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MARCH 1972 The American Journal of Medicine VOLUME 52. NUMBER 3 EDITORIAL Lead Poisoning VINCENT F. GUINEE, M.D., M.P.H. New York, New York * from the Bureau of Lead Poisoning Con trol, New York City Department of Health, Health Services Administration, New York, New York. Requests for reprints should be addressed to Dr. V. F. Guinee, Bureau of Lead Poisoning Control, 377 Broadway, New York, New York 10013. Manuscript received November 15,1971. Lead poisoning is a common medical problem and has been for centuries [1]. It is known to cause death and mental retardation after severe exposure. But, the sequelae of prolonged low level exposure to lead remain unknown. Its basic treatment has been removal of the patient from the source of exposure--a treatment better suited to an individual than a community. Lead exposure can be divided into three categories: occupa tional, community and individual. It is the impression of industrial physicians that lead in toxication is now an infrequent mild disease. But as recently as 1913, Hoffman [2] recorded 164 cases of chronic lead poisoning among 915 workers in five large storage battery fac tories. And, Aub et al. [3] noted a 13.5 per cent incidence of plumbism among the men and women who glazed and decorated pottery. During the eleven years 1914-1924, 841 painters in the United States registration area died of lead poisoning [2]. They accounted for one half of the total reported mortality from lead poisoning for that time period. At least a painter or miner was likely to be aware of his ex posure to lead. The consumer of lead products may not be as fortunate. In colonial America, for example, the entire popula tion was exposed daily to lead in pewter plates and vessels and inadequately glazed pottery [4,5]. This chronic diet of lead was the cause of the "dry gripes," an ailment which was widespread in the colonies until the 1780's, it appeared in Europe under several names including Colica Pictonum and Poitou Colic. Distillers of alcohol have apparently escaped occupational exposure to lead but are likely to have succumbed as con- GLD35133 tEAD POISONiNG -- GUINEE sumers. The use of lead to sweeten wine was common until the 18th century. The use of lead in stills became recognized as a hazard to good business if not health. The Massachusetts Bay Colony on September 3r 1723, promulgated a law "For preventing abuses in distilling of rum or other strong liquors with leaden heads or pipes" [6]. It provided for inspectors; and fines. The action was prompted by their customers in North Carolina who attributed a high incidence of "dry bellyache" to use of Massachusetts Bay rum. It is of note that the law was passed before the classic studies naming lead as the cause of the Devonshire colic by Sir George Baker and James Hardy (17671778). The former investigator demonstrated that lead used to line cider presses and vats appeared in the product [7]. The latter supported his col league, but also pointed out that the cider was shipped, stored and drunk from cheap lead-glazed earthenware jugs which, he demonstrated, quickly gave up their lead to acid cider [8]. Hardy [9] de fended his hypothesis convincingly. "If the 30th part of a grain of iron taken daily for a few weeks can produce the most salutary effects, is it diffi cult to believe one half of that same quantity of a noxious mineral dissolved in wine taken occa sionally for a number of years, should ultimately prove injurious?" The gradual disappearance of lead colic was largely due to cultural, economic and technologic changes in society without sig nificant intervention by the medical profession. Exposure of the individual to lead has often been caused by an unusual set of circumstances, such as a child swallowing a foreign body [10,11]. It has been lead gone astray from its usual path, such as the lead poisoning that occurred in fami lies which burned old battery cases to heat their homes [12-14]. Often it has been a flash-back to bygone days--the use of inadequately glazed pot tery [15-17] or decorative pewter for food con tainers; the making of home-made wine [18-20] or "moonshine whiskey" [22-23], and the use of products, such as cosmetics [24,25], from coun tries with less stringent product regulation. The child, at the turn of the century, lived in a world of lead, as Ruddock