Inequality in the Distribution of Air Pollution Attributable Mortality Within Canadian Cities.

Recent studies have identified inequality in the distribution of air pollution attributable health impacts, but to our knowledge this has not been examined in Canadian cities. We evaluated the extent and sources of inequality in air pollution attributable mortality at the census tract (CT) level in seven of Canada's largest cities. We first regressed fine particulate matter (PM2.5) and nitrogen dioxide (NO2) attributable mortality against the neighborhood (CT) level prevalence of age 65 and older, low income, low educational attainment, and identification as an Indigenous (First Nations, Métis, Inuit) or Black person, accounting for spatial autocorrelation. We next examined the distribution of baseline mortality rates, PM2.5 and NO2 concentrations, and attributable mortality by neighborhood (CT) level prevalence of these characteristics, calculating the concentration index, Atkinson index, and Gini coefficient. Finally, we conducted a counterfactual analysis of the impact of reducing baseline mortality rates and air pollution concentrations on inequality in air pollution attributable mortality. Regression results indicated that CTs with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality. Concentration index, Atkinson index, and Gini coefficient values revealed different degrees of inequality among the cities. Counterfactual analysis indicated that inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities. Reducing inequality in air pollution attributable mortality requires reducing disparities in both baseline mortality and air pollution exposure.

The prevalence of household air conditioning in Canada.

Background: Household air conditioning is one of the most effective approaches for reducing the health impacts of heat exposure; however, few studies have measured the prevalence of household air conditioning in Canada. Data and methods: Data were obtained from the 2017 Canadian Community Health Survey and the 2017 Households and the Environment Survey. Statistics Canada linked the survey respondents and created survey weights. Four heat-vulnerable populations were defined: older adults, older adults living alone, older adults with at least one health condition associated with reduced thermoregulation and older adults living alone and with a health condition associated with reduced thermoregulation. Weighted ratios and logistic regression models were used to analyze person-level air conditioning rates for national, regional and heat-vulnerable populations. Results: Approximately 61% of the national population had household air conditioning. Regional rates ranged between 32% in British Columbia and 85% in Ontario. People living alone and people who did not own a home were significantly less likely to have air conditioning in Canada and in most regions. One heat vulnerable group, older adults living alone, had significantly lower air conditioning rates compared with the national and Ontario averages, at 56% and 81%, respectively. Interpretation: This study is the first to quantify air conditioning prevalence in Canada at the person-level. The results of this study may inform heat-health policies and climate change adaptation strategies that aim to identify populations with high risks of heat-related mortality or morbidity and low access to household air conditioning.

Using Parametric g-Computation to Estimate the Effect of Long-Term Exposure to Air Pollution on Mortality Risk and Simulate the Benefits of Hypothetical Policies: The Canadian Community Health Survey Cohort (2005 to 2015).

BACKGROUND: Numerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter ≤2.5µm in aerodynamic diameter (PM2.5)] on mortality even at relatively low levels. However, methodological challenges remain to consider potential regulatory intervention's complexity and provide actionable evidence on the predicted benefits of interventions. We propose the parametric g-computation as an alternative analytical approach to such challenges. METHOD: We applied the parametric g-computation to estimate the cumulative risks of nonaccidental death under different hypothetical intervention strategies targeting long-term exposure to PM2.5 in the Canadian Community Health Survey cohort from 2005 to 2015. On both relative and absolute scales, we explored the benefits of hypothetical intervention strategies compared with the natural course that a) set the simulated exposure value at each follow-up year to a threshold value if exposure was above the threshold (8.8 µg/m3, 7.04 µg/m3, 5 µg/m3, and 4 µg/m3), and b) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average PM2.5 concentration with 1-y lag at the postal code of respondents' annual mailing addresses as their long-term exposure to PM2.5. We considered baseline and time-varying confounders, including demographics, behavior characteristics, income level, and neighborhood socioeconomic status. We also included the R syntax for reproducibility and replication. RESULTS: All hypothetical intervention strategies explored led to lower 11-y cumulative mortality risks than the estimated value under the natural course without intervention, with the smallest reduction of 0.20 per 1,000 participants (95% CI: 0.06, 0.34) under the threshold of 8.8 µg/m3, and the largest reduction of 3.40 per 1,000 participants (95% CI: -0.23, 7.03) under the relative reduction of 10% per interval. The reductions in cumulative risk, or numbers of deaths that would have been prevented if the intervention was employed instead of maintaining the status quo, increased over time but flattened toward the end of the follow-up period. Estimates among those ≥65 years of age were greater with a similar pattern. Our estimates were robust to different model specifications. DISCUSSION: We found evidence that any intervention further reducing the long-term exposure to PM2.5 would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient PM2.5. The parametric g-computation used in this study provides flexibilities in simulating real-world interventions, accommodates time-varying exposure and confounders, and estimates adjusted survival curves with clearer interpretation and more information than a single hazard ratio, making it a valuable analytical alternative in air pollution epidemiological research. https://doi.org/10.1289/EHP11095.

