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Background: The 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., Methods: We 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 (PM 2.5 ), nitrogen dioxide (NO 2 ) and ground-level ozone (O 3 ), 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., Results: Among 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 PM 2.5 (1.70 μg/m 3 ), 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 NO 2 . 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 O 3 for hospital admission, ICU admission and death, respectively., Interpretation: Chronic exposure to air pollution may contribute to severe outcomes after SARS-CoV-2 infection, particularly exposure to O 3 ., Competing Interests: Competing interests: Jeff Kwong is supported by a Clinician Scientist Award from the Department of Family and Community Medicine, University of Toronto. Chen Chen reports receiving salary support by the funding of this project, from Health Canada. Megan Kirby-Mcgregor reports receiving doctoral student funding from Health Canada, paid through McGill University. Jay Kaufman reports receiving payments from Health Canada (paid to institution) for student salaries and other research expenses associated with this work. Hong Chen reports receiving support for the present manuscript from Health Canada. No other competing interests were declared., (© 2022 CMA Impact Inc. or its licensors.)

Background: Air pollution has been associated with increased mortality. However, updated evidence from cohort studies with detailed information on various risk factors is needed, especially in regions with low air pollution levels. We investigated the associations between long-term exposure to air pollution and mortality in a prospective cohort., Methods: We studied 88,615 participants aged ≥30 years from an ongoing cohort study in Ontario, Canada from 2009 to 2017. Exposure to ambient fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) was estimated at participants' residence. Cox proportional hazard models were used to investigate the associations between air pollution and non-accidental, cardiovascular, and respiratory mortality, adjusted for a wide array of individual-level and contextual covariates. Potential effect modification by socio-demographic and behavioral factors was also examined in exploratory stratified analyses., Results: The fully adjusted hazard ratios (HRs) per 1 µg/m 3 increment in PM 2.5 were 1.037 [95% confidence interval (CI): 1.018, 1.057]¸ 1.083 (95% CI: 1.040, 1.128) and 1.109 (95% CI: 1.035, 1.187) for non-accidental, cardiovascular, and respiratory mortality, respectively. Positive associations were also found for NO 2 ; the corresponding HRs per 1 ppb increment were 1.027 (95% CI: 1.021, 1.034), 1.032 (95% CI: 1.019, 1.046) and 1.044 (95% CI: 1.020, 1.068). We found suggestive evidence of stronger associations in physically active participants, smokers, and those with lower household income., Conclusions: Long-term exposure to PM 2.5 and NO 2 was associated with increased risks for non-accidental, cardiovascular, and respiratory mortality, suggesting potential benefits of further improvement in air quality even in low-exposure environments., (Copyright © 2021. Published by Elsevier Ltd.)

Owing to their greater outdoor activity and ongoing lung development, children are particularly vulnerable to the harmful effects of exposure to fine particulate matter (PM 2.5 ) . However, the effects of PM 2.5 components are poorly understood. This study aimed to use a longitudinal birth cohort of children with physician-diagnosed incident asthma to investigate the effect of PM 2.5 components at birth on morbidity measured by health services utilization. Of 1277 Toronto Child Health Evaluation Questionnaire (T-CHEQ) participants, the study population included 362 children diagnosed with asthma who were followed for a mean of 13 years from birth until March 31, 2016, or loss-to-follow-up. Concentrations of PM 2.5 and its components were assigned based on participants' postal codes at birth. Study outcomes included counts of asthma, asthma-related, and all-cause health services use. Poisson regression in single-, two-, and multi-pollutant models was used to estimate rate ratios (RR) per interquartile range (IQR) increase of exposures. Covariates were included in all models to further adjust for potential confounding. The adjusted RR for sulfate (SO 4 ) and all-cause hospitalizations was statistically significant with RR = 2.23 (95% confidence interval [CI]: 1.25-3.96) in a multi-pollutant model with nitrogen dioxide (NO 2 ) and ozone (O 3 ). In multi-pollutant models with oxidants, the adjusted RRs for SO 4 of all-cause hospitalizations and emergency department (ED) visits were also statistically significant with RR = 2.31 (95% CI: 1.32-4.03) and RR = 1.39 (95% CI: 1.02-1.90), respectively. While unadjusted single-pollutant RRs for asthma-specific and asthma-related health services use with the SO 4 component of PM 2.5 were above one, none were statistically significant. This study found significant associations with exposure to SO 4 in PM 2.5 and all-cause acute care, chiefly for hospitalizations, in children with asthma., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)

