Background: Ambient air pollution has been linked to adverse birth outcomes, but the role of industrial emissions remains understudied. We examined the association between maternal exposure to industrial air pollutants during pregnancy and the risk of preterm birth (PTB) and small-for-gestational-age (SGA) birth. Methods: We conducted a retrospective cohort study of 1,199,516 singleton live births in Quebec, Canada, from 2002 to 2016. Exposure to PM2.5, NO2, and SO2 emitted by industries within 7.5 km of the maternal residence was estimated using an indicator combining residential proximity, emissions, and wind data. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for PTB and SGA comparing exposed to unexposed individuals. We assessed the modifying effects of maternal comorbidities using subgroup analyses. Results: The cohort comprised 71,699 PTB and 105,894 SGA cases. Compared with unexposed participants, exposure to industrial air pollutants during pregnancy increased the risk of extreme and very PTB and SGA. For extreme PTB, adjusted ORs (95% CI) comparing exposed with unexposed were 1.08 (1.00, 1.17) for PM2.5, 1.11 (1.03, 1.19) for NO2, and 1.05 (0.98, 1.12) for SO2. For SGA, the corresponding values were 1.03 (1.02, 1.05) for PM2.5, 1.03 (1.02, 1.04) for NO2, and 1.05 (1.04, 1.06) for SO2. Exposure to NO2 was associated with a higher risk of extreme and very PTB among mothers with preeclampsia (OR: 1.26; 95% CI: 1.12, 1.42) compared with no preeclampsia (OR:1.07; 95% CI: 1.01, 1.12). Conclusion: Exposure to industrial air emissions during pregnancy may increase the risk of extreme and very PTB and SGA, especially among women with preeclampsia.
Félicitée Mumbanza, A. Mariet, Nathalie Auger et al.· Environmental Epidemiology· 0 citations
Concerns are growing regarding the relationship of air pollution (especially fine particulate matter, PM2.5) in diseases like systemic lupus erythematosus (SLE). It is unclear which chemical components of ambient PM2.5 may be most harmful, and whether other air pollutants play additional roles. We aimed to evaluate the association between the mixture of PM2.5 components and SLE onset, quantifying their relative contributions to SLE risk, and potential effect modification by ambient ozone levels.
Using MarketScan® administrative health data, we assembled an urban open cohort of all enrollees ≥18-year-old (without prior SLE) with residential core-based statistical area (CBSA) information. Each year after 2013, eligible individuals entered the cohort and were followed until SLE onset, death, insurance disenrollment, or study end (Dec. 2023). SLE incident cases were identified by ≥1 hospitalization or ≥2 physician billing diagnostic codes. From the cohort, all SLE cases and a 20% random baseline sub-cohort were combined into a case-cohort sample. Concentrations of PM2.5 components (ammonium, black carbon, mineral dust, sulfate, nitrate, organic matter, sea salt) and ambient ozone for 2 years before cohort entry were estimated by satellite- and ground-based models and assigned based on CBSAs at cohort entry. Extended quantile g-computation models assessed potential associations of SLE onset with the mixture of PM2.5components, ozone and their interaction, adjusting for sex, age, baseline chronic obstructive pulmonary disease (as a proxy for smoking), geographic region, and year of cohort entry. Index weights estimated by quantile g-computation models quantified the relative contributions of individual PM2.5 components to SLE risk.
Our case-cohort sample numbered 8,345,067 individuals including 21,485 new SLE cases. At the median ozone referent level (ie, 36.1 parts per billion), the adjusted hazard ratio for SLE onset was 1.142 (95% confidence interval, CI 1.107-1.179) per every quartile increase in all PM2.5 components (Table 1). Ozone was also associated with increased risk of SLE (HR 1.009, 95% CI 1.001-1.017). There was effect modification such that the HR for PM2.5 was highest when ozone level was lowest (Table 1). Similar results were seen in sub-groups stratified by sex or age. Mineral dust consistently had the largest index weight across different sub-groups and ozone levels.
Table 1.
Systemic Lupus Erythematosus Risk: Hazard Ration (HR) estimates for effects of PM
2.5
component mixture, ozone, and the interaction between the exposures, at different referent levels of ozone.
PM2.5 and ozone were associated with SLE onset; mineral dust was an important contributor. Mineral dust triggers pulmonary inflammation and is a plausible trigger of autoimmunity and SLE onset. Addressing sources of ambient mineral dust (road traffic, construction, farming) may help reduce SLE incidence.
Naizhuo Zhao, S. Bernatsky, Sharon Dowell et al.· Journal of Rheumatology· 0 citations
