## Electronic Filing

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# 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 Jolm Therriault Assistant Clerk ofthe Board James R. Thompson Center 100 W Randolph Suite 11-500 Chicago, Illinois 60601

Re: DocketNo. 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 aboutPotential HealthEffects during the Hearing (August 1, 2012) on Ameren Energy Resources (AER) Request for Variance from the Illinois Sulfur Dioxide (S02) Multi-Pollutant Standard (MPS)

DearMembers ofthe Illinois Pollution Control Board:
Thepurpose ofthis letteris to provide a toxicologist's perspective on the statements about potential health effects made inthe hearing (August 1, 2012) onAmeren Energy Resources (AER) request for variance from the 2015 and 2017 SulfurDioxide (S02) emissionrate provisions ofthe Illinois Multi-Pollutant Standard (MPS). Myknowledge ofthe statements made during the hearing comes from the transcript ofthe hearing, which was providedto me by Amy Antoniolli ofSchiffHardinLLP.
Discussions aboutthe potential for adverse health effects providedin this letter are predicatedonthe 

### assumption thatthere is a causal relationship between S02 exposures and adverse health effects. However, most epidemiological evidencepoints towardparticulate matter as a stronger causal agent for mortality and morbidity (i.e., effects otherthan mortality) than gaseous S02. Because S02 isusually found in association withparticulate pollution, (S02 is the precursor for fine sulfateparticles) andbecause only limited evaluation ofpotential confounding (intervening variables thatmakes it appear that au effectis caused by a particular agent whenthe effect is actually due to something else) has been conductedin most epidemiological studies, separatingthe health effects ofthese two pollutants has been very difficult.
The Board should be aware that more studies thannothave failed to find statistically significant associations between long-term and short-term S02 concentrations and adverse health outcomes, indicatingthatthe apparent associations maywell be due to other factors. In

### fact, EPAhas concludedthatthere is not a causal relationship between long-term 802 exposure and respiratory effects ormortality. While EPAhas concludedthat theresults of clinical studies inwhichhumans are exposedto S02 concentrations muchhigher than those found in ambient air support a causal relationship betweenrespiratory morbidity and shortterm exposure to S02, nine ofthe 10 primary epidemiology studies attempting to correlate short-term exposure to asthma-related emergency room visits or hospitalizations reliedupon

## 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 onlysuggestive 

### ofa causal relationship with mortality. Therefore, despite the dogmatism with which health effects from S02 are asserted, whenthe studies providing the underlying support for such declarations are more closely examined, it becomes clearthatthe association between S02 exposure and respiratory health effects and mortality isnotnearly as certain as typically portrayedbythe media, regulators and activists. Asthmais the health effect most commonly citedbythese groups as associated with S02 exposure, and they pointto the rise in asthma in the US population as proofofeffect. However, there are many theories about the rise in asthma over the past 30 years, and exposure to outdoorpollutionis probablythe leastplausible explanation given thatthe air quality in Illinois and the nation as a whole has improved dramatically during the same time period over which asthma prevalencehas increased, as discussed in more detail in the specificresponses to public comments. Although it canbe universally agreed that respiratory effects such as asthma attacks and chronic obstructivepulmonary disease (COPD) represent adverse or harmful effects, simply establishing that apersonwho has possiblybeen exposedto S02 in an environmental setting experiencedbronchoconstriction or a reduced expiratory volume is notproofthat the potential exposure causedthe effect. This is because in any individual, these effects could have been causedby a number ofdifferent factors, for example, indoor or outdoor allergens, smoking orpassive exposure to cigarette smoke, or viralpathogens. Likewise, the fact that a powerplantmay emit S02 does notnecessarilymeanthat off-site air concentrations will be high enough to elicit adverse health effects.
Moredetails aboutresearch onthe potentialhealth effects ofS02 are providedin the specific responses topublic comments. Background
The MPS and the AER Requested Variance 

### The MPS specifies a 0.5lb/MMBtu S02 emissionrate until2014 when the required emission rate is decreased to 0.43 lb/MMBtu, followed by a decrease to 0.25 lb/MMBtu in 2015. Underthe MPS, the S02 emission rate is further decreased to 0.23 lb/MMBtu in2017. AER has requested a variance from meeting the 0.25 lb/MMBtu S02 emission rate requiredby the provisions ofthe MPS in 2015 and the 0.23 lb/MMBtu emissionrate thatis required in 2017. However, AERhas proposed amitigation emissionrate of0.35 lb/MMBtu that would take effectin 2013, resulting in AERtaking actionto reduce S02 emissions earlier than required bythe MPS. AER would comply withthe 0.35 lb/MMBtu mitigation emissionrate from 2013 to 2019, withthe 2017 MPS emissionrate of0.23 lb/MMBtubeing metby2020. The figure belowprovides a comparison ofAER's S02 emissions under the provisions ofthe MPS and the S02 variance.

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

2010 

### Ameren Energy 

### Resources Variance 502.UmitComparison**to~**

### tile CurrentMPS

Zflll 11}:12 101'3 2014 2015 Year 2016 2017 Z018**-'i"-AllP.~;~)Jie Emi5.~lon>** **~.Me(l** onMPS**Bi!~eliue Rat~**  -+-**Total.fl,lture&n!~s.ion~** B<UE:\! c.·n Ama-en Varianq--Rnte 2019 1.010



### The blue line represents AER's baseline emissions underthe MPS and the blackline represents emissions under the S02variance. As canbe seenin the figure, AER's emissions under the S02variance are considerably lower than the MPS emissions between 2012 and 2014 and are slightlyhigher from 2015 to 2019. However, the area representing the difference betweenthe MPS and S02variance emissions from 2012 to 2014 is larger than the area betweenthe MPS and S02variance emissions from 2015 and 2019. Therefore, there is an overall net improvement (i.e., decline) in S02 emissions under the S02 variance proposedbyAER. It

### should also be noted that AER has voluntarily operated at lower S02 emissionrates than allowable under the MPS since 2010, demonstrating its commitmentto reducing emissions. Ifthe reduced S02 emissions starting in2010 are taken into consideration, the positive difference betweenAER's S02 variance emissions andthose allowableunderMPS is even larger.

Overall Net Health Benefit ofthe Variance 

### Overthe course ofthe entire variance period, betweennow and 2020, the total tons ofS02 reduced in the atmosphere will be greater iftheAER-requested variance is granted than ifit is not. The source ofreduction in S02 emissions over the course ofthe variance periodis two-fold: 1) AERwill emit less S02via amitigationrate representing a 19% to 30% reduction in theMPS allowable S02through 2014; and 2) AERhas agreedto keep two of its coal-firedpowerplants shut down during the variance period, which will result in less coal beingburned. Assuming that the S02 emissions from the AER coal fleet are at levels that couldpotentially resultin off-site ambient concentrations high enough to cause adverse health effects under the provisions ofthe MPS, which is not a foregone conclusion, granting the variance would resultin an overall net health benefit. For example, ifa hypotheticalriskrelationship ofone additional asthma-related emergencyroom (ER) visitper 100 tons ofS02 emittedis 

### assumed, there will have been 77 fewer ERvisits over the duration ofthe S02 variance than 3

## Electronic Filing
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ifAER complies withthe MPS on schedule. Please note,however, that this assumed risk relationship is purelyhypothetical, as riskrelationships ofthis nature are typically expressed
on a per capitaper ton basis, taking into account the size ofthepotentially 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 whatthe scientific research is telling us, as described above and further elaborated upon below.
There appears to be a continuous 'spectrum ofsensitivity to S02, with some peoplebeing completelyunaffectedby concentrations that lead to severebronchoconstriction in others. Asthmatics are particularly sensitive to the effects ofS02 and the effects are enhanced if S02 reaches the lowerregions ofthelungs, which is more likely to occur during mouth breathing (as opposedto breathing throughthe nose) and exercise. Maximum effects ofS02
occurwithin a few minutes and continued exposure does nottypically increase the response and the effects are generally short-lived and completelyreversible (WHO, 2006).
Illinois Attorney General's Office 

