TY - JOUR
T1 - Inhalation coexposure to carbon black and acrolein suppresses alveolar macrophage phagocytosis and tnf-α release and modulates peritoneal macrophage phagocytosis
AU - Jakab, George J.
AU - Hemenway, David R.
N1 - Funding Information:
This work was supported by Grant ES05429 from the National Institutes of Health and Grant P30 ES03819 from the National Institute of Environmental Health Sciences. The authors thank Dr. Terence H. Risby for his thought and support of this investigation and Robert Hmieleski for his excellent technical assistance.
PY - 1993
Y1 - 1993
N2 - Acrolein, a hydrophilic vapor that is efficiently absorbed in the upper respiratory tract, is often emitted with respirable particles by combustion sources. If acrolein is adsorbed on respirable particles it may be deposited in the deep lung and interact with cells in the lung parenchyma. To test this hypothesis, mice were coexposed to target concentrations 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 lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α production were assessed. AM phagocytosis was suppressed at 1 through 11 days after exposure, with recovery of phagocytic activity at day 20. TNF-a production was a/so initially impaired but was reestablished by day 20. Suppression of AM phagocytosis and TNF-α production were not observed following exposure to either agent alone. Coexposure to target 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 performed at 4 days after cessation of exposure resulted in an initial suppression 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 modulatory effect on peritoneal macrophage (PM) phagocytosis. An initial enhancement for approximately a week after exposure was followed by suppression of PM phagocytosis. These data indicate the importance of the interaction of acrolein with an inert particle and that the pulmonary toxicity of acrolein may depend on its ability to bypass the absorptive surfaces of the upper respiratory tract, thereby allowing it to reach the alveolar region of the lung. In addition, the data also point toward the potential adverse systemic effects of acrolein inhalation.
AB - Acrolein, a hydrophilic vapor that is efficiently absorbed in the upper respiratory tract, is often emitted with respirable particles by combustion sources. If acrolein is adsorbed on respirable particles it may be deposited in the deep lung and interact with cells in the lung parenchyma. To test this hypothesis, mice were coexposed to target concentrations 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 lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α production were assessed. AM phagocytosis was suppressed at 1 through 11 days after exposure, with recovery of phagocytic activity at day 20. TNF-a production was a/so initially impaired but was reestablished by day 20. Suppression of AM phagocytosis and TNF-α production were not observed following exposure to either agent alone. Coexposure to target 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 performed at 4 days after cessation of exposure resulted in an initial suppression 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 modulatory effect on peritoneal macrophage (PM) phagocytosis. An initial enhancement for approximately a week after exposure was followed by suppression of PM phagocytosis. These data indicate the importance of the interaction of acrolein with an inert particle and that the pulmonary toxicity of acrolein may depend on its ability to bypass the absorptive surfaces of the upper respiratory tract, thereby allowing it to reach the alveolar region of the lung. In addition, the data also point toward the potential adverse systemic effects of acrolein inhalation.
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U2 - 10.3109/08958379308998385
DO - 10.3109/08958379308998385
M3 - Article
AN - SCOPUS:0001550871
SN - 0895-8378
VL - 5
SP - 275
EP - 289
JO - Inhalation Toxicology
JF - Inhalation Toxicology
IS - 3
ER -