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Background: Exposure to fine particulate matter (PM 2.5 ) has been linked to an increased risk of atherosclerosis. However, it remains unclear whether specific compounds within PM 2.5 , rather than the overall mass, serve as a better indicator of adverse cardiovascular health outcomes associated with air pollution., Methods: In this cross-sectional study, we included 3257 participants (aged 37-51 years) from the Coronary Artery Risk Development in Young Adults (CARDIA) study. Exposure to PM 2.5 and its constituent compounds, black carbon (BC), ammonium, nitrate, organic matter, sulfate, mineral dust, and sea salt were included in the analyses. Carotid intima media thickness (cIMT; the average of common, bulb, and internal carotid) was measured by carotid ultrasonography. We assessed the cross-sectional associations of one-year exposure to PM 2.5 and its compounds with mean cIMT using linear regression models adjusting for participants' demographics, individual- and neighborhood-level socioeconomic status, behavioral components, and health conditions. We also adopted Bayesian kernel machine regression (BKMR) models to investigate the association between the PM 2.5 compound mixture and cIMT as well as the contribution of each compound to the association., Results: Greater exposure to BC was associated with higher cIMT (mm) (β =0.034, 95 % CI = 0.019-0.049, per IQR increase [0.56 μg/m 3 ] of BC) among participants with a mean age of 45.0, consisting of 45.9 % Black and 54.1 % White males and females. The association was generally consistent across participants' demographic characteristics. In our BKMR analysis, BC exhibited a dose-response association with cIMT with a high contribution to the association of cIMT with PM 2.5 compound as a mixture (posterior inclusion probability [PIP]: 1.00)., Conclusions: Our findings suggest that certain compounds of PM 2.5 , such as BC, may offer more reliable indications of the impact of air pollution on cardiovascular health., Competing Interests: Declaration of competing interest V. Murthy owns stock in General Electric, Cardinal Health, Viatris, Pfizer, Amgen, Merck and Johnson & Johnson and stock options in Ionetix. He is a paid consultant for INVIA Medical Imaging Solutions & Siemens Healthineers. V. Murthy has received research support through his institution from Siemens Healthineers., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Living in greener areas of cities was linked to increased physical activity levels, improved mental well-being, and lowered harmful environmental exposures, all of which may affect human health. However, whether living in greener areas may be associated with lower risk of cardiovascular disease incidence, progression, and premature mortality is unclear., Objectives: We conducted a cohort study to examine the associations between residential green spaces and the incidence of acute myocardial infarction (AMI) and heart failure (HF), post-AMI and HF hospital readmissions, and mortality., Methods: We simultaneously followed four large population-based cohorts in Ontario, Canada, including the entire adult population, adults free of AMI and HF, and survivors of AMI or HF from 2000 to 2014. We estimated residential exposure to green spaces using satellite-derived observations and ascertained health outcomes using validated disease registries. We estimated the associations using spatial random-effects Cox proportional hazards models. We conducted various sensitivity analyses, including further adjusting for property values and performing exploratory mediation analysis., Results: Each interquartile range increase in residential greenness was associated with a 7% [95% confidence interval (CI): 4%, 9%] decrease in incident AMI and a 6% (95% CI: 4%, 7%) decrease in incident HF. Residential greenness was linked to a ∼ 10 % decrease in cardiovascular mortality in both adults free of AMI and HF and the entire adult population. These associations remained consistent in sensitivity analyses and were accentuated among younger adults. Additionally, we estimated that the decreases in AMI and HF incidence associated with residential greenness explained ∼ 53 % of the protective association between residential greenness and cardiovascular mortality. Conversely, residential greenness was not associated with any delay in readmission or mortality among AMI and HF patients., Conclusions: Living in urban areas with more green spaces was associated with improved cardiovascular health in people free of AMI and HF but not among individuals who have already developed these conditions. https://doi.org/10.1289/EHP6161.

Background: Immigrants make up 20% of the Canadian population; however, little is known about the mortality impacts of fine particulate matter (PM 2.5 ) air pollution on immigrants compared with non-immigrants, or about how impacts may change with duration in Canada., Data and Methods: This study used the 2001 Canadian Census Health and Environment Cohort, a longitudinal cohort of 3.5 million individuals, of which 764,000 were classified as immigrants (foreign-born). Postal codes from annual income tax files were used to account for mobility among respondents and to assign annual PM 2.5 concentrations from 1998 to 2016. Exposures were estimated as a three-year moving average prior to the follow-up year. Cox survival models were used to determine hazard ratios (HRs) for cause-specific mortality, comparing the Canadian and foreign-born populations, with further stratification by year of immigration grouped into 10-year cohorts., Results: Differences in urban-rural settlement patterns resulted in greater exposure to PM 2.5 for immigrants compared with non-immigrants (mean = 9.3 vs. 7.5 μg/m 3 ), with higher exposures among more recent immigrants. In fully adjusted models, immigrants had higher HRs per 10 μg/m 3 increase in PM 2.5 concentration compared with Canadian-born individuals for cardiovascular mortality (HR [95% confidence interval] = 1.22 [1.12 to 1.34] vs. 1.12 [1.07 to 1.18]) and cerebrovascular mortality (HR = 1.25 [1.03 to 1.52] vs. 1.03 [0.93 to 1.15]), respectively. However, tests for differences between the two groups were not significant when Cochran's Q test was used. No significant associations were found for respiratory outcomes, except for lung cancer in non-immigrants (HR = 1.10 [1.02 to 1.18]). When stratified by year of immigration, differences in HRs across varied by cause of death., Discussion: In Canada, PM 2.5 is an equal-opportunity risk factor, with immigrants experiencing similar if not higher mortality risks compared with non-immigrants for cardiovascular-related causes of death. Some notable differences also existed with cerebrovascular and lung cancer deaths. Continued reductions in air pollution, particularly in urban areas, will improve the health of the Canadian population as a whole.

Lung and female breast cancers are highly prevalent worldwide. Although the association between exposure to ambient fine particulate matter (PM 2.5 ) and lung cancer has been recognized, there is less evidence for associations with other common air pollutants such as nitrogen dioxide (NO 2 ) and ozone (O 3 ). Even less is known about potential associations between these pollutants and breast cancer. We conducted a population-based cohort study to investigate the associations of chronic exposure to PM 2.5 , NO 2 , O 3 and redox-weighted average of NO 2 and O 3 (O x ) with incident lung and breast cancer, using the Ontario Population Health and Environment Cohort (ONPHEC), which includes all long-term residents aged 35-85 years who lived in Ontario, Canada, 2001-2015. Incident lung and breast cancers were ascertained using the Ontario Cancer Registry. Annual estimates of exposures were assigned to the residential postal codes of subjects for each year during follow-up. We used Cox proportional-hazards models adjusting for personal- and neighborhood-level covariates. Our cohorts for lung and breast cancer analyses included ~4.9 million individuals and ~2.5 million women, respectively. During follow-up, 100,146 incident cases of lung cancer and 91,146 incident cases of breast cancer were diagnosed. The fully adjusted analyses showed positive associations of lung cancer incidence with PM 2.5 (hazard ratio [HR] = 1.02 [95% CI: 1.01-1.05] per 5.3 μg/m 3 ) and NO 2 (HR = 1.05 [95% CI: 1.03-1.07] per 14 ppb). No associations with lung cancer were observed for O 3 or O x . Relationships between PM 2.5 and NO 2 with lung cancer exhibited a sublinear shape. We did not find compelling evidence linking air pollution to breast cancer., (© 2019 UICC.)

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.

