Abstract  Rationale: Growing evidence suggests that long-term exposure to fine particulate matter (PM2.5) air pollution contributes to risk of cardiovascular disease (CVD) morbidity and mortality. There is uncertainty regarding who are most susceptible. Individuals with underlying cardiometabolic disorders, including hypertension, diabetes, and obesity, may be at greater risk. PM2.5 pollution may also contribute to cardiometabolic disorders, augmenting CVD risk. Objective: This analysis evaluates relationships between long-term PM2.5 exposure and cardiometabolic disease on risk of death from CVD and cardiometabolic conditions. Methods and Results: Data on 669,046 participants from the American Cancer Society, Cancer Prevention Study II cohort were linked to modeled PM2.5 concentrations at geocoded home addresses. Cox proportional hazards regression models were used to estimate adjusted hazards ratios (HR) for death from CVD and cardiometabolic diseases based on death-certificate information. Effect modification by pre-existing cardiometabolic risk factors on the PM2.5-CVD mortality association was examined. PM2.5 exposure was associated with CVD mortality, with the HR (95% CI) per 10 µg/m(3) increase in PM2.5 equal to 1.12 (1.10-1.15). Deaths linked to hypertension and/or diabetes (mentioned on death certificate as either primary or contributing cause of death) were also associated with PM2.5. There was no consistent evidence of effect modification by cardiometabolic disease risk factors on the PM2.5-CVD mortality association. Conclusions: Pollution-induced CVD mortality risk is observed for those with and without existing cardiometabolic disorders. Long-term exposure may also contribute to the development or exacerbation of cardiometabolic disorders, increasing risk of CVD and cardiometabolic disease mortality.

Abstract  #Using the photographs and optical measurements taken during a summer field program (REVEAL) designed to examine the chemical and physical characteristics of visibility impairment in the Fraser Valley, southwestern British Columbia, a protocol for gauging public perception of visibility in this region was devised and tested in a pilot survey. This paper details the protocol (which is based on previous studies conducted in the United States of America) and analysis techniques for survey responses. A preliminary assessment of the results of the pilot study is also presented. A public perception survey conducted in Denver (Ely et al., 1991), resolved a visibility standard for Denver of bext (total light extinction) = 0.076 Î 10-3 m-1. Assuming a homogeneous atmosphere, this level of bext is approximately equal to a visual range of 50 km. Using a similar protocol, responses from this pilot study were used to extrapolate visibility standards for two suburban locations in the Fraser Valley of b(ext) (approx) 0.09 Î 10-3-0.105 Î 10-3 m-1 (bsp (particle light scattering) (approx) 0.051 Î 10-3-0.063 Î 10-3 m-1) and b(sp) (approx) 0.39 Î 10-3 m-1. These levels of light extinction (bsp is the largest component of b(ext)) relate to approximate visual range of between 40 and 60 km in a homogeneous atmosphere. Possible reasons for the apparent discrepancies between locations are discussed and the effect of survey group are addressed.

Abstract  RATIONALE: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease. OBJECTIVES: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction (MI) and stroke, as well as all-cause and cause-specific mortality. METHODS: We estimated long-term residential air pollution exposure for over 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals. We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident MI and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models. MEASUREMENTS AND MAIN RESULTS: We found elevated hazard ratios linking long-term exposure to fine particulate matter (PM2.5, scaled to an increment of 10 µg/m3) with mortality from ischemic heart disease (IHD) (1.20, 95% C.I. 1.02-1.41) and, particularly among post-menopausal women, incident stroke (1.19, 95% C.I. 1.02-1.38). Long-term exposure to particulate matter less than 10 µm aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06, 95% C.I. 0.99-1.14) and incident stroke 1.06 (95% CI: 1.00-1.13), while nitrogen oxides were associated with elevated risks for cardiovascular as well as IHD mortality. CONCLUSIONS: Long-term exposures to PM2.5 and PM10 were associated with increased risks of incident stroke and death from IHD; exposures to nitrogen oxides were associated with all cardiovascular as well as IHD mortality.

Abstract  Background: We and others have shown that increases in particulate air pollutant (PM) concentrations in the previous hours and days have been associated with increased risks of myocardial infarction, but little is known about the relationships between air pollution and specific subsets of myocardial infarction, such as ST-elevation myocardial infarction (STEMI) and non ST-elevation myocardial infarction (NSTEMI). Methods: Using data from acute coronary syndrome patients with STEMI (n = 338) and NSTEMI (n = 339) and case-crossover methods, we estimated the risk of STEMI and NSTEMI associated with increased ambient fine particle (<2.5 um) concentrations, ultrafine particle (10-100 nm) number concentrations, and accumulation mode particle (100-500 nm) number concentrations in the previous few hours and days. Results: We found a significant 18% increase in the risk of STEMI associated with each 7.1 mu g/m(3) increase in PM2.5 concentration in the previous hour prior to acute coronary syndrome onset, with smaller, non-significantly increased risks associated with increased fine particle concentrations in the previous 3, 12, and 24 hours. We found no pattern with NSTEMI. Estimates of the risk of STEMI associated with interquartile range increases in ultrafine particle and accumulation mode particle number concentrations in the previous 1 to 96 hours were all greater than 1.0, but not statistically significant. Patients with pre-existing hypertension had a significantly greater risk of STEMI associated with increased fine particle concentration in the previous hour than patients without hypertension. Conclusions: Increased fine particle concentrations in the hour prior to acute coronary syndrome onset were associated with an increased risk of STEMI, but not NSTEMI. Patients with pre-existing hypertension and other cardiovascular disease appeared particularly susceptible. Further investigation into mechanisms by which PM can preferentially trigger STEMI over NSTEMI within this rapid time scale is needed.

