Document 91pr00QqZRBeJOjr0d3yRnr6q

* Acknowledgment The Public Health Service gratefully acknowl edges the assistance of the Advisory Committee to the Surgeon General on Lead Poisoning in the preparation of this pamphlet. The members of the Committee are: Dr. Elston L. Belknap, Professor of Occupational and En vironmental Medicine. Marquette University School of Medicine; Dr. Samuel Bessman, Asso ciate Professor of Pediatrics, University of Mary land Hospital. Baltimore; Dr. R. A. Kehoe. Director. Kettering Laboratory, College of Medi cine, University of Cincinnati; Dr. Lewis W. Spolyar, Director. Bureau of Preventive Medi cine, Indiana State Board of Health; Mr. Jerome Trichter, Assistant Commissioner. Environ mental Sanitation, New York City, Department of Health. 21 cases of lead poisoning in children were un covered in Chicago. Twelve oi these cases were recognized at one hospital The clinicians at this hospital had become interested in the problem and. as a result became quite astute in recognizing cases. Later an. cases ware found in other Chicago hospitals when these hospitals became familiar with the problem. In Cincinnati, 45 c o m* warn seen in two boa* pitals btwen the years oi 1928 and 1950, and than, in association with heightened concern among local pediatricians, 79 cases were seen during the next five years. Since that time, about 20 cases have been seen annually. The mortality has ranged from 25 to 30 percent from year to year. Incidence In 1955, sixty-four deaths horn lead poisoning were reported for the United States. Doubtless, additional deaths were certified as encepha litis of unknown origin, status epilepticus, and other severe neurological conditions, but were actually due to lead intoxication. Of these 64 deaths, 47 (73 percent) were in children under five years of age. Studies in New York, Balti more, Cincinnati, and Chicago have shown that lead poisoning in childhood almost always oc curs in children between the ages of one and five, the largest number of cases falling in the second year--the teething, mouth-centered ac tivity age. Consideration of this age incidence gives insight into the etiological factors involved in lead poisoning in children. The disease is more likely to be seen in lower economic groups--in children whose frrmiiue * NCA*nO 01012 or* likely to live in old house* in which the walls have had many coats of lead paint, applied throughout several decades. Of interest and significance, but still unex plained. is the increased incidence of cases occurring in the summer. This observation should serve to keep physicians on the alert to signs of lead poisoning during this season. Etiology Etiologic factors involved in any accidental poisoning are the host, the agent, and the en vironment. In lead poisoning the host is usually a child between one and five, with pica--the abnormal craving for and the indiscriminate eating of non-food substances. The agent is, of course, lead--almost always lead paint The environment is the home, usually an aid run-down dwelling where coat after coat of lead paint has been applied to the walls. The paint flakes with age. The child with pica picks these flakes from surfaces, such as walls and window sills, and swallows them. In some cases parents have repainted cribs and other types of baby furni ture. The infant sucks or chews on this furni ture and thus ingests the lead-containing paint 3 NCA'OO 01013 There are reports of lead poisoning in children from old and discarded lead storage battery cas ings. These casings are a cheap source of fuel in the home; the fumes and ashes contain lead, and they are poisonous. The combination of pica and available lead paint is certainly a diagnostic clue and calls for further investigation. Diagnosis A history of pica is enough to raise a sus picion of lead poisoning. The onset of the disease is often insidious. Lack of appetite, vague abdominal pain, slight listlessness or increased irritability, constipa tion. and occasional vomiting may appear to parents to be the consequences of "too much hot weather." "worms," and a host of other minor ailments. However, it is just in this guise that the