Toxic effects of dietary methylmercury on immune system development in nestling American kestrels (Falco sparverius)

This study evaluated the effects of dietary methylmercury (MeHg) on immune system development in captive‐reared nestling American kestrels (Falco sparverius) to determine whether T cell–mediated and antibody‐mediated adaptive immunity are targets for MeHg toxicity at environmentally relevant concentrations. Nestlings received various diets, including 0 (control), 0.6, and 3.9 µg/g (dry wt) MeHg for up to 18 d posthatch. Immunotoxicity endpoints included cell‐mediated immunity (CMI) using the phytohemagglutinin (PHA) skin‐swelling assay and antibody‐mediated immune response via the sheep red blood cell (SRBC) hemagglutination assay. T cell– and B cell–dependent histological parameters in the spleen, thymus, and bursa of Fabricius were correlated with the functional assays. For nestlings in the 0.6 and 3.9 µg/g MeHg groups, CMI was suppressed by 73 and 62%, respectively, at 11 d of age. Results of this functional assay were correlated with T cell–dependent components of the spleen and thymus. Dose‐dependent lymphoid depletion in spleen tissue directly affected the proliferation of T‐lymphocyte populations, insofar as lower stimulation indexes from the PHA assay occurred in nestlings with lower proportions of splenic white pulp and higher THg concentrations. Nestlings in the 3.9 µg/g group also exhibited lymphoid depletion and a lack of macrophage activity in the thymus. Methylmercury did not have a noticeable effect on antibody‐mediated immune function or B cell–dependent histological correlates. We conclude that T cell–mediated immunosuppression is the primary target of MeHg toward adaptive immunity in developing kestrels. This study provides evidence that environmentally relevant concentrations of MeHg may compromise immunocompetence in a developing terrestrial predator and raises concern regarding the long‐term health effects of kestrels that were exposed to dietary MeHg during early avian development. Environ. Toxicol. Chem. 2011; 30:1328–1337. © 2011 SETAC