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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 (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.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 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.Interpretation: Chronic exposure to air pollution may contribute to severe outcomes after SARS-CoV-2 infection, particularly exposure to O3. [ABSTRACT FROM AUTHOR]

Several epidemiological studies have investigated the possible role that living in areas with greater amounts of greenspace has on the incidence of childhood asthma. These findings have been inconsistent, and few studies explored the relevance of timing of exposure. We investigated the role of residential surrounding greenness on the risk of incident asthma using a population-based retrospective cohort study. We included 982,131 singleton births in Ontario, Canada between 2006 and 2013. Two measures of greenness, the Normalized Difference Vegetation Index (NDVI) and the Green View Index (GVI), were assigned to the residential histories of these infants from pregnancy through to 12 years of age. Longitudinally-based diagnoses of asthma were determined by using provincial administrative health data. The extended Cox hazards model was used to characterize associations between greenness measures and asthma (up to age 12 years) while adjusting for several risk factors. In a fully adjusted model, that included a term for traffic-related air pollution (NO 2), we found no association between an interquartile range increase (0.08) of the NDVI during childhood and asthma incidence (HR = 0.99; 95 % CI = 0.99–1.01). In contrast, we found that an 0.08 increase in NDVI during childhood reduced the risk of asthma in children 7–12 years of age by 14 % (HR = 0.86, 95 % CI:0.79–0.95). Seasonal differences in the association between greenness and asthma were noted. Our findings suggest that residential proximity to greenness reduces the risk of asthma in children aged 7–12. • In a cohort of nearly one million infants, we investigated links between residential greenness and asthma. • Greenness exposure during childhood was associated with a lower risks asthma among children 7–12 years of age. • The association between greenness and incidence was modified by season of birth. [ABSTRACT FROM AUTHOR]

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 (PM2.5), nitrogen dioxide (NO2), ozone (O3), and the redox-weighted average of NO2 and O3 (Ox) 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 PM2.5 per interquartile-range (IQR) increase of 3.4 μg/m3 (hazard ratio, 1.07; 95% confidence interval, 1.06-1.08), NO2 per IQR increase of 13.9 ppb (1.04; 1.02-1.05), O3 per IQR increase of 6.3 ppb (1.04; 1.03-1.04), and Ox 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 PM2.5, NO2, O3, and Ox, 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. [ABSTRACT FROM AUTHOR]

Lung and female breast cancers are highly prevalent worldwide. Although the association between exposure to ambient fine particulate matter (PM2.5) and lung cancer has been recognized, there is less evidence for associations with other common air pollutants such as nitrogen dioxide (NO2) and ozone (O3). 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 PM2.5, NO2, O3 and redox‐weighted average of NO2 and O3 (Ox) 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 PM2.5 (hazard ratio [HR] = 1.02 [95% CI: 1.01–1.05] per 5.3 μg/m3) and NO2 (HR = 1.05 [95% CI: 1.03–1.07] per 14 ppb). No associations with lung cancer were observed for O3 or Ox. Relationships between PM2.5 and NO2 with lung cancer exhibited a sublinear shape. We did not find compelling evidence linking air pollution to breast cancer. What's new? Although exposure to ambient fine particulate matter has been associated with lung cancer, there is less evidence for associations with other common air pollutants such as NO2 and O3. Even less is known about potential associations between these pollutants and breast cancer. In this large population‐based cohort study in Ontario, Canada, exposures to PM2.5 and NO2 but not O3 were associated with increased lung cancer incidence. Using a newly developed class of concentration‐response models, the authors observed sublinear relationships of PM2.5 and NO2 with lung cancer. No strong evidence of a relationship between air pollutants and breast cancer was observed. [ABSTRACT FROM AUTHOR]

