Search

This paper consists of an investigation of the structural arrangement of the sp2 phase in amorphous unhydrogenated carbon nitride (a-CNx) films and its effect on their physical properties. The a-CNx films (0.161020/cm3) and the EPR linewidth (of a few gausses) along with a decrease in nitrogen content. Visible Raman measurements indicate that these effects are accompanied by an increase in the degree of disorder of the sp2 phase, as inferred from the broadening and downshift of the G Raman band, and a reduction of the CN triple bond signal. The analysis of these results in terms of the structural configuration and bonding in the films, show that an enhancement of the connectivity of the sp2 phase in the layers, takes place when deposition is performed at high laser intensities. These structural modifications are strongly correlated to a decrease in the optical gap from 0.61 to 0.21 eV as well as to an increase of the hardness value of the films from 12 to 24 GPa. The transition from a reduced to an enhanced connectivity of the sp2 phase occurs when the nitrogen content decreases below 22 at. %, as a result of the detected reduction of the triply bonded CN species in the layers. [ABSTRACT FROM AUTHOR]

Studies the effect of deposition temperature on the optical transmission and paramagnetic centers in pulsed laser deposited amorphous silicon. Measurement of density of paramagnetic defects by electron paramagnetic resonance (EPR); Increase of the EPR linewidth with deposition temperature; Analysis of the thermal dependence of the EPR linewidth.

The investigation of the structural arrangement of the sp(super 2) phase in amorphous unhydrogenated carbon nitride (a-CN(sub x)) films and its effect on their physical properties were conducted. The analysis of these results in terms of the sp(super 2) phase in the layers, takes place when deposition was performed at higher laser intensities.

We report a theoretical and experimental investigation of the interaction of a coupled electron–nuclear spin system with three electromagnetic fields: two equally intense microwave fields resonant with the electron spin, and one radio-frequency field resonant with the nuclear spin. This is an electron–nuclear double-resonance experiment where the effect of the nuclear transition is detected via changes of the electron multiple photon transitions (MQ-EPR) rather than steady-state saturation and, therefore, is called multiquantum electron–nuclear double resonance (MQ-ENDOR). The theoretical framework previously developed for the description of multiple photon phenomena in a two level system is extended to the case of a four level system. The equation of motion of the density matrix is solved in the presence of three fields, which results in five master equations relating various populations and coherences. A ten photon approximation is used to study the functional dependence on spectral parameters and determine the sensitivity of this technique to spin relaxation rates. The experimental investigation is carried out on a sample of tri-t-butyl phenoxyl radical dissolved in mineral oil. At low values of the electron saturation factor Se, the rf-swept MQ-ENDOR is a de-enhancement of the 3Q-EPR signal (i.e., the first intermodulation sidebands). As the microwave field strength increases, the MQ-ENDOR signal changes phase by 180° due to dominance of generalized saturation. Higher order MQ-EPR signals (i.e., higher order sidebands) have larger negative enhancement and tend to display smaller positive enhancement. Line splitting results if the microwave frequency difference or field strength is increased. The dependence of MQ-ENDOR displays on various spectral parameters was found to be consistent with the general trends predicted by the theory. These displays provide a convenient way to estimate electron and nuclear relaxation rates. [ABSTRACT FROM AUTHOR]

Hyperfine selectivity is demonstrated in a continuous wave electron–nuclear double resonance (ENDOR) experiment. A multiquantum electron–electron double resonance (ELDOR) signal is monitored as a function of the nuclear radio frequency. The signs and relative intensities of the ENDOR lines permit separating the case where both ELDOR and ENDOR frequencies match hyperfine couplings from the cases where this condition is not satisfied. © 1996 American Institute of Physics. [ABSTRACT FROM AUTHOR]

Abstract: Magnetization and magnetic susceptibility of dimeric polyoxoanions [M4(H2O)2(GeW9O34)2]12− (M=Mn2+, Cu2+) were investigated using an isotropic exchange coupling model with two coupling constant (J and J′) within the spin quartet formed by M4O16 (M=Mn2+, Cu2+). The exchange couplings were found to be antiferromagnetic for both samples with the values (J/k B=−0.91±0.04K and J′/k B=−1.18±0.02K) and (J/k B=−13.5±0.5K and J′/k B=−66±4K) for the samples containing Mn2+ and Cu2+, respectively. Furthermore, X- and Q-Band powder electron paramagnetic resonance (EPR) measurements on the sample containing Cu2+ were investigated and the experimental spectra were simulated using a triplet spin state and , and including a small axial distortion D term. This leads to spin-Hamiltonian parameters of: |D|=0.44±0.01GHz, g ||=2.415±0.005, g ⊥=2.070±0.005, A ||=(40±1)G. [Copyright &y& Elsevier]