Rationale: Current evidence on the relationship between long-term exposure to air pollution and new onset of chronic lung disease is inconclusive. Objectives: To examine associations of incident chronic obstructive pulmonary disease (COPD) and adult-onset asthma with past exposure to fine particulate matter ≤ 2.5 μm in diameter (PM 2.5 ), nitrogen dioxide (NO 2 ), ozone (O 3 ), and the redox-weighted average of NO 2 and O 3 (O x ) and characterize the concentration-response relationship. Methods: We conducted a population-based cohort study of all Ontarians, aged 35-85 years, from 2001 to 2015. A 3-year moving average of residential exposures to selected pollutants with a 1-year lag were estimated during follow-up. We used Cox proportional hazard models and Aalen additive-hazard models to quantify the pollution-disease associations and characterized the shape of these relationships using newly developed nonlinear risk models. Measurements and Main Results: Among 5.1 million adults, we identified 340,733 and 218,005 incident cases of COPD and asthma, respectively. We found positive associations of COPD with PM 2.5 per interquartile-range (IQR) increase of 3.4 μg/m 3 (hazard ratio, 1.07; 95% confidence interval, 1.06-1.08), NO 2 per IQR increase of 13.9 ppb (1.04; 1.02-1.05), O 3 per IQR increase of 6.3 ppb (1.04; 1.03-1.04), and O x per IQR increase of 4.4 ppb (1.03; 1.03-1.03). By contrast, we did not find strong evidence linking these pollutants to adult-onset asthma. In addition, we quantified that each IQR increase in pollution exposure yielded 3.0 (2.4-3.6), 3.2 (2.0-4.3), 1.9 (1.3-2.5), and 2.3 (1.7-2.9) excess cases of COPD per 100,000 adults for PM 2.5 , NO 2 , O 3 , and O x , respectively. Furthermore, most pollutant-COPD relationships exhibited supralinear shapes. Conclusions: Air pollution was associated with a higher incidence of COPD but was not associated with a higher incidence of adult-onset asthma.

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: A growing number of epidemiological studies have linked air pollution exposure to psychological conditions. Laboratory studies indicate that air pollutants can activate the neuroendocrine stress axis and modulate stress hormone levels, which could contribute to the development or exacerbation of psychological distress. The present study examined the spatial associations between air pollutants (fine particulate matter [PM 2.5 ], nitrogen dioxide [NO 2 ] and ground-level ozone [O 3 ]) and psychological distress among subjects in the most populous provinces in Canada., Data and Methods: Subjects were sampled from the Canadian Community Health Survey in three regions (Quebec in 2005 [n=25,800], British Columbia and Alberta in 2005 [n=23,000], and Ontario in 2011 [n=36,000]), and were assigned estimates of annual exposure to three ambient air pollutants (PM 2.5 , NO 2 and O 3 ) for the same years. Individual psychological distress was assessed using the Kessler Psychological Distress Scale (K10), based on anxiety and depressive symptoms in the past month. Regression models (both ordinary least squares and simultaneous autoregressive models) were applied to estimate associations between K10 distress scores and each air pollutant, after adjusting for individual (demographic, socioeconomic and behavioural) and neighbourhood covariates.., Results: Psychological distress was positively associated with PM 2.5 and NO 2 in all three regions, and with O 3 in Quebec. However, after further adjusting for individual and neighbourhood covariates, the associations between distress and air pollution remained statistically significant only in Quebec., Discussion: Some evidence for positive associations between psychological distress and ambient air pollution after adjusting for spatial autocorrelation was found.