Abstract  OBJECTIVES: Develop statistical methods for survival models to indirectly adjust hazard ratios of environmental exposures for missing risk factors.

METHODS: A partitioned regression approach for linear models is applied to time to event survival analyses of cohort study data. Information on the correlation between observed and missing risk factors is obtained from ancillary data sources such as national health surveys. The relationship between the missing risk factors and survival is obtained from previously published studies. We first evaluated the methodology using simulations, by considering the Weibull survival distribution for a proportional hazards regression model with varied baseline functions, correlations between an adjusted variable and an adjustment variable as well as selected censoring rates. Then we illustrate the method in a large, representative Canadian cohort of the association between concentrations of ambient fine particulate matter and mortality from ischemic heart disease.

RESULTS: Indirect adjustment for cigarette smoking habits and obesity increased the fine particulate matter-ischemic heart disease association by 3%-123%, depending on the number of variables considered in the adjustment model due to the negative correlation between these two risk factors and ambient air pollution concentrations in Canada. The simulations suggested that the method yielded small relative bias (<40%) for most cohort designs encountered in environmental epidemiology.

CONCLUSIONS: This method can accommodate adjustment for multiple missing risk factors simultaneously while accounting for the associations between observed and missing risk factors and between missing risk factors and health endpoints.

Abstract  Epidemiological studies have observed between city heterogeneity in PM2.5-mortality risk estimates. These differences could potentially be due to the use of central-site monitors as a surrogate for exposure which do not account for an individual's activities or ambient pollutant infiltration to the indoor environment. Therefore, relying solely on central-site monitoring data introduces exposure error in the epidemiological analysis. The amount of exposure error produced by using the central-site monitoring data may differ by city. The objective of this analysis was to cluster cities with similar exposure distributions based on residential infiltration and in-vehicle commuting characteristics. Factors related to residential infiltration and commuting were developed from the American Housing Survey (AHS) from 2001 to 2005 for 94 Core-Based Statistical Areas (CBSAs). We conducted two separate cluster analyses using a k-means clustering algorithm to cluster CBSAs based on these factors. The first only included residential infiltration factors (i.e. percent of homes with central air conditioning (AC) mean year home was built, and mean home size) while the second incorporated both infiltration and commuting (i.e. mean in-vehicle commuting time and mean in-vehicle commuting distance) factors. Clustering on residential infiltration factors resulted in 5 clusters, with two having distinct exposure distributions. Cluster 1 consisted of cities with older, smaller homes with less central AC while homes in Cluster 2 cities were newer, larger, and more likely to have central AC. Including commuting factors resulted in 10 clusters. Clusters with shorter in-vehicle commuting times had shorter in-vehicle commuting distances. Cities with newer homes also tended to have longer commuting times and distances. This is the first study to employ cluster analysis to group cities based on exposure factors. Identifying cities with similar exposure distributions may help explain city-to-city heterogeneity in PM2.5 mortality risk estimates.

Abstract  Background and Methods Atrial fibrillation is associated with an increased risk of ischemic stroke. Data on individual patients were pooled from five recently completed randomized trials comparing warfarin (all studies) or aspirin (the Atrial Fibrillation, Aspirin, Anticoagulation Study and the Stroke Prevention in Atrial Fibrillation Study) with control in patients with atrial fibrillation. The purpose of the analysis was to (1) identify patient features predictive of a high or low risk of stroke, (2) assess the efficacy of antithrombotic therapy in major patient subgroups (eg, women), and (3) obtain the most precise estimate of the efficacy and risks of antithrombotic therapy in atrial fibrillation. For the warfarin-control comparison there were 1889 patient-years receiving warfarin and 1802 in the control group. For the aspirin-placebo comparison there were 1132 patient-years receiving aspirin and 1133 receiving placebo. The daily dose of aspirin was 75 mg in the Atrial Fibrillation, Aspirin, Anticoagulation Study and 325 mg in the Stroke Prevention in Atrial Fibrillation Study. To monitor warfarin dosage, three studies used prothrombin time ratios and two used international normalized ratios. The lowest target intensity was a prothrombin time ratio of 1.2 to 1.5 and the highest target intensity was an international normalized ratio of 2.8 to 4.2. The primary end points were ischemic stroke and major hemorrhage, as assessed by each study. Results At the time of randomization the mean age was 69 years and the mean blood pressure was 142/82 mm Hg. Forty-six percent of the patients had a history of hypertension, 6% had a previous transient ischemic attack or stroke, and 14% had diabetes. Risk factors that predicted stroke on multivariate analyses in control patients were increasing age, history of hypertension, previous transient ischemic attack or stroke, and diabetes. Patients younger than 65 years who had none of the other predictive factors (15% of all patients) had an annual rate of stroke of 1.0%, 95% confidence interval (CI) 0.3% to 3.0%. The annual rate of stroke was 4.5% for the control group and 1.4% for the warfarin group (risk reduction, 68%; 95% CI, 50% to 79%). The efficacy of warfarin was consistent across all studies and subgroups of patients. In women, warfarin decreased the risk of stroke by 84% (95% CI, 55% to 95%) compared with 60% (95% CI, 35% to 76%) in men. The efficacy of aspirin was not as consistent. The risk reduction with 75 mg of aspirin in the Atrial Fibrillation, Aspirin, Anticoagulation Study was 18% (95% CI, 60% to 58%), and with 325 mg of aspirin in the Stroke Prevention in Atrial Fibrillation Study the risk reduction was 44% (95% CI, 7% to 66%). When both studies were combined the risk reduction was 36% (95% CI, 4% to 57%). The annual rate of major hemorrhage (intracranial bleeding or a bleed requiring hospitalization or 2 units of blood) was 1.0% for the control group, 1.0% for the aspirin group, and 1.3% for the warfarin group. Conclusion In these five randomized trials warfarin consistently decreased the risk of stroke in patients with atrial fibrillation (a 68% reduction in risk) with virtually no increase in the frequency of major bleeding. Patients with atrial fibrillation younger than 65 years without a history of hypertension, previous stroke or transient ischemic attack, or diabetes were at very low risk of stroke even when not treated. The efficacy of aspirin was less consistent. Further studies are needed to clarify the role of aspirin in atrial fibrillation.

