Document 6425368

 July 10, 2013
Bryce Bird, Director
Martin D. Gray, Manager
New Source Review Section
John Jenks, Engineer
Utah Division of Air Quality
PO Box 144820
Salt Lake City, UT 84114-4820
Via: Email
Re: Intent to Approve: May 22, 2013 Intent to Approve: Tesoro (Gasoline Hydrotreater
Conversion Project (Project Number: N10335-0062; DAQE-IN103350062-13)
Dear Mr. Bird, Mr. Gray and Mr. Jenks,
Thank you for the opportunity to comment on the May 22, 2013 Intent to Approve:
Tesoro (Tesoro Refining and Marketing Company) Gasoline Hydrotreater Conversion Project
(Project Number: N10335-0062; DAQE-IN103350062-13) and the documents that purport to
support that Intent to Approve (we refer to the projects as the “GHT Project,” the Intent to
Approve/Proposed Approval Order as “Proposed Permit” and the company as “Tesoro”) issued
by the Utah Division of Air Quality and Executive Secretary of the Air Quality Board and/or the
Director of the Division of Air Quality (collectively “Executive Secretary”). We submit these
comments on behalf of Utah Physicians for a Healthy Environment, Friends of Great Salt Lake
and Western Resource Advocates (collectively “Utah Physicians”).
Before reaching our substantive comments, we would like to express our appreciation of
your willingness to extent the public comment period to allow for more meaningful review of the
GHT Project.
As these comments make clear, we are troubled by the Proposed Permit, the terms and
conditions of which appear insufficiently rigorous to control and monitor emissions from the
Tesoro facility. Before addressing these concerns, we turn first to an analysis of the significant
adverse health and environmental impacts from the air pollutants emitted by refineries in general
and the Tesoro facility specifically.
Utah Physicians hereby incorporates by reference into its comments any and all
comments submitted by the U.S. Environmental Protection Agency (“EPA”) on GHT Project and
the Proposed Permit. As such, Utah Physicians has met it burden to sufficiently raise, for the
purposes of putting the Executive Secretary on notice as to the legal deficiencies of his
permitting process and decision, any issues raised by EPA in that agency’s comments.
Health and Environmental Impacts of Air Pollution
Utah Physicians
Utah Physicians for a Healthy Environment (UPHE) is the largest community service
organization of health professionals in the state of Utah. UPHE and its members are health
professionals, toxicologists, biologists, chemists and engineers dedicated to protecting the health
and well-being of the citizens of Utah. We are troubled by the health risks that currently exist in
our environment and we seek to give policy makers a better understanding of how environmental
degradation, and air pollution in particular, adversely affects our own health, and the health of
our patients and families.
In carrying out its mission, UPHE has met with former Governor John Huntsman Jr.,
Gov. Gary Herbert, the Utah Air Quality Board, the Utah Public Service Commission, several
local mayors, local business leaders, media and concerned citizens. We have repeatedly
submitted comments to state and federal regulators and decision makers relative to specific
projects and rule making that impact and influence the condition of Utah’s environment and the
health of the people living here.
UPHE and its members have a strong legal interest in the and the ITA based on the
Clean Air Act and Utah Air Conservation Act’s protection of public health and the environment.
UPHE members, their families and their patients are harmed by air pollution, including that
pollution currently emitted and that will be emitted from the Tesoro facility. They are harmed
because air pollution adversely affects their health, quality of life, recreational pursuits and
aesthetic sense. Therefore, UPHE and its members have a protectable legal interest in ensuring
that the Executive Secretary regulates Tesoro Refinery to the maximum extent required by the
Clean Air Act and the Utah Air Conservation Act and that emissions, including fugitive
emissions, from the facility are properly modeled, monitored, reported, recorded, quantified,
characterized and minimized as required by the law.
F RIENDS of Great Salt Lake
FRIENDS of Great Salt Lake has, as its mission, the preservation and protection of the
Great Salt Lake ecosystem. The organization seeks to increase public awareness and
appreciation of the Lake through education, research, and advocacy. FRIENDS has long been
involved in the protection and restoration of Great Salt Lake and its ecosystems, advocating for
ways in which the public may enjoy these resources by fishing, birdwatching, boating,
photographing, hiking and studying these natural areas. Importantly, The Clean Air Act
identifies two types of national ambient air quality standards. Primary standards provide public
2 health protection, including the health of sensitive populations such as children, the elderly and
asthmatics. 42 U.S.C. § 7409(b)(1). Secondary standards provide public welfare protection,
including protection against decreased visibility and damage to animals, crops, vegetation, and
buildings. Id. at § 7409(b)(2).
Therefore, FRIENDS of Great Salt Lake, its staff and its members have a strong legal
interest in the GHT Project and the Proposed Permit based on the Clean Air Act and Utah Air
Conservation Act’s protection of public health as well as the environment, including water
quality in Great Salt Lake, the well-being of the birds and other wildlife that inhabit the Lake and
the habitat on which they rely. FRIENDS, its staff and its members also have a legal interest in the
Clean Air Act’s protection of visibility – without which members cannot undertake bird
watching or enjoy the stunning views of Great Salt Lake. It goes without saying that emissions
from Tesoro do and will adversely impact Great Salt Lake as well as the health of the people
who recreate there. Therefore, FRIENDS, its staff and its members have a protectable legal
interest in ensuring that the Executive Secretary regulates Tesoro Refinery to the maximum
extent required by the Clean Air Act and the Utah Air Conservation Act and that emissions,
including fugitive emissions, from the facility are properly modeled, monitored, reported,
recorded, quantified, characterized and minimized as required by the law.
UPHE and FRIENDS have a protected legal interest and standing sufficient to make these
comments and to administratively and judicially appeal any adverse decision on the GHT Project
on behalf of the organizations themselves and their members. This is because: 1) their members
have standing to comment and sue in their own right; 2) the interests at stake are germane to
purposes of the organizations; and 3) neither the claims asserted nor the relief requested requires
the organizations’ members to participate directly in the lawsuit. See Hunt v. Washington State
Apple Advertising Commission, 432 U.S. 333, 343 (1977). The members of UPHE and FRIENDS
have standing to sue in their own right because they will have suffered an injury in fact, there
will be a causal connection between their injury and the conduct of the Executive Secretary, and
a favorable decision on the merits will likely redress the injury. See Lujan v. Defenders of
Wildlife, 504 U.S. 555, 560-61 (1992).
The Air Pollution Consequences of Utah’s Refineries
According to official inventory figures reported to the Executive Secretary, the five oil
refineries in North Salt Lake and South Davis County represent the second largest source of
industrial pollution along the Wasatch Front, after the Kennecott mining operation. However,
there is evidence that the refineries actually emit many times the amount of pollution, volatile
organic compounds (“VOCs”) and hazardous air pollutants (HAPs) in particular, than is reported
to the Executive Secretary.
On April 22, 2010 the Associated Press reported that, “[t]he nation’s oil and chemical
plants are spewing a lot more pollution than they report to the Environmental Protection Agency
– and the EPA knows it. Records, scientific studies and interviews suggest pollution from
petrochemical plants is at least 10 times greater than what is reported to the government and the
public.” The report went on to explain that oil refineries vastly underreport leaks from valves to
federal and state regulators and that these unreported fugitive emissions from oil refineries add
millions of pounds of harmful pollutants to the atmosphere each year, including over 80 million
3 pounds of VOCs and over 15 million pounds of toxic HAPs. These emissions could be
eliminated if refineries complied with the requirements of the Clean Air Act.
One of the sources for the Associated Press story was an EPA internal memo from July
27, 2007, which stated that, “emissions of VOCs from refineries are significantly higher (10 to
20 times) than amounts estimated using standard techniques.” There is no reason to believe that
the refineries in Utah are also not seriously underestimating their emissions. While it is well
accepted that the refineries are a significant air pollution source, it is very likely they are, in fact,
a much larger contributor to Wasatch Front air pollution than is acknowledged by state
regulators.
Year after year, the major urban areas on the west side of the Wasatch Mountains
consistently rank in the top ten worst cities in the country for acute spikes in air pollution, and
the American Lung Association gives many of these cities the grade of “F” for both particulate
matter (PM) and ozone. Three of the last four winters have been plagued by recurrent and
prolonged inversion episodes. This year the northern counties of Utah have had the highest
levels of PM2.5 in the country on several days, including one day where the PM2.5 levels reached
the dangerous value of 140 µg/m3 – exceeding the 35 µg/m3 National Ambient Air Quality
Standards (NAAQS) by 400%. Even worse, during dust storms in the last few years Salt Lake
County has seen PM2.5 values apparently in excess of the maximum ability of the monitoring
stations to calculate the concentrations, about 250 ug/m3.
