376 THE THRESHOLD OF LEAD TOXICITY IN CHILDREN

Abstract

The elevation of erythrocyte protoporphyrin (EP) is a sensitive indicator of childhood Pb poisoning, reflecting interference of Pb with mitochondrial function. This study was directed to establish the minimum blood Pb level (BPb, μg/dl) at which this metabolic evidence of toxicity becomes apparent in children. Venous blood samples were obtained for screening purposes from 1944 apparently normal N.Y.C. children (aged 2-12, median 4.7). BPb was measured by atomic absorption and EP by fluorometry; 1816 children had BPb < 30, the accepted “normal” limit. Up to BPb 15 there was no correlation with EP; above BPb 15 the EP increased exponentially, with a slope similar to that reported for children with BPb > 30. The threshold BPb for EP elevation was determined, by probit analysis and by two different segmented curve-fitting techniques, to be 15.5 (c.l. 14.7 to 16.7). To exclude that the elevation of EP could be due to greater absorption of Pb by children with Fe deficiency, the Fe status of 164 children was estimated by serum ferritin (SF) and transferrin saturation (TS). There was no significant difference in either SF or TS between children with BPb below or above 15, confirming that the elevation of EP observed in the latter group results from the Pb toxicity. This study indicates detectable metabolic Pb toxicity at a level of BPb which is well below the value presently accepted as “normal.” This evidence, and the recent demonstration that in remote human populations BPb is negligible, indicate an unacceptable degree of exposure to Pb of urban children.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account

Continue with Google

Continue with ORCiD