Air Pollution as a Risk Factor for Incident Chronic Obstructive Pulmonary Disease and Asthma. A 15-Year Population-based Cohort Study.

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.

A Population-Based Cohort Study of Respiratory Disease and Long-Term Exposure to Iron and Copper in Fine Particulate Air Pollution and Their Combined Impact on Reactive Oxygen Species Generation in Human Lungs.

Metal components in fine particulate matter (PM2.5) from nontailpipe emissions may play an important role in underlying the adverse respiratory effects of PM2.5. We investigated the associations between long-term exposure to iron (Fe) and copper (Cu) in PM2.5 and their combined impact on reactive oxygen species (ROS) generation in human lungs, and the incidence of asthma, chronic obstructive pulmonary disease (COPD), COPD mortality, pneumonia mortality, and respiratory mortality. We conducted a population-based cohort study of ∼0.8 million adults in Toronto, Canada. Land-use regression models were used to estimate the concentrations of Fe, Cu, and ROS. Outcomes were ascertained using validated health administrative databases. We found positive associations between long-term exposure to Fe, Cu, and ROS and the risks of all five respiratory outcomes. The associations were more robust for COPD, pneumonia mortality, and respiratory mortality than for asthma incidence and COPD mortality. Stronger associations were observed for ROS than for either Fe or Cu. In two-pollutant models, adjustment for nitrogen dioxide somewhat attenuated the associations while adjustment for PM2.5 had little influence. Long-term exposure to Fe and Cu in PM2.5 and estimated ROS concentration in lung fluid was associated with increased incidence of respiratory diseases, suggesting the adverse respiratory effects of nontailpipe emissions.

Exposure to ambient air pollution and the incidence of lung cancer and breast cancer in the Ontario Population Health and Environment Cohort.

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.

Estimates of healthcare utilisation and deaths from waterborne pathogen exposure in Ontario, Canada.

Burden of disease analyses can quantify the relative impact of different exposures on population health outcomes. Gastroenteritis where the causative pathogen was not determined and respiratory illness resulting from exposure to opportunistic pathogens transmitted by water aerosols have not always been considered in waterborne burden of disease estimates. We estimated the disease burden attributable to nine enteric pathogens, unspecified pathogens leading to gastroenteritis, and three opportunistic pathogens leading primarily to respiratory illness, in Ontario, Canada (population ~14 million). Employing a burden of disease framework, we attributed a fraction of annual (year 2016) emergency department (ED) visits, hospitalisations and deaths to waterborne transmission. Attributable fractions were developed from the literature and clinical input, and unattributed disease counts were obtained using administrative data. Our Monte Carlo simulation reflected uncertainty in the inputs. The estimated mean annual attributable rates for waterborne diseases were (per 100 000 population): 69 ED visits, 12 hospitalisations and 0.52 deaths. The corresponding 5th-95th percentile estimates were (per 100 000 population): 13-158 ED visits, 5-22 hospitalisations and 0.29-0.83 deaths. The burden of disease due to unspecified pathogens dominated these rates: 99% for ED visits, 63% for hospitalisations and 40% for deaths. However, when a causative pathogen was specified, the majority of hospitalisations (83%) and deaths (97%) resulted from exposure to the opportunistic pathogens Legionella spp., non-tuberculous mycobacteria and Pseudomonas spp. The waterborne disease burden in Ontario indicates the importance of gastroenteritis not traced back to a particular pathogen and of opportunistic pathogens transmitted primarily through contact with water aerosols.

Urban green space and the risks of dementia and stroke.