### James Gignac, the Assistant Attorney General (pg 84 ofTranscript) stated in the hearing that there is a harm that would occur, despite AER's calculations demonstrating an overall reduction inthe tonnage ofS02 emissions over the 12-yearperiod. The basis for his statements regarding potentialharmis theincrease in emissions thatwouldbe allowed betweenthe years of2015 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 betweenthe years of2012 and 2014 andbecause the magnitude ofthe emissionreductions during the earlyyears is greater than the increased S02 emissions that will occurbetween 2015 and 2019, there wouldbe fewer adverse health effects overall. Therefore, the healthbenefits ofapproving the variance requested byAER outweighthehealth costs, resulting in an overall health benefit, whenthe entire period ofthe variance is taken into account. Assuming that one accepts thatthe current emissions pose a healththreat, not approving the variance represents a tradeoffbetween greaterreductions in health effects from 2012 and 2014 in exchange for smallerreductions inhealth effects between the years of2015 and 2019.
As mentioned in the beginning ofthis letter, the above discussion is predicated on the assumption that the C-R (concentration-response) relationships reported in epidemiological studies indicate causalrelationships betweenthe S02 exposures and adverse health effects. However, inmost studies thathave examinedthe potential for confoundingby other copollutants (particulates, ozone, nitrogen oxides), the small associations observedbetween ambient S02 concentrations and adverse health outcomes usuallybecome null whentwopollutantmodels are used, indicating that the associations are strongerfor the other pollutants
orthat there is no association with S02 (EPA, 2008; EPA, 2009; Goodman et al., 2010). As
aresult, more studies than nothave 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 ownIntegrated Science Assessment (ISA, EPA, 2008) prepared in support ofthe most recent S02NationalAmbient Air Quality Standards (NAAQS) review, "Overall, the epidemiologic studies do notprovide sufficient evidence to infer a causalrelationship between long-tenn exposure to S02 and asthma, bronchitis, orrespiratory symptoms". The EPA ISA also concludedthat "The available epidemiologic evidence onthe effect oflongterm exposure to S02 on mortality is inadequate to infer a causal relationship at this time" (EPA, 2008).
The EPAISA does conclude that "thehumanclinical, epidemiologic, and animal toxicological data are sufficientto conclude thatthere is a causal relationship between respiratory morbidity and short-term exposure to S02" and that 'The evidence is suggestive ofa causal relationship between short-term exposure to S02 and mortality". However, ofthe 10 primary epidemiology studies attempting to correlate short-term (daily) S02 exposures to adverse health outcomes relied uponbyEPA, nine found either no association or very small positive associationsbetween daily S02 concentrations and asthma-related emergencyroom visits orhospitalizations. Amongthe studies for whichweakpositive associations were observed, conclusions were either: 1) basedonly onresults from single-pollutantmodels (i.e., multiplepollutantmodels were notused, which are applied to determine confounding by co-pollutants); or 2) based onresults from single-pollutantmodels thatwere not statistically significantin two-pollutant models.
Statistical significance is keyto determining ifexposure and effect are causally associated. Determining whether the effect is isolated, independent, or secondary to a known effect of exposure is also importantbecausethese types ofeffects maybe the result ofother factors not related to the exposure ofinterest (Goodman eta!., 2010). Isolated effects occurin only a few test subjects and independent effects are those which occurin the absence ofother effects expected viathe same mechanism ofaction. The fact thatthese effects occur inconsistently andlackbiologicalplausibilityis an indicationthat they are more likely due to another factor ormeasurement errorrather than exposure related. A test ofstatistical significance helps determine whether effects are .causedbythe exposure under study. These tests compare differences between exposed and non-exposed groups oftest subjects as opposed to evaluating effects inindependent individuals. Ifthe difference between exposed and non-exposed groups is not statistically significant, the exposure is eitherinsufficient to cause the effectunder study orthe study is not sufficientlypowered, most likely due to having too few test subjects. Only one ofthe I0 epidemiological studies (NYSDOH, 2006) correlating daily S02 concentrations to adverse health outcomes relied uponbyEPA in the latestNAAQS review found a marginally statistically significant association with increased S02 levels inboth single-andtwo-pollutantmodels. However, the authors ofthat one study acknowledgedthat correlationsbetween co-pollutants made these results difficult to interpret.


### Peoria Families against Toxic Waste A representative for the PeoriaFamilies against ToxicWaste, Tracey Cox, indicated that health experts understand andhavepointed outthat cumulative S02 reductions do nothing to help communities with short-termpollution impacts and it is those short-term impacts that happento children and the elderly population across the state. 5

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Itis not correct that cumulative S02 reductions do nothing to abate short-termpollutant impacts. Long-term concentrations are not completely independent ofshort-term concentrations ofthe same pollutant. In fact, EPAhas performed extensive evaluations to determine relationships between short-term and longer-term concentrations ofvarious pollutants andhas on occasion set a longer-term standardto limit the relative frequency with which shorter-tenn exposures will exceed aparticular level. In

### addition, EPA's screening modeling guidance indicates that for a point source it canbe assumed that the maximum daily average concentration is 0.4 ofthe maximum 1-hour and thatthe maximum annual concentration is 0.08 ofthe max 1-hr (http:llwww.colorado.gov/airguality/permitslscreen.pdf). Fromthis we can infer 24-hourto annual ratio of0.4/0.08 = 

### 5. Thus, it is widely accepted thatlong-term and short-term concentrations are related to one another. Forthis reason, the overall netreduction in S02providedbythe variance in comparisonto the MPS regulatory schedule is also expectedto have an effect orreducing short-term exposures over the variance time period.
Sierra Club 

### A representative ofthe Sierra Club raisedthe issue ofthe increasing incidence ofasthma in childrenthathas been observed overthe last several decades, indicatingthat inhisjob as a school social worker, he has seen the effects ofS02 in terms ofasthma. Nationwide, S02 concentrations fell32% between 1980 and 1990 alone. The distribution of asthma in other countries also fails to implicate S02 or otherpollutants as an aggravating factor. Some ofthe highest asthma mortalityrates occurin Australia andNew Zealand, whichhave excellent air quality. Asthmais more prevalent in rural areas ofthe Scottish highlands, whichhave some ofthe lowestozone concentrations inthe world, than in more urban andpollutedparts ofthe United Kingdom, according to a recentreport (Friebele, 1996). Changes in the diagnostic coding ofasthma and survey questions in self-reporting asthma questionnaires overthe last 30years have likely altered the diagnosis ofasthma cases and caused changes inprevalence and incidence statistics. The International Classification of Diseases (ICD) providedbythe World Health Organization (WHO) was revised in 1978 (9th revision) and 1990 (1Oth revision) resulting in a change to the coding ofasthma. Inthe ICD 8, a patientwith "asthmaticbronchitis" wouldhave beencodedunderbronchitis, while in ICD 9this sameperson wouldbe codedunder asthma (Marcus andBraman, 2010). One study that analyzed asthma patientrecords found an increase inpatients with an asthma classificationthathada history ofsmoking in the 1980s versus the 1970s. The cause ofthis difference was attributed to the change in classification ofasthmatic bronchitis from a bronchitis heading to an asthma heading, resulting in asthmatic bronchitis patientsnow falling under the umbrella ofasthma inthe 1980s (Marcus andBraman, 2010). This change in coding may also influence the validity ofepidemiology studies thatlook at hospital ER visits for asthma as potential indicators ofan associationbetween ambient pollutant concentrations and respiratory effects over years during which changes in the asthma definition has changed.

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A large source ofasthma surveillance data is compiledby the N a tiona! Centerfor Health Statistics ofthe Centers for Disease Control and Prevention (CDC) under the National Health Interview Survey (NHIS). The NHIS questions usedto evaluate asthmaprevalence changed in 1997 and 2001, resulting in three separate types ofquestions thatcould impact asthma prevalence estimates from 1980 to 1996, 1997 to 2000, and 2001 to the present (National Heart andLung Institute; www.nhlbi.nih.gov/health/prof/lung/asthma!surveil.htm). These changes prevent comparisons ofreported 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 ofasthma informationis requested (lifetime incidence versus episodes in thepast 12 months, for example).
The increase inasthma cases may also bepartially explainedbyfactors relating to changes in healthcare access andphysicianperceptions. The diagnosis ofasthma may have become
more likely than a similar diagnosis ofbronchitis 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 backgroundincreases found for other diseases with similar symptoms over thattime period (Manfreda eta!., 1993). The study attributes some ofthe increase to an increase inthe likelihood ofasthma diagnoses.
Another factor that may have contributed to the apparent increase in childhood asthma prevalence is that children spendmuchmore time indoors todaythan they did 30 years ago. In addition to contributingto the development ofasthma, exposure to various indoor air initants can also exacerbate asthma symptoms. Cat, cockroach, andhouse mite dust allergens have all beencausally linked to exacerbation ofasthma symptoms in.sensitive individuals, and environmentaltobacco smoke exposurehas also been causally linked to exacerbation ofasthma symptoms in young children (Institute ofMedicine, 2000). Therefore, the suggestion byMr. Coxthat S02 emissions (pg. 133 oftranscript) are significant contributors to the rise inreported asthma cases (and other diseases) is not supportedby evidence in the literature.
ELPC 

### Jennifer Cassel from the ELPC read a letter from Illinois health professionals opposing AER's variancerequest. The letter stated that "High levels ofS02 andNOx can exacerbate respiratory systems in at-risk individuals, including children andthe elderly, including asthma and COPD attacks." (pg 144 oftranscript). The operative wordin this statementis "high" levels. There are many controlledhuman studies thathave exposed healthy and asthmatic testpopulations to S02 andthathave measured smalllung function decrements in the asthmatic population, particularly athigher than normal exertionlevels. However, most fail to show a statistically significantresponse, and evenin asthmatics (a sensitive subpopulation), responses are only seen athigh concentrations on the order of250ppb (715 J.lg/m3) 

### over a 10 minute period (WHO, 2006). Peak exposures in the range of4,000 ppb (11,440 J.lg/m3) 

### to 5,000 ppb (14,330 J.lg/m3) 

### are required for reductions in mean lung function innormal (non-asthmatic) individuals at rest. No significant changes in group mean

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lung function in healthy individuals have been seenbelow short-term exposures of 1000 ppb (2860**~g/m ),**  

