Ray Copes

Living near major roads and the incidence of dementia, Parkinson's disease, and multiple sclerosis: a population-based cohort study

BACKGROUND Emerging evidence suggests that living near major roads might adversely affect cognition. However, little is known about its relationship with the incidence of dementia, Parkinsons disease, and multiple sclerosis. We aimed to investigate the association between residential proximity to major roadways and the incidence of these three neurological diseases in Ontario, Canada. METHODS In this population-based cohort study, we assembled two population-based cohorts including all adults aged 20-50 years (about 4·4 million; multiple sclerosis cohort) and all adults aged 55-85 years (about 2·2 million; dementia or Parkinsons disease cohort) who resided in Ontario, Canada on April 1, 2001. Eligible patients were free of these neurological diseases, Ontario residents for 5 years or longer, and Canadian-born. We ascertained the individuals proximity to major roadways based on their residential postal-code address in 1996, 5 years before cohort inception. Incident diagnoses of dementia, Parkinsons disease, and multiple sclerosis were ascertained from provincial health administrative databases with validated algorithms. We assessed the associations between traffic proximity and incident dementia, Parkinsons disease, and multiple sclerosis using Cox proportional hazards models, adjusting for individual and contextual factors such as diabetes, brain injury, and neighbourhood income. We did various sensitivity analyses, such as adjusting for access to neurologists and exposure to selected air pollutants, and restricting to never movers and urban dwellers. FINDINGS Between 2001, and 2012, we identified 243 611 incident cases of dementia, 31 577 cases of Parkinsons disease, and 9247 cases of multiple sclerosis. The adjusted hazard ratio (HR) of incident dementia was 1·07 for people living less than 50 m from a major traffic road (95% CI 1·06-1·08), 1·04 (1·02-1·05) for 50-100 m, 1·02 (1·01-1·03) for 101-200 m, and 1·00 (0·99-1·01) for 201-300 m versus further than 300 m (p for trend=0·0349). The associations were robust to sensitivity analyses and seemed stronger among urban residents, especially those who lived in major cities (HR 1·12, 95% CI 1·10-1·14 for people living <50 m from a major traffic road), and who never moved (1·12, 1·10-1·14 for people living <50 m from a major traffic road). No association was found with Parkinsons disease or multiple sclerosis. INTERPRETATION In this large population-based cohort, living close to heavy traffic was associated with a higher incidence of dementia, but not with Parkinsons disease or multiple sclerosis. FUNDING Health Canada (MOA-4500314182).

Risk of Incident Diabetes in Relation to Long-term Exposure to Fine Particulate Matter in Ontario, Canada

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 follow-up. 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.

Spatial association between ambient fine particulate matter and incident hypertension

Background— Laboratory studies suggest that exposure to fine particulate matter (⩽2.5 &mgr;m in diameter) (PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension. Methods and Results— We assembled a cohort of 35 303 nonhypertensive adults from Ontario, Canada, who responded to 1 of 4 population-based health surveys between 1996 and 2005 and were followed up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants’ postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adjusting for various individual and contextual risk factors including body mass index, smoking, physical activity, and neighbourhood-level unemployment rates. We conducted various sensitivity analyses to assess the robustness of the effect estimate, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time. Between 1996 and 2010, we identified 8649 incident cases of hypertension and 2296 deaths. For every 10-µg/m3 increase of PM2.5, the adjusted hazard ratio of incident hypertension was 1.13 (95% confidence interval, 1.05–1.22). Estimated associations were comparable among all sensitivity analyses. Conclusions— This study supports an association between PM2.5 and incident hypertension.

Temporal and spatial variability of traffic-related noise in the City of Toronto, Canada.

The majority of studies that assessed population-level exposure to traffic-related noise were conducted in European countries and less is known about the exposure to traffic noise in North America, particularly in Canadian cities. This study explored the temporal and spatial variability of traffic noise in the City of Toronto, the largest city in Canada. We conducted two cycles of intensive field measurement campaign to collect real-time measurements of traffic noise at 554 locations across Toronto between June 2012 and January 2013. At each site, we collected measurements for a period of 30 min during daytime. Repeated measurements were made in cycle two at 62 locations randomly selected from cycle one, which exhibited high correlation (Pearsons correlation coefficient (r): 0.79). In addition, continuous measurements of noise were recorded for seven days at ten sites. We observed that noise variability was predominantly spatial in nature, rather than temporal: spatial variability accounted for 60% of the total observed variations in traffic noise. Traffic volume, length of arterial road, and industrial area were three most important variables, explaining the majority of the spatial variability of noise (R(2)=0.68 to 0.74, depending on the cycle). In comparison to the 16-h equivalent sound level guideline for outdoor locations set out by the Ministry of the Environment of the Province of Ontario, 80% of our sampled locations exceeded this guideline (i.e. 55 dBA,16 h). These findings suggested ubiquitous traffic noise exposure across Toronto and that noise variability was explained mostly by spatial characteristics.