INTRODUCTION: It is unknown whether urban green space is associated with reduced risk of major neurological conditions, especially dementia and stroke. METHODS: Retrospective, population-based cohorts were created for each study outcome, including 1.7 and 4.3 million adults in Ontario, Canada for dementia and stroke, respectively. Residential green space was quantified using the satellite-derived Normalized Difference Vegetation Index. Incidence was ascertained using health administrative data with validated algorithms. Mixed-effects Cox models were used to estimate hazard ratios per interquartile range increase in green space exposure. RESULTS: Between 2001 and 2013, 219,013 individuals were diagnosed with dementia and 89,958 had a stroke. The hazard ratio per interquartile range increase in green space was 0.97 (95% CI: 0.96-0.98) for dementia and 0.96 (0.95-0.98) for stroke. Estimates remained generally consistent in sensitivity analyses. DISCUSSION: Increased exposure to urban green space was associated with reduced incidence of dementia and stroke. To our knowledge, this is the first population-based cohort study to assess these relationships.

An approach to estimating the environmental burden of cancer from known and probable carcinogens: application to Ontario, Canada.

BACKGROUND: Quantifying the potential cancer cases associated with environmental carcinogen exposure can help inform efforts to improve population health. This study developed an approach to estimate the environmental burden of cancer and applied it to Ontario, Canada. The purpose was to identify environmental carcinogens with the greatest impact on cancer burden to support evidence-based decision making. METHODS: We conducted a probabilistic assessment of the environmental burden of cancer in Ontario. We selected 23 carcinogens that we defined as "environmental" (e.g., pollutants) and were relevant to the province, based on select classifications provided by the International Agency for Research on Cancer. We evaluated population exposure to the carcinogens through inhalation of indoor/outdoor air; ingestion of food, water, and dust; and exposure to radiation. We obtained or calculated concentration-response functions relating carcinogen exposure and the risk of developing cancer. Using both human health risk assessment and population attributable fraction models in a Monte Carlo simulation, we estimated the annual cancer cases associated with each environmental carcinogen, reporting the simulation summary (e.g., mean and percentiles). RESULTS: We estimated between 3540 and 6510 annual cancer cases attributable to exposure to 23 environmental carcinogens in Ontario. Three carcinogens were responsible for over 90% of the environmental burden of cancer: solar ultraviolet (UV) radiation, radon in homes, and fine particulate matter (PM2.5) in outdoor air. Eight other carcinogens had an estimated mean burden of at least 10 annual cancer cases: acrylamide, arsenic, asbestos, chromium, diesel engine exhaust particulate matter, dioxins, formaldehyde, and second-hand smoke. The remaining 12 carcinogens had an estimated mean burden of less than 10 annual cancer cases in Ontario. CONCLUSIONS: We found the environmental burden of cancer in Ontario to fall between previously estimated burdens of alcohol and tobacco use. These results allow for a comparative assessment across carcinogens and offer insights into strategies to reduce the environmental burden of cancer. Our analysis could be adopted by other jurisdictions and repeated in the future for Ontario to track progress in reducing cancer burden, assess newly classified environmental carcinogens, and identify top burden contributors.

Time Trends of the Incidence, Prevalence, and Mortality of Parkinsonism.

OBJECTIVES: We assessed trends in the incidence, prevalence, and post-diagnosis mortality of parkinsonism in Ontario, Canada over 18 years. We also explored the influence of a range of risk factors for brain health on the trend of incident parkinsonism. METHODS: We established an open cohort by linking population-based health administrative databases from 1996 to 2014 in Ontario. The study population comprised residents aged 20-100 years with an incident diagnosis of parkinsonism ascertained using a validated algorithm. We calculated age- and sex-standardized incidence, prevalence, and mortality of parkinsonism, stratified by young onset (20-39 years) and mid/late onset (≥40 years). We assessed trends in incidence using Poisson regression, mortality using negative binomial regression, and prevalence of parkinsonism and pre-existing conditions (e.g., head injury) using the Cochran-Armitage trend test. To better understand trends in the incidence of mid/late-onset parkinsonism, we adjusted for various pre-existing conditions in the Poisson regression model. RESULTS: From 1996 to 2014, we identified 73,129 incident cases of parkinsonism (source population of ∼10.5 million), of whom 56% were male, mean age at diagnosis was 72.6 years, and 99% had mid/late-onset parkinsonism. Over 18 years, the age- and sex-standardized incidence decreased by 13.0% for mid/late-onset parkinsonism but remained unchanged for young-onset parkinsonism. The age- and sex-standardized prevalence increased by 22.8%, while post-diagnosis mortality decreased by 5.5%. Adjustment for pre-existing conditions did not appreciably explain the declining incidence of mid/late-onset parkinsonism. CONCLUSION: Young-onset and mid/late-onset parkinsonism exhibited differing trends in incidence over 18 years in Ontario. Further research to identify other factors that may appreciably explain trends in incident parkinsonism is warranted.