Objective: To assess the associations between ambient temperatures and hospitalisations for coronary heart disease (CHD) and stroke.Methods: Our study comprised all residents living in Ontario, Canada, 1996-2013. For each of 14 health regions, we fitted a distributed lag non-linear model to estimate the cold and heat effects on hospitalisations from CHD, acute myocardial infarction (AMI), stroke and ischaemic stroke, respectively. These effects were pooled using a multivariate meta-analysis. We computed attributable hospitalisations for cold and heat, defined as temperatures above and below the optimum temperature (corresponding to the temperature of minimum morbidity) and for moderate and extreme temperatures, defined using cut-offs at the 2.5th and 97.5th temperature percentiles.Results: Between 1996 and 2013, we identified 1.4 million hospitalisations from CHD and 355 837 from stroke across Ontario. On cold days with temperature corresponding to the 1st percentile of temperature distribution, we found a 9% increase in daily hospitalisations for CHD (95% CI 1% to 16%), 29% increase for AMI (95% CI 15% to 45%) and 11% increase for stroke (95% CI 1% to 22%) relative to days with an optimal temperature. High temperatures (the 99th percentile) also increased CHD hospitalisations by 6% (95% CI 1% to 11%) relative to the optimal temperature. These estimates translate into 2.49% of CHD hospitalisations attributable to cold and 1.20% from heat. Additionally, 1.71% of stroke hospitalisations were attributable to cold. Importantly, moderate temperatures, rather than extreme temperatures, yielded the most of the cardiovascular burdens from temperatures.Conclusions: Ambient temperatures, especially in moderate ranges, may be an important risk factor for cardiovascular-related hospitalisations. [ABSTRACT FROM AUTHOR]

Background: Daily changes in aeroallergens during pregnancy could trigger early labor, but few investigations have evaluated this issue. This study aimed to investigate the association between exposure to aeroallergens during the week preceding birth and the risk of early delivery among preterm and term pregnancies.Methods: We identified data on 225,234 singleton births that occurred in six large cities in the province of Ontario, Canada, from 2004 to 2011 (April to October) from a birth registry. We obtained daily counts of pollen grains and fungal spores from fixed-site monitoring stations in each city and assigned them to pregnancy period of each birth. Associations between exposure to aeroallergens in the preceding week and risk of delivery among preterm (<37 gestational weeks), early-term (37-38 weeks), and full-term (≥39 weeks) pregnancies were evaluated with Cox regression models, adjusting for maternal characteristics, meteorologic parameters, and air pollution concentrations, and pooled across the six cities.Results: The risk of delivery increased by 3% per interquartile range width (IQRw = 22.1 grains/m) increase in weed pollen the day before birth among early-term (hazard ratio [HR] = 1.03; 95% confidence interval [CI]: 1.01, 1.05) and full-term pregnancies (HR = 1.03; 95% CI: 1.01, 1.04). Exposure to fungal spores cumulated over 0 to 2 lagged days was associated with increased risk of delivery among full-term pregnancies only (HR = 1.07; 95% CI: 1.01, 1.12). We observed no associations among preterm deliveries.Conclusions: Increasing concentrations of ambient weed pollen and fungal spores may be associated with earlier delivery among term births. [ABSTRACT FROM AUTHOR]

Ambient extreme temperatures have been associated with mental and behavior disorders (MBDs). However, few studies have assesed whether vulnerability factors such as ambient air pollution, pre-existing mental health conditions and residential environmental factors increase susceptibility. This study aims to evaluate the associations between short-term variations in outdoor ambient extreme temperatures and MBD-related emergency department (ED) visits and how these associations are modified by vulnerability factors. We conducted a case-crossover study of 9,958,759 MBD ED visits in Alberta and Ontario, Canada made between March 1st, 2004 and December 31st, 2020. Daily average temperature was assigned to individual cases with ED visits for MBD using gridded data at a 1 km × 1 km spatial resolution. Conditional logistic regression was used to estimate associations between extreme temperatures (i.e., risk of ED visit at the 2.5th percentile temperature for cold and 97.5th percentile temperature for heat for each health region compared to the minimal temperature risk) and MBD ED visits. Age, sex, pre-existing mental health conditions, ambient air pollution (i.e. PM 2.5 , NO 2 and O 3) and residential environmental factors (neighborhood deprivation, residential green space exposure and urbanization) were evaluated as potential effect modifiers. Cumulative exposure to extreme heat over 0–5 days (odds ratio [OR] = 1.145; 95% CI: 1.121–1.171) was associated with ED visits for any MBD. However, cumulative exposure to extreme cold was associated with lower risk of ED visits for any MBD (OR = 0.981; 95% CI: 0.976–0.987). We also found heat to be associated with ED visits for specific MBDs such as substance use disorders, dementia, neurotic disorders, schizophrenia and personality behavior disorder. Individuals with pre-existing mental health conditions, those exposed to higher daily concentrations of NO 2 and O 3 and those residing in neighborhoods with greater material and social deprivation were at higher risk of heat-related MBD ED visits. Increasing tree canopy coverage appeared to mitigate risks of the effect of heat on MBD ED visits. Findings provide evidence that the impacts of heat on MBD ED visits may vary across different vulnerability factors. • Extreme heat associations with mental and behavior disorder. • Higher risk with daily concentrations of NO2 and O3. • Greater risk in neighborhoods with highest material and social deprivation. • Extreme heat may exacerbate pre-existing mental health conditions. • Tree canopy coverage may be beneficial in mitigating the effect of extreme heat. [ABSTRACT FROM AUTHOR]

