Increased T-lymphocyte dependent antibody production in female SJL/J mice following exposure to commercial grade malathion.

Abstract The organophosphate pesticide, malathion, was evaluated for effects on immune function in female SJL/J mice. Commercial grade malathion was dissolved in corn oil and administered at doses of 0.018–180 mg/kg to mice via oral gavage on alternate days for 28 days. Exposure to malathion did not alter brain acetylcholinesterase activity, body weight gain, organ/body weight ratios or food and water consumption during the treatment period. Malathion enhanced the primary IgM antibody response to sheep red blood cells (SRBCs) by approximately 150% ( P 6 viable spleen cells and per spleen. B-lymphocyte blastogenesis induced by lipopolysaccharide (LPS, P =0.10) was not affected by malathion exposure. T-lymphocyte blastogenesis induced by concanavalin A (ConA, P =0.23) and phytohemagglutinin (PHA-P, P =0.24) also was unaffected by treatment with malathion. Malathion had no effect on splenic macrophage phagocytosis ( P >0.11). These results indicate that repeated oral administration of commercial-grade malathion increased antibody production following immunization with a T-lymphocyte dependent antigen at doses as low as 0.018 mg/kg, which is below the human allowable daily intake (0.02 mg/kg). These changes occurred in the absence of B- or T-lymphocyte hyper responsiveness or alterations in macrophage phagocytosis. Immune system alterations at a sub-clinical level following exposure to a commercial formulation of malathion may have an important impact on human and animal health risk assessment. Therefore, further investigation into the mechanisms responsible for the increased antibody production is warranted.