Inhaled chemicals may enhance allergic airway inflammation in ovalbumin-sensitised mice.

Occupational allergy and asthma is a challenging issue in the developing countries. Chemicals inhaled in the workplaces may act not only as allergens but also as immune response modifiers, contributing to asthma exacerbation. In this study, we tested the adjuvant effect of 20 ppm chloroform, 10 ppm 1,1-dichloroethylene, and 100 ppm styrene in mice. Female BALB/c mice were sensitised to ovalbumin (OVA) without using alum. During the OVA-sensitisation period, these mice were exposed by inhalation to the chemicals studied for 6h/day for four consecutive days. After two OVA-intratracheal challenges, a mild Th2 immune response was observed in the OVA-exposed groups. This response was characterised by a mild increase in serum specific IgE level, in local Th2 cytokine production, and in lung inflammatory reaction. Exposure to styrene or chloroform alone slightly increased Th2 cytokine production by lung-draining lymph node cells cultured with concanavaline A, except for the IL-4 level in the chloroform exposure group, which decreased. On the other hand, exposure to 1,1-dichloroethylene alone markedly increased the Th2 cytokine levels compared to those observed in the groups exposed to OVA alone. In the combined OVA+chemical-treated groups, styrene potentiated IL-4, -5 and -13 production efficiently (approximately two, four and three times higher, respectively), resulting in an increase in the total IgE levels and inflammatory reaction. On the other hand, the enhanced IgE levels and the exacerbation of the inflammatory response by 1,1-dichloroethylene or chloroform were associated with only minor changes in local cytokine levels. These findings suggest that exposure to chemicals through inhalation may aggravate the allergic lung inflammation. And this, depending on the chemical exposure conditions, may result from the synergistic effect of chemicals and allergen on local Th2 cytokine production.