Electronic Filing - Received, Clerk's Office, 08/15/2012 

EXIDBIT3 
Electronic Filing- Received, Clerk's Office, 08/15/2012 A:COM AECOM 5124724519 tel 

Wednesday, August 15, 2012 

Illinois Pollution Control Board 

C/0 J olm Therriault 

Assistant Clerk of the Board 

James R. Thompson Center 

100 W Randolph 

Suite 11-500 

Chicago, Illinois 60601 

Re: Docket No. PCB 2012-126 

400 West 15lh Street 512 472 7519 fax 

Suite 500 

Austin, Texas 78701 

www.aecom.com 

A Toxicologist's Perspective on Statements made about Potential Health Effects 

during the Hearing (August 1, 2012) on Ameren Energy Resources (AER) Request 

for Variance from the Illinois Sulfur Dioxide (S02) Multi-Pollutant Standard (MPS) 

Dear Members of the Illinois Pollution Control Board: 

The purpose of this letter is to provide a toxicologist's perspective on the statements about 

potential health effects made in the hearing (August 1, 2012) on Ameren Energy Resources 

(AER) request for variance from the 2015 and 2017 Sulfur Dioxide (S02) emission rate 

provisions of the Illinois Multi-Pollutant Standard (MPS). My knowledge of the statements 

made during the hearing comes from the transcript of the hearing, which was provided to me 

by Amy Antoniolli of Schiff Hardin LLP. 

Discussions about the potential for adverse health effects provided in this letter are 

predicated on the assumption that there is a causal relationship between S02 exposures and 

adverse health effects. However, most epidemiological evidence points toward particulate 

matter as a stronger causal agent for mortality and morbidity (i.e., effects other than 

mortality) than gaseous S02. Because S02 is usually found in association with particulate 

pollution, (S02 is the precursor for fine sulfate particles) and because only limited evaluation 

of potential confounding (intervening variables that makes it appear that au effect is caused 

by a particular agent when the effect is actually due to something else) has been conducted in 

most epidemiological studies, separating the health effects of these two pollutants has been 

very difficult. 

The Board should be aware that more studies than not have failed to find statistically 

significant associations between long-term and short-term S02 concentrations and adverse 

health outcomes, indicating that the apparent associations may well be due to other factors. 

In fact, EPA has concluded that there is not a causal relationship between long-term 802 

exposure and respiratory effects or mortality. While EPA has concluded that the results of 

clinical studies in which humans are exposed to S02 concentrations much higher than those 

found in ambient air support a causal relationship between respiratory morbidity and shortterm exposure to S02, nine of the 10 primary epidemiology studies attempting to correlate 

short-term exposure to asthma-related emergency room visits or hospitalizations relied upon 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

by EPA found either no association or very small positive associations. EPA further 

concludes that the evidence on short-term S02 exposure is only suggestive of a causal 

relationship with mortality. Therefore, despite the dogmatism with which health effects from 

S02 are asserted, when the studies providing the underlying support for such declarations are 

more closely examined, it becomes clear that the association between S02 exposure and 

respiratory health effects and mortality isnot nearly as certain as typically portrayed by the 

media, regulators and activists. Asthma is the health effect most commonly cited by these 

groups as associated with S02 exposure, and they point to the rise in asthma in the US 

population as proof of effect. However, there are many theories about the rise in asthma over 

the past 30 years, and exposure to outdoor pollution is probably the least plausible 

explanation given that the air quality in Illinois and the nation as a whole has improved 

dramatically during the same time period over which asthma prevalence has increased, as 

discussed in more detail in the specific responses to public comments. 

Although it can be universally agreed that respiratory effects such as asthma attacks and 

chronic obstructive pulmonary disease (COPD) represent adverse or harmful effects, simply 

establishing that a person who has possibly been exposed to S02 in an environmental setting 

experienced bronchoconstriction or a reduced expiratory volume is not proof that the 

potential exposure caused the effect. This is because in any individual, these effects could 

have been caused by a number of different factors, for example, indoor or outdoor allergens, 

smoking or passive exposure to cigarette smoke, or viral pathogens. Likewise, the fact that a 

power plant may emit S02 does not necessarily mean that off-site air concentrations will be 

high enough to elicit adverse health effects. 

More details about research on the potential health effects of S02 are provided in the specific 

responses to public comments. 

Background 

The MPS and the AER Requested Variance 

The MPS specifies a 0.5lb/MMBtu S02 emission rate until2014 when the required emission 

rate is decreased to 0.43 lb/MMBtu, followed by a decrease to 0.25 lb/MMBtu in 2015. 

Under the MPS, the S02 emission rate is further decreased to 0.23 lb/MMBtu in 2017. AER 

has requested a variance from meeting the 0.25 lb/MMBtu S02 emission rate required by the 

provisions of the MPS in 2015 and the 0.23 lb/MMBtu emission rate that is required in 2017. 

However, AER has proposed a mitigation emission rate of 0.35 lb/MMBtu that would take 

effect in 2013, resulting in AER taking action to reduce S02 emissions earlier than required 

by the MPS. AER would comply with the 0.35 lb/MMBtu mitigation emission rate from 

2013 to 2019, with the 2017 MPS emission rate of 0.23 lb/MMBtu being met by 2020. The 

figure below provides a comparison of AER's S02 emissions under the provisions of the 

MPS and the S02 variance. 

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2010 

Ameren Energy Resources Variance 502. Umit Comparison to~ tile Current MPS 

Zflll 11}:12 101'3 2014 2015 

Year 

2016 2017 Z018 

-'i"-AllP.~;~)Jie Emi5.~lon> ~.Me(l on M PS Bi!~eliue Rat~ -+-Total.fl,lture&n!~s.ion~ B<UE:\! c.·n Am a-en Varianq--Rnte 

2019 1.010 

The blue line represents AER's baseline emissions under the MPS and the black line 

represents emissions under the S02 variance. As can be seen in the figure, AER's emissions 

under the S02 variance are considerably lower than the MPS emissions between 2012 and 

2014 and are slightly higher from 2015 to 2019. However, the area representing the 

difference between the MPS and S02 variance emissions from 2012 to 2014 is larger than 

the area between the MPS and S02 variance emissions from 2015 and 2019. Therefore, 

there is an overall net improvement (i.e., decline) in S02 emissions under the S02 variance 

proposed by AER. It should also be noted that AER has voluntarily operated at lower S02 

emission rates than allowable under the MPS since 2010, demonstrating its commitment to 

reducing emissions. If the reduced S02 emissions starting in 2010 are taken into 

consideration, the positive difference between AER's S02 variance emissions and those 

allowable under MPS is even larger. 

Overall Net Health Benefit of the Variance 

Over the course of the entire variance period, between now and 2020, the total tons of S02 

reduced in the atmosphere will be greater ifthe AER-requested variance is granted than if it 

is not. The source of reduction in S02 emissions over the course of the variance period is 

two-fold: 1) AER will emit less S02 via a mitigation rate representing a 19% to 30% 

reduction in the MPS allowable S02 through 2014; and 2) AER has agreed to keep two of 

its coal-fired powerplants shut down during the variance period, which will result in less 

coal being burned. 

Assuming that the S02 emissions from the AER coal fleet are at levels that could potentially 

result in off-site ambient concentrations high enough to cause adverse health effects under 

the provisions of the MPS, which is not a foregone conclusion, granting the variance would 

result in an overall net health benefit. For example, if a hypothetical risk relationship of one 

additional asthma-related emergency room (ER) visit per 100 tons of S02 emitted is 

assumed, there will have been 77 fewer ER visits over the duration of the S02 variance than 

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if AER complies with the MPS on schedule. Please note, however, that this assumed risk 

relationship is purely hypothetical, as risk relationships of this nature are typically expressed 

on a per capita per ton basis, taking into account the size of the potentially exposed 

population. 

Health Effects Concerns Raised during the Hearing 

While concerns about potential health effects associated with exposure to S02 are 

understandable, there are misconceptions about what the scientific research is telling us, as 

described above and further elaborated upon below. 

There appears to be a continuous 'spectrum of sensitivity to S02, with some people being 

completely unaffected by concentrations that lead to severe bronchoconstriction in others. 

Asthmatics are particularly sensitive to the effects of S02 and the effects are enhanced if 

S02 reaches the lower regions ofthe lungs, which is more likely to occur during mouth 

breathing (as opposed to breathing through the nose) and exercise. Maximum effects of S02 

occur within a few minutes and continued exposure does not typically increase the response 

and the effects are generally short-lived and completely reversible (WHO, 2006). 

Illinois Attorney General's Office 

James Gignac, the Assistant Attorney General (pg 84 of Transcript) stated in the hearing that 

there is a harm that would occur, despite AER' s calculations demonstrating an overall 

reduction in the tonnage of S02 emissions over the 12-year period. The basis for his 

statements regarding potential harm is the increase in emissions that would be allowed 

between the years of 2015 and 2019 under the variance. 

While there could, theoretically, be additional adverse health outcomes between the years of 

2015 and 2019, there would be fewer between the years of 2012 and 2014 and because the 

magnitude of the emission reductions during the early years is greater than the increased S02 

emissions that will occur between 2015 and 2019, there would be fewer adverse health 

effects overall. Therefore, the health benefits of approving the variance requested by AER 

outweigh the health costs, resulting in an overall health benefit, when the entire period of the 

variance is taken into account. Assuming that one accepts that the current emissions pose a 

health threat, not approving the variance represents a tradeoff between greater reductions in 

health effects from 2012 and 2014 in exchange for smaller reductions in health effects 

between the years of 2015 and 2019. 

As mentioned in the beginning of this letter, the above discussion is predicated on the 

assumption that the C-R (concentration-response) relationships reported in epidemiological 

studies indicate causal relationships between the S02 exposures and adverse health effects. 

However, in most studies that have examined the potential for confounding by other copollutants (particulates, ozone, nitrogen oxides), the small associations observed between 

ambient S02 concentrations and adverse health outcomes usually become null when twopollutant models are used, indicating that the associations are stronger for the other pollutants 

or that there is no association with S02 (EPA, 2008; EPA, 2009; Goodman et al., 2010). As 

a result, more studies than not have failed to find statistically significant associations between 

long-term and short-term S02 concentrations and adverse health outcomes. According to the 

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EPA's own Integrated Science Assessment (ISA, EPA, 2008) prepared in support of the most 

recent S02 National Ambient Air Quality Standards (NAAQS) review, "Overall, the 

epidemiologic studies do not provide sufficient evidence to infer a causal relationship 

between long-tenn exposure to S02 and asthma, bronchitis, or respiratory symptoms". The 

EPA ISA also concluded that "The available epidemiologic evidence on the effect of longterm exposure to S02 on mortality is inadequate to infer a causal relationship at this time" 

(EPA, 2008). 

The EPA ISA does conclude that "the human clinical, epidemiologic, and animal 

toxicological data are sufficient to conclude that there is a causal relationship between 

respiratory morbidity and short-term exposure to S02" and that 'The evidence is suggestive 

of a causal relationship between short-term exposure to S02 and mortality". However, of the 

10 primary epidemiology studies attempting to correlate short-term (daily) S02 exposures to 

adverse health outcomes relied upon by EPA, nine found either no association or very small 

positive associations between daily S02 concentrations and asthma-related emergency room 

visits or hospitalizations. Among the studies for which weak positive associations were 

observed, conclusions were either: 1) based only on results from single-pollutant models 

(i.e., multiple pollutant models were not used, which are applied to determine confounding 

by co-pollutants); or 2) based on results from single-pollutant models that were not 

statistically significant in two-pollutant models. 

Statistical significance is key to determining if exposure and effect are causally associated. 

Determining whether the effect is isolated, independent, or secondary to a known effect of 

exposure is also important because these types of effects may be the result of other factors 

not related to the exposure of interest (Goodman eta!., 201 0). Isolated effects occur in only a 

few test subjects and independent effects are those which occur in the absence of other 

effects expected via the same mechanism of action. The fact that these effects occur 

inconsistently and lack biological plausibility is an indication that they are more likely due to 

another factor or measurement error rather than exposure related. A test of statistical 

significance helps determine whether effects are .caused by the exposure under study. These 

tests compare differences between exposed and non-exposed groups of test subjects as 

opposed to evaluating effects in independent individuals. If the difference between exposed 

and non-exposed groups is not statistically significant, the exposure is either insufficient to 

cause the effect under study or the study is not sufficiently powered, most likely due to 

having too few test subjects. 

Only one of the I 0 epidemiological studies (NYSDOH, 2006) correlating daily S02 

concentrations to adverse health outcomes relied upon by EPA in the latest NAAQS review 

found a marginally statistically significant association with increased S02 levels in both 

single-and two-pollutant models. However, the authors of that one study acknowledged that 

correlations between co-pollutants made these results difficult to interpret. 

Peoria Families against Toxic Waste 

A representative for the Peoria Families against Toxic Waste, Tracey Cox, indicated that 

health experts understand and have pointed out that cumulative S02 reductions do nothing to 

help communities with short-term pollution impacts and it is those short-term impacts that 

happen to children and the elderly population across the state. 

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It is not correct that cumulative S02 reductions do nothing to abate short-term pollutant 

impacts. Long-term concentrations are not completely independent of short-term 

concentrations of the same pollutant. In fact, EPA has performed extensive evaluations to 

determine relationships between short-term and longer-term concentrations of various 

pollutants and has on occasion set a longer-term standard to limit the relative frequency with 

which shorter-tenn exposures will exceed a particular level. In addition, EPA's screening 

modeling guidance indicates that for a point source it can be assumed that the maximum 

daily average concentration is 0.4 of the maximum 1-hour and that the maximum annual 

concentration is 0.08 of the max 1-hr (http:llwww.colorado.gov/airguality/permitslscreen.pdf). 

From this we can infer 24-hour to annual ratio of0.4/0.08 = 5. Thus, it is widely accepted 

that long-term and short-term concentrations are related to one another. For this reason, the 

overall net reduction in S02 provided by the variance in comparison to the MPS regulatory 

schedule is also expected to have an effect or reducing short-term exposures over the 

variance time period. 

Sierra Club 

A representative of the Sierra Club raised the issue of the increasing incidence of asthma in 

children that has been observed over the last several decades, indicating that in his job as a 

school social worker, he has seen the effects of S02 in terms of asthma. 

Nationwide, S02 concentrations fell32% between 1980 and 1990 alone. The distribution of 

asthma in other countries also fails to implicate S02 or other pollutants as an aggravating 

factor. Some of the highest asthma mortality rates occur in Australia and New Zealand, 

which have excellent air quality. Asthma is more prevalent in rural areas of the Scottish 

highlands, which have some of the lowest ozone concentrations in the world, than in more 

urban and polluted parts of the United Kingdom, according to a recent report (Friebele, 

1996). 

Changes in the diagnostic coding of asthma and survey questions in self-reporting asthma 

questionnaires over the last 3 0 years have likely altered the diagnosis of asthma cases and 

caused changes in prevalence and incidence statistics. The International Classification of 

Diseases (ICD) provided by the World Health Organization (WHO) was revised in 1978 (9th 

revision) and 1990 (1Oth revision) resulting in a change to the coding of asthma. In the ICD 

8, a patient with "asthmatic bronchitis" would have been coded under bronchitis, while in 

ICD 9 this same person would be coded under asthma (Marcus and Braman, 2010). One 

study that analyzed asthma patient records found an increase in patients with an asthma 

classification that had a history of smoking in the 1980s versus the 1970s. The cause of this 

difference was attributed to the change in classification of asthmatic bronchitis from a 

bronchitis heading to an asthma heading, resulting in asthmatic bronchitis patients now 

falling under the umbrella of asthma in the 1980s (Marcus and Braman, 2010). This change 

in coding may also influence the validity of epidemiology studies that look at hospital ER 

visits for asthma as potential indicators of an association between ambient pollutant 

concentrations and respiratory effects over years during which changes in the asthma 

definition has changed. 

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A large source of asthma surveillance data is compiled by the N a tiona! Center for Health 

Statistics of the Centers for Disease Control and Prevention (CDC) under the National Health 

Interview Survey (NHIS). The NHIS questions used to evaluate asthma prevalence changed 

in 1997 and 2001, resulting in three separate types of questions that could impact asthma 

prevalence estimates from 1980 to 1996, 1997 to 2000, and 2001 to the present (National 

Heart and Lung Institute; www.nhlbi.nih.gov/health/prof/lung/asthma!surveil.htm). These 

changes prevent comparisons of reported asthma rates from 1980 to 1997 to the more recent 

data set from 1997 to 2001 and illustrate the potential variability in reported asthma 

prevalence depending on how asthma questions are phrased, and what sort of asthma 

information is requested (lifetime incidence versus episodes in the past 12 months, for 

example). 

The increase in asthma cases may also be partially explained by factors relating to changes in 

healthcare access and physician perceptions. The diagnosis of asthma may have become 

more likely than a similar diagnosis of bronchitis or chronic obstructive pulmonary disease 

(COPD) among patients with similar symptoms. One study looked at healthcare data from 

Manitoba, Canada from 1980-1990 and found a statistically significant increase in asthma 

diagnosis above background increases found for other diseases with similar symptoms over 

that time period (Manfreda eta!., 1993). The study attributes some of the increase to an 

increase in the likelihood of asthma diagnoses. 

Another factor that may have contributed to the apparent increase in childhood asthma 

prevalence is that children spend much more time indoors today than they did 30 years ago. 

In addition to contributing to the development of asthma, exposure to various indoor air 

initants can also exacerbate asthma symptoms. Cat, cockroach, and house mite dust 

allergens have all been causally linked to exacerbation of asthma symptoms in. sensitive 

individuals, and environmental tobacco smoke exposure has also been causally linked to 

exacerbation of asthma symptoms in young children (Institute of Medicine, 2000). 

Therefore, the suggestion by Mr. Cox that S02 emissions (pg. 133 of transcript) are 

significant contributors to the rise in reported asthma cases (and other diseases) is not 

supported by evidence in the literature. 

ELPC 

Jennifer Cassel from the ELPC read a letter from Illinois health professionals opposing 

AER's variance request. The letter stated that "High levels of S02 and NOx can exacerbate 

respiratory systems in at-risk individuals, including children and the elderly, including 

asthma and COPD attacks." (pg 144 of transcript). The operative word in this statement is 

"high" levels. There are many controlled human studies that have exposed healthy and 

asthmatic test populations to S02 and that have measured small lung function decrements in 

the asthmatic population, particularly at higher than normal exertion levels. However, most 

fail to show a statistically significant response, and even in asthmatics (a sensitive 

subpopulation), responses are only seen at high concentrations on the order of250 ppb (715 

J.lg/m3

) over a 10 minute period (WHO, 2006). Peak exposures in the range of 4,000 ppb 

(11,440 J.lg/m3

) to 5,000 ppb (14,330 J.lg/m3) are required for reductions in mean lung 

function in normal (non-asthmatic) individuals at rest. No significant changes in group mean 

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lung function in healthy individuals have been seen below short-term exposures of 1000 ppb 

(2860 ~g/m ), even with exercise (WHO, 2006). 

