TCEQ AIR QUALITY PERMIT NUMBER 76338L002 Docket # 2019-0946-AIR

APPLICATION BY AUSTIN ASPHALT, INC HOT MIX ASPHALT PLANT DALLAS, DALLAS COUNTY

DOWNWINDERS AT RISK’S RESPONSE TO EXECUTIVE DIRECTOR’S RESPONSE TO PUBLIC COMMENT

Downwinders at Risk files this Response to the Executive Director’s Response to Public Comment on the New Source Review Authorization application.

Executive Director recommends denial of Downwinders at Risk’s request for a contested case hearing for Joppa resident Jabrille Mc Duffie. This denial is based on Executive’s Director assertion that “the emissions authorized by this permit are protective of both human health and the environment.”

That conclusion in turn is based on two other assertions:

1) TCEQ’s “Effect Screening Levels” are protective of human health, as are the EPA’s National Ambient Air Quality Standards from which they are partially derived, and,

2) Potential impacts from Austin Asphalt air pollution have been evaluated in the past and found sufficiently protective.

Both of these assertions are incorrect.

I. TCEQ’s ESL and EPS’s NAAQS for Particulate Matter (PM) 2.5 air pollution are not protective of human health

There’s no peer-reviewed journal published study of human health proving TCEQ’s ESLs and EPA’s NAAQS for PM2.5 are protective of human health. On the other hand, almost every peer-reviewed journal published study in the last ten years examining the health effects of Particulate Matter has concluded harms to human health can occur at levels of exposure to PM 2.5 well below the NAAQS for PM 2.5, or even a fraction of the NAAQS as reflected in the TCEQ’s ESL. These include:

1. 2017’s “Air Pollution and Mortality in the Medicare Population”( Qian Di, M.S., Yan Wang, M.S., Antonella Zanobetti, Ph.D., Yun Wang, Ph.D., Petros Koutrakis, Ph.D., Christine Choirat, Ph.D., Francesca Dominici, Ph.D., and Joel D. Schwartz, Ph.D.N Engl J Med 2017; 376:2513-2522 June 29, 2017 DOI: 10.1056/NEJMoa1702747).

This was the largest study to date on the effects of Particulate Matter pollution on US public health examining all Medicare beneficiaries from 2000 through 2012, a population of 61 million, with 460 million person-years of follow-up. According to the authors “The enormous sample size in this study, which includes the entire Medicare cohort, allowed for unprecedented accuracy in the estimation of risks among racial minorities and disadvantaged subgroups.”

This study concluded: “There was a significant association between PM2.5 exposure and mortality when the analysis was restricted to concentrations below 12 μg per cubic meter, with a steeper slope below that level.

This association indicated that the health-benefit-per-unit decrease in the concentration of PM2.5 is larger for PM2.5 concentrations that are below the current annual NAAQS than the health benefit of decreases in PM2.5 concentrations that are above that level.

Moreover, we found no evidence of a threshold value — the concentration at which PM2.5 exposure does not affect mortality — at concentrations as low as approximately 5 μg per cubic meter - this finding is similar to those of other studies.

The estimate of effect size for PM2.5 exposure was greatest among male, black, and Medicaid-eligible persons.

It is critical to estimate the health effects of low levels of air pollution — below the current NAAQS — to determine whether these levels are adequate to minimize the risk of death. ”

2. “Longitudinal Analysis of Particulate Air Pollutants and Adolescent Delinquent Behavior in Southern California.” Journal of Abnormal Child Psychology, ISSN: 1573-2835, Vol: 46, Issue: 6, Page: 1283-1293 2018 Kiros T. Berhane; Meredith Franklin

This University of Southern California study examined whether juvenile delinquent behavior is affected by levels of PM2.5 exposures below the EPA’s NAAQS before and during adolescence. It involved 682 children from the Risk Factors for Antisocial Behavior Study conducted in a multi-ethnic cohort of twins born in 1990–1995.

The study concluded:

“The results suggest that PM2.5 exposure at baseline and cumulative exposure during follow-up was significantly associated (p < 0.05) with increased delinquent behavior. The estimated effect sizes (per interquartile increase of PM2.5 by 3.12–5.18 μg/m3) were equivalent to the difference in delinquency scores between adolescents who are 3.5–4 years apart in age… Overall, these findings suggest long- term PM2.5 exposure may increase delinquent behavior of urban-dwelling adolescents, with the resulting neurotoxic effect aggravated by psychosocial adversities.

3. “Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models” Cacciottolo M, Wang X, Driscoll I, Woodward N, Saffari A, Reyes J, Serre ML, Vizuete W, Sioutas C4, Morgan TE, Gatz M Chui HC, Shumaker SA, Resnick SM, Espeland MA, Finch CE, Chen JC. Transl Psychiatry. 2017 Jan 31;7(1):e1022. doi: 10.1038/tp.2016.280.

University of Southern California researchers looked at over 1,400 women without dementia who were initially enrolled in a large health study from 1996 to 1998. Researchers measured their brain volume with M.R.I. scans in 2005 and 2006, when the women were 71 to 89 years old.

4. “Socioeconomic disparities and sexual dimorphism in neurotoxic effects of ambient fine particles on youth IQ: A longitudinal analysis” Wang , Tuvblad , Younan, Franklin, Lurmann, Wu, Baker, Chen Plos One December 5, 2017 https://doi.org/10.1371/journal.pone.0188731

This was the first longitudinal study examining whether exposure to ambient PM 2.5 at residential locations affects intelligence quotient (IQ). It looked at exposures during pre-/early- adolescence (ages 9–11) and emerging adulthood (ages 18–20) in a demographically-diverse population (N = 1,360) residing in Southern California.

The study concluded:

“Exposure to ambient particulate air pollutants, including PM2.5 (particulate matter [PM] with aerodynamic diameter <2.5 μm), has emerged as a novel environmental neurotoxin affecting brain development in children…We found strong evidence for a decreased PIQ score with higher exposure to ambient PM2.5 estimated at residential locations, even after adjusting for socio-demographic factors, spatial characteristics of residential neighborhoods, and parents’ cognitive abilities…For each 3 inter-quartile (7.73 μg/m ) increase in one-year PM2.5 preceding each assessment, the average PIQ score decreased by 3.08 points (95% confidence interval = [-6.04, -0.12]) The adverse effect was 150% greater in low SES families and 89% stronger in males, compared to their counterparts.

5. “The 2016 global and national burden of diabetes mellitus attributable to PM2·5 air pollution” Bowe, MPH , Xie, MPH , Li, MD , Yan, MD , Xian, PhD , Al-Aly, MD The Lancet, July, 2018DOI: https://doi.org/10.1016/S2542-5196(18)30140-2

This study… provides evidence that ambient PM2·5 pollution is associated with increased risk of diabetes. We examined the association in a longitudinal cohort of about 1.7 million US veterans, in which we control for relevant individual-level variables and ecological characteristics. The integrated exposure response function was non-linear in that risk increased substantially above PM2·5 concentrations of 2·4 μg/m3, and then exhibited a more moderate increase in risk at concentrations above 10 μg/m3.

