2,3,7,8-Tetrachlorodibenzo-p-dioxin is a well-known immunosuppressive environmental pollutant. TCDD interferes with physiological signaling of the arylhydrocarbon receptor, leading to cell-specific changes in gene transcription and cell differentiation. With respect to the immune system, the T-cell lineage and B-cell lineages are particularly affected. Although a single dose given to mice is excreted within weeks, these changes in differentiation may have long-term consequences for immune competence. We studied the effects of a single dose of TCDD given to young mice on some parameters of their immune system after they had aged almost to the end of their lifespan. Groups of 15 mice were given either 2.5 microg TCDD/kg b.w. or 25 microg TCDD/kg b.w. at the age of 8-12 weeks, and were analyzed between 16 and 21 months of age. Survival was equal in all groups. Blood glucose levels did not differ, and glucose tolerance after oral challenge was normal in old control mice and TCDD-exposed mice. No differences in the frequencies of B-cells, T-cells, or NK-cells were detectable. TCDD-exposed mice at both doses had a significantly higher titer of IgM compared to controls. Histological examination of pancreas, liver, kidney, spleen, and lungs yielded no differences, except for the lungs, where a significantly higher number of animals displayed activated BALT. In conclusion, our data suggest that a single dose of TCDD in young mice is correlated to activated secondary lymphoid tissues and high IgM titers. Both findings are congruent with a weakened immune system.