Toxicity of aluminum exposure during lactation to the maternal and suckling rabbit.

To assess aluminum toxicity to the A1-exposed lactating organism and her suckling offspring, lactating rabbits received 20, sc, A1 lactate injections (0, 25, 100, 400, or 800 mumol A1/kg/inj) between Days 4 and 29 postpartum. Offspring were weaned Day 30 postpartum. Weight gain in the first 12 postnatal weeks was slightly greater in 25 and 100 mumol offspring and somewhat less in 400 and 800 mumol offspring than in controls. Significant weight loss was seen in the 400 and 800 mumol group does. Does in the 800 mumol group died within 10 days after completion of the A1 injections. Every fifth day postpartum, after 24-hr isolation of the doe from her offspring, a milk sample was obtained and the weight of milk consumed by the offspring was determined. Does receiving higher A1 exposures had increased milk A1 concentration [e.g., 6.0 micrograms/g (220 microM)] in the 800 mumol group vs 1.3 micrograms/g in controls) and decreased milk production (105 g/day vs 219 g/day). Based on milk consumption and milk A1 concentration, no more than 2% of the A1 injected into the does in any of the treatment groups was found in the milk 24 hr later. During the 1 month postpartum, each suckling offspring of a 800-mumol group doe received a cumulative oral A1 exposure of about 300 mumol/kg, whereas each doe received a total of 16,000 mumol/kg, sc, and approximately 60,000 mumol/kg in her diet. When measured 1 week after weaning, offspring had no elevations in tissue A1 concentration, whereas their does had a considerable increase 5 and 9 weeks after weaning. Other than the decreased weight gain of 400 and 800 mumol offspring, probably caused by the decreased milk production of the does, no detrimental effects of the A1 treatment of lactating does were observed in the offspring. The lack of effects in the offspring is probably explained by their low levels of A1 exposure from milk compared to typical adult rabbit A1 intakes.