6. “Autism Spectrum Disorder and Particulate Matter Air Pollution before, during, and after Pregnancy: A Nested Case–Control Analysis within the Nurses’ Health Study II Cohort” Raz, Roberts, Lyall ,Hart , Just, Laden, Weisskopf Environmental Health Perspectives Vol. 123, No. 3 March 2015 https://doi.org/10.1289/ehp.1408133

“In our nested case–control study of nurses from across the continental United States, ambient PM2.5 concentrations during pregnancy were significantly associated with having a child diagnosed with ASD…The average (± SD) levels of PM2.5 and PM10–2.5 during pregnancy were 14.6 ± 3.3 and 9.9 ± 4.9 μg/m3, respectively.”

7. “Association of ambient particulate matter with heart failure incidence and all-cause readmissions in Tasmania: an observational study” Huynh, Blizzard, Marwick, Negishi BMJ Open 2018 Vol 8 Issue 5

“PM2.5 was detrimentally associated with HF incidence (risk ratio (RR)=1.29 (1.15– 1.42)) and weakly so with readmission (RR=1.07 (1.02–1.17)), with 1 day time lag. In multivariable analyses, PM2.5 significantly predicted HF incidence (RR=1.12 (1.01– 1.24)) but not readmission (RR=0.96 (0.89–1.04)). HF incidence was similarly low 3 3 when PM <4 µg/m and only started to rise when PM2.5≥4 µg/m . Conclusions: PM2.5 predicted HF incidence, independent of other environmental 3 factors. A possible threshold of PM2.5=4 µg/m is far below the daily Australian national standard of 25 µg/m3.”

8. “Particulate matter air pollution and national and county life expectancy loss in the USA: A spatiotemporal analysis” Bennett, Helen Tamura-Wicks, Robbie M. Parks, Richard T. Burnett, C. Arden Pope III, Matthew J. Bechle, Julian D. Marshall, Goodarz Danaei, Majid Ezzati PLOS Medicine July 23, 2019 https://doi.org/10.1371/journal.pmed.1002856

9. “Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects” Raaschou-Nielsen, PhD , Andersen, PhD , Beelen, PhD , Samoli, PhD , Stafoggia, MSc , et al. The Lancet July 10, 2013 https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(13)70279- 1/fulltext

“Particulate matter air pollution contributes to lung cancer incidence in Europe. Lung cancer risks went up 18% with each increase of 5 migrograms of PM 2.5. Researchers noted that they did not find a level of pollution for where there was no risk, and the results indicated "the more the worse, the less the better" when it came to pollution.”

A more complete list of recent studies of the impacts of PM 2.5 air pollution on human health is provided in Appendix A.

Neither TCEQ’s ESLs nor EPA’s NAAQS have incorporated any of this science into their regulatory standards. The EPA NAAQS for PM 2.5 has not been revised since 2012 and it reflects science even older than that.

Despite asserting ESL’s are health-based, TCEQ has no evidence that its ESL for PM 2.5 is protective of human health in light of new scientific research showing otherwise.

The Executive Director statement about the protective nature of ESLs and the NAAQS is an hypothesis not supported by the science. However the statement that there appears to be no level of exposure to Particulate Matter 2.5 incapable of causing human health harm has been robustly tested repeatedly by scientists and proven correct.

To win this permit, Austin Asphalt or TCEQ must show the PM 2.5 emissions from the facility are protective of human health as the Executive Director claims. But neither of them has proven those emissions will produce benign levels of PM pollution, either via an epidemiological study citing no health impacts from similar levels of PM exposure, or as we’re about to see, from any previous risk assessments of the Austin Asphalt facility.

II. The only previous evaluation of this facility’s health impacts is fatally flawed.

According to the TCEQ the Austin Asphalt facility is a portable asphalt operation. It was originally sited in Hockley County in a rural part of Northwest Texas in 2002. It moved to its current location in the Joppa community of the City of Dallas in 2008.

Also according to the TCEQ, the Commission used a SCREEN3 air model in 2002 to determine if emissions were a threat to local residents or other receptors. Besides this initial modeling Austin Asphalt has has not been subject to any additional impacts evaluation. TCEQ is relying on this single model run to claim Austin Asphalt pollution releases are not injuring human health.

The “SCREEN3” air modeling run for this facility in 2002 - the only one ever performed - was done while it was still in rural Hockley County. There has been no air modeling of Austin Asphalt in its current location in Joppa. Besides the obvious difference in population density between unincorporated Hockley County and urban Dallas and the location of “receptors,” i.e. residents and property, there’s a series of variables in the modeling that apply only to the Hockley County location. Meteorology, stack height, and surrounding terrain among them. In fact, the entire model was defaulted to a “rural” versus “urban” option in 2002. This renders the modeling useless in its current location in Joppa. (Appendix B).

There’s also the matter of the age and limitations of the SCREEN3 model. The EPA defines the SCREEN3 model as a “a single source Gaussian plume model which provides maximum ground-level concentrations for point, area, flare, and volume sources.” It also makes sure to say it’s replaced the SCREEN3 model with something better: “AERSCREEN uses the EPA's preferred near-field dispersion model AERMOD in screening mode and represents the state of the science versus the outdated algorithms of SCREEN3… we feel that there are no valid technical reasons to retain SCREEN3 as a recommended screening model.” (https://www.federalregister.gov/documents/2017/01/17/2016-31747/revisions-to- the-guideline-on-air-quality-models-enhancements-to-the-aermod-dispersion- modeling)

According to the Arizona Department of Environmental Quality, “The current recommended model for screening sources in simple and complex terrain is the most recent version of EPA’s AERSCREEN model. The AERSCREEN model can be downloaded from EPA’s Support Center for Regulatory Air Models (SCRAM) website at http://www.epa.gov/ttn/scram. The AERSCREEN model has replaced the previous SCREEN3 model as the recommended screening model (U.S. EPA, 2011a). Analyses performed with SCREEN3 will no longer be accepted by ADEQ for permitting purposes.” (https://legacy.azdeq.gov/environ/air/download/modeling.pdf)

According to Alex De Visscher, Associate Professor and Canada Research Chair in Air Quality and Pollution Control Engineering at the University of Calgary, writing in an 2013 text book entitled “Air Dispersion Modeling: Foundations and Applications,” SCEEN3 is a “product of a previous generation of air dispersion modeling” and “is no longer a recommended model… it does not allow for multiple sources, and it does not include atmospheric chemistry or deposition.” (https://onlinelibrary.wiley.com/doi/10.1002/9781118723098.ch13)

These exclusions are important. There are multiple sources of Particulate Matter 2.5 air pollution at Austin Asphalt in its Joppa location, including piles of raw material, and industrial combustion at the site. SCREEN 3 modeling didn’t and wouldn’t reflect these multiple sources of pollution.

