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Background: Prenatal exposure to ambient air pollution has been associated with adverse birth outcomes, but the potential modifying effect of maternal comorbidities remains understudied. Our objective was to investigate whether associations between prenatal air pollution exposures and birth outcomes differ by maternal comorbidities., Methods: A total of 818,400 singleton live births were identified in the province of Ontario, Canada from 2005 to 2012. We assigned exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ozone (O3) to maternal residences during pregnancy. We evaluated potential effect modification by maternal comorbidities (i.e. asthma, hypertension, pre-existing diabetes mellitus, heart disease, gestational diabetes and preeclampsia) on the associations between prenatal air pollution and preterm birth, term low birth weight and small for gestational age., Results: Interquartile range (IQR) increases in PM2.5 (2μg/m(3)), NO2 (9ppb) and O3 (5ppb) over the entire pregnancy were associated with a 4% (95% CI: 2.4-5.6%), 8.4% (95% CI: 5.5-10.3%) and 2% (95% CI: 0.5-4.1%) increase in the odds of preterm birth, respectively. Increases of 10.6% (95% CI: 0.2-2.1%) and 23.8% (95% CI: 5.5-44.8%) in the odds of preterm birth were observed among women with pre-existing diabetes while the increases were of 3.8% (95% CI: 2.2-5.4%) and 6.5% (95% CI: 3.7-8.4%) among women without this condition for pregnancy exposure to PM2.5 and NO2, respectively (Pint<0.01). The increase in the odds of preterm birth for exposure to PM2.5 during pregnancy was higher among women with preeclampsia (8.3%, 95% CI: 0.8-16.4%) than among women without (3.6%, 95% CI: 1.8-5.3%) (Pint=0.04). A stronger increase in the odds of preterm birth was found for exposure to O3 during pregnancy among asthmatic women (12.0%, 95% CI: 3.5-21.1%) compared to non-asthmatic women (2.0%, 95% CI: 0.1-3.5%) (Pint<0.01). We did not find statistically significant effect modification for the other outcomes investigated., Conclusions: Findings of this study suggest that associations of ambient air pollution with preterm birth are stronger among women with pre-existing diabetes, asthma, and preeclampsia., (Crown Copyright © 2016. Published by Elsevier Inc. All rights reserved.)

Numerous studies have examined the association of air pollution with preterm birth and birth weight outcomes. Traffic-related air pollution has also increasingly been identified as an important contributor to adverse health effects of air pollution. We employed a national nitrogen dioxide (NO2) exposure model to examine the association between NO2 and pregnancy outcomes in Canada between 1999 and 2008. National models for NO2 (and particulate matter of median aerodynamic diameter <2.5µm (PM2.5) as a covariate) were developed using ground-based monitoring data, estimates from remote-sensing, land use variables and, for NO2, deterministic gradients relative to road traffic sources. Generalized estimating equations were used to examine associations with preterm birth, term low birth weight (LBW), small for gestational age (SGA) and term birth weight, adjusting for covariates including infant sex, gestational age, maternal age and marital status, parity, urban/rural place of residence, maternal place of birth, season, year of birth and neighbourhood socioeconomic status and per cent visible minority. Associations were reduced considerably after adjustment for individual covariates and neighbourhood per cent visible minority, but remained significant for SGA (odds ratio 1.04, 95%CI 1.02-1.06 per 20ppb NO2) and term birth weight (16.2g reduction, 95% CI 13.6-18.8g per 20ppb NO2). Associations with NO2 were of greater magnitude in a sensitivity analysis using monthly monitoring data, and among births to mothers born in Canada, and in neighbourhoods with higher incomes and a lower proportion of visible minorities. In two pollutant models, associations with NO2 were less sensitive to adjustment for PM2.5 than vice versa, and there was consistent evidence of a dose-response relationship for NO2 but not PM2.5. In this study of approximately 2.5 million Canadian births between 1999 and 2008, we found significant associations of NO2 with SGA and term birth weight which remained significant after adjustment for PM2.5, suggesting that traffic may be a particularly important source with respect to the role of air pollution as a risk factor for adverse pregnancy outcomes., (Crown Copyright © 2016. Published by Elsevier Inc. All rights reserved.)