Abstract: SiC thin films were grown on Si (100) substrates by excimer laser ablation of a SiC target in vacuum. The effect of deposition temperature (up to 950°C), post-deposition annealing and laser energy on the nanostructure, bonding and crystalline properties of the films was studied, in order to elucidate their transition from an amorphous to a crystalline phase. Infra-red spectroscopy shows that growth at temperatures greater than 600°C produces layers with increasingly uniform environment of the Si–C bonds, while the appearance of large crystallites is detected, by X-ray diffraction, at 800°C. Electron paramagnetic resonance confirms the presence of clustered paramagnetic centers within the sp2 carbon domains. Increasing deposition temperature leads to a decrease of the spin density and to a temperature-dependent component of the EPR linewidth induced by spin hopping. For films grown below 650°C, post-deposition annealing at 1100°C reduces the spin density as a result of a more uniform Si–C nanostructure, though large scale crystallization is not observed. For greater deposition temperatures, annealing leads to little changes in the bonding properties, but suppresses the temperature dependent component of the EPR linewidth. These findings are explained by a relaxation of the stress in the layers, through the annealing of the bond angle disorder that inhibits spin hopping processes. [Copyright &y& Elsevier]

Background: Outdoor fine particulate air pollution, <2.5 µm (PM 2.5 ) mass concentrations can be constructed through many different combinations of chemical components that have varying levels of toxicity. This poses a challenge for studies interested in estimating the health effects of total outdoor PM 2.5 (i.e., how much PM 2.5 mass is present in the air regardless of composition) because we must consider possible confounders of the version of treatment-outcome relationships., Methods: We evaluated the extent of possible bias in mortality hazard ratios for total outdoor PM 2.5 by examining models with and without adjustment for sulfate and nitrate in PM 2.5 as examples of potential confounders of version of treatment-outcome relationships. Our study included approximately 3 million Canadians and Cox proportional hazard models were used to estimate hazard ratios for total outdoor PM 2.5 adjusting for sulfate and/or nitrate and other relevant covariates., Results: Hazard ratios for total outdoor PM 2.5 and nonaccidental, cardiovascular, and respiratory mortality were overestimated due to the confounding version of treatment-outcome relationships, and associations for lung cancer mortality were underestimated. Sulfate was most strongly associated with nonaccidental, cardiovascular, and respiratory mortality suggesting that regulations targeting this specific component of outdoor PM 2.5 may have greater health benefits than interventions targeting total PM 2.5 ., Conclusions: Studies interested in estimating the health impacts of total outdoor PM 2.5 (i.e., how much PM 2.5 mass is present in the air) need to consider potential confounders of the version of treatment-outcome relationships. Otherwise, health risk estimates for total PM 2.5 will reflect some unknown combination of how much PM 2.5 mass is present in the air and the kind of PM 2.5 mass that is present., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Background: Studies across the globe generally reported increased mortality risks associated with particulate matter with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ) exposure with large heterogeneity in the magnitude of reported associations and the shape of concentration-response functions (CRFs). We aimed to evaluate the impact of key study design factors (including confounders, applied exposure model, population age, and outcome definition) on PM 2.5 effect estimates by harmonizing analyses on three previously published large studies in Canada [Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE), 1991-2016], the United States (Medicare, 2000-2016), and Europe [Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), 2000-2016] as much as possible., Methods: We harmonized the study populations to individuals 65 + years of age, applied the same satellite-derived PM 2.5 exposure estimates, and selected the same sets of potential confounders and the same outcome. We evaluated whether differences in previously published effect estimates across cohorts were reduced after harmonization among these factors. Additional analyses were conducted to assess the influence of key design features on estimated risks, including adjusted covariates and exposure assessment method. A combined CRF was assessed with meta-analysis based on the extended shape-constrained health impact function (eSCHIF)., Results: More than 81 million participants were included, contributing 692 million person-years of follow-up. Hazard ratios and 95% confidence intervals (CIs) for all-cause mortality associated with a 5 - μ g / m 3 increase in PM 2.5 were 1.039 (1.032, 1.046) in MAPLE, 1.025 (1.021, 1.029) in Medicare, and 1.041 (1.014, 1.069) in ELAPSE. Applying a harmonized analytical approach marginally reduced difference in the observed associations across the three studies. Magnitude of the association was affected by the adjusted covariates, exposure assessment methodology, age of the population, and marginally by outcome definition. Shape of the CRFs differed across cohorts but generally showed associations down to the lowest observed PM 2.5 levels. A common CRF suggested a monotonically increased risk down to the lowest exposure level. https://doi.org/10.1289/EHP12141.

