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• We studied 43,931 new SARD diagnoses from 12 million Canadian adults. • We found positive associations between SARD onset and mixed industrial emissions. • PM 2.5 contributed more to SARD onset than NO 2 and SO 2 in the industrial mixture. • Similar associations and contributions were seen in stratified analyses. Past investigations of air pollution and systemic autoimmune rheumatic diseases (SARDs) typically focused on individual (not mixed) and overall environmental emissions. We assessed mixtures of industrial emissions of fine particulate matter (PM 2.5), nitrogen dioxide (NO 2), and sulfur dioxide (SO 2) and SARDs onset in Ontario, Canada. We assembled an open cohort of over 12 million adults (without SARD diagnoses at cohort entry) based on provincial health data for 2007–2020 and followed them until SARD onset, death, emigration, or end of study (December 2020). SARDs were identified using physician billing and hospitalization diagnostic codes for systemic lupus, scleroderma, myositis, undifferentiated connective tissue disease, and Sjogren's. Rheumatoid arthritis and vasculitis were not included. Average PM 2.5 , NO 2 , and SO 2 industrial emissions from 2002 to one year before SARDs onset or end of study were assigned using residential postal codes. A quantile g-computation model for time to SARD onset was developed for the industrial emission mixture, adjusting for sex, age, income, rurality index, chronic obstructive pulmonary disease (as a proxy for smoking), background (environmental overall) PM 2.5 , and calendar year. We conducted stratified analyses across age, sex, and rurality. We identified 43,931 new SARD diagnoses across 143,799,564 person-years. The adjusted hazard ratio for SARD onset for an increase in all emissions by one decile was 1.018 (95% confidence interval 1.013–1.022). Similar positive associations between SARDs and the mixed emissions were observed in most stratified analyses. Industrial PM 2.5 contributed most to SARD risk. Industrial air pollution emissions were associated with SARDs risk. [ABSTRACT FROM AUTHOR]

Several epidemiological studies have investigated the possible role that living in areas with greater amounts of greenspace has on the incidence of childhood asthma. These findings have been inconsistent, and few studies explored the relevance of timing of exposure. We investigated the role of residential surrounding greenness on the risk of incident asthma using a population-based retrospective cohort study. We included 982,131 singleton births in Ontario, Canada between 2006 and 2013. Two measures of greenness, the Normalized Difference Vegetation Index (NDVI) and the Green View Index (GVI), were assigned to the residential histories of these infants from pregnancy through to 12 years of age. Longitudinally-based diagnoses of asthma were determined by using provincial administrative health data. The extended Cox hazards model was used to characterize associations between greenness measures and asthma (up to age 12 years) while adjusting for several risk factors. In a fully adjusted model, that included a term for traffic-related air pollution (NO 2), we found no association between an interquartile range increase (0.08) of the NDVI during childhood and asthma incidence (HR = 0.99; 95 % CI = 0.99–1.01). In contrast, we found that an 0.08 increase in NDVI during childhood reduced the risk of asthma in children 7–12 years of age by 14 % (HR = 0.86, 95 % CI:0.79–0.95). Seasonal differences in the association between greenness and asthma were noted. Our findings suggest that residential proximity to greenness reduces the risk of asthma in children aged 7–12. • In a cohort of nearly one million infants, we investigated links between residential greenness and asthma. • Greenness exposure during childhood was associated with a lower risks asthma among children 7–12 years of age. • The association between greenness and incidence was modified by season of birth. [ABSTRACT FROM AUTHOR]