disease may appear. On the other hand, the child may develop convulsions suddenly with no previous con vulsive history. In this case, unless die con vulsions are intractable or the poet ictal depression is prolonged, the physician may be misled by such deceptive dues as a "head in- 4 NCA'OO 01014 ' ii f'weeks ago or th pressnee of fever TmSf toad to a diagnosis of febrile con* Other findings of lead encephalopathy may include hypertension. ataxia, weakness or paralysis of an upper motor nsuron typo, and changes in behavior. Permanent neurologic damage may occur as a result of lead encephalopathy. Adults with lead poisoning often exhibit a lead line at the gum margins. This is rarely observed in children. The laboratory can aid in making a diagnosis of lead poisoning. A microcytic hypochromic anemia occurs. The red blood cells may show basophilic stippling in a Wrights stained periph eral blood smear. Urinary excretion of exces sive amounts of coproporphyrin can be detected. A semiquantitative test for coproporphyria can be performed in the physician's office on a single voided urine specimen. X-rays of the long bones show fines of in creased density at the metaphyseal margins. Variable degrees of elevation of the levels of lead concentration in the urine and the blood, support the clinical impression of lead intales and absorption. NCA`00 01015 Edathamil calcium disodlum (Ca-EDTA} is ft* medical treatment of choice, at present. in lead poisoning. The drug is given parsnterally for acute intoxication. Ca-EDTA is superior to BAL as a de-leading agent The de-leading process is not the only factor involved in the treatment of lead poison ing. A period of 48-72 hours of Ca-EDTA ad ministration is usually required to reduce to lees toxic levels highly dangerous concentrations of lead initially present in the tissues. ft is in this period, after onset of symptoms, that most of the deaths from acute lead encephalopathy occur. Edathamil has not significantly reduced mor tality from lead poisoning. It seems to be no more effective than BAL for terminating the acute episode of lead encephalopathy, but seems to be mars effective than BAL in reduc ing the incidence of residual neurologic damage. There is good evidence that the lethal factor in lead encephalopathy in children may be in creased intracranial pressure. Extensive crani ectomy with opening of the dura appears to havs saved lives and to have prevented in some in stances, irreversible brain damage. NCA'HO 01016 E5b.":3^5 djagncau* nscsssary to mducs mor- Wdftjr, ssquslas, and mortality from lead poi soning. A child undsr fivs, with a history af pica, who is whihiHii^ miM gcatrointsstinal symptoms and changss in bsharior should b* invsstigatsd lor lsad poisoning. Anemia, basophilic stippling of rsd blood colls, copro porphyrinuria and slsvated blood and urins concsntratioas of load will add in ths diagnosis. Initial appsarancs of convulsions in a child with pica should also males tbs physician sus picious of load poisoning. Local health dspartmsnts should bs nodfisd in ths svsnt of suspsetsd cans of load poisoo- ing to psrmit follow-upactivities by public hsatfe nursss or sanitarians. Tbs information thus ob- tainsd will bs mads available to physicians and will bs of substantial assistance in diftsrsnttal diagnosis. Treatment with Ca-EDTA has somewhat im proved ths prognosis of dais dissoss in children, but rigorous prevention of exposure to lsad is nscsssary to protset against furtbsr acute spi- sodss of lsad intoxication. (tCA'HO 01017 1) . Williams. H.; Kapkm, E; Couchman. C. E; and Sayers, R. R.: Lead Poisoning in Young Children, Pub. Health Rep. 67:230. 1952. 2) . McLaughlin. M. C.: Lead Poisoning in Chil dren in New York City, 1950-1954. An Epidemiologic Study, New York State J. Med. .56: 3711. 1956. 3X Jenkins, C. D.; and Mellins, R. B.: Lead Poi soning in Children, A. M. A. Arch. NeuroL Psychiat 77:70, 1957. 4). Chisolm. J. J. Jr. and Harrison. H. E: The Ex posure of Children to Lead. Pediatrics 18: 943. 1956. SL Chisolm. J. J. Jr. and Harrison. H. E: The Treatment oi Acute Lead Encephalopathy in Children. Pediatrics 19: 2. 19S7. If. $ O-- I NCA"HO 01018