According to the TCEQ itself (TCEQ APDG 6232v4, Revised 09/18 Air Quality Modeling Guidelines Page 80 of 110 Appendix N - Surface Characteristics of the Modeling Domain): “Air dispersion models utilize dispersion coefficients to determine the rate of dispersion for a plume. Dispersion coefficients are influenced by factors such as land-use / land-cover (LULC), terrain, averaging period, and meteorological conditions. Evaluating the LULC within the modeling domain is an integral component to air dispersion modeling. The data obtained from a LULC analysis can be used to determine representative dispersion coefficients. The selection of representative dispersion coefficients may be as simple as selecting between rural or urban land- use types. For more complex analyses, representative dispersion coefficients can be determined by parameters that are directly related to the LULC within the modeling domain. LULC Analysis for ISC, ISC-PRIME, and SCREEN3.

For the ISC, ISC-PRIME, and SCREEN3 models, the dispersion coefficients are based on whether the area is predominately rural or urban. The classification of the land use in the vicinity of sources of air pollution is needed because dispersion rates differ between rural and urban areas.

In general, urban areas cause greater rates of dispersion because of increased turbulent mixing and buoyancy-induced mixing. This mixing is due to the combination of greater surface roughness caused by more buildings and structures and greater amounts of heat released from concrete and similar surfaces. The Environmental Protection Agency (EPA) guidance provides two procedures to determine whether the character of an area is predominantly rural or urban. One procedure is based on land-use typing and the other is based on population density. Both procedures require an evaluation of characteristics within a three-kilometer radius from a source. The land-use typing method is based on the work of August Auer (Auer, 1978) and is preferred because it is more directly related to the surface characteristics of the evaluated area that affects dispersion rates.”(https://www.tceq.texas.gov/assets/public/permitting/air/Modeling/g uidance/airquality-mod-guidelines6232.pdf)

The TCEQ’s own guidelines for air modeling say it makes a fundamental difference whether the model is run for urban or rural terrain. Yet TCEQ and Austin Asphalt have used the results of a model run for a rural location to inappropriately reassure urban residents that the facility posed no air pollution harm.

Moreover, the SCREEN3 modeling performed in 2002 for Austin Asphalt in Hockley County only examined “asphalt vapors,” a generic pollutant category that can’t be monitored or measured. It didn’t examine Particulate Matter 2.5 pollution or specific Volatile Organic Compounds that make up those “vapors” and was therefore incomplete in the extreme.

In summary, the only air modeling ever done for this facility was performed 17 years ago in a sparsely-populated rural location 400 miles vastly different from its current densely-populated urban site with what TCEQ admits are inaccurate modeling inputs. It didn’t include all priority pollutants or even all sources of air pollution from the facility and the model used is now considered obsolete by EPA, modeling experts, and other state environmental agencies.

Joppa residents deserve better.

Downwinders at Risk specifically requests TCEQ delay further regulatory action on this permit renewal until it can conduct a modern comprehensive air modeling impact analysis for Austin Asphalt’s current operation in Joppa that requires an evaluation of all on-site sources of pollution, including fugitive and mobile sources, on the Austin Asphalt site, off-site near-by sources of pollution within a three kilometer (1.86 mile) radius of Austin Asphalt’s facility, and representative monitored background concentrations obtained from local Joppa neighborhood monitoring as well as modeling of permitted maximums emission rates form all sources.

III. Lack of a cumulative risk assessment prevents this permit from being “protective of public health”

The idea that TCEQ can judge whether Austin Asphalt’s Particulate Matter 2.5 pollution levels are protective of human health in Joppa separate from the emissions of other industrial sources only yards away is not supported by the science.

Many of the same studies concluding there appears to be no level of exposure to PM 2.5 that cannot cause harm also conclude that cumulative lifetime exposure to PM 2.5 is causing increased human health damage, i.e. "the more the worse, the less the better.”

“…the more bad air a child inhaled, the more likely they were to engage in delinquent activity.” (“Longitudinal Analysis of Particulate Air Pollutants and Adolescent Delinquent Behavior in Southern California”)

“For each increase of 3.49 micrograms per cubic centimeter (μg/m3) cumulative exposure to PM, there was an associated 6.23 cubic centimeter reduction in the subject's brain white matter, the equivalent of one to two years of brain aging.“(“Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models” )

"With each percentile of pollutant exposure, the presence of autism increased." (“Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ HealthStudy II Participants”)

“The more Ozone and Particulate Matter pollution a baby in the womb is exposed to, the more likely he or she will be born with autism.” (“Residential Proximity to Freeways and Autism in the CHARGE Study”)

“We found that as PM 2.5 exposure rises, the larger the heart gets and the worse it performs. Both of these measures are associated with increased morbidity and mortality from heart disease.” (“Association Between Ambient Air Pollution and Cardiac Morpho-Functional Phenotypes”)

Joppa, the site of an historic Freedmen’s Town, is also the location of more industrial pollution per capita than any other neighborhood in Dallas. Based on the close proximity of multiple large industrial sources, its residents are already routinely exposed to higher than average levels of PM2.5 air pollution. In this regard Joppa’s plight is a microcosm of a national phenomenon identified by an EPA report published last year by the current Administration.

According to “Disparities in Distribution of Particulate Matter Emission Sources by Race and Poverty Status” (Am J Public Health. 2018; 108:480–485. doi:10.2105 AJPH.2017.304297) “For PM of 2.5 micrometers in diameter or less, those in poverty had 1.35 times higher burden than did the overall population, and non- Whites had 1.28 times higher burden. Blacks, specifically, had 1.54 times higher burden than did the overall population. These patterns were relatively unaffected by sensitivity analyses, and disparities held not only nationally but within most states and counties as well.”

Joppa residents don’t breathe the PM 25 pollution from Austin Asphalt in isolation from the PM 2.5 pollution from the Union Pacific locomotives in the company’s switchyard or the PM 2.5 pollution from the TAMKO asphalt shingle manufacturing plant. Their lungs inhale the combined pollution of all of those sources, plus others.

That combination of PM 2.5 air pollution has already been shown to be of concern in Joppa. In March of 2018 calibrated portable monitors were deployed in the neighborhood by Downwinders at Risk to measure ambient levels of PM 2.5 pollution (AEROQUAL Series 500 PM10/PM2.5 portable particulate monitor). 133 separate measurements were taken on a north to south transect through the neighborhood, allowing the calculation of one-hour PM2.5 concentrations throughout the neighborhood in order to compare with the closest stationary PM monitor from the TCEQ, located at 1415 Hinton St., approximately nine miles from Joppa.

Findings showed elevated levels of PM2.5 during all monitored periods in the Joppa neighborhood. PM2.5 levels in Joppa on 15 March 2018 averaged 38.5 µg/m3 , 55% higher than TCEQ measurements (21 µg/m3) during the 7:00-8:00 hour and 40% higher than the TCEQ 8:00-9:00 hour average (27 µg/m3) . For 18 March 2018, average PM2.5 levels, 23.8 µg/m3, were 33% greater than TCEQ levels (17 µg/m3).

As far as we know, this remains the only ambient air monitoring evre conducted in Joppa.

Unless the TCEQ is assessing total current PM 2.5 air pollution burdens for Joppa residents, it can’t be protecting their health with the addition of a renewed permit because it has no baseline to judge what the level of threat to their health is from “pre-existing” PM 2.5 air pollution. Just as a physician needs to know what pre- existing conditions affect their patient before knowing if a treatment will help, make no difference, or make things worse, so the TCEQ must know what levels of PM 2.5 pollution Joppa residents are routinely exposed to now in order to know if this permit renewal will make a critical difference to community health burdens.