remarked. There was lead paint on the walls, woodwork and window sills, porch railings, furniture, play-pens and cribs. Lead chromate was used as a coloring for food [26]. Toys were made of lead and painted with lead paint. Even young infants were unprotected; lead was used for nipple shields. Holt [27] described an eight month old girl with no teeth whose source of lead was found to be a lead acetate ointment, "diachylon compound," used by the mother on her breast for eczema. In Japan, lead salts were used in the manufacture of toilet powders causing lead meningitis in hundreds of infants [28]. Many of these sources could be effectively removed from the market place and the home, but house paint once applied became a source of lead for fu ture decades. The widespread prevalence of lead paint poison ing in childhood was brought to medical attention by the Australian workers Gibson [29] and Turner [30] in the 1890's. Gibson [31] traced, the prin cipal source of lead exposure to house paint which he said turned a home into "a simple lead trap." He postulated that the paint,, especially on porches, powdered in the hot Queensland sun and that the children ingested what stuck on their hands or accumulated.under their fingernails. It was about 1920 when clinfcians in the United States began linking paint, pica and the possi bility of unsuspected lead poisoning. Blackfan [32] in 1917 described four children with lead poisoning..In one instance, a father stated that the patient, age two and a half years, and his brother had recently ruined a set of parlor furni ture by eating the paint off it--a striking example of what a patient may have to do to bring our at tention to a problem. Blackfan concluded, "I would urge that .energetic prophylactic measures be taken with children who habitually eat painted articles, In order to guard against the develop ment of lead poisoning. Since my attention has been directed to lead-poisoning, 1 have found a number of children who nibble the white p^int from enameled cribs." Strong [33] confirmed paint as a cause of lead poisoning in a nineteen month old boy.. It was Ruddock [34] in 1924 who first pre sented a strong case for the association of pica and lead poisoning in children. He also recog nized that there were many unsuspected mild cases of lead poisoning in children. By 1926, McKhann [35] stated that lead poisoning was a relatively frequent occurrence in children: "In our cases it has usually been associated with pica ... which causes ingestion of lead paint." Reports from hospitals and health departments in the United States have documented the con tinuing occurrence of lead poisoning due to paint ingestion. More accurately documented than the cases themselves has been the variability of medical interest in this disease. In a Chicago hospital, Tanis [36] attributed the finding of thirteen children with plumbism in 1953 to in- 1V JT t * Z 284 The American Journal of Medicine LEAD POISONING -- GUINEE creased physician interest. In fact, this repre sented such an increase in cases that it prompted a request by the city for aid from the Communi cable Disease Center because they thought it might be ah epidemic of viral meningitis [37]. From 1931 to 1955, 462 children were admitted to Baltimore hospitals with lead ingestion [38]. In New York City, McLaughlin [39] reported 143 cases and thirty-nine deaths from 1950 to 1955. Ingalls et al. \[40j reported approximately fifty cases yearly in Philadelphia in the 1955--1960 period. The 338 cases in New York City in 1963 were contrasted by Jacobziner [41] with the single case reported in 1950. In 1966, Chicago began the first mass screening program using a blood lead test to detect lead poisoning in children living-in low income neigh borhoods [42]..Over a two year period, 68,800 children, one to six years old were tested; 5.7 per cent had blood lead levels of 50 ^g/100 ml or higher, a total of 3,935 cases. In smaller studies etevated blood lead levels had been reported in up to 40 per cent of those tested, but it was noted that in this large scale survey there had been no prior screening of the children by another test or history of pica. Old paint is a formidable source of lead expo sure for children. It is estimated that 450,000 apartment units in New York City are in such a state of disrepair that children living in them will be exposed