Rationale: Fine particulate air pollution (PM2.5; particulate matter 2.5 μm or less in diameter) is thought to contribute to acute respiratory morbidity in part through oxidative stress.Objectives: To examine the association between PM2.5 oxidative burden and emergency room visits for respiratory illnesses.Methods: We conducted a case-crossover study in Ontario, Canada between 2004 and 2011, including 127,836 cases of asthma, 298,751 cases of chronic obstructive pulmonary disease, and more than 1.1 million cases of all respiratory illnesses. Daily air pollution data were collected from ground monitors, and city-level PM2.5 oxidative potential was measured on the basis of a synthetic respiratory tract lining fluid containing the antioxidants glutathione and ascorbate. Conditional logistic regression was used to estimate associations between air pollution concentrations and emergency room visits, adjusting for time-varying covariates.Measurements and Main Results: Three-day mean PM2.5 concentrations were consistently associated with emergency room visits for all respiratory illnesses. Among children (<9 yr), each interquartile change (5.92 μg/m(3)) in 3-day mean PM2.5 was associated with a 7.2% (95% confidence interval, 4.2-10) increased risk of emergency room visits for asthma. Glutathione-related oxidative potential modified the impact of PM2.5 on emergency room visits for respiratory illnesses (P = 0.001) but only at low concentrations (≤10 μg/m(3)). Between-city differences in ascorbate-related oxidative potential did not modify the impact of PM2.5 on respiratory outcomes.Conclusions: Between-city differences in glutathione-related oxidative potential may modify the impact of PM2.5 on acute respiratory illnesses at low PM2.5 concentrations. This may explain in part how small changes in ambient PM2.5 mass concentrations can contribute to acute respiratory morbidity in low-pollution environments. [ABSTRACT FROM AUTHOR]

Few studies have examined the acute cardiovascular effects of airborne allergens. We conducted a case-crossover study to evaluate the relationship between airborne allergen concentrations and emergency room visits for myocardial infarction (MI) in Ontario, Canada. In total, 17,960 cases of MI were identified between the months of April and October during the years 2004-2011. Daily mean aeroallergen concentrations (pollen and mold spores) were assigned to case and control periods using central-site monitors in each city along with daily measurements of meteorological data and air pollution (nitrogen dioxide and ozone). Odds ratios and their 95% confidence intervals were estimated using conditional logistic regression models adjusting for time-varying covariates. Risk of MI was 5.5% higher (95% confidence interval (CI): 3.4,7.6) on days in the highest tertile of total pollen concentrations compared with days in the lowest tertile, and a significant concentration-response trend was observed (P< 0.001). Higher MI risk was limited to same-day pollen concentrations, with the largest risks being observed during May (odds ratio =1.16, 95% CI: 1.00,1.35) and June (odds ratio =1.10, 95% CI: 1.00,1.22), when tree and grass pollen are most common. Mold spore concentrations were not associated with MI. Our findings suggest that airborne pollen might represent a previously unidentified environmental risk factor for myocardial infarction. [ABSTRACT FROM AUTHOR]

It is unknown whether urban green space is associated with reduced risk of major neurological conditions, especially dementia and stroke. 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. 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. 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. • Residential green space was associated with reduced incidence of dementia and stroke. • Reductions in risk for dementia and stroke were 3% and 4%, respectively, per 0.12 increase in NDVI exposure. • Estimates were generally robust to sensitivity and stratified analyses considered. • Results suggests that green space may be a protective factor against both outcomes. [ABSTRACT FROM AUTHOR]