Introduction: It is unknown whether urban green space is associated with reduced risk of major neurological conditions, especially dementia and stroke., Methods: Retrospective, population-based cohorts were created for each study outcome, including 1.7 and 4.3 million adults in Ontario, Canada for dementia and stroke, respectively. Residential green space was quantified using the satellite-derived Normalized Difference Vegetation Index. Incidence was ascertained using health administrative data with validated algorithms. Mixed-effects Cox models were used to estimate hazard ratios per interquartile range increase in green space exposure., Results: Between 2001 and 2013, 219,013 individuals were diagnosed with dementia and 89,958 had a stroke. The hazard ratio per interquartile range increase in green space was 0.97 (95% CI: 0.96-0.98) for dementia and 0.96 (0.95-0.98) for stroke. Estimates remained generally consistent in sensitivity analyses., Discussion: Increased exposure to urban green space was associated with reduced incidence of dementia and stroke. To our knowledge, this is the first population-based cohort study to assess these relationships., Competing Interests: Declaration of competing interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

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: Studies have reported increasing incidence rates of paediatric diabetes, especially among those aged 0-5 years. Epidemiological evidence linking ambient air pollution to paediatric diabetes remains mixed., Objective: This study investigated the association between maternal and early-life exposures to common air pollutants (NO 2 , PM 2.5 , O 3 , and oxidant capacity [Ox; the redox-weighted average of O 3 and NO 2 ]) and the incidence of paediatric diabetes in children up to 6 years of age., Methods: All registered singleton births in Ontario, Ca nada occurring between April 1st , 2006 and March 31st , 2012 were included through linkage from health administrative data. Monthly exposures to NO 2 , PM 2.5 , O 3 , and O x were estimated across trimesters, the entire pregnancy period and during childhood. Random effects Cox proportional hazards models were used to assess the relationships with paediatric diabetes incidence while controlling for important covariates. We also modelled the shape of concentration-response (CR) relationships., Results: There were 1094 children out of a cohort of 754,698 diagnosed with diabetes before the age of six. O 3 exposures during the first trimester of pregnancy were associated with paediatric diabetes incidence (hazard ratio (HR) per interquartile (IQR) increase = 2.00, 95% CI: 1.04-3.86). The CR relationship between O 3 during the first trimester and paediatric diabetes incidence appeared to have a risk threshold, in which there was little-to-no risk below 25 ppb of O 3 , while above this level risk increased sigmoidally. No other associations were observed., Conclusion: O 3 exposures during a critical period of development were associated with an increased risk of paediatric diabetes incidence., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Crown Copyright © 2020. Published by Elsevier Inc. All rights reserved.)

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.)