to the hazard of lead paint poisoning. Approximately 120,000 children are living in these dwellings. The New York City Health Code banned the use of high content lead paint on interior sur faces in 959. However, most deteriorating hous ing stock was built before World War II. In January 1970, the New York City Health Department cre ated the Bureau of Lead Poisoning Control [43]. The Bureau's approach has been to seek out and attempt to protect the child who is most likely to suffer from lead poisoning. It is recognized that the long-term solution is to replace the deteriorating housing of the inner city. When a child is found to have a blood lead level of 60 fig/100 ml, the Health Department notifies the physician submitting a specimen. A nurse and sanitarian visit the home to plan for medical super vision and to determine the source of lead avail able to the child. If Health Department laboratory analysis finds paint samples with more than 1 per cent lead content, the owner of the building is ordered to correct the condition within five days. If he fails to comply, the work is done by the city's Emergency Repair Program. When we speak of a case of lead poisoning, "case" has a connotation of symptoms and "poi soning" has a connotation of damage; neither is necessarily true. However, we have been unable to find any other verbal designation which describes the situation more succinctly. New York City's cur rent definition of a "case" is a child who, on a single occasion, has a blood lead level of 60 pg/ 100 m! or greater. These children, as a rule, do not have symptoms which can be attributed to lead intoxication. We believe this level does indicate that the child has access to lead in his environ ment and is taking the lead into his system. That this situation is not unusual can be seen in the ac companying tables. The distribution of blood lead levels (analyzed by Atomic Absorption Spectrophotometry) of chil dren from the lower socioeconomic areas of New York City is presented in Table i. Comparing 1969 and 1970, we see the effect of a change in the pop ulation screened from a restrictive program based on a child's history of pica toward a community screening program stressing the character of hous ing in the neighborhood. In 1970, a greater per- TABLE I Lead Content of Blood Specimens Drawn from New York City Children--1969-1971 Blood Level (pg/100 ml) 1969* No. % 1970 No. % Total Blood Samples 1/1-9/24/1971 No. % 10 20 30 40 50 60 70-100 110+ 157 5.9 5,050 6.0 5,428 6.2 552 20.8 26,650 31.6 33,577 38.3 738 27.8 28,422 33.7 27,882 31.8 556 21.0 13,582 16.1 11.730 13.4 319 12.0 5,619 6.6 4,979 5.7 156 5.9) 2,757 3.3] 2,282 2.7) 135 5.2>12.5 2,134 2.576.0 1,569 1.874.6 35 1.4) 154 0.2) 112 0-1) 2,648 '100.0 84.368 100.0 87,559 100.0 * Data available on 2,648 of approximately 10,000 samples. Velum* 52, March 1972 First Blood Samples 1/1-9/24/1971 No. 5,310 32,910 26,941 10,623 3.953 1,137 702 50 % 6.5 40.3 33.0 13.0 4.8 1.4) 0.9>2.4 0.1) 91.626 100.0 GLP35135 I LEAD POISONING -- GUINEE TT TABLE II Per Cent of Screened New York City Children and above, the total number of tests was double with Lead Levels in First Blood Sample of 0 pg/100 ml or More, by Age and Race--January 1-September 30f 1971 the number of first blood specimens. Over-all, 6.8 per cent of the blood specimens were "repeat sam ples." in this table a first biood specimen repre kale per 100 Children Screened sents the first sample obtained from an individual Age (yr) <1 1 2 3 4 5 6 7 >7 Unknown Black 2 5 6 4 3 2 1 1 1 0.5 Puerto Rican 1 1 2 1 1 1 1 1 1 0.1 Other Unknown Total 1 1 -2 2 23 2 13 2 12 0.4 1 1 1 0.4 1 0.4 1 1 0.4 0.4 1 0 0.4 1 0 0.1 2 in 1971. It is the closest we have to true point prevalence of blood lead levels in this age group. The twelve month totals for 1971 may show a slight increase in the percentage of blood speci mens with lower levels of lead, as the lead levels of blood specimens drawn during the last three months of the year might be expected to be some what lower than the levels in blood drawn in the summer months. It has been thought that the predominance of cases among black children reflected a greater l >I! I a< centage of children appeared in the group with blood lead levels In the 20 and 30 pg range, whereas the percentage of children with blood lead levels in the range of 60 and above dropped from 12.5 to 6 per cent. In 