### even with exercise (WHO, 2006).
To putthe 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/m 3**  

### (15 ppb) and45**~g/m 3**  

### (17 ppb) in2009. The statewide average 1-hourhigh in 2010 was 197**~g/m 3**  

### (75 ppb), compared with 212**~g/m 3**  

### (81 ppb) in 2009 and 335**~g/m 3**  

### (128 ppb) in 2008. Therefore, not onlyhave the air concentrations monitored in Illinois been wellbelow 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 bythe National Research Council (NRC) thatindicated that annual healthrelated damages from particulate, S02 andN02 cost 62 billiondollars in 2005 alone. The concentration-response (C-R) relationship used in the NRC Health ImpactAssessment (HIA) to estimate damages associated with S02-related hospital admissions was from a study conductedby Sheppard et al. (1999). However, this study, like most S02 epidemiology studies, failed to fm(l an associationbetween ambient S02 concentrations and asthma-relatedhospital admissions, as was clearly acknowledged by the authors.
The C-R function is a key component ofIDAs because it is this function that allows the effect ofinterestto be linkedin a quantitative way to incremental changes in concentrations by assuming a response continuum. However, C-Rrelationships are calculated for all pollutants andhealth endpoints examined in a scientific studybythe authors, even for those pollutant-health effectpairings that are determined through statistics not to be associated with the exposure ofinterest. Therefore, it is up to those conductingthe HIA (individuals other thanthe scientific study authors) to choose appropriate C-R relationships for use in modeling. Itdefies logic that the NRC study woulduse a C-R function from a study inwhich the ambient S02 concentrations and asthma-related hospital admissions were determined notto be correlated and casts doubt onthe validity ofthe entire NRC report. This is a clear example ofhow fmdings publishedinthe scientific literature are often misinterpreted and inadvertently or intentionallymisusedby activist groups. Comments of Samuel Dorevitch, MD 

### Comments from Dr. Dorevitchwere providedbyAndrewArmstrong withthe ELPC. Mr. 

### Armstrong read excerpts from Dr. Dorevitch's written comments, which statedthat research has demonstratedthat evenmoderate levels ofS02 are associated withbronchospasmbut provided no information onwhichresearch he was referring to or whathe considers a moderate concentration ofS02. However, the doctor does cite the EPA's ISA (EPA, 2008) andnotes thatit states that "epidemiologic studies observedrespiratory effects in areas where the S02 concentrationwas belowthe regulatory level in place at the time." The evidence of respiratory effects belowthe 24-hourNAAQS referenced in the ISA comes entirely from epidemiological studies. To putthis fmding into contextitis importantto understand what epidemiological studies can and cannot do.

. Observational epidemiological studies attemptto determine which factors are associated with diseases (riskfactors), and which factors mayprotectpeople or animals against disease 8

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

(protective factors). However, epidemiological studies ca1motprove that a specific risk factor actually causes the disease being studied. This is because epidemiological studies cannot control for, norcanthey necessarily identify, all ofthe factors that may influence a health outcome. Therefore, they are plaguedwith issues ofconfounding. For example, if coffee drinkers were more likely to also be cigarette smokers, and a study was conductedto explore potential associations between coffee drinking and lung cancer, without taking the smoking habits ofthe coffee drinkers into account, smoking wouldbe a confounder and the results may seem to show that coffee drinking increases the risk oflung cancer. Epidemiological evidence can only show that a risk factor is or is not associated (correlated) with ahigherincidence ofdisease in the population exposedto thatrisk factor. The higher the correlation, the more certain the association; but causation Catlf\Ot be proven in these studies. Therefore, the fact thatthere maybe studies showing that hospital admissions or emergencyroom visits were increased inan area where short-term S02 concentrations were below the NAAQS does notnecessarily meanthat the S02 concentrations causedthe increase inhospital admissions.
Studies thatuse populationlevel data, such as respiratory hospital admissions or emergency room visits obtainedfrom databases without collecting any data onthe individuals involved,
are proneto what is known as "ecologic fallacy". This occurs when a correlation observed at the population level is assumed to apply atthe individual level. Withoutinformation on whether the correlations were statistically significant and whether co-pollutants and other intervening variables were properly controlledfor, itis notpossibleto know whatthe implications ofthe findings are orifthe statement even accurately characterizes the fmdings. Thus, while EPA's ISA mayhave notedthatepidemiologic studies observedrespiratory effects in

### areas where the S02 concentration was belowthe regulatory level inplace at the time, the respiratory effects were notnecessarily due to S02 exposure. 

### Prairie Rivers Network A representative from the Prairie Rivers Network indicatedthatthe air pollutionthatis released from the Newton facility kills about 25 peopleperyear (pg. 186 oftranscript). This value appears to be from the PowerPlantImpactEstimator Software Tool located at http://www.catf.us/resources/publications/view/138 and another report entitled, "Toll from Coal: 

### An UpdatedAssessment ofDeath and Disease from America's DirtiestEnergy Source". This study was commissionedbythe Clean Air Task.Force (CATF, 2010). However, even upon examination ofthe technical support document for the estimator tool and Toll from Coalreport (Abt, 2010), the underlying assumptions usedin deriving these numbers are notparticularlytransparent. However, one thing noted is that the C-R relationship for S02 exposure and asthma-related hospital admissions used inthe tool was from a study (Sheppard eta!., 1999) that failed to find an associationbetween ambient S02 concentrations and asthma-relatedhospital admissions. Although these types ofevaluations
are becoming increasingly more common, use ofthese C-R relationships are subjectto significantuncertaintyrelated to their generalizability and accuracy. One thing is certain, CR relationships from studies that fail to establish an associationbetweenthe exposure and effect ofconcern should notbe extrapolatedto other situations in the hopes ofproviding

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accurate predictions ofadverse health outcomes. The other comments made above about CR relationships and theiruse apply here as well.
Miscellaneous Comments 

### Many commenters made vague statements such as "Coal power plants kill people.", "Hundreds ofpeople in Illinois die from what comes out ofcoal-fired powerplant stacks:" etc, but gave no support for these statements.
The public debate on air pollution coupled with the sensationalized air pollutionhealth stories inthe mediahave createdthe appearance thatharm from air pollution is much greater and more certainthan suggestedbythe underlying scientific evidence. According to Dr. Joel Schwartz (2006), whose work on the relationship betweenrespiratory hospital admissions and ambient airpollutants is amongst some ofthe mosthighly cited and one ofthe premier authors ofmany epidemiological studies thathave beenrelied uponbyEPAin establishing andre-evaluating US NAAQS, "the incentives in airpollution healthresearch encourage risk exaggeration

...Through exaggeration, m,nission ofcontrary evidence, and lackofcontext, regulators, activists, and even many health scientists misrepresent the results ofairpollution health studies and the overall weight ofthe evidence from the research literature" (Schwartz, 2006). Dr. Schwartz across multiple fields, including Clinical Medicine, Environment & 

### Ecology, Biology & 

### Biochemistry, andPharmacology & 

### Toxicology. http://www.esitopics.com/airpoll/interviews/JoelSchwartz.html
It

### is not surprising that ordinary citizens perpetuate the misinformation that is rampant in the mediainhearings such as the one onAER's request for variance from the S02MPS. We urge the boardto considerthe scientific evidence onthe health effects ofS02 rather than statements from citizens that havebeenmisleadbythe news media andreports publishedby activist groups. In support ofthis perspective, we have attached a copy of"AirPollution and Health: Do PopularPortrayals Reflect the ScientificEvidence?"byJoel Schwartz, which provides several case studies aimed atdemonstrating thatmisinformation about air pollution is a pervasiveproblem. The Schwartz (2006) article demonstrates why it is so important for those involved in evaluating and setting healthpolicy to look deeper thanthe summaries of studies providedby other governmental agencies, health scientists in press conferences, and activists inhearings. Likewise, because itis not uncommon for even those who shouldknow betterto inadvertentlymisrepresent the evidence, interpreting airpollutionhealth effects informationpublishedinthe mediarequires a level ofvigilancethatfew citizens are capable ofand as a result, while citizensmaybelievethat their health effects canbe attributed to AER's emissions, they are oftenmisinformed or evenmanipulatedby the local activists.
There is no question thatvery high levels ofpollution can kill, as occurred during the "London Fog" of 1952, when soot and S02were at levels orders ofmagnitude higher than those experiencedin developed countries today andvisibility was less than 20 feet. However, claims that low levels ofpollutants cause death is basedpurely on scientific evidence from observational studies that are incapable ofcontrolling for co-pollutants, lifestyle variables, and usually do noteven contemplate regional disease patterns that have nothing to do with air pollution. It

### is noteworthy thatresearchers havebeenunable to evoke adverse health outcomes in animals with S02 concentrations anywhere near as low as those found in ambient air today. 10

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Sincerely,

AECOM

LucyFraiser, PhD, DABT Associate Vice President/Senior Toxicologist

Enclosures: Attachment I. References Lisa JN Bradley, PhD, DABT Vice President/Senior Toxicologist

Attachment2. Schwartz, J. 

### 2006. Air Pollution and Health: Do PopularPortrayals Reflect the Scientific Evidence? AmericanEnterprises Institute for Public Policy Research. Envirorunental Policy Outlook, No. 2. Attachment 3. Resume ofDr. Lucy Fraiser Attachment 4. Resume ofDr. LisaBradley

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Attachment 1: References

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References
Abt, 2010. AbtAssociates Inc. Teclmical Support Documentfor the Powerplant Impact Estimator Software Tool
CATF, 2010. Clean Air Task Force. Toll from Coal: AnUpdated Assessment ofDeath and Disease from America's DirtiestEnergy Source. September.
Friebele, E. (1996). The attack ofAsthma. EnvironHealth Persp., 104: 22-25. Goodman, J.E., Dodge, D.G., and Bailey, L.A. (2010). A framework for assessing causality and adverse effects inhumans with a case study ofsulfur dioxide. Reg. Toxicol. Pharmacal. 58:308-322.