Salt Lake County, home to more than 1 million people, including 300,000 children under
the age of 18, continues to experience repeated episodes of severe PM pollution. In 2009,
country residents were exposed to pollution levels above the 24-hour NAAQS on 19 days. The
maximum 24-hour average concentration for 2009 was 74.1 µg/m3, more than double the healthbased standard of 35 µg/m3. Similarly, in 2010, Salt Lake County residents were exposed to
pollution levels above the 24-hour PM2.5 NAAQS for a total of 16 days and a maximum 24-hour
average concentration of 76.4 µg/m3, again, more than twice the relevant standard.
Moreover, Salt Lake County is currently failing to meet the NAAQS for SO2. Salt Lake
and Utah counties are non-attainment for the PM10 NAAQS. All the counties along the Wasatch
Front, including Salt Lake and Davis, are in non-attainment status for PM2.5. Finally, the Utah
governor has requested that EPA declare Salt Lake, Davis and part of Weber County as not
meeting the 8-hour ground level NAAQS for ozone, or smog. Although this request was
recently recalled, it shows that levels of ozone pollution in the valley hover close to the NAAQS.
The violation of ozone, PM10, PM2.5 and SO2 standards is particularly relevant to refinery
emissions because these facilities produce PM10, PM2.5 and SO2 directly and emit precursors to
PM10, PM2.5 and ozone.
Human Health Impacts of Air Pollution
Medical research in the last ten years clearly indicates that, certainly for PM2.5, and likely
also for ozone, there is no “safe level” of exposure. Even levels previously thought to be benign
we now know are not. There is no threshold below which there is no health effect and all
persons are adversely affected, regardless of age and/or overall state of health.
4 Most Utahns are exposed to high levels of ozone in the summer and PM2.5 in the winter,
as well as PM10 and SO2 year-round, meaning that a large percentage of Utah’s population is
exposed repeatedly to unhealthy levels of pollution throughout the year. There is now evidence
that exposure to ozone and PM2.5 can act synergistically, increasing the adverse health effects
from these air pollutants. 1.
PM2.5 air pollution at the levels experienced by residents of the northern counties of Utah
has the approximately same type and magnitude of biologic effect as living with an active
smoker. E.g. 71 Fed. Reg. at 61157. That should not be a surprise, because most of the
chemicals found in tobacco smoke are also found in fine particulate matter. As with smoking,
particulate matter pollution and ozone cause increased systemic oxidative stress leading to
pathologic vascular changes, including progression of atherosclerotic plaques to vulnerable
forms, prothrombotic states, endothelial dysfunction and altered autonomic nervous system
control. 2.
For the last several years, the research-based conventional wisdom has been that with
each 10 µg/m3 increase in PM2.5 long-term average, there is an increase in community mortality
rate of about 10%. 3. New research draws an even stronger correlation, i.e. a mortality rate of
14% for each 10 µg/m3 increase. 4. The elderly and those with existing morbidities are
particularly vulnerable to air pollution consequences.
Since the late 1980s, more than 150 epidemiological studies have reported associations
between daily changes in particulate air pollution and respiratory and cardiovascular mortality,
hospitalizations and other related health endpoints. 5; 71 Fed. Reg. at 61150-61162. These
adverse effects are seen at low and “common” concentrations of particulate pollution. A Dutch
study demonstrated risks for cardiopulmonary mortality even at what are considered
“background” levels of particulate pollution. 6. A study done in our own area demonstrated that
each short-term 10 µg/m3 increase in PM2.5 was associated with an increase in the risk of acute
ischemic coronary artery events (unstable angina and myocardial infarction) of 4.5%. 7.
Not only does PM2.5 result in an increase in death from cardiovascular causes, but there is
also an increased risk for non-fatal events. 71 Fed. Reg. at 61151-52. For each 10 µg/m3
increase in PM2.5 there is a 24% increase in risk of a cardiovascular event and a 76% increase in
the risk of death from that event. There is also an increased risk of cerebrovascular events. 8, 9,
10. It should be noted that this rate of increase approaches that demonstrated from a chronic
active smoking habit. 71 Fed. Reg. at 61157.
Regrettably, some Utah lawmakers and agency staff often dismiss the significance of our
PM2.5 spikes with the observation that our annual average fine particulate matter concentrations
are not extraordinarily high. This is false comfort and reflects a poor understanding of the
existing research. Many medical studies show that impacts from pollution are seen very quickly
and can last long after the air has cleared. 71 Fed. Reg. at 61164. For example, within as little as
30 minutes, exposure to particulate matter is associated with increases in blood pressure,
followed within hours by increased rates of heart attacks and strokes. Community mortality rates
stay elevated for 30 days after a spike in PM10 even if the episode lasts less than 24 hours. 11.
5 Within one hour, exposure to traffic pollution, including particulate matter, is associated
with increased rates of heart attacks as much as 300% compared to non-exposed individuals. 12.
Other studies show rates of strokes and heart attacks in the community increase within hours
after spikes in PM10. 13. Quoting from the American Heart Association (AHA) scientific
statement published in May 2010:
The overall evidence from time-series analyses conducted worldwide since publication of
the first AHA statement confirms the existence of a small, yet consistent association
between increased mortality and short-term elevations in PM10 and PM2.5 approximately
equal to a 0.4% to 1.0% increase in daily mortality (and cardiovascular death
specifically) due to a 10 µg/m3 elevation in PM2.5 during the preceding 1 to 5 days.
Confirming the strong correlation between modest, short term spikes in PM and serious
health consequences are three new studies that showed spikes of as little as one day in PM10 were
associated with higher rates of heart attacks, 14, daily spikes of either PM10 or PM2.5 were
associated with significant increases in emergency room visits for hypertensives crisis, 15, and
less than 24 hours of a spike in PM2.5 of 15-40 µg/m3 increased rates of strokes 34%, with the
peak increase occurring within 12 hours. 16.
Not only have numerous studies shown that there is no safe level of PM exposure, but a
recent landmark study published in the flagship journal of the AHA, using data from over 1
million people, demonstrated that when cardiac mortality, the signature air pollution health
outcome, was plotted against particulate matter from air pollution, first and second-hand
cigarette smoke, all three sources showed a steep curve at low doses. In other words, per unit
dose of exposure, low levels of PM caused higher rates of mortality. 17. Long-term exposure to
particulate matter air pollution is associated with an average rise in blood pressure for
populations chronically exposed. Average blood pressure was found to rise 1.7 mmHg for an
increase of 2.4 µg/m3 in PM2.5. A similar association was found with the coarser PM10. The rise
was found in both systolic and diastolic blood pressure. 18.
Chronic exposure to particulate matter has been shown to increase the thickening of
arterial walls, which is a known end result of higher blood pressure. A chronic increase in PM10
of 5.2 µg/m3 is associated with a 5% increase in the intima-media thickness of the carotid artery,
which is one of many end results of the biologic process described above. 19.
Another study showed a remarkable correlation between chronic exposure to PM2.5 and
narrowing in the tiny arteries in the back of the eye. Chronic exposure to 3 µg/m3 of PM2.5 (one
fifth of the NAAQS) was associated with narrowing equivalent to seven years of aging. 20.
These finding are especially significant because they demonstrate community-wide effects,
acceleration of the aging process, and impairing the health of everyone exposed, not just a
susceptible population.
Based on extrapolations from numerous studies and the aforementioned AHA scientific
statement, UPHE estimates that between 1,400 and 2,000 premature deaths occur every year in
Utah from PM2.5. The AHA has estimated that residents of most cities in the United States lose
between one and three years of life expectancy due to fine particulate air pollution. 21.
6 Furthermore, studies show that even small reductions in air pollution improve community life
expectancy. 22.
There is a remarkable correlation between rates of deep vein thrombosis and increased
levels of PM10, beginning at very modest levels. 23. A likely mechanism of this clinical
outcome is revealed by studies that show PM10 causes excessive platelet aggregation in diabetics.
24.
Throughout the age spectrum, from infants to the elderly, air pollution has been shown to
impair brain function. Oxidative stress (OS) appears to be the biological genesis of numerous
diseases processes and a major contributor to the aging phenomenon. OS is the mechanism
behind the role of particulate matter and carbon monoxide pollution in central nervous system
dysfunction, neuroinflammation, cortical stress, cognitive impairment and memory loss in
children and neuro-degenerative diseases such as Alzheimer’s disease. 25, 26. Numerous
studies show such specific outcomes as impaired intellect, and penetration of particle matter and
Alzheimer type protein deposition among children who grow up breathing more particulate air
pollution. 27, 28, 29. Human volunteers exposed to typical urban levels of diesel exhaust
demonstrate brain cortical stress measured by EEG. 30.
Children exposed to more air pollution or whose mothers were more exposed during
pregnancy show an IQ loss of five to nine points. 31, 32, 33. Rates of neurobehavioral disorders
correlate with NOx and PM10 levels. 34. Children exposed to more vehicle pollution show a
doubling in rates of autism. 35. Older people show accelerated cognitive decline if chronically
exposed to more traffic generated air pollution. 36, 37. A very recent landmark study showed
that chronic exposure to 10 µg/m3 of either PM2.5 or PM2.5-PM10 was associated with faster
cognitive decline in older women, equivalent to about two years of aging. 38.