• High-income nations have the highest rates of inflammatory bowel disease. • Exposure to O x during childhood was associated with IBD < 18 years. • Ambient air pollution is suspected to be associated with risk of IBD. High-income nations have the highest rates of inflammatory bowel disease (IBD). The incidence of pediatric-onset IBD is increasing faster than IBD diagnosed in older individuals. Previous epidemiological studies have shown that air pollution might be a risk factor for development of earlier-onset IBD, but results remain mixed. The objective of this study was to evaluate the associations between maternal and early-life exposures to nitrogen dioxide (NO 2), fine particulate matter (PM 2.5), ozone (O 3 ,) and oxidant capacity (O x) and risk of pediatric-onset IBD diagnosis. We conducted a retrospective cohort study using linked population-based health administrative data. Singleton livebirths in Ontario, Canada between April 1st, 1991 and March 31st, 2014 were included. We investigated the association between weekly exposures during pregnancy and annual exposures from birth until the age of 18 years, and IBD diagnosed <18 years of age using Cox proportional hazards models. We reported hazard ratios (HR) and 95% confidence intervals (CI) for an associated increase in the interquartile range (IQR) of each pollutant. Models were mutually adjusted for exposures in both prenatal and postnatal periods, as well as for sex, rurality of residence at birth, maternal IBD, and neighborhood income. 2,218,789 newborns were included in this study, of whom 2491 developed IBD during follow-up. Increased associations with pediatric-onset IBD were noted for childhood exposure to O x (HR 1.08, 95% CI 1.01–1.16). IBD development was also associated with O x during the second trimester (HR 1.21, 95% CI 1.03–1.42), but not the overall pregnancy period (HR 1.12, 95% CI 0.79–1.59). There were no associations of IBD with exposure to NO 2 , PM 2.5 , or O 3. Exposure to O x during childhood was associated with IBD < 18 years. This suggests that air pollution may impact the developing child physiology in such a way that leads to early onset of IBD. [ABSTRACT FROM AUTHOR]

• Air pollution was associated with the incidence of diabetes, in particular NO 2. • Air pollution was also associated with cardiovascular and diabetes mortality among persons with prevalent diabetes. • The strongest associations were observed between NO 2 and diabetes mortality. • Results may suggest that traffic-related pollution has the greatest effect on outcomes of diabetes. 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. 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. 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). 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. [ABSTRACT FROM AUTHOR]

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). • PM 2.5 , NO 2 , O 3 , and O x were associated to increased congestive heart failure incidence. • Exposure to PM 2.5 , O 3 , and O x was associated with acute myocardial infarction (AMI). • A near-linear concentration-response relationship was found for PM 2.5 and AMI. • Non-linear patterns were observed for other pollutant and outcome combinations. • There was some evidence of effect modification by age and income. [ABSTRACT FROM AUTHOR]

Importance: Air pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated., Objective: To evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada., Design, Setting, and Participants: Population-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022., Exposures: Weekly average concentrations of ambient fine particulate matter with a diameter 2.5 μm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data., Main Outcome and Measures: CP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years., Results: The present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 μg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk., Conclusions and Relevance: In this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.

Background: Ambient air pollution is thought to contribute to increased risk of COVID-19, but the evidence is controversial., Objective: To evaluate the associations between short-term variations in outdoor concentrations of ambient air pollution and COVID-19 emergency department (ED) visits., Methods: We conducted a case-crossover study of 78 255 COVID-19 ED visits in Alberta and Ontario, Canada between 1 March 2020 and 31 March 2021. Daily air pollution data (ie, fine particulate matter with diameter less than 2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ) and ozone were assigned to individual case of COVID-19 in 10 km × 10 km grid resolution. Conditional logistic regression was used to estimate associations between air pollution and ED visits for COVID-19., Results: Cumulative ambient exposure over 0-3 days to PM2.5 (OR 1.010; 95% CI 1.004 to 1.015, per 6.2 µg/m 3 ) and NO 2 (OR 1.021; 95% CI 1.015 to 1.028, per 7.7 ppb) concentrations were associated with ED visits for COVID-19. We found that the association between PM 2.5 and COVID-19 ED visits was stronger among those hospitalised following an ED visit, as a measure of disease severity, (OR 1.023; 95% CI 1.015 to 1.031) compared with those not hospitalised (OR 0.992; 95% CI 0.980 to 1.004) (p value for effect modification=0.04)., Conclusions: We found associations between short-term exposure to ambient air pollutants and COVID-19 ED visits. Exposure to air pollution may also lead to more severe COVID-19 disease., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY. Published by BMJ.)

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.)