IEPA, 2010. Illinois Environmental Protection Agency. Illinois 2009 AnnualAir Quality Report. November 2010. http://www.epa.state.il.us/air/air-qualityreport/2009/index.htm.
Institute ofMedicine. (2000). Clearingthe Air: Asthma andIndoorAir Exposures. National AcademyPress. 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 asthmaprevalence inManitobabetween 1980 and 1990. Chest, 103:151-157. NYSDOH, 2006. April. NewYork State, Dept. ofHealth. A study ofambient air contaminants and asthma inNew York City. PartA: a comparison ofambient air 

### quality in the Bronx andManhattan. Part B: air contaminants and emergency departmentvisits for asthmainthe Bronx and Manhattan (Final). Report to Agency for Toxic Substances and Disease Registry (ATSDR); NewYork State, Energy Research andDevelopmentAuthority. NTIS PB2006-113523, July, 260p. http://www.nyserda.nv.gov

### Ien/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 PopularPortrayals Reflectthe Scientific Evidence? AmericanEnterprises 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. ParticulateMatter, ozone, nitrogen dioxide andsulfurdioxide. WorldHealth Organization Regional Office for Europe. 2006.

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Attachment 2: Schwartz, 

## J. 2006. Air Pollution and Health: Do Popular Portrayals Reflect the Scientific Evidence? American Enterprises Institutefor Public Policy Research. Environmental Policy Outlook, No. 2.

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## AmericanEnterpriseInstitutefor PublicPolicyResearch



## No.2,2006


# Air Pollution and Health: Do Popular Portrayals Reflect the Scientific Evidence? By Joel Schwartz
Envi-ronmentalists, regulawrs, health scientists, andjournaUsts are the main pun. 1 

### eyors ofinfonnation on ai-r pollution health risks. Unfortunatd)', these groups create the appearance that 

### ha:nnfrom airpollution is much greater and more cerr:ain r.han suggested 

### by the underl:;iing evidence. The incentives in airpollution health research encourage risk exaggeration, because infonnation purveyors depend on

### publicfear to nurintain rheir funding and influence. Investigative reporters are in 

### the bestposition to assess how the political economy ofenvironmental health research affects the production andportrayal ofthe evidence. Public debate on airpollution will continue to

### proceedfrom false premises untiljournalists 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 ofAmericans said they worry about air pollution "a fair**~mount"** or "a great deal."2 Public fear ofair 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 Healthresearchers often issue alarming summaries ofthe1r 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 andTiny Particles of Soot," "USC Study Shows Arr Pollution May Trigger Asthma inYoung 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 avisicingfellow atAEI.

1150 Seventeenth Street, N.W, Washington, 

### D.C. 20036menacing 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 amongNation's Most Toxic," and uAstlnna Riskfor- Children Soars with High Ozone Levels."5 Headlin_es like these m_ight be warranted ifthey accurately reflected the weight 

### ofthe scientific evidence. But they do not. Through exaggeration, omission ofcontrary evidence, and lack of**con~** text, regulators, activists, and even manyhealth scientists misrepresent the results 

### ofair 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 ofmedia air_pollution health stories are sensationalized exaggerations ofair 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 ofair pollution is out ofall proportion to the minor risks posed by current, historicallylow airpollution levels.

202.862.5800 wwv?.aei.org

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## 08/15/2012

False Alarm on Asthma and Air Pollution
Beginning in 1993, the CaliforniaAirResources 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·welve communities with air pollution ranging from near-background to the worst in the nation. 

### At a jointpress conference in 

### 2002) the USC researchers and CARB managers reported Infact, 

### by che time ofits 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 ofthe Air that childrenwho played three or more team sports were more rhan three times 

### Through exaggeration, Resources Board claimed: "This study illustrates the neednot to retreatbut 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 pushingforward in our efforts to strengd"len air pollution regulations."ll But 

### ifanyrhing, 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 ofthe 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 showedjust the opposite. While higher ozone \Vas associated with a greater risk ofdeveloping asthma for children who played three or more team sports (8 percent ofchildren in the study), higher

ozone was associated \:vith a 30 percent 

### lower risk ofdeveloping asthma in the full sample ofchildren 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 limitedjust 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 ofNew York at 

### overall weight of the

evidence from the research literature.
Higher levels ofother pollutants, including nitrogen dioxide and particulate matter (PM 10), 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 offour (rather than two groups of six), the association ofozone 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 ofthe countrywas also false. The four high-ozone areas inthe study averaged 

### 89 days peryear exceedmg the federal eight,hour ozone standard and 59 days peryear exceeding the one-hour standard during 

### 1994-1997, the years used to assess pollution exposure in the study.lONo

area ofthe United States, outside ofa few parts ofCali, fomia, has 

### ever had ozone levels this high evenfor a sin, gle year, much less for several years running. Stony Brook, who has since become the American Lung Association's medical director, claimed:

1This is notjust a Southern California problem. There

are communities across the nation thathave 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 stateplan to reduce ozone_nl3 The director ofthepediatric asthma program at theUniversity ofCalifon1ia atDavis claimed

11Sacramento is a very high ozone area, so 

### this [the CHS asd1ma study] is going to be very relevant to us."14 Notonly were all ofthese nominal experts wrong about whether the study 1s relevant to actual ozone**lev~ls** in the United States, all ofthem completely miSsed the fact that ozone and other air pollutants were associated with an overall lowerrisk ofdeveloping asthma. In a recent commentary on air pollution and asthma in the ]

### ournal ofthe American Medical Association, two prominent air pollutionhealth researchers cla'iroed:

## Electronic Filing

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## _Clerk's Office, 08/15/2012

"Some ev1dence suggests rhat air pollution may have contributed to the increasing prevalence ofasthma.''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-andThreat-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. Afterfollowing more than 1,700 children from ages ten to eighteen (years 1993 co 2001), CHS scientists reported thatthere 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 peryear during rhe study period.l8 Once again, no area outside Cahfo1nia has everhad anywhere near this frequency ofelevated ozone, even for a single year, so we can conclude that ozone is not causing anyreduction in children's lung capacity. This has not stopped environmental groups from claiming otherwise. For example, in 

### Impacts ofOzone on Our 

### Health, the Carolinas Clean Air Coalition claims: "Childrenhave a 10 percent decrease in lung function growth when theygrmv up in more polluted 

### air."19 The Children's Health Study also suggests thatfine particular matter (PM2

### .s) is causing little orno 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 inforced expiratory volume in one second (FEV1) and a 

### 1.3 percent decrease inforce vital capacity (FVC), both measures oflung capacity. But even this small effect drastically inflates the apparent 1mportance ofthe results. First, no location outside ofthe CHS communities has P!vf 25 levels anywherenear 

### 32 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 tenyears 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 Ifit 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 

### 1percentdecrease in

### FEY1 and a 

### 0.5 percent decrease in FVC. Thus) taking 

### the CHS results atface value, ozone is having no effect on children's lung development anywhere in theUnited States. 

### Plv1 2.5 is having virtually no effect. Nevertheless, the USCresearchers' press release on the study created an unwananted appearance ofserious harm. Titled "Smog May Cause Lifelong Lung Deficits," the press release asserted: "By age 18, the lungs ofmany childrenwho gro\V up in smoggy areas are underdeveloped andwill likely never recover."22 The National Institutes ofHealth (NIH) also misled the public about the study's findings and relevance. The director ofthe National lnstitme ofEnvironmental Health Sciences claimed the study ushows thatcurrent levels 

### ofairpollution have adverse effects on lung development in children."23 Furthermore, although the study is relevant only 

### co a few areas ofCalifornia with uniquely high air pollution levels, by asserting that it applies 

### co all 

### "smoggy areas" and to "cw-rent levels ofair pollution," NIH and USC created the false impression that the study applies to much ofche United States. The scientists were able to create these false**impres~** sions, because thejournal article on the study, which

was published in the prestigious 

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

### ti1e percentage change canbe calculatedby combining infonnation found in three differentplaces 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. Theresearchers reported a different outcome**meas~** ure in their NEJM paper: the percent of children in

## Electronic Filing

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each community with a lung capacity of less than 80 percent ofthe "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 per

### centage, from about 1.6 percent ofchildren 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 ofsome 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 ofCalifornia 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 ofexposure to occasional ozone smog-for example as itoccurs in the Sacrament.o area." capacityfor 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 ofchildren 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 ofthemagnitude ofthese 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 Statesneverreaches even 

### 0.25 ppm for

onehour, 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 withonly a 

### 2 percentdecrease in lungcapacitywould 

### nothave caused much alarm. This probably explains why thatnumber is nowhere to be fmmd in d1e 

### NEJM. report or thepress releases on it. 

## statistical correlations

are telling us something real about the effects of low-level air pollution. NIH took advantage ofthis 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 childrenwould be at 100 percent 

### ifthere were
no air pollution. This is exactly tl1e mistake environmentalistshave made inpromoting the study. For example, the American Lung Association's (ALA) 

### State ofthe 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 CleanAirCoalition 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 ofMedicine 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 ofYoung Monkeys Drastically Changedwhen Exposed to Ozone Pollution," the AmericanLung 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 contaminatedwith 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 thatreaders are 

### supposed to conclude that ozone is causing Americans to develop asthma.


## OfMice and Men
By far the most serious health claim about air pollution is that it kills tens ofthousan_ds ofAmericans eachyear, 

