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Ed 092 563 Title Institution Report No Pub Date Note Available from Edrs Price Descriptors Identifiers Document Resume- Sp 008 1 DOCUMENT RESUME- ED 092 563 SP 008 167 TITLE Poisoning and Intoxication by Trace Elements in Children. At Abstract Review of the Worldwide Medical. Literature 1966-1971. INSTITUTION Public Health Service (DREW), Washington, D.C. Bureau of Community Environmental Management. REPORT NO DREW-HSM-73-10005 PUB DATE 73 NOTE 104p. AVAILABLE FROM Superintendent of Documents, U.S. Government Printing Office, Washington, D.C. 20402 (No price quoted) EDRS PRICE MF-$0.75 HC-$5.40 PLUS POSTAGE DESCRIPTORS *Abstracts; Accidents; *Annotated Bibliographies; Clinical Diagnosis; *Health; Lead Poisoning; *Medical Case Histories; *Physiology; Safety IDENTIFIERS *Poisons ABSTRACT This annotated bibliography of 247 entries is divided into the following categories:(a) general aspects and reviews; (b) sources of poisoning, epideE-,..ology, and pica studies; (c) clinico-pathological studies;(d) diagnosis and screening; (e) laboratory methods; and (f) treatment and prevention. A subject and author index is included. (PD) ca° POISONING AND INTOXICATION BY TRACE ELEMENTS U.S. DEPARTMENT OF HEALTH. IN CHILDREN EDUCATICN IL WELFARE NATIONAL INSTITUTE OF EDUCATION THIS DOCUMENT HAS SEEN REPRO- DUCED EXACTLY AS RECEIVED FROM THE PERSON OR ORGANIZATION ORIGIN- ATING IT. POINTS OF VIEW OR OPINIONS STATED DO NOT NECESSARILY REPRE. SENT OFFICIAL NATIONAL INSTITUTE OF EDUCATION POSITION OR POLICY. an abstract review of the worldwide medical literature 1966-1971 DHEW Publication No. (HSM) 73-10005 U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service Health Services and Mental Health Administration Bureau of Community Environmental Management Division of Community injury Control For sale by the Superintendent ae Documents, U.S. Government Printing Office, Washington, D.C. 20402 PREPARED BY EXCERPTA MEDICA THE INTERNATIONAL MEDICAL ABSTRACTING SERVICE Acknowledgement The Project upon which this publication is based was performed pursuant to Contract no. HSM 99-72-79 with theHealth Services and Mental Health Administration, Department of Health, Education, and Welfare. Contents General nects and reviews Sources of poisoning,b,'demiology and Ws:. studies 20 Clinico-pathological studies 41 Diagonosis and screening 54 Laboratory methods 61 Treatment and prevention 76 Subject index 85 Index of authors 97 General aspects and reviews I. Plombism exists todayReddick L.P., Bowman Gray Sch. of Med., Wake Forrest Univ., Winston-Salem, N.Car.STH MED. J. (BGHAM, ALA.) 1971, 64/4 (446-450) Although lead poisoning accounts for only a small proportion of cases of accidental poi- soning, the high mortality associated with the condition makes it by far the most common cause of death due to accidental poisoning. Most cases of lead poisoning are due to pica in children who ingest old house paint from the structure and furniture of their housing. Less common sources reported include the application of an eye cosmetic containing lead sulphide to the eyelids and conjunctivae of a 3 year old boy and the swallowing of a lead button by a 2 year old child who subsequently died. In adults illegally distilled whisky, home brewed alcoholic drinks in lead-lined containers and soft or acid drinking water in lead pipes are important sources as well as industrial exposure. Smokers have slightly but consistently higher concentrations of serum lead than non-smokers due to lead arsenate spraying of the soil in which tobacco is grown. 2. Asymptomatic lead poisoning in 85 Chicago children. Some diagnostic, therapeutic, prog- nostic and sociologic considerationsRennert 0.M., Weiner P. and Madden J., Dept. of Ped., Univ. of Florida Coll. of Med., Gainesville, Fla.CLIN. PEDIAT. 1970, 9/1 (9-13) Eighty-five children with blood lead levels higher than 60 pg./ 100 ml. were found as the result of a door-to-door survey in high-risk neighborhoods of almost all children under 7 years. The children were aged from II months to 7 years with 35% being 2 years old. Ninety per cent of the children were asymptomatic but 10% had significant Loproporphyrinnria and 6% had significant anemia. All patients were give a course of intramuscular chelation therapy with dimercaprol and EDTA. Those with blood lead levels greater than 150 ,ug./ 100 ml. were hospitalized for treatment. There were wide discrepancies between blood lead values reported by different laboratories. This posed a problem both in diagnosis and evaluation of the results of chelation therapy. Since none of the children had any symp- toms before therapy, the overall effects of treatment were not clearly demonstrated. To eliminate childhood plumbism requires massive rebuilding of slums. However emotional factors may also be involved aside from the availability of paint chips and plaster. Usu- ally only one child in a family, most often the youngest, is affected and it is possible that pica may be an indicator of emotional deprivation. 