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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 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.

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 Toronto, Canada, chronic exposure to road traffic noise was associated with elevated risks for AMI and CHF incidence. https://doi.org/10.1289/EHP5809.

BackgroundSurvivors of acute myocardial infarction (AMI) are at increased risk of dying within several hours to days following exposure to elevated levels of ambient air pollution. Little is known, however, about the influence of long-term (months to years) air pollution exposure on survival after AMI.ObjectiveWe conducted a population-based cohort study to determine the impact of long-term exposure to fine particulate matter ≤ 2.5 μm in diameter (PM2.5) on post-AMI survival.MethodsWe assembled a cohort of 8,873 AMI patients who were admitted to 1 of 86 hospital corporations across Ontario, Canada in 1999-2001. Mortality follow-up for this cohort extended through 2011. Cumulative time-weighted exposures to PM2.5 were derived from satellite observations based on participants' annual residences during follow-up. We used standard and multilevel spatial random-effects Cox proportional hazards models and adjusted for potential confounders.ResultsBetween 1999 and 2011, we identified 4,016 nonaccidental deaths, of which 2,147 were from any cardiovascular disease, 1,650 from ischemic heart disease, and 675 from AMI. For each 10-μg/m3 increase in PM2.5, the adjusted hazard ratio (HR10) of nonaccidental mortality was 1.22 [95% confidence interval (CI): 1.03, 1.45]. The association with PM2.5 was robust to sensitivity analyses and appeared stronger for cardiovascular-related mortality: ischemic heart (HR10 = 1.43; 95% CI: 1.12, 1.83) and AMI (HR10 = 1.64; 95% CI: 1.13, 2.40). We estimated that 12.4% of nonaccidental deaths (or 497 deaths) could have been averted if the lowest measured concentration in an urban area (4 μg/m3) had been achieved at all locations over the course of the study.ConclusionsLong-term air pollution exposure adversely affects the survival of AMI patients.CitationChen H, Burnett RT, Copes R, Kwong JC, Villeneuve PJ, Goldberg MS, Brook RD, van Donkelaar A, Jerrett M, Martin RV, Brook JR, Kopp A, Tu JV. 2016. Ambient fine particulate matter and mortality among survivors of myocardial infarction: population-based cohort study. Environ Health Perspect 124:1421-1428; http://dx.doi.org/10.1289/EHP185.

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. [ABSTRACT FROM AUTHOR]

BACKGROUND: Epidemiological 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. OBJECTIVES: We evaluated the associations between long-term exposure to road traffic noise and the incidence of AMI and CHF. METHODS: Our 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]. RESULTS: During 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. CONCLUSION: In this large cohort study in Toronto, Canada, chronic exposure to road traffic noise was associated with elevated risks for AMI and CHF incidence. [ABSTRACT FROM AUTHOR]

BACKGROUND: Laboratory studies suggest that fine particulate matter (≤ 2.5 µm in diameter; [PM.sub.2.5]) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating [PM.sub.2.5] and diabetes is sparse, particularly for incident diabetes. OBJECTIVES: We conducted a population-based cohort study to determine whether long-term exposure to ambient [PM.sub.2.5] is associated with incident diabetes. METHODS: We assembled a cohort of 62,012 nondiabetic adults who lived in Ontario, Canada, and completed one of five population-based health surveys between 1996 and 2005. Follow-up extended until 31 December 2010. Incident diabetes diagnosed between 1996 and 2010 was ascertained using the Ontario Diabetes Database, a validated registry of persons diagnosed with diabetes (sensitivity = 86%, specificity = 97%). Six-year average concentrations of [PM.sub.2.5] at the postal codes of baseline residences were derived from satellite observations. We used Cox proportional hazards models to estimate the associations, adjusting for various individual-level risk factors and contextual covariates such as smoking, body mass index, physical activity, and neighborhood-level household income. We also conducted multiple sensitivity analyses. In addition, we examined effect modification for selected comorbidities and sociodemographic characteristics. RESULTS: There were 6,310 incident cases of diabetes over 484,644 total person-years of followup. The adjusted hazard ratio for a 10-µg/[m.sup.3] increase in [PM.sub.2.5] was 1.11 (95% CI: 1.02, 1.21). Estimated associations were comparable among all sensitivity analyses. We did not find strong evidence of effect modification by comorbidities or sociodemographic covariates. CONCLUSIONS: This study suggests that long-term exposure to [PM.sub.2.5] may contribute to the development of diabetes. KEY WORDS: cohort study, diabetes, particulate air pollution. Environ Health Perspect 121:804-810 (2013). http://dx.doi.org/10.1289/ehp.1205958 [Online 26 April 2013], Diabetes mellitus and its associated macrovascular (Kannel and McGee 1979; Manson et al. 1991a) and microvascular (Watkins and Edmonds 1983) complications constitute a serious threat to global human health and [...]

