180
Trace Elements in Abiotic and Biotic Environments
are considered to be an important factor. This reflects the success in reducing Pb
contamination in food, due to replacement of soldered cans, banning of Pb in wine
bottles, and the phasing out of leaded petrol. The largest contributors to overall Pb
exposure are cereals and cereal products and vegetables.
Dietary exposures of the general U.K. population have declined from 0.12 mg/day
estimated in 1980 to 0.006 mg/day in 2006 (Rose et al. 2010). The United States
reported declines in Pb exposure for all age groups, with the greatest decline in
teenage males (from 0.07mg/day in 1976 to 0.00345 mg/day in 2000); Canada and
France have also reported a 50% decline in Pb exposure over the past 10–15 years
(WHO 2011c). Lead intake by people of China, in 1990–2000, were much higher
than in some other countries (e.g., the United States, the United Kingdom, Australia,
and Japan), and were in the range of 0.084–0.392 mg/day; it was caused by the large
consumption of Pb-contaminated rice (Sun et al. 2011b).
24.7 ANIMALS
Cattle, especially young calves, are extremely susceptible to Pb toxicity. In domestic animals, Pb poisoning (plumbism) is mainly one of acute toxicity, whereas the
chronic form occurs most often in humans. Lead is one of the most frequently
reported causes of poisoning in farm animals, especially in cattle, as well as in other
ruminants.
Susceptibility to Pb poisoning is affected by the type of its compounds, ruminal or intestinal acidity, animal species, and stage of lactating and/or pregnancy.
In some instances, as little as 6 mg Pb/kg bw (300 mg/kg in the total diet) over 60
days was fatal for cattle. In all domestic species, Pb poisoning causes derangement
of the central nervous system, gastrointestinal tract, muscular coordination, and
red blood cell synthesis. In cattle, signs of toxicity include a depressed appearance,
blindness, grinding of teeth, muscular twitching, snapping of eyelids, and convulsive seizures. With sheep, Pb toxicity results in depression, anorexia, abdominal pain, and usually diarrhea. Anemia is common during chronic Pb ingestion.
Osteoporosis has been observed in young grazing lambs and abortions in ewes
grazing in lead-mining areas.
Chronic oral exposure of experimental animals to inorganic Pb has effects on
multiple organs, including kidney and liver, and systems, as well as the cardiovascular, hematological, immune, reproductive, and nervous systems. In horses, Pb toxicity syndrome induces anemia, depression, stupor, knuckling at the fetlocks, and
laryngeal paralysis, which produces an obstruction in the air passage. Large amounts
of dietary Zn decrease or prevent clinical signs of Pb toxicity in horses. Protective
effect occurs despite an increase in Pb retention in several soft tissues, with the high
Zn uptake. Also, lower than optimal amounts of dietary Ca (and P, to a lesser extent)
increase liver Pb in the young horses.
About 90% of Pb in animal blood is associated with red blood cells. Lead inhibits the utilization of Fe and the biosynthesis of heme, thus causing anemia. Lead
may displace metals from enzymes, thereby causing their inactivation. Nuclei,
microsomes, and mitochondria seem particularly susceptible to Pb. Lead inhibits