Screening for hand dermatitis in healthcare workers: Comparing workplace screening with dermatologist photo screening.

BACKGROUND: Healthcare workers are at increased risk for occupational contact dermatitis, owing to wet work exposure. Early detection and management improves outcomes. Although several diagnostic tools are available, none is appropriate for rapid screening. OBJECTIVES: To assess the validity and feasibility of the Hand Dermatitis Screening Tool in the acute healthcare sector. METHODS: Screening of 508 employees at three hospitals in Ontario, Canada was performed with the Hand Dermatitis Screening Tool either by an occupational health nurse (N = 225) or by self-administration (N = 283). Two occupational dermatologists rated photographs of participants' hands. RESULTS: Of the participants, 30.5% screened positive for hand dermatitis. A positive screen was associated with wet work, history of eczema, dermatitis, or other rash, and currently having a rash. Ninety-four per cent of participants reported that using the tool took <2 minutes, 99% indicated that the tool was easy to use, and 86% stated that workplace screening was very important. Workplace and dermatologist photo screening showed fair agreement. CONCLUSIONS: The prevalence of hand dermatitis and identified risk factors were consistent with the literature. These findings, along with positive feasibility results, support further testing of the tool despite only fair agreement between workplace and dermatologist screening.

Estimated Annual Deaths, Hospitalizations, and Emergency Department and Physician Office Visits from Foodborne Illness in Ontario.

Public Health Ontario is working to estimate the burden of disease from environmental hazards in Ontario, Canada. As part of this effort, we estimated deaths and health care utilization resulting from exposure to pathogens and toxic substances in food. We applied fractions for the proportion of illness attributable to foodborne transmission to the annual (2008-2012) counts of deaths, hospitalizations, emergency department (ED) visits, and physician office visits for 15 diseases (13 pathogen-specific diseases and 2 nonspecific syndromes) captured by administrative health data. Nonspecific gastroenteritis (causative agent unknown) was the dominant disease, accounting for 98% of ED visits, 94% of hospitalizations, and 88% of deaths annually attributed to the 15 diseases. We estimated that foodborne nonspecific gastroenteritis results in ∼137,000 physician office visits (1000/100,000 population), 40,000 ED visits (310/100,000), 6200 hospitalizations (47/100,000), and 59 deaths (0.45/100,000) in Ontario per year (mean estimates). Our results indicate that pathogen-specific approaches to foodborne disease surveillance can substantially underestimate the deaths and illness resulting from exposure to foodborne pathogens and other causes of foodborne illness.

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, Parkinson's 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 Parkinson's 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 individual's proximity to major roadways based on their residential postal-code address in 1996, 5 years before cohort inception. Incident diagnoses of dementia, Parkinson's disease, and multiple sclerosis were ascertained from provincial health administrative databases with validated algorithms. We assessed the associations between traffic proximity and incident dementia, Parkinson's 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 Parkinson's 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 Parkinson's 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 Parkinson's disease or multiple sclerosis. FUNDING: Health Canada (MOA-4500314182).

Exposure to Ambient Ultrafine Particles and Nitrogen Dioxide and Incident Hypertension and Diabetes.