Abstract  Spatial estimations are increasingly used to estimate geocoded ambient particulate matter (PM) concentrations in epidemiologic studies because measures of daily PM concentrations are unavailable in most U.S. locations. This study was conducted to a) assess the feasibility of large-scale kriging estimations of daily residential-level ambient PM concentrations, b) perform and compare cross-validations of different kriging models, c) contrast three popular kriging approaches, and d) calculate SE of the kriging estimations. We used PM data for PM with aerodynamic diameter </= 10 microm (PM10) and aerodynamic diameter </= 2.5 microm (PM2.5) from the U.S. Environmental Protection Agency for the year 2000. Kriging estimations were performed at 94,135 geocoded addresses of Women's Health Initiative study participants using the ArcView geographic information system. We developed a semiautomated program to enable large-scale daily kriging estimation and assessed validity of semivariogram models using prediction error (PE) , standardized prediction error (SPE) , root mean square standardized (RMSS) , and SE of the estimated PM. National- and regional-scale kriging performed satisfactorily, with the former slightly better. The average PE, SPE, and RMSS of daily PM10 semivariograms using regular ordinary kriging with a spherical model were 0.0629, -0.0011, and 1.255 microg/m3, respectively ; the average SE of the estimated residential-level PM10 was 27.36 microg/m3. The values for PM2.5 were 0.049, 0.0085, 1.389, and 4.13 microg/m3, respectively. Lognormal ordinary kriging yielded a smaller average SE and effectively eliminated out-of-range predicted values compared to regular ordinary kriging. Semiautomated daily kriging estimations and semivariogram cross-validations are feasible on a national scale. Lognormal ordinary kriging with a spherical model is valid for estimating daily ambient PM at geocoded residential addresses.

Abstract  The Interagency Monitoring of Protected Visual Environments (IMPROVE) network is the basis for monitoring visibility in Class I Areas throughout the United States. Monitoring is conducted by collecting PM2.5 and PM10 samples every third day at over 150 remote and rural sites nationwide, with PM2.5 samples being analyzed for chemical composition. Light extinction is reconstructed using an algorithm that relates speciated mass to light extinction based on aerosol mass and size (second IMPROVE equation). In addition, the National Park Service directly measures light scattering at a subset of IMPROVE sites using Optec NGN-2 integrating nephelometers. The optical measurements serve as a check of the reconstructed scattering, in that measured scattering from the nephelometers and reconstructed scattering from the second IMPROVE equation should be equivalent. During its development, the second IMPROVE equation was shown to accurately estimate light scattering for a broad range of aerosol compositions and loadings for samples collected through 2003. Here reconstructed scattering is assessed from the second IMPROVE equation by comparing measured light scattering from nephelometers to reconstructed light scattering at 11 collocated sites over a 16 year period (2001–2016). The comparisons suggest that the relationship between measured and reconstructed light scattering has changed over time and that in recent years the second IMPROVE equation has underestimated light scattering at many sites. This shift toward poorer agreement corresponds to periods with relatively large decreases in sulfate and organic mass concentrations. These decreases lead to biases in reconstructed scattering calculated with the second IMPROVE equation, due to the assumed relationship between mass concentration and size distribution. This relationship, referred to as the split component algorithm, appears to be flawed as currently implemented. A potential approach is explored that scales the split component algorithm each year and at each site, based on measured mass concentrations at the site. The proposed approach appears to reduce the biases in the second IMPROVE equation.

