||Limited Toxicity of Inhaled Acetonitrile on the Immune System of Mice with Cover Letter dated 01/26/1984 and EPA Acknowledgement dated 03/09/1984.
||Immuquest Labs., Inc., Fairfax, VA.;Environmental Protection Agency, Washington, DC. Office of Toxic Substances.
Immune system ;
Immune response ;
Humoral immunity ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
||Hematological, cellular and humoral immune responses as well as clinical chemistry parameters of mice exposed to acetonitrile by inhalation were examined following observations that 800 ppm (10 treatment days) of this agent induced thymic atrophy in mice and rats. B(sub 6)C(sub 3)F(sub 1) mice received ten 6-hour exposures to 0, 100, 200, or 400 ppm of acetonitrile during a fourteen day period and were evaluated by a battery of immunological assays. Hematological parameters including hematocrit, hemoglobin, RBC and WBC were significantly depressed (P< 0.05) at increasing concentrations of the chemical. Lymphocyte proliferative responses to T-cell mitogens were depressed along with a somewhat depressed host susceptibility to transplantable tumor cell challenge, although neither of these responses were dose dependent. Studies of B-lymphocyte function indicated that levels of serum IgG were significantly depressed (P< 0.05) with increasing concentrations of acetonitrile while concentrations of IgA and IgM were unchanged. Other assays of B-cell function, including Cunningham plaque assay responses to sheep RBC and B-cell proliferative responses to mitogens, were not significantly altered by acetonitrile. Delayed hypersensitivity responses to keyhole limpet hemocyanin responses were not affected by acetontrile treatment.
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||PC A03/MF A01