Six-week-old female CD-1 mice were administered the n-butylester of 2,4-dichlorophenoxyacetic acid (2,4-D). The 2,4-D ester was applied dermally at dosages ranging from 0 to 500 mg/kg (2,4-D content) in the acute studies and 0 to 300 mg/kg in the 3 week subacute studies. Following acute exposure, antibody production against sheep red blood cells was suppressed at higher exposure levels. Evidence of clinical toxicity, myotonia and depression, and histopathological alterations in the central nervous system including perivascular edema and ganglial cell necrosis, was also seen in the mice. No alterations were observed in the T- and B-lymphocyte proliferative responses induced by concanavalin A, a T-lymphocyte mitogen, or Escherichia coli lipopolysaccharide, a B-lymphocyte mitogen. Subacute 2,4-D ester exposure which produced minimal clinical or pathological alterations, had no effect on antibody production, but did enhance the B- and T-lymphocyte proliferative responses. The immunosuppressive effects of acute 2,4-D ester exposure which were observed in this study, were unlikely a direct immunological alteration, but rather a secondary manifestation of the clinical syndrome. Since the subacute exposure levels may be more comparable to occupational or environmental exposure, it is unlikely that 2,4-D esters will have any major immunotoxicological significance in agricultural communities.