Enhanced human IgE production results from exposure to the aromatic hydrocarbons from diesel exhaust: Direct effects on B-cell IgE production

Abstract

Epidemiologic and experimental studies suggest that air pollution, and particularly diesel exhaust particles (DEPs) may play a role in the increasing prevalence and severity of airway allergic disease. We show that the extract of polyaromatic hydrocarbons (PAHs) from DEPs (PAH-DEP) enhances human IgE production from purified B cells. Interleukin-4 plus CD40 monoclonal antibody–stimulated IgE production was enhanced 20% to 360% by the addition of PAH-DEP over a period of 10 to 14 days. This effect was increased when PAH-DEP was added 2 to 5 days after cultures were initiated. PAH-DEP itself did not induce IgE production or synergize with interleukin-4 alone to induce IgE from purified B cells, suggesting that it was enhancing ongoing IgE production rather than inducing germline transcription or isotype switching. The prototype nonmetabolized aromatic hydrocarbon 2,3,7,8 tetracholorodibenzo- p-dioxin, which functions solely through activation of the cytosolic aromatic hydrocarbon receptor complex, also increased IgE production. Additionally, the pattern of mRNAs coding for distinct isoforms of the ϵ chain was altered by PAH-DEP, and B-cell expression of the low-affinity IgE receptor was upregulated by PAH-DEP. Enhanced IgE production in the human airway, resulting from exposure to PAH-DEP, may be an important factor in the increase in airway allergic disease. (J A LLERGY C LIN I MMUNOL 1995;95:103-115)