TY - JOUR
T1 - Relationship between carbon black particulate-bound formaldehyde, pulmonary antibacterial defenses, and alveolar macrophage phagocytosis
AU - Jakab, George J.
N1 - Funding Information:
The research described in this article was conducted under contracts to the Health Effects Institute (HEI), an organization that is jointly funded by the U.S. Environmental Protection Agency (EPA) and automotive manufacturers. Publication here implies nothing about the view of the contents by HE1 or its research sponsors. Additionally, although the work described in this document has been funded in part by the EPA under assistance agreement X808859 with HEI, the contents do not necessarily reflect the views and policies of the agency; nor does mention of trade names or commercial products constitute endorsement or recommendation for use.
PY - 1992
Y1 - 1992
N2 - The goal of this study was to investigate whether exposure to formaldehyde vapors decreases resistance to respiratory infections through dysfunctions of the alveolar macrophage phagocytic system. Additionally, the study explored whether the interactions of formaldehyde and respirable carbon black particles result in an altered susceptibility through delivery of the absorbed formaldehyde to the deep lung with the inhaled particle. This aim was accomplished through in vivo studies of alveolar macrophage-dependent intrapulmonary killing of Staphylococcus au-reus and ex vivo alveolar macrophage k-receptor-mediated phagocytosis. Exposure to 15 ppm formaldehyde impaired lung antibacterial defenses when exposure followed bacterial challenge; however, this effect was found at 1 ppm when formaldehyde exposure preceded and was continued after bacterial challenge. Coexposure to target concentration of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde or 10 mg/m3 carbon black and 5 ppm formaldehyde for 4 h after bacterial challenge had no effect on intrapulmonary staphylococcal killing; nor was there any bactericidal dysfunction found in mice coexposed for 4 h/day for 4 days followed by bacterial challenge 1 day after cessation of exposure. To determine whether any possible effect was delayed, a surrogate assay for alveolar macrophage phagocytosis, Fc-receptor-mediated phagocytosis, was performed at 1- 3- 5- 10- 14-, 25-, and 40-day intervals after cessation of exposure to target concentrations of 10 mg/m3 carbon black and 5 ppm formaldehyde for 4 h/day for 4 days. Alveolar macrophage phagocytosis was progressively suppressed through day 25, and thereafter the phagocytic potential recovered by day 40. Exposure to target concentration of either 10 mg/mg3 carbon black or 5 pprn formaldehyde alone had no such effect. These data demonstrate that the coexposures to carbon black and formaldehyde suppress alveolar macrophage phagocytosis whereas exposure to either agent alone has no effect.
AB - The goal of this study was to investigate whether exposure to formaldehyde vapors decreases resistance to respiratory infections through dysfunctions of the alveolar macrophage phagocytic system. Additionally, the study explored whether the interactions of formaldehyde and respirable carbon black particles result in an altered susceptibility through delivery of the absorbed formaldehyde to the deep lung with the inhaled particle. This aim was accomplished through in vivo studies of alveolar macrophage-dependent intrapulmonary killing of Staphylococcus au-reus and ex vivo alveolar macrophage k-receptor-mediated phagocytosis. Exposure to 15 ppm formaldehyde impaired lung antibacterial defenses when exposure followed bacterial challenge; however, this effect was found at 1 ppm when formaldehyde exposure preceded and was continued after bacterial challenge. Coexposure to target concentration of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde or 10 mg/m3 carbon black and 5 ppm formaldehyde for 4 h after bacterial challenge had no effect on intrapulmonary staphylococcal killing; nor was there any bactericidal dysfunction found in mice coexposed for 4 h/day for 4 days followed by bacterial challenge 1 day after cessation of exposure. To determine whether any possible effect was delayed, a surrogate assay for alveolar macrophage phagocytosis, Fc-receptor-mediated phagocytosis, was performed at 1- 3- 5- 10- 14-, 25-, and 40-day intervals after cessation of exposure to target concentrations of 10 mg/m3 carbon black and 5 ppm formaldehyde for 4 h/day for 4 days. Alveolar macrophage phagocytosis was progressively suppressed through day 25, and thereafter the phagocytic potential recovered by day 40. Exposure to target concentration of either 10 mg/mg3 carbon black or 5 pprn formaldehyde alone had no such effect. These data demonstrate that the coexposures to carbon black and formaldehyde suppress alveolar macrophage phagocytosis whereas exposure to either agent alone has no effect.
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U2 - 10.3109/08958379209145312
DO - 10.3109/08958379209145312
M3 - Article
AN - SCOPUS:0342795847
SN - 0895-8378
VL - 4
SP - 325
EP - 342
JO - Inhalation Toxicology
JF - Inhalation Toxicology
IS - 4
ER -