Document jgaxOdQG3QXzmkDmrBLBkQz0p

l/J) 11 ) 4 R e p r in t e d fr o m M A R C H I952 Volume 67 Number 3 P ublic HEALTH EPORTS V} In this issue Lead Poisoning in Young Children FEDERAL SECURITY AGENCY PUBLIC HEALTH SERVICE Lead Poisoning in Young Children By HUNTINGTON WILLIAMS, M.D., EMANUEL KAPLAN, Sc.D., CHARLES E. COUCHMAN, and R. R. SAYERS, M.D, Lend poisoning in young children associated with eating lead-containing paint has been in creasingly recognized until it ranks as one of the most common causes of child mortality due to poisoning. However, lead poisoning is not a reportable disease and, therefore, there is a lack of adequate morbidity data (7). The widespread occurrence of lead poisoning throughout the United States and Canada is evident from reports of cases in which eat ing lead-containing paints was mentioned as the cause of poisoning in infants and young children (-37). Although 19 different com munities are mentioned, most of the cases were from large cities such as Baltimore and Boston, where children's hospitals or local health au thorities were especially interested in the prob lem. During the period 1931-40, the city of Baltimore alone reported 24.3 percent of all the child deaths from lead poisoning reported from the entire United States registration area (1). From January 1, 1931, to June 30, 1951, a total of 293 cases of lead poisoning was reported in Baltimore children. Of these, 83 died (2). The most common cause of lead poisoning is Dr. Williams is commissioner of health of the Baltimore City Health Department; Dr. Kap lan is chief of the division of chemistry; Mr. Couchman is director of the bureau of indus trial hygiene; and Dr. Sayers, a medical director (retired) of the Public Health Service, is senior medical supervisor of occupational diseases. For several years he was director of the Bureau of Mines, Department of the Interior. apparently the habit of chewing paint from cribs, toys, furniture, woodwork such as win dow sills, and the eating of painted plaster and fallen paint flakes. The tendency to put things in the mouth, though normal in the first year of life, is considered abnormal if continued into the latter part of infancy, and is referred to as pica, or perverted appetite (6, 30). Pica is the usual forerunner of lead poisoning. Although pica docs not exist on a seasonal basis, a striking number of lead-poisoning cases resulting from this habit occur in the hot sum mer months. For this, no satisfactory explana tion is available, although several investigators have commented on the tendency for lead poisoning to occur in children during the warmer weather (, 1, 6, 37-40). Diagnosis, Prognosis, and Soqutlao Unrecognized plumbism, lead poisoning, in children may explain many obscure nervous conditions and convulsions of undetermined etiology (1, ). Errors have been made in operating on cases presenting symptoms indi cating a need for surgery but which were caused by lead intoiication (14,31). Lead poisoning is cumulative. Some weeks or months following the continued ingestion of small amounts of lead, symptoms begin to ap pear. Early symptoms may be only irritability, fretfulness, or disturbed gastrointestinal func tion characterized by lack of appetite, consti pation, vomiting, or cramps. A secondary anemia with resulting pallor is often present. More severe intoxication results in lead en- 230 Public H ealth Report* i oephalitis due to increased intracranial pressure because of cerebral edema. The acute stages of the disease are manifested in changes in mental state, ataxia, persistent vomiting, muscle weakness or paralysis, delirium, stupor, coma, convulsions, and, not infrequently, death. Diagnosis involves correlation of a history of paint-eating or pica with the physical findings, laboratory and X-ray data. The importance of eliciting a history of pica cannot be over emphasized in the early recognition of the disease. Examination of blood smears often shows stippling of the red blood cells. Por phyrinuria is frequently found. The demon stration by roentgenogram of an increased density in the growing ends of the long bones is a cardinal sign of lead poisoning (34). In recent years, the quantitative determination of lead in blood or urine as an index of abnormal lead absorption has proved an invaluable aid in diagnosis (41, 4%) Lead poisoning in chil dren differs considerably from the disease in adults. Central nervous system involvement or encephalopathy, rarely seen in adults, is com mon in children, whereas peripheral neuritis, lead line on the gums, and colic are usually absent. The prognosis in lead encephalitis in children is poor; the high mortality rate, as well as the incidence of severe, lifelong, residual nervous system injury, has been commented on by many investigators (&5). The mental development of even the less severe cases may be seriously impaired (16). Baltimore Experience Thomas and Blackfan (3) of the Johns Hop kins Hospital were the first to point out in American pediatric literature the frequency of occurrence of lead encephalopathy in children. Subsequently, studies at the same institution provided