3. Lead poisoning in children - a disease of the environmentRoffman H. and Finberg L. HLTH NEWS 1969, 46/7 (3-5) The high risk of lead poisoning in children which exists in the ghetto districts of large cit- ies has dearly been demonstrated. This risk mainly affects the children between the ages of 1 and 3 due to the pica common to 20-30% of children in this age group. The lead is absorbed and distributed in soluble form through the soft tissues and later deposited in the bone as an insoluble phosphate compound. The toxic effect of lead, which predominantly affects 1 the nervous system, blood, kidneys and gastrointestinal tract, is produced by the soluble form and the amount of damage done therefore depends on the level of lead in the soft tissues, which may vary according to intake and mobilization from the bones. Seasonal variations, probably caused by variations in the absorption from the intestinal tract, have thus been observed. The symptomatology of lead poisoning may vary and individual symp- toms produced also by other diseases. However, the diagnosis can he confirmed by deter- mination of urinary coproporphyrin and 6-aminolevulinic acid of blood, blood and urinary levels of lead, morphological examination of red cells and X-rays of bones and abdomen. Two agents, which form a complex with soluble lead and thereby give rise to a precipitate excretion, are widely used in the treatment of lead poisoning. Lead poisoning is a recurrent disease by the nature of the social and economic conditions which foster its existence. Mass investigations with screening tests such as urinary, coproporphyrin leveis and blood levels, as well as the newer inexpensive techniques such as urinary 6-aminolevulinic acid determinations serve to detect and should ultimately eradicate this preventable disease. 4. Iron poisoningJ. AMER. MED. ASS. 1966, 198/ 12 (165-166) Acute iron intoxication is one of the most common lethal childhood poisonings in the US. It almost invariably occurs in the pediatric age group, and the poison is usually in the form of ferrous sulfate tablets prescribed for a pregnant woman in the household of the poisoned child. Ingestion of as few as 10 to 15 5-grain tablets has been lethal. Typically, in the child who has ingested ferrous sulfate, symptoms develop within 30 to 90 minutes, with signs of shock, coma, acidosis, vomiti.,g, diarrhea, and melena. The child may sub- sequently appear to improve somewhat, but within 10 to 14 hours further acidosis and coma, bleeding, and irreversible shock develop, and the child dies. Autopsy reveals no anatomic cause of death. The pathophysiology remains obscure. The iron chelater, defer- oxamine, promises to reduce substantially the mortality of acute iron intoxication. It is most effective when given relatively early. Moreover, some question has arisen as to the occasional toxicity (principally hypotension) of deferoxamine or the iron-deferoxamine complex. A delineation of the mechanisms of iron toxicity is, therefore, considered im- portant in crder to improve the management and therapy of the poisoned individual, es- pecially the patient who is not seen soon after iron ingestion, or in whom deferoxamine therapy fails. Animal experiments have shown that acute iron overload results in hyper- ventilation, profound acidosis with lactic and citric acidemia, and death. These findings suggest that a disturbance in oxidative metabolism is rapidly created by iron overload. Massive intravenous iron overloading of rabbits results in the development of hepatic necrosis. A study of the enzyme histochemical changes induced in the livers of acutely iron-overloaded rabbits has shown alterations in several enzymes involved in oxidative rtl etabolism. Electron-microscopic studies of animals exposed to the same experimental pro- cedures show early and severe mitochondrial injury, indicating that these organelles may be the site of the observed disturbances. The mechanism of this injury is not yet evident, but the experimental protocol provides a potential means of further acute iron poisoning. 5. More leads on leadFD. COSMET. TOXICOL. 1967, 5 (414-418) Lesions in chronic lead poisoning include kidney damage and cardiovascular disease. There is evidence that chronic lead poisoning during childhood can produce renal failure in later life. There is a significant increase in deaths from cardiovascular disease in retired lead workers which is related to vascular damage rather than hypertension. Blood hemoglobin levels are of little value in detecting incipient lead poisoning. Blood lead levels and urine excretion levels of 6-aminolevulinic acid (ALA) are the only valuable indicators of
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