Mortality inequalities of Black adults in Canada.

Background: Mortality rates in Canada have been shown to vary by population group (e.g., Indigenous peoples, immigrants) and social economic status (e.g., income levels). Mortality patterns for some groups, including Black individuals, are not as well known. The objective of this study was to assess cause-specific mortality for Black adults living in Canada. Methods: Mortality inequalities between Black and White cohort members were estimated by sex using Cox proportional hazard models, based on data from the 2001, 2006 and 2011 Canadian Census Health and Environment Cohorts (CanCHECs). The CanCHEC cycles were combined and followed for mortality between Census Day and December 31, 2016 or 2019, resulting in a follow-up period of 15.6, 13.6 or 8.6 years, depending on the CanCHEC cycle. Results: Ischemic heart disease mortality was the leading cause of death among adult Black males (12.9%) and females (9.8%), as it is for adult White males (16.4%) and females (12.4%). Despite reduced risk of all-cause mortality among Black males and females, compared with White cohort members, there was notable increased risk for some cause-specific mortality. For instance, in the age-adjusted model, among the 25 causes of death examined, Black males had an increased risk of dying from four causes (HIV/AIDS, prostate cancer, diabetes mellitus and cerebrovascular disease), compared with White males. Similarly, Black females were at an increased risk for 6 causes of death (HIV/AIDS, stomach cancer, corpus uteri cancer, lymphomas and multiple myeloma, diabetes mellitus, and endocrine disorders) out of the 27 causes of death examined. These relative increased risks persisted for most causes of death after adjustment for differences in important social determinants of health. Interpretation: Results showed substantial variability in the risk of dying by cause of death between Black and White cohort members. An important step in reducing health inequities is the routine identification and surveillance of different health outcomes by population groups. This study helps fill that information gap.

Impact of lowering fine particulate matter from major emission sources on mortality in Canada: A nationwide causal analysis.

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

Long-term Exposure to Oxidant Gases and Mortality: Effect Modification by PM 2.5 Transition Metals and Oxidative Potential.

BACKGROUND: Populations are simultaneously exposed to outdoor concentrations of oxidant gases (i.e., O 3 and NO 2 ) and fine particulate air pollution (PM 2.5 ). Since oxidative stress is thought to be an important mechanism explaining air pollution health effects, the adverse health impacts of oxidant gases may be greater in locations where PM 2.5 is more capable of causing oxidative stress. METHODS: We conducted a cohort study of 2 million adults in Canada between 2001 and 2016 living within 10 km of ground-level monitoring sites for outdoor PM 2.5 components and oxidative potential. O x exposures (i.e., the redox-weighted average of O 3 and NO 2 ) were estimated using a combination of chemical transport models, land use regression models, and ground-level data. Cox proportional hazards models were used to estimate associations between 3-year moving average O x and mortality outcomes across strata of transition metals and sulfur in PM 2.5 and three measures of PM 2.5 oxidative potential adjusting for possible confounding factors. RESULTS: Associations between O x and mortality were consistently stronger in regions with elevated PM 2.5 transition metal/sulfur content and oxidative potential. For example, each interquartile increase (6.27 ppb) in O x was associated with a 14.9% (95% CI = 13.0, 16.9) increased risk of nonaccidental mortality in locations with glutathione-related oxidative potential (OP GSH ) above the median whereas a 2.50% (95% CI = 0.600, 4.40) increase was observed in regions with OP GSH levels below the median (interaction P value <0.001). CONCLUSION: Spatial variations in PM 2.5 composition and oxidative potential may contribute to heterogeneity in the observed health impacts of long-term exposures to oxidant gases.