Because of strong evidence that particulate air pollution's neurotoxicity is related to
attached metals, 39, 40, 41, the oil refineries contribution to Wasatch Front pollution takes on
additional public health significance.
It is intuitive that short-term exposure to fine particulate matter would have adverse
impacts on the pulmonary system. 71 Fed. Reg. at 61145 & 61152. Indeed, numerous studies
show increased rates of asthma and virtually all other respiratory diseases including lung cancer
where short-term PM2.5 is higher. Id. at 61154-61155 & 61157. Equally disturbing are less
obvious outcomes. Even young healthy people demonstrate rapid decrease in lung function from
brief exposure to particulate matter that persists for several days after the exposure has ended.
Id. at 61152, 61154 & 61169; 42, 43. Again, this contradicts any comfort derived from the
perspective that Utah’s fine particulate matter air pollution problem is episodic and therefore less
of a problem.
An unusually large proportion of Utah’s population is young. Census-based estimates
indicate that nearly a third of Utah residents are under age 18 and one of every 10 residents is
under age five, figures approximately 40 percent higher than the national average. This means
that Utah’s unhealthy levels of air pollution constitute a public health crisis that endangers its
most vulnerable populations. 74 Fed. Reg. at 58690.
7 The physiology of children differs from that in adults in many important ways, causing
them to be affected more profoundly by air pollution than adults. A child has a higher metabolic
rate, meaning their oxygen demand is higher, they breathe faster and have higher heart rates and
blood flows on a per weight basis than an adult. Combined with their rapidly growing organ size
and function, this physiologic difference makes them more susceptible to the adverse influence
of air pollution. Children who breathe more air pollution can experience a permanent stunting of
their lung growth. Just as chronic exposure to second-hand cigarette smoke causes a permanent
loss of lung function growth in children, so does long-term exposure to PM2.5 air pollution.
44,45; 71 Fed. Reg. at 61154, 61172; see also id. at 61169. Not only does short-term exposure to
PM2.5 air pollution permanently impair the exercise capacity of individuals so affected, 46, few
physiologic outcomes have more of an ultimate impact on longevity than lung function.
Various forms of cancer such as lung, cervical, stomach and brain cancer show increased
rates with higher concentrations of community particulate matter. 47, 48; 71 Fed. Reg. at 61152.
Each 10 µg/m3 increase in long term PM2.5 concentration is associated with a 15-27% increase in
lung cancer mortality. 49. Especially troubling are the numerous studies that show increases in
childhood leukemia among more exposed populations, 50, 51, and a significant association
between nitrogen oxide concentrations and rates of breast cancer. 52.
The precipitation of oxidative stress, as mentioned above, is the likely explanation for
new studies that show higher rates of numerous other, seemingly unrelated diseases, among
populations subjected to more air pollution; such as type II diabetes, obesity, arthritis, and lupus.
53, 54, 55, 56, 57.
Air pollution, especially particulate matter, may have its largest impact on public health
through its effect on the human embryo. A study in laboratory animals demonstrated a change in
morphology of the placenta that compromised blood flow to the fetus. 58, 46. Exposure of
pregnant women to various components of traffic-related air pollution, including PM10, results in
intrauterine growth retardation, including smaller head size, increased rates of spontaneous
abortions, premature births and low birth weight syndrome. Genetic damage and epigenetic
changes can have virtually identical consequences and both can be passed on to subsequence
generations. Newborn babies whose mothers are exposed to more air pollution show increases in
both, and the life-long disease burden that results can include higher rates of metabolic disorders,
reactive airway disease, cardiovascular disease, cancer, Alzheimer’s and all the diseases
consequent to immuno-suppression. Epigenetic changes can be seen within three days after
exposure to PM2.5 and perhaps even as soon as minutes after exposure. 59-66. There is strong
evidence for a persistence of epigenetic changes from one generation to another. Medical
science is now learning that the air pollution today can adversely affect the health of future
generations. For example, episodic air pollution, the type that occurs along the Wasatch Front,
has been shown to be associated with fragmentation of DNA in human sperm. 67.
The common assumption about particulate air pollution has been that internalizing the
particles and their adsorbed compounds like heavy metals occurs through the lungs. Smaller
particles are assumed more dangerous because they can penetrate more deeply into the lungs and
are cleared by the lung cilia less readily. However, there is new evidence to suggest that
atmospheric particulate matter is also swallowed, leading to toxicity of internal organs and
increased carcinogenic risk. This is of particular relevance for increasing childhood risk. 68.
8 That all these above mentioned adverse health outcomes can be the result of pregnant
women smoking is easy for physicians and the lay public alike to comprehend and the sight of a
pregnant woman smoking is now repulsive to society at large. It is a new thought process, but
equally scientifically based, to think that the same thing happens when a pregnant woman has to
breathe particulate air pollution. Again, regarding impact on the human embryo there appears to
be no safe threshold of exposure.
As a manifestation of the evidence for severe health affects from air pollution, virtually
every major medical organization in the United States has called for stricter NAAQS for annual
PM2.5 and for ozone, including the American Medical Association, the American Thoracic
Society, the American Lung Association, the American Academy of Pediatrics, the American
College of Cardiology, the American Heart Association, the American Cancer Society, the
American Public Health Assoc., and the National Association of Local Boards of Health, and the
EPA’s Clean Air Scientific Advisory Committee (considered the nation's premier air pollution
experts).
Unique Toxicity of Refinery Emissions
While the oil refineries contribute to the overall air pollution burden along the Wasatch
Front, their uniquely toxic emissions makes their health impact even greater, per unit dose of
particulate emissions, than most other common sources of urban air pollution. Refinery
pollution has high concentrations of HAPs including heavy metals and polycyclic aromatic
hydrocarbons (PAHs). The only station that monitors HAPs on a continuous basis is near the oil
refineries for good reason. Tesoro’s NOI admits to an increase in HAPs emissions of over 328
pounds per year.
Many of the studies mentioned above identifying air pollution's association with
diminished intelligence, chromosomal/epigenetic dysfunction and cancer measured specifically
levels of PAHs and/or heavy metals. Furthermore, children living near petrochemical industries
have higher PAH levels than adults, contributing to more DNA damage, and affecting a more
vulnerable population. 69. Industrial based pollution has been shown to be more toxic to DNA
than traffic based pollution. 70. In homes near refineries indoor air sampling has revealed
higher levels of refinery air toxics than outdoors. The heavy metals vanadium and nickel were
especially elevated in those homes. 71.
Emission of HAPs is undoubtedly the reason why epidemiologic studies show that rates
of leukemia are double in populations living in the vicinity of oil refineries. 72. Benzene is one
of the primary HAPs in refinery emissions. The Department of Health and Human Services, the
International Agency for Research on Cancer, the National Toxicology Program, and the EPA
have all determined that benzene is carcinogenic to humans. The American Cancer Society has
stated that studies with pregnant animals show that breathing benzene has harmful effects on the
developing fetus. These effects include low birth weight, delayed bone formation, and bone
marrow damage. Long-term exposure to benzene primarily harms the bone marrow resulting in
anemia, low white blood cell count, and low platelet counts. 73.
Exposure to benzene near the legally permissible limit is associated with sperm
aneuploidy (wrong number of chromosomes). 74. Exposure to petrochemicals, specifically
9 benzene, gasoline, and hydrogen sulfide is significantly associated with increased frequency of
spontaneous abortion. 75. PAHs act as developmental and reproductive toxicants and fall into
the broad category of “endocrine disruptors.” The Endocrine Society, physicians who specialize
in endocrinology, issued a special scientific statement on endocrine disruptors in 2009 which
included this statement: “Even infinitesimally low levels of exposure indeed, any level of
exposure at all, may cause endocrine or reproductive abnormalities, particularly if exposure
occurs during a critical developmental window. Surprisingly, low doses may even exert more
potent effects than higher doses.”
The main finding of a new report, three years in the making, published March 14, 2012,
by a team of twelve scientists who study hormone-altering chemicals was: Small doses can have
big health effects and there are no safe doses for endocrine disruptors. 76.
A recent article in the world’s most prestigious medical journal, The New England
Journal of Medicine, made this statement: “Mutagenic effects theoretically can result from a
single molecular DNA alteration. Regulatory prudence has led to the use of “one-hit models” for
mutagenic end points, particularly cancer, in which every molecule of a carcinogen is presumed
to pose a risk. The carcinogens of concern in crude oil are benzene and polycyclic aromatic
hydrocarbons (PAHs).” 77. Highlighting the toxicity of chemicals volatilized from oil, the
authors went on to say, “Pregnant women should particularly avoid dermal contact with oil and
should avoid areas with visible oil contamination or odors.”