Introduction: Environmental factors related to urbanization and industrialization are believed to be involved in inflammatory bowel disease (IBD) development, but no study has looked at the association between greenspace and IBD., Methods: We conducted a retrospective cohort study using linked population-based health administrative and environmental data sets. The study population comprised 2,715,318 mother-infant pairs from hospital births in Ontario, Canada, between April 1, 1991, and March 31, 2014. We measured the exposure to residential greenspace using the normalized difference vegetation index derived using remote-sensing methods. Average greenspace was estimated for the pregnancy and childhood periods. We used mixed-effects Cox proportional hazard models to assess potential associations between residential greenspace and the risk of developing IBD before 18 years while adjusting for covariates including sex, maternal IBD, rural/urban residence at birth, and neighborhood income., Results: There were 3,444 IBD diagnoses that occurred during follow-up. An increase in the interquartile range of residential greenspace during the childhood period was associated with a lower risk of developing pediatric-onset IBD (hazard ratio [HR] 0.77, 95% confidence interval [CI] 0.74-0.81). This relationship was significant for both ulcerative colitis (HR 0.72 95% CI 0.67-0.78) and Crohn's disease (HR 0.81, 95% CI 0.76-0.87). There was a linear dose response across increasing quartiles of greenspace (P < 0.0001). No consistent association was detected between maternal intrapartum greenspace exposure and pediatric-onset IBD., Discussion: Higher exposure to residential greenspace during childhood was associated with a reduced risk of IBD, suggesting a novel avenue to prevent IBD in children., (Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)

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.

Past health impact assessments of ambient fine particulate matter (particles with an aerodynamic diameter ≤2.5 μm; PM 2.5 ) have generally considered mass concentration only, despite PM 2.5 being a heterogeneous mixture. Given constant changes in the concentration and the composition of atmospheric aerosol, uncertainty exists as to whether the current focus on PM 2.5 mass or individual components may fully characterize the health burden of PM 2.5 . We proposed a component-adjusted method that jointly estimates the health impacts of PM 2.5 and its major components while allowing for a potential nonlinear PM 2.5 -outcome relationship. Using this method, we quantified the effects of PM 2.5 on the risks of developing acute myocardial infarction (AMI) and dying from cardiovascular causes in comparison to three traditional approaches in the entire adult population across Ontario, Canada. We observed that PM 2.5 was positively associated with AMI incidence and cardiovascular mortality with all four methods. Compared to the traditional approaches, however, the new component-adjusted approach demonstrated a significant improvement in explaining the health impacts of PM 2.5 , especially in the presence of a nonlinear PM 2.5 -outcome relationship. Using the new approach, we found that the effects of PM 2.5 on AMI incidence and cardiovascular mortality may be 10% to 27% higher than what would be estimated from the conventional approaches examining PM 2.5 alone.

The purpose of this study was to examine the spatial variability of asthma outcomes in Ontario, Canada and broad environmental factors that contribute to this variability. Age-/sex-standardized asthma prevalence and health services use rates (2003-2013) were obtained from a provincial cohort of asthma patients. Employing an ecological-level study design, descriptive and Bayesian spatial regression analyses were used to examine patterns of asthma outcomes and their relationship to physical environment, socioeconomic environment and healthcare factors. Significant spatial variation in asthma outcomes was found between southern urban/suburban areas and northern/rural areas. Rurality was found to have a substantial effect on all asthma outcomes, except hospitalizations. For example, the most rural areas were associated with lower asthma prevalence and physician visits [RR = 0.708, 95% credible interval (CI): 0.636-0.795 and RR = 0.630, 95% CI: 0.504-0.758, respectively], and with higher ED visits (RR = 1.818, 95% CI: 1.194-2.858), when compared to urban areas. Strong associations were also found between material deprivation and ED visits (RR = 1.559, 95% CI: 1.358-1.737) and hospitalizations (RR = 1.259, 95% CI: 1.143-1.374). Associations between asthma outcomes and environmental variables such as air pollution and temperature were also found. Findings can be expected to inform the development of improved public health strategies, which take into account local environmental, socioeconomic and healthcare characteristics., Competing Interests: The authors have declared that no competing interests exist.

