Effects of asphalt fume condensate exposure on acute pulmonary responses

Citation
Jyc. Ma et al., Effects of asphalt fume condensate exposure on acute pulmonary responses, ARCH TOXIC, 74(8), 2000, pp. 452-459
Citations number
38
Categorie Soggetti
Pharmacology & Toxicology
Journal title
ARCHIVES OF TOXICOLOGY
ISSN journal
03405761 → ACNP
Volume
74
Issue
8
Year of publication
2000
Pages
452 - 459
Database
ISI
SICI code
0340-5761(200010)74:8<452:EOAFCE>2.0.ZU;2-I
Abstract
Objective: The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macr ophage (AM) functions and to monitor acute pulmonary responses to in vivo A FC exposure in rats. Methods: For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degreesC. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium t o monitor AM function. The effect of AFC on chemiluminescence (CL) generate d by resting AM or AM in response to zymosan or PMA stimulation was also de termined as a marker of AM activity. For in vivo studies, rats received eit her (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0. 5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of salin e, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar la vage were measured to monitor inflammation. Acellular LDH and protein conte nt in the first lavage fluid were measured to monitor damage. CL generation , TNF-alpha and IL-1 production by AM were assayed to monitor AM function. Results: In vitro AFC exposure at <200 <mu>g/ml did not induce cytotoxicity , oxidant generation, or IL-1 production by AM, but it did cause a small bu t significant increase in TNF-alpha release from AM. In vitro exposure of A M to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induc e significant neutrophil infiltration or alter LDH or protein content in ac ellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control macrophages. Conclus ions: These results suggest that: (1) in vitro AFC exposure did not adverse ly affect cell viability or induce the release of high levels of inflammato ry cytokines or oxidants; and (2) exposure of rats to AFC did not cause acu te pulmonary inflammation or injury, and did not significantly alter AM fun ctions.