Fifteen applicators of dichloropropene (DCP) were studied for personal air exposure to DCP, excretion of the metabolite of DCP (3CNAC), and excretion of the renal tubular enzyme, N-acetyl glucosaminidase (NAG). Each was studied for four 6-8 h consecutive intervals following baseline determinations of 3CNAC and NAG excretion. In accord with pilot data, 24-h urinary excretion of 3CNAC (mg) correlated well with exposure product for DCP (min exposed.mg/m3), r = 0.854, p less than .001. A more precise correlation of the air exposure product with urinary excretion of 3CNAC was discerned by using the morning urine after the previous day of exposure (micrograms/mg of creatinine), r = 0.914, p less than .001. Four workers had clinically elevated activity of NAG (greater than 4 mU/mg creatinine) in any of their urine collections after baseline. Nine workers showed greater than 25% increases in NAG excretion when compared to baseline. Dichloropropene air exposure products of greater than 700 mg.min/m3 or excretion of greater than 1.5 mg 3CNAC/d distinguished abnormally high daily excretion of NAG. These data demonstrate a firm positive relationship between air exposure and internal exposure, and a possible subclinical nephrotoxic effect in DCP workers.