Our objective is to analyse the association between long term ozone exposure and cardiovascular related mortality while accounting for climate, location, and socioeconomic factors. We assigned subjects with 16 years of follow-up in the Canadian Census Health and Environment Cohort (CanCHEC) to one of seven regions based on spatial synoptic classification (SSC) weather types and examined the interaction of exposure to both fine particulate matter (PM2.5) and ground level ozone and cause of death using survival analysis, while adjusting for socioeconomic characteristics and individual confounders. Correlations between ozone and PM2.5 varied across SSC zones from -0.02 to 0.7. Comparing zones using the most populated SSC zone as a reference, a 10 ppb increase in ozone exposure was associated with increases in hazard ratios (HRs) that ranged from 1.007 (95% CI 0.99, 1.015) to 1.03 (95% CI 1.02, 1.041) for cardiovascular disease, 1.013 (95% CI 0.996, 1.03) to 1.058 (95% CI 1.034, 1.082) for cerebrovascular disease, and 1.02 (95% CI 1.006, 1.034) for ischemic heart disease. HRs remained significant after adjustment for PM2.5. Long term exposure to ozone is related to an increased risk of mortality from cardiovascular and cerebrovascular diseases; the risk varies by location across Canada and is not attenuated by adjustment for PM2.5. This research shows that the SSC can be used to define geographic regions and it demonstrates the importance of accounting for that spatial variability when studying the long term health effects of air pollution., (Crown Copyright © 2016. Published by Elsevier Ltd. All rights reserved.)

Rationale: Tropospheric ozone (O3) is potentially associated with cardiovascular disease risk and premature death. Results from long-term epidemiological studies on O3 are scarce and inconclusive., Objectives: In this study, we examined associations between chronic ambient O3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults., Methods: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 μm [PM2.5]) and NO2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual- and ecological-level covariates., Measurements and Main Results: In single-pollutant models, we observed significant positive associations between O3, PM2.5, and NO2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM2.5, significant positive associations remained between O3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO2. We also observed positive mortality associations with both PM2.5 (both near source and regional) and NO2 in multipollutant models., Conclusions: Findings derived from this large-scale prospective study suggest that long-term ambient O3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O3 concentrations.

Previous evidence suggests that exposure to outdoor air pollution during pregnancy could alter fetal metabolic function, which could increase the risk of obesity in childhood. However, to our knowledge, no epidemiologic study has investigated the association between prenatal exposure to air pollution and indicators of fetal metabolic function. We investigated the association between maternal exposure to nitrogen dioxide and fine particulate matter (aerodynamic diameter ≤2.5 µm) and umbilical cord blood leptin and adiponectin levels with mixed-effects linear regression models among 1,257 mother-infant pairs from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, conducted in Canada (2008-2011). We observed that an interquartile-range increase in average exposure to fine particulate matter (3.2 µg/m(3)) during pregnancy was associated with an 11% (95% confidence interval: 4, 17) increase in adiponectin levels. We also observed 13% (95% confidence interval: 6, 20) higher adiponectin levels per interquartile-range increase in average exposure to nitrogen dioxide (13.6 parts per billion) during pregnancy. Significant associations were seen between air pollution markers and cord blood leptin levels in models that adjusted for birth weight z score but not in models that did not adjust for birth weight z score. The roles of prenatal exposure to air pollution and fetal metabolic function in the potential development of childhood obesity should be further explored., (© The Author 2016. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Backround: Fine particulate air pollution (PM2.5) is known to contribute to cardiorespiratory mortality but it is not clear how PM2.5 oxidative burden (i.e. the ability of PM2.5 to cause oxidative stress) may influence long-term mortality risk., Methods: We examined the relationship between PM2.5 oxidative burden and cause-specific mortality in Ontario, Canada. Integrated PM2.5 samples were collected from 30 provincial monitoring sites between 2012 and 2013. The oxidative potential (% depletion/µg) of regional PM2.5 was measured as the ability of filter extracts to deplete antioxidants (glutathione and ascorbate) in a synthetic respiratory tract lining fluid. PM2.5oxidative burden was calculated as the product of PM2.5 mass concentrations and regional estimates of oxidative potential. In total, this study included 193,300 people who completed the Canadian long-form census in 1991 and who lived within 5km of a site where oxidative potential was measured. Deaths occurring between 1991 and 2009 were identified through record linkages and Cox proportional hazard models were used to estimate hazard ratios (and 95% confidence intervals) for interquartile changes in exposure adjusting for individual-level covariates and indirect-adjustment for smoking and obesity., Results: Glutathione-related oxidative burden was associated with cause-specific mortality. For lung cancer specifically, this metric was associated with a 12% (95% CI: 5.0-19) increased risk of mortality whereas a 5.0% (95% CI: 0.1, 10) increase was observed for PM2.5. Indirect adjustment for smoking and obesity decreased the lung cancer hazard ratio for glutathione-related oxidative burden but it remained significantly elevated (HR=1.07, 95% CI: 1.005, 1.146). Ascorbate-related oxidative burden was not associated with mortality., Conclusions: Our findings suggest that glutathione-related oxidative burden may be more strongly associated with lung cancer mortality than PM2.5 mass concentrations., (Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.)

