Exposure to diesel exhaust enhances total IgE in non-atopic dockers

Diesel exhaust particles (DEPs) containing polycyclic aromatic hydrocarbons stimulate the formation of IgE in humans following single and acute exposure. The aim of the present study was to ascertain whether long-standing occupational exposure to DEPs carries a risk of enhanced serum IgE, and of rhinitis or asthma.

In this cross-sectional study, findings in 76 dockers were compared with those in 63 reference subjects. Among the dockers, drivers and laborers were exposed to diesel emission from forklifts or trucks in the ship-holds, where benzopyrene levels averaged 4.9 ng/m(3). Serum IgE levels were measured by the UNICAP method. Atopy, an evident source of high IgE levels, was assessed by the Phadiatop test. The subjects' clinical and occupational histories were collected. Interval variables were analyzed with Student's t- and Levene's F-tests. The odds ratio (OR) with the 95% confidence interval (CI) was obtained by the exact method at univariate and multivariate (logistic regression) analysis.

In view of the large difference in serum IgE (P=0.00001) and the prevalence of respiratory diseases ( P=0.009) between atopic and non-atopic subjects, we analyzed their data separately. For non-atopic subjects, the risk of presenting high IgE was significantly higher (OR=11.4; CI=1.44-526; P=0.013) and the risk of respiratory disease was significantly lower (OR=0.09; CI=0.00-0.73; P=0.016) in drivers and laborers as a whole than in the reference subjects. None of the ORs was significant among atopic individuals.

In non-atopic dockers, long-standing exposure to DEPs at concentrations similar to those in heavily polluted cities increased serum IgE levels but not the incidence of rhinitis or asthma.