To put the S02 concentrations above into context, according to the Illinois EPA 2009 Air 

Quality Report (IEPA, 2010), the statewide average 24-hour S02 concentration for 2010 was 

39 ~g/m3 (15 ppb) and 45 ~g/m3 (17 ppb) in 2009. The statewide average 1-hour high in 

2010 was 197 ~g/m3 (75 ppb), compared with 212 ~g/m3 (81 ppb) in 2009 and 335 ~g/m3 

(128 ppb) in 2008. Therefore, not only have the air concentrations monitored in Illinois been 

well below levels demonstrated to cause respiratory effects in healthy and asthmatic 

individuals, there has been an overall downward trend in S02 concentrations in the state. 

The letter also references a 2010 study conducted by the National Research Council (NRC) 

that indicated that annual health related damages from particulate, S02 and N02 cost 62 

billion dollars in 2005 alone. The concentration-response (C-R) relationship used in the 

NRC Health Impact Assessment (HIA) to estimate damages associated with S02-related 

hospital admissions was from a study conducted by Sheppard et al. (1999). However, this 

study, like most S02 epidemiology studies, failed to fm(l an association between ambient 

S02 concentrations and asthma-related hospital admissions, as was clearly acknowledged by 

the authors. 

The C-R function is a key component of IDAs because it is this function that allows the 

effect of interest to be linked in a quantitative way to incremental changes in concentrations 

by assuming a response continuum. However, C-R relationships are calculated for all 

pollutants and health endpoints examined in a scientific study by the authors, even for those 

pollutant-health effect pairings that are determined through statistics not to be associated with 

the exposure of interest. Therefore, it is up to those conducting the HIA (individuals other 

than the scientific study authors) to choose appropriate C-R relationships for use in modeling. 

It defies logic that the NRC study would use a C-R function from a study in which the 

ambient S02 concentrations and asthma-related hospital admissions were determined not to 

be correlated and casts doubt on the validity of the entire NRC report. This is a clear 

example of how fmdings published in the scientific literature are often misinterpreted and 

inadvertently or intentionally misused by activist groups. 

Comments of Samuel Dorevitch, MD 

Comments from Dr. Dorevitch were provided by Andrew Armstrong with the ELPC. Mr. 

Armstrong read excerpts from Dr. Dorevitch's written comments, which stated that research 

has demonstrated that even moderate levels of S02 are associated with bronchospasm but 

provided no information on which research he was referring to or what he considers a 

moderate concentration of S02. However, the doctor does cite the EPA's ISA (EPA, 2008) 

and notes that it states that "epidemiologic studies observed respiratory effects in areas where 

the S02 concentration was below the regulatory level in place at the time." The evidence of 

respiratory effects below the 24-hour NAAQS referenced in the ISA comes entirely from 

epidemiological studies. To put this fmding into context it is important to understand what 

epidemiological studies can and cannot do. . 

Observational epidemiological studies attempt to determine which factors are associated with 

diseases (risk factors), and which factors may protect people or animals against disease 

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(protective factors). However, epidemiological studies ca1mot prove that a specific risk 

factor actually causes the disease being studied. This is because epidemiological studies 

cannot control for, nor can they necessarily identify, all of the factors that may influence a 

health outcome. Therefore, they are plagued with issues of confounding. For example, if 

coffee drinkers were more likely to also be cigarette smokers, and a study was conducted to 

explore potential associations between coffee drinking and lung cancer, without taking the 

smoking habits of the coffee drinkers into account, smoking would be a confounder and the 

results may seem to show that coffee drinking increases the risk of lung cancer. 

Epidemiological evidence can only show that a risk factor is or is not associated (correlated) 

with a higher incidence of disease in the population exposed to that risk factor. The higher 

the correlation, the more certain the association; but causation Catlf\Ot be proven in these 

studies. Therefore, the fact that there may be studies showing that hospital admissions or 

emergency room visits were increased in an area where short-term S02 concentrations were 

below the NAAQS does not necessarily mean that the S02 concentrations caused the 

increase in hospital admissions. 

Studies that use population level data, such as respiratory hospital admissions or emergency 

room visits obtained from databases without collecting any data on the individuals involved, 

are prone to what is known as "ecologic fallacy". This occurs when a correlation observed at 

the population level is assumed to apply at the individual level. Without information on 

whether the correlations were statistically significant and whether co-pollutants and other 

intervening variables were properly controlled for, it is not possible to know what the 

implications of the findings are or if the statement even accurately characterizes the fmdings. 

Thus, while EPA's ISA may have noted that epidemiologic studies observed respiratory 

effects in areas where the S02 concentration was below the regulatory level in place at the 

time, the respiratory effects were not necessarily due to S02 exposure. 

Prairie Rivers Network 

A representative from the Prairie Rivers Network indicated that the air pollution that is 

released from the Newton facility kills about 25 people per year (pg. 186 of transcript). This 

value appears to be from the Power Plant Impact Estimator Software Tool located at 

http://www.catf.us/resources/publications/view/138 and another report entitled, "Toll from 

Coal: An Updated Assessment of Death and Disease from America's Dirtiest Energy 

Source". This study was commissioned by the Clean Air Task.Force (CATF, 2010). 

However, even upon examination of the technical support document for the estimator tool 

and Toll from Coal report (Abt, 2010), the underlying assumptions used in deriving these 

numbers are not particularly transparent. However, one thing noted is that the C-R 

relationship for S02 exposure and asthma-related hospital admissions used in the tool was 

from a study (Sheppard eta!., 1999) that failed to find an association between ambient S02 

concentrations and asthma-related hospital admissions. Although these types of evaluations 

are becoming increasingly more common, use of these C-R relationships are subject to 

significant uncertainty related to their generalizability and accuracy. One thing is certain, CR relationships from studies that fail to establish an association between the exposure and 

effect of concern should not be extrapolated to other situations in the hopes of providing 

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accurate predictions of adverse health outcomes. The other comments made above about CR relationships and their use apply here as well. 

Miscellaneous Comments 

Many commenters made vague statements such as "Coal power plants kill people.", 

"Hundreds of people in Illinois die from what comes out of coal-fired power plant stacks:" 

etc, but gave no support for these statements. 

The public debate on air pollution coupled with the sensationalized air pollution health 

stories in the media have created the appearance that harm from air pollution is much greater 

and more certain than suggested by the underlying scientific evidence. According to Dr. Joel 

Schwartz (2006), whose work on the relationship between respiratory hospital admissions 

and ambient air pollutants is amongst some of the most highly cited and one of the premier 

authors of many epidemiological studies that have been relied upon by EPA in establishing 

and re-evaluating US NAAQS, "the incentives in air pollution health research encourage risk 

exaggeration ... Through exaggeration, m,nission of contrary evidence, and lack of context, 

regulators, activists, and even many health scientists misrepresent the results of air pollution 

health studies and the overall weight of the evidence from the research literature" (Schwartz, 

2006). Dr. Schwartz across multiple fields, including Clinical Medicine, Environment & 

Ecology, Biology & Biochemistry, and Pharmacology & Toxicology. http://www.esitopics.com/airpoll/interviews/JoelSchwartz.html 

It is not surprising that ordinary citizens perpetuate the misinformation that is rampant in the 

media in hearings such as the one on AER's request for variance from the S02 MPS. We 

urge the board to consider the scientific evidence on the health effects of S02 rather than 

statements from citizens that have been mislead by the news media and reports published by 

activist groups. In support of this perspective, we have attached a copy of "Air Pollution and 

Health: Do Popular Portrayals Reflect the Scientific Evidence?" by Joel Schwartz, which 

provides several case studies aimed at demonstrating that misinformation about air pollution 

is a pervasive problem. The Schwartz (2006) article demonstrates why it is so important for 

those involved in evaluating and setting health policy to look deeper than the summaries of 

studies provided by other governmental agencies, health scientists in press conferences, and 

activists in hearings. Likewise, because it is not uncommon for even those who should know 

better to inadvertently misrepresent the evidence, interpreting air pollution health effects 

information published in the media requires a level of vigilance that few citizens are capable 

of and as a result, while citizens may believe that their health effects can be attributed to 

AER's emissions, they are often misinformed or even manipulated by the local activists. 

There is no question that very high levels of pollution can kill, as occurred during the 

"London Fog" of 1952, when soot and S02 were at levels orders of magnitude higher than 

those experienced in developed countries today and visibility was less than 20 feet. 

However, claims that low levels of pollutants cause death is based purely on scientific 

evidence from observational studies that are incapable of controlling for co-pollutants, 

lifestyle variables, and usually do not even contemplate regional disease patterns that have 

nothing to do with air pollution. It is noteworthy that researchers have been unable to evoke 

adverse health outcomes in animals with S02 concentrations anywhere near as low as those 

found in ambient air today. 

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Sincerely, 

AECOM 

Lucy Fraiser, PhD, DABT 

Associate Vice President/Senior Toxicologist 

Enclosures: 

Attachment I. References 

Lisa JN Bradley, PhD, DABT 

Vice President/Senior Toxicologist 

Attachment 2. Schwartz, J. 2006. Air Pollution and Health: Do Popular Portrayals 

Reflect the Scientific Evidence? American Enterprises Institute for 

Public Policy Research. Envirorunental Policy Outlook, No. 2. 

Attachment 3. Resume of Dr. Lucy Fraiser 

Attachment 4. Resume of Dr. Lisa Bradley 

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Attachment 1: References 

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References 

Abt, 2010. Abt Associates Inc. Teclmical Support Document for the Power plant Impact 

Estimator Software Tool 

CATF, 2010. Clean Air Task Force. Toll from Coal: An Updated Assessment of Death and 

Disease from America's Dirtiest Energy Source. September. 

Friebele, E. (1996). The attack of Asthma. Environ Health Persp., 104: 22-25. 

Goodman, J.E., Dodge, D.G., and Bailey, L.A. (2010). A framework for assessing causality 

and adverse effects in humans with a case study of sulfur dioxide. Reg. Toxicol. 

Pharmacal. 58:308-322. 

IEP A, 2010. Illinois Environmental Protection Agency. Illinois 2009 Annual Air Quality 

Report. November 2010. http://www.epa.state.il.us/air/air-qualityreport/2009/index.htm. 

Institute of Medicine. (2000). Clearing the Air: Asthma and Indoor Air Exposures. National 

Academy Press. Executive Summary. 

http://www.nap.edu/ openbook.php?isbn=0309064961. 

Manfreda, J., Becker, A. B., Wang, P. Z., Roos, L. L., and Anthonisen, N. R .. (1993). 

Trends in physician-diagnosed asthma prevalence in Manitoba between 1980 and 

1990. Chest, 103:151-157. 

NYSDOH, 2006. April. New York State, Dept. of Health. A study of ambient air 

contaminants and asthma in New York City. Part A: a comparison of ambient air 

quality in the Bronx and Manhattan. Part B: air contaminants and emergency 

department visits for asthma in the Bronx and Manhattan (Final). Report to Agency 

for Toxic Substances and Disease Registry (ATSDR); New York State, Energy 

Research and Development Authority. NTIS PB2006-113523, July, 260p. 

http://www .nyserda.nv. gov I en/Publications/Research -and-Development/ 

Environmental/ EMEP- Publications/-/media/Files/Publications/ 

Research/Environmental/ EMEP/Report%2006 02 web.ashx 

Schwartz, J. 2006. Air Pollution and Health: Do Popular Portrayals Reflect the Scientific 

Evidence? American Enterprises Institute for Public Policy Research. 

Environmental Policy Outlook, No. 2. www.aei.org. 

U.S. EPA. (2008). Integrated Science Assessment for Sulfur Oxides-Health Criteria. EPA600/R-08/047F. September 

WHO. 2006. Air Quality Guidelines, Global Update 2005. Particulate Matter, ozone, 

nitrogen dioxide and sulfur dioxide. World Health Organization Regional Office for 

Europe. 2006. 

13 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

Attachment 2: Schwartz, J. 2006. Air Pollution and Health: Do Popular 

Portrayals Reflect the Scientific Evidence? American Enterprises Institute for 

Public Policy Research. Environmental Policy Outlook, No. 2. 

14 
American Enterprise Institute for Public Policy Research 

No.2,2006 

Air Pollution and Health: Do Popular Portrayals Reflect 

the Scientific Evidence? 

By Joel Schwartz 

Envi-ronmentalists, regulawrs, health scientists, and journaUsts are the main pun.1eyors of infonnation on ai-r 

pollution health risks. Unfortunatd)', these groups create the appearance that ha:nn from air pollution is much 

greater and more cerr:ain r.han suggested by the underl:;iing evidence. The incentives in air pollution health 

research encourage risk exaggeration, because infonnation purveyors depend on public fear to nurintain rheir 

funding and influence. Investigative reporters are in the best position to assess how the political economy of environmental health research affects the production and portrayal of the evidence. Public debate on air pollution 

will continue to proceed from false premises until journalists take up this challenge. 

In a nationwide survey in 2004, 85 percent of 

Americans rated air pollution as a "very serious" 

or "somev.;hat serious" problem, \Vith similar 

results for state surveys.l In a recent Gallup Poll, 

78 percent of Americans said they worry about 

air pollution "a fair ~mount" or "a great deal."2 

Public fear of air pollution is understandable, 

because most popular information about air pol~ 

lution is indeed alarmin§;. 

Acnvist groups regularly issue reports with scary 

titles such as Danger in the Air_; Death, Disease and 

Dirty Power; Highway Health Hazards; Plagued by 

Pollution; and Children at Risk..l Health researchers 

often issue alarming summaries of the1r research as 

well. Recent press-release headlines from health 

research institutes include "Smog May Cause Life~ 

long Lung Deftctts," "Link Strengthened between 

Lung Cancer, Heart Deaths and Tiny Particles of 

Soot," "USC Study Shows Arr Pollution May 

Trigger Asthma in Young Athletes," and 1

'Traffic 

Exhaust Poisons Home Air."4 

Regulators declare "code orange" and ucode 

red" alerts on days when air pollution is pre~ 

dieted to exceed federal health standards. And 

news stories on atr pollution ofcen feature 

Joel Schwartz (jschwartz@aei.org) is a visicing fellow at AEI. 

1150 Seventeenth Street, N.W, Washington, D.C. 20036 

menacing headlmes such as "Air Pollution's 

Threat Proving Worse than Believed," 'rDon't 

Breathe Deeply," ''Study Finds Smog Raises 

Death Rate," "State's Air Is among Nation's 

Most Toxic," and uAstlnna Risk for- Children 

Soars with High Ozone Levels."5 

Headlin_es like these m_ight be warranted if they 

accurately reflected the weight of the scientific 

evidence. But they do not. Through exaggeration, 

omission of contrary evidence, and lack of con~ 

text, regulators, activists, and even many health 

scientists misrepresent the results of air pollution 

health studies and the overall weight of the evi~ 

dence from the research literature. They crear.e 

the appearance that harm from air pollution is 

much greater and more certain than suggested by 

the underlying evidence. 

Jomnalists are the final line of-defense bet~een 

the publlc and the proponents of air pollution 

health scares. Unfortunately, d1e majority of media 

air _pollution health stories are sensationalized 

exaggerations of air pollution's risks. 

Through several case studies, this essay shows 

chac misinformation on air pollution and health is 

a pervasive problem. As a result, public fear of air 

pollution is out of all proportion to the minor risks 

posed by current, historically low air pollution levels. 

202.862.5800 wwv?.aei.org 
Electronic Filing - Receive_d2_Cierk's Office, 08/15/2012 

False Alarm on Asthma and Air Pollution 

Beginning in 1993, the California Air Resources Board 

(CARB) funded the Children's Health Study (CHS). 

Researchers from the University of $outhem Calrfon~ia 

(USC) tracked several thousand California children living in t·we lve communities with air pollution ranging 

from near-background to the worst in the nation. 

At a joint press conference in 2002) the USC 

researchers and CARB managers reported 

In fact, by che time of its release in February 2002, 

the study no longer applied even in che southern California areas where 1t was performed. Eight -hour ozone 

exceedances had declined 55 percent, and one-hour 

exceedances had declmed 78 p~rcent in the interim. By 

2002, communities that were "high-ozone" areas during 

rhe study had become umedium~ozone" areas, for wh1ch 

ozone had no effect on astb_ma risk. 

At the press conference releasing the CHS asthma 

results, d1e chairman of the Air 

that children who played three or more 

team sports were more rhan three times Through exaggeration, 

Resources Board claimed: "This study 

illustrates the need not to retreat but to 

as likely to develop asthma if they lived 

in the si.-x highest,ozone communities in 

the srudy, when compared with the six 

lowest,ozone communir_ies.6 They also 

claimed the study's results applied to cities 

across the United Stares. 

omission of contrary continue pushing forward in our efforts 

to strengd"len air pollution regulations. "ll 

But if anyrhing, the CHS asthma study 

showed that current standards already 

include a large safery margin. Ozone \\'as 

not assocrated with a change in asthma 

risk in the medium,ozone areas of the 

study. Yet these areas exceeded federal 

ozone standards by large margins-an 

average of 41 eight,hour exceedance days 

per year and 17 one~hour exceedances. 

evidence, and lack of 

context, regulators, 

activists, and even 

Ironically, the CHS asthma srudy acrually showed just the opposite. While 

higher ozone \Vas associated with a greater 

risk of developing asthma for children 

who played three or more team sports (8 

percent of children in the study), higher 

ozone was associated \:vith a 30 percent 

lower risk of developing asthma in the full 

sample of children in the study.7 While 

this fact was discussed in a journal article 

on the study, it was not mentioned at the 

press conference.8 

many health scientists 

misrepresent the 

results of air pollution 

health studies and the False information on the CHS asthma 

results was not limited just to CARB officials or USC scientists. Health experts 

from around the country Inisinterpreted 

the study's results. For example, on d1e 

day the study was released, a professor at 

the State University of New York at 

overall weight of the 

evidence from the 

research literature. 

Higher levels of other pollutants, 

including nitrogen dioxide and particulate matter 

(PM10), were also associated with a lower asthma risk9 

Also mentioned in the journal article, but not at the 

press conference, was that when the researchers divided 

the twelve communities in three groups of four (rather 

than two groups of six), the association of ozone with 

increased asthma prevalence in child athletes applied 

only to the four communities in the highest ozone 

group and not to the medium,ozone group. 

The assertion that the study is relevant for other parts 

of the country was also false. The four high-ozone areas 

in the study averaged 89 days per year exceedmg the federal eight,hour ozone standard and 59 days per year 

exceeding the one-hour standard during 1994-1997, the 

years used to assess pollution exposure in the study.lO No 

area of the United States, outside of a few parts of Cali, 

fomia, has ever had ozone levels this high even for a sin, 

gle year, much less for several years running. 