Abstract  Background: Long-term exposure to particulate matter <2.5 µm in diameter (PM2.5) and ozone has been associated with the development and progression of cardiovascular disease and, in the case of PM2.5, higher cardiovascular mortality. Whether exposure to PM2.5 and ozone is associated with patients' health status and quality of life is unknown. We used data from 2 prospective myocardial infarction (MI) registries to assess the relationship between long-term PM2.5 and ozone exposure with health status outcomes 1 year after an MI. Methods and Results: TRIUMPH (Translational Research Investigating Underlying Disparities in Acute Myocardial Infarction) and PREMIER (Prospective Registry Evaluating Myocardial Infarction: Events and Recovery) enrolled patients presenting with MI at 31 US hospitals between 2003 and 2008. One year later, patients were assessed with the disease-specific Seattle Angina Questionnaire, and 5-year mortality was assessed with the Centers for Disease Control's National Death Index. Individual patients' exposures to PM2.5 and ozone over the year after their MI were estimated from the Environment Protection Agency's Fused Air Quality Surface Using Downscaling tool that integrates monitoring station data and atmospheric models to predict daily air pollution exposure at the census tract level. We assessed the association of exposure to ozone and PM2.5 with 1-year health status and mortality over 5 years using regression models adjusting for age, sex, race, socioeconomic status, date of enrollment, and comorbidities. In completely adjusted models, higher PM2.5 and ozone exposure were independently associated with poorer Seattle Angina Questionnaire summary scores at 1-year (β estimate per +1 SD increase =-0.8 [95% CI, -1.4 to -0.3; P=0.002] for PM2.5 and -0.9 [95% CI, -1.3 to -0.4; P<0.001] for ozone). Moreover, higher PM2.5 exposure, but not ozone, was independently associated with greater mortality risk (hazard ratio =1.13 per +1 SD [95% CI, 1.07-1.20; P<0.001]). Conclusions: In our study, greater exposure to PM2.5 and ozone was associated with poorer 1-year health status following an MI, and PM2.5 was associated with increased risk of 5-year death.

Abstract  It has been posited that populations being exposed to long-term air pollution are more susceptible to COVID-19. Evidence is emerging that long-term exposure to ambient PM2.5 (particulate matter with aerodynamic diameter 2.5 μm or less) associates with higher COVID-19 mortality rates, but whether it also associates with the speed at which the disease is capable of spreading in a population is unknown. Here, we establish the association between long-term exposure to ambient PM2.5 in the United States (US) and COVID-19 basic reproduction ratio R0- a dimensionless epidemic measure of the rapidity of disease spread through a population. We inferred state-level R0 values using a state-of-the-art susceptible, exposed, infected, and recovered (SEIR) model initialized with COVID-19 epidemiological data corresponding to the period March 2-April 30. This period was characterized by a rapid surge in COVID-19 cases across the US states, implementation of strict social distancing measures, and a significant drop in outdoor air pollution. We find that an increase of 1 μg/m3 in PM2.5 levels below current national ambient air quality standards associates with an increase of 0.25 in R0 (95% CI: 0.048-0.447). A 10% increase in secondary inorganic composition, sulfate-nitrate-ammonium, in PM2.5 associates with ≈10% increase in R0 by 0.22 (95% CI: 0.083-0.352), and presence of black carbon (soot) in the ambient environment moderates this relationship. We considered several potential confounding factors in our analysis, including gaseous air pollutants and socio-economical and meteorological conditions. Our results underscore two policy implications - first, regulatory standards need to be better guided by exploring the concentration-response relationships near the lower end of the PM2.5 air quality distribution; and second, pollution regulations need to be continually enforced for combustion emissions that largely determine secondary inorganic aerosol formation.

Abstract  BACKGROUND: The temporal and spatial scales of exposure assessment may influence observed associations between fine particulate air pollution (PM2.5) and mortality, but few studies have systematically examined this question.

METHODS: We followed 2.4 million adults in the 2001 Canadian Census Health and Environment Cohort for nonaccidental and cause-specific mortality between 2001 and 2011. We assigned PM2.5 exposures to residential locations using satellite-based estimates and compared three different temporal moving averages (1, 3, and 8 years) and three spatial scales (1, 5, and 10 km) of exposure assignment. In addition, we examined different spatial scales based on age, employment status, and urban/rural location, and adjustment for O3, NO2, or their combined oxidant capacity (Ox).

RESULTS: In general, longer moving averages resulted in stronger associations between PM2.5 and mortality. For nonaccidental mortality, we observed a hazard ratio of 1.11 (95% CI = 1.08, 1.13) for the 1-year moving average compared with 1.23 (95% CI = 1.20, 1.27) for the 8-year moving average. Respiratory and lung cancer mortality were most sensitive to the spatial scale of exposure assessment with stronger associations observed at smaller spatial scales. Adjustment for oxidant gases attenuated associations between PM2.5 and cardiovascular mortality and strengthened associations with lung cancer. Despite these variations, PM2.5 was associated with increased mortality in nearly all of the models examined.

CONCLUSIONS: These findings support a relationship between outdoor PM2.5 and mortality at low concentrations and highlight the importance of longer-exposure windows, more spatially resolved exposure metrics, and adjustment for oxidant gases in characterizing this relationship.

Abstract  BACKGROUND: In studies showing associations between ambient air pollution and myocardial infarction (MI), data have been lacking on the inherent spatial variability of air pollution. The aim of this study was to determine whether the long-term spatial distribution of air pollution influences short-term temporal associations between air pollution and admission to hospital for MI.

METHODS: We identified adults living in Calgary who were admitted to hospital for an MI between 2004 and 2012. We evaluated associations between short-term exposure to air pollution (ozone [O3], nitrogen dioxide [NO2], sulfur dioxide [SO2], carbon monoxide [CO], particulate matter < 10 μm in diameter [PM10] and particulate matter < 2.5 μm in diameter [PM2.5]), and hospital admissions for MI using a time-stratified, case-crossover study design. Air Quality Health Index (AQHI) scores were calculated from a composition of O3, NO2 and PM2.5. Conditional logistic regression models were stratified by low, medium and high levels of neighbourhood NO2 concentrations derived from land use regression models; results of these analyses are presented as odds ratios (ORs) with 95% confidence intervals (CIs).

