Record Display for the EPA National Library Catalog


Main Title Biological Effects of Short Term, High Concentration Exposure to Methyl Isocyanate (In Vitro and In Vivo Complement Activation Studies) with Cover Letter 12/15/86.
CORP Author Cytotech, Inst., San Diego, CA. ;Mellon Inst.-Union Carbide Corp., Export, PA. Bushy Run Research Center. ;Union Carbide Corp., Danbury, CT.;Environmental Protection Agency, Washington, DC. Office of Toxic Substances.
Publisher 22 Dec 1986
Year Published 1986
Report Number 8HEQ-1286-0392;
Stock Number OTS-0204924-2
Additional Subjects Toxicity ; In vitro analysis ; In vivo analysis ; Exposure(Physiology) ; Pigs ; Laboratory tests ; Concentration(Composition) ; Vapors ; Chemical analysis ; Laboratory animals ; Hemolysis ; Methyl isocyanate ; Union Carbide Corporation
Library Call Number Additional Info Location Last
NTIS  OTS-0204924-2 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 27p
The ability of MIC to induce complement activation in vitro and in vivo was investigated. For the in vitro studies, both human and guinea pig serum or EDTA-plasma sample were exposed to 1167-1260 ppm MIC vapor for 15 min at room temperature. The human serum samples exposed to MIC showed significant reductions in Factor B, C2, C4, C3, C5, and total hemolytic complement CH50 activity levels. C6 functional activity was unaffected. The C3, C5 and CH50 functional activities in guinea pig serum (the only functional tests conducted on these samples) were more sensitive to MIC mediated reduction than the corresponding activity reductions observed in the human serum samples. The human and guinea pig EDTA-plasma samples exposed to MIC vapor showed no evidence of C3 consumption but did show significant reductions in CB50 levels. Thus, MIC vapor was able to activate, and thereby reduce serum complement C3 activity in vitro by a complement-dependent process. However, at least one complement component other than C3 was inactivated in EDTA-plasma by a complement-independent mechanism.