Wildfires and the Changing Landscape of Air Pollution-related Health Burden in California.

Rationale: Wildfires are a growing source of pollution including particulate matter ⩽2.5 µm in aerodynamic diameter (PM2.5), but associated trends in health burden are not well characterized. Objectives: We investigated trends and disparities in PM2.5-related cardiorespiratory health burden (asthma, chronic obstructive pulmonary disease, and all-cause respiratory and cardiovascular emergency department [ED] visits and hospital admissions) for all days and wildfire smoke-affected days across California from 2008 to 2016. Methods: Using residential Zone Improvement Plan code and daily PM2.5 exposures, we estimated overall and subgroup-specific (age, gender, race and ethnicity) associations with cardiorespiratory outcomes. Health burden trends and disparities were evaluated on the basis of relative risk, attributable number, and attributable fraction by demographic and geographic factors and over time. Measurements and Main Results: PM2.5-attributed burden steadily decreased, whereas the fraction attributed to wildfire smoke varied by fire season intensity, constituting up to 15% of the annual PM2.5-burden. The highest relative risk and PM2.5-attributed burden (92 per 100,000 people) was observed for respiratory ED visits, accounting for 2.2% of the respiratory annual burden. Disparities in overall morbidity in the oldest age, Black, and "other" race groups were also reflected in PM2.5-attributed burden, whereas Asian populations had the highest risk rate in respiratory outcomes and thus the largest fraction of the total burden attributed to the exposure. In contrast, high wildfire PM2.5-attributed burden rates in rural, central, and northern California populations occurred because of differential exposure. Conclusions: In California, wildfires' impact on air quality offset the public health gains achieved through reductions in nonsmoke PM2.5. Disproportionate effects could be attributed to differences in subpopulation susceptibility, relative risk, and differential exposure.

Using Geospatial Data and Random Forest To Predict PFAS Contamination in Fish Tissue in the Columbia River Basin, United States.

Decision makers in the Columbia River Basin (CRB) are currently challenged with identifying and characterizing the extent of per- and polyfluoroalkyl substances (PFAS) contamination and human exposure to PFAS. This work aims to develop and pilot a methodology to help decision makers target and prioritize sampling investigations and identify contaminated natural resources. Here we use random forest models to predict ∑PFAS in fish tissue; understanding PFAS levels in fish is particularly important in the CRB because fish can be a major component of tribal and indigenous people diet. Geospatial data, including land cover and distances to known or potential PFAS sources and industries, were leveraged as predictors for modeling. Models were developed and evaluated for Washington state and Oregon using limited available empirical data. Mapped predictions show several areas where detectable concentrations of PFAS in fish tissue are predicted to occur, but prior sampling has not yet confirmed. Variable importance is analyzed to identify potentially important sources of PFAS in fish in this region. The cost-effective methodologies demonstrated here can help address sparsity of existing PFAS occurrence data in environmental media in this and other regions while also giving insights into potentially important drivers and sources of PFAS in fish.

Feasibility and acceptability of home monitoring with portable spirometry in young adults with asthma.

OBJECTIVE: Self-monitoring asthma control is a key component of asthma management. Few studies have reported usability and acceptability of portable spirometry among young adults with asthma. Portable spirometry offers a practical solution to monitoring airway narrowing at home. The purpose of this paper was to determine if self-administered spirometry is feasible and acceptable in young adults with asthma and whether regular monitoring resulted in improved airway function as measured by forced expiratory volume in one second (FEV1). METHODS: Sixty-seven young adults (18-26 years) with self-reported asthma participated in a clinical trial during wildfire season which measured FEV1 as an outcome measure. Data was collected at baseline, week 4, and week 8 using a portable spirometer linked to a smartphone application. A subset of intervention participants completed spirometry twice daily. Acceptability of self-administered spirometry was evaluated after the trial among participants that volunteered to submit a survey and be interviewed. RESULTS: At baseline, all 67 participants (100.0%) completed their scheduled spirometry readings which declined to 94.0% (n = 63) at week 4 and 86.6% (n = 58) at week 8. Daily readings were completed 83.2% of the time in the mornings and 84.3% of the time in the evenings. Mean FEV1 values were lower than predicted values, but above the lower limit of expected. FEV1 remained steady throughout the study period. Over two-thirds of participants used the notes feature in the application and described symptoms, asthma triggers, mitigating actions and test-taking issues. CONCLUSIONS: Young adults in our sample were highly compliant with regular, self-administered spirometry.