### mainly due to**expo~ure** 

### to PM2_5· 

### There is no question that high levels ofair pollution canhlL About

### 4,000 Londoners died dunng the infamous**five~day** 

### "London Fog" ofDecember 1952, when sooc and sulfur dioxide 

### soared to levels tens oftimes greater than the highest levels experienced in developed countries today, and visibility dropped to less than 

### 20 feet34 However, current fears center onwhether today's comparatively low levels of air pollution are also deadly. 

### An embarrassmentfor proponents oflow-level air pollution as a cause ofdeath is that the evidence is almost solely circumstantial, beingbased on sratiscical studies reporting small correlations betweenlong- or short-term air pollution levels an_d risk ofdying. 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 ofair pollution' Observational studies could be caken more seriously ifthey were supported by evidence -fi:om randomized, controlled studies that eliminate the possibility ofconfounding by non-pollution factors. Such studies cannot, ofcourse, 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 ofparticulate matter toxicology concluded:

Itremains the case thatno fom1 ofambient 

### 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 ofthe 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 airfor six hours per day for six months, or about one-fourth ofa typical mouse life span.36 Mice fed a high-fat diet and exposed to PMz.s had

more than 

### a 

### 50 percent greater rate ofatherosclerosis (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 linkbetween exposure to fine particle air pollution and the development ofatherosclerosis

... [The study] may explainwhypeople who live in highly polluted areas have a higherrisk ofheart 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 enthusiasticreception, there is much less here than meets the eye. The mice used m the study

were genetically engineered inways d1.at make them nnrepresentative ofeven real-world mice, much less of humans. The mice were designed to lack the genefor apolipoproteinE (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 thannormalmice ·when fed regular ratchow. ApoEknockout 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 cholesterollevel in Amelican men.40 Only

one in 

### SO Amencanmen 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 gulfbetween 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 Ifyou build a house outofcards, you would expect
even a gentle breeze to knock itdown. But rhis does not tell you much about rhe ability ofa real house to withstand a gentlebreeze. Likewise, 

### ifyou design an artificial

mouse that cannotregulate its fat or cholesterollevels, 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 onpeople. Unfortunately, news artieles on th_e study failed to provide 

### the context that \vould showthat studyhas 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 ofheart 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 ofthe 

### 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 ofconcentrations found in the air around majormecropolitan areas.'' The press release also quotes one of rhe study's authors saying that ';the**aver~** age exposure over the course ofthe 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 ofeach week, and filtered air the rest ofthe time. Over the six,month study period, this does indeed average out to about 15 )lg/m3, the level ofthe 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 PM2.5 levels in the countryhave far fewer hours ofhigh 

### Plv12 

## .s than were uSed in the mouse study. For example, Riverside Califor, nia averaged 

### 27**~1g/m3** 

### PM25 overthe pastyear, buthad 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 

### 8all atonce each day. Erther way, your average dose is 

### 8aspirins per day. But you are more likely to suffer 

### ill effects ifyou 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 inprinciple. It shows thatwhen 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 ofPM2 _5, that PM 25 increases the extent ofheart 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 nowfind a summary ofthe 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 Marchmeeting of the California Air Resources Board, staffmembers gave a detailedpresentation on jerrett eta!. (2005)-a new epidemiological study of the Los Angeles region thatreported a stronger link between PM2.5 and mortality than suggested m previous research regulators have used to supporttougher PM2

## .s standards.46 What CARE's staffdid not tell its board is that right around the same trme thatJerret.[ et al. was published, another study ofPM25 rioks in Californiaby 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

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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 ofattention 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 ofthe e1•idence. each year.54 The Bush administration, a constant target ofenvironmental groups for supposedly "gutting" power plant pollution requirements, last year adopced the Clean Air lntersrate Rule (CAJR).55 CAIR requires that powerplants 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 mainfonn of

### P!viz.s from power plants. EPA claims these PM1

## .s The AmericanLung Association's website includes an area called Medical Jomnal Watch, which summarizes**hun~** dreds ofair 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, orJames Enscrom-all of whom have provided evidence againsr. a connectionbetween**lm:~,r-level** airpollution andrisk ofdeath.49 

### Environmental groups want to increase reductions will prevent 

### 17,000 premature deaths eachyear.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 compoundnot expected to have any health effects-in studies of the health effects ofac1dic aerosols59 If

The ALA also excludes specific studies and portions ofsrudies thatfail to find any harmfrom air pollution. For e..xample, Medical]ournalWatch does notmention Gong et al. 

### (2003) and Holgate ec al. 

### (2003), whichfound hcrle orno adverse health effects in human volunteers who breathedhigh levels ofPM2.5 and diesel
sooc, respectively.50 The ALA does summarize the CHS findings on children's lungcapacitydiscussed earl1er, but does not mention that the study found that

even thehighesc ozone levels in the country had no effect onlung 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 powerplants 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 detailedreport summarizing ozone health effects research. The report analyzes hundreds ofhealch studies in nearly 1,000 pages, but fails to mention a studyreporting that 

### higher ozone was associated with a 

### lowerrate ofhospital visits in California's Central Valley.6l CARB was cerrainly

aware ofthe existence of th1s study, because CARB funded and published it. EPA also failed to mention the study in its latestreview ofthefederal 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 Medicaljournal Watch. CARB likewise cites only the first study in its review ofCalifornia's ozone standard.53 

### 500,000 Americans in 

### fifty cities from 

### 1982
to 

### 1989 and looked for cmTelations betweenPM2

_ 5levels and risk ofdeath.63 ThemostrecentACS report covered the periodfrom 

### 1982 to 

### 1998 and reported that each 

### 10**~tg/m3** increase in long-term PM2

## .s levels is associated with a 

### 4percent increase in risk ofdeath.64 Coal-fired power plants havebeen one ofenviron- mentalists' premier targets during the last several years. In reports such as 

### Danger in 

### the Air; 

### Death, Disease andDirty 

### Power; Power to Kill; 

### Children at Risk; and many more, environmental groups claim that particulate pollution from power plants is killing thousands ofAmericans The validity ofepidemiological studies, such as the ACS study, depends on rhe assumption that correlations between air pollution and health outcomes represent genuine causalrelationships. The implicit assumption is that after researchers have controlled fornon-pollution

## Electronic Filing

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- health factors 111.:e income or smoking, any residual**cor~** relation between air pollunon and healthrepresents a genuine causal linkage. Experience has shown that this assumption is false. For example, a reanalysis ofthe ACS data showed 

### that the apparent PM2

### smortality link was spurious. According to sensitivity analyses ofthe ACS data, PMz.s apparently kills men, but not women; those with

no more than a

### high school degree, but notthose 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 ofvarious dries

over time were added to the statiscical model relating PM2.S and risk ofdeach, che apparent effect ofPM2.5 disappeared.66 Cities that losr population during the**1980s~l\1idwest** "rust belf' cities-also had higher Pl\1 2.5 levels. People left these cities, ·which were in**eco~** nomic decline 1 in search ofwork in more economically dynamic parts ofthe country. Butpeople who work and have the wherewithal to migrate also tend to be healthier than the average person. Hence, what appeared to be an effect ofPM25 \Vas actually 

### the result of**differen~** rial migracion. Migration\\'as just one ofseveral**con~** founding factors that diminished or erased th_e apparent harmfrom PM2

_ 5, but thar were not accounted for by the 

### ACS researchers. This problem ofspurious air pollutionnsk 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 oflowlevel air pollution.


## The Politics of

## Air Pollution Health Science

Most public mformation on air pollution andhealth

comes from environmental activists, regulators, and health researchers. As these case studies show, their claims ofharm from cunent, historically low air**pollu~** tion levels are atbesc exaggerattons and at worst**fabri~** cations. The result is unwan-anted public fear, and continued supportfor ever more costlyregulatory 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 ofthe vast majority of**Ameri~** cans. Environmental groups want to increase support for

ever more stringent regulations, maintain and enhance their control over otherpeople's lives, and bring in the donations that support their activism. Regulamrs want to show the success oftheir efforts to reduce air**pollu~** non, but d1ey also want tojustify the need to preserve
or expand their powers andbudgets. Maintaining a**eli~** mate ofcrisis andpessimism meets d1ese institutional 

### ' goals, but at the expense ofencouraging 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 ofscience and scientists tlows from the power ofscientific 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 absentfrom more explicitly polirical endeavors. Environmental health research nevertheless suffers from its own set ofpressures that militate against evenhanded inquiry and dispassionace analysis and presentation ofevidence. 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 ofthe research intended to demonstrate the severity ofthe 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 attractviewers. As a result, journalists and editors are more likely to cover studies claiming harmfrom 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 ofspecific studies. But continuing

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-

to rely on scientific authoricy 

### will only petVetuate the 

### problem ofrisk exaggeration. Among the major providers ofpublic information on environmental risks, investigative reporters are in the best position to assess hmv rhe political economy ofenvironmental health research affects the production and portrayal ofsciennficevidence. 

