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Suppression of Pulmonary Host Defenses and Enhanced Susceptibility to Respiratory bacterial Infection in mice Following Inhalation Exposure to Trichloroethylene and Chloroform
Citation:
SELGRADE, M. AND M. I. GILMOUR. Suppression of Pulmonary Host Defenses and Enhanced Susceptibility to Respiratory bacterial Infection in mice Following Inhalation Exposure to Trichloroethylene and Chloroform. JOURNAL OF IMMUNOTOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, 7(4):35--356, (2010).
Impact/Purpose:
This paper provides dose responses and Noel's for effects of inhalation exposure to Trichloroethylene and chloroform on pulmonary host defenses and susceptibility to bacterial infection in mice. Experiments were actually done some time ago, initially because superfund was interested in these chemicals. Both chemicals are also among 33 air pollutants identified in the U.S. Environmental Protection Agency's Integrated Urban Air Toxics Strategy as presenting the greatest threat to public health in the largest number of urban areas. Limited studies on systemic immunotoxicty following oral exposure are available, but little on inhalation exposures and local host defenses. There is and RID for both chemicals in IRIS, but RfC is still pending
Description:
Numerous epidemiologic studies have associated episodes of increased air pollution with increased incidence of respiratory disease, including pneumonia, croup, and bronchitis. Trichloroethylene (TCE) and chloroform are among 33 hazardous air pollutants identified by the U.S. Environmental Protection Agency as presenting the greatest threat to public health in the largest number of urban areas. Also, both are common indoor air pollutants. Here we assessed the potential effects of TCE and chloroform on resistance to pulmonary bacterial infection and related alveolar macrophage (AM) function. CD-l mice were exposed by inhalation to filtered air (control) or concentrations of TCE ranging from 5 to 200 ppm, or concentrations of chloroform ranging from 100 to 2000 ppm. Immediately following exposure mice were challenged with an aerosol of Streptococcus zooepidemicus and monitored for clearance of bacteria from the lung and mortality. In separate experiments exposed mice were injected intratracheally with viable bacteria and phagocytic function was evaluated in macrophages obtained from lung washes 30 minutes later. The NOEL for enhanced mortality to infection was 25 ppm for TCE and 500 ppm for chloroform. Relative to the air controls, differences in clearance of bacteria from the lung were noted in mice exposed to TCE (NOEL 50 ppm) and to chloroform (NOEL 100 ppm), while differences in AM phagocytic index were noted for TCE (NOEL 100 ppm) and for chloroform (NOEL <100 ppm). The data support the utility of the S. zooepidemicus infectivity model in assessing potential increased risk of respiratory infection and suggest that delayed clearance of bacteria from the lung or decreased phagocytosis are viable alternatives to mortality as an endpoint. Collectively, these endpoints are among the most sensitive health effects reported for TCE. U.S. Environmental Protection Agency and approved for publication. Approval does not signify that the contents necessarily reflects the views and policies of the Agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use.
