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Metal Disease OccupationLead Renal toxicity Battery and ammunition workers, foundry workers, spray painting, radiator repair Anemia, colic Peripheral neuropathy Insomnia, fatigue Cognitive deficits Mercury Renal toxicity Chlorine-alkali industry Muscle tremors, dementia Cerebral palsy Mental retardation Arsenic Cancer of skin, lung, liver Miners, smelters, oil refinery workers, farm workers Beryllium Acute lung irritant Beryllium refining, aerospace manufacturing, ceramics Chronic lung hypersensitivity ? Lung cancer Cobalt and tungsten carbide Lung fibrosis Toolmakers, grinders, diamond polishers Asthma Cadmium Renal toxicity Battery workers, smelters, welders, soldering ? Prostate cancer Chromium Cancer of lung and nasal cavity Pigment workers, smelters, steel workers Nickel Cancer of lung and nasal sinuses Smelters, steel workers, electroplating Data from Levi PE: Classes of toxic chemicals. In Hodgson E, Levi PE (eds): A Textbook of Modern Toxicology. Stamford, CT, Appleton & Lange, 1997, p. 229; and Sprince NL: Hard metal disease. In Rom WN (eds): Environmental and Occupational Medicine, 2nd ed. Boston, Little, Brown, 1992, p. 791. has been shown to be associated with an increased risk of leukemia. Plastics are widely used in consumer products, including food and beverage containers. Public exposure to plasticizers, such as phthalate esters, and to additives such as bisphenol-A raises concern about potential adverse reproductive effects of these synthetic chemicals. Phthalate esters have been shown to induce testicular injury in rats, and bisphenol-A mimics the proliferative effects of estrogen. Metals Occupational exposure to metals in mining and manufacturing is associated with acute and chronic toxicity, as well as carcinogenicity, as summarized in Table 9-13 .[43] Occupational as well as environmental exposure to lead continues to be a serious public health problem. Agricultural exposure to arsenic-containing pesticides is discussed subsequently. The pulmonary effects of beryllium are described in Chapter 15 . The health effects of inorganic and organic mercury were discussed earlier in this chapter under "Mechanisms of Toxicity." The untoward effects of some of the remaining metals listed in Table 9-13 are described here. Lead. More than 4 million tons of lead are produced each year for use in batteries, alloys, exterior red lead paint, and ammunition. Workers employed in these industries as well as in mining, smelting, spray painting, recycling, and radiator repair are exposed to lead. In some countries, tetraethyl lead is still used as a gasoline additive, thus polluting the air. Inhalation is the most important route of occupational exposure. Environmental sources of lead are urban air due to use of leaded gasoline, soil contaminated with exterior lead paint, the water supply due to lead plumbing, and house dust in homes with interior lead paint. Consumers may be exposed to lead-glazed ceramics, lead solder in food and soft drink cans, and illegally produced alcoholic beverages (moonshine). Lead ingested in this manner is absorbed through the gastrointestinal tract. Intestinal absorption of lead is enhanced by calcium, iron, or zinc deficiency; compared with adults, the absorption is greater in children and infants and hence they are particularly vulnerable to lead toxicity. Absorbed lead is mainly (80% to 85%) taken up by bone and developing teeth in children; the blood accumulates 5% to 10%, and the remainder is distributed throughout the soft tissues. Lead clears rapidly from blood, but that deposited in bones has a half-life of 30 years. Thus, the presence of lead in blood indicates recent exposure, and it does not allow the determination of total body burden. The toxicity of lead is related to its multiple biochemical effects: • High affinity for sulfhydryl groups. The most important enzymes inhibited by lead due to this mechanism are involved in heme biosynthesis: d-aminolevulinic acid dehydratase and ferroketolase. These enzymes catalyze the incorporation of iron into the heme molecule, and hence patients develop hypochromic anemia. • Competition with calcium ions. As a divalent cation, lead competes with calcium and is stored in bone. It also interferes with nerve transmission and brain development. • Inhibition of membrane-associated enzymes. Lead inhibits 5'-nucleotidase activity and sodium-potassium ion pumps, leading to decreased survival of red blood cells (hemolysis), renal damage, and hypertension. • Impaired production of 1,25-dihydroxyvitamin D, the active metabolite of vitamin D. Lead contributes to multiple chronic health effects, illustrated in Figure 9-9 . Injury to the central and peripheral nervous systems causes headache, dizziness, memory deficits, and decreased nerve conduction velocity. Blood changes occur early and are characteristic. Because lead interferes with heme biosynthesis, it causes a microcytic hypochromic anemia; punctate basophilic stippling of erythrocytes is characteristic. There is also an element of hemolysis because lead inhibits membrane-associated red cell enzymes. Because lead inhibits incorporation of iron into heme, the iron is displaced, and zinc protoporphyrin is formed. Thus, an elevated blood level of zinc protoporphyrin or its product, free erythrocyte protoporphyrin, is an important indicator of lead poisoning. Gastrointestinal symptoms include colic and anorexia. The kidneys are a major route of excretion of lead. Acutely, there is damage to the proximal tubules, with intranuclear lead inclusions and clinical evidence of renal tubule dysfunction. Chronically, lead can cause diffuse interstitial fibrosis, gout, and renal failure. Even in the absence of overt clinical symptoms of kidney damage, lead causes hypertension. Lead can cause infertility in men due to testicular injury; failure of implantation of the fertilized ovum can occur in women.[44] Infants and children are especially vulnerable to lead toxicity. It is estimated by the CDC that in the year 2000 approximately 454,000 children in the United States had blood lead levels greater than 10 μg/dL. A recent study indicates that even below this level there is an inverse correlation between blood lead concentration and IQ scores. Very slightly elevated blood levels (~3 μg/dL) in young females have also been reported to delay puberty.[45] Thus, lead toxicity continues to be a matter of concern. Lead may be mobilized from the maternal skeleton during pregnancy and it readily crosses the placental barrier. Hence Figure 9-9Consequences of lead exposure. TABLE 9-14-- Health Effects of Agricultural Pesticides Date: 2016-04-22; view: 795
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