How low can you go? Air pollution affects mortality at very low levels.

The World Health Organization (WHO) recently released new guidelines for outdoor fine particulate air pollution (PM2.5) recommending an annual average concentration of 5 µg/m3. Yet, our understanding of the concentration-response relationship between outdoor PM2.5 and mortality in this range of near-background concentrations remains incomplete. To address this uncertainty, we conducted a population-based cohort study of 7.1 million adults in one of the world's lowest exposure environments. Our findings reveal a supralinear concentration-response relationship between outdoor PM2.5 and mortality at very low (<5 µg/m3) concentrations. Our updated global concentration-response function incorporating this new information suggests an additional 1.5 million deaths globally attributable to outdoor PM2.5 annually compared to previous estimates. The global health benefits of meeting the new WHO guideline for outdoor PM2.5 are greater than previously assumed and indicate a need for continued reductions in outdoor air pollution around the world.

Neighbourhood walkability and mortality: Findings from a 15-year follow-up of a nationally representative cohort of Canadian adults in urban areas.

BACKGROUND: Using a nationally representative cohort of Canadian adults, we assessed associations between neighbourhood walkability and cause-specific mortality and investigated whether they differed by socioeconomic status. METHODS: The study population was drawn from the 2001 Canadian Census Health and Environment Cohort, which contains individual-level data from a random sample of 20% of Canadian households mandated to complete the long-form census. We included those aged ≥ 25 years at baseline who lived in urban and suburban areas. The national death registry was used to ascertain annual vital status. Linkages to annual income tax data provided place of residence. The Canadian Active Living Environments, a national index that summarizes walkability across Canadian neighbourhoods, was assigned to individuals' residential history. The Cox proportional hazards model was used to assess associations between walkability and cause-specific mortality. RESULTS: A total of 1.8 million participants (52.5% female) accrued 27.3 million person-years and 265 710 deaths during the 15-year follow-up. The adjusted hazard ratio (HR) for living in a highly walkable neighbourhood relative to living in the least walkable neighbourhoods was associated with a 9% (HR: 0.91 [0.88, 0.95]) and 3% (HR: 0.97 [0.94, 0.99]) reduced risk of cardiovascular and all non-accidental mortality, respectively. The strongest benefits of walkability were found among individuals within the lowest education and household income categories, and who lived in the most deprived neighbourhoods. There were no significant associations (most [class 5] versus least [class 1] walkable HR: 0.84 [0.61-1.16]) seen for accidental traffic mortality. CONCLUSIONS: Canadian adults who live in walkable neighbourhoods have lower rates of cardiovascular and non-accidental mortality, with the greatest benefits seen in those from the lowest socioeconomic groups.

Residential proximity to greenness and adverse birth outcomes in urban areas: Findings from a national Canadian population-based study.

