Pro-inflammatory effects of Dunkerque city air pollution particulate matter 2.5 in human epithelial lung cells (L132) in culture

Exposure to urban airborne particulate matter (PM) has been associated with adverse health effects. The majority of research articles published on air pollution PM relate to PM,. However, increasing emphasis and stringent regulations have been placed on PM,.,,. The mechanisms for PM-induced adverse health effects are not well understood, but inflammation seems to be of importance. We focused our attention also on the capacity of air pollution PM,., to induce cytotoxic and inflammatory responses in human epithelial lung cells (L132) in culture. Particulate matter was collected in Dunkerque, a French seaside city characterized by the proximity of industrial activity and heavy motor vehicle traffic. Size distribution results showed that the cumulative frequency of PM,., was 92.15% and their specific surface area was 1 m(2) g(-1). inorganic and organic chemicals usually associated with the natural environment but also so-called anthropogenic elements were found in PM, suggesting that much of the PM was derived from wind-borne dust from the industrial complex and the heavy diesel motor vehicle. We observed PM concentration-dependent cytotoxic effects in L132 cells (LC10 = 18.84 mu g PM ml(-1); LC50 = 75.36 mu g PM ml(-1)). We showed that exposure to Dunkerque City's PM2.5 induced significant increases (in a concentration- and time-dependent manner) in protein secretion and/or gene expression of inflammatory cytokines (i.e. TNF-alpha IL-1 beta, IL-8, GM-CSF, IL-6, TGF-beta 1). We hypothesized also that the occurrence of the acute inflammatory response might rely on the capacity of such air pollutants to generate oxidative species, which have been implicated in the stringent regulation of the cytokine network. Hence, we suggest that the development of inflammatory effects that worsen over time stems from the cytotoxicity in Dunkerque City's PM2.5-exposed L132 cells in culture. Copyright (c) 2005 John Wiley E Sons, Ltd.