pioneer information on the diagno sis (4, SG, 34, lfi) and treatment (S3, Ifi) of plumbism in infancy. The Baltimore City Health Department in 1932 began studies of nonindustrial lead poisoning in children in an investigation of cases resulting from the use of storage battery casings for fuel (43). A fter wards, all cases of lead poisoning brought to the attention of the department were routinely investigated to ascertain the source of the lead. Blood-Laad Laboratory Servico A6 an aid in diagnosis, since early in 1935, the bureau of laboratories of the Baltimore City Health Department has maintained a free routine analytical service for the quantitative estimation of lead in the blood of cases of sus pected plumbism (41). The dithizone method is used. Especially prepared lead-free blood specimen collection containers known as "bloodlead outfits" are distributed to the local hos pitals and physicians in the same manner as outfits regularly provided for specimens in cases of communicable diseases. Since 1935, almost 3.000 specimens of blood from about 1,800 children have been tested for lead. Increase in this service, as well as the increased number of cases diagnosed during the last 4 years in contrast to the preceding 13 years, is shown in the accompanying table. Undoubtedly, the improved educational activi ties in lead poisoning prevention in recent years have been a prominent factor in this increase. (m poH M fl o f blood-Uod laboratory Mrvl< U it i and c o m b of Wod poisoning in Baltimore children for th periods 19 4b --51 nd 1935-47 Period N um ber chil- Diagnoaed cases dren given lead of lead poison- teat ing T o tal A verage per year T o tal A verage per year 194&-51 (4 y e a r s ) . . . 1, 007 1035--47 (13 y e a r s ) . . 772 252 166 59 161 41 12. 4 Field Investigation Field work, associated with a follow-up of the blood-lead laboratory service, has enabled the Baltimore City Health Department to ac quire relatively accurate data concerning the incidence of lead poisoning in the community (1). A report of each blood analysis was for warded to the bureau of industrial hygiene, which investigated cases in which the "blood showed an abnormal absorption of lead. The Vol. 67, No. 3, M arch 1952 231 Figure T. Lead poisoning cases reported in Baltimore, according to month of report, 1931--51. upper limit of normal is considered to be 0.05 to 0.06 mg. percent of lead. Adequate clinical and laboratory data were usually available because nearly all of the children were diagnosed and treated in hospitals. After learning the medical history, a field worker visited the home of the affected child to obtain pertinent information, particularly concerning exposure to lead. Almost without exception, the cause of poisoning was found to be pica associated with the ingestion of paint. This was confirmed at the time of the home visit by obtaining for analysis a sample of paint scrapings, approximately 0.5 to 1 gm., from surfaces where the child had chewed paint. Lead Poisoning in Children Over the past two decades, 347 cases of lead poisoning have been diagnosed in Baltimore children. These do not include the storage bat tery cases referred to earlier. Of the 347 cases, 54 have been reported since June 30, 1951. A study of these cases has led to the discovery of interesting patterns in the seasonal incidence of the disease, age and color distribution of the children, and the types of houses involved. It is evident from figure 1 that more cases were reported in July and August than in any other months. There was no significant difference in incidence between sexes. Sixty percent of the cases occurred among children in their second year of life, at teething age, when they have a greater tendency to put things into the mouth. Only 2.3 percent of the cases, were in children above 5 years of age. The annual attack rate for the age segment under 5 years during the period 1931-51 was 7.5 times as high among the Negro population (71 per 100,000) as it was among the white 232 Public H ealth Reporta population (0.5 ]>er 100,000). When the more recent experience of the past 4 years is con sidered, the attack rates for both white and Negro children as well as the difference be tween races are significantly elevated above tho average experience cited. The high rates among Negro children are a problem of con siderable public health significance since 30 percent of Baltimore's preschool population is Negro. The racial difference in incidence is believeil to be due to environmental factors probably resulting chiefly from economic dis advantage. For the past few years information has been collected on home ownership in neighborhoods where child lead poisoning cases occurred. Al most 90 percent of the houses were tenantoccupied. In the early years of the study some of the cases arose in well-kept property, but with the continued community education by press and radio, cases in this category have liecome relatively rare. The problem in Balti more at present involves chiefly slum or blighted-area properties. The. cases are con centrated in two areas which arc of known slum status and where the houses