BACKGROUND: Over the last decade, several studies have reported that residential proximity to vegetation, or 'greenness', is associated with improved birth outcomes, including for term birth weight (TBW), preterm birth (PTB), and small for gestational age (SGA). However, there remain several uncertainties about these possible benefits including the role of air pollution, and the extent to they are influenced socioeconomic status. METHODS: We addressed these gaps using a national population-based study of 2.2 million singleton live births in Canadian metropolitan areas between 1999 and 2008. Exposures to greenness, fine particulate matter (PM2.5), and nitrogen dioxide (NO2) were assigned to infants using the postal code of their mother's residence at the time of birth. The Normalized Difference Vegetation Index (NDVI) was used to characterize greenness, while estimates of ambient PM2.5 and NO2 were estimated using remote sensing, and a national land-use regression surface, respectively. Multivariable regression analysis was performed to describe associations between residential greenness and the birth outcomes. Stratified analyses explored whether these associations were modified by neighbourhood measures of socioeconomic status. RESULTS: Mothers who lived in greener areas had a lower risk of low TBW, PTB, and SGA babies. These associations persisted after adjustment for ambient NO2 and PM2.5. Specifically, in fully adjusted models, an interquartile range (IQR = 0.16) increase in the NDVI within a residential buffer of 250 m yielded odds ratios of 0.93 (95% confidence interval (CI): 0.92, 0.94), 0.94 (95% CI: 0.92, 0.95), and 0.94 (95% CI: 0.93, 0.95) for the outcomes of PTB, low TBW, and SGA, respectively. Similarly, an IQR increase in greenness was associated with a 16.3 g (95% CI: 15.3, 17.4) increase in TBW. We found inverse associations between greenness and the occurrence of adverse birth outcomes regardless of the socioeconomic status of the neighbourhood. INTERPRETATION: Our findings support the hypothesis that residential greenness contributes to healthier pregnancies, that these associations are independent from exposure to air pollution. , and that proximity to greenness benefits all mothers regardless of socioeconomic status.

Ambient air pollution and the risk of acute myocardial infarction and stroke: A national cohort study.

We used a large national cohort in Canada to assess the incidence of acute myocardial infarction (AMI) and stroke hospitalizations in association with long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3). The study population comprised 2.7 million respondents from the 2006 Canadian Census Health and Environment Cohort (CanCHEC), followed for incident hospitalizations of AMI or stroke between 2006 and 2016. We estimated 10-year moving average estimates of PM2.5, NO2, and O3, annually. We used Cox proportional hazards models to examine the associations adjusting for various covariates. For AMI, each interquartile range (IQR) increase in exposure was found to be associated with a hazard ratio of 1.026 (95% CI: 1.007-1.046) for PM2.5, 1.025 (95% CI: 1.001-1.050) for NO2, and 1.062 (95% CI: 1.041-1.084) for O3, respectively. Similarly, for stroke, an IQR increase in exposure was associated with a hazard ratio of 1.078 (95% CI: 1.052-1.105) for PM2.5, 0.995 (95% CI: 0.965-1.030) for NO2, and 1.055 (95% CI: 1.028-1.082) for O3, respectively. We found consistent evidence of positive associations between long-term exposures to PM2.5, and O3, and to a lesser degree NO2, with incident AMI and stroke hospitalizations.

The influence of outdoor PM2.5 concentration at workplace on nonaccidental mortality estimates in a Canadian census-based cohort.

BACKGROUND: Associations between mortality and exposure to ambient air pollution are usually explored using concentrations of residential outdoor fine particulate matter (PM2.5) to estimate individual exposure. Such studies all have an important limitation in that they do not capture data on individual mobility throughout the day to areas where concentrations may be substantially different, leading to possible exposure misclassification. We examine the possible role of outdoor PM2.5 concentrations at work for a large population-based mortality cohort. METHODS: Using the 2001 Canadian Census Health and Environment Cohort (CanCHEC), we created a time-weighted average that incorporates employment hours worked in the past week and outdoor PM2.5 concentration at work and home. We used a Cox proportional hazard model with a 15-year follow-up (2001 to 2016) to explore whether inclusion of workplace estimates had an impact on hazard ratios for mortality for this cohort. RESULTS: Hazard ratios relying on outdoor PM2.5 concentration at home were not significantly different from those using a time-weighted estimate, for the full cohort, nor for those who commute to a regular workplace. When exploring cohort subgroups according to neighborhood type and commute distance, there was a notable but insignificant change in risk of nonaccidental death for those living in car-oriented neighborhoods, and with commutes greater than 10 km. CONCLUSIONS: Risk analyses performed with large cohorts in low-pollution environments do not seem to be biased if relying solely on outdoor PM2.5 concentrations at home to estimate exposure.

