Search

In this study, the long-term mortality effects associated with exposure to PM 10 (particles with an aerodynamic diameter smaller than or equal to 10 µm), PM 2.5 (particles with an aerodynamic diameter smaller than or equal to 2.5 µm), BC (black carbon), and NO x (nitrogen oxides) were analyzed in a cohort in southern Sweden during the period from 1991 to 2016. Participants (those residing in Malmö, Sweden, born between 1923 and 1950) were randomly recruited from 1991 to 1996. At enrollment, 30,438 participants underwent a health screening, which consisted of questionnaires about lifestyle and diet, a clinical examination, and blood sampling. Mortality data were retrieved from the Swedish National Cause of Death Register. The modeled concentrations of PM 10 , PM 2.5 , BC, and NO x at the cohort participants' home addresses were used to assess air pollution exposure. Cox proportional hazard models were used to estimate the associations between long-term exposure to PM 10 , PM 2.5 , BC, and NO x and the time until death among the participants during the period from 1991 to 2016. The hazard ratios (HRs) associated with an interquartile range (IQR) increase in each air pollutant were calculated based on the exposure lag windows of the same year (lag0), 1-5 years (lag1-5), and 6-10 years (lag6-10). Three models were used with varying adjustments for possible confounders including both single-pollutant estimates and two-pollutant estimates. With adjustments for all covariates, the HRs for PM 10 , PM 2.5 , BC, and NO x in the single-pollutant models at lag1-5 were 1.06 (95% CI: 1.02-1.11), 1.01 (95% CI: 0.95-1.08), 1.07 (95% CI: 1.04-1.11), and 1.11 (95% CI: 1.07-1.16) per IQR increase, respectively. The HRs, in most cases, decreased with the inclusion of a larger number of covariates in the models. The most robust associations were shown for NO x , with statistically significant positive HRs in all the models. An overall conclusion is that road traffic-related pollutants had a significant association with mortality in the cohort.

While prenatal exposure to ambient air pollution has been shown to be associated with reduced birth weight, there is substantial heterogeneity across studies, and few epidemiological studies have utilized source-specific exposure data. The aim of the present study was, therefore, to investigate the associations between local, source-specific exposure to fine particulate matter (PM2.5) during pregnancy and birth weight. An administrative cohort comprising 40,245 singleton births from 2000 to 2009 in Scania, Sweden, was combined with data on relevant covariates. Investigated sources of PM2.5 included all local sources together as well as tailpipe exhaust, vehicle wear-and-tear, and small-scale residential heating separately. The relationships between these exposures, represented as interquartile range (IQR) increases, and birth weight (continuous) and low birth weight (LBW; <2500 g) were analyzed in crude and adjusted models. Each local PM2.5 source investigated was associated with reduced birth weight; average decreases varied by source (12−34 g). Only small-scale residential heating was clearly associated with LBW (adjusted odds ratio: 1.14 (95% confidence interval: 1.04−1.26) per IQR increase). These results add to existing evidence that prenatal exposure to ambient air pollution disrupts fetal growth and suggest that PM2.5 from both vehicles and small-scale residential heating may reduce birth weight.