Lead (Pb) is a well-known environmental contaminant of food and water. Previous rodent studies have shown that Pb exposure can alter blood physiology, induce neural and renal toxicity and affect nutrient absorption. In birds the primary route of exposure, with similar indications of toxicity, is by oral ingestion of Pb particles as grit or mistakenly as food. However, no data existed tracking the retention and clearance of these Pb pellets in the bird GI tract while linking toxicity and blood accumulated lead levels. Further, no data existed on the effects of oral Pb bullet fragment exposure in birds. To begin to address these gaps in the data, Northern Bobwhite quail were orally gavaged with spent lead shot (0, 1, 5 and 10 spent Pb shot/bird) or bullet fragments (0, 1, and 5 fragments/bird), radiographed and evaluated for changes in peripheral blood, neural, renal, and immune parameters. The majority of the pellets and fragments were voided within 7 to 14 days post exposure with no detection by radiograph by day 21. In the quail, Pb exposure resulted in severe weight loss, hemodynamic compromise, koilin degeneration, and at doses exceeding five 50 mg pellets, mortality from complications of emaciation. Pb inhibited -ALAD activity, a marker of heme synthesis, by as much as 90% with doses as low as one 24 mg fragment after just one week of exposure. Initial functional immune evaluation in the quail was inconclusive, so we evaluated the effect of Pb at blood concentrations commonly seen in vivo on a model of antigen presenting cells (APCs), the RAW 267.4 cell line. Recent data had shown that APCs may play a major role in the upregulation of the adaptive immune response to antigen through altered surface expression of MHC and co-stimulatory molecules after exposure to Pb. In the present study, 2.5- 5.0 M Pb dysregulated cellular metabolism in RAW 267.4 cells cultured for 17 hr resulting in enhanced autophagy, increased MIIC trafficking leading to increased surface expression of MHC-II and co-stimulatory proteins critical to T-helper type 2 activation suggesting an alternate mechanism of autoimmune induction, in vitro.