Changes in exposure to ambient fine particulate matter after relocating and long term survival in Canada: quasi-experimental study.

OBJECTIVE: To investigate the association between changes in long term residential exposure to ambient fine particulate matter (PM2.5) and premature mortality in Canada. DESIGN: Population based quasi-experimental study. SETTING: Canada. PARTICIPANTS: 663 100 respondents to the 1996, 2001, and 2006 Canadian censuses aged 25-89 years who had consistently lived in areas with either high or low PM2.5 levels over five years preceding census day and moved during the ensuing five years. INTERVENTIONS: Changes in long term exposure to PM2.5 arising from residential mobility. MAIN OUTCOME MEASURES: The primary outcome was deaths from natural causes. Secondary outcomes were deaths from any cardiometabolic cause, any respiratory cause, and any cancer cause. All outcomes were obtained from the national vital statistics database. RESULTS: Using a propensity score matching technique with numerous personal, socioeconomic, health, and environment related covariates, each participant who moved to a different PM2.5 area was matched with up to three participants who moved within the same PM2.5 area. In the matched groups that moved from high to intermediate or low PM2.5 areas, residential mobility was associated with a decline in annual PM2.5 exposure from 10.6 µg/m3 to 7.4 and 5.0 µg/m3, respectively. Conversely, in the matched groups that moved from low to intermediate or high PM2.5 areas, annual PM2.5 increased from 4.6 µg/m3 to 6.7 and 9.2 µg/m3. Five years after moving, individuals who experienced a reduction in exposure to PM2.5 from high to intermediate levels showed a 6.8% (95% confidence interval 1.7% to 11.7%) reduction in mortality (2510 deaths in 56 025 v 4925 deaths in 101 960). A greater decline in mortality occurred among those exposed to a larger reduction in PM2.5. Increased mortality was found with exposure to PM2.5 from low to high levels, and to a lesser degree from low to intermediate levels. Furthermore, the decreases in PM2.5 exposure were most strongly associated with reductions in cardiometabolic deaths, whereas the increases in PM2.5 exposure were mostly related to respiratory deaths. No strong evidence was found for the changes in PM2.5 exposure with cancer related deaths. CONCLUSIONS: In Canada, decreases in PM2.5 were associated with lower mortality, whereas increases in PM2.5 were associated with higher mortality. These results were observed at PM2.5 levels considerably lower than many other countries, providing support for continuously improving air quality.

Long-term ozone exposure and mortality from neurological diseases in Canada.

BACKGROUND: There is increasing interest in the health effects of air pollution. However, the relationships between ozone exposure and mortality attributable to neurological diseases remain unclear. OBJECTIVES: To assess associations of long-term exposure to ozone with death from Parkinson's disease, dementia, stroke, and multiple sclerosis. METHODS: Our analyses were based on the 2001 Canadian Census Health and Environment Cohort. Census participants were linked with vital statistics records through 2016, resulting in a cohort of 3.5 million adults/51,045,700 person-years, with 8,500/51,300/43,300/1,300 deaths from Parkinson's/dementia/stroke/multiple sclerosis, respectively. Ten-year average ozone concentrations estimated by chemical transport models and adjusted by ground measurements were assigned to subjects based on postal codes. Cox proportional hazards models were used to calculate hazard ratios (HRs) for deaths from the four neurological diseases, adjusting for eight common demographic and socioeconomic factors, seven environmental indexes, and six contextual covariates. RESULTS: The fully adjusted HRs for Parkinson's, dementia, stroke, and multiple sclerosis mortalities related to one interquartile range increase in ozone (10.1 ppb), were 1.09 (95% confidence interval 1.04-1.14), 1.08 (1.06-1.10), 1.06 (1.04-1.09), and 1.35 (1.20-1.51), respectively. The covariates did not influence significance of the ozone-mortality associations, except airshed (i.e., broad region of Canada). During the period of 2001-2016, 5.66%/5.01%/ 3.77%/19.11% of deaths from Parkinson's/dementia/stroke/multiple sclerosis, respectively, were attributable to ozone exposure. CONCLUSIONS: We found positive associations between ozone exposure and mortality due to Parkinson's, dementia, stroke, and multiple sclerosis.

