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Background Understanding the shape of the relationship between long-term exposure to ambient fine particulate matter (PM 2.5 ) concentrations and health risks is critical for health impact and risk assessment. Studies evaluating the health risks of exposure to low concentrations of PM 2.5 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 PM 2.5 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 PM 2.5 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 PM 2.5 . HRs were generally greater than most literature values, and adjusting for behavioural covariates served to reduce HR estimates slightly.

Background Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM 2.5 ). In general, cohort studies of mortality and outdoor PM 2.5 concentrations have limited information on individuals exposed to low levels of PM 2.5 as well as covariates such as smoking behaviours, alcohol consumption, and diet which may confound relationships with mortality. This study provides an updated and extended analysis of the Canadian Community Health Survey-Mortality cohort: a population-based cohort with detailed PM 2.5 exposure data and information on a number of important individual-level behavioural risk factors. We also used this rich dataset to provide insight into the shape of the concentration-response curve for mortality at low levels of PM 2.5 . Methods Respondents to the Canadian Community Health Survey from 2000 to 2012 were linked by postal code history from 1981 to 2016 to high resolution PM 2.5 exposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PM 2.5 concentrations (measured as a three-year average with a one-year lag) adjusted for socio-economic, behavioural, and time-varying contextual covariates. Results In total, 50,700 deaths from non-accidental causes occurred in the cohort over the follow-up period. Annual average ambient PM 2.5 concentrations were low (i.e. 5.9 μg/m 3 , s.d. 2.0) and each 10 μg/m 3 increase in exposure was associated with an increase in non-accidental mortality (HR = 1.11; 95% CI 1.04–1.18). Adjustment for behavioural covariates did not materially change this relationship. We estimated a supra-linear concentration-response curve extending to concentrations below 2 μg/m 3 using a shape constrained health impact function. Mortality risks associated with exposure to PM 2.5 were increased for males, those under age 65, and non-immigrants. Hazard ratios for PM 2.5 and mortality were attenuated when gaseous pollutants were included in models. Conclusions Outdoor PM 2.5 concentrations were associated with non-accidental mortality and adjusting for individual-level behavioural covariates did not materially change this relationship. The concentration-response curve was supra-linear with increased mortality risks extending to low outdoor PM 2.5 concentrations.

Background Agricultural workers may be exposed to potential carcinogens including pesticides, sensitizing agents and solar radiation. Previous studies indicate increased risks of hematopoietic cancers and decreased risks at other sites, possibly due to differences in lifestyle or risk behaviours. We present findings from CanCHEC (Canadian Census Health and Environment Cohort), the largest national population-based cohort of agricultural workers. Methods Statistics Canada created the cohort using deterministic and probabilistic linkage of the 1991 Canadian Long Form Census to National Cancer Registry records for 1992–2010. Self-reported occupations were coded using the Standard Occupational Classification (1991) system. Analyses were restricted to employed persons aged 25–74 years at baseline ( N  = 2,051,315), with follow-up until December 31, 2010. Hazard ratios (HR) and 95% confidence intervals (CI) were modeled using Cox proportional hazards for all workers in agricultural occupations ( n  = 70,570; 70.8% male), stratified by sex, and adjusted for age at cohort entry, province of residence, and highest level of education. Results A total of 9515 incident cancer cases (7295 in males) occurred in agricultural workers. Among men, increased risks were observed for non-Hodgkin lymphoma (HR = 1.10, 95% CI = 1.00–1.21), prostate (HR = 1.11, 95% CI = 1.06–1.16), melanoma (HR = 1.15, 95% CI = 1.02–1.31), and lip cancer (HR = 2.14, 95% CI = 1.70–2.70). Decreased risks in males were observed for lung, larynx, and liver cancers. Among female agricultural workers there was an increased risk of pancreatic cancer (HR = 1.36, 95% CI = 1.07–1.72). Increased risks of melanoma (HR = 1.79, 95% CI = 1.17–2.73), leukemia (HR = 2.01, 95% CI = 1.24–3.25) and multiple myeloma (HR = 2.25, 95% CI = 1.16–4.37) were observed in a subset of female crop farmers. Conclusions Exposure to pesticides may have contributed to increased risks of hematopoietic cancers, while increased risks of lip cancer and melanoma may be attributed to sun exposure. The array of decreased risks suggests reduced smoking and alcohol consumption in this occupational group compared to the general population.