Adverse Effects of Air Pollution on Wildlife and the Environment
Air pollution has significant direct and indirect adverse effects on wildlife. Generally,
animals are exposed to air pollutants via three pathways: 1) inhalation of gases or small particles;
2) ingestion of particles suspended in food or water; and 3) absorption of gases through the skin.
In general, only soft-bodied invertebrates, such as earthworms, or animals with thin, moist skin,
such as amphibians, are affected by the absorption of pollutants.
Birds are impacted directly by industrial emission, which can damage avian respiratory
systems. Ozone, sulfur dioxide, and nitrogen dioxide primarily affect the respiratory system, and
it is likely that birds are even more susceptible to gaseous pollutant injury than mammals due to
their higher respiratory rates. Metals damage the circulatory, respiratory, gastrointestinal, and
central nervous systems of animals. Often organs such as the kidney, liver, and brain are
targeted. Entire populations can be affected as metal contamination can cause changes in birth,
growth, and death rates. Air pollution from industrial sources also includes organic compounds
that are toxic to animals, including birds.
Insects are very susceptible to air pollution. Small fluctuations in air quality force certain
insects to relocate, affecting other plants and animals connected to them. Insects that are more
resilient to air pollution are those that digest organic waste less effectively, which can result in a
buildup of organic waste when air pollution rises in an area.
Air pollution has been linked to changes in both physiology and behavior in toads and
other amphibians. Ozone impairs immune systems in human beings and studies show it affects
toads in a similar way.
10 In addition to affecting individual animals or populations directly, air pollutants also
affect wildlife indirectly by causing changes in the ecosystem. Vegetation affords cover for
protection from predators and weather, provides breeding and nesting habitat, and also serves as
a food source. Therefore, any change in vegetation could indirectly affect wildlife populations.
Many studies have found that invertebrates show a preference for, or are better able to establish
themselves in, air pollution-injured vegetation.
Vegetation can be injured when exposed to high concentrations of various air pollutants.
Injury ranges from visible markings on the foliage, to reduced growth and yield, to premature
death of the plant. The development and severity of the injury depends not only on the
concentration of the particular pollutant, but also on a number of other factors. These include the
length of exposure to the pollutant, the plant species and its stage of development, as well as the
environmental factors conducive to a build-up of the pollutant and to the preconditioning of the
plant, which make it either susceptible or resistant to injury. Ozone injury to vegetation has been
reported and documented in many areas throughout North America, while sulfur dioxide enters
the leaves mainly through the stomata (microscopic openings), leading to both acute and chronic
damage to the plant. Ammonia injury to vegetation has also been observed frequently and
particulate matter deposited on vegetation can inhibit the normal respiration and photosynthesis
mechanisms within the leaf.
Air pollution also indirectly harms wildlife because emissions adversely impact water
quality. Nitrogen compounds supply an unnatural amount of nutrients to a body of water, which
can cause a rapid increase in the growth of algae. For example, studies show that up to one-third
of the nitrogen that pollutes the Chesapeake Bay and its rivers comes from the air. An
overabundance of algae can reduce available oxygen in the water, cause fish-kills, clog
waterways and otherwise upset the balance of the ecosystem. Some algal blooms are toxic, and
since algae are at the base of the food web, their toxins can be transmitted to a wide variety of
organisms. In addition to contributing to algal blooms, nitrogen pollution can also contribute to
water bodies becoming more acidic.
Sulfur dioxide and nitrogen oxides undergo chemical transformation in the atmosphere,
and occur as sulfate, nitrate, and hydrogen ions when dissolved in precipitation known as “acid
rain.” Well-buffered soils can adsorb sulfate and neutralize acidity, resulting in soil water and
stream water composition being maintained in a range acceptable to organisms. The adsorption
capacity of even well-buffered soils is limited, however, and long-term deposition of acidic
compounds depletes the supply of base cations in the soils that buffer these inputs. The build-up
of sulfates and nitrates in soils can result in delayed acidification of surface waters once
saturation is reached in sensitive watersheds.
Certain fish and animals, such as frogs, have a hard time adapting to and reproducing in
an acidic environment. At pH 5, most fish eggs cannot hatch, and at lower pH levels some fish
die. In fact, some acid lakes have no fish at all. Also, aluminum is released from soils into lakes
and streams as acid rain flows through soils in a watershed. This aluminum is harmful to fish as
well.
The effects of decreasing pH on aquatic invertebrates and fish have been repeatedly
catalogued. Insect taxa differ greatly in their response to acidity, with some species affected at
11 pH levels near 6.0. In the early stages of acidification, acid-sensitive species are replaced by
acid-tolerant ones. However, as pH levels continue to drop, more species are lost. Acid
deposition is a possible cause of declines in amphibian populations. The larval stages of aquatic
amphibian species are most affected by acidic water.
Many studies have demonstrated that surface water acidification can lead to a decline in,
and loss of, fish populations. A decrease in pH is often associated with an increase in metal
availability, being particularly true for aluminum and mercury. Decreased pH and elevated
aluminum have been shown to increase fish mortality, decrease fish growth, decrease egg
production and embryo survival, and result in physiological impairment of adult fish. In general,
embryos, fry, and juveniles are less acid-tolerant than adult fish. Aluminum can precipitate onto
fish gills, inhibiting diffusion and resulting in respiratory stress.
Finally, CO2 emissions trap heat in the earth’s atmosphere and worsen climate change.
Climate change adversely effects wildlife in a multitude of ways, including by destroying
habitat, increasing disease and altering migrations patterns.
The Possibility of “Refinery Row” Hot Spot of Carbon Monoxide
While less emphasis has been placed on CO pollution by regulators, there is more than
enough research to suggest it too has long term public health impacts, such as reduction in the
production of proteins critical to cerebellar formation during prenatal development. 78. Even
more alarming, this was found to occur at concentrations well below the NAAQS one hour CO
standard. Apparently, the closest monitoring station to the refineries is miles away at the
Hawthorne station and modeling is no replacement for monitoring of ambient air quality. As a
result, the Executive Secretary has no way of knowing if this project is to be permitted in an area
that already has exceedances of the CO NAAQS or whether there are localized exceedances of
the CO NAAQS. Given the CO emissions from the other refineries in the vicinity, this is likely
to be a completely unassessed health hazard and potential violation of the NAAQS.
More Detailed Comments on the Proposed Permit
In Making These Comments, Utah Physicians is Necessarily Restricted to the Record.
Utah Physicians is necessarily in a position to comment only on that analysis and those
issues evidenced in the record and cannot be required to raise matters that are not manifest in
those documents. By the same token, the adequacy of the Executive Secretary’s permitting
decision must be evaluated based solely on that same record.
Should the Executive Secretary Decide to Supplement the Record or His Analysis in Any
Way, the Public Must be Given the Opportunity to Comment on the Additional Material.
To the extent that the Executive Secretary considers new information and undertakes new
analysis, the public and commenting agencies such as EPA, must be given the opportunity to
review and comment on this new material.
12 Moreover, we also note that if the Executive Secretary supplements the record with
additional data and investigation, he should undertake a corresponding reevaluation of his
permitting decision. To do otherwise would be to provide a legally untenable post hoc
rationalization for his previous decision, rather than a comprehensive review of that decision
based on the new information before him. Not only, then, does the law require that new
information and analysis be subject to public notice and comment, but also that the Executive
Secretary consider his decision anew based on the supplemental evidence and review and
comments submitted by the public.
That Tesoro Has No Title V Permit is a Violation of the Clean Air Act.
That Tesoro is required to have a Title V permit is clear under both federal law and state
law. 40 C.F.R. part 70; Utah Admin. Code R307-415. After all, the Tesoro facility is a major
source and thus bound by R307-415. Utah Admin. Code R307-415-4(1)(a); see also R307-4154(2) (none of the exemptions apply).
As a result, all of the requirements of Utah’s Title V program apply to the permitting of
the facility, including, but not limited to, a permit application that provides: 1) identification and
description of all points of emission; 2) descriptions of fuels, fuel use, raw materials, production
rates, and operating schedules; 3) citation and description of all applicable requirements; 4) a
compliance plan; 5) a compliance schedule; 6) and, a schedule for submission of certified
progress reports. Utah Code Ann. R307-415-5c. Yet, the Proposed Permit fails to meet these
requirements.
In addition, a proper Title V permit must meet all the requirements listed in R307-415-6a,
including; 1) emission limitations and standards, including those operational requirements and
limitations that assure compliance with all applicable requirements at the time of permit
issuance; and 2) monitoring and related recordkeeping and reporting requirements. The permit
must also meet the requirements of R307-415-6b and 6c. Yet, the proposed AO fails to meet
these standards.
Finally, “no Part 70 source may operate after the time that it is required to submit a
timely and complete application, except in compliance with a permit issued under these rules.”
Utah Admin. Code R307-415-7b(1).1 Therefore, Tesoro is illegally operating and will continue
to do so until it receives a valid Title V permit.
Suggestions that the Proposed Permit is analogous to a Title V permit are without merit.