Stony Brook, who has since become the 

American Lung Association's medical director, claimed: 1

This is not just a Southern California problem. There 

are communities across the nation that have high 

ozone."12 According to the Houston Chronicle, Houston 

asthma specialists said the study showed that "Houston 

[should] step up its efforts to implement a state plan to 

reduce ozone_nl3 The director of the pediatric asthma 

program at the University of Califon1ia at Davis claimed 11Sacramento is a very high ozone area, so this [the CHS 

asd1ma study] is going to be very relevant to us."14 

Not only were all of these nominal experts wrong 

about whether the study 1s relevant to actual ozone lev~ls 

in the United States, all of them completely miSsed the 

fact that ozone and other air pollutants were associated 

with an overall lower risk of developing asthma. 

In a recent commentary on air pollution and asthma 

in the ] ournal of the American Medical Association, two 

prominent air pollution health researchers cla'iroed: 
Electronic Filing - Receive_~~ _Clerk's Office, 08/15/2012 

"Some ev1dence suggests rhat air pollution may have 

contributed to the increasing prevalence of asthma.''15 

The "evidence'' they cite is the CHS asthma study. 

Journalists also often act as cheerleaders for air poilu~ 

tion alarmists when reporting on air pollution and 

healch. For example, a recent editorial headline in the 

Sacramento Bee declared "Smog and Asthma: The 

Link-and Threat-Are Real."l6 The Bee's source for 

this claim? Once again, the CHS asthma study. 

Much Ado about Very Little 

The Children's Health Study also suggests that even the 

highest air pollution levels in the nation are having lit~ 

de or no effect on children's lung development. BUt 

once again, the sclentists involved ill the study obscured 

that fact. 

After following more than 1,700 children from ages 

ten to eighteen (years 1993 co 2001), CHS scientists 

reported that there was no association bet\veen ozone 

and lung~function growrh.l7 This is despir.e the fact that 

rhe twelve communities in d1e study ranged from zero 

to more than_ 120 eight~hour ozone exceedance days 

per year, and zero to more than' 70 one~ hour ozone 

exceedance days per year during rhe study period.l8 

Once again, no area outside Cahfo1nia has ever had 

anywhere near this frequency of elevated ozone, even 

for a single year, so we can conclude that ozone is not 

causing any reduction in children's lung capacity. This 

has not stopped environmental groups from claiming 

otherwise. For example, in Impacts of Ozone on Our 

Health, the Carolinas Clean Air Coalition claims: 

"Children have a 10 percent decrease in lung function 

growth when they grmv up in more polluted air."19 

The Children's Health Study also suggests that fine 

particular matter (PM2.s) is causing little or no longterm hann to lung growth. Unlike ozone, PM2.s actually 

was associated with a small effect on lung development. 

Annual-average PM2.s levels ranged from about 6 to 32 

micrograms per cubic meter (pgfm3) in the twelve communities in the study.20 Across this range, PM25 was 

associated with about a 2 percent decrease in forced 

expiratory volume in one second (FEV1) and a 1.3 percent decrease in force vital capacity (FVC), both measures of lung capacity. 

But even this small effect drastically inflates the 

apparent 1mportance of the results. First, no location 

outside of the CHS communities has P!vf25 levels anywhere near 3 2 lJgfm3. In fact, outside California there is 

not a single area \:vith P!\1z.s above 21 pgfm3. And by 

rhe time the study \\'as published in 2004, even the 

highest Plv12.s area in California V·las at 25 )Jg/m3. 

It is also worth noting that the children in rhe CHS 

i'-'ere already ten years old ·when they entered the sn1dy 

in 1993 and had therefore been breathing the evenhigher air pollutant levels extant during the 1980s m 

southetn Califmnia. For example, Riverside averaged 

about 48 flg/ml PM1.s during the 1980s, or about 50 

percent greater than the highest Ph-12_5 level measured 

during ti1e CHS years21 If it were really these higher 

1980s PM25 levels that caused the lung-function 

declines, dten the current worst P1.1z.5 in the country 

would be causing about a 1 percent decrease in FEY 1 

and a 0.5 percent decrease in FVC. Thus) taking the 

CHS results at face value, ozone is having no effect on 

children's lung development anywhere in the United 

States. Plv12.

5 is having virtually no effect. 

Nevertheless, the USC researchers' press release on 

the study created an unwananted appearance of serious 

harm. Titled "Smog May Cause Lifelong Lung Deficits," 

the press release asserted: "By age 18, the lungs of many 

children who gro\V up in smoggy areas are underdeveloped and will likely never recover."22 The National 

Institutes of Health (NIH) also misled the public about 

the study's findings and relevance. The director of the 

National lnstitme of Environmental Health Sciences 

claimed the study ushows that current levels of air pollution have adverse effects on lung development in 

children."23 

Furthermore, although the study is relevant only co a 

few areas of California with uniquely high air pollution 

levels, by asserting that it applies co all "smoggy areas" 

and to "cw-rent levels of air pollution," NIH and USC 

created the false impression that the study applies to 

much of che United States. 

The scientists were able to create these false impres~ 

sions, because the journal article on the study, which 

was published in the prestigious New England]oumal of 

Medicine (NEJM), does not explicitly reveal the magnitude of the percentage change in children's lung capacity. Instead, readers have to be vigilant enough to realize 

that ti1e percentage change can be calculated by combining infonnation found in three different places in 

the arcicle. 24 It is odd that a study whose main outcome 

measure is changes in lung capacity never actually staces 

the percentage change explicicly. 

The researchers reported a different outcome meas~ 

ure in their NEJM paper: the percent of children in 
Electronic Filing - Received, Clerk's Office, 08/15/2012 - 4-

each community with a lung capacity of less than 80 

percent of the "predicted" value for the1r age.25 Betvveen 

the least and most polluted communities) PM2_5 was 

associated with nearly a five-fold increase in this percentage, from about 1.6 percent of children in the 

lowes_r-PM2_5 community, up to about 7.9 percent in the 

highest-PM25 commumty. 

Th_is seems like a large effect, but lt is not. \Vhat is 

going on is that the 2 percent average decline in lung 

function in the highest-PM2_5 community relative to the 

lowest meant a shift of some children who were at, say, 

80 or 81 percent "of "predicted" lung 

not requiring that 1ts article on the study explicitly state 

the percentage change in lung capacity associated with 

air pollution. 

Monkey Business 

A University of California at Davis press release begins 

"Primate Research Shows Link bet\veen Ozone Pollution, Asthma.".3° The press release goes on to claim the 

ozone exposures in the study "mimic the effect of exposure to occasional ozone smog-for example as it occurs 

in the Sacrament.o area." 

capacity for their age, down to maybe 78 

or 79 percent. Because lung-capacicy 

scores have a bell-curve distribution, and 

few children have low lung capacity, there 

are many more children slightly above 80 

percent than slightly below SO percent. A 

small shift in average lung~capaciry scores 

therefore results in a large change in the 

fraction of children scoring below a given 

cutoffleveJ.26 

Scientists, regulators, In fact, the ozone exposures in the 

study were far higher d,an the actual 

ozone levels in American air-including 

the air in Sacramento. The monkeys 

\vere exposed to 0.5 parts per million 

(ppm) ozone for eighc hours a day for five 

days in a row, followed by nine days of 

clean air. This cycle was repeated eight 

times. To give you an idea of the magnitude of these ozone exposures, during the 

iast thirty years only one site in the U.S. 

has ever exceeded 0.5 ppm mane for 

even one hour, and that happened in 

1976. Today, the worsr site in the United 

States never reaches even 0.25 ppm for 

one hour, and the average site never 

reaches 0.11 ppm. 

and environmentalists 

have ignored these 

weaknesses and 

continue to make 

believe these spurious 

Reporting that even the highest air pol~ 

lution leyels in the cmmtry were associated with only a 2 percent decrease in 

lung capacity would not have caused 

much alarm. This probably explains why 

that number is nowhere to be fmmd in d1e 

NEJM. report or the press releases on it. 

statistical correlations 

are telling us 

something real about 

the effects of low-level 

air pollution. 

NIH took advantage of this omission 

in its press release, which begins: "Children who live in 

polluted communities are five times more likely to have 

clinically low lung function-less chan SO percent of 

the lung function expected for their age."27 Note how 

this scatement creates the appearance Of a decline of 

more than 20 percent m average lung function by lead~ 

ing readers to tacitly make the incorrect assumption 

that all children would be at 100 percent if there were 

no air pollution. 

This is exactly tl1e mistake environmentalists have 

made in promoting the study. For example, the American 

Lung Association's (ALA) State of the Air 2005 report 

claims the "average drop in lung function was 20 percent 

below what was expected for the child's age."28 The 

Carolinas Clean Air Coalition made a similar error.29 

The ALA clearly did not understand the srudy's 

results. But NIH and rhe USC researchers created tbe 

confusion. The editors and peer reviewers at the New 

England] ournal of Medicine also bear responsibilicy for 

Despite che real-world irrelevance of 

this study, environmental acnvists cite it to support 

claims that ozone is causing pennanent lung damage in 

people. For example, under the headline "Lung Devel~ 

opment of Young Monkeys Drastically Changed when 

Exposed to Ozone Pollution," the American Lung Association concludes, "This study presents data suggesting 

that the changes caused by ozone pollution are longlasting, and maybe even pennanent."31 

Some reporters also failed to compare ozone levels 

in the study to real~world ozone levels. For example, 

according to the l\1odesto Bee, "Monkeys were exposed 

to air contaminated with ozone, mimicking the smog 

in the [Central] valley."32 But even more nuanced sto~ 

ries still took an alarmist tack. For example, the Sac-ra~ 

menta Bee explicitly compared ozone levels in the 

Sacramento region with the far higher ozone levels 

used in the study.33 But you have to go halhvay into 

the 1,100-word story to find this infonnation. The story's headline-uStudy Suggests Asthma Culprit; Young 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

- 5 -

Lungs Exposed to Ozone Seem lvfore Prone to Problems 

with Developmene'-leaves no doubt that readers are 

supposed to conclude that ozone is causing Americans 

to develop asthma. 

Of Mice and Men 

By far the most serious health claim about air pollution 

is that it kills tens of thousan_ds of Americans each year, 

mainly due to expo~ure to PM2_5· There is no question 

that high levels of air pollution can hlL About 4,000 

Londoners died dunng the infamous five~day "London 

Fog" of December 1952, when sooc and sulfur dioxide 

soared to levels tens of times greater than the highest 

levels experienced in developed countries today, and 

visibility dropped to less than 20 feet34 

However, current fears center on whether today's 

comparatively low levels of air pollution are also deadly. 

An embarrassment for proponents of low-level air pollution as a cause of death is that the evidence is almost 

solely circumstantial, being based on sratiscical studies 

reporting small correlations between long- or short-term 

air pollution levels an_d risk of dying. These "observational" studies are not based ·on randomized trials, but on 

non~random data that inherently suffer from confound~ 

ing by non~pollution factors w1rh much larger effects on 

health than the purported effects of air pollution' 

Observational studies could be caken more seriously 

if they were supported by evidence -fi:om randomized, 

controlled studies that eliminate the possibility of confounding by non-pollution factors. Such studies cannot, of course, be done with people, but they can be 

done with animals. However, researchers have been 

unable to kill animals with air pollution at levels anywhere near as low as the levels found in ambient air. 

As a recent review of particulate matter toxicology 

concluded: 

It remains the case that no fom1 of ambient PMother than viruses, bacteria, and biochemical 

antigens-has been shown) experimentally or 

clinically, to cause disease or death at concentra, 

tions remotely close to U.S. ambient levels.35 

This seemingly changed in December 2005 when 

the Journal of the Ame1ican Medical Association UAMA) 

published the results of a study that claimed PM2.s at 

current ambient levels is increasing Americans' risk of 

developing heart disease. The srudy exposed mice to 

85 pg/m3 of PM25 concentrated fi.-om ambient air for six 

hours per day for six months, or about one-fourth of a 

typical mouse life span.36 

Mice fed a high-fat diet and exposed to PMz.s had 

more than a 50 percent greater rate of atherosclerosis 

(as measured by arterial plaque area) and other signs of 

heart disease, \vhen compared with a conrrol group that 

was fed a high-fat diet, but not exposed to PMz.s· PM2.5 

was associated with greater atherosclerosis in mice on a 

low-fat diet as well, but the effect was not statistically 

significant. 

NIH highlighted the study with a press release that 

begin_s: "Test results with laboratory mice show a direct 

cause,and-effect link between exposure to fine particle 

air pollution and the development of atherosclerosis ... 

[The study] may explain why people who live in highly 

polluted areas have a higher risk of heart d1sease."37 

The study caused a minor media sensation, ·with both 

journalists and health ex-perts claiming the srudy pro~ 

vides strong evidence that Pl\125 is causing serious harm 

to human beings)S 

Despite the enthusiastic reception, there is much less 

here than meets the eye. The mice used m the study 

were genetically engineered in ways d1.at make them 

nnrepresentative of even real-world mice, much less of 

humans. The mice were designed to lack the gene for 

apolipoprotein E (ApoE), a key substance for fat and 

cholesterol metabolism. As a result, these ApoE "knockout" mice have blood cholesterol levels 5 to 6 times 

greater than normal mice ·when fed regular rat chow. 

ApoE knockout mice have 14 times the cholesterol of 

normal mice when both are fed a high, fat diet.39 

These are stupendous cholesterol levels. For compari~ 

son, medical authorities define ;'high cholesterol" as a 

serum cholesterol level greater than 240 milligrams per 

deciliter (mg/dl), which is about 20 percent greater than 

the average cholesterol level in Amelican men.40 Only 

one in SO Amencan men exceeds 1.5 times the U.S. 

average, and only one in 500 exceeds twice the average.41 

The very reason for using such grossly unrealistic 

mice to study PM25 is that PM2.s does not kill regular 

mice or other anhnals at PJ\1 concentrations relevant 

to real,world human exposures. For that matter, PM2.5 

did not actually kill the high-cholesterol mtce in the 

study either. 

NIH downplayed the vast gulf between the generically engmeered mice and nonnal mice, stating only 

that they were ugenetically programmed to develop ath~ 

erosclerosis at a higher-than~normal rate." This is a bit 
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like doing a study on people ·who weigh 500 pounds and 

refening to them merely as "ove1weight.n 

If you build a house out of cards, you would expect 

even a gentle breeze to knock it down. But rhis does not 

tell you much about rhe ability of a real house to withstand a gentle breeze. Likewise, if you design an artificial 

mouse that cannot regulate its fat or cholesterol levels, it 

is not smprising that even a mmor environmental insult 

can cause it some health problems. But this does not tell 

you much about the effects oflow~level air pollution 

levels on regular mice or on people. 

Unfortunately, news artie les on th_e study failed to 

provide the context that \vould show that study has little real,world relevance. A Nexis search turned up ten 

news reports on the study. Seven did not even mention 

that the mice had been genetically engineered, leaving 

the impression that real,world PM2.S levels caused heart 

disease in normal mice. 

Three other news outlets followed NIH's lead, creating the impression that the mice in the study were 

merely analogous to people with a higher,rhan~average 

risk of heart drsease. For example, according ro the Los 

Angeles Times, the mice were "bred to be susceptible to 

developing heart disease."42 

NIH and the study authors also misled reporters 

about the relevance of the PMz.s doses to real~world 

PM2_5 levels. According to NIH, "The fine panicle 

IPM2.5] concentrations used in the study were well 

withm the range of concentrations found in the air 

around major mecropolitan areas.'' The press release also 

quotes one of rhe study's authors saying that ';the aver~ 

age exposure over the course of the study was 15 micro, 

grams per cubic meter, which is typical of the particle 

concentrations that urban area residents would be 

exposed to, and well below the federal air quality srandard of 65 )lg/m3 over a 24,hour period.ll43 

In fact, the PMz.s levels in the study were nothing 

like real-world PM2.5 levels. The mice were exposed to 

PM2.5 at 85 J.lgfm3 for six hours in a row during five days 

of each week, and filtered air the rest of the time. Over 

the six,month study period, this does indeed average 

out to about 15 )lg/m3, the level of the federal PM2.

5 

annual standard. But in the real world, areas that aver, 

age 15 )lg/m3 ofPM2.5 over a year rarely approach shortterm PM25 levels of 85 )lg/ml_ 

For example, in the mouse study, the mice spent the 

equivalent of 1,560 hours per year breathing 85 )lg/mJ 

PM2.5 (30 hours per week times 52 weeks per year). 

In contrast, Modesto California averaged 16 Jlgfm3 

of Plv1z.5 over the past year, but spent only 80 hours 

at 85 )lg/m3 or above. 44 Furthermore, 40 percent of 

those high,PM25 hours occurred between 11 p.m. and 

6 a.m., when most people are in bed. There were only 

420 hours when Modesto exceeded even 50 pgfm3 

ofPM2.s· 

Even areas with the highest PM 2.5 levels in the 

country have far fewer hours of high Plv12.s than were 

uSed in the mouse study. For example, Riverside Califor, 

nia averaged 27 ~1g/m3 PM25 over the past year, but had 

only 135 hours at or above 85 )lg/m3, and 1,055 hours 

above 50 )lg/m3. 

Health effects depend not only on th_e average dose, 

but on the acute dose. For example, you could take 2 

aspirins 4 times per day, or you could take 8 all at once 

each day. Erther way, your average dose is 8 aspirins per 

day. But you are more likely to suffer ill effects if you 

take the asprrins all at once. The mice received an 

analogously unrealisric daily PM2.5 exposure. NIH and 

the scientists involved in the scudy then created the 

false appearance that this unrealistic exposure schedule 

has some relevance to the real world. 

There is nothing wrong wirh the JA'v!A mouse study 

in principle. It shows that when you take a mouse spe, 

cially designed to have unrealistically stupendous cho, 

lesterollevels, feed it a high-fat diet, and repeatedly 

expose it to unrealistiCally high acute levels of PM2_5, 

that PM 25 increases the extent of heart disease. The 

problem arose when the study's proponents cla1med that 

this has something to do with PM2.5 risks faced by 

human beings. 

You can now find a summary of the scudy on-NIH's 

website. Its title? "Particulate Air Pollution and a High 

Fat D1eto A Potentially Deadly Combination."45 

Sins of Omission 

At the March meeting of the California Air Resources 

Board, staff members gave a detailed presentation on 

jerrett eta!. (2005)-a new epidemiological study of 

the Los Angeles region that reported a stronger link 

between PM2.5 and mortality than suggested m previous 

research regulators have used to support tougher PM2.s 

standards.46 What CARE's staff did not tell its board is 

that right around the same trme that Jerret.[ et al. was 

published, another study of PM25 rioks in California by 

Enstrom (2005) concluded that PM2.