Background: Evidence suggests a link between air pollution and dementia. Cardiovascular disease (CVD) may be a potential determinant of dementia. This motivated us to quantify the contribution of CVD to the association between air pollution and dementia., Methods: A cohort of Canadian-born residents of Ontario, who participated in the 1996-2003 Canadian Community Health Surveys, was followed through 2013 or until dementia diagnosis. Exposure to nitrogen dioxide (NO2) and fine particulate matter (PM2.5) was estimated with a 3-year average and 5-year lag before dementia diagnosis. Incident CVD was evaluated as a mediator. We used multi-level Cox proportional and Aalen additive hazard regression models, adjusting for individual- and neighbourhood-level risk factors to estimate associations with NO2 and PM2.5. We estimated the total, direct and indirect effects of air pollution on dementia through cardiovascular disease., Results: This study included 34 391 older adults. At baseline, the mean age of this cohort was 59 years. The risk of dementia was moderately higher among those more exposed to NO2 (hazard ratio (HR) 1.10, 95% confidence interval (CI) 0.99-1.19; and 100 additional cases per 100 000 [standard error (SE) <100x10-5]) and PM2.5 [(HR 1.29, 95% CI 0.99-1.64; 200 additional cases per 100 000] [SE 100x10-5]) after adjusting for covariates; however, these estimates are imprecise. A greater proportion of the relationship between PM2.5 and dementia was mediated through CVD than NO2 for both scales., Conclusions: These results suggest some of the association between air pollution and dementia is mediated through CVD, indicating that improving cardiovascular health may prevent dementia in areas with higher exposure to air pollution., (© The Author(s) 2019; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Purpose: Growing evidence implicates ambient air pollutants in the development of major chronic diseases and premature mortality. However, epidemiologic evidence linking air pollution to diabetes remains inconclusive. This study sought to determine the relationships between selected air pollutants (nitrogen dioxide [NO 2 ], fine particulate matter [PM 2.5 ], ozone [O 3 ], and oxidant capacity [Ox; the redox-weighted average of O 3 and NO 2 ]) and the incidence of diabetes, as well as the risk of cardiovascular or diabetes mortality among individuals with prevalent diabetes., Research Design and Methods: We followed two cohorts, which included 4.8 million Ontario adults free of diabetes and 452,590 Ontario adults with prevalent diabetes, from 2001 to 2015. Area-level air pollution exposures were assigned to subjects' residential areas, and outcomes were ascertained using health administrative data with validated algorithms. We estimated hazard ratios for the association between each air pollutant and outcome using Cox proportional hazards models, and modelled the shape of the concentration-response relationships., Results: Over the study period, 790,461 individuals were diagnosed with diabetes. Among those with prevalent diabetes, 26,653 died from diabetes and 64,773 died from cardiovascular diseases. For incident diabetes, each IQR increase in NO 2 had a hazard ratio of 1.04 (95% CI: 1.03-1.05). This relationship was relatively robust to all sensitivity analyses considered, and exhibited a near-linear shape. There were also positive associations between incident diabetes and PM 2.5 , O 3 , and Ox, but these estimates were somewhat sensitive to different models considered. Among those with prevalent diabetes, almost all pollutants were associated with increased diabetes and cardiovascular mortality risk. The strongest association was observed between diabetes mortality and exposure to NO 2 (HR = 1.08, 95% CI: 1.02-1.13)., Conclusions: Selected air pollutants, especially NO 2 , were linked to an increased risk of incident diabetes, as well as risk of cardiovascular or diabetes mortality among persons with prevalent diabetes. As NO 2 is frequently used as a proxy for road traffic exposures, this result may indicate that traffic-related air pollution has the strongest effect on diabetes etiology and survival after diabetes development., (Crown Copyright © 2019. Published by Elsevier Ltd. All rights reserved.)

Fine particulate matter (PM 2.5 ) is a well-established risk factor for public health. To support both health risk assessment and epidemiological studies, data are needed on spatial and temporal patterns of PM 2.5 exposures. This review article surveys publicly available exposure datasets for surface PM 2.5 mass concentrations over the contiguous U.S., summarizes their applications and limitations, and provides suggestions on future research needs. The complex landscape of satellite instruments, model capabilities, monitor networks, and data synthesis methods offers opportunities for research development, but would benefit from guidance for new users. Guidance is provided to access publicly available PM 2.5 datasets, to explain and compare different approaches for dataset generation, and to identify sources of uncertainties associated with various types of datasets. Three main sources used to create PM 2.5 exposure data are ground-based measurements (especially regulatory monitoring), satellite retrievals (especially aerosol optical depth, AOD), and atmospheric chemistry models. We find inconsistencies among several publicly available PM 2.5 estimates, highlighting uncertainties in the exposure datasets that are often overlooked in health effects analyses. Major differences among PM 2.5 estimates emerge from the choice of data (ground-based, satellite, and/or model), the spatiotemporal resolutions, and the algorithms used to fuse data sources. Implications : Fine particulate matter (PM 2.5 ) has large impacts on human morbidity and mortality. Even though the methods for generating the PM 2.5 exposure estimates have been significantly improved in recent years, there is a lack of review articles that document PM 2.5 exposure datasets that are publicly available and easily accessible by the health and air quality communities. In this article, we discuss the main methods that generate PM 2.5 data, compare several publicly available datasets, and show the applications of various data fusion approaches. Guidance to access and critique these datasets are provided for stakeholders in public health sectors.

Background: Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM 2.5 ). In general, cohort studies of mortality and outdoor PM 2.5 concentrations have limited information on individuals exposed to low levels of PM 2.5 as well as covariates such as smoking behaviours, alcohol consumption, and diet which may confound relationships with mortality. This study provides an updated and extended analysis of the Canadian Community Health Survey-Mortality cohort: a population-based cohort with detailed PM 2.5 exposure data and information on a number of important individual-level behavioural risk factors. We also used this rich dataset to provide insight into the shape of the concentration-response curve for mortality at low levels of PM 2.5 ., Methods: Respondents to the Canadian Community Health Survey from 2000 to 2012 were linked by postal code history from 1981 to 2016 to high resolution PM 2.5 exposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PM 2.5 concentrations (measured as a three-year average with a one-year lag) adjusted for socio-economic, behavioural, and time-varying contextual covariates., Results: In total, 50,700 deaths from non-accidental causes occurred in the cohort over the follow-up period. Annual average ambient PM 2.5 concentrations were low (i.e. 5.9 μg/m 3 , s.d. 2.0) and each 10 μg/m 3 increase in exposure was associated with an increase in non-accidental mortality (HR = 1.11; 95% CI 1.04-1.18). Adjustment for behavioural covariates did not materially change this relationship. We estimated a supra-linear concentration-response curve extending to concentrations below 2 μg/m 3 using a shape constrained health impact function. Mortality risks associated with exposure to PM 2.5 were increased for males, those under age 65, and non-immigrants. Hazard ratios for PM 2.5 and mortality were attenuated when gaseous pollutants were included in models., Conclusions: Outdoor PM 2.5 concentrations were associated with non-accidental mortality and adjusting for individual-level behavioural covariates did not materially change this relationship. The concentration-response curve was supra-linear with increased mortality risks extending to low outdoor PM 2.5 concentrations.

Background: Ambient fine particulate air pollution with aerodynamic diameter ≤ 2.5   μ m ( PM 2.5 ) is an important contributor to the global burden of disease. Information on the shape of the concentration-response relationship at low concentrations is critical for estimating this burden, setting air quality standards, and in benefits assessments., Objectives: We examined the concentration-response relationship between PM 2.5 and nonaccidental mortality in three Canadian Census Health and Environment Cohorts (CanCHECs) based on the 1991, 1996, and 2001 census cycles linked to mobility and mortality data., Methods: Census respondents were linked with death records through 2016, resulting in 8.5 million adults, 150 million years of follow-up, and 1.5 million deaths. Using annual mailing address, we assigned time-varying contextual variables and 3-y moving-average ambient PM 2.5 at a 1 × 1   km spatial resolution from 1988 to 2015. We ran Cox proportional hazards models for PM 2.5 adjusted for eight subject-level indicators of socioeconomic status, seven contextual covariates, ozone, nitrogen dioxide, and combined oxidative potential. We used three statistical methods to examine the shape of the concentration-response relationship between PM 2.5 and nonaccidental mortality., Results: The mean 3-y annual average estimate of PM 2.5 exposure ranged from 6.7 to 8.0   μ g / m 3 over the three cohorts. We estimated a hazard ratio (HR) of 1.053 [95% confidence interval (CI): 1.041, 1.065] per 10 - μ g / m 3 change in PM 2.5 after pooling the three cohort-specific hazard ratios, with some variation between cohorts (1.041 for the 1991 and 1996 cohorts and 1.084 for the 2001 cohort). We observed a supralinear association in all three cohorts. The lower bound of the 95% CIs exceeded unity for all concentrations in the 1991 cohort, for concentrations above 2   μ g / m 3 in the 1996 cohort, and above 5   μ g / m 3 in the 2001 cohort., Discussion: In a very large population-based cohort with up to 25 y of follow-up, PM 2.5 was associated with nonaccidental mortality at concentrations as low as 5   μ g / m 3 . https://doi.org/10.1289/EHP5204.

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 ([Formula: see text]), nitrogen dioxide ([Formula: see text]), and ozone ([Formula: see text]) from satellite-derived data, a land-use regression model, and a fusion-based method, respectively, as well as redox-weighted averages of [Formula: see text] and [Formula: see text] ([Formula: see text]) 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 [Formula: see text], [Formula: see text], [Formula: see text], and [Formula: see text] 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 [Formula: see text], whereas [Formula: see text], [Formula: see text]-, and [Formula: see text] 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.