Background: Understanding the shape of the relationship between long-term exposure to ambient fine particulate matter (PM2.5) concentrations and health risks is critical for health impact and risk assessment. Studies evaluating the health risks of exposure to low concentrations of PM2.5 are limited. Further, many existing studies lack individual-level information on potentially important behavioural confounding factors., Methods: A prospective cohort study was conducted among a subset of participants in a cohort that linked respondents of the Canadian Community Health Survey to mortality (n = 299,500) with satellite-derived ambient PM2.5 estimates. Participants enrolled between 2000 and 2008 were followed to date of death or December 31, 2011. Cox proportional hazards models were used to estimate hazard ratios (HRs) for mortality attributed to PM2.5 exposure, adjusted for individual-level and contextual covariates, including smoking behaviour and body mass index (BMI)., Results: Approximately 26,300 non-accidental deaths, of which 32.5 % were due to circulatory disease and 9.1 % were due to respiratory disease, occurred during the follow-up period. Ambient PM2.5 exposures were relatively low (mean = 6.3 μg/m(3)), yet each 10 μg/m(3) increase in exposure was associated with increased risks of non-accidental (HR = 1.26; 95 % CI: 1.19-1.34), circulatory disease (HR = 1.19; 95 % CI: 1.07-1.31), and respiratory disease mortality (HR = 1.52; 95 % CI: 1.26-1.84) in fully adjusted models. Higher hazard ratios were observed for respiratory mortality among respondents who never smoked (HR = 1.97; 95 % CI: 1.24-3.13 vs. HR = 1.45; 95 % CI: 1.17-1.79 for ever smokers), and among obese (BMI ≥ 30) respondents (HR = 1.76; 95 % CI: 1.15-2.69 vs. HR = 1.41; 95 % CI: 1.04-1.91 for normal weight respondents), though differences between groups were not statistically significant. A threshold analysis for non-accidental mortality estimated a threshold concentration of 0 μg/m(3) (+95 % CI = 4.5 μg/m(3))., Conclusions: Increased risks of non-accidental, circulatory, and respiratory mortality were observed even at very low concentrations of ambient PM2.5. HRs were generally greater than most literature values, and adjusting for behavioural covariates served to reduce HR estimates slightly.

Background: Numerous studies have examined associations between air pollution and pregnancy outcomes, but most have been restricted to urban populations living near monitors., Objectives: We examined the association between pregnancy outcomes and fine particulate matter in a large national study including urban and rural areas., Methods: Analyses were based on approximately 3 million singleton live births in Canada between 1999 and 2008. Exposures to PM2.5 (particles of median aerodynamic diameter ≤ 2.5 μm) were assigned by mapping the mother's postal code to a monthly surface based on a national land use regression model that incorporated observations from fixed-site monitoring stations and satellite-derived estimates of PM2.5. Generalized estimating equations were used to examine the association between PM2.5 and preterm birth (gestational age < 37 weeks), term low birth weight (< 2,500 g), small for gestational age (SGA; < 10th percentile of birth weight for gestational age), and term birth weight, adjusting for individual covariates and neighborhood socioeconomic status (SES)., Results: In fully adjusted models, a 10-μg/m(3) increase in PM2.5 over the entire pregnancy was associated with SGA (odds ratio = 1.04; 95% CI 1.01, 1.07) and reduced term birth weight (-20.5 g; 95% CI -24.7, -16.4). Associations varied across subgroups based on maternal place of birth and period (1999-2003 vs. 2004-2008)., Conclusions: This study, based on approximately 3 million births across Canada and employing PM2.5 estimates from a national spatiotemporal model, provides further evidence linking PM2.5 and pregnancy outcomes.

