scallop
50
7/
07
/
14 93
/0
7
21 /93
/0
7/
28 93
/0
7/
9
4/ 3
08
11 /93
/0
8
18 /93
/0
8
25 /93
/0
8/
9
1/ 3
09
/9
8/ 3
09
15 /93
/0
9/
93
0
Time
Figure 2.6:
Comparison of levels of PSP in mussels (species not specified in
database), tuatua (Paphies subtriangulata) and scallop (Pecten
novaezelandiae) at Waihi Beach July 1993 to September 1993.
39
50
45
40
35
30
Mussel
25
Scallop
20
15
10
5
0
3
3
3
3
3
3
3
3
3
3
/9
/9
/9
/9
/9
/9
/9
/9
/9
/9
07 /08 /08 /09 /09 /10 /10 /11 /11 /12
/
8
6
3
1
28
11
25
22
20
17
Time
Figure 2.7:
Comparison of levels of PSP in mussels (species not specified in
database) and scallops (Pecten novaezelandiae) in Rangaunu Bay,
Northland from July 1993 to December 1993.
In addition to the data illustrated, several one-off comparisons have been made:
Concurrent samples taken from Ngunguru (Northland) in October 1993 indicated that
pipi (Paphies australis) from the site had a level of 34.5 µg PSP/100g tissue, while
cockles (Austrovenus stutchburyi) had no detectable PSP. Blue mussels (Mytilus
edulis aoteanus) from Tairua Harbour (eastern Coromandel Peninsula) on 11/07/99
had no detectable levels of PSP, whereas tuatua sampled concurrently from the same
site had a level of 95 µg PSP/100g tissue (which was above the regulatory limit of 80
µg/100g.
Only the data comparing the PSP levels in Greenshell™ mussels and tuatua at Ohope
Beach (Figure 2.5) have sufficient samples to undertake robust quantitative analysis.
A two-sample t-test, assuming unequal variance, indicated that the toxin levels in
Greenshell™ mussels and tuatua from Ohope Beach were significantly different
(p<0.05) over the time period of the recorded data, identifying that on average tuatua
had higher levels of PSP than mussels.
In the ten-month study at Ohope Beach (Figure 2.5), 35.1% of tuatua samples were
above the regulatory limit for PSP, compared to only 5.9% of GreenshellTM mussel
samples over the same time. This is of potential significance in terms of the risk of
PSP to consumers of non-commercially gathered shellfish.
Qualitative examination of the data suggests that not only do tuatua retain PSP toxins
longer, but they also accumulate comparatively more toxin than mussels when a toxic
event occurs in the phytoplankton. However, in terms of maximum toxin levels
measured to date, GreenshellTM mussels may also accumulate high levels of PSP toxin
e.g. D41-Whangaparoa, on the 22 April 1996, with a level of 556 µg PSP/100g tissue.
Similarly, the data suggest that scallops may accumulate and retain PSP toxins to a
40
greater extent than mussels, but to a lesser extent than tuatua. There may also be
differences in accumulation and retention of PSP toxins between pipi and cockles.
Whether these differences are from environmental or physiological causes is unable to
be identified from the data available in this study. However, inter-specific differences
in accumulation of PSP toxins have been observed in controlled field experiments
undertaken overseas (e.g. Shumway et al., 1990).
The results of our analysis are not in any way definitive, and much more data
collection would be required to investigate this further. However, they do suggest that
differences between species in PSP toxin accumulation and retention have the
potential to impact significantly on the risk of PSP to consumers, and that these
differences should be taken into consideration in the design of the marine biotoxin
monitoring programme.
2.4.2
Phytoplankton monitoring data on the FoodNet database had been recorded for an
insufficient period for a meaningful analysis of temporal patterns. However, some
analysis of seasonal patterns in potentially toxic Alexandrium species in Zone G was
possible using the data supplied by the Marlborough Sounds Shellfish Quality
Assurance Programme. Five years of data (1994-1999) were analysed to investigate
seasonal patterns in occurrence as described in Section 2.2.3(b). The results showed
that in the Marlborough Sounds in the winters of 1995-1999, 1.1% of phytoplankton
samples contained potentially toxic Alexandrium species above the level to trigger
flesh testing (N=1361), while in the summers (1994-1999), 7.1% of samples
contained this level (N=1625). In spring and autumn, these percentages were 3.3%
(N=1619) and 3.0% (N=1647) respectively. While these results are rudimentary, this
suggests that there may be a higher chance of occurrence of PSP toxins in shellfish in
the Marlborough Sounds in summer than in winter.
The seasonality of PSP toxin occurrence in shellfish was analysed using data from
sample sites that had been regularly and consistently monitored from 1/7/93 to
30/6/99 as described in Section 2.2.7. This analysis was based on the incidence of
PSP toxins above the detectable level in shellfish, for each zone, because the
incidence of PSP toxins above the regulatory level was low (implying a relatively low
risk to consumers). The data were standardised to take account of differences in the
number of sites per zone. Data from 48 sites were included in the analysis. Fourteen
of these sites were in Zone G. There were no data available from Zones J or K (due to
discontinuous sampling at all sites in these zones). Due to the fact that regular weekly
sampling was discontinued in sites in Zone D with persistent levels of PSP toxins in
tuatua, these sites were not included in this analysis.
The risk of PSP to consumers is related to both the occurrence of PSP events, and the
duration of retention of toxins in the shellfish. In this analysis, it is assumed that the
presence of any PSP toxins in shellfish is indicative of an increased likelihood of PSP
levels sufficient to be a risk to public health. As depicted in Figure 2.8, there appears
to be no clear seasonal pattern relating to the potential risk of PSP to consumers of
shellfish.
41
Cumulative No. of PSP
"Detects" per Month by Zone
3.00
2.50
2.00
1.50
1.00
0.50
0.00
Jan Feb Mar Apr May Jun
Jul
Aug Sept Oct Nov Dec
Month
Figure 2.8:
Zone A
Zone B
Zone H
Zone I
Zone C
Zone D
Zone E
Zone F
Zone G
The six-year cumulative incidence of PSP toxins above the
detectable level at sites within each zone by month, recorded from
1st July 1993 to 30th June 1999. The data has been standardised to
account for differences in the number of sites per zone.
PSP Level (µgSTX/100g Tissue)
Using the same set of data, the variation in PSP toxin occurrence from year to year
was investigated, as described in Section 2.2.7. The temporal distribution of PSP
levels above the detectable level in shellfish samples from the same consistently
sampled sites is presented in Figure 2.9.
600
500
400
300
200
100
0
9
8
7
6
5
4
3
9
8
6
7
5
4
3
9
8
7
6
5
4
3
-9
l-9 v-9 ar-9 ul-9 v-9 ar-9 ul-9 v-9 ar-9 ul-9 v-9 ar-9 ul-9 v-9 ar-9 ul-9 v-9 ar-9 ul-9 v-9
ar
J
J
J
J
J
J
Ju No
M
M
M
M
M
M
M
No
No
No
No
No
No
Time
Zone A
Figure 2.9:
Zone B
Zone D
Zone G
Zone H
Distribution of detectable levels of PSP toxin in shellfish from
consistently monitored sites from July 1993 to June 1999.
This figure shows that that the frequency of occurrence of detectable levels of PSP in
shellfish from each zone may vary from year to year, for example, PSP toxins
occurred in Zone G sites in 1993-94 and again in the summer of 1997-98. With the
42
exception of the period from July 1993 to July 1994, when there were relatively high
numbers of PSP detects below the regulatory level, there appear to be no obvious year
to year patterns. It should be noted however, that there is not a consistent seasonal
occurrence from year to year of PSP toxins within each zone: for example, PSP
toxicity occurred in Zone G in the summer of 1993-94, but was absent in the summer
of 1994-95. Similarly, PSP toxicity was not recorded at the Zone D sites included in
this analysis prior to the summer of 1995. There are similar variations in the
incidence of PSP toxicity in Zone A. This is important in terms of risk analysis.
While analysis of PSP toxin data on a purely geographical basis might suggest that
Zones A and D are the areas of highest risk to shellfish consumers with respect to
PSP, the temporal data suggests that extrapolation of historical data to predict future
occurrence of PSP toxicity by area should be undertaken with great caution.
A summary of the occurrence of El Nino/La Nina climate patterns over this time
period is presented in Appendix III. There appears to be no obvious correlation
between the occurrence of PSP toxins, (either across NZ as a whole, or within zones)
with these broad climate patterns. More information on the population dynamics of
potentially toxic Alexandrium species in each area is required before any
predictability of risk would be possible.
Most Alexandrium species have a life cycle that involves alternation between asexual
and sexual reproduction. Anderson (1998) discusses the physiology and bloom
dynamics of toxic Alexandrium species overseas. Anderson (1998) suggests that
generally Alexandrium blooms have a “life-span” – a relatively short period of time in
which these species are found in the water column as motile vegetative cells. At other
times, Alexandrium species reside in the sediments as resting cysts (hypnozygotes). It
is commonly thought that cyst “seedbeds” provide the inoculum for many
Alexandrium blooms. These may not necessarily be discrete beds of cysts, but may be
due to a widespread distribution of cysts in the sediment in general. The dynamics of
Alexandrium species life cycles (for example, the triggers to encystment and
excystment) are complex and not particularly well understood. They appear to
involve the interaction of a series of factors such as temperature, nutrient availability,
oxygen availability and endogenous rhythms (internal clock mechanisms) (Anderson,
1998).
The bloom dynamics of Alexandrium species are the result of the interaction between
the biological and behavioural characteristics of Alexandrium (e.g. life cycle,
dormancy times of hypnozygotes, swimming behaviour, diel vertical migration
through the water column etc.) and environmental and hydrographical factors
(temperature, nutrients, salinity, currents, tides, wind etc.). Patterns of occurrence of
Alexandrium may also be influenced by larger-scale factors such as El Nino/La Nina
weather patterns (Erickson & Nishitahi, 1985), and 18.6 year cycles of lunar tidal
modulation (White, 1987). There are insufficient data available to analyze the
occurrence of Alexandrium species in significant densities in New Zealand in terms of
the interaction of these micro- and meso-scale factors. While some seasonal
differences in Alexandrium occurrence in Zone G may be indicated from the
phytoplankton monitoring data over the last five years, there are no apparent seasonal
patterns in the occurrence of PSP toxins in shellfish in New Zealand overall, and there
are inter-annual differences in PSP occurrence by zone. Predictions of risk based on
historical data would be inappropriate until a much greater depth of understanding
43
about the dynamics of Alexandrium blooms in New Zealand is gained through longterm studies.
2.4.3
Phytoplankton as a Predictor of PSP in Shellfish
The phytoplankton monitoring data and shellfish toxin testing data on the FoodNet
database were analysed to determine the probability that phytoplankton monitoring
would fail to predict the occurrence of PSP above the regulatory level in shellfish.
(Refer to Section 2.2.4 for methodology). Prior to the commencement of
phytoplankton records on the database at the beginning of May 1997, there were
residual low levels of PSP in tuatua at sites in the Bay of Plenty. Some level of
activity in this area continued through to the end of the period of analysis in June
1999. During this time there were four instances at Ohope Beach (Site D37) in which
the level of PSP increased from consistently below the regulatory level (around 30-40
µg/100g) to over the regulatory level of 80 µg/100g. Three of these occasions were
associated with levels of potentially toxic Alexandrium species above the level to
trigger industry voluntary closure to harvest (500 cells/L). In the fourth instance,
early in June 1999, when there was an increase in toxin level from 48 µg/100g to 139
µg/100g, no potentially toxic Alexandrium species were detected in the phytoplankton
samples concurrent with the shellfish tests, or the week before, although 200 cells/L
of Alexandrium margalefii (a species considered to be non-toxic) were identified in
the sample the week before the occurrence of elevated toxin levels. However, there
were 100 cells/L of Alexandrium catenella in the phytoplankton sample two weeks
prior to the elevated toxin levels. Assuming that the identification of Alexandrium
margalefii was made correctly, and that it does not produce PSP toxins, these results
suggest that either only low numbers of Alexandrium catenella are required to
increase shellfish toxicity from residual levels of 48 µg/100g to 139 µg/100g, or that a
low level of precision in the phytoplankton sampling or counting methods resulted in
failure to detect toxic species that were present.
The lack of a consistent relationship between apparent increases in PSP content in
shellfish containing initial residual levels of PSP toxin and potentially toxic
phytoplankton, could be due not only to changes in shellfish toxin levels over time,
but to a high degree of variability between shellfish at any one time. Studies on
overseas shellfish species have shown a high variation in toxin levels between
individual shellfish in the same area. The degree of variation between individuals was
found to increase with decreasing toxin levels (White et al., 1993). We have been
unable to find any instances recorded on the FoodNet database of replicate sampling
to measure the variation between individuals or pooled samples of the same species at
one time. It is suggested that such information could be significant in the
determination of the risk of PSP to shellfish consumers in New Zealand. It would
also assist in the interpretation of monitoring data for management purposes.
The results of the above analysis support the continuation of weekly shellfish testing
for PSP when there are residual levels of PSP below the regulatory level present in
shellfish.
There were no instances of PSP toxin rising from zero levels to above the regulatory
level for public warnings/closure to industry harvesting at any shellfish monitoring
sites associated with phytoplankton sites during the time over which phytoplankton
44
data are recorded on the FoodNet database. This meant that we were unable to
investigate the probability that phytoplankton levels would fail to indicate the
presence of PSP toxin in shellfish. However, we did investigate the relationship
between detectable levels of PSP in shellfish and the presence of potentially toxic
Alexandrium species. In six out of eight instances where PSP toxins rose to detectable
levels in shellfish, potentially toxic phytoplankton species were recorded above the
level to trigger shellfish testing or voluntary closure by industry. In the two instances
with no associated phytoplankton levels, the PSP levels in the shellfish were relatively
low (33 µg/100g and 35 µg/100g). Further long-term data are required in order to
ascertain the reliability of phytoplankton monitoring as a predictor of levels of PSP
above the regulatory level in shellfish.
A wide range of factors impact on the ability to predict shellfish toxicity by sampling
phytoplankton. Characteristics of shellfish species with respect to their feeding, and
accumulation and retention of toxins over a period of time, combined with temporal
and spatial variability in phytoplankton abundance, complicate the use of weekly
phytoplankton monitoring in prediction of shellfish toxicity. However, good
sampling design, incorporating appropriate site selection, appropriate levels of
precision in both sampling and counting of phytoplankton, combined with action
levels that are appropriate for limitations of the sampling design, potentially result in a
sound monitoring programme.
Consideration of the phytoplankton data with respect to PSP toxicity in shellfish
suggests that low numbers of potentially toxic Alexandrium species may be
significant. Where low numbers are significant, precision in sampling and counting
may be significant factors.
Precision is the variability of repeated sample estimates of mean abundance, and is
limited by the effort that can be expended to collect and analyse samples (i.e. cost).
The measurement of precision provides information that is important in deciding the
value to be placed on any quantitative result. In a robust marine biotoxin monitoring
programme, the phytoplankton trigger levels take into consideration the precision of
sampling – i.e. at a lower level of precision, the trigger levels are set more
conservatively. In the case of monitoring for PSP, the levels at which Alexandrium
species trigger shellfish sampling are set at the level of detection for the
phytoplankton counting method used.
Numbers of toxic species in a phytoplankton sample are based on counting cells
settled out from one 10 mL sample (Kirsten Todd, Cawthron Institute, pers. comm.).
A level of 100 cells/L (which is the concentration that triggers shellfish sampling)
thus equates to a count of 1 cell in 10 mL. In counting phytoplankton, the level of
precision is related to the number of individuals counted. There has been much
discussion in the literature regarding the number of cells that should be counted to
give a satisfactory level of precision, and a variety of approaches have been proposed.
Based on an assumption of a non-aggregated distribution of individuals, it has been
suggested that for counts less than 50, the limits of expectation of population means
based on single estimates of abundance may be obtained from fiducial limits to the
Poisson distribution. For more than 50 cells per sample, the individuals may be
distributed normally (Lund et al., 1958, Venrick, 1978). This information can be used
for comparing different counts. If one actual count lies within the confidence limits of
45
the other, there is no significant difference between them (Lund et al., 1958). The
marine biotoxin monitoring programme for non-commercially harvested shellfish has
two phytoplankton trigger levels for Alexandrium species (100 cells/Litre to trigger
shellfish monitoring, and 5,000 cells/Litre to trigger a Public Warning). It is noted
that, at a 95% confidence level, the respective limits of expectation indicate that
counts representing these two trigger levels are significantly different under the
current counting protocol.
However, using the current counting protocol,
determination of the limits of expectation at a 95% confidence level indicate that the
two lower trigger levels in the shellfish industry programme (100 cells/Litre and 500
cells/Litre), are not significantly different (based on methods described in Lund et al.,
1958; also Figure 29 - Venrick, 1978; Table 7 - Andersen, 1996). While this does not
directly relate to the marine biotoxin monitoring programme for non-commercially
harvested shellfish, it does raise the question of whether the precision of the counting
methods has been sufficiently considered in the determination of phytoplankton
monitoring methods.
2.4.4
Conclusions
Despite the challenges presented by data collection not designed with long-term
analysis in mind, several conclusions regarding the risk of PSP to shellfish consumers
in New Zealand may be drawn from the analysis of biotoxin monitoring data
undertaken in this review. These are summarised below.
•
Alexandrium species and PSP toxicity in shellfish are widespread around New
Zealand and have occurred in a variety of marine environments. Latitude or
biogeographic region does not limit their occurrence.
•
If it can be assumed that the monitoring programme is representative of shellfish
harvesting in New Zealand, the incidence of PSP toxins in shellfish at a level that
represents a potential risk to consumers has been comparatively low in most areas.
Levels above the regulatory level of 80 µg/100g have been detected in only Zones
A, D, and G in 0.03%, 2.14%, and 0.03% of the total samples respectively.
•
Analysis of the temporal distribution of PSP toxins in shellfish in New Zealand
indicates there may be some year to year variation in the number of samples with
detectable levels of PSP. Overseas research suggests that long-term cycles in
abundance of toxic Alexandrium species occur (e.g. 18.6 year cycles). A better
understanding of the factors controlling the incidence of Alexandrium blooms in
New Zealand, based on robust long-term data collection, is required to facilitate a
good assessment of the risk of occurrence of PSP toxins in shellfish at levels that
are harmful to consumers.
•
The monitoring data collected over the last six years suggest that there were
differences in occurrence of PSP toxins between zones. In addition, temporal
analysis indicates that occurrence of biotoxins varied inter-annually by zone.
Overseas research suggests that Alexandrium blooms are controlled by the
interaction of a complex set of variables, some of which operate over long time
scales. It is therefore suggested that historical data may not provide a good
46
estimate of risk in the future with respect to differences between zones in the
distribution of PSP toxins in New Zealand.
•
While five years of phytoplankton monitoring data from the Marlborough Sounds
suggested that there may be some seasonal differences in the frequency of
occurrence of potentially toxic Alexandrium species, there were no similar
patterns obvious in the occurrence of PSP toxins in shellfish by zone across New
Zealand. This suggests that until further long term phytoplankton data are
available, any seasonal variations in the marine biotoxin monitoring programme
for PSP toxins should arise from seasonal differences in shellfish harvesting
patterns, not assumptions about seasonal variations in the occurrence of PSP.
•
Limited data are available to investigate the differences in uptake and
accumulation of PSP toxins between different species of shellfish, and further data
are required for rigorous analysis. However, analysis of existing data suggests
that differences between species in accumulation and retention of PSP toxins have
the potential to impact significantly on the risk of PSP to consumers. It needs to
be ensured that these differences are taken into account in the design of the marine
biotoxin monitoring programme.
•
There were no data available to test the probability that phytoplankton monitoring
would fail to detect levels of PSP above the level to trigger shellfish testing.
However, in 25% of instances where lower levels of PSP were detected in
shellfish, there were no potentially toxic Alexandrium species recorded in the
phytoplankton monitoring either concurrently or in the previous week.
Phytoplankton monitoring also failed to detect any potentially toxic Alexandrium
species associated with the increase of residual low levels of PSP in shellfish to
above the regulatory level in 25% of the cases for which there are data. Both
these instances are based on small sample sizes, and further data are required to
test the robustness of the phytoplankton monitoring programme with respect to
detection of PSP toxins in shellfish. However, the results of the latter analysis
support the continuation of weekly shellfish testing for PSP when there are
residual levels of PSP below the regulatory level present in shellfish.
47
2.5
RESULTS OF ANALYSIS – ASP
2.5.1
The distribution of Pseudo-nitzschia species throughout New Zealand is shown in
Figure 2.10. These data are drawn from the phytoplankton monitoring data on
FoodNet, as described in Section 2.2.3. Unfortunately, on the database there is no
distinction between potentially toxic and non-toxic species, so the map represents the
geographic distribution of all Pseudo-nitzschia species around the New Zealand coast,
both non-toxic and potentially toxic. The distribution of potentially toxic species may
not necessarily correlate with that of all species collectively.
Figure 2.11 shows the sites throughout New Zealand where ASP toxins above the
regulatory level, and above the level of detection, have been found in shellfish tested
in the marine biotoxin monitoring programme. (Refer to Section 2.2.7 for details of
the method of analysis used).
Neither of these figures provides quantitative information about the frequency of
occurrence of potentially toxic phytoplankton or ASP in shellfish samples. However,
they do indicate that Pseudo-nitzschia species have been found at all the
phytoplankton monitoring sites throughout New Zealand. The distribution of ASP
toxins in shellfish is also widespread throughout New Zealand. ASP toxins have been
detected in shellfish from the far north of the North Island to the south of the South
Island, on both western and eastern coasts, and also in the Chatham Islands to the east.
These figures suggest that latitude, or biogeographic zone, does not limit the
distribution of Pseudo-nitzschia species, and that given the right environmental
conditions, ASP toxicity in shellfish could potentially occur anywhere in New
Zealand.
Table 2.7 shows the occurrence, and levels above regulatory limits of Pseudonitzschia species by Biotoxin Zone in New Zealand, as described in Section 2.2.3.
Note that there are no phytoplankton monitoring sites in Zones F or K. This table
represents an analysis summary for two sets of data: the first (“Total Samples”) is the
data set of all the phytoplankton samples recorded on the FoodNet and Marlborough
Sounds Shellfish Quality Assurance Programme databases. The second set of data
includes all the samples recorded on these databases within an “Identified Time
Interval” (i.e. 19/12/97-25/5/99).
The percentage occurrence of Pseudo-nitzschia species measured from the full data
set (Total Samples) suggests that Pseudo-nitzschia species are commonly found in the
phytoplankton (percentage occurrence ranges from 58% in Zone C to 80.5% of the
samples in Zone H). All zones have had levels of Pseudo-nitzschia species sufficient
to trigger shellfish testing for ASP, and 78% of the zones have had levels sufficient to
trigger an industry voluntary closure (all zones except Zones H and J).
The data relating to the occurrence of Pseudo-nitzschia species using the total number
of samples on the database is the best information that we have on an individual zone
basis. The quantity of data varies considerably from zone to zone – most zones
include data from late 1997 to May 1999, but data for the Marlborough Sounds in
48
Distribution of Pseudo-nitzschia
species in New Zealand
Pseudo-nitzschia species detected
at all 26 phytoplankton sites in the
Marlborough Sounds
Pseudo-nitzschia species
detected
No Pseudo-nitzschia
species detected
Figure 2.10: Distribution of Pseudo-nitzschia species at sites where
phytoplankton has been monitored throughout New Zealand (to
June 1999).
49
Distribution of ASP in
New Zealand
shellfish sample sites in the
Marlborough Sounds area. ASP
above the regulatory level has
occurred in shellfish at one site.
ASP has been detected in all but 9
other regularly monitored sites.
ASP detected at one
site at the Chatham
Islands
Sites with samples above regulatory
level for ASP
Sites at which ASP has been detected
Frequently sampled sites where ASP
has not been detected
Figure 2.11: Distribution of ASP at shellfish sample sites at two levels (above
the level of detection and above the regulatory level of 20 µg
Domoic acid/g shellfish tissue) throughout New Zealand (to June
1999).
50
Zone G are available from 1994 to 1999, from the Marlborough Sounds Shellfish
Quality Assurance Programme database. However, in order to compare the relative
occurrence of Pseudo-nitzschia species between zones, the data relating to the
identified time interval must be used.
From analysis of the “Identified Time Interval” data set, the zones can be ranked in
descending order of frequency of occurrence of Pseudo-nitzschia species as follows:
J, I, A, B and H, G, D, E, C. However, it must be remembered that this analysis is
based on only 17 months of recorded data, which is a comparatively short time.
Zone
Total samples (%).
N=
Percentage of Total
samples with 50,000199,900 cells/L (%)
Percentage of Total
samples with 200,000
cells/L or more (%)
identified time interval
(%)
N=
the identified time
interval with 50,000199,900 cells/L (%)
the identified time
interval with 200,000
cells/L or more (%)
Table 2.7:
A
B
C
D
E
G
H
I
J
73.3
72.9
58.0
77.2
75.7
63.1
80.5
72.0
74.0
438
107
584
622
243
6486
82
468
104
6.2
6.5
0.5
7.9
4.5
7.6
3.7
8.3
1.9
1.1
5.6
0.3
5.0
0.4
2.5
0.0
3.8
0.0
76.6
73.7
48.9
66.7
64.5
71.5
73.7
78.3
81.6
304
76
456
532
152
1941
76
304
76
4.3
5.3
0.4
5.3
5.3
8.9
3.9
8.6
2.6
3.9
3.9
0.2
2.4
0.0
2.9
0.0
5.6
0.0
Percentage occurrence of Pseudo-nitzschia species, and percentage
occurrence above the regulatory levels (50,000 cells/L and
≥ 200,000 cells/L, assuming that Pseudo-nitzschia species are
greater than 50% of the total phytoplankton) in the Total Samples
and in the samples from 19/12/97 to 25/5/99 (the “Identified Time
Interval”) by zone.
To display the spread of the data in the “Identified Time Interval” data set, the same
ranges of data (50,000-199,000 cells/L and ≥ 200,000 cells/L) have been represented
graphically as “Box and Whisker Plots” (where five of more data points exist) or
where there are less than five data points, as numbers simply stated. This summary is
presented in Figure 2.12.
51
200x103
150x103
100x103
50x103
Zone B:
N=13 N=28 N=8 N=173 N=26
0
A
D
E
G
I
Zone
Closure Level (>200 000 cells/Litre)
Range of data above the Flesh Testing Trigger
Level (50 000 to 199 900 cells/Litre)
Pseudo-nitzschia
250x103
Pseudo-nitzschia
7x106
6x106
5x106
4x106
3x106
N=12 N=13
N=57 N=17
2x106
1x106
0
A
D
G
I
Zone
Above Flesh Testing Trigger Level (50 000 cells/L): 95 000,
72 000, 61 000, 89 000
Above Industry Voluntary Closure Level (200 000 cells/L):
273 000, 427 000, 219 000
Zone C:
76 000
Above Industry Voluntary Closure Level (200 000 cells/L):
236 000
Zone H:
58 000, 187 000
Zone J:
80 000
Figure 2.12: Box and whisker plots showing the frequency distribution of (a)
Pseudo-nitzschia species above the level to trigger flesh testing
(50,000 cells/L) by zone, and (b) Pseudo-nitzschia species above the
level to trigger a voluntary closure to commercial harvesting
(200,000 cells/L) in the four zones (A, D, G and I) where these
levels occur.
Most Pseudo-nitzschia samples in the range to trigger shellfish testing (i.e. 50,000199,000 cells/L) occurred at the lower end of the range – 75% of all samples were less
52
than 125,000 cells/L. In the upper range of samples with 200,000 cells/L or more,
75% of samples are less than 1,000,000 cells/L. The maximum density found was one
sample in Zone G (Whangakoko Bay, on 29/12/97), which was in excess of 6,000,000
cells/L.
Overall, these data indicate that Pseudo-nitzschia species are common throughout
New Zealand waters, and can occur in very high densities. While there are molecular
probes available to distinguish between potentially toxic and non-toxic species of
Pseudo-nitzschia, these are not used as part of the regulatory monitoring programme.
They are however used informally, particularly by the commercial shellfish industry
to determine whether voluntary closures to harvesting should be implemented. Had
these results been recorded on the database, there would have been information
available regarding the occurrence of individual toxic species of Pseudo-nitzschia.
However, studies undertaken by Rhodes et al., (1998a), on the composition of
Pseudo-nitzschia blooms around New Zealand in 1996 using whole cell DNA probes
and immunochemical assays indicated that species assemblages may differ regionally.
The occurrence of Domoic acid in Northland scallops coincided with a bloom
dominated by P. australis, and toxicity in the Bay of Plenty occurred during a bloom
of P. turgidula and P. fraudulenta.
A summary of ASP toxin occurrence in shellfish for all sites, in all zones, from July
1993 to June 1999 is provided in Table 2.8.
Zone
Total No.
of
Samples
A
B
C
D
E
F
G
H
I
J
K
2007
879
1698
2285
743
1276
5069
591
1418
714
215
Table 2.8:
Number of
samples in
which ASP
was
detected
294
78
53
262
12
11
172
3
30
16
2
Percentage
of samples
in which
ASP was
detected
14.6
8.9
3.1
11.5
1.6
0.9
3.4
0.5
2.1
2.2
0.9
No. of
samples
above the
regulatory
level
33
0
0
1
1
0
1
0
0
0
0
Percentage
of samples
above the
regulatory
level
1.64
0.00
0.00
0.04
0.13
0.00
0.02
0.00
0.00
0.00
0.00
Maximum
toxin level
(µg/g)
600
72
22
187
Summary by zone of the total occurrence of ASP toxins detected in
shellfish samples, and ASP toxins above the regulatory level of 20
µg/g detected in shellfish samples from 1/7/93 to 30/6/99.
These results indicate that ASP toxin has been detected in all zones. However,
samples above the regulatory level have occurred in only Zones A, D, E, and G. They
occurred as comparatively low percentages of the total samples tested – in Zones D, E
and G there was only one sample each above the regulatory level out of all the
samples tested. In Zone E, this sample was only just above the regulatory level (2
µg/g of Domoic acid above the regulatory level of 20 µg/g). However, the samples
from the other zones were significantly higher – particularly from Zone A, which had
a maximum Domoic acid level of 600 µg/g (a scallop sample from Doubtless Bay on
53
28/11/94). Closer examination of the data and questioning of ESR revealed that this
sample was the gut portion of the scallop (P. Truman, ESR, pers. comm.) – a sample
of whole scallops from the same site on the same day had a level of 136 µg/g. This
variation between toxin levels in different parts of the scallop may contribute to an
over estimation of the maximum value in Zone A. The maximum level of toxin in
whole scallop samples (as distinct from a portion of shellfish) in Zone A was 210
µg/g from the Cavelli Islands on 2/11/93.
As reported in the previous review of the marine biotoxin monitoring data (Wilson &
Sim, 1996), different anatomical parts of scallops appear to retain different levels of
Domoic acid. This highlights a potential problem with the consistency and accuracy
of reporting of scallop data with respect to parts of the scallop analysed in specific
samples in the early years of the monitoring programme. However, it appears from
the limited amount of data (See Table 2.9) that the highest levels of Domoic acid are
found in the gut and skirt of the scallop (which is the portion that is most commonly
not eaten). Lower levels are found in the roe, and still lower levels in the muscle.
These differences are taken into account in the testing for commercial harvesting, but
to a lesser extent with respect to the non-commercial harvesting of scallops.
Date/Site code
5/11/96/A05A
17/11/96/A05A
28/11/94/A06A
7/12/94/A06A
14/12/94/A06A
14/11/95/A08A
19/11/95/A08A
27/12/95/A08A
Table 2.9:
Domoic acid
level in
sample of
whole
scallops
(µg/g)
136
80
Domoic acid
level in
sample of
scallop guts
and skirt
(µg/g)
600
471
445
Domoic acid
level in
sample of
scallop roe
(µg/g)
Domoic acid
level in sample
of scallop
muscle and roe
(µg/g)
90
60
25
23
26
47
21
29
34
30
10
12
22
21
7
Results of analysis for ASP in whole and portions of scallops
sampled from the same site at the same time.
Table 2.9 tends to suggest that scallop muscle has the lowest levels of Domoic acid
when compared to other parts of the scallop. However on one occasion (19/11/95)
levels in the combined muscle and roe were identical to that found in the roe alone.
Examination of the events in which Domoic acid had been detected at levels above
the regulatory level revealed that most of the samples were scallops from the far north
of New Zealand. We therefore undertook further analysis of the geographical
distribution taking into consideration the potential differences between shellfish
species.
It should be noted that the analysis presented in Table 2.8 did not use standardized
data, and that potential differences in toxin accumulation characteristics between
shellfish, the clumping of sample sites and variations in sampling regimes (both
through time and between sample sites), have been ignored. In an attempt to reduce
some of this bias, a similar analysis was carried out using data from a single species
only, from sites that had been consistently monitored over the whole time period, as
54
described in Section 2.2.7. Because they were the most widely sampled species, with
consistent year-round sampling, GreenshellTM mussels were chosen as the sample
species. The data were standardized to account for the changes in the shellfish
sampling programme since the introduction of phytoplankton sampling, as described
in Section 2.2.7.
Table 2.10 provides a summary of ASP occurrence in GreenshellTM mussels by zone
from July 1995 to the end of June 1999. The scope of the data is less than that in
Table 2.8 as GreenshellTM mussels had only been consistently monitored at sites in
Zones C, D, G, H and I over that time period. No data were available from the other
zones. This summary suggests that the occurrence of Domoic acid in GreenshellTM
mussels in Zone D was higher than in the other zones. No samples of GreenshellTM
mussels above the regulatory level were found over this period.
Zone
C
D
G
H
I
Table 2.10:
Zone
A
C
D
F
Table 2.11:
Total No. of
Samples
816
179
2480
396
205
with ASP above
Detectable Levels (%)
0.3
14.0
0.0
0.0
2.9
with ASP above the
0.0
0.0
0.0
0.0
0.0
Summary by zone of occurrence of ASP toxins in GreenshellTM
30/6/99.
Total No. of
Samples
129
136
508
245
with ASP above
Detectable Levels (%)
74.4
8.1
26.6
2.5
with ASP above the
7.75
0.00
0.00
0.00
Summary, by zone, of occurrence of ASP toxins in scallops from
sample sites consistently monitored over the same time period each
year (beginning of July to end of January, excluding February to
June each year) from 1/794 to 31/1/99.
Table 2.11 presents a similar summary of the occurrence of Domoic acid in scallops
from sites that had been consistently monitored over the same months each year for
the years 1994-1999. Since scallops are only monitored seasonally when the scallop
harvesting season is open, a time period when the maximum of scallop sample sites
were regularly monitored each year was identified for this analysis. This period was
for seven months each year, from the 1st of July one year, through to the 31st of
January the following year, beginning July 1994, and finishing January 1999. Only 8
sites from 4 zones (Zones A, C, D and F) had consistent data for this period over all
years.
The summary presented in Table 2.11 shows that scallops in Zone A had a higher
number of samples in which Domoic acid was detected over this period. Zone A was
55
the only zone of the four that had samples with Domoic acid levels above the
regulatory level of 20 µg/g.
The results presented in Tables 2.10 and 2.11 suggest that the differences between
zones in total occurrence of Domoic acid (Table 2.8) in shellfish may not merely be
due to the varying species composition of shellfish samples taken in each zone, as
results for the same shellfish species were highly variable between zones. The factors
influencing blooms of potentially toxic Pseudo-nitzschia species and the production
of Domoic acid appear complex and are not well understood. Overseas studies have
shown that toxin production may be linked to the balance of nitrogen and silicate in
the water (Bates et al., 1998). Toxin production has been observed when pulses of
nitrate (for example due to run-off from rainfall after prolonged dry periods) occur
when silicates are limiting growth. There has also been speculation that human
activities, such as marine farming, may cause changes in the nutrient levels that
promote Domoic acid production. There has recently been some lively discussion on
the “Phycotoxins List” (phycotoxins@lists.listquest.com) debating this issue with
respect to a long-running ASP event in Scotland. To date, no studies have been
undertaken relating Domoic acid production to environmental factors in New Zealand.
However, an environmental study being undertaken by shellfish farmers in the
Marlborough Sounds (Zone G), Coromandel and the Mahurangi Harbour (Zone C)
could provide data for the basis of such a study.
Given that there is potential for the accumulation of ASP to differ between species,
provides a summary of the occurrence of ASP in the major shellfish species sampled
in the marine biotoxin monitoring programme. It should be noted that while there
may be potential for planktivorous fish to accumulate ASP toxins (e.g. Work et al.
1993), there is no record on the FoodNet database of planktivorous fish species in
New Zealand having been tested for ASP.
Species
Total
No. with
detectable
levels of
ASP
Percentage of
samples
above
detectable
level
No. of
samples
above the
regulatory
level
Percentage
above the
regulatory
level
133
29
29
2
790
12
1
9
3
1.57
2.02
1.23
0.44
31.14
0.99
0.11
1.50
1.27
5
0
0
0
41
0
0
0
0
0.06
0.00
0.00
0.00
1.62
0.00
0.00
0.00
0.00
TM
Greenshell
mussel
Blue mussel
Pacific oyster
Dredge oyster
Scallop
Tuatua
Pipi
Cockle
Paua
Table 2.12:
8451
1438
2362
451
2537
1211
928
599
236
Summary of occurrence of ASP toxins in the major shellfish
species sampled in the marine biotoxin monitoring programme
from 1/7/93 to 30/6/99.
56
These data indicate that a higher percentage of scallop samples contained a detectable
level of ASP than other shellfish species sampled, and that scallop samples also had a
greater percentage of ASP levels above the regulatory level of 20 µg/g. However,
these data alone are not sufficient to indicate species differences with respect to
biotoxin accumulation and retention, since the toxin accumulation might be site
specific rather than species specific.
While the data are scarce, several species of shellfish from the same site have been
monitored concurrently and tested for ASP on a few occasions. The most
comprehensive data are summarised in Figures 2.13 and 2.14. Note that in these
figures sample results below the level of detection have been depicted as zero.
1.8
1.6
ASP Level (µg/g)
1.4
1.2
1
Greenshell Mussel
Scallop (Roe)
0.8
0.6
0.4
0.2
8
8
19
/1
0/
9
12
/1
0/
9
8
8
8
5/
10
/9
8
28
/0
9/
9
21
/0
9/
9
14
/0
9/
9
7/
09
/9
8
0
Time
Figure 2.13: Comparison of levels of ASP in Greenshell™ mussels (Perna
canaliculus) and scallop (Pecten novaezelandiae) at Takaka River
(site G07) over a six week period. (Note the scallop samples were
roe only).
57
3
ASP Level ( µg/g)
2.5
2
Greenshell mussel
Scallop (Roe)
1.5
Cockle
1
0.5
0
8 98 98 98 98 98 98 98 98
/9
/
/
/
/
/
/
/
/
09 /09 /09 /09 /10 /10 /10 /10 /11
/
7 14 21 28
5 12 19 26
2
Time
Figure 2.14: Comparison of levels of ASP in Greenshell™ mussels (Perna
canaliculus), scallop (Pecten novaezelandiae), and cockles
(Austrovenus stutchburyi) at Four Fathom Bay (site G87) over a
two month period.
Figures 2.13 and 2.14 identify that at the same site different shellfish species can
accumulate toxin very differently, with scallops tending to accumulate the highest
amounts of ASP. Note that the scallop samples tested were roe only, so based on
previous comparisons of ASP levels between different parts of the scallop (refer to
Table 2.9), the toxin levels in the whole scallops would have been much higher.
Several one-off comparison were made between Domoic acid levels in mussels and
whole scallops:
Sample Site
Cavelli Is. (A08A)
Cavelli Is. (A08A)
Cavelli Is. (A08A)
Rangaunu Bay (A05A)
Rangaunu Bay (A05A)
Rangaunu Bay (A05A)
Table 2.13:
Date
Domoic acid level in
scallop sample (µg/g)
2/11/93
15/11/93
29/11/93
29/9/93
5/10/93
15/11/93
210
48.6
44.6
8.6
16.2
11.7
Domoic acid level
in GreenshellTM
mussel sample
(µg/g)
11.4
4.0
4.8
0
0
2.0
Comparison of Domoic acid levels in scallop (Pecten
novaezelandiae) and mussel (Perna canaliculus) samples taken
concurrently from the same sites.
The data in Table 2.13 also suggest that there may be differences in toxicity levels
between species at the same site. In the three sets of samples from the Cavelli Islands,
the toxin levels in all the mussel samples were below the regulatory level of 20 µg/g,
while all three scallop samples had toxin levels significantly above this level.
58
Unfortunately none of these comparisons have sufficient data to allow any rigorous
quantitative analysis. It should be noted that while sample results are recorded as
having been taken from the same site, it is uncertain how closely the samples were
actually sited. With the limited data available to date it is not possible to comment on
the possible differences in toxin retention time between species.
The results of this analysis are not in any way definitive, and much more data
collection would be required to investigate this further. The differences may be due to
physiological differences between species, or environmental differences. However,
these results do suggest that differences between species in ASP toxin accumulation
have the potential to impact significantly on the risk of ASP to consumers, and that
these differences should be taken into consideration in the design of the marine
biotoxin monitoring programme.
2.5.2
The results of phytoplankton monitoring for Pseudo-nitzschia species from three sites
in the Hauraki Gulf (from January 1995 to July 1999), 25 sites in the Marlborough
Sounds and Port Underwood (from January 1995 to July 1999) and one site at
Collingwood (from August 1996 to July 1999) are presented in Appendix IV(B). (A
map showing the sites in the Marlborough Sounds is presented in Appendix IV(A)).
Sites in the Marlborough Sounds (Zone G) tended to have a greater range of cell
densities of Pseudo-nitzschia sp. than those sites from the Hauraki Gulf area
(Appendix IV(B)). An easy comparison can be made by comparing the number of
cases at each site where Pseudo-nitzschia levels were above 200 000 cells/L. Only 2
instances above this level were recorded in the Hauraki Gulf sites, one from the
Tamaki Strait on the 14 August 1995, and one at Kopake on the 21 January 1997 (see
Appendix IV(B), 1).). In comparison, over the same time period (January 1995-1
July, 1999), the Marlborough Sounds sites commonly consisted of periods above this
arbitrary level. At the Hauraki Gulf sites no clear seasonal trends were apparent
between years. However, some seasonality was apparent in the Marlborough Sounds
area (see Appendix IV(B), 2).).
Both Kenepuru Entrance (G08) and Schnapper Point (G35) showed increased levels
of Pseudo-nitzschia (generally >100,000 cells/L) between August and September each
year. Little Nikau Bay (G44), Nikau Bay (G36), Nydia Bay (G09), and Southeast
Bay (G38) all showed increased levels (>100,000 cells/L) in March/April of all years
except 1999, as well as an increase in cell density (>100 000 cells/L) in August and
September, similar to that mentioned for the previous site grouping.
Crail Bay (G15), Laverique Bay (G37), West Beatrix Bay(G31), and Brightlands
Bay(G27) did not show any consistent seasonal patterns over the period of interest.
The period from October 1995 to early January 1997 was defined by consistently
lower numbers of Pseudo-nitzschia sp. at all sites, when compared to the long term
data series.
Hallam Cove (G10), Richmond Bay (G28), Waitata Bay (G26), Ketu Bay (G41) and
Cannon Bay (G16) did not show any consistent seasonal patterns over the period of
interest. As described for the Crail Bay group, the period from October 1995 to early
59
January 1997 was defined by consistently lower numbers of Pseudo-nitzschia sp. at
all sites, when compared to the long term data series.
Forsyth Bay (G39), Anakoha Bay (G17), Puketea Bay (G18) and Oyster Bay (G13)
did not show any consistent seasonal patterns over the period of interest. However, at
Forsyth Bay increases in cell density were apparent seasonally from December to
January in every year except 1995. Pseudo-nitzschia sp. density for these sites
reached exceedingly high levels of up to 1,560,000 cells/L.
East Bay (G19), Horohora Bay (G12), Whangakoko Bay (G11) and Opihi Bay (G40)
appeared to have a consistently high density (> 100,000 cells/L) of Pseudo-nitzschia
sp. over most of the yearly cycle. However very low densities were consistently
recorded in the months of June and July of all years studied. Pseudo-nitzschia sp.
density for these sites reached high levels of up to 2,430,000 cells/L.
Samples from Collingwood Farms in Golden Bay (monitoring began in August 1996)
did show increased density in September/October of each year sampled.
Phytoplankton monitoring data on the FoodNet database has been recorded for an
insufficient period for a meaningful analysis of temporal patterns in other zones.
The seasonality of ASP toxin occurrence in shellfish was analysed using data from
30/6/99 as described in Section 2.2.7. (This excluded data from sampling of scallops,
which are only monitored during the scallop harvesting season). This analysis is
based on the incidence of ASP toxins above the level of detection in shellfish, for
each zone, because the incidence of ASP toxins above regulatory levels was low
(implying a relatively low risk to consumers). The data were standardized to take into
account differences in the number of sites per zone. Data from 48 sites were included
in the analysis. Fourteen of these sites were in Zone G. There were no consistently
monitored sites in Zone K (Chatham Islands) over this time period.
The risk of ASP to consumers is related to both the occurrence of ASP events, and the
duration of retention of toxins in shellfish. As depicted in Figure 2.15, there appears
to be a possible broad seasonal pattern with increased risk of ASP to consumers of
shellfish from mid winter (August) to mid summer (December). This contrasts with
seasonal patterns in North America, where blooms of Pseudo-nitzschia tend to occur
predominantly in the late summer and autumn (Bates et al., 1998).
60
Cumulative No. of ASP
4.00
3.00
2.00
1.00
0.00
Jan Feb Mar
Apr May Jun
Jul
Aug Sept Oct
Nov Dec
Month
Zone A
Zone H
Zone B
Zone I
Zone C
Zone J
Zone D
Zone E
Zone F
Zone G
Figure 2.15: The six-year cumulative incidence of ASP toxins above the level of
detection at sites within each zone by month, recorded from 1st
July 1995 to 30th June 1999. The data have been standardized to
account for differences in the number of sites per zone.
ASP Level (µg/g)
35
30
25
20
15
10
5
0
5
7
6
8
9
7
5
6
5
7
6
8
8
r-9 ug-9 ec-9 pr-9 ug-9 ec-9 pr-9 ug-9 ec-9 pr-9 ug-9 ec-9 pr-9
Ap
A
A
A
A
A
A
D
D
A
D
A
D
Time
Zone A
Zone B
Zone C
Zone D
Zone G
Zone I
Zone J
Figure 2.16: Distribution of detectable levels of ASP toxin, in shellfish from
consistently monitored sites from April 1995 to April 1999.
Using the same set of data, the variation in ASP toxin occurrence from year to year
was investigated, as described in Section 2.2.7. The temporal distribution of ASP
sampled sites is presented in Figure 2.16. This figure shows that the frequency of
occurrence of detectable levels of ASP in shellfish from each zone may vary from
year to year. However, Zone A appeared to have the most consistent seasonal pattern
with detectable levels of ASP toxin between August and December of all years
analysed. Overseas studies suggest that different species of Pseudo-nitzschia bloom
in different environmental conditions, resulting in seasonal differences in abundance
61
of individual species (Bates et al., 1998). There have been no studies on the dynamics
of Pseudo-nitzschia blooms in New Zealand.
The overall occurrence of Domoic acid in shellfish across all zones also varies from
year to year. A summary of the broad El Nino/La Nina climate patterns is presented
in Appendix III. There appears to be no obvious correlation between the occurrence
of ASP toxins (either across New Zealand as a whole, or within zones) with these
broad climate patterns. For example, the most intensive periods of detectable levels
of ASP have been from August to December in 1996 and 1998. In August/September
1996, La Nina conditions prevailed, turning to El Nino from October 1996 through to
June 1998. From July 1998, the conditions were once again typical of La Nina.
While environmental conditions no doubt do impact on the occurrence of blooms of
Pseudo-nitzschia, the relationship is not so simple as to allow prediction of risk by
such broad climate patterns. At this early stage, it is not possible to tell whether the
pattern of increased incidence of detectable levels of ASP in the months of August to
December indicates a long-term temporal trend.
2.5.3
Phytoplankton Monitoring as a Predictor of ASP in Shellfish
The ability of phytoplankton counts to reliably indicate the potential presence of
Domoic acid above the regulatory level could not be rigorously investigated due to the
paucity of phytoplankton monitoring data – there was only one instance recorded at
this level in the time period for which phytoplankton data were available. (Most high
levels of ASP occur in scallops, and in general there is no phytoplankton monitoring
on scallop beds). The relationships between levels of Pseudo-nitzschia species in the
water, and two ranges of toxicity in shellfish (<1 µg DA/g shellfish tissue and 1-19.9
µg DA/g shellfish tissue) were therefore investigated. Because levels of toxin are
greatest in the stationary phase of a Pseudo-nitzschia bloom, and shellfish toxicity
may not occur until after this, Pseudo-nitzschia numbers were examined in
phytoplankton for up to three weeks prior to the date of the shellfish sample.
There was one instance of Domoic acid in shellfish above the regulatory level of 20
µg/g – this was a level of 187 µg/g in a sample of GreenshellTM mussels from
Kenepuru Entrance (Zone G, Marlborough Sounds) on 20/12/94. None of the levels
of Pseudo-nitzschia species in the phytoplankton samples either concurrent with the
shellfish sample, or in any of the four preceding weeks exceeded the level to trigger
shellfish testing at this site. (The maximum level recorded in this time was 27,300
cells/L). However, very high numbers of Pseudo-nitzschia species were recorded at
many other sample sites in the Marlborough Sounds over this period, with no
associated shellfish toxicity. It is likely that this particular phytoplankton sampling
site does not provide a good indication of the toxin status of the shellfish present, as it
is positioned in a current from the outer Sounds. This may increase the temporal
variation of phytoplankton populations at the site.