5 was having no 

effect on mortality.47 Several California papers, including the Los Angeles Times, covered the alarming findings 
Electronic Filing- Received, Clerk's Office, 08/15/2012 - 7-

ofJerretc ec al. But none covered che bemgn results 

reponed by Enstrom. 

This is a typical partetn. Studies that report harm 

from air pollution receive a great deal of attention from 

regulators, environmentaliscs, and journalists. Studies 

finding no ha1m from air pollution are ignored. As a 

result, claims o~ hann from air pollution appear more 

consistent and robust than suggested by the actual 

weight of the e1•idence. 

each year. 54 The Bush administration, a constant target 

of environmental groups for supposedly "gutting" power 

plant pollution requirements, last year adopced the 

Clean Air lntersrate Rule (CAJR).55 CAIR requires 

that power plants reduce their sulfur dioxide emissions 

by more than 70 percent below cun·ent levels'.56 Some 

sulfur dioxide is converted to ammonium sulfate in the 

atmosphere) and this is the main fonn of P!viz.s from 

power plants. EPA claims these PM1.s 

The American Lung Association's 

website includes an area called Medical 

Jomnal Watch, which summarizes hun~ 

dreds of air pollution health studres. 48 But 

the site omits studies that do nm report 

any harm from air pollution. For example, the site does not include any studies 

by Fred Lipfert, Suresh Moolgavkar, 

Richard Smith, Gary Koop, William 

Keatinge, or James Enscrom-all of 

whom have provided evidence againsr. a 

connection between lm:~,r-level air pollution and risk of death.49 

Environmental groups 

want to increase 

reductions will prevent 17,000 premature 

deaths each year.57 

There is just one problem: anunonium 

sulfate is not toxic, even at levels many 

times d1.ose ever found in ambient air. 58 In 

fact, ammonium sulfate is used as an inert 

control-that is, a compound not expected 

to have any health effects-in studies of 

the health effects of ac1dic aerosols59 If 

The ALA also excludes specific studies 

and portions of srudies that fail to find any 

harm from air pollution. For e..xample, 

Medical] ournal Watch does not mention 

Gong et al. (2003) and Holgate ec al. 

(2003 ), which found hcrle or no adverse 

health effects in human volunteers who 

breathed high levels of PM2.5 and diesel 

sooc, respectively. 50 The ALA does summarize the CHS findings on children's 

lung capacity discussed earl1er, but does 

not mention that the study found that 

even the highesc ozone levels in the 

country had no effect on lung growth. 

Three studies have used CHS dara to 

assess whether ozone is associated with 

increases in school absences. One study 

support for ever more 

stringent regulations, 

maintain and enhance 

their control over 

other people's lives, 

and bring in the 

donations that support 

their activism. 

Regulators want to 

show the success of 

their efforts to reduce 

air pollution, but they 

also want to justify the 

need to preserve or 

expand their powers 

and budgets. 

ammonium sulfate is not toxic, then the 

campaign againsr PM25 from power plants 

is based on a false premise. 

Last year CARB adopted a tougher 

ozone standard for California.60 To justify 

the tougher standard, CARB prepared a 

detailed report summarizing ozone health 

effects research. The report analyzes hundreds of healch studies in nearly 1,000 

pages, but fails to mention a study reporting that higher ozone was associated with a 

lower rate of hospital visits in California's 

Central Valley.6l CARB was cerrainly 

aware of the existence of th1s study, 

because CARB funded and published it. 

EPA also failed to mention the study in its 

latest review of the federal ozone standard.62 

EPA based its annual PM2.s standard 

mainly on the American Cancer Society 

(ACS) study, which followed more rl'an 

reported an increase. 51 Two reported no effect. 52 The 

ALA mentions only the first study on Medical journal 

Watch. CARB likewise cites only the first study in its 

review of California's ozone standard. 53 

500,000 Americans in fifty cities from 1982 

to 1989 and looked for cmTelations between PM2_5 levels 

and risk of death. 63 The most recent ACS report covered 

the period from 1982 to 1998 and reported that each 

10 ~tg/m3 increase in long-term PM2.s levels is associCoal-fired power plants have been one of environ- ated with a 4 percent increase in risk of death.64 

mentalists' premier targets during the last several years. In 

reports such as Danger in the Air; Death, Disease and Dirty 

Power; Power to Kill; Children at Risk; and many more, 

environmental groups claim that particulate pollution 

from power plants is killing thousands of Americans 

The validity of epidemiological studies, such as the 

ACS study, depends on rhe assumption that correlations 

between air pollution and health outcomes represent 

genuine causal relationships. The implicit assumption is 

that after researchers have controlled for non-pollution 
Electronic Filing - Received, Clerk's Office, 08/15/2012 - 8 -

health factors 111.:e income or smoking, any residual cor~ 

relation between air pollunon and health represents a 

genuine causal linkage. Experience has shown that this 

assumption is false. 

For example, a reanalysis of the ACS data showed 

that the apparent PM2smortality link was spurious. 

According to sensitivity analyses of the ACS data, 

PMz.s apparently kills men, but not women; those with 

no more than a high school degree, but not those with 

at least some college; and those who said they \Vere 

moderately active, but not the very active or the sedentary65 Results like these are biologically implausible and 

suggest a failure to adequately control for confounding 

by non-pollution factors. 

When migration rates into and out of various dries 

over time were added to the statiscical model relating 

PM2.S and risk of deach, che apparent effect of PM2.5 

disappeared.66 Cities that losr population during the 

1980s~l\1idwest "rust belf' cities-also had higher 

Pl\12.5 levels. People left these cities, ·which were in eco~ 

nomic decline 1 in search of work in more economically 

dynamic parts of the country. But people who work and 

have the wherewithal to migrate also tend to be healthier than the average person. Hence, what appeared to 

be an effect of PM25 \Vas actually the result of differen~ 

rial migracion. Migration \\'as just one of several con~ 

founding factors that diminished or erased th_e apparent 

harm from PM2_5, but thar were not accounted for by 

the ACS researchers. 

This problem of spurious air pollution nsk estimates 

is not .limited ro the ACS study, but is endemic co air 

pollution epidemiology and to epidemiology in gen~ 

eral.67 Nevertheless, scientists, regulators, and environ~ 

mentalists have ignored these weaknesses and continue 

to make believe these spurious statisrical correlations 

are telling us someching real about the effects of lowlevel air pollution. 

The Politics of Air Pollution Health Science 

Most public mformation on air pollution and health 

comes from environmental activists, regulators, and 

health researchers. As these case studies show, their 

claims of harm from cunent, historically low air pollu~ 

tion levels are at besc exaggerattons and at worst fabri~ 

cations. The result is unwan-anted public fear, and 

continued support for ever more costly regulatory 

requirements that deliver little or no benefit in 

exchange for their high costs. 

Regulators, environmentalists, and scientists enjoy 

substantial credibility with the public and che press. But 

like other interest groups, therr goals often do not coin~ 

Cide with the interests of the vast majority of Ameri~ 

cans. Environmental groups want to increase support for 

ever more stringent regulations, maintain and enhance 

their control over other people's lives, and bring in the 

donations that support their activism. Regula mrs want 

to show the success of their efforts to reduce air pollu~ 

non, but d1ey also want to justify the need to preserve 

or expand their powers and budgets. Maintaining a eli~ 

mate of crisis and pessimism meets d1ese institutional 

' goals, but at the expense of encouraging people to exag~ 

gerate the risks they face. 

While it is not surprising that activists and regulators 

exaggerate air pollution risks, they \\'ould not be taken 

as seriously wirhout scientific authority co back them 

up. The credibllit:y of science and scientists tlows from 

the power of scientific methods to uncover truths about 

the world, and from the perceived objectivity of scien~ 

tisrs themselves. As the case studies above show, aust in 

scientific authority is often misplaced. 

Scientific and medical research does have checks 

and balances that are absent from more explicitly 

polirical endeavors. Environmental health research 

nevertheless suffers from its own set of pressures that 

militate against evenhanded inquiry and dispassionace 

analysis and presentation of evidence. Studies that 

report harm from air pollution are more likely to be 

published than studies that do not. Regulacory agen~ 

cies, whose power and budgets depend on the perception that air pollution is a serious health problem1 are 

also major funders of the research intended to demonstrate the severity of the problem. Scientists who 

believe air pollut10n is a serious health threat and who 

report larger health effects are more likely to attract 

research funding. It is not a big leap to conclude that 

there is a great deal of selection bias in who does environmental health research, what questions they ask, 

and how they report their resulcs. 

journalists should be acting as a check on air pollution misinformation, but they are not. Media outlets 

face their mvn pressures to sensationalize stmies. Good 

news does not sell newspapers or attract viewers. As a 

result, journalists and editors are more likely to cover 

studies claiming harm from air pollution, and to pass 

along these claims with little or no critical review. 

True, few journalists have the expertise to evaluate 

the r.echnical merits of specific studies. But continuing 
Electronic Filing - Received, Clerk's Office, 08/15/2012 - 9 -

to rely on scientific authoricy will only petVetuate the 

problem of risk exaggeration. Among the major 

providers of public information on environmental risks, 

investigative reporters are in the best position to assess 

hmv rhe political economy of environmental health 

research affects the production and portrayal of sciennfic evidence. It would be a breach of fresh air if journalists and editors took up this challenge. 

AEI editor Scott R. Palmer worhed tvith Mr. Schwart:;. w edit and 

produce thrs Environmental Policy Oudook. 

Notes 

1. The Em..n'romnental Deficic: Surve:y on American Attitudes 

on the Ent'ironment (New Haven, Cf: Yale Center for Environmental Law and Pohcy, May 2004), available a[ WV.lw.yale.edu/ 

forescry/downloads/yale_poll_globalwanning.pdf. For slm1lar 

results in state surveys, see Recent Texas Statewide Survey Findings 

Prepared for Public Citizen and the Seed Coalition (Alexandna,-

VA: American Viewpoint, 2002); New York Conservation 

Education FU11.d, Key Findings of a State'U!ide Survey Of New York 

State Residents on Environmental Issues (New York: New York 

League of Conservation Voters, 2001 ); Sprawl: New ]erseyans 

Disbke the Problerns, and the Solutions (New Brunswick, NJ: 

Newark Star~Ledger/Eagleton,Rutgers, September 29, 2002), 

available at http://slerp.rutgers.edu/retrieve.php?id= 138~6; and 

M. Baldassare, PPIC Sratewzde Survey: Special Survey on Califor, 

nians and the Environment (San Francisco: Public Policy Insri, 

tute of California, july 2004 ). 

2. Water Pollution Tops Americans' Environmenr.al Concerns 

(Washington, D.C Gallup Poll, April21, 2006), available ar 

http//poll.gallup.com/content/Defau lt.aspx ?ct ~ 22492& 

VERSION~p. 

3. Death, Disease and Dirty Power: Mortality and Health 

Damage Due to Air Pollution from Power Plants (Boston: 

Clean Air Task Force, October 2000), available at www. 

cleartheair.org/fctct/morrality/mortalitylowres.pdf; Our Children at Risk ("W,!ashmgton, D.C.: Natural Resources Defense 

Council, November 1997), available at W\Vw.mdc.org/ 

heal th/hds/ocar/ocarlnx.asp; Children at Risk: How Air Pol/.u~ 

tion fmm Power Plants Threatens the Health of America's Children (Boston: Physicians for Social Responsibility, May 2002), 

available at wv.rv,r.cleartheair.org/fact/children/ children_at_ 

risk. pdf; Danger in the Air (WashingtOn, D.C.: Public Inter, 

est Research Group [PIRG], August 2003 ); Plagued by Pollution (Washington, D.C PIRG, January 2006), available at 

http://cleanairnow.org/pdfs/plaugedbypollutron.pdf; and 

Highway Health Hazards (Washington, D.C.: Sierra Club, 

July 2004 ), available ac 'vww.sierradub.org/sprawl/repott04_ 

highwayhealth/report.pdf. 

4. Johns Hopkms School of Public Health News Center, 

"Traffic Exhaust Poisons Home Air," nev.:s release, August 31, 

1999. available at v-.rww.jhsph.edu/PublicHealtlu"-..Jews/Pre~_ 

Releases/PR_l999/traffic_e.xhamt.hcml; A. Di Rado, ''USC 

Study Shows Air Pollutron May Trigger Asthma in Young 

Athletes," news release, February 1, 2002, available at li'I'VI'\\'.usc. 

edu/hsc/info/pr/1 vol8/803/air.html; A. Di Rado, "Smog May 

Cause Ltfelong Lung Deflcits," Universrty of Southem Cahfor, 

nia, September 8, 2004, available at Vt"l.\w.usc.edu/uscnews/ 

scories/10495.html; and Nationallnstitures of Health (NIH), 

"Link Screngrhened between Lung Cancer, Heart Deachs and 

Tiny Particles of Soot," March .5, 2002, available at www.niehs. 

nih.gov/oc/news/lchltnk.htm. 

5. T. Avril, "Air Pollution's 11wear Proving Worse than 

Believed," Philadelphia Inqwrer, November 17, 2004; M. Cone, 

"State's Air Is among Nation's Most Toxic," Los Angeles Times, 

March 22, 2006, a·vadable at www.latimes.com/news/ 

printedition/la,me-cancer22mar22, 1, 708733 6.story; M. Cone, 

"Study Finds Smog Raises Death Rate," Los Angeles Times, 

November 17, 2004; T. Freemantle, ''Asthma Risk for Children 

Soars wich High Ozone Levels-Study," Houston Chronicle, 

February 1, 2002; and T Webber, "Don't Breathe Deeply," 

Indianapolis Star, june 23, 2005. 

6. California Air Resources Board, "Study Links Air Poilu, 

tlon and As1:hma," news release, January 31, 2002, avallable at 

wv.w.arb.ca.gov/nev.rsrel]nr0131 02.htm. 

7. TI1e risk of developing asthma was 30 percent lower based 

on one,hour ozone levels and was statistically s1gnificant. Asthma 

1isk was 20 percen~ lower based on eight,hour ozone levels and 

was just a hair shan of statistical significance. (The cop of rhe 

9 5 percent confidence interval ±Or relative risk was 1.0. Anything 

less than that would have been statistically significant.) 

8. The journal article is. R. McConnell, K T Berhane, F. 

Gilliland e1: al., "Asthma in Exercising Children Exposed to 

Ozoneo A Cohort Study," Lancer 359 (2002)o 386--91. 

9. Once again the risk was 20 percent lO\:ver and was just 

barely short of statistical significance. 

10. Pollution monitoring data from the Children's Health 

Study were provided by CARB's staff. 

11. California Air Resources Board, "Study Links Air Pollu, 

tion and Asthma," news release, January 31, 2002, available at 

wv.•":"r .arb.ca.gov /newsrel/nr0131 02.htm. 

12. Dr. No!rnan Edelman, quoted inS. Borenstein, "Air 

Pollution Is a Cause of Asthma, Study Contends," Philadelphia 

Inquirer, February 1, 2002. 

13. T. Freemamle, "Asthma Risk for Children Soars with 

High Ozone Levels-Study." 
Electronic Filing - Received, Clerk's Office, 08/15/2012 - 10-

14. In fact, even the worst areas of Sacramenro never aver, 

age more than a few days per year exceeding the one, hour 

ozone standard and 20 or so days per year exceedtng the 

eight, hour standard--ozone levels typical of the ''medium, 

ozone" CHS communities, in which there \Vas n.o relationship 

between air pollution and asthma risk. Dr. Jesse Joad, quored in 

C. Bowman, "Asthma's Tall: A New Smdy Links Chtldren's 

Sporrs Activ1ties m Smoggy Areas to rhe Illness," Sacramento 

Bee, February 1, 2002. 

15. G. D. Thurston an_d D. V. Bates, "Air Pollution as an 

Underappreciated Cause of Asthma Symptoms," ]ou:rnal of the 

American Medical Association 290 (2003 )o 1915-17. 

16. "Smog and Asthma: The Link-and Threat-Are 

Real," Sacramento Bee, May 6, 2003. 

17. W.]. Gauderrnan, E. A vol, F. Gilliland et al., "The 

Effect of Air Pollution on Lung Development from 10 to 18 

Years of Age," New England]oumal of Medicine 351 (2004): 

1057-67. 

18. The CHS study set up special-purpose monitors co 

measure pollution levels in the communities where the 

study was performed. CARB staff provided data from these 

monitors. 

19. Impacts of Ozone on Our Health (Charlotte, NC Carolinas Clean Atr Coalition, undated), available at http://003af56. 

nersolliost.com/air_basics_ozone_impact.htm. 

20. Based on research by CARB staff, these values have 

been adjusted upward by 13.6 percent to make "!:hem comparable wlrh PM25 levels determined by the Federal Reference 

Method, which has been used nationwide since 1999 for 

der.erminlng compliance with federal PM2.5 standards. SeeN. 

Motallebi, J. Taylor, A. Clincon, B. E. Croes et al., "Particu~ 

late Mateer rp California: Part 1-lntercomparison of Several 

PM2.

5, PM 10~I.5• and PM10 Monitoring Net\>.rorks," .Journal of 

rhe Air & Waste Management Association 53 (2003): 1.509-16. 

21. Based on lPN data for Riverside collected in the early 

1980s, and PM1.s data collected by Ci\RB in 1988 and 1989 

and retrieved from CARB's 2006 Air Pollution Data CD, 

~.rww.arb.ca.gov/aqd/aqdcd/aqdcd.htm. Once again_, I have corrected these values for the change in measurement methods. 

22. Di Rado, "Smog May Cause Lifelong Lung Deficits." 

23. Dr. Kenneth Olden_, quoted in NIH, "New Research 

Shows Air Pollution Can Reduce Children's Lung Ftmction," 

news release, September 9, 2004, www.nih.gov/news/pr/ 

sep2004/nieh.s-08a.htm. 

24. Here's how: First, note from table-3 of the NE]M article 

that PM2_5 was associated with a 79.7 tmllilirer (ml) reduction 

in FEV1 between the least and most polluted community. Then 

from table 2, note that at eighteen years of age average FEV1 

was 3,332 ml for girls and 4,464 ml for boys. Given that d1ere 

were 876 giTls and 883 boys in the srudy (p. 1,059, column 1), 

the weighted average FEV 1 for the smdy population was 3,900 

ml. The percentage decline is then 79.7/3,900 = 0.02 or 2 per~ 

cent. A similar calculation can be done to show that the aver~ 

age declin_e in FVC was 1..3 percent. Gauderman, Avol, 

Gilliland et al., ''The Effect of Air Pollution on Lung Develop~ 

mentfrom 10 to-18 Years of Age." 

25. The researchers used a regresston model to create this 

"predicted" value. 

26. This is assurnmg the "predicted" lung capacity values are 

valid. The NEJM paper provides few details on the model or 

the underlying distribution of lung~funcrion test scores by community. Thus, another problem with this outcome measLITe is 

that it depends on something that was not actually measured! 