1970 and 1971, the children screened were comparable according to age and race. There again was some shift in the distribution to lower blood lead levels, but it was not as marked as in 1969-1970. Comparing the total number of blood specimens obtained in the first nine months of 1971 with the inumber of first blood specimens obtained from in ! Idividuals for the same period, the distribution of biood lead levels was similar. As expected, the higher the blood lead level of the first specimen, the more likely was a repeat blood analysis per formed. Roughly, tests were repeated in one of ten children with levels of 40 pg and in one of four with levels of 50 pg. In those with levels of 60 pg chance of a black child being tested. In Table II we see that in each year of age up to and including five years, the black child was indeed more likely to have a blood lead level of 60 pg or greater. This is surprising, since both black and Puerto Rican populations in New York City apparently live in housing of similar disrepair. Although previous case reports pointed to chil dren in the one to four year age group as being the most affected, it was also true that children at these ages were most likely to be tested. The risk of lead poisoning for-each year of age can be com pared in Table II. For categories other than black, the variability from year to year is not striking. However, in black children there is a sharp de crease in the incidence with increasing age. The data in Table ii are based on the first blood sample ever taken from an individual. Equal num bers of black and Puerto Rican children were tested. The data oh white chiidren-are included in ! l ) t > r / c r c 2 t i r c t TABLE III Lead Poisoning Cases (Blood Lead >60 j<g/100 ml) by Month In New York City-- 1969-1971 the "Other" column; The percentages shown are based only on cases'uncovered by a first blood sample. Thus, the data for a child who had been 0 t Year found to have a lead level of 60 pg nrhis second or Month 1969 1970 1971 third blood sample would not be included in this January 71 29 103 calculation. Thus this eliminates a potential error February 58 44 119 which might arise if one group was more likely to March 50 85 177 be retested than another. April May June July 59 112 124 The monthly incidence of lead poisoning re 85 84 177 146 325 232 ported over the past three years in New York City 77 376 251 is presented in Table Ml. The increase in cases be August 72 471 234 ginning in March 1970 reflects the initiation of a September October November December 55 43 33 40 383 251 1..8.8* large scale community testing program. Whereas roughly 10,000 blood tests were performed in 217 . 179 ... 1969, over 80,000 were performed in 1970. There was a steady testing program of approximately Total 727 2.649 ... 10,000 biood samples a month in 1971. Although Provisional. more cases become apparent in the summer GL035136 266 Tha American Journal of Madlcina LEAD POISONING --GUINE6 mths, a significant number of cases can be unTovered by screening throughout the year. Varia tions from month to month may be influenced by the pattern of screening, age group, neighborhood [43] and season [44]. After April 1971 there were fewer cases each month than in the same month of the preceding year. This suggests that some progress has been made through the- program's educational and housing repair efforts. The decrease might best be explained by considering in theory the number of cases found in the first and second year of any screening program. * example, the annual in cidence of a disease.condition is 2,500 and its duration three years, its prevalence would be 7,500 cases (Prevalence^ Incidence X Duration). Given a screening program that is 100 per cent effective, the yield would be 7,500 cases during the first year and 2,50Q.new cases the second year. In effect, the first year would be a prevalence rate; the second year would be an incidence rate. A decline in reported cases in the first two years of a program would therefore not necessarily rep resent a change in the incidence of the disease condition. Cases which occurred in the first nine months of 1971 are presented according.to.age and race in Table IV. More cases of lead poisoning occurred in black 'children than in all other children com bined. The. unknown column may indicate simply a clerical omission or may represent