Wildfire smoke exposure and early childhood respiratory health: a study of prescription claims data.

Wildfire smoke is associated with short-term respiratory outcomes including asthma exacerbation in children. As investigations into developmental wildfire smoke exposure on children's longer-term respiratory health are sparse, we investigated associations between developmental wildfire smoke exposure and first use of respiratory medications. Prescription claims from IBM MarketScan Commercial Claims and Encounters database were linked with wildfire smoke plume data from NASA satellites based on Metropolitan Statistical Area (MSA). A retrospective cohort of live infants (2010-2016) born into MSAs in six western states (U.S.A.), having prescription insurance, and whose birthdate was estimable from claims data was constructed (N = 184,703); of these, gestational age was estimated for 113,154 infants. The residential MSA, gestational age, and birthdate were used to estimate average weekly smoke exposure days (smoke-day) for each developmental period: three trimesters, and two sequential 12-week periods post-birth. Medications treating respiratory tract inflammation were classified using active ingredient and mode of administration into three categories:: 'upper respiratory', 'lower respiratory', 'systemic anti-inflammatory'. To evaluate associations between wildfire smoke exposure and medication usage, Cox models associating smoke-days with first observed prescription of each medication category were adjusted for infant sex, birth-season, and birthyear with a random intercept for MSA. Smoke exposure during postnatal periods was associated with earlier first use of upper respiratory medications (1-12 weeks: hazard ratio (HR) = 1.094 per 1-day increase in average weekly smoke-day, 95%CI: (1.005,1.191); 13-24 weeks: HR = 1.108, 95%CI: (1.016,1.209)). Protective associations were observed during gestational windows for both lower respiratory and systemic anti-inflammatory medications; it is possible that these associations may be a consequence of live-birth bias. These findings suggest wildfire smoke exposure during early postnatal developmental periods impact subsequent early life respiratory health.

Association Between Long-term Ambient PM2.5 Exposure and Cardiovascular Outcomes Among US Hemodialysis Patients.

