Experimental Lead Paint Poisoning in Nonhuman Primates

Bc, Zook; Wt, London; Jl, Sever; Rm, Sauer

doi:10.1159/000459904

Cited by 17 publications

(23 citation statements)

References 20 publications

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“…Young animals are more sensitive to the toxic effects of lead than juvenile or adult animals (3,(25)(26)(27). The increased susceptibility of young animals is due in part to their increased capacity to absorb lead from the gastrointestinal tract (3,4,(27)(28)(29).…”

Section: Discussionmentioning

confidence: 99%

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Rader¹,

Peeler²,

Mahaffey³

1981

Environ Health Perspect

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The relative toxicity of low doses of lead acetate provided steadily in drinking water or by mouth once per week was studied in weanling and adult rats. Free erythrocyte protoporphyrin and urinary 8-aminolevulinic acid levels were measured, as well as lead levels in blood and kidney. The accumulation of lead in brain tissue and in bone (femur) was measured to determine the effect of age and schedule of administration on tissue distribution and retention of lead. Total intakes of lead during the 60-week experimental period were: weanling and adult rats exposed to drinking water supplemented with 200 ,g of lead acetate/ml: 127 + 10 mg and 160 ± 16 mg, respectively; weanling and adult rats dosed with lead acetate orally once per week: 132 mg and 161 mg, respectively. Increased toxic effects of lead in the weanling animals were apparent in most of the parameters measured (urinary 8-aminolevulinic acid and blood, brain, femur and kidney lead levels). This pattern was observed in weanling rats exposed to lead steadily through drinking water or dosed orally with an equivalent quantity of lead once per week. Lead levels in blood were highly correlated with the accumulation of lead in brain, femur, and kidney tissue in both groups of weanling rats. In adult rats, significant correlations between blood lead and kidney lead and between blood lead and femur lead were found only in the rats receiving lead steadily in drinking water.

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Section: Discussionmentioning

confidence: 99%

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Rader¹,

Peeler²,

Mahaffey³

1981

Environ Health Perspect

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“…Gross findings at necropsy revealed few lesions that were not observed clinically, i.e., Burtonian lines, focal alopecia, decreased body fat; and were pre viously reported (31). Considerable amounts of ground paint were observed in the intestinal contents.…”

Section: Necropsy Findingsmentioning

confidence: 87%

“…Lead poisoning occurs naturally in simian primates resulting in a disease closely resembling lead poisoning in man (11,14,24,(30)(31)(32)(33). Surprisingly, how ever nonhuman primates have seldom been used as an experimental model of lead intoxication.…”

Section: Introductionmentioning

confidence: 99%

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Experimental Lead Paint Poisoning in Nonhuman Primates

et al. 1980

J Med Primatol

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Necropsies were performed on 25 rhesus monkeys, three cebus monkeys and three baboons which had been fed leaded paint or lead acetate at various doses up to 666 days. The 31 test primates and six controls ranged in age from five days to about eight years. In addition, the brains of 13 subadult squirrel monkeys fed lead oxide and two controls were studied grossly and microscopically. Lead content of liver, kidney and brain correlated with clinical outcome and typical histologic changes. Neuropathologie lesions, most severe in the young, occurred in 28 of 43 test primates despite a paucity of neurological signs. Brain lesions were similar to those occurring in human lead encephalopathy and included degenerative and proliferative changes of small vessels, ring hemorrhages, edema, perivascular hyalin droplets, rosette-like deposits of proteinaceous exudates, focal loss of myelin, astrogliosis and necrosis of hippocampal neurons.

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“…Details concer ning the experimental subjects and procedures, methods of analysis and other data have been reported (37).…”

Section: Methodsmentioning

confidence: 99%

Experimental Lead Paint Poisoning in Nonhuman Primates II. Clinical Pathologie Findings and Behavioral Effects

Bc¹,

Wt²,

Jf³

et al. 1980

J Med Primatol

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Oral administration of lead-containing paint to rhesus monkeys induced anemia, more profound in older primates. Erythrocytes were microcytic and hypochromic, but tended to become macrocytic terminally. Stippled erythrocytes were increased in all poisoned monkeys, especially in those with high blood lead levels and anemia. Proteinuria, glycosuria, casts and sloughed tubular cells containing acid-fast inclusion bodies were found on urinalysis. Terminal elevations of blood urea nitrogen were associated with profound anemia and renal tubular damage. Repeated blood lead values over 200 μg/dl were associated with a moribund termination while monkeys which had levels under 100 μg/dl remained apparently healthy. Behavioral studies in a small number of subclinically poisoned juveniles and neonates failed to reveal deficiencies of visual acuity or cognitive ability, nor was there evidence of alterations in levels of activity.

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Experimental Lead Paint Poisoning in Nonhuman Primates

Cited by 17 publications

References 20 publications

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

Experimental Lead Paint Poisoning in Nonhuman Primates

Experimental Lead Paint Poisoning in Nonhuman Primates II. Clinical Pathologie Findings and Behavioral Effects

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