MONITORING ACRYLIC FIBER WORKERS FOR LIVER TOXICITY AND EXPOSURE TO DIMETHYLACETAMIDE .2. SERUM CLINICAL-CHEMISTRY RESULTS OF DIMETHYLACETAMIDE-EXPOSED WORKERS

Worker exposure to N,N-dimethylacetamide (DMAC) in an acrylic fiber manufacturing facility was measured, over a 1-year study period by full-shift (12 hours) personal air monitoring for DMAC and biological monitoring for levels of DMAC, N-methylacetamide (MMAC) and acetamide in post-shift spot urine samples. Evidence of liver toxicity was assessed by serum clinical chemistry tests (serum levels of total bilirubin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transpeptase) at least once during the study period for all 127 male workers in the two study departments and for 217 male in-plant controls with no previous or current exposure to DMAC. If a worker's biomonitoring results exceeded one of two ''trigger'' values established for the study (60 mg MMAC/g creatinine or 136 mg DMAC equivalent/g creatinine), additional serum clinical chemistry tests were conducted at weekly intervals for 3 weeks. DMAC-exposed workers were classified as either high exposure, if one or more biomonitoring result exceeded one of the trigger values, or unspecified exposure if none of them did. Control-group employees were classified as no-exposure. Mean DMAC in air levels for the high- and unspecified-exposure groups appeared do differ (geometric mean DMAC in air levels of 1.9 and 1.3 ppm 12-hour time-weighted average, respectively). No significant DMAC exposure-related trends in hepatic serum clinical chemistry results were detected. Neither transient increases in serum analyte levels after a ''high'' biomonitoring result (one that exceeded a trigger value) nor an elevated mean level over the study period when compared with in-plant controls were observed. These results suggest that brief threshold limit value-level exposures and chronic low-level exposure (maximum likelihood estimate of the arithmetic mean for DMAC in air for the high-exposure group over the study period was 3.0 ppm 12-hour time-weighted average) do not cause hepatotoxic clinical chemistry responses.