Background: Indirect adjustment via partitioned regression is a promising technique to control for unmeasured confounding in large epidemiological studies. The method uses a representative ancillary dataset to estimate the association between variables missing in a primary dataset with the complete set of variables of the ancillary dataset to produce an adjusted risk estimate for the variable in question. The objective of this paper is threefold: 1) evaluate the method for non-linear survival models, 2) formalize an empirical process to evaluate the suitability of the required ancillary matching dataset, and 3) test modifications to the method to incorporate time-varying exposure data, and proportional weighting of datasets., Methods: We used the association between fine particle air pollution (PM 2.5 ) with mortality in the 2001 Canadian Census Health and Environment Cohort (CanCHEC, N = 2.4 million, 10-years follow-up) as our primary dataset, and the 2001 cycle of the Canadian Community Health Survey (CCHS, N = 80,630) as the ancillary matching dataset that contained confounding risk factor information not available in CanCHEC (e.g., smoking). The main evaluation process used a gold-standard approach wherein two variables (education and income) available in both datasets were excluded, indirectly adjusted for, and compared to true models with education and income included to assess the amount of bias correction. An internal validation for objective 1 used only CanCHEC data, whereas an external validation for objective 2 replaced CanCHEC with the CCHS. The two proposed modifications were applied as part of the validation tests, as well as in a final indirect adjustment of four missing risk factor variables (smoking, alcohol use, diet, and exercise) in which adjustment direction and magnitude was compared to models using an equivalent longitudinal cohort with direct adjustment for the same variables., Results: At baseline (2001) both cohorts had very similar PM 2.5 distributions across population characteristics, although levels for CCHS participants were consistently 1.8-2.0 μg/m 3 lower. Applying sample-weighting largely corrected for this discrepancy. The internal validation tests showed minimal downward bias in PM 2.5 mortality hazard ratios of 0.4-0.6% using a static exposure, and 1.7-3% when a time-varying exposure was used. The external validation of the CCHS as the ancillary dataset showed slight upward bias of -0.7 to -1.1% and downward bias of 1.3-2.3% using the static and time-varying approaches respectively., Conclusions: The CCHS was found to be fairly well representative of CanCHEC and its use in Canada for indirect adjustment is warranted. Indirect adjustment methods can be used with survival models to correct hazard ratio point estimates and standard errors in models missing key covariates when a representative matching dataset is available. The results of this formal evaluation should encourage other cohorts to assess the suitability of ancillary datasets for the application of the indirect adjustment methodology to address potential residual confounding., (Crown Copyright © 2019. Published by Elsevier Inc. All rights reserved.)

Background: Epidemiological studies have consistently demonstrated that exposure to fine particulate matter (PM 2.5 ) 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 PM 2.5 , greenness, and mortality., Methods: We investigated the role of residential greenness in modifying associations between long-term exposures to PM 2.5 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 PM 2.5 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 PM 2.5 and mortality (e.g., hazard ratios (HRs) and 95% confidence intervals (CIs) per interquartile range increase in PM 2.5 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 PM 2.5 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 PM 2.5 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 PM 2.5 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., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Rationale: Little is known regarding the impact of ambient ultrafine particles (UFPs; <0.1 μm) on childhood asthma development. Objectives: To examine the association between prenatal and early postnatal life exposure to UFPs and development of childhood asthma. Methods: A total of 160,641 singleton live births occurring in the City of Toronto, Canada between April 1, 2006, and March 31, 2012, were identified from a birth registry. Associations between exposure to ambient air pollutants and childhood asthma incidence (up to age 6) were estimated using random effects Cox proportional hazards models, adjusting for personal- and neighborhood-level covariates. We investigated both single-pollutant and multipollutant models accounting for coexposures to particulate matter ≤2.5 μm in aerodynamic diameter (PM 2.5 ) and NO 2 . Measurements and Main Results: We identified 27,062 children with incident asthma diagnosis during the follow-up. In adjusted models, second-trimester exposure to UFPs (hazard ratio per interquartile range increase, 1.09; 95% confidence interval, 1.06-1.12) was associated with asthma incidence. In models additionally adjusted for PM 2.5 and nitrogen dioxide, UFPs exposure during the second trimester of pregnancy remained positively associated with childhood asthma incidence (hazard ratio per interquartile range increase, 1.05; 95% confidence interval, 1.01-1.09). Conclusions: This is the first study to evaluate the association between perinatal exposure to UFPs and the incidence of childhood asthma. Exposure to UFPs during a critical period of lung development was linked to the onset of asthma in children, independent of PM 2.5 and NO 2 .

Background: Despite recent studies linking air pollution to neurodegenerative illness, evidence relating air pollution and Parkinson's disease (PD) remains scarce. We conducted a population-based cohort study in Ontario, Canada, to determine the association between air pollution and incident PD., Methods: Using health administrative databases, we identified all adults aged 55-85 years, free of PD, and who lived in Ontario on 1 April 2001 (∼2.2 million). Individuals were followed up until 31 March 2013. We derived long-term average exposures to fine particulate matter (particles ≤2.5 µm in diameter, or PM2.5), nitrogen dioxide (NO2) and ozone from satellite-based estimates, land-use regression models and optimal interpolation methods, respectively. Using 2-year lags in exposures, we linked these estimates to individuals' annual postal codes from 1994 (7 years before cohort inception). We applied spatial random-effects Cox proportional hazards models, adjusting for individual- and area-level characteristics. We also performed sensitivity analyses, such as considering longer lags in exposures and stratifying by selected characteristics., Results: During the study period, we identified 38 745 newly diagnosed cases of PD. Each interquartile increment (3.8 µg/m3) of PM2.5 was associated with a 4% increase in incident PD (95% confidence interval, 1.01-1.08) after adjusting for various covariates. We also found positive associations for NO2 and ozone [hazard ratios (HRs) ranged from 1.03 to 1.04]. The associations for all exposures were unaltered with various sensitivity analyses except for considering longer lags, which somewhat attenuated the estimates, particularly for NO2 and ozone., Conclusions: Exposure to air pollution, especially PM2.5, was found to be related to incident PD.

Background: Evidence of the adverse neurological effects of exposure to ambient air pollution is emerging, but little is known about its effect on the development of multiple sclerosis (MS), the most common autoimmune disease of the central nervous system., Objectives: To investigate the associations between MS incidence and long-term exposures to fine particles (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) METHODS: We conducted a population-based cohort study to investigate the associations between long-term exposures to PM 2.5 , NO 2 , and O 3 and the incidence of MS. Our study population included all Canadian-born residents aged 20-40 years who lived in the province of Ontario, Canada from 2001 to 2013. Incident MS was ascertained from a validated registry. We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during the 13 years of follow-up. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for each pollutant separately using random-effects Cox proportional hazards models. We conducted various sensitivity analyses, such as lagging exposure up to 5 years and adjusting for access to neurological care, annual average temperature, and population density., Results: Between 2001 and 2013, we identified 6203 incident cases of MS. The adjusted HR of incident MS was 0.96 (95% CI: 0.86-1.07) for PM 2.5 , 0.91(95% CI: 0.81-1.02) for NO 2 , and 1.09 (95% CI: 0.98-1.23) for O 3 . These results were robust to various sensitivity analyses conducted., Conclusions: In this large population-based cohort, we did not observe significant associations between MS incidence and long-term exposures to PM 2.5 , NO 2 , and O 3 in adults in Ontario, 2001-2013., (Crown Copyright © 2018. Published by Elsevier Inc. All rights reserved.)

Exposure to ambient fine particulate matter (PM 2.5 ) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM 2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM 2.5 -mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM 2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM 2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations., Competing Interests: Conflict of interest statement: J.V.S. is an independent consultant and not benefiting commercially from the results of this research., (Copyright © 2018 the Author(s). Published by PNAS.)

Background: Previous studies reported that long-term exposure to traffic-related air pollution may increase the incidence of hypertension and diabetes. However, little is known about the associations of ultrafine particles (≤0.1 μm in diameter) with these two conditions., Methods: We conducted a population-based cohort study to investigate the associations between exposures to ultrafine particles and nitrogen dioxide (NO2) and the incidence of diabetes and hypertension. Our study population included all Canadian-born residents aged 30 to 100 years who lived in the City of Toronto, Canada, from 1996 to 2012. Outcomes were ascertained using validated province-wide databases. We estimated annual concentrations of ultrafine particles and NO2 using land-use regression models and assigned these estimates to participants' annual postal code addresses during the follow-up period. Using random-effects Cox proportional hazards models, we calculated hazard ratios (HRs) and 95% confidence intervals (CIs) for ultrafine particles and NO2, adjusted for individual- and neighborhood-level covariates. We considered both single- and multipollutant models., Results: Each interquartile change in exposure to ultrafine particles was associated with increased risk of incident hypertension (HR = 1.03; 95% CI = 1.02, 1.04) and diabetes (HR = 1.06; 95% CI = 1.05, 1.08) after adjusting for all covariates. These results remained unaltered with further control for fine particulate matter (≤2.5 μm; PM2.5) and NO2. Similarly, NO2 was positively associated with incident diabetes (HR = 1.06; 95% CI = 1.05, 1.07) after controlling for ultrafine particles and PM2.5., Conclusions: Exposure to traffic-related air pollution including ultrafine particles and NO2 may increase the risk for incident hypertension and diabetes. See video abstract at, http://links.lww.com/EDE/B337.