First, there is no provision that allows substitutions for Title V permits. Secondly, according to
the Executive Secretary, for the very reason that he chooses not to require a Title V permit of
Tesoro – because the permit would not comply with the SIP and would be rejected by EPA –
establishes that the Proposed Permit is not the same as or equivalent to a Title V permit.
1
At a minimum, the AO must comply with all applicable requirements of R307-415.
This appendix may be found at:
https://yosemite.epa.gov/R8/R8Sips.nsf/b2af5baa99cc429287256b5f0054df73/7868fa249dc40d8
2
13 Tesoro Must be Required to Address Condensable Emissions.
Emission estimates for GHT Project appear to be filterable only estimates and Tesoro
must be required to characterize fully both filterable and condensable emissions for any emission
units. Tesoro must provide total filterable plus condensable PM, PM10 and PM2.5 emissions for
purposes of Table 3-1 analysis of emission increases and net emission increase determinations
for purposes of, inter alia, R307-401-5(b) and 40 C.F.R. §52.21(a)(2)(iv)(a) analysis.
Similarly, Condition II.B.6.a provides that condensable particle emissions shall not be
used for compliance demonstration, but shall be used for inventory purposes. The effect of this
provision is to clearly indicate that the condensable PM emissions shall not be considered in the
determination of whether the FCCU emission limitation contained in the provision. This fails to
assure compliance with the NAAQS and protect increment and is otherwise illegal under R307401-8.
The Permit Does Not Comply with the Federally Enforceable PM10 SIP.
The federally enforceable PM10 SIP applicable to Tesoro was approved by EPA in 1994.
Appendix A to that SIP establishes the applicable emission limits, emission factors and other
requirements for the facility.2 Comparing the Appendix A emission limits, emission factors and
other requirements for the Tesoro facility with the proposed permit limits shows non-compliance
with the SIP. It is also evident under the SIP that any new emission unit not covered by the SIP
would be required to have an individual emission limit.
The Proposed Permit Impermissibly Lacks a PM2.5 Limit on the FCCU and Indeed Lacks
Any PM2.5 Emission Limits.
There is no PM2.5 limit on the FCCU Unit. This fails to demonstrate compliance with
NAAQS and protection of increment. In addition, there are no emission limits in the entire
proposed permit that limit PM2.5 emissions. This fails to ensure compliance with the PM2.5
NAAQS in the area of the facility, as well as the annual PM2.5 NAAQS and during times when
the relevant airshed is not exceeding the NAAQS and is a violation of, inter alia, R307-401-8.
The Proposed AO Impermissibly Lacks Emission Limits on the Flares.
Condition II.B.4.f of the Proposed Permit is illegal. It states that the flares, which the
Executive Secretary admits are emission units, “shall not be regulated for SO2 or NOX emissions
nor shall they be included in the emission limitation totals.” This provision fails to ensure
compliance with NAAQS, fails to protect increment, fails to provide a federally enforceable
emission limit on these emission units and otherwise is illegal under the Clean Air Act, the Utah
Air Conservation Act and R307-401-8. Moreover, this provision violates the requirement that
Tesoro operate its facility in compliance with good operating practices and to minimize
2
This appendix may be found at:
https://yosemite.epa.gov/R8/R8Sips.nsf/b2af5baa99cc429287256b5f0054df73/7868fa249dc40d8
987256bad00746ebc?OpenDocument. 14 emissions. It also fails to meet the requirement that emissions be monitored on a continuous
basis and that this monitoring be reported. Any suggestion that emissions from flares cannot be
monitored or regulated is without basis, particularly given EPA’s regulation of flares as part of
its New Source Performance Standards and the analysis that supports those standards.
The NSPS exempts flaring of fuel gas from the standards for sulfur oxides and
monitoring requirements only when there is a process upset or an emergency malfunction. 40
C.F.R. 60.104(a)(1). This exemption applies only to true emergencies, and other flaring must be
monitored and comply with emission limits.
Acid gas flaring is not a federally permitted operation and may not occur except where
there is a “sudden, infrequent, and not reasonably preventable failure of equipment or processes
to operate in a normal or usual manner.” 40 C.F.R. 60.2. Only rare flaring can be considered a
malfunction and all other occurrences must be regulated. Acid gas flaring that is routine or
preventable violates the NSPS requirement for operating consistent with ‘Good Air Pollution
Control Practices’ to minimize emissions at refineries with NSPS fuel gas combustion devices
and affected facilities including SRPs. 40 C.F.R. 60.11(d).
As with acid gas flaring, good air pollution control practices include investigating the
causes of flaring events and taking corrective action to avoid or reduce the probability of their
recurrence. One way to address these potential compliance issues may be through the proper
design, operation and maintenance of flare gas recovery system. Without such efforts, any
claims that flaring is an emergency operation are unsupportable.
Finally, under 40 C.F.R. 60.100a(c), if between June 2008 and the present day, Tesoro
has added any flare piping connections outside of the limited list of allowed exceptions, its flares
have been “modified” and it must achieve compliance with all NSPS Ja flare requirements by
November 2015.
There is No Federally Enforceable Emission Limit on the FCCU.
The Proposed Permit lacks a federally enforceable limit on the FCCU. In a case in which
no emission-unit-specific time rate of mass emissions reflecting BACT have been imposed on an
emission unit specific basis, the failure to incorporate a federally enforceable throughput
limitation on FCCU means there is no assurance that the FCCU will limit emissions of criteria
pollutants to the values indicated in relevant emission characterization and to the levels of
emissions that were used in air quality modeling demonstrations. Similarly, Tesoro cannot argue
that its modification is minor.
The Proposed Permit is Inadequate Because it Does Not Include Emission Limits on Each
Subject Emission Unit and Does Not Protect Short Term NAAQS.
EPA guidance related to the one-hour SO2 NAAQS states:
Because compliance with the new SO2 NAAQS must be demonstrated on the basis of a
1-hour averaging period, the reviewing authority should ensure that the source’s PSD
permit defines a maximum allowable hour emission limitation for SO2 regardless of
15 whether it is derived from the BACT top-down approach or is the result of an air-quality
based emissions rate. Hourly limits are important because they are the foundation of the
air quality modeling demonstration relative to the 1-hour SO2 NAAQS.
EPA 1-Hour SO2 NAAQS Guidance Memo at 7. In the present case, compliance with this
provision is particularly important given that Salt Lake County is not meeting SO2 the standard.
Although EPA’s one-hour NO2 NAAQS guidance is silent on this issue, significant
portions of the one-hour SO2 NAAQS guidance echo the language in the one-hour NO2 NAAQS
guidance. Based on this analysis, the EPA Environmental Appeals Board (“EAB”) stated:
“Accordingly, the Board believes that it is reasonable to infer that U.S. EPA expects ‘PSD
permit[s] [to] define a maximum allowable hour emission limitation’ for NOX to protect the onehour NO2 NAAQS.” In Re: Mississippi Lime, PSD Appeal No. 11-01 (August 9, 2011); 2011
WL 3557194 at 17. As a result of this analysis, the EBA determined that
On remand, IEPA must either include maximum allowable hourly emissions limitations
for SO2 and NOx and explain how it concluded that the limitations are protective of the
respective one-hour NAAQS or provide sufficient rationale for not including such
emissions limitations. In either case, IEPA must reopen the public comment period to
provide the public with an opportunity to submit comments.
Id. at 18.
Applying this reasoning to the present matter indicates that the Proposed Permit fails on
several grounds. First, the proposed AO lacks an enforceable emission limit for each subject
emission unit at the source and for each pollutant subject to review that is emitted from the
source. This approach fails to assure compliance with the NAAQS and protect increment and
otherwise violates the Clean Air Act, the Utah Air Conservation Act and R307-401-8. At a
minimum, the FCCU should have an individually enforceable hourly and annual mass rate
emission limitation for PM, CO, SO2 and NOX that reflect BACT or an air quality based
emission.
For example, there are no emission limits (other than opacity/visibility) on the flares.
There are no emission limits to control PM2.5 and therefore none of the PM2.5 emission units has
an associated enforceable emission limit. There are no emission limits on VOCs and therefore
none of the VOC emission units has an associated enforceable emission limit. The only emission
units with SO2 emission limits are the SRU and the FCCU. Proposed Permit at II.B.3.b, II.B.4.b
& 4.c. Therefore, none of the remaining SO2 emission units has an associated enforceable
emission limit. The only PM emission unit with an emission limit is the FCCU. Proposed Permit
at II.B.6.a. Therefore, none of the remaining PM emission units has an associated enforceable
emission limit. Likewise, there is no CO emission unit with a CO emission limit. Condition
II.B.4.c.1(e) may purport to regulate emissions from the FCCU, but the provision is worded as a
condition of monitoring rather than operation. Therefore, none of the CO emission units has an
associated enforceable emission limit. Similarly, other than the FCCU and the K1 Compressor,
no NOX emission units are controlled by emission limits. These failures to control the emissions
of air pollutants from the facility constitute a violation of the Clean Air Act and Utah Air
Conservation Act. Moreover, any calculations of emissions from the refinery or estimates of
16 increased emissions must be determined by assuming that the unregulated unit will be
uncontrolled.
