December 16 | 2019

Early Life Exposure to Air Pollution and Incidence of Childhood Asthma, Allergic Rhinitis and Eczema.

To T, Zhu J, Stieb D, Gray N, Fong I, Pinault L, Jerrett M, Robichaud A, Ménard R, van Donkelaar A, Martin RV, Hystad P, Brook JR, Dell S.

Eur Respir J. 2019 Dec 5. pii: 1900913. DOI: 10.1183/13993003.00913-2019  [Epub ahead of print]




There is growing evidence that air pollution may contribute to the development of childhood asthma and other allergic diseases. In this follow-up of the Toronto Child Health Evaluation Questionnaire (T-CHEQ) study, we examined associations between early life exposures to air pollution and incidence of asthma, allergic rhinitis and eczema from birth through adolescence.


1286 T-CHEQ participants were followed from birth until outcome, March 31, 2016, or loss-to-follow-up with a mean of 17 years of follow-up. Concentrations of NO2, O3 and PM2.5 from January 1, 1999, to December 31, 2012 were assigned to participants based on their postal codes at birth using ground observations, chemical/meteorological models, remote sensing and land use regression (LUR) models. Study outcomes included incidence of physician-diagnosed asthma, allergic rhinitis and eczema. Cox proportional hazard regression models were used to estimate hazard ratios (HR) per interquartile range of exposures and outcomes, adjusting for potential confounders.


HRs of 1.17 (95%CI: 1.05, 1.31) for asthma and 1.07 (95%CI: 0.99, 1.15) for eczema were observed for total oxidants (O3 and NO2) at birth. No significant increase in risk was found for PM2.5.


Exposures to oxidant air pollutants (O3 and NO2), but not PM2.5 were associated with an increased risk of incident asthma and eczema in children. This suggests that improving air quality may contribute to the prevention of asthma and other allergic disease in childhood and adolescence.

Making the Most of Residential History | February 4th | 2020


It’s a fact – people move! Join our panel of experts to hear more about how this impacts environmental health research, and how you can take advantage of residential history data now in Canada’s major cohorts.

Why do we care about residential history?

  • Paul Villeneuve,  Professor in the School of Mathematics and Statistics, with appointments in the Department of Health Sciences and in the Departments of Health Sciences and Neurosciences at Carleton University
Statistics Canada residential history program. 
  • Michael Tjepkema, Principal Researcher, Statistics Canada, Division of Health Analysis
CANUE data and cohorts with residential history.
  • Dany Doiron, Research Associate, Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Centre (RI-MUHC); CANUE data linkage expert.
Case Study – Examples from the Canadian Census Health and Environment Cohort.
  • Dan Crouse, Consulting Senior Scientist, Health Effects Institute, Boston, MA.
Case Study – Examples from the BC Generations CPTP cohort.
  • Trevor Dummer, Co-National Scientific Director of the Canadian Partnership for Tomorrow Project (CPTP).

December 9 | 2019

Effects of greenspace morphology on mortality at the neighbourhood level: a cross-sectional ecological study.

Huaqing Wang, MSc, Prof Louis G Tassinary, PhD

The Lancet Planetary Health  VOLUME 3, ISSUE 11, PE460-E468, NOVEMBER 01, 2019

November, 2019 DOI:




The association between urban greenspace and mortality risk is well known, but less is known about how the spatial arrangement of greenspace affects population health. We aimed to investigate the relation between urban greenspace distribution and mortality risk.


We did a cross-sectional study in Philadelphia, PA, USA, using high-resolution landcover data for 2008 from the Pennsylvania Spatial Data Access database. We calculated landscape metrics to measure the greenness, fragmentation, connectedness, aggregation, and shape of greenspace, including and omitting green areas 83·6 m2 or smaller, using Geographical Information System and spatial pattern analysis programs. We analysed all-cause and cause-specific mortality (related to heart disease, chronic lower respiratory diseases, and neoplasms) recorded in 2006 for 369 census tracts (small geographical areas with a population of 2500–8000 people). We did negative binomial regression and principal component analyses to assess associations between landscape spatial metrics and mortality, controlling for geographical, demographic, and socioeconomic factors.