sre old and have had many coats of paint, usually lead paint, applied throughout several decades. A typi cal home where a case of lead poisoning oc curred is shown in figure 2. Methods of Prevention Education and Publicity In an effort to prevent lead poisoning, re peated public warnings about this child health hazard have been given by the Baltimore City Health Department in the press, by radio, and on television. The Baltimore Health News-- mailed each month to over 10,000 persons, in cluding 1,800 local physicians and 0,000 school teachers--devoted a number of issues (S, 1C, 47) to the subject. The bureau of child hy giene issued a leaflet (44) entitled "Lead Poi soning in Children, a Disease You Can Pre vent." The leaflet directs attention to 220 cases and 78 deaths from lead poisoning in Balti more during the past 18 years, makes sugges tions to parents for preventing children from contracting the disease, lists the warning sig nals to be watched for, and stresses the im portance of early diagnosis and treatment. It is not unusual now for a mother to take a child to a physician and to volunteer infor mation on pica and suggest that the child may be suffering from lead poisoning. The Public Health Nurse One of the most promising advances in tinprevention of child plumhism was the assign ment several years ago of a public health nurse supervisor to investigate lead poisoning cases. AVith the knowledge gained by intimate associa tion with the problem, the supervisor was able to interest other public health nurses. They not only make home visits and disseminate in formation in the most-affected areas of the city, but may take part in well-baby clinics, where mothers are told of the dangers connected with pica. l*ead Paint Removal For the past 1 years, landlords of properties where lead poisoning has occurred have been notified, in accordance with the Baltimore ordi nance on the hygiene of housing (44), to remove lead paint from the surfaces where there is flaking or where a child has chewed. Of 90 such notices during this period only 2 were not complied with in tire time allotted. Both owners were summoned to the Magistrate's Court, where they were found guilty and fined; only then did they fully comply with the health department's orders. Many sanitarians on the health department staff who inspect property, primarily on the basis of other types of com plaints or because of rodent and housing sur veys, also require correction of a flaking paint condition in the notice sent to the propertyowner. The sanitarians are instrumental in the distribution to slum dwellers of the leaflet on the lead poisoning prevention (44). Legislation Because of the danger to small children, man ufacturers of cribs and toys have for many years (9, 17, 44) used paints free of lead pigment. For various reasons legislation against the use of lead paint has existed in widely sepa rated jurisdictions for a number of decades. Germany has had a national law on the matter Vol. 67, No. 3, March 19S2 233 Figure 2. House doorway in home of patient with lead poisoning. since about 1900. Regulations prohibiting the use of lead-containing paints on toys, children's furniture, and for interior work have been en forced in France since 1917 (17). As early as 1922, the nations adhering to the International Labor Office in Geneva pro|>oscd a convention prohibiting the use of white-lead paint in in terior painting of buildings as a health meas ure affecting painters.(.9). Since 193*2, factory legislation in Ontario has required all leadcontaining paints supplied to plants manufac turing children's toys and furniture to be so labeled (77, 4$). No cases of lead poisoning related to chewing on new furniture or painted toys have been reported in recent times. When such objects are involved, the source of lead has been repainted furniture--parents frequently use lead-base paints for repainting jobs. Never theless, the Maryland State Legislature in 1949 enacted chapter 517 of the Acts of 1949, which made it compulsory to affix a label to any toy or to any children's furniture decorated with paint or other material containing lead or any other poisonous substance, stating clearly the poisonous nature of the paint or decoration. Unenforceable, the law was repealed a year later. On June 27, 1951, regulation No. 17 was adopted by the commissioner of health of Baltimore under the ordinance on the hygiene of housing. The text follows: I nt e r i or Pai nt inn. S o p a in t sh all be u sed fo r in terior painting of any dwelling or dwelling unit or a n y p a rt th e re o f unless th e p a in t is free fro m an y lead pigm ent. The wording was studied carefully so as nut to prohibit the use of paints containing either lead driers, usually present in amounts corre sponding to less than 1 percent of lead in the finished paint, or pigments contaminated with 23-S P u b lic H e a lth R eports traces of lead. The use of the term "lead-free paint" was purposely avoided, since it is doubt ful if the usual commercial product could be made without having a detectable amount of lead present. This regulation has had pro nounced salutary