RATIONALE & OBJECTIVE: Ambient PM2.5 (particulate matter with a diameter of 2.5 microns) is a ubiquitous air pollutant with established adverse cardiovascular (CV) effects. However, quantitative estimates of the association between PM2.5 exposure and CV outcomes in the setting of kidney disease are limited. This study assessed the association of long-term PM2.5 exposure with CV events and cardiovascular disease (CVD)-specific mortality among patients receiving maintenance in-center hemodialysis (HD). STUDY DESIGN: Retrospective cohort study. SETTINGS & PARTICIPANTS: 314,079 adult kidney failure patients initiating HD between 2011 and 2016 identified from the US Renal Data System. EXPOSURE: Estimated daily ZIP code-level PM2.5 concentrations were used to calculate each participant's annual average PM2.5 exposure based on the dialysis clinics visited during the 365 days before the outcome. OUTCOME: CV event and CVD-specific mortality were ascertained based on ICD-9/ICD-10 diagnostic codes and recorded cause of death from Centers for Medicare & Medicaid Services form 2746. ANALYTICAL APPROACH: Discrete time hazards models were used to estimate hazards ratios per 1 µg/m3 greater annual average PM2.5, adjusting for temperature, humidity, day of the week, season, age at baseline, race, employment status, and geographic region. Effect measure modification was assessed for age, sex, race, and baseline comorbidities. RESULTS: Each 1 µg/m3 greater annual average PM2.5 was associated with a greater rate of CV events (HR, 1.02 [95% CI, 1.01-1.02]) and CVD-specific mortality (HR, 1.02 [95% CI, 1.02-1.03]). The association was more pronounced for people who initiated dialysis at an older age, had chronic obstructive pulmonary disease (COPD) at baseline, or were Asian. Evidence of effect modification was also observed across strata of race, and other baseline comorbidities. LIMITATIONS: Potential exposure misclassification and unmeasured confounding. CONCLUSIONS: Long-term ambient PM2.5 exposure was associated with CVD outcomes among patients receiving maintenance in-center HD. Stronger associations between long-term PM2.5 exposure and adverse effects were observed among patients who were of advanced age, had COPD, or were Asian. PLAIN-LANGUAGE SUMMARY: Long-term exposure to air pollution, also called PM2.5, has been linked to adverse cardiovascular outcomes. However, little is known about the association of PM2.5 and outcomes among patients receiving dialysis, who are individuals with high cardiovascular disease burdens. We conducted an epidemiological study to assess the association between the annual PM2.5 exposure and cardiovascular events and death among patients receiving regular outpatient hemodialysis in the United States between 2011 and 2016. We found a higher risk of heart attacks, strokes, and related events in patients exposed to higher levels of air pollution. Stronger associations between air pollution and adverse health events were observed among patients who were older at the start of dialysis, had chronic obstructive pulmonary disease, or were Asian. These findings bolster the evidence base linking air pollution and adverse health outcomes and may inform policy makers and clinicians.

Effects of short-term ambient PM2.5 exposure on cardiovascular disease incidence and mortality among U.S. hemodialysis patients: a retrospective cohort study.

BACKGROUND: Ambient PM2.5 is a ubiquitous air pollutant with demonstrated adverse health impacts in population. Hemodialysis patients are a highly vulnerable population and may be particularly susceptible to the effects of PM2.5 exposure. This study examines associations between short-term PM2.5 exposure and cardiovascular disease (CVD) and mortality among patients receiving maintenance in-center hemodialysis. METHODS: Using the United State Renal Data System (USRDS) registry, we enumerated a cohort of all US adult kidney failure patients who initiated in-center hemodialysis between 1/1/2011 and 12/31/2016. Daily ambient PM2.5 exposure estimates were assigned to cohort members based on the ZIP code of the dialysis clinic. CVD incidence and mortality were ascertained through 2016 based on USRDS records. Discrete time hazards regression was used to estimate the association between lagged PM2.5 exposure and CVD incidence, CVD-specific mortality, and all-cause mortality 1 t adjusting for temperature, humidity, day of the week, season, age at baseline, race, employment status, and geographic region. Effect measure modification was assessed for age, sex, race, and comorbidities. RESULTS: Among 314,079 hemodialysis patients, a 10 µg/m3 increase in the average lag 0-1 daily PM2.5 exposure was associated with CVD incidence (HR: 1.03 (95% CI: 1.02, 1.04)), CVD mortality (1.05 (95% CI: 1.03, 1.08)), and all-cause mortality (1.04 (95% CI: 1.03, 1.06)). The association was larger for people who initiated dialysis at an older age, while minimal evidence of effect modification was observed across levels of sex, race, or baseline comorbidities. CONCLUSIONS: Short-term ambient PM2.5 exposure was positively associated with incident CVD events and mortality among patients receiving in-center hemodialysis. Older patients appeared to be more susceptible to PM2.5-associated CVD events than younger hemodialysis patients.

Omega-3 fatty acids attenuate cardiovascular effects of short-term exposure to ambient air pollution.