27. NIH, "New Research Shows Air Pollution Can Reduce 

Chtldten's Lung Function." 

28. Amen can Lung Association, State of rh£ Air 2005 

(Washington, D.C.: May 2005), 60. 

29. N. Bryant, "What Air Quality Problem?" Charlotre 

Observer, September 1, 2005, available at \\'\Vw.charlotte.corn/ 

mld/charlotte/news/opinion/12530112.htm1BMIDS= 13194. 

30. A. Fell, ''Primate Research Shows Lmk between Ozone 

Pollution, Asthma," U.C.~Davis news release, October 13, 2000, 

available at 'N\vw.dateline.ucdavis.edu/101300/DL_asthma.htmL 

31. Recent Scientific Finclings on Healrh Effects of Air PoUutwn 

and Diesel Exhaust (Oakland, CA: American Ltmg Association 

of Califomia, 2003 ), available a( v;vlw.californialung.org/ 

spotllght/c leanair03 _research.html. 

32. Melanie T um.er, "Kids Focus of Air Quality Study 

Researcher Looking for Link Becween. Ozone, Asthma in 

Yauch," Modesto Bee, May 11, 2001. 

33. Edie Lau, "Study Suggests Asthma Culpri(; Young Lungs 

Exposed to Ozone Seem More Prone to Problems with Devel~ 

oproent," Sacramento Bee, April15, 2001. 

34.!. M. Goklany, Clearing the hro The Real Stmy of the War 

on Air PoUution (Washington, D.C.: Cato Institute, 1999). 

35. L. C. Green and S. R. Armstrong, "Particulate Maner in 

Amblent Air and Mortality: Toxlcologic Perspec(ives," Regula.~ 

tory Toxicology and Phannacology 38 (2003 ): 326-35. 

36. Q. Sun, A. Wang, X. Jm et al., "Long~ Term A1r Pollu~ 

tion Exposure and Acceleration of Atherosclerosis and Vascu~ 

lar Inflammation in an Animal Model," ]oumal of the American 

Medical Association 294 (2005)o 3003-10. 

37. NIH, "Air Pollution, High~ Fat Diet Cause Atherosclero~ 

sis in Laboratory Mice," news release, December 22, 2005, 

available at www.nih.gov/news/pr/dec2005/nieh.s~22.htm. 

38. Newspapers caii)'mg articles-on the study included the 

Los Angeles Times, Houston Chronicle, Philadelphia Inquirer, and 

several others. 
Electronic Filing- Received, Clerk's Office, 08/15/2012 - II -

39. A. S. Plump, J.D. Smith, T. Hayek et al., "Severe 

HypeTCholesterolemia and Atherosclerosts m Apolipoprotem 

E~Deficiem Mice Created by Homologous Recombination in 

Es Cells," CeU 71 (1992): 34.3-53; and S. H. Zhang, R. L. Reddick, J. A. Piedrahita et al., "Spontaneous Hypercholes~ 

terolemia and Arterial Lesions m Mice Lacking Apohpoprotein 

E," Science 258 (1992): 468-71. 

40. See table 70 in National Cemer for Health Stanstics, 

Health, United States, 2005 (Hyattsville, MD: U.S. Department 

of Health and Human Services, 2005), available at 

wv\'w.cdc.gov/nchs/data;hus/hus05.pdf.:;o-070. 

41. Based on National Health and Nutmion Exarnin.ation 

Survey (NHANES) daca on 4,090 adult men collected from 

1999-2002. Data were dov,nloaded from Vl\.Vw.cdc.gov/nchs/ 

nhanes.hcm. 

42. M. Bustillo and M. Cone, "EPA Issues New Plan to 

Limit Soot; Critics Say the Revised Standard Is Too \Veak 

to Properly Prm:ect che Pubhc from Health Dangers Caused 

by Breathing Particulates," Los Angeles Times, December 21, 

2005. 

43. NIH, "Air Pollution, High~ Fat Diet Cause Atherosclero~ 

sis in Laboratory Mice." 

44. Hourly PM2 5 data were dm:~,•nloaded from CARE at 

W\Vw.arb.ca.gov/aqrnis2/paqdselect.php. 

45. M. Lippmann, L C. Chen, and S. Rajagopalan, "Par~ 

riculate Air Pollution and a High Fat Diet: A Potentially 

Deadly Combination," NIH, available ac \'>'Ww.mehs.nih. 

gov / dert /p rofi les/h ilt tes/2 00 5/ p rn ~diet. htm. 

46. Stronger Relationship bett{}een Particulate Matter (PM) and 

Premature Death (Sacramento: California Air Resources Board, 

March 23, 2006), available ac ftp://ftp.arb.ca.gov/carbis/board/ 

books/2006/032306/06~3-1pres.pdf. This presentation was based 

on the results ofM. Jerrett, R. T. Burnett, R. Ma et al., "Spatial 

Analysis of Air Pollution and Mortality m Los Angele.o;," EpJ,.. 

demio/ogy 16 (2005): 727-36. 

4 7. J. E. Enstrom, "Fine Particulate Air Pollution and Total 

Morrality among Elderly Californians, 1973-2002,'' Inhalntion 

Toxicology 17 (2005): 803-16. 

48. American Lung Associacion, "Clean Air Standards," 

Medical J oumal Warch, available ac www .cleanairstandards. 

org/listing/journal\V atch. 

49. Based on a search of the Medical Journal .Watch website 

on /\pril 6, 2006. 

50. H. Gong Jr., W. S. Lilm, C. Sioutas et al., ''Controlled 

Exposures ofHealrhy and Asthmatic Volunteers to Concencrared Ambient Fme Particles in Los Angeles," Inhalation T oxico/ogy 15 (2003): 305-25; S. T. Holgate, T. Sandstrom, A. J. 

Frew et aL, "Health. Effects of Acute Exposure to Air Pollution. 

Part I: Heah:hy and Asthmatic Subjects Exposed to Diesel 

Exhaust," Research Report/Health E.ffecr..~ lmtiture (2003 }: 1-30, 

discussions 51--67. 

51. F. D. Gilliland, K. Berhane, E. B. Rappaport et al., 

"The Effects of Ambient Air Pollution on School Absenre~ism Due to Respiratory Illnesses," Epidemiology 12 (2001): 

43-54. 

52. K. Berhane and D. C. Thomas, l(A Two~Stage Model for 

Multiple Time Series Daca of COLmts," Biostatistics 3 (2002): 

21-32; :md V. Rondeau, K. Berhane, and D. C. Thomas, "A 

Three-Level Model for Binary Time-Series Data: The Effects of 

Air Pollution on School Absences in the South em Califomia 

Children's Health Study," Swrisrics in Medicine 24 (2005): 

1103-15. 

53. Ret,iew of the California Ambient Air Qwility Standard for 

Ozone (Sacramento: Cahfomia Au Resources Board, March 

2005 ), available at \1-.rww.arb.ca.gov/research/aaqs/ozone~rs/ 

ozone-final/ozone-final.htm; J. Schwartz, "Rethinkmg the 

California Air Resources Board's Ozone Standards" (working 

paper, AEI, Washington, D.C., September 2005), v.nv.r-w.aei.org/ 

publicationl3145. 

54. Death, Disease and Dirty Potver, Clean Air Task Force; 

Power to ]\ill: Death and Disease from Power Plants Charged with 

Violating the Clean Air Act (Boston: Clean Atr Task Force, July 

2001); Children at Risk: How Air Pollution from Power Plants 

Threate:ns the Health of America's Children, Physicia115 for Socml 

Responsibilicy; Danger in the Air, PIRG. 

55. Envitonn1ental Protection Agency (EPA), "Clean Air 

Intersmre Rule," available at V.lWV?.epa.gov/cair/. 

56. "Clean A.ir Interstate Rule: Charrs and Table," EPA, 

available at ·wwv;'.epa.gov/catr/charts.html. 

57. Clean Air Inte.rstare Rule (CAIR): Reducing Power Plant 

Emissions .for Cleaner Air, Healthier People, and a Strong America 

(Washington, D.C.: EPA, March 2005), avaHable at wv,,\v.epa. 

gov/cair/charts_files/c.arr_final_presentation.pdf. 

58. L. C. Green and S. R. Armstrong, "Particulate Marter in 

~Ambient Air and Mortality: Toxicologic Perspectives"; M.A. 

Sackner, D. Ford, and R. Fernandez, "Effect of Sulf8.te Aerosols 

on Cardiopulmonary Function ofNonnal Humans," American 

Review of Respiratory Disease 115 (1977): 240: and M. J. Utell, 

P. E. Morrow, D. M. Speers et al., "Ainvay Responses to Sulfate 

and Sulfuric Acid Aerosols in Asilimat1cs. An Exposure~ 

Response Relationship," Amencan Review of Respimtory Disease 

128 (1983): 444-50. 

59. J. Q. Koenig, K. Dumler, V. Rebolledo et al., "Respiratory Effects of Inhaled Sulfuric Acid on Senior Asthmatics and 

Nonasthmatics," Archives of Environmental Health 48 ( 1993): 

171-75. 

60. Retriew of the Califomia Ambient Air Quality Standard for 

Ozone, C/\RB. 
Electronic Filing - Received, Clerk's Office, 08/15/2012 - 12-

61. J. Schwartz, ''Rethinking the California Air Resource::: 

Board's OZone Standards"; S. F. van den Eeden, C. P. Quesen~ 

berry,]. Shan et al., Particulate Azr Pollution and Morbidity in 

rhe Califomia Cenrra! Valley: A High Particulate Pollution Region 

(Sacramemo' CARB, july 2002). 

62. Air Qualit)' Crireria for Ozone and Relared Photochemical 

Oxidanrs {Second Enernal Review D-raft) Volumes I-III (\YJashington, D.C.: EPA, August 2005), available at wv.,·w.epa.gov/ 

ttn/naaqs/smndards/ozone/s_o3_cr_cd.html. 

63. C. A. Pope rii, M.]. Thun, M. 1:vL Namboodirl et al., 

"Paniculate Air Pollution as a Prediccor of Monalicy in a 

Prospective Scudy of U.S. Adults," American Journal of Respiratory mld Crirical Care Medicine !51 (1995)o 669-74. 

64. C. A. Pope III, R. T. Burnett, M.]. 1lmn et al., "Lung 

Cancer, Cardiopulmonary Mortaiity, and Long,Term Exposure 

m Fine Paniculate Air Pollution," Journal of ir.e American Medical Association 287 (2002 ), 1132-4 I. 

65. D. Krewski, R. T. Burnett, M.S. Goldberg et al., 

Reanalysis of the Harvard Six Cities Study and the American 

Cancer Society Study of Particulate Air Ponution and Mortaliry 

(Cambridge, MA: Health Effects Insntute, July 2000); Pope, 

Burnett, Thun et al., "Lung Cancer, Cardiopulmonary 

Mortality." 

66 Ibid. 

67. J. P. loa.J.midis, "Why Most Published Research Findin_gs 

Are False," PLoS Medicine 2 (2005): el24; W. R. Keatinge and 

G. C. Donaldson, "Heat Acclimatization and Sunshine Cause 

False Indications of Mortality Due to Ozone,'' Ewuironment.al 

Research 100 (2006)o 387-93; G Koop and L. Tole, "Measuring 

the Health Effects of Air Pollution: To \X/hat Extent Can We 

Really Say That People Are Dying from Bad Air?" Journal of 

Em.n'ronmenta[ Economics and Management 4 7 (2004): 30-54; T. 

Lumley and L. Sheppard, "Time Series Analyses of Air Pollution and Healch: Stralning at Gnats and Swa)lowing Camels?" 

Epidemiology 14 (2003): 13-14; S. H. Moolgavkar, "A Review 

and Cricique of the EPA's· Rationale fot a Fal.e Particle Standard," Regulato!J To,icology and Pharmacology 42 (2005), 123-44; 

G. D. Smith, "Reflections on the Limitations ro Epidemiology," 

Journal ofCunical Epidemio/ngy 54 (200]), 325-31; G. Taubes, 

';Epidemiology Faces Its Limits," Science 269 (1995): 164--69. 

#20036 May 2, 2006 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

Attachment 3: Resume of Dr. Lucy Fraiser, PhD, DABT 

16 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

Lucy H. Fraiser, Ph.D., DABT 

Senior Toxicologist/Associate Vice President 

Professional History 

AECOM Corporation 

Signature Science, LLC 

MFG Inc. 

URS Corporation 

Texas Natura! Resource 

Conservation Commission 

Radian Corporatbn 

Education 

PhD (Toxicology) University of 

Texas at Austin 

BA (Psychology) University of 

Texas at Austin 

Years of Experience 25 

Technical Specialties 

Toxfcologfcal Evaluations 

Risk Assessments 

Risk Communication 

Litigation Support 

Agency Negotiations 

Development of Innovative RiskBased Approaches 

Exposure Modeling 

Professional Affiliations 

Dlplomat of the American Board of 

Toxicology 

National Member, Air & Waste 

Management Association 

Society of Environmental 

Toxicology and Chemistry 

Dr. Fraiser is a Senior Consulting Toxicologist, Operations Manager for 

AECOM Environment's Austin and Dallas offices, and Associate Vice 

President of AECOM Environment North America (Austin, Texas). She 

has 21 years of experience in the areas of human health risk assessment, 

development of quantitative toxicity criteria, health effects and toxicology 

research, risk communication, and litigation support. While she has 

extensive experience in all areas of risk assessment, she specialized in air 

quality risk assessment. She has acted as Health Risk Assessment Team 

Lead and/or Project Manager for numerous human health and ecological 

risk assessments of air pollutants emitted from chemical plants, waste 

management facilities, army depots, cement kilns and power plants. She 

is part of a successful proposal team for a study on the development of 

POP (persistent organic pollutant) inventory and monitoring program in the 

Philippines and will act as the Project Manager and Health Risk 

Assessment Team Leader on that project. Dr. Fraiser was the Health Risk 

Assessment Team Lead for a recently completed Phase 1 Engineering 

Investigation and Environmental Study conducted by AECOM for the siting 

of a Municipal Solid Waste Incinerator in Hong Kong. Because of her 

extensive experience with human health risk assessments for hazardous 

waste combustion units, Dr. Fraiser was invited, along with several others 

at AECOM, to develop U.S. Environmental Protection Agency (EPA) 

training materials on various aspects of the U.S. National Emission 

Standards for Hazardous Air Pollutants (NESHAPs) regulations for 

Hazardous Waste Combustors and ~o teach the site-specific risk 

assessment component of the training in 2008. 

Representative project experience follows. 

Experience 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. As part of a federal litigation case on 

behalf of a major multi-national petrochemical company, 

developed a health-based effects screening level for hydrogen 

sulfide in air. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Developed interim Effects Screening 

Levels (air action levels) forT oluene Diisocyanate and 

17 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

· Hexamethylene Diisocyanate on behalf of a major chemical 

company for use in permitting Maintenance, Startup, Shutdown 

activities at the facility. A report documenting the development of 

the Effects Screening Levels is currently being reviewed by the 

Texas Commission on Environmental Quality. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Researched toxicity and risk-based 

criteria information on Perfluorooctanic Acid (PFOA) and 

Perfuorooctane Sulfonate (PFOS) to educate management and 

potential client on the toxicity and status of risk-based criteria 

development for perfluorinated compounds. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Developed a risk-based soil cleanup 

objective for insoluble inorganic mercury based on a review of 

available toxicity, bioavailability, and plant uptake studies for 

insoluble mercury salts. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Critically reviewed an Air Quality Health 

Consultation conducted by the Texas Department of State Health 

Services (DSHS) and the Agency for Toxic Substances and 

Disease Registry (ATSDR) on behalf of a commercial client. 

Responsibilities included working with the client's attorney to 

develop formal comments and representing the client in meetings 

with the DSHS and ATSDR. Health department data on birth 

defects were reviewed to evaluate whether community concerns 

about birth defects were likely related to emissions from the 

client's hazardous waste combustion unit. Constituents of 

concern included aldehydes, chlorinated and non-chlorinated 

volatile organic compounds, and metals. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Evaluated potential health effects 

associated with methanol and ethanol emissions from tailpipe 

emissions under different test scenarios. The exhaust 

concentrations were derived from composite emission results 

from two different diesel engines. It was determined that ethanol 

and methanol concentrations in tailpipe exhaust are below acute 

and chronic health protective concentrations. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Developed an alternate to EPA's acute 

inhalation toxicity benchmark for nickel and nickel compounds on 

behalf of a commercial client based on site-specific speciation 

data and information from the toxicological literature. 

18 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Used the National Library of Medicine's 

ChemiDPius database to search for compounds with similar 

chemical structures to dye constituents and information on 

chemical structure to identify appropriate surrogate health 

benchmarks for dyestuffs lacking health benchmarks. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Developed an Emergency Response 

Planning Guideline (ERPG) for a reactant (thionyl chloride) used 

in organic synthesis, which involved estimating toxicological 

properties of the previously uncharacterized compound on the 

basis of knowledge of chemistry concepts (i.e., stoichiometry of 

hydrolysis). 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Developed water quality criteria for 

methyl isobutyl ketone and methyl isobutyl carbinol that are 

protective of human health and domestic animals utilizing criteria 

set forth in the Illinois Environmental Protection Agency Water 

Quality Standards. Reviewed available toxicology data and 

recommended a suitable chemical for use as a surrogate in 

calculating aquatic criteria in the absence of toxicological data for 

methyl isobutyl carbinol. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Performed a human health exposure 

and risk assessment for Rodeo® herbicide based on its intended 

use patterns, including applicator exposure, consumer safety, 

and terrestrial wildlife. The product subsequently received 

registration approval in the state of Connecticut. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Reviewed toxicity data and derived an 

inhalation reference concentration (RfC) for cesium oxide, a 

gasoline additive that is used in France, using EPA's "Interim 

Methods for Development of Inhalation Reference 

Concentrations" on behalf of a commercial client. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Served as primary author on a 

successful delisting petition for di-n-octylphthalate in which 

similarly-structured phthalates were evaluated. 

Toxicological Evaluations and Risk-Based Regulatory 

Criteria Development. Reviewed toxicity studies from the 

chemical inventory of a large chemical company and made 

19 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

recommendations for submittal under TSCA BE (Toxic 

Substances Control Act). 

Air Quality Risk Assessment. Health Risk Assessment Advisor 

for a study recently completed on behalf of the Electric Power 

Research Institute (EPRI) that evaluated the potential health risk 

from emissions of coal fired power plants throughout the U.S. 

Responsibilities included consultation with project risk assessors 

on various technical issues, senior review of human health risk 

assessments and associated calculations, and presentation of 

information in a joint EPRI/Utility Air Research Group meeting in 

May, 2012. 