RESULTS: From 2004 to 2012, 6142 MIs were recorded in Calgary. Individuals living in neighbourhoods with higher long-term air pollution concentrations were more likely to be admitted to hospital for MI after short-term elevations in air pollution (e.g., 5-day average NO2: OR 1.20, 95% CI 1.03-1.40, per interquartile range [IQR]) as compared with regions with lower air pollution (e.g., 5-day average NO2: OR 0.90, 95% CI 0.78-1.04, per IQR). In high NO2 tertiles, the AQHI score was associated with MI (e.g., 5-day average OR 1.13, 95% CI 1.02-1.24, per IQR; 3-day average OR 1.13, 95% CI 1.04-1.23, per IQR).

INTERPRETATION: Our results show that the effect of air pollution on hospital admissions for MI was stronger in areas with higher NO2 concentrations than that in areas with lower NO2 concentrations. Individuals living in neighbourhoods with higher traffic-related pollution should be advised of the health risks and be attentive to special air quality warnings.

Abstract  BACKGROUND: Although growing evidence links air pollution to stroke incidence, less is known about the effect of air pollution on atrial fibrillation (AF), an important risk factor for stroke. OBJECTIVES: We assessed the associations between air pollution and incidence of AF and stroke. We also sought to characterize the shape of pollutant–disease relationships. METHODS: The population-based cohort comprised 5,071,956 Ontario residents, age 35–85 y and without the diagnoses of both outcomes on 1 April 2001 and was followed up until 31 March 2015. AF and stroke cases were ascertained using health administrative databases with validated algorithms. Based on annual residential postal codes, we assigned 5-y running average concentrations of fine particulate matter (PM2:5), nitrogen dioxide (NO2), and ozone (O3) from satellite-derived data, a land-use regression model, and a fusion-based method, respectively, as well as redox-weighted averages of NO2 and O3 (Ox) for each year. Using Cox proportional hazards models, we estimated the hazard ratios (HRs) and 95% confidence intervals (95% CIs) of AF and stroke with each of these pollutants, adjusting for individual- and neighborhood-level variables. We used newly developed nonlinear risk models to characterize the shape of pollutant–disease relationships. RESULTS: Between 2001 and 2015, we identified 313,157 incident cases of AF and 122,545 cases of stroke. Interquartile range increments of PM2:5, NO2, O3, and Ox were associated with increases in the incidence of AF [HRs (95% CIs): 1.03 (1.01, 1.04), 1.02 (1.01, 1.03), 1.01 (1.00, 1.02), and 1.01 (1.01, 1.02), respectively] and the incidence of stroke [HRs (95% CIs): 1.05 (1.03, 1.07), 1.04 (1.01, 1.06), 1.05 (1.03, 1.06), and 1.05 (1.04, 1.06), respectively]. Associations of similar magnitude were found in various sensitivity analyses. Furthermore, we found a near-linear association for stroke with PM2:5, whereas Ox-stroke, PM2:5-, and Ox-AF relationships exhibited sublinear shapes. CONCLUSIONS: Air pollution was associated with stroke and AF onset, even at very low concentrations. https://doi.org/10.1289/EHP4883

Abstract  INTRODUCTION: Effects of more than one-year exposure to air pollution on atherosclerosis is seldom studied. This paper aims to examine the association between five-year exposure to particulate matter ≤2.5 μm (PM2.5), ozone (O3) and atherosclerosis observed about seven years later in late midlife women.

MATERIAL AND METHODS: This study was conducted among 1188 women of the Study of Women's Health Across the Nation (SWAN) from five sites, Detroit, MI; Oakland, CA; Pittsburgh, PA; Chicago, IL; and Newark, NJ, with available data on both air pollutant exposure and carotid ultrasound scans. Five-year mean annualized exposure levels of two air pollutants, PM2.5 and ozone (O3), were collected during 5 SWAN visits (1999-2005) from monitors 20 km within the participant's residential address. Linear regression models were used to estimate the association of prior five-year mean annualized exposure to PM2.5 and O3 with common carotid intima-media thickness (cIMT) and inter-adventitial diameter (IAD) examined approximately seven years later (2009-2013). Logistic and multinomial logistic regressions were applied to assess the associations of air pollutants with plaque presence and plaque index, respectively.

RESULTS: At time of carotid ultrasound scan, women were on average 59.6 (±2.7) years old and a majority was postmenopausal (88.4%). The women were White (48.4%), Black (31.2%), Chinese (13.3%) and Hispanic (7.1%). A 1 μg/m3 higher 5-year mean annualized exposure to PM2.5 was associated with an 8.0 μm (95% CI: 1.0-15.1) greater maximum cIMT at a later mid-life, adjusting for cardiovascular disease risk factors; but was only related to IAD after adjusting for site. No association was found between either pollutant and plaque presence or plaque index.

CONCLUSIONS: Long-term exposure to PM2.5 may contribute to elevated risk of atherosclerosis in the post-menopausal period.

Abstract  Importance: Air pollution is associated with cardiovascular outcomes. Specifically, fine particulate matter measuring 2.5 μm or less (PM2.5) is associated with thrombosis, stroke, and myocardial infarction. Few studies have examined particulate matter and stroke risk in individuals with atrial fibrillation (AF).