Background: Large cohort studies have been used to characterise the association between long-term exposure to fine particulate matter (PM 2.5 ) air pollution with non-accidental, and cause-specific mortality. However, there has been no consensus as to the shape of the association between concentration and response., Methods: To examine the shape of this association, we developed a new cohort based on respondents to the 2001 Canadian census long-form. We applied new annual PM 2.5 concentration estimates based on remote sensing and ground measurements for Canada at a 1km spatial scale from 1998 to 2011. We followed 2.4 million respondents who were non-immigrants aged 25-90 years and did not reside in an institution over a 10 year period for mortality. Exposures were assigned as a 3-year mean prior to the follow-up year. Income tax files were used to account for residential mobility among respondents using postal codes, with probabilistic imputation used for missing postal codes in the tax data. We used Cox survival models to determine hazard ratios (HRs) for cause-specific mortality. We also estimated Shape Constrained Health Impact Functions (a concentration-response function) for selected causes of death., Results: In models stratified by age, sex, airshed, and population centre size, and adjusted for individual and neighbourhood socioeconomic variables, HR estimates for non-accidental mortality were HR = 1.18 (95% CI: 1.15-1.21) per 10μg/m 3 increase in concentration. We observed higher HRs for cardiovascular disease (HR=1.25; 95% CI: 1.19-1.31), cardio-metabolic disease (HR = 1.27; 95% CI: 1.21-1.33), ischemic heart disease (HR = 1.36; 95% CI: 1.28-1.44) and chronic obstructive pulmonary disease (COPD) mortality (HR = 1.24; 95% CI: 1.11-1.39) compared to HR for all non-accidental causes of death. For non-accidental, cardio-metabolic, ischemic heart disease, respiratory and COPD mortality, the shape of the concentration-response curve was supra-linear, with larger differences in relative risk for lower concentrations. For both pneumonia and lung cancer, there was some suggestion that the curves were sub-linear., Conclusions: Associations between ambient concentrations of fine particulate matter and several causes of death were non-linear for each cause of death examined., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels., Methods: We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM 2·5 ) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure-response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure-response functions spanning the global range of exposure., Findings: Ambient PM 2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM 2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM 2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000-422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015., Interpretation: Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM 2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction., Funding: Bill & Melinda Gates Foundation and Health Effects Institute., (Copyright © 2017 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Remote sensing (RS) is increasingly used for exposure assessment in epidemiological and burden of disease studies, including those investigating whether chronic exposure to ambient fine particulate matter (PM 2.5 ) is associated with mortality., Objectives: We compared relative risk estimates of mortality from diseases of the circulatory system for PM 2.5 modeled from RS with that for PM 2.5 modeled using ground-level information., Methods: We geocoded the baseline residence of 668,629 American Cancer Society Cancer Prevention Study II (CPS-II) cohort participants followed from 1982 to 2004 and assigned PM 2.5 levels to all participants using seven different exposure models. Most of the exposure models were averaged for the years 2002-2004, and one RS estimate was for a longer, contemporaneous period. We used Cox proportional hazards regression to estimate relative risks (RRs) for the association of PM 2.5 with circulatory mortality and ischemic heart disease., Results: Estimates of mortality risk differed among exposure models. The smallest relative risk was observed for the RS estimates that excluded ground-based monitors for circulatory deaths [RR = 1.02, 95% confidence interval (CI): 1.00, 1.04 per 10 μg/m 3 increment in PM 2.5 ]. The largest relative risk was observed for the land-use regression model that included traffic information (RR = 1.14, 95% CI: 1.11, 1.17 per 10 μg/m 3 increment in PM 2.5 )., Conclusions: We found significant associations between PM 2.5 and mortality in every model; however, relative risks estimated from exposure models using ground-based information were generally larger than those estimated using RS alone.

Background: Exposure to ambient fine particulate matter (PM2.5) has been associated with a greater risk of non-accidental, cardiovascular and respiratory mortality in Canada. Research based on Canadian cohorts suggests that exposure to PM2.5 varies by demographic and socioeconomic characteristics. Studies of NO₂, another pollutant, indicate that persons of lower socioeconomic status and some visible minority groups have greater exposure in urban centres., Data and Methods: National residential PM2.5 was estimated from a ~1 km² spatial layer for respondents to the 2006 Census long-form questionnaire. Weighted PM2.5 estimates from personal-level estimates were determined for white, Aboriginal, visible minority and immigrant populations, as well as for socioeconomic groups (household income, educational attainment) and stratified by urban core, urban fringe and rural residence. Descriptive statistics were provided for selected comparisons., Results: In Canada, PM2.5 exposure was 1.61 μg/m³ higher for visible minority (versus white) populations, and 1.55 μg/m³ higher for immigrants (versus non-immigrants). When the relatively high percentages of these groups in large cities were taken into account, exposure differences in urban cores were much smaller. Exposure among urban immigrants did not decrease substantially with time since immigration (< 0.5 μg/m³ between any two years). In urban cores, residents of low-income households had marginally higher exposure (0.56 μg/m³) than did people who were not in low-income households., Interpretation: Differences between specific population groups in exposure to PM2.5 are due, at least in part, to higher percentages of these groups living in urban cores where air pollution levels are elevated.

Objectives: Atmospheric fine particulate matter (PM 2.5 ) has multiple adverse effects on human health. Global atmospheric levels of PM 2.5 increased by 0.55 μg/m 3 /year (2.1%/year) from 1998 through 2012. There is evidence of a causal relationship between atmospheric PM 2.5 and breast cancer (BC) incidence, but few studies have investigated BC mortality and atmospheric PM 2.5 . We investigated BC mortality in relation to atmospheric PM 2.5 levels among patients living in Varese Province, northern Italy., Methods: We selected female BC cases, archived in the local population-based cancer registry, diagnosed at age 50-69 years, between 2003 and 2009. The geographic coordinates of each woman's place of residence were identified, and individual PM 2.5 exposures were assessed from satellite data. Grade, stage, age at diagnosis, period of diagnosis and participation in BC screening were potential confounders. Kaplan-Meir and Nelson-Aalen methods were used to test for mortality differences in relation to PM 2.5 quartiles. Multivariable Cox proportional hazards modelling estimated HRs and 95% CIs of BC death in relation to PM 2.5 exposure., Results: Of 2021 BC cases, 325 died during follow-up to 31 December 2013, 246 for BC. Risk of BC death was significantly higher for all three upper quartiles of PM 2.5 exposure compared to the lowest, with HRs of death: 1.82 (95% CI 1.15 to 2.89), 1.73 (95% CI 1.12 to 2.67) and 1.72 (95% CI 1.08 to 2.75)., Conclusions: Our study indicates that the risk of BC mortality increases with PM 2.5 exposure. Although additional research is required to confirm these findings, they are further evidence that PM 2.5 exposure is harmful and indicate an urgent need to improve global air quality., Competing Interests: Conflicts of Interest: None declared., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Backround: Fine particulate air pollution (PM2.5) is known to contribute to cardiorespiratory mortality but it is not clear how PM2.5 oxidative burden (i.e. the ability of PM2.5 to cause oxidative stress) may influence long-term mortality risk., Methods: We examined the relationship between PM2.5 oxidative burden and cause-specific mortality in Ontario, Canada. Integrated PM2.5 samples were collected from 30 provincial monitoring sites between 2012 and 2013. The oxidative potential (% depletion/µg) of regional PM2.5 was measured as the ability of filter extracts to deplete antioxidants (glutathione and ascorbate) in a synthetic respiratory tract lining fluid. PM2.5oxidative burden was calculated as the product of PM2.5 mass concentrations and regional estimates of oxidative potential. In total, this study included 193,300 people who completed the Canadian long-form census in 1991 and who lived within 5km of a site where oxidative potential was measured. Deaths occurring between 1991 and 2009 were identified through record linkages and Cox proportional hazard models were used to estimate hazard ratios (and 95% confidence intervals) for interquartile changes in exposure adjusting for individual-level covariates and indirect-adjustment for smoking and obesity., Results: Glutathione-related oxidative burden was associated with cause-specific mortality. For lung cancer specifically, this metric was associated with a 12% (95% CI: 5.0-19) increased risk of mortality whereas a 5.0% (95% CI: 0.1, 10) increase was observed for PM2.5. Indirect adjustment for smoking and obesity decreased the lung cancer hazard ratio for glutathione-related oxidative burden but it remained significantly elevated (HR=1.07, 95% CI: 1.005, 1.146). Ascorbate-related oxidative burden was not associated with mortality., Conclusions: Our findings suggest that glutathione-related oxidative burden may be more strongly associated with lung cancer mortality than PM2.5 mass concentrations., (Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.)

