The effects of lead (7439921) on skeletal development were studied in rats. Female Sprague-Dawley-rats were administered 0, 250, or 1,000 parts per million (ppm) lead as lead-acetate-trihydrate (6080564) in their drinking water starting 49 days before mating and continuing through delivery. At delivery, control dams were given drinking water containing 250 or 1,000ppm lead. Dams given 250 or 1,000ppm lead before were continued on these protocols. At weaning, the dams were killed and blood samples were collected and analyzed for lead, calcium, and phosphorus. The tibial bones were removed and examined for morphological changes. Growth plate widths were measured. The bones were ashed and analyzed for lead, calcium, and phosphorus. The offspring were killed 3 days after weaning, weighed, and their tail lengths were measured. The tibias were removed and examined for morphological changes. Maternal blood lead concentrations increased in a dose and time related manner. Lead did not affect litter size or offspring viability. Tibial lead concentrations were significantly higher in dams dosed from mating up throughout lactation than those dosed only during lactation. Tibial calcium and phosphorus concentrations were significantly decreased only in dams dosed continuously. Lead did not significantly affect maternal tibial morphology or growth plate width. Offspring body weights and tail lengths were significantly decreased by 250 and 1,000ppm lead following continuous exposure and by 1,000ppm lead in those dosed during lactation only. Blood calcium and phosphorus concentrations were significantly decreased in offspring continuously exposed to 1,000ppm lead. Tibial calcium and phosphorus concentrations were not affected. Offspring exposed to 1,000ppm lead continuously had significantly increased tibial growth plate widths. The degree of chondrocyte orientation was disrupted, the metaphyseal trabecula was widened, and the amount of nonmineralized cartilage in the growth plates was increased in these animals. The authors conclude that prenatal and lactational exposure to lead impairs skeletal development in the offspring. The impaired skeletal development may reflect local effects on growth plate chondrogenesis and metaphyseal mineralization.
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