Pulmonary effects of exposure to acetaldehyde or benzaldehyde in ovalbumin-sensitized Guinea-pigs

The pulmonary effects of two environmentally relevant aldehydes were investigated in ovalbumin (OA)-sensitized guinea-pigs (GP). Four week-old male Hartley GP, weighing about 300 g, were intraperitoneally injected with 1 ml of a NaCl solution containing 100 µg OA and 100 mg Al(OH)3. They were then exposed either to acetaldehyde or benzaldehyde (500 ppb each) during 4 weeks (6 hours/day, 5 days/week). At the end of exposure, GP were challenged with an OA aerosol (0.1% in NaCl) and pulmonary functions were measured. The day after, guinea-pigs were anesthetized and several endpoints related to inflammatory and allergic responses were assessed in : blood (numeration, formula, biochemistry), whole lung (histology), and bronchoalveolar lavage (BAL) (differential cell count, protein and eicosanoid concentrations). Sensitized non-exposed GP (n = 8) had an increased number of eosinophils in blood and BAL, together with an increase in total protein and leukotrien (LTB4 and LTC4/D4/E4) contents in BAL. In non-sensitized GP (n = 8), exposure to acetaldehyde or benzaldehyde did not induce any change in the tested parameters, with the exception of a slight irritation of the respiratory tract as detected by histology and an increased number of alveolar macrophages in animals exposed to acetaldehyde (21.9 +- 1.6 and 42.2 +- 5.4 x 106 cells in control and exposed GP respectively). In sensitized GP, exposure to acetaldehyde induced a moderate irritation of the respiratory tract but no change in biological parameters linked to the inflammatory and allergic responses. In contrast, exposure to benzaldehyde induced : a decrease in both OA-induced bronchoconstriction and neutrophil number in BAL, an increase in the bronchodilatator mediator PGE2 and a decrease in the bronchoconstrictor mediators LTC4/D/E4. Further investigations are needed to determine if the attenuated response observed in sensitized GP exposed to benzaldehyde is due to an alteration of the mechanism of sensitization or to a more direct effect on various mechanisms of the allergic response.