Air Quality Risk Assessment. Recently provided comments on 

Boiler MACT Health Based Emissions Limitations on behalf of 

the American Forest and Paper Association. 

Air Quality Risk Assessment. Health Risk Assessment Team 

Leader responsible for overseeing the conduct of a risk 

assessment as part of an engineering investigation (EI) and 

environmental impact assessment (EIA) study for two potential 

sites of an Integrated Waste Management Facility in Hong Kong. 

The project entailed using air dispersion and deposition modeling 

to evaluate exposure, and calculating potential risk associated 

with both stack and fugitive air emissions from the facilities. 

Air Quality Risk Assessment. Recently acted as project 

manager for multi-pathway risk assessment updates for two 

chemical plants in the U.S. (Houston Texas and Baton Rouge 

Louisiana) to support permitting activity that reflected the 

installation of new sulfur dioxide (S02) abatement equipment on 

sulfuric acid regeneration units. 

Air Quality Risk Assessment. Conducted a Best Available Control 

Technology (BACT) analysis for carbon monoxide (CO), particulate 

matter, sulfur dioxide (502), nitrogen oxides (NOx), and volatile organic 

compounds (VOCs) on behalf of a meat processing and rendering plant 

in Texas. 

Air Quality Risk Assessment. Health risk assessment lead for vapor 

intrusion evaluation, using crawl-space soil vapor and ambient air 

samples collected beneath and near a house in the vicinity of a crude oil 

release from a buried flow line. 

Air Quality Risk Assessment. Health risk assessment lead for vapor 

intrusion evaluation, using indoor and ambient air samples at 

manufacturing facility. 

20 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

Air Quality Risk Assessment. Served as task leader for over 

two dozen human health risk assessments conducted in support 

of RCRA Part B permit applications for hazardous waste 

combustion units at chemical plants. waste management 

facilities, army depots, and cement kilns. Responsibilities 

included oversight and coordination of staff conducting modeling, 

reporting for the project, representation of clients in Agency 

meetings, and complete responsibility for all financial and 

technical aspects of the risk assessments. Primary risk drivers 

routinely consisted of Polycyclic Aromatic Hydrocarbons (PAHs), 

mercury, chromium, phthalates, and dioxins. 

Air Quality Risk Assessment. Evaluated the potential for 

health effects associated with particulates and metals present in 

air samples collected by neighbourhood volunteers when noxious 

odors were detected. 

Air Quality Risk Assessment. Completed formal technical 

comments on behalf of a power plant client on the Strategic Toxic 

Air Reduction (STAR) program, a risk-based program intended to 

significantly reduce levels of toxic air contaminants in Louisville, 

KY. 

Air Quality Risk Assessment. Conducted a risk evaluation of 

site operations that described potential impacts to on-site 

workers, the surrounding community, and ecological receptors. In 

combination with information on chemical hazards, local 

exposure patterns, and available local media concentrations, 

toxic release inventory (TRI) data were used to identify chemical 

release and material handling practices at the plant that may 

warrant further study or action. 

Air Quality Risk Assessment. Served as project manager and 

technical lead for multipathway exposure and risk assessments 

conducted for three lignite-fired utility plants. Toxic Release 

Inventory (TRI) data were used as the basis for emission 

estimates. 

Air Quality Risk Assessment. Served as project manager and 

technical lead for mercury exposure and risk assessments 

conducted for three lignite-fired utility plants in which the Electric 

Power Research Institute's (EPRI's) Dynamic Mercury Cycling 

model was used. TRI data were used as the basis for emission 

estimates. 

Air Quality Risk Assessment. Developed technical comments 

on EPA Risk Assessment Protocols for Hazardous Waste 

21 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

Combustion Facilities on behalf of the Louisiana Chemical 

Association (LCA) and the Cement Kiln Recycling Coalition 

(CKRC). Included evaluating chemical-specific approaches, 

including those for Polycyclic Aromatic Hydrocarbons (PAHs). In 

particular, the benefit of including a metabolism factor for PAHs 

in calculating PAH concentrations in beef, milk, pork, poultry, 

eggs, and fish was evaluated and commented upon. 

Air Quality Risk Assessment. Had primary responsibility within 

the Toxicology & Risk Assessment Section for implementation of 

the Texas Natural Resource Conservation Commission's 

(TNRCC) Combustion Strategy. Was instrumental in recognizing 

issues associated with high Polycyclic Aromatic Hydrocarbon 

(PAH) detection limits typical in environmental media samples 

and spear-headed the development of guidance/approaches for 

ensuring that high PAH detection do not artificially inflate risk 

estimates. 

Air Quality Risk Assessment. Represented the TNRCC in an 

EPA work group to evaluate Maximum Achievable Control 

Technology (MACT) standards developed under the Clean Air 

Act for hazardous waste incinerators, cement kilns, and 

lightweight aggregate kilns. Highly advanced technical support 

documentation was critically reviewed and concerns and ideas 

regarding each standard were conveyed to EPA during the preproposal stage. 

Air Quality Risk Assessment. Served as an external peer 

reviewer for a draft exposure and risk assessment guidance 

document developed by EPA Region 6 for conducting exposure 

and risk assessments at facilities that burn hazardous waste 

("Protocol for Screening Level Human Health Risk Assessment at 

Hazardous Waste Combustion Facilities" and "Screening Level 

Ecqlogical Risk Assessment Protocol for Hazardous Waste 

Combustion Facilities") while employed by the TNRCC. 

Evaluated and commented upon various chemical-specific 

approaches, including those for Polycyclic Aromatic 

Hydrocarbons (PAHs ). 

Risk Based Corrective Action. Served as task leader for over 

75 human health risk assessments and/or risk-based evaluations 

conducted in support of Resource Conservation Recovery Act 

(RCRA) closures or under the Comprehensive Environmental 

Response, Compensation, and Liability Act (CERCLA) for both 

commercial companies (petrochemical, agrochemical/pesticide, 

gas supply, aluminum, electric utility, cement kiln) and 

government clients (Army Corp of Engineers [USAGE], Air Force 

22 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

Center for Environmental Excellence [AFCEE], Air Force Bases 

[Cannon, Davis-Monthan, Holloman, Langley, Maxwell]). 

Responsibilities included oversight and coordination of staff 

conducting modeling and reporting, representation of clients in 

Agency meetings, and complete responsibility for all financial and 

technical aspects of the risk assessments. 

Risk Based Corrective Action. Currently acting as Health Risk 

Assessment Lead for a multi-media health risk assessment for a 

high school at which incinerator ash was used as fill material 

beneath several sports fields. The primary constituents of 

concern are polychlorinated biphenyls (PCBs). 

Risk Based Corrective Action. Currently acting as Health Risk 

Assessment Lead for a multi-media health risk assessment for a 

former refinery. 

Risk Based Corrective Action. Recently completed a human 

health and screening ecological risk assessment for several 

areas within a former refinery in Southeast Asia in preparation for 

divestment. 

Risk Based Corrective Action. Currently supporting an 

evaluation of a historical polychlorinated biphenyl (PCB) release 

under the risk-based provisions of 40 CFR 761.61(c) of the TSCA 

regulations for an Independent School District in the Northeast. 

Risk Based Corrective Action. Currently providing risk 

assessment and toxicology support on a very large remediation 

project for a former battery manufacturing company. 

Contaminants of concern include mercury and lead. 

Risk Based Corrective Action. Currently providing toxicology 

and risk-based corrective action support to a consortium of 

Potentially Responsible Parties on a remediation project for a 

river segment in the Northeast. Primary contaminants of concern 

include dioxins, polychlorinated biphenyls, polycyclic aromatic 

hydrocarbons (PAHs), arsenic, lead, mercury. 

Risk Based Corrective Action. Currently involved in 

conducting a risk-based evaluation of a former production well 

site for submittal to the Texas Railroad Commission. 

Risk Based Corrective Action. Currently involved in 

developing a risk-based strategy for achieving regulatory closure 

of numerous oil field leases at a very large Texas oil field. 

Responsibilities include developing site-specific standard 

23 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

operating procedures, preparing reports on risk-based 

evaluations for submittal to the Texas Railroqd Commission, and 

representing the client in Agency meetings. 

Risk Based Corrective Action. Performed detailed human 

health and screening ecological risk assessments for a former 

lube oil refinery intended for divestiture in Southeast Asia. 

Responsibilities included interpretation of sampling data 

generated by another contractor for use in the risk assessment, 

coordination of groundwater modeling, exposure modeling, 

reporting, and complete responsibility for all financial and 

technical aspects of the risk assessment project. The risk 

assessment was conducted in a manner consistent with 

International guidance on the conduct of risk assessments. An 

extensive exposure pathway analysis was conducted for the site, 

including inhalation of vapors from in indoor and outdoor air, 

dermal contact with water and soil, ingestion of water and soil, 

and uptake through the food chain (i.e., vegetables). 

Risk Based Corrective Action. Performed a post-remediation 

human health risk assessment for an active petroleum depot in 

Southeast Asia. Responsibilities included modeling and 

reporting for the project, representation of the client before a 

health panel of scientists convened to review the risk 

assessments, and complete responsibility for all financial and 

technical aspects of the risk assessment project. The risk 

assessment was conducted in a manner consistent with 

International guidance on the conduct of risk assessments. 

Risk Based Corrective Action. Performed a human health risk 

assessment for an operational petroleum dispensing station in 

Southeast Asia. Responsibilities included coordination with both 

U.S. and Asian staff conducting sampling, modeling, and 

reporting for the project, representation of the client before a 

health panel of scientists convened to review the risk 

assessments, and complete responsibility for all financial and 

technical aspects of the risk assessment project. The risk 

assessment was conducted in a manner consistent with 

International guidance on the conduct of risk assessments. An 

extensive exposure pathway analysis was conducted for the site, 

including inhalation of vapors from in indoor and outdoor air, 

dermal contact with water, ingestion of water, and uptake through 

the food chain (i.e., vegetables, chicken, and eggs). 

Risk Based Corrective Action. Served as task leader for three 

human health risk assessments and one ecological risk 

assessment for an active petroleum depot in Southeast Asia. 

24 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

Responsibilities included oversight and coordination of both U.S. 

and Asian staff conducting sampling, modeling, and reporting for 

the project. representation of the client before a health panel of 

scientists convened to review the risk assessments, and 

complete responsibility for all financial and technical aspects of 

the risk assessment project. The risk assessment was conducted 

in a manner consistent with International guidance on the 

conduct of risk assessments. An extensive exposure pathway 

analysis was conducted for the site, including inhalation of vapors 

from in indoor and outdoor air, dermal contact with soil and 

water, ingestion of soil and water, and uptake through the food 

chain (i.e., vegetables, chicken, and eggs). 

Risk Based Corrective Action. Developed numerous 

approaches to ensure internal consistency in risk assessments 

conducted by Texas Natural Resource Conservation Commission 

(TNRCC) personnel, the review of risk assessments submitted to 

the TNRCC, and data collection procedures while employed by 

the TNRCC. Dr. Fraiser also played a critical role in developing a 

risk-based corrective action rule package (Texas Risk Reduction 

Program) and technical support guidance documents for the 

proposed rule. 

Risk Based Corrective Action. Significant involvement in a 

large-scale project in which risk-based tools for use by the Air 

Force were evaluated and recommended. Risk-based cleanup 

options at Installation Restoration Program (IRP) and Resource 

Conservation and Recovery Act (RCRA) sites located on Air 

Force Bases were reviewed to identify Records of Decision 

(RODs) amenable to modification. 

Risk Based Corrective Action. Participated in the development 

of an approach for establishing cleanup criteria for Air Force 

Bases nationwide as part of the Rational National Standards 

Initiative (RNSI). During the course of the project, Dr. Fraiser 

was involved in negotiations with military personnel and 

regulators. 

Testifying and Litigation Support. Currently providing litigation 

support in a federal case on behalf of a major multi-national 

petrochemical company. Constituents of concern include sulfur 

dioxide, hydrogen sulfide, nitrogen oxides, ozone and volatile 

organic compounds associated with emissions from a refinery, a 

chemical plant, and an olefins plant. The case also involves 

evaluating potential odor nuisances. Dr. Fraiser was deposed on 

June 20, 2012 and the hearing is expected to take place in the 

fall of 2012. 

25 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

Testifying and Litigation Support. Provided testimony on 

potential risks associated with permitting of a rock crusher. 

Constituents of concern for the case are anticipated to be PM10, 

PM2.5, and crystalline silica. Hearing took place in 2011 and 

construction permit was granted. 

Testifying and Litigation Support. Consulting toxicologist on 

behalf plaintiff in a lawsuit brought against a steel tank 

manufacturer by the State of Texas. 

Testifying and Litigation Support. Provided toxicological 

support and testified in a contested case hearing involving a 

Texas rock crusher. Constituents of concern for the case are 

PM1 0, PM2.5, limestone and crystalline silica. The permit was 

granted in December 2010. 

Testifying and Litigation Support. Criteria Pollutant, Air 

Taxies, and Odor Nuisance Litigation Support: Currently 

providing Jiti§ation support in a federal case on behalf of a major 

multi-national petrochemical company. Constituents of concern 

include sulfur dioxide, hydrogen sulphide. nitrogen oxides, ozone 

and volatile organic compounds associated with emissions from 

a refinery, a chemical plant, and an olefins plant. Dr. Fraiser will 

be deposed on June 20, 2012 and the hearing is expected to 

take place in the fall of 2012. 

Testifying and Litigation Support. Developed an opinion 

regarding the likelihood that a level of exposure sufficient to 

cause known health effects could have occurred as a result of a 

hydrogen sulfide (H2S) and/or sulfur dioxide (S02) release from 

a Sulfur Recovery Unit at a Refinery in Texas. Development of 

the opinion entailed review of medical records, air dispersion 

model results, depositions, and discovery responses of the 

defendant and plaintiff. The case settled in 2009. 

Testifying and Litigation Support. Testified on potential risks 

associated with permitting of a concrete batch plant. 

Constituents of concern for the case were PM10. PM2.5, total 

suspended particulate and crystalline silica. Dr. Fraiser was 

deposed and prepared pre-filed testimony in this case. Permit 

was granted. 

Testifying and Litigation Support. Testified on potential risks 

associated with permitting of a copper smelter on behalf of the 

City of El Paso. Constituents of concern for the case were 

metals, PM10, PM2.5, nitric oxide, sulfur dioxide, and sulfuric 

acid. Hearing took place in July 2005. Permit was denied. 

26 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

Testifying and Litigation Support. Testified on potential risks 

associated with permitting of a rock crusher. Constituents of 

concern for the case are PM1 0. PM2.5, and crystalline silica. Dr. 

Fraiser was deposed and prepared pre-filed testimony in this 

case. Hearing took place July 2005. 

Testifying and Litigation Support. Provided critical testimony 

on potential risks associated with emissions from a commercial 

hazardous waste incinerator. The Kentucky Department of 

Environmental Protection attempted to revoke the facility's RCRA 

Interim Status Part B permit for alleged violations of RCRA and 

the Clean Air Act. As a result of the combined testimony of Dr. 

Fraiser and one of her colleagues, the client's request for a 

restraining order was granted and 75 employees kept their jobs. 

Testifying and Litigation Support. Developed expert opinion 

and provided testimony in a criminal case hearing regarding the 

potential for health effects associated with relatively short-term 

exposure to benzene concentrations above the Maximum 

Contaminant Level (MCL) in groundwater. Case was lost. 

Testifying and Litigation Support. Prepared to provide expert 

testimony on potential risks associated with lead and total 

petroleum hydrocarbon (TPH) levels detected in street 

sweepings for a criminal case hearing. Issues considered 

included potential risk associated with contaminant levels that 

were detected and potential for matrix interferences associated 

with laboratory methods. The case settled before going to trial. 

Testifying and Litigation Support. Served as an expert 

witness on toxicology and risk assessment issues in a contested 

case hearing involving the Texas Natural Resource Conservation 

Commission (TNRCC) and the first Boiler & Industrial Furnace 

(BIF) to be permitted under Subpart H of 40 CFR 266 in the state 

of Texas (only second BIF to be permitted in the nation). 

Televised Press Conference. Peer reviewed of a paper entitled 

"Proximity to Point Sources of Environmental Mercury Release 

as a Predictor of Autism Prevalence" and conducted a televised 

press conference on the findings of the paper on behalf of the 

Clean Coal Technology Foundation of Texas. 

Testimony Before Regulatory Agencies/Bodies. Provided 

technical support to the American Clean Coal Coalition for 

Electricity, a non-profit group dedicated to protecting the viability 

of coal-based electricity, in meetings with various state regulatory 

agencies (Texas Commission on Environmental Quality. North 

27 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

Carolina Department of Environment and Natural Resources) 

and regulatory bodies (Environmental Regulations Committee of 

Texas House of Representatives and the Cultural, Recreation 

and Tourism Committee of Texas Senate) on mercury emission 

issues. 

Publications, Presentations, and Training Courses 

Fraiser, L.H. and Vosnakis, KAS. Evolution of PCB Regulations 

and Toxicity Assessment: Impact on Environmental 

Management. 27~ Annual International Conference on Soils, 

Sediments, Water and Energy, Amherst, Massachusetts. 

October 17-19,2011. 

Fraiser, L.H. Toxicology & Risk Assessment in the News: Recent 

EPA Proposals with Broad Implications. Houston Air & Waste 

Management Association. June 2010. 

Fraiser, L.H., Quintin, A. Durocher, K. Szembek, C. Heinold, D. 

EPRI Human Health and Environmental Risk Assessment 

Process. February 18,2010. 

Fraiser, L.H. Trends in International Risk-Based Screening 

Levels (RBSLs). Society of Toxi~ology and Chemistry, New 

Orleans, Louisiana. November 19- 23, 2009. 

Fraiser, L.H. Risk Assessment: How it Can Inform Site Closure 

Decisions. Invited Short Course presented to the Department of 

Environment Malaysia, Kuala Lumpur. March 4- 5, 2009. 

Fraiser, L.H. Incinerator Risk Assessment: Principles and 

Practices, Hong Kong. Regional Conference on Sustainable 

Waste Management in Carbon-Conscious Cities. December 

2008. 

Fraiser, L.H. and Quintin, A. International Screening Levels. 

White Paper prepared for Exxon Mobil, Fairfax, VA. December, 

2008. 

Site-Specific Risk Assessments, RCRA Omnibus Provision and 

Combining Risk Burns and Comprehensive Performance Tests. 

MACT EEE EPA Training Workshop, Dallas, TX. November 3-

8, 2008. 

Fraiser, L.H., Quintin, A. and Ng, H.S. Comparison of 

International Risk-Based Screening Levels. Brownfield Asia 

2008, Third International Conference on Remediation and 

Management of Contaminated Land: Focus on Asia October 21 -

28 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

23, 2008, Kuala Lumpur, Malaysia. 