BACKGROUND: Survivors of acute myocardial infarction (AMI) are at increased risk of dying within several hours to days following exposure to elevated levels of ambient air pollution. Little is known, however, about the influence of long-term (months to years) air pollution exposure on survival after AMI. OBJECTIVE: We conducted a population-based cohort study to determine the impact of long-term exposure to fine particulate matter ≤ 2.5 µm in diameter (PM2.5) on post-AMI survival. METHODS: We assembled a cohort of 8,873 AMI patients who were admitted to 1 of 86 hospital corporations across Ontario, Canada in 1999-2001. Mortality follow-up for this cohort extended through 2011. Cumulative time-weighted exposures to PM2.5 were derived from satellite observations based on participants' annual residences during follow-up. We used standard and multilevel spatial random-effects Cox proportional hazards models and adjusted for potential confounders. RESULTS: Between 1999 and 2011, we identified 4,016 nonaccidental deaths, of which 2,147 were from any cardiovascular disease, 1,650 from ischemic heart disease, and 675 from AMI. For each 10-µg/m³ increase in PM2.5, the adjusted hazard ratio (HR10) of nonaccidental mortality was 1.22 [95% confidence interval (CI): 1.03, 1.45]. The association with PM2.5 was robust to sensitivity analyses and appeared stronger for cardiovascular-related mortality: ischemic heart (HR10 = 1.43; 95% CI: 1.12, 1.83) and AMI (HR10 = 1.64; 95% CI: 1.13, 2.40). We estimated that 12.4% of nonaccidental deaths (or 497 deaths) could have been averted if the lowest measured concentration in an urban area (4 µg/m³) had been achieved at all locations over the course of the study. CONCLUSIONS: Long-term air pollution exposure adversely affects the survival of AMI patients. [ABSTRACT FROM AUTHOR]

Background: Laboratory studies suggest that fine particulate matter (≤ 2.5 µm in diameter; PM2.5) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating PM2.5 and diabetes is sparse, particularly for incident diabetes. Objectives: We conducted a population-based cohort study to determine whether long-term exposure to ambient PM2.5 is associated with incident diabetes. Methods: We assembled a cohort of 62,012 nondiabetic adults who lived in Ontario, Canada, and completed one of five population-based health surveys between 1996 and 2005. Follow-up extended until 31 December 2010. Incident diabetes diagnosed between 1996 and 2010 was ascertained using the Ontario Diabetes Database, a validated registry of persons diagnosed with diabetes (sensitivity = 86%, specificity = 97%). Six-year average concentrations of PM2.5 at the postal codes of baseline residences were derived from satellite observations. We used Cox proportional hazards models to estimate the associations, adjusting for various individual-level risk factors and contextual covariates such as smoking, body mass index, physical activity, and neighborhood-level household income. We also conducted multiple sensitivity analyses. In addition, we examined effect modification for selected comorbidities and sociodemographic characteristics. Results: There were 6,310 incident cases of diabetes over 484,644 total person-years of followup. The adjusted hazard ratio for a 10-µg/m3 increase in PM2.5 was 1.11 (95% CI: 1.02, 1.21). Estimated associations were comparable among all sensitivity analyses. We did not find strong evidence of effect modification by comorbidities or sociodemographic covariates. Conclusions: This study suggests that long-term exposure to PM2.5 may contribute to the development of diabetes. [ABSTRACT FROM AUTHOR]