BACKGROUND: Previous studies reported that long-term exposure to traffic-related air pollution may increase the incidence of hypertension and diabetes. However, little is known about the associations of ultrafine particles (≤0.1 µm in diameter) with these two conditions. METHODS: We conducted a population-based cohort study to investigate the associations between exposures to ultrafine particles and nitrogen dioxide (NO2) and the incidence of diabetes and hypertension. Our study population included all Canadian-born residents aged 30 to 100 years who lived in the City of Toronto, Canada, from 1996 to 2012. Outcomes were ascertained using validated province-wide databases. We estimated annual concentrations of ultrafine particles and NO2 using land-use regression models and assigned these estimates to participants' annual postal code addresses during the follow-up period. Using random-effects Cox proportional hazards models, we calculated hazard ratios (HRs) and 95% confidence intervals (CIs) for ultrafine particles and NO2, adjusted for individual- and neighborhood-level covariates. We considered both single- and multipollutant models. RESULTS: Each interquartile change in exposure to ultrafine particles was associated with increased risk of incident hypertension (HR = 1.03; 95% CI = 1.02, 1.04) and diabetes (HR = 1.06; 95% CI = 1.05, 1.08) after adjusting for all covariates. These results remained unaltered with further control for fine particulate matter (≤2.5 µm; PM2.5) and NO2. Similarly, NO2 was positively associated with incident diabetes (HR = 1.06; 95% CI = 1.05, 1.07) after controlling for ultrafine particles and PM2.5. CONCLUSIONS: Exposure to traffic-related air pollution including ultrafine particles and NO2 may increase the risk for incident hypertension and diabetes. See video abstract at, http://links.lww.com/EDE/B337.

Long-term exposure to air pollution and the incidence of multiple sclerosis: A population-based cohort study.

BACKGROUND: Evidence of the adverse neurological effects of exposure to ambient air pollution is emerging, but little is known about its effect on the development of multiple sclerosis (MS), the most common autoimmune disease of the central nervous system. OBJECTIVES: To investigate the associations between MS incidence and long-term exposures to fine particles (PM2.5), nitrogen dioxide (NO2), and ozone (O3) METHODS: We conducted a population-based cohort study to investigate the associations between long-term exposures to PM2.5, NO2, and O3 and the incidence of MS. Our study population included all Canadian-born residents aged 20-40 years who lived in the province of Ontario, Canada from 2001 to 2013. Incident MS was ascertained from a validated registry. We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during the 13 years of follow-up. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for each pollutant separately using random-effects Cox proportional hazards models. We conducted various sensitivity analyses, such as lagging exposure up to 5 years and adjusting for access to neurological care, annual average temperature, and population density. RESULTS: Between 2001 and 2013, we identified 6203 incident cases of MS. The adjusted HR of incident MS was 0.96 (95% CI: 0.86-1.07) for PM2.5, 0.91(95% CI: 0.81-1.02) for NO2, and 1.09 (95% CI: 0.98-1.23) for O3. These results were robust to various sensitivity analyses conducted. CONCLUSIONS: In this large population-based cohort, we did not observe significant associations between MS incidence and long-term exposures to PM2.5, NO2, and O3 in adults in Ontario, 2001-2013.

Exploring nighttime road traffic noise: A comprehensive predictive surface for Toronto, Canada.

Road traffic noise can adversely impact the health of city residents, particularly when it occurs at night. The objective of this study was to evaluate nighttime traffic ambient noise in Toronto, Canada using measured and model-estimated noise levels. Road traffic noise was measured at 767 locations over 3 seasonal sampling campaigns between June 2012 and October 2013 to fully capture noise variability in Toronto. Temporal and campaign-specific spatial models, developed using the noise measurements, were used to build a final predictive surface. The surface was capable of estimating noise across the city over a 24-hr time frame. Measured and surface-estimated noise levels were compared with guidelines from the World Health Organization and the Province of Ontario to identify areas where noise may pose a health risk. Measured mean nighttime noise in Toronto exceeded World Health Organization (40 dBA) guidelines and mean daytime noise exceeded provincial (55 dBA) guidelines. The final predictive surface, incorporating spatial variables and daily cycles in noise levels, provides noise estimates geocoded for the entire study area. This tool could be used for epidemiological studies and to inform noise mitigation efforts. Based on surface-estimated noise levels during the quietest time of night (2 a.m.-2:30 a.m.), 100% of Toronto has nighttime noise exceeding 40 dBA (mean = 57 dBA, range = 49-110 dBA). A predictive surface was developed to estimate geocoded noise levels and facilitate further study of noise in Toronto. This tool can be used to assess road traffic noise, particularly at night, as an environmental health hazard.