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., Competing Interests: The authors declare no conflicts of interest relevant to this study., (© 2023 His Majesty the King in Right of Canada and The Authors. Reproduced with the permission of the Minister of Health 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.

The World Health Organization (WHO) recently released new guidelines for outdoor fine particulate air pollution (PM 2.5 ) recommending an annual average concentration of 5 μg/m 3 . Yet, our understanding of the concentration-response relationship between outdoor PM 2.5 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 PM 2.5 and mortality at very low (<5 μg/m 3 ) concentrations. Our updated global concentration-response function incorporating this new information suggests an additional 1.5 million deaths globally attributable to outdoor PM 2.5 annually compared to previous estimates. The global health benefits of meeting the new WHO guideline for outdoor PM 2.5 are greater than previously assumed and indicate a need for continued reductions in outdoor air pollution around the world.

Introduction: Mortality is associated with long-term exposure to fine particulate matter (particulate matter ≤2.5 μm in aerodynamic diameter; PM 2.5 ), although the magnitude and form of these associations remain poorly understood at lower concentrations. Knowledge gaps include the shape of concentration-response curves and the lowest levels of exposure at which increased risks are evident and the occurrence and extent of associations with specific causes of death. Here, we applied improved estimates of exposure to ambient PM 2.5 to national population-based cohorts in Canada, including a stacked cohort of 7.1 million people who responded to census year 1991, 1996, or 2001. The characterization of the shape of the concentration-response relationship for nonaccidental mortality and several specific causes of death at low levels of exposure was the focus of the Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE) Phase 1 report. In the Phase 1 report we reported that associations between outdoor PM 2.5 concentrations and nonaccidental mortality were attenuated with the addition of ozone (O 3 ) or a measure of gaseous pollutant oxidant capacity (O x ), which was estimated from O 3 and nitrogen dioxide (NO 2 ) concentrations. This was motivated by our interests in understanding both the effects air pollutant mixtures may have on mortality and also the role of O 3 as a copollutant that shares common sources and precursor emissions with those of PM 2.5 . In this Phase 2 report, we further explore the sensitivity of these associations with O 3 and O x , evaluate sensitivity to other factors, such as regional variation, and present ambient PM 2.5 concentration-response relationships for specific causes of death., Methods: PM 2.5 concentrations were estimated at 1 km 2 spatial resolution across North America using remote sensing of aerosol optical depth (AOD) combined with chemical transport model (GEOS-Chem) simulations of the AOD:surface PM 2.5 mass concentration relationship, land use information, and ground monitoring. These estimates were informed and further refined with collocated measurements of PM 2.5 and AOD, including targeted measurements in areas of low PM 2.5 concentrations collected at five locations across Canada. Ground measurements of PM 2.5 and total suspended particulate matter (TSP) mass concentrations from 1981 to 1999 were used to backcast remote-sensing-based estimates over that same time period, resulting in modeled annual surfaces from 1981 to 2016., Annual exposures to PM 2.5 were then estimated for subjects in several national population-based Canadian cohorts using residential histories derived from annual postal code entries in income tax files. These cohorts included three census-based cohorts: the 1991 Canadian Census Health and Environment Cohort (CanCHEC; 2.5 million respondents), the 1996 CanCHEC (3 million respondents), the 2001 CanCHEC (3 million respondents), and a Stacked CanCHEC where duplicate records of respondents were excluded (Stacked CanCHEC; 7.1 million respondents). The Canadian Community Health Survey (CCHS) mortality cohort (mCCHS), derived from several pooled cycles of the CCHS (540,900 respondents), included additional individual information about health behaviors. Follow-up periods were completed to the end of 2016 for all cohorts. Cox proportional hazard ratios (HRs) were estimated for nonaccidental and other major causes of death using a 10-year moving average exposure and 1-year lag. All models were stratified by age, sex, immigrant status, and where appropriate, census year or survey cycle. Models were further adjusted for income adequacy quintile, visible minority status, Indigenous identity, educational attainment, labor-force status, marital status, occupation, and ecological covariates of community size, airshed, urban form, and four dimensions of the Canadian Marginalization Index (Can-Marg; instability, deprivation, dependency, and ethnic concentration). The mCCHS analyses were also adjusted for individual-level measures of smoking, alcohol consumption, fruit and vegetable consumption, body mass index (BMI), and exercise behavior., In addition to linear models, the shape of the concentration-response function was investigated using restricted cubic splines (RCS). The number of knots were selected by minimizing the Bayesian Information Criterion (BIC). Two additional models were used to examine the association between nonaccidental mortality and PM 2.5 . The first is the standard threshold model defined by a transformation of concentration equaling zero if the concentration was less than a specific threshold value and concentration minus the threshold value for concentrations above the threshold. The second additional model was an extension of the Shape Constrained Health Impact Function (SCHIF), the eSCHIF, which converts RCS predictions into functions potentially more suitable