Moreover, because TCEQ has never monitored or modeled Austin Asphalt’s air pollution in Joppa, it has no idea what the facility is actually releasing into the air or in what volumes. A knee-jerk approval of this permit is giving permission for one unknown PM 2.5 air pollution impact to operate in an area with many unknown PM 2.5 air pollution impacts that have never been collectively assessed despite operating adjacent to a densely populated neighborhood. For all TCEQ knows, levels of PM 2.5 could already be exceeding the EPA’s NAAQS and TCEQ’s ESLs in Joppa.

EPA considers cumulative impact assessments critical. “The combined, incremental effects of human activity, referred to as cumulative impacts, pose a serious threat to the environment. While they may be insignificant by themselves, cumulative impacts accumulate over time, from one or more sources, and can result in the degradation of important resources.” (https://www.epa.gov/sites/production/files/2014-08/documents/cumulative.pdf)

Other state regulatory agencies recognize the necessity of accounting for cumulative exposures before awarding new permits. The Minnesota Pollution Control Agency states: “People’s health is affected by many outside factors including multiple sources of pollution and other social conditions and stressors. Some people and communities are burdened by higher levels of pollution and more social stressors than others. Minnesotans are increasingly interested in understanding the impact on their health from all of these multiple pollution sources and stressors combined together. This is referred to as a cumulative impact analysis.”

“The 2008 Minnesota Legislature passed a law that affects how the MPCA evaluates air permit applications for a very specific part of South Minneapolis. This law requires the MPCA to analyze and consider “cumulative levels and effects of past and current pollution” before a permit may be issued for a facility located in the area described by the statute.” (https://www.pca.state.mn.us/air/air- permitting-south-minneapolis)

California EPA's Office of Environmental Health Hazard Assessment uses an environmental justice screening tool, CalEnviroScreen, to consider 20 indicators of pollution burden, population characteristics (e.g., poverty level, income, education level), and health conditions, like low-birth weight, that increase a population's vulnerability to pollution. Its model derives a single score by census tract, ranking overall pollution burden and vulnerability for that land tract. Scoring above the 75th percentile marks a community for investments to reduce pollution —such as public transit, renewable energy and clean vehicle initiatives.

Not accounting for the historic total Particulate Matter 2.5 pollution burden Joppa is already suffering under in deciding whether to renew Austin Asphalt’s permit is an act of discrimination against the community’s residents. It ignores the inequity of exposure already documented on the ground as well as the science of cumulative impacts. It’s contributing to the long record of environmental racism that has made Joppa a Dallas dumping ground.

Downwinders at Risk again specifically requests TCEQ delay further regulatory action on this permit renewal until it can conduct a modern comprehensive air modeling impact analysis for Austin Asphalt’s current operation in Joppa that requires an evaluation of all on-site sources of pollution, including fugitive and mobile sources, on the Austin Asphalt site, off-site near-by sources of pollution within a three kilometer (1.86 mile) radius of Austin Asphalt’s facility, and representative monitored background concentrations obtained from local Joppa neighborhood monitoring as well as modeling of permitted maximums emission rates form all sources.

IV. No assurance of compliance because there’s no monitoring of compliance

Despite the claim of the Executive Director that the TCEQ regional office “is required to perform regular investigations” of the Austin Asphalt plant, no member of the TCEQ staff in either Austin or Fort Worth could identify when such an investigation might have taken place in more than 10 years the facility has been located in Joppa when Downwinders requested to see evidence of any such inspections.

Since there’s been no monitoring of the facility by TCEQ and no continuous emission monitoring is required of the company, TCEQ has no idea if Austin Asphalt is currently in compliance with the permit it’s applying to renew.

Downwinders again requests a contested case hearing for this permit renewal so that residents can make clear their concern for the pollution this facility releases into their community and argue for inclusion of special provisions in a new permit, including continuous monitoring of PM and VOC pollution from Austin Asphalt stacks and fence line monitoring on the south-southeast/community-facing side of the facility. Such monitoring is the only way to know for sure what air pollution Austin Asphalt is releasing into the adjacent neighborhood.

Submitted By Downwinders at Risk, on behalf of Joppa resident Jabrille McDuffie.

Jim Schermbeck Director Downwinders at Risk

APPENDIX A

SUMMARY OF RECENT STUDIES ON PM POLLUTION HEALTH HARMS

______LOSS OF IQ

1. “The impact of exposure to air pollution on cognitive performance” Proceedings of the National Academy of Sciences of the United States of America PNAS September 11, 2018 https://doi.org/10.1073/pnas.1809474115 “We find that long-term exposure to air pollution impedes cognitive performance in verbal and math tests. We provide evidence that the effect of air pollution on verbal tests becomes more pronounced as people age, especially for men and the less educated. The damage on the aging brain by air pollution likely imposes substantial health and economic costs, considering that cognitive functioning is critical for the elderly for both running daily errands and making high-stake decisions.”

2. “Socioeconomic Disparities and Sexual Dimorphism in Neurotoxic Effects of Ambient Fine Particles on Youth IQ: A Longitudinal Analysis” (PLOS ONE) December 5, 2017 http://healthpolicy.ucla.edu/publications/search/pages/detail.aspx?PubID=1707

“Mounting evidence indicates that early-life exposure to particulate air pollutants pose threats to children’s cognitive development, but studies about the neurotoxic effects associated with exposures during adolescence remain unclear. Study authors examined whether exposure to ambient fine particles (PM2.5) at residential locations affects intelligence quotient (IQ) during pre-/early- adolescence (ages 9–11) and emerging adulthood (ages 18–20) in a demographically-diverse population (N = 1,360) residing in Southern California. Increased ambient PM2.5 levels were associated with decreased IQ scores. This association was more evident for Performance IQ (PIQ), but less for Verbal IQ, assessed by the Wechsler Abbreviated Scale of Intelligence.

3. “Air pollution can affect memory and IQ” Journal of Alzheimer’s Disease, February 18, 2015 https://pdfs.semanticscholar.org/e3d5/8109827f3020c60a1efef6db47f494072bac.pdf

“….two groups of children living in Mexico City were compared including multiple variables, such as age, gender, socioeconomic status and education, among others. Then, differences between children carrying the variant epsilon 4 with carriers of the epsilon 3 variant were analyzed. They found that the former had three notable changes: They showed short-term memory deficits, an IQ within the normal limits but 10 average points lower, and key metabolic changes in the brain, which resemble those of people with Alzheimer’s disease. ______

DIABETES 1. “The 2016 global and national burden of diabetes mellitus attributable to PM2·5 air pollution” The Lancet Volume 2, ISSUE 7, Pe301-e312, July 01, 2018 https://www.thelancet.com/journals/lanpla/article/PIIS2542-5196(18)30140-2/fulltext

“The global toll of diabetes attributable to PM2·5 air pollution is significant. Reduction in exposure will yield substantial health benefits.”