Fraiser, L.H. Involvement of Local Governments in Air Taxies 

Regulation. Texas Chemical Council/ Association of Chemical 

Industry of Texas's EH&S Seminar Moody Gardens Hotel, 

Galveston Texas. June 10, 2008. 

Fraiser, L.H. Chemical and Microbial Risk Assessment: 

Establishing Environmental Endpoints for use in Regulatory 

Decision-Making. Presented at a meeting jointly organized by 

the Hong Kong Institute of Environmental Impact Assessment 

and Chartered Institution of Water and Environmental 

Management. May 9, 2008. 

Coal-fired Power Plants: Assessing the Positive Health Benefits 

of Reliable and Low Cost Electricity. White Paper prepared for 

Center for Energy and Economic Development. March 2007. 

Introduction to Toxin Threat Agents, Confidential Government 

Client, AUstin, TX. January 2006. 

Toxins as Threat Agents, Confidential Government Client, Austin, 

TX. July 2003. 

Environmental Risk and Impact: What Do the Numbers Really 

Mean? Society of Women Engineers, Atlanta, GA. October 11, 

2003. 

TRRP-13- Review and Reporting of COC [chemical of concern] 

Concentration Data, Central Texas Chapter of the Air & Waste 

Management Association, 301 Congress Avenue, Room 360, 

Austin, TX. January 16, 2003. 

Health Studies Conducted in Midlothian, TX, Tarrant County 

Medical Society, Renaissance Hotel, Austin, TX. January 18, 

2002: 

Fraiser, L.H., and Chaudhuri, I. Short-Term Toxicity Benchmark 

for Nickel Oxide. To be presented at the 42nd Annual Society of 

Toxicology Meeting, Salt Lake City, Utah. March 9- 14,2002. 

Fraiser, L.H., and Ruffle, B. Chemical Regulations with Business 

Implications. Environmental Protection. June, 2002. 

Fraiser, L.H ., and Chaudhuri, I. Short-Term Toxicity Benchmark 

for Nickel Oxide. International Conference on Incineration & 

Thermal Treatment Technologies Proceedings, New Orleans, 

Louisiana. May 13 -17, 2002. 

29 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

Fraiser, L.H., and Chaudhuri, I. Short-Term Toxicity Benchmark 

for Nickel Oxide. Proceedings of the Air & Waste Management 

Association, StLouis, Missouri. April16- 19 2002. 

Fraiser, LH., Chaudhuri, I, and Smith, D. EPA's Dioxin 

Reassessment- Potential Impacts to the Regulated Community. 

Proceedings of the Air & Waste Management Association, 

Orlando, Florida. June 24-28, 2001. 

Fraiser, LH., Reeck, D., and Smith, D. New Developments in 

Dioxin Regulation- Potential impacts on the Regulated 

Community. International Conference on Incineration & Thermal 

Treatment Technologies Proceedings, Philadelphia, 

Pennsylvania. May 14-18, 2001. 

Fraiser, LH., Reeck, D., and Smith, D. Current Environment of 

Hazardous Waste Combustion. International Conference on 

Incineration & Thermal Treatment Technologies Proceedings, 

Philadelphia, Pennsylvania. May 14-18, 2001. 

Fraiser, L.H., and Pope, P.G. 'Hazardous Waste Combustion 

Risk Assessment- Artifact or True Risk?' International 

Conference on Incineration & Thermal Treatment Technologies 

Proceedings., Portland, Oregon. May 8-12,2000. 

Fraiser, L.H., and Lewis, D. 'Detection Limits: Practical 

Implications for Risk Assessments Conducted on Hazardous 

Waste Combustion Units.' Presented before the Louisiana 

Chemical Association. Baton Rouge, Louisiana. September 9, 

1999. 

Fraiser, LH., Tachovsky, JA, King, ML, McCoy, J.T., and 

Haws, LC. 'Hazardous Waste Combustion Risk Assessment 

Experience in the State of Texas: International Conference on 

Incineration & Thermal Treatment Technologies Proceedings. pp. 

189-196, Salt Lake City, Utah. May 11-15, 1998. 

Fraiser, L., McCoy, J.T., Perry, C., King, M., and Haws, LC. 

Screening Risk Analysis for the Bayer Corporation Facility in 

Baytown, Texas. TNRCC publication number AS-120, AS-120A, 

and AS-120B. November 1996. 

Fraiser, L, Lund, L, Tyndall, K., King, M., Schultz, D., and Haws, 

L 'Case Studies in Risk Assessment for Hazardous Waste 

Burning Cement Kilns in Waste Combustion' in Boilers and 

Industrial Furnaces Proceedings. pp.208-225. Kansas City, 

Missouri. March 26-27, 1996. 

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Fraiser, L., Lund, L., Hueske, K., and Haws, L.C. 'Indirect Risk 

Assessment: Case Studies of Hazardous Waste Combustors'. 

Toxicologist 30:6, 1996. 

Fraiser, L., Lund, L., Hueske, K., King, M., and Haws, L.C. 

Screening Risk Analysis for the North Texas Cement Company 

(NTCC) Facility in Midlothian, Texas. TNRCC publication number 

AS-71, AS-71A, and AS-71B. January 31, 1996. 

Fraiser, L., Lund, L., Hueske, K., King, M., and Haws, L.C. 

Screening Risk Analysis for the Texas Industries (TXI) Facility in 

Midlothian, Texas. TNRCC publication number AS-72, AS-72A, 

and AS-72B. November 2, 1995. 

Ramu, K., Fraiser, L., Mamiya, B., Ahmed, T., and Kehrer, J.P. 

'Acrolein Mercapturates: Synthesis, Characterization, and 

Assessment of Their Role in the Bladder Toxicity of 

Cyclophosphamide.' Chern. Res. Toxicol. 8:515-524, 1995. 

Fraiser, L., and Kehrer, J.P. 'Effect of Indomethacin, Aspirin, 

Nordihydroguairetic Acid, and Piperonly Butoxide on 

Cyclophosphamide-Induced Bladder Damage.' Drug Chern. 

Toxicol. 16(2):117-133, 1993. 

Fraiser, L., Barnett, J.W., and Hixson, E.J. 'Toxicity Equivalents 

for Chlorinated Hydrocarbon Pesticides Lacking EPA-Verified 

Toxicity Values.' Toxicologist 14: 1540, 1994. 

Kanekal, S., Fraiser, L., and Kehrer, J.P. 'Pharmacokinetics, 

Metabolism, and Lung Toxicity of Cyclophosphamide in C57/BI6 

and ICR Mice.' Toxicol. Appl. Pharmacal. 114:1-8, 1992. 

Fraiser, L., and Kehrer, J.P. 'Murine Strain Differences in Bladder 

Toxicity of Cyclophosphamide.' Toxicol. 75:257-272, 1992. 

Fraiser, L., Kanekal, S., and Kehrer, J.P. 'Cyclophosphamide 

Toxicity: Characterizing and Avoiding the Problem.' Drugs. 

42(5):781 -795, 1991. 

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Attachment 4: Resume of Dr. Lisa Bradley, PhD, DABT 

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Lisa J. N. Bradley, Ph.D., DABT 

Vice President and Senior Toxicologist 

Professional History 

AECOM (formerly ENSR) 

r .. 1assachusetts lilstitute of 

Technology 

University of !daho 

Education 

PhD (Toxicology) Massachusetts 

Institute ofTechnology, 1991 

BS (Zoology) University of Idaho, 

1983 

BS (Chemistry) University of 

Idaho, 1983 

Years of Experience 25 

Technical Specialties 

Toxicology 

Risk Assessment 

Environmental Communication 

Regulatory Negotiatfon 

Site Strategy Development 

Professional Affiliations 

Diplomate, American Board of 

Toxicology, 1994 

Society of Toxicology 

Phi Beta Kappa 

Dr. Lisa Bradley is a Senior Toxicologist/Risk Assessor and Vice 

President with AECOM. She has a Ph.D. in toxicology from the 

Massachusetts Institute of Technology. She has 25 years of experience 

in risk assessment and toxicology, and is certified by the American Board 

of Toxicology. She has managed risk assessments for hazardous waste 

sites in many EPA Regions, and under many state programs. Dr. Bradley 

has also served as an advisor on strategic risk assessment issues for 

clients in the natural gas, utility, and railroad industries. She has 

developed the risk assessment approach for a large multi-site program 

for a railroad client, for a national steel client, and developed and 

managed the risk evaluation component of a large multi-site, multi-state 

federal program for a natural gas client. Dr. Bradley is experienced in 

public speaking and environmental communications, and she has 

published articles in peer reviewed scientific journals based on both her 

laboratory and risk assessment work. Dr. Bradley is the global risk 

practice technical lead for AECOM. She is the manager and technical 

lead for AECOM's coal combustion product (CCP) initiative and was 

recently elected to the Executive Committee of the American Coal Ash 

Association. 

Experience 

A. Representative Superfund Experience 

Pines Area of Investigation, Indiana, USEPA Region 5 . . 

Serving as project manager for a multi-disciplinary team 

conducting the Remediallnvestigation/Feasibility Study for the 

Respondents of an Administrative Order on Consent (AOC) being 

administered under the Superfund Alternative program in US EPA 

Region 5. The AOC addresses the placement of coal combustion 

by-products (CCBs) within a local permitted landfill and allegedly 

used as fill in other locations within the Area of investigation. 

Activities to date include agency negotiations on the AOC and 

scope of work; submission of a Site Management Strategy 

document, and subsequent approval by the Agency; submittal of 

the Rl/FS Work Plan (including a Field Sampling Plan, Human 

Health and Ecological Risk Assessment Work Plans, HASP, 

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QAPP, and a Quality Management Plan), and subsequent 

approval by the agency; submission of additional Sampling and 

Analysis Plans; and communications activities (including a 

website- www.pinesupdate.com -and regular mailings of 

information updates to the community). Regular communications 

with the agency is also a cornerstone of the project. As the site 

covers not a facility, but a town and surrounding area, executing 

access agreements with the land owners for sampling and well 

installation was a critical task. Four rounds of sampling and 

analysis have been successfully completed. The Final Rl Report 

has been approved, and the Draft Human Health Risk 

Assessment Report and the Draft Ecological Risk Assessment 

Report have been submitted to the agency. Approved project 

documents to date are available on US EPA's website: 

http://www. epa. qov/reqion 5/sites/pines/index. htm. 

Delaware Sand & Gravel Remedial Trust, Delaware, USEPA 

Region 3. A human health risk assessment (HHRA) focusing on 

evaluation of the vapor intrusion exposure pathway was 

performed for the PRPs at a former drum disposal area to 

evaluate the effectiveness of a Bioremediation System installed as 

a result of an EPA Superfund Record of Decision Amendment. A 

tiered vapor intrusion assessment was performed consistent with 

USEPA guidance using groundwater and then soil gas data. It 

was successfully concluded, with acceptance from EPA Region 3, 

that no unacceptable risk to human health was posed to 

occupants of on-site buildings via the vapor intrusion inhalation 

pathway. 

Solutia, Inc., Human Health Risk Assessment, Sauget Area 1, 

Illinois, USEPA Region 5. Prepared a human health risk 

assessment work plan to follow Superfund guidelines for several 

abandoned landfill areas and areas downgradient of the landfills. 

The work plan was accepted by U.S. EPA Region V. A 

comprehensive human health risk assessment was prepared that 

evaluated the former land fill areas as well as local residential 

areas, a creek, and a borrow pit lake. A total of 64 receptor and 

area scenarios were quantitatively evaluated. Supporting risk 

modeling included indoor and outdoor air from subsurface soil and 

groundwater. Activities included site visits, meetings with 

personnel from USEPA Region 5 and their contractors, and 

preparations of responses to comments and document revisions. 

The human health risk assessment has been accepted by the 

agency, and the results have been used to guide the feasibility 

study and remedy selection. Constituents of interest included 

PCBs in ditch sediments. The final report is available on EPA's 

website: http://www. epa. gov/reqion5/ cleanu p/saugetarea 1 /pdfs/ 

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sauget1_deadcreek_final_remedy_200604.pdf 

Sauget Area 2 Sites Group, Human Health Risk Assessment, 

Illinois, USEPA Region 5. Serving as the senior human health 

risk assessment manager for a multi-party PRP group. Prepared 

a human health risk assessment work plan to follow Superfund 

guidelines for a set of sites that include abandoned landfill areas. 

Conducted the multi-receptor, multi-pathway human health risk 

assessment, including vapor intrusion modeling for both indoor 

and outdoor air for the multiple multi-acre sites within the project 

area. Activities included a site visit, meetings and negotiations 

with US EPA Region 5 and their contractors, and preparation of 

responses to comments. 

Columbia Gas Transmission, Strategic Risk Assessment 

Advisor, West Virginia, USEPA Region 3. Served as strategic 

risk assessment advisor to a multi-site, ten-state AOC with U.S. 

EPA Region Ill to assess environmental conditions along their 

pipeline system in the Mid-Atlantic States. Provided strategic risk 

assessment advice and technical support on the design and 

implementation of the program, and developed a programmatic 

approach to the evaluation of risk across the program. Was 

responsible for: review of other contractor reports, development 

of a common strategy for TPH and mercury to be used across the 

program, revi.ew and summary of risk assessment regulations and 

guidance for each of the states (Ohio, Pennsylvania, West 

Virginia, Virginia, Kentucky, North Carolina, Delaware, New 

Jersey, Maryland, New York, and Louisiana), conducted risk 

assessments, provided critical review of individual site 

characterization reports prepared by other contractors, and 

provided support in negotiations and meetings with regulators. 

Additional constituents of interest include PCBs, arsenic, and 

PAHs. 

Tippecanoe Landfill, Human Health Risk Assessment, 

Indiana, USEPA Region 5. Conducted agency negotiations 

(U.S. EPA Region V) concerning the human health risk 

assessment for a Superfund site. Because arsenic concentrations 

in groundwater were of concern to the agency, researched and 

reviewed the toxicological information available for arsenic, and 

prepared a literature review and evaluation of the dose-response 

values developed by the U.S. EPA for arsenic. 

lndustri-Piex CERCLA Site, Risk Assessment Review and 

Strategy for PRP Group, Massachusetts, US EPA Region 1. 

Provided risk assessment review and strategy for PRP group, and 

developed risk assessment work plan to address surface water 

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and groundwater exposure pathways. 

Tennessee Valley Authority, Human Health Risk Assessment, 

Tennessee, USEPA Region 4. Prepared human health risk 

assessment and developed target cleanup levels for an 

abandoned battery manufacturing site. Primary constituent was 

lead and both child and adult lead models were used in the 

evaluation. 

Confidential Client, Human Health Risk Assessment, New 

Jersey, USEPA Region 5. Conducted a human health risk 

assessment for a school district's baseball fields located adjacent 

to a potential Superfund site. Report was prepared for community 

distribution, and results presented at a public meeting. 

Mateo Superfund Site, Review of AIC for Volatile Organics, 

Texas, USEPA Region 6. Reviewed U.S. EPA-developed acute 

inhalation criteria (AIC) for volatile organics. Developed a 

consistent and scientifically-defensible methodology for AIC 

development, and applied this methodology to provide alternative 

AICs for use at the site. 

Brio Site Task Force, Texas, USEPA Region 6. Developed 

acute inhalation criteria for use in a remedial program for 

benzene, 1, 1-dichloroethane, 1 ,2-dichloroethane, ethyl benzene, 

methylene chloride, styrene, toluene, 1,1, 1-trichloroethane, 1,1 ,2-

trichloroethane, and vinyl chloride. 

B. RepresentatiVe RCRA Experience 

Sol uti a, Inc., Human Health Risk Assessment Oversight for 

the J.F. Queeny Facility, St. Louis, Missouri. Provided 

oversight for the human health risk assessment prepared for the 

facility under an order with US EPA Region 6. The risk 

assessment is designed to meet the requirements of both USEPA 

and the State of Missouri Risk-Based Corrective Action Program. 

Sol uti a, Inc., Human Health Risk Assessment for the W.G. 

Krummrich Facility, Sauget, Illinois, USEPA Region 5. 

Developed the human health risk assessment workplan and report 

for the RCRA Sampling Plan for Solutia's W.G. Krumm rich 

Facility. The workplan was designed to permit evaluation of the 

"Human Exposures Environmental Indicator'' as well as human 

health risk. Used risk assessment and data visualization to 

identify extent of areas for remediation such that total site risk 

would not exceed target risk levels once remediation is complete. 

Also used the risk assessment to identify remedial treatment 

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objectives for soils and groundwater. Target chemicals included 

PCBs and chlorinated compounds. 

U.S. Steel, Human Health Risk Assessment, Gary, Indiana, 

USEPA Region 5. Developed the RCRA RFI Human Health Risk 

Assessment Workplan for the U.S. Steel Gary Works. Activities 

included response to regulatory comments on previous reports, 

site visits, review of reports generated both by USS and by local 

groups about the facility and its environs, development of the riskrelated portions of the facility-wide RCRA RFI workplan, in 

addition to the HHRA workplan, and agency negotiation. 

Participated in strategy development for and preparation of the 

human health sections of the Sampling and Analysis Plans for 

each of the Solid Waste Management Areas being addressed at 

Gary Works under RCRA (13 in total). Managed and prepared 

the human health risk evaluation of perimeter groundwater data. 

Work included conducting a two tiered well-by-well screening (55 

wells total). The first tier comparison was to generic and readily 

available standards, and the second tier took into account 

background and dilution into receiving water bodies, and 

evaluated construction worker and indoor air scenarios. 

U.S. Steel, Human Health Risk Assessment, Fairless Hills, 

Pennsylvania, USEPA Region 3. Prepared the human health 

risk evaluation under RCRA Corrective Action for a parcel of 

property to be leased by U.S. Steel at Fairless Works. The work 

was conducted to satisfy Pennsylvania Department of 

Environmental Protection (PADEP) requirements under the 

Pennsylvania Act 2 program, as well as USEPA Region 3 

requirements. Activities included site visit, meetings and 

presentations to both agencies, as well as preparation of 

memoranda and reports. Included in the evaluation was a 

sensitivity analysis of the parameters used to evaluate a 

construction worker scenario; site-specific parameters, 

parameters from the scientific literature, and parameters provided 

by the agency were evaluated. 

U.S, Steel, Human Health Risk Assessment, Fairfield, 

Alabama, USEPA Region 4. Developed the RCRA RFI Human 

Health Risk Assessment Workplan for the U.S. Steel Fairfield 

Works under USEPA Region 4 and Alabama Department of 

Environmental Management (ADEM) requirements. Activities 

included site visits, preparation of strategy, review of the full RFI 

workplan to ensure consistency with risk objectives, and 

preparation of responses to agency comments. Work included a 

detailed evaluation of US EPA's current and proposed adult soil 

ingestion rates. 

