Pregnant women are uniquely susceptible to adverse effects of air pollution exposure due to vulnerabilities and health consequences during pregnancy (e.g., hypertensive disorders of pregnancy [HDP]) compared to the general population. Because the Clean Air Act (CAA) creates a duty to protect at-risk groups, the regulatory assessment of at-risk populations has both policy and scientific foundations. Previously, pregnant women have not been specially protected in establishing the margin of safety for the ozone and particulate matter (PM) standards. Due to physiological changes, pregnant women can be at greater risk of adverse effects of air pollution and should be considered an at-risk population. Women with preexisting conditions, women experiencing poverty, and groups that suffer systematic discrimination may be particularly susceptible to cardiac effects of air pollutants during pregnancy. We rigorously reviewed 11 studies of over 1.3 million pregnant women in the United States to characterize the relationship between ozone or PM exposure and HDP. Findings were generally mixed, with a few studies reporting a joint association between ozone or PM and social determinants or pre-existing chronic health conditions related to HDP. Adequate evidence associates exposure to PM with an adverse effect of HDP among pregnant women not evident among non-gravid populations.

Exposures to industrial chemicals are widespread and can increase the risk of adverse health effects such as cancer, developmental disorders, respiratory effects, diabetes, and reproductive problems. The amended Toxic Substances Control Act (amended TSCA) requires the U.S. Environmental Protection Agency (EPA) to evaluate risks of chemicals in commerce, account for risk to potentially exposed and susceptible populations, and mitigate risks for chemicals determined to pose an unreasonable risk to human health and the environment. This analysis compares EPA’s first 10 chemical risk evaluations under amended TSCA to best scientific practices for conducting risk assessments. We find EPA’s risk evaluations underestimated human health risks of chemical exposures by excluding conditions of use and exposure pathways; not considering aggregate exposure and cumulative risk; not identifying all potentially exposed or susceptible subpopulations, and not quantifying differences in risk for susceptible groups; not addressing data gaps; and using flawed systematic review approaches to identify and evaluate the relevant evidence. We present specific recommendations for improving the implementation of amended TSCA using the best available science to ensure equitable, socially just safeguards to public health. Failing to remedy these shortcomings will result in continued systematic underestimation of risk for all chemicals evaluated under amended TSCA.

Wildland fire smoke exposure affects a broad proportion of the U.S. population and is increasing due to climate change, settlement patterns and fire seclusion. Significant public health questions surrounding its effects remain, including the impact on cardiovascular disease and maternal health. Using atmospheric chemical transport modeling, we examined general air quality with and without wildland fire smoke PM 2.5 . The 24-h average concentration of PM 2.5 from all sources in 12-km gridded output from all sources in California (2007-2013) was 4.91 µg/m 3 . The average concentration of fire-PM 2.5 in California by year was 1.22 µg/m 3 (~25% of total PM 2.5 ). The fire-PM 2.5 daily mean was estimated at 4.40 µg/m 3 in a high fire year (2008). Based on the model-derived fire-PM 2.5 data, 97.4% of California's population lived in a county that experienced at least one episode of high smoke exposure ("smokewave") from 2007-2013. Photochemical model predictions of wildfire impacts on daily average PM 2.5 carbon (organic and elemental) compared to rural monitors in California compared well for most years but tended to over-estimate wildfire impacts for 2008 (2.0 µg/m 3 bias) and 2013 (1.6 µg/m 3 bias) while underestimating for 2009 (−2.1 µg/m 3 bias). The modeling system isolated wildfire and PM 2.5 from other sources at monitored and unmonitored locations, which is important for understanding population exposure in health studies. Further work is needed to refine model predictions of wildland fire impacts on air quality in order to increase confidence in the model for future assessments. Atmospheric modeling can be a useful tool to assess broad geographic scale exposure for epidemiologic studies and to examine scenario-based health impacts.