### It would be a breach offresh air ifjour

### nalists and editors took up this challenge.
AEI editor Scott 

### R. Palmerworhedtvith 

### Mr. Schwart:;. 

### w editand 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 Preparedfor Public Citizen and the Seed Coalition (Alexandna,- VA: American Viewpoint, 2002); New York Conservation Education FU11.d, Key Findings of aState'U!ide Survey OfNew York State Residents onEnvironmental Issues (New York: New York League ofConservationVoters, 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, PPICSratewzde Survey: Special Survey on Califor, nians and 

### the Environment (San Francisco: Public Policy Insri,
tute ofCalifornia,july 2004). 2. Water Pollution Tops Americans' Environmenr.al Concerns 

### (Washington, D.C Gallup Poll, April21, 2006), available ar http//poll.gallup.com/content/Default.aspx?ct**~**

### 22492&**VERSION~p.** 3. Death, Disease and Dirty Power: Mortality andHealth Damage Due to AirPollutionfrom 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/ health/hds/ocar/ocarlnx.asp; Children at Risk: How Air**Pol/.u~** tionfmm Power Plants Threatens the Health ofAmerica's Chil

### dren (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 ofPublic HealthNews 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 AirPollutron May Trigger Asthma in Young Athletes," news release, February 1, 2002, available at li'I'VI'\\'.usc. 

### edu/hsc/info/pr/1vol8/803/air.html; A. 

### Di Rado, "Smog May Cause Ltfelong Lung Deflcits," Universrty 

### ofSouthem Cahfor, nia, September 8, 2004, available atVt"l.\w.usc.edu/uscnews/ scories/10495.html; 

### and Nationallnstitures 

### ofHealth 

### (NIH), "Link Screngrhened between Lung Cancer, Heart Deachs and Tiny Particles ofSoot," 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-cancer22mar22,1,7087336.story; M. Cone, "Study Finds Smog Raises Death Rate," LosAngeles Times, November 17, 2004; T. Freemantle, ''AsthmaRisk for Children Soars wich High Ozone Levels-Study," Houston Chronicle, February 1, 2002; and T Webber, "Don'tBreathe Deeply," 

### Indianapolis Star, 

### june 23, 2005. 6. CaliforniaAirResources Board, "Study Links AirPoilu, tlon andAs1:hma," news release, January 31, 2002, avallable at wv.w.arb.ca.gov/nev.rsrel]nr013102.htm. 7. TI1e risk ofdeveloping asthma was 30percent 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 ofstatistical significance. (The cop of rhe 9 5 percentconfidence interval±Orrelative riskwas 1.0. Anything less than that would have been statistically significant.) 8. Thejournal article is. R. McConnell, K T Berhane, F. Gilliland e1: al., "Asthma inExercising Children Exposed to 

### Ozoneo A Cohort Study," Lancer

### 359 (2002)o 386--91. 9. Once again the risk was 20 percentlO\:ver andwas just barely short ofstatistical significance. 10. Pollution monitoring data from theChildren'sHealth Studywere provided by CARB's staff. 11. CaliforniaAirResources Board, "StudyLinks AirPollu, tion and Asthma," news release, January 31, 2002, available at wv.•":"r.arb.ca.gov/newsrel/nr013102.htm. 12. Dr. No!rnanEdelman, quoted inS. Borenstein, "Air Pollution Is a Cause ofAsthma, Study Contends," Philadelphia Inquirer, February 1, 2002. 13. T. Freemamle, "AsthmaRisk for ChildrenSoars with High Ozone Levels-Study."

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14. In fact, even theworst areas ofSacramenro never aver, age more than a few days peryear exceeding the one, hour

ozone standard and 20 or so days per yearexceedtng the eight, hour standard--ozone levels typical ofthe ''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 SporrsActiv1ties 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 ofAsthma Symptoms,"]ou:rnal ofthe American MedicalAssociation 290 (2003)o 1915-17. 16. "Smog and Asthma: The Link-and Threat-Are Real," Sacramento Bee, May 6, 2003. 17. W.]. Gauderrnan, E. Avol, F. Gilliland et al., "The Effect ofAir Pollution onLung Development from 10 to 18 Years ofAge," 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 staffprovided data from these monitors. 19. Impacts ofOzone on OurHealth (Charlotte, NC Carolinas Clean Atr Coalition, undated), available at http://003af56. nersolliost.com/air_basics_ozone_impact.htm. 20. Based on researchby CARB staff, these values have been adjusted upward 

### by 13.6 percent to make "!:hem comparable wlrh PM25 levels determinedby the Federal Reference Method, which has been used nationwide since 1999 for der.erminlng compliance withfederal PM2.5 standards. SeeN. Motallebi,

## J. Taylor, A. Clincon, B. E. Croes et al.,**"Particu~** late Mateer rp California: Part 1-lntercomparisonofSeveral PM2.5,**PM 10** **~I.5•** and 

### PM 10 Monitoring Net\>.rorks," .Journal of rhe Air & Waste ManagementAssociation 53 (2003): 1.509-16. 21. Based on 

### lPN datafor 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 inmeasurementmethods. 22. Di Rado, "Smog May Cause Lifelong Lung Deficits." 23. Dr. Kenneth Olden_, quoted inNIH, "New Research ShowsAir PollutionCanReduce Children's Lung Ftmction,"

news release, September9, 2004, www.nih.gov/news/pr/ sep2004/nieh.s-08a.htm. 24. Here's how: First, note from table-3 

### ofthe NE]M article that PM2

_ 5 was associated with a 79.7 tmllilirer (ml) reduction in FEV1between the least and mostpolluted community. Then from table 2, note that at eighteen years ofage average FEV1
was 3,332 mlfor girls and 4,464 mlfor boys. Given that d1ere were 876 giTls and 883 boys in the srudy (p. 1,059, column 1), the weighted average FEV1 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 FVCwas 1..3 percent. Gauderman, Avol, Gilliland et al., ''The Effect ofAir Pollution on Lung**Develop~** mentfrom 10 to-18 Years ofAge." 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 paperprovides few details on the model or the underlying distribution 

### of**lung~funcrion** test scores by community. Thus, anotherproblem with this outcome measLITe is that it depends on something that was not actually measured! 27. NIH, "New Research ShowsAir PollutionCan Reduce Chtldten's LungFunction." 28. Amencan LungAssociation, State of

### rh£Air 2005 (Washington, D.C.: May 2005), 60. 29. N. Bryant, "WhatAir Quality Problem?" Charlotre Observer, September 1, 2005, available at \\'\Vw.charlotte.corn/ mld/charlotte/news/opinion/12530112.htm 1BMIDS= 13194. 30. A. Fell, ''Primate Research ShowsLmk between Ozone Pollution, Asthma,"**U.C.~Davis** news release, October 13, 2000, available at 'N\vw.dateline.ucdavis.edu/101300/DL_asthma.htmL 31. RecentScientific Finclings onHealrh Effects 

### ofAir PoUutwn andDiesel Exhaust (Oakland, CA: American Ltmg Association ofCalifomia, 2003), available a( v;vlw.californialung.org/ spotllght/cleanair03_research.html. 32. MelanieTum.er, "Kids Focus ofAir Quality Study ResearcherLookingfor 

### Link Becween. Ozone, Asthma in Yauch," 

### Modesto Bee, May 11, 2001. 33. EdieLau, "Study Suggests Asthma Culpri(; YoungLungs 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 AirPoUution (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 andPhannacology 38 (2003): 326-35. 36. Q. Sun, 

### A. Wang, 

### X. Jm et al.,**"Long~**Term

### A1r**Pollu~** tion Exposure and Acceleration 

### ofAtherosclerosis and**Vascu~** lar Inflammation inanAnimal Model," ]oumal of

### the American Medical Association 294 (2005)o 3003-10. 

### 37. NIH, "Air Pollution,**High~**Fat DietCause**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, HoustonChronicle, 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 andAtherosclerosts 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 ofHealth and Human Services, 2005), available at wv\'w.cdc.gov/nchs/data;hus/hus05.pdf.:;o-070. 41. Based on NationalHealth 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 andM. 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~**FatDiet Cause**Atherosclero~** sis inLaboratoryMice." 44. Hourly PM25 datawere**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 /profiles/h

### ilttes/200 5/prn**~diet.**htm. 46. StrongerRelationship bett{}een Particulate Matter (PM) and Premature Death (Sacramento: CaliforniaAir 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 ofAir Pollution and Mortality m Los Angele.o;," 

### EpJ,.. demio/ogy 16 (2005): 727-36. 47.

### J. E. Enstrom, "Fine ParticulateAir Pollution andTotal Morrality amongElderly Californians, 1973-2002,'' Inhalntion Toxicology 17 (2005): 803-16. 48. AmericanLungAssociacion, "Clean Air Standards," Medical

### J oumalWarch, available ac www.cleanairstandards. org/listing/journal\Vatch. 49. Based on a search ofthe MedicalJournal .Watch website

on/\pril 6, 2006. 50. H. GongJr., W. S. Lilm, C. Sioutas et al., ''Controlled Exposures ofHealrhy and Asthmatic Volunteers to Concencrared AmbientFme Particles in Los Angeles," Inhalation Toxico/ogy 15 (2003): 305-25; S. T. Holgate, T. Sandstrom, A. 