Uptake of cadmium from Pacific oysters (Crassostrea gigas) in British Columbia oyster growers

BACKGROUND Pacific oysters along the North American coast from Washington to Alaska contain concentrations of cadmium (Cd) that are high by comparison with Atlantic oysters, frequently exceeding 2mug/g wet weight, but it is unclear whether this Cd is absorbed by consumers. OBJECTIVES To determine the effect of oyster consumption on Cd in blood and urine among a group with high oyster consumption. METHODS Sixty-one non-smoking oyster growers and family members with a mean age of 47.3+/-7.6 years (range 33-64) were interviewed by telephone to assess their oyster consumption and other sources of Cd exposure at present and 5 years prior to the start of oyster farming. Their blood and urine Cd concentrations were measured. RESULTS The geometric mean Cd concentration in blood was 0.83mug/L and in urine was 0.76mug/g creatinine. Thirty-six percent of participants had urinary Cd levels above 1mug/g creatinine and 5% were above 2mug/g creatinine. Recent (last 12 months) and long-term oyster consumptions were positive predictors of blood Cd but did not directly predict urinary Cd. The optimal model for predicting the variance in blood Cd included recent intake of oyster-derived Cd, serum iron concentration and recent ketchup consumption (R(2)=0.34, p=0.00004), with the latter two variables showing a protective effect. The factors found to predict urinary Cd were blood Cd concentration and duration of oyster farming. A rise in blood Cd was observed after 12 years of farming oysters, likely caused by higher consumption of oysters during this period. CONCLUSIONS Oyster-derived Cd is bioavailable and affects body stores of the metal.

Neighborhood walkability: differential associations with self-reported transport walking and leisure-time physical activity in Canadian towns and cities of all sizes.

OBJECTIVE To estimate associations between walkability and physical activity during transportation and leisure in a national-level population. METHODS Walkability was measured by Walk Score® (2012-2014) and physical activity by the Canadian Community Health Survey (2007-2012) for urban participants who worked or attended school. Multiple linear regression was done on the total study population, four age subgroups (12-17, 18-29, 30-64, 65+) and three population center subgroups (1000-29,999, 30,000-99,999, 100,000+). RESULTS 151,318 respondents were examined. Comparing highest to lowest Walk Score® quintiles, covariate-adjusted energy expenditure on transport walking [95% confidence interval] was 0.17 [0.15, 0.18] kcal/kg/day higher in the total study population, and significantly higher in all age and population center subgroups. Leisure physical activity was lower in the age 18-29 subgroup (-0.28 [-0.43, -0.12]) and population centers 100,000+ subgroup (-0.10 [-0.18, -0.03]), but higher in the population centers 1000-29,999 subgroup (0.30 [0.12, 0.48]). Total physical activity was higher in the following subgroups: age 30-64 (0.19 [0.12, 0.26]), population centers 100,000+ (0.12 [0.04, 0.19]) and population centers 1000-29,999 (0.40 [0.20, 0.59]). CONCLUSIONS Walkability is associated with transport walking in all age groups and towns and cities of all sizes. Walkabilitys inverse associations with leisure physical activity among young adults and in large population centers may offset energy expenditure gains, while positive associations with leisure physical activity in small centers may add to energy expenditure.

Ambient Fine Particulate Matter and Mortality among Survivors of Myocardial Infarction: Population-Based Cohort Study.

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. Citation: Chen 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

Hospitalizations from Hypertensive Diseases, Diabetes, and Arrhythmia in Relation to Low and High Temperatures: Population-Based Study.