Background Numerous studies have examined the association between air pollution and preterm birth (< 37 weeks gestation) but findings have been inconsistent. These associations may be more difficult to detect than associations with other adverse birth outcomes because of the different duration of exposure in preterm vs. term births, and the existence of seasonal cycles in incidence of preterm birth. Methods We analyzed data pertaining to 1,001,700 singleton births occurring between 1999 and 2008 in 24 Canadian cities where daily air pollution data were available from government monitoring sites. In the first stage, data were analyzed in each city employing Cox proportional hazards models using gestational age in days as the time scale, obtaining city-specific hazard ratios (HRs) with their 95% confidence intervals (CIs) expressed per interquartile range (IQR) of each air pollutant. Effects were examined using distributed lag functions for lags of 0–6 days prior to delivery, as well as cumulative lags from two to six days. We accounted for the potential nonlinear effect of daily mean ambient temperature using a cubic B-spline with three internal knots. In the second stage, we pooled the estimated city-specific hazard ratios using a random effects model. Results Pooled estimates across 24 cities indicated that an IQR increase in ozone (O 3 , 13.3 ppb) 0–3 days prior to delivery was associated with a hazard ratio of 1.036 (95% CI 1.005, 1.067) for preterm birth, adjusting for infant sex, maternal age, marital status and country of birth, neighbourhood socioeconomic status (SES) and visible minority, temperature, year and season of birth, and a natural spline function of day of year. There was some evidence of effect modification by gestational age and season. Associations with carbon monoxide, nitrogen dioxide, particulate matter, and sulphur dioxide were inconsistent. Conclusions We observed associations between daily O 3 in the week before delivery and preterm birth in an analysis of approximately 1 million births in 24 Canadian cities between 1999 and 2008. Our analysis is one of a limited number which have examined these short term associations employing Cox proportional hazards models to account for the different exposure durations of preterm vs. term births.

Statistics Canada uses two self-report measures - Ancestry and Identity - in the Canadian Census to identify First Nations, Inuit and Métis (FNIM) peoples. How these measures are employed alone or in combination to assess definitional impact on the reporting of health conditions has not been investigated. To illustrate, we assessed how these measures, alone or in combination, estimate colorectal cancer rates. A working group comprised of Indigenous and non-Indigenous academics assessed the response patterns to the Identity and Ancestry questions in the 2006 Canadian Census Health and Environment Cohort and categorised the responses into groups: A) Identity only; B) Ancestry only; C) any Ancestry or Identity; D) both Ancestry and Identity. We then assessed concordance, and subsequently examined the way these groupings may impact the reporting of colorectal cancer rates (2010-2015). FNIM responses varied across the different combinations of the Ancestry and Identity questions. Concordance for FNIM was 76%, 81%, and 18% respectively for single responses, which impacted the estimation of colorectal cancer rates. To improve health reporting, it is essential that research teams choose the most appropriate definition in partnership with FNIM and urban Indigenous organisations to ensure the right data are analysed to align with community priorities.

Métis people are 1 of 3 Aboriginal groups recognized by the Canadian constitution. We estimated site-specific incidence rates and survival for the most common cancers among Métis adults in Canada and compared these with rates among non-Aboriginal adults in Canada. We examined responses to the 1991 long-form census, including self-reported Métis ancestry linked to national mortality and cancer databases for followup from 1992 to 2009. We estimated age-standardized incidence rates and 5-year relative survival. We determined relative risk (RR) of cancer among Métis and non-Aboriginal adults using Poisson regression, and estimated excess mortality rate ratios using ethnicity-specific life tables. For all cancers and both sexes combined, cancer incidence was similar for Métis and non-Aboriginal adults. However, incidence was significantly higher among Métis adults than among non-Aboriginal adults for the following cancers: female breast (RR 1.18, 95% confidence interval [CI] 1.02–1.37), lung (RR 1.34, 95% CI 1.18–1.52), liver (RR 2.09, 95% CI 1.30–3.38), larynx (RR 1.60, 95% CI 1.03–2.48), gallbladder (RR 2.35, 95% CI 1.12–4.96) and cervix (RR 1.84, 95% CI 1.23–2.76). Métis people had poorer survival for prostate cancer (excess mortality rate ratio 2.60, 95% CI 1.52–4.46). We found higher incidence for several cancers and poorer survival after prostate cancer among Métis adults. Several of these disparities may be related to lifestyle factors (including tobacco use, obesity and lack of cancer screening), providing evidence to support development of public health policy and health care to address cancer burden in the Métis people of Canada.