In 97.5% of the events in which trace levels of Domoic acid occurred in shellfish
(N=41), Pseudo-nitzschia species were present in the phytoplankton samples either
concurrently with the shellfish sample, or up to three weeks prior to the shellfish
sample.
62
With levels of Domoic acid between 1.0 - 19.9 µg DA/g shellfish tissue, 100% of the
events coincided with the presence of Pseudo-nitzschia species in phytoplankton
samples (N=14) either concurrently with the shellfish sample or up to three weeks
prior to the shellfish sample.
Because the species of Pseudo-nitzschia present in the phytoplankton samples are not
reported individually, and different species (and strains within species) differ in
toxicity, it is not possible to meaningfully investigate the relationship between
numbers of Pseudo-nitzschia cells and toxin levels in shellfish using the data available
from the FoodNet database. Analysis is further complicated by the lack of
independence of the variables, since levels of Pseudo-nitzschia species in excess of
50,000 cells/L may trigger shellfish sampling. This becomes significant if
quantitatively analyzing events based on the incidence of any level of shellfish
toxicity, resulting in the necessity to distinguish between routine shellfish samples and
shellfish samples triggered by phytoplankton levels.
It is pertinent to comment however, that in the data analysis it was noted that some
levels of Pseudo-nitzschia species associated with trace levels of toxicity in shellfish
were very low: in four instances Pseudo-nitzschia counts were less than 1,000 cells/L.
However, Pseudo-nitzschia species occur commonly as a component of the
phytoplankton in many areas, and thus these trace levels may be residual toxin levels
arising from low numbers of toxic species.
From the data available, it is not possible to conclude whether the levels of cell counts
that trigger shellfish sampling in the marine biotoxin monitoring programme are
appropriate for New Zealand Pseudo-nitzschia species, or whether phytoplankton
monitoring is a robust proxy indicator of the presence of Domoic acid in shellfish.
The data certainly suggest that phytoplankton monitoring may not always predict
significant levels of Domoic acid in shellfish. However, the sample sizes are very
small, and further data are required for a robust analysis.
2.5.4
The Use of Whole Cell DNA Probes for Pseudo-nitzschia Species as a
Predictor of Risk of Shellfish Toxicity
At the request of the Ministry of Health, the effectiveness of the use of whole cell
DNA probes as an indicator of the risk of ASP toxicity in shellfish, was investigated.
Whole cell DNA probes have been developed by Cawthron Institute, as a means of
easily identifying species of Pseudo-nitzschia. These probes (commonly referred to
as “gene probes”) are used by the shellfish industry in the event of Pseudo-nitzschia
numbers high enough to trigger a voluntary closure, to determine whether a voluntary
closure should be implemented pending shellfish test results. The probes also appear
to have been used in the non-commercial monitoring programme in deciding whether
shellfish samples in addition to routine samples should be taken for toxin testing when
Pseudo-nitzschia numbers reach trigger levels. The probes distinguish Pseudonitzschia australis, P. fraudulenta, P. multiseries, P. delicatissima, P. pungens, P.
heimii, and P. pseudodelicatissima. There is some cross-reactivity between the probe
for P. australis (a toxin-producing species), and the non-toxic P. multistriata.
However, these species are easily distinguishable by shape under a light microscope
63
(P. multistriata has a distinctive sigmoid shape). P. delicatissima and P. turgidula are
detected by the same probe, but these species are thought to be identical, with closely
similar toxicity and morphology (L. Rhodes, Cawthron Institute, pers. comm.).
The results of gene probe analyses undertaken for the shellfish industry and Ministry
of Health, and as part of Dr Lesley Rhodes’ doctoral research project, were supplied
to us by Cawthron Institute. These results include only the results of the gene probe
tests, and for the most part, data on total Pseudo-nitzschia numbers and total
phytoplankton numbers for each sample were obtained from the FoodNet database. In
some cases where the phytoplankton samples were not taken as part of the regulatory
monitoring programme, these data were obtained from Cawthron Institute. Upon
requesting information regarding the interpretation of the results of the gene probe
tests, we were initially informed that there was no formal or written protocol for this
(K. Todd, Cawthron Institute, pers. comm.). (Lack of protocols is potentially an area
of concern, as it can lead to inconsistency in the interpretation of test results).
However, Cawthron Institute subsequently provided us with a written protocol for the
interpretation of gene probe results, and the guidelines from this protocol have been
used in our analysis. (These guidelines are outlined in Table 2.14). It should be noted
that our analysis is based on advice from results of gene probe tests that would be
given based on these stated protocols, and has not examined the actual advice given to
industry or Ministry of Health at the time the tests were done.
Species of Pseudonitzschia
P. australis, P. pungens and
P. multiseries
P. delicatissima and P.
pseudodelicatissima
P. fraudulenta
P. heimii and
P. multistriata
Table 2.14
Risk Assessment Guidelines
Trigger flesh testing when the combined cell density is greater
than 50, 000 cells/L
Trigger flesh testing at 100, 000 cells/L when they comprise >
50% of the total phytoplankton biomass
Trigger flesh testing at 250, 000 cells/L when they comprise <
Trigger flesh testing at 500, 000 cells/L when they comprise <
Trigger flesh testing at 1, 000, 000 cells/L when they
comprise < 50% of the total phytoplankton biomass
Risk assessment guidelines for toxin flesh testing in shellfish, for
various species of the genus Pseudo-nitzschia.
In our analysis, a total of 171 phytoplankton samples from September 1997 to June
1999 were examined to investigate the use of whole cell gene probes in differentiating
potentially toxic or non-toxic species of the Pseudo-nitzschia genus as a predictor of
the risk of shellfish toxicity.
Density estimates of each Pseudo-nitzschia species identified by the whole cell gene
probes were matched to concurrent and subsequent shellfish toxin testing results, to
identify the relationships between risk assessment guideline trigger levels and
subsequent detection of Domoic acid in shellfish tissue. Because the peak in Domoic
acid found in shellfish tissue may not coincide with the peak Pseudo-nitzschia density
64
in phytoplankton samples (because Domoic acid may be released as the bloom
crashes), shellfish samples for 2 weeks after each phytoplankton sample was collected
were included in our analysis.
Over all the instances in which whole cell gene probes had been applied to
phytoplankton samples, there were no instances of shellfish toxin tissue testing over
the regulatory level of 20 µg Domoic acid/g shellfish tissue. This is unfortunate, as in
order to conclusively validate the method we need to be sure that the risk of
significant shellfish toxicity would be predicted by the results of the gene probe tests
and the accompanying protocols for interpretation of results. Consequently, no
conclusive inference can be made about the effectiveness of whole cell gene probes in
identifying species composition, and consequently risk assessment at this level. All
analysis is based on extremely low trace levels of Domoic acid in shellfish.
Had shellfish toxicity been measured weekly for three weeks after each gene probe
test, the total shellfish sample data would have equated to 513 shellfish tests for the
171 phytoplankton samples investigated (i.e. 171 x 3, one test in the initial week of
the phytoplankton sample and 2 follow up samples in subsequent weeks). Complete
coverage by shellfish toxin testing was not obtained, with 119 (70%) shellfish toxin
tests undertaken in the week the initial phytoplankton sample was obtained, and 101
(59%) and 106 (62%) in the second and third weeks respectively. This lack of
comprehensive coverage of follow up in shellfish toxin testing reduces the robustness
of assessment of the gene probe test and the current risk assessment guidelines for
Pseudo-nitzschia sp. in relation to subsequent Domoic acid accumulation in shellfish
tissue.
The results of the gene probe tests for Pseudo-nitzschia species, and corresponding
results from shellfish toxicity testing are presented in Appendix V. In this analysis
0.5 µg Domoic acid/g shellfish tissue indicates a trace level of Domoic acid only.
Note also that no data are provided for P. multistriata, which is a non-toxic species.
In five cases (3%), cell densities of Pseudo-nitzschia sp. above the risk assessment
guidelines, as identified by whole cell probes, were related to trace levels (0.5 µg/g)
of Domoic acid in shellfish toxin tissue testing (see Table 1, Appendix V). In only
one case (at Blueskin Bay, 4 Feb 1998) was the level of Domoic acid significantly
higher than this, but still well below the regulatory level of 20 µg Domoic acid/g
shellfish tissue.
In 8 cases (5%) the cell densities for Pseudo-nitzschia sp. were below the risk
assessment guidelines, as identified by whole cell probes, but were still associated
with trace levels of Domoic acid in shellfish toxin tissue testing (see Table 2,
Appendix V). This may simply be due to the breakdown of Domoic acid from
previously declining blooms, which is almost certainly the case for site A08
(Whangaroa), where trace levels of Domoic acid were apparent from August 1998
continuously through until the sample analysed there in early November. Similarly
for site G19, (East Bay), where trace levels of Domoic acid were apparent from
August 1998 continuously through until the sample analysed there in late September,
and G01 (Collingwood), where a trace was detected a week prior to the phytoplankton
levels measured on the 28th September 1998. For the other sites outlined in Table 3,
there are no trace levels apparent in previous shellfish toxin tissue testing samples.
65
Interestingly the samples from A03 (Houhora) and the samples from B14 (Marsden
Point) are comprised of 100% P. heimii, which may suggest extremely low levels of
toxicity below the risk assessment guidelines in this species. The trace level found at
Kennedy Bay (D06, 31/8/98) cannot be currently explained.
From the total samples tested, there were 41 cases for which the whole cell gene
probe data indicated phytoplankton densities above the risk assessment guidelines, but
for which no corresponding toxicity was found in shellfish toxin tissue testing (Table
3, Appendix V). Of these samples, 24 phytoplankton samples (60%) did not have
consistent shellfish toxin tissue testing for the full three-week period after the initial
sample was taken. Because of this, no clear statement can be made about the
relationship between cell density (as identified by the whole cell probe) and possible
shellfish toxicity in these samples as identified by the risk assessment guidelines. Of
the remaining 17 samples, most (70.6%) contained combined numbers of Pseudonitzschia australis, P. pungens, and P. multiseries sufficient to trigger shellfish
toxicity testing (refer to Table 3, Appendix V).
The lack of data relating to the use of whole cell gene probes in events where there
have been significant levels of Domoic acid in shellfish tissue means that definitive
conclusions cannot be drawn about the robustness of the method as an indicator of the
risk of toxicity in shellfish. However, this is a potentially useful tool in biotoxin
monitoring. It is suggested that some effort should be made to collect this information
so that the method can be properly validated.
The succession of Pseudo-nitzschia species within a bloom is of potential interest
with respect to the use of whole cell gene probes, as an indicator of potential toxicity.
There are a few instances when gene probes have been applied to a series of
consecutive weekly samples, providing information about the species composition of
Pseudo-nitzschia within a bloom. Unfortunately, most of these data have been
collected in blooms of comparatively low densities. These data are presented in
Appendix VI. From the small amount of data available, it is apparent that within a
Pseudo-nitzschia species bloom, the dominant species can change over time. Thus, it
cannot be assumed that a bloom that initially appears to be composed of non-toxic
Pseudo-nitzschia species will continue with the same species composition. For this
reason, in the absence of shellfish toxin testing, identification of the species
composition of a bloom should continue at regular intervals.
2.5.5
Conclusions
The following points summarise the conclusions that can be drawn from analysis of
the marine biotoxin monitoring programme regarding the risk of ASP to shellfish
consumers:
•
Pseudo-nitzschia species occur throughout New Zealand, and have been found at
all phytoplankton monitoring sites. They are common components of the
phytoplankton assemblage from all zones. However, the data available do not
distinguish between potentially toxic and non-toxic species of Pseudo-nitzschia.
66
•
Shellfish samples containing ASP above the level of detection are also widespread
throughout New Zealand, and have been found at the majority of sampling sites.
The distribution of ASP toxicity does not appear to be limited by latitude or broad
biogeographic patterns.
•
If it can be assumed that the monitoring programme is representative of shellfish
harvesting in New Zealand, the incidence of ASP toxins at a level that represents a
potential risk to consumers has been comparatively low in most areas. Such levels
have been detected in only Zones A (in 1.64% of total samples), D (0.04%), E
(0.13%), and G (0.02%).
•
There appears to be a possible broad seasonal pattern in the occurrence of Domoic
acid in shellfish, with increased risk of ASP to consumers of shellfish from midwinter (August) to mid-summer (December).
•
The frequency of Domoic acid above the level of detection in shellfish may vary
from year to year, within zones and across all zones. Zone A appeared to have the
most consistent seasonal pattern, with detectable levels of ASP toxin between
August and December each year. However, there are insufficient data for
predictions about future occurrence to be made.
•
The distribution of Domoic acid throughout shellfish organs and tissues is not
uniform, and this impacts on the risk to shellfish consumers. Customary practices
that include the consumption of scallop and paua guts (and possibly whole
planktivorous fish) need to be considered in the design of the monitoring
programme.
•
Limited data were available to investigate the differences in uptake and
accumulation of ASP toxins between different species of shellfish, and further
data are required for rigorous analysis. However, initial observations suggest that
inter-specific differences between shellfish, whether arising from physiological or
environmental causes, have the potential to impact significantly on the risk of ASP
to consumers.
•
Limited data were available to investigate the robustness of the use of whole cell
DNA probes in determining the risk of ASP toxins in shellfish, so no definitive
conclusions could be drawn. It is suggested that this should be investigated
further so this potentially useful method can be properly validated. The possibility
that the dominant Pseudo-nitzschia species within a Pseudo-nitzschia bloom may
change suggests that if reliance were to be placed on gene probes as an indicator
of risk, they should be applied regularly through the course of a bloom.
67
2.6
RESULTS OF ANALYSIS – DSP
2.6.1
The distributions of the causative agents of DSP, Dinophysis species and
Prorocentrum lima, in New Zealand are shown in Figures 2.17 and 2.18 respectively.
These data are drawn from the phytoplankton monitoring data on FoodNet, as
described in Section 2.2.3. Figure 2.17 indicates that both Dinophysis acuta and D.
acuminata have been found at most sites throughout New Zealand. Prorocentrum
lima appears to be less widely distributed. However, it is an epibenthic phytoplankton
that is normally found associated with sand, sediments and macroalgae.
Consequently, plankton samples taken from the water column are not a good measure
of its abundance, since they may only be suspended in the water column after rough
weather. It is thus likely that the distribution of Prorocentrum lima is wider than as
recorded in the phytoplankton monitoring database. It is certainly common in the
Hauraki Gulf (B. Hay, pers. obs.) and has also been recorded in the Marlborough
Sounds from phytoplankton samples (Marlborough Sounds Shellfish Quality
Assurance Programme database of phytoplankton monitoring results), and Cable Bay
(Nelson) and Stewart Island (L. Rhodes, Cawthron Institute, pers. comm.).
Figure 2.19 shows the sites throughout New Zealand where DSP toxins above the
regulatory level, and above the level of detection, have been found in shellfish tested
in the marine biotoxin monitoring programme (Refer to Section 2.2.7 for details of the
method of analysis used). While there are many sites where DSP has not been
detected, the sites where DSP has occurred are widely distributed, and are not limited
by latitude. DSP has occurred at sites on both the eastern and western coasts.
None of these figures provide quantitative information about the frequency of
occurrence of DSP-producing phytoplankton, or DSP in shellfish samples. However,
it can be seen that DSP-producing phytoplankton are found throughout New Zealand.
DSP toxins have been recorded in shellfish at sites from both eastern and western
coasts and do not appear to be limited by latitude.
Table 2.15 shows the occurrence, and levels above regulatory limits, of potentially
toxic Dinophysis acuminata by Biotoxin Zone in New Zealand, as described in
Section 2.2.3. Table 2.16 shows the same data for Dinophysis acuta. (Note that there
are no phytoplankton monitoring sites in Zones F or K. Note also the differences in
the regulatory levels between the two species due to differences in toxicity). These
tables summarise the results of analysis of two sets of data: the first (“Total Samples”)
is the data set of all the phytoplankton samples recorded on the FoodNet and
Time Interval” (i.e. 19/12/97-25/5/99).
As can be seen from Table 2.15, Dinophysis acuminata occurred in less than 10% of
the total samples in all zones, except Zones E and I. Zone I had the highest
percentage occurrence.
68
Distribution of Dinophysis
Species in New Zealand
Dinophysis acuta detected at 15 out of 26
sites in the Marlborough Sounds.
Dinophysis species detected at all 26
sites.
Dinophysis acuta and
Dinophysis acuminata detected
Dinophysis species but no
Dinophysis acuta
No Dinophysis species detected
Figure 2.17: Distribution of potentially toxic species of Dinophysis throughout
69
Distribution of Prorocentrum
lima.
Prorocentrum lima has not been
detected in routine samples recorded on
FoodNet at any of 26 sites in the
Marlborough Sounds.
Prorocentrum lima
detected at site
No Prorocentrum lima
detected at site
Figure 2.18: Distribution of potentially toxic Prorocentrum lima throughout
70
Distribution of DSP in
New Zealand
shellfish sample sites in the
Marlborough Sounds area. DSP
toxicity above the regulatory level
has been found in shellfish at 1 site.
DSP toxicity in shellfish has been
detected in all but 11 other regularly
monitored sites.
Sites with samples above regulatory
level for DSP
Sites at which DSP has been detected
Frequently sampled sites where DSP
has not been detected
Figure 2.19: Distribution of DSP at shellfish sample sites at two levels (above
the level of detection, and above the regulatory level of 20 µg
DSP/100g shellfish tissue) throughout New Zealand (to June 1999).
71
Zone
Total samples (%).
N=
Percentage of Total
samples with 1,000-1,900
cells/L (%)
Percentage of Total
samples with 2,000
cells/L or more (%)
(%)
N=
with 1,000-1,900 cells/L
(%)
with 2,000 cells/L or more
(%)
Table 2.15:
A
B
C
D
E
G
H
I
J
9.5
4.7
0.7
3.7
12.1
1.34
2.4
18.2
0.0
432
107
583
618
240
6486
82
468
104
0.5
0.0
0.0
0.2
0.0
0.9
0.0
2.4
0.0
0.0
0.0
0.0
0.0
0.0
0.7
0.0
0.4
0.0
8.9
1.3
0.0
3.0
15.8
7.9
2.6
16.8
0.0
304
76
456
532
152
1941
76
304
76
0.0
0.0
0.0
0.2
0.0
1.1
0.0
1.6
0.0
0.0
0.0
0.0
0.0
0.0
0.5
0.0
0.0
0.0
Percentage occurrence of Dinophysis acuminata, and percentage
occurrence above the regulatory levels (1,000–1,900 cells/L, and ≥
2,000 cells/L) in the total samples, and in samples from 19/12/9725/6/99 (the “Identified Time Interval”) by zone.
The data relating to the occurrence of Dinophysis using the total number of samples
on the database are the best information that we have on an individual zone basis.
The quantity of data varies considerably from zone to zone – for example, a full set of
data from the beginning of 1994 through to June 1999 has been included for most
sites in Zone G (from the Marlborough Sounds Shellfish Quality Assurance
Programme database), but most other zones have data only from the end of 1997.
However, in order to compare the relative occurrence of DSP-producing species
between zones, the data relating to the “Identified Time Interval” must be used.
From the analysis of the “Identified Time Interval” data set, it can be seen that
Dinophysis acuminata has occurred in all zones except zones C and J. But in only
three zones: D, G, and I, at levels of ≥ 1,000 cells/L. The data presented indicate that
the zones can be ranked in a descending order of frequency of occurrence of D.
acuminata levels as follows: I, E, A, G, D, H, and B. Prior to the 19/12/97, the only
other zone that contained levels above the regulatory level was Zone A. Zone G was
the only zone to obtain levels high enough for an industry voluntary closure.
However, it must be remembered that this analysis is based on only 17 months of
recorded data, which is a comparatively short time interval.
ranges of data (1,000-1,900 cells/L and ≥ 2,000 cells/L) have been represented
72
Closure Level (>2 000 cells/Litre)
Level (1 000 to 1 900 cells/Litre)
graphically as “Box and Whisker Plots” (where five or more data points exist).
Where there are less than five data points, numbers are simply stated. This analysis is
Dinophysis acuminata
2000
1800
1600
1400
1200
1000
800
N=21
N=5
600
400
200
0
G
Zone
I
10000
8000
6000
4000
2000
N=9
0
G
Zone
Zone D: Above Flesh Testing Trigger Level (1000 cells/L): 1 500
Dinophysis acuminata above the level to trigger shellfish testing
(1,000-1,900 cells/L), and (b) Dinophysis acuminata above the level
to trigger a voluntary closure to commercial harvesting ( ≥ 2,000
cells/L) for Zone G where these levels occurred.
Zone D had only one sample above the level to trigger shellfish testing ( ≥ 1,000
cells/L). The median value of samples in the range to trigger shellfish testing in Zone
G was 1,300 cells/L, with 75% of the samples below 1,400 cells/L, and 95% of the
samples below 1,700 cells/L. The median of the samples in the range to trigger
shellfish testing in Zone I was 1,500 cells/L, with 75% of samples less than 1,550
cells/L, and 95% of the samples below 1,580 cells/L. The median value for samples
above the level to trigger an industry voluntary closure in Zone G was 3,600 cells/L,
with 75% of samples less than 4,200 cells/L and 95% of samples less than 8,120
cells/L. The maximum cell count was 9,400 cells/L (from Opihi Bay on 8/3/99).
73
Zone
A
B
C
D
E
G
H
I
J
4.2
5.6
0.0
1.8
1.7
5.3
3.7
13.1
1.0
432
107
583
618
238
6486
82
466
104
Percentage of Total
cells/L (%)
0.0
0.0
0.0
0.2
0.0
0.4
0.0
1.3
0.0
Percentage of Total
samples with 1,000
cells/L or more (%)
Percentage occurrence
in identified time
interval (%)
N=
Percentage of samples
in the identified time
cells/L (%)
interval with 1,000
cells/L or more (%)
0.0
0.0
0.0
0.0
0.0
0.7
0.0
1.7
0.0
3.3
5.3
0.0
2.1
2.6
1.1
3.9
9.2
0.1
304
76
456
532
152
1941
76
304
76
0.0
0.0
0.0
0.2
0.0
0.3
0.0
0.3
0.0
0.0
0.0
0.0
0.0
0.0
1.0
0.0
1.0
0.0
in Total samples (%).
N=
Table 2.16:
Percentage occurrence of Dinophysis acuta, and percentage
occurrence above the regulatory levels (500-900 cells/L and
≥ 1000cells/L) in total samples and in samples from 19/12/97 to
25/6/99 (the “Identified Time Interval”) by zone.
The occurrence of Dinophysis acuta (Table 2.16) was relatively low: it occurred in
less than 10% of the total samples in all zones except Zone I, where it was present in
13.1% of samples. D. acuta did not occur at all in Zone C over the time period for
which we have data. Table 2.16 identified that D. acuta in excess of the levels to
trigger shellfish testing ( ≥ 500 cells/L), occurred in only three zones: Zones D, G, and
I. Only Zones G and I had samples with cell densities above the level to trigger
voluntary industry closure ( ≥ 1,000cells/L). The “Identified Time Interval” data set
showed that Zones G and I had the greatest frequency of occurrence of cell densities
of D. acuta above the regulatory level of 500 cells/L. The data presented indicate that
the zones can be ranked in a descending order of frequency of occurrence of D. acuta
levels as follows: I, B, H, A, E, D, G, J and C.
ranges of data (500-900 cells/L and ≥ 1,000 cells/L) have been represented
graphically as “Box and Whisker Plots” (where five or more data points exist).
Where there are less than five data points, numbers are simply stated. This analysis is
74
800
600
400
N=5
200
0
G
Zone
Closure Level (›1 000 cells/Litre)
Level (500 to 900 cells/Litre)
Dinophysis acuta
1000
Dinophysis acuta
12000
N=20
10000
8000
6000
4000
2000
0
G
Zone
Zone D:
Above Flesh Testing Trigger Level (500 cells/L): 800
Zone I:
Above Flesh Testing Trigger Level (500 cells/L): 500
Above Industry Voluntary Closure Level (1000 cells/L): 1 000,
1 200, 6 700
Dinophysis acuta above the level to trigger shellfish testing (500900 cells/L), and (b) Dinophysis acuta above the level to trigger a
voluntary closure to commercial harvesting ( ≥ 1,000 cells/L). Data
from zones with less than 5 data points is also presented.
Zone D had only one sample above the level to trigger shellfish testing ( ≥ 500
cells/L). The median of the samples in the range to trigger shellfish testing in Zone G
was 600 cells/L, with 75% of the samples below 700 cells/L, and 95% of the samples
below 780 cells/L. Zone I had only one sample above the level to trigger shellfish
testing ( ≥ 500 cells/L). The median value for samples above the level to trigger an
industry voluntary closure in Zone G was 3,400 cells/L, with 75% of samples less
than 4,800 cells/L and 95% of samples less than 7,340 cells/L. The maximum cell
count from Zone G was 10,000 cells/L (from Wedge Point on 8/12/98). Zone I also
contained 3 counts above the industry voluntary closure level, with the highest count
reaching 6,700 cells/L (from Caroline Bay, on 3/5/99).
75
Zone
A
B
C
D
E
G
H
I
J
0.5
0.0
0.0
0.2
0.4
0.1
0.0
0.4
0.0
432
107
583
618
240
6486
82
468
104
Percentage of Total
cells/L (%)
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
Percentage of Total
samples with 1,000
cells/L or more (%)
in identified time
interval (%)
N=
cells/L (%)
interval with 1,000
cells/L or more (%)
0.5
0.0
0.0
0.0
0.0
0.0
0.0
0.2
0.0
0.0
0.0
0.0
0.2
0.0
0.0
0.0
0.3
0.0
304
76
456
532
152
1941
76
304
76
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.3
0.0
N=
Table 2.17:
Zone I:
Percentage occurrence of Prorocentrum lima, and percentage
occurrence above the regulatory levels (500-900 cells/L and
≥ 1000cells/L) in total samples, and in samples from 19/12/97 to
25/6/99 by zone.
Above Industry Voluntary Closure Level (1000 cells/L): 1 600
The occurrence of Prorocentrum lima was exceptionally low (Table 2.17). P. lima
only occurred in samples in Zones A, D, E, G, and I. The only incidence of P. lima
being higher than the industry voluntary closure level of 1,000 cells/L was at Akaroa
on the 8/6/98 at 1,600 cells/L.
76
Zone
Total No.
of
Samples
A
B
C
D
E
F
G
H
I
J
K
2113
1009
2085
2111
772
1468
5796
682
1519
817
200
Table 2.18:
Number of
samples in
which DSP
was
detected
32
3
13
3
4
2
137
3
27
5
0
Percentage
of samples
in which
DSP was
detected
1.5
0.3
0.6
0.1
0.5
0.1
2.4
0.4
1.8
0.6
0
No. of
samples
above
regulatory
level
2
0
0
0
1
0
71
0
8
0
0
Percentage
of samples
above
regulatory
level
0.09
0.00
0.00
0.00
0.13
0.00
1.22
0.00
0.53
0.00
0.00
Maximum
toxin
level
(µg/100g)
33
39
96
86
Summary by zone of the total occurrence of DSP toxins detected in
shellfish samples, and DSP toxins above the regulatory level of 20
µg/100g detected in shellfish samples from 1/9/94 to 30/6/99.
“Total No. of Samples” includes all acetone screen tests, plus DSP
ELISA tests done without a prior acetone screen test.
A summary of DSP toxin occurrence in shellfish for all sites, in all zones, from
September 1994 until the end of June 1999 is presented in Table 2.18. The
percentages are calculated as percentages of the total Acetone Screen tests plus the
DSP ELISA’s done without a prior acetone screen, not the total DSP ELISA tests
alone. This full total is used because the Acetone Screen test and the DSP ELISA
together constitute the test for DSP in the Marine Biotoxin Monitoring Programme.
It can be seen that the overall percentage occurrence of detectable levels of DSP was
relatively low, and that there were only four zones in which levels of DSP above the
regulatory level of 20 µg/100g have been detected: Zones A, E, G and I. Most of the
DSP detected in Zone G was from one site, Wedge Point (G23) in the Marlborough
Sounds. Blue mussels at this site contained persistent levels of DSP from November
1994-August 1995, November 1995 to July 1996, and October 1996 to March 1997.
The DSP in Zone I was also predominantly from one site, Akaroa Harbour (I04),
where shellfish toxicity persisted from February 1995 to October 1995. The shellfish
species sampled at this site were also Blue mussels. It is interesting to note that both
these long-running events occurred in relatively protected waters. Blooms of
Dinophysis species in Europe have been associated with persistent stratification over
summer, fed with nutrients from upwelling pulses (Reguera et al., 1993; Palma et al.,
1998). We are uncertain as to the influence of these factors in the New Zealand
events.
It should be noted that the analysis of data presented in Table 2.18 did not use
standardized data, and that differences in toxin accumulation characteristics between
shellfish species, the clumping of sample sites, and variations in sampling regimes,
both through time and between sample sites, have been ignored. In an attempt to
reduce some of this bias, a similar analysis was carried out using data from a single
species, from sites that had been consistently monitored over the whole time period,
77
as described in Section 2.2.7. Because they were the most widely sampled species,
Greenshell™ mussels were chosen as the sample species. The data were standardized
to cope with the changes in the shellfish sampling programme since the introduction
of phytoplankton sampling, as described in Section 2.2.7.
Table 2.19 provides a summary of the DSP toxin occurrence in Greenshell™ mussels,
by zone, from September 1994 to the end of June 1999. The scope of the data is less
than that in the previous table as Greenshell™ mussels had only been consistently
monitored at sites in Zones C, D, G, H, and I over that time period. No data were
available from the other zones. None of the Greenshell™ mussel samples had levels
of DSP above the regulatory level. The percentage of samples with DSP above the
level of detection was low. The greatest percentage occurrence was in Zone I.
Zone
Total No. of
Samples
C
D
G
H
I
816
179
2480
396
205
Percentage of
Samples with DSP
above Detectable
Levels (%)
0.5
0.0
0.4
0.3
1.0
with DSP above the
Regulatory Level
0.0
0.0
0.0
0.0
0.0
Table 2.19:
Summary by zone of occurrence of DSP toxins in Greenshell™
30/6/99.
Given that there is potential for the accumulation of DSP to differ between species,
provides a summary of the occurrence of DSP in the major shellfish species sampled
in the marine biotoxin monitoring programme from 1/9/94 to 30/6/99.
Species
Total
(Acetone
Screen
tests)
No. with
detectable
levels of
DSP by
ELISA
Percentage of
samples
above
detectable
level
No. of
samples
above the
regulatory
level
Percentage
above the
regulatory
level
8670
1403
2332
412
1958
1220
1202
503
296
18
127
15
3
0
5
2
0
5
0.21
9.05
0.64
0.73
0.00
0.41
0.17
0.00
1.69
1
77
2
0
0
0
0
0
1
0.01
5.49
0.09
0.00
0.00
0.00
0.00
0.00
0.34
TM
Greenshell
mussel
Blue mussel
Pacific oyster
Dredge oyster
Scallop
Tuatua
Pipi
Cockle
Paua
Table 2.20:
Summary of occurrence of DSP toxins in the major shellfish
species sampled in the marine biotoxin monitoring programme
from 1/9/94 to 30/6/99.
This summary indicates that a higher percentage of Blue mussel samples contained
detectable levels of DSP than any other shellfish species sampled, and that Blue
78
mussels also had a greater percentage of DSP levels above the regulatory level of 20
µg/100g shellfish tissue. Greenshell™ mussels, Pacific oysters and paua (that is,
whole paua including the gut) also included samples with levels of DSP above the
regulatory level.
The data in Table 2.20 are not sufficient to indicate species differences with respect to
biotoxin accumulation and retention, since the toxin accumulation could be site
specific rather than species-specific. Unfortunately, the only occasions recorded on
the FoodNet database where different species have been sampled concurrently from
the same site and tested for DSP have been times when no DSP toxins have been
detected in any of the samples. However, a study was undertaken by Lincoln
Mackenzie from the Cawthron Institute in which both GreenshellTM mussels (Perna
canaliculus) and Blue mussels (Mytilus edulis aoteanus) were sampled concurrently
from the same site (Wedge Point, Site G23) during a multi-species dinoflagellate
bloom in the spring of 1996 (Mackenzie et al., 1998b). The predominant species in
the bloom were Dinophysis acuta and Protoceratium reticulatum. Mouse bioassays
using the acetone screen test indicated that both the Blue mussels and the
GreenshellTM mussels contained significant toxin levels. While significant amounts of
Okadaic acid were found in both the Blue mussels and plankton concentrates from
water samples, only trace amounts of Okadaic acid and DTX-1 were detected in the
GreenshellTM mussels. However, HPLC analysis of plankton from the GreenshellTM
mussel gut, and from P. reticulatum cultures from water samples, indicated the
presence of yessotoxin derivatives. This suggested that two different species of
mussel feeding on the same phytoplankton assemblage accumulate different toxins.
The apparent differences in DSP toxin occurrence between Wedge Point and other
adjacent sampling sites in the Marlborough Sounds may be due to differences in the
species of shellfish sampled, rather than toxin occurrence.
The DSP ELISA Check-Kit does not detect DTX-3 or Okadaic acid diol esters. It is
thus possible that the incidence of DSP is under-reported in the data. In addition,
because the marine biotoxin monitoring programme does not incorporate monitoring
for yessotoxin or pectenotoxin, there are no records available regarding the
occurrence of these toxins on the FoodNet database.
2.6.2
The results of phytoplankton monitoring for Dinophysis species from three sites in the
Hauraki Gulf (from January 1995 to July 1999), 25 sites in the Marlborough Sounds
and Port Underwood (from January 1995 to July 1999), and one site at Collingwood
(from August 1996 to July 1999) are presented in Appendix IV(C). (A map showing
the location of sites in the Marlborough Sounds is presented in Appendix IV(A)).
Sites in the Marlborough Sounds (Zone G) tended to have a greater range of cell
densities of Dinophysis sp. than those sites from the Hauraki Gulf area (Appendix
IV(C)). An easy comparison can be made by comparing the number of cases at each
site in which Dinophysis levels were above 1,000 cells/L. Only 3 instances above this
level were recorded in the Hauraki Gulf sites, two from the Tamaki Strait (on the 28
June and the 17 July 1995), and one at Kopake on the 24 August 1995 (see Appendix
IV(C), 1).). In comparison, over the same time period (January 1995-1 July, 1999),
the majority of the Marlborough Sounds sites also had low numbers of counts above
79
this level (see Appendix IV(C), 2).), except for the composite group of sites
encompassing East Bay (G19), Horohora Bay (G12), Whangakoko Bay (G11) and
Opihi Bay (G40), which had consistently high numbers of counts above this level
over the total sampling period. At the Hauraki Gulf sites no clear seasonal trends
were apparent between years. The Marlborough Sounds sites were also largely
characterised by a lack of seasonality in increased cell density of Dinophysis sp.
However, East Bay (G19), Horohora Bay (G12), Whangakoko Bay (G11) and Opihi
Bay (G40) appeared to have a consistently high density (>1,000 cells/L) of
Dinophysis sp. over most of the yearly cycle. Very low densities were consistently
recorded in the months of June to August of all years studied. Dinophysis sp. density
for these sites reached exceedingly high levels of up to 10,600 cells/L.
Other sites to reach comparatively high densities of Dinophysis sp. were Hallam Cove
(G10) with a maximum density of 7,200 cells/L, and Wedge Point (G23) with a
maximum density of 23,400 cells/L.
The 17 months of phytoplankton data recorded on the FoodNet database for other
zones were insufficient for temporal analysis of seasonal patterns.
Cumulative No. of DSP
The seasonality of DSP toxin occurrence in shellfish was analysed using data from
30/6/99 as described in Section 2.2.7. (There were no such sites in Zone K). This
analysis is based on the incidence per zone of DSP toxins above the level of detection
in shellfish. The data were standardized to take into account differences in the
number of sites per zone. Data from 48 sites were included in the analysis. Fourteen
of these sites were in Zone G. While an analysis of DSP toxins above the regulatory
level would perhaps have been more pertinent in terms of measuring risk to shellfish
consumers, there were insufficient instances of such toxin levels within the
standardized data set.
3.00
2.50
2.00
1.50
1.00
0.50
0.00
Jan Feb Mar
Apr May Jun
Jul
Aug Sept Oct
Nov Dec
Month
Zone A
Zone H
Zone B
Zone I
Zone C
Zone J
Zone D
Zone E
Zone F
Zone G
Figure 2.22: The four year cumulative incidence of DSP toxins above the level
of detection at sites within each zone by month, recorded from
1/7/95 to 30/6/99. The data has been standardized to account for
differences in the number of sites per zone.
80
The risk of DSP to consumers is related to both the occurrence of DSP events, and the
duration of retention of toxins in shellfish. As depicted in Figure 2.22 (see previous
page), there appears to be a possible broad seasonal pattern with a slightly decreased
risk of DSP to consumers of shellfish over the winter months.
Using the same set of data, the variation in DSP toxin occurrence from year to year
was investigated, as described in Section 2.2.7. The temporal distribution of DSP
sampled sites is presented in Figure 2.23. This figure shows that the frequency of
occurrence of detectable levels of DSP in shellfish from each zone may vary from
year to year. On a New Zealand-wide basis, the occurrence of toxins also varies from
year to year: for example, overall there were fewer samples containing detectable
levels of DSP from September 1997 to September 1998 than in previous years. A
summary of the broad El Nino/La Nina climate patterns is presented in Appendix III.
There appears to be no obvious relationship between the occurrence of DSP toxins
(either across New Zealand as a whole, or within zones) with these broad climate
patterns.
DSP Level (µg/100g)
120
100
80
60
40
20
0
9
8
7
6
5
8
6
5
99
98
97
96
95
97
94
y-9
y-9 ep-9
y-9
y-9 ep-9
y-9 ep-9
nnnnnppJa
Ja
Ja
Ja
Ja
S
Se
S
S
Se
Ma
Ma
Ma
Ma
Ma
Time
Zone A
Zone B
Zone C
Zone G
Zone H
Zone I
Figure 2.23: Distribution of detectable levels of DSP toxin in shellfish from
consistently monitored sites from September 1994 to May 1999.
2.6.3
Reliability of Acetone Screen
The inability of the DSP ELISA Check Kit to detect DTX-3 and Okadaic acid diol
esters has already been mentioned. However, there are also other discrepancies
between the acetone screen test and the DSP ELISA Check Kit.
There are 349 instances in which a DSP ELISA was undertaken even though the
result of the preceding (or in some cases concurrent) acetone screen test was negative.
81
Of these, there were 50 instances in which the acetone screen test was recorded as a
“Not Detect” but a DSP ELISA produced a positive result.
Normally a DSP ELISA is not undertaken unless the acetone screen test is positive, so
the validity of these results was queried with ESR. Checking by ESR revealed that
some of these anomalies were as a result of misreporting of data (P. Truman, ESR,
pers. comm.). Table 2.21 (see following page) lists the corrected results, based on
investigation by Penny Truman of ESR, who checked the results with the original
laboratory records.
It can be seen from Table 2.21 that there are 33 instances in which the results are
misreported: 32 that were reported as “Not Detected” instead of “Detected”, and one
in which an ELISA test was not undertaken at all, but was reported as “Not Detected”.
There are sixteen instances in which the acetone screen assay was correctly reported
as negative (i.e. a “Not Detect” result), but a DSP ELISA result was positive. This
represents 4.6% of the total tests in which DSP ELISA was undertaken when the
screen test was negative. These positive results range from 10 to 42 µg/100g. A total
of 4 results (1.1% of the total tested by DSP ELISA when the acetone screen was
negative) were over the regulatory limit of 20 µg/100g, and 9 of them (2.6%) were
equal to, or greater than 16 µg/100g.
Investigation by ESR indicated that in two cases, (Site I04, Laboratory Numbers
951438 and 954517), the ELISA test was undertaken because the mice in the acetone
screen assay were very sick at 24 hours (but still alive, so reported as “Not Detected”).
The DSP ELISA found toxin levels of 22 µg/100g and 11µg/100g respectively in
these samples.
Of the remaining thirteen samples, one was from Site C05 (Coromandel), one from
Site D03 (Port Charles), one from Site G10 (Hallam Cove), four from Site I04
(Akaroa Harbour) and eight from Site G23 (Wedge Point). ESR records show that the
mice in the assays of samples from Site I04 exhibited symptoms of some toxin
activity: they became very sick, but subsequently recovered (P. Truman, ESR, pers.
comm.). There is currently no definitive explanation for the anomalous results in any
of these thirteen samples.
These results could suggest one of two things: that the acetone screen test is not 100%
reliable in detecting levels of DSP above the regulatory level, as recorded by the DSP
ELISA Check Kit, or that cross-reactivity in the DSP-ELISA Check Kit can cause
false positives. Inconsistencies in the DSP-ELISA Check Kit have been reported
elsewhere (Cembella et al., 1995a). Whatever the reasons for these discrepancies, the
difference between a negative acetone screen result and a level of 42 µg/100g
measured by the DSP ELISA Check Kit could potentially be significant. This
requires further investigation.
82
SITECODE
DATE
A05
A05A
A08
A08A
A13
A15
A18A
B11
C05
C05
C09
C10
C10
D03
E13
F01
F12
G03
G05
G10
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G23
G31
H03
I04
I04
I04
I04
I04
I04
J16
02/11/94
30/01/95
06/12/94
03/01/95
01/11/94
02/11/94
02/11/94
01/02/95
24/01/95
31/01/95
31/01/95
02/11/94
08/02/95
23/10/95
28/11/94
03/10/94
24/01/95
23/01/95
23/01/95
18/12/95
28/11/94
05/12/94
19/12/94
09/01/95
23/01/95
30/01/95
06/02/95
13/02/95
20/02/95
26/02/95
06/03/95
13/03/95
20/03/95
17/04/95
24/04/95
29/05/95
05/06/95
31/07/95
01/07/96
15/07/96
25/11/97
10/01/95
07/12/94
28/03/95
04/04/95
05/09/95
12/09/95
10/10/95
10/10/95
01/11/94
Table 2.21:
LABNO
946164
950550
946761
950079
946168
946179
946181
950584
950402
950554
950556
946173
950717
954719
946621
945685
950426
950390
950391
955636
946545
946695
946969
950143
950383
950505
950617
950774
950874
950976
951104
951203
951308
951706
951830
952338
952430
953315
962398
962603
972914
950176
946749
951438
951541
953934
954062
954517
954518
946178
SCREEN
DET
DET
DET
DET
DET
DET
DET
DET
DET
NOT DET
DET
DET
DET
NOT DET
DET
DET
DET
DET
DET
NOT DET
DET
DET
DET
DET
DET
DET
DET
DET
NOT DET
DET
DET
DET
DET
NOT DET
NOT DET
NOT DET
NOT DET
NOT DET
NOT DET
NOT DET
DET
DET
NOT DET
NOT DET
DET
NOT DET
NOT DET
NOT DET
DET
ELISA
(µg/100g)
10
12
11
18
11
10
11
11
13
16
10
12
11
11
39
11
12
13
11
12
35
33
32
50
30
44
12
34
17
44
42
39
70
42
26
15
18
22
19
10
19
13
10
22
12
15
17
11
11
11
SPECIES
OYST-P
SCALR
OYST-P
SCALR
OYST-P
OYST-P
PIPI
SCALMR
GMUSS
GMUSS
GMUSS
OYST-P
OYST-P
GMUSS
PAUA-G
TUATUA
OYST-P
SCALMR
SCALMR
GMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
GMUSS
TUATUA
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
BMUSS
GMUSS
The corrected results for the samples recorded in FoodNet as
having negative Acetone Screen test results, but positive DSP
ELISA results. (DET= Detected; NOT DET= Not detected.)
83
2.6.4
Phytoplankton Monitoring as a Predictor of DSP in Shellfish
The phytoplankton monitoring data and shellfish toxin testing data on the FoodNet
database and the Marlborough Sounds Quality Assurance Programme database were
analysed to determine the probability that phytoplankton monitoring would fail to
predict the occurrence of DSP above the regulatory level in shellfish. (Refer to
Section 2.2.4 for methodology). The only shellfish samples where DSP levels
exceeded the regulatory level of 20 µg/100g over a time period for which there are
phytoplankton monitoring data available, were from the long-running toxicity events
in blue mussels at Wedge Point (G23) in the Marlborough Sounds. Over some
periods, the toxin levels varied widely from week to week (for example, range 10-93
µg/100g over 20/11/95-22/7/96) in the absence of any Dinophysis or Prorocentrum
lima species recorded in the phytoplankton. It would have been useful if the variation
within samples had been measured by some replicate sampling during this time, to
determine the extent of the unexplained increases in DSP toxin levels.
There were two instances in which DSP toxin levels rose from zero to above the
regulatory level (as distinct from increasing from long-running residual levels).
Neither of these instances was associated with Dinophysis sp. or Prorocentrum lima
densities above the regulatory level to initiate shellfish testing. Of the three instances
where detectable levels of DSP occurred (in the range 10-12 µg/100g), one was
associated with Dinophysis acuta densities of 2,800 cells/L, one with 400 cells/L of
Dinophysis acuminata, while for the third event, no Dinophysis species or
Prorocentrum lima were recorded.
It should be noted that the current sampling methods used in phytoplankton
monitoring may not be appropriate for detecting densities of Prorocentrum lima that
reflect the exposure of shellfish to this species. Prorocentrum lima (and other species
of epibenthic phytoplankton of potential concern such as Ostreopsis and Coolia
species, that may produce toxins of other kinds) live in close association with
substrata such as seaweed and sediment that may be in proximity to a range of
shellfish species. (Prorocentrum lima has also been found on mussel ropes – L
Rhodes, Cawthron Institute, pers. comm.) As such, they are not generally distributed
through the water column except after turbulent weather, but may be consumed by
shellfish due to their proximity. Their absence in phytoplankton samples taken from
the water column may thus not reflect the exposure of shellfish to potentially toxic
species. This requires further investigation.
Further data are necessary for rigorous investigation of the relationship between the
numbers of potentially toxic phytoplankton and DSP toxicity in shellfish.
84
2.6.5
Conclusions
the marine biotoxin monitoring programme regarding the risk of DSP for shellfish
consumers:
•
Dinophysis species occur widely around the coastline of New Zealand.
Prorocentrum lima occurs less widely in phytoplankton samples taken from the
water column, but has been recorded in both the North and South Islands.
Information from sources other than the marine biotoxin monitoring programme
database suggests that this species is also widely distributed.
•
The incidence of DSP toxicity is also widely distributed, and is not limited by
latitude. Detectable levels of DSP have occurred on both eastern and western
coasts.
•
If it can be assumed that the marine biotoxin monitoring programme is
representative of shellfish harvesting in New Zealand, the incidence of DSP toxins
at a level that represent a risk to consumers has been comparatively low in most
areas.
•
There may be a slightly lower risk of DSP in the winter months.
•
The frequency of DSP occurrence may vary from year to year across the whole of
New Zealand, and between zones within New Zealand. There is insufficient data
for predictions about future occurrence to be made.
•
Based on a very limited amount of data, the relationship between the presence of
species of phytoplankton known to produce DSP toxins and DSP toxicity in
shellfish does not appear to be predictive. More data are required to investigate
this further.
•
The DSP ELISA Check-Kit does not detect DTX-3 or Okadaic acid diol esters. It
is thus possible that the incidence of DSP is under-reported in the data. In
addition, because the marine biotoxin monitoring programme does not incorporate
monitoring for yessotoxin or pectenotoxin, there are no records available
regarding the occurrence of these toxins on the FoodNet database.
•
There are some discrepancies between the performance of the acetone screen test
and the DSP ELISA Check Kit. These would become more significant if the
regulatory level of DSP toxins were lowered from 20 µg/100g to 16 µg/100g.
This requires further investigation.
85
2.7
RESULTS OF ANALYSIS – NSP AND RESPIRATORY IRRITATION
SYNDROME
2.7.1
Introduction
As discussed in the introduction, the causative agents for both NSP and Respiratory
Irritation Syndrome (RIS) are Gymnodinium species and Gyrodinium galatheanum.
The marine biotoxin monitoring programme does not specifically encompass RIS at
present. However, because RIS results from blooms of Gymnodinium species,
components of the monitoring programme do provide an indication of the risk of RIS
also. For this reason, both NSP and RIS are discussed in this section.
The method of testing for NSP using an ether extraction method and mouse bioassay
is not specific for brevetoxins, and may also detect other lipid soluble toxins. The
extent to which other lipid soluble toxins found in New Zealand phytoplankton (such
as, for example, DSP toxins, gymnodimine, and “Wellington Harbour toxin”)
confound the results of the bioassay for NSP is not well understood. While the mouse
death times and symptoms can provide some indication of the presence of unexpected
toxins, these observations provide limited information. To date, such observations
have not been recorded in the database of monitoring results. Some resolution of
results can be obtained by additional testing: for example, by NSP ELISA or
neuroblastoma assays to confirm NSP, by DSP ELISA, and by LC-MS or HPLC.
However, such methods are not used routinely as part of the monitoring programme,
and where they have been undertaken as part of a research programme, the results
have not been recorded on the FoodNet database.
In the absence of results from additional testing, the results of phytoplankton
monitoring could potentially be used to reduce uncertainty about historical NSP
results. However, prior to 1997 there are few phytoplankton data from outside the
Marlborough Sounds or the Hauraki Gulf. There have been no distinctions made
between the various “Gymnodinium mikimotoi” species (refer to Section 1.3.4), and
not all known brevetoxin producers are monitored.
For these reasons, the interpretation of “NSP” results is problematical. It would have
been helpful for risk analysis if any additional information collected about positive
“NSP” results had been recorded on the database.
In this analysis and discussion, “NSP toxins” refer to the group of toxins detected in
the ether extraction mouse bioassay. Where there is evidence that indicates particular
toxin events can be attributed to known toxins other than brevetoxins, this is noted.
2.7.2
The distribution of potentially toxic Gymnodinium species, Gymnodinium c.f. breve
and Gymnodinium c.f. mikimotoi is shown in Figure 2.24. These data are drawn from
the phytoplankton monitoring data on FoodNet, as described in Section 2.2.3.