Little is known about the extent to which ambient temperatures contribute to the burden of hospitalizations from hypertensive diseases, diabetes, and arrhythmia. To fill this knowledge gap, we conducted a time-series study comprising entire population of Ontario, Canada during 1996–2013. A distributed lag non-linear model was developed to estimate the cumulative effect of temperatures over a 21-day lag period. We computed the burden of hospitalizations attributable to cold and heat. Furthermore, we separated the burden into components related to mild and extreme temperatures. Compared to the temperature with minimum risk of morbidity, cold temperatures (1st percentile) were associated with a 37% (95% confidence interval: 5%, 78%) increase in hypertension-related hospitalizations whereas no significant association with hot temperatures (99th percentile) was observed. Cold and hot temperatures were also associated with a 12% (1%, 24%) and a 30% (6%, 58%) increase in diabetes-related hospitalizations, respectively. Arrhythmia was not linked to temperatures. These estimates translate into ~10% of hypertension-related hospitalizations attributable to total cold, and ~9% from mild cold. Similarly, ~11% of diabetes-related hospitalizations were due to total heat, virtually all of which were from mild heat. In conclusion, ambient temperatures, especially in moderate ranges, contribute to excess hospitalizations from hypertension and diabetes.

Assessment of the effect of cold and hot temperatures on mortality in Ontario, Canada: a population-based study

BACKGROUND Ambient high temperature is associated with death; however, heat-related risk of death has not been quantified systematically in Ontario, the most populous province in Canada. Less is known about cold-related risk in this population. Our objective was to quantify the health impact from cold and hot temperatures in Ontario. METHODS The study population consisted of all residents of Ontario who died between Jan. 1, 1996, and Dec. 31, 2010, from any nonaccidental cause. A case-crossover analysis was applied to assess the relation between daily temperature fluctuation and deaths from nonaccidental and selected causes in cold (December-February) and warm (June-August) seasons, respectively, adjusting for various potential confounders. Risk estimates were obtained for each census division, then pooled across Ontario. We examined potential effect modification for selected comorbidities and sociodemographic characteristics. RESULTS In warm seasons, each 5°C increase in daily mean temperature was associated with a 2.5% increase in nonaccidental deaths (95% confidence interval [CI] = 1.3% to 3.8%) on the day of exposure (lag 0). In cold seasons, each 5°C decrease in daily temperature was associated with a 3.0% (95% CI 1.8% to 4.2%) increase in nonaccidental deaths, which persisted over 7 days (lag 0-6). The cold-related effects (lag 0-6) were stronger for cardiovascular-related deaths (any cardiovascular death: 4.1%, 95% CI 2.3% to 5.9%; ischemic heart disease: 5.8%, 95% CI 3.6% to 8.1%), especially among people less than 65 years of age (8.0%, 95% CI 3.0% to 13.0%). Conversely, heat most strongly increased respiratory-related deaths during admission to hospital (26.0%, 95% CI 0% to 61.4%). Across Ontario, each 5°C change in daily temperature was estimated to induce 7 excess deaths per day in cold seasons and 4 excess deaths in warm seasons. INTERPRETATION Heat contributed to excess deaths in Ontario, although the effect of cold weather appeared to be greater. Further work is required to better define high-risk subgroups, which might include the homeless and people with inadequately heated housing.

Cohort Profile: The ONtario Population Health and Environment Cohort (ONPHEC)

Cohort Profile: The ONtario Population Health and Environment Cohort (ONPHEC) Hong Chen*, Jeffrey C. Kwong, Ray Copes, Paul J. Villeneuve, Mark S. Goldberg, Scott Weichenthal, Aaron van Donkelaar, Michael Jerrett, Randall V. Martin, Jeffrey R. Brook, Alexander Kopp and Richard T. Burnett Public Health Ontario, Toronto, ON, Canada, Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada, Institute for Clinical Evaluative Sciences, Toronto, ON, Canada, Department of Family and Community Medicine, University of Toronto, Toronto, ON, Canada, CHAIM Research Centre, Carleton University, Ottawa, ON, Canada, Department of Medicine, McGill University, Montreal, QC, Canada, Division of Clinical Epidemiology, Research Institute of the McGill University Health Centre, Montreal, QC, Canada, Air Health Effects Science Division, Health Canada, Ottawa, ON, Canada, Department of Physics and Atmospheric Science, Dalhousie University, Halifax, NS, Canada, Department of Environmental Health Sciences, Jonathan and Karin Fielding School of Public Health, University of California, Los Angeles, CA, USA, Harvard-Smithsonian Centre for Astrophysics, Cambridge, MA, USA, Air Quality Research Division, Environment Canada, Toronto, ON, Canada and Population Studies Division, Health Canada, Ottawa, ON, Canada