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 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. 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. 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.

OBJECTIVES:To examine socio-economic inequalities in cause-specific mortality by examining the independent effects of education, occupation and income in a population-based study of working-age Canadian adults. METHODS:This is a secondary analysis of data from the 1991–2006 Canadian Census mortality and cancer follow-up study (n=2.7 million persons). For this analysis, the cohort was restricted to 2.3 million persons aged 25 to 64 at cohort inception, of whom 164,332 died during the follow-up period. Hazard ratios were calculated by educational attainment (4 levels), occupational skill (6 categories) and income adequacy (5 quintiles) for all-cause mortality and major causes of death. Models were run separately for men and women, controlled for multiple variables simultaneously, and some were stratified by 10-year age cohorts. RESULTS:The magnitude of socio-economic inequalities in mortality differed by indicator of socio-economic position (education, occupation, or income), age group, sex, and cause of death. Compared to age-adjusted models, hazard ratios were attenuated but remained significant in models that adjusted for both age and all three indicators of socio-economic position simultaneously. Socio-economic inequalities in mortality were evident for most of the major causes of death examined. CONCLUSION:This study demonstrates that education, occupation and income were each independently associated with mortality and were not simply proxies for each other. When evaluating socio-economic inequalities in mortality, it is important to use different indicators of socio-economic position to provide a more complete picture.

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 (PM 2.5 ) and nitrogen dioxide (NO 2 ) 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, PM 2.5 and NO 2 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. Is air pollution attributable mortality equally distributed within cities? What population characteristics drive inequalities? Does the degree of inequality differ between cities? To what extent are inequalities in air pollution attributable mortality driven by exposure inequalities versus baseline mortality inequalities? In this study of seven Canadian cities, we found that neighborhoods with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality. However, there were different degrees of inequality among the cities. Inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities. Census tracts with a higher prevalence of low income and Indigenous identity had significantly higher air pollution attributable mortality The magnitude of inequality differed among seven Canadian cities Inequality in air pollution attributable mortality tended to be driven more by baseline mortality inequalities than exposure inequalities

Background Cause-specific (CS) and net survival in a relative survival framework (RS) are two of the most common methods for estimating cancer survival. In this paper, we assess the differences in results produced by two permutations of cause-specific and relative survival applied to estimating cancer survival and disparities in cancer survival, using data from First Nations and non-Aboriginal populations in Canada. Methods Subjects were members of the 1991 Canadian Census Mortality Cohort, a population-based cohort of adult respondents to the 1991 Long Form Census who have been followed up for incident cancers and death through linkage to administrative databases. We compared four methods: relative survival analyses with ethnicity-specific life tables (RS-ELT); relative survival with general population life tables (RS-GLT); cause-specific survival with a broad definition of cancer death (CS-Broad); and cause-specific survival with a narrow definition of cause of death (CS-Narrow) and applied these to the nine most common cancers among First Nations. Results Apart from breast and prostate cancers, RS-ELT, RS-GLT, and CS-Broad tended to produce similar estimates of age-standardized five-year survival, whereas CS-Narrow yielded higher estimates of survival. CS-Narrow estimates were particularly unlike those based on the other methods for cancers of the digestive and respiratory tracts. Estimates of disparities in survival were generally comparable across the four methods except for breast and prostate cancers. Conclusions Cancer surveillance efforts in sub-populations defined by race, ethnicity, geography, socioeconomic status, or similar factors are necessary for identifying disparities and monitoring progress toward reducing them. In the absence of routine monitoring of cancer survival and cancer survival disparities in these populations, estimates generated by different methods will inevitably be compared over time and across populations. In this study, we demonstrate that caution should be exercised in making these comparisons, particularly in interpreting cause-specific survival rates with an unknown or narrow definition of cancer death and in estimates of breast and prostate cancer survival and/or disparities in survival generated by different methods.