Because Gyrodinium galatheanum is less than 10 micron in size, no data have been
86
collected through the phytoplankton monitoring programme on the distribution or
abundance of this species (K. Todd, Cawthron Institute, pers. comm.).
This figure does not provide quantitative information about the frequency of
occurrence of potentially toxic phytoplankton. However, it does indicate that the
distribution of potentially toxic Gymnodinium species is widespread around the New
Zealand coastline.
Gymnodinium c.f. mikimotoi has been found at most
phytoplankton monitoring sites in New Zealand. There are many sites where
Gymnodinium c.f. breve has not been found. However, its distribution includes both
the North and South Islands. Unfortunately, there are no phytoplankton data from the
western coast or Chatham Islands to provide additional information in the assessment
of whether or not NSP could potentially occur there.
87
Figure 2.24: Distribution of potentially
throughout New Zealand.
toxic
species
of
Gymnodinium
Distribution of Potentially
Toxic Gymnodinium species
in New Zealand
Gymnodinium mikimotoi detected at
20 out of 26 sites in the Marlborough
Sounds
Gymnodinium cf breve and
Gymnodinium mikimotoi
detected
Gymnodinium mikimotoi
detected
No potentially toxic
Gymnodinium species
detected
88
Table 2.22 outlines the occurrence, and levels above the regulatory limits of
Gymnodinium c.f. breve by Biotoxin Zone in New Zealand, as described in Section
2.2.3. (Note that there are no phytoplankton monitoring sites in Zones F or K). This
table summarizes the results of analysis of two sets of data: the first (“Total Samples”)
is the data set of all the phytoplankton samples recorded on the FoodNet and
Time Interval” (i.e. 19/12/97-25/5/99).
Zone
Total samples (%).
N=
Percentage of Total
samples with 1,000 to
4,900 cells/L (%)
Percentage of Total
samples with 5,000
cells/L or more (%)
(%)
N=
the identified time
interval with 1,000 to
4,900 cells/L (%)
the identified time
interval with 5,000 cells/L
or more (%)
Table 2.22:
A
B
C
D
E
G
H
I
J
0.2
4.7
0.9
1.8
1.2
0.0
0.0
0.0
1.0
436
106
583
621
242
6486
82
466
104
0.0
1.9
0.0
0.2
0.0
0.0
0.0
0.0
0.0
0.0
0.9
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.3
2.6
1.1
2.1
2.0
0.0
0.0
0.0
0.0
304
76
456
532
152
1941
76
304
76
0.0
1.3
0.0
0.2
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
Percentage occurrence of Gymnodinium c.f. breve, and percentage
occurrence above the regulatory levels (1,000 to 4,900 cells/L, and
≥ 5,000 cells/L) in total samples and in samples from 19/12/97 to
25/5/99 (the “Identified Time Interval”) by zone.
Over the entire sampling period only Zones G, H and I have not encountered
Gymnodinium c.f. breve. In the “Identified Time Interval” only Zones B and D have
had samples with levels above the level to trigger shellfish testing (i.e. ≥ 1,000
cells/L). These specific cases are outlined below:
Zone B:
Above Shellfish Testing Trigger Level (1,000 cells/L): 3 000
Zone D:
Above Shellfish Testing Trigger Level (1,000 cells/L): 1 100
89
Over the “Identified Time Interval” no cases above the level to trigger industry
voluntary closure have been recorded for Gymnodinium c.f. breve.
Table 2.23 summarizes the occurrence of Gymnodinium c.f. mikimotoi, (now
identified as three separate potentially toxic species) in two density ranges: 1,0004,900 cells/L, and >5,000 cells/L, as described in Section 2.2.3.
Zone
N=
Percentage of Total
samples with 1,0004,900 cells/L (%)
Percentage of Total
samples with 5,000
cells/L or more (%)
in identified time
interval (%)
N=
interval with 1,0004,900 cells/L (%)
interval with 5,000
cells/L or more (%)
Table 2.23:
A
B
C
D
E
G
H
I
J
6.9
13.9
22.8
6.1
6.6
8.0
23.2
0.9
1.9
436
108
583
621
242
6486
82
466
104
1.1
4.8
4.5
1.0
0.8
2.6
3.7
0.0
0.0
0.2
0.0
0.5
0.0
0.0
0.7
7.3
0.0
0.0
8.9
10.5
22.8
6.4
9.2
16.5
25.0
1.0
2.6
304
76
456
532
152
1941
76
304
76
1.6
1.3
5.0
0.8
1.3
3.9
3.9
0.0
0.0
0.3
0.0
0.7
0.0
0.0
1.8
7.9
0.0
0.0
Percentage occurrence of Gymnodinium c.f. mikimotoi and
percentage occurrence above defined density levels (1,000 to 4,900
cells/L and ≥ 5,000 cells/L) in total samples and in samples from
19/12/97 to 25/5/99 (the “Identified Time Interval”) by zone.
Gymnodinium c.f. mikimotoi appears to have a more uniform distribution around the
New Zealand coastline than G. c.f. breve, being identified within all the sampled
zones (Table 2.23). However over the “Identified Time Interval” G. c.f. mikimotoi
has not occurred above the defined densities in either zones I or J. The zones where it
has been within these ranges can be ranked in descending order of frequency of
occurrence as follows: H, C, G, A, E, B, and D. Zone H appears to have a greater
percentage of samples in the upper density range (>5,000) than any other zone. Note
that the different species that comprise the Gymnodinium c.f. mikimotoi group may
have different distributions. However, because these data have been grouped we have
no way of identifying this from the available information.
90
Gymnodinium c.f. mikimotoi
5000
4000
3000
2000
1000
N=5
N=23
N=76
C
G
0
A
Range of data above 5 000 cells/Litre.
Range of data between 1 000 to 4 900 cells/Litre.
ranges of data (1,000 to 4,900 cells/L and ≥ 5,000 cells/L) have been represented
graphically as “Box and Whisker Plots” (where five or more data points exist), or
where there are less than five data points, numbers are simply stated. This summary
is presented in Figure 2.25.
250x103
N=6
200x103
150x103
100x103
50x103
N=34
0
G
H
Zone
Zone
Zone A:
Above 5 000 cells/L: 20 000
Zone B:
Above 1 000 cells/L: 2 800
Zone C:
Above 5 000 cells/L: 6 200, 6 600, 6 800
Zone D:
Above 1 000 cells/L: 2 600, 2 200, 1 500, 1 400
Zone E:
Above 1 000 cells/L: 1 800, 1 400
Zone H:
Above 1 000 cells/L: 1 600, 1 600, 4 200
Figure 2.25: Box and Whisker plots showing the frequency distribution of (a)
potentially toxic Gymnodinium c.f. mikimotoi above 1,000
cells/Litre (Zones A, C, and G), and (b) potentially toxic G. c.f.
mikimotoi above 5,000 cells/Litre (Zones G and H).
Figure 2.25 clearly outlines the distribution of toxin occurrence for each zone. Four
zones contained counts above 5,000 cells/L. Zone A had one sample containing
20,000 cells/L at Tapeka Point on 8/12/98. Zone C had three samples just over the
5,000 cells/L cut-off point, one at Tamaki Strait on 23/2/98 (6,200 cells/L), and two at
91
Waimangu Point: 6,800 cells/L on 22/2/98 and 6,600 cells/L on 22/3/98. Zone G had
34 samples above the 5,000 cells/L cut-off point, with a median value of 9,500
cells/L. However, three extreme outliers in Zone G were obvious, two of these
samples were from one episode at the Oyster Bay site: 192,000 cells/L on 20/4/98 and
140,000 cells/L on 27/4/98. The remaining outlier of 48,000 cells/L was from Wedge
Point on 11/5/99. In comparison to the other zones, Zone H had a far higher median
value of 54,500 cells/L. One extreme outlier was also apparent in Zone H, a density
of 170,000 cells/L at Dorset Point on 16/3/98. These densities were associated with a
large bloom of Gymnodinium c.f. mikimotoi in the early months of 1998 (Chang et al.,
1998a). This Gymnodinium species has now been identified as a separate species, and
named Gymnodinium brevisulcatum (Dr Hoe Chang, NIWA, pers. comm.).
Chang et al. (1998a) described the blooms of Gymnodinium c.f. mikimotoi on the
eastern coast and in Wellington Harbour in the summer of 1998. The following
description is summarized from that work: From Mid-January to early February 1998,
sporadic kills of fish and marine fauna were reported off the Wairarapa and Kaikoura
Coasts. In early February there were also reports of human respiratory symptoms in
several areas of the Wairarapa coast. Respiratory irritation was also reported in
Hawkes Bay, and Cape Palliser areas in February. In Wellington Harbour, there were
a small number of Gymnodinium c.f. mikimotoi in samples taken in January. These
numbers increased rapidly, and peaked in about mid-March, with the highest recorded
cell concentration being 33 million cells/L at Mahanga Bay (note: this sample is not
recorded on the FoodNet database). People in Wellington also reported respiratory
irritation, and there was extensive mortality of marine flora and fauna in the harbour.
“Results from two voyages conducted off the East coast of the North Island between
January and February 1998 showed that Gymnodinium c.f. mikimotoi was widespread
in low numbers from Cape Brett in the north to Cape Palliser in the south of the North
Island”. Environmental data collected on the same voyages “indicates that the 20o
isotherm offshore extended further southwards than usual, associated with a strong
southward directed current. During this period, the cooling effects of El Nino on sea
surface temperatures, as experienced in the spring months around New Zealand, were
reversed. The warming of nearshore waters by incursions of warm oceanic waters,
and the entrainment of nutrient-rich waters by upwelling were observed at several
locations along the North Island east coast. The build-up of Gymnodinium species off
Wairarapa and Hawkes Bay between January and February suggests that this species
might have been brought into the nutrient rich inshore waters as seed stock, by
shoreward intrusions of oceanic waters. In March at Foxton on the North Island
western coast, a small number of Gymnodinium c.f. mikimotoi were also recorded
after fish kills were reported in the area. The distribution of sea surface temperatures
in early 1998 suggest it is more likely that the Gymnodinium sp. was introduced into
Wellington from the west coast than from the east coast” (Chang et al., 1998a).
The sample of 20,000 cells/L at Tapeka Point in Zone A in December 1998
(mentioned above) may have resulted from similar processes. This bloom was almost
immediately blown offshore again by a strong easterly wind, so no potential public
health impacts resulted (T. Beauchamp, Northland Health, pers. comm.).
92
Zone
Total No.
of
Samples
A
B
C
D
E
F
G
H
I
J
K
2112
1015
2101
2094
763
1459
5627
675
1471
811
198
Table 2.24:
Number of
samples in
which lipid
soluble
toxins (ether
extract)
were
detected
31
4
41
10
0
0
3
1
4
22
1
Percentage
of samples
in which
lipid soluble
toxins (ether
extract)
were
detected (%)
1.5
0.4
2.0
0.5
0.0
0.0
0.1
0.1
0.3
2.7
0.5
No. of
samples
above
regulatory
level
Percentage
of samples
above
regulatory
level (%)
Maximum
toxin level
(mouse
units)
9
0
3
6
0
0
2
1
0
4
1
0.43
0.00
0.14
0.29
0.00
0.00
0.04
0.15
0.00
0.49
0.50
26
26
44
27
22
23
21
Summary by zone of the total occurrence of lipid soluble toxins
detected in shellfish samples by ether extract mouse bioassay, and
lipid soluble toxins above the regulatory level of 20 mouse units
detected in shellfish samples from 1/9/94 to 30/6/99.
A summary of the occurrence of lipid soluble toxins detected by ether extract mouse
bioassay in shellfish for all sites, in all zones from 1/9/94 to 30/6/99 is provided in
Table 2.24. Note that the analysis of data presented did not use standardized data, and
that differences in toxin accumulation characteristics between shellfish species, the
clumping of sample sites, and variations in sampling regimes, both through time and
between sample sites have been ignored. It can be seen from Table 2.24 that “NSP”
was detected in only a small percentage of all the samples tested, and that Zones C
and J had the highest percentage detected at 2% and 2.7% respectively. However,
Zones K, and J had the highest percentage of samples above the regulatory levels,
closely followed by Zone A. Zone D had the highest recorded level of 44 mouse units
(Port Fitzroy on 22/2/98) (20 mouse units is the regulatory level).
Closer examination of the data, and additional data gathered by ESR, provide further
information about the identity of some of the “NSP” results above the regulatory
level. Of the nine instances of results above the regulatory level of 20 mouse units in
Zone A, seven were from Pacific oysters from the Rangaunu Harbour between
26/9/94 and 8/2/95, and one other from the same site on 14/2/96. There are limited
data from phytoplankton monitoring at this time, although some data from September
1995 appears on the database. During this time, only 200 cells/L of Gymnodinium
species (species not identified) were present. However, there were several records of
Gymnodinium cysts (up to 19,200 on 27/9/94). There are no phytoplankton data from
this site for early 1996. The Rangaunu Harbour has experienced persistent toxicity in
the acetone screen test with in general no positive results from the DSP ELISA, or
ether extract mouse bioassay. Samples of oysters containing “Rangaunu Harbour
toxin” have produced negative results when tested for brevetoxins by neuroblastoma
assay (Dr Penny Truman, ESR, pers. comm.). David Stirling of ESR is currently
elucidating the identity of the “Rangaunu Harbour toxin”. It is thought that the
93
compound dubbed the “Rangaunu Harbour toxin” would not be detected in the ether
extract mouse bioassay (Dr David Stirling, ESR, pers. comm.). It is therefore possible
that the positive results above the regulatory level in the ether extract mouse bioassay
from Rangaunu Harbour could have been low levels of brevetoxin, but this has not
been confirmed by a definitive test method.
The other result above the regulatory level in the ether extract mouse bioassay from
Zone A was from a sample of tuatua from Tokerau Ramp on 25/1/95. There are no
phytoplankton data for this site at this time, and no additional tests have been
undertaken to confirm the identity of the toxin in this sample.
Of the three positive results above the regulatory level in Zone C, (GreenshellTM
mussels from Sites C02 (Kopake) on 27/11/95 and C38 (Awakiriapa Bay) on
26/12/95; and Pacific oysters from Site C10 (Pakihi) on 10/5/95), only two were
associated with the presence of Gymnodinium species. The sample from Site C10
(Pakihi) on 10/5/95 had associated phytoplankton counts of Gymnodinium c.f.
mikimotoi of 400 cells/L on 9/5/95, but 9,200 cells/L on 15/5/95. The sample from
Site C02 (Kopake) on 27/11/95 had a Gymnodinium c.f. mikimotoi density of 1,200
cells/L on the same day. Both brevetoxin and yessotoxin have recently been detected
concurrently by LC-MS and neuroblastoma assay techniques in historic samples from
Zone C, taken in 1995 (P. Truman, ESR, pers. comm.). It is known that yessotoxin
can be detected by the ether extract mouse bioassay. The identity of the toxin present
in these particular samples that were above the regulatory level remains unconfirmed,
but could have been either brevetoxin, yessotoxin, or a mixture of both.
The six samples above the regulatory level for NSP from Zone D were all from
GreenshellTM mussels from Port Fitzroy (D01) taken between late January and early
March 1998. It has now been confirmed by LC-MS that these results were due to the
presence of yessotoxin. Neuroblastoma assays indicated that there was no brevetoxin
in these shellfish (P. Truman, ESR, pers. comm.).
The two samples above the regulatory level from Zone G were both from Blue mussel
samples taken from Wedge Point (G23), on 4/11/96 and 11/11/96 respectively. The
positive results in the ether extract mouse bioassay coincided with low levels of DSP
(22 µg/100g and 16 µg/100g respectively). There is some uncertainty about whether
Okadaic acid is detected by the ether extract mouse bioassay (P. Truman, ESR, pers.
comm.). There are no phytoplankton data available for this time. In this case, the
identity of the toxins detected remains uncertain – they could be either brevetoxin or
Okadaic acid, or indeed, yessotoxin.
The sample above the regulatory level from Zone H was a sample of GreenshellTM
mussels from Dorset Point on 31/3/98. This coincided with a very dense bloom of
Gymnodinium c.f. mikimotoi, which was subsequently identified as Gymnodinium
brevisulcatum. This bloom produced a toxin known as “Wellington Harbour toxin”.
It appears that this compound may be extracted by the ether extraction method
(although the extent to which this occurs appears variable) (P. Truman, ESR, pers.
comm.). Gymnodinium brevisulcatum is also known to produce brevetoxins (A.
Haywood, Cawthron Institute, pers. comm.) It is thus possible that this positive
sample result in the ether extract mouse bioassay could have been due to the presence
of either “Wellington Harbour toxin”, or brevetoxin.
94
The four samples from Zone J above the regulatory level for NSP were dredge oyster
samples taken from Foveaux Strait in September and December 1994. There are no
phytoplankton data relating to these samples. Zone J is an area in which
gymnodimine, produced by Gymnodinium selliforme, has been detected in shellfish.
Gymnodimine is a compound that is extracted by the acetone extraction method, and
kills mice rapidly (within 20 minutes, or not at all) in the acetone screen mouse
bioassay. These results were unlikely to have been produced by gymnodimine, as the
mice died more slowly than this. However, in a range of samples that have been
tested from Zone J by neuroblastoma assay, there has been no brevetoxin detected (P
Truman, ESR, pers. comm.). The identity of the toxin in these samples thus remains
unconfirmed.
The sample above the regulatory level from Zone K (Chatham Islands) consisted of
Blue mussels collected from site K01 on 16/1/95. There are no concurrent
phytoplankton data, or data from further analysis of the toxin available. Thus, in this
case also, the identity of the toxin remains unconfirmed as brevetoxin.
In summary therefore, the regulatory test for NSP using the ether extraction mouse
bioassay is not a specific test for brevetoxin. There is a range of other compounds
found in New Zealand phytoplankton potentially detected by this method. These
include yessotoxin, and possibly gymnodimine and “Wellington Harbour toxin”.
Rangaunu Harbour toxin and pectenotoxin are unlikely to be detected by this method.
The lack of specificity of the test method means that it is difficult to assess the
incidence of brevetoxin in shellfish. Of the 25 samples that have been recorded as
“NSP positive” (i.e. had levels of toxins above 20 mouse units in an ether extract
mouse bioassay), six have been confirmed as resulting from yessotoxin not
brevetoxin, and none of the others have had brevetoxin specifically confirmed. In
three cases the presence of another toxin that could confound the results was
confirmed. It thus appears that although the presence of brevetoxins in shellfish has
been confirmed by investigation outside the marine biotoxin monitoring programme,
the incidence of brevetoxins above the regulatory level in New Zealand since
September 1994 has been extremely low, if not negligible.
There are no data from the marine biotoxin monitoring programme that compare the
uptake of NSP between different shellfish species. However, some differences have
been observed in laboratory situations. Attempts by Fletcher et al., (1998) to induce
toxicity above the regulatory level of 20 mouse units in GreenshellTM mussels by
feeding them with the Florida strain of Gymnodinium breve were unsuccessful. When
fed G. breve with a mixture of non-toxic species, there was some evidence of
selective feeding on the non-toxic species. In contrast, Pacific oysters fed G. breve in
the same quantities readily ingested the algae, and subsequent mouse bioassays
indicated 24-100 mouse units of NSP in the oyster tissue (Fletcher et al., 1998).
While these observations are not definitive, they do suggest that there could be
significant differences in the accumulation, retention and /or detoxification processes
for NSP between shellfish species.
95
2.7.3
Investigation of the temporal distribution of NSP in New Zealand is limited by the
short history of phytoplankton monitoring in most areas, and the non-specific shellfish
toxin testing methods. However, the temporal distribution of Gymnodinium c.f.
mikimotoi in the Hauraki Gulf (3 sites), Marlborough Sounds (24 sites) and at
Collingwood (Golden Bay) was analysed using phytoplankton data from 1994 to
1999. There was insufficient occurrence for similar analysis of Gymnodinium c.f.
breve, and no data has been collected for Gyrodinium galatheanum. Graphs of the
abundance of G. c.f. mikimotoi over time are presented in Appendix IV(D). Sites in
the Marlborough Sounds have been grouped into geographical areas, and graphed
accordingly. Unfortunately, these data do not distinguish between the three different
species that are now known to form the “Gymnodinium c.f. mikimotoi group”. Each
species may have different characteristics with respect to temporal distribution.
As can be seen from the graphs in Appendix IV(D), sites in the Marlborough Sounds
(Zone G) tended to have a greater range of cell densities of G. c.f. mikimotoi than
those sites from the Hauraki Gulf area. An easy comparison can be made by
comparing the number of cases at each site where G. c.f. mikimotoi levels were above
2,000 cells/L. Only 6 cases above this level were recorded at the Hauraki Gulf sites,
one from Kopake on the 18 December 1998, and five from Tamaki Strait on the 15
and 23 May 1995, 11 July 1995, 5 November 1995 and 21 February 1995
respectively. Some sites in the Marlborough sounds also had low numbers above
these levels –the Kenepuru Entrance group, Little Nikau Bay group and East
Bay/Horahora group. The remaining other site groups contained large numbers above
this level. Interestingly G. c.f. mikimotoi was not detected at several sites until after
January 1997.
At the Hauraki Gulf sites, no clear seasonal trends were apparent between years. The
Marlborough Sites did show some seasonality of occurrence. The site groupings
relating to Little Nikau Bay, Crail Bay, Hallam Cove and Forsyth Bay, all showed
increased levels of G. c.f. mikimotoi between January and July from 1997 to 1999.
Interestingly, Collingwood Farms (G01) only showed increased cell densities of G.
c.f. mikimotoi from January to July in 1998, but not in 1997 or 1999.
Extrapolation of these data in the prediction of the occurrence of NSP toxins in
shellfish in the future should be undertaken with caution. The differences in temporal
distribution between the Hauraki Gulf and Marlborough Sounds suggest that patterns
of occurrence may differ significantly between different geographic locations. There
are also noticeable differences in abundance of Gymnodinium c.f. mikimotoi between
years. These differences do not appear to be related to the broad climate patterns
caused by El Nino/La Nina (refer to Appendix III for a summary of these patterns).
There is no clear relationship able to be determined between the occurrence of
Gymnodinium species in the phytoplankton and the occurrence of shellfish toxicity, as
detected by the ether extract mouse bioassay (refer to the discussion of shellfish toxin
results above the regulatory level in the previous section). Detection of such a
relationship is probably confounded by the non-specific toxin testing, and the lack of
analysis of Gymnodinium c.f. mikimotoi species to a species level. The lack of
reporting of the potentially brevetoxin-producing Gyrodinium galatheanum could also
96
potentially impact on the ability of phytoplankton monitoring to predict NSP toxicity
in shellfish.
2.7.4
Conclusions
the monitoring programme regarding the risk of NSP for shellfish consumers:
•
Gymnodinium c.f. breve is widespread around New Zealand, but there are many
phytoplankton sampling sites where it has not been recorded. The distribution of
Gymnodinium c.f. mikimotoi is also widespread, and it has been recorded at most
phytoplankton sampling sites. Distribution of the three species that make up the
G. c.f. mikimotoi group is at this stage unknown.
•
There have been few occurrences of Gymnodinium c.f. breve above the level to
trigger shellfish testing, and none above the level to trigger a voluntary shellfish
industry closure to harvesting or the issuing of a public health warning.
•
Gymnodinium c.f. mikimotoi (or the species now known as Gymnodinium
brevisulcatum) has been associated with RIS and fish kills. “Wellington Harbour
toxin” has been implicated in one of these events. In the case of several major
Gymnodinium bloom events, there is evidence to suggest that the seed stock for
the bloom originated offshore.
•
It is thought that the Gymnodinium bloom in Wellington Harbour in the summer
of 1998 originated from the western coast of New Zealand. This suggests that the
commonly held assumption that there is lower risk of toxins arising from
Gymnodinium species on the western coast may be unfounded.
•
The incidence of “NSP toxicity” in shellfish, as reported from the ether extract
mouse bioassay, is comparatively low, as are the maximum levels of toxicity
recorded. Some of this apparent “NSP” toxicity may be due to the presence of
other lipid soluble toxins.
•
There are possible differences in NSP toxin uptake/detoxification processes
between shellfish species. These might impact significantly on the risk of NSP to
shellfish consumers.
•
Occurrence of potentially brevetoxin-producing phytoplankton may vary by year
within zones. In some areas, these phytoplankton may also vary in abundance
seasonally.
•
Further data are required to determine the reliability of phytoplankton monitoring
as an indicator of shellfish NSP toxicity. Currently however, not all known
potentially brevetoxin-producing species are included in the phytoplankton
monitoring programme.
97
SECTION 3:
3.1
NON-COMMERCIAL SHELLFISH GATHERING AND
CONSUMPTION IN NEW ZEALAND
INTRODUCTION
The risk of exposure to marine biotoxins through non-commercial shellfish harvesting
not only depends upon the patterns of biotoxin occurrence as described in the last
section, but also upon patterns of shellfish gathering and consumption. These patterns
may be affected by geographical, social and temporal components.
The following sections describe the patterns of shellfish gathering in New Zealand,
and the factors that influence them.
3.2
DISTRIBUTION OF SHELLFISH IN NEW ZEALAND
Underlying all non-commercial shellfish gathering patterns in New Zealand is the
availability of shellfish species desired by consumers. The many non-commercially
gathered shellfish in New Zealand live in a wide range of habitats, of varying
accessibility to man. The habitats and ranges of the most commonly gathered species
are summarized very briefly below, followed by a summary of the species available in
each “Biotoxin Zone”. Except where referenced separately, this information has been
collated from personal observations, from Health Protection Officers in each area, and
from Morton & Miller (1973), and Tortell (1981).
Because of their mode of feeding, bivalve shellfish are the species of most concern
with respect to the risk of biotoxins to consumers. Bivalve species can live in a range
of habitats, and are widely distributed throughout New Zealand. All of the biotoxin
zones contain some bivalve species that are gathered by the public.
The bivalve with one of the widest distributions in New Zealand is the green-lipped
(GreenshellTM) mussel, Perna canaliculus, which is found on rocky shores from low
water down. It can be found in a wide range of habitats, from on wharf piles in the
protected waters of harbours, to rocks on exposed open shores, and in dense beds on
the bottom in moderately protected areas. It may be collected from the shore at low
water, by snorkeling in the less exposed areas, or by dredging.
The blue mussel, Mytilus edulis aoteanus has a more southerly distribution, being
found very commonly only as far north as Wellington, and with a more patchy
distribution in the North Island. Where the blue and green-lipped mussels co-exist,
blue mussels tend to live in places with less wave action.
Several commonly gathered bivalves are associated with rocky shores. These include
the native rock oyster, Saccostrea glomerata, and the introduced Pacific oyster,
Crassostrea gigas, both of which live most frequently in harbour or estuarine areas.
Native rock oysters are most common in the very north of the North Island, but may
occur as far south as Taranaki on the western coast, and East Cape on the east coast.
Similarly, the Pacific oyster is most common in the north of the North Island, but also
occurs as far south as some parts of the Marlborough Sounds, although it is rare in the
98
south of the North Island. Both species of oyster live intertidally (i.e. between the low
water and high water marks), and are thus relatively easily accessible to shellfish
gatherers at low tide.
Tuatua (Paphies subtriangulata, and Paphies donacina) are the most common
bivalves on exposed open sandy beaches, and are found in the sand at the low water
mark throughout New Zealand. On extremely exposed coasts, they are replaced by
the toheroa (Paphies ventricosa), which lives higher up the shore than tuatua. Both
tuatua and toheroa are accessible from the shore at low water. On exposed sandy
shores below low water, venerid and mactrid clams are found (e.g. Bassina yatei,
Dosinia anus). These species are less easy to gather, since the conditions are
generally too rough for easy dredging.
Pipi (Paphies australis) and cockles (Austrovenus stutchburyi) are other New
Zealand-wide inhabitants of soft shores favoured by shellfish gatherers. These
species can tolerate higher levels of silt and lower salinity, and live in the more
sheltered waters of harbours and estuaries. Both are accessible at low tide: pipi live in
the intertidal zone in coarser sand, and cockles on the tidal flats in finer silt at neap
low water. In some areas, (for example, harbours or estuaries adjacent to large cities)
the gathering of pipi and cockles for consumption is restricted by the water quality of
the environment in which they live (M. Hart, Healthcare Hawkes Bay, pers. comm.; P.
Wood, MidCentral Health, pers. comm.; B. Munro, Tairawhiti Healthcare, pers.
comm.).
On soft bottoms in open water and harbours throughout New Zealand, scallops
(Pecten novaezelandiae) are found. These may be collected in some places by
wading out into the water at low spring tide, but are most commonly gathered by
dredging or diving.
Another species that is commonly dredged is the dredge oyster (also known as the flat
oyster), Tiostrea chilensis. Dredge oysters occur throughout New Zealand, but are
most commonly associated with the cooler waters of the South Island. They live subtidally in beds from the low spring water down to 500 feet deep.
While bivalves represent the highest risk to consumers with respect to marine
biotoxins, several other species that are frequently gathered may represent a lower
potential risk. These include species that graze on benthic phytoplankton or eat
macroalgae covered by benthic phytoplankton, and species that are carnivores and
may accumulate biotoxins from their prey.
The most commonly gathered gastropods are paua (Haliotis spp.), of which the largest
is Haliotis iris. Paua live sub-tidally in rocky platform reefs in the high salinity
waters of the open coasts. They are found throughout New Zealand, but are more
common (and larger) toward the south. Less commonly harvested are the smaller
gastropods: pupu, the mud snail (Amphibola crenata), found in protected harbours and
estuaries, and the rocky reef dwellers, the cats-eye (Turbo smaragdus), the topshell
(Melagraphis aethiops), Cooks turban (karakea, toitoi or ngaruru) (Cookia sulcata),
the whelks (kawari) (Cominella spp.) and limpets (ngakihi) (Cellana spp.).
99
The sea urchin, kina, (Evechinus chloroticus) is found throughout New Zealand in
rocky reef areas. Kina feed on macroalgae. In more protected waters they are found
in low tidal areas, but on open, exposed shores may be found in pools in the mid-tidal
zone. They are more common sub-tidally, nestling in cracks, under ledges and in
hollows, and are usually gathered by snorkeling.
The most sought-after crustacean is the crayfish. The most common species is the red
rock lobster (Jasus edwardsii), which is found throughout New Zealand, living subtidally in rocky crevices and caves on open coasts. Crayfish are gathered by diving.
One potential source of biotoxins currently not considered in the marine biotoxin
monitoring programme is planktivorous fish. The linking of the mortality of sea lions
along the central California coast to a bloom of Pseudo-nitzschia australis (Scholin et
al., 2000), indicates the potential for ASP to be passed up through the food chain. A
range of planktivorous fish are found widely distributed throughout the New Zealand
coastline, particularly in rocky reef areas.
One of the underlying factors influencing the shellfish gathering activities in each
biotoxin zone is the availability of desirable species. This is a function of the ecology
of the area, which is partly determined by the topography of the coast, and the degree
of wave exposure.
The western coast of Zone A consists of an exposed sandy coastline (Ninety Mile
Beach) between Ahipara and Scott Point. (Refer to Appendix II(A) for the location of
the zones). Tuatua and toheroa are dominant species in the sand of the beach. Both
species are patchy in distribution, and local knowledge is usually necessary to locate
denser beds. Toheroa have been exploited to such an extent that harvesting is highly
restricted, but tuatua are still present in numbers that make the species attractive to
gather. Associated with the rocky outcrops (e.g. at Ahipara, The Bluff, and Scott
Point) are mussels, paua, kina and crayfish, and in much lower numbers, rock oysters.
While there is relatively little road access to this area, vehicles are able to drive long
distances along the beach at low tide, so the whole length of the beach is accessible.
The same shellfish species are gathered further south in Zone F from the long
exposed sandy beaches broken occasionally by rocky reefs and headlands. The
Herekino, Whangape, Hokianga, and Kaipara Harbours that lead off these long
exposed beaches provide an environment for species that thrive in more sheltered and
silty environments. Species gathered here include native and Pacific oysters, dredge
oysters, cockles, horse mussels, and pipi. There are scallop beds in the Kaipara
Harbour, and green-lipped mussels can be dredged from beds near the harbour mouth.
The Manukau Harbour also has abundant shellfish, although in places the ability to
harvest these is compromised by the bacteriological water quality. Due to
overfishing, the Auckland Regional Council has banned the gathering of shellfish on
some of the beaches between the Manukau and Kaipara Harbours, and a lower daily
bag limit for cockles applies in the Auckland Regional Council area. Further south,
green-lipped mussels and cockles are common in the Raglan Harbour, and pipi,
cockles and mussels in the Kawhia Harbour. The Manukau and Kaipara Harbours are
easily accessible from Auckland, and the coast of the Hokianga Harbour is easily
accessible by car and boat. The Whangape and Herekino Harbours further north are
much more remote. The most popular access to the open sandy beaches in the north
100
of the zone is via Dargaville. Here, and on Muriwai Beach, and the beaches south of
the Manukau Heads, cars are able to drive along the beach at low tide, so infrequent
road access does not necessarily significantly limit access to the length of the beach.
Southwards, the coast curves westwards into the North Taranaki Bight. As the rocky
reef habitat increases, green mussels, paua and kina are more abundant, and some
tuatua are found in sandy areas. The southern part of Zone F from Urenui to Cape
Egmont consists of gravel, cobble and boulder beaches, providing habitat for paua,
kina and green-lipped mussels.
Paua, kina, green-lipped mussels and pipi are abundant in the South Taranaki Bight in
the north of Zone H. Further south, the coast changes to coarse-grained sandy
beaches with mactrid clams, tuatua, toheroa and pipi present. The rocky areas
adjacent from Paekakariki south and then east to Cape Palliser provide habitat for
paua, kina and crayfish. Cockles are found in the estuarine areas near Paremata.
Zone J, the western coast of the South Island, is a long exposed rocky coastline,
interspersed with mixed shingle and sand beaches. With the exception of mussels on
the rocky reefs, there are few bivalves suitable for gathering – crayfish are the main
non-commercially gathered species other than finfish. Similar coastline extends south
to the sounds in Fiordland, where scallops, paua, kina mussels and crayfish are
available. In the Sounds the cliffs drop straight into the sea, and there are very few
places where the intertidal zone is other than vertical. Lack of road access in much of
this area limits the gathering of shellfish. At the south of the South Island, paua and
kina are present as the coast runs in an easterly direction, with toheroa and mactrid
clams present in Te WaeWae Bay, and toheroa at Oreti Beach. The coastline of
Stewart Island is convoluted and rocky, with the major species of interest to noncommercial harvesters being mussels, paua and dredge oysters. Paterson Inlet has a
wider variety of species with the addition of kina, scallops, pipi and cockles. The
Foveaux Strait is famous for its abundance of dredge oysters. These are conserved
through seasonal bans on harvesting. Due to the impact of Bonamia disease on the
oyster population, the seasons have been highly restricted through the 1990’s, but the
beds now appear to have recovered. The longer “Bluff oyster” seasons now expected
will increase the risk of exposure of consumers to biotoxins in this area.
Zone I includes the eastern coast of the South Island. This coast is more sheltered
from the prevailing south-westerlies than the western coast. The major species for
much of this rocky coast are still mussels, paua and crayfish. The mixed sand and
gravel beaches from Oamaru north to Banks Peninsula provide little opportunity for
the settlement of bivalve shellfish, paua or crayfish. In contrast, these species are
found in the rocky reefs around Banks Peninsula, and the harbours and estuaries
contain cockles and pipi. There are significant beds of cockles at Papanui. North of
Banks Peninsula is a stretch of steep coarse grained sandy beach with beds of cockles
present. From Amberley Beach north, the coast is comprised of exposed rocky reefs
where crayfish and paua are the major species of interest to non-commercial
harvesters. North of Kaikoura, the coast is well known for its abundance of paua.
The eastern coast of Zone G is predominantly rocky and gravel beaches, with paua,
kina and crayfish found in reefs. Mussels are found at Port Underwood. To the west
inside the Marlborough Sounds and Croiselles Harbour, the coastline is steep and
101
rocky, with very few intertidal areas. The main species gathered here are mussels
(Blue, and green-lipped (GreenshellTM)), and scallops. While road access is limited in
much of the Marlborough Sounds, most areas are easily and safely accessible by boat.
Paua and crayfish are present on the outer shores of the Sounds where the coast is
more exposed to wave action. To the west, dredge oysters and scallops are the major
bivalve species in Tasman and Golden Bays, and significant beds of cockles occur in
Tapu Bay and Pakawau Beach. Crayfish are taken from the rocky reefs of the coast
that separates the two major bays.
On the south-eastern coast of the North Island, paua, kina and crayfish are the
predominant species of interest to non-commercial harvesters in Zone E. Some
mussels are also present, and cockle and pipi occur in the few sheltered areas. The
coast is a mixture of rocky reefs, rock platforms, and steeply graded coarse sand
beaches interspersed in Hawke’s Bay with rocky beaches. Much of this coastline is
relatively remote, with poor road access.
Similar species are found on the east-facing coast of Zone D, from Cape Runaway
into the Bay of Plenty. In the sandy beaches from Opotiki to Waihi Beach, tuatua are
found. Pipi, oysters, cockles and mussels are found in the harbours in this bay. On
the western side of the Bay of Plenty, scallop beds lie off shore and in Tauranga
Harbour, and these continue north up the Coromandel Peninsula. From Waihi
northwards, the coastline is again rocky, but interspersed with harbours and estuaries
where oysters, pipi and cockles are found. The rocky open shores provide good
habitat for crayfish, and green-lipped mussels, paua and kina are also present. There
is good road access to much of this area.
The range of species potentially available for non-commercial gathering for
consumption by the public is related to the range of habitats available in an area – the
more homogenous the environment, the less diversity in terms of desirable species for
consumption. Zone C, the Hauraki Gulf and Great Barrier Island, encompasses a
very large range of habitats, and thus species for consumption by the public. These
range from species found in sheltered estuarine and harbour areas, through to those in
moderately protected areas, and a few areas that face open water. The zone thus
contains cockles, pipi, Pacific and native rock oysters, tuatua, green-lipped mussels,
scallops, kina, paua and crayfish. The shellfish gathering areas in this zone are in
general highly accessible to the public – the coast is well supplied with roads and boat
launching facilities. However, there are some local restrictions on the gathering of
shellfish, designed both to conserve shellfish stocks, and to prevent illness in
consumers.
The eastern coast of Zone A and Zone B in the north-east of the North Island have a
similarly wide diversity of marine habitats, providing a wide range of seafood for
non-commercial harvest. As with the Bay of Plenty northwards, this coastline is
protected from the prevailing south-westerly swells, but is subject to wind and waves
from north-easterly directions. The coastline is irregular and convoluted. The
orientation of the beaches in the area, and their fetch lengths and directions are highly
variable. These substantial differences in exposure and shelter result in rapid changes
in beach type over quite small distances. This variability contrasts with most of the
other zones except Zone C. The result of this is that Zones A, B, and C, despite that
fact that they are relatively small compared to other zones, all contain most of the
102
commonly gathered species of shellfish (with the exception of course of those species
that do not extend this far north, such as the Blue mussel). One species not found in
this area is toheroa, which prefer sandy coasts with greater wave exposure.
The coastline in both Zones A and B are relatively easily accessible. Zone B is well
serviced by roads, with numerous places where it is possible to launch a boat. While
some of the coastline in Zone A is relatively remote with fewer roads, most areas are
easily accessible by boat.
Zone K is the Chatham Islands. Chatham Island itself consists of several sandy
beaches, separated by rocky coasts. Paua and crayfish are common on the rocky
coasts, and scallops and tuatua occur in Hansen and Petrie Bays. The adjacent Pitt
Island has only two small sandy bays with the rest of the coastline being formed by
rocky reefs and eroding rock platforms. Paua and crayfish occur on this coast also.
The Chatham Islands are unusual in the absence of the Green-lipped mussel, and Blue
mussels are also rare.
In considering the shellfish available for non-commercial harvest and their relative
potentials to accumulate and retain biotoxins (as discussed in the previous chapter), it
is apparent that biotoxin zones may vary considerably in biotoxin risk. One issue that
has not been examined in our discussion of where different shellfish species occur, is
the abundance of various species. We have merely stated that particular species occur
in the habitats available in each zone. There are several reasons for this: firstly, there
is very little objective data available to assist in this – few surveys of shellfish
abundance have been undertaken in this detail, and most information available is at
the level of casual observation. Secondly, abundance of shellfish is something that
may change significantly from year to year through over-exploitation, environmental
factors or disease. At a local level this is something that needs to be monitored in
order to keep an appropriate level of biotoxin monitoring – there is little point in
monitoring for biotoxins at a site where shellfish species are no longer available for
harvest by the public.
If the differences between species in accumulation and retention of biotoxins are
considered along with the distribution and accessibility of the shellfish species, it is
evident that there are differences between biotoxin zones. Zones A, B, C, D, F and G
all contain significant proportions of coastline where bivalve shellfish are present, and
that are readily accessible to the public. If it can be assumed that tuatua and scallops
represent shellfish with a significantly higher level of accumulation and retention of
biotoxins than some other species, then these zones would represent areas where the
range of available shellfish for harvest presents the greatest risk. While some other
common shellfish species are absent, the Chatham Islands (Zone K) are also home to
the high risk species. The west coast portion of Zone J represents a low risk area due
to the relatively low numbers of bivalve shellfish available for non-commercial
harvest, and the relative inaccessibility of some areas of coast. However, the Foveaux
Strait area of Zone J has a significant number of dredge oysters, toheroa and scallops,
and this presents a greater risk. The harbour/estuarine areas, which contain higher
numbers of bivalve shellfish than the open stony beaches, may also represent areas of
relatively greater risk potential. In this respect, Zone I is similar to Zone J, except
there is a greater diversity of habitats, with more extensive harbour and estuarine
species. The most abundant habitats in Zone E support species with a low risk of
103
biotoxin contamination, like paua and kina. However, bivalve species such as
mussels also occur on the open coast, and estuaries and harbours support those
bivalves normally found in such habitats.
Obviously the occurrence of readily available shellfish with the potential to
accumulate biotoxins is just one small factor in the assessment of the risk of TSP to
consumers. However, it is significant in the design of marine biotoxin monitoring
programmes.
3.3
SHELLFISH GATHERING
In addition to the availability of shellfish for non-commercial harvest, the quantity of
shellfish harvested and consumed, and the identity of the consumers are important in
biotoxin risk analysis.
There have been surprisingly few published studies undertaken on non-commercial
shellfish gathering in New Zealand. Results from a study on marine recreational (i.e.
non-commercial) fishing done by Sylvester et al. (1991), based on a telephone survey
in 1987, have been presented in a previous review of the marine biotoxin monitoring
programme (Wilson, 1996). These will not be presented in detail again here except in
comparison to more recent data.
A more recent National Marine Recreational Fishing Survey has been undertaken for
the Ministry of Fisheries (Fisher & Bradford, 1998). This study was based on a
national telephone and diary survey. The survey used a preliminary telephone survey
to determine the number of households that contain marine non-commercial fishers
from a random selection of households with a phone. One randomly selected fisher
from each of these households was asked to keep a diary of their recreational (i.e.
non-commercial) fishing trips during the year. The figures provided by the diarists
were scaled to give estimates for the total marine non-commercial fishing population
of New Zealand. The data collected in this survey is likely to be of better quality than
that collected in the telephone survey in 1987, which relied on participants to recall
their fishing activities some time after the event.
In both these studies, the population surveyed included only those people that have
telephone connections. It is possible that those people who do not have telephones
may be more reliant on non-commercially harvested seafood as a source of food.
Table 3.1 shows the number of trips by survey respondents targeting the main
shellfish species in each Biotoxin Zone, except Zone K (Chatham Islands) for which
there are no data. These data are reworked from Fisher and Bradford (1998) so that
the fishing areas in the survey data correspond with the Biotoxin Zones used in the
marine biotoxin monitoring programme. Due to the positioning of the boundaries of
fishing areas used in the original analysis of data by Fisher and Bradford, Zone F data
from Tirua Point southwards has been included with data from Zone H. Most other
area boundaries were similar to the boundaries of the Biotoxin Zones. The “Oyster”
category includes Pacific oysters, native rock oysters, and oysters of unspecified type.
Some of the oysters in this category in Zone G and all in Zone I are likely to be
dredge oysters. The species of mussel targeted are not detailed.
104
If all the main non-finfish species that are non-commercially harvested are
considered, the data suggest that the greatest level of gathering activity occurs in Zone
D, with significant levels in Zones E, G and B. Comparatively low levels of activity
occur in Zones A and H. If trips targeting bivalve species only are considered, Zone
D again has the highest level of activity, closely followed by Zone G. Comparatively
high levels of activity are also indicated in Zones B, C and F, with Zones A, E, H, I
and J having comparatively lower levels. Over all areas, scallops are the most
actively targeted species, followed by mussels and pipi. (Note that the ability of the
general public to distinguish between pipi and tuatua may be limited, so there may be
some confusion between these two classes).
Comparison of the percentage of trips targeting each bivalve species within each zone
(Table 3.2) indicates that scallops are the most actively targeted species in 6 of the 10
zones (Zones A, B, C, D, F and G).
Mussels are the most actively targeted species in Zones E and J, and pipi in Zone H.
With the exception of Dredge oysters in Zones G, I and J, oysters are the species that
are least frequently targeted. In both zones A and D, tuatua and pipi are the next most
frequently targeted species after scallops.
105
Table 3.1
Zone
Bivalve Species
Cockle Mussel Oyster D Oyster
Pipi
A
B
C
D
E
F
G
H
I
J
Total
%
Zone
A
B
C
D
E
F
G
H
I
J
2
16
11
13
7
4
29
6
15
8
111
7.8
3
30
35
72
20
34
37
7
14
39
291
20.5
2
5
3
7
1
13
11
0
2
0
44
3.1
0
0
0
0
0
0
35
0
9
14
58
4.1
9
55
17
85
7
16
12
9
10
2
222
15.6
Scallop
31
59
72
111
0
110
178
0
0
10
571
40.2
Tuatua
9
13
9
74
1
15
0
0
5
0
126
8.9
Total
Bivalves
56
178
147
362
36
192
302
22
55
73
1423
% Total
Bivalves
3.9
12.5
10.4
25.5
2.5
13.5
21.3
1.5
3.9
5.1
Other Species
Paua
Cray Kina
4
7
4
26
122
9
21
21
61
50
325
13
126
98
329
273
14
71
33
46
68
1071
3
22
4
16
14
6
2
7
6
9
89
Total All
Species
% All
Species
76
333
253
733
445
221
396
83
168
200
2908
2.6
11.5
8.7
25.2
15.3
7.6
13.6
2.9
5.8
6.9
Table 3.1: Number of trips targeting the main
shellfish species in each Biotoxin Zone recorded by
diarists in 1996. (Data from Fisher & Bradford
(1998)). D Oyster = Dredge oyster; Oyster=Oysters
including native rock and Pacific oysters, and
unspecified species; Cray=Crayfish
Distribution of Targeted Species Within Each Zone (% of Zone
Total)
Cockle Mussel Oyster D Oyster
Pipi
Scallop Tuatua
3.6
5.4
3.6
0.0
16.1
55.4
16.1
9.0
16.9
2.8
0.0
30.9
33.1
7.3
7.5
23.8
2.0
0.0
11.6
49.0
6.1
3.6
19.9
1.9
0.0
23.5
30.7
20.4
19.4
55.6
2.8
0.0
19.4
0.0
2.8
2.1
17.7
6.8
0.0
8.3
57.3
7.8
9.7
12.4
3.7
11.7
4.0
59.5
0.0
27.3
31.8
0.0
0.0
40.9
0.0
0.0
27.3
25.5
3.6
16.4
18.2
0.0
9.1
11.0
53.4
0.0
19.2
2.7
13.7
0.0
Table 3.2: Distibution of targeted bivalve shellfish
species within each zone as a percentage of the total
target trips for each zone. (Data from Fisher &
Bradford (1998)). D Oyster = Dredge oyster;
Oyster=Oysters including native rock and Pacific
oysters, and unspecified species; Cray = Crayfish
Table 3.2
106
Table 3.3 shows the numbers of each species taken from each biotoxin zone by
respondents in the same survey. These data reflect both gathering activity, and the
availability of each species in each zone. The highest numbers of mussels, pipi,
tuatua and crayfish were gathered from Zone D, while the highest number of scallops,
dredge oysters and cockles were harvested from Zone G. With respect to oysters
(rock and unspecified), 45% were taken from Zone F, along with 15% of the mussels.
Paua and crayfish were the predominant species harvested in Zone E, which recorded
the highest number of paua, and second highest number of crayfish taken.
The results of the survey undertaken by Fisher & Bradford (1998) show that most
people surveyed generally fish near home. Some exceptions to this are the
respondents from Auckland fishing in the eastern Coromandel area (Zone D). The
Marlborough Sounds (Zone G) are also a popular destination for fishers residing
outside that area. Respondents from both Wellington and Christchurch made a
number of trips to Pelorus and Queen Charlotte Sounds. There were only a small
number of trips made by South Island respondents to the North Island.
The data collected in the 1996 Marine Recreational Fishing Survey (Fisher and
Bradford, 1998) described here represent the most comprehensive nation-wide data
that are currently available. The results are not inconsistent with what could be
predicted from the ecology of the coast, the accessibility of the coast, and the location
with respect to centers of population. If one can assume that the figures from this
survey provide a reasonably realistic picture of the distribution of non-commercial
shellfish gathering, then with some knowledge of biotoxin distribution throughout
New Zealand, and the accumulation and retention of TSP toxins in different species of
shellfish, risk assessment on a zone by zone basis should be possible.