Effectiveness of N95 respirators versus surgical masks in protecting health care workers from acute respiratory infection: a systematic review and meta-analysis.

BACKGROUND: Conflicting recommendations exist related to which facial protection should be used by health care workers to prevent transmission of acute respiratory infections, including pandemic influenza. We performed a systematic review of both clinical and surrogate exposure data comparing N95 respirators and surgical masks for the prevention of transmissible acute respiratory infections. METHODS: We searched various electronic databases and the grey literature for relevant studies published from January 1990 to December 2014. Randomized controlled trials (RCTs), cohort studies and case-control studies that included data on health care workers wearing N95 respirators and surgical masks to prevent acute respiratory infections were included in the meta-analysis. Surrogate exposure studies comparing N95 respirators and surgical masks using manikins or adult volunteers under simulated conditions were summarized separately. Outcomes from clinical studies were laboratory-confirmed respiratory infection, influenza-like illness and workplace absenteeism. Outcomes from surrogate exposure studies were filter penetration, face-seal leakage and total inward leakage. RESULTS: We identified 6 clinical studies (3 RCTs, 1 cohort study and 2 case-control studies) and 23 surrogate exposure studies. In the meta-analysis of the clinical studies, we found no significant difference between N95 respirators and surgical masks in associated risk of (a) laboratory-confirmed respiratory infection (RCTs: odds ratio [OR] 0.89, 95% confidence interval [CI] 0.64-1.24; cohort study: OR 0.43, 95% CI 0.03-6.41; case-control studies: OR 0.91, 95% CI 0.25-3.36); (b) influenza-like illness (RCTs: OR 0.51, 95% CI 0.19-1.41); or (c) reported workplace absenteeism (RCT: OR 0.92, 95% CI 0.57-1.50). In the surrogate exposure studies, N95 respirators were associated with less filter penetration, less face-seal leakage and less total inward leakage under laboratory experimental conditions, compared with surgical masks. INTERPRETATION: Although N95 respirators appeared to have a protective advantage over surgical masks in laboratory settings, our meta-analysis showed that there were insufficient data to determine definitively whether N95 respirators are superior to surgical masks in protecting health care workers against transmissible acute respiratory infections in clinical settings.

Arsenic from community water fluoridation: quantifying the effect.

Community water fluoridation is a WHO recommended strategy to prevent dental carries. One debated concern is that hydrofluorosilicic acid, used to fluoridate water, contains arsenic and poses a health risk. This study was undertaken to determine if fluoridation contributes to arsenic in drinking water, to estimate the amount of additional arsenic associated with fluoridation, and compare this to the National Sanitation Foundation/American National Standards Institute (NSF/ANSI) standard and estimates from other researchers. Using surveillance data from Ontario drinking water systems, mixed effects linear regression was performed to examine the effect of fluoridation status on the difference in arsenic concentration between raw water and treated water samples. On average, drinking water treatment was found to reduce arsenic levels in water in both fluoridated and non-fluoridated systems by 0.2 µg/L. However, fluoridated systems were associated with an additional 0.078 µg/L (95% CI 0.021, 0.136) of arsenic in water when compared to non-fluoridated systems (P = 0.008) while controlling for raw water arsenic concentrations, types of treatment processes, and source water type. Our estimate is consistent with concentrations expected from other research and is less than 10% of the NSF/ANSI standard of 1 µg/L arsenic in water. This study provides further information to inform decision-making regarding community water fluoridation.

