PMID- 11097382
OWN - NLM
STAT- MEDLINE
DCOM- 20010301
LR  - 20190906
IS  - 0340-5761 (Print)
IS  - 0340-5761 (Linking)
VI  - 74
IP  - 8
DP  - 2000 Oct
TI  - Effects of asphalt fume condensate exposure on acute pulmonary responses.
PG  - 452-9
AB  - OBJECTIVE: The present study was carried out to characterize the effects of in 
      vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage 
      (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure 
      in rats. METHODS: For in vitro studies, rat primary AM cultures were incubated 
      with various concentrations of AFC for 24 h at 37 degrees C. 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 to monitor AM function. The 
      effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response 
      to zymosan or PMA stimulation was also determined as a marker of AM activity. For 
      in vivo studies, rats received either (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 saline, 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 lavage were measured to monitor inflammation. 
      Acellular LDH and protein content 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 microg/ml did not 
      induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did 
      cause a small but significant increase in TNF-alpha release from AM. In vitro 
      exposure of AM 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 
      induce significant neutrophil infiltration or alter LDH or protein content in 
      acellular 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. CONCLUSIONS: These 
      results suggest that: (1) in vitro AFC exposure did not adversely affect cell 
      viability or induce the release of high levels of inflammatory cytokines or 
      oxidants; and (2) exposure of rats to AFC did not cause acute pulmonary 
      inflammation or injury, and did not significantly alter AM functions.
FAU - Ma, J Y
AU  - Ma JY
AD  - Health Effects Laboratory Division, National Institute for Occupational Safety 
      and Health, Morgantown, West Virginia 26505-2888, USA. jym1@cdc.gov
FAU - Barger, M W
AU  - Barger MW
FAU - Kriech, A J
AU  - Kriech AJ
FAU - Castranova, V
AU  - Castranova V
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Arch Toxicol
JT  - Archives of toxicology
JID - 0417615
RN  - 0 (Hydrocarbons)
RN  - 0 (Interleukin-1)
RN  - 0 (Polycyclic Aromatic Hydrocarbons)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 8052-42-4 (asphalt)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Hydrocarbons/*toxicity
MH  - In Vitro Techniques
MH  - Interleukin-1/biosynthesis
MH  - Luminescent Measurements
MH  - Lung/*drug effects/pathology
MH  - Macrophages, Alveolar/*drug effects/physiology
MH  - Male
MH  - Occupational Exposure
MH  - Polycyclic Aromatic Hydrocarbons/toxicity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tumor Necrosis Factor-alpha/biosynthesis
EDAT- 2000/11/30 11:00
MHDA- 2001/03/07 10:01
CRDT- 2000/11/30 11:00
PHST- 2000/11/30 11:00 [pubmed]
PHST- 2001/03/07 10:01 [medline]
PHST- 2000/11/30 11:00 [entrez]
AID - 10.1007/s002040000145 [doi]
PST - ppublish
SO  - Arch Toxicol. 2000 Oct;74(8):452-9. doi: 10.1007/s002040000145.