BACKGROUND: Exposure to air pollution is associated with elevated cardiovascular risk. Evidence shows that omega-3 polyunsaturated fatty acids (omega-3 PUFA) may attenuate the adverse cardiovascular effects of exposure to fine particulate matter (PM2.5). However, it is unclear whether habitual dietary intake of omega-3 PUFA protects against the cardiovascular effects of short-term exposure to low-level ambient air pollution in healthy participants. In the present study, sixty-two adults with low or high dietary omega-3 PUFA intake were enrolled. Blood lipids, markers of vascular inflammation, coagulation and fibrinolysis, and heart rate variability (HRV) and repolarization were repeatedly assessed in 5 sessions separated by at least 7 days. This study was carried out in the Research Triangle area of North Carolina, USA between October 2016 and September 2019. Daily PM2.5 and maximum 8-h ozone (O3) concentrations were obtained from nearby air quality monitoring stations. Linear mixed-effects models were used to assess the associations between air pollutant concentrations and cardiovascular responses stratified by the omega-3 intake levels. RESULTS: The average concentrations of ambient PM2.5 and O3 were well below the U.S. National Ambient Air Quality Standards during the study period. Significant associations between exposure to PM2.5 and changes in total cholesterol, von Willebrand factor (vWF), tissue plasminogen activator, D-dimer, and very-low frequency HRV were observed in the low omega-3 group, but not in the high group. Similarly, O3-associated adverse changes in cardiovascular biomarkers (total cholesterol, high-density lipoprotein, serum amyloid A, soluable intracellular adhesion molecule 1, and vWF) were mainly observed in the low omega-3 group. Lag-time-dependent biphasic changes were observed for some biomarkers. CONCLUSIONS: This study demonstrates associations between short-term exposure to PM2.5 and O3, at concentrations below regulatory standard, and subclinical cardiovascular responses, and that dietary omega-3 PUFA consumption may provide protection against such cardiovascular effects in healthy adults.

Can disposable masks be worn more than once?

Disposable facemasks are a primary tool to prevent the transmission of SARS-COV-2 during the COVID-19 pandemic. However, plastic waste generated from their disposal represents a significant environmental problem that can be reduced by maximizing the service life of disposable masks. We evaluated the effect of repeated wearing on the fitted filtration efficiency (FFE) of N95, KF94, KN95, and procedure/surgical masks. The FFEs of masks were compared following extended wearing with and without washing. Results reveal that most disposable facemasks can retain a high level of their baseline FFE after extended wearing, even after 40 h of wearing. Laundering disposable masks degraded FFE in some instances. We conclude that the durability of disposable facemask performance is considerably longer than their intended single use indication, suggesting that reusing disposable masks is a safe means of reducing plastic waste in the environment.

Circulating microRNAs as putative mediators in the association between short-term exposure to ambient air pollution and cardiovascular biomarkers.

BACKGROUND: Exposure to ambient air pollution is associated with increased cardiovascular morbidity and mortality. Circulating microRNAs (miRNAs) may mediate cardiovascular effects of exposure to air pollution. This study aims to investigate whether circulating miRNAs mediate the associations between short-term human exposure to ambient air pollution and cardiovascular biomarkers. METHODS: Twenty-four healthy adults residing in the Research Triangle area of North Carolina, USA were enrolled between December 2016 and July 2019. Circulating miRNAs, protein, and lipid biomarkers were assessed repeatedly for 3 sessions separated by at least 7 days. Linear mixed-effects models were used to assess the associations between air pollutant concentrations obtained from nearby air quality monitoring stations and miRNAs controlling for covariates including omega-3 index, relative humidity, and temperature. miRNAs that were significantly altered were then matched with protein or blood lipid biomarkers using either Ingenuity Pathway Analysis or a literature search. A mediation analysis was performed to test the statistical significance of miRNA's mediating effects between exposure to air pollution and cardiovascular biomarkers. RESULTS: Short-term exposure to ambient fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) was associated with changes in 11, 9, and 24 circulating miRNAs, respectively. Pathway analysis showed that several miRNAs including miR-125b-5p, miR-144-5p, miR-26a-5p, and miR-34a-5p may mediate the effects of air pollutant exposure on the changes of downstream protein / lipid biomarkers including serum amyloid A (SAA), C-reactive protein (CRP), soluble vascular adhesive molecules 1 (sICAM1), total cholesterol, and high-density lipoproteins (HDL). Mediation analysis showed that only miR-26a-5p significantly mediated air pollutant (PM2.5 and NO2)-induced effects on blood CRP and total cholesterol levels. For example, 34.1% of PM2.5-associated changes in CRP were significantly mediated by miR-26a-5p at lag4 [indirect effects, 0.06 (0.02, 0.10), P = 0.005]. Similarly, the proportions of indirect effects of miR-26a-5p on the association between NO2 exposure and CRP were 46.8% at lag2 [0.06 (0.02, 0.11), P = 0.003], 61.2% at lag3 [0.05 (0.00, 0.09), P = 0.04], and 30.8% at 5-day moving average [0.06 (0.02, 0.10), P = 0.01]. In addition, omega-3 index may be a significant modifying factor of the mediated effects of miRNAs. CONCLUSIONS: This study demonstrates that short-term exposure to ambient PM2.5, O3, and NO2 was associated with specific circulating miRNAs, and some of which may mediate their effects on the downstream inflammation and blood lipid markers.