Background: Living in unwalkable neighborhoods has been associated with heightened risk for diabetes and hypertension. However, highly walkable environments may have higher concentrations of traffic-related air pollution, which may contribute to increased cardiovascular disease risk. We therefore aimed to assess how walkability and traffic-related air pollution jointly affect risk for hypertension and diabetes., Methods: We used a cross-sectional, population-based sample of individuals aged 40-74 years residing in selected large urban centres in Ontario, Canada on January 1, 2008, assembled from administrative databases. Walkability and traffic-related air pollution (NO 2 ) were assessed using validated tools and linked to individuals based on neighborhood of residence. Logistic regression was used to estimate adjusted associations between exposures and diagnoses of hypertension or diabetes accounting for potential confounders., Results: Overall, 2,496,458 individuals were included in our analyses. Low walkability was associated with higher odds of hypertension (lowest vs. highest quintile OR = 1.34, 95% CI: 1.32, 1.37) and diabetes (lowest vs. highest quintile OR = 1.25, 95% CI: 1.22, 1.29), while NO 2 exhibited similar trends (hypertension: OR = 1.09 per 10 p.p.b., 95% CI: 1.08, 1.10; diabetes: OR = 1.16, 95% CI: 1.14, 1.17). Significant interactions were identified between walkability and NO 2 on risk for hypertension (p < 0.0001 and diabetes (p < 0.0001). At higher levels of pollution (40 p.p.b.), differences in the probability of hypertension (lowest vs. highest walkability quintile: 0.26 vs. 0.25) or diabetes (lowest vs. highest walkability quintile: 0.15 vs. 0.15) between highly walkable and unwalkable neighborhoods were diminished, compared to differences observed at lower levels of pollution (5 p.p.b.) (hypertension, lowest vs. highest walkability quintile: 0.21 vs. 0.13; diabetes, lowest vs. highest walkability quintile: 0.09 vs. 0.06)., Conclusions: Walkability and traffic-related air pollution interact to jointly predict risk for hypertension and diabetes. Although walkable neighborhoods appear to have beneficial effects, they may accentuate the harmful effects of air pollution on cardiovascular risk factors., (Crown Copyright © 2019. Published by Elsevier Ltd. All rights reserved.)

Long-term exposure to ambient air pollution has been linked to cardiovascular mortality, but the associations with incidence of major cardiovascular diseases are not fully understood, especially at low concentrations. We aimed to investigate the associations between exposure to fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), ozone (O 3 ), redox-weighted average of NO 2 and O 3 (O x ) and incidence of congestive heart failure (CHF) and acute myocardial infarction (AMI). Our study population included all long-term residents aged 35-85 years who lived in Ontario, Canada, from 2001 to 2015 (~5.1 million). Incidence of CHF and AMI were ascertained from validated registries. We assigned estimates of annual concentrations of pollutants to the residential postal codes of subjects for each year during follow-up. We estimated hazard ratios (HRs) and 95% CIs for each pollutant separately using Cox proportional hazards models. We examined the shape of concentration-response associations using shape-constrained health impact functions. From 2001 to 2015, there were 422,625 and 197,628 incident cases of CHF and AMI, respectively. In the fully adjusted analyses, the HRs of CHF corresponding to each interquartile range increase in exposure were 1.05 (95% CI: 1.04-1.05) for PM 2.5 , 1.02 (95% CI: 1.01-1.04) for NO 2 , 1.03 (95% CI: 1.02-1.03) for O 3 , and 1.02 (95% CI: 1.02-1.03) for O x, respectively. Similarly, exposure to PM 2.5 , O 3 , and O x were positively associated with AMI. The concentration-response relationships were different for individual pollutant and outcome combinations (e.g., for PM 2.5 the relationship was supralinear with CHF, and linear with AMI)., (Crown Copyright © 2019. Published by Elsevier Ltd. All rights reserved.)

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: 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.)

Although individuals spend the majority of their time indoors, most epidemiological studies estimate personal air pollution exposures based on outdoor levels. This almost certainly results in exposure misclassification as pollutant infiltration varies between homes. However, it is often not possible to collect detailed measures of infiltration for individual homes in large-scale epidemiological studies and thus there is currently a need to develop models that can be used to predict these values. To address this need, we examined infiltration of fine particulate matter (PM(2.5)) and identified determinants of infiltration for 46 residential homes in Toronto, Canada. Infiltration was estimated using the indoor/outdoor sulphur ratio and information on hypothesized predictors of infiltration were collected using questionnaires and publicly available databases. Multiple linear regression was used to develop the models. Mean infiltration was 0.52 ± 0.21 with no significant difference across heating and non-heating seasons. Predictors of infiltration were air exchange, presence of central air conditioning, and forced air heating. These variables accounted for 38% of the variability in infiltration. Without air exchange, the model accounted for 26% of the variability. Effective modelling of infiltration in individual homes remains difficult, although key variables such as use of central air conditioning show potential as an easily attainable indicator of infiltration.