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Hartford Working Group, Hartford Hydrocarbon Plume Site, 

Hartford, 1/linois, USEPA Region 5. Provided toxicology and 

risk assessment services to the PRP group for the Hartford 

Hydrocarbon Plume site in Hartford. IL. Provided review of indoor 

air screening levels developed by the Agencies for benzene. 

butane, isopentane. trimethylbenzene and other petroleum-related 

constituents used in vapor intrusion evaluations. 

C. Representative Risk Assessment Experience Under Other 

Programs 

NiSource, Risk Assessment Issues, Columbus, Ohio. Serving 

as the human health risk assessment expert for NiSource's 

environmental programs. Have addressed issues related to PCBs 

(including conducting employee informational meetings), MGPrelated constituents (benzene, PAHs), radon, and mercury. 

Confidential Utility. Have provided PCB expert support for 

issues related to PCBs in natural gas pipeline systems and 

potential residential and commercial exposures. 

Bureau of Land Management, Environmental Impact 

Statement, Western States. Developed human health risk 

assessment to evaluate five pesticides proposed for use in. BLM 

vegetation treatment programs. Risk assessment uses standard 

USEPA Office of Pesticide Policy risk assessment methods and 

includes use of the AgDRIFT model to evaluate off-site spray drift 

and deposition, and transport models to evaluate surface water 

impacts. Worker, public and Native American subsistence 

receptors were evaluated. Work has included interagency 

seeping meetings. Report available at: 

http://www.blm.gov/wo/stlen/proq/more/veg eis.html. 2007. 

Bureau of Land Management, Environmental Impact 

Statement, Western States. Conducting human health risk 

assessment for additional pesticides for the BLM vegetation 

treatment programs following the protocol developed for the 2007 

BLM Vegetation EIS. 

Confidential Client, Indiana. Evaluated groundwater and soil 

gas data for vapor intrusive to indoor air using the US EPA version 

of the Johnson and Ettinger model. Used the Johnson (2002) 

sensitivity analysis method to ensure that critical model 

parameters were within acceptable/realistic ranges. Provided 

deposition testimony and testimony in a court hearing on both the 

vapor intrusion pathway risk assessment and the toxicology of 

benzene. 

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U.S. Steel, Development of a Standardized Risk Evaluation 

Guidance Manual, Pennsylvania. Worked in conjunction with 

another firm and USS personnel to develop a standardized Risk 

Evaluation Guidance Manual for USS. The manual addresses 

important issues in human health and ecological risk assessment, 

provides background for the issues, USS strategy to address the 

issues, and examples of standard language and references to be 

used in future USS reports. The manual will allow for more costeffective and consistent risk evaluations to be conducted for USS 

facilities and sites. 

U.S. Steel, Review and Comment on Indiana's RISC Program, 

Indiana. Reviewed several draft versions of Indiana's "Risk 

Integrated System for Closure" guidance, and submitted 

comments to the agency. Detailed comments were provided on 

the following topics: construction worker soil ingestion rate, soil 

saturation limit, arbitrary caps for metals concentrations in soil. 

Have also prepared comments on Indiana's draft groundwater 

policy and The User's Guide that details how the RISC program 

will be applied to RCRA sites under state authority. 

U.S. Steel, Human Health Risk Assessment, Fairfield, 

Alabama. Conducted a human health risk evaluation for a parcel 

of property to be leased by U.S. Steel at Fairfield Works. 

Activities included <ovaluation of a construction worker scenario, 

and use of the Johnson & Ettinger and ASTM models to evaluate 

indoor and outdoor air. 

West Virginia Manufacturer's Association, West Virginia. 

Worked with the WVMA on a committee to review and provide 

language to the West Virginia Department of Environmental 

Protection in development of their tiered site closure guidance. 

Indiana Department of Environmental Management, Indiana. 

Served on an IDEM committee to review and provide language in 

the development of revisions to the "Risk Integrated System for· 

Closure" guidance. 

D. Representative Toxicology Experience 

Utility Solid Waste Activities Group (USWAG), Washington, 

DC. Reviewed and developed comments on the risk assessment 

aspects of USEPA's June 2010 proposed rulemaking for the 

disposal of coal combustion residuals (CCRs). Comments 

focused on a critique of the USEPA's updated human health and 

ecological risk assessment, a critique of the USEPA's fugitive dust 

model report, and a critique of USEPA's proposed listing of CCRs 

as a hazardous waste under RCRA Subtitle C. 

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Utility Solid Waste Activities Group (USWAG), Washington, 

DC. Reviewed and developed comments on the USEPA"s risk 

assessment for coal combustion wastes. The risk assessment 

was released in 2007, and comments were submitted under 

USWAG cover in January 2008. AECOM addressed all aspects of 

the risk assessment including human health, ecological risk and 

fate and transport. Provided oral comments during a national 

teleconference. 

Utility Solid Waste Activities Group (USWAG}, Washington, 

DC. Developed information sheet on "What is Coal Ash" for use 

by the USWAG membership for community relations. 

Electric Power Research Institute, Palo Alto, CA. Developed 

the report ··comparison of Risks for Leachate from Coal 

Combustion Product Landfills and Impoundments with Risks for 

Leachate from Municipal Solid Waste Landfill Facilities,"" EPRI 

Report Number 1020555. available at www.epri.com. 

Prairie State Energy Campus, Washington County, fL. 

Provided presentation to county board on coal ash composition 

and health risk issues. 

We Energies, Milwaukee, WI. Reviewed the basis of the state 

and USEPA screening levels and toxicity values for molybdenum, 

and demonstrated the over-conservatism used in their derivation. 

Provided the review to the state agency, and developed a fact 

sheet on molybdenum in groundwater for communications with a 

local community. 

We Energies, Milwaukee, WI. Reviewed the basis of the state 

screening levels and toxicity values for aluminum as part of review 

of the Wisconsin Department of Natural Resources proposed 

groundwater standards under NR 140. Provided testimony for a 

board hearing, and met with the state regulators, and 

demonstrated the over-conservatism used in their derivation. 

Ameren UE, St. Louis, MO. Developed a human health and 

ecological risk assessment to support the regulatory closure under 

the state agency of a former ash impoundment located along a 

major river at the Hutsonville, IL Power Station. Boron and 

molybdenum were constituents of interest. Pathways evaluated in 

the risk assessment included use of groundwater for irrigation 

purposes and the migration of groundwater to the river and 

potential impact on the benthic community. Work included 

negotiation meeting with the local agency. 

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Ameren UE, St. Louis, MO. Serving as an expert for a landfill 

siting project in Missouri, for issues related to exposure, toxicity 

and risk assessment. Provided public testimony at a county board 

meeting as well as written comments that have been submitted 

into the record. 

AES, New York. Provided expert testimony on the lack of human 

health effects of ammonia in groundwater associated with coal 

ash landfills. Developed expert opinion, reviewed and critiqued 

opposing opinions, and testified at hearing. 

AES, Puerto Rico. Provided review and synthesis of data 

associated with a beneficial use product, AGREMAXTM 

manufactured by AES Puerto Rico using bottom ash and fly ash 

from the coal-fired power plant. Specifically, evaluation of data on 

metals content, leaching of metals, and radionuclides were shown 

not to pose a human health or environmental risk based on the 

beneficial uses of AGREMAXTM. Testified on AES behalf at a 

Puerto Rican Senate subcommittee hearing on coal ash issues. 

South Carolina Electric & Gas, Columbia, SC. Provided 

presentation materials for use in a landfill siting and zoning 

process. Materials addressed the comparison of arsenic and 

other metals and radionuclides in coal ash and in our natural 

environment, and background levels of arsenic in foods and 

background levels of exposure to radioactivity in our natural 

environment. 

Utility Solid Waste Activities Group (USWAG), Washington, 

DC. Provided oversight of comments developed on the proposed 

listing of naphthalene as a carcinogen by the National Toxicology 

Program, and on the US EPA's childhood cancer document. 

Electric Power Research Institute, California. Worked with 

another ENSR toxicologist to develop a critique of the 

benzo(a)pyrene toxicity value developed by the United Kingdom 

for their Contaminated Lands program. 

Confidential Natural Gas Client, Toxicity Assessment, Ohio. 

Provided toxicity assessment of cleaning compounds proposed for 

use in the decommissioning of a natural gas pipeline laid on the 

bed of a reservoir that serves as the primary drinking water source 

for a community. Demonstrated that even should a catastrophic 

release of cleaning fluid and/or PCBs occur, human and 

ecological health would not be adversely affected and that 

concentrations at the drinking water intake would be much lower 

than health-based values or detection limits. 

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Confidential Client, Toxicology Review, Indiana. Provided a 

review of the toxicology and potential carcinogenicity of two 

structurally similar proprietary industrial chemicals. Used recent 

data on the nongenotoxic/cytotoxic mechanism of action of a class 

of potential carcinogens to demonstrate that a safe level for 

worker exposure exists. 

U.S. Environmental Protection Agency, Literature Review. 

Developed a strategy for evaluating absorption data in the 

literature and applied it to the development of absorption 

adjustment factors for oral and dermal exposures to soil and water 

for 5 metals of concern at hazardous waste sites (arsenic, 

cadmium, chromium Ill, chromium VI, inorganic mercury, organic 

mercury, and nickel) based on a thorough review of the literature. 

Georgia Pacific, Literature Review, Georgia. Reviewed 

literature and summarized the current scientific knowledge of the 

endogenous synthesis of halogenated compounds in humans. 

E. Representative MGP Experience 

Natural Gas Company, Risk Assessment Advisor, Ohio. 

Serving as strategic risk assessment advisor to the manager of 

MGP sites. Work includes conducting risk assessments for MGP 

sites under various state programs, evaluation of program-wide 

vapor intrusion data, regulatory negotiations, environmental 

communications, and employee meetings. 

Natural Gas Company, Former MGP Site Advisor, Wisconsin. 

Have reviewed remediation plans and fenceline monitoring plans, 

gave presentation at public meetings discussing the air monitoring 

plan, and have reviewed fenceline monitoring data for a 

remediation project. 

Energy Company, Former MGP Site Review, Rhode Island. 

Provided senior review of an air monitoring program and identified 

where fiexibility can be used in the development of fenceline air 

monitoring standards. 

Village of Oak Park, Former MGP Site Advisor, Illinois. 

Provid.ed senior review of remediation plans, and fenceline 

monitoring plans, and provided air monitoring data evaluation. 

Was involved in regulatory meetings, negotiations, and 

presentations to the Village council, including public meetings 

concerning air monitoring aspects of the project. 

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Committees 

Leader of AECOM's Risk Assessment Technical Practice Group 

including practitioners internationally within AECOM with 

specialties in human health and ecological risk assessment and 

other supporting disciplines. 

Leader of AECOM's Coal Combustion Product (CCP) Initiative; 

responsible for following regulatory developments, and keeping 

AECOM staff and clients updated on the issues. 

Elected member of the American Coal Ash Association (ACAA) 

Executive Committee, and member of the Government Relations 

Committee, and the Women's Leadership Forum. 

Task group leader for AECOM's Women's Leadership 

Collaborative program. 

Publications and Presentations 

"Hexavalent Chromium in Perspective" Presentaf1on and invited 

Chair- Human Health Risk Panel, MGP 2012, Chicago, IL, March 

29,2012. 

"Health Risk of CCPs." Presented at the EUCI conference on 

CCR Management: Impacts of Regulations and Technological 

Advances. , Nashville, TN, February 28-29, 2012. 

"Risk Assessment: How the EPA Looks at Coal Combustion 

Products." Presented at the ACAA Fall meeting, Indianapolis, IN, 

September 27, 2011. 

"Risk assessment: An overview of how the U.S. Environmental 

Protection Agency looks at coal combustion residuals." Presented 

at the American Chemical Society meeting in Denver, CO, August 

28,2011. 

"Is Coal Ash Toxic?" Keynote Presentation at the World of Coal 

Ash May 1 0-12, 2011, and invited presentation at The Coal 

lnstitute/NCCI meeting July 11,2011. 

"Potential Effect of Proposed Coal Combustion Residuals 

Regulation and Alternative Leach Testing on Beneficial Reuse." 

World of Coal Ash May 10-12, 2011. 

"Comparison of Risks for Leachate from Coal Combustion Product 

Landfills and Impoundments with Risks for Leachate from 

Municipal Solid Waste Landfill Facilities." World of Coal Ash May 

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10-12, 2011, and poster at Society ofToxicology March 6-10, 

2011. 

"Overview of Coal Ash Regulatory Issues." NCASI Northern 

Regional Meeting May 18-19, 2011. 

"Perspectives on Health Risks Associated with Beneficial Re-Use 

of Byproducts of Coal Combustion." Mcilvaine Hot Topic Hour. 

April 28, 2011. 

"Risk Assessment: How the EPA Looks at Coal Combustion 

Products." EUCI March 13-14,2011. 

"Risk Assessment: How the EPA Looks at Coal Combustion 

Products." Presented at the EUCI conference on Future of Coal 

Combustion Products (CCPs): Regulatory, Legal, Technical, and 

New Markets, March 2011, Denver, CO. 

"Development of a Realistic Risk Assessment Conceptual Site 

Model for an Urban River Sediment Site." B. Ruffie, L. Bradley, K. 

Durocher, and L. Fraiser. Battelle Sediment Conference February 

7-10, 2011. 

Press Conference with ACAA (American Coal Ash Association), 

October 27,2010, Knoxville, TN. 

"US EPA's Proposed rule for Coal Combustion Residual (CCRs): 

Beneficial Use Aspects." Keynote address given at the June 2010 

meeting of the American Coal Ash Association, Baltimore, MD. 

Bradley, L.J.N, and A. Ellis. 

"Overview of a CCP Site Investigation Conducted Under the 

Superfund Alternative Program." Presented at the ACAA spring 

meeting, March 2010, Nashville, TN. 

"Coal Ash Business Planning and Management: Addressing 

Risks and Liabilities in a Changing Regulatory Environment." 

Workshop presented at the EUCI Conference on the Future of 

Coal Combustion Products, March 2010, Houston, TX. L.J.N. 

Bradley, J. Trast, J. Matus, and A. Kier. 

"PAHs and Dioxins Not Present in Fly Ash at Levels of Concern." 

World of Coal Ash, May 2009 and Society ofT oxicology, March 

2009. 

Bradley, L.J.N., G.M. Fen!, and S.W. Casteel. "In Vivo 

Bioavailability of Arsenic in Coal Combustion By-Products." 

44 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

Poster presented at the Society of Toxicology 2008 annual 

meeting in Seattle, WA. 

Bradley, L.J.N., K. Sullivan, and M. Garcia. "Background Levels 

of Benzene in Indoor and Outdoor Air." Paper presented at the 

Gas Technology Institute's Natural Gas Technologies II 

Conference, Phoenix, Arizona. February, 2004 

Bradley, L.J.N., and K.A. Sullivan. "Risk-Based Action Levels for 

Remediation Project Fence-Line Air Monitoring Programs." The 

Toxicologist. 72(S-1): 395. March, 2003 

Bradley, L.J.N., and M. Gerath. "Generic Risk and Fate Analysis 

for Mercury at Natural Gas Meters." Paper presented at the 

December 1998 Society for Risk Analysis Annual Meeting, 

Phoenix, AZ. 

Bradley, L.J.N., K.B. Lemieux, M.C. Garcia, A.H. Parsons, and 

D.E. Rabbe. "Comparison of Concentrations of Selected Metals 

and Organics in Fish Tissue and Sediment ·,n the Grand River, 

Ohio, and the Southern Lake Erie Drainage Basin." Human and 

Ecological Risk Assessment 4(1 ):57-74 (1998). 

Bradley, L.J.N. "TPH Analyses Provide Means of Direct 

Assessment of Diesel Releases." Paper presented at the October, 

1997, Contaminated Soils Conference, Amherst, MA. 

Bradley, L.J.N. "Risk Assessment of Hazardous Air Pollutants in 

Arizona." Paper presented at the December, 1996 Society for Risk 

Analysis Annual Meeting, New Orleans, LA. 

Bradley, L.J.N. "Cost-Effective Use of Tiered Approaches in Risk 

Assessment." Paper presented at the October, 1996 Annual 

Conference on Contaminated Soils, Amherst, MA. 

Bradley, L.J.N. "Role of Risk Assessment in Environmental 

Management." Invited paper presented at the West Virginia 

Manufacturers Association Environmental Compliance 

Conference, May, 1996, Charleston, WV. 

Bradley, L.J.N. "New Toxicology Data for Chloroform: 

Implications for the Pulp and Paper Industry." Proceedings of the 

1996 Environmental Conference of the Technical Association of 

the Pulp and Paper Industry. Vol1, pp. 13-16 (1996). 

Bradley, L.J.N. "Ingested Arsenic- Are the Taiwanese Data 

Appropriate for Risk Assessment in the U.S." Paper presented at 

45 
Electronic Filing- Received, Clerk's Office, 08/15/2012 

the December, 1994, Society of Risk Analysis Conference, 

Baltimore, MD. 

Magee, B.H., and L.J.N. Bradley. "Absorption Adjustment Factors 

for Use in Risk Assessment." Proceedings of the International 

Congress on the Health Effects of Hazardous Waste. (1994). 

Bradley, L.J.N., B. H. Magee, and S.L. Allen. "Background Levels 

of Polycyclic Aromatic Hydrocarbons and Selected Metals in New 

England Urban Soils." J. Soil Contam. 3(4):349-361. (1994). 

Magee, B.H., L.J.N. Bradley, E.L. Butler, A. Dasinger, J. 

Grabowski. "Risk-Based Target Clean-Up Levels for TPH in 

Soils." In: Hydrocarbon Contaminated Soils. Vol. 3. pp. 303-319. 

Edited by P.T. Kostecki and E.J. Calabrese. 1993. 

Bradley, L.J.N. "Human Health Risk Assessment Workshop." 

Presented at the September, 1992, Hydrocarbon Contaminated 

Soils Conference, Amherst, MA. 

46 
Electronic Filing - Received, Clerk's Office, 08/15/2012 

EXHIBIT4 
12 

2019 

2020 

lotal I 

Amersn Energy Raaot~rcea AH&rn&tfve S02 Ltmit Com.parlaon to the Current MPS 

39, . 

39,151 

VariencaS02 

T >n& 

39 151 

6ll' 

7, 

7, 

Note for Ula -cumula~ve S02 Ver\ance Fledu:ed Tons• CJOIUml\, a positive number lndioates an em~ decrease (b5Mfit), 

51 

51 

31.452 

594.690 

i=!eductions il"' 

SOZ Variance 

.,.. 

~.S'i2 

~Tons shown for ~010 ,end 2011 ara be.s&d on aciu.aJ SOO emissions, ReWCed tons~ toe 2012-2020 are bas&d 0t1 the notoparating HutsorMJle 

end Meredosia less !XJiooti&iS02 eml~ !rom Futvra.Gen 2. 

Ameren Alternative $02. Emis$on Umit