INHALATION COEXPOSURE TO CARBON-BLACK AND ACROLEIN SUPPRESSES ALVEOLAR MACROPHAGE PHAGOCYTOSIS AND TNF-ALPHA RELEASE AND MODULATES PERITONEAL MACROPHAGE PHAGOCYTOSIS

Citation
Gj. Jakab et Dr. Hemenway, INHALATION COEXPOSURE TO CARBON-BLACK AND ACROLEIN SUPPRESSES ALVEOLAR MACROPHAGE PHAGOCYTOSIS AND TNF-ALPHA RELEASE AND MODULATES PERITONEAL MACROPHAGE PHAGOCYTOSIS, Inhalation toxicology, 5(3), 1993, pp. 275-289
Citations number
35
Categorie Soggetti
Toxicology
Journal title
ISSN journal
08958378
Volume
5
Issue
3
Year of publication
1993
Pages
275 - 289
Database
ISI
SICI code
0895-8378(1993)5:3<275:ICTCAA>2.0.ZU;2-1
Abstract
Acrolein, a hydrophilic vapor that is efficiently absorbed in the uppe r respiratory tract, is often emitted with respirable particles by com bustion sources. If acrolein is adsorbed on respirable particles it ma y be deposited in the deep lung and interact with cells in the lung pa renchyma. To test this hypothesis, mice were coexposed to target conce ntrations of 10 mg/m3 of carbon black and 2.5 ppm acrolein for 4 hours /day for 4 days and alveolar macrophage (AM) phagocytosis and lipopoly saccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) produ ction were assessed. AM phagocytosis was suppressed at 1 through 11 da ys after exposure, with recovery of phagocytic activity at day 20. TNF -alpha production was also initially impaired but was reestablished by day 20. Suppression of AM phagocytosis and TNF-alpha production were not observed following exposure to either agent alone. Coexposure to t arget concentrations of 10 mg/m3 of carbon black and 5 ppm of acrolein for 4 hours/day for either 2, 4, 6, or 8 days with AM phagocytosis pe rformed at 4 days after cessation of exposure resulted in an initial s uppression of phagocytosis followed by an adaptive response, as shown by reestablishment of phagocytosis with prolonged exposure. Coexposure to carbon black and acrolein or acrolein alone also resulted in a mod ulatory effect on peritoneal macrophage (PM) phagocytosis. An initial enhancement for approximately a week after exposure was followed by su ppression of PM phagocytosis. These data indicate the importance of th e interaction of acrolein with an inert particle and that the pulmonar y toxicity of acrolein may depend on its ability to bypass the absorpt ive surfaces of the upper respiratory tract, thereby allowing it to re ach the alveolar region of the lung. In addition, the data also point toward the potential adverse systemic effects of acrolein inhalation.