Second, the Proposed Permit lacks the short-term emission limits necessary to protect
short-term PSD increment and short term NAAQS. For example, there are no hourly emission
limits on the FCCU necessary to protect the one hour NO2 and SO2 NAAQS. Indeed, the FCCU
is limited, at the shortest, by 7-day average emission limits. One of the most significant SO2
emission limit – that on the SRU – is a tons per day limit and therefore fails to protect short-term
air quality standards. No NOX emission limit on a particular unit has a shorter timeframe than a
year, while the limit on the NOX cap sources is stated in tons per day. Moreover, there are no
short- term emission limits sufficient to protect the secondary, three-hour SO2 NAAQS or the
eight hour ozone NAAQS, or even the 24 hour PM2.5 and PM10 NAAQS. After all, there are no
limits on PM2.5 in the permit and the shortest term PM emission limit is pounds per day, the
shortest term SO2 limit is tons per day, the shortest term NOX limit (other than the compressor) is
tons per day and there are no VOC emission limits. Moreover, as not every emission unit has an
emission limit, the issue of failing to protect NAAQS and increment extends beyond those
emission limits in the proposed AO.
The Proposed Permit’s practice of bubbling PM, NOX and SO2 mass rate limitations
across multiple emission units or on a source-wide basis is an impediment to regulated source
accountability for its emissions. The Proposed Permit does not contain any mass rate limits that
can be enforced on an individual emission unit basis. For a source located in an area with serious
overall air quality concerns, such multiple emission unit or source-wide bubbling of emission
limitations can only serve to reduce accountability of a source for maintaining both compliance
and environmentally acceptable emissions and therefore is illegal.
The Proposed Permit Fails to Require Compliance with Emission Limits on a Continuous
Basis.
Condition II.B.6.a. addresses compliance with the PM10 emission limit at the FCCU. The
condition limits compliance evaluation to only a single stack test per year. This condition must
be revised to additionally address parameter monitoring and the need to assure compliance with
this limitation on a continuous basis as required by law.
Production Rates During Compliance Stack Tests are Inadequate to Protect NAAQS and
Increment.
Condition II.B.6.a of the Proposed Permit provides for stack testing to be done at 90% of
the maximum production rate under a three year average. This means that Tesoro is being
allowed to conduct stack tests at times when the tested equipment will be operating a less than
95% of the physicaloperational capacity of the unit. Allowing Tesoro to test its equipment at a
production rate less than a maximum potential to emit rate fails to properly regulation the subject
facility and therefore is illegal.
17 Tesoro Must Certify the NOI and all Compliance and Monitoring Reports.
Apparently, the application materials did not contain a signed certification statement
attesting to the accuracy of claims made in Tesoro’s Notice of Intent. If Tesoro has not signed a
NSR Section Form 1 certification statement attesting to the accuracy of the submitted Notice of
Intent (or a functionally equivalent statement submitted under certification by a designated
corporate officer), then NOI and requested Executive Secretary approval order should be denied
In addition, the Proposed Permit should be amended to require that all compliance and
monitoring reports and other presentations, submittals and filings by Tesoro also be accompanied
by the requirement for a signed certification statement consistent with Part 70 requirements for
such certification.
The Proposed AO Lacks Adequate Enforceability.
The NSR Manual provides that a PSD permit must, among other things, provide for
adequate reporting and recordkeeping so that the permitting agency can determine the
compliance status of the source. However, many of the stack tests set forth in the AO are to be
performed once every five years, and others, every three years. Testing every three or five years
is not frequent enough to satisfy the requirements of the Act and the regulations for practical
enforceability and periodic testing and inspection of stationary sources. See, e.g., Sections
110(a)(2)(A), (C), and (F) of the Act; 40 CFR 51.210, 51.212.
The Proposed AO Lacks Throughput or Production Limits
The proposed permit impermissibly lacks production or operation limits. A lack of
production or operation limits fails to satisfy the requirements of the Act and the regulations that
mandate practical enforceability of stationary sources.
Conclusion
We request that the Proposed Permit be amend based on the above comments. Once
again, we appreciate the opportunity to comment on this permit. Please inform us directly of any
further action you take with regard to the Proposed Permit or the GHT Project. We hope that you
will carefully review our comments and reconsider your decision in light of what we say here.
_____________________
Joro Walker
Rob Dubuc
Attorney for Utah Physicians, et al.
18 REFERENCES
1. Mauderly J.L., Samet J.M., Is There Evidence for Synergy Among Air Pollutants in
Causing Health Effects?, 117 Environ. Health Perspect. 1-6 (2009).
2. Peters, A., Air Quality and Cardiovascular Health: Smoke and Pollution Matter,
120(11) EPUB 924-27 (2009).
3. Brook R., Rajagopalan S., Pope C.A., Brook J., Bhatnagar A., et al., AHA Scientific
Statement: Particulate Matter Air Pollution and Cardiovascular Disease; An Update to the
Scientific Statement From the American Heart Association, Circulation, American Heart
Association 121:2331-2378 (2010).
4. Lepeule J, Laden F, Dockery D, Schwartz J. Chronic Exposure to Fine Particles and
Mortality: An Extended Follow-Up of the Harvard Six Cities Study from 1974 to 2009. Environ
Health Perspect. 2012 Mar 28. [Epub ahead of print].
5. Zanobetti A., Schwartz J., Samoli E., Gryparis A., Touloumi G., Peacock J., Anderson
R.H., Le Tertre A., Bobros J., Celko M., Goren A., Forsberg B., Michelozzi P., Rabczenko D.,
Hoyos S.P., Wichmann H.E., and Katsouyanni K., The Temporal Pattern of Respiratory and
Heart Disease Mortality in Response to Air Pollution, 111(9) ENVIRON. HEALTH PERSPECT.
1188-1193 (2003).
6. Peters, A., and Pope, C.A., III, Editorial, LANCET. Vol. 360, Oct 19, 2002.
7. Pope C.A. III, Muhlestein J.B., May H.T., et al., Ischemic Heart Disease
EventsTriggered by Short-term Exposure to Fine Particulate Air Pollution, 114(23) EPUB 244348 (2006).
8. Dockery D.W., Stone P.H.. Cardiovascular Risks from Fine Particulate Air Pollution,
356(5) N. ENGL. J. MED. 511-13 (2007).
9. Miller K.A., Siscovick D.S., Sheppard L. et al., Long-term Exposure to Air Pollution
and Incidence of Cardiovascular Events in Women, 356(5) N. ENGL. J. MED. 447-58 (2007).
10. Peters, A., Air Quality and Cardiovascular Health: Smoke and Pollution Matter,
120(11) EPUB 924-27 (2009).
11. Urch B, Silverman F, Corey P, et al. Acute Blood Pressure Responses in Healthy
Adults during Controlled Air Pollution Exposures, 113 (8) ENVIRON. HEALTH PERSPECT.
1052-55 (2005).
12. Peters A., von Klot S., Heier M., et al., Exposure to Traffic and the Onset of
Myocardial Infarction, 351 (17) N. ENGL. J. MED. 1721-30 (2004).
19 13. Shang-Shyue Tsai, William B. Goggins, Hui-Fen Chiu, and Chun-Yuh Yang,
Evidence for an Association between Air Pollution and Daily Stroke Admissions in Kaohsiung,
Taiwan, 34 (11) STROKE 2612-16 (2003).
14. Mustafić H, Jabre P, Caussin C, Murad M, et al. Main Air Pollutants and
Myocardial Infarction: A Systematic Review and Meta-analysis. JAMA 2012. vol 307, no. 7 pg
713-721.
15. Szyszkowicz M, Rowe BH, Brook RD. Even Low Levels of Ambient Air Pollutants
Are Associated With Increased Emergency Department Visits for Hypertension. Can J Cardiol.
2011 Sep 23. [Epub ahead of print].
16. Wellenius G, Burger M, Coull B, Schwartz J, et al. Ambient Air Pollution and the
Risk of Acute Ischemic Stroke. Arch Intern Med. 2012;172(3):229-234.
doi:10.1001/archinternmed.2011.732.
16. Calle E, Thun M, Pope CA, Burnett R, et al. Cardiovascular Mortality and
Exposure to Airbourne Fine Particulate Matter and Cigarette Smoke, Circulation, American
Heart Association 120:941-948 (2009).
17. Hoffman B., Higher Blood Pressure Found in People Living in Urban Areas,
Presentation, American Thoracic Society (May 17, 2010).
18. Kunzil N., Jerrett M., Garcia-Esteban, R., et al., Ambient Air Pollution and the
Progression of Atherosclerosis in Adults, 5(2) PLOS ONE e9096 DOI:
10.1371/journal.pone.0009096 (2010).