Estimates of the total quantity of non-commercial harvest of species within the
Ministry of Fisheries Quota Management System are provided in the Report from the
Fisheries Assessment Plenary, based on telephone and diary surveys (Annala &
Sullivan, 1996). This report suggests that the total non-commercial harvest of cockles
per year is 62 tonne. The estimate of non-commercial harvest of paua is 205 tonne
per year, with an additional illegal commercial harvest of 275 tonne. The accuracy of
these data is uncertain. A study was undertaken by Kearney (1999) of the ecology
and management of cockles in the Whangateau Harbour, north of Auckland. This
study was conducted over a 12-month period from December 1997 to December
1998, using structured sampling regimes and interviewing all harvesters on the beach
during sampling times. From the data collected in his study, Kearney estimated that
the total annual harvest of cockles from Lew’s Bay, Whangateau Harbour, from
December 1997 to December 1998 was 27,950 kg. The contrasts with the results of
the Ministry of Fisheries 1993-94 telephone and diary survey, which estimated that
the total non-commercial cockle harvest in QMA1 (Cape Reinga to Cape Runaway)
was 55 tonne (Annala & Sullivan, 1996).
Given that the data from Kearney’s study are based on actual observation from only
one of many harvestable populations in this area, this would suggest that the Ministry
of Fisheries survey grossly underestimated the non-commercial harvest of cockles in
QMA1. If this underestimation extends to other shellfish species also, there are
obviously implications in terms of quantification of risk in the event of the occurrence
of marine biotoxins.
107
Quantity of Species Taken by Diarists
Cockle
Zone
Mussel
% of
Total
Cockle
No.
No.
Oyster
% of
Total
Mussel
D Oyster
% of
Total
Oyster
No.
Pipi
% of
Total D
Oyster
No.
Scallop
% of
Total
Pipi
No.
Tuatua
% of
Total
Scallop
No.
Paua
% of
Total
Tuatua
No.
No.
Cray
% of
Total
Paua
No.
Kina
% of
Total
Cray
No.
% of
Total
Kina
A
30
0.3
100
0.8
200
5.4
0
0.0
715
3.6
685
3.3
1250
10.8
30
1.0
42
1.1
42
1.2
B
1770
20.2
1344
11.1
306
8.2
0
0.0
5870
29.9
1259
6.0
1259
10.9
96
3.1
505
13.3
1069
29.7
C
1134
12.9
1515
12.6
32
0.9
0
0.0
1591
8.1
2003
9.5
635
5.5
22
0.7
270
7.1
221
6.1
D
1133
12.9
2935
24.3
925
24.8
0
0.0
7822
39.8
2435
11.6
5890
50.9
171
5.6
1252
32.9
944
26.3
E
215
2.5
568
4.7
30
0.8
0
0.0
433
2.2
0
0.0
20
0.2
1229
40.0
1045
27.4
433
12.0
F
350
4.0
1885
15.6
1693
45.3
0
0.0
1767
9.0
2516
11.9
1907
16.5
71
2.3
53
1.4
326
9.1
G
2236
25.5
1137
9.4
490
13.1
1221
43.3
575
2.9
12003
57.0
0
0.0
164
5.3
199
5.2
16
0.4
H
253
2.9
308
2.6
0
0.0
0
0.0
412
2.1
0
0.0
0
0.0
263
8.6
113
3.0
307
8.5
I
1029
11.7
540
4.5
58
1.6
843
29.9
391
2.0
0
0.0
621
5.4
584
19.0
138
3.6
98
2.7
611
7.0
1723
14.3
1
0.0
754
26.8
87
0.4
172
0.8
0
0.0
440
14.3
190
5.0
139
3.9
J
TOTAL
8761
12055
3735
2818
19663
21073
11582
3070
Table 3.3: Numbers of the main shellfish species caught by diarists in
each Biotoxin Zone (Data from Fisher & Bradford, 1998).
D. Oyster=Dredge oyster; Oyster=Oysters including native rock and
Pacific oyster, and unspecified species;Cray=Crayfish
108
3807
3595
3.4
POPULATION STRUCTURE AND SHELLFISH CONSUMPTION
The question of whether some sectors of the population are more at risk because of
proportionately higher rates of consumption of non-commercially harvested shellfish,
is one that needs to be considered in biotoxin risk management.
Kaimoana (seafood) has traditionally been extremely important to Maori, not merely
as a food source, but also as a way of upholding customary obligations within and
between whanau, hapu and iwi (Te Puni Kokiri, 1993). Kaimoana is still very
important to Maori today. A survey of Maori households in Te Hiku o Te Ika (the far
north of the North Island) showed that 11% of the households collected seafood more
than once a week, 31% collected seafood at least weekly, and 52% at least fortnightly.
Only 9% did not collect seafood at least monthly (n = 499) (Hay, 1996).
As noted by Wilson (1996) in the last review of the marine biotoxin monitoring
programme, some species of shellfish are of particular cultural significance to iwi or
hapu. This may be associated with a cultural history through which particular species
are regarded in a special relationship (as in the case of Te Uri o Hau with respect to
toheroa), or with the traditional use of shellfish at particular times (for example, the
consumption of a particular kind of shellfish by a person who is dying).
Traditionally, seafood has also been important to Pacific Island and Asian peoples,
and this is potentially reflected in shellfish harvesting patterns also.
The population of each regional authority area by ethnic origin is presented in Figure
3.1. It can be seen that there are significant differences in the ethnic composition of
the population in different regions.
There has been little data gathered on non-commercial shellfish harvesting by people
of different ethnic origins in New Zealand. Wilson (1996) presented data drawn from
the 1987 Marine Recreational Fishing Survey, and this is summarized in Table 3.4.
Ethnicity
Maori
Pacific Islands
Other Ethnic Groups
Non-Specified
Table 3.4:
Gathering (%)
14
2
84
1
Diving (%)
16
2
82
0
Estimated percentage of non-commercial shellfish harvesting
(either by gathering or diving) by ethnicity, per year, throughout
New Zealand. (Summarized from Wilson, 1996).
109
Northland
(137 052)
Auckland
(1 068 654)
Waikato
(350 130)
Nelson
(40 275)
Taranaki
(106 587)
Bay of Plenty
(224 361)
Manawatu-Wanganui
(228 768)
Gisborne
(45 789)
Tasman
(37 974)
Hawke's Bay
(142 794)
Wellington
(414 081)
West Coast
(32 514)
Marlborough
(38 403)
Canterbury
(468 036)
Southland
(97 095)
Figure 3.1:
Otago
(185 079)
European
Maori
Pacific Island
Asian
Other
Not Specified
Population distribution by ethnic origin for each regional
authority within New Zealand (data extracted from the 1996
census, Statistics New Zealand).
110
Somewhat different data have been obtained from surveys based on observations of
non-commercial shellfish gathering in a qualitative survey of intertidal harvesting by
amateur fishers in the Auckland Metropolitan area. This survey was conducted over
the summer of 1991-92 (Drey & Hartill, 1993). In this study, it was concluded that
there were distinct differences in the ethnic composition of people harvesting
intertidal organisms at various beaches. Although the “relatively low number of
interviews conducted at many sites render any characterization of user populations at
these sites suspect” (Drey & Hartill, 1993), the data did suggest that the distribution of
shellfish gatherers by ethnic origin was not representative of the composition of the
population as a whole, with people of New Zealand European origin being underrepresented and Maori, Asian and Pacific Island peoples generally being overrepresented. This study also suggested that the most favoured species of shellfish
taken from hard and soft shores differed with ethnicity. Given the potential for
different species of shellfish to differ with respect to accumulation and retention of
biotoxins, this may also result in differing levels of risk with respect to ethnicity.
A more recent, and much more detailed study has been undertaken by Kearney
(1999), in his study of the ecology and management of cockles in the Whangateau
Harbour, north of Auckland (discussed previously). Table 3.5 presents data gathered
from observations and interviews in his study.
Ethnic Group
Maori
NZ European
Asian
Pacific Island
Other
Total
Table 3.5:
Total Weight
Harvested (kg)
5853
2022
1703
958
106
10,642
Percentage of
Total
Harvested (%)
55
19
16
9
1
100
Number of
Harvesters
893
430
248
66
17
1654
Percentage of
Total
Harvesters (%)
54
26
15
4
1
100
Numbers and percentages of the total weight of cockles harvested,
and harvesting population structure by ethnic group at Lews Bay,
Whangateau Harbour (n = 1654). (From Kearney, 1999).
It is interesting to note that the majority of harvesters (82%) were not resident in the
surrounding district. Most had residency in Manukau City (South Auckland).
These studies by Drey & Hartill (1993) and Kearney (1999), while localised and
undertaken within reasonable driving distance of Auckland, suggest that based on the
percentage of shellfish gatherers, the risk of TSP may not necessarily be the same for
all ethnic groups. Further studies are required to ascertain the differences in risk with
respect to ethnicity. It should be noted that this may vary with location also – in more
remote coastal areas there may be a greater reliance by people of all ethnic origins on
gathered seafood.
111
3.5
TEMPORAL PATTERNS
Studies by Hartill & Cryer (1999) and Kearney (1999) have shown seasonal
differences in non-commercial harvesting activity. These studies have shown that for
a range of intertidal shellfish, non-commercial harvesting is highest in the summer,
and lowest in the winter, with harvesting activity in autumn and spring at intermediate
levels and varying with the species harvested. Obviously, in addition to these patterns
of activity, harvesting of some species (such as scallops and dredge oysters) may be
prevented by seasonal restrictions for conservation reasons.
The type of day also affects the extent of non-commercial shellfish harvest, with
greatest harvesting activity occurring on public holidays or weekends attached to
public holidays. Harvesting activity is significantly greater on weekends compared to
weekdays (Hartill & Cryer, 1999, Kearney, 1999). Anecdotal evidence also suggests
that in some areas harvesting activity may increase significantly in the days before
public holidays or long weekends. Mussel spat harvesters drive along Ninety Mile
Beach in the north of Northland several times each day. They report that harvesting
activity, particularly by Maori, is greatest in the days before public holidays or long
weekends, and suggest that this is a result of preparation for visits by whanau from
outside the area (C. & R. Hensley, pers. comm.).
Many Health Protection Officers have reported that there are large increases in their
local populations over summer, as holiday-makers from the cities move to coastal
areas over the summer holidays. Seasonal variations in shellfish gathering may thus
result from both an increase in activity by local residents in summer, and through a
temporary increase in population over holiday periods.
3.6
CONCLUSION
An investigation of available data on non-commercial shellfish gathering suggests that
based on differences in shellfish availability, shellfish gathering activity and shellfish
species collected, the risk of TSP varies across the Biotoxin Zones in New Zealand.
Although there are insufficient data for this to be quantified, data also suggest that this
risk may vary with ethnicity. Thus differences in population structure in different
areas with respect to ethnicity may also impact on the risk of TSP in each zone.
Temporal patterns in shellfish gathering also impact on the risk of TSP. It should be
noted that times at which shellfish gathering activity is high may coincide with an
increased risk of toxic phytoplankton blooms in the warmer months (See Section 2).
In general, the ability to assess the risks presented by the occurrence of marine
biotoxins in shellfish would greatly benefit from the collection of high quality data
through studies focussed on this issue.
112
SECTION 4:
4.1
INTRODUCTION
Environmental surveillance for public health with respect to marine biotoxins in New
Zealand is primarily reliant on hazard surveillance at present – that is, monitoring for
toxic phytoplankton and biotoxins in shellfish. However, outcome surveillance in the
form of reporting the incidence of cases of Toxic Shellfish Poisoning (TSP), is also
undertaken. The current outcome surveillance system is designed to fulfill the
following objectives (Baker & McNicholas, 1995):
•
•
•
•
•
To identify cases of TSP so that the incidence and distribution of this illness, and
the associated biotoxin(s), can be monitored.
To identify shellfish contaminated by marine biotoxins that were not detected by
routine shellfish biotoxin monitoring, so that control measures can be taken.
To assist in characterising the illness caused by biotoxins, including the doseresponse relationship between biotoxin exposure and illness.
To assist in identifying other biotoxins that are not detected by current shellfish
biotoxin testing.
To assess the effectiveness of control measures.
Cases of TSP are identified by general practitioners and hospital clinicians, and
reported to local Medical Officers of Health. In some instances, (for example, where
they have not consulted a medical practitioner) members of the public may report
cases directly. Notified cases are investigated by public health staff, and recorded
locally by them on the notifiable disease database, EpiSurv. “Confirmed” or
“probable” cases are defined as being those where TSP symptoms occur within
relevant time frames, and which are associated with toxicity in shellfish sufficient to
account for those symptoms. Where these conditions are not met, cases may either
remain in the “suspect” category, or may be discounted depending on the outcome of
the investigation (Ministry of Health, 1997a).
Epidemiology of TSP is severely limited by the lack of biomarkers for exposure to
marine biotoxins in humans (i.e. there are no recognised human diagnostic tests to
determine whether a person has been exposed to marine biotoxins). There is also a
lack of knowledge about the clinical symptoms of TSP, and this results in a
comparative under reporting of the incidence of TSP (Fleming et al., 1995; Fleming et
al., 1998). Fleming et al., (1998) summarise the situation as follows:
“The lack of progress in phycotoxin disease epidemiology is due to the lack of disease
and exposure biomarkers in humans. The only way to study these diseases
epidemiologically has been identification through their clinical presentation, and
more recently, by applying the appropriate laboratory testing to the ingested seafood.
Because diagnosis could not be made accurately for either the clinical diseases or the
asymptomatic cases associated with these phycotoxin exposures, it has not been
possible to investigate their true incidence in human populations. Nor has it been
possible, without human biomarkers, to accurately evaluate the true clinical course,
treatment and prognosis of the marine toxin diseases.”
113
Any analysis of the epidemiological data relating to TSP in New Zealand should
consider the limitations of the knowledge framework within which the data were
gathered.
4.2
METHODOLOGY AND ASSUMPTIONS IN ANALYSIS
The Institute for Environmental & Scientific Research (ESR) has supplied the data
used in this analysis. These data were drawn from several separate databases that
record cases of TSP in New Zealand (an Excel spreadsheet of 1993 cases, a database
of summarized monthly reports to the Ministry of Health (1994-July 1996), an Excel
spreadsheet of cases from 1994 and January to July 1996, and the current EpiSurv
database (July 1996-June 1999)). Note that the details of the cases from 1995 were
only available in summary form from the summarised monthly reports to the Ministry
of Health.
Until 1996, assessments of the status of cases were based on the following criteria:
Unlikely:
The case does not meet case definition, and/or shellfish testing
(leftovers/same site) was negative for PSP or NSP.
Suspected:
The case meets the case definition, but no shellfish (leftovers/same
site) were available for testing.
Confirmed:
The case meets the case definition, and shellfish testing (leftovers/same
site) was positive for PSP, or NSP.
The case definition included the presence of one or more neurological symptoms
within 24 hours of eating shellfish (which includes neurosensory, neuromuscular, and
neurocerebellar symptoms).
Subsequent to a review of the epidemiological surveillance system for cases of TSP
(Baker & McNicholas, 1995), the case definitions were re-written to include all four
toxins (PSP, NSP, ASP and DSP). The current case definitions are given in Section C
of the Manual for Public Health Surveillance in New Zealand (ESR Communicable
Disease Centre, 1996). The revised status definitions separate the previous
“Confirmed” status into “Probable” and “Confirmed”, as follows:
Probable:
Meets case definition for suspect case, AND detection of relevant
biotoxin at or above the regulatory limit in shellfish obtained from near
or same site (not leftovers) within seven days of collection of shellfish
consumed by case;
Confirmed:
Meets case definition for suspect case, AND detection of biotoxin in
leftover shellfish at a level resulting in the case consuming a dose
likely to cause illness: Current dose level:
ASP: 0.05 mg/kg body weight
DSP: ingestion of 48 µg or 12 MU
NSP: 0.3 MU/kg body weight
PSP:10 MU/kg body weight(approx. 2 µg/kg body wt.)
114
As procedures within the surveillance system have improved, and toxin test methods
have become more specific, the quality of the epidemiological data collected has
improved.
Data for 1993 were provided as two sets of data – one containing all the cases
reported at the time, and the other only those cases that fit the case definitions for TSP
(Yvonne Galloway, ESR, pers. comm.). It has been assumed that all the cases in the
latter set of data could be assessed as “suspected”. In general there was no testing of
left-over meals or shellfish harvested concurrently from the same sites as the shellfish
consumed, so all these cases remain in the “suspected” category. The symptoms
exhibited by some cases suggest strongly that had shellfish samples been available,
there is a possibility that they might have established TSP as a cause of illness. In
other cases, the symptoms exhibited could have resulted from a range of causes, and it
is due to the lack of confirmatory tests that they remain in the TSP “suspected”
category rather than being considered “unlikely”.
There is no detailed computerised database of the 43 cases reported from 1995.
Copies of the original questionnaires filled out relating to each case are unable to be
located by ESR. Analysis is therefore based on the Results summary for reported
cases of illness following the consumption of shellfish, supplied by ESR to the
Ministry of Health. These summaries do not contain data about individual cases, so
no information regarding age, ethnicity, hospitalisation, weight, amount of seafood
consumed etc. are available over this time period. They do, however, contain an
assessment of the case status from the results of the combined questionnaire data and
shellfish testing for each case.
For the purposes of analysis in this review, current case definitions have been used.
All cases of “confirmed” status prior to July 1996 have been revised according to the
current status definitions, so that they are separated into “probable” or “confirmed”
status. This is unable to be done for two “probable” cases of DSP in 1995, as the data
on body weights and quantities of shellfish consumed with which to calculate likely
toxin doses, are not available. These two cases thus remain as “probable”. In the
course of our analysis we noted some inconsistencies in the assessments made over
this time period – for example, the assessment of several cases as “unlikely” where
the symptoms were recorded as fitting the case definition, but samples tested as
having been free of detectable levels of PSP or NSP. However, the samples were not
tested for ASP. Given that these cases resulted from the consumption of scallops,
which have a tendency to accumulate and retain ASP, it is our view that these cases
should have been assessed as “suspected” under the stated criteria. However, given
that we had only a summary of the information available to ESR, we have not altered
these assessments in our analysis of the data.
Data from July 1996 to June 1999, as recorded on the questionnaire forms for each
reported case, are collected in the “EpiSurv” database. We have revised the status of
some cases where microbiological results have subsequently provided additional
information and the case status had not been updated. Of the 17 cases recorded on
EpiSurv from July 1996 to the end of June 1999, two cases entered were recorded as
having no known symptoms, and a further three cases had microbiological test results
that strongly suggested that the symptoms were caused by bacterial contamination of
the shellfish. One further case did not fit the case definitions and there were no results
115
from shellfish testing, so the status of this case was revised from “probable” to
“unlikely”.
Epidemiological data for TSP collected from January 1993 until the end of June 1999
were analyzed with respect to: numbers of “unlikely”, “suspected”, “probable” and
“confirmed” cases each year; numbers of “suspected” and “probable”, cases arising
from non-commercial shellfish gathering as compared to commercial harvest;
shellfish species implicated in “suspected” and “probable” cases; and the areas from
which non-commercially harvested shellfish were gathered in “suspected” and
“probable” cases. The incidence of “probable” cases of TSP in New Zealand were
compared to the incidence of other food-borne diseases here. The distribution of
gender, age and ethnicity in “suspected” and “probable” cases from 1993 and 1994,
and January 1996 to June 1999 were also analyzed (these data were unavailable for
the intervening period).
4.3
RESULTS
Table 4.1 provides a summary of the total reported cases of TSP in New Zealand by
year, and their assessment as being “unlikely”, “suspected”, “probable” or
“confirmed” to have been caused by marine biotoxins in shellfish consumed.
Year
1993
1994
1995
1996
1997
1998
1999
(6
months)
Total number
of cases
reported
302
82
43
21
3
1
5
Number
assessed as
unlikely
163
55
13
11
2
1
0
Number
assessed as
suspected
139
26
23
10
2
0
4
Number
assessed as
probable
0
1
7
0
0
0
1
Number
assessed as
confirmed
0
0
0
0
0
0
0
Table 4.1:
Summary of the reported cases of TSP by year as assessed with
respect to the likelihood of the causative agents being PSP, ASP,
NSP or DSP toxins.
116
Over the time-period analysed (1993 to mid 1999) no confirmed cases of TSP have
been reported in New Zealand (consequently further analysis does not include this
category). Of all the TSP cases identified as “probable” from 1993 to June 1999, data
on hospitalisation are only available for one case. This case was not hospitalised.
The incidences of “probable” cases of TSP are compared with the incidence of two
other illnesses associated with the consumption of shellfish in Table 4.2.
Campylobacter is the most common food-borne illness, predominantly associated
with poor food handling. Vibrio parahaemolyticus is a halophilic bacterium that is
naturally present in marine waters and silts, and that can become concentrated in
shellfish due to their filter-feeding activity.
Because illness from Vibrio
parahaemolyticus is not notifiable, it is possible that these numbers are understated
(hence not being stated as an official rate per 100,000 in Table 4.2). It can be seen
that the incidence of TSP is very much lower than that of Campylobacter, and very
slightly lower than that of Vibrio parahaemolyticus.
Year
1994
1995
1996
1997
1998
Table 4.2:
TSP
Number of Rate per
cases
100,000
1
0.03
7
0.19
0
0
0
0
0
0
Campylobacter
Number
Rate per
of cases
100,000
7,714
213.2
7,442
205.7
7,628
210.8
8,848
244.5
11,578
320.0
Vibrio parahaemolyticus
Number of cases
Not available
2
3
3
6
Comparison of the numbers of cases and rates per 100,000 people
in New Zealand between “probable” cases of TSP, and illnesses
caused by Campylobacter and Vibrio parahaemolyticus. (Source:
Epidemiology Group, ESR).
Of the “suspected” and “probable” cases of TSP in 1993-94, and from January 1996
to June 1999, 48.3% were male, and 50.6% were female (N=178). The gender of
1.1% of the cases was not recorded. Data were not available for 1995 cases.
Of the total “suspected” and “probable” cases from January 1993 to June 1999
(N=213), 30.0% were from commercially harvested shellfish, and 67.7% from noncommercially harvested shellfish. In 2.3% of the cases, the shellfish source was not
recorded on the database.
Most of the cases in 1993 occurred prior to the instigation of a comprehensive marine
biotoxin monitoring programme. Of the total cases in 1993 (N=139), 21.6% were
from commercially harvested shellfish, and 74.8% from non-commercially harvested
shellfish. The source of 3.6% of the shellfish was not recorded. Of the “suspected”
and “probable” cases from the beginning of 1994 to June 1999 (i.e. excluding the
cases from 1993), 45.9% were from commercially harvested shellfish, and 54.1%
from non-commercially harvested shellfish (N=74). However, eight of the nine
“probable” cases (88.9%) arose from non-commercially harvested seafood, and 11.1%
from commercially harvested seafood. The case arising from commercially harvested
shellfish meets the case definition for NSP, and arose from the consumption of
mussels, harvested from Big Glory Bay in Zone J. Of the cases arising from non117
commercially harvested shellfish, one was a case of PSP arising from tuatua gathered
at Ohope Beach (Zone D), and 7 cases of DSP were from mussels gathered at Akaroa
(Zone I).
The age distribution of the “suspected” and “probable” cases of TSP in 1993-94 and
from January 1996 to June 1999 is shown in Table 4.3 with reference to the New
Zealand population as a whole. Data were not available for 1995 cases.
Age (years)
<10
10-19
20-29
30-39
40-49
50-59
60-69
70-79
80+
Not recorded
Table 4.3:
Percentage of
Total Cases
(%)
1.1
5.1
14.6
26.4
25.8
14.0
6.7
3.4
0.6
2.3
Number
2
9
26
47
46
25
12
6
1
4
Age Structure of New
Zealand Population
(%)
15.7
14.7
14.2
15.9
13.7
10.7
7.3
5.1
2.7
Age distribution of the “suspected” and “probable” cases of TSP in
1993-94, and from January 1996 to June 1999, compared to the
age structure of the total New Zealand population (based on 1996
Census data, Statistics NZ).
Table 4.4 shows an analysis of the “suspected” and “probable” cases of TSP in 199394 and from January 1996 to June 1999 by ethnic origin, with reference to the ethnic
composition of the New Zealand population as a whole. Data were not available for
cases from 1995.
Ethnic Origin
NZ European
Maori
Pacific Island
Other
Not recorded
Total No. of
cases (N)
Table 4.4:
Percentage of Cases
from NonCommercially
Harvested Seafood (%)
78.0
14.6
4.1
2.4
0.9
Percentage of Cases
from Commercially
Harvested Seafood
(%)
85.5
9.1
1.8
0.0
3.6
123
55
Percentage of
Total New Zealand
Population (%)
71.7
14.5
4.8
9.0
Analysis of “suspected” and “probable” cases of TSP from noncommercially and commercially harvested seafood in 1993-94 and
from January 1996 to June 1999 by ethnic origin, compared to the
ethnic composition of the NZ population. (NZ population figures
from 1996 census data, Statistics NZ).
For all the “suspected” and “probable” cases of TSP from 1993-94 and 1996-June
1999, the source of seafood (i.e. non-commercially harvested or commercially
118
harvested) for each ethnic group was analysed. These results are presented in Table
4.5. Data were not available for cases from 1995.
Ethnic Origin
NZ European
Maori
Pacific Island
Other
Not Recorded
Table 4.5:
Percentage from
Non-Commercially
Harvested Seafood
(%)
67.1
78.3
83.3
100.0
33.3
Number of Cases
143
23
6
3
3
Percentage from
Commercially
Harvested Seafood
(%)
32.9
21.7
16.7
0.0
66.7
Analysis of source of seafood by ethnic group for “suspected” and
“probable” cases from 1993-1994 and 1996-June 1999.
The cases arising from non-commercial gathering of shellfish have been analyzed
with respect to the areas from which shellfish were taken. For this purpose, the
Biotoxin Zones A-K have been used. The results of this analysis are presented in
Table 4.6. A map illustrating the geographical areas covered by each zone and a
summary of these data are presented in Figure 4.1.
Number of Cases in each Zone
1993
1994
1995
1996
1997
1998
1999 (6
months)
7
36
17
13
13
5
0
1
3
0
0
3
1
0
2
0
4
0
0
0
0
0
0
0
3
4
0
1
4
0
6
3
0
1
0
0
0
0
1
1
0
0
0
0
0
0
0
1
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
1
0
0
4
0
0
0
0
11
37
20
21
13
11
9
1
9
3
0
Total No.
of Cases
excluding
1993
4
1
3
8
0
6
9
0
6
3
0
9
0
0
0
0
0
0
9
0
Zone
A
B
C
D
E
F
G
H
I
J
K
Not
known
Table 4.6:
Total
No. of
Cases
Geographical distribution of sites from which shellfish were
gathered in “suspected” and “probable” cases of TSP arising from
non-commercially harvested shellfish January 1993-June 1999.
(Zones are illustrated in Figure 4.1).
119
Zone B: Cape Brett to Cape
Rodney. Cases: 37 (1)
Zone A: Tauroa Point to Cape Brett
Cases: 11 (4)
Zone C: Cape Rodney to Cape
Colville. Cases: 20 (3)
Zone D: Cape Colville to Cape
Runaway. Cases: 21 (8)
Zone F: Tauroa Point to Cape
Egmont. Cases: 11 (6)
Zone G: Cape Farewell
to Cape Campbell.
Cases: 9 (9)
H
G
Zone E: Cape Runaway
to Cape Palliser. Cases:
13 (0)
Zone J: Cape Farewell
to Bluff. Cases: 3 (3)
Zone H: Cape Egmont to
Cape Palliser.
Cases: 1 (0)
Zone K: Chatham
Islands. Cases: 0 (0)
Zone I: Cape
Campbell to Bluff.
Cases: 9 (6)
Figure 4.1:
Distribution of “suspected” and “probable” cases of TSP arising
from non-commercially harvested shellfish. Number of cases =
Total number of cases from January 1993-June 1999; (Number in
brackets = Number of cases January 1994-June 1999).
120
s
Sc el
om allo
bi p
na
tio
Tu n
at
ua
Pi
p
O i
ys
te
r
Pa
u
C
ra a
yf
is
h
Ki
n
C a
oc
kl
e
C
ra
b
40
35
30
25
20
15
10
5
0
C
M
us
Number of Cases
An analysis of the shellfish species consumed in the “suspected” and “probable” cases
of TSP arising from non-commercially and commercially harvested shellfish is
presented in Figure 4.2. Where several shellfish species were consumed and it is not
possible to either identify the individual species, or identify separately which of
several species is implicated in the TSP, the shellfish has been classified as
“Combination”.
Shellfish Species
Commercially harvested species
Recreationally harvested species
Figure 4.2:
Graph showing the number of “suspected” and “probable” cases
of TSP from January 1993 to June 1999 arising from the
consumption of different seafood species. Figures for cases arising
from non-commercially harvested seafood and commercially
harvested seafood are shown separately.
ESR does not collect data regarding the incidence of respiratory irritation syndrome
caused by brevetoxins or other lipid soluble toxins. There have been three incidents
of respiratory irritation syndrome in New Zealand. One occurred in Orewa, north of
Auckland in the summer of 1993 (Bates et al. 1993), one on the east coast of the
North Island from Hawkes Bay to Cape Palliser in the summer of 1998, and the other
in the Wellington Harbour area, also in the summer of 1998 (Chang et al., 1998a). In
the two former events, several hundred people living on the coast or visiting the beach
were affected. Approximately 80 people reported symptoms associated with the
Wellington Harbour event. Symptoms included sore throat, dry coughing, and nose
and eye irritation. People swimming in the Wairarapa area also reported skin
irritation. It has been reported that asthmatic people may be more seriously affected
than others (Catherine Hayes, Health Protection Officer, Wairarapa Health district,
Hutt Valley Health, pers. comm.).
121
4.4
DISCUSSION
Because of the large number of variables impacting on the reported incidence of TSP
in New Zealand, interpretation of the epidemiological data needs to be undertaken
with care and caution. Interpretation of the data needs to take into consideration the
following factors:
•
The amount of good data quality data is limited: Although 457 cases potentially
related to TSP have been reported between January 1993 and June 1999, only 9 of
these (1.97%) have been corroborated as probably being some form of TSP (i.e.
established as “probable” or “confirmed” status). There have been increases over
time in the range and specificity of tests undertaken for toxins in leftover/same site
samples of shellfish. In 1993, tests were not done on leftover/same site samples,
so no cases could be either downgraded to “unlikely”, or up-graded to
“confirmed”. Similarly, the testing of leftover/same site samples for only one or
two toxin groups in the early years means that cases that may have resulted from,
say ASP or DSP (which were commonly excluded from testing at that time), have
not been established as “probable’ or “confirmed” cases. In addition, where tests
from leftover or same site samples have been taken, and microbiological tests
have been undertaken, the results have frequently not been entered into the
database. A distortion of the proportion of cases in the “suspected” category is the
result of these inconsistencies, and this must be considered when trying to draw
conclusions from year-to-year comparisons. The lack of leftover samples, failure
to collect “same site” samples in a timely manner, and incomplete data from 1995
(resulting in the inability to calculate the dose received in two cases with
“probable” status), have also resulted in failure to corroborate “suspected” cases
as “probable” or “confirmed”.
•
It is not known what percentage of TSP cases actually get reported to the medical
authorities. It is likely that people suffering from neurological symptoms after
consuming shellfish would seek the advice of their doctor, since these symptoms
are somewhat unusual and likely to worry the sufferer. The level of familiarity of
doctors with the symptoms of TSP, the proportion of cases that are recognised and
reported as such, and the incidence of asymptomatic cases, are not known.
•
It is likely that the incidence of DSP is under-reported in these data. The
symptoms of DSP are similar to those of many illnesses of microbiological
sources related to shellfish consumption. In addition, cases arising from
pectenotoxin, or from a suite of DSP toxins in which DTX-3 is predominant, will
not be identified as TSP under the present surveillance system. Similarly, the
surveillance system does not include yessotoxin.
•
Data on the incidence of NSP prior to the introduction of testing using the acetone
extraction method as a screen test, followed by a bioassay using an ether
extraction method (refer to section 1.2) may not accurately reflect the incidence of
NSP. This may impact on the validity of the confirmation of an NSP case prior to
September 1994, (currently assessed as “probable”).
122
•
Due to the absence of biomarkers, there are no recorded data on the effects of
long-term exposure to low levels of any of the biotoxins.
The epidemiological data suggest that there is a general trend toward a reduction in
the number of cases of TSP being reported (Table 4.1). There are several factors that
could potentially contribute to this trend: a) the overall decrease in marine biotoxin
events since 1993; b) an increasingly effective marine biotoxin monitoring
programme, ensuring that fewer people are exposed to marine biotoxins; and c) a
decreasing awareness amongst medical practitioners of the symptoms of TSP. It is
suggested that medical practitioners be reminded of the symptoms of TSP, and the
requirement to report suspected cases. One general practitioner questioned about TSP
by the authors commented that “the general public are kept better informed about TSP
than are medical practitioners”.
While the gender distribution of TSP cases is similar to that of the general population
in New Zealand, the age structure appears somewhat different (Table 4.3). There
appears to be a lower than expected number of cases of people less than 20 and 80+
years old, and a higher than expected number of cases in the 30-59 age group. While
this could potentially be due to an increased susceptibility of the 30-59 age group to
TSP, it may also be a result of a higher level of consumption of shellfish. Similarly,
the lower level in the younger and older age groups could result from lower levels of
shellfish consumption.
Within the limits of the data collected, the distribution of cases of TSP from noncommercially harvested seafood with respect to ethnic origin is similar to that of the
total population in New Zealand (Table 4.3). With respect to commercially harvested
shellfish, the higher than expected percentage of NZ European cases, and slightly
lower percentage of Maori and Pacific Island cases may be a reflection of how
shellfish is obtained by these groups. In cases arising from both commercially and
non-commercially harvested shellfish, people of ethnic origin other than NZ
European, Maori or Pacific Island have lower reported incidence of TSP than would
be predicted from the population structure. The results are also surprising given the
data on ethnicity of shellfish gatherers presented in Section 3, which suggests that
Maori and Asian populations potentially form a much more significant percentage of
non-commercial harvesters of shellfish (for example, 54% and 15% respectively in
one study in the Whangateau Harbour). The distribution of cases of TSP does not
reflect this activity. One reason for this could be differences in medical presentation
and reporting rates between people of different ethnic origins.
Except in cases where ethnic origin has not been recorded, a greater percentage of
cases in all ethnic groups arose from non-commercially harvested seafood (Table 4.5).
NZ Europeans were the group with the lowest percentage of cases from noncommercially harvested seafood. This may be a reflection of a lower level of noncommercial harvesting activity by this group.
With respect to a comparison between the incidence of cases of TSP arising from
commercial and non-commercial harvesting, the high percentage of cases related to
non-commercial harvesting in 1993 is a reflection of the geographical location of
shellfish contaminated with biotoxins, and the location of major commercial
123
harvesting areas elsewhere. The event also occurred over a summer holiday season
when non-commercial harvesting was particularly high.
The comparison between the incidence of cases of TSP from commercial and noncommercial harvesting since the institution of the marine biotoxin monitoring
programme is more pertinent to the comparative effectiveness of commercial and noncommercial programmes. The percentage of total cases from non-commercial
harvesting is only slightly higher than that from commercially harvested shellfish
(54.1% compared to 45.9%). However, if only the “probable” cases of TSP are
considered, the result is somewhat different: eight out of nine “probable” cases
(88.9%) arose from the consumption of non-commercially harvested shellfish. This
suggests that the non-commercial marine biotoxin monitoring programme is less
effective at protecting public health than the commercial marine biotoxin monitoring
programme. This is not surprising, given the differences between the programmes
with respect to the level of control over harvesting in the event of biotoxin occurrence.
124
SECTION 5:
5.1
RISK ASSESSMENT
INTRODUCTION
A commonly used public health risk analysis model consists of three phases: risk
assessment, risk management, and risk communication (USEPA, 1993). This section
of the report provides a risk assessment with respect to Toxic Shellfish Poisoning
(TSP) arising from consumption of non-commercially harvested shellfish in New
Zealand.
“Risk assessment defines the potential safety and health effects from exposure of
individuals and populations to hazardous materials and situations” (USEPA, 1993).
The USEPA risk analysis model outlines four interrelated steps to risk assessment
(USEPA, 1993). These are:
•
Hazard identification: identification of the environmental agent of concern, its
adverse effects, target populations and conditions of exposure.
•
Dose-response assessment: determination of the degree of the effects at different
doses.
•
Exposure assessment: estimation of the magnitude, duration and frequency of
human exposure to pollutants of concern, and the number of people exposed via
different pathways.
•
Risk characterisation: combination of the information obtained from the hazard
identification, dose-response assessment, and exposure assessment to estimate the
risk associated with each exposure scenario considered, and to present information
on uncertainties in the analysis.
The following sections contain a risk assessment for each of PSP, ASP, DSP, NSP
and respiratory irritation syndrome.
5.2
PARALYTIC SHELLFISH POISONING
5.2.1
Hazard Identification
The toxins that cause Paralytic Shellfish Poisoning (PSP) comprise a suite of naturally
occurring neurotoxic tetrahydropurine derivatives, which act as sodium channel
blocking agents. Cembella et al., (1995b) summarised the toxin syndromes of PSP:
“Paralytic Shellfish Poisoning is a neurotoxic syndrome resulting primarily from the
blockage of neuronal and muscular Na+ channels. Binding to the Na+ channel
prevents propagation of the action potential that is essential to the conduction of nerve
impulse and muscle contraction. In vertebrates, the peripheral nervous system is
particularly affected; typical symptoms of poisoning include tingling and numbness of
the extremities, progressing to muscular incoordination, respiratory distress, and
muscular paralysis leading to death by asphyxiation in extreme cases”. Initial
symptoms occur within 30 minutes of ingestion, and in extreme cases, respiratory
paralysis may occur within 2-24 hours after ingestion (Hallegraeff, 1995). The
125
fatality rate may exceed 10%, particularly when medical attention is not available
(Wilson, 1996). There are no known antidotes to the toxin. Treatment includes
pumping out the patient’s stomach, and the application of artificial respiration. In
cases that are not fatal, there are no lasting effects (Hallegraeff, 1995). Exposure to
the toxin does not confer immunity.
In New Zealand, several species of the dinoflagellate Alexandrium produce biotoxins
known to cause PSP. They include Alexandrium angustitabulatum, A. minutum, A.
ostenfeldii, and an unidentified species isolated from Marsden Point in Northland.
Alexandrium tamarense is known to produce PSP toxins overseas, but as yet the New
Zealand strains have not been tested or implicated in the occurrence of PSP toxins in
shellfish. Given possible variations in toxin production between different strains of
the same species, and that phytoplankton monitoring has not always identified the
origin of detectable levels of PSP in shellfish, it is possible that other species of
Alexandrium in New Zealand waters will also produce PSP toxins.
Different strains of Alexandrium have different toxin profiles (Cembella et al., 1987).
Since different toxin derivatives have different toxicity, the toxin profile impacts on
the overall toxicity of the strain.
Because of the tendency of shellfish to accumulate PSP toxins from toxic
phytoplankton, shellfish consumers are exposed to PSP toxins when they consume
shellfish that have been harvested from areas where PSP-producing phytoplankton are
present. Shellfish consumers are thus the target population for PSP. Shellfish
consumers are reliant on a marine biotoxin monitoring programme to determine
whether shellfish are contaminated with PSP toxins – it is not possible to ascertain
this by the appearance of the shellfish, or the water from where they are harvested.
The comparatively low densities of toxic Alexandrium species required to produce
significant PSP levels in shellfish are not obvious as a “bloom” in the water. The
preparation of the shellfish may impact on the risk of PSP to the consumer – for
example, whole scallops are more toxic than scallop roe. However, exclusion of high
risk portions of the shellfish is the only step that can be taken in the preparation of
shellfish for consumption to reduce the risk of PSP. Cooking does not destroy PSP
toxins.
The risk of PSP varies not only with the degree of exposure of the shellfish to PSPproducing phytoplankton and the toxin profile of the phytoplankton, but also with the
species of shellfish. Analysis of coincident monitoring data suggests that the presence
of PSP-producing Alexandrium species in shellfish growing water results in
significantly higher levels of toxicity in tuatua than in GreenshellTM mussels.
Qualitative analysis of a very limited amount of data on toxicity levels in other
species suggests that scallops do not become as toxic as tuatua, but accumulate higher
PSP toxin levels than GreenshellTM mussels, pipi and cockles. These differences may
be related to differences in ingestion of toxin, or in detoxification processes within the
shellfish. These results are not in any way definitive, and more data collection is
required to investigate this further.
126
5.2.2
Dose-Response Assessment
A summary of international data on PSP dose-response relationships for adults was
provided in the previous review of the marine biotoxin monitoring programme
(Wilson, 1996). Wilson (1996) concluded that “It is estimated that 200 to 500 µg of
saxitoxin will produce at least mild symptoms, 500 to 2,000 µg is likely to cause
moderate to severe symptoms, and consumption of over 2,000 µg is likely to produce
serious and possibly lethal consequences. However, the variability in PSP toxicity is
quite marked”. There has been one probable case of PSP in New Zealand. The
patient had consumed an estimated 50 g of tuatua taken from Ohope Beach in January
1999. Tuatua taken from the same site two days later were tested and found to
contain 230 µg STX eq./100g. If it can be assumed that the PSP level in the shellfish
had not decreased significantly over the two day interval, this suggests an estimated
dose of 115 µg of saxitoxin was consumed by the 60 kg patient. Symptoms
experienced included: nausea, vomiting, diarrhoea, numbness and tingling sensation
in face and hands, unstable walking, blurred vision, difficulty swallowing, slurred
speech, weakness and drowsiness, a rash on the skin, headaches, back pain and aching
joints.
5.2.3
Exposure Assessment
Given the data available, it is extremely difficult to provide a meaningful exposure
assessment that is in any way quantitative. Analysis of marine biotoxin monitoring
data in Section 2 identified that PSP toxin levels in shellfish varied within zones from
year to year, and that overall occurrence of PSP in shellfish also varied annually
across New Zealand as a whole. As a result of this, and in consideration of the
complex set of variables that may impact on PSP toxin occurrence, it was concluded
that predictions of risk based on historical data would be inappropriate until a much
greater depth of understanding about the dynamics of Alexandrium blooms in New
Zealand has been gained through long-term studies. Exposure assessment related to
the consumption of non-commercially gathered shellfish is further complicated by
potential differences in toxin ingestion and detoxification between different shellfish
species, variations in the distribution of shellfish species, and lack of robust data
regarding the location and quantity of shellfish gathered and consumed by noncommercial harvesters.
However, the following observations regarding the risk of exposure to PSP can be
made:
•
The frequency of occurrence of PSP levels in shellfish above the level that
represents a risk to consumers has been relatively low (one or two samples over 6
years) or zero in most areas since July 1993. An exception to this is in the Bay of
Plenty, where there has been a long-running occurrence of PSP, with levels both
above and below the regulatory level in many of the months between March 1995
and the present. It is not possible to quantify the overall frequency of occurrence
of PSP toxin levels that represent a potential risk to consumers, due to temporal
and spatial stratification in the sampling regime.
127
•
With exception to the Bay of Plenty, the maximum toxin levels in most areas have
been low (82 µg/100g and 127 µg/100g compared to a regulatory level of 80
µg/100g ). The maximum toxin level in the Bay of Plenty (Zone D) was 1007
µg/100g, which is high enough to cause moderate to severe symptoms in human
consumers. In the Bay of Plenty, the site with the greatest number of samples
with PSP toxin levels above the regulatory level between 1/7/93 and 30/6/99, (Site
D37, Ohope Beach), contained PSP toxin levels in samples over 18 weeks that
were sufficient to produce mild symptoms in consumers (PSP >115 µg/100g and
<500 µg/100g). PSP levels sufficient to produce moderate to severe symptoms
(>500 µg/100g and <2,000 µg/100g) occurred on 1 week during this period at this
site. This is potentially an understatement of risk, since sampling was
discontinued when toxin levels were high. At one of the most consistently
monitored sites in this area, D41 (Whangaparoa), PSP toxin levels sufficient to
produce mild symptoms occurred on 4 weeks, and levels sufficient to produce
moderate to severe symptoms on 1 week. At Tokata (D38), a sample site that has
not been consistently monitored, toxin levels sufficient to produce mild symptoms
were recorded on 2 weeks, and sufficient to produce moderate to severe symptoms
on 3 weeks. Again, this is probably understated, as sampling was discontinued at
times when toxin levels were high. PSP toxin levels in shellfish at other sites in
the Bay of Plenty that were inconsistently monitored had between 1 week and 12
weeks on which toxin levels were sufficient to produce mild symptoms in
shellfish consumers. The numbers of people that would have been potentially
exposed to PSP toxins in this area in the absence of a marine biotoxin monitoring
programme are uncertain, due to inadequate data on non-commercial harvesting of
shellfish. However, the diary survey of Fisher & Bradford (1998) suggested that
Zone D is an area where a comparatively high level of non-commercial shellfish
gathering activity has occurred (25% of the total New Zealand fishing trips
targeting bivalve species).
•
Available data suggest that the risk of exposure to PSP toxins varies with the
species of shellfish, with tuatua being a shellfish that represents a high risk.
Further work is required to clarify these differences.
•
Phytoplankton monitoring indicates that potentially toxic Alexandrium species are
widely distributed in New Zealand. The mechanisms related to the disappearance
of previously persistent PSP toxicity in shellfish at Tokerau Beach, and the
persistence of PSP toxicity in the Bay of Plenty are not understood. Until they
are, it cannot be assumed that PSP will persist in the Bay of Plenty, or not occur
elsewhere.
•
There are no obvious seasonal patterns in the occurrence of PSP toxicity in
shellfish. However, research suggests that for a range of inter-tidal shellfish, noncommercial harvesting is highest in the summer, and lowest in the winter
(Kearney, 1999; Hartill & Cryer, 1999).
5.2.4
Risk Characterisation
Meaningful quantitative assessment of the risks associated with PSP through the
consumption of non-commercially harvested shellfish is not possible due to the lack
of robust information about consumption of non-commercially harvested shellfish.
128
Data collected from the marine biotoxin monitoring programme, combined with
research results overseas, are insufficient to make robust predictions about the
frequency of occurrence, or location of PSP toxins in New Zealand in the future.
However, several scenarios are presented in order to examine the kinds of human
impacts that PSP could have in New Zealand. (Even these scenarios are difficult to
construct, due to the discontinuity of sampling in Zone D at times when PSP toxins
were present).
Data from the diary survey of recreational fishing in New Zealand by Fisher &
Bradford (1998) indicated that diarists recorded taking 4,341 tuatua from Zone D in
the 12 months of the survey. Fisher and Bradford (1998) apply a scaling factor of
139.9 to calculate the total non-commercial harvest figures from the figures recorded
by the diarists. Using this scaling factor, and if an average meal size of tuatua is
100g, equating to 12 tuatua, the average number of meals per week of noncommercially harvested tuatua from Zone D would be 973. In a year like July 1995June 1996, there were approximately 2 weeks when PSP levels in shellfish in the Bay
of Plenty would produce moderate to severe symptoms in consumers, and 2 weeks
when consumption of shellfish would result in mild PSP symptoms. (These figures
are estimated over all the tuatua sites where PSP toxin levels occurred, taking into
account discontinuities in the sampling). This suggests that in the absence of a marine
biotoxin monitoring programme, and assuming that there is no communication of risk
that prevents consumers eating shellfish in the event of PSP occurrence, 1,946 people
could suffer moderate to severe PSP symptoms, and 1,946 people mild PSP symptoms
each year. These figures are calculated from estimated consumption of tuatua alone
(apparently the species that represents the greatest risk, and harvested from the area in
Zone D where the toxin occurred), and do not include exposure to toxins through
consumption of other species of shellfish. In reality, communication of the risk
through media reports means that the actual number of people likely to become ill
would be somewhat lower. In contrast, in a scenario similar to the July 1994-June
1995 year, there would be no cases of PSP in Zone D, and none from elsewhere.
Data from Hay (1996) found that 31% of Maori households in the far north of New
Zealand collected seafood for consumption at least once a week, and 52% at least
fortnightly.
Information from a variety of Maori informants suggests that
approximately 30% of this seafood is shellfish. This means that in the Far North,
approximately 10% of the Maori households collect shellfish at least weekly, and
about 16% at least fortnightly. If similar toxin levels as occurred in Zone D in 199596 were to occur in the far north, then a significant percentage of the Maori
population would be at risk from PSP.
At this point it is worth considering these scenarios somewhat objectively. The wide
disparity between the results of the Fisher & Bradford (1998) diary survey, and the
results of the study by Kearney (1999) with respect to non-commercial harvest of
cockles, brings into question the reliability of the harvest data used in these scenarios.
This highlights the need for more comprehensive and robust data in order to estimate
the risk of PSP and other marine biotoxins accumulated by shellfish in New Zealand.
129
5.3
AMNESIC SHELLFISH POISONING
5.3.1
Amnesic Shellfish Poisoning is caused by Domoic acid (Wright et al., 1989). Domoic
acid is an excitatory amino acid derivative acting as a glutamate agonist on the
Kainate receptors of the central nervous system (Cembella et al., 1995b). “This
secondary amino acid is considered to be a more potent neuroexcitor than Kainic acid,
which when systemically injected into specific parts of the brain is known to have
degenerative effects. Domoic acid is considered to be the primary toxin involved in
ASP, although isomeric forms (e.g. iso-domoic acid) of lesser potency also occur
naturally”(Cembella et al., 1995b).
Pennate diatoms within the genus Pseudo-nitzschia produce Domoic acid implicated
in ASP. Domoic acid has been confirmed in some but not all New Zealand isolates of
Pseudo-nitzschia australis, P. pungens, P. turgidula, (Rhodes et al., 1996), P.
delicatissima and P. pseudodelicatissima (Rhodes et al., 1998b). Two other species
are a frequent component of Pseudo-nitzschia blooms: P. heimii and P. multistriata
(L. Rhodes, Cawthron Institute, pers. comm.), but to date neither have been found to
be toxic.
A mild case of ASP causes nausea, vomiting, diarrhoea, and abdominal cramps,
within 3-5 hours. In severe cases, patients suffer a decreased reaction to deep pain,
dizziness, hallucinations, confusion, short term memory loss, and seizures
(Hallegraeff, 1995). Most severe cases have been found to show continued selective
memory loss, particularly short-term memory (Todd, 1993).
