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 rouped 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 exretion 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 pg 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 pg. 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. Whether urine NAG is an early indicator of lead nephropathy is still unconclusive, and long-term follow- up in our study is needed to detail these relations.
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