### J. Frew et aL, "Health.Effects ofAcute 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 

### ofAmbient Air Pollution on School Absen**re~ism** Due to Respiratory Illnesses," Epidemiology 12 (2001): 43-54. 52. K. Berhane and 

### D. C. Thomas, l(A**Two~Stage** Modelfor Multiple Time Series Daca ofCOLmts," Biostatistics 3 (2002): 21-32; :md V. Rondeau, K. Berhane, andD. C. Thomas, "A Three-Level Modelfor BinaryTime-Series Data: The Effects of Air Pollution on School Absences in the SouthemCalifomia Children's Health Study," Swrisrics in Medicine 

### 24 (2005): 1103-15. 53. Ret,iew of

### the California AmbientAir Qwility Standardfor 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 CaliforniaAirResources Board's OzoneStandards" (working paper, AEI, Washington, D.C., September2005), v.nv.r-w.aei.org/ publicationl3145. 54. Death, Disease andDirty Potver, CleanAirTaskForce; Power to ]\ill: Death andDiseasefrom PowerPlants Charged with Violating the CleanAirAct (Boston: Clean

### AtrTask Force, July 2001); Children atRisk: How AirPollutionfrom PowerPlants Threate:ns the Health of America's Children, Physicia115 for Socml Responsibilicy; Danger in the Air, PIRG. 55. Envitonn1ental Protection Agency (EPA), "Clean Air IntersmreRule," available atV.lWV?.epa.gov/cair/. 56. "Clean A.ir InterstateRule: Charrs andTable," EPA, available at ·wwv;'.epa.gov/catr/charts.html. 57. CleanAirInte.rstare Rule (CAIR): Reducing Power Plant Emissions.for CleanerAir, Healthier People, anda StrongAmerica (Washington, D.C.: EPA, March 2005), avaHable atwv,,\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 ofSulf8.te Aerosols

on CardiopulmonaryFunction ofNonnal Humans,"American Review of Respiratory Disease 115 (1977): 240: and M. 

### J. Utell, P. E. Morrow, D. M. Speers etal., "AinvayResponses 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 ofInhaled Sulfuric Acid on SeniorAsthmatics and Nonasthmatics,"Archives ofEnvironmentalHealth 48 (1993): 171-75. 60. Retriew ofthe CalifomiaAmbientAir Quality Standardfor Ozone, C/\RB.

## Electronic Filing

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- 12-

61.

### J. Schwartz, ''Rethinking the California AirResource::: Board's OZone Standards"; S. F. van denEeden, 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)' Crireriafor Ozone and Relared Photochemical Oxidanrs {Second Enernal Review D-raft) Volumes I-III (\YJashington, 

### D.C.: EPA, August 2005), available atwv.,·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 ofMonalicy in a Prospective Scudy ofU.S. Adults,"American Journal ofRespiratory mld Crirical Care Medicine !51 (1995)o 669-74. 64. C. A. Pope III, R. 

### T. Burnett, M.]. 1lmnet al., "Lung Cancer, Cardiopulmonary Mortaiity, and Long,Term Exposure

m Fine Paniculate Air Pollution,"Journal 

### ofir.e AmericanMedicalAssociation 287 (2002), 1132-4I. 65. D. Krewski, R. T. Burnett, M.S. Goldberg et al., Reanalysis ofthe Harvard Six Cities Study and the American Cancer Society Study ofParticulate AirPonution 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 MostPublished ResearchFindin_gs Are False," PLoS Medicine 2 (2005): el24;W. R. Keatinge and 

### G. C. Donaldson, "HeatAcclimatization 

### and Sunshine Cause False Indications ofMortality Due to Ozone,'' Ewuironment.al Research 100 (2006)o 387-93; G Koop and L. Tole, "Measuring the Health Effects ofAirPollution: To \X/hat Extent CanWe Really Say That People Are Dyingfrom Bad Air?"Journal of Em.n'ronmenta[Economics and Management 

### 47 (2004): 30-54; T. Lumley and L. Sheppard, "Time Series Analyses ofAir Pollution

### and Healch: Stralning at Gnats and Swa)lowing Camels?" Epidemiology 

### 14 (2003): 13-14; S. H. Moolgavkar, "A Review and Cricique ofthe EPA's· Rationale fot a Fal.e Particle Standard," Regulato!J To,icology andPharmacology 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 atAustin

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 oftheAmerican Board of Toxicology National Member, Air &Waste ManagementAssociation Society of Environmental Toxicology and Chemistry Dr. Fraiser is a Senior Consulting Toxicologist, Operations Managerfor AECOM Environment's Austin and Dallas offices, and Associate Vice President ofAECOM 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 Managerfor numerous human health and ecological risk assessments of air pollutants emitted from chemical plants, waste managementfacilities, army depots, cement kilns and power plants. She is part ofa successful proposal team for a study on the developmentof 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. Fraiserwas invited, along with several others at AECOM, to develop U.S. Environmental Protection Agency (EPA) training materials on various aspects ofthe U.S. National Emission Standards for Hazardous Air Pollutants (NESHAPs) regulations for Hazardous Waste Combustors and**~o** teach the site-specific risk assessment component ofthe training in 2008. Representative project experience follows. Experience 

### Toxicological Evaluations andRisk-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 andRisk-Based Regulatory Criteria Development. Developed interim Effects Screening Levels (air action levels) forToluene 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 andRisk-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 developmentfor perfluorinated compounds.
ToxicologicalEvaluations andRisk-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. ToxicologicalEvaluations andRisk-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.
ToxicologicalEvaluations andRisk-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. 

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

Toxicological Evaluations andRisk-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 andRisk-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 ofthe previously uncharacterized compound on the basis of knowledge ofchemistry concepts (i.e., stoichiometry of hydrolysis).


### Toxicological Evaluations andRisk-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 andRisk-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 andRisk-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 andRisk-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 ofa large chemical company and made 

### 19

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recommendations for submittal under TSCA BE (Toxic Substances Control Act).

AirQualityRiskAssessment. Health Risk Assessment Advisor for a study recently completed on behalf ofthe 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 ajoint EPRI/Utility Air Research Group meeting in May, 2012.

AirQualityRiskAssessment. Recently provided comments on Boiler MACT Health Based Emissions Limitations on behalf of the American Forest and Paper Association.

Air QualityRiskAssessment. Health Risk Assessment Team Leader responsible for overseeing the conduct of a risk assessment as part ofan engineering investigation (EI) and environmental impact assessment (EIA) study for two potential sites ofan 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.

AirQuality RiskAssessment. Recently acted as project managerfor 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 QualityRiskAssessment. 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.

AirQualityRiskAssessment. 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.

AirQualityRiskAssessment. Health risk assessment lead for vapor intrusion evaluation, using indoor and ambient air samples at manufacturing facility.

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## Electronic Filing

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AirQualityRiskAssessment. 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 ofstaff conducting modeling, reporting for the project, representation ofclients in Agency meetings, and complete responsibility for all financial and technical aspects ofthe risk assessments. Primary risk drivers routinely consisted of Polycyclic Aromatic Hydrocarbons (PAHs), mercury, chromium, phthalates, and dioxins.



### AirQualityRiskAssessment. 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 QualityRiskAssessment. Completed formal technical comments on behalf ofa 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.



### AirQualityRiskAssessment. 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 oraction.



### AirQualityRiskAssessment. 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.



### AirQualityRiskAssessment. 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.



### AirQualityRiskAssessment. Developed technical comments on EPA RiskAssessment Protocols for Hazardous Waste 

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Combustion Facilities on behalf ofthe 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.



### AirQualityRiskAssessment. 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.



### AirQualityRiskAssessment. Represented the TNRCC in an EPAwork 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.



### AirQualityRiskAssessment. 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 CorrectiveAction. 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 underthe 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 

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## 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 ofthe risk assessments.



### RiskBased 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).



### RiskBased CorrectiveAction. Currently acting as Health Risk Assessment Lead for a multi-media health risk assessment for a former refinery.



### RiskBased CorrectiveAction. Recently completed a human health and screening ecological risk assessment for several areas within a former refinery in Southeast Asia in preparation for divestment.



### RiskBased CorrectiveAction. Currently supporting an evaluation ofa historical polychlorinated biphenyl (PCB) release underthe risk-based provisions of40 CFR 761.61(c) ofthe 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 ofconcern include mercury and lead.



### RiskBased CorrectiveAction. 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 ofconcern include dioxins, polychlorinated biphenyls, polycyclic aromatic hydrocarbons (PAHs), arsenic, lead, mercury.



### RiskBased Corrective Action. Currently involved in conducting a risk-based evaluation of a former production well site for submittal to the Texas Railroad Commission.



### RiskBased CorrectiveAction. 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 

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operating procedures, preparing reports on risk-based evaluations for submittal to the Texas Railroqd Commission, and representing the client in Agency meetings.



### RiskBased 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 ofsampling data generated by another contractor for use in the risk assessment, coordination ofgroundwater modeling, exposure modeling, reporting, and complete responsibility for all financial and technical aspects ofthe 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 ofvapors from in indoor and outdoor air, dermal contact with water and soil, ingestion ofwater and soil, and uptake through the food chain (i.e., vegetables).



### RiskBased CorrectiveAction. Performed a post-remediation human health risk assessment for an active petroleum depot in Southeast Asia. Responsibilities included modeling and reporting forthe project, representation of the client before a health panel ofscientists convened to review the risk assessments, and complete responsibility for all financial and technical aspects ofthe risk assessment project. The risk assessment was conducted in a manner consistent with International guidance on the conduct of risk assessments.



### RiskBased CorrectiveAction. 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 forthe project, representation of the client before a health panel ofscientists convened to review the risk assessments, and complete responsibility for all financial and technical aspects ofthe 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 ofvapors from in indoor and outdoor air, dermal contact with water, ingestion ofwater, and uptake through the food chain (i.e., vegetables, chicken, and eggs).