Because of the tendency of shellfish to accumulate ASP toxins from toxic
phytoplankton, shellfish consumers are exposed to ASP toxins when they consume
shellfish that have been harvested from areas where ASP-producing phytoplankton
are present. Shellfish consumers are thus the target population for ASP. The age of
the consumer may affect the severity of the symptoms of ASP experienced. For
example, there appears to be a close association between memory loss and age: those
people under 40 years old are more likely to have diarrhoea, and those over 50 to have
memory loss (Todd, 1993). Other symptoms are not related to age. However, people
in poor health are more likely to be more severely affected (Todd, 1993).
Shellfish consumers are reliant on a marine biotoxin monitoring programme to
determine whether shellfish are contaminated with ASP – it is not possible to
ascertain this by the appearance of the shellfish or the water from where they are
harvested. Risk may be reduced somewhat in the preparation of the shellfish for
eating: toxin levels may vary with the parts of the shellfish consumed (for example,
scallop guts tend to contain higher levels of ASP toxins than the roe or muscle).
Exclusion of the high risk portions of shellfish can reduce the risk of ASP. It has been
suggested that cooking, and subsequent discarding of the cooking water, might reduce
the risk of ASP since the toxins are water soluble (Wilson, 1996). Experiments with
Dungeness crabs showed that cooking appears to decrease the level of Domoic acid in
the viscera while translocating small amounts into the meat (Loscutoff, 1992).
However, how this applies to shellfish is unknown.
130
The risk of ASP may also vary with shellfish species consumed. Limited data from
concurrent sampling of different shellfish species from the same sites suggest that
scallops accumulate and retain higher levels of Domoic acid than mussels or cockles.
More data are required to investigate this further.
5.3.2
A summary of international data on ASP dose-response relationships for adults was
provided in the previous review of the marine biotoxin monitoring programme
(Wilson, 1996). Wilson concluded: The minimal dose for acute symptoms has been
estimated as being in the 5-10 mg range, with moderate to severe symptoms,
including memory loss, associated with doses in the 60-290 mg range. There have
been no confirmed cases of ASP in New Zealand.
5.3.3
Exposure Assessment
The following observations can be made regarding the risk of exposure to ASP:
•
The frequency of occurrence of ASP levels in shellfish above the level that
represents a risk to consumers has been relatively low, with zero or only one
sample over 6 years in most zones. An exception to this very low frequency is in
Zone A, where 33 samples above the regulatory level have occurred since July
1993.
•
The frequency of occurrence of Domoic acid, above the level of detection in
shellfish, may vary from year to year, within zones, and across all zones. Both
Pseudo-nitzschia species, and the occurrence of low levels of Domoic acid in
shellfish, are widely distributed throughout New Zealand. There are insufficient
data for robust predictions about future occurrence to be made.
•
In Zone A, all Domoic acid levels above the regulatory level have occurred in
scallop samples, with the exception of three GreenshellTM mussel samples. In
Zone A, 7.75% of scallop samples taken between 1/7/94 and 30/6/99 contained
levels of ASP above the regulatory level (Note that scallop sampling is seasonal,
and includes the time of year when ASP is most frequent). Qualitative analysis
suggests that there may be significant differences in accumulation and retention of
Domoic acid between different shellfish species, and that scallops may be a
species that represents a comparatively high risk to consumers. 74.4% of Zone A
scallop samples taken in the harvesting season between 1/7/94 and 30/6/99
contained detectable levels of Domoic acid, as did 26.6% of scallop samples in
Zone D. While there are currently no known chronic effects caused by long-term
ingestion of low levels of Domoic acid, these frequencies would be a cause for
concern should this be the case.
•
Inconsistent sampling confounds quantification of the magnitude of toxin levels.
Observations suggest that the toxin levels vary in different parts of scallops, with
the highest levels found in the gut and skirt, and lower levels in the roe and
muscle. The maximum level of Domoic acid found in whole scallops was 210
µg/g, while a level of 600 µg/g was found in the gut and skirt in another sample.
131
The maximum level in GreenshellTM mussels was 187 µg/g. Assuming that mild
symptoms of ASP arise from a dose that is 50 µg/g – 599 µg/g (i.e. 5-59.9
mg/100g), then consumers of non-commercially harvested shellfish in Zones D &
G would have been exposed to ASP for one week at one site over 6 years.
Domoic acid level in scallops (either whole, or muscle and roe only) from Zone A
were sufficient to produce mild ASP symptoms in consumers of 100g of shellfish
for 2 weeks in July 1993-June 1994, 3 weeks in 1994-95, and 1 week in 1996-97.
None of the levels in mussels in Zone A were sufficient to produce even mild
symptoms assuming consumption of only 100g.
•
There appears to be a possible broad seasonal pattern in the occurrence of Domoic
acid in shellfish, with increased risk of exposure to ASP for consumers of shellfish
from August to December. Research suggests that for a range of inter-tidal
shellfish, non-commercial harvesting is highest in the summer, lowest in the
winter, and at intermediate levels in spring and autumn (Kearney, 1999; Hartill &
Cryer, 1999). However, there are no data available regarding seasonality of noncommercial harvest of sub-tidal shellfish such as scallops (although the time
period when scallops may be legally harvested runs from July through to
February).
5.3.4
Quantitative estimation of the risk of ASP in New Zealand can only be undertaken if
large assumptions about non-commercial harvesting patterns and consumption are
made. If scenarios are created using the occurrence of ASP in scallop beds in Zone A
as a model, assumptions need to be made about the level of non-commercial
harvesting from each bed. A range of scallop beds in Zone A appears to have
exhibited ASP toxicity above regulatory levels in different years: the
Whangaroa/Cavelli Islands area in 1993 and 1995, Doubtless Bay in 1994, and
Rangaunu Bay/Houhora Bay in 1996-97.
From the diary survey of Fisher & Bradford (1998), the total non-commercial harvest
of scallops in Zone A can be estimated. An assumption is made that the harvest is
divided equally across the beds in all areas, and that the non-commercial harvest of
scallops from Spirits Bay (in the far north) is negligible because it is less accessible to
small boats, and further from population bases. It is assumed that the average scallop
meal from non-commercially harvested scallops would consist of 12 scallops,
equating to 200g in weight. Under these assumptions, there would be 83 meals of
scallops harvested from each bed each week of the scallop harvest season. In a year
similar to July 1996-June 1997, there would be 9 weeks over which Domoic acid
levels were sufficient to produce mild symptoms of ASP, provided that only the
muscle and roe of the scallops were consumed. In the absence of any publicity about
illness, this would mean that 747 people could potentially be exposed to ASP.
However, given that the occurrence of Domoic acid is likely to be in consecutive
weeks, and some publicity of illness is likely, then the number of mild cases of ASP is
likely to be somewhere between 747 and 83. Conversely, in a year similar to 199798, there would be no cases of ASP from this area.
132
The widely recognised cultural importance of seafood for Maori, and some survey
data (e.g. Kearney, 1999) suggest that Maori may be disproportionately affected by
marine biotoxins. As discussed previously, results from a survey by Hay (1996) and
subsequent discussion with Maori informants suggest that 10% of Maori households
eat non-commercially harvested shellfish each week, and approximately 16% at least
once a fortnight. Data from the diary survey of Fisher & Bradford (1998) indicates
that in Zone A, 55% of non-commercial fishing trips targeting bivalve shellfish target
scallops. If it could be assumed that harvest quantities are proportional to target trips
(a very large assumption) then it follows that 5.5% of the Maori community consume
scallops each week in Zone A and approximately 8.8% at least fortnightly. This
suggests that a significant proportion of the Maori population would be exposed to
mild ASP in a year similar to 1996-97.
The scenarios presented have utilised Zone A as a model, because this is the area
where Domoic acid has most frequently occurred to date. However, given the wide
distribution of both low levels of Domoic acid in shellfish and Pseudo-nitzschia
species, ASP events could potentially occur in other areas also. If for example,
similar toxin levels as occurred in Zone A in 1996-97 were to occur in the eastern
Coromandel area (Zone D), in one of three major scallop harvesting areas (Mercury
Islands, Slipper Island, or Whangamata to Waihi), the potential cases of ASP would
be higher. Using harvest data from the diary survey of Fisher & Bradford in the
Eastern Coromandel, it is estimated that there are 687 200g meals of scallops
consumed every week over the scallop season. If these are distributed equally over
the scallop beds, and a toxin scenario similar to that in Zone A in 1996-97 were to
occur at one location, then in the absence of a marine biotoxin monitoring
programme, there would potentially be 2,061 mild cases of ASP in the year. (This
assumes that there is no publicity to prevent continuing exposure). Should a similar
incident occur in the Nelson area, then harvest figures suggest that the number of
cases could be up to five times higher.
The risk of exposure, and the severity of the impact, are increased if the shellfish guts
(particularly scallop guts) are consumed. There are no robust data on the numbers of
people who consume whole scallops, as distinct from muscle and roe. Forty-four
percent of cases on the epidemiological databases who had eaten scallops had
consumed the whole shellfish. However, this proportion is not representative of
scallop consumers in general, since those who eat whole scallops are more at risk of
TSP, and thus more likely to be represented on the epidemiological database. It does
however, indicate that whole scallops are consumed by some members of the
community. It should be noted that discarding parts of the shellfish is contrary to
Maori traditional practices related to moumou kai. Moumou kai requires that people
gather just what they need, and that they eat all that is gathered without waste (Wyllie,
1995). However, in scenarios like those presented from Zone A, the consumption of
whole scallops would not increase the numbers of moderate to severe ASP cases.
However, if only the gut and skirt were consumed, then it is likely that a greater
number of severe cases of ASP would occur under this scenario. Although the
scenarios presented have resulted in only mild cases of ASP, the dose-response
figures are not adjusted for body weight. It has also been assumed that only 200g of
shellfish are consumed. Variations in body weight, and amount of shellfish consumed
will also cause variation in the severity of ASP symptoms.
133
5.4
DIARRHETIC SHELLFISH POISONING
As discussed in Section 1.3.3, there are several different toxins in the “DSP group”.
However, because they are frequently found together, and are all extracted by the
acetone extraction method, they tend to be grouped together. All these toxins,
whether diarrheagenic or not, are included in the risk assessment in this section.
5.4.1
The toxins in the “DSP group” can be sub-divided into several groups: Okadaic acid
and the closely related dinophysistoxins: the pectenotoxins, which are polyether
lactones consisting of three compounds with known structure (PTX 1-3) and at least
two additional compounds with presumed slightly modified skeletons; and thirdly,
yessotoxin (YTX), with two sulphate esters, which resemble the brevetoxins (Aune &
Yndestad, 1993).
The DSP toxins Okadaic acid and dinophysistoxins DTX1 and DTX3, produce
diarrheagenic effects. (DTX-3 hydrolyses back to the more toxic DTX-1 in the body).
These substances are potent inhibitors of at least two sub-classes of protein
phosphatases (PP1 and PP2A), and this mode of action may be linked to diarrhoea,
degenerative changes in the absorptive epithelium of the small intestine, and to
tumour production. Symptoms of human intoxication occur within 30 minutes to a
few hours (seldom more than 12 hours) and include diarrhoea, nausea, vomiting, and
abdominal pain (Hallegraeff, 1995). Although no human mortalities have been
reported, the affliction can be highly debilitating for several days.
The longer term potential effects of OA and DTX1 are of more concern. Okadaic
acid and DTX1 have tumour-promoting activity through their inhibition of the activity
of protein phosphatases 1 and 2 (Bialojan & Takai, 1988). In laboratory tests,
Okadaic acid has also been shown to exhibit some mutagenic properties and
immunotoxic effects (Aune & Yndestad, 1993; Fessard, 1998). Laboratory trials have
also suggested that DTX1 has enterotoxic effects (Terao et al., 1990).
There is some discussion about whether OA and DTX1 have long term tumour
promoting and mutagenic effects if only low levels of toxin are ingested. This
remains controversial. Most, but not all, research on this has been done using high
toxin levels and administration by intraperitoneal injection. Fessard (1998)
summarised the research on the potential carcinogenic effects of OA, and concluded
that “It can be suggested that OA can be considered as a genotoxic compound
forming (directly or indirectly) DNA adducts and that its promotion capacity is in fact
due to the Tumour Necrosis Factor ∝ (TNF- µ ∝ ) induction. In that case, we must be
aware that the risks incurred for human health, mainly during chronic intoxications,
are underestimated. Therefore, the toxin levels allowed for consumption should be
reconsidered”. A Working Group on Toxicology of Yessotoxins, Pectenotoxins and
the Okadaic Group Toxins has been set up by the European Community Reference
Laboratory on Marine Biotoxins. At a meeting of this Group in February 1999, it was
concluded that “According to the data on tumour promotion activity of Okadaic acid,
there is no evidence that there may be a risk of a long term hazard for shellfish
consumers under the current regulations regarding diarrheagenic substances. There
134
is no good evidence of the genotoxic potential of OA. Only the diarrheagenic activity
of OA should be a matter of concern to establish regulatory limits for these toxins”.
It was suggested that the level of 16 µg/100g should offer sufficient protection to
consumers (note that the regulatory level in New Zealand is currently 20 µg/100g).
Few studies have yet been undertaken on the impact of yessotoxin. Pathological
effects on the heart and liver have been shown after intraperitoneal injection of mice.
Experimental studies based on oral ingestion have suggested that high levels of
yessotoxin produce pathogenic effects in the gastrointestinal tract. More recent
studies suggest that yessotoxin may have little impact when ingested orally at the
levels likely to be encountered in shellfish (Ogino et al., 1997). Until recently,
research on yessotoxin was hindered by a lack of knowledge of causative agents
limiting the toxin available to work with.
However, the identification of
Protoceratium reticulatum as a producer of yessotoxin (Satake et al., 1997) will
facilitate research in this area. In the mean time, the limited knowledge of the toxicity
of yessotoxin means that it remains a public health risk because of potential long-term
effects.
Research into the toxic effects of pectenotoxin is severely limited by the inability to
culture Dinophysis species (the known producers of pectenotoxins) in the laboratory.
Until recently, there was no evidence of human illness caused by pectenotoxins.
However, pectenotoxin has been implicated in a TSP incident that occurred in New
South Wales, Australia, in which a number of people became ill, with symptoms that
included vomiting, and diarrhoea (P. Truman, ESR, pers. comm.). Mackenzie et al.
(1999) suggest that the pectenotoxins PTX-2 and PTX-2 Seco acid may be the
predominant DSP-toxins in New Zealand, and may be of greater concern to human
health than Okadaic acid. This conclusion was based on the following (Mackenzie et
al., 1999):
•
PTX-2 induces diarrhetic symptoms and severe mucosal injuries in the small
intestine of mice by intraperitoneal injection and oral administration (Ishige et
al., 1988; Terao et al., 1986)
•
PTX-2 causes liver necrosis in mice by oral administration (Terao et al., 1986)
•
PTX-2 has potent and selective cyto-toxicity against human lung, colon and
breast cancer cell lines (Jung et al., 1995).
•
PTX-2 is implicated in cases of gastro-intestinal illness in Australia.
Yessotoxin and PTX-2 and its derivatives are detected by the current mouse bioassay
screening procedures but are not detected by confirmatory ELISA (DSP Check-Kit) or
protein phosphatase inhibition assays.
Okadaic acid and dinophysistoxins are produced by dinoflagellates in the genera
Dinophysis and Prorocentrum. Species that have been found to be toxic in New
Zealand include Dinophysis acuta and Prorocentrum lima (Rhodes & Syhre, 1995).
Low levels of DSP toxins in shellfish have also been associated with Dinophysis
acuminata in the water (L. Mackenzie, Cawthron Institute, pers. comm.). Yessotoxin
is produced by Protoceratium reticulatum (Satake et al., 1997, Mackenzie et al.
135
1998b). In New Zealand, Dinophysis acuta has been found to produce the
pectenotoxins PTX-2 and Pectenotoxin-2 Seco acid (Daiguji et al., 1998).
Because of the tendency of shellfish to accumulate DSP toxins from toxic
phytoplankton, shellfish consumers are exposed to DSP toxins when they consume
shellfish that have been harvested from areas where DSP-producing phytoplankton
are present. Shellfish consumers are thus the target population for DSP from Okadaic
acid, dinophysistoxins, yessotoxin and pectenotoxin. Shellfish consumers are reliant
on the marine biotoxin monitoring programme to determine whether shellfish are
contaminated with DSP toxins – it is not possible to ascertain this by the appearance
of the shellfish, or the water from where they are harvested. It is possible that the
portions of the shellfish eaten may vary in toxin content.
The risk of DSP (including poisoning from Okadaic acid, dinophysistoxin, yessotoxin
and pectenotoxin) may vary not only with the degree of exposure of the shellfish to
the toxic phytoplankton, and the toxin profile of the phytoplankton, but also with the
species of shellfish consumed (Mackenzie et al., 1998b; Rhodes et al., 2000). More
research is required to investigate this further.
5.4.2
Overseas experience suggests that diarrheagenic effects from Okadaic acid and DTX
toxins start at ingested amounts of 40 µg and 30 µg respectively (Aune & Yndestad,
1993). Cases from consumption of New Zealand shellfish suggest that 20-30 µg of
DSP toxins may produce symptoms (Wilson, 1996). However, it is possible that
some of these symptoms may have resulted from ingestion of coincident pectenotoxin
that would not have been detected by the DSP ELISA. There is no information on the
long term mutagenic and immunotoxic effects of Okadaic acid or dinophysistoxins
ingested orally by humans. Similarly, there is no dose response information for the
oral ingestion of yessotoxin by humans, with regard to either short-term or long-term
effects. Illness has been reported in New South Wales, Australia, following the
consumption of shellfish contaminated with pectenotoxin. Information from this
event suggests that 30-60 µg of pectenotoxin was ingested by the people affected
(Mike Quilliam, National Research Council of Canada, pers. comm.). However, the
dose response information arising from this incident has not been published, and there
is no information regarding long-term impacts or the impact of long-term ingestion at
low levels.
5.4.3
Exposure Assessment
The following observations regarding the risk of exposure to DSP toxins can be made:
•
The Dinophysis species producing Okadaic acid, dinophysistoxins, and
pectenotoxin are widely distributed throughout New Zealand, and have been
found at most sample points. There are inadequate data to determine the
distribution of phytoplankton producing the other “DSP” toxins: Prorocentrum
lima, and Protoceratium reticulatum.
136
•
“Classic DSP” toxins (i.e. Okadaic acid and dinophysistoxins) above the
regulatory level of 20 µg/100g shellfish tissue have occurred relatively rarely in
New Zealand since monitoring for DSP began. They occurred in only 4 zones
(Zones A, E, G, and I) from 1/4/94 to 30/6/99. The highest frequency of
occurrence was in Zone G, where 71 samples (1.36% of total samples) above the
regulatory level were recorded. Most of the DSP detected in Zone G was from
one site, Wedge Point (G23) in the Marlborough Sounds. Blue mussels at this site
contained persistent levels of DSP from November 1994-August 1995, November
1995 to July 1996, and October to March 1997. The DSP in Zone I (the area with
the next highest frequency of occurrence of DSP toxins in shellfish) was also
predominantly from one site, Akaroa Harbour (I14), where shellfish toxicity
persisted from February 1995 to October 1995. The shellfish species sampled at
this site were also blue mussels. There are insufficient data to comment on the
distribution and frequency of occurrence of yessotoxin and pectenotoxin in
shellfish in New Zealand.
•
There is some indication that there may be differences in accumulation and
retention of DSP toxins between different species of shellfish, but further
investigation is required to determine these differences. Blue mussels are a
species of shellfish that are relatively infrequently sampled in the marine biotoxin
monitoring programme, but exhibited a significantly higher frequency of
occurrence of DSP toxins than other species.
•
The maximum DSP toxin levels (as determined by the DSP ELISA) in Zones A,
E, G and I were 33, 39, 96 and 86 µg/100g respectively. At Wedge Point (G23),
where the highest frequency of samples containing DSP levels above the
regulatory level occurred, the mean of these values was 46.8 µg/100g, and the
median 44 µg/100g. If it is assumed, as suggested by Wilson (1996), that ingested
levels of Okadaic acid/dinophysistoxins as low as 20 µg/100g can produce DSP
symptoms, then levels sufficient to produce at least mild symptoms of DSP
occurred in 82 weeks in the time period between 1/9/94 and 30/6/99.
•
There are insufficient data to comment on the levels of pectenotoxin or yessotoxin
in shellfish in New Zealand with respect to risk to shellfish consumers.
•
The frequency of occurrence of Okadaic acid and dinophysistoxins has varied
significantly between years since shellfish monitoring began. There are
insufficient data to be able to predict future occurrence.
•
There is a possibility that there is a slightly lower risk of DSP in the winter
months, but further data are required to clarify this. If this were the case, the times
of higher risk would coincide with the times of higher non-commercial shellfish
harvest activity (Kearney, 1999; Hartill & Cryer, 1999).
5.4.4
Lack of robust data makes estimation of the risks associated with DSP very difficult.
There are no data on the occurrence of pectenotoxin and yessotoxin on which to base
meaningful analysis. Neither is definitive information available about effective doses,
137
nor chronic effects of ingestion of these toxins over a longer period of time. These
uncertainties effectively increase the potential risks associated with the occurrence of
pectenotoxin and yessotoxin in New Zealand.
There is a dearth of robust data on which to base sensible quantitative estimation of
risks associated with “classic DSP”. While data for non-commercial harvesting of
shellfish are available from the Fisher & Bradford (1998) diary survey for Queen
Charlotte Sound (the sound within which lies Wedge Point), there are no noncommercial harvesting data available for Akaroa Harbour alone. This limits the
construction of scenarios based on previous events. However, given that Wedge Point
is the site where DSP toxins have been found most frequently, it is worthwhile to
consider estimations of risk in various scenarios from that site.
In these scenarios, it is assumed that an effective dose may be as low as 20 µg/100g
(Wilson, 1996). It is also assumed that the level of toxin at Wedge Point is indicative
of toxin levels in shellfish throughout Queen Charlotte Sound (there are insufficient
data from other sample points in the Sound to test this assumption and none from
where the same species of shellfish have been sampled). From 1/9/94 to 30/6/95,
samples of mussels contained a minimum of 20 µg/100g of DSP toxins in 26 weeks.
In subsequent years (from 1/7 to 30/6 the following year) the frequency of DSP toxins
at this level were as follows: 30 weeks in 1995-96, 12 weeks in 1996-97, 1 week in
1997-98; and 1 week in 1998-99. Data from the Fisher & Bradford (1996) diary
survey suggests that the non-commercial harvest of mussels from Queen Charlotte
Sound is approximately equivalent to 60 100g meals of mussels per week (assuming
10 mussels equals 100g meat weight). Based on a year like 1995-96, in the absence
of a marine biotoxin monitoring programme, there could be 1,800 cases of DSP
arising from consumption of mussels alone from Queen Charlotte Sound. Other
species of shellfish are also harvested from the area, including cockles, crayfish, paua,
pipi and scallops, so the number of cases could be higher depending upon the
propensity of these other species to accumulate and retain DSP toxins. In contrast, in
a year like 1997-98, there would only be 60 cases of DSP arising from consumption
of mussels from the same area. However, reservations about the reliability of
shellfish harvest data expressed in previous sections potentially apply to this analysis
also.
As is the case with toxins discussed in previous sections, the occurrence of DSP
toxins in shellfish is likely to impact disproportionately on Maori, and to a lesser
extent on Pacific and Asian peoples in some areas (Kearney, 1999). Based on data
from Maori households in the Far North (Hay 1996), up to 16% of Maori would be
exposed to DSP if there were no publicity of the risk of DSP within a fortnight of the
initiation of an event. In particular, the potential impacts of long-term consumption of
low levels of DSP toxins are also likely to impact disproportionately on Maori, since
they are more regular consumers of shellfish.
138
5.5
NEUROTOXIC SHELLFISH POISONING
5.5.1
Neurotoxic shellfish poisoning, (NSP), is caused by lipophilic polycyclic ether
compounds, known as brevetoxins. There are many brevetoxin derivatives. All these
derivatives exert their toxic effect by specific binding to site-5 of voltage sensitive
Na+ channels, leading to channel activation at normal resting potential (i.e., they act as
sodium channel activators) (Cembella et al., 1995b).
The symptoms of NSP occur within 3-5 hours. Symptoms of a mild case include:
chills, headache, diarrhoea, muscle weakness and joint pain, nausea and vomiting.
Severe symptoms include paraesthesia, altered perception of hot and cold, difficulty in
breathing, double vision, trouble in walking and swallowing (Hallegraeff, 1995).
Death may occur as a result of respiratory arrest.
Species of phytoplankton known to produce NSP toxins in New Zealand include
Gymnodinium c.f. breve, Gymnodinium c.f. mikimotoi, (which is now known to
include three separate species), Gyrodinium galatheanum and a species of
Heterosigma (Mackenzie et al., 1995a, Haywood, 1998). The NSP toxins found
isolated from New Zealand shellfish include previously known brevetoxins, and new
analogues (Ishida et al., 1994; Ishida et al., 1995; Morohashi et al., 1995; Murata et
al., 1998). At this stage the specific toxicity of the new analogues is unknown.
Because of the tendency of shellfish to accumulate NSP toxins from toxic
phytoplankton, shellfish consumers are exposed to NSP toxins when they consume
shellfish that have been harvested from areas where NSP-producing phytoplankton
are present. Shellfish consumers are thus the target population for NSP. As with
other marine biotoxins, shellfish consumers are reliant on a marine biotoxin
monitoring programme to determine whether shellfish are contaminated with NSP
toxins – it is not possible to ascertain this from the appearance of the water or the
shellfish themselves.
The risk of NSP may vary with the species of shellfish consumed. For example,
based on a very limited amount of data, it appears that Pacific oysters might
accumulate brevetoxins from Gymnodinium breve more readily than GreenshellTM
mussels. These results are not definitive, and more rigorous research is required to
investigate these differences further.
5.5.2
There are several limitations to dose-response estimation for NSP toxins in New
Zealand. Some of the brevetoxin derivatives observed in New Zealand shellfish in the
1993 event had not previously been observed elsewhere. There have been no
confirmed cases of NSP in New Zealand. There is thus no dose-response relationship
for some of the brevetoxins found in New Zealand.
139
Wilson (1996) extrapolated overseas data to obtain some tentative dose-response
relationships that were adjusted for the acetone extraction mouse bioassay results that
were used in New Zealand prior to the introduction of the acetone screen test followed
by the ether extraction mouse bioassay for NSP. It is apparent from dose-response
data published by Hemmert (1975) that, not surprisingly, the impact of a dose of NSP
toxin depends on the body weight of the consumer. His data, drawn from cases from
Florida red tide events, showed that in adults no symptoms were evident at a dose of
0.3-3.6 mouse units/kg of body weight. Mild symptoms, including distal paraesthesia,
occurred at 5.1-6.8 mouse units/kg body weight, and extreme symptoms, including
difficulty walking, occurred at 5.1-6.8 mouse units/kg body weight. The dose for
children was much lower, with extreme symptoms occurring at 3.1-4.4mouse units/kg
of body weight. These data, plus other international data, were summarised by
Wilson (1996) in terms of the concentration of NSP toxin in the shellfish consumed
(so that it can be related to the mouse bioassay results). This combination of data
showed that doses (in adult consumers) as low as 54 mouse units/100g may produce
tingling in the mouth, 115 mouse units/100g may produce mild symptoms.
Conversely, 295 mouse units/100g may produce no symptoms. Distal paraesthesia,
and in some cases, extreme symptoms such as difficulty in walking, may occur at
340-350 mouse units/100g. Doses as low as 94 mouse units/100g may result in
extreme cases in children. It is not known how well these data fit the brevetoxins
found in New Zealand shellfish.
5.5.3
Exposure Assessment
The following observations can be made regarding the risk of exposure to NSP toxins
through consuming non-commercially harvested shellfish in New Zealand:
•
The distribution of potentially toxic Gymnodinium species is widespread
throughout New Zealand, and they have been detected at most sample sites. The
distribution of NSP toxicity in shellfish is not well understood due to the nonspecific test methods employed in the marine biotoxin monitoring programme, the
results of which may be confounded by other lipid soluble toxins. However, the
presence of brevetoxins in shellfish has been confirmed at Rangaunu Harbour,
Coromandel and the Bay of Plenty (Ishida et al., 1994; Ishida et al., 1995;
Morohashi et al., 1995; Murata et al., 1998), in oysters, mussels and cockles.
•
Since the introduction of the ether extraction mouse bioassay in September 1994,
“NSP” levels above the regulatory level of 20 mouse units/100g have occurred
relatively rarely. This toxin level has not occurred at all in Zones B, D, E, F, or I.
Recorded instances in Zones G and H are unlikely to be due to brevetoxin (most
likely to be Okadaic acid/yessotoxin, and “Wellington Harbour” toxin,
respectively). They occurred at a frequency of less than 0.5% of samples in each
of the other zones between 1/9/94 and 30/6/99. Temporal and geographic
stratification of the sampling regime means that this level is indicative only.
However, it is apparent that the incidence of possible NSP has been very low.
•
The maximum “NSP” toxin levels in Zones A, C, G, H, J and K were all less than
30 mouse units/100g. (There were no “NSP” toxins above the regulatory level in
140
samples from the other zones). These levels are unlikely to produce significant
illness in adult human consumers.
•
There is little doubt that NSP occurred in shellfish in New Zealand in 1993.
However, there are insufficient data to determine the frequency of occurrence,
magnitude, or duration of the event, since the monitoring results are confounded
by the acetone extraction method used at the time, and the lack of differentiation
between NSP and other lipid soluble toxins (such as gymnodimine, DSP toxins,
yessotoxin, pectenotoxin etc.). While the frequency and magnitude of presumed
NSP toxins in shellfish in New Zealand since September 1994 have been very
low, it is pertinent to note that significant blooms of Gymnodinium species
producing other lipid soluble compounds have occurred during this time. Should
such a bloom of a brevetoxin-producing species occur, then there would be a
significant risk of exposure to NSP through the consumption of shellfish.
•
It is likely that there are differences in accumulation and retention of NSP toxins
between different shellfish species, and that this impacts on the risk of exposure to
consumers. However, research is required to investigate this rigorously.
•
To date, NSP (i.e. the occurrence of brevetoxins in shellfish) has only been
confirmed from the Bay of Plenty northwards, on the eastern coast. However,
there are insufficient data to predict a greater level of risk in some areas than
others.
5.5.4
As with toxin groups discussed previously, the characterisation of risks associated
with NSP in New Zealand is hampered by lack of robust data. Based on available
information, in a future scenario similar to any of the years from 1994-1999, it is
unlikely that there would be any significant illness in adults due to NSP (assuming a
meal size of 100-200g, with no adjustment for variations due to body weight). There
are insufficient dose-response data available to determine whether illness would occur
in children at the maximum toxin levels that occurred in these years. It has been
assumed that the toxicity of the brevetoxin derivatives found in New Zealand is
similar to those in Gymnodinium breve in Florida.
However, it cannot be assumed that there is no risk of NSP in the future. The
occurrence of significant Gymnodinium blooms containing other lipid soluble
bioactive compounds (possibly seeded from oceanic populations), and the occurrence
of some NSP toxicity in shellfish in 1993 (albeit unquantifiable), suggest that there is
potential for NSP to occur in shellfish here. There are insufficient data to quantify the
impact of such an event in terms of the likely number of cases. However, data from
Kearney (1999) suggests that Maori might be significantly disproportionately at risk,
and to a lesser extent, Pacific and Asian peoples also. Data from Hay (1996)
discussed elsewhere suggests that in the far north, up to 16% of the Maori population
would be exposed to NSP toxins during such an event if there were no publicity of the
risk within a fortnight of the initiation of the event.
141
While not NSP, it is also pertinent to comment on the potential risk associated with
“Wellington Harbour toxin”. This toxin was detected in shellfish, and killed mice by
IP injection (Hoe Chang, NIWA, pers. comm.). However, there were no reported
cases of TSP resulting from this event. The oral toxicity of the compound is as yet
unknown.
5.6
RESPIRATORY IRRITATION SYNDROME
5.6.1
Respiratory Irritation Syndrome (RIS) is caused by aerosolised marine biotoxins
arising from blooms of toxic phytoplankton in the sea. Toxins known to cause RIS
include brevetoxins (for example, from Gymnodinium breve) (Pierce, 1986), and the
as yet unidentified toxin that was isolated from the newly identified Gymnodinium
brevisulcatum in Wellington Harbour during the summer of 1998 (Hoe Chang,
NIWA, pers. comm.). In the laboratory, purified brevetoxins block neuromuscular
transmission, and cause a severe bronchoconstriction in animal models. The mode of
action of the “Wellington Harbour toxin” is unknown.
During blooms of the toxic phytoplankton, the toxins become aerosolised in the
process of the bursting of bubbles caused by wind-generated whitecaps and breaking
waves. The presence of toxic algal cells is not necessary for the occurrence of toxins
in sea spray – with brevetoxins, sea spray containing fragments of Gymnodinium
breve cells, and cell-free extracts have both been found toxic. This suggests that
toxicity in aerosols can persist for some time after the algal cells have disappeared
from the water column, so phytoplankton monitoring is unlikely to provide a good
estimate of the risk of persistence of a RIS event.
The toxin profiles of the aerosolised toxins may not be in the same proportions as the
toxins in the phytoplankton. Pierce (1986) suggested that factors such as solubility,
volatility, surface sorption characteristics, and the presence of other naturally
occurring organic surface active substances would have an important effect on the
extent to which each toxin is aerosolised, potentially altering toxin aerosol
composition even within the same red tide bloom event. Selective accumulation in
aerosols of four most potent brevetoxins to levels 20 to 25 times that in the algal cells
has been shown for aerosols from G. breve (Baden et al., 2000).
Brevetoxin is rapidly absorbed into the body by inhalation. It is highly soluble in
cellular lipid, and crosses cell membranes with high efficiency (Baden et al., 2000). It
is likely that some of the effects of aerosolised brevetoxins are systemic, arising from
brevetoxins absorbed into the body across membrane surfaces. There is no
information on the mode of absorption of the “Wellington Harbour toxin”.
Most of the airborne toxin effect is experienced near the surf zone. The respiratory
irritation is observed most intensively within a few kilometres of the beach, indicating
a rapid settling or dispersion of the aerosolised toxins (Pierce, 1986).
Symptoms of RIS caused by brevetoxins include sore throats, eye and nose irritation,
involuntary dry coughing and sneezing, watery eyes, copious rhinnorhea, and
142
difficulty breathing. Aerosolised “Wellington Harbour toxin” produced similar
symptoms, but also caused headaches and skin rash (reported by marine hatchery
workers at NIWA, Wellington, J. Illingworth, pers. comm.).
People with pre-existing lung disease appear to have more lower airway symptoms
from aerosolised brevetoxins than people with no prior history of reactive lung
disease (Kirkpatrick et al., 2000), and elderly people are more susceptible than young
people (Dr S. Shumway, Southampton College, pers. comm.). Asthmatics are
affected by contact with both brevetoxin and “Wellington Harbour toxin” aerosols.
Studies of RIS caused by brevetoxin overseas found that exposure induced asthma
attacks in 80% of the asthmatics studied (Baden et al., 2000).
Those people living in coastal areas, or visiting the coast, are affected. There may
also be some occupational exposure by people working on the coast – for example, by
lifeguards, hatchery workers, shellfish farmers and fishermen. Wearing cotton face
masks, or moving into air-conditioned space indoors immediately reduces, and
subsequently eliminates, respiratory irritation. Residue remaining on skin and
mucous membranes can re-intoxicate by rubbing or touching previously affected areas
(Baden et al., 2000). Anecdotal accounts of repeated exposure to brevetoxin aerosols
from Florida red tides suggest sensitisation, but this has not been verified or
quantified (Baden et al., 2000). The long-term impacts of repeated exposure to
aerosolised brevetoxin and “Wellington Harbour toxin” are unknown.
5.6.2
There is no dose-response information available for human exposure to aerosolised
brevetoxins or aerosolised “Wellington Harbour toxin”. A study that includes an
investigation of the dose-response to aerosolised brevetoxins in humans is currently
being undertaken by Baden and co-workers. The results of this study are not yet
available. However, studies of aerosolised brevetoxins using sheep have shown that
exposure to femtomolar concentrations produce bronchoconstriction. Environmental
inhalation of aerosolised brevetoxins produced a massive mortality of manatees in
1996 (158 deaths) (Baden et al., 2000).
5.6.3
Exposure Assessment
There have been several respiratory irritation events recorded in New Zealand since
the beginning of 1993. The first event, at Orewa in the summer of 1993, is presumed
to have been caused by brevetoxins, but no identification of aerosol toxins was
undertaken. However, shellfish in some areas in the Hauraki Gulf did accumulate
brevetoxins over this time, as confirmed by toxin analysis in shellfish tissue (Ishida et
al., 1994; Ishida et al., 1995; Morohashi et al., 1995; Murata et al., 1998). The second
series of events occurred in the summer of early 1998, on the coasts of Wairarapa and
Hawkes Bay, and in Wellington Harbour. The nature of the aerosolised toxins that
were causative agents in this series of events is unknown (the “Wellington Harbour
toxin”), as is the quantity of toxin in the aerosol. There is no formal record of the
duration of any of these events, nor of the numbers of people affected. Anecdotal
evidence suggests that several hundred people were affected in each event, over a
period of several weeks.
143
If it can be assumed that the limited data that has been gathered can be used to predict
future exposure to RIS in New Zealand, then the following might be expected:
•
Gymnodinium sp. blooms with the potential to cause RIS may occur every three
years. In the years when these blooms occur, widespread and/or several events
might occur. These blooms may last for up to three months, and may change
location on the coast during this time. The conditions that cause exposure to RIS
are likely to occur at some time during this period and may continue for up to
several weeks.
•
RIS is more likely to occur in the months December-March. Since this is the
period of high recreational use of the coastline, exposure to RIS is not just limited
to the population normally resident in coastal areas, but may be several orders of
magnitude higher.
•
The location of RIS events appears more likely on the eastern coast of the North
Island, but events on the western coast, or further south may also be possible.
•
The most intense exposure to RIS occurs at the coast, but may be experienced up
to a few kilometres inland from the shore, depending on the quantity of toxin in
the aerosol and the strength and direction of the wind.
The numbers of people likely to be exposed to RIS are difficult to predict, since they
depend on the specific location of Gymnodinium blooms. It is not possible to predict
such specific locations from the data available. Obviously, if the blooms occur in
areas where the adjacent coast is highly populated by residents and visitors, the
numbers of people exposed are likely to be higher than in areas that are largely
uninhabited or sparsely populated.
5.6.4
Given the uncertainties in the analysis, it is difficult to present an overall estimation of
the risk associated with RIS in New Zealand. The variations in occurrence of
Gymnodinium sp. blooms with the potential to cause RIS are likely to occur over a
much longer period than the period for which we have data available. The events that
have been recorded so far have occurred in somewhat different hydrographic and
environmental conditions, and at different locations. In addition, there is no
information available about the toxicity or mode of action of the “Wellington Harbour
toxin”, nor any data on human dose-response or long-term impacts of either the
“Wellington Harbour toxin” or aerosolised brevetoxins. Predictions of risk therefore
need to be made with great caution.
There are several scenarios that can be considered in estimating the risks associated
with RIS in New Zealand. One scenario is years like 1994-1997 and 1999, in which
no cases of RIS occurred. Based on the data that are currently available, it is likely
that some years in the future will match this scenario.
144
The potential risks associated with blooms of Gymnodinium producing RIS toxins
vary according to the size, density and location of the blooms, and the wind
conditions at the time. The numbers of people affected could vary from thousands
(for example in the event of a dense bloom associated with a strong on-shore breeze
off Auckland’s North Shore or Northland holiday resorts) to few. Amongst those
people exposed, asthma sufferers are likely to be most seriously affected, with the
possibility that 80% may suffer asthma attacks upon contact with the toxins. In New
Zealand, 20% of children under the age of 15, and 10% of adults, suffer from asthma
(statistics from the Asthma Society Inc. Auckland). This suggests that approximately
9.8% of people exposed to RIS could potentially suffer asthma attacks as a result
(based on approximately 23% of the population being under the age of 15). This
needs to be considered in the management of risk associated with RIS.
Other considerations in the estimation of risk of RIS in New Zealand are the factors
that are unknown with respect to the “Wellington Harbour toxin”. These include the
unknown mode of action of the toxin, the lack of information about effects of
prolonged exposure, or likely chronic effects.
145
SECTION 6:
SUMMARY BY AREA
Following is a brief summary of the factors impacting on the risk of TSP, and local
issues in each Biotoxin Zone. The location of each zone is presented on a map in
Appendix I(D).
6.1
ZONE A
Zone A extends from Tauroa Point on the north-west coast of Northland around to
Cape Brett on the eastern coast.
The western coast of Zone A consists of an exposed sandy coastline (Ninety Mile
Beach) between Ahipara and Scott Point. Tuatua and toheroa are dominant species in
the sand of the beach. Both species are patchy in distribution, and local knowledge is
usually necessary to locate denser beds. Associated with the rocky outcrops (e.g. at
Ahipara, The Bluff, and Scott Point) are mussels, paua, kina and crayfish, and in
much lower numbers, rock oysters. While there is relatively little road access to this
area, vehicles are able to drive long distances along the beach at low tide, so the
whole length of the beach is accessible. Locals report a consistently high level of
shellfish harvesting off this beach: “Hundreds of shellfish come off this beach every
day, all year round”. There are high levels of harvesting before public holidays, as
people prepare for visits from whanau from outside the area (C & R Hensley, mussel
spat collectors, Ninety Mile Beach, pers .comm.).
The eastern coast of Zone A has a wide diversity of marine habitats, providing a wide
range of seafood for non-commercial harvest. The coastline is irregular and
convoluted. The orientation of the beaches in the area, and their fetch lengths and
directions are highly variable. These substantial differences in exposure and shelter
result in rapid changes in beach type over quite small distances. This coast in Zone A
contains most of the commonly gathered species of shellfish (with the exception of
course, of those species that do not extend this far north, such as the blue mussel).
One species not found in this area is toheroa, which prefer sandy coasts with greater
wave exposure.
A survey by Fisher & Bradford (1998) indicated that scallops are the most actively
targeted species for non-commercial harvest in this area, followed by crayfish, tuatua
and pipi. Paua, mussels, cockles, oysters and kina are also targeted (Table 3.1,
Section 3). The same survey showed that the trips targeting bivalve shellfish species
from this zone comprised only 3.9% of the total trips in New Zealand. If trips
targeting paua, kina and crayfish are included, the trips from Zone A only represent
2.6% of the total trips in New Zealand. These low figures may be in part due to the
comparatively small size of this zone compared to most other zones. It is also
possible that significant harvesting activity has not been reported in the survey, which
was undertaken for the Ministry of Fisheries – for example, the harvesting of toheroa,
which is prohibited by regulation except for customary purposes. A survey of
consumption of non-commercially harvested seafood in the north of this zone by Hay
(1996) showed that 11% of Maori households collected seafood more than once a
week, 31% at least weekly, and 52% at least monthly. If 30% of that seafood were
shellfish species (as suggested from anecdotal evidence), Maori consume significant
quantities of non-commercially harvested shellfish in this region.
146
The coastline is relatively easily accessible. While some of the eastern coastline in
Zone A is relatively remote with fewer roads, most areas are easily accessible by boat.
The population of Northland is not high, but it is within proximity of the dense
population in the Auckland area. Maori are a significant proportion of the population.
There are large increases in population over the summer holiday period.
Low levels of PSP have been found in shellfish from both the western and eastern
coasts of Zone A. Most of these occurred in 1993 and early 1994, with some activity
late in 1995 (October- December) on the eastern coast at Houhora Bay and the Cavelli
Islands, and in January 1996 at Waipapakauri (on the western coast). Most of the
instances of PSP arose in samples of tuatua taken from Tokerau Beach between July
1993 and October 1996. Tuatua exhibited residual low levels of PSP throughout this
time. Only one sample above the regulatory level was detected in Zone A between
1/7/93 and 30/6/99 – this occurred at Houhora Harbour in November 1996. This level
was only 83 µg/100g (the regulatory level is 80 µg/100g). Since 1996, the PSP
activity in Zone A has been very low, with only two samples with very low levels
detected in 1997, and none in 1998 or 1999. The current monitoring regime has been
designed on the premise that there is likely to be little toxin activity on the western
coast of New Zealand. This is not supported by the data collected across New
Zealand. (Author note: Subsequent to the preparation of this report a large bloom of
Gymnodinium catenatum has occurred on the western coast of Zone A).
Shellfish from Zone A contained ASP levels above the regulatory level (20 µg/g) in
33 samples taken between 1/7/93 and 30/6/99. All except three of these samples were
scallops. Detectable levels were found in 294 samples (14.6%) over the same time
period. The highest level found in a whole shellfish was 210 µg/g in scallops from
the Cavelli Islands on 2/11/93.
DSP above the regulatory level of 20 µg/100g was detected in two shellfish samples
taken from Zone A between 1/9/94 and 30/6/99. These were samples of Pacific
oysters taken in consecutive weeks in July 1995 from Rangaunu Harbour, and had
DSP levels of 33 µg/100g and 26 µg/100g respectively. Detectable levels of DSP
were found in 32 shellfish samples (1.5% of total samples taken) over the same time
period. These included a sample from Waipapakauri on the western coast of the zone.
An unidentified toxin, called “Rangaunu Harbour toxin” has caused persistent toxicity
in shellfish in the Rangaunu Harbour. The identity and oral toxicity of this toxin is
unknown. However there is no evidence of any human illness having resulted from
the consumption of shellfish from the Rangaunu Harbour.
There are 9 instances of shellfish samples from the period 1/9/94 to 30/6/99 that have
contained toxins above the regulatory level of 20 mouse units when tested with the
ether extract mouse bioassay for NSP. Seven of these were from shellfish taken from
the Rangaunu Harbour, some of them at a time when significant numbers of
Gymnodinium cysts were identified from phytoplankton samples. It is thus possible
that these toxin levels were due to brevetoxin.
There have been no probable or confirmed cases of TSP from Zone A, and four
suspected cases since the beginning of 1994.
147
6.2
ZONE B
Zone B extends from Cape Brett to Cape Rodney.
Zone B has wide diversity of marine habitats, providing a wide range of seafood for
non-commercial harvest, including most of the commonly gathered species of
shellfish. One species not found in this area is toheroa, which prefer sandy coasts
with greater wave exposure.
A survey by Fisher & Bradford (1988) suggested that crayfish, scallops, pipi and
mussels were the most actively targeted species for non-commercial harvesting in this
area, followed by kina and cockles. Tuatua, paua and oysters are also targeted (Table
3.1, Section 3). The same survey also indicated that trips in this zone targeting
bivalve species represent 12.5% of all trips in New Zealand. If trips targeting paua,
kina and crayfish are included, trips in this zone represent 11.5% of all trips in New
Zealand. If it can be assumed that the results of this survey are representative of noncommercial harvesting activity, this suggests that Zone B has a comparatively
significant level of non-commercial harvesting for shellfish.
Zone B is well serviced by roads, with numerous places where it is possible to launch
a boat. It has a comparatively low population, with Whangarei being the major
population centre. However, the zone is in close proximity to the dense population in
the Auckland area, and there are large increases in the population in the zone over the
holiday periods in the summer months.
There have been no instances of PSP above the regulatory level in shellfish between
1/7/93 and 30/6/99. The 48 instances of low levels of PSP occurred predominantly at
in tuatua at Oakura and Waipu in 1993-95. Only one sample was above the regulatory
level in 1996 (again, in tuatua at Oakura) and one in 1998 in pipi from Waipu. These
samples reflect the tendency of tuatua to hold low residual levels of PSP for long
periods of time.
No shellfish from Zone B contained ASP levels above the regulatory level (20 µg/g)
in shellfish samples taken between 1/7/93 and 30/6/99. Detectable levels were found
in 78 samples (8.9% of total samples taken) over the same time period. All these
were samples of scallops from the Bream Bay area between 1994 and 1997.
DSP above the regulatory level of 20 µg/100g was not detected in any shellfish
samples taken from Zone B between 1/9/94 and 30/6/99. Detectable levels of DSP
period.
There have been no shellfish samples above the regulatory level of 20 mouse units
using the ether extract mouse bioassay over the period 1/9/94 to 30/6/99. However,
four samples over this time had detectable levels of toxin using this assay. The
identity of this toxin has not been confirmed as brevetoxin.
There have been no probable or confirmed cases of TSP in Zone B, and one suspected
case since the beginning of 1994 to June 1999.
148
6.3
ZONE C
Zone C includes the Hauraki Gulf from Cape Rodney to Cape Colville at the north of
the Coromandel Peninsula, including Great Barrier Island.
Zone C encompasses a very large range of habitats, and thus species for consumption
by the public. These range from species found in sheltered estuarine and harbour
areas, through to those in moderately protected areas, and a few areas that face open
water. The zone thus contains cockles, pipi, Pacific and native rock oysters, tuatua,
green-lipped mussels, scallops, kina, paua and crayfish. The shellfish gathering areas
in this zone are in general highly accessible to the public – the coast is well supplied
with roads and boat launching facilities. However, there are some local restrictions on
the gathering of shellfish, designed both to conserve shellfish stocks, and to prevent
illness in consumers.
A survey by Fisher & Bradford (1998) indicated that crayfish and scallops were by far
the most frequently targeted species in this area, followed by mussels, pipi, cockles
and tuatua. Lower numbers of trips targeted paua, kina and oysters (Table 3.1,
Section 3). The same survey showed that trips targeting bivalve shellfish in this zone
represent10.4% of total non-commercial harvesting trips in New Zealand.
