Acetaldehyde (CH3CHO) production in rodent lung after exposure to metal-rich particles.

Epidemiological reports demonstrate an association between increased human morbidity and mortality with exposure to air pollution particulate matter (PM). Metal-catalyzed oxidative stress has been postulated to contribute to lung injury in response to PM exposure. We studied the effects of residual oil fly ash (ROFA), a component of ambient air PM, on the formation of lung carbonyls that are indicators of lipid peroxidation. Rats were instilled intratracheally with ROFA (62.5-1000 micrograms) and underwent lung lavage. Lavage fluid carbonyls were derivatized with 2,4-dinitrophenylhydrazine, and measured by high performance liquid chromatography with UV detection. Dose-dependent increases in a peak that eluted with the same retention time as the acetaldehyde (CH3CHO) derivative was observed in rats treated with ROFA 15 min after instillation (up to 25-fold greater than saline treated controls). The identification of CH3CHO was confirmed using gas chromatography-mass spectroscopy. ROFA-induced increases in other lavage fluid carbonyls were not seen. Increased CH3CHO in lavage fluid was observed as late as 8 h later. No increase in CH3CHO was observed in plasma from ROFA-treated rats. An increased formation of CH3CHO was observed in a human airway epithelial cell line incubated with ROFA suggesting a pulmonary source of CH3CHO production. Instillation of solutions of metals (iron, vanadium, nickel) contained in ROFA, or instillation of another ROFA-type particle containing primarily iron, also induced a specific increase in CH3CHO. These data support the hypothesis that metals were involved in the increased CH3CHO formation. Thus metals on PM may mediate lung responses through induction of lipid peroxidation and carbonyl formation.