Ambient PM2.5 exposure exacerbates severity of allergic asthma in previously sensitized mice.

Objective: Epidemiological studies have shown that elevated concentrations of ambient particulate matter (aerodynamic diameter ≤2.5 μm; PM2.5) correlates with increased incidence of asthma. The aim of this study was to determine whether PM2.5 participates in the exacerbation of asthma.

Methods: Effects of 1, 10 and 100 μg PM2.5 instilled intratracheally in ovalbumin (OVA)-sensitized or asthmatic mice were compared.

Results: PM2.5 exposure in the OVA-sensitized and especially asthmatic groups increased Mch responsiveness in a dose-dependent manner. In OVA-sensitized groups, exposure to 1 μg of PM2.5 caused no detectable lung inflammation, while 10 and 100 μg of PM2.5 resulted in a slightly increased trend in numbers of neutrophils and macrophages. Compared with the asthmatic control group, both 10 and 100 μg of PM2.5 provoked a significant increase in eosnophils and neutrophils whereas only 100 μg of PM2.5 noticeably enhanced lymphocytes. In asthmatic groups, administration of 100 μg of PM2.5 greatly increased levels of the pro-inflammatory cytokine TNF-α and Th2-related cytokines IL-4 and IL-10 in bronchoalveolar lavage fluid, but it decreased Th1-related INF-γ. In addition, 10 and 100 μg of PM2.5 exacerbated inflammatory infiltration, goblet cell metaplasia and lung ultrastructure lesions in asthmatic mice.

Conclusions: Our results suggested that acute exposure of PM2.5 could synergize with allergens in the subsequent challenge to aggravate the severity of asthma in sensitized mice, possibly by promoting a Th2-biased immune response.