Self-rated stress, distress, mental health, and health as modifiers of the association between long-term exposure to ambient pollutants and mortality.

BACKGROUND: Individual and neighbourhood-scale socioeconomic characteristics modify associations between exposure to air pollution and mortality. The role of stress, which may integrate effects of social and environmental exposures on health, is unknown. We examined whether an individual's perspective on their own well-being, as assessed using self-rated measures of stress and health, modifies the pollutant-mortality relationship. METHODS: The Canadian Community Health Survey (CCHS)-mortality cohort includes respondents from surveys administered between 2001 and 2012 linked to vital statistics and postal codes from 1981 until 2016. Annual fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) exposure estimates were attached to a sample of cohort members aged 30-89 years (n = 398,300 respondents/3,848,400 person-years). We examined whether self-rated stress, distress, mental health, and general health modified associations between long-term exposure to each pollutant (three-year moving average with one-year lag) and non-accidental mortality using Cox survival models, adjusted for individual- (i.e. socioeconomic and behavioural) and neighbourhood-scale covariates. RESULTS: In fully-adjusted models, the relationship between exposure to pollutants and mortality was stronger among those with poor self-rated mental health, including a significant difference for NO2 (hazard ratio (HR) = 1.15, 95% CI 1.06-1.25 per IQR) compared to those with very good/excellent mental health (HR = 1.05, 95% CI 1.01-1.08; Cochran's Q = 4.01; p < 0.05). Poor self-rated health was similarly associated with higher pollutant-associated HRs, but only in unadjusted models. Stress and distress did not modify pollutant-mortality associations. CONCLUSIONS: Poor self-rated mental and general health were associated with increased mortality attributed to exposure to ambient pollutants.

The association between ambient air pollution concentrations and psychological distress.

BACKGROUND: A growing number of epidemiological studies have linked air pollution exposure to psychological conditions. Laboratory studies indicate that air pollutants can activate the neuroendocrine stress axis and modulate stress hormone levels, which could contribute to the development or exacerbation of psychological distress. The present study examined the spatial associations between air pollutants (fine particulate matter [PM2.5], nitrogen dioxide [NO2] and ground-level ozone [O3]) and psychological distress among subjects in the most populous provinces in Canada. DATA AND METHODS: Subjects were sampled from the Canadian Community Health Survey in three regions (Quebec in 2005 [n=25,800], British Columbia and Alberta in 2005 [n=23,000], and Ontario in 2011 [n=36,000]), and were assigned estimates of annual exposure to three ambient air pollutants (PM2.5, NO2 and O3) for the same years. Individual psychological distress was assessed using the Kessler Psychological Distress Scale (K10), based on anxiety and depressive symptoms in the past month. Regression models (both ordinary least squares and simultaneous autoregressive models) were applied to estimate associations between K10 distress scores and each air pollutant, after adjusting for individual (demographic, socioeconomic and behavioural) and neighbourhood covariates.. RESULTS: Psychological distress was positively associated with PM2.5 and NO2 in all three regions, and with O3 in Quebec. However, after further adjusting for individual and neighbourhood covariates, the associations between distress and air pollution remained statistically significant only in Quebec. DISCUSSION: Some evidence for positive associations between psychological distress and ambient air pollution after adjusting for spatial autocorrelation was found.

Accuracy of matching residential postal codes to census geography.

