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BACKGROUND: The effects of the COVID-19 pandemic have been more pronounced for socially disadvantaged populations. We sought to determine how access to SARS-CoV-2 testing and the likelihood of testing positive for COVID-19 were associated with demographic factors, socioeconomic status (SES) and social determinants of health (SDH) in three Canadian provinces. METHODS: An observational population-based cross-sectional study was conducted for the provinces of Ontario, Manitoba and New Brunswick between March 1, 2020 and April 27, 2021, using provincial health administrative data. After excluding residents of long-term care homes, those without current provincial health insurance and those who were tested for COVID-19 out of province, records from provincial healthcare administrative databases were reviewed for 16,900,661 healthcare users. Data was modelled separately for each province in accordance to a prespecified protocol and follow-up consultations among provincial statisticians and collaborators. We employed univariate and multivariate regression models to examine determinants of testing and test results. RESULTS: After adjustment for other variables, female sex and urban residency were positively associated with testing, while female sex was negatively associated with test positivity. In New Brunswick and Ontario, individuals living in higher income areas were more likely to be tested, whereas in Manitoba higher income was negatively associated with both testing and positivity. High ethnocultural composition was associated with lower testing rates. Both high ethnocultural composition and high situational vulnerability increased the odds of testing positive for SARS-CoV-2. DISCUSSION: We observed that multiple demographic, income and SDH factors were associated with SARS-CoV-2 testing and test positivity. Barriers to healthcare access identified in this study specifically relate to COVID-19 testing but may

Emissions of fine particulate matter (PM2.5) from human activities have been linked to substantial disease burdens, but evidence regarding how reducing PM2.5 at its sources would improve public health is sparse. We followed a population-based cohort of 2.7 million adults across Canada from 2007 through 2016. For each participant, we estimated annual mean concentrations of PM2.5 and the fractional contributions to PM2.5 from the five leading anthropogenic sources at their residential address using satellite observations in combination with a global atmospheric chemistry transport model. For each source, we estimated the causal effects of six hypothetical interventions on 10-y nonaccidental mortality risk using the parametric g-formula, a structural causal model. We conducted stratified analyses by age, sex, and income. This cohort would have experienced tangible health gains had contributions to PM2.5 from any of the five sources been reduced. Compared with no intervention, a 10% annual reduction in PM2.5 contributions from transportation and power generation, Canada's largest and fifth-largest anthropogenic sources, would have prevented approximately 175 (95%CI: 123-226) and 90 (95%CI: 63-117) deaths per million by 2016, respectively. A more intensive 50% reduction per year in PM2.5 contributions from the two sources would have averted 360 and 185 deaths per million, respectively, by 2016. The potential health benefits were greater among men, older adults, and low-income earners. In Canada, where PM2.5 levels are among the lowest worldwide, reducing PM2.5 contributions from anthropogenic sources by as little as 10% annually would yield meaningful health gains.

BackgroundLiving 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.ObjectivesWe 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.MethodsWe 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.ResultsEach 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.ConclusionsLiving in urb

Background Exposure to road traffic noise has been linked to cardiometabolic complications, such as elevated blood pressure and glucose dysregulation. However, epidemiologic evidence linking road traffic noise to diabetes mellitus and hypertension remains scarce. We examined associations between road traffic noise and the incidence of diabetes mellitus and hypertension in Toronto, Canada. Methods and Results Using the Ontario Population Health and Environment Cohort, we conducted a retrospective, population-based cohort study of long-term residents of Toronto, aged 35 to 100 years, who were registered for provincial publicly funded health insurance, and were without a history of hypertension (n=701 174) or diabetes mellitus (n=914 607). Road traffic noise exposure levels were assessed by the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day and the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). Noise exposures were assigned to subjects according to their annual residential postal codes during the 15-year follow-up. We used random-effect Cox proportional hazards models adjusting for personal and area-level characteristics. From 2001 to 2015, each interquartile range increase in the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day (10.0 dBA) was associated with an 8% increase in incident diabetes mellitus (95% CI, 1.07-1.09) and a 2% increase in hypertension (95% CI, 1.01-1.03). We obtained similar estimates with the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). These results were robust to all sensitivity analyses conducted, including further adjusting for traffic-related air pollutants (ultrafine particles and nitrogen dioxide). For both hypertension and diabetes mellitus, we observed stronger associations with the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day among women and younger adults