Background: Air pollution is associated with morbidity and premature mortality. Satellite remote sensing provides globally consistent decadal-scale observations of ambient nitrogen dioxide (NO2) pollution., Objective: We determined global population-weighted annual mean NO2 concentrations from 1996 through 2012., Methods: We used observations of NO2 tropospheric column densities from three satellite instruments in combination with chemical transport modeling to produce a global 17-year record of ground-level NO2 at 0.1° × 0.1° resolution. We calculated linear trends in population-weighted annual mean NO2 (PWMNO2) concentrations in different regions around the world., Results: We found that PWMNO2 in high-income North America (Canada and the United States) decreased more steeply than in any other region, having declined at a rate of -4.7%/year [95% confidence interval (CI): -5.3, -4.1]. PWMNO2 decreased in western Europe at a rate of -2.5%/year (95% CI: -3.0, -2.1). The highest PWMNO2 occurred in high-income Asia Pacific (predominantly Japan and South Korea) in 1996, with a subsequent decrease of -2.1%/year (95% CI: -2.7, -1.5). In contrast, PWMNO2 almost tripled in East Asia (China, North Korea, and Taiwan) at a rate of 6.7%/year (95% CI: 6.0, 7.3). The satellite-derived estimates of trends in ground-level NO2 were consistent with regional trends inferred from data obtained from ground-station monitoring networks in North America (within 0.7%/year) and Europe (within 0.3%/year). Our rankings of regional average NO2 and long-term trends differed from the satellite-derived estimates of fine particulate matter reported elsewhere, demonstrating the utility of both indicators to describe changing pollutant mixtures., Conclusions: Long-term trends in satellite-derived ambient NO2 provide new information about changing global exposure to ambient air pollution. Our estimates are publicly available at http://fizz.phys.dal.ca/~atmos/martin/?page&#95;id=232.

Background: Understanding the shape of the relationship between long-term exposure to ambient fine particulate matter (PM2.5) concentrations and health risks is critical for health impact and risk assessment. Studies evaluating the health risks of exposure to low concentrations of PM2.5 are limited. Further, many existing studies lack individual-level information on potentially important behavioural confounding factors., Methods: A prospective cohort study was conducted among a subset of participants in a cohort that linked respondents of the Canadian Community Health Survey to mortality (n = 299,500) with satellite-derived ambient PM2.5 estimates. Participants enrolled between 2000 and 2008 were followed to date of death or December 31, 2011. Cox proportional hazards models were used to estimate hazard ratios (HRs) for mortality attributed to PM2.5 exposure, adjusted for individual-level and contextual covariates, including smoking behaviour and body mass index (BMI)., Results: Approximately 26,300 non-accidental deaths, of which 32.5 % were due to circulatory disease and 9.1 % were due to respiratory disease, occurred during the follow-up period. Ambient PM2.5 exposures were relatively low (mean = 6.3 μg/m(3)), yet each 10 μg/m(3) increase in exposure was associated with increased risks of non-accidental (HR = 1.26; 95 % CI: 1.19-1.34), circulatory disease (HR = 1.19; 95 % CI: 1.07-1.31), and respiratory disease mortality (HR = 1.52; 95 % CI: 1.26-1.84) in fully adjusted models. Higher hazard ratios were observed for respiratory mortality among respondents who never smoked (HR = 1.97; 95 % CI: 1.24-3.13 vs. HR = 1.45; 95 % CI: 1.17-1.79 for ever smokers), and among obese (BMI ≥ 30) respondents (HR = 1.76; 95 % CI: 1.15-2.69 vs. HR = 1.41; 95 % CI: 1.04-1.91 for normal weight respondents), though differences between groups were not statistically significant. A threshold analysis for non-accidental mortality estimated a threshold concentration of 0 μg/m(3) (+95 % CI = 4.5 μg/m(3))., Conclusions: Increased risks of non-accidental, circulatory, and respiratory mortality were observed even at very low concentrations of ambient PM2.5. HRs were generally greater than most literature values, and adjusting for behavioural covariates served to reduce HR estimates slightly.

Most studies on the association between exposure to fine particulate matter (PM2.5) and mortality have considered only total concentration of PM2.5 or individual components of PM2.5, and not the combined effects of concentration and particulate composition. We sought to develop a method to estimate the risk of death from long-term exposure to PM2.5 and the distribution of its components, namely: sulphate, nitrate, ammonium, organic mass, black carbon, and mineral dust. We decomposed PM2.5 exposure into the sum of total concentration and the proportion of each component. We estimated the risk of death due to exposure using a cohort of ~2.4 million Canadians who were followed for vital status over 16 years. Modelling the concentration of PM2.5 with the distribution of the proportions of components together was a superior predictor for mortality than either total PM2.5 concentration alone, or all component concentrations modelled together. Our new approach has the advantage of characterizing the toxicity of the atmosphere in its entirety. This is required to fully understand the health benefits associated with strategies to improve air quality that may result in complex changes not only in PM2.5 concentration, but also in the distribution of particle components.

Exposure to ambient air pollution is a major risk factor for global disease. Assessment of the impacts of air pollution on population health and evaluation of trends relative to other major risk factors requires regularly updated, accurate, spatially resolved exposure estimates. We combined satellite-based estimates, chemical transport model simulations, and ground measurements from 79 different countries to produce global estimates of annual average fine particle (PM2.5) and ozone concentrations at 0.1° × 0.1° spatial resolution for five-year intervals from 1990 to 2010 and the year 2013. These estimates were applied to assess population-weighted mean concentrations for 1990-2013 for each of 188 countries. In 2013, 87% of the world's population lived in areas exceeding the World Health Organization Air Quality Guideline of 10 μg/m(3) PM2.5 (annual average). Between 1990 and 2013, global population-weighted PM2.5 increased by 20.4% driven by trends in South Asia, Southeast Asia, and China. Decreases in population-weighted mean concentrations of PM2.5 were evident in most high income countries. Population-weighted mean concentrations of ozone increased globally by 8.9% from 1990-2013 with increases in most countries-except for modest decreases in North America, parts of Europe, and several countries in Southeast Asia.

Background: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution., Methods: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian meta-regression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol., Findings: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa., Interpretation: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks., Funding: Bill & Melinda Gates Foundation., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: Long-term exposure to fine particulate matter (PM2.5) has been associated with increased mortality, especially from cardiovascular disease. There are, however, uncertainties about the nature of the exposure-response relation at lower concentrations. In Canada, where ambient air pollution levels are substantially lower than in most other countries, there have been few attempts to study associations between long-term exposure to PM2.5 and mortality., Methods: We present a prospective cohort analysis of 89,248 women who enrolled in the Canadian National Breast Screening Study between 1980 and 1985, and for whom residential measures of PM2.5 could be assigned. We derived individual-level estimates of long-term exposure to PM2.5 from satellite observations. We linked cohort records to national mortality data to ascertain mortality between 1980 and 2005. We used Cox proportional hazards models to characterize associations between PM2.5 and several causes of death. The hazard ratios (HRs) and 95% confidence intervals (CIs) computed from these models were adjusted for several individual and neighborhood-level characteristics., Results: The cohort was composed predominantly of Canadian-born (82%) and married (80%) women. The median residential concentration of PM2.5 was 9.1 μg/m(3) (standard deviation = 3.4). In fully adjusted models, a 10 μg/m(3) increase in PM2.5 exposure was associated with elevated risks of nonaccidental (HR: 1.12; 95% CI = 1.04, 1.19), and ischemic heart disease mortality (HR: 1.34; 95% CI = 1.09, 1.66)., Conclusions: The findings from this study provide additional support for the hypothesis that exposure to very low levels of ambient PM2.5 increases the risk of cardiovascular mortality.

Background: More than a decade of satellite observations offers global information about the trend and magnitude of human exposure to fine particulate matter (PM2.5)., Objective: In this study, we developed improved global exposure estimates of ambient PM2.5 mass and trend using PM2.5 concentrations inferred from multiple satellite instruments., Methods: We combined three satellite-derived PM2.5 sources to produce global PM2.5 estimates at about 10 km × 10 km from 1998 through 2012. For each source, we related total column retrievals of aerosol optical depth to near-ground PM2.5 using the GEOS-Chem chemical transport model to represent local aerosol optical properties and vertical profiles. We collected 210 global ground-based PM2.5 observations from the literature to evaluate our satellite-based estimates with values measured in areas other than North America and Europe., Results: We estimated that global population-weighted ambient PM2.5 concentrations increased 0.55 μg/m3/year (95% CI: 0.43, 0.67) (2.1%/year; 95% CI: 1.6, 2.6) from 1998 through 2012. Increasing PM2.5 in some developing regions drove this global change, despite decreasing PM2.5 in some developed regions. The estimated proportion of the population of East Asia living above the World Health Organization (WHO) Interim Target-1 of 35 μg/m3 increased from 51% in 1998-2000 to 70% in 2010-2012. In contrast, the North American proportion above the WHO Air Quality Guideline of 10 μg/m3 fell from 62% in 1998-2000 to 19% in 2010-2012. We found significant agreement between satellite-derived estimates and ground-based measurements outside North America and Europe (r = 0.81; n = 210; slope = 0.68). The low bias in satellite-derived estimates suggests that true global concentrations could be even greater., Conclusions: Satellite observations provide insight into global long-term changes in ambient PM2.5 concentrations. Satellite-derived estimates and ground-based PM2.5 observations from this study are available for public use.