Promoting risk reduction among young adults with asthma during wildfire smoke: A feasibility study.

OBJECTIVE(S): This study explored the feasibility, acceptability, preliminary impact, and functionality of two risk reduction mobile application (app) interventions on asthma outcomes as compared to a control arm during wildfire season. DESIGN: Three-arm, 8-week randomized clinical trial. SAMPLE: Sixty-seven young adults with asthma were enrolled. MEASUREMENTS: The Asthma Control Test, forced expiratory volume in one second (FEV1 ) and the System Usability Scale were measured at baseline, 4, and 8 weeks. The Research Attitude Scale was administered at 8 weeks. Twenty participants from the two intervention arms completed an optional survey and six were interviewed after completing the study. INTERVENTION: Both intervention arms could access Smoke Sense Urbanova, an app that supports reducing risks from breathing wildfire smoke. The Smoke Sense Urbanova Plus arm also monitored their daily FEV1 , received air quality notifications, and accessed preventive tips and a message board. RESULTS: Most participants agreed the app and spirometer were usable and their privacy and confidentiality were maintained. No adverse events were reported. CONCLUSIONS: Participant-identified recommendations will support intervention refinement and testing. This research supports asthma self-management tools that public health nurses and community health workers can recommend for at-risk populations.

Trends in Fire Danger and Population Exposure along the Wildland-Urban Interface.

The increased risk of wildfires and associated smoke exposure in the United States is a growing public health problem, particularly along the Wildland-Urban Interface (WUI). Using the measure of fire danger, the Energy Release Component, we define fire danger as the onset and duration of fire season, in the continental US, between 1979 and 2016. We then combine the measure of fire danger with census data to quantify changes in population fire exposure across the WUI. We determined that the largest increases in fire danger were observed in the Southwest, Intermountain, and Pacific Southwest regions. The increased fire danger, specifically during peak fire season, accounted for 6.1 more fires each year and 78,000 more acres burned each year, underscoring the link between fire danger and the risks of large fire occurrence and burn acreage. Finally, we observed significant population growth (121.2% between 1990 and 2010) within high-danger WUI areas, further implying significant increases in potential fire exposure.

The influence of dietary intake of omega-3 polyunsaturated fatty acids on the association between short-term exposure to ambient nitrogen dioxide and respiratory and cardiovascular outcomes among healthy adults.