inability on the part of the observer to decide racial character istics of the patient. The age pattern for 1970 In \ew York City was the same except that more :ases occurred in the two-year old group than in he one year ojd age group. This age distribution if cases is similar to that found over the past iventy years in major U.S. cities. When apartments of children with lead poisonig (affected children) have been visited, lead aint and deteriorating surfaces have often been umd [45]. It could be, however, that the home ivironments of these children and their "normal" 'mng neighbors provide equal exposure to lead, it that the affected children have less parental ipervision or more pronounced pica. To investi* te this question, the Bureau of Lead Poisoning ntrof undertook a study in which apartments of 5 affected children were compared with apart?nts of a control group. The affected group con- ted of one, two and three year old children with >od lead levels of 60 ng or greater. The control up was matched by age and had blood lead els of 10 or 20 ^g. JW 52, March J972 Lead Poisoning Cases (Blood Lead Level >60 jtg/100 ml) in New York City, by Age and Race--January l-September 30, 1971 Age (yr) <1 1 2 3 4 5 6 7 >7 Unknown Black 17 280 229 150 111 79 43 22 12 5 Puerto Un Rican Other known Total No. % 10 2 3 32 2.0 78 22 50 430 27.3 91 16 42 378 24.0 59 11 33 253 16.1 37 3 21 172 10.9 40 6 24 149 9.5 28 1 17 89 5.7 12 1 4 ` 39 2.5 903 24 1.5 102 8 0.5 365 62 199 1,574 100.0 The results of apartment inspection are given in Table V. In only four of 135 cases did the sani tarian find an apartment with intact interior sur faces indicating "no cause for action." In con trast, sixty-four of 233 (27.5 per cent) apartments of the control group were in good condition. If peeling paint was found, the paint samples con tained illegal amounts of lead about 80 per cent of the time in the apartments of the affected chil dren and 50 per cent of the time in the apartments of the control group. Over-all, a potential source of lead within the apartment was uncovered in 76.3 per cent of the investigations of affected children, but in only 37.7 per cent of the investiga tions in the control group. Until recently our knowledge of lead poisoning was based primarily on retrospective observations of symptomatic cases. This left us in much the same situation as if we knew diabetes only through observations of patients seen in hospitals. The increasing availability of mass screening tech nology which can measure the lead exposure of large segments of populations is creating a new opportunity to delineate the natural history of lead poisoning. TABLE V Apartment Inspection for Lead Exposure of Children with Lead Poisoning and a Control Group--New York City 1971 Children with Lead Poisoning Control Group Result of Inspection No. % No. % No cause for action 4 3.0 64 27.5 Samples taken, negative 28 20.7 81 34.8 Samples taken, positive 103 76.3 88 37.7 Total 135 100.0 233 100.0 GLD35137 287 u .t HI; 5: 5i *1? t-EAO POISONING -- GUINEE SUMMARY Lead poisoning is a common disease, its reported incidence varies widely according to physician in terest. A mass screening program in New York City has uncovered over 4,000 children with blood lead levels of 60 /ig/100 ml or higher. Black chil dren were at greatest risk. Analysis of homes of affected children and comparable controls showed significantly more lead paint available to the child who became a ``case." New screening technology will enable us to better delineate the natural his tory of lead exposure and its toxicity. REFERENCES 1. Hammond PB: Lead poisoning. An old problem with a new dimension. Essays in Toxicology, vol 1 (Blood FR, ed). New York, Academic Press, 1969. 2. Hoffman Ft: Deaths from lead poisoning. Bull US Bureau Labor Statistics, No. 426,1927. 3. Aub JC, Fairhiil LT, Minot AS, Reznikoff P: Lead poisoning. Medicine 4: 226,1925. 4. McCord CP: Lead and lead poisoning in Early America, lead compounds. Industr Med Surg, February 1954, p 75. 5. McCord CP: Lead and lead poisoning in Early America, the pewter era. Industr Med Surg, De cember 1953, p 573. 6. McCord CP: Lead and lead poisoning in Early Amer ica, Benjamin Franklin and lead poisoning. Industr Med Surg, September 1953, p 394. 7. Baker G: An essay concerning the cause of the endemial colic of Devonshire. Reprinted by the Delta Omega Society, 1958. 