Comparison of lead bioavailability in F344 rats fed lead acetate, lead oxide, lead sulfide, or lead ore concentrate from Skagway, Alaska
- 1 May 1993
- journal article
- research article
- Published by Taylor & Francis in Journal of Toxicology and Environmental Health
- Vol. 39 (1), 79-93
- https://doi.org/10.1080/15287399309531737
Abstract
An animal model using rats was developed to initiate investigations on the bioavailability of different sources of environmental lead. Lead must be absorbed and transported to target organs like brain, liver, kidney, and bone, before susceptible cells can be harmed. The bioavailability and therefore the toxicity of lead are dependent upon the route of exposure, dose, chemical structure, solubility, particle size, matrix incorporation, and other physiological and physicochemical factors. In the present study male F344 rats were fed ≤ 38 μm size particles of lead sulfide, lead oxide, lead acetate, and a lead ore concentrate from Skagway, Alaska, mixed into the diet at doses of 0, 10, 30, and 100 ppm as lead for 30 d. No mortality or overt symptoms of lead toxicity were observed during the course of the study. Maximum blood lead concentrations attained in the 100 ppm groups were ∼80 μg/dl in rats fed lead acetate and lead oxide, and were ∼10 μg/dl in those fed lead sulfide and lead ore concentrate. Maximum bone lead levels in rats fed soluble lead oxide and lead acetate were much higher (∼200 μg/g) than those seen in rats fed the less soluble lead sulfide and lead ore (∼10 μg); kidney lead concentrations were also about 10‐fold greater in rats fed the more soluble compared to the less soluble lead compounds. However, strong correlations between dose and tissue lead concentrations were observed in rats fed each of the four different lead compounds. Kidney lesions graded as minimal occurred in 7/10 rats fed 30 ppm and in 10/10 rats fed 100 ppm lead acetate, but not at lower doses or from other lead compounds. Similarly, urinary aminolevulinic acid excretion, a biomarker for lead toxicity, was increased in rats fed 100 ppm lead acetate or lead oxide, but was unaffected at lower doses or by the less soluble lead compounds. Although the histological and biochemical responses to lead toxicity were restricted to the more soluble lead compounds in this study, lead from Skagway lead ore concentrate and lead sulfide was also bioavailable, and accumulated in proportion to dose in vulnerable target organs such as bone and kidney. Longer‐term studies with different mining materials are being conducted to determine if tissue lead continues to increase, and whether the levels attained are toxic. Data from such studies can be used to compare the toxicity and bioavailability of lead from different sources in the environment.Keywords
This publication has 15 references indexed in Scilit:
- Relative bioavailability of lead from mining waste soil in ratsFundamental and Applied Toxicology, 1992
- Experimental model of lead nephropathyEnvironmental Research, 1992
- An Update on Exposure and Effects of LeadFundamental and Applied Toxicology, 1992
- An Integrated Exposure/ Pharmacokinetic Based Approach to the Assessment of Complex ExposuresToxicology and Industrial Health, 1991
- Introduction and summary. International workshop on lead in bone: implications for dosimetry and toxicology.Environmental Health Perspectives, 1991
- Assessing the contribution from lead in mining wastes to blood leadRegulatory Toxicology and Pharmacology, 1990
- The Long-Term Effects of Exposure to Low Doses of Lead in ChildhoodNew England Journal of Medicine, 1990
- Deficits in Psychologic and Classroom Performance of Children with Elevated Dentine Lead LevelsNew England Journal of Medicine, 1979
- Changes in sodium and potassium in urine and serum of lead-intoxicated ratsToxicology and Applied Pharmacology, 1979
- Acute effects of lead on renal electrolyte excretion and plasma renin activityToxicology and Applied Pharmacology, 1978