2. “Air Pollution as a Risk Factor for Type 2 Diabetes” US National Library of Medicine, National Institutes of Health 2015 Feb https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4306726/ “From the University of Maryland comes a report that concludes air pollution increases inflamation of the heart which leads to diabetes when combined with a high fat diet – the kind so many Americans are still eating. Sedentary mice were fed the high-fat diet and then forced to breath Beijing-like levels of air pollution. Exposure to that bad air, primarily high levels of particulate matter, increased the likelihood of the mice developing diabetes by 2 to 4 times, and increased he severity of the disease as well. “

MENTAL ILLNESS

1. “Spatiotemporal influence of temperature, air quality, and urban environment on cause- specific mortality during hazy days” Environment International Volume 112, March 2018, Pages 10-22 https://www.ncbi.nlm.nih.gov/pubmed/29245038

“A Hong Kong university study published in the upcoming March edition of Environment International concludes the risk of death for people with mental and behavioral disorders rises sharply on days when particulate matter and other kinds of air pollution reaches toxic peaks. Reviewing a decade of death statistics revealed a 16% increase in mortality risk on the first day of haze and a 27% increase on the second day compared to better air days. If the haze was accompanied by high ozone pollution, the risk of death increased by 79%.”

2. “Association between neighbourhood air pollution concentrations and dispensed medication for psychiatric disorders in a large longitudinal cohort of Swedish children and adolescents” BMJ OPEN · Volume 6, Issue 6 https://bmjopen.bmj.com/content/6/6/e010004.full

This Swedish study is the first to report linking air pollution to mental illness in children. It found that relatively small increases in air pollution were associated with a significant increase in treated psychiatric problems.

ANTI-SOCIAL BEHAVIOR/CRIME

1. “Longitudinal Analysis of Particulate Air Pollutants and Adolescent Delinquent Behavior in Southern California” Journal of Abnormal Child Psychology, August 2018, Volume 46, Issue 6, pp 1283–1293 https://link.springer.com/article/10.1007/s10802-017-0367-5

“The first study to look at the effects of PM pollution exposure on the social behavior of children found that that the more bad air a child inhaled, the more likely they were to engage in delinquent activity. “

“Multilevel mixed-effects models were used to examine the association between PM2.5 exposure and individual trajectories of delinquent behavior, adjusting for within-family/within-individual correlations and potential confounders. The results sμggest that PM2.5 exposure at baseline and cumulative exposure during follow-up was significantly associated (p < 0.05) with increased delinquent behavior.”

2. “Traffic-Related Air Pollution Exposure in the First Year of Life and Behavioral Scores at 7 Years of Age “ Environmental Health Perspectives June 1 2013 https://ehp.niehs.nih.gov/doi/10.1289/ehp.1205555

“We explored the association between early-life exposure to TRAP using a surrogate, elemental carbon attributed to traffic (ECAT), and attention deficit/hyperactivity disorder (ADHD) symptoms at 7 years of age. Results: Exposure to the highest tertile of ECAT during the child’s first year of life was significantly associated with Hyperactivity T-scores in the “at risk” range at 7 years of age, after adjustment [adjusted odds ratio (aOR) = 1.7; 95% CI: 1.0, 2.7]. Stratification by maternal education revealed a stronger association in children whose mothers had higher education (aOR = 2.3; 95% CI: 1.3, 4.1).” Conclusions: ECAT exposure during infancy was associated with higher Hyperactivity scores in children; this association was limited to children whose mothers had more than a high school education.”

3. “Prenatal and childhood traffic-related air pollution exposure and childhood executive function and behavior.” Neurotoxicol Teratol. Sept 2016 https://www.ncbi.nlm.nih.gov/pubmed/27350569

“Traffic-related air pollution exposure may influence brain development and function and thus be related to neurobehavioral problems in children, but little is known about windows of susceptibility. Using validated spatiotemporal models, we estimated exposure to black carbon (BC) and fine particulate matter (PM2.5) in the third trimester of pregnancy, from birth to 3 years, from birth to 6 years, and in the year before behavioral ratings. We also measured residential distance to major roadways and near-residence traffic density at birth and in mid-childhood. We estimated associations of BC, PM2.5, and other traffic exposure measures with BRIEF and SDQ scores, adjusted for potential confounders. Children with higher mid-childhood exposure to BC and greater near- residence traffic density in mid-childhood had greater problems with behavioral regulation as assessed by classroom teachers, but not as assessed by parents. “

BRAIN DISEASE/DEMENTIA

1. “Long-Term Exposure to Fine Particulate Matter, Residential Proximity to Major Roads and Measures of Brain Structure“ STROKE American Heart Association Journal April 3 2015 https://www.ahajournals.org/doi/full/10.1161/STROKEAHA.114.008348

“Exposure to elevated levels of PM2.5 was associated with smaller total cerebral brain volume, a marker of age-associated brain atrophy, and with higher odds of covert brain infarcts. These findings suggest that air pollution is associated with insidious effects on structural brain aging even in dementia- and stroke-free persons.”

2. “Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models” Translational Psychiatry January 31 2017 University of Southern California researchers looked at over 1,400 women without dementia who were initially enrolled in a large health study from 1996 to 1998. Researchers measured their brain volume with M.R.I. scans in 2005 and 2006, when the women were 71 to 89 years old.

Using residential histories and air pollution monitoring data, they estimated their exposure to PM air pollution from 1999 to 2006. For each increase of 3.49 micrograms per cubic centimeter (μg/m3) cumulative exposure to PM, there was an associated 6.23 cubic centimeter reduction in the subject's brain white matter, the equivalent of one to two years of brain aging. The current EPA standard for 24 PM exposure is 35 μg/m3, while the annual average standard is 12 μg/m3, although many leading scientists now believe there's no "safe" level of exposure to PM pollution. That is, any amount of exposure is capable of doing some damage. 3. “The emerging risk of exposure to air pollution on cognitive decline and Alzheimer's disease – Evidence from epidemiological and animal studies “ Biomedical Journal Published online 2018 Jul 17 https://www.ncbi.nlm.nih.gov/pubmed/30080655 “In this review, we summarize recent evidence supporting exposure to air pollution as a risk for cognitive decline at all ages and AD at later lifetime. Additionally, we review the current body of work investigating the molecular mechanisms by which air pollutants mediate damage in the CNS.”

4. “Fine Particulate Matter Air Pollution and Cognitive Function Among U.S. Older Adults” The Journals of Gerontology March 2015 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351385/

In a study involving approximately 15,000 people, the U.S. National Institute on Aging found that higher levels of exposure to fine particulate matter pollution, or soot, is prematurely aging the brain of those 50 and older by up to three years.

