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Occupational lead exposures anemia from

Biochemical changes such as increased aminolaevulinate excretion and inhibition of amino-laevulinate dehydrase may be detected in urine and blood, respectively, at blood lead levels of 0.4 to 0.6 mg mL-1. Anemia is a late feature, however. Neurotoxicity may be detectable at blood lead levels of 0.8 to 1.0 mg mL-1. At blood lead levels greater than 1.2 mg mL-1, encephalopathy occurs. Peripheral nerve palsies are rare, and the foot and wrist drop, which were once characteristic of occupational lead poisoning, only occur after excessive exposure and are now rarely seen. Similarly, seizures and impaired consciousness may result from involvement of the CNS. Bone changes are usually seen in children and are detected as bands at the growing ends of the bones and a change in bone shape. [Pg.392]

Lead is an acute and a chronic toxicant. Acute effects are ataxia, headache, vomiting, stupor, hallucination, tremors and convulsions. Chronic symptoms from occupational exposure include weight loss, anemia, kidney damage and memory loss. (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substarwes, 2nbrain damage has been noted among children. Lead bioaccumulates in bones and teeth. The metal is classified as an environmental priority pollutant by the US EPA. [Pg.458]


See other pages where Occupational lead exposures anemia from is mentioned: [Pg.253]    [Pg.87]    [Pg.310]    [Pg.18]    [Pg.204]    [Pg.149]    [Pg.91]    [Pg.735]   
See also in sourсe #XX -- [ Pg.601 , Pg.602 ]




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