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Lead poisoning acute

Colic is also a symptom of lead poisoning in children. EPA (1986a) has identified a LOAEL of approximately 60-100 pg/dL for children. This value apparently is based on a National Academy of Sciences (NAS 1972) compilation of unpublished data from the patient groups originally discussed in Chisolm (1962, 1965) and Chisolm and Harrison (1956) in which other signs of acute lead poisoning, such as severe constipation, anorexia, and intermittent vomiting, occurred at 60 pg/dL. [Pg.60]

Full Fanconi syndrome has been reported to be present in some children with lead encephalopathy (Chisolm 1968 Chisolm et al. 1955). According to the National Academy of Sciences (NAS 1972), the Fanconi syndrome is estimated to occur in approximately one out of three children with encephalopathy and PbB levels of approximately 150 pg/dL. Aminoaciduria occurs at PbB levels >80 pg/dL in children with acute symptomatic lead poisoning (Chisolm 1962). The aminoaciduria and symptoms of lead toxicity disappeared after treatment with chelating agents (Chisolm 1962). [Pg.72]

Accidental or intentional ingestion of folk remedies containing lead (discussed in Section 5.5) represents another source for potential lead-poisoning in children. Acute lead encephalopathy in early infancy has been reported in a Middle Eastern study for 14 infants following the use of Bint al Thahab, a traditional... [Pg.434]

Marino PE, Franzblau A, Lilis R, et al. 1989. Acute lead poisoning in construction workers The failure of current protective standards. Arch Environ Health 44 140-145. [Pg.548]

Suggested Alternatives for Differential Diagnosis Salmonellosis, pasteurellosis, enterotox-emia due to . coli, rabies, pregnancy toxemia, polioencephalomalatia, acute rumen impaction, louping-ill hypocalcemia, hypomagnesemia, and acute lead poisoning. [Pg.504]

Suggested Alternatives for Differential Diagnosis Sheep Scrapie, pregnancy toxemia, hypocalcemia, tetanus, listeriosis, tick pyemia, hypocuprosis, rabies, hydatid disease, and various plant poisons. Cattle Malignant catarrhal fever, listeriosis, pseudorabies, bovine spongiform encephalopathy, rabies, hypomagnesemia, hypocalcemia, acute lead poisoning, and certain plant poisons. [Pg.554]

Gill, C.E. and K.M. Langelier. 1994. Acute lead poisoning in a bald eagle secondary to bullet ingestion. Canad. Veterin. Jour. 35 303-304. [Pg.331]

Aminolevulinate now leaves the mitochondria. In the cytoplasm, two molecules condense to form porphobilinogen, a compound that already contains the pyrrole ring. Porphobilinogen synthase is inhibited by lead ions. This is why acute lead poisoning is associated with increased concentrations of ALA in the blood and urine. [Pg.192]

Drug may produce same signs of renal damage as severe acute lead poisoning (proteinuria, microscopic hematuria). Transient anemia/bone marrow depression, hypercalcemia (constipation, drowsiness, dry mouth, metallic taste) occurs occasionally. [Pg.415]

Acute inorganic lead poisoning is uncommon today. It usually results from industrial inhalation of large quantities of lead oxide fumes or, in small children, from ingestion of a large oral dose of lead in the form of lead-based paint chips small objects, eg, toys coated or fabricated from lead or contaminated food or drink. The onset of severe symptoms usually requires several days or weeks of recurrent exposure and manifests as signs and symptoms of encephalopathy or colic. Evidence of hemolytic anemia (or anemia with basophilic stippling if exposure has been subacute), and elevated hepatic aminotransferases may be present. [Pg.1230]

Dimercaprol is FDA-approved as single-agent treatment of acute poisoning by arsenic and inorganic mercury and for the treatment of severe lead poisoning when used in conjunction with edetate calcium disodium (EDTA see below). Although studies of its metabolism in humans are limited, intramuscularly administered dimercaprol appears to be readily absorbed, metabolized, and excreted by the kidney within 4-8 hours. Animal models indicate that it may also undergo biliary excretion, but the role of this excretory route in humans and other details of its biotransformation are uncertain. [Pg.1240]


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See also in sourсe #XX -- [ Pg.1131 ]




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