PMID- 8806881
OWN - NLM
STAT- MEDLINE
DCOM- 19961031
LR  - 20071114
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 140
IP  - 1
DP  - 1996 Sep
TI  - Characterization of the early pulmonary inflammatory response associated with 
      PTFE fume exposure.
PG  - 154-63
AB  - Heating of polytetrafluoroethylene (PTFE) has been described to release fumes 
      containing ultrafine particles (approximately 18 nm diam). These fumes can be 
      highly toxic in the respiratory tract inducing extensive pulmonary edema with 
      hemorrhagic inflammation. Fischer-344 rats were exposed to PTFE fumes generated 
      by temperatures ranging from 450 to 460 degrees C for 15 min at an exposure 
      concentration of 5 x 10(5) particles/cm3, equivalent to approximately 50 
      micrograms/m3. Responses were examined 4 hr post-treatment when these rats 
      demonstrated 60-85% neutrophils (PMNs) in their lung lavage. Increases in 
      abundance for messages encoding the antioxidants manganese superoxide dismutase 
      and metallothionein (MT) increased 15- and 40-fold, respectively. For messages 
      encoding the pro- and anti-inflammatory cytokines: inducible nitric oxide 
      synthase, interleukin 1 alpha, 1 beta, and 6 (IL-1 alpha, IL-1 beta, and IL-6), 
      macrophage inflammatory protein-2, and tumor necrosis factor-alpha (TNF alpha) 
      increases of 5-, 5-, 10-, 40-, 40-, and 15-fold were present. Vascular 
      endothelial growth factor, which may play a role in the integrity of the 
      endothelial barrier, was decreased to 20% of controls. In situ sections were 
      hybridized with 33P cRNA probes encoding IL-6, MT, surfactant protein C, and TNF 
      alpha. Increased mRNA abundance for MT and IL-6 was expressed around all airways 
      and interstitial regions with MT and IL-6 demonstrating similar spatial 
      distribution. Large numbers of activated PMNs expressed IL-6, MT, and TNF alpha. 
      Additionally, pulmonary macrophages and epithelial cells were actively involved. 
      These observations support the notion that PTFE fumes containing ultrafine 
      particles initiate a severe inflammatory response at low inhaled particle mass 
      concentrations, which is suggestive of an oxidative injury. Furthermore, PMNs may 
      actively regulate the inflammatory process through cytokine and antioxidant 
      expression.
FAU - Johnston, C J
AU  - Johnston CJ
AD  - Department of Environmental Medicine, University of Rochester, New York 14642, 
      USA.
FAU - Finkelstein, J N
AU  - Finkelstein JN
FAU - Gelein, R
AU  - Gelein R
FAU - Baggs, R
AU  - Baggs R
FAU - Oberdorster, G
AU  - Oberdorster G
LA  - eng
GR  - ES01247/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Cytokines)
RN  - 0 (Endothelial Growth Factors)
RN  - 0 (Protein C)
RN  - 63231-63-0 (RNA)
RN  - 9002-84-0 (Polytetrafluoroethylene)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
SB  - IM
MH  - Animals
MH  - Atmosphere Exposure Chambers
MH  - Blotting, Northern
MH  - Cytokines/*metabolism
MH  - Endothelial Growth Factors/analysis
MH  - In Situ Hybridization
MH  - Lung/chemistry/*drug effects/immunology
MH  - Male
MH  - Nitric Oxide Synthase/analysis
MH  - Polytetrafluoroethylene/administration & dosage/*toxicity
MH  - Protein C/analysis
MH  - RNA/analysis
MH  - Rats
MH  - Rats, Inbred F344
OTO - NASA
OT  - NASA Discipline Environmental Health
OT  - Non-NASA Center
FIR - Clarkson, T W
IR  - Clarkson TW
IRAD- U Rochester, NY
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
AID - S0041-008X(96)90208-2 [pii]
AID - 10.1006/taap.1996.0208 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 1996 Sep;140(1):154-63. doi: 10.1006/taap.1996.0208.