Abstract

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 < .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 (μg/mg of creatinine), r = 0.914, p < .001. Four workers had clinically elevated activity of NAG (> 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 > 700 mg · min/m³ or excretion of > 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.