Susceptibility to Lead Toxicity

When infant rhesus monkeys were exposed to lead via the addition of lead acetate (0.5-9 mg/kg body weight) to their formula or by the consumption of lead particles from lead-based surrogate mothers, they developed symptoms of lead intoxication within 6 weeks. Seizures, muscular tremors, and altered social interaction were the predominant changes. Visual impairment was also apparent in the more severely affected animals. In the animals showing obvious symptoms lead levels varied between 300 to 500 ,g/100 ml of blood. Even in those animals having blood lead levels below 100 ,ug, hyperactivity and insomnia were observed. When the exposure to lead was eliminated, seizures subsided and visual impairment was reduced; however, the abnormal social interaction persisted. These animals also experienced a gradual decline in hematocrit and hemoglobin values during the period of examination. Liver and kidney biopsies obtained from these leadexposed animals revealed characteristic intranuclear inclusions.When adolescent and adult monkeys were exposed to doses of lead acetate similar to those employed in the infant experiments, lead levels in excess of 200 Mg/100 ml of blood were recorded. However, there were no obvious behavioral abnormalities observed. There were, however, numerous lead inclusion bodies in kidney biopsy specimens from these animals.These data suggest that, like man, the infant nonhuman primate is much more susceptible to lead intoxication than is the adult. The clinical and behavioral changes recorded in these infant rhesus monkeys suggest their use as an experimental model to evaluate lead intoxication.The injurious effects of excessive exposure to lead by man and lower animals have been known since ancient times. In spite of r-

Section: Experimental Observationsmentioning

confidence: 99%

Pathobiological and Behavioral Effects of Lead Intoxication in the Infant Rhesus Monkey

Allen¹,

McWey²,

Suomi³

1974

“…This is especially true in the case of lead poisoning, the severity of which is influenced by a wide variety of nutrients (1)(2)(3)(4)(5). The importance of dietary factors in determining the degree of lead poisoning is emphasized by the observation of Morrison et al (6) that the dietary content of certain major minerals often had greater effects on the toxicity and tissue content of lead than did a doubling of the dietary lead content itself.…”

Section: Introductionmentioning

confidence: 99%

Lead toxicity and nutritional deficiencies.

Levander¹

1979

Under appropriate conditions, deficiencies of certain minerals and vitamins as well as high intakes of dietary fat increase the toxicity of a given dose of lead in experimental animals. The severity of lead poisoning can also be increased by the consumption of either deficient or excessive levels of protein. Mineral deficiencies appear to have some of the most profound effects on lead toxicity, since the consequences of plumbism can be exaggerated by feeding diets low in calcium, phosphorus, iron, zinc, and in some cases, copper. Evidence for an antagonism between lead and nutritional levels of selenium is inconclusive. Vitamin E deficiency and lead poisoning interact to produce an anemia in rats that is more severe than that caused by either treatment alone. Lead apparently exerts a pro-oxidant stress on the red cell, thereby causing its accelerated destruction. One of the biochemical mechanisms of lead poisoning may be the disruption of normal membrane architecture, thereby leading to peroxidative damage. Epidemiological surveys have suggested a negative correlation between the poor nutritional status of children with regard to calcium and the concentration of lead in blood. Other examples of potential interactions of mineral status and lead poisoning in humans include the hypothesized hazards of soft water to public health in areas with lead plumbing and the possible role of mineral deficiencies in the etiology of pica. Experimental studies have shown that in some situations combined nutritional deficiencies can have an additive effect in potentiating lead toxicity.

“…Susceptibility to lead (Pb) toxicity is known to be influenced by a number of physiological and environmental factors (1 ): (1) age; (2) season of the year (body temperature, dehydration, ultraviolet light); (3) calcium, phosphorus and vitamin D; (4) dietary protein; (5) ascorbic acid; (6) nicotinic acid; (7) alcohol; (8) other heavy metals. The types of factors involved in alteration of vulnerability vary widely but include dietary and metabolic effects.…”

mentioning

confidence: 99%

Nutritional Factors and Susceptibility to Lead Toxicity

Mahaffey¹

1974

Self Cite

Although the quantities of lead (Pb) to which individuals are exposed vary widely, susceptibility of an individual to the effects of a specific level of exposure is another highly important factor in development of lead toxicity. For example, susceptibility to lead toxicity can be modified by several dietary factors. Low dietary intakes of calcium or iron (20% of recommended levels) substantially increase the toxicity of the same level of lead exposure to rats. In the studies of calcium effect, when calcium was fed to rats at 1/5 of the recommended intake, 12 jg Pb/ml drinking water produced the same degree of toxicity as did 200 jig Pb/mI with a normal calcium diet. The maximal dose for a 10-week period that does not impair heme synthesis or renal function in the rat has been established to be 200 jg Pb/ml drinking water. The role of low calcium diet on increasing susceptibility to lead has been confirmed in several species.Mechanisms explaining the effect of calcium on lead toxicity may be related to absorption of lead from the gastrointestinal tract or renal tubule or to function of the parathyroid. Preliminary histological investigations on the parathyroids of control and lead-treated rats on normal and low calcium diets show no effect of lead.Studies are currently underway to evaluate the lead, calcium and iron contents of the diets of children with normal and elevated concentrations of blood lead.