Lead
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.
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.
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.
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.
Mechanism of toxicity
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.
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 compartments in the bone (half-life, years to decades). Approximately 70% of lead excretion occurs via the urine, with smaller amounts eliminated via the feces and scant amounts via the hair, nails, and sweat. Greater than 90% of the lead burden in adults and more than two-thirds of the burden in young children occur in the skeleton. Slow redistribution of lead from bone to soft tissues may elevate blood lead concentrations for months to years after a patient with chronic high-dose exposure has been removed from external sources. In patients with a high bone lead burden, pathologic states associated with rapid bone turnover or demineralization, such as hyperthyroidism and immobilization osteoporosis, have resulted in symptomatic lead intoxication.
Toxic dose
Dermal absorption is minimal with inorganic lead but may be substantial with organic lead compounds, which may also cause skin irritation.
Ingestion. In general, absorption of lead compounds is directly proportional to solubility and inversely proportional to particle size. Gastrointestinal lead absorption is increased by iron deficiency and low dietary calcium. Absorption can increase substantially in a fasted state.
Acute symptomatic intoxication is rare after a single exposure but may occur within hours after ingestion of gram quantities of soluble lead compounds or days after GI retention of swallowed lead objects, such as fishing weights and curtain weights.
Studies have not established a low-dose threshold for adverse subclinical effects of lead. Recent epidemiologic studies in children have observed effects of lead on cognitive function at blood lead concentrations of less than 5 mcg/dL, and other studies suggest that background levels of lead exposure in recent decades may have been associated with hypertension in some adults. The geometric mean blood lead concentration in the United States during 2003–2004 was estimated to be 1.43 mcg/dL; background dietary lead intake may be in the range of 1–4 mcg/d.
The US Environmental Protection Agency (EPA) action level for lead in drinking water is 15 ppb (parts per billion). However, the maximum contaminant level (MCL) goal for drinking water is 0 ppb, and EPA has set no “reference dose” for lead because of the lack of a recognized low-dose threshold for adverse effects.
Inhalation. Unprotected exposure to the massive airborne lead levels (>2500 mcg/m3
Related posts:
Full access? Get Clinical Tree
