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Lead is a soft, malleable metal that is obtained chiefly by the primary smelting and refining of natural ores or by the widespread practice of recycling and secondary smelting of scrap lead products. Recycling accounts for nearly 85% of domestic lead consumption, approximately 85% of which is used in the manufacture of lead acid batteries. Lead is used for weights and radiation shielding, and lead alloys are used in the manufacture of pipes; cable sheathing; brass, bronze, and steel; ammunition; and solder (predominantly electric devices and automotive radiators). Lead compounds are added as pigments, stabilizers, or binders in paints, ceramics, glass, and plastic.

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Although the use of lead in house paint has been curtailed since the 1970s, industrial use of corrosion-resistant lead-based paint continues, and high-level exposure may result from renovation, sandblasting, torching, or demolition. Corrosion of lead plumbing in older homes may increase the lead concentration of tap water. Young children are particularly at risk from repeated ingestion of lead-contaminated house dust, yard soil, or paint chips or from mouthing toy jewelry or other decorative items containing lead. Children may also be exposed to lead carried into the home on contaminated work clothes worn by adults. Regular consumption of game meat harvested with lead ammunition and contaminated with lead residues may increase blood lead above background levels, particularly in children.

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Lead exposure may occur from the use of lead-glazed ceramics or containers for food or beverage preparation or storage. Certain folk medicines (eg, the Mexican remedies azarcon and greta, the Dominican remedy litargirio, and some Indian Ayurvedic preparations) may contain high amounts of lead salts.

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Consumer protection legislation enacted in 2008 lowered the permissible concentration of lead in paint and other surface coatings for consumer use to 0.009% (90 ppm). By 2011, the lead content of children's products must not exceed 100 ppm.

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  1. Mechanism of toxicity

    1. The multisystem toxicity of lead is mediated by several mechanisms, including inactivation or alteration of enzymes and other macromolecules by binding to sulfhydryl, phosphate, or carboxyl ligands and interaction with essential cations, most notably calcium, zinc, and iron. Pathologic alterations in cellular and mitochondrial membranes, neurotransmitter synthesis and function, heme synthesis, cellular redox status, and nucleotide metabolism may occur. Adverse impacts on the nervous, renal, GI, hematopoietic, reproductive, and cardiovascular systems can result.

    2. Pharmacokinetics. Inhalation of lead fume or other fine, soluble particulate results in rapid and extensive pulmonary absorption, the major although not exclusive route of exposure in industry. Nonindustrial exposure occurs predominantly by ingestion, particularly in children, who absorb 45–50% of soluble lead, compared with approximately 10–15% in adults. After absorption, lead is distributed via the blood (where 99% is bound to the erythrocytes) to multiple tissues, including trans-placental transport to the fetus, and CNS transport across the blood-brain barrier. Clearance of lead from the body follows a multicompartment kinetic model, consisting of “fast” compartments in the blood and soft tissues (half-life, 1–2 months) and slow ...

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