BACKGROUND: Short-term exposure to ambient nitrogen dioxide (NO2) is associated with adverse respiratory and cardiovascular outcomes. Supplementation of omega-3 polyunsaturated fatty acids (PUFA) has shown protection against exposure to fine particulate matter. This study aims to investigate whether habitual omega-3 PUFA intake differentially modify the associations between respiratory and cardiovascular responses and short-term exposure to ambient NO2. METHODS: Sixty-two healthy participants were enrolled into low or high omega-3 groups based on their habitual omega-3 PUFA intake. Each participant was repeatedly assessed for lung function, blood lipids, markers of coagulation and fibrinolysis, vascular function, and heart rate variability (HRV) in up to five sessions, each separated by at least 7 days. This study was carried out in the Research Triangle area of North Carolina, USA between October 2016 and September 2019. Daily ambient NO2 concentrations were obtained from an area air quality monitoring station on the day of outcome assessment (Lag0), 4 days prior (Lag1-4), as well as 5-day moving average (5dMA). The associations between short-term exposure to NO2 and the measured indices were evaluated using linear mixed-effects models stratified by omega-3 levels and adjusted by covariates including relative humidity and temperature. RESULTS: The average concentration of ambient NO2 during the study periods was 5.3±3.8 ppb which was below the National Ambient Air Quality Standards (NAAQS). In the high omega-3 group, an interquartile range (IQR) increase in short-term NO2 concentrations was significantly associated with increased lung function [e.g. 1.2% (95%CI: 0.2%, 2.2%) in FVC at lag1, 2.6% (95%CI: 0.4%, 4.8%) in FEV1 at 5dMA], decreased blood lipids [e.g. -2.6% (95%CI: -4.4%, -0.9%) in total cholesterol at lag2, -3.1% (95%CI: -6.1%, 0.0%) in HDL at 5dMA, and -3.1% (95%CI: -5.5%, -0.7%) in LDL at lag2], improved vascular function [e.g. 8.9% (95%CI: 0.6%, 17.2%) increase in FMD and 43.1% (95%CI: -79.8%, -6.3%) decrease in endothelin-1 at 5dMA], and changed HRV parameters [e.g. -7.2% (95%CI: -13.6%, -0.8%) in HFn and 13.4% (95%CI: 0.2%, 28.3%) in LF/HF ratio at lag3]. In the low omega-3 group, an IQR increase in ambient NO2 was associated with elevations in coagulation markers (von Willebrand Factor, D-dimer) and a decrease in HRV (very-low frequency); however, null associations were observed between short-term NO2 exposure and changes in lung function, blood lipids, and vascular function. CONCLUSIONS: The results in this study imply that dietary omega-3 PUFA consumption may offer respiratory and vascular benefits in response to short-term exposure of healthy adults to NO2 levels below the NAAQS. TRIAL REGISTRATION: ClinicalTrials.gov ( NCT02921048 ).

Mortality in US Hemodialysis Patients Following Exposure to Wildfire Smoke.

BACKGROUND: Wildfires are increasingly a significant source of fine particulate matter (PM2.5), which has been linked to adverse health effects and increased mortality. ESKD patients are potentially susceptible to this environmental stressor. METHODS: We conducted a retrospective time-series analysis of the association between daily exposure to wildfire PM2.5 and mortality in 253 counties near a major wildfire between 2008 and 2012. Using quasi-Poisson regression models, we estimated rate ratios (RRs) for all-cause mortality on the day of exposure and up to 30 days following exposure, adjusted for background PM2.5, day of week, seasonality, and heat. We stratified the analysis by causes of death (cardiac, vascular, infectious, or other) and place of death (clinical or nonclinical setting) for differential PM2.5 exposure and outcome classification. RESULTS: We found 48,454 deaths matched to the 253 counties. A 10-µg/m3 increase in wildfire PM2.5 associated with a 4% increase in all-cause mortality on the same day (RR, 1.04; 95% confidence interval [95% CI], 1.01 to 1.07) and 7% increase cumulatively over 30 days following exposure (RR, 1.07; 95% CI, 1.01 to 1.12). Risk was elevated following exposure for deaths occurring in nonclinical settings (RR, 1.07; 95% CI, 1.02 to 1.12), suggesting modification of exposure by place of death. "Other" deaths (those not attributed to cardiac, vascular, or infectious causes) accounted for the largest portion of deaths and had a strong same-day effect (RR, 1.08; 95% CI, 1.03 to 1.12) and cumulative effect over the 30-day period. On days with a wildfire PM2.5 contribution >10 µg/m3, exposure accounted for 8.4% of mortality. CONCLUSIONS: Wildfire smoke exposure was positively associated with all-cause mortality among patients receiving in-center hemodialysis.

