P. Factorlitvak et al., HYPERPRODUCTION OF ERYTHROPOIETIN IN NONANEMIC LEAD-EXPOSED CHILDREN, Environmental health perspectives, 106(6), 1998, pp. 361-364
Lead (Pb) poisoning has numerous effects on the erythropoietic system,
but the precise mechanism whereby high dose exposure causes anemia is
not entirely clear. We previously reported that ph exposure is associ
ated with depressed serum erythropoietin (EPO) in pregnant women resid
ing in a ph mining town and in a nonexposed town in Kosovo, Yugoslavia
. In a prospective study, we tested the hypothesis that blood Pb conce
ntration (BPb) may be associated with depressed EPO in children. BPb,
hemoglobin (Hgb), and serum EPO were measured at ages 4.5, 6.5, and 9.
5 years in 211, 178, and 234 children, respectively. At 4.5 years of a
ge, mean BPbs were 38.9 and 9.0 mu g/dl in the exposed and nonexposed
towns, respectively; BPbs gradually declined to 28.2 and 6.5 mu g/dl,
respectively, by age 3.5 years. No differences were found in Hgb at an
y age. At age 4.5 years, a positive association between BPb and EPO (b
eta = 0.21; p = 0.0001), controlled for Hgb, was found. The magnitude
of this association declined to 0.11 at age 6.5 years (p = 0.0103) and
0.03 at age 9.5 years (p = 0.39). These results were confirmed using
repeated measures analyses. We concluded that in ph-exposed children,
the maintenance of normal Hgb requires hyperproduction of EPO. With ad
vancing age land continuing exposure), this compensatory mechanism app
ears to be failing, suggesting a gradual loss of renal endocrine funct
ion due to ph exposure.