BackgroundEpidemiological evidence for the association between traffic-related noise and the incidence of major cardiovascular events such as acute myocardial infarction (AMI) and congestive heart failure (CHF) is inconclusive, especially in North America.ObjectivesWe evaluated the associations between long-term exposure to road traffic noise and the incidence of AMI and CHF.MethodsOur study population comprised ∼1 million people 30-100 years of age who lived in Toronto, Canada, from 2001 to 2015 and were free of AMI (referred to as the AMI cohort) or CHF (the CHF cohort) at baseline. Outcomes were ascertained from health administrative databases using validated algorithms. Annual average noise levels were estimated as the A-weighted equivalent sound pressure level over the 24-h period (LAeq24) and during nighttime (LAeqNight), respectively, using propagation modeling, and assigned to participants' annual six-digit postal code addresses during follow-up. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) for incident AMI and CHF in relation to LAeq24 and LAeqNight using random-effects Cox proportional hazards models adjusting for individual- and census tract-level covariates, including traffic-related air pollutants [e.g., ultrafine particles (UFPs) and nitrogen dioxide].ResultsDuring follow-up, there were 37,441 AMI incident cases and 95,138 CHF incident cases. Each interquartile range change in LAeq24 was associated with an increased risk of incident AMI (HR=1.07; 95% CI: 1.06, 1.08) and CHF (HR=1.07; 95% CI: 1.06, 1.09). Similarly, LAeqNight was associated with incident AMI (HR=1.07; 95% CI: 1.05, 1.08) and CHF (HR=1.06; 95% CI: 1.05, 1.07). These results were robust to various sensitivity analyses and remained elevated after controlling for long-term exposure to UFPs and nitrogen dioxide. We found near-linear relationships between noise and the incidence of AMI and CHF with no evidence of threshold values.ConclusionIn this large cohort study in

BackgroundLiving 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.ObjectivesWe 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.MethodsWe 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.ResultsEach 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.ConclusionsLiving in urb

BackgroundEpidemiological evidence for the association between traffic-related noise and the incidence of major cardiovascular events such as acute myocardial infarction (AMI) and congestive heart failure (CHF) is inconclusive, especially in North America.ObjectivesWe evaluated the associations between long-term exposure to road traffic noise and the incidence of AMI and CHF.MethodsOur study population comprised ∼1 million people 30-100 years of age who lived in Toronto, Canada, from 2001 to 2015 and were free of AMI (referred to as the AMI cohort) or CHF (the CHF cohort) at baseline. Outcomes were ascertained from health administrative databases using validated algorithms. Annual average noise levels were estimated as the A-weighted equivalent sound pressure level over the 24-h period (LAeq24) and during nighttime (LAeqNight), respectively, using propagation modeling, and assigned to participants' annual six-digit postal code addresses during follow-up. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) for incident AMI and CHF in relation to LAeq24 and LAeqNight using random-effects Cox proportional hazards models adjusting for individual- and census tract-level covariates, including traffic-related air pollutants [e.g., ultrafine particles (UFPs) and nitrogen dioxide].ResultsDuring follow-up, there were 37,441 AMI incident cases and 95,138 CHF incident cases. Each interquartile range change in LAeq24 was associated with an increased risk of incident AMI (HR=1.07; 95% CI: 1.06, 1.08) and CHF (HR=1.07; 95% CI: 1.06, 1.09). Similarly, LAeqNight was associated with incident AMI (HR=1.07; 95% CI: 1.05, 1.08) and CHF (HR=1.06; 95% CI: 1.05, 1.07). These results were robust to various sensitivity analyses and remained elevated after controlling for long-term exposure to UFPs and nitrogen dioxide. We found near-linear relationships between noise and the incidence of AMI and CHF with no evidence of threshold values.ConclusionIn this large cohort study in

Background Exposure to road traffic noise has been linked to cardiometabolic complications, such as elevated blood pressure and glucose dysregulation. However, epidemiologic evidence linking road traffic noise to diabetes mellitus and hypertension remains scarce. We examined associations between road traffic noise and the incidence of diabetes mellitus and hypertension in Toronto, Canada. Methods and Results Using the Ontario Population Health and Environment Cohort, we conducted a retrospective, population-based cohort study of long-term residents of Toronto, aged 35 to 100 years, who were registered for provincial publicly funded health insurance, and were without a history of hypertension (n=701 174) or diabetes mellitus (n=914 607). Road traffic noise exposure levels were assessed by the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day and the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). Noise exposures were assigned to subjects according to their annual residential postal codes during the 15-year follow-up. We used random-effect Cox proportional hazards models adjusting for personal and area-level characteristics. From 2001 to 2015, each interquartile range increase in the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day (10.0 dBA) was associated with an 8% increase in incident diabetes mellitus (95% CI, 1.07-1.09) and a 2% increase in hypertension (95% CI, 1.01-1.03). We obtained similar estimates with the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). These results were robust to all sensitivity analyses conducted, including further adjusting for traffic-related air pollutants (ultrafine particles and nitrogen dioxide). For both hypertension and diabetes mellitus, we observed stronger associations with the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day among women and younger adults

BackgroundEvidence 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.MethodsA 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.ResultsThis 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.ConclusionsThese 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.