8. Childs St JR: Sir George Baker and the dry belly ache. Bull Hist Med 44: 213,1970. 9. Waldron HA: James Hardy and the Devonshire colic. Med Hist 13: 74,1969. 10. Biehusen FC, Pulaski EJ: Lead poisoning after in gestion of a foreign body retained in the stomach. New Eng J Med 254:1179,1956. 11. Forsby N, Fristedt B, Kjellman B: Acute, lethal poisoning after ingestion of metallic lead. Acta Paediat Scand suppl 177, p 107,1967. 12. Travers E, Rendle-Short J, Harvey CC: The Rother ham .lead-poisoning outbreak. Lancet 2: 113, 1956. 13. Turner W, Bamford FN, Dodge JS: Lead poisoning at Bradford. Brit Med J 3: 56,1967. 14. Giltet JA: An outbreak of lead poisoning In the Canktow district of Rotherham. Lancet 1: 1118, 1955. 15. Klein M, Namer R, Harpur E, Corbin R: Earthen ware containers as a source of fatal lead poi soning. Case study and public-health considera tions. New Eng J Med 283:669,1970. 16. Harris RW, Etsea VR: Ceramic glaze 8S a source of lead poisoning. JAMA 202:544.1967. 17. Beritic T, Stahuljak D: Lead poisoning from leadglazed pottery. Lancet 1:669,1961. 18. Harben EF, Reid DP: A case of "dry gripes/' Med J Aust 2:193,1969. 19. Whitehead TP, Prior AP: Lead poisoning from home made wine. Lancet 2:1343,1960. 20. Lane CR, Lawrence A: Home-made wine as a cause of lead poisoning. Report of case. Brit Med J 2:939,1961. 21. Crutcher JC: Clinical manifestations and therapy of acute lead intoxication due to the ingestion of il licitly distilled alcohol. Ann Intern Med 59: 707, 1963. 22. Palmisano PA. Sneed RC, Cassady G: Untaxed whiskey and fatal lead exposure. J Pediat 75; 869,1969. 23. Patterson M, Jernigan WCT: Lead intoxication from "moonshine." GP 40:126,1969. 24. Warley MA, Blackledge P, O'Gorman P; Lead pot- soning from eye cosmetic. Brit Med J 1: 117, 1968. 25. Fernandes MT: An outbreak of lead poisoning. Med Offr, August 1969, p 88. 26. Stewart DD: Lead convulsions, a study of sixteen cases. Amer J Med Sci 109: 288,1895. 27. Holt LE: Lead poisoning in infancy._Amer J Dis Child 25:229,1923. 28. Kato K: Lead meningitis In Infants. Resume of Japanese contributions on the diagnosis of lead poisoning in nurslings. Amer J Dis Child 44: 569,1932. ** 29. Gibson JL, Love W, Hardie D, Bancroft P, Turner AJ: Notes on lead poisoning as observed among children In Brisbane. Proceedings of the Inter colonial Medical Congress of Australasia, Third Session, 1B92, p 76. 30. Turner AJ: Lead-poisoning among Queensland chil dren. Aust Med Gaz, October 1897, p 475. 31. Gibson JL: A plea for painted railings and painted walls of rooms as the source of lead poisoning amongst Queensland children. Aust Med Gaz, April 1904, p 149. 32. Blackfan KD: Lead poisoning In children with espe cial reference to lead as a cause of convulsions. Amer J MerfScl 153:877,1917. 33. ' Strong RA: Meningitis, caused by lead poisoning, in a child of nineteen months. Arch Pediat 37: 532, 1920. 34. Ruddock JC: Lead-poisoning In children with spe cial reference to pica. JAMA 82: 1682, 1924. 35. McKhann CF: Lead poisoning In children with notes on therapy. Amer J Dis Child 32: 386, 1926. 36. Tanis AL: Lead poisoning In children including nine cases treated with edathamll calcium-disodium. Amer J Dis Child 89:325,1955. / 37. Mellins RB. Jenkins CD: Epidemiological and psy chological study of lead poisoning'In children. JAMA 158:15,1955. 38. Bradley JE, Powell AE, Niermann W, McGrady KR, Kaplan E: The incidence of abnormal blood levels of lead In a- metropolitan pediatric clinic. J Pediat 49:1,1956. 39. McLaughlin MC: Lead poisoning in children in New York City 1950-1954. NY J Med*$6:3711,1956. 40. Ingalls TH, Tibonl EA, Werrin M: .Lead poisoning in Philadelphia, 1955-1960. Arch .Environ Hlth 3: 575,1961. 41. Jacobziner H: Lead poisoning In childhood: epide miology, manifestations, and prevention. Clin Pediat 5:277,1966. 42. Blanksma LA, Sachs HK, Murray EF, O'Connel MJ: Incidence of high blood lead levels In Chicago children. Pediatrics 44:661,1969. 43. Guinee VF: Lead poisoning in New York City. Trans NY Acad Sci 33:539.1971. 44. Chisolm JJ: Lead poisoning. Sci Amer 224:15,1971. 45. Airborne lead in perspective. Committee on Bio logic Effects of Atmospheric Pollutants of the Division of Medical Sciences, National Research Council, National Academy of Sciences, Wash ington, D.C., 1971, to be published. GLD35138 288 The American Journal of Medlcln*