BACKGROUND: Postal codes are often the only geographic identifier available to match subjects in a health dataset to census geography. This paper describes the characteristics of postal codes reported by the Canadian population on the census and, as an indicator of geocoding accuracy, the proportion that are linked to a single dissemination area (DA). DATA AND METHODS: Postal codes reported on the 2016 Census questionnaire were matched to a combination of the Postal Code Conversion File (PCCF) and the Postal Code Conversion File Plus (PCCF+ version 7B) (reference date November 2018) to calculate population-weighted counts and the number of matches to DAs by province or territory, delivery mode type (DMT), population centre or rural area size, and census metropolitan area. The number of single matches to census tracts (CTs), census subdivisions (CSDs) and census divisions (CDs) was also calculated. RESULTS: In Canada, 72.6% of the population reported postal codes that matched to a single DA. This proportion was higher in urban cores (87.1%) and among postal codes for an urban street address (DMT=A) (85.3%) or apartment building (DMT=B) (95.3%), and was lower in rural areas (26.2% to 38.1%) and among rural postal codes (13.9%). In comparison, 89.3% and 95.4% of the population reported postal codes matching to a single CSD or CD, respectively, while 92.1% of the population that live within CT boundaries were matched to a single CT. DISCUSSION: Matching postal codes to census geography is relatively accurate and frequently one to one in urban centres. In rural areas and for some types of postal code DMTs, alternative approaches to using the PCCF and PCCF+ for attaching census geography might be explored.

Disease assimilation: The mortality impacts of fine particulate matter on immigrants to Canada.

BACKGROUND: Immigrants make up 20% of the Canadian population; however, little is known about the mortality impacts of fine particulate matter (PM2.5) air pollution on immigrants compared with non-immigrants, or about how impacts may change with duration in Canada. DATA AND METHODS: This study used the 2001 Canadian Census Health and Environment Cohort, a longitudinal cohort of 3.5 million individuals, of which 764,000 were classified as immigrants (foreign-born). Postal codes from annual income tax files were used to account for mobility among respondents and to assign annual PM2.5 concentrations from 1998 to 2016. Exposures were estimated as a three-year moving average prior to the follow-up year. Cox survival models were used to determine hazard ratios (HRs) for cause-specific mortality, comparing the Canadian and foreign-born populations, with further stratification by year of immigration grouped into 10-year cohorts. RESULTS: Differences in urban-rural settlement patterns resulted in greater exposure to PM2.5 for immigrants compared with non-immigrants (mean = 9.3 vs. 7.5 µg/m3), with higher exposures among more recent immigrants. In fully adjusted models, immigrants had higher HRs per 10 µg/m3 increase in PM2.5 concentration compared with Canadian-born individuals for cardiovascular mortality (HR [95% confidence interval] = 1.22 [1.12 to 1.34] vs. 1.12 [1.07 to 1.18]) and cerebrovascular mortality (HR = 1.25 [1.03 to 1.52] vs. 1.03 [0.93 to 1.15]), respectively. However, tests for differences between the two groups were not significant when Cochran's Q test was used. No significant associations were found for respiratory outcomes, except for lung cancer in non-immigrants (HR = 1.10 [1.02 to 1.18]). When stratified by year of immigration, differences in HRs across varied by cause of death. DISCUSSION: In Canada, PM2.5 is an equal-opportunity risk factor, with immigrants experiencing similar if not higher mortality risks compared with non-immigrants for cardiovascular-related causes of death. Some notable differences also existed with cerebrovascular and lung cancer deaths. Continued reductions in air pollution, particularly in urban areas, will improve the health of the Canadian population as a whole.

Use of a Canadian Population-Based Surveillance Cohort to Test Relationships Between Shift Work and Breast, Ovarian, and Prostate Cancer.

