Traffic policemen are the most exposed population to lead (Pb) from automobile exhaust. There has been increasing concern about the possible harmful effects of Pb from automobile exhaust on health of traffic policemen. However, no such study was concerned with the impact of Pb exposure on renal function among them. Therefore, we aimed to study the effect of Pb exposure from automobile exhaust on renal integrity among traffic policemen.
Markers of tubular damage [urinary excretion of beta(2)-microglobulin (beta(2)M), N-acetyl-beta-D-glucosaminidase (NAG), alkaline phosphatase (ALP) and gamma-glutamyl transferase (gamma-GT)], a marker of glomerular injury (albuminuria), and markers of glomerular filtration [serum creatinine, serum beta(2)M and blood urea nitrogen (BUN)] were determined in 43 traffic policemen (Pb-exposed group) and 52 matched healthy persons (control group). Pb levels in blood, urine, hair and nails were determined in the two groups as exposure indices of Pb.
The results obtained show that the Pb-exposed group had higher Pb levels in blood, urine, hair and nails than the controls. Among the Pb-exposed group, Pb levels in blood, hair and nails showed significant and positive correlations with the duration of exposure to Pb which is measured as the duration of employment. Among the studied markers of kidney damage, urinary excretion of NAG and albumin were significantly higher in the Pb-exposed group than in the controls. Urinary excretion of NAG was positively correlated with duration of exposure, blood Pb and nail Pb. Urinary albumin was positively correlated with duration of exposure, blood Pb and hair Pb. The other markers of kidney damage were neither elevated nor correlated with exposure indices of Pb.
Traffic policemen are liable to Pb toxicity, and the determination of Pb in blood, hair and nails are good markers of such toxicity. In these exposure conditions, kidney damage is possible. Such damage is both tubular and glomerular in nature and can be documented by determination of the urinary excretion of NAG and albumin.