Effect of asphalt fume inhalation exposure at simulated road paving conditions prior to bacterial infection on lung defense responses in rats.
Asphalt fume inhalation has been suspected of affecting immune function in exposed workers. The objective of this study was to evaluate the effect of asphalt exposure on lung immune responses in rats using a bacterial infectivity model. Pathogen-free male Sprague-Dawley rats were exposed by inhalation to asphalt fumes (72.6 +/- 4.95 mg/m3) or filtered air for 6 h/day for 5 days. One day after the final asphalt exposure, rats were intratracheally inoculated with 5 x 10(5) Listeria monocytogenes. At 0 (prior to bacterial inoculation), 3, and 7 days after L. monocytogenes instillation, the lungs of each animal were divided. Bronchoalveolar lavage (BAL) was performed on right lungs. The recovered BAL cells were then differentiated and counted, and alveolar macrophage (AM) function was determined. Albumin and lactate dehydrogenase (LDH), two indices of lung injury, were measured in the acellular BAL fluid. To assess bacterial clearance, the left lungs were removed, homogenized, and bacterial colony-forming units (CFUs) were counted. In addition, lung-draining lymph nodes were removed, and lymphocyte phenotype and lymphocyte-induced cytokine production were examined. Asphalt fume exposure did not cause lung injury or inflammation in rats in the absence of infection. Infection induced elevations in AMs, neutrophils (PMNs), albumin, and LDH. Importantly, no significant differences were seen when comparing the asphalt group with the air and nonexposed naive groups at any time before or after infection. Also, asphalt fume inhalation exposure did not affect the rate of pulmonary clearance of L. monocytogenes or AM production of reactive oxygen and nitrogen species. However, asphalt-related increases in lymphocyte secretion of interferon (IFN)-gamma, interleukin (IL)-6, and IL-10 were observed at different times after bacterial infection, whereas the total number of lymph-node cells and the percentage of CD4+ and CD8+ cells were not significantly different among the treatment groups. Despite the asphalt-induced changes observed in lymphokine secretion, adaptive immune function seemed to function properly in lung defense against bacterial infection. Because innate nonspecific lung responses and pulmonary clearance of L. monocytogenes were unaffected by asphalt fume exposure, lung defenses were sufficient to control the infection. It was concluded that acute inhalation of asphalt fumes at a high concentration had a minimal effect on lung immune responses to infection in rats.
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505, USA. jga6@cdc.gov
James M
JM
Antonini
Jenny R
JR
Roberts
Michael D
MD
Taylor
Xuejun
X
Yin
Samuel
S
Stone
Amy
A
Moseley
Joseph K-H
JK
Ma
David G
DG
Frazer
Vincent
V
Castranova
Jane Y C
JY
Ma
D000818:Animals; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D006838:Hydrocarbons / Q000008:administration & dosage / Q000506:poisoning*; D017745:Incineration; D019570:Inhalation Exposure; D008089:Listeria monocytogenes / Q000472:pathogenicity; D008088:Listeriosis / Q000276:immunology*; D008168:Lung / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D008171:Lung Diseases / Q000209:etiology / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology / Q000502:physiology; D008297:Male; D016273:Occupational Exposure; D010641:Phenotype; D051381:Rats; D017207:Rats, Sprague-Dawley
D016207:Cytokines; D006838:Hydrocarbons; C006647:asphalt