The Auckland region in Zone C is a highly populated area, with significant ethnic
diversity, including comparatively high numbers of Maori, Pacific Island people, and
people of Asian origin. The more remote areas in this zone, such as Coromandel
Peninsula, are still within easy access of Auckland, and this is reflected in the increase
in population over holiday periods.
Zone C has exhibited an extremely low level of PSP activity, with no samples found
above the regulatory level of 80 µg/100g, and only six samples with detectable levels
(5 of them in November-December 1993).
No shellfish from Zone C contained ASP levels above the regulatory level (20 µg/g)
in shellfish samples taken between 1/7/93 and 30/6/99. Detectable levels (but
extremely low levels) were found in 53 samples (3.1% of total samples taken) over
the same time period.
samples taken from Zone C between 1/9/94 and 30/6/99. Detectable levels of DSP
period.
There have been three shellfish samples above the regulatory level of 20 mouse units
using the ether extract mouse bioassay over the period 1/9/94 to 30/6/99. Two of
these were associated with the presence of Gymnodinium c.f. mikimotoi in the
phytoplankton. However, the identity of this toxin has not been confirmed as
brevetoxin.
There have been no probable or confirmed cases of TSP in Zone C, and 3 suspected
cases from the beginning of 1994 to June 1999.
149
6.4
ZONE D
Zone D extends from Cape Colville to Cape Runaway.
In the sandy beaches from Opotiki to Waihi Beach, tuatua are found. Pipi, oysters,
cockles and mussels are found in the harbours in this bay. On the western side of the
Bay of Plenty, scallop beds lie off shore and in Tauranga Harbour, and these continue
north up the Coromandel Peninsula. From Waihi northwards, the coastline is rocky,
but interspersed with harbours and estuaries where oysters, pipi and cockles are
found. The rocky open shores provide good habitat for crayfish, and green-lipped
mussels, paua and kina are also present. There is good road access to much of this
area.
A survey by Fisher & Bradford (1998) indicated that crayfish and scallops were the
most frequently targeted species by non-commercial harvesters. Significant numbers
of pipi, tuatua and mussels were also targeted, followed by paua, kina, and cockles
(Table 3.1, Section 3). The same survey also indicated that 25.5% of all noncommercially harvested shellfish (bivalves) come from Zone D. This was the highest
percentage for any zone.
Maori form a significant proportion of the population, and there is a significant
component of non-commercial harvesting by Maori, as well as gathering by the
general public. Early in the biotoxin programme, concern was expressed by Maori in
the western Bay of Plenty that the sampling programme did not specifically monitor
their gathering sites.
There has been a problem with persistent PSP toxicity in the Bay of Plenty, over a
time period spanning 1993-1999. This has occurred in the open beach sites,
predominantly in tuatua, which have a tendency to retain PSP toxins. Over this time,
91 samples above the regulatory level of 80 µg PSP/100g shellfish tissue, have been
recorded. The maximum level was 1007 µg/100g. For the period 1993-June 1999,
this area exhibited the highest frequency of PSP toxin activity of any area in New
Zealand, and also the highest toxin levels. These levels represent a potential risk to
consumers. While some of the persistent toxicity may be as a result of long-term
sequestering in tuatua tissue, there may also be seed beds of cysts of Alexandrium
species, causing repeated blooms in the area. It is not possible to determine this from
available information.
One shellfish sample from Zone D contained ASP levels above the regulatory level
(20 µg/g) in shellfish samples taken between 1/7/93 and 30/6/99. This was a sample
of scallop meat and roe taken in December 1994 from Rangiwaea. Detectable levels
(but extremely low levels) were found in 262 samples (11.5% of total samples taken)
over the same time period.
samples taken from Zone D between 1/9/94 and 30/6/99. Detectable levels of DSP
period.
150
There have been six shellfish samples above the regulatory level of 20 mouse units
using the ether extract mouse bioassay over the period 1/9/94 to 30/6/99 in this zone.
However, the identity of this toxin has been confirmed as yessotoxin, not brevetoxin.
There has been one probable case of TSP in Zone D, and 7 suspected cases between
the beginning of 1994 and June 1999. The probable case of PSP arose from the
consumption of tuatua gathered from Ohope Beach. It is highly likely that one of the
suspected cases was also PSP, since a phytoplankton sample gathered from the nearest
sample site the following day, contained 10,300 cells/L of Alexandrium catenella.
A suggestion has been made that public warnings with respect to marine biotoxins in
shellfish should be species specific, to allow some continued harvesting of species
that have not accumulated biotoxins (E. Ashcroft, Pacific Health, pers. comm.). This
would involve monitoring several species of shellfish at each site, and would thus be
more expensive. It would have advantages in allowing some food source to remain
available for harvest, and in the maintenance of credibility that is lost when the public
harvest seafood in the face of a warning, but do not get sick. In addition to other
factors, the effectiveness of public warnings in this case would depend on the ability
of the public to absorb and interpret a more complicated warning message, and to
competently distinguish between different species of shellfish.
6.5
ZONE E
Zone E extends from Cape Runaway to Cape Palliser.
Paua, kina and crayfish are the predominant species of interest to non-commercial
harvesters in Zone E. Some mussels are also present, and cockle and pipi occur in the
few sheltered areas. The coast is a mixture of rocky reefs, rock platforms, and steeply
graded coarse sand beaches interspersed in Hawke’s Bay with rocky beaches. Much
of this coastline is relatively remote, with poor road access.
A survey by Fisher & Bradford (1998) showed that most non-commercial harvesting
in this area is targeted at crayfish and paua. Of the bivalve species, mussels are the
most frequently targeted, with much lower numbers of trips targeting cockles and pipi
(Table 3.1, Section 3). The same survey found that this zone only represents 2.5% of
the total trips targeting bivalve shellfish. However, if paua, crayfish and kina are
included in the shellfish species, this zone represents 15.3% of total trips targeting
shellfish – an indication of the significance of these latter species in the noncommercial harvesting in the region.
The northern part of the zone is comparatively sparsely populated, with the main
population centre being Gisborne. Napier and Hastings form the major population
centres further south. Regional data indicate that the area has the highest proportion of
Maori, relative to other regions.
There have been no shellfish samples with levels of PSP above the regulatory level of
80 µg/100g in this zone, and only 9 samples (0.73%) above the detectable level. This
suggests that the PSP activity in the area has been low. Samples with detectable
levels comprised a variety of shellfish, in several different years at different sites.
151
However, it is noticeable that all 9 samples occurred in the months November to
February.
One shellfish sample from Zone E contained ASP levels above the regulatory level
(20 µg/g) in shellfish samples taken between 1/7/93 and 30/6/99. This was a sample
of GreenshellTM mussels from Te Araroa Beach in October 1995 (22 µg/g).
Detectable levels (but extremely low levels) were found in 12 samples (1.6% of total
samples taken) over the same time period.
DSP above the regulatory level of 20 µg/100g was detected in one shellfish sample
taken from Zone E between 1/9/94 and 30/6/99. This was from paua gut from a
sample taken from Riversdale Beach in November 1994 (39 µg/100g). Detectable
levels of DSP were found in 4 shellfish samples (0.5% of total samples taken) over
the same time period. All these results were from tests on paua gut.
using the ether extract mouse bioassay over the period 1/9/94 to 30/6/99 in this zone,
nor any detectable levels of toxin identified using this assay.
There were no suspected, probable or confirmed cases of TSP in Zone E between the
beginning of 1994 and June 1999.
6.6
ZONE F
Zone F extends from Tauroa Point to Cape Egmont on the west coast of the North
Island.
Tuatua and toheroa are present on the long exposed sandy beaches broken
occasionally by rocky reefs and headlands. The predominant species in the rocky
areas include mussels, kina, paua and crayfish. The Herekino, Whangape, Hokianga,
and Kaipara Harbours that lead off these long exposed beaches provide an
environment for species that thrive in more sheltered and silty environments. Species
gathered here include native and Pacific oysters, dredge oysters, cockles, horse
mussels, and pipi. There are scallop beds in the Manukau and Kaipara Harbours, and
green-lipped mussels can be dredged from beds near the Kaipara Harbour mouth. The
Manukau Harbour also has abundant shellfish, although in places the ability to harvest
these is compromised by the bacteriological water quality. Due to overfishing, the
Auckland Regional Council has banned the gathering of shellfish on some of the
beaches between the Manukau and Kaipara Harbours, and a lower daily bag limit for
cockles applies in the Auckland Regional Council area. Further south, green-lipped
mussels and cockles are common in the Raglan Harbour, and pipi, cockles and
mussels in the Kawhia Harbour. The Manukau and Kaipara Harbours are easily
accessible from Auckland, and the coast of the Hokianga Harbour is easily accessible
by car and boat. The Whangape and Herekino Harbours further north are much more
remote. The most popular access to the open sandy beaches in the north of the zone is
via Dargaville. Here, and on Muriwai Beach, and the beaches south of the Manukau
Heads, cars are able to drive along the beach at low tide, so infrequent road access
does not necessarily significantly limit access to the length of the beach.
152
Southwards, the coast curves westwards into the North Taranaki Bight. As the rocky
reef habitat increases, green mussels, paua and kina are more abundant, and some
tuatua are found in sandy areas. The southern part of Zone F from Urenui to Cape
Egmont consists of gravel, cobble and boulder beaches, providing habitat for paua,
kina and green-lipped mussels.
A survey by Fisher & Bradford (1998) indicated that scallops are the most frequently
targeted shellfish species in this zone, followed by mussels, with lower numbers of
trips targeting pipi, tuatua, oysters and cockles. Non-bivalve species targeted include
crayfish, followed by paua and kina (Table 3.1, Section 3). The same survey found
that trips targeting bivalve shellfish species in this zone represent 13.5% of the total
non-commercial harvesting trips in New Zealand. This suggests that non-commercial
harvesters collect significant quantities of shellfish off this coast.
There were no shellfish samples above the detectable level for PSP in this zone
between 1/7/93 and 30/6/99 and only 2 samples (0.11% of total samples taken) above
the detectable level for PSP. If we were to rely on the predictive nature of historic
data, this would suggest that Zone F is a low risk area for PSP. However, as this
report is being prepared, there is a very large bloom of Gymnodinium catenatum off
this coast, resulting in high levels of PSP in shellfish. This is a good example of how
unreliable short-term historic data can be in predicting the future risk of TSP.
No shellfish from Zone F contained ASP levels above the regulatory level (20 µg/g)
in shellfish samples taken between 1/7/93 and 30/6/99. Detectable levels (but
samples taken from Zone F between 1/9/94 and 30/6/99. Detectable levels of DSP
period.
using the ether extract mouse bioassay over the period 1/9/94 to 30/6/99 in this zone,
nor any detectable levels of toxin identified using this assay.
There have been no probable or confirmed cases in Zone F, and six suspected cases
between the beginning of 1994 and June 1999.
6.7
ZONE G
Zone G includes the north of the South Island, from Farewell Spit in the west, to Cape
Campbell in the east.
The eastern coast of Zone G is predominantly rocky and gravel beaches, with paua,
kina and crayfish found in reefs. Mussels are found at Port Underwood. Inside the
Marlborough Sounds and Croiselles Harbour, the coastline is steep and rocky, with
very few intertidal areas. The main species gathered here are mussels (blue and
green-lipped), and scallops. There are significant numbers of cockles gathered from
153
Pelorus Sound and Croiselles Harbour. While road access is limited in much of the
Marlborough Sounds, most areas are easily and safely accessible by boat. Paua and
crayfish are present on the outer shores of the Sounds where the coast is more exposed
to wave action. There is a high level of non-commercial fishing activity in Tory
Channel, where mussels, kina, crayfish and paua are collected.
The Marlborough Sounds are easily accessible from the more densely populated area
of Wellington, and there are significant increases in population during holiday
periods. Maori account for approximately 10% of the population in the Sounds.
To the west, dredge oysters and scallops are the major bivalve species in Tasman and
Golden Bays, and significant beds of cockles occur in Tapu Bay and Pakawau Beach.
Crayfish are taken from the rocky reefs of the coast that separates the two major bays.
A survey by Fisher & Bradford (1998) indicated that the most frequently targeted
species in this zone are scallops, followed by crayfish and dredge oysters, mussels and
cockles. Other species targeted include pipi, and paua, with lower numbers of kina
targeted. The same survey showed that trips targeting bivalve shellfish species from
this zone comprise 21.3% of the total New Zealand trips. This was the second highest
percentage, indicating that this zone is an area of significant non-commercial harvest
of bivalves.
Between 1/7/93 and 30/6/99, levels of PSP above the regulatory level of 80 µg/100g
have only been found in two shellfish samples in Zone G: these were consecutive
samples of GreenshellTM mussels from Anakoha Bay in January 1994. PSP has been
detected in a very low percentage of samples (0.36%), mostly from Oyster Bay in
1993-94 and Anakoha Bay in January-February 1994 and November-December 1997.
Two samples with detectable levels of PSP also occurred in Melville Cove in
February-March 1998. There have been no detectable levels of PSP in any sites in
Tasman or Golden Bays.
Only one shellfish sample from Zone G contained ASP levels above the regulatory
level (20 µg/g) in shellfish samples taken between 1/7/93 and 30/6/99. This was from
Kenepuru Entrance in December 1994, in a sample of GreenshellTM mussels. The
sample contained a level of 187 µg/g Domoic acid. Detectable levels (but extremely
low levels) were found in 172 samples (3.4% of total samples taken) over the same
time period.
DSP above the regulatory level of 20 µg/100g was detected in 71 shellfish samples
taken from Zone G between 1/9/94 and 30/6/99. Detectable levels of DSP were found
in 137 shellfish samples (2.4% of total samples taken) over the same time period.
Most of these samples were from Wedge Point (G23). Blue mussels from this site
contained persistent levels of DSP from November 1994-August 1995, November
1995 to July 1996, and October 1996 to March 1997. It is possible that the hydrology
of the Wedge Point area, combined with the diurnal phytoplankton migration favours
the establishment of resident populations of Dinophysis. However, it is noted that
there is a significant year to year variation in the occurrence of DSP in mussels at
Wedge Point.
154
Several samples with detectable levels of DSP were located in Tasman Bay (The Glen
and Port Motueka). There were no detectable levels found in Golden Bay.
There have been two shellfish samples above the regulatory level of 20 mouse units
However, there is a possibility that these results may be due to Okadaic acid (or
possibly, yessotoxin), not brevetoxin. The presence of brevetoxin in shellfish samples
has not been confirmed in this zone.
Between the beginning of 1994 and June 1999, there were seven probable cases of
TSP in Zone G, and two suspected cases. All the probable cases were from noncommercially harvested shellfish. These are likely to have been caused by DSP
toxins or pectenotoxin.
6.8
ZONE H
Zone H is situated at the south-west of the North Island, and extends from Cape
Egmont in the west, around to Cape Palliser at the south of the North Island.
Paua, kina, green-lipped mussels and pipi are abundant in the South Taranaki Bight in
the north of Zone H. Further south, the coast changes to coarse-grained sandy
beaches with mactrid clams, tuatua, toheroa and pipi present. The rocky areas
adjacent from Paekakariki south and then eastwards to Cape Palliser provide habitat
for paua, kina and crayfish. Cockles are found in the estuarine areas near Paremata.
A survey by Fisher & Bradford (1998) indicated that the most frequently targeted
species by non-commercial harvesters in this area is crayfish, followed by paua, with
lower numbers of trips targeting pipi, mussels, cockles and kina (Table 3.1, Section
3). The same survey indicated that the trips targeting bivalve shellfish in this zone
comprise only 1.5% of the total trips in New Zealand. If trips to target paua, kina and
crayfish are also included with the bivalve species, the trips targeting all these species
in Zone H only comprise 2.9% of the New Zealand total. If one can assume that the
results of this survey are representative of non-commercial harvesting activity for
these species, this suggests that Zone H is an area where non-commercial harvest of
shellfish is less significant than most other zones in New Zealand.
There were no shellfish samples detected with levels of PSP above the regulatory
level (80 µg/100g) between 1/7/93 and 30/6/99. PSP has been detected in three
shellfish samples: two at Ohawe Beach (68 µg/100g on 8/11/95 and 30 µg/100 on
25/5/98), and one at Dorset Point (36 µg/100g, 7/9/98).
No shellfish samples from Zone H contained ASP levels above the regulatory level
(20 µg/g) in shellfish samples taken between 1/7/93 and 30/6/99. Detectable levels
(but extremely low levels) were found in 3 samples (0.5% of total samples taken) over
samples taken from Zone H between 1/9/94 and 30/6/99. Detectable levels of DSP
155
period.
There has been one shellfish sample above the regulatory level of 20 mouse units
However, there is a possibility that this might have been due to Wellington Harbour
toxin, not brevetoxin, as it occurred at Dorset Point during a dense bloom of
Gymnodinim c.f. mikimotoi (in this case, Gymnodinium brevisulcatum) that is known
to have been producing “Wellington Harbour toxin”.
There were no suspected, probable or confirmed cases of TSP in Zone H between the
beginning of 1994 and June 1999.
6.9
ZONE I
Zone I extends down the eastern coast of the South Island, from Cape Campbell to
Bluff.
The major species for much of this rocky coast are mussels, paua and crayfish.
Tuatua are also found in some sandy beach areas (for example, Moeraki, Kaitiki
Beach, and Warrington), and dredge oysters are found at Blueskin Bay. The mixed
sand and gravel beaches from Oamaru north to Banks Peninsula provide little
opportunity for the settlement of bivalve shellfish, paua or crayfish. In contrast, these
species are found in the rocky reefs around Banks Peninsula, and the harbours and
estuaries contain cockles and pipi. There are significant beds of cockles at Papanui.
North of Banks Peninsula is a stretch of steep coarse-grained sandy beaches with beds
of cockles present. From Amberley Beach north, the coast is comprised of exposed
rocky reefs where crayfish and paua are the major non-commercially harvested
species. North of Kaikoura, the coast is well known for its abundance of paua.
A survey by Fisher & Bradford (1998) indicated that the species most frequently
targeted for non-commercial harvest on this coast are paua and crayfish, with lower
numbers of trips targeting cockles, mussels and pipi. Other species collected include
dredge oysters, kina and tuatua (Tale 3.1, Section 3). The same survey indicated that
the trips targeting bivalve shellfish species in this zone comprised only 3.9% of the
total trips in New Zealand. If trips targeting paua, kina, and crayfish are included
with the trips targeting bivalve species, the total trips from Zone I are only 5.8% of
the trips in New Zealand. If the results of this survey can be assumed to be
representative of non-commercial harvesting for shellfish in New Zealand, these
results suggest that Zone I has a comparatively low level of non-commercial shellfish
gathering.
level (80 µg/100g) between 1/7/93 and 30/6/99. PSP has been detected in one
shellfish sample (0.05% of total samples) over this time period: at Bull Creek in
September 1995 (32 µg/100g). (Note that subsequently the Gymnodinium catenatum
bloom in 2000 has resulted in high levels of PSP in shellfish in this area).
156
No shellfish samples from Zone I contained ASP levels above the regulatory level (20
µg/g) in shellfish samples taken between 1/7/93 and 30/6/99. Detectable levels (but
DSP above the regulatory level of 20 µg/100g was detected in 8 shellfish samples
taken from Zone I between 1/9/94 and 30/6/99. Detectable levels of DSP were found
in 27 shellfish samples (2.4% of total samples taken) over the same time period. Most
of these samples were from Akaroa Harbour (I04). Blue mussels from this site
contained persistent levels of DSP from February 1995 to October 1995.
There have been no probable or confirmed cases of TSP in Zone I, and 6 suspected
cases between the beginning of 1994 and June 1999.
6.10
ZONE J
Zone J encompasses all the west coast of the South Island, from Cape Farewell in the
north, down to Bluff in the south, and includes Stewart Island.
The western coast of the South Island is a long exposed rocky coastline, interspersed
with mixed shingle and sand beaches. With the exception of mussels on the rocky
reefs, there are few bivalves suitable for gathering – crayfish are the main noncommercially gathered species other than finfish. White-baiting is an important
recreational and commercial fishery. Similar coastline extends south to the sounds in
Fiordland, where scallops, paua, kina mussels and crayfish are available. In the
Sounds the cliffs drop straight into the sea, and there are very few places where the
intertidal zone is other than vertical. Lack of road access in much of this area limits
the gathering of shellfish. At the south of the South Island, paua and kina are present
as the coast runs in an easterly direction, with toheroa and mactrid clams present in Te
WaeWae Bay, and toheroa at Oreti Beach. The coastline of Stewart Island is
convoluted and rocky, with the major species of interest to non-commercial harvesters
being mussels, paua and dredge oysters. Paterson Inlet has a wider variety of species
with the addition of kina, scallops, pipi and cockles. The Foveaux Strait is famous for
its abundance of dredge oysters. These are conserved through seasonal bans on
harvesting. Due to the impact of Bonamia disease on the oyster population, the
seasons have been highly restricted through the 1990’s, but the beds now appear to
have recovered. The longer “Bluff oyster” seasons now expected will increase the
risk of exposure of consumers to biotoxins in this area.
A survey by Fisher & Bradford (1998) indicated that the species most frequently
targeted for non-commercial harvest are crayfish, paua and mussels, with lower
numbers of trips targeting dredge oysters, scallops, cockles, kina and pipi (Table 3.1,
Section 3). The same survey showed that the trips targeting bivalve species in this
zone comprised 5.1% of the total trips in New Zealand. If paua, kina and crayfish are
included among the species targeted, the trips from this zone comprise 6.9% of the
157
total. Most of this activity is concentrated in the southern part of the zone, as large
stretches of the western coastline (in the north and south) are relatively inaccessible.
level (80 µg/100g) between 1/7/93 and 30/6/99. PSP has been detected in 10 shellfish
samples (0.79% of total samples) over this time period. One was from blue mussels
sampled from Mussel Rocks (on the West Coast) in May 1997 (32 µg/100g), and the
others from Foveaux Strait (8 in February/March 1994, 1 in February 1996), all
dredge oysters.
No shellfish samples from Zone J contained ASP levels above the regulatory level (20
µg/g) in shellfish samples taken between 1/7/93 and 30/6/99. Detectable levels (but
the same time period. These included two samples containing traces of ASP from
Mussel Rocks on the West Coast, as well as samples from the southern sites in the
zone.
samples taken from Zone J between 1/9/94 and 30/6/99. Detectable levels of DSP
period.
There have been four shellfish samples above the regulatory level of 20 mouse units
using the ether extract mouse bioassay over the period 1/9/94 to 30/6/99 in this zone
(equating to 0.49% of the total samples taken over this period). These samples were
Dredge oysters taken from Foveaux Strait in September and December 1994. The
identity of the toxin in these samples was not confirmed as brevetoxin, but is unlikely
to have been gymnodimine.
There has been one probable case of TSP in Zone J, and three suspected cases
between the beginning of 1994 and June 1999. The probable TSP case in 1994 arose
from the consumption of commercially harvested mussels from Big Glory Bay. It
should be noted that the NSP assay at this time utilised an acetone extraction method,
which also extracts gymnodimine. Initial rat-feeding trials, and the lack of any
epidemiological evidence of illness arising from the consumption of shellfish
containing gymnodimine, suggest that this compound is not orally toxic. The current
marine biotoxin monitoring programme does not include gymnodimine.
Note that low levels of PSP and ASP have been detected at the one sample site on the
western coast of the South Island, indicating that these toxins may occur in this
environment. It is questionable as to whether this one site adequately protects
consumers of non-commercially harvested shellfish along the whole length of the
coast.
6.11
ZONE K
Zone K encompasses the Chatham Islands, which lie to the east of the main islands of
New Zealand. Chatham Island itself consists of several sandy beaches, separated by
rocky coasts. Paua and crayfish are common on the rocky coasts, and scallops and
158
tuatua occur in Hansen and Petrie Bays. The adjacent Pitt Island has only two small
sandy bays, with the rest of the coastline being formed by rocky reefs and eroding
rock platforms. Paua and crayfish occur on this coast also. The Chatham Islands are
unusual in the absence of the GreenshellTM mussel, and Blue mussels are also rare.
Zone K is relatively small compared to other Biotoxin Zones. Based on 1996 Census
figures, the total population of the Chatham Islands is 729, with a relatively high
proportion (57%) of the population being Maori (Data from Statistics New Zealand).
There is little information available about the non-commercial harvest of seafood in
the Chatham Islands. However scallops and tuatua, species that appear to readily
accumulate and retain PSP and ASP toxins, are available for harvest. Anecdotal
evidence suggests that crayfish and paua are important species harvested noncommercially. A commercial scallop fishery exists in the area, and marine biotoxin
monitoring, (weekly scallop samples), is undertaken by the scallop fishery during the
scallop season. Weekly monitoring for marine biotoxins in non-commercially
harvested shellfish was discontinued in Zone K in November 1996, and the seasonal
scallop monitoring by the scallop industry currently represents the only monitoring for
marine biotoxins in the zone.
Due to the low level of monitoring, there are only limited data regarding the
occurrence of marine biotoxins in this zone. However, the available data indicate that
there were no shellfish samples with levels of PSP above the regulatory level (80
µg/100g), or above the level of detection, between 1/7/93 and 30/6/99.
No shellfish samples from Zone K contained ASP levels above the regulatory level
(20 µg/g) in shellfish samples taken between 1/7/93 and 30/6/99. Detectable levels
(but extremely low levels) were found in 2 samples of scallop roe (0.9% of total
samples taken) over the same time period.
No DSP toxins above the regulatory level of 20 µg/100g, or above the level of
detection, were found in any of the shellfish samples taken from Zone K between
1/9/94 and 30/6/99.
There has been one shellfish sample above the regulatory level of 20 mouse units
using the ether extract mouse bioassay over the period 1/9/94 to 30/6/99 in this zone
(equating to 0.5% of the total samples taken over this period). This occurred in a
sample of Blue mussels taken from Site K01 in January 1995. The identity of the
toxin in these samples was not confirmed as brevetoxin.
There were no reported cases of TSP from Zone K in the period from January 1993 to
June 1999.
The lack of phytoplankton data from this area, and the inconsistent sampling since
1996, means that the prediction of the risk of marine biotoxin occurrence based on
available data should be undertaken with great caution. There is insufficient evidence
to conclude that marine biotoxins are less likely to occur in the Chatham Islands than
in other areas of New Zealand. Based on data from other areas (Hay, 1996; Kearney,
1999), the high proportion of Maori in the Chatham Islands population suggests that,
if shellfish are available for harvest, there would be a comparatively high proportion
159
of the population at risk from TSP in the event of the occurrence of marine biotoxins.
Further data, including patterns of the occurrence of potentially toxic phytoplankton,
and non-commercial shellfish harvesting patterns, are required before a robust
assessment of the risk of marine biotoxins in this zone can be undertaken.
160
SECTION 7:
7.1
BIOTOXIN MANAGEMENT IN NEW ZEALAND AND
OVERSEAS
EDUCATION AND COMMUNICATION STRATEGIES
Two components of biotoxin management in New Zealand have been discussed in
previous sections of this report: the monitoring programme that encompasses hazard
surveillance, and the outcome surveillance by reporting of cases of TSP. Educational
strategies form another component of the management of biotoxins in New Zealand.
These strategies are designed to perform a variety of functions:
•
•
•
•
Provide an immediate warning to the public not to consume shellfish from an
affected area when a biotoxin event occurs.
Ensure that the public has sufficient background knowledge to be able to interpret
the public warnings and take appropriate action.
Encourage people to use safe practices in the consumption of shellfish to reduce
the risk of TSP (for example, not to eat the gut of scallops or paua).
Ensure that cases of TSP are reported rapidly to local health authorities.
Communication strategies include a range of different actions, some of which may be
modified to suit local situations. During a biotoxin event, local health protection
officers advise the public not to consume shellfish through a variety of media: press
releases to news media, including local newspapers, and local radio stations
(including iwi radio stations); signs posted at boat ramps and access points to shellfish
gathering areas; and in some cases, signs in local stores, and messages on marine
radio. A range of different languages may be used in these communications. In the
event of very high or persistent toxicity, national media statements may also be made.
The information to be included in the media statements in the event of a biotoxin
event is specified in the Marine Biotoxin Management Plan. In the non-commercial
scallop season, this also recommends the inclusion of a message that people should
never eat the skirt and gut from scallops, even when taken from areas that are not
subject to warnings about biotoxins. Health protection officers in many cases also
directly contact local marae and iwi organisations, and local boating clubs. They may
also alert local medical practitioners.
It is a requirement of the National Marine Biotoxin Management Plan that Medical
Officers of Health should regularly ensure that general practitioners in their areas are
aware of the need to notify suspected cases so that these cases can be followed up
(Section 5.1) (N.Z. Marine Biotoxin Management Board, 1995). General practitioners
may also be reminded about TSP through reports of events in the NZ Public Health
Report, or through newsletters from local public health service providers. However,
due to the lack of major biotoxin events in most areas in the last few years, it appears
from discussion with local Health Protection Officers that there has been little
communication of this sort recently. (Author note: This may have changed due to the
recent bloom of Gymnodinium catenatum).
Educational strategies have also encompassed a variety of methods. When the 199293 biotoxin event occurred in New Zealand, most of the New Zealand public had
never heard of marine biotoxins or TSP. The publicity through the media (television,
radio and newspapers) of this event increased the awareness of the public of these
161
issues. Until the restructuring of the management of marine biotoxins in New
Zealand in 1997, the Communications Committee of the Marine Biotoxin
Management Board was responsible for ensuring that mechanisms were in place to
keep the public informed about marine biotoxins. As part of the management of
biotoxins, several formal initiatives were made to educate the public about the risks of
marine biotoxins. These included:
•
The preparation in 1994 of a leaflet “Beginners Guide to Marine Biotoxins”,
containing basic information about marine biotoxins, toxic phytoplankton, closure
and opening of areas to shellfish harvesting, and the management of marine
biotoxins in New Zealand. The prime target group for this leaflet was reporters,
so that the information publicised through the media was accurate and
informative.
•
Data from the 1993 biotoxin event suggested that Maori and Pacific Island people
were possibly more likely to have reported illness after eating shellfish (19% and
3.4% respectively). The Public Health Commission identified the need to inform
whanau, hapu and iwi about the potential risks of TSP for Maori by developing
the Mataitai Health Education Resource Kit. This resource kit includes posters,
pamphlets, and a video, about marine biotoxins, and is presented in both Maori
and English. In late 1994, twelve consultation hui were held throughout the
country to promote the Mataitai resource. They spanned whanau, hapu and iwi
groupings in locations that were inland, estuarine and coastal. These hui
recognised the preference for kanohi ki te kanohi (face to face) interaction, and
were designed as “training for trainers” hui to introduce the resource to iwi. This
enabled further dissemination of the resource to those who could not attend the
hui. The facilitator was Tutekawa Wyllie, and technical support was provided by
Public Health Commission analysts and local health protection officers (Wyllie,
1995).
Discussion in the hui covered key themes including tikanga and traditional
conservation practices, and the relationship between whanau, hapu, iwi and the
Crown acting through local and central governments.
A number of
recommendations arose from the hui, and were presented in a report by Wyllie
(1995). This report also includes valuable information about traditional practices
that impact on effective management of the risk of TSP for Maori (for example,
practices relating to moumou kai).
The Public Health Commission distributed the Mataitai Health Resource
Education Kits to marae, iwi organisations and general practitioners. The
pamphlets and booklets available as part of this resource were reprinted in 1996,
and are still available from Public Health Services.
•
At a local level (for example, in Northland) pamphlets were distributed at boat
ramps advising people about the risks of marine biotoxins, and advising them not
to eat the guts of scallop or paua.
There have been no studies undertaken in New Zealand to evaluate the effectiveness
of the current education and communication strategies with respect to TSP. It is
suggested that this would be a valuable exercise, both in terms of ensuring the cost162
effectiveness of the management of risk of biotoxins, and in interpretation of
epidemiological data that have been collected. Various factors may impact on the
effectiveness of these strategies. These include factors related to whether people
receive the communications, and whether they are acted upon:
•
•
•
•
•
Language – it is noted that the languages used on signage may not adequately
target those people at highest risk – Maori, Pacific Island, and Asian people.
Especially in areas where there are high numbers of new Asian immigrants with
limited English skills, the use of appropriate language on signage would improve
communication of risk.
In some isolated areas it is difficult to post adequate signage (for example,
Marlborough Sounds, where access to many isolated bays is possible by boat, and
people may be away from public boat ramps/piers for many days).
Method of communication must be culturally appropriate – At the Mataitai hui in
1994 it was suggested the news media were not an effective method of
communication of public warnings to Maori. They identified a need for the
HPO’s to work in partnership with kaumatua in each area to ensure that the
message is received appropriately: “the message is more effective coming from
iwi Maori instead of Health Protection Officers” (Wyllie, 1995).
This
recommendation has been acted upon in some areas, but there is no evidence of
any investigation of the most effective means of communicating with other “high
risk” groups.
There may be cultural pressure not to act on warnings – for example, several such
issues were identified as a result of the Mataitai hui. Concern was expressed that
the discarding of parts of shellfish is contrary to Maori traditional practices related
to moumou kai. In addition, it was suggested that “a significant factor to Maori
non-compliance concerned those iwi who lived at the moana and retained kaitiaki
responsibility whereby the impact of closures affected their mana, tikanga and
their identity” (Wyllie, 1995). While there has been some effort to identify such
issues with respect to Maori, there has been little effort to investigate issues
relating to other ethnic groups identified as being at a high risk from TSP. Such
issues may impact on whether public warnings are heeded by these groups.
There is little feedback to reinforce compliance with public warnings. In general,
anecdotal evidence suggests that those members of the public who have not
heeded warnings have not become ill (often due to the fact that the regulatory
toxin levels are set with a safety margin), and this may result in a level of
complacency in complying with warnings.
It is noted that there appears to be no strategy targeting people at the most risk with
respect to respiratory irritation syndrome (e.g. people with asthma). It is suggested
that protocols for communicating this risk to the public in the event of a bloom
producing toxins that cause RIS, could usefully be added into the section on “Marine
Biotoxin Control” in the Ministry of Health “Food Administration Manual” (Ministry
of Health, 1997a).
163
7.2
OVERSEAS MARINE BIOTOXIN MONITORING PROGRAMMES
AND TECHNOLOGY DEVELOPMENTS
In the course of this review, the Ministry of Health indicated that they were interested
in examining overseas marine biotoxin monitoring programmes, to determine whether
there were any management options that could be of benefit in New Zealand. The
following section briefly discusses marine biotoxin monitoring programmes overseas
and associated developments in biotoxin technology.
During this project, health authorities overseas were questioned by Dorothy-Jean
McCoubrey (MAF Verification Authority) about the marine biotoxin monitoring
programmes for non-commercially harvested shellfish in their countries. Countries
where inquiries were made included Australia, Canada, Spain, Denmark, Ireland,
United Kingdom, Philippines and USA. The results are summarised below.
Many countries do not have a separate monitoring programme for non-commercially
harvested shellfish outside the monitoring programme for the shellfish industry. This
may be because either there is not a strong tradition of non-commercial harvesting
(e.g. Denmark) or because non-commercial harvest of shellfish is forbidden, to protect
over-exploited shellfish beds (e.g. Galicia, Spain). In Canada, most of the noncommercial harvesting areas are covered by the sampling programme that covers
commercial harvesting, with some additional sampling, particularly from within
National Parks. In the USA, the monitoring criteria in the National Shellfish
Sanitation Programme only covers commercial shellfish that are transferred interstate,
and each harvesting state develops its own programme for non-commercially
harvested shellfish. In some states, such as Maine, the two programmes are
integrated. Recreational harvesting in Texas and Florida is based on monitoring
phytoplankton counts for Gymnodinium breve. University researchers undertake
monitoring in Texas, and areas are closed when the cell counts are high.
Most countries advertise public warnings through the news media, but advertising the
status of shellfish gathering areas on a web page on the Internet is common. Another
common method of disseminating such information appears to be through a telephone
hotline where callers can dial in for recorded information.
In the USA, there is a much higher level of community involvement in monitoring for
biotoxins than in New Zealand. In California, Maine and Massachusetts, “volunteer
observer networks” have been set up to monitor for potentially toxic phytoplankton.
These are run in conjunction with volunteer groups that monitor water quality in
general. We were also provided with an example of community involvement in
education, in which a teacher from Maine who had her students involved in the
phytoplankton monitoring programme had some students develop a fact sheet about
biotoxins that went to all the doctors in their immediate region. The comment was “It
was very low budget, cute, and probably got the attention of the docs. Local is always
better in the US” (Paul Anderson, University of Maine, U.S.A, pers. comm.).
As knowledge of the causative agents of TSP increase, there appears to be an
increasing trend toward the inclusion of phytoplankton monitoring in marine biotoxin
monitoring programmes. Phytoplankton is cost-effective, can provide early warning
of shellfish intoxication, and the results are available promptly (Todd, 1999).
164
Monitoring for toxic phytoplankton species requires equipment (i.e. plankton
samplers, microscopes) and the ability to recognize potentially toxic species. The
level of technical expertise required is related to the number of different potentially
toxic species, and the type of species – as discussed earlier, toxic and non-toxic
species may not be readily distinguishable. In some countries there is a shortage of
people with the necessary skills to analyze plankton samples. In Korea, this is being
overcome by the use of remote television monitoring network: microscopic images
from local laboratories are transmitted to a central institute in Pusan. An expert in a
central institute can identify the algae from the transmitted microscopic image, thus
reducing the need for large numbers of highly trained staff (Kim, 1999).
A different kind of approach to phytoplankton monitoring is being taken in some
states in the USA. As mentioned, in California, Maine and Massachusetts, “volunteer
observer networks” have been set up to monitor for potentially toxic phytoplankton.
They have been trained in sampling techniques and phytoplankton identification, and
are equipped with nets and field microscopes (Anon, 1998; Hall, 1999). Monitoring
is qualitative rather than quantitative, providing a rough estimate of numbers only.
Samples may be preserved and sent to a laboratory for identification if required.
While these plankton observations do not replace toxicity testing, they make the
monitoring programme more cost effective by focussing toxicity testing on times,
locations and toxins of greatest concern. The net sampling method used in the
programme is not suitable for sampling Gymnodinium species, since they are too
fragile and disintegrate when sampled through a net. The system would therefore
have to be modified for use in areas such as New Zealand, where NSP is a potential
problem. Whether or not such a system would be feasible in areas where greater
numbers of species of potentially toxic phytoplankton need to be identified is also a
relevant consideration in regard to the use of this system elsewhere.
More automated methods of analyzing phytoplankton samples are also being
investigated - for example, the use of flow cytometry (Hofstraat et al., 1994), visual
identification using neural network techniques (Culverhouse, 1995), and as mentioned
earlier, the use of gene probes (Rhodes et al., 1997). However, at this stage analysis
of phytoplankton samples for potentially toxic species is generally undertaken with
the use of a light microscope. In New Zealand, molecular probes are being used
successfully to distinguish between potentially toxic and non-toxic species of Pseudonitzschia, and probes are becoming available for Alexandrium species. Overseas, an
instrument for autonomous collection and real-time detection of harmful algae using
species-specific molecular probes is being developed (Chris Scholin, HABTech
Workshop presentation, Nelson, February 2000). This instrument is being designed to
collect discrete water samples autonomously, concentrate particles contained within
those samples onto filter discs, and automate application of species-specific DNA
probes to identify and quantify particular organisms so captured. In addition to
archiving discrete samples, the instrument is also capable of transmitting results of the
probe assays in real-time to a remote location for data processing and interpretation.
While this is useful as a measure of risk, this technique does not indicate toxin levels,
since strains within species may differ in toxin production. However, DNA probes
are currently proving useful to the New Zealand shellfish industry when trying to
decide whether to implement a voluntary closure to harvesting based on
phytoplankton sample results, and as knowledge of toxin production in phytoplankton
increases, so too will the effectiveness of this technology.
165
The use of remote sensing techniques in monitoring to provide early warning of algal
blooms is also being investigated overseas (Satsuki et al., 1989; Millie et al., 1992;
Belliss, 1993; Wiebe, 1995; Tester et al., 1998). Given the low cell densities of some
toxic phytoplankton that result in shellfish toxicity (e.g. Alexandrium sp.), these
techniques are unlikely to be useful as early warning indicators in New Zealand.
The most widely used toxin test method in shellfish samples is still the mouse
bioassay, although HPLC is used by five of the seven countries/regions that test for
ASP (Andersen, 1996). Except for ASP, there is a large variation between countries
in the critical toxin concentration limits. Concern about this is frequently expressed in
the literature. This is especially an issue in Europe, where the borders between EC
member states are disappearing. In order to deal with this issue, the EC has
nominated National Reference Laboratories on marine biotoxin analysis, and a
Community Reference Laboratory with the aim of establishing an information
exchange network about analytical methodology and to coordinate the standardization
of these criteria (Fernandez et al., 1996).
New test methods for biotoxins found in New Zealand are being developed both in
New Zealand and overseas, to replace mouse bioassays. These include methods based
on chemical analysis (for example HPLC, LC-MS), and in vitro assay methods that
may be broadly categorized into two general sub-types: functional assays, or
structural assays (Cembella et al., 1995a). Cembella et al. (1995a) summarise these as
follows:
“Functional assays are based upon biochemical action of the toxin (e.g. binding to the
ion channels of neuroreceptors), and hence quantitation will tend to correlate well
with the specific toxicity of the analyte. In the case of matrices which contain several
toxic components with a similar mode of biological activity, but which vary in specific
potency, such assays should yield an accurate estimate of net toxicity.
In contrast, structural assays are dependent upon the conformation interaction of the
analyte (toxin) with the assay recognition factor (e.g. epitopic binding sites in
immunoassays). Thus cross-reactivity in such structural immunoassays is limited to
components with compatible epitopic sites and often does not reflect relative
biological activity or specific toxicity. This lack of broad-spectrum cross-reactivity
for toxic, naturally occurring analogs is a major drawback to the use of quantitative
immunoassays for screening phycotoxins in naturally contaminated samples.”
Functional assays for marine biotoxins include cell culture (cytotoxicity) bioassays
(e.g. neuroblastoma assays), and enzymatic tests (e.g. protein phosphatase inhibition
assays). Structural assays include immunoassays of various kinds (e.g. ELISA
techniques).
Each method has advantages and disadvantages. Chemical analysis methods are
accurate in their determination of what toxins are present, but may lack sensitivity.
They require expensive analytical instruments, and often involve complex sample
extraction procedures. Thus they can only be performed in centralised laboratories.
Analytical instrumental detection methods are based on sequential processing of
samples, so it is more difficult to process large numbers of samples (Cembella et al.,
166
1995b). In New Zealand, LC-MS methods are being developed for detection of
yessotoxin and pectenotoxin, but accessibility to equipment may be a problem if large
numbers of samples need to be processed. (Author note: Recent developments
initiated by the shellfish industry have resolved this issue). On the other hand, the
processing of large numbers of samples may reduce the cost, since the set-up times
per sample would be reduced.
Neuroblastoma assays, based on the activity in sodium channels, are being developed
in New Zealand to test for brevetoxins (NSP) and saxitoxins (PSP). These techniques
are relatively sensitive, and are specific to toxin activity. Neuroblastoma assays could
also be combined with biosensor technology to produce a test that can be undertaken
outside a laboratory by relatively unskilled people.
The protein phosphatase inhibition assays have been developed to detect DSP toxin
analogues, Okadaic acid and DTX1 in both shellfish samples and phytoplankton. The
protein phosphatase type-2 inhibition assay is more sensitive than the DSP-ELISA
Check Kit (P. Truman, ESR, pers. comm.), and may be useful if the regulatory limits
for DSP were to be lowered in New Zealand.
Functional assays also include neuroreceptor binding assays, such as the saxitoxin
radio receptor binding assay. This is basically a competitive displacement assay in
which radiolabelled and unlabelled STX and/or its derivatives compete for a given
number of available receptor sites in a preparation of rat-brain synaptosomes. The
disadvantage of these types of assays is the use of vertebrate animals. Work is
progressing on the use of cloned receptors in these assays.
Immunoassays are structural assays. ELISA techniques and sandwich hybridization
assays currently present a promising option for “dock-side” techniques. ELISA
technology is well established, and widely used in other applications. However, these
techniques do have disadvantages, including the susceptibility for generating false
positives due to the presence of non-toxic (or less toxic) congeners, or failure to detect
all toxigenic components when a complex suite of toxin analogues is present. One of
the difficulties in developing immunoassays is the difficulty in obtaining a supply of
toxins to work with. Currently this is particularly pertinent to pectenotoxins, since the
phytoplankton that produce these toxins cannot be cultured in the laboratory
sufficiently well to obtain quantities of toxin.
There are currently very limited options for mitigation or control of toxic algal events.
Because of the economic impact of harmful algal blooms, research into the control of
algal blooms is being undertaken overseas. There are several potential methods of
controlling blooms being investigated. These include the use of bacteria and viruses
to kill phytoplankton populations (Nagasaki et al., 1995, Imai et al., 1995, Yoshinaga
et al., 1995a & 1995b, Gastrich et al., 1998, Nagai & Imai, 1998, Yoshinaga et al.,
1998), and the use of clay flocculents to disperse blooms (Kim, 1998; Bae et al., 1999;
Sun et al., 1999; Sengco et al., 1999; Sengco et al., 2000). The environmental impacts
of releasing algicidal bacteria or viruses into algal blooms have not been determined,
and at this stage would seem to be a high-risk option for control. Clay flocculents are
being used successfully in Korea to control blooms, and this may present a viable
option for the control of large blooms in the future. However, this technique may be
more applicable to blooms of a non-toxic nature (such as those that impact on
167
aquaculture), and would need to be approached with some caution. An attempt was
made to control a Gymnodinium breve red tide in Florida in the 1950’s with the
application of copper, which lysed the algal cells. This was unsuccessful in terms of
toxin reduction, since the lysed cells released the toxin into the water, which resulted
in increased and persistent toxicity in the water (Steidinger, 1983). It is possible that
the application of flocculents might have a similar effect on Gymnodinium species, or
indeed other species here. The issues of the environmental impact of applying large
quantities of clay into our coastal waters would also have to be investigated, and
weighed against the impact of toxic phytoplankton blooms.
Although some research is being undertaken to investigate the environmental
conditions under which toxic algal blooms occur in New Zealand (e.g. Sharples et al.,
1998), these processes are still not well understood. Data from an environmental
monitoring programme established by the mussel farming industry in the
Marlborough Sounds, and more recently by the oyster farming industry at
Coromandel and Mahurangi Harbour, could provide valuable information if linked
with data from the marine biotoxin monitoring programme. Currently there is little
action able to be taken to prevent the occurrence of toxic phytoplankton in New
Zealand. However, the threat of introduction of new species of toxic algae to New
Zealand by ballast water is being addressed in a Government strategy under which
new international regulations request ships to exchange ballast water in mid-ocean
away from coastal influences. There are technical difficulties associated with
exchanging ballast water on large ships, and research to determine alternative
practicable measures to reduce the risk from ballast water is being undertaken
(Ministry of Fisheries, 1998).
7.3
NEW ZEALAND BIOTOXIN MANAGEMENT IN A GLOBAL
CONTEXT
In a review of New Zealand’s non-commercial marine biotoxin monitoring
programme, it is pertinent to consider some factors from a wider context than those
covered by the risk analysis model, which has a very sharp focus. Some of these
factors are summarised below:
•
There is an apparent increase and/or increasing awareness, of marine biotoxins
globally. This may be linked to global warming, the distribution of toxic algal
species via ballast water in ships, and/or increasing concern and understanding
about health issues globally.
•
People are becoming more concerned about environmental quality. There is an
awareness of the potential for human activities to impact on the occurrence of
marine biotoxins, and a concomitant lack of understanding about the processes
that cause toxic phytoplankton blooms.
•
Social values are changing in the western world, including New Zealand, with
respect to animal rights. It is suggested that the mouse bioassay will not continue
to be acceptable as a toxin detection technique.
168
•
New toxin detection techniques are being developed, presenting opportunities for
improvement in monitoring techniques.
•
On a world-wide scale, New Zealand is unusual in that a wide range of marine
biotoxins have been detected here. This adds a level of complexity to the process
of monitoring for marine biotoxins that is not found elsewhere.
Along with the specific assessment of risk, these factors provide part of a broad
framework within which options for management of the risk of TSP and respiratory
irritation syndrome are developed.
169
SECTION 8:
DISCUSSION AND CONCLUSION
This section provides a summary of the conclusions drawn from analysis presented in
previous sections, and outlines potential options for cost-effective management of the
risk presented by marine biotoxins in New Zealand. More detailed discussion of
options is provided in Part 2 of this report under separate cover (Hay et al., 2000).
Following the analysis and collation of information presented in previous chapters,
some broad observations relating to the risk of TSP and RIS can be made:
•
In broad overview, the situation in New Zealand with respect to marine biotoxins
is characterised by:
• Wide distribution of potentially toxin-producing phytoplankton throughout
New Zealand.
•
Periods of low frequency of biotoxin occurrence followed by periods of
higher frequencies, generally in relatively localised areas. Biotoxins may
then persist in a localised area for a period of time, sometimes in one
shellfish species/at one location.
• Possible seasonal patterns in the occurrence of some biotoxins in shellfish
(for example, ASP), and not in others (e.g. PSP).
• In periods of low biotoxin activity, some toxins are present very rarely (e.g.
NSP toxins) and others are common at low levels in some areas (e.g.
Domoic acid).
• Possible differences in the accumulation and retention of biotoxins by
different New Zealand shellfish species. These differences are potentially
significant in terms of the risk of TSP to consumers.
•
Currently there is a poor understanding, both here and internationally, of the
factors influencing the occurrence of toxic phytoplankton blooms. There is
insufficient information to be able to predict the future occurrence of marine
biotoxins in New Zealand with confidence.
•
There is a possibility that the impact of human activity may increase the risk of
marine biotoxins – for example, through global warming, addition of nutrients to
the marine environment, and transportation of toxic species from place to place.
This would suggest that there might be an increasing risk of TSP and RIS in the
future.