Most studies on the association between exposure to fine particulate matter (PM2.5) and mortality have considered only total concentration of PM2.5 or individual components of PM2.5, and not the combined effects of concentration and particulate composition. We sought to develop a method to estimate the risk of death from long-term exposure to PM2.5 and the distribution of its components, namely: sulphate, nitrate, ammonium, organic mass, black carbon, and mineral dust. We decomposed PM2.5 exposure into the sum of total concentration and the proportion of each component. We estimated the risk of death due to exposure using a cohort of ~2.4 million Canadians who were followed for vital status over 16 years. Modelling the concentration of PM2.5 with the distribution of the proportions of components together was a superior predictor for mortality than either total PM2.5 concentration alone, or all component concentrations modelled together. Our new approach has the advantage of characterizing the toxicity of the atmosphere in its entirety. This is required to fully understand the health benefits associated with strategies to improve air quality that may result in complex changes not only in PM2.5 concentration, but also in the distribution of particle components.

Background: Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up., Objective: We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians., Methods: We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects' residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2., Results: PM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2., Conclusions: In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2., Citation: Crouse DL, Peters PA, Hystad P, Brook JR, van Donkelaar A, Martin RV, Villeneuve PJ, Jerrett M, Goldberg MS, Pope CA III, Brauer M, Brook RD, Robichaud A, Menard R, Burnett RT. 2015. Ambient PM2.5, O3, and NO2 exposures and associations with mortality over 16 years of follow-up in the Canadian Census Health and Environment Cohort (CanCHEC). Environ Health Perspect 123:1180-1186; http://dx.doi.org/10.1289/ehp.1409276.

The independent and joint effects of within- and between-city contrasts in air pollution on mortality have been investigated rarely. To examine the differential effects of between- versus within-city contrasts in pollution exposure, we used both ambient measurements and land use regression models to assess associations with mortality and exposure to nitrogen dioxide (NO2) among ~735,600 adults in 10 of the largest Canadian cities. We estimated exposure contrasts partitioned into within- and between-city contrasts, and the sum of these as overall exposures, for every year from 1984 to 2006. Residential histories allowed us to follow subjects annually during the study period. We calculated hazard ratios (HRs) adjusted for many personal and contextual variables. In fully-adjusted, random-effects models, we found positive associations between overall NO2 exposures and mortality from non-accidental causes (HR per 5 p.p.b.: 1.05; 95% confidence interval (CI): 1.03-1.07), cardiovascular disease (HR per 5 p.p.b.: 1.04; 95% CI: 1.01-1.06), ischaemic heart disease (HR per 5 p.p.b.: 1.05; 95% CI: 1.02-1.08) and respiratory disease (HR per 5 p.p.b.: 1.04; 95% CI: 0.99-1.08), but not from cerebrovascular disease (HR per 5 p.p.b.: 1.01; 95% CI: 0.96-1.06). We found that most of these associations were determined by within-city contrasts, as opposed to by between-city contrasts in NO2. Our results suggest that variation in NO2 concentrations within a city may represent a more toxic mixture of pollution than variation between cities.