OBJECTIVES: Shift work with circadian disruption is a suspected human carcinogen. Additional population-representative human studies are needed and large population-based linkage cohorts have been explored as an option for surveillance shift work and cancer risk. This study uses a surveillance linkage cohort and job-exposure matrix to test relationships. METHODS: We estimated associations between shift work and breast, ovarian, and prostate cancer using the population-based Canadian Census Health and Environment Cohort (CanCHEC), linking the 1991 Canadian census to national cancer registry and mortality databases. Prevalence estimates from population labour survey data were used to estimate and assign probability of night, rotating, or evening shifts by occupation and industry. Cohort members were assigned to high (>50%), medium (>25 to 50%), low (>5 to 25%), or no (<5%) probability of exposure categories. Cox proportional hazards modelling was used to estimate associations between shift work exposure and incidence of prostate cancer in men and ovarian and breast cancer in women. RESULTS: The cohort included 1 098 935 men and 939 520 women. Hazard ratios (HRs) indicated null or inverse relationships comparing high probability to no exposure for prostate cancer: HR = 0.96, 95% confidence interval (CI) = 0.91-1.02; breast cancer: HR = 0.94, 95% CI = 0.90-0.99; and ovarian cancer: HR = 0.99, 95% CI = 0.87-1.13. CONCLUSIONS: This study showed inverse and null associations between shift work exposure and incidence of prostate, breast, or ovarian cancer. However, we explore limitations of a surveillance cohort, including a possible healthy worker survivor effect and the possibility that this relationship may require the nuanced exposure detail in primary collection studies to be measurable.

Socioeconomic disparities in life and health expectancy among the household population in Canada.

BACKGROUND: Life expectancy (LE) and health expectancy have increased throughout much of the world. However, these gains have not been shared equally across all population groups. Socioeconomic disparities exist, though varied methodologies and data sources have made it difficult to ascertain changes over time in Canada. DATA AND METHODS: The 1996 and 2011 Canadian Census Health and Environment Cohorts, with a five-year mortality follow-up, were used to estimate the LE of the household population at ages 25 and 65, according to individual-level education and income. Health status was measured by the Health Utilities Index Mark 3 instrument in two national population health surveys and was used to adjust LE to estimate health-adjusted life expectancy (HALE). Disparities in LE and HALE, and differences between cohorts, were examined. RESULTS: LE, HALE and the ratio of HALE to LE were greater at higher levels of education or income. A stepwise gradient was also observed by level of education within and across income quintiles, with people in the lowest combined education and income categories at the greatest disadvantage. Disparities were wider in the 2011 cohort compared with the 1996 cohort, but not necessarily to the same extent for both sexes or at different ages. DISCUSSION: In Canada, education-related and income-related disparities in life and health expectancy persist and may be wider than they were in the past. This underscores the importance of ongoing data development for routine monitoring of trends in mortality and morbidity, which can, in turn, inform policy development and planning to advance health equity.

Within-city Spatial Variations in Ambient Ultrafine Particle Concentrations and Incident Brain Tumors in Adults.

BACKGROUND: Ambient ultrafine particles (UFPs, <0.1 µm) can reach the human brain, but to our knowledge, epidemiologic studies have yet to evaluate the relation between UFPs and incident brain tumors. METHODS: We conducted a cohort study of within-city spatial variations in ambient UFPs across Montreal and Toronto, Canada, among 1.9 million adults included in multiple cycles of the Canadian Census Health and Environment Cohorts (1991, 1996, 2001, and 2006). UFP exposures (3-year moving averages) were assigned to residential locations using land-use regression models with exposures updated to account for residential mobility within and between cities. We followed cohort members for malignant brain tumors (ICD-10 codes C71.0-C71.9) between 2001 and 2016; Cox proportional hazards models (stratified by age, sex, immigration status, and census cycle) were used to estimate hazard ratios (HRs) adjusting for fine particle mass concentrations (PM2.5), nitrogen dioxide (NO2), and various sociodemographic factors. RESULTS: In total, we identified 1,400 incident brain tumors during the follow-up period. Each 10,000/cm increase in UFPs was positively associated with brain tumor incidence (HR = 1.112, 95% CI = 1.042, 1.188) after adjusting for PM2.5, NO2, and sociodemographic factors. Applying an indirect adjustment for cigarette smoking and body mass index strengthened this relation (HR = 1.133, 95% CI = 1.032, 1.245). PM2.5 and NO2 were not associated with an increased incidence of brain tumors. CONCLUSIONS: Ambient UFPs may represent a previously unrecognized risk factor for incident brain tumors in adults. Future studies should aim to replicate these results given the high prevalence of UFP exposures in urban areas.