for use in health impact assessments. Given the RCS parameter estimates and their covariance matrix, 1,000 realizations of the RCS were simulated at concentrations from the minimum to the maximum concentration, by increments of 0.1 μg/m 3 . An eSCHIF was then fit to each of these RCS realizations. Thus, 1,000 eSCHIF predictions and uncertainty intervals were determined at each concentration within the total range., Sensitivity analyses were conducted to examine associations between PM 2.5 and mortality when in the presence of, or stratified by tertile of, O 3 or O x . Additionally, associations between PM 2.5 and mortality were assessed for sensitivity to lower concentration thresholds, where person-years below a threshold value were assigned the mean exposure within that group. We also examined the sensitivity of the shape of the nonaccidental mortality-PM 2.5 association to removal of person-years at or above 12 μg/m 3 (the current U.S. National Ambient Air Quality Standard) and 10 μg/m 3 (the current Canadian and former [2005] World Health Organization [WHO] guideline, and current WHO Interim Target-4). Finally, differences in the shapes of PM 2.5 -mortality associations were assessed across broad geographic regions (airsheds) within Canada., Results: The refined PM 2.5 exposure estimates demonstrated improved performance relative to estimates applied previously and in the MAPLE Phase 1 report, with slightly reduced errors, including at lower ranges of concentrations (e.g., for PM 2.5 <10 μg/m 3 )., Positive associations between outdoor PM 2.5 concentrations and nonaccidental mortality were consistently observed in all cohorts. In the Stacked CanCHEC analyses (1.3 million deaths), each 10-μg/m 3 increase in outdoor PM 2.5 concentration corresponded to an HR of 1.084 (95% confidence interval [CI]: 1.073 to 1.096) for nonaccidental mortality. For an interquartile range (IQR) increase in PM 2.5 mass concentration of 4.16 μg/m 3 and for a mean annual nonaccidental death rate of 92.8 per 10,000 persons (over the 1991-2016 period for cohort participants ages 25-90), this HR corresponds to an additional 31.62 deaths per 100,000 people, which is equivalent to an additional 7,848 deaths per year in Canada, based on the 2016 population. In RCS models, mean HR predictions increased from the minimum concentration of 2.5 μg/m 3 to 4.5 μg/m 3 , flattened from 4.5 μg/m 3 to 8.0 μg/m 3 , then increased for concentrations above 8.0 μg/m 3 . The threshold model results reflected this pattern with -2 log-likelihood values being equal at 2.5 μg/m 3 and 8.0 μg/m 3 . However, mean threshold model predictions monotonically increased over the concentration range with the lower 95% CI equal to one from 2.5 μg/m 3 to 8.0 μg/m 3 . The RCS model was a superior predictor compared with any of the threshold models, including the linear model., In the mCCHS cohort analyses inclusion of behavioral covariates did not substantially change the results for both linear and nonlinear models. We examined the sensitivity of the shape of the nonaccidental mortality-PM 2.5 association to removal of person-years at or above the current U.S. and Canadian standards of 12 μg/m 3 and 10 μg/m 3 , respectively. In the full cohort and in both restricted cohorts, a steep increase was observed from the minimum concentration of 2.5 μg/m 3 to 5 μg/m 3 . For the full cohort and the <12 μg/m 3 cohort the relationship flattened over the 5 to 9 μg/m 3 range and then increased above 9 μg/m 3 . A similar increase was observed for the <10 μg/m 3 cohort followed by a clear decline in the magnitude of predictions over the 5 to 9 μg/m 3 range and an increase above 9 μg/m 3 . Together these results suggest that a positive association exists for concentrations >9 μg/m 3 with indications of adverse effects on mortality at concentrations as low as 2.5 μg/m 3 ., Among the other causes of death examined, PM 2.5 exposures were consistently associated with an increased hazard of mortality due to ischemic heart disease, respiratory disease, cardiovascular disease, and diabetes across all cohorts. Associations were observed in the Stacked CanCHEC but not in all other cohorts for cerebrovascular disease, pneumonia, and chronic obstructive pulmonary disease (COPD) mortality. No significant associations were observed between mortality and exposure to PM 2.5 for heart failure, lung cancer, and kidney failure., In sensitivity analyses, the addition of O 3 and O x attenuated associations between PM 2.5 and mortality. When analyses were stratified by tertiles of copollutants, associations between PM 2.5 and mortality were only observed in the highest tertile of O 3 or O x . Across broad regions of Canada, linear HR estimates and the shape of the eSCHIF varied substantially, possibly reflecting underlying differences in air pollutant mixtures not characterized by PM 2.5 mass concentrations or the included gaseous pollutants. Sensitivity analyses to assess regional variation in population characteristics and access to healthcare indicated that the observed regional differences in concentration-mortality relationships, specifically the flattening of the concentration-mortality relationship over the 5 to 9 μg/m 3 range, was not likely related to variation in the makeup of the cohort or its access to healthcare, lending support to the potential role of spatially varying air pollutant mixtures not sufficiently characterized by PM 2.5 mass concentrations., Conclusions: In several large, national Canadian cohorts, including a cohort of 7.1 million unique census respondents, associations were observed between exposure to PM 2.5 with nonaccidental mortality and several specific causes of death. Associations with nonaccidental mortality were observed using the eSCHIF methodology at concentrations as low as 2.5 μg/m 3 , and there was no clear evidence in the observed data of a lower threshold, below which PM 2.5 was not associated with nonaccidental mortality., (© 2022 Health Effects Institute. All rights reserved.)