19. Tonne C, Yanosky JD, Beevers S, Wilkinson P, Kelly FJ. PM Mass Concentration
and PM Oxidative Potential in Relation to Carotid Intima-media Thickness. Epidemiology. 2012
Mar 23. [Epub ahead of print].
20. Adar SD, Klein R, Klein BE, Szpiro AA, Cotch MF, Wong TY, O'Neill MS, Shrager
S, Barr RG, Siscovick DS, Daviglus ML, Sampson PD, Kaufman JD. Air Pollution and the
Microvasculature: A Cross-Sectional Assessment of In Vivo Retinal Images in the PopulationBased Multi-Ethnic Study of Atherosclerosis (MESA). PLoS Med. 2010 Nov
30;7(11):e1000372.
21. Pope CA, Ezzate M, Dockery D. Fine-Particulate Air Pollution and Life Expectancy
in the United States, 360(4) N. ENGL. J. MED. 376-86 (2009).
22. 101. Correia A, Pope CA, Dockery D, Wang Y, Ezzati M, Dominici F. Effect of
Air Pollution Control on Life Expectancy in the United States: An Analysis of 545 U.S. Counties
for the Period from 2000 to 2007 Epidemiology. 3 December 2012 doi:
10.1097/EDE.0b013e3182770237
23. Baccarelli A., Martinelli A., Zanobetti A., et al., Exposure to Particulate Air
Pollution and Risk of Deep Vein Thrombosis, 168 ARCH. INTERN MED. 920-27 (2008).
20 24. Jacobs L., Emmerechts J., Mathieu C., Hoylaerts M.F., Fierens F., Hoet P.H.,
Nemery B., Nawrot T.S. Air Pollution Related Prothrombotic Changes in Persons with Diabetes,
118(2) ENVIRON. HEALTH PERSPECT. 191-96 (2010).
25. Hartz A., Bauer B., Block M., Diesel Exhaust Particles Induce Oxidative Stress,
Proinflammatory signaling, and P-Glycoprotein, Up-Regulation at the Blood-Brain Barrier,
THE FASEB JOURNAL 2723-33 (2008).
26. Lopez I, Acuna D, Beltran-Parrazal L, et al. Evidence for oxidative stress in the
developing cerebellum of the rat after chronic mild carbon monoxide exposure (0.0025% in air).
BMC Neuroscience 2009, 10:53doi:10.1186/1471-2202-10-53.
27. Calderon-Garciduenas L., Mora-Tiscareno A., Ontiveros E., et al., AIR
POLLUTION, COGNITIVE DEFICITS AND BRAIN ABNORMALITIES: A PILOT STUDY
WITH CHILDREN AND DOGS, 68(2) BRAIN COGN. 117-27 (2008).
28. Calderon-Garciduenas L., Solt A.C., et al., Long-Term Air Pollution Exposure is
Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the
Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid Beta-42
and Alpha-Synuclein in Children and Young Adults, 36(2) TOXICOL. PATHOL. 289-310
(2008).
29. Calderon-Garciduenas L., Franco-Lira M., Torres-Jardon R., Pediatric Respiratory
and Systemic Effects of Chronic Air Pollution Exposure: Nose, Lung, Heart, and Brain
Pathology, 35(1) TOXICOL. PATHOL.154-162 (2007).
30. Cruts B., van Etten L., Tornquvist H., et al., Exposure to Diesel Exhaust Induces
Changes in EEG in Human Volunteers, 5(4) PART FIBRE TOXICOL. dol:1186/1743-8977-5-4
(2008).
31. Suglia S.F., et al., Association of Black Carbon with Cognition among Children in a
Prospective Birth Cohort Study, 167 AM. J. EPIDEMIOLOGY 280-86 (2008).
32. Edwards SC, Jedrychowski W, Butscher M, Camann D, Kieltyka A, Mroz E, et al.
2010. Prenatal Exposure to Airborne Polycyclic Aromatic Hydrocarbons and Children’s
Intelligence at Age 5 in a Prospective Cohort Study in Poland. Environ Health Perspect :-.
doi:10.1289/ehp.0901070.
33. Perera, FP, L Zhigang, R Whyatt, L Hoepner, S Wang, D Camann and V Rauh.
2009. 2009. Prenatal airborne polycyclic aromatic hydrocarbon exposure and child IQ at age 5
years. Pediatrics doi: 10.1542/peds.2008-3506.
34. Wang, Z., Zeng, X, Zeng, Y, Wang, S. Chen, S., Association of Traffic-Related Air
Pollution with Children’s Neurobehavioral Functions in Quanzhou, China, 117(10) ENVIRON.
HEALTH PERSPECT. 1612-18 (2009).
21 35. Volk H, Hertz-Picciotto I, Delwiche L , Lurmann F, McConnell R. Residential
Proximity to Freeways and Autism in the CHARGE study. Environ Health Perspect. 2010 Dec
13. [Epub ahead of print] PMID: 21156395.
36. Power MC, Weisskopf MG, Alexeeff SE, Coull BA, Spiro Iii A, Schwartz J.
Traffic-Related Air Pollution and Cognitive Function in a Cohort of Older Men. Harvard School
of Public Health. Environ Health Perspect. 2010 Dec 20. [Epub ahead of print].
37. Ranft U, Schikowski T, Sugiri D, Krutmann J, Krämer U. Long-term exposure to
traffic-related particulate matter impairs cognitive function in the elderly. Environ Res. 2009
Nov;109(8):1004-11. Epub 2009 Sep 4.
38. Weuve J, Puett R, Schwartz J, Yanosky J, Laden F, Grodstein F. Exposure to
Particulate Air Pollution and Cognitive Decline in Older Women Arch Intern Med.
2012;172(3):219-227. doi:10.1001/archinternmed.2011.683.
39. Calderón-Garcidueñas L, Serrano-Sierra A, Torres-Jardón R, Zhu H, Yuan Y, Smith
D, Delgado-Chávez R, Cross JV, Medina-Cortina H, Kavanaugh M, Guilarte TR. The impact of
environmental metals in young urbanites' brains. Exp Toxicol Pathol. 2012 Mar 19. [Epub ahead
of print].
40. Ciesielski T, Weuve J, Bellinger DC, Schwartz J, Lanphear B, Wright RO 2012.
Cadmium Exposure and Neurodevelopmental Outcomes in U.S. Children. Environ Health
Perspect :-. http://dx.doi.org/10.1289/ehp.1104152.
41. Henn BC, Schnaas L, Ettinger AS, Schwartz J, Lamadrid-Figueroa H, HernándezAvila M, et al. 2011. Associations of Early Childhood Manganese and Lead Coexposure with
Neurodevelopment. Environ Health Perspect 120:126-131.
http://dx.doi.org/10.1289/ehp.1003300.
42. Schelegle, E., Morales, C., Walby, W., et al, 6.6 Hour Inhalation of Ozone
Concentrations from 60 to 87 Parts per Billion in Healthy Humans, 180 AMERICAN JOURNAL
OF RESPIRATORY AND CRITICAL CARE MEDICINE 265-72 (2009).
43. Thaller, E., Petronella, S., Hochman, D. et al., Moderate Increases in Ambient PM
2.5 and Ozone are Associated with Lung Function Decreases in Beach Lifeguards, 50(2)
JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE 202-11 (2008).
44. Gauderman W.J., Gilliland G.F., Vora H., et al., Association between Air Pollution
and Lung Function Growth in Southern California Children: Results from a Second Cohort, 166
AM. J. RESPIR. CRIT. CARE MED. 76-84 (2002).
45. Gauderman W.J., Gilliland G.F., Vora H., et al., The Effect of Air Pollution on Lung
Development from 10 to 18 Years of Age, 351(11) N. ENGL. J. MED. 1057-67 (2004).
22 46. Cakmak S, Dales R, Leech J, Liu L. The influence of air pollution on cardiovascular
and pulmonary function and exercise capacity: Canadian Health Measures Survey (CHMS).
Environ Res. 2011 Oct 13. [Epub ahead of print].
47. Raaschou-Nielsen O, Andersen ZJ, Hvidberg M, Jensen SS, Ketzel M, Sorensen M,
Hansen J, Loft S, Overvad K, Tjonneland A. Air pollution from traffic and cancer incidence: a
Danish cohort study. Environ Health. 2011 Jul 19;10(1):67. [Epub ahead of print].
48. Raaschou-Nielsen O, Andersen Z, Hvidberg M, Jensen SS, Ketzel M, Sørensen M,
Loft S, Overvad K, Tjønneland A. Lung Cancer Incidence and Long-Term Exposure to Air
Pollution from Traffic. Environ Health Perspect. 2011 Jan 12. [Epub ahead of print].
49. Turner MC, Krewski D, Pope Iii CA, Chen Y, Gapstur SM, Thun MJ. Long-Term
Ambient Fine Particulate Matter Air Pollution and Lung Cancer in a Large Cohort of Never
Smokers. Am J Respir Crit Care Med. 2011 Oct 6. [Epub ahead of print].
