Suppression of pulmonary host defenses and enhanced susceptibility to respiratory bacterial infection in mice following inhalation exposure to trichloroethylene and chloroform

Selgrade, MK; Gilmour, MI

HERO ID

730119

Reference Type

Journal Article

Year

2010

Language

English

PMID

20925451

HERO ID 730119
In Press No
Year 2010
Title Suppression of pulmonary host defenses and enhanced susceptibility to respiratory bacterial infection in mice following inhalation exposure to trichloroethylene and chloroform
Authors Selgrade, MK; Gilmour, MI
Journal Journal of Immunotoxicology
Volume 7
Issue 4
Page Numbers 350-356
Abstract Numerous epidemiological 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-1 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 min 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), and 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.
Doi 10.3109/1547691X.2010.520139
Pmid 20925451
Wosid WOS:000284316600012
Is Certified Translation No
Dupe Override No
Comments Source: Web of Science WOS:000284316600012Scopus URL: https://www.scopus.com/inward/record.uri?eid=2-s2.0-78649294595&doi=10.3109%2f1547691X.2010.520139&partnerID=40&md5=a03d02457c3db639a021dd0d0c4c808c
Is Public Yes
Language Text English
Keyword Host resistance; trichloroethylene; chloroform; respiratory infection; risk assessment
Is Qa No