5. “Non-Phosphorylated Tau in Cerebrospinal Fluid is a Marker of Alzheimer’s Disease Continuum in Young Urbanites Exposed to Air Pollution” Journal of Alzheimer's Disease, vol. 66, no. 4, pp. 1437-1451, 2018 https://content.iospress.com/articles/journal-of-alzheimers-disease/jad180853 “Long-term exposure to fine particulate matter (PM2.5) and ozone (O3) above USEPA standards is associated with Alzheimer’s disease (AD) risk. “

AUSTISM

1. “Echoes of Autism? Inhaled Ultrafine Particles and Brain Changes in Mice” Environmental Health Perspectives, September 2014 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4154204/

"Epidemiological evidence has raised the possibility that exposure to air pollution could be a risk factor for autism spectrum disorders (ASDs) and schizophrenia. The team, led by Deborah Cory- Slechta of the University of Rochester Medical Center (URMC), found that exposure to ultrafine particles early in life produced brain changes in mice suggestive of those in humans with ASDs and schizophrenia. Notably, the brains of exposed male mice showed enlarged lateral ventricles, a condition called ventriculomegaly. “That’s alarming, because ventriculomegaly in humans has behavioral consequences” including ASDs6 and schizophrenia, says Cory-Slechta.

2. “Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ HealthStudy II Participants” Environmental Health Perspectives June 18, 2013 https://ehp.niehs.nih.gov/doi/10.1289/ehp.1206187 “We estimated associations between U.S. Environmental Protection Agency–modeled levels of hazardous air pollutants at the time and place of birth and ASD in the children of participants in the Nurses’ Health Study II (325 cases, 22,101 controls). For most pollutants, associations were stronger for boys (279 cases) than for girls (46 cases) and significantly different according to sex. Conclusions: Perinatal exposure to air pollutants may increase risk for ASD.”

“Women in the U.S. exposed to high levels of air pollution while pregnant were up to twice as likely to have a child with autism as women who lived in areas with low pollution, according to a new study from Harvard School of Public Health (HSPH). It is the first large national study to examine links between autism and air pollution across the U.S.”

"What you see is the mothers with the 20 percent least exposure to pollutants, their children are least likely to have autism," lead researcher Dr. Andrea Roberts of the Harvard School of Public Health told The Standard-Times. "With each percentile of pollutant exposure, the presence of autism increased."

3. “Autism Spectrum Disorder and Particulate Matter Air Pollution before, during, and after Pregnancy: A Nested Case–Control Analysis within the Nurses’ Health Study II Cohort” Environmetnal Health Perspectives August 2015 https://ehp.niehs.nih.gov/doi/10.1289/ehp.1408133

“We explored the association between maternal exposure to particulate matter (PM) air pollution and odds of ASD in her child. The association between ASD and PM2.5 was stronger for exposure during the third trimester (OR = 1.42 per IQR increase in PM2.5; 95% CI: 1.09, 1.86) than during the first two trimesters (ORs = 1.06 and 1.00) when mutually adjusted. Conclusions: Higher maternal exposure to PM2.5 during pregnancy, particularly the third trimester, was associated with greater odds of a child having ASD.”

4. “Residential Proximity to Freeways and Autism in the CHARGE Study” Environmeental Health Perspectives March 1 2013 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114825/ “The more Ozone and Particulate Matter pollution a baby in the womb is exposed to, the more likely he or she will be born with autism according to a new UCLA study. It's the largest study of its kind to date and is the first to link autism with ozone, or smog, levels.

“Researchers compared levels of air pollutants, mostly related to vehicle traffic, during pregnancy gestation periods of 7,603 children with autism and 75,635 children without autism, born from 1995 to 2006 in Los Angeles. Babies at the 75th percentile of exposure to toxins had a 8 percent to 10 percent higher risk of autism than babies at the bottom 25th percentile, the study said. Ozone and fine particulates had the strongest association with autism.”

5. “Early life exposure to particulate matter air pollution (PM1, PM2.5 and PM10) and autism in Shanghai, China: A case-control study.” Environment International Volume 121, Part 2, December 2018 https://www.sciencedirect.com/science/article/pii/S0160412018313242?via%3Dihub

“A case-control study was performed in Shanghai with a multi-stage random sampling design. Children's exposures to PM1, PM2.5 and PM10 (particulate matter with aerodynamicdiameter < 1 μm, < 2.5 μm and < 10 μm, respectively) during the first three years after birth were estimated with satellite remote sensing data. Conditional logistic regression was used to examine the PM-ASD association.”

“Conclusions: Exposures to PM1, PM2.5 and PM10 during the first three years of life were associated with the increased risk of ASD and there appeared to be stronger effects of ambient PM pollution on ASD in the second and the third years after birth.”

HEART DISEASE/ATTACKS

1. “Association Between Ambient Air Pollution and Cardiac Morpho-Functional Phenotypes” Circulation Vol 138 No 20 August 2, 2018 https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.118.034856 “Exposure to ambient air pollution is strongly associated with increased cardiovascular morbidity and mortality. Little is known about the influence of air pollutants on cardiac structure and function. We aim to investigate the relationship between chronic past exposure to traffic-related pollutants and the cardiac chamber volume, ejection fraction, and left ventricular remodeling patterns after accounting for potential confounders.”

“Conclusions: In a large asymptomatic population with no prevalent cardiovascular disease, higher past exposure to particulate matter with an aerodynamic diameter <2.5 µm and nitrogen dioxide was associated with cardiac ventricular dilatation, a marker of adverse remodeling that often precedes heart failure development.” “We found that as PM 2.5 exposure rises, the larger the heart gets and the worse it performs. Both of these measures are associated with increased morbidity and mortality from heart disease.” 2. “Combustion- and friction-derived magnetic air pollution nanoparticles in human hearts” Environmental Research Volume 176, September 2019, 108567 https://www.sciencedirect.com/science/article/pii/S0013935119303640

“Iron-rich, strongly magnetic combustion- and friction-derived nanoparticles are present in abundance in young urbanites' hearts. Mexico City residents have up to ∼22 billion magnetic NPs/g of ventricular tissue.. Oxidative and endoplasmic reticulum (ER) stress are significant in human ventricular tissues. Exposure to solid NPs appears to be directly associated with early and significant cardiac damage.”

3. “Air Pollution Exposure and Cardiovascular Disease” Toxicological Research, June 30 2014 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112067/

“Ambient air pollution (AAP) and particulate matters (PM) have been closely associated with adverse health effects such as respiratory disease and cardiovascular diseases. Previous studies have examined the adverse health effects associated with short- and long-term exposure to AAP and outdoor PM on respiratory disease. Both PM2.5and PM10 air pollution concentrations have a marked and close association with adverse health effect, such as heart disease, stroke, blood pressure, and cardiovascular diseases. Nevertheless, epidemiological studies exhibit a stronger correlation of adverse health effects with PM2.5 than with PM10. “

4. “Air Pollution and Cardiovascular Disease A JACC State-of-the-Art Review” Journal of the American College of Cardiology October 17, 2018 http://www.onlinejacc.org/content/72/17/2054

“Fine particulate matter <2.5 μm (PM2.5) air pollution is the most important environmental risk factor contributing to global cardiovascular (CV) mortality and disability. Short-term elevations in PM2.5 increase the relative risk of acute CV events by 1% to 3% within a few days. Longer-term exposures over several years increase this risk by a larger magnitude (∼10%), which is partially attributable to the development of cardiometabolic conditions (e.g., hypertension and diabetes mellitus). As such, ambient PM2.5 poses a major threat to global public health.