Objective: To assess the association of residential-level pollution exposure in 1 year and ischemic stroke in individuals with AF.

Design, Setting, and Participants: This cohort study included 31 414 individuals with AF from a large regional health care system in an area with historically high industrial pollution. All participants had valid residential addresses for geocoding and ascertainment of neighborhood-level income and educational level. Participants were studied from January 1, 2007, through September 30, 2015, with prospective follow-up through December 1, 2017. Data analysis was performed from March 14, 2018, to October 9, 2019.

Exposures: Exposure to PM2.5 ascertained using geocoding of addresses and fine-scale air pollution exposure surfaces derived from a spatial saturation monitoring campaign and land-use regression modeling. Exposure to PM2.5 was estimated annually across the study period at the residence level.

Main Outcomes and Measures: Multivariable-adjusted stroke risk by quartile of residence-level and annual PM2.5 exposure.

Results: The cohort included 31 414 individuals (15 813 [50.3%] female; mean [SD] age, 74.4 [13.5] years), with a median follow-up of 3.5 years (interquartile range, 1.6-5.8 years). The mean (SD) annual PM2.5 exposure was 10.6 (0.7) μg/m3. A 1-SD increase in PM2.5 was associated with a greater risk of stroke after both adjustment for demographic and clinical variables (hazard ratio [HR], 1.08; 95% CI, 1.03-1.14) and multivariable adjustment that included neighborhood-level income and educational level (HR, 1.07; 95% CI, 1.00-1.14). The highest quartile of PM2.5 exposure had an increased risk of stroke relative to the first quartile (HR, 1.36; 95% CI, 1.18-1.58). After adjustment for clinical covariates, income, and educational level, risk of stroke remained greater for the highest quartile of exposure relative to the first quartile (HR, 1.21; 95% CI, 1.01-1.45).

Conclusions and Relevance: This large cohort study of individuals with AF identified associations between PM2.5 and risk of ischemic stroke. The results suggest an association between fine particulate air pollution and cardiovascular disease and outcomes.

Abstract  BACKGROUND: Air pollution has been associated with increased mortality. However, updated evidence from cohort studies with detailed information on various risk factors is needed, especially in regions with low air pollution levels. We investigated the associations between long-term exposure to air pollution and mortality in a prospective cohort.

METHODS: We studied 88,615 participants aged ≥30 years from an ongoing cohort study in Ontario, Canada from 2009 to 2017. Exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) was estimated at participants' residence. Cox proportional hazard models were used to investigate the associations between air pollution and non-accidental, cardiovascular, and respiratory mortality, adjusted for a wide array of individual-level and contextual covariates. Potential effect modification by socio-demographic and behavioral factors was also examined in exploratory stratified analyses.

RESULTS: The fully adjusted hazard ratios (HRs) per 1 µg/m3 increment in PM2.5 were 1.037 [95% confidence interval (CI): 1.018, 1.057]¸ 1.083 (95% CI: 1.040, 1.128) and 1.109 (95% CI: 1.035, 1.187) for non-accidental, cardiovascular, and respiratory mortality, respectively. Positive associations were also found for NO2; the corresponding HRs per 1 ppb increment were 1.027 (95% CI: 1.021, 1.034), 1.032 (95% CI: 1.019, 1.046) and 1.044 (95% CI: 1.020, 1.068). We found suggestive evidence of stronger associations in physically active participants, smokers, and those with lower household income.

CONCLUSIONS: Long-term exposure to PM2.5 and NO2 was associated with increased risks for non-accidental, cardiovascular, and respiratory mortality, suggesting potential benefits of further improvement in air quality even in low-exposure environments.

Abstract  BACKGROUND: Epidemiological studies have consistently demonstrated that exposure to fine particulate matter (PM2.5) is associated with increased risks of mortality. To a lesser extent, a series of studies suggest that living in greener areas is associated with reduced risks of mortality. Only a handful of studies have examined the interplay between PM2.5, greenness, and mortality.

METHODS: We investigated the role of residential greenness in modifying associations between long-term exposures to PM2.5 and non-accidental and cardiovascular mortality in a national cohort of non-immigrant Canadian adults (i.e., the 2001 Canadian Census Health and Environment Cohort). Specifically, we examined associations between satellite-derived estimates of PM2.5 exposure and mortality across quintiles of greenness measured within 500 m of individual's place of residence during 11 years of follow-up. We adjusted our survival models for many personal and contextual measures of socioeconomic position, and residential mobility data allowed us to characterize annual changes in exposures.

RESULTS: Our cohort included approximately 2.4 million individuals at baseline, 194,270 of whom died from non-accidental causes during follow-up. Adjustment for greenness attenuated the association between PM2.5 and mortality (e.g., hazard ratios (HRs) and 95% confidence intervals (CIs) per interquartile range increase in PM2.5 in models for non-accidental mortality decreased from 1.065 (95% CI: 1.056-1.075) to 1.041 (95% CI: 1.031-1.050)). The strength of observed associations between PM2.5 and mortality decreased as greenness increased. This pattern persisted in models restricted to urban residents, in models that considered the combined oxidant capacity of ozone and nitrogen dioxide, and within neighbourhoods characterised by high or low deprivation. We found no increased risk of mortality associated with PM2.5 among those living in the greenest areas. For example, the HR for cardiovascular mortality among individuals in the least green areas was 1.17 (95% CI: 1.12-1.23) compared to 1.01 (95% CI: 0.97-1.06) among those in the greenest areas.

