The Canadian Urban Environmental Health Research Consortium - A protocol for building a national environmental exposure data platform for integrated analyses of urban form and health

Background: Multiple external environmental exposures related to residential location and urban form including, air pollutants, noise, greenness, and walkability have been linked to health impacts or benefits. The Canadian Urban Environmental Health Research Consortium (CANUE) was established to facilitate the linkage of extensive geospatial exposure data to existing Canadian cohorts and administrative health data holdings. We hypothesize that this linkage will enable investigators to test a variety of their own hypotheses related to the interdependent associations of built environment features with diverse health outcomes encompassed by the cohorts and administrative data. Methods: We developed a protocol for compiling measures of built environment features that quantify exposure; vary spatially on the urban and suburban scale; and can be modified through changes in policy or individual behaviour to benefit health. These measures fall into six domains: air quality, noise, greenness, weather/climate, and transportation and neighbourhood factors; and will be indexed to six-digit postal codes to facilitate merging with health databases. Initial efforts focus on existing data and include estimates of air pollutants, greenness, temperature extremes, and neighbourhood walkability and socioeconomic characteristics. Key gaps will be addressed for noise exposure, with a new national model being developed, and for transportation-related exposures, with detailed estimates of truck volumes and diesel emissions now underway in selected cities. Improvements to existing exposure estimates are planned, primarily by increasing temporal and/or spatial resolution given new satellite-based sensors and more detailed national air quality modelling. Novel metrics are also planned for walkability and food environments, green space access and function and life-long climate-related exposures based on local climate zones. Critical challenges exist, for example, the quantity and quality of input data to many of the models and metrics has changed over time, making it difficult to develop and validate historical exposures. Discussion: CANUE represents a unique effort to coordinate and leverage substantial research investments and will enable a more focused effort on filling gaps in exposure information, improving the range of exposures quantified, their precision and mechanistic relevance to health. Epidemiological studies may be better able to explore the common theme of urban form and health in an integrated manner, ultimately contributing new knowledge informing policies that enhance healthy urban living

Traffic-Related Air Pollution and Carotid Plaque Burden in a Canadian City With Low-Level Ambient Pollution

Background The association between fine particulate matter and cardiovascular disease has been convincingly demonstrated. The role of traffic-related air pollutants is less clear. To better understan

Ambient PM2.5, O3, and NO2 exposures and associations with mortality over 16 years of follow-up in the canadian census health and environment cohort (CanCHEC)

Background: Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up. Objective: We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 μm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians. Methods: We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects’ residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 μg/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2. Results: PM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associa-tions with NO2. conclusions: In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2

Effect modification of perinatal exposure to air pollution and childhood asthma incidence

Perinatal exposure to ambient air pollution has been associated with childhood asthma incidence; however, less is known regarding the potential effect modifiers in this association. We examined whether maternal and infant characteristics modified the association between perinatal exposure to air pollution and development of childhood asthma. 761 172 births occurring between 2006 and 2012 were identified in the province of Ontario, Canada. Associations between exposure to ambient air pollutants and childhood asthma incidence (up to age 6 years) were estimated using Cox regression models. 110 981 children with asthma were identified. In models adjusted for postnatal exposures, secondtrimester exposures to particulate matter with a 50% cut-off aerodynamic diameter ≤2.5 μm (hazard ratio (HR) per interquartile range (IQR) increase 1.07, 95% CI 1.06-1.09) and nitrogen dioxide (HR per IQR increase 1.06, 95% CI 1.03-1.08) were associated with childhood asthma development. Enhanced impacts were found among children born to mothers with asthma, who smoked during pregnancy or lived in urban areas during pregnancy, males and children born preterm or of low birthweight. Prenatal exposure to air pollution may have a differential impact on the risk of asthma development, according to maternal and infant characteristics

Maternal exposure to ambient air pollution and risk of early childhood cancers: A population-based study in Ontario, Canada

Background: There are increasing concerns regarding the role of exposure to ambient air pollution during pregnancy in the development of early childhood cancers. Objective: This population based study examined whether prenatal and early life (<1year of age) exposures to ambient air pollutants, including nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters ≤2.5μm (PM2.5), were associated with selected common early childhood cancers in Canada. Methods: 2,350,898 singleton live births occurring between 1988 and 2012 were identified in the province of Ontario, Canada. We assigned temporally varying satellite-derived estimates of PM2.5 and land-use regression model estimates of NO2 to maternal residences during pregnancy. Incident cases of 13 subtypes of pediatric cancers among children up to age 6 until 2013 were ascertained through administrative health data linkages. Associations of trimester-specific, overall pregnancy and first year of life exposures were evaluated using Cox proportional hazards models, adjusting for potential confounders. Results: A total of 2044 childhood cancers were identified. Exposure to PM2.5, per interquartile range increase, over the entire pregnancy, and during the first trimester was associated with an increased risk of astrocytoma (hazard ratio (HR) per 3.9μg/m3=1.38 (95% CI: 1.01, 1.88) and, HR per 4.0μg/m3 =1.40 (95% CI: 1.05-1.86), respectively). We also found a positive association between first trimester NO2 and acute lymphoblastic leukemia (ALL) (HR=1.20 (95% CI: 1.02-1.41) per IQR (13.3ppb)). Conclusions: In this population-based study in the largest province of Canada, results suggest an association between exposure to ambient air pollution during pregnancy, especially in the first trimester and an increased risk of astrocytoma and ALL. Further studies are required to replicate the findings of this study with adjustment for important individual-level confounders