To understand the relationship between chronic low-level lead exposure and renal function, residents living nearby a lead battery factory for more than 10 years were selected and entered in this cross-section study. The residents living in the 1st village, within 500 m from the factory, were grouped in group 1; those in the 2nd village, within 1,000-1,500 m, in group 2, and those in the 3rd village, far from any lead-contaminated sources, in group 3. Twenty-four-hour urinary N-acetyl-glucosaminidase (NAG) was detected as early indicator of renal damage, and an ethylenediamine-tetraacetic acid mobilization test was performed to estimate total body lead burden of lead-exposed persons. Blood lead level (BLL) showed a significant difference among the three study groups. The further the distance between the group and the factory, the higher BLL. The results showed a significant high prevalence of abnormal urine NAG excretion in the chronic lead-exposed group, although BLL and body lead burden of these persons were within the 'normal' range. A significant correlation between body lead burden less than 200 micrograms and 24-hour urine NAG excretion and a dose-response relationship between them were found. These observations suggested that lead was the possible cause of abnormal renal tubular function in persons with chronic low-level lead exposure, but this effect became blunt when body lead burden was more than 200 micrograms. The possible explanation may be that high body lead burden from long-term exposure will deplete the kidney of NAG or render it insensitive to the effects of lead exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylglucosaminidase Body Burden