•
The oral toxicity of some of the marine biotoxins found in New Zealand,
including the effect of long-term ingestion of low levels of toxin, are still
unknown. The current outcome surveillance may not detect these impacts. This
uncertainty needs to be taken into account in the management of risk of biotoxins.
170
•
The estimation of the risk of TSP and RIS in New Zealand is limited by a
significant lack of robust data. This includes data regarding interspecific and
intraspecific differences in toxin accumulation and retention by shellfish for each
toxin type, and long-term data regarding geographic and temporal patterns in
biotoxin occurrence. There are very significant discrepancies between the few
studies that have been undertaken on non-commercial shellfish harvesting, and
this suggests that further studies are required in this field.
•
The potential risks presented by marine biotoxins in New Zealand are not
distributed evenly across the population. There is a disproportionate potential
impact on sectors of the population that consume more non-commercially
harvested shellfish (for example, Maori, and possibly Pacific and Asian peoples),
on older people or people in poor health, and on asthmatics. Any change to the
management of risk of marine biotoxins needs to consider any strategic health
objectives or goals relevant to the sectors impacted. The objectives contained in
the current strategy for public health specifically mention the improvement,
promotion and protection of the health of Maori and Pacific Island peoples, and
the reduction of disability and death rates from asthma in children.
•
The options for the public to minimise or avoid the risk of TSP in the absence of a
marine biotoxin monitoring programme are limited. Risk can be reduced by
avoidance of consumption of high-risk portions of shellfish, such as scallop and
paua guts. However, in the absence of a marine biotoxin monitoring programme,
the only way of avoiding the risk of TSP is by not consuming non-commercially
harvested shellfish. Some sectors, such as Maori, to whom seafood is of cultural
and economic importance, are likely to find this option unacceptable (Wyllie,
1995).
•
The options for effective surveillance for TSP and RIS are limited. Environmental
surveillance for public health involves three types of complementary surveillance:
hazard, exposure and outcome surveillance. Monitoring for toxic phytoplankton
and biotoxins in shellfish constitutes hazard surveillance, and this is the method of
surveillance that is strongly relied upon both in New Zealand and internationally.
Other forms of surveillance are limited by lack of knowledge: there is a lack of
biomarkers to detect the exposure of humans to marine biotoxins, and this means
that exposure surveillance is not possible. Outcome surveillance is also hindered
by lack of knowledge about the clinical symptoms of TSP, resulting in an underreporting of cases (Fleming et al., 1995; Fleming et al., 1998). At present, chronic
effects caused by long term consumption of low levels of toxins are highly
unlikely to be recognised as arising from marine biotoxins at all. Until these
issues are resolved, reliance on hazard surveillance in the management of marine
biotoxins with respect to public health remains the most effective option.
Within the strategic framework for public health (Section 1.4), and the global context
discussed in Section 7, a range of broad issues relating to the management of marine
biotoxins in New Zealand require consideration. These encompass both strategic and
technical issues.
In the course of this review it has become apparent that there is a dearth of
information on which to base robust risk analysis, and that the mere passage of time
171
on the present course of action will not significantly alter this situation. Uncertainty
increases the overall level of risk. The marine biotoxin monitoring programme is
currently focused only on utilising the data gathered for immediate needs (i.e. is it
currently safe to harvest shellfish from this area?). It is suggested that a more
proactive, strategic approach to the collection and use of data would result in
substantial improvements in cost-effectiveness in the future. This would involve:
a) Improved management of the data collected in the marine biotoxin
monitoring programme. This would ensure that all relevant information is
recorded consistently and in a manner that is accessible for informed analysis,
preferably on a central database. In addition to many problems associated
with the recording of historical data, current deficiencies include: differences
between laboratories in the way in which low levels of toxins are quantified on
the database, and lack of facility (e.g. fields in the database) to record all
relevant data. Relevant data include information about changes to protocols
(e.g. changes in test methods, changes in phytoplankton species names etc.),
environmental data, results of determination of phytoplankton species by gene
probe, results of any additional testing undertaken in addition to regulatory
requirements (e.g. LC-MS, neuroblastoma or ELISA assays for NSP) and
information about mouse deaths in mouse bioassays. An annual audit of the
epidemiological data would be beneficial to ensure the quality of the data
entered, and to identify cases where results from testing have not been entered,
or case status updated.
b) A sampling strategy to ensure that robust, long-term data are available to
detect patterns in the geographic and temporal distribution of biotoxins.
Monitoring data need to be gathered consistently and regularly from sufficient
representative sites within each zone. The initiation of additional monitoring
is suggested in some areas, for example, the collection of regular
phytoplankton data from suitable sites on the western coast (such as sites
within harbours). The Chatham Islands (Zone K) also represents an area from
which very little data have been collected. The collection of phytoplankton
data from this area, possibly through the use of volunteers, would be beneficial
in future risk assessment.
c) A co-ordinated management strategy that ensures sampling and
analytical techniques used in the monitoring programme are scientifically
validated, and that changes in the programme are consistent with the
results of risk analysis and long-term strategies to increase costeffectiveness. Co-ordination is required to ensure that the marine biotoxin
monitoring programme does not progressively change in a “piecemeal”
fashion.
As part of a strategy to improve the long-term cost-effectiveness of the marine
biotoxin monitoring programme for non-commercially harvested shellfish, an
increased emphasis on advocacy and facilitation of relevant research is suggested.
172
This includes research to:
•
•
•
•
•
•
Determine inter-specific differences between shellfish with respect to
biotoxin uptake, accumulation and detoxification processes.
Determine the oral toxicity, including the impacts of long-term ingestion
of low levels of toxin, for those compounds currently known to be toxic to
mice by IP injection, but for which oral toxicity is unknown.
Relate environmental parameters and processes to the occurrence of toxic
phytoplankton, and toxin levels within species.
Validate new toxin testing methods for biotoxins found in New Zealand
(such as the PSP MISTTM Alert Kit).
Rigorously determine non-commercial shellfish harvest patterns.
Evaluate the effectiveness of education and communication strategies with
respect to the management of the risk of marine biotoxins in New Zealand.
The Biotoxin Research Strategy provides a forum for facilitating relevant research.
An increased emphasis on promotion of research relevant to the risk of marine
biotoxins from non-commercially harvested seafood need not result in additional cost
to the Ministry of Health. One of the cross-cutting themes identified as underpinning
all public health goals, objectives and targets is “Building strategic alliances”
(Ministry of Health, 1997b; see Section 1.4 of this report). While participation in the
Biotoxin Technical Committee is an example of such an alliance, increased
incorporation of this theme in the strategy for management of marine biotoxins could
have some benefit. For example, there are environmental data being collected by a
range of other organisations (such as shellfish industry associations, Regional
Councils etc.) for other uses. Similarly, a range of organisations such as the Ministry
of Fisheries, Regional Councils, Maori, and community groups, are interested in noncommercial harvest of shellfish. Strategic alliances with organisations with research
interests in common could assist in facilitation of these research outcomes.
Maintenance of cost-effectiveness in the marine biotoxin monitoring programme is
obviously very important. It is pertinent to consider whether, in the light of a reevaluation of risk arising from analysis of historical data, costs could be reduced by
broad reduction in temporal or spatial components of the monitoring programme.
Several factors are relevant to consideration of this issue:
•
There are sufficient data to suggest that in the absence of a non-commercial
marine biotoxin monitoring programme, a significant number of people could
become ill as a result of TSP in some years. Some of these people would be
severely ill, with the risk of death. For example, one scenario suggests that 50%
of the PSP cases (amounting to nearly 2000 people) would have moderate to
severe symptoms. The long-term effects of ingestion of “DSP” toxins, including
Okadaic acid, dinophysistoxins, yessotoxin and pectenotoxin, are unknown, but
potentially present a risk. The incidences of these two latter toxins are unknown
because they are not currently included in the monitoring programme. The levels
of Domoic acid detected in shellfish to date would only produce relatively mild
symptoms of ASP in adults, (although one scenario suggested that up to 750
people could be affected). The potential impact of NSP remains somewhat
unknown due to a lack of robust data on shellfish toxicity levels from the 1993
event, but has been very low in subsequent years.
173
•
In reviewing the non-commercial marine biotoxin monitoring programme, the
relevance of historical data in predicting future occurrence of marine biotoxins
needs to be considered. There are now 5-6 years data from monitoring the
occurrence of biotoxins in shellfish. Temporal and geographic stratification of
sampling, and inconsistent monitoring data (for example, discontinuities and
changing sample sites) mean that the actual historical occurrence of biotoxins in
shellfish throughout New Zealand cannot be rigorously quantified. International
data suggest that there may be long-term cycles (e.g. 18-19 years) in the
occurrence of biotoxins (White, 1987). The time over which marine biotoxins
have been monitored in New Zealand is thus relatively short. Internationally,
there are many instances where significant levels of toxins have “unexpectedly”
appeared. These factors, plus the widespread distribution of potentially toxic
phytoplankton, suggest that the use of present historical data in the prediction of
future risk of marine biotoxins should be undertaken with extreme caution.
•
The risk of exposure of the New Zealand public to TSP from the consumption of
non-commercially harvested shellfish is dependent, not just on the occurrence of
biotoxins in the marine environment, but also on the patterns of non-commercial
shellfish harvesting and potential differences in accumulation and retention of
biotoxins by different species of shellfish. Definitive data are lacking in both
these areas.
If the short-comings outlined in the last two paragraphs could be ignored, and it could
be assumed that the occurrence of marine biotoxins will not increase (as a result of
human activities, changes to the environment such as global warming, or the spread of
toxic phytoplankton species through the ballast water of ships), then one could
possibly conclude that cost savings through a reduction in monitoring could be
achieved without a resulting increase in the risk of TSP to the public. However, it is
suggested that these short-comings are too comprehensive to be totally ignored.
Consequently, any cost-saving reductions in marine biotoxin monitoring (either in the
temporal or spatial components of the monitoring regime, or reduction in
effectiveness of biotoxin detection) must be considered in light of the question:
Would an increased level of risk to the public resulting from marine biotoxins be
acceptable under the current strategy for public health? This issue is significantly
complicated by the lack of robust data allowing the impact of changes in the
management of the risk of biotoxins to be accurately quantified. In consideration of
the current public health strategy (refer to Section 1.4), it appears that an increased
level of risk would be inconsistent with the strategy unless the money saved by the
change could be more effectively used elsewhere. Within the scope of this review,
and the data available, we are unable to assess this.
Education of the public about the risks associated with marine biotoxins, and
communication of risk in the event of marine biotoxin occurrence, are important
aspects of the way in which the risk of marine biotoxins are managed. The issues
associated with effective communication regarding marine biotoxins are not simple.
As the public become more aware of the marine biotoxin monitoring programme
through communication of public warnings via the news media, there is potentially an
increased expectation that the marine biotoxin monitoring programme will provide
174
protection from the risk of marine biotoxins. On the other hand, the effectiveness of
the monitoring programme is diminished when the public consumes shellfish in
defiance of a public warning, but individuals do not get sick. As one Health
Protection Officer commented recently: “The public test shellfish when we warn
them, and if they get sick they tell nobody. If they do not get sick, they tell
everybody” (T. Beauchamp, Northland Health, oral presentation at the Marine
Biotoxin Science Workshop, November 2000). It is apparent that communication of
the risk of marine biotoxins to the public is not always effective. However, the extent
to which this is the case is unknown, as are the impacts of this: People who have
consumed shellfish in the face of a public warning are unlikely to report consequent
illness unless it is very serious, and the health impacts of consistent consumption of
shellfish containing low levels of biotoxins are unknown.
In areas where consumption of non-commercially harvested shellfish is of particular
cultural or economic importance to a comparatively high proportion of the local
population, and that are subject to long closures due to biotoxin persistence in one
shellfish species only, the introduction of species-specific closures could be
considered. This would require knowledge of the dynamics of accumulation and
detoxification of biotoxins in each shellfish species. Some additional testing to clear a
species for harvest would also be required. The education and communication
requirements with respect to species specific public warnings would be greater than in
the case of implementation of public warnings that apply to all shellfish types.
Protection from the risk of biotoxins would rely not only on the public understanding
the implications of a public warning sufficiently well to take heed, but also on the
ability to discriminate between different shellfish species when they are collecting
them. More complex public warnings may be harder for the public to recall in detail.
In this case, the use of a telephone “hotline”, containing regularly updated recorded
messages of the biotoxin status of each area, could be beneficial. In addition to the
benefits to the public in terms of increased access to shellfish, species specific public
warnings at the end of biotoxin events would assist in maintaining the credibility of
the marine biotoxin monitoring programme, by restricting the application of public
warnings to only those shellfish species that actually contain marine biotoxins.
In discussing potential broad changes to the marine biotoxin monitoring programme,
it is noted that there is currently no specific surveillance or management of risk with
respect to RIS. One option would be to utilise the current phytoplankton monitoring
programme to detect the risk of RIS based on high numbers of relevant Gymnodinium
species, and to issue public warnings based on this data. In effect, this is what
currently happens, and only formalisation of the protocols is required. Provision of
information to medical practitioners about the risks of RIS to asthmatics is also
suggested.
There is currently a high level of co-operation and co-ordination between the Ministry
of Health and MAF and the shellfish industry with respect to monitoring for
biotoxins. Any changes proposed to the marine biotoxin monitoring programme for
non-commercially harvested shellfish need to take into consideration any impacts on
the marine biotoxin monitoring programme for commercially harvested shellfish also.
The impacts of any changes proposed in the commercial monitoring programme on
the non-commercial marine biotoxin monitoring programme also need to be
considered. Currently the Ministry of Health pays the shellfish industry for data
175
received from their monitoring programme. Both industry and the Ministry of Health
programmes use the same test methods. This has advantages in terms of cost, since it
means economies of scale are able to be achieved by the testing laboratories. The
volume of monitoring, (in terms of sample numbers), undertaken in the commercial
programme is approximately twice that of the public health programme (Janet Young,
Ministry of Health, pers. comm.). This means that the shellfish industry is in a more
dominant economic position in driving any changes with respect to testing methods.
In addition to concerns about the health of shellfish consumers, the design of the
marine biotoxin monitoring programme for commercially harvested shellfish is
influenced by several other issues. These include:
•
•
The attitude and regulations regarding various new biotoxins in overseas markets;
and
The methods overseas markets use to test for biotoxins in incoming products.
Currently the shellfish industry is planning to initiate testing for DSP group toxins
(Okadaic acid, DTX-1, DTX-2, DTX-3, Okadaic diol esters, pectenotoxin and
yessotoxin), using LC-MS. The shellfish industry is also aware of the unacceptability
of continuing to use mouse bioassays in toxin testing.
The moves initiated by the shellfish industry provide the Ministry of Health with the
opportunity to consider alternative toxin test methods in an environment where either
economies of scale, or competition for business between competing testing
laboratories, have the potential to provide downward pressure on cost. Technical
developments in the field of testing for biotoxins provide opportunities for more
definitive information about the identity of biotoxins in shellfish samples than the
mouse bioassay currently used. Testing that focuses more specifically on identifying
particular toxins, or, in the case of functional assays, specific modes of toxic activity,
has advantages in the reduction of “false positive” toxicity results that may occur in
mouse bioassays. However, a move to testing for specific biotoxins or types of toxin
activity would remove the hazard surveillance for new biotoxins currently provided
by the mouse bioassays. In this situation, robust outcome surveillance would be of
increased importance. Some new biotoxin assay methods may offer cost advantages
over the mouse bioassays currently used. Specific options with respect to the
potential use of new test methods are discussed in Part 2 of this report under separate
cover.
Phytoplankton monitoring plays an important role in the monitoring of marine
biotoxins in New Zealand. It can provide early warning of shellfish toxicity, and
additional information that is important in the management of the risk of biotoxins.
Our analysis suggests that further data are required to confirm the robustness of the
current phytoplankton monitoring programme in predicting shellfish toxicity. This
applies to both monitoring using counts of potentially toxic phytoplankton species,
and the use of whole cell DNA probes for identification of potentially toxic Pseudonitzschia species. However, review of the phytoplankton monitoring data highlighted
several technical issues. With respect to some phytoplankton species, the impact of
the low level of precision in the phytoplankton methods currently used, and whether
any additional assurance gained by improving this precision justifies additional cost,
needs to be considered. In addition, the impact of succession of Pseudo-nitzschia
species within a Pseudo-nitzschia bloom on the protocols for use of gene probes
176
within the monitoring programme, requires further investigation. As mentioned
earlier, validation of the protocols for use of whole cell DNA probes in the monitoring
programme should be undertaken before they are used in decisions not to undertake
shellfish toxicity testing.
In addition to the technical issues raised by our review of the robustness of the
phytoplankton monitoring programme, one other important issue was highlighted.
This concerns the quality of critiquing of sampling protocols and analytical techniques
prior to their introduction to the monitoring programme. While the quality assurance
programmes of the organisations delivering sampling or analytical services to the
programme ensure a consistent quality, they do not necessarily address the issue of
whether the protocols used are designed to deliver the required result. Many of the
technical issues that require consideration in biotoxin monitoring are complex and
specialised, and the Marine Biotoxin Technical Committee regularly seeks expert
advice. However, it is suggested that the Marine Biotoxin Technical Committee
could benefit from consistently seeking independent advice from appropriately
qualified technical specialists to peer review technical proposals when considering
major changes to the marine biotoxin monitoring programme.
In conclusion, the analysis of biotoxin data undertaken as part of this review identified
some broad patterns relating to the occurrence of biotoxins in New Zealand. Also
identified were a number of very key areas where lack of information prevents a
robust assessment of the risks to public health presented by biotoxins. Robust
quantification of changes in risk resulting from changes to the monitoring programme
is thus not possible. We therefore cannot recommend any broad cost-saving changes
in the frequency or distribution of monitoring for marine biotoxins, especially as the
sectors of the public most probably disproportionately at risk include those for which
there are specific strategic objectives and goals to improve public health. An
alternative is to address the current barriers to risk analysis, and ensure that the data
being collected in the monitoring programme is used more effectively to obtain the
information required for robust risk analysis in the future. The options suggested in
this review address both specific technical issues that have been highlighted in the
review process, and broader issues that will improve the cost-effectiveness of the
programme in the longer term. Particularly in the latter case, strategic relationships
with outside organisations will be important in determining synergies with respect to
both effectiveness and cost.
177
LITERATURE CITED
Andersen, P. (1996) Design and implementation of some harmful algal monitoring
systems. Intergovernmental Oceanographic Commission Technical Series 44,
UNESCO, Paris. 102 pp.
Anderson, D. M. (1998) Physiology and bloom dynamics of toxic Alexandrium
species, with emphasis on life cycle transitions. In: Physiological ecology of
harmful algal blooms. Anderson, D. M., Cembella, A. D., & Hallegraeff, G. M.
(Eds.). Springer-Verlag, Berlin. Pp. 29-47
Anderson, D. M. & Wall, D. (1978) The potential importance of benthic cysts of
Gonyaulax tamarensis and Gonyaulax excavata in initiating toxic dinoflagellate
blooms. J. Phycol. 14:224-234
Annala, J. H. & Sullivan, K. J. (1996) Report from the Fishery Assessment Plenary
April-May 1996: Stock assessments and yield estimates. Ministry of Fisheries.
308 pp.
Anon (1998) “Early warning system” for shellfish poisoning. Volunteer Monitor,
Fall ’98. Pp. 4-7
Aune, T. & Yndestad, M. (1993) Chapter 5: Diarrhetic Shellfish Poisoning. In:
Algal toxins in seafood and drinking water. Falconer, I. (Ed.). Academic Press,
San Diego. Pp. 87-103
Baden, D. G. (1989) Brevetoxins: Unique polyether dinoflagellate toxins. FASEBJ
3:1807-1817
Baden, D. G., Abraham, W., Backer, L., Benson, J., Bossart, G., Cheng, Y. S.,
Fleming, L., Pierce, R., Rowan, A. & Wanner, A. (2000). What is the
respiratory irritant released during Florida Red Tides? A poster presentation
at the Harmful Algal Bloom 2000 Conference, Hobart, Australia.
Bae, H. M., Yoon S. J. & Kim, H. G. (1999) Control of the HAB’s by yellow loess
dispersion. Abstract from the First Conference on Harmful Algal Management
and Mitigation. Subic Bay, Philippines, 10 – 14 May, 1999. Pp. 7
Baker, M. & McNicholas, A. (1995) A review of the surveillance system for cases of
toxic shellfish poisoning. A report prepared by the Epidemiology Group, ESR.
27 pp.
Balech, E. (1995) The genus Alexandrium Halim (Dinoflagellata). Sherkin Island
Marine Station, Sherkin Island, Co. Cork, Ireland.
Bates, M., Baker, M., Wilson, N., Lane, L. & Handford, S. (1993) Epidemiologic
overview of the New Zealand shellfish toxicity outbreak. In: Marine Biotoxins
and New Zealand Shellfish. Jasperse, J. A. (Ed.). Proceedings of a workshop
on research issues 10-11 June 1993. The Royal Society of N.Z. Miscellaneous
Series 24. Pp. 35-40
178
Bates, S. S., Leger, C., & Smith, K. M. (1996) Domoic Acid production by the diatom
Pseudo-nitzschia multiseries as a function of division rate in silicate-limited
chemostat culture. In: Harmful and toxic algal blooms. Yasumoto, T., Oshima,
Y. & Fukuyo, Y. (Eds.). Intergovernmental Oceanographic Commission of
UNESCO, Paris, France. Pp. 163-166
Bates, S. S., Garrison, D. L. & Horner, R. A. (1998) Bloom dynamics and physiology
of Domoic-Acid-producing Pseudo-nitzschia species. In: Physiological ecology
of harmful algal blooms. Anderson, D. M., Cembella, A. D. & Hallegraeff, G.
M. (Eds.). NATO ASI Series, Sub-series G “Ecological Sciences” Vol. 41,
Springer. 662 pp.
Belliss, S. E. (1993) The potential use of airborne scanning for monitoring algal
dynamics in Australasian waters. Unpublished report of a Workshop session
with Graham Harris of COSSA, 27 July 1993. 14 pp.
Bialojan, C. & Takai, A. (1988) Inhibitory effect of marine sponge Okadaic acid on
protein phosphatases: specificity and kinetics. Biochem. J. 256:283-290
Bricelj, V. M., Cembella, A. D., Laby, D., Shumway, S. E. & Cucci, T. L. (1996)
Comparative physiological and biochemical responses to two PSP toxins in two
bivalve molluscs, the softshell clam Mya arenaria and the surf clam Spisula
solidissima. In: Harmful and toxic algal blooms.. Yasumoto, T., Oshima, Y. &
Fukuyo, Y. (Eds.). Intergovernmental Oceanographic Commission, UNESCO,
Paris, France. Pp. 405-408
Briggs, L., Rhodes, L., Munday, R. & Towers, N. (1998) Detection of palytoxin using
a haemolysis neutralisation assay. Proceedings of the Marine Biotoxin Science
Workshop No. 10 (20th November 1998). Pp. 91-97
Burns, D. A. & Mitchell, J. S. (1982) Dinoflagellates of the genus Dinophysis
Ehrenberg from New Zealand coastal waters. N.Z. J. Mar. Freshw. Res.
16:289-298
Carter, L., Garlick, R. D., Sutton, P., Chiswell, S., Oien, N. A., & Stanton, B. R.
(1998) Ocean Circulation New Zealand. NIWA Chart Miscellaneous Series
No.76.
Cembella, A. D., Sullivan, J. J., Boyer, G. L., Taylor, F. J. R. & Anderson, R. J.
(1987)
Variation in paralytic shellfish toxin composition within the
Protogonyaulax tamarensis/catenella species complex. Biochem. System. Ecol.
15:171-186
Cembella, A. D., Turgeon, J., Therriault, J. C., & Boland, P. (1988) Spatial
distribution of Protogonyaulax tamarensis resting cysts in nearshore sediments
along the north coast of the lower St Lawrence Estuary. J. Shellfish Res. 7:
597-610
179
Cembella, A. D., Shumway, S. E., & Lewis, N. I. (1993) Anatomical distribution and
spatio-temporal variation in paralytic shellfish toxin composition in two bivalve
species from the Gulf of Maine. J. Shellfish Res. 12:389-403
Cembella, A. D., Milenkovic, L. V. & Doucette, G. J. (1995a) In vitro biochemical
and cellular assays. In: Manual on harmful marine microalgae. Hallegraeff,
G. M., Anderson, D. M., Cembella, A. D. and Enevoldsen, H. O. (Eds.). Intergovernmental Oceanographic Commission Manuals and Guides No. 33,
UNESCO. Pp. 181-211
Cembella, A. D., Milenkovic, L., Doucette, G. & Fernandez, M. (1995b) In vitro
biochemical methods and mammalian bioassays for phycotoxins. In: Manual on
harmful marine microalgae. Hallegraeff, G. M., Anderson, D. M., Cembella,
A. D. and Enevoldsen, H. O. (Eds.). Inter-governmental Oceanographic
Commission Manuals and Guides No. 33, UNESCO. Pp. 177-179
Chang, F. H. (1996) A review of knowledge of a group of closely related
economically important toxic Gymnodinium/Gyrodinium (Dinophyceae) species
in New Zealand. J. Royal Soc. N.Z. 26:381-394
Chang, F. H., Anderson, C., Boustead, N. C. (1990) First record of a Heterosigma
(Raphidophyceae) bloom with associated mortality of cage-reared salmon in
Big Glory Bay, New Zealand. N.Z. J. Mar. Freshw. Res. 24:461-469
Chang, F. H., Anderson, D. M., Kulis, D. M., & Till, D. G. (1997) Toxin production
of Alexandrium minutum (Dinophyceae) from the Bay of Plenty, New Zealand.
Toxicon 35:393-409
Chang, F. H., Redfearn, P., Diggles, B., Glasby, C., & Allen, S. (1998a) Some
characteristics of the Wellington Harbour Gymnodinium toxins: impacts on
marine animals and algae. In: Proceedings of the Marine Biotoxin Science
Workshop No. 10 (20 November 1998), Marine Biotoxin Management Board
Technical Committee.
Chang, F. H., McKoy, J. & Uddstrom, M. (1998b) The summer 1998 Gymnodinium
c.f. mikimotoi blooms on the East Coast and in Wellington Harbour of New
Zealand. In: Proceedings of the Marine Biotoxin Science Workshop No. 9 (1
May 1998) Marine Biotoxin Science Committee. Pp. 38-43
Culverhouse, P. F. (1995) Automatic methods for the detection of harmful algae. In:
Harmful algal marine blooms: Proceedings of the sixth international conference
on toxic marine phytoplankton, October 1993, Nantes, France. Lassus, P.,
Arzul, G. Erard, E., Gentien, P. & Marcaillou, C. (Eds.) Intercept Ltd., Andover,
UK. Pp. 695-706
Daiguji, M., Satake, M., James, K., Bishop, A., Mackenzie, L., Naoki, H. &
Yasumoto, T. (1998) Structures of new pectenotoxin analogs Pectenotoxin-2
Seco Acid and 7-epi-Pectenotoxin-2 Seco Acid, isolated from a dinoflagellate
and Greenshell mussels. Chem. Lett. 7:653-654
180
Delaney, J. E. (1985) Chapter 4: Bioassay procedures for shellfish toxins. In:
Laboratory procedures for the examination of seawater and shellfish. 5th Ed.
Greenburg, & Hunt, (Eds.). American Public Health Association Inc.,
Washington, DC. Pp. 66-78
Drey, B. & Hartill, B. (1993) A qualitative survey of intertidal harvesting by amateur
fishers in the Auckland metropolitan area. Northern Fisheries Region Internal
Report No. 11. 22 pp.
Erickson, G. & Nishitani, L. (1985) The possible relationship of El Nino/Southern
Oscillation events to interannual variations in Gonyaulax populations as shown
by records of shellfish toxicity. In: Proceedings of the Meeting on El Nino
effects in the Eastern Subarctic Pacific. Wooster W. S. et al., (Eds.).
Washington Sea Grant Program, University of Washington. Pp. 283-290
ESR Communicable Disease Centre (1996) Instructions for completing case report
forms. Manual for Public Health Surveillance in New Zealand: Section C. A
publication of ESR Communicable Disease Centre.
Fernandez, M. I., Miguez, A., Cacho, E. & Martinez, A. (1996) Sanitary control of
marine biotoxins in the European Union: National References Laboratories
Network. . In: Harmful and toxic algal blooms. Yasumoto, T., Oshima, Y. &
Fessard, V. (1998) Okadaic acid and carcinogenesis. IOC Harmful Algal News.
17:10-11. April.
Fisher, D. & Bradford, E. (1998) National marine recreational fishing survey 1996:
catch and effort results by fishing zone. Final Research Report of Ministry of
Fisheries Project REC9701, National Institute of Water & Atmospheric
Research. 7 pp.
Fleming, L. E., Bean, J. A. & Baden, D. G. (1995) Epidemiology and public health.
In: Manual on harmful marine microalgae. Hallegraeff, G. M., Anderson, D.
M. & Cembella, A. D. (Eds.). Intergovernmental Oceanographic Commission
Manuals and Guides 33, UNESCO. Pp. 475-486
Fleming, L. E., Baden, D. G., Bean, J. A., Weissman, R. & Blythe, D. G. (1998)
Seafood toxin diseases: Issues in epidemiology and community outreach. In:
Harmful Algae: Proceedings of the VIII International Conference of Harmful
Algae. Reguera, B., Blanco, J., Fernandez, L. & Wyatt, T. (Eds.) Vigo, Spain,
25-29th June 1997. Xunta de Galicia, Intergovernmental Oceanographic
Commission of UNESCO. Pp. 245-248
Fletcher, G., Hay, B. & Scott, M. (1998) Uptake and elimination of NSP and
Yessotoxin by GreenshellTM mussels. In: Proceedings of the Marine Biotoxin
Science Workshop No. 10 (20 Nov. 1998) MAF, Wellington.
181
Gainey, L. F. & Shumway, S. E. (1988) A compendium of the responses of bivalve
molluscs to toxic dinoflagellates. J. Shellfish Res. 7:623-628
Gastrich, M. D., Anderson, R. O., Benmayor, S. S. & Cosper, E. M. (1998) Fine
structure analysis of viral infection in the harmful brown tide alga Aureococcus
anophagefferens. In: Harmful Algae: Proceedings of the VIII International
Conference of Harmful Algae. Reguera, B., Blanco, J., Fernandez, L. & Wyatt,
T. (Eds.). Vigo, Spain, 25-29th June 1997. Xunta de Galicia, Intergovernmental
Oceanographic Commission of UNESCO. Pp. 419-421
Hall, S. (1991) Interim revision to the PSP mouse bioassay protocol. 4th January
1991, United States Food & Drug Administration, Washington. A modification
to: Irwin, N. (Chairman) (1970). Recommended procedures for the examination
of seawater and shellfish. 5th Edition. American Public Health Association Inc.
Washington. Pp. 74-79
Hall, S. (1999) Volunteer phytoplankton programme. In: Proceedings of the Sixth
Canadian Workshop on Harmful Marine Algae. Martin, J. L. & Haya, K.
(Eds.). Canadian Technical Report of Fisheries and Aquatic Sciences No. 2261.
30 pp.
Hallegraeff, G. M. (1995) Harmful algal blooms: A global overview. In: Manual on
harmful marine microalgae. Hallegraeff, G. M., Anderson, D. M., Cembella,
A. D. and Enevoldsen, H. O. (Eds.) Intergovernmental Oceanographic
Commission, Manuals and Guides No. 33, UNESCO. Pp. 1-22
Hannah, D. J., Till, D. G., Benseman, B., Jones, P. D., Pickston, L. & Walker, N.
(1993) Toxins and assay techniques. In: Marine Biotoxins and New Zealand
Shellfish. J. A. Jasperse (Ed.). Proceedings of a workshop on research issues
10-11 June 1993. The Royal Society of NZ Miscellaneous Series 24. Pp.28-30
Hannah, D. J., Till, D. G., Deverall, T., Jones, P. D. & Fry, J. M. (1995) Extraction of
lipid-soluble marine biotoxins. J. AOAC International 78: 480-483
Hartill, B. & Cryer, M. (1999) User survey of shellfish harvesting in the Auckland
metropolitan area. Progress Report for Ministry of Fisheries Research Project
REC9707, National Institute of Water & Atmospheric Research.
Hay, B. E. (1996) Marine resources of Te Hiku o te Ika. In: Sustainable development
in Tai Tokerau Case Study Two: Te Hiku o te Ika. Report published by James
Henare Maori Research Centre, University of Auckland. Pp. 24-55
Hay, B. E., Grant, C.M. & McCoubrey, D-J. (2000) A review of the marine biotoxin
monitoring programme for non-commercially harvested shellfish. Part 2:
Options and Recommendations. A report prepared for the NZ Ministry of
Health. 16pp.
182
Haywood, A. (1998) Toxic Gymnodinium update. In: Proceedings of the Marine
Biotoxin Science Workshop No. 10 (20 November 1998) Marine Biotoxin
Hemmert, W. H. (1975). The public health implications of Gymnodinium breve red
tides: A review of the literature and recent events. In: Proceedings of the first
international conference on toxic dinoflagellate blooms. Massachusetts
Institute of Technology, April 1975. Pp. 489-497.
Hofstraat, J. W., van Zeijl, W. J. M, de Vreeze, M. E. J., Peeters, J. C. H., Peperzak,
L., Colijn, F. & Rademaker, T. W. M. (1994) Phytoplankton monitoring by
flow cytometry. J. Plankton Res. 16:1197-1224
Imai, I., Ishida, Y., Sakaguchi, K. & Hata, Y. (1995) Algicidal marine bacteria
isolated from Northern Hiroshima Bay, Japan. Fish. Sci. 61: 628-636
Ishida, H., Nozawa, A., Nukaya, H., Tsuji, K., Kaspar, H., Berkett, N., & Kosuge, T.
(1994) Isolation and structure determination of a new marine neurotoxin from
the New Zealand shellfish Austrovenus stutchburyi. Toxicon 32:1672-1674
Ishida, H., Nozawa, A., Totoribe, K., Muramatsu, N., Nukaya, H., Tsuji, K.,
Yamaguchi, K., Yasumoto, T., Kaspar, H. F., Berkett, N. & Kosuge, T. (1995).
Brevetoxin B1, a new polyether marine toxin from the New Zealand shellfish
Austrovenus stutchburyi. Tetrahedron Letts. 36:725-728
Ishige, M., Satoh, N., & Yasumoto, T. (1988) Pathological studies on mice
administered with the causative agent of diarrhetic shellfish poisoning (Okadaic
acid and Pectenotoxin-2). Bulletin Hokkaido Institute of Public Health 38:1819
Jackson, A. E., Marr, J. C. & McLachan, J. L. (1993) The production of Diarrhetic
shellfish toxins by an isolate of Prorocentrum lima from Nova Scotia, Canada.
In: Toxic phytoplankton blooms in the sea. Smayda, T. J. & Shimizu Y. (Eds.)
Elsevier Science Publishers. Pp. 513-518
Jung, J. H., Sim, S., & Lee, C. O. (1995) Cytotoxic compounds from a two-sponge
association. J. Nat. Products 58:1722
Kearney, M. B. (1999) Ecology and management of Austrovenus stutchburyi in the
Whangateau Harbour. M.Sc. Thesis, School of Environmental and Marine
Science, University of Auckland. 135 pp.
Kim, H. G. (1998) Cochlodinium polykrikoides in Korean coastal waters and their
mitigation.
In: Harmful Algae: Proceedings of the VIII International
Conference of Harmful Algae. Reguera, B., Blanco, J., Fernandez, L. & Wyatt,
T. (Eds.). Vigo, Spain, 25-29th June 1997. Xunta de Galicia, Intergovernmental
183
Kim, H. G. (1999) Remote televisual HABs monitoring system. Abstract from paper
presented at the first Conference on Harmful Algae Management and
Mitigation, Subic Bay, Philippines, 10-14 May 1999.
Kirkpatrick, B., Hautamaki, P., Kane, T., Henry, M., Lyons, J. & Pierce, R. (2000). A
pilot study to explore the relationship of occupational exposure to
Gymnodinium breve toxin and pulmonary function. A poster presented at the
Harmful Algal Bloom 2000 Conference, Hobart, Australia.
Lawrence, J. F. & Menard, C. (1991) Confirmation of domoic acid in shellfish using
butyl isothioncyanate and reversed-phase liquid chromatography.
J.
Chromatography 550:595-601
Lawrence, J. F., Charbonneau, C. F. & Menard, C. (1991). Liquid chromatographic
determination of domoic acid in mussels, using AOAC paralytic shellfish poison
extraction procedure: Collaborative study. J. Assoc. Off. Anal. Chem. 74:6872
Lee, J. S., Igarashi, T., Fraga, S., Dahl, E., Horgaard, P. & Yasumoto, T. (1989)
Determination of Diarrhetic shellfish toxins in various dinoflagellate species. J.
Appl. Phycol. 1:147-152
Loscutoff, S. (1992) West Coast experience – Overview. In: Domoic Acid Workshop
Proceedings. Feb 6-8, 1992, San Pedro, California.
Lund, J. W. G., Kipling, C. & Le Cren, E. D. (1958) The inverted microscope method
of estimating algal numbers and the statistical basis of estimations by counting.
Hydrobiologia 11(2):143-170
Mackenzie, A. L. (1992) A report on the examination of oyster gut contents and
phytoplankton during a “Red Tide” event in Akaroa Harbour 1-5 July 1992.
An unpublished report for the NZ Shellfish Sanitation Committee, July 1992.
Mackenzie, L. (1994) More blooming problems – toxic algae and shellfish biotoxins
in the South Island (January-May 1994). Seafood New Zealand, June 94. Pp.
47-52
Mackenzie, A. L., Rhodes, L. L. & White, D. (1992) An investigation of algal
biotoxins in plankton and mussels from the Coromandel area 8-10 November,
1992. An unpublished report for the Ministry of Agriculture and Fisheries,
Thames.
Mackenzie, A. L., White, D. A., Sim, P. G., Holland, J. A. (1993) Domoic Acid and
In: Toxic
the New Zealand Greenshell mussel (Perna canaliculus).
phytoplankton blooms in the sea. Smayda, T. J., & Shimizu, Y. (Eds.). Elsevier
Science Publishers. Pp. 607-612
Mackenzie, L., White, D., Rhodes, L., Berkett, N., Burke, B., & Haywood, A. (1994)
Alexandrium and PSP in New Zealand – Another chapter in the marine biotoxin
saga. Seafood New Zealand, July ’94. Pp. 72-75
184
Mackenzie, L., Syhre, M., Todd, K., Haywood, A., Truman, P. Garthwaite, I. &
Towers, N. (1995a) DSP and NSP in New Zealand, Some recent findings. In:
Proceedings of the Marine Biotoxin Science Workshop No. 4. Marine Biotoxin
Mackenzie, L., Rhodes, L., Till, D., Chang, F. H., Kaspar, H., Haywood, A., Kapa, J.,
& Walker, B. (1995b) A Gymnodinium sp. bloom and the contamination of
shellfish with lipid soluble toxins in New Zealand. In: Harmful marine algal
blooms: Proceedings of the sixth international conference on toxic marine
phytoplankton, October 1993, Nantes, France. Lassus, P., Arzul, G. Erard, E.,
Gentien, P. & Marcaillou, C. (Eds.) Intercept Ltd., Andover, UK. Pp. 795-800
Mackenzie, L., Adamson, J., White, D., & Todd, K., (1996a) Alexandrium catenella
and PSP-toxin contamination of shellfish in the Bay of Plenty: Progress to date
on an investigation of the April/May 1996 bloom. In: Proceedings of the
Marine Biotoxin Science Workshop No. 6 (18 October 1996), MAF.
Mackenzie, L., Haywood, A., Adamson, J., Truman, P., Till, D., Seki, T., Satake, M.,
& Yasumoto, T. (1996b) Gymnodimine contamination of shellfish in New
Zealand. In: Harmful and toxic algal blooms. Yasumoto, T., Oshima, Y. &
Mackenzie, L., Adamson, J. & Todd, K. (1997) Alexandrium and associated PSP
toxin contamination of shellfish on the North Island East Coast during 1997.
In: Proceedings of the Marine Biotoxin Science Workshop No. 8 (10 November
1997), MAF.
Mackenzie, L., Adamson, J. & Todd, K. (1998a) A recent Alexandrium bloom in the
Coromandel: What species and why no toxicity? In: Proceedings of the Marine
Biotoxin Science Workshop No. 9 (1 May 1998), MAF. Pp. 128-145
Mackenzie, L., Truman, P., Satake, M., Yasumoto, T., Adamson, J., Mountfort, D. &
White, D. (1998b) Dinoflagellate blooms and associated DSP toxicity in
shellfish in New Zealand. In: Harmful Algae: Proceedings of the VIII
International Conference of Harmful Algae.
Reguera, B., Blanco, J.,
Fernandez, L. & Wyatt, T. (Eds.). Vigo, Spain, 25-29th June 1997. Xunta de
Galicia, Intergovernmental Oceanographic Commission of UNESCO. Pp. 7477
Mackenzie, L., Suzuki, T., & Adamson, J. (1999) DSP toxin profiles in Dinophysis
acuta and mussels from Wedge Point, Queen Charlotte Sound. In: Proceedings
of the Marine Biotoxin Science Workshop No. 11, Marine Biotoxin Technical
Committee. Pp. 77-83
Marsden, I. (1993) Effects of algal blooms on shellfish biology and metabolism. In:
Proceedings of a Workshop on research issues 10-11 June 1993. Royal Society
of New Zealand Miscellaneous Publications Series 24. Pp. 23-27
185
Millie, D. F., Baker, M. C., Tucker, C. S., Vinyard, B. T. & Dionigi, C. P. (1992)
High resolution airborne remote sensing of bloom-forming phytoplankton. J.
Phycol. 28: 281-290
Ministry of Agriculture & Fisheries (1993a) Ministry of Agriculture and Fisheries
Contingency plans for emergencies. Section 4. Marine biotoxin emergencies.
Pg. 21-26
Ministry of Agriculture & Fisheries (1993b) National management plan for Marine
Biotoxin Control in New Zealand. In: Contingency plans for emergencies. An
internal report, MAF, February 1993.
Ministry of Fisheries (1998) Ballast water and ship’s hull de-fouling: A Government
Strategy. Ministry of Fisheries, January 1998. 41 pp.
Ministry of Health (1997a) Food Administration Manual Section 27: Marine
Biotoxin Control. Version 1.0: June 1997.
Ministry of Health (1997b) Strengthening public health action: The strategic
direction to improve, promote and protect public health. A paper developed by
the Public Health Group, Ministry of Health.
Morohashi, A., Satake, M., Murata, K., Naoki, H., Kaspar, H. F. & Yasumoto, T.
(1995). Brevetoxin B3, a new brevetoxin analog isolate from the Greenshell
mussel Perna canaliculus involved in neurotoxic shellfish poisoning in New
Zealand. Tetrahedron Letts. 36:8995-8998
Morton, J. & Miller, M. (1973) The New Zealand Sea Shore. 2nd Ed. William Collins
& Sons, Glasgow. 653 pp.
Murakami, Y., Oshima, Y., & Yasumoto, T. (1982) Identification of Okadaic acid as
a toxic component of a marine dinoflagellate Prorocentrum lima. Bull. Jpn.
Soc. Sci. Fish. 48:69-72
Murata, K., Satake, M., Naoki, H., Kaspar, H. F. & Yasumoto, T. (1998). Isolation
and structure of a new brevetoxin analog, Brevetoxin B2, from Greenshell
mussels from New Zealand. Tetrahedron Letts. 54:735-742
Nagai, S. & Imai, I. (1998) Killing of a giant diatom Coscinodiscus wailesii Gran by
a marine bacterium Alteromonas sp. isolated from the Seto Inland Sea of Japan.
In: Harmful Algae: Proceedings of the VIII International Conference of
Harmful Algae. Reguera, B., Blanco, J., Fernandez, L. & Wyatt, T. (Eds.).
Vigo, Spain, 25-29th June 1997. Xunta de Galicia, Intergovernmental
Nagasaki, K., Imai, I., Itakura, S., Ando, M. & Ishida, Y. (1995) Viral infection in
Heterosigma akashiwo (Raphidophyceae): A possible termination mechanism of
the noxious red tide. In: Harmful algal marine blooms: Proceedings of the sixth
international conference on toxic marine phytoplankton, October 1993, Nantes,
186
France. Lassus, P., Arzul, G. Erard, E., Gentien, P. & Marcaillou, C. (Eds.).
Intercept Ltd., Andover, UK. Pp. 639-644
New Zealand Fishing Industry Board (1995) Phytoplankton monitoring: A tool for
predicting the presence of marine biotoxins in shellfish in New Zealand – A
discussion paper. A discussion paper presented to the New Zealand Marine
Biotoxin Management Board Technical Committee, June 1995.
New Zealand Marine Biotoxin Management Board (1995) National Marine Biotoxin
Management Plan. August 1995.
Nishitani, L. & Chew, K. (1988) PSP toxins in the Pacific Coast states: Monitoring
programs and effects on bivalve industries. J. Shellfish Res. 7: 653-669
Ogino, H., Kamagi, M. & Yasumoto, T. (1997) Toxicologic evaluation of yessotoxin.
Natural Toxins 5: 255-259
Palma, A. S., Vilarinho, G., & Moita, M. T. (1998) Interannual trends in the
longshore distribution of Dinophysis species off the Portuguese coast. In:
Harmful algae: Proceedings of the VIII International Conference of Harmful
Algae. Reguera, B., Blanco, J., Fernandez, M. L., & Wyatt, T. (Eds.). Vigo,
Spain, 25-29th June 1997. Xunta de Galicia, Intergovernmental Oceanographic
Pierce, R. H. (1986) Red tide (Ptychodiscus brevis) toxin aerosols: A review.
Toxicon 24:955-965
Redondo, J., Fiedler, B., Scheiner-Bobis, G. (1996) Palytoxin induced Na+ influx into
yeast cells expressing the mammalian sodium pump is due to the formation of a
channel within the enzyme. Mol. Pharmacol. 49:49-57
Reguera, B., Marino, J., Campos, M. J., Bravo, I., Fraga, S, & Carbonell, A. (1993)
Trends in the occurrence of Dinophysis spp. in Galician waters. In Toxic
phytoplankton blooms in the sea. Smayda, T. J. & Shimizu, Y. (Eds.)
Proceedings of the Vth International Conference on Toxic Marine
Phytoplankton. Elsevier Science Publishers. Pp. 559-564
Reyes-Vasquez, G., Ferraz-Reyes, E., & Vasquez, E. (1979) Toxic dinoflagellate
blooms in northeastern Venezuaela during 1977. In: Toxic Dinoflagellate
Blooms. Taylor, D. L. & Seliger, H. H. (Eds.). Proc. Int. Conf. (2nd) Elsevier,
Holland.
Rhodes, L. L. & Syhre, M. (1995) Okadaic acid production by New Zealand
Prorocentrum lima isolate. N.Z. J. Mar. Freshw. Res. 29:367-370
Rhodes, L. L. & Thomas, A. E. (1997) Coolia monotis (Dinophyceae): A toxic
epiphytic microalgal species found in New Zealand. N.Z. J. Mar. Freshw. Res.
31:139-141
187
Rhodes, L. L., Haywood, A. J., Ballantine, W. J. & Mackenzie, A. L. (1993) Algal
blooms and climatic anomalies in north-east New Zealand August-December
1992. N.Z. J. Mar. Freshw. Res. 27:419-430
Rhodes, L., White, D., Syhre, M. & Atkinson, M. (1996) Pseudo-nitzschia species
isolated from New Zealand coastal waters: Domoic Acid production in vitro
and links with shellfish toxicity. In: Harmful and toxic algal blooms.
Yasumoto, T., Oshima, Y. & Fukuyo, Y. (Eds.).
Intergovernmental
Oceanographic Commission of UNESCO, Paris, France. Pp. 155-158
Rhodes, L. L., Thomas, A., Mackenzie, L., Bowen, J. & Todd, K. (1997) Gene
probes and shellfish biotoxin management. Seafood New Zealand 5: 35-36
Rhodes, L., Adamson, J. & Todd, K. (1998a) MMP: More molecular probes. In:
Proceedings of the marine biotoxin science workshop No. 10. (20 November
1998). Marine Biotoxin Technical Committee. Pp. 145-151
Rhodes, L., Scholin, C., Garthwaite, I., Haywood, A. & Thomas, A. (1998b). Domoic
Acid producing Pseudo-nitzscha species educed by whole cell DNA probe-based
and immunochemical assays. In: Harmful algae: Proceedings of the VIII
International Conference of Harmful Algae.
Reguera, B., Blanco, J.,
Fernandez, M. C., & Wyatt, T. (Eds.). .). Vigo, Spain, 25-29th June 1997.
Xunta de Galicia and Intergovernmental Oceanographic Commission of
UNESCO. Pp. 274-277
Rhodes, L., Suzuki, T., Adamson, J., and Mountford, D. (2000). Esterified Okadaic
Acid in New Zealand strains of Prorocentrum lima. Oral presentation at
Harmful Algal Blooms 2000 Conference, February 2000, Hobart, Australia.
Roszell, L. E., Schulman, L. S., & Baden, D. G. (1990) Toxin profiles are dependent
In: Toxic Marine
in growth stages in cultured Ptychodiscus brevis.
Phytoplankton. Graneli, E., Sundstroen, B., Edler, L., & Anderson, D. M.
(Eds.). Elsevier Science Publishing Co. Pp. 403-407
Satake, M., Mackenzie, L. & Yasumoto, T., (1997) Identification of Protoceratium
reticulatum as the biogenetic origin of Yessotoxin. Natural Toxins 5:164-167
Satsuki, M., Fukushima, H. & Sugimori, Y. (1989) Remotely sensed phytoplankton
pigment concentrations around Japan using the coastal zone scanner. In: Red
Tides: Biology, environmental science and toxicology. Okaichi, T. Anderson, D.
