Inhaled particle-bound sulfate: Effects on pulmonary inflammatory responses and alveolar macrophage function

Robert W. Clarke, James M. Antonini, David R. Hemenway, Robert Frank, Steven R. Kleeberger, George J. Jakab

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


Acid sulfate-coated solid particles are a significant environmental hazard produced primarily by the combustion of fossil fuels. We have previously described a system for the nascent generation of carbonaceous particles surface coated with approximately 140 μg/m3 acid sulfate [cpSO42-; 10 mg/m3 carbon black (CB) and 10 ppm sulfur dioxide (SO2) at 85% relative humidity (RH)]. The effects of inhaled cpSO42- on pulmonary host defenses are assessed in the present work. Mice were acutely exposed (4 h) to either 10 mg/m3 CB, 10 ppm SO2, or their combination at 10% or 85% RH in a nose-only inhalation chamber. No evidence of an inflammatory response was found following any of the exposures as assessed by total cell counts and differential cell counts from bronchoalveolar lavage fluid. However, alveolar macrophage Fc receptor-mediated phagocytosis decreased only following exposure to 140 μg cpSO42-, significant suppression occurred after 24 h, maximal suppression occurred at 3 days postexposure, and recovery to preexposure levels required 7-14 days. Intrapulmonary bactericidal activity (IBA) was also suppressed only after exposure to 140 μg cpSO42-; suppression was maximal at 1 day postexposure and recovered by day 7. To assess the effects of lower cpSO42- concentrations, mice were repeatedly exposed to 1 mg/m3 CB and 1 ppm SO2 at 85% RH (~20 μg/m3 cpSO42- for 4 h/day) for up to 6 days. A significant decrement in IBA was observed following 5 and 6 days of exposure. These studies indicated that acute or repeated exposure to cpSO42- could alter pulmonary host defense mechanisms.

Original languageEnglish (US)
Pages (from-to)169-186
Number of pages18
JournalInhalation Toxicology
Issue number3
StatePublished - Mar 2000

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis


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