A few recent studies have reported positive associations between long-term exposure to traffic-related air pollution and the incidence of breast cancer. We capitalized on an existing Canadian multi-site population-based case-control study to further investigate this association. We used the National Enhanced Cancer Surveillance System, a population-based case-control study conducted in eight of 10 Canadian provinces from 1994 to 1997. A total of 1569 breast cancer cases and 1872 population controls who reported at least 90% complete self-reported addresses over the 1975-1994 exposure period were examined. Mean exposure levels to nitrogen dioxide (NO2) (an indicator of traffic-related air pollution) were estimated for this period using three different measures: (1) satellite-derived observations; (2) satellite-derived observations scaled with historical fixed-site measurements of NO2; and (3) a national land-use regression (LUR) model. Proximity to major roads was also examined. Using unconditional logistic regression, stratified by menopausal status, we estimated odds ratios (ORs) adjusted for many individual-level and contextual breast cancer risk factors. We observed positive associations between incident breast cancer and all three measures of NO2 exposure from 1975 to 1994. In fully adjusted models for premenopausal breast cancer, a 10ppb increase in NO2 exposure estimated from the satellite-derived observations, the scaled satellite-derived observations, and the national LUR model produced ORs of 1.26 (95% confidence intervals (CIs): 0.92-1.74), 1.32 (95% CI: 1.05-1.67) and 1.28 (95% CI: 0.92-1.79). For postmenopausal breast cancer, we found corresponding ORs of 1.10 (95% CI: 0.88-1.36), 1.10 (95% CI: 0.94-1.28) and 1.07 (95% CI: 0.86-1.32). Substantial heterogeneity in the ORs was observed across the eight Canadian provinces and reduced ORs were observed when models were restricted to women who had received routine mammography examinations. No associations were found for road proximity measures. This study provides some support for the hypothesis that traffic-related air pollution may be associated with the development of breast cancer, especially in premenopausal women. With the few studies available, further research is clearly needed., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Objective: Recent studies suggest that chronic exposure to air pollution can promote the development of diabetes. However, whether this relationship actually translates into an increased risk of mortality attributable to diabetes is uncertain., Research Design and Methods: We evaluated the association between long-term exposure to ambient fine particulate matter (PM2.5) and diabetes-related mortality in a prospective cohort analysis of 2.1 million adults from the 1991 Canadian census mortality follow-up study. Mortality information, including ∼5,200 deaths coded as diabetes being the underlying cause, was ascertained by linkage to the Canadian Mortality Database from 1991 to 2001. Subject-level estimates of long-term exposure to PM2.5 were derived from satellite observations. The hazard ratios (HRs) for diabetes-related mortality were related to PM2.5 and adjusted for individual-level and contextual variables using Cox proportional hazards survival models., Results: Mean PM2.5 exposure levels for the entire population were low (8.7 µg/m3; SD, 3.9 µg/m3; interquartile range, 6.2 µg/m3). In fully adjusted models, a 10-µg/m3 elevation in PM2.5 exposure was associated with an increase in risk for diabetes-related mortality (HR, 1.49; 95% CI, 1.37-1.62). The monotonic change in risk to the population persisted to PM2.5 concentration<5 µg/m3., Conclusions: Long-term exposure to PM2.5, even at low levels, is related to an increased risk of mortality attributable to diabetes. These findings have considerable public health importance given the billions of people exposed to air pollution and the worldwide growing epidemic of diabetes.

The 1991 Canadian Census Cohort is the largest population-based cohort in Canada (N=2,734,835). Prior to the creation of this Cohort, no national population-based Canadian cohort was available to examine mortality by socioeconomic indicators. The 1991 Canadian Census Cohort was created via the linkage of a sub-sample of respondents from the mandatory 1991 Canadian Census long-form to historical tax summary files, Canadian Mortality Database, Canadian Cancer Database, 1991 Health and Activity Limitation Survey and a sub-sample of the Longitudinal Worker File. Overall ascertainment of mortality and cancer is anticipated to be nearly complete and the Cohort is broadly representative of most groups in the Canadian population. The Cohort has been used to examine mortality outcomes by different indicators of socioeconomic status, occupational categories, ethnic groups, educational attainment, and for exposure to ambient air pollution. Results have shown that the estimated remaining years of life at age 25 differed substantially by income adequacy quintile, educational attainment, housing type and Aboriginal ancestry.