Objective: To assess the associations between ambient temperatures and hospitalisations for coronary heart disease (CHD) and stroke., Methods: Our study comprised all residents living in Ontario, Canada, 1996-2013. For each of 14 health regions, we fitted a distributed lag non-linear model to estimate the cold and heat effects on hospitalisations from CHD, acute myocardial infarction (AMI), stroke and ischaemic stroke, respectively. These effects were pooled using a multivariate meta-analysis. We computed attributable hospitalisations for cold and heat, defined as temperatures above and below the optimum temperature (corresponding to the temperature of minimum morbidity) and for moderate and extreme temperatures, defined using cut-offs at the 2.5 th and 97.5 th temperature percentiles., Results: Between 1996 and 2013, we identified 1.4 million hospitalisations from CHD and 355 837 from stroke across Ontario. On cold days with temperature corresponding to the 1 st percentile of temperature distribution, we found a 9% increase in daily hospitalisations for CHD (95% CI 1% to 16%), 29% increase for AMI (95% CI 15% to 45%) and 11% increase for stroke (95% CI 1% to 22%) relative to days with an optimal temperature. High temperatures (the 99 th percentile) also increased CHD hospitalisations by 6% (95% CI 1% to 11%) relative to the optimal temperature. These estimates translate into 2.49% of CHD hospitalisations attributable to cold and 1.20% from heat. Additionally, 1.71% of stroke hospitalisations were attributable to cold. Importantly, moderate temperatures, rather than extreme temperatures, yielded the most of the cardiovascular burdens from temperatures., Conclusions: Ambient temperatures, especially in moderate ranges, may be an important risk factor for cardiovascular-related hospitalisations., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

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.)

The Geospatial Determinants of Health Outcomes Consortium (GeoDHOC) study investigated ambient air quality across the international border between Detroit, Michigan, USA and Windsor, Ontario, Canada and its association with acute asthma events in 5- to 89-year-old residents of these cities. NO2, SO2, and volatile organic compounds (VOCs) were measured at 100 sites, and particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs) at 50 sites during two 2-week sampling periods in 2008 and 2009. Acute asthma event rates across neighborhoods in each city were calculated using emergency room visits and hospitalizations and standardized to the overall age and gender distribution of the population in the two cities combined. Results demonstrate that intra-urban air quality variations are related to adverse respiratory events in both cities. Annual 2008 asthma rates exhibited statistically significant positive correlations with total VOCs and total benzene, toluene, ethylbenzene and xylene (BTEX) at 5-digit zip code scale spatial resolution in Detroit. In Windsor, NO2, VOCs, and PM10 concentrations correlated positively with 2008 asthma rates at a similar 3-digit postal forward sortation area scale. The study is limited by its coarse temporal resolution (comparing relatively short term air quality measurements to annual asthma health data) and interpretation of findings is complicated by contrasts in population demographics and health-care delivery systems in Detroit and Windsor.

Background: Extreme ambient temperatures are an increasing public health concern. The aim of this study was to assess if persons with comorbid health conditions were at increased risk of adverse cardiorespiratory morbidity during temperature extremes., Methods: A time series study design was applied to 292,666 and 562,738 emergency room (ER) visits for cardiovascular and respiratory diseases, respectively, that occurred in Toronto area hospitals between April 1st 2002 and March 31st 2010. Subgroups of persons with comorbid health conditions were identified. Relative risks (RRs) and their corresponding 95% confidence intervals (CIs) were estimated using a Poisson regression model with distributed lag non-linear model, and were adjusted for the confounding influence of seasonality, relative humidity, day-of-the-week, outdoor air pollutants and daily influenza ER visits. Effect modification by comorbid health conditions was tested using the relative effect modification (REM) index., Results: Stronger associations of cardiovascular disease ER visits were observed for persons with diabetes compared to persons without diabetes (REM = 1.12; 95% CI: 1.01 - 1.27) with exposure to the cumulative short term effect of extreme hot temperatures (i.e. 99th percentile of temperature distribution vs. 75th percentile). Effect modification was also found for comorbid respiratory disease (REM = 1.17; 95% CI: 1.02 - 1.44) and cancer (REM = 1.20; 95% CI: 1.02 - 1.49) on respiratory disease ER visits during short term hot temperature episodes. The effect of extreme cold temperatures (i.e. 1st percentile of temperature distribution vs. 25th percentile) on cardiovascular disease ER visits were stronger for individuals with comorbid cardiac diseases (REM = 1.47; 95% CI: 1.06 - 2.23) and kidney diseases (REM = 2.43; 95% CI: 1.59 - 8.83) compared to those without these conditions when cumulated over a two-week period., Conclusions: The identification of those most susceptible to temperature extremes is important for public health officials to implement adaptation measures to manage the impact of extreme temperatures on population health.