5. “Association of ambient particulate matter with heart failure incidence and all-cause readmissions in Tasmania: an observational study” BMJ Journals BMJ Open Volume 8, Issue 5 https://bmjopen.bmj.com/content/8/5/e021798

PM2.5 was detrimentally associated with HF incidence (risk ratio (RR)=1.29 (1.15–1.42)) and weakly so with readmission (RR=1.07 (1.02–1.17)), with 1 day time lag. In multivariable analyses, PM2.5 significantly predicted HF incidence (RR=1.12 (1.01–1.24)) but not readmission (RR=0.96 (0.89–1.04)). HF incidence was similarly low when PM <4 µg/m3 and only started to rise when 3 PM2.5≥4 µg/m . Stratified analyses showed that PM2.5 was associated with readmissions among patients not taking beta-blockers but not among those taking beta-blockers (pinteraction=0.011). Conclusions PM2.5 predicted HF incidence, independent of other environmental factors. A possible 3 3 threshold of PM2.5=4 µg/m is far below the daily Australian national standard of 25 µg/m . Our data suggest that beta-blockers might play a role in preventing adverse association between air pollution and patients with HF.

6. “Cardiovascular and Cerebrovascular Emergency Department Visits Associated With Wildfire Smoke Exposure in California in 2015” Journal of the Amerian Heart Association, April 18, 2018 https://www.ahajournals.org/doi/10.1161/JAHA.117.007492

“Wildfire smoke is known to exacerbate respiratory conditions; however, evidence for cardiovascular and cerebrovascular events has been inconsistent, despite biological plausibility. Analysis of an extensive wildfire season found smoke exposure to be associated with cardiovascular and cerebrovascular ED visits for all adults, particularly for those over aged 65 years.”

7. “Global association of air pollution and heart failure: a systematic review and meta- analysis” The Lancet July 10, 2013 https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)60898-3/fulltext

Increases in particulate matter concentration were associated with heart failure hospitalisation or death 3 3 (PM2·5 2·12% per 10 μg/m , 95% CI 1·42–2·82; PM10 1·63% per 10 μg/m , 95% CI 1·20–2·07). Strongest associations were seen on the day of exposure, with more persistent effects for PM2·5. In the USA, we 3 estimate that a mean reduction in PM2·5 of 3·9 μg/m would prevent 7978 heart failure hospitalisations and save a third of a billion US dollars a year. Air pollution has a close temporal association with heart failure hospitalisation and heart failure mortality. Although more studies from developing nations are required, air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy. ______

LEUKEMIA/CANCER

1. “Residential Traffic Exposure and Childhood Leukemia” American Journal of Preventive Medicine April 2014 https://www.ajpmonline.org/article/S0749-3797%2813%2900619-3/abstract

“After a review of over 30 years of studies, the Centers for Disease Control concluded that children living near high-volume roads and highways were 50% more likely to suffer from childhood leukemia. The cancer risk is linked to postnatal exposure. Out of nine relevant studies, seven, covering approximately 8,000 children, reveled a correlation between exposure and leukemia.”

2. “The International Agency for Research on Cancer (IARC) evaluation of the carcinogenicity of outdoor air pollution: focus on China.” Chinese Journal of Cancer April 2014 https://www.ncbi.nlm.nih.gov/pubmed/24694836 “The air you breathe CAN kill you, at least according to the World Health Organization, which officially classified air pollution as a cause of lung cancer. The move came after the group released a report earlier this year estimating that over 220,000 people died from lung cancer worldwide from exposure to bad air. Most of those deaths are occurring in countries in Asia. Mostly these deaths are due to Particulate Matter pollution, the ubiquitous tiny particles of soot that are produced when things burn, like gas in cars, coal or gas or waste in power plants and cement kilns, and diesel engines and flares in the the gas fields.”

3. “Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects” The Lancet July 10, 2013 https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(13)70279-1/fulltext “Interpretation: Particulate matter air pollution contributes to lung cancer incidence in Europe. Lung cancer risks went up 18% with each increase of 5 migrograms of PM 2.5. Researchers noted that they did not find a level of pollution for where there was no risk, and the results indicated "the more the worse, the less the better" when it came to pollution.”

NEONATAL

1. “Air pollution linked to increase in newborn intensive care admissions” Annals of Epidemiology. July 19, 2019 https://www.sciencedirect.com/science/article/abs/pii/S1047279719300572

“Infants born to women exposed to high levels of air pollution ((pollution particles less than 2.5 microns in diameter or PM2.5 ) in the week before delivery are more likely to be admitted to a newborn intensive care unit (NICU). ‘Short-term exposure to most types of air pollutants may increase the risk for NICU admission,’ Dr. Mendola said. "If our findings are confirmed, they suggest that pregnant women may want to consider limiting their time outdoors when air quality advisories indicate unhealthy conditions. Depending on the type of pollution, chances for NICU admission increased from about 4% to as much as 147%, compared to infants whose mothers did not encounter high levels of air pollution during the week before delivery. “

2. “Ambient air pollution and the risk of pregnancy loss: a prospective cohort study” January 2018Volume 109, Issue 1, Pages 148–153 https://www.fertstert.org/article/S0015-0282(17)31973-8/fulltext

“Average chronic whole pregnancy exposures to ozone and PM2.5 were positively associated with the risk of pregnancy loss. An IQR increase (from the 25th to 75th percentile) in ozone and PM2.5 exposures were, respectively, associated with a 12% (HR 1.12, 95% CI 1.07–1.17), and 13% (HR 1.13, 95% CI 1.13–1.24) increased risk of pregnancy loss. These findings suggest that chronic exposure may be more detrimental than acute exposures during sensitive windows.”

3. “Impact of London's road traffic air and noise pollution on birth weight: retrospective population based cohort study” The British Medical Journal 05 December 2017 https://www.bmj.com/content/359/bmj.j5299

“The findings suggest that air pollution from road traffic in London is adversely affecting fetal growth. To our knowledge, this is the largest UK study on air pollution and birth weight, and the first UK study and largest study worldwide of birth weight and noise exposure. We observed that long term exposure during pregnancy to NO2, NOx, PM2.5 overall and specifically from traffic exhaust and non-exhaust sources, and PM10, were all associated with increased risk of LBW at term, across London. Our findings from two air pollutant models suggest that associations between term LBW and air pollutants emitted from vehicle exhausts may be driven by the fine particulate matter (PM2.5 traffic exhaust) component rather than the gaseous NOx component. “

4. “Exposures to fine particulate matter (PM2.5) and birthweight in a rural-urban, mother-child cohort in Tamil Nadu, India.” Environmental Research Volume 161, February 2018, https://www.sciencedirect.com/science/article/pii/S0013935117312276?via%3Dihub

3 Results: A 10-μg/m increase in pregnancy period PM2.5 exposures was associated with a 4 g (95% CI: 1.08 g, 6.76 g) decrease in birthweight and 2% increase in prevalence of low birthweight [odds ratio(OR) = 1.02; 95%CI:1.005,1.041] after adjusting for gestational age, infant sex, maternal BMI, maternal age, history of a previous low birth weight child, birth order and season of conception.