Background: Wildfires emit many carcinogenic pollutants that contaminate air, water, terrestrial, and indoor environments. However, little is known about the relationship between exposure to wildfires and cancer risk. We aimed to assess the associations between residential exposure to wildfires and the incidence of several cancer outcomes (lung cancer, brain cancer, non-Hodgkin lymphoma, multiple myeloma, and leukaemia) in Canada., Methods: We did a population-based observational cohort study of participants in the 1996 Canadian Census Health and Environment Cohort. The 1996 Canadian Census Health and Environment Cohort is a nationally representative sample of Canadian adults, followed up for cancer incidence and mortality from 1996 to 2015. For this analysis, we excluded participants who lived in major Canadian cities (with a population size greater than 1·5 million people), recent immigrants, and individuals younger than 25 years or 90 years of age or older at baseline. Exposures to wildfires were assigned on the basis of area burned within a 20 km or 50 km radius of residential locations and updated for annual residential mobility. Multivariable Cox proportional hazards models were used to estimate associations between exposure to wildfires and specific cancers associated with carcinogenic compounds released by wildfires, including lung and brain cancer, non-Hodgkin lymphoma, multiple myeloma, and leukaemia, adjusted for many personal and neighbourhood-level covariates., Findings: Our analyses included more than 2 million people followed up for a median of 20 years, for a total of 34 million person-years. Wildfire exposure was associated with slightly increased incidence of lung cancer and brain tumours. For example, cohort members exposed to a wildfire within 50 km of residential locations in the past 10 years had a 4·9% relatively higher incidence (adjusted hazard ratio [HR] 1·049, 95% CI 1·028-1·071) of lung cancer than unexposed populations, and a 10% relatively higher incidence (adjusted HR 1·100, 1·026-1·179) of brain tumours. Similar associations were observed for the 20 km buffer size. Wildfires were not associated with haematological cancers in this study, and concentration-response trends were not readily apparent when area burned was modelled as a continuous variable., Interpretation: Long-term exposure to wildfires might increase the risk of lung cancer and brain tumours. Further work is needed to develop long-term estimates of wildfire exposures that capture the complex mixture of environmental pollutants released during these events., Funding: Canadian Institute for Health Research and Fonds de recherche du Quebec., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

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., (Crown Copyright © 2022. Published by Elsevier Ltd. All rights reserved.)

Background: Associations between mortality and exposure to ambient air pollution are usually explored using concentrations of residential outdoor fine particulate matter (PM 2.5 ) 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 PM 2.5 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 PM 2.5 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 PM 2.5 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 PM 2.5 concentrations at home to estimate exposure., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)