CONCLUSIONS: Studies that do not account for greenness may overstate the air pollution impacts on mortality. Residents in deprived neighbourhoods with high greenness benefitted by having more attenuated associations between PM2.5 and mortality than those living in deprived areas with less greenness. The findings from this study extend our understanding of how living in greener areas may lead to improved health outcomes.

Abstract  Epidemiologic studies on acute effects of air pollution have generally been limited to larger cities, leaving questions about rural populations behind. Recently, we had developed a spatiotemporal model to predict daily PM2.5 level at a 1 km(2) using satellite aerosol optical depth (AOD) data. Based on the results from the model, we applied a case-crossover study to evaluate the acute effect of PM2.5 on mortality in North Carolina, South Carolina, and Georgia between 2007 and 2011. Mortality data were acquired from the Departments of Public Health in the States and modeled PM2.5 exposures were assigned to the zip code of residence of each decedent. We performed various stratified analyses by age, sex, race, education, cause of death, residence, and environmental protection agency (EPA) standards. We also compared results of analyses using our modeled PM2.5 levels and those imputed daily from the nearest monitoring station. 848,270 non-accidental death records were analyzed and we found each 10 μg/m(3) increase in PM2.5 (mean lag 0 and lag 1) was associated with a 1.56% (1.19 and 1.94) increase in daily deaths. Cardiovascular disease (2.32%, 1.57-3.07) showed the highest effect estimate. Blacks (2.19%, 1.43-2.96) and persons with education ≤8 year (3.13%, 2.08-4.19) were the most vulnerable populations. The effect of PM2.5 on mortality still exists in zip code areas that meet the PM2.5 EPA annual standard (2.06%, 1.97-2.15). The effect of PM2.5 below both EPA daily and annual standards was 2.08% (95% confidence interval=1.99-2.17). Our results showed more power and suggested that the PM2.5 effects on rural populations have been underestimated due to selection bias and information bias. We have demonstrated that our AOD-based exposure models can be successfully applied to epidemiologic studies. This will add new study populations in rural areas, and will confer more generalizability to conclusions from such studies.Journal of Exposure Science and Environmental Epidemiology advance online publication, 26 August 2015; doi:10.1038/jes.2015.47.

Abstract  The impact of chronic exposure to fine particulate matter (PM2.5) on respiratory disease and lung cancer mortality is poorly understood. In a cohort of 18.9 million Medicare beneficiaries (4.2 million deaths) living across the conterminous United States between 2000 to 2008, we examined the association of chronic PM2.5 exposure and cause-specific mortality, and evaluated confounding through adjustment of neighborhood behavioral covariates and decomposition of PM2.5 into two spatiotemporal scales. We found significantly positive associations of 12-month moving average PM2.5 exposures (per 10 ug/m3 increase) with respiratory, chronic obstructive pulmonary disease and pneumonia mortality, with risk ratios ranging from 1.10 to 1.24. We also found significant PM2.5-associated elevated risks for cardiovascular-related and lung cancer mortality. Risk ratios generally increased with longer moving averages; e.g., elevation in 60-month moving averaged PM2.5 exposures was linked to 1.33 times the lung cancer mortality risk (95% confidence interval: 1.24, 1.40), as compared to 1.13 (95% confidence interval: 1.11, 1.15) for 12-month moving averaged exposures. Observed associations were robust in multivariable models, although evidence of unmeasured confounding remained. In our large cohort of American elderly, we provide important new evidence that long-term PM2.5 exposure is significantly related to increased respiratory-, lung cancer and cardiovascular-related mortality.

Abstract  BACKGROUND: Many studies have identified an inequitable distribution of exposure to PM2.5 (particulate matter less than 2.5 microns) by race. We investigated the association of PM2.5 and cardiovascular mortality considering both the decedents' race and neighborhood racial composition as potential modifiers.

METHODS: We obtained geocoded cardiovascular mortality records of all black and white decedents from urban block-groups in Massachusetts between 2001 and 2011 (n = 130,863). We examined the association between PM2.5 and cardiovascular mortality, and assessed effect modification by three types of racial modifiers: decedents' race, census block-group percent black and white, and two novel measures of racial segregation. The Racial Residential Segregation (RRS) quantifies the concentration of non-Hispanic blacks and whites in each block-group. The Index of Racial Dissimilarity measures dissimilarity in non-Hispanic black and white racial distribution between the smaller census block-group and larger tract.

RESULTS: We found a 2.35%(95%CI: 0.92%;3.79%) increase in mortality for each 10μg/m3 increase in two-day average exposure to PM2.5. The effect was modified by the block-group racial composition, with higher risks in block-groups with the highest percentage of black residents (interaction p-value = 0.04), and in block-groups with the lowest RRS (i.e. higher black to white resident ratio, interaction p-value = 0.072). Racial dissimilarity did not modify the associations.

CONCLUSION: Current levels of PM2.5 are associated with increased cardiovascular deaths in Massachusetts, with different risks between areas with different racial composition and segregation. This suggests that pollution reductions in neighborhoods with the highest percentage of non-Hispanic blacks would be most beneficial in reducing cardiovascular mortality and disparities.