Conclusions: The study provides some of the first quantitative effects estimates for linking rural- urban PM2.5exposures and birthweight in India, adding important evidence for this association from high exposure settings in LMICs, that also experience dual health burdens from ambient and household air pollution. Study results also point to the need for considering maternal PM2.5exposures alongside other risk factors for low birthweight in India.”

5. “The association between air pollution and pretem birth and low birth weight in Guangdong, China “ BMC Public Healthvolume 19, Article number: 3 (2019) https://bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-018-6307-7 “A mountain of evidence has shown that people’s physical and mental health can be affected by various air pollutions. Poor pregnancy outcomes are associated with exposure to air pollution. Therefore, this study aims to investigate the association between air pollutions (PM2.5, PM10, SO2, NO2, CO, and O3) and preterm birth/low birth weight in Guangdong province, China. Conclusion: This study provides further evidence for the relationships between air pollutions and preterm birth/low birth weight. Pregnant women are recommended to reduce or avoid exposure to air pollutions during pregnancy, especially in the early and late stages of pregnancy.”

6. “Ambient PM2.5 and birth outcomes: Estimating the association and attributable risk using a birth cohort study in nine Chinese cities” Environment International Volume 126, May 2019, Pages 329-335 https://www.sciencedirect.com/science/article/pii/S0160412018326473

“We examined associations in a birth cohort of 1,455,026 mother-and-live-birth pairs who were followed up from the first hospital visit for pregnancy until the birth of the baby during 2014–2017 in nine cites of the Pearl River Delta (PRD) region, China. The PM2.5 exposures were estimated based on the air pollution concentrations of the nearby monitors. Cox proportional hazards regressions were employed to examine the associations. The results indicate that maternal PM2.5 exposure is a risk factor for both LBW and PTB, and responsible for considerable burdens of PTB and LBW in the Pearl River Delta region.”

7. “Ambient Fine Particulate Matter, Nitrogen Dioxide, and Term Birth Weight in New York, New York “ American Journal of Epidemiology, Volume 179, Issue 4, 15 February 2014, Pages 457–466, https://academic.oup.com/aje/article/179/4/457/127797

“Using NYCCAS air monitoring data, the research team examined to the associations of PM2.5 and NO2 in ambient air with birth weights of 252,967 babies born to New York City mothers at full term from 2008-2010. Our results add support to the possible impact of common air pollutants, specifically PM2.5 and nitrogen dioxide, on fetal growth. The results of this study showed that for every of 10-µg/m3 increase in PM2.5 exposure over the entire pregnancy, birth weight was reduced by 48.4 g. Similarly, results show that for every 10-ppb increase in NO2 exposure over the entire pregnancy, birth weights were reduced by 18.0 g.”

8. “Exposure to Ambient Particulate Matter during Specific Gestational Periods Produces Adverse Obstetric Consequences in Mice” Environmental Health Perspectives.July 27, 2017 https://ehp.niehs.nih.gov/doi/10.1289/EHP1029

“The study, conducted in mice, found that exposure to air pollution during the equivalent of the first or second trimester in humans was linked to more negative birth outcomes than exposure later in pregnancy. Researchers studied the effects of fine particulate air pollution, which is made up of particles less than one ten-thousandth of an inch in diameter, or PM2.5. Inhalable and almost invisible to the eye, this type pollution comes from car exhaust, coal-fired power plants, and other industrial processes. PM2.5exposure has previously been linked to risk for asthma and heart disease. According to the US Centers for Disease Control and Prevention, preterm birth and low birth weight increase risk for vision and hearing problems, learning problems and even death.” 9. “Periconception Exposure to Air Pollution and Risk of Congenital Malformations” The Journal of Pediatrics September 2017 https://www.jpeds.com/article/S0022-3476(17)31330-6/fulltext

Using birth certificate data from the Ohio Department of Health (2006-2010) and PM2.5 data from the US Environmental Protection Agency's 57 monitoring stations located throughout Ohio, the geographic coordinates of the mother's residence for each birth were linked to the nearest PM2.5 monitoring station and monthly exposure averages were calculated. Conclusions: Increased exposure to PM2.5 in the periconception period is associated with some modest risk increases for congenital malformations. The most susceptible time of exposure appears to be the 1 month before and after conception. Although the increased risk with PM2.5 exposure is modest, the potential impact on a population basis is noteworthy because all pregnant women have some degree of exposure.

EARLY DEATH

1. “Associations of PM2.5 Constituents and Sources with Hospital Admissions: Analysis of Four Counties in Connecticut and Massachusetts (USA) for Persons ≥ 65 Years of Age” Environmental Health Perspectives Vol. 122, No. 2 February 2014 https://ehp.niehs.nih.gov/doi/10.1289/ehp.1306656

“Results: PM2.5 total mass and PM2.5 road dust contribution were associated with cardiovascular hospitalizations, as were the PM2.5 constituents calcium, black carbon, vanadium, and zinc. For respiratory hospitalizations, associations were observed with PM2.5 road dust, and sea salt as well as aluminum, calcium, chlorine, black carbon, nickel, silicon, titanium, and vanadium.”

“Our work indicates that some constituents of PM2.5 may be more toxic than others and therefore regulating PM total mass alone may not be sufficient to protect human health,” the authors wrote in Environmental Health Perspectives.

2. “New evidence on the impact of sustained exposure to air pollution on life expectancy from China’s Huai River Policy” Proceedings of the National Academy of Science September 11, 2017 https://www.pnas.org/content/early/2017/09/05/1616784114.full

‘”This paper finds that a 10-μg/m3 increase in airborne particulate matter [particulate matter smaller than 10 μm (PM10)] reduces life expectancy by 0.64 years (95% confidence interval = 0.21–1.07). Furthermore, the shorter lifespans are almost entirely caused by elevated rates of cardiorespiratory mortality, suggesting that PM10 is the causal factor. The estimates imply that bringing all of China into compliance with its Class I standards for PM10 would save 3.7 billion life-years.”

3. “Particulate matter air pollution and national and county life expectancy loss in the USA: A spatiotemporal analysis” PLOS Medicine July 23, 2019 https://doi.org/10.1371/journal.pmed.1002856 “Exposure to fine particulate matter pollution (PM2.5) is hazardous to health. Our aim was to directly estimate the health and longevity impacts of current PM2.5 concentrations and the benefits of reductions from 1999 to 2015, nationally and at county level, for the entire contemporary population of the contiguous United States.”

3 “PM2.5 pollution in excess of the lowest observed concentration (2.8 μg/m ) was responsible for an estimated 15,612 deaths (95% credible interval 13,248–17,945) in females and 14,757 deaths (12,617–16,919) in males. These deaths would lower national life expectancy by an estimated 0.15 years (0.13–0.17) for women and 0.13 years (0.11–0.15) for men. The life expectancy loss due to PM2.5 was largest around Los Angeles and in some southern states such as Arkansas, Oklahoma, and Alabama. At any PM2.5 concentration, life expectancy loss was, on average, larger in counties with lower income and higher poverty rate than in wealthier counties.”

APPENDIX B : 2002 SCREEN3 MODELING RUN FOR AUSTIN ASPHALT