Epidemiologic and health impact studies are inhibited by the paucity of global, long-term measurements of the chemical composition of fine particulate matter. We inferred PM2.5 chemical composition at 0.1° × 0.1° spatial resolution for 2004-2008 by combining aerosol optical depth retrieved from the MODIS and MISR satellite instruments, with coincident profile and composition information from the GEOS-Chem global chemical transport model. Evaluation of the satellite-model PM2.5 composition data set with North American in situ measurements indicated significant spatial agreement for secondary inorganic aerosol, particulate organic mass, black carbon, mineral dust, and sea salt. We found that global population-weighted PM2.5 concentrations were dominated by particulate organic mass (11.9 ± 7.3 μg/m(3)), secondary inorganic aerosol (11.1 ± 5.0 μg/m(3)), and mineral dust (11.1 ± 7.9 μg/m(3)). Secondary inorganic PM2.5 concentrations exceeded 30 μg/m(3) over East China. Sensitivity simulations suggested that population-weighted ambient PM2.5 from biofuel burning (11 μg/m(3)) could be almost as large as from fossil fuel combustion sources (17 μg/m(3)). These estimates offer information about global population exposure to the chemical components and sources of PM2.5.

Background: Few studies have examined the relationship between long-term exposure to ambient fine particulate matter (PM2.5) and nonaccidental mortality in rural populations., Objective: We examined the relationship between PM2.5 and nonaccidental and cardiovascular mortality in the U.S. Agricultural Health Study cohort., Methods: The cohort (n = 83,378) included farmers, their spouses, and commercial pesticide applicators residing primarily in Iowa and North Carolina. Deaths occurring between enrollment (1993-1997) and 30 December 2009 were identified by record linkage. Six-year average (2001-2006) remote-sensing derived estimates of PM2.5 were assigned to participants' residences at enrollment, and Cox proportional hazards models were used to estimate hazard ratios (HR) in relation to a 10-μg/m(3) increase in PM2.5 adjusted for individual-level covariates., Results: In total, 5,931 nonaccidental and 1,967 cardiovascular deaths occurred over a median follow-up time of 13.9 years. PM2.5 was not associated with nonaccidental mortality in the cohort as a whole (HR = 0.95; 95% CI: 0.76, 1.20), but consistent inverse relationships were observed among women. Positive associations were observed between ambient PM2.5 and cardiovascular mortality among men, and these associations were strongest among men who did not move from their enrollment address (HR = 1.63; 95% 0.94, 2.84). In particular, cardiovascular mortality risk in men was significantly increased when analyses were limited to nonmoving participants with the most precise exposure geocoding (HR = 1.87; 95% CI: 1.04, 3.36)., Conclusions: Rural PM2.5 may be associated with cardiovascular mortality in men; however, similar associations were not observed among women. Further evaluation is required to explore these sex differences.

Background: Laboratory studies suggest that exposure to fine particulate matter (≤2.5 μm in diameter) (PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension., Methods and Results: We assembled a cohort of 35 303 nonhypertensive adults from Ontario, Canada, who responded to 1 of 4 population-based health surveys between 1996 and 2005 and were followed up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants' postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adjusting for various individual and contextual risk factors including body mass index, smoking, physical activity, and neighbourhood-level unemployment rates. We conducted various sensitivity analyses to assess the robustness of the effect estimate, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time. Between 1996 and 2010, we identified 8649 incident cases of hypertension and 2296 deaths. For every 10-µg/m(3) increase of PM2.5, the adjusted hazard ratio of incident hypertension was 1.13 (95% confidence interval, 1.05-1.22). Estimated associations were comparable among all sensitivity analyses., Conclusions: This study supports an association between PM2.5 and incident hypertension.

Background: Laboratory studies suggest that fine particulate matter (≤ 2.5 µm in diameter; PM(2.5)) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating PM2.5 and diabetes is sparse, particularly for incident diabetes., Objectives: We conducted a population-based cohort study to determine whether long-term exposure to ambient PM(2.5) is associated with incident diabetes., Methods: We assembled a cohort of 62,012 nondiabetic adults who lived in Ontario, Canada, and completed one of five population-based health surveys between 1996 and 2005. Follow-up extended until 31 December 2010. Incident diabetes diagnosed between 1996 and 2010 was ascertained using the Ontario Diabetes Database, a validated registry of persons diagnosed with diabetes (sensitivity = 86%, specificity = 97%). Six-year average concentrations of PM2.5 at the postal codes of baseline residences were derived from satellite observations. We used Cox proportional hazards models to estimate the associations, adjusting for various individual-level risk factors and contextual covariates such as smoking, body mass index, physical activity, and neighborhood-level household income. We also conducted multiple sensitivity analyses. In addition, we examined effect modification for selected comorbidities and sociodemographic characteristics., Results: There were 6,310 incident cases of diabetes over 484,644 total person-years of follow-up. The adjusted hazard ratio for a 10-µg/m(3) increase in PM(2.5) was 1.11 (95% CI: 1.02, 1.21). Estimated associations were comparable among all sensitivity analyses. We did not find strong evidence of effect modification by comorbidities or sociodemographic covariates., Conclusions: This study suggests that long-term exposure to PM2.5 may contribute to the development of diabetes.

Background: The effect of ambient air pollution on global variations and trends in asthma prevalence is unclear., Objectives: Our goal was to investigate community-level associations between asthma prevalence data from the International Study of Asthma and Allergies in Childhood (ISAAC) and satellite-based estimates of particulate matter with aerodynamic diameter < 2.5 µm (PM₂.₅) and nitrogen dioxide (NO₂), and modelled estimates of ozone., Methods: We assigned satellite-based estimates of PM₂.₅ and NO₂ at a spatial resolution of 0.1° × 0.1° and modeled estimates of ozone at a resolution of 1° × 1° to 183 ISAAC centers. We used center-level prevalence of severe asthma as the outcome and multilevel models to adjust for gross national income (GNI) and center- and country-level sex, climate, and population density. We examined associations (adjusting for GNI) between air pollution and asthma prevalence over time in centers with data from ISAAC Phase One (mid-1900s) and Phase Three (2001-2003)., Results: For the 13- to 14-year age group (128 centers in 28 countries), the estimated average within-country change in center-level asthma prevalence per 100 children per 10% increase in center-level PM₂.₅ and NO₂ was -0.043 [95% confidence interval (CI): -0.139, 0.053] and 0.017 (95% CI: -0.030, 0.064) respectively. For ozone the estimated change in prevalence per parts per billion by volume was -0.116 (95% CI: -0.234, 0.001). Equivalent results for the 6- to 7-year age group (83 centers in 20 countries), though slightly different, were not significantly positive. For the 13- to 14-year age group, change in center-level asthma prevalence over time per 100 children per 10% increase in PM₂.₅ from Phase One to Phase Three was -0.139 (95% CI: -0.347, 0.068). The corresponding association with ozone (per ppbV) was -0.171 (95% CI: -0.275, -0.067)., Conclusion: In contrast to reports from within-community studies of individuals exposed to traffic pollution, we did not find evidence of a positive association between ambient air pollution and asthma prevalence as measured at the community level.

Background: Few epidemiological studies of air pollution have used residential histories to develop long-term retrospective exposure estimates for multiple ambient air pollutants and vehicle and industrial emissions. We present such an exposure assessment for a Canadian population-based lung cancer case-control study of 8353 individuals using self-reported residential histories from 1975 to 1994. We also examine the implications of disregarding and/or improperly accounting for residential mobility in long-term exposure assessments., Methods: National spatial surfaces of ambient air pollution were compiled from recent satellite-based estimates (for PM2.5 and NO2) and a chemical transport model (for O3). The surfaces were adjusted with historical annual air pollution monitoring data, using either spatiotemporal interpolation or linear regression. Model evaluation was conducted using an independent ten percent subset of monitoring data per year. Proximity to major roads, incorporating a temporal weighting factor based on Canadian mobile-source emission estimates, was used to estimate exposure to vehicle emissions. A comprehensive inventory of geocoded industries was used to estimate proximity to major and minor industrial emissions., Results: Calibration of the national PM2.5 surface using annual spatiotemporal interpolation predicted historical PM2.5 measurement data best (R2 = 0.51), while linear regression incorporating the national surfaces, a time-trend and population density best predicted historical concentrations of NO2 (R2 = 0.38) and O3 (R2 = 0.56). Applying the models to study participants residential histories between 1975 and 1994 resulted in mean PM2.5, NO2 and O3 exposures of 11.3 μg/m3 (SD = 2.6), 17.7 ppb (4.1), and 26.4 ppb (3.4) respectively. On average, individuals lived within 300 m of a highway for 2.9 years (15% of exposure-years) and within 3 km of a major industrial emitter for 6.4 years (32% of exposure-years). Approximately 50% of individuals were classified into a different PM2.5, NO2 and O3 exposure quintile when using study entry postal codes and spatial pollution surfaces, in comparison to exposures derived from residential histories and spatiotemporal air pollution models. Recall bias was also present for self-reported residential histories prior to 1975, with cases recalling older residences more often than controls., Conclusions: We demonstrate a flexible exposure assessment approach for estimating historical air pollution concentrations over large geographical areas and time-periods. In addition, we highlight the importance of including residential histories in long-term exposure assessments. For submission to: Environmental Health.