50. Pearson R.L., Wachtel H., Ebi K.L., Distance-Weighted Traffic Density in Proximity
to a Home is a Risk Factor for Leukemia and Other Childhood Cancers, 50(2) J. AIR WASTE
MANAG. ASSOC. 175-180 (2000).
51. Weng H.H., Tsai S.S., Chen C.C., et al., Childhood Leukemia Development and
Correlation with Traffic Air Pollution in Taiwan Using Nitrogen Dioxide as an Air Pollutant
Marker, 71(7) J. TOXICOL. ENVIRON. HEALTH A. 434-8 (2008).
52. Crouse DL, Goldberg MS, Ross NA, Chen H, Labrèche F 2010. Postmenopausal
Breast Cancer Is Associated with Exposure to Traffic-Related Air Pollution in Montreal, Canada:
A Case–Control Study. Environ Health Perspect 118:1578-1583. doi:10.1289/ehp.1002221.
53. Xu X, Liu C, Xu Z, Tzan K, et al. Long-term Exposure to Ambient Fine
Particulate Pollution Induces Insulin Resistance and Mitochondrial Alteration in Adipose Tissue.
Toxicological Sciences Volume 124, Issue 1Pp. 88-98.
54. Zou M. Is NAD(P)H Oxidase a Missing Link for Air Pollution–Enhanced Obesity?
Arterioscler Thromb Vasc Biol. 2010;30:2323-2324, doi:10.1161/ATVBAHA.110.216648.
55. Zeft AS, Prahala S, Lefevre S, et al. Juvenile idiopathic arthritis and exposure to
fine particulate air pollution. Clin Exp Rheumotol 2009 Sep-Oct; 27(5):877-84.
56. Krämer U, Herder C, Sugiri D, Strassburger K, Schikowski T, Ranft U, et al. 2010.
Traffic-related Air Pollution and Incident Type 2 Diabetes: Results from the SALIA Cohort
Study. Environ Health Perspect :-. doi:10.1289/ehp.0901689.
57. Puett RC, Hart JE, Schwartz J, Hu FB, Liese AD, Laden F 2011. Are Particulate
Matter Exposures Associated with Risk of Type 2 Diabetes? Environ Health Perspect 119:384389. doi:10.1289/ehp.1002344.
23 58. Veras M.M., Damaceno-Rodregues N., Caldini E., Ribeiro A., et al., Particulate
Urban Air Pollution Affects the Functional Morphology of Mouse Placenta, 79(3) BIOLOGY
OF REPRODUCTION 578-84 (2008).
59. Perera F., Tang W., Herbstman J., Relation of DNA Methylation of 5-CpG Island of
ACSL3 to Transplacental Exposure to Airborne PAH and Childhood Asthma, 4(2) PLOS ONE
e4488 (2009).
60. Hansen C., Barnett A., Prichard G., The Effect of Ambient Air Pollution during
Early Pregnancy on Fetal Ultrasound Measurements during Mid-Pregnancy, 116(3) ENVIRON
HEALTH PERSP. 362-69 (2008).
61. Bocskay K., Tang D., Orjuela M., et al., Chromosomal Aberrations in Cord Blood
Are Associated with Prenatal Exposure to Carcinogenic Polycyclic Aromatic Hydrocarbons.
CANCER EPIDEM. BIOMARKERS AND PREV. 506-511 (2005).
62. Perera F., Tang D., Tu Y., Biomarkers in Maternal and Newborn Blood Indicate
Heightened Fetal Susceptibility to Procarcinogenic DNA Damage, 112(10) ENVIRON.
HEALTH PERSP. 1133-36 (2004).
63. Pilsner J.R., Hu H., Ettinger A., Sanchez B.N., et al., Influence of Prenatal Lead
Exposure on Genomic Methaylation of Cord Blood DNA, 117 (9) ENVIRON HEALTH
PERSP., 1466-71 (2009).
64. Baccarelli A., Breathe Deeply into Your Genes!: Genetic Variants and Air Pollution
Effects, 179(6) AM. J. RESPIR. CRIT. CARE MED., 431-2 (2009).
65. Baccarelli A., Wright R.O., Bollati V., Tarantini L., Litonjua A.A., Suh H.H.,
Zanobetti A, Sparrow D., Vokonas P.S., Schwartz J., Rapid DNA Methylation Changes after
Exposure to Traffic Particles, 179(7) AM. J. RESPIR. CRIT. CARE MED., 523-4 (2009).
66. Yan Zhong, Steven G. Carmella, Pramod Upadhyaya, J. Bradley Hochalter, Diane
Rauch, Andrew Oliver, Joni Jensen, Dorothy Hatsukami, Jing Wang, Cheryl Zimmerman,
Stephen S. Hecht. Immediate Consequences of Cigarette Smoking: Rapid Formation of
Polycyclic Aromatic Hydrocarbon Diol Epoxides. Chemical Research in Toxicology, 2010;
101227010050010 DOI: 10.1021/tx100345x.
67. Rubes J, Selevan S, Evenson D, Zudova D, Vozdova M, Zudova Z, Robbins W,
Perreault S. Episodic air pollution is associated with increased DNA fragmentation in human
sperm without other changes in semen quality. Human Reproduction Vol.20, No.10 pp. 2776–
2783, 2005 doi:10.1093/humrep/dei122. Advance Access publication June 24, 2005.
68. Møller P, Folkmann JK, Danielsen PH, Jantzen K, Loft S. Oxidative Stress
Generated Damage to DNA by Gastrointestinal Exposure to Insoluble Particles. Curr Mol Med.
2012 Jan 27. [Epub ahead of print].
24 69. Sánchez-Guerra M, Pelallo-Martínez N, Díaz-Barriga F, Rothenberg SJ, HernándezCadena L, Faugeron S, Oropeza-Hernández LF, Guaderrama-Díaz M, Quintanilla-Vega B.
Environmental polycyclic aromatic hydrocarbon (PAH) exposure and DNA damage in Mexican
children. Mutat Res. 2011 Dec 17. [Epub ahead of print].
70. Topinka J, Rossner P Jr, Milcova A, Schmuczerova J, Svecova V, Sram RJ. DNA
Adducts and Oxidative DNA Damage Induced by Organic Extracts From PM2.5 in an Acellular
Assay. Toxicol Lett. 2011 Feb 14. [Epub ahead of print].
71. Brody, J.G., R. Morello-Frosch, A. Zota, P. Brown, C. Perez and R. Rudel. 2009.
Linking Exposure Assessment Science with Policy Objectives for Environmental Justice and
Breast Cancer Advocacy: The Northern California Household Exposure Study. American
Journal of Public Health, 99: S600-S609.
72. Barregard L, E Holmberg and G Sallsten. 2009. Leukaemia incidence in people
living close to an oil refinery. Environmental Research 109:985-990.
73. Toxicological Profile for Benzene, 2005 Draft for Public Comment Agency for
Toxic Substances and Disease Registry United States Public Health Service.
74. Xing C, Marchetti F, Li G, et al. Benzene exposure near the US permissible limit is
associated with sperm aneuploidy. Environ Health Perspect 2010;118:833-839.
75. Xu, Xiping, Sung-Il Cho, et al.. “Association of petrochemical exposure with
spontaneous abortion.” Occupational and Environmental Medicine. 55: 31-36. 1998.
76. Vandenberg LN, Colborn T, Hayes TB, Heindel JJ, Jacobs DR Jr, Lee DH, Shioda T,
Soto AM, Vom Saal FS, Welshons WV, Zoeller RT, Myers JP. Hormones and EndocrineDisrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses. Endocr Rev.
2012 Mar 14. [Epub ahead of print].
77. Goldstein B, Osofsky H, Lichtveld M. The Gulf Oil Spill. N Engl J Med 2011;
364:1334-1348. April 7, 2011.
78. A Lopez 1, Acuna D, Beltran-Parrazal L, et al. Evidence for oxidative stress in the
developing cerebellum of the rat after chronic mild carbon monoxide exposure (0.0025% in air).
BMC Neuroscience 2009,10:53 doi10.1186/1471-2202-10-53
79. Silverman DT, Samanic CM, Lubin JH, et al. The diesel exhaust in miners study: a
nested case-control study of lung cancer and diesel exhaust. J Natl Cancer Inst. March 2, 2012.
doi:10.1093/jnci/djs034.
80. Attfield MD, Schlieff PL, Lubin JH, et al. The diesel exhaust in miners study: a
cohort mortality study with emphasis on lung cancer. J Natl Cancer Inst. March 2, 2012.
doi:10.1093/jnci/djs035.
25 81. Fisher J, et al. Synapse Energy Economics. Co-Benefits of Energy Efficiency and
Renewable Energy in Utah, March 24, 2010.
82. Hammond PB. Valuing Health Risks, Costs, and Benefits for Environmental
Decision Making. National Research Council...EPA 1983, 1985.
26