Objectives: There is a paucity of information on environmental risk factors for prostate cancer. We conducted a case-control study in Montreal to estimate associations with exposure to ground-level nitrogen dioxide (NO2), a marker for traffic-related air pollution., Methods: Cases were 803 men with incident prostate cancer, ≤75 years of age, and diagnosed across all French hospitals in Montreal. Concurrently, 969 controls were drawn from electoral lists of French-speaking individuals residing in the same electoral districts as the cases and frequency-matched by age. Concentrations of NO2 were measured across Montreal in 2005-2006. We developed a land use regression model to predict concentrations of NO2 across Montreal for 2006. These estimates were back-extrapolated to 1996. Estimates were linked to residential addresses at the time of diagnosis or interview. Unconditional logistic regression was used, adjusting for potential confounding variables., Results: For each increase of 5 parts per billion of NO2, as estimated from the original land use regression model in 2006, the OR5ppb adjusted for personal factors was 1.44 (95% CI 1.21 to 1.73). Adding in contextual factors attenuated the OR5ppb to 1.27 (95% CI 1.03 to 1.58). One method for back-extrapolating concentrations of NO2 to 1996 (about 10 years before the index date) gave the following OR5ppb: 1.41 (95% CI 1.24 to 1.62) when personal factors were included, and 1.30 (95% CI 1.11 to 1.52) when contextual factors were added., Conclusions: Exposure to ambient concentrations of NO2 at the current address was associated with an increased risk of prostate cancer. This novel finding requires replication.

Background: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM(2.5))]. This is the first national-level cohort study to investigate these risks in Canada., Objective: We investigated the association between long-term exposure to ambient PM(2.5) and cardiovascular mortality in nonimmigrant Canadian adults., Methods: We assigned estimates of exposure to ambient PM(2.5) derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models., Results: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m(3) increase in concentrations of PM(2.5). Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities., Conclusions: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM(2.5). Associations were observed with exposures to PM(2.5) at concentrations that were predominantly lower (mean, 8.7 μg/m(3); interquartile range, 6.2 μg/m(3)) than those reported previously.

Background: Only about 30% of cases of breast cancer can be explained by accepted risk factors. Occupational studies have shown associations between the incidence of breast cancer and exposure to contaminants that are found in ambient air., Objectives: We sought to determine whether the incidence of postmenopausal breast cancer is associated with exposure to urban air pollution., Methods: We used data from a case-control study conducted in Montreal, Quebec, in 1996-1997. Cases were 383 women with incident invasive breast cancer, and controls were 416 women with other incident, malignant cancers, excluding those potentially associated with selected occupational exposures. Concentrations of nitrogen dioxide (NO2) were measured across Montreal in 2005-2006. We developed a land-use regression model to predict concentrations of NO2 across Montreal for 2006, and developed two methods to extrapolate the estimates to 1985 and 1996. We linked these estimates to addresses of residences of subjects at time of interview. We used unconditional logistic regression to adjust for accepted and suspected risk factors and occupational exposures., Results: For each increase of 5 ppb NO2 estimated in 1996, the adjusted odds ratio was 1.31 (95% confidence interval, 1.00-1.71). Although the size of effect varied somewhat across periods, we found an increased risk of approximately 25% for every increase of 5 ppb in exposure., Conclusions: We found evidence of an association between the incidence of postmenopausal breast cancer and exposure to ambient concentrations of NO2. Further studies are needed to confirm whether NO2 or other components of traffic-related pollution are indeed associated with increased risks.

Some neighbourhoods in urban areas are characterised by concentrations of socially and materially deprived populations. Additionally, levels of ambient air pollution in a city can be variable at the local scale and can create disparities in air quality between neighbourhoods. Socioeconomic and physical characteristics of neighbourhood environments can affect the health and well-being of local residents. In this paper we identify whether neighbourhoods in Montreal, Canada characterised by social and material deprivation have higher levels of ambient air pollution than do others. We collected two-week integrated samples of nitrogen dioxide (NO(2)) at 133 sites in Montreal during three seasons between 2005 and 2006. We used these data in a geographic information system, along with data describing characteristics of land use, roads, and traffic, to create a spatial model of predicted mean annual concentrations of NO(2) across Montreal. Next, we collected neighbourhood socioeconomic information for 501 census tracts and overlaid their boundaries on the pollution surface. We calculated Pearson correlation coefficients and 95% confidence intervals (CI) between neighbourhood-level indicators of deprivation and levels of ambient NO(2). We found associations between concentrations of NO(2) and neighbourhood-level indicators of material deprivation, including median household income, and with indicators of social deprivation, including proportion of people living alone. We identified specific neighbourhoods that were characterised by a double burden of high levels of deprivation and high concentrations of ambient NO(2). Because of the particular social geography in Montreal, we found that not all deprived neighbourhoods had high levels of pollution and that some affluent neighbourhoods in the downtown core had high levels. Our results underscore the importance of considering social contexts in interpreting general associations between social and environmental risks to population health.