Vaccine safety signals require investigation, which may be done rapidly at the population level using ecological studies, before embarking on hypothesis-testing studies. Incidence rates were used to assess a signal of narcolepsy following AS03-adjuvanted monovalent pandemic H1N1 (pH1N1) influenza vaccination among children and adolescents in Sweden and Finland in 2010. We explored the utility of ecological data to assess incidence of narcolepsy following exposure to pandemic H1N1 virus or vaccination in 10 sites that used different vaccines, adjuvants, and had varying vaccine coverage. We calculated incidence rates of diagnosed narcolepsy for periods defined by influenza virus circulation and vaccination campaign dates, and used Poisson regression to estimate incidence rate ratios (IRRs) comparing the periods during which wild-type virus circulated and after the start of vaccination campaigns vs. the period prior to pH1N1 virus circulation. We used electronic health care data from Sweden, Denmark, the United Kingdom, Canada (3 provinces), Taiwan, Netherlands, and Spain (2 regions) from 2003 to 2013. We investigated interactions between age group and adjuvant in European sites and conducted a simulation study to investigate how vaccine coverage, age, and the interval from onset to diagnosis may impact the ability to detect safety signals. Incidence rates of narcolepsy varied by age, continent, and period. Only in Taiwan and Sweden were significant time-period-by-age-group interactions observed. Associations were found for children in Taiwan (following pH1N1 virus circulation) and Sweden (following vaccination). Simulations showed that the individual-level relative risk of narcolepsy was underestimated using ecological methods comparing post- vs. pre-vaccination periods; this effect was attenuated with higher vaccine coverage and a shorter interval from disease onset to diagnosis. Ecological methods can be useful for vaccine safety assessment but the results are influ

BACKGROUND: In 2010, a safety signal was detected for narcolepsy following vaccination with Pandemrix, an AS03-adjuvanted monovalent pandemic H1N1 influenza (pH1N1) vaccine. To further assess a possible association and inform policy on future use of adjuvants, we conducted a multi-country study of narcolepsy and adjuvanted pH1N1 vaccines.METHODS: We used electronic health databases to conduct a dynamic retrospective cohort study to assess narcolepsy incidence rates (IR) before and during pH1N1 virus circulation, and after pH1N1 vaccination campaigns in Canada, Denmark, Spain, Sweden, Taiwan, the Netherlands, and the United Kingdom. Using a case-control study design, we evaluated the risk of narcolepsy following AS03- and MF59-adjuvanted pH1N1 vaccines in Argentina, Canada, Spain, Switzerland, Taiwan, and the Netherlands. In the Netherlands, we also conducted a case-coverage study in children born between 2004 and 2009.RESULTS: No changes in narcolepsy IRs were observed in any periods in single study sites except Sweden and Taiwan; in Taiwan incidence increased after wild-type pH1N1 virus circulation and in Sweden (a previously identified signaling country), incidence increased after the start of pH1N1 vaccination. No association was observed for Arepanrix-AS03 or Focetria-MF59 adjuvanted pH1N1 vaccines and narcolepsy in children or adults in the case-control study nor for children born between 2004 and 2009 in the Netherlands case-coverage study for Pandemrix-AS03.CONCLUSIONS: Other than elevated narcolepsy IRs in the period after vaccination campaigns in Sweden, we did not find an association between AS03- or MF59-adjuvanted pH1N1 vaccines and narcolepsy in children or adults in the sites studied, although power to evaluate the AS03-adjuvanted Pandemrix brand vaccine was limited in our study.

BACKGROUND: In 2010, a safety signal was detected for narcolepsy following vaccination with Pandemrix, an AS03-adjuvanted monovalent pandemic H1N1 influenza (pH1N1) vaccine. To further assess a possible association and inform policy on future use of adjuvants, we conducted a multi-country study of narcolepsy and adjuvanted pH1N1 vaccines.METHODS: We used electronic health databases to conduct a dynamic retrospective cohort study to assess narcolepsy incidence rates (IR) before and during pH1N1 virus circulation, and after pH1N1 vaccination campaigns in Canada, Denmark, Spain, Sweden, Taiwan, the Netherlands, and the United Kingdom. Using a case-control study design, we evaluated the risk of narcolepsy following AS03- and MF59-adjuvanted pH1N1 vaccines in Argentina, Canada, Spain, Switzerland, Taiwan, and the Netherlands. In the Netherlands, we also conducted a case-coverage study in children born between 2004 and 2009.RESULTS: No changes in narcolepsy IRs were observed in any periods in single study sites except Sweden and Taiwan; in Taiwan incidence increased after wild-type pH1N1 virus circulation and in Sweden (a previously identified signaling country), incidence increased after the start of pH1N1 vaccination. No association was observed for Arepanrix-AS03 or Focetria-MF59 adjuvanted pH1N1 vaccines and narcolepsy in children or adults in the case-control study nor for children born between 2004 and 2009 in the Netherlands case-coverage study for Pandemrix-AS03.CONCLUSIONS: Other than elevated narcolepsy IRs in the period after vaccination campaigns in Sweden, we did not find an association between AS03- or MF59-adjuvanted pH1N1 vaccines and narcolepsy in children or adults in the sites studied, although power to evaluate the AS03-adjuvanted Pandemrix brand vaccine was limited in our study.