Spatial association between ambient fine particulate matter and incident hypertension.

BACKGROUND: Laboratory studies suggest that exposure to fine particulate matter (≤2.5 µm 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/m(3) 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.

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. Walkability's 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.

Lung cancer risk from radon in Ontario, Canada: how many lung cancers can we prevent?

PURPOSE: To calculate the burden of lung cancer illness due to radon for all thirty-six health units in Ontario and determine the number of radon-attributable lung cancer deaths that could be prevented. METHODS: We calculated the population attributable risk percent, excess life-time risk ratio, life-years lost, the number of lung cancer deaths due to radon, and the number of deaths that could be prevented if all homes above various cut-points were effectively reduced to background levels. RESULTS: It is estimated that 13.6 % (95 % CI 11.0, 16.7) of lung cancer deaths in Ontario are attributable to radon, corresponding to 847 (95 % CI 686, 1,039) lung cancer deaths each year, approximately 84 % of these in ever-smokers. If all homes above 200 Bq/m(3), the current Canadian guideline, were remediated to background levels, it is estimated that 91 lung cancer deaths could be prevented each year, 233 if remediation was performed at 100 Bq/m(3). There was important variation across health units. CONCLUSIONS: Radon is an important contributor to lung cancer deaths in Ontario. A large portion of radon-attributable lung cancer deaths are from exposures below the current Canadian guideline, suggesting interventions that install effective radon-preventive measures into buildings at build may be a good alternative population prevention strategy to testing and remediation. For some health units, testing and remediation may also prevent a portion of radon-related lung cancer deaths. Regional attributable risk estimates can help with local public health resource allocation and decision making.

Peak event analysis: a novel empirical method for the evaluation of elevated particulate events.

BACKGROUND: We report on a novel approach to the analysis of suspended particulate data in a rural setting in southern Ontario. Analyses of suspended particulate matter and associated air quality standards have conventionally focussed on 24-hour mean levels of total suspended particulates (TSP) and particulate matter <10 microns, <2.5 microns and <1 micron in diameter (PM10, PM2.5, PM1, respectively). Less emphasis has been placed on brief peaks in suspended particulate levels, which may pose a substantial nuisance, irritant, or health hazard. These events may also represent a common cause of public complaint and concern regarding air quality. METHODS: Measurements of TSP, PM10, PM2.5, and PM1 levels were taken using an automated device following local complaints of dusty conditions in rural south-central Ontario, Canada. The data consisted of 126,051 by-minute TSP, PM10, PM2.5, and PM1 measurements between May and August 2012. Two analyses were performed and compared. First, conventional descriptive statistics were computed by month for TSP, PM10, PM2.5, and PM1, including mean values and percentiles (70th, 90th, and 95th). Second, a novel graphical analysis method, using density curves and line plots, was conducted to examine peak events occurring at or above the 99th percentile of per-minute TSP readings. We refer to this method as "peak event analysis". Findings of the novel method were compared with findings from the conventional approach. RESULTS: Conventional analyses revealed that mean levels of all categories of suspended particulates and suspended particulate diameter ratios conformed to existing air quality standards. Our novel methodology revealed extreme outlier events above the 99th percentile of readings, with peak PM10 and TSP levels over 20 and 100 times higher than the respective mean values. Peak event analysis revealed and described rare and extreme peak dust events that would not have been detected using conventional descriptive statistics. CONCLUSIONS: Peak event analysis underscored extreme particulate events that may contribute to local complaints regarding intermittently dusty conditions. These outlier events may not appear through conventional analytical approaches. In comparison with conventional descriptive approaches, peak event analysis provided a more analytical and data-driven means to identify suspended particulate events with meaningful and perceptible effects on local residents.