From 1999–2014, obesity prevalence increased among adults and youth. Obese individuals may be uniquely susceptible to the proinflammatory effects of ozone because obese humans and animals have been shown to experience a greater decline in lung function than normal-weight subjects. Obesity is independently associated with limitations in lung mechanics with increased ozone dose. However, few epidemiologic studies have examined the interaction between excess weight and ozone exposure among adults. Using PubMed keyword searches and reference lists, we reviewed epidemiologic evidence to identify potential response-modifying factors and determine if obese or overweight adults are at increased risk of ozone-related health effects. We initially identified 170 studies, of which seven studies met the criteria of examining the interaction of excess weight and ozone exposure on cardiopulmonary outcomes in adults, including four short-term ozone exposure studies in controlled laboratory settings and three community epidemiologic studies. In the studies identified, obesity was associated with decreased lung function and increased inflammatory mediators. Results were inconclusive about the effect modification when data were stratified by sex. Obese and overweight populations should be considered as candidate at-risk groups for epidemiologic studies of cardiopulmonary health related to air pollution exposures. Air pollution is a modifiable risk factor that may decrease lung function among obese individuals with implications for environmental and occupational health policy.

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Wildland fire smoke exposure affects a broad proportion of the U.S. population and is increasing due to climate change, settlement patterns and fire seclusion. Significant public health questions surrounding its effects remain, including the impact on cardiovascular disease and maternal health. Using atmospheric chemical transport modeling, we examined general air quality with and without wildland fire smoke PM 2.5 . The 24-h average concentration of PM 2.5 from all sources in 12-km gridded output from all sources in California (2007-2013) was 4.91 µg/m 3 . The average concentration of fire-PM 2.5 in California by year was 1.22 µg/m 3 (~25% of total PM 2.5 ). The fire-PM 2.5 daily mean was estimated at 4.40 µg/m 3 in a high fire year (2008). Based on the model-derived fire-PM 2.5 data, 97.4% of California's population lived in a county that experienced at least one episode of high smoke exposure ("smokewave") from 2007-2013. Photochemical model predictions of wildfire impacts on daily average PM 2.5 carbon (organic and elemental) compared to rural monitors in California compared well for most years but tended to over-estimate wildfire impacts for 2008 (2.0 µg/m 3 bias) and 2013 (1.6 µg/m 3 bias) while underestimating for 2009 (−2.1 µg/m 3 bias). The modeling system isolated wildfire and PM 2.5 from other sources at monitored and unmonitored locations, which is important for understanding population exposure in health studies. Further work is needed to refine model predictions of wildland fire impacts on air quality in order to increase confidence in the model for future assessments. Atmospheric modeling can be a useful tool to assess broad geographic scale exposure for epidemiologic studies and to examine scenario-based health impacts.

The 2016 Frank Lautenberg Chemical Safety for the 21st Century Act (Lautenberg TSCA) amended the 1976 Toxic Substances Control Act (TSCA) to mandate protection of susceptible and highly exposed populations. Program implementation entails a myriad of choices that can lead to different degrees of public health protections. Well-documented exposures to multiple industrial chemicals occur from air, soil, water, food, and products in our workplaces, schools, and homes. Many hazardous chemicals are associated with or known to cause health risks; for other industrial chemicals, no data exist to confirm their safety because of flaws in 1976 TSCA. Under the 2016 Lautenberg amendments, the United States Environmental Protection Agency (EPA) must evaluate chemicals against risk-based safety standards under enforceable deadlines, with an explicit mandate to identify and assess risks to susceptible and highly exposed populations. Effective public health protection requires EPA to implement the Lautenberg TSCA requirements by incorporating intrinsic and extrinsic factors that affect susceptibility, adequately assessing exposure among vulnerable groups, and accurately identifying highly exposed groups. We recommend key scientific and risk assessment principles to inform health-protective chemical policy such as consideration of aggregate exposures from all pathways and, when data are lacking, the use of health-protective defaults.

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