Ambient air pollution is associated with numerous adverse health impacts. Previous assessments of global attributable disease burden have been limited to urban areas or by coarse spatial resolution of concentration estimates. Recent developments in remote sensing, global chemical-transport models, and improvements in coverage of surface measurements facilitate virtually complete spatially resolved global air pollutant concentration estimates. We combined these data to generate global estimates of long-term average ambient concentrations of fine particles (PM(2.5)) and ozone at 0.1° × 0.1° spatial resolution for 1990 and 2005. In 2005, 89% of the world's population lived in areas where the World Health Organization Air Quality Guideline of 10 μg/m(3) PM(2.5) (annual average) was exceeded. Globally, 32% of the population lived in areas exceeding the WHO Level 1 Interim Target of 35 μg/m(3), driven by high proportions in East (76%) and South (26%) Asia. The highest seasonal ozone levels were found in North and Latin America, Europe, South and East Asia, and parts of Africa. Between 1990 and 2005 a 6% increase in global population-weighted PM(2.5) and a 1% decrease in global population-weighted ozone concentrations was apparent, highlighted by increased concentrations in East, South, and Southeast Asia and decreases in North America and Europe. Combined with spatially resolved population distributions, these estimates expand the evaluation of the global health burden associated with outdoor air pollution.

BACKGROUND: Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. METHODS: In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). RESULTS: Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032-1.053) vs OR = 1.009 (95% CI, 0.996-1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019-1.047), RERI = 0.039 (95% CI, 0.025-0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. CONCLUSIONS: The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users.

BackgroundNumerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter ≤2.5μm in aerodynamic diameter (PM2.5)] on mortality even at relatively low levels. However, methodological challenges remain to consider potential regulatory intervention's complexity and provide actionable evidence on the predicted benefits of interventions. We propose the parametric g-computation as an alternative analytical approach to such challenges.MethodWe applied the parametric g-computation to estimate the cumulative risks of nonaccidental death under different hypothetical intervention strategies targeting long-term exposure to PM2.5 in the Canadian Community Health Survey cohort from 2005 to 2015. On both relative and absolute scales, we explored the benefits of hypothetical intervention strategies compared with the natural course that a) set the simulated exposure value at each follow-up year to a threshold value if exposure was above the threshold (8.8 μg/m3, 7.04 μg/m3, 5 μg/m3, and 4 μg/m3), and b) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average PM2.5 concentration with 1-y lag at the postal code of respondents' annual mailing addresses as their long-term exposure to PM2.5. We considered baseline and time-varying confounders, including demographics, behavior characteristics, income level, and neighborhood socioeconomic status. We also included the R syntax for reproducibility and replication.ResultsAll hypothetical intervention strategies explored led to lower 11-y cumulative mortality risks than the estimated value under the natural course without intervention, with the smallest reduction of 0.20 per 1,000 participants (95% CI: 0.06, 0.34) under the threshold of 8.8 μg/m3, and the largest reduction of 3.40 per 1,000 participants (95% CI: -0.23, 7.03) under the relative reduction of 10% per interval. The reductions in cumulative risk, or numbers of deaths that would have been prevented if the intervention was employed instead of maintaining the status quo, increased over time but flattened toward the end of the follow-up period. Estimates among those ≥65 years of age were greater with a similar pattern. Our estimates were robust to different model specifications.DiscussionWe found evidence that any intervention further reducing the long-term exposure to PM2.5 would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient PM2.5. The parametric g-computation used in this study provides flexibilities in simulating real-world interventions, accommodates time-varying exposure and confounders, and estimates adjusted survival curves with clearer interpretation and more information than a single hazard ratio, making it a valuable analytical alternative in air pollution epidemiological research. https://doi.org/10.1289/EHP11095.

This retrospective cohort study examined associations of autism spectrum disorder (ASD) with prenatal exposure to major fine particulate matter (PM2.5) components estimated using two independent exposure models. The cohort included 318 750 mother-child pairs with singleton deliveries in Kaiser Permanente Southern California hospitals from 2001 to 2014 and followed until age five. ASD cases during follow-up (N = 4559) were identified by ICD codes. Prenatal exposures to PM2.5, elemental (EC) and black carbon (BC), organic matter (OM), nitrate (NO3-), and sulfate (SO42-) were constructed using (i) a source-oriented chemical transport model and (ii) a hybrid model. Exposures were assigned to each maternal address during the entire pregnancy, first, second, and third trimester. In single-pollutant models, ASD was associated with pregnancy-average PM2.5, EC/BC, OM, and SO42- exposures from both exposure models, after adjustment for covariates. The direction of effect estimates was consistent for EC/BC and OM and least consistent for NO3-. EC/BC, OM, and SO42- were generally robust to adjustment for other components and for PM2.5. EC/BC and OM effect estimates were generally larger and more consistent in the first and second trimester and SO42- in the third trimester. Future PM2.5 composition health effect studies might consider using multiple exposure models and a weight of evidence approach when interpreting effect estimates.

Background Long-term exposure to outdoor fine particulate matter (PM2.5) is the leading environmental risk factor for premature mortality worldwide. Characterizing important pathways through which PM2.5 increases individuals' mortality risk can clarify the PM2.5-mortality relationship and identify possible points of interventions. Recent evidence has linked PM2.5 to the onset of diabetes and cardiovascular disease, but to what extent these associations contribute to the effect of PM2.5 on mortality remains poorly understood. Methods and Results We conducted a population-based cohort study to investigate how the effect of PM2.5 on nonaccidental mortality is mediated by its impacts on incident diabetes, acute myocardial infarction, and stroke. Our study population comprised ≈200 000 individuals aged 20 to 90 years who participated in population-based health surveys in Ontario, Canada, from 1996 to 2014. Follow-up extended until December 2017. Using causal mediation analyses with Aalen additive hazards models, we decomposed the total effect of PM2.5 on mortality into a direct effect and several path-specific indirect effects mediated by diabetes, each cardiovascular event, or both combined. A series of sensitivity analyses were also conducted. After adjusting for various individual- and neighborhood-level covariates, we estimated that for every 1000 adults, each 10 μg/m3 increase in PM2.5 was associated with ≈2 incident cases of diabetes, ≈1 major cardiovascular event (acute myocardial infarction and stroke combined), and ≈2 deaths annually. Among PM2.5-related deaths, 31.7% (95% CI, 17.2%-53.2%) were attributable to diabetes and major cardiovascular events in relation to PM2.5. Specifically, 4.5% were explained by PM2.5-induced diabetes, 22.8% by PM2.5-induced major cardiovascular events, and 4.5% through their interaction. Conclusions This study suggests that a significant portion of the estimated effect of long-term exposure to PM2.5 on deaths can be attributed to its effect on diabetes and cardiovascular diseases, highlighting the significance of PM2.5 on deteriorating cardiovascular health. Our findings should raise awareness among professionals that improving metabolic and cardiovascular health may reduce mortality burden in areas with higher exposure to air pollution.

BackgroundThe tremendous global health burden related to COVID-19 means that identifying determinants of COVID-19 severity is important for prevention and intervention. We aimed to explore long-term exposure to ambient air pollution as a potential contributor to COVID-19 severity, given its known impact on the respiratory system.MethodsWe used a cohort of all people with confirmed SARS-CoV-2 infection, aged 20 years and older and not residing in a long-term care facility in Ontario, Canada, during 2020. We evaluated the association between long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ground-level ozone (O3), and risk of COVID-19-related hospital admission, intensive care unit (ICU) admission and death. We ascertained individuals' long-term exposures to each air pollutant based on their residence from 2015 to 2019. We used logistic regression and adjusted for confounders and selection bias using various individual and contextual covariates obtained through data linkage.ResultsAmong the 151 105 people with confirmed SARS-CoV-2 infection in Ontario in 2020, we observed 8630 hospital admissions, 1912 ICU admissions and 2137 deaths related to COVID-19. For each interquartile range increase in exposure to PM2.5 (1.70 μg/m3), we estimated odds ratios of 1.06 (95% confidence interval [CI] 1.01-1.12), 1.09 (95% CI 0.98-1.21) and 1.00 (95% CI 0.90-1.11) for hospital admission, ICU admission and death, respectively. Estimates were smaller for NO2. We also estimated odds ratios of 1.15 (95% CI 1.06-1.23), 1.30 (95% CI 1.12-1.50) and 1.18 (95% CI 1.02-1.36) per interquartile range increase of 5.14 ppb in O3 for hospital admission, ICU admission and death, respectively.InterpretationChronic exposure to air pollution may contribute to severe outcomes after SARS-CoV-2 infection, particularly exposure to O3.