A Review of Spatial Causal Inference Methods for Environmental and Epidemiological Applications.

The scientific rigor and computational methods of causal inference have had great impacts on many disciplines but have only recently begun to take hold in spatial applications. Spatial causal inference poses analytic challenges due to complex correlation structures and interference between the treatment at one location and the outcomes at others. In this paper, we review the current literature on spatial causal inference and identify areas of future work. We first discuss methods that exploit spatial structure to account for unmeasured confounding variables. We then discuss causal analysis in the presence of spatial interference including several common assumptions used to reduce the complexity of the interference patterns under consideration. These methods are extended to the spatiotemporal case where we compare and contrast the potential outcomes framework with Granger causality and to geostatistical analyses involving spatial random fields of treatments and responses. The methods are introduced in the context of observational environmental and epidemiological studies and are compared using both a simulation study and analysis of the effect of ambient air pollution on COVID-19 mortality rate. Code to implement many of the methods using the popular Bayesian software OpenBUGS is provided.

Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Findings from a Multisite Case-Control Study.

BACKGROUND: Epidemiologic studies have reported associations between prenatal and early postnatal air pollution exposure and autism spectrum disorder (ASD); however, findings differ by pollutant and developmental window. OBJECTIVES: We examined associations between early life exposure to particulate matter ≤2.5 µm in diameter (PM2.5) and ozone in association with ASD across multiple US regions. METHODS: Our study participants included 674 children with confirmed ASD and 855 population controls from the Study to Explore Early Development, a multi-site case-control study of children born from 2003 to 2006 in the United States. We used a satellite-based model to assign air pollutant exposure averages during several critical periods of neurodevelopment: 3 months before pregnancy; each trimester of pregnancy; the entire pregnancy; and the first year of life. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for study site, maternal age, maternal education, maternal race/ethnicity, maternal smoking, and month and year of birth. RESULTS: The air pollution-ASD associations appeared to vary by exposure time period. Ozone exposure during the third trimester was associated with ASD, with an OR of 1.2 (95% CI: 1.1, 1.4) per 6.6 ppb increase in ozone. We additionally observed a positive association with PM2.5 exposure during the first year of life (OR = 1.3 [95% CI: 1.0, 1.6] per 1.6 µg/m increase in PM2.5). CONCLUSIONS: Our study corroborates previous findings of a positive association between early life air pollution exposure and ASD, and identifies a potential critical window of exposure during the late prenatal and early postnatal periods.

Low levels of fine particulate matter increase vascular damage and reduce pulmonary function in young healthy adults.

BACKGROUND: Fine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies. METHODS: To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 µg/m3, SD 6.5), and filtered air (mean: 2.1 µg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure. RESULTS: Low-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 µg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure. CONCLUSIONS: This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard. CLINICAL TRIAL REGISTRATION INFORMATION: clinicaltrials.gov ; Identifier: NCT03232086 . The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

Effects of ambient ozone exposure on circulating extracellular vehicle microRNA levels in coronary artery disease patients.

