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 i
ntratracheally with ROFA (62.5-1000 mu g) and underwent lung lavage. Lavage
fluid carbonyls were derivatized with 2,4-dinitrophenylhydrazine, and meas
ured by high performance liquid chromatography with UV detection. Dose-depe
ndent increases in a peak that eluted with the same retention time as the a
cetaldehyde (CH3CHO) derivative was observed in rats treated with ROFA 15 m
in after instillation (up to 25-fold greater than saline treated controls).
The identification of CH3CHO was confirmed using gas chromatography-mass s
pectroscopy. ROFA-induced increases in other lavage fluid carbonyls were no
t 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 in
creased 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 i
ron, also induced a specific increase in CH3CHO, These data support the hyp
othesis that metals were involved in the increased CH3CHO formation. Thus m
etals on PM may mediate lung responses through induction of lipid peroxidat
ion and carbonyl formation. (C) 1999 Elsevier Science Inc.