Short-term effects of PM10 sources and oxidative potential on child lung function.

Exposure to particulate matter (PM10) poses a significant threat to human health. We investigated the effects of short-term exposures to PM10 sources and oxidative potential (OP), an indicator of PM related to its toxicity, on lung function in early childhood. The study is based on 435 children from the SEPAGES cohort in Grenoble, with lung function measured at 6-8 weeks (N2 multiple breath washout and tidal breathing flow-volume loop) and 3 years (oscillometry, including resistance and reactance). PM10 chemical composition and OP (ascorbic acid - AA and dithiothreitol - DTT assays) were measured on filters collected at an urban background station. PM10 concentrations were attributed to 10 different sources using a source apportionment method. Associations of short-term exposure (1-, 3-, 7- and 14-day) to each source and OP with lung function were estimated by regression models. Increased acute exposure to PM10 from traffic was associated with parameters indicating impaired lung function at 6-8 weeks and 3 years. Increased exposure to PM10 from biomass burning and primary biogenic sources was associated with lower intra-breath reactance at 3 years. Total PM10 mass and other sources showed no association, or were associated with higher lung function. Increased OPAA was consistently associated to lower child lung function. The greatest magnitude was found between 2-week exposure to mass-normalized OPAA and reduced 7-Hz-reactance at 3 years (β = -0.52 hPa×s/L 95%CI: -0.88, -0.15 per 0.07 nmol/min/μg increase). This study suggests that short-term exposure to PM10 from primary biogenic and local anthropogenic sources, mainly traffic and biomass burning, and to OP may have detrimental effects on early life lung function.