BackgroundLittle is known about the long-term health effects of ambient ultrafine particles (

RationaleAlthough substantial scientific evidence suggests that chronic exposure to ambient air pollution contributes to premature mortality, uncertainties exist in the size and consistency of this association. Uncertainty may arise from inaccurate exposure assessment.ObjectivesTo assess the associations of three types of air pollutants (fine particulate matter, ozone [O3], and nitrogen dioxide [NO2]) with the risk of mortality in a large cohort of California adults using individualized exposure assessments.MethodsFor fine particulate matter and NO2, we used land use regression models to derive predicted individualized exposure at the home address. For O3, we estimated exposure with an inverse distance weighting interpolation. Standard and multilevel Cox survival models were used to assess the association between air pollution and mortality.Measurements and main resultsData for 73,711 subjects who resided in California were abstracted from the American Cancer Society Cancer Prevention II Study cohort, with baseline ascertainment of individual characteristics in 1982 and follow-up of vital status through to 2000. Exposure data were derived from government monitors. Exposure to fine particulate matter, O3, and NO2 was positively associated with ischemic heart disease mortality. NO2 (a marker for traffic pollution) and fine particulate matter were also associated with mortality from all causes combined. Only NO2 had significant positive association with lung cancer mortality.ConclusionsUsing the first individualized exposure assignments in this important cohort, we found positive associations of fine particulate matter, O3, and NO2 with mortality. The positive associations of NO2 suggest that traffic pollution relates to premature death.

Background: Populations are simultaneously exposed to outdoor concentrations of oxidant gases (i.e., O 3 and NO 2 ) and fine particulate air pollution (PM 2.5 ). Since oxidative stress is thought to be an important mechanism explaining air pollution health effects, the adverse health impacts of oxidant gases may be greater in locations where PM 2.5 is more capable of causing oxidative stress.Methods: We conducted a cohort study of 2 million adults in Canada between 2001 and 2016 living within 10 km of ground-level monitoring sites for outdoor PM 2.5 components and oxidative potential. O x exposures (i.e., the redox-weighted average of O 3 and NO 2 ) were estimated using a combination of chemical transport models, land use regression models, and ground-level data. Cox proportional hazards models were used to estimate associations between 3-year moving average O x and mortality outcomes across strata of transition metals and sulfur in PM 2.5 and three measures of PM 2.5 oxidative potential adjusting for possible confounding factors.Results: Associations between O x and mortality were consistently stronger in regions with elevated PM 2.5 transition metal/sulfur content and oxidative potential. For example, each interquartile increase (6.27 ppb) in O x was associated with a 14.9% (95% CI = 13.0, 16.9) increased risk of nonaccidental mortality in locations with glutathione-related oxidative potential (OP GSH ) above the median whereas a 2.50% (95% CI = 0.600, 4.40) increase was observed in regions with OP GSH levels below the median (interaction P value <0.001).Conclusion: Spatial variations in PM 2.5 composition and oxidative potential may contribute to heterogeneity in the observed health impacts of long-term exposures to oxidant gases. [ABSTRACT FROM AUTHOR]

BACKGROUND: Preharvest burning of sugarcane is a common agricultural practice in Florida, which produces fine particulate matter [particulate matter (PM) with aerodynamic diameter ≤ 2.5 µm (PM2.5)] that is associated with higher mortality. OBJECTIVES: We estimated premature mortality associated with exposure to PM2.5 from sugarcane burning in people age 25 y and above for 20 counties in South Florida. METHODS: We combined information from an atmospheric dispersion model, satellites, and surface measurements to quantify PM2.5 concentrations in South Florida and the fraction of PM2.5 from sugarcane fires. From these concentrations, estimated mortalities attributable to PM2.5 from sugarcane fires were calculated by census tract using health impact functions derived from literature for six causes of death linked to PM2.5. Confidence intervals (CI) are provided based on Monte Carlo simulations that propagate uncertainty in the emissions, dispersion model, health impact functions, and demographic data. RESULTS: Sugarcane fires emitted an amount of primary PM2.5 similar to that of motor vehicles in Florida. PM2.5 from sugarcane fires is estimated to contribute to mortality rates within the Florida Sugarcane Growing Region (SGR) by 0.4 death per 100,000 people per year (95% CI: 0.3, 1.6 per 100,000). These estimates imply 2.5 deaths per year across South Florida were associated with PM2.5 from sugarcane fires (95% CI: 1.2, 6.1), with 0.16 in the SGR (95% CI: 0.09, 0.6) and 0.72 in Palm Beach County (95% CI: 0.17, 2.2). DISCUSSION: PM2.5 from sugarcane fires was estimated to contribute to mortality risk across South Florida, particularly in the SGR. This is consistent with prior studies that documented impacts of sugarcane fire on air quality but did not quantify mortality. Additional health impacts of sugarcane fires, which were not quantified here, include exacerbating nonfatal health conditions such as asthma and cardiovascular problems. Harvesting sugarcane without field burning would likely reduce PM2.5 and health burdens in this region. [ABSTRACT FROM AUTHOR]

BACKGROUND: Experimental evidence and studies of children and adolescents suggest that ambient fine particulate matter [particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5)] air pollution may be obesogenic, but the relationship between PM2.5 and the risk of body weight gain and obesity in adults is uncertain. OBJECTIVES: Our goal was to characterize the association between PM2.5 and the risks of weight gain and obesity. METHODS: We followed 3,902,440 U.S. Veterans from 2010 to 2018 (median 8.1 y, interquartile range: 7.3–8.4) and assigned time-updated PM2.5 exposures by linking geocoded residential street addresses with satellite-based estimates of surface-level PM2.5 mass (at ~1-km² resolution). Associations with PM2.5 were estimated using Cox proportional hazards models for incident obesity [body mass index (BMI) ≥30 kg/m²] and a 10-lb increase in weight relative to baseline and linear mixed models for associations with intra-individual changes in BMI and weight. RESULTS: A 10-μg/m³ higher average annual PM2.5 concentration was associated with risk of incident obesity [푛=2,325,769; hazard ratio (HR)=1.08 (95% CI: 1.06, 1.11)] and the risk of a 10-lb (4.54 kg) increase in weight [HR=1.07 (95% CI: 1.06, 1.08)] and with higher intra-individual changes in BMI [0.140 kg/m² per year (95% CI: 0.139, 0.142)] and weight [0.968 lb/y (95% CI: 0.955, 0.981)]. Nonlinear exposure– response models indicated associations at PM2.5 concentrations below the national standard of 12 μg/m³. As expected, a negative exposure control (ambient air sodium) was not associated with obesity or weight gain. Associations were consistent in direction and magnitude across sensitivity analyses that included alternative outcomes and exposures assigned at different spatial resolutions. DISCUSSION: PM2.5 air pollution was associated with the risk of obesity and weight gain in a large predominantly male cohort of U.S. Veterans. Discussions about health effects of PM2.5 should include its association with obesity, and deliberations about the epidemiology of obesity should consider its association with PM2.5. Investigation in other cohorts will deepen our understanding of the relationship between PM2.5 and weight gain and obesity. [ABSTRACT FROM AUTHOR]

Background: Exposure to fine particulate (PM2.5) air pollution is associated with increased cardiovascular disease (CVD), but less is known about its specific components, such as metals originating from non-tailpipe emissions. We investigated the associations of long-term exposure to metal components [iron (Fe) and copper (Cu)] in PM2.5 with CVD incidence.Methods: We conducted a population-based cohort study in Toronto, Canada. Exposures to Fe and Cu in PM2.5 and their combined impact on the concentration of reactive oxygen species (ROS) in lung fluid were estimated using land use regression models. Incidence of acute myocardial infarction (AMI), congestive heart failure (CHF) and CVD death was ascertained using health administrative datasets. We used mixed-effects Cox regression models to examine the associations between the exposures and health outcomes. A series of sensitivity analyses were conducted, including indirect adjustment for individual-level cardiovascular risk factors (e.g. smoking), and adjustment for PM2.5 and nitrogen dioxide (NO2).Results: In single-pollutant models, we found positive associations between the three exposures and all three outcomes, with the strongest associations detected for the estimated ROS. The associations of AMI and CHF were sensitive to indirect adjustment, but remained robust for CVD death in all sensitivity analyses. In multi-pollutant models, the associations of the three exposures generally remained unaltered. Interestingly, adjustment for ROS did not substantially change the associations between PM2.5 and CVD, but attenuated the associations of NO2.Conclusions: Long-term exposure to Fe and Cu in PM2.5 and their combined impact on ROS were consistently associated with increased CVD death. [ABSTRACT FROM AUTHOR]