A 1% increase in the percentage of greenspace was predicted to reduce all-cause mortality by 0·419% (95% CI 0·050–0·777), with no effect on cause-specific mortality. All-cause mortality was negatively associated with the area of greenspace. A 1 m2 increase in the mean area of greenspace led to a 0·011% (95% CI 0·004–0·018) fall in all-cause mortality and a 0·019% (0·007–0·032) decrease in cardiac mortality; considering only green areas larger than 83·6 m2 would contribute to a 0·002% (95% CI 0·001–0·003) decrease in all-cause mortality and a 0·003% (0·001–0·006) reduction in cardiac deaths. Census tracts with more connected, aggregated, coherent, and complex shape greenspaces had a lower risk of all-cause and cause-specific mortality. The negative association between articulated landscape parcels and all-cause mortality varied with age and education, such that the relation was stronger for census tracts with a higher percentage of older and less well-educated adults.


A significant modest association exists between the spatial distribution of greenspace in cities and mortality risk. The overall amount of greenspace alone is probably failing to capture significant variance in local health outcomes and, thus, environment-based health planning should consider the shape, form, and function of greenspace.

December 4 | 2019

Examining the Shape of the Association between Low Levels of Fine Particulate Matter and Mortality across Three Cycles of the Canadian Census Health and Environment Cohort.

Pappin AJ, Christidis T, Pinault LL, Crouse DL, Brook JR, Erickson A, Hystad P, Li C, Martin RV, Meng J, Weichenthal S, van Donkelaar A, Tjepkema M, Brauer M, Burnett RT.

Environ Health Perspect. 2019 Oct;127(10):107008. doi: 10.1289/EHP5204 Epub 2019 Oct 22.



Ambient fine particulate air pollution with aerodynamic diameter ≤2.5 μm (PM2.5) is an important contributor to the global burden of disease. Information on the shape of the concentration-response relationship at low concentrations is critical for estimating this burden, setting air quality standards, and in benefits assessments.


We examined the concentration-response relationship between PM2.5 and nonaccidental mortality in three Canadian Census Health and Environment Cohorts (CanCHECs) based on the 1991, 1996, and 2001 census cycles linked to mobility and mortality data.


Census respondents were linked with death records through 2016, resulting in 8.5 million adults, 150 million years of follow-up, and 1.5 million deaths. Using annual mailing address, we assigned time-varying contextual variables and 3-y moving-average ambient PM2.5 at a 1×1 km spatial resolution from 1988 to 2015. We ran Cox proportional hazards models for PM2.5 adjusted for eight subject-level indicators of socioeconomic status, seven contextual covariates, ozone, nitrogen dioxide, and combined oxidative potential. We used three statistical methods to examine the shape of the concentration-response relationship between PM2.5 and nonaccidental mortality.


The mean 3-y annual average estimate of PM2.5 exposure ranged from 6.7 to 8.0 μg/m3 over the three cohorts. We estimated a hazard ratio (HR) of 1.053 [95% confidence interval (CI): 1.041, 1.065] per 10-μg/m3 change in PM2.5 after pooling the three cohort-specific hazard ratios, with some variation between cohorts (1.041 for the 1991 and 1996 cohorts and 1.084 for the 2001 cohort). We observed a supralinear association in all three cohorts. The lower bound of the 95% CIs exceeded unity for all concentrations in the 1991 cohort, for concentrations above 2 μg/m3 in the 1996 cohort, and above 5 μg/m3 in the 2001 cohort.


In a very large population-based cohort with up to 25 y of follow-up, PM2.5 was associated with nonaccidental mortality at concentrations as low as 5 μg/m3.