effect as shown by an increas ing interest on the part of home owners, health agencies, and local paint manufacturers, some of whom hare recently advertised paints free from lead pigment. Lead Content of Paint The health departments suggestions to parents interested in the purchase of "leadfree" paint emphasizes a selection based upon the labeled composition of the product. A l though there is no Maryland law on the subject, many of the paints sold locally contain a state ment of composition on the label. Such labels provide information on the presence of lead bearing compounds and are adequate except in those instances where the terms "chrome yel low," "chrome green," or "chrome orange" cam ouflage the fact that these pigments contain substantial amounts of lead chromate. For this reason, when inquiry is made, it has been recommended that no yellow, green, or orange colors be used in refinishing articles of furni ture intended for use by children unless the pigment composition as declared on the label clearly eicludes the presence of lead. Summary Lead poisoning in children caused by in gesting lead from surfaces coated with leadcontaining paint is apparently widespread throughout many parts of the Xation. The disease has a high rate of incidence in the city of Baltimore, where it occurs in chil dren of teething age living in old, run-down rented properties where lead paint had been used indoors for many years. Public health education, coupled with a "lead consciousness" on the part of physicians and the pediatric clinics of local hospitals, and with a blood-lead laboratory service offered by the city health department has resulted in a marked in crease in case recognition. It is hoped that the application of principles in v o lv in g education an d th e en fo rcem en t o f m easures reg u latin g th e use of le ad -co n tain in g p ain ts w ill resu lt in a m a terial red u ctio n an d th e eventual erad icatio n of ch ild lead p o iso n in g in B a ltim o re C ity. ACKNOWLEDGMENTS The authors are Indebted to M atthew L. Taback, di rector of the bureau of blostatistlca, and to M argaret G albreath, suj>ervisor assigned by the b u reau of public health nursin g to the bureau of In d u stria l hygiene, for assistance in the preparation of this article. REFEIENCES ( / ) M cD onald, J . M., and K ap la n , E . : In cid en ce of lead poisoning In th e city o f B altim ore. J . A. M. A. 119: 870-872 (1042). (2) W illiam s, H u n tin g to n : Load po iso n in g killed S3 children. B altim ore H ealth N ew s 28: 113-11G (1031). (5 ) T hom as, H. M.. an d B la ck fan , K . D . : R e c u rre n t m eningitis due to lead In a child of five years. Am. J. Dis. Child. 8: S77-3S0 (1914). (4) B la ck fan , K. D .: Lead p o isoning In c h ild ren w ith especial reference to lead as a cause of con vulsions. Am. J. Med. Sc. 183:877-887 (1917). (5) Strong, R. A.: M eningitis caused by lead poison ing in a child of nineteen m onths. Arch. Ped. 37: 532-337 (1020). 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(56) M cKbann, C. F .: Lead poisoning. I n Brennenm nn's P ractice of P ed ia tric s, H ag ersto w n , Md.. W. F. P rio r Co., Inc., 1948. vol. 1, ch. 18, p. 1-8. (57) Feldm an. II. T .: Lead poisoning. S alient fe a tures in its diagnosis and treatm en t. Clin. Proc. Child. Hosp. 7: 194-205 (1951). (5S) B rien l, A., an d Young, W . J . : T h e o cc u rre n ce of lead poisoning am ong N orth Q ueensland chil dren. Ann. Trop. Med. 8: 575-589 (1914-15). (39) F u k u sb lm a, M., and M alsu m a to , 'l l . : S ta tis tic s of 298 cases of In fantile lead poisoning. O ri ental J. Dls. In fa n ts 3: 27-31 (1928). (40) Shelling. D. H., and H opper, K. B .: C alcium and phosphorus studies. Bull. Jo h n s H opkins Hosp. 5S: 137-211 (1930). ( 4 /) K aplan, E., and M cDonald, J . M .: Blood-lead determ inations as a health departm ent labora tory service. Am. J. Pub. H ealth 32: 4S1-486 (1942). (42) Blumberg. H.. and Scott, T. F. M e.: T he q u a n ti tative spectrographlc estim ation of blood lead and Its value In the diagnosis of lead poisoning. Bull. Johns H opkins Hosp. 56: 276-293 (1935). (43) W illiam s, H untington, Schulze, W. H., Rothchild. H. B., B row n, A. S., an d S m ith , F . R ., J r . : L e a d poisoning from the burning of battery casings. J . A. M. A. 100:1485-1489 (1933). (44) B altim o re o rd in a n ce on th e hy g ie n e of h o u sin g . No. 384, approved M arch 6, 1941, as am ended by No. 902, a p p ro v e d `M arch 29, 1943. (45) Lead poisoning In ch ild ren -- A d isease you can prevent Baltim ore City H ealth D epartm ent L e a fle t 1949. (46) Lead poisoning In children. B altim o re H e a lth News 14: 109-110 (1937). (47) Lead poisoning In children Is preventable and ca n be fa ta l. B altim o re H e a lth N ew s 26: 122124 (1949). (4 8 ) J e p h c o tt, C. M .: Lead in c e rta in colored ch a lk s and their danger to children. Canad. Pub. H ealth J. 28 : 391-393 (1937). (40) H am ilton, A lice: Recent changes in the painters* trade. U. S. D epartm ent of Labor, D ivision of L abor S tatistic s, B u lletin No. 7, 1937, p. 40. S3 Public H ealth R eports