M. & Nemoto, T. (Eds.). Elsevier Science Publishing, New York. Pp. 185-188
Scholin, C. A.; Marin III, R.; Miller, P. E.; Doucette, G. J.; Van Dolah, F. M.; Powell,
C. L.; Busman, M.; Moeller, P. D. R.; Gulland, F.; Haulena, M.; Lowenstine, L.;
Silvangi, P.; Silver, M.; Lefebvre, K. & Trainer, V. (2000). Mortality of sea
lions along the central Californian coast linked to a toxic diatom bloom. Oral
presentation at Harmful Algal Blooms 2000 Conference, February 2000,
Hobart, Australia.
188
Seki, T., Satake, M., Mackenzie, L., Kaspar, H. F. & Yasumoto, T. (1995)
Gymnodimine, an new marine toxin of unprecedented structure isolated from
New Zealand oysters and the dinoflagellate Gymnodinium sp. Tetrahedron
Letts. 36:7093-7096
Seki, T., Satake, M., Mackenzie, L., Kaspar, H. F. & Yasumoto, T. (1996)
Gymnodimine, an novel toxic imine isolated from the Foveaux Strait oysters and
Gymnodinium sp. In: Harmful and toxic algal blooms. Yasumoto, T., Oshima,
Y. & Fukuyo, Y. (Eds.). Intergovernmental Oceanographic Commission,
Sengco, M. R., Tugend, K., Li, A., Kulis, D. & Anderson, D. M. (1999) The use of
clay minerals to control harmful algal blooms (HAB’s) in the United States:
experiments with Gymnodinium breve. Abstract from the First Conference on
Harmful Algal Management and Mitigation. Subic Bay, Philippines, 10 – 14
May, 1999. 26 pp.
Sengco, M. R., Li, A., & Anderson, D. M. (2000) The control of harmful algal
blooms using clay minerals. Abstract from Harmful Algal Blooms 2000
Conference. Tasmania, Australia, 7-11 February, 2000. Downloaded from the
website- http://ftp.utas.edu.au/docs/plant_science/HAB2000/abstracts/
Sharples, J., Greig, M. & Oliver M. (1998) Understanding algal blooms: the annual
arrival of subtropical water along the coast on northeast New Zealand.
Seafood New Zealand, March 1998. Pp. 34-37.
Shumway, S. E., Sherman-Casswell, S. & Hurst, J. W. (1988) Paralytic shellfish
poisoning in Maine: Monitoring a monster. J. Shellfish Res. 7:643-652
Shumway, S. E., Barter, J., & Sherman-Casswell, S. (1990) Auditing the impact of
toxic algal blooms on oysters. Environmental Auditor. 2(1):41-56
Statistics New Zealand (1996) 1996 New Zealand Census of Population and
Dwellings – Regional Summary. Statistics New Zealand. Pp.60-61
Steidinger, K. A. (1983) A re-evaluation of toxic dinoflagellate biology and ecology.
Prog. Phycol. Res. 2:147-188
Steidinger, K. A. & Joyce, Jr., E. A. (1973) Florida red tides. Fla. Dep. Nat. Resour.
Mar. Res. Lab. Educ. Ser. No. 17. 26 pp.
Sun, X., Zou, J. & Yu, Z. (1999) Coagulation of Heterosigma akashiwo with
modified clay. Abstract from the First Conference on Harmful Algal
Management and Mitigation. Subic Bay, Philippines, 10 – 14 May, 1999. 27
pp.
Sylvester, T., Sharples, D., & Hartill, B. (1991) Marine recreational fishing survey
(1987). A report on a survey conducted by the Department of Statistics on
behalf of the Ministry of Agriculture and Fisheries. MAF Fisheries North.
189
Taylor, F. J. R. (1984) Toxic dinoflagellates: Taxonomic and biogeographic aspects
with emphasis on Protogonyaulax. In: Amer. Chem. Soc. Symposium Series.
Ragelis, E. (Ed.). Washington, D.C. Pp. 77-97
Taylor, F. J., Taylor, N. J., Walsby, J. R. (1988) A bloom of the planktonic diatom
Ceratium pelagica off the coast of north-eastern New Zealand in 1983 and its
contribution to an associated mortality of fish and benthic fauna. Internationale
Revue der gesamten Hydrobiologie. 70:773-795
Te Puni Kokiri (1993) Nga Kai o te Moana: Kaupapa Tiakina- Customary
Fisheries: Philosophy and practices, legislation and change. Ministry for
Maori Development, June 1993.
Terao, K., Ito, E., Yanagi, T. & Yasumoto, T. (1986) Histopathological studies on
experimental marine toxin poisoning 1. Ultrastructural changes in the small
intestine and liver of suckling mice induced by Dinophysistoxin-1 and
Pectenotoxin-1. Toxicon 24:1141-1151
Terao, K., Ito, E., Yasumoto, T. & Yamaguchi, K. (1990) Enterotoxic, hepatotoxic
and immunotoxic effects of dinoflagellate toxins on mice. In: Toxic marine
phytoplankton. Graneli, E., Sundstroen, B., Edler, L., & Anderson, D. M.
(Eds.). Proceedings from the International Conference on Toxic Marine
Phytoplankton, Lund, Sweden, June 1989.
Tester, P. A., Stumpf, R. P. & Steidinger, K. (1998) Ocean color imagery: Whats the
minimum detection level for Gymnodinium breve blooms? In: Harmful Algae:
Proceedings of the VIII International Conference of Harmful Algae. Reguera,
B., Blanco, J., Fernandez, L. & Wyatt, T. (Eds.). Vigo, Spain, 25-29th June
1997. Xunta de Galicia, Intergovernmental Oceanographic Commission of
UNESCO. Pp. 149-151
Till, D. G., (1993) Public health issues. In: Marine Biotoxins and New Zealand
Shellfish. Jasperse, J. A. (Ed.). Proceedings of a workshop on research issues
10-11 June 1993. The Royal Society of New Zealand Miscellaneous Series 24.
Pp. 41-44
Todd, E. C. D. (1993) Domoic acid and Amnesic Shellfish Poisoning – A review. J.
Food Protection. 56:69-83
Todd, K., (1999) Harmful algae monitoring is an essential prerequisite to successful
management. Abstract from paper presented at the first Conference on Harmful
Algae Management and Mitigation, Subic Bay, Philippines, 10-14 May 1999.
Tortell, P. (1981) New Zealand Atlas of Coastal Resources. Tortell P. (Ed.).
Commission for the Environment. P.D. Hasselberg (Publ.), Government
Printer, Wellington.
Towers, N. (1994) Summary of Southland toxin rat feeding trials. In: Proceedings of
the Marine Biotoxin Science Workshop No. 2 (21 September 1994). Marine
Biotoxin Technical Committee.
190
Trusewich, W., Sim, J., Busby, P. & Hughs, C. (1996) Management of marine toxins
in New Zealand. In: Harmful and toxic algal blooms. Yasumoto, T., Oshima,
Y. & Fukuyo, Y. (Eds.). Intergovernmental Oceanographic Commission,
United States Environment Protection Agency (1993) A guidebook to comparing
risks and setting priorities. Washington USEPA Office of Policy, Planning &
Evaluation.
Venrick, E. L. (1978) How many cells to count? In: Phytoplankton Manual. Sournia,
A. (Ed.) UNESCO. Pp. 167-180
White, A. W. (1987) Relationships of environmental factors to toxic dinoflagellate
blooms in the Bay of Fundy. Rapp. P.-v Reun. Cons. Int. Explor. Mer. 187:3846
White, A. W., Shumway, S. E., Nassif, J., and Whittaker, D. K. (1993) Variation in
levels of paralytic shellfish toxins among individual shellfish. In: Toxic
phytoplankton blooms in the sea. Smayda, T. J. and Shimizu, Y. (Eds.).
Elsevier Science Publishers. Pp. 441-446
Wiebe, P. (1995) Developing a high-frequency system to remotely “see” plankton
distributions. Oceanus 38:14-16
Wilson, N. (1996) Review of the surveillance and control of toxic shellfish poisoning
from non-commercially gathered shellfish in New Zealand. A report for the
Public Health Commission and Ministry of Health, revised and updated July
1995, with a July 1996 postscript. 192 pp.
Wilson, N. & Sim, J. (1996) Review of the New Zealand Marine Biotoxin Monitoring
Programme Data. A report for the Public Health Group, New Zealand Ministry
of Health, October 1996.
Wright, J. L. C., Boyd, R. K., deFreitas, A. S. W., Falk, M., Foxall, R. A., Jamieson,
W. D., Laycock, M. V., McCulloch, A. W., McInnes, A. G., Odense, P., Pathak,
V. P., Quilliam, M. A., Rogan, M. A., Sim, P. G., Thibault, P., Walter, J. A.,
Gilgan, M., Richard, D. J. A., & Dewar, D. (1989) Identification of Domoic
Acid, a neuroexcitatory amino acid, in toxic mussels from eastern Prince
Edward Island. Can. J. Chem. 67:481-490
Work, T. M., Beale, A. M., Frtiz, L., Quillam, M. A., Silver, M., Buck, K. & Wright,
J. L. C. (1993). Domoic acid intoxication of Brown Pelicans and Cormorants in
Santa Cruz, California. In: Toxic Phytoplankton Blooms in the Sea. Smayda,
T. J. & Shimizu, Y. (Eds.). Elsevier Science Publishers. Amsterdam. Pp. 643649.
Wyllie, T. (1995). Report to the Public Health Commission on the Mataitai Hui
Unpublished Report to the Public Health Commission, 1995.
191
Yasumoto, T., Oshima, Y., & Yamaguchi, M. (1978) Occurrence of a new type of
toxic shellfish poisoning in the Tohuku district. Bull Jpn. Soc. Sci Fish.
44:1249-1255
Yasumoto, T. & Satake, M. (1998) New toxins and their toxicological evaluations.
In: Harmful Algae: Proceedings of the VIII International Conference of
Harmful Algae. Reguera, B., Blanco, J., Fernandez, L. & Wyatt, T. (Eds.).
Vigo, Spain, 25-29th June 1997. Xunta de Galicia, Intergovernmental
Yoshinaga, I., Kawai, T. & Ishida, Y. (1995a) Lysis of Gymnodinium nagasakiense
by marine bacteria. In: Harmful algal marine blooms: Proceedings of the sixth
international conference on toxic marine phytoplankton, October 1993, Nantes,
France. Lassus, P., Arzul, G., Erard, E., Gentien, P. & Marcaillou, C. (Eds.).
Intercept Ltd., Andover, UK. Pp. 687-692
Yoshinaga, I., Kawai, T., Takeuchi, T. & Ishida, Y. (1995b) Distribution and
fluctuation of bacteria inhibiting the growth of a marine red tide phytoplankton
Gymnodinium mikimotoi in Tanabe Bay (Wakayama Pref., Japan). Fish. Sci.
61:780-786
Yoshinaga, I., Ishida, Y., Kim, M. C., Katanozaka, N., Kimura, N., Imai, I. & Uchida,
A. (1998) Dynamics and population analysis of algicidal bacteria targeting
marine microalgae during red tides by RFLP of 16S ribosomal RNA gene. In:
Harmful Algae: Proceedings of the VIII International Conference of Harmful
Algae. Reguera, B., Blanco, J., Fernandez, L. & Wyatt, T. (Eds.). Vigo, Spain,
25-29th June 1997. Xunta de Galicia, Intergovernmental Oceanographic
192
APPENDICES
193
APPENDIX I(A): PHYTOPLANKTON TRIGGER LEVELS
Phytoplankton Species
Alexandrium minutum
Alexandrium ostenfeldii
Alexandrium catenella
Alexandrium tamarense
Alexandrium
angustitabulatum
(>50% total biomass)
(<50% total biomass)
Gymnodinium c.f. breve
Dinophysis acuta
Prorocentrum lima
Toxin
PSP
PSP
PSP
PSP
PSP
Level in
composite
sample to
trigger flesh
sampling
(Cells/L)
100
100
100
100
100
Industry
voluntary
closure
pending flesh
testing results
(Cells/L)
500
500
500
500
500
5,000
5,000
5,000
5,000
5,000
ASP
50,000
200,000
N/A
ASP
100,000
500,000
N/A
NSP
DSP
DSP
DSP
1,000
500
1,000
500
5,000
1,000
2,000
1,000
5,000
N/A
N/A
N/A
194
Issue public
health
warning
(Cells/L)
APPENDIX I(B) THE COMMERCIAL AND NON-COMMERCIAL
MONITORING PROGRAMME SAMPLING REGIMES
1) Non-Commercial Phytoplankton Monitoring Programme
Location
Marsden Point
Bay of Islands (Tapeka
Point)
Whangaroa
Whatuwhiwhi
Houhora Bay
Rangaunu Harbour
Waimangu Point
Tiritiri/Whangaparaoa
Port Fitzroy
Waiheke
Kennedy Bay
Tairua
Steels Reef
Matakana Bank
Motiti Island
Ohope Beach
Te Kaha
Tolaga Bay Wharf
Hicks Bay Wharf
Hawkes Bay
Wellington Harbour entrance
Collingwood Farms
The Glen – Tasman Bay
Port Motueka – Tasman Bay
Takaka River/Tata Island
Wedge Point
Tory Channel
Kaikoura
Akaroa (The Kaik)
Taylors Mistake
Caroline Bay/Timaru
Blueskin Bight/Heyward
Point
Riverton/Colac Bay
Site
No.
P021
P020
P059
P023
P023
P024
P028
P019
P027
P032
P017
P018
P001
Frequency
Weekly
Weekly
P033
P006
P026
P025
P014
P011
P012
P013
P015
Weekly when industry not sampling
Weekly
Weekly
Weekly
Weekly
Weekly
Weekly 1 September to 15 February
Fortnightly 1 July to 31 August
Weekly
Weekly
Weekly
Weekly
Weekly
Weekly
Weekly
Weekly
Weekly
Weekly
Fortnightly: 1 November-31 March
Weekly
Weekly
Weekly
Weekly
P016
Weekly
P002
P003
P005
P004
P008
P010
P007
P009
P034
195
2) Non-Commercial Shellfish Sampling Programme
Location
Langs Beach
Waipu
One Tree Point
Ngunguru/Tutukaka
Oakura
Te Haumi
Waiaua Bay
Whangaroa
Tokerau Beach
Houhora
Parengarenga
Waipapakauri
Hokianga
Glinks Gully
Manukau Harbour
Kaipara Harbour
Waimangu Point
Kawau Island
Port Fitzroy (Nagle Cove)
Port Fitzroy
Awakiriapa (Waiheke)
Kennedy Bay
Tairua
Mercury Island
Slipper Island
Raglan
Waihi
Pukehina
Site
No.
B25C
B10
B15B
Species/Frequency
Oyster- Monthly
Tuatua/Pipi- Monthly
Pipi-Monthly when industry not
sampling
B05
Oyster- Monthly 1 April- 1 Sept.
otherwise fortnightly
B01
Tuatua/Pipi/Oyster Monthly 1
April-1 Sept. otherwise weekly
A18
Pipi-Monthly when industry not
sampling
A09
Tuatua –Monthly
A08A Oyster – Monthly when industry
not sampling
A21
Tuatua – Monthly
Tuatua – Weekly
A02
Oyster/mussel – monthly when
industry not sampling
A01
Oyster – Monthly when industry
not sampling
A27
Tuatua –Monthly 1 May-1 Sept,
otherwise fortnightly
F22
Oyster – Monthly
F01
Tuatua – Monthly
F15/
Scallop – Fortnightly 7 months
F11
Mussel – Fortnightly 5 months
F08A/ Scallop – Fortnightly 7 months
F08C Oyster– Fortnightly 5 months
C09
Mussel – Monthly when
C36
Scallop – Monthly for 7 months
D02A Scallop – Monthly for 7 months
D01
Mussel – Monthly for 3 months
C38
Mussel – Monthly for 3 months
when industry not sampling
D06
Mussel – Monthly
D12
Mussel – Monthly
D05
Scallop – Weekly Dec-Feb
D13
Scallop – Weekly Dec-Feb
Scallop – Fortnightly Jul-Aug
F16
Mussel – Fortnightly
D17
Tuatua – Weekly
Tuatua - Monthly
D28
Tuatua – Weekly
Tuatua - Monthly
196
Toxins
All
All
All
All
All
All
PSP, ASP
All
All
PSP, ASP
All
All
All
All
All
All
All
All
All
All
ASP
ASP
All
All
All
All
ASP
ASP
ASP
All
PSP
All
PSP
All
Non-Commercial Shellfish Sampling Programme continued…
Location
“A” Buoy
Kauri Point
Site
No.
D19
D21
Rangiwaea
D31
Motiti Island
D29
Whangaparaoa
D41
Tokata
D38
Ohope
D37
Te Araroa
Tolaga Bay
Pania Reef (Napier)
Ohawe
Oakura
Himitangi Beach
Riversdale
Dorset Point
Collingwood Farms
E15
E01
E07
H01
F20
E13
H07
G01
The Glen- Tasman Bay
G03
Port Motueka
G05
Takaka River/Tata Island
G07
Wedge Point
G23
Tory Channel
Oaro
Akaroa (The Kaik)
G22
I01
I04
Taylors Mistake
Dashing Rocks
I21
I09
Species/Frequency
Toxins
Mussel – Monthly
Scallop – Fortnightly 1 July-31
August
Scallop – Weekly 1 Sept-15 Feb
August
August
Mussel – Weekly
Mussel – Monthly
Mussel – Weekly
Mussel – Monthly
Tuatua – Weekly
Tuatua – Monthly
Mussel – Monthly
Mussel – Monthly
Mussel – Monthly
Mussel – Monthly
Tuatua – Fortnightly
Paua gut – Weekly
Mussel – Monthly
Mussel – Monthly when
Dredge oyster/Scallop –
Monthly when industry not
sampling
sampling
sampling
Mussel – Monthly
Mussel – Weekly
Mussel – Monthly
Mussel – Monthly 1 Apr-31 Oct
Mussel – Weekly
Mussel – Monthly
Mussel – Monthly
Mussel – Monthly
All
ASP, PSP
197
ASP, PSP
ASP, PSP
ASP, PSP
ASP, PSP
ASP, PSP
PSP
All
PSP
All
PSP
All
All
ASP, PSP
All
All
All
All
All
All
All
All
All
All
All
All
DSP
All
All
DSP
All
All
All
Non-Commercial Shellfish Sampling Programme continued…
Location
Mussel Rocks
Mopoutahi Pt (Aramoana)
Site
No.
J03
I14
Riverton/Colac Bay
J20
Species/Frequency
Toxins
Mussel - Fortnightly
Mussel – Monthly
Mussel – Weekly at high risk
times (plus I11, I16 & I17 at
high risk times)
Mussel – Monthly
All
All
All
All
3). Commercial Phytoplankton and Shellfish Monitoring Programme
Location
Site
No.
Phytoplankton
Frequency
Frequency
Toxins
North Island
Parengarenga,
Kauanga
Houhora
A01
Weekly
A02
Weekly
Houhora Bay
A03
Weekly
Rangaunu Hbr
A05
Whangaroa Hbr
A08
Weekly at lease
site
Weekly
Kerikeri/Te Puna
Inlet
Paroa Bay,
Orongo Bay,
Waikare Inlet
Parua Bay, Snake
Bank, Mair Bank
A14
Weekly
A15
Weekly at
Tapeka Point
B07, Weekly
B13,
B14,
B15
198
Fortnightly
Monthly
Summer - Weekly
Winter - Monthly
Summer –Fortnightly
Winter - Monthly
Summer – Fortnightly
Summer – Monthly
Winter - Monthly
Weekly
Monthly
Summer – Monthly
Winter – Fortnightly
Winter - Monthly
Fortnightly
Monthly
Fortnightly
Monthly
NSP/DSP
ASP,PSP
ASP,PSP
Summer – Monthly
Winter - Monthly
NSP/DSP
ASP,PSP
ASP,PSP,NSP/DSP
NSP/DSP
ASP
PSP
NSP/DSP
ASP,PSP,NSP/DSP
NSP/DSP
ASP,PSP
ASP,NSP/DSP
PSP
ASP
PSP, NSP/DSP
NSP/DSP
ASP,PSP
NSP/DSP
ASP,PSP
Commercial Phytoplankton and Shellfish Monitoring Programme continued…
Location
Kaipara Pahi
Inlet
Mahurangi
Kaipara Hbr
Mouth
Great Barrier
Island
Waiheke Island,
Kauri Bay and
Waimangu Point
Whitianga
Port Charles
Kennedy Bay
Coromandel
Ohiwa
Site
No.
F03
Phytoplankton
Frequency
None
Frequency
Toxins
Fortnightly
ASP,PSP,NSP/DSP
C33
None
F25
None
Fortnightly
Monthly
Fortnightly, if F08A
indicates toxicity
Fortnightly
Monthly
Fortnightly
Monthly
NSP/DSP
ASP,PSP
ASP,PSP,NSP/DSP
Monthly
Weekly
Monthly
Summer - Weekly
Summer –
Fortnightly
Winter - Fortnightly
Summer –
Fortnightly
Weekly
Fortnightly
ASP,PSP,NSP/DSP
ASP,PSP,NSP/DSP
ASP,PSP,NSP/DSP
NSP/DSP
ASP,PSP
ASP,PSP,NSP/DSP
D01,
D01A
C38,
C10,
C09
D07
D03
D06
C02,
C05,
C29
Weekly
D33
Weekly
Scallop Areas
Weekly
None
Weekly
Weekly
Weekly
None
ASP,NSP/DSP
PSP
NSP/DSP
ASP,PSP
PSP
ASP
PSP,NSP/DSP
South Island
Nydia Bay
G9
Weekly
Waitaria Bay
G14
Weekly
Crail Bay
G15
Weekly
Pukatea Bay
G18
Weekly
Brightlands
G27
Weekly
West Beatrix
G31
Weekly
Laverique Bay
G37
Weekly
Weekly
Monthly
Weekly
Monthly
Weekly
Monthly
Weekly
Monthly
Weekly
Monthly
Weekly
Monthly
Weekly
Monthly
199
NSP/DSP
ASP,PSP
NSP/DSP
ASP,PSP
NSP/DSP
ASP,PSP
NSP/DSP
ASP,PSP
NSP/DSP
ASP,PSP
NSP/DSP
ASP,PSP
NSP/DSP
ASP,PSP
Location
Hallam Cove
Site
No.
G10
Phytoplankton
Frequency
Weekly
Whangakoko
G11
Weekly
Horahora
G12
Weekly
Cannon Hill
G16
Weekly
Richmond Bay
G28
Weekly
Oyster Bay,
Croisilles
Anakoha
G13
Weekly
G17
Weekly
Kenepuru
G8
Entrance
East Bay
G19
Opihi Bay,
Waitata,
Schnapper Point,
Nikau Bay, South
East Bay, Little
Nikau Bay,
Forsyth Bay
Port Gore
G50
Frequency
Toxins
None
Weekly
Fortnightly
Monthly
Weekly
Fortnightly
Monthly
Weekly
Fortnightly
Monthly
Weekly
Fortnightly
Monthly
Weekly
Fortnightly
Monthly
Weekly
Monthly
Weekly
Fortnightly
Weekly
NSP/DSP
ASP
PSP
NSP/DSP
ASP
PSP
NSP/DSP
ASP
PSP
NSP/DSP
ASP
PSP
NSP/DSP
ASP
PSP
PSP,NSP/DSP
ASP
PSP,NSP/DSP
ASP
ASP,PSP,NSP/DSP
Weekly
Weekly
Weekly
None
ASP,PSP,NSP/DSP
Weekly-when
harvesting
Weekly-when
harvesting
Weekly-when
harvesting
Fortnightly
Monthly
ASP,PSP,NSP/DSP
Monthly
Weekly-when
harvesting
ASP,PSP,NSP/DSP
ASP,PSP,NSP/DSP
Port Hardy
G85
Weekly-when
harvesting
Occasionally
Clifford and
Cloudy Bays
Pakawau
&Collingwood
[one site covers
both]
Tapu Bay
Wainui Farms
G30
None
G1
Weekly
G6
Weekly
None
200
ASP,PSP,NSP/DSP
ASP,PSP,NSP/DSP
NSP/DSP
ASP,PSP
Location
Dredge Oyster
Fisheries
[seasonal, March
to 31 August]
Scallop
[seasonal]
Tasman/Golden
Bays /
Marlborough
Sounds
Papanui Inlet
Blueskin Bay
Site
No.
I14
Continental Shelf
I20
Big Glory
Foveaux Strait
Dredge Oysters
J13
J6
Phytoplankton
Frequency
None
Frequency
Toxins
Weekly
ASP,PSP,NSP/DSP
None
Weekly
ASP,PSP,NSP/DSP
Info from
recreational
weekly site
None
Weekly
ASP,PSP,NSP/DSP
Weekly-when
harvesting
Weekly
Weekly-Seasonal
ASP,PSP,NSP/DSP
None
201
ASP,PSP,NSP/DSP
ASP,PSP,NSP/DSP
APPENDIX I(C) FLOW DIAGRAM ILLUSTRATING SHELLFISH TISSUE
TESTING FOR NSP AND DSP
202
APPENDIX I (D) MAP SHOWING LOCATION OF BIOTOXIN ZONES
Zone B: Cape Brett to Cape
Rodney
Zone A: Tauroa Point to Cape Brett
Zone C: Cape Rodney to Cape
Colville.
Zone D: Cape Colville to Cape
Runaway.
Zone F: Tauroa Point to Cape
Egmont
Zone G: Cape Farewell to
Cape Campbell.
Zone E: Cape Runaway
to Cape Palliser.
G
Zone J: Cape Farewell to
Bluff.
Zone H: Cape Egmont to
Cape Palliser.
Zone K: Chatham
Islands.
Zone I: Cape Campbell to Bluff.
203
APPENDIX II PHYTOPLANKON SITES INCLUDED IN ANALYSIS OVER
THE “IDENTIFIED TIME INTERVAL”
Zone A:
P060 Keri Keri Inlet
P059 Patricks Point
P020 Tapeka Point
P023 Whatuwhiwhi
Zone B:
P021 Marsden Point
Zone C:
P029 C2
P030 C5
P031 Te Kapa
P032 Tamaki Strait
P028 Waimangu Point
P019 Whangaparoa
Zone D:
P017 Kennedy Bay
P002 Matakana Bank
P003 Motiti Island
P005 Ohope
P027 Port Fiztroy
P004 Te Kaha
P018 Tairua
Zone E:
P007 Napier
P008 Tolaga Bay
Zone G:
G08 Kenepuru Entrance
P035 Schnapper Point
P036 Waitaria Bay
P037 Little Nikau Bay
P038 Nikau Bay
P039 Nydia Bay
P040 South East Bay
P041 Crail Bay
P042 Laverique Bay
P044 Brightlands Bay
P043 West Beatrix Bay
P045 Hallam Cove
P046 Richmond Bay
P047 Waitata Bay
G041 Ketu Bay
P048 Cannon Bay
P049 Forsyth Bay
P050 Anakoha Bay
P051 Puketea Bay
P052 Oyster Bay
204
Phytoplankton sites included in analysis over the “Identified Time Interval”
continued…
P053 East Bay
P054 Horahora Bay
P055 Whangakoko Bay
P056 Opihi Bay
P026 Wedge Point
P034 Collingwood Farms
Zone H:
P009 Fort Dorset
Zone I:
P011 Akaroa
P013 Caroline Bay
P015 Blueskin Bay
P012 Taylors Mistake
Zone J:
P016 Riverton
205
APPENDIX III TEMPORAL PERIODICITY OF EL NINO/LA NINA
WEATHER CONDITIONS
Year
1992
1993
1994
1995
1996
1997
1998
1999
Jan-Mar
El Nino
El Nino
El Nino
El Nino
La Nina
El Nino
El Nino
La Nina
Apr-Jun
El Nino
El Nino
El Nino
El Nino
La Nina
El Nino
El Nino
La Nina
Jul-Sep
El Nino
El Nino
El Nino
La Nina
La Nina
El Nino
La Nina
La Nina
Oct-Dec
El Nino
El Nino
El Nino
La Nina
El Nino
El Nino
La Nina
La Nina
Summarised from a website of the NOAA Climate Prediction Centrehttp://www.cpc.ncep.noaa.govt/products/analysis_monitoring/ensostuff/ensoyears.html
206
APPENDIX IV(A) MAP SHOWING THE LOCATION OF SAMPLING SITES
IN THE MARLBOROUGH SOUNDS (ZONE G)
G08-Kenepuru Entrance
G14-Waitara Bay
G36-Nikau Bay
G38-South East Bay
G37-Laverique Bay
G27-Brightlands
G28-Richmond Bay
G41-Ketu Bay
G35-Schnapper Point
G44-Little Nikau Bay
G09-Nydia Bay
G15-Crail Bay
G31-West Beatrix Bay
G10-Hallam Bay
G26-Waitata Bay
G16-Cannon Bay
207
Continuation of sample sites…
G39-Forsyth Bay
G18-Pukatea Bay
G19-East Bay
G11-Whangakoko Bay
G23-Wedge Point
G17-Anakoha Bay
G13-Oyster Bay
G12-Horohora Bay
G40-Opihi Bay
G01-Collingwood Farm
208
APPENDIX IV(B) SITE COMPARISONS OF PSEUDO-NITZSCHIA
OCCURRENCE IN THE HAURAKI GULF AND MARLBOROUGH
SOUNDS/COLLINGWOOD
1). Hauraki Gulf (Zone C, 1995-1999)
Pseudo-nitzschia
1200000
Cell Density/L
1000000
Kopake (Coromandel)
MAF Farms (Coromandel)
Tamaki Strait
800000
500000
400000
300000
200000
100000
0
95 95 95 95 95 95 96 96 96 96 96 96 97 97 97 97 97 97 98 98 98 98 98 98 99 99 99
n- r- y- l- p- v- n- r- y- l- p- v- n- r- y- l- p- v- n- r- y- l- p- v- n- r- yJa Ma Ma Ju Se No Ja Ma Ma Ju Se No Ja Ma Ma Ju Se No Ja Ma Ma Ju Se No Ja Ma Ma
Sampling Date
The scale of the Y-axis is the same as that used for the Marlborough sites.
2). Marlborough Sounds/Collingwood (Zone G, 1994-1999)
All Marlborough sites are grouped on the following 7 graphs, with the same Yaxis scale to show the relative abundance of Pseudo-nitzschia between sites. In
some cases Pseudo-nitzschia numbers were greater than the given scale-bar.
Pseudo-nitzschia
1200000
1000000
Cell Density/L
800000
500000
A
Kenepuru Entrance (G08)
Schnapper Point (G35)
Waitaria Bay (G14)
400000
300000
200000
100000
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Ju Sep Nov JanMa May Ju Sep Nov JanMa May Ju Sep Nov JanMa May Ju Sep Nov JanMa May Ju Sep Nov JanMa May
209
Marlborough Sounds/Collingwood (Zone G, 1994-1999) continued…
Pseudo-nitzschia
1200000
1000000
B
800000
500000
Little Nikau Bay (G44)
Nikau Bay (G36)
Nydia Bay (G09)
South East Bay (G38)
400000
300000
200000
100000
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
1200000
1000000
C
Cell Density/L
800000
500000
Crail Bay (G15)
Laverique Bay (G37)
West Beatrix Bay (G31)
Brightlands Bay (27)
Points omitted-Laverique Bay-678 000
West Beatrix Bay-574 000
400000
300000
200000
100000
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
1200000
1000000
800000
500000
D
Hallam Cove (G10)
Richmond Bay (G28)
Waitata Bay (G26)
Ketu Bay (G41)
Cannon Bay (G16)
Point omitted-Hallam Cove 719 000
400000
300000
200000
100000
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
210
Pseudo-nitzschia
1200000
E
1000000
800000
500000
Forsyth Bay (G39)
Anakoha Bay (G17)
Puketea Bay (G18)
Oyster Bay (G13)
400000
300000
200000
100000
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
1200000
1000000
F
East Bay (G19)
Horohora Bay (G12)
Whangakoko Bay (G11)
Opihi Bay (G40)
Cell Density/L
800000
500000
400000
300000
200000
100000
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
1200000
1000000
G
Collingwood Farms (G01)
Wedge Point (G23)
800000
500000
400000
300000
200000
100000
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
Note: Collingwood Farms (G01) site was not monitored until late August 1996.
Wedge Point (G23) site data missing from 29-Oct 1996 to 30-Apr 1997.
211
APPENDIX IV(C) SITE COMPARISONS OF DINOPHYSIS OCCURRENCE
IN THE HAURAKI GULF AND MARLBOROUGH
SOUNDS/COLLINGWOOD
Dinophysis
2000
1800
Kopake (Coromandel)
MAF Farm (Coromandel)
Tamaki Strait
1600
Cell Density/L
1400
1200
1000
800
600
400
200
0
95 95 95 95 95 95 96 96 96 96 96 96 97 97 97 97 97 97 98 98 98 98 98 98 99 99 99
Sampling Date
All Marlborough sites are grouped on the following 7 graphs, with the same Yaxis scale to show the relative abundance of Dinophysis between sites. In some
cases Dinophysis numbers were greater than the given scale-bar.
Dinophysis sp.
5000
4500
-1
Cell Density (L )
4000
A
Waitaria Bay (G14)
3500
3000
2500
2000
1500
1000
500
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
212
Dinophysis sp.
5000
4500
B
4000
3500
Nikau Bay (G36)
Nydia Bay (G09)
3000
2500
2000
1500
1000
500
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
5000
4500
C
Crail Bay (G15)
Laverique Bay (G37)
Brightlands Bay (G27)
Cell Density/L
4000
3500
3000
2500
2000
1500
1000
500
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
5000
4500
D
Hallam Cove (G10)
Richmond Bay (G28)
Waitata Bay (G26)
Ketu Bay (G41)
Cannon Bay (G16)
4000
3500
3000
2500
2000
1500
1000
500
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
213
Dinophysis sp.
5000
4500
E
Forsyth Bay (G39)
Anakoha Bay (G17)
Puketea Bay (G18)
Oyster Bay (G13)
4000
3500
3000
2500
2000
1500
1000
500
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
5000
4500
East Bay (G19)
Horohora Bay (G12)
Whangakoko Bay
(G11)
Opihi Bay (G40)
F
Cell Density/L
4000
3500
3000
2500
2000
1500
1000
500
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
5000
4500
4000
G
Wedge Point (G23)
3500
3000
2500
2000
1500
1000
500
0
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
Wedge Point (G23) site data missing from 29-Oct 1996 to 30-Apr 1997.
214
APPENDIX IV(D) SITE COMPARISONS OF GYMNODINIUM c.f.
MIKIMOTOI OCCURRENCE IN THE HAURAKI GULF AND
MARLBOROUGH SOUNDS/COLLINGWOOD
10000
Kopake (Coromandel)
MAF Farms (Coromandel)
Tamaki Strait
Cell Density/L
8000
6000
4000
2000
0
95 95 95 95 95 95 96 96 96 96 96 96 97 97 97 97 97 97 98 98 98 98 98 98 99 99 99
Sampling Date
All Marlborough sites are grouped on the following 7 graphs, with the same Yaxis scale to show the relative abundance of G. c.f. mikimotoi between sites. In
some cases G. c.f. mikimotoi numbers were greater than the given scale-bar.
Cell Density/L
6000
5500
5000
4500
4000
3500
3000
2500
2000
1500
1000
500
0
Waitaria Bay (G14)
A
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
215
6000
5500
5000
4500
4000
3500
3000
2500
2000
1500
1000
500
0
Nikau Bay (G36)
Nydia Bay (G09)
B
Cell Density/L
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
6000
5500
5000
4500
4000
3500
3000
2500
2000
1500
1000
500
0
C
Crail Bay (G15)
Laverique Bay (G37)
Brightlands Bay (G27)
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
6000
5500
5000
4500
4000
3500
3000
2500
2000
1500
1000
500
0
Hallam Cove (G10)
Richmond Bay (G28)
Waitata Bay (G26)
Ketu Bay (G41)
Cannon Bay (G16)
D
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
216
6000
5500
5000
4500
4000
3500
3000
2500
2000
1500
1000
500
0
Forsyth Bay (G39)
Anakoha Bay (G17)
Puketea Bay (G18)
Oyster Bay (G13)
E
Cell Density/L
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
6000
5500
5000
4500
4000
3500
3000
2500
2000
1500
1000
500
0
East Bay (G19)
Horohora Bay (G12)
Whangakoko Bay (G11)
Opihi Bay (G40)
F
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
6000
5500
5000
4500
4000
3500
3000
2500
2000
1500
1000
500
0
Wedge Point (G23)
G
4 4 4 5 5 5 5 5 5 6 6 6 6 6 6 7 7 7 7 7 7 8 8 8 8 8 8 9 9 9
l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9 l-9 -9 -9 -9 r-9 -9
Sampling Date
1996. Wedge Point (G23) site data missing from 29-Oct 1996 to 30-Apr 1997.
217
APPENDIX V RESULTS FROM WHOLE CELL DNA PROBES FOR PSEUDO-NITZSCHIA SPECIES
Site
No
Site
Name
Date
Total
Biomass
Pseudonitzschia
Biomass
Shellfish Toxin Results
(weeks after initial
phytoplankton test)
Wk 1
Wk 2
Wk 3
Relative density of each Pseudo-nitzschia species from whole
cell gene probes
P. australis &
P. pungens &
P. multiseries
P. pseudodelicatissima & P.
delicatissima
P. fradulenta
P. heimii
Cells/L
Cells/L
(% of Total
Biomass)
Cells/L
(% of Total
Biomass)
Cells/L
(% of Total
Biomass)
56000
(8.7)
174330
(18.7)
0
19-Oct-98
640,200
224,000
0.50
1.00
0.50
112000
G07
Patricks
Point
Takaka
8-Dec-97
929,975
871,650
0.50
0.50
n.t.
43583
56000
(8.7)
0
G28
Richmond
15-Dec-97
330,485
155,490
0.50
0.00
0.00
77745
0
I13
Blueskin
Bay
Blueskin
Bay
23-Dec-97
631545
417,480
0.50
0.00
0.00
208740
0
4-Feb-98
221,000
219,000
12.00
0.00
0.00
0
219000
(99.1)
A08
I13
Table 1.
208740
(33.1)
0
0
653738
(70.3)
77745
(23.5)
0
0
Cases of cellular density above the risk assessment guidelines for Pseudo-nitzschia sp. (relative densities obtained from
whole cell gene probes) associated with positive shellfish testing results (Domoic Acid, µg/g shellfish tissue). Cell densities
above the risk assessment guidelines are given in italics. n.t. = No shellfish toxin testing for that particular week.
218
Site
No
Site Name
Date
Total
Biomass
Pseudonitzschia
Biomass
Shellfish Toxin
Results (weeks after
initial phytoplankton
test)
Wk 1 Wk 2
Wk 3
Relative density of each Pseudo-nitzschia species from whole
cell gene probes
P. australis &
P. pungens &
P. multiseries
delicatissima
P. fradulenta
P. heimii
Cells/L
Cells/L (% of
Total Biomass)
Cells/L
(% of Total
Biomass)
Cells/L
(% of Total
Biomass)
A03
Houhora
25-Nov-97
74,890
60,705
0.50
0.00
0.00
0
0
0
A08
Whangaroa
10-Nov-98
495,800
377,000
0.50
0.00
0.00
37700
B14
25-Nov-97
2,287,340
225,780
0.50
0.50
0.50
0
124410
(25.1)
0
9-Dec-97
1,832,670
680,535
0.50
0.50
0.50
0
0
0
15-Dec-97
426,555
12,000
0.50
0.50
0.00
0
0
0
D06
G01
Marsden
Point
Marsden
Point
Marsden
Point
Kennedy Bay
Collingwood
18850
(3.8)
0
31-Aug-98
28-Sep-98
20,000
93,600
10,000
6,400
0.50
0.50
n.t.
0.00
n.t.
n.t.
10000
5824
G19
G19
30-Sep-98
71,000
53,000
2.50
0.50
n.t.
44520
0
64
(0.1)
3710
(5.2)
0
64
(0.1)
4240
(6.0)
B14
B14
Table 2.
60705
(81.1)
188500
(38.0)
225780
(9.9)
680535
(37.1)
12000
(2.8)
0
0
0
Cases of cellular density below the risk assessment guidelines for Pseudo-nitzschia sp. (relative densities obtained from
whole cell gene probes) associated with positive shellfish testing results (Domoic Acid, µg/g tissue). n.t. = No shellfish toxin
testing for that particular week.
219
Table 3.
Site No
Cases of cellular density above the risk assessment guidelines for Pseudo-nitzschia sp. (relative densities obtained from
whole cell gene probes) associated with no incidence of domoic acid in shellfish testing results (Domoic acid, µg/g tissue).
Cell densities above the risk assessment guidelines are given in italics. n.t. = No shellfish toxin testing for that particular
week. ** = cell density would be lower than this density as only an approximate % was given.
Site Name
Date
Total
Bio
Pseudonitzschia
Biomass
phytoplankton test)
Wk 1
Wk 2
Wk 3
Relative density of each Pseudo-nitzschia species from whole cell gene
probes
P. australis & P.
pungens & P.
multiseries
delicatissima
P. fradulenta
P. heimii
Cells/L (% of
Total Biomass)
Cells/L (% of
Total Biomass)
Cells/L (% of
Total Biomass)
Cells/L (% of
Total Biomass)
A03
Houhora
12-Nov-98
938,400
935,000
0.00
n.t.
0.00
28050
A03
Houhora
28-Apr-99
425,800
382,000
0.00
0.00
n.t.
3820
B14
B14
Marsden Point
Marsden Point
9-Feb-98
13-May-98
176,400
293,400
52,000
95,000
0.00
0.00
n.t.
n.t.
n.t.
0.00
52000
76000
9350
(1.0)
370540
(87.0)
0
0
B14
Marsden Point
21-Oct-98
474,000
89,000
n.t.
0.00
n.t.
55180
0
C02
D06
Coromandel
Kennedy Bay
13-Apr-98
18-May-98
386,800
154,300
121,000
130,000
n.t.
0.00
0.00
0.00
n.t.
0.00
60500
104000
0
0
D12
Tairua
7-Nov-98
789,400
507,000
0.00
n.t.
n.t.
5070
D19
Matakana
11-Nov-97
195,400
166,600
0.00
0.00
n.t.
133280
5070
(0.6)
0
D19
Matakana
8-Feb-98
618,000
564,000
n.t.
n.t.
0.00
0
D19
Matakana
13-Apr-98
224,600
176,000
n.t.
0.00
n.t.
88000
E15
Hicks Bay
13-Dec-98
2,608,000
2,419,000
n.t.
0.00
n.t.
846650
220
564000
(91.3)
88000
(39.2)
725700
(27.8)
9350
(1.0)
3820
(0.9)
0
19000
(6.5)
0
0
26000
(16.9)
456300
(57.8)
33320
(17.1)
0
906950
(96.6)
3820
(0.9)
0
0
32930
6.9
0
0
40560
(5.1)
0
0
0
0
120950
(4.6)
725700
(27.8)
Table 3 continued
Site No
Site Name
Date
Total
Bio
Pseudonitzschia
Biomass
phytoplankton test)
Wk 1
Wk 2
Wk 3
Relative density of each Pseudo-nitzschia species from whole cell gene
probes
G01
Collingwood
19-Jan-98
11,442,000
1,066,000
0.00
n.t.
n.t.
P. australis & P.
pungens & P.
multiseries
Cells/L (% of Total
Biomass)
106600**
G10
G10
10-Nov-97
172,400
101,800
n.t.
0.00
0.00
97728
0
G10
G10
24-Nov-97
542,535
399,325
0.00
0.00
0.00
199663
0
G13
G13
10-Jun-98
203,800
153,000
0.00
0.00
0.00
18360
G16
G16
10-Nov-97
118,200
86,400
0.00
0.00
0.00
82944
130050
(63.8)
0
G17
G17
5-Jan-98
1,663,265
1,499,520
0.00
0.00
0.00
14996
0
G28
G28
10-Nov-97
103,200
83,400
0.00
0.00
0.00
80064
0
G28
G28
Richmond
Richmond
17-Nov-97
28-Dec-97
176,000
328,555
89,800
224,715
0.00
0.00
0.00
0.00
0.00
0.00
89800
112358
0
0
G28
Richmond
5-Jan-98
957,770
473,925
0.00
0.00
0.00
0
G28
G28
Richmond
Richmond
23-Feb-98
28-Dec-98
330,800
518,000
96,000
198,000
n.t.
0.00
0.00
0.00
n.t.
0.00
96000
75240
473925
(49.5)
0
0
G28
Richmond
4-Jan-99
180,800
86,000
0.00
0.00
0.00
77400
0
G31
G37
G31
G37
14-Sep-98
13-Apr-98
266,400
579,000
60,000
147,000
0.00
0.00
0.00
0.00
0.00
0.00
60000
139650
0
0
G39
G39
10-Nov-97
129,100
73,125
n.t.
n.t.
n.t.
70200
0
221
delicatissima
Cells/L (% of
Total Biomass)
0
P. fradulenta
P. heimii
Cells/L (% of
Total Biomass)
959400
(8.4)
1018
(0.6)
199663
(36.8)
7650
(3.8)
864
(0.7)
149952
(9.0)
834
(0.8)
0
112358
(34.2)
0
Cells/L (% of
Total Biomass)
10660
(0.1)
0
0
61380
(11.8)
4300
(2.4)
0
1470
(0.3)
732
(0.6)
0
61380
(11.8)
4300
(2.4)
0
1470
(0.3)
0
0
0
0
1349568
(81.1)
0
0
0
0
Table 3 continued
Site
No
Site Name
Date
Total
Pseudo-
Bio nitzschia
Biomass
Shellfish Toxin
Results (weeks after
initial phytoplankton
test)
Wk 1 Wk 2 Wk 3
Relative density of each Pseudo-nitzschia species from whole cell
gene probes
P. australis & P.
pungens & P.
multiseries
Cells/L (% of
Total Biomass)
delicatissima
Cells/L (% of
Total Biomass)
1,381,325
1,167,240
n.t.
n.t.
n.t.
23345
0
28-Dec-98
449,800
282,000
0.00
0.00
n.t.
56400
G40
10-Feb-98
681,800
493,000
0.00
0.00
0.00
295800
11280
(2.5)
0
G44
G44
13-Apr-98
287,800
207,000
n.t.
n.t.
n.t.
103500
G50
G50
10-Feb-98
2,030,800
573,000
0.00
0.00
n.t.
28650
I01
Kaikoura
10-Aug-98
306,900
178,000
n.t.
n.t.
n.t.
5340
I04
I04
Akaroa
Akaroa
5-Jan-98
9-Nov-98
363,365
2,116,200
309,915
1,900,000
0.00
0.00
0.00
0.00
0.00
0.00
309915
0
I04
Akaroa
29-Dec-98
132,700
132,000
0.00
n.t.
n.t.
13200
I04
Akaroa
1-Jun-99
1,212,600
217,000
0.00
n.t.
0.00
65100
I21
Taylor's
Mistake
Taylor's
Mistake
Taylor's
Mistake
16-Mar-98
626,000
313,000
n.t.
n.t.
n.t.
65730
16-Aug-98
965,000
809,000
0.00
0.00
0.00
24270
29-Nov-98
1,249,000
177,000
0.00
0.00
n.t.
169920
G39
G39
5-Jan-98
G39
G39
G40
I21
I21
222
82800
(28.8)
178000
(58.0)
0
1254000
(59.3)
112200
(84.6)
0
93900
(15.0)
776640
(80.5)
0
P. fradulenta
P. heimii
Cells/L
(% of Total
Biomass)
Cells/L
(% of Total
Biomass)
11672.4
(0.8)
169200
(37.6)
197200
(28.9)
10350
(3.6)
544350
(26.8)
1780
(0.6)
0
627000
(29.6)
6600
(5.0)
32550
(2.7)
0
1108878
(80.3)
45120
(10.0)
0
40450
(4.2)
1770
(0.1)
0
0
0
0
0
0
130200
(10.7)
156500
(25.0)
0
1770
(0.1)
APPENDIX VI PSEUDO-NITZSCHIA SPECIES COMPOSITION AT THE
SAME SITE OVER CONSECUTIVE WEEKS, DETERMINED BY WHOLE
CELL GENE PROBES
Marsden Point
500000
Cell Density/L
400000
60000
50000
40000
30000
20000
10000
0
19-Oct-98 26-Oct-98 2-Nov-98
Sampling Date
Matakana
250000
Cell Density/L
200000
150000
100000
50000
0
10-Nov-97 17-Nov-97 24-Nov-98
Sampling Date
223
P. australis
P. pungens
P. multiseries
P. delicatissima
P. fraudulenta
P. heimii
Pseudo-nitzschia species composition at the same site over consecutive weeks,
determined by whole cell gene probe, continued…
Richmond
Richmond
100000
20000
80000
Cell Density/L
25000
15000
60000
10000
40000
5000
20000
0
0
-99
-98
-99
-98
-98
ec
ec
ec
an
an
J
J
D
D
D
1
4
1
28
21
16
98
98
98
98
ararprprA
A
M
M
6
13
31
23
Beatrix Bay
Richmond
60000
40000
50000
30000
Cell Density/L
40000
30000
20000
20000
10000
10000
0
0
-98 -98 -98 -98 -98 -98 -98 -98
ug Aug Aug Aug -Sep -Sep -Sep -Sep
A
7 14 21 28
10 17 24 31
Sampling Date
-M
31
P. australis
P. pungens
P. multiseries
P. delicatissima
P. fraudulenta
P. heimii
224
98
ar-
98
98
98
prprprA
A
A
6
20
13
Sampling Date

a review of the marine biotoxin monitoring

Transcription

Similar documents

Shellfish Allergies Fact Sheet

Summer 2016 - Shellfish Culture Ltd

Wild Maine Mussels

Report on a visit to Canada 22 June to 4 July 2009

Midnight Club 3: DUB Edition

Vibrio vulnificus

Feeling good

Marine tourism - Dezanove House

Spring 2015 - Marlborough District Libraries

erspective - De La Salle-College of Saint Benilde