### RiskBased Corrective Action. Served as task leader for three human health risk assessments and one ecological risk assessment for an active petroleum depot in SoutheastAsia. 

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## 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 ofvapors 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.

RiskBased 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 ofthe Rational National Standards Initiative (RNSI). During the course ofthe 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 of2012. 

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Testifying andLitigation Support. Provided testimony on potential risks associated with permitting of a rock crusher. Constituents ofconcern for the case are anticipated to be PM10, PM2.5, and crystalline silica. Hearing took place in 2011 and construction permit was granted.
Testifying andLitigation Support. Consulting toxicologist on behalf plaintiff in a lawsuit brought against a steel tank manufacturer by the State ofTexas.
Testifying andLitigation 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 andLitigation Support. Criteria Pollutant, Air Taxies, and Odor Nuisance Litigation Support: Currently providingJiti§ation support in a federal case on behalf ofa major multi-national petrochemical company. Constituents ofconcern 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. Fraiserwill be deposed on June 20, 2012 and the hearing is expected to take place in the fall of2012.
Testifying andLitigation Support. Developed an opinion regarding the likelihood that a level ofexposure 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 ofthe defendant and plaintiff. The case settled in 2009.
Testifying andLitigation Support. Testified on potential risks associated with permitting ofa concrete batch plant. Constituents of concern forthe 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 ofthe City of El Paso. Constituents ofconcern for the case were metals, PM10, PM2.5, nitric oxide, sulfur dioxide, and sulfuric acid. Hearing took place in July 2005. Permit was denied. 

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

Testifying andLitigation 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 andLitigation 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 ofthe combined testimony of Dr. Fraiser and one of her colleagues, the client's request for a restraining orderwas granted and 75 employees kept theirjobs. 

### 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 andLitigation 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 of40 CFR 266 in the state ofTexas (only second BIF to be permitted in the nation).



### Televised Press Conference. Peer reviewed ofa paper entitled "Proximity to Point Sources of Environmental Mercury Release
as a Predictor ofAutism Prevalence" and conducted a televised press conference on the findings ofthe paper on behalf ofthe Clean Coal Technology Foundation of Texas.


### TestimonyBefore RegulatoryAgencies/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 ofTexas 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 ExxonMobil, Fairfax, VA. December, 

### 2008.
Site-Specific Risk Assessments, RCRA Omnibus Provision and Combining Risk Burns and Comprehensive Performance Tests. MACT 

### EEE EPATraining 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 ofContaminated Land: Focus on Asia October 

### 21

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23, 2008, Kuala Lumpur, Malaysia.
Fraiser, L.H. Involvement of Local Governments in Air Taxies Regulation. Texas Chemical Council/ Association of Chemical Industry ofTexas'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 meetingjointly organized by the Hong Kong Institute of Environmental Impact Assessment and Chartered Institution ofWater 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 ofthe 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. 

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Fraiser, L.H., and Chaudhuri, 

### I. Short-Term Toxicity Benchmark for Nickel Oxide. Proceedings ofthe 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 HazardousWaste 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 ofTheir Role in the BladderToxicity 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 ofCyclophosphamide.' 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 RiskAssessment Environmental Communication Regulatory Negotiatfon Site Strategy Development
Professional Affiliations Diplomate, American Board of Toxicology, 1994 Society ofToxicology 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 scientificjournals 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 ofthe American Coal Ash Association. 

### Experience

A. Representative Superfund Experience 

### PinesArea ofInvestigation, 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 USEPA Region 5. The AOC addresses the placement ofcoal 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 ofwork; 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 USEPA's website: http://www.epa.qov/reqion5/sites/pines/index.htm.

Delaware Sand& Gravel Remedial Trust, Delaware, USEPA Region 3. A human health risk assessment (HHRA) focusing on evaluation ofthe 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 RiskAssessment, 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 ofthe 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/cleanup/saugetarea1 /pdfs/ 34

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sauget1_deadcreek_final_remedy_200604.pdf 

### SaugetArea 2 Sites Group, Human Health RiskAssessment, 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 ofsites 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 USEPA Region 5 and their contractors, and preparation of responses to comments.



### Columbia Gas Transmission, Strategic RiskAssessment 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 ofthe program, and developed a programmatic approach to the evaluation of risk across the program. Was responsible for: review ofother 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 ofthe 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 RiskAssessment, 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 ofthe dose-response values developed by the U.S. EPA for arsenic.



### lndustri-Piex CERCLA Site, RiskAssessmentReview and Strategy forPRP Group, Massachusetts, USEPA 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 ValleyAuthority, Human Health RiskAssessment, 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 RiskAssessment, 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 SuperfundSite, Review

### ofAIC 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 

### Soluti 

### a, Inc., Human Health RiskAssessment Oversightfor the J.F. QueenyFacility, 

### St. Louis, Missouri. Provided oversightfor the human health risk assessment prepared for the facility under an order with USEPA Region 6. The risk assessment is designed to meet the requirements of both USEPA and the State of Missouri Risk-Based Corrective Action Program.



### Soluti 

### a, Inc., Human Health RiskAssessmentfor 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 ofareas 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 RiskAssessment, 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 HHRAworkplan, and agency negotiation. Participated in strategy developmentfor and preparation ofthe human health sections ofthe Sampling and Analysis Plans for each ofthe Solid Waste ManagementAreas 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 RiskAssessment, 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 underthe 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 ofthe 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 RiskAssessment, 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 ofthe full RFI workplan to ensure consistency with risk objectives, and preparation of responses to agency comments. Work included a detailed evaluation of USEPA'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, RiskAssessmentIssues, 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 ofLandManagement, 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 ofthe 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 ofLandManagement, EnvironmentalImpact 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 USEPA version ofthe 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

### ofa StandardizedRiskEvaluation 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 ofstandard 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 draftversions 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 howthe RISC program will be applied to RCRA sites under state authority.

U.S. Steel, Human Health RiskAssessment, 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 ofthe 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 oftheir tiered site closure guidance. Indiana Department

### ofEnvironmental 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 ofcoal combustion residuals (CCRs). Comments focused on a critique of the USEPA's updated human health and ecological risk assessment, a critique ofthe 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 PowerResearch 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 ofthe 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 groundwaterfor communications with a local community.

We Energies, Milwaukee, WI. Reviewed the basis ofthe state screening levels and toxicity values for aluminum as part of review ofthe Wisconsin Department of Natural Resources proposed groundwater standards under NR 140. Provided testimony for a board hearing, and metwith 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 atthe Hutsonville, 

### IL Power Station. Boron and molybdenum were constituents of interest. Pathways evaluated in the risk assessment included use of groundwaterfor 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 ofdata 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 ofAGREMAXTM. 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 ofarsenic in foods and background levels of exposure to radioactivity in our natural environment. 

### Utility Solid Waste Activities Group (USWAG), Washington, DC. Provided oversight ofcomments developed on the proposed listing of naphthalene as a carcinogen by the National Toxicology Program, and on the USEPA's childhood cancer document.



### Electric PowerResearch Institute, California. Worked with another ENSR toxicologist to develop a critique ofthe benzo(a)pyrene toxicity value developed by the United Kingdom fortheir Contaminated Lands program.


### Confidential Natural Gas 

### Client, ToxicityAssessment, 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, ToxicologyReview, Indiana. Provided a review ofthe toxicology and potential carcinogenicity oftwo 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. EnvironmentalProtection 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 ofthe literature. 

### Georgia Pacific, Literature Review, Georgia. Reviewed literature and summarized the current scientific knowledge ofthe endogenous synthesis of halogenated compounds in humans.

E. Representative MGP Experience 

### Natural Gas 

### Company, RiskAssessmentAdvisor, 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, FormerMGP 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, FormerMGP Site Review, Rhode Island. Provided senior review ofan air monitoring program and identified where fiexibility can be used in the development offenceline air monitoring standards.


### Village ofOakPark, FormerMGP 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 ofthe project.



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Committees Leader ofAECOM'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 ofAECOM's Coal Combustion Product (CCP) Initiative; responsible for following regulatory developments, and keeping AECOM staff and clients updated on the issues. Elected member ofthe American Coal Ash Association (ACAA) Executive Committee, and member ofthe 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 ofCCPs." 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 10-12, 2011, and invited presentation atThe 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 ofCoal 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 HotTopic Hour. April 28, 2011.

"Risk Assessment: Howthe EPA Looks at Coal Combustion Products." EUCI March 13-14,2011.

"Risk Assessment: Howthe EPA Looks at Coal Combustion Products." Presented at the EUCI conference on Future ofCoal Combustion Products (CCPs): Regulatory, Legal, Technical, and New Markets, March 2011, Denver, CO.
"Development ofa 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.

"USEPA's Proposed rule for Coal Combustion Residual (CCRs): Beneficial Use Aspects." Keynote address given at the June 2010 meeting ofthe 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 ofToxicology, March 2009.
Bradley, L.J.N., G.M. Fen!, and S.W. Casteel. "In Vivo Bioavailability ofArsenic in Coal Combustion By-Products." 

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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 ofConcentrations 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 ofTiered 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 ofthe 1996 Environmental Conference ofthe 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 ofthe 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.

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## EXHIBIT412

2019 2020 lotal I Amersn Energy**Raaot~rcea** AH&rn&tfve S02 Ltmit Com.parlaon tothe Current MPS

39,

. 39,151 VariencaS02 T>n&

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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"' SOZVariance 

# .,..**~.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