Exposure to ambient air pollutants such as ozone (O3) and particulate matter (PM) is associated with increased cardiovascular morbidity and rate of mortality, but the underlying biological mechanisms have yet to be described. Emerging evidence shows that extracellular vehicle (EV) microRNAs (miRNAs) may facilitate cell-to-cell and organ-to-organ communications and play a role in the air pollution-induced cardiovascular effects. This study aims to explore the association between air pollutant exposure and miRNA changes related to cardiovascular diseases. Using a panel study design, 14 participants with coronary artery diseases were enrolled in this study. Each participant had up to 10 clinical visits and their plasma samples were collected and measured for expression of miRNA-21 (miR-21), miR-126, miR-146, miR-150, and miR-155. Mixed effects models adjusted for temperature, humidity, and season were used to examine the association between miRNA levels and exposure to 8-hr O3 or 24-hr PM2.5 up to 4 days prior. Results demonstrated that miR-150 expression was positively associated with O3 exposure at 1-4 days lag and 5day moving average while miR-155 expression tracked with O3 exposure at lag 0. No significant association was found between miRNA expression and ambient PM2.5 at any time point. ß-blocker and diabetic medication usage significantly modified the correlation between O3 exposure and miR-150 expression where the link was more prominent among non-users. In conclusion, evidence indicated an association between exposure to ambient O3 and circulating levels of EV miR-150 and miR-155 was observed. These findings pointed to a future research direction involving miRNA-mediated mechanisms of O3-induced cardiovascular effects.

Fine particulate matters: The impact of air quality standards on cardiovascular mortality.

BACKGROUND: In 1997 the U.S. Environmental Protection Agency set the first annual National Ambient Air Quality Standard (NAAQS) for fine particulate matter (PM2.5). Although the weight of scientific evidence has determined that a causal relationship exists between PM2.5 exposures and cardiovascular effects, few studies have concluded whether NAAQS-related reductions in PM2.5 led to improvements in public health. METHODS: We examined the change in cardiovascular (CV) mortality rate and the association between change in PM2.5 and change in CV-mortality rate before (2000-2004) and after implementation of the 1997 annual PM2.5 NAAQS (2005-2010) among U.S. counties. We further examined how the association varied with respect to two factors related to NAAQS compliance: attainment status and design values (DV). We used difference-in-differences and linear regression models, adjusted for sociodemographic confounders. FINDINGS: Across 619 counties, there were 1.10 (95% CI: 0.37, 1.82) fewer CV-deaths per year per 100,000 people for each 1µg/m3 decrease in PM2.5. Nonattainment counties had a twofold larger reduction in mean annual PM2.5, 2.1µg/m3, compared to attainment counties, 0.97µg/m3. CV-mortality rate decreased by 0.59 (95% CI: -0.54, 1.71) in nonattainment and 1.96 (95% CI: 0.77, 3.15) deaths per 100,000 people for each 1µg/m3 decrease in PM2.5 in attainment counties. When stratifying counties by DV, results were similar: counties with DV greater than 15µg/m3 experienced the greatest decrease in mean annual PM2.5 (2.29µg/m3) but the smallest decrease in CV-mortality rate per unit decrease in PM2.5, 0.73 (95% CI: -0.57, 2.02). INTERPRETATION: We report a significant association between the change in PM2.5 and the change in CV-mortality rate before and after the implementation of NAAQS and note that the health benefits per 1µg/m3 decrease in PM2.5 persist at levels below the current national standard. FUNDING: US EPA intermural research.

Community Vulnerability to Health Impacts of Wildland Fire Smoke Exposure.

Identifying communities vulnerable to adverse health effects from exposure to wildfire smoke may help prepare responses, increase the resilience to smoke and improve public health outcomes during smoke days. We developed a Community Health-Vulnerability Index (CHVI) based on factors known to increase the risks of health effects from air pollution and wildfire smoke exposures. These factors included county prevalence rates for asthma in children and adults, chronic obstructive pulmonary disease, hypertension, diabetes, obesity, percent of population 65 years of age and older, and indicators of socioeconomic status including poverty, education, income and unemployment. Using air quality simulated for the period between 2008 and 2012 over the continental U.S. we also characterized the population size at risk with respect to the level and duration of exposure to fire-originated fine particulate matter (fire-PM2.5) and CHVI. We estimate that 10% of the population (30.5 million) lived in the areas where the contribution of fire-PM2.5 to annual average ambient PM2.5 was high (>1.5 µg/m3) and that 10.3 million individuals experienced unhealthy air quality levels for more than 10 days due to smoke. Using CHVI we identified the most vulnerable counties and determined that these communities experience more smoke exposures in comparison to less vulnerable communities.