Biomedical subjects
Publications and source records attributed to S I Lerner.
A qualitative screening method to detect inorganic lead on skin and other surfaces is described. It is based on the development of a brownish to black lead sulfide when sodium sulfide solution reacts with inorganic lead. The procedure can facilitate worker training and assist in reducing excessive exposure to lead of workers and their families.
Histochemical and microscopic studies have shown that a characteristic renal response to lead exposure is the formation of discrete, dense, staining intranuclear inclusion bodies in renal tubular epithelial cells. Cytologic examination of urinary sediment showed that four of 19 (21%) lead workers had exfoliated inclusion-bearing cells of proximal renal tubular origin. These lead-induced inclusion-bearing cells appeared distinctly different from viral-induced inclusions, degenerative or nonspecific intranuclear inclusions seen with tubular necrosis, or macronucleoli seen in reparative renal tubular epithelium. While their presence indicates cytologic evidence of tubular injury, the clinical significance of these cells and their application to medical monitoring is not clearly understood.
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The expected relationship between the apparent half-life of blood lead (PbB) and the length of previous exposure is compared with the observed relationship in a group of workers on strike from a primary smelter where they had been employed for from a few months to ten years. Within this group, the apparent PbB half-life was positively correlated both with pre-strike PbB and with length of exposure to lead. It is likely that the dependence of apparent half-life on pre-strike PbB is primarily a reflection of interindividual differences in lead kinetics in these men. The direct dependence of apparent half-life on duration of lead exposure is consistent with published data from former lead workers and from human subjects experimentally exposed to lead.
A lead-intoxicated patient with extremely high blood lead levels and unexpectedly mild symptoms was studied prior to and following treatment with calcium disodium edetate (ethylenediaminetetraacetic acid) and then prior to and following oral administration of zinc sulfate. During chelation therapy, erythrocyte (delta)-aminolevulinic acid dehydratase (ALAD) activity decreased as blood lead levels fell. Urinary excretion of zinc increased and was more than 3.5 times greater than that of lead. The ratio of blood lead to serum zinc was greatest (1.47) when ALAD activity was lowest. Oral administration of zinc sulfate following chelation therapy resulted in a significant increase in mean ALAD activity. In vitro additions of zinc chloride to the patient's erythrocytes resulted in reactivation of ALAD activity. These studies suggest that zinc is an important element in the ALAD system in man. Zinc may play a protective role in lead toxicity, and zinc supplementation may be a useful adjunct to chelation therapy for lead toxicity.