Abstract  The Integrated Science Assessment (ISA) for Oxides of Nitrogen, Oxides of Sulfur and Particulate Matter Ecological Criteria is a comprehensive evaluation and synthesis of the most policy relevant science aimed at characterizing the ecological effects caused by oxides of nitrogen, oxides of sulfur, and particulate matter. The ISA provides the scientific foundation necessary for the review of ecological effects associated with the secondary (welfare based) National Ambient Air Quality Standards (NAAQS) for these three criteria pollutants under the Clean Air Act. Welfare effects according to the Clean Air Act include, but are not limited to, effects on soils, water, crops, vegetation, animals, wildlife and climate. Oxides of nitrogen, oxides of sulfur, and particulate matter are three of six criteria pollutants for which EPA has established NAAQS. Periodically, EPA reviews the scientific basis for these standards by preparing an ISA (formerly called an Air Quality Criteria Document). The intent of the ISA, as described in the Clean Air Act (CAA), is to 'accurately reflect the latest scientific knowledge expected from the presence of [a] pollutant in ambient air.' It includes scientific research from atmospheric sciences, exposure and deposition, biogeochemistry, hydrology, soil science, marine science, plant physiology, animal physiology, and ecology conducted at multiple scales (e.g., population, community, ecosystem, landscape levels). Key information and judgments formerly found in the Air Quality Criteria Documents for oxides of sulfur, oxides of nitrogen and particulate matter for ecological effects are included; appendices provide additional details supporting the ISA. Together, the ISA and appendices serve to update and revise the 2008 Integrated Science Assessment for Oxides of Nitrogen and Oxides of Sulfur - Ecological Criteria and the ecological portion of the last particulate matter ISA which was published in 2009. Additionally, the Clean Air Scientific Advisory Committee (CASAC) is an independent science advisory committee whose review and advisory functions are mandated by Section 109(d)(2) of the Clean Air Act, and charged (among other things) with performing an independent scientific review of all the EPA’s air quality criteria.

Abstract  BACKGROUND: Evidence indicates that air pollution contributes to cardiopulmonary mortality. There is ongoing debate regarding the size and shape of the pollution–mortality exposure–response relationship. There are also growing appeals for estimates of pollution–mortality relationships that use public data and are based on large, representative study cohorts.

OBJECTIVES: Our goal was to evaluate fine particulate matter air pollution ([Formula: see text]) and mortality using a large cohort that is representative of the U.S. population and is based on public data. Additional objectives included exploring model sensitivity, evaluating relative effects across selected subgroups, and assessing the shape of the [Formula: see text]–mortality relationship.

METHODS: National Health Interview Surveys (1986–2014), with mortality linkage through 2015, were used to create a cohort of 1,599,329 U.S. adults and a subcohort with information on smoking and body mass index (BMI) of 635,539 adults. Data were linked with modeled ambient [Formula: see text] at the census-tract level. Cox proportional hazards models were used to estimate [Formula: see text]–mortality hazard ratios for all-cause and specific causes of death while controlling for individual risk factors and regional and urban versus rural differences. Sensitivity and subgroup analyses were conducted and the shape of the [Formula: see text]–mortality relationship was explored.

RESULTS: Estimated mortality hazard ratios, per [Formula: see text] long-term exposure to [Formula: see text], were 1.12 (95% CI: 1.08, 1.15) for all-cause mortality, 1.23 (95% CI: 1.17, 1.29) for cardiopulmonary mortality, and 1.12 (95% CI: 1.00, 1.26) for lung cancer mortality. In general, [Formula: see text]–mortality associations were consistently positive for all-cause and cardiopulmonary mortality across key modeling choices and across subgroups of sex, age, race-ethnicity, income, education levels, and geographic regions.

DISCUSSION: This large, nationwide, representative cohort of U.S. adults provides robust evidence that long-term [Formula: see text] exposure contributes to cardiopulmonary mortality risk. The ubiquitous and involuntary nature of exposures and the broadly observed effects across subpopulations underscore the public health importance of breathing clean air. https://doi.org/10.1289/EHP4438.

Abstract  Visible Multifilter Rotating Shadowband Radiometer (vis-MFRSR) data were collected at Storm Peak Laboratory (SPL), a mountain-top facility in northwest Colorado, from 1999 to 2011 and in 2013. From 2011 to 2014, in situ measurements of aerosol light scattering were also obtained. Using these data sets together, the seasonal impact of dust and biomass burning is considered for the western USA. Analysis indicates that the median contributions to spring and summer aerosol optical depth (AOD) from dust and biomass-burning aerosols across the data set are comparable. The mean AOD is slightly greater in the summer, with significantly more frequent and short-duration high AOD measurements due to biomass-burning episodes than in the spring. The angstrom ngstrom exponent showed a significant increase in the summer for both the in situ and vis-MFRSR data, suggesting an increase in combustion aerosols. Spring dust events are less distinguishable in the in situ data than the column measurement, suggesting that a significant amount of dust may be found above the elevation of SPL, 3220 ma.s.l. Twenty-two known case studies of intercontinental dust, regional dust, and biomass-burning events were investigated. These events were found to follow a similar pattern, in both aerosol loading and angstrom ngstrom exponent, as the seasonal mean signal in both the vis-MFRSR and ground-based nephelometer. This data set highlights the wide-scale implications of a warmer, drier climate on visibility in the western USA.