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MARCH 1972 The American Journal off ileciioine 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. Guinea, Bureau of Lead Poisoning Control, 377 Broadway, New York, New York 100*13. 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- Volume 52, March 1972 2S3 LEAD POISONING--GUINEE mmm anis sumers. The use of lead to sweeten wine was common until the 18th century. The use of lead "diachylon compound," used by the mother on her breast for eczema. In Japan, lead salts were I 1 in stills became recognized as a hazard to good used in the manufacture of toilet powders causing I business if not health. The Massachusetts Bay lead meningitis in hundreds of infants [28]. Many I Colony on September 3, 1723, promulgated a law of these sources could be effectively removed f "For preventing abuses in distilling of rum or other strong liquors with leaden heads or pipes" [6], from the market place and the home, but house paint once applied became a source of lead for fu- I I It provided for inspectors and fines. The action ture decades. I was prompted by their customers in North Carolina The widespread prevalence of lead paint poison- I who attributed a high incidence of "dry bellyache" ing in childhood was brought to medical attention i to use of Massachusetts Bay rum. It is of note that by the Australian workers Gibson [29] and Turner | the law was passed before the classic studies [30] in the 1890's. Gibson [31] traced the prin- l naming lead as the cause of the Devonshire colic by Sir George Baker and James Hardy (1767- cipal source of lead exposure to house paint which he said turned a home into "a simple lead trap." I f 1778). The former investigator demonstrated that He postulated that the paint, especially on lead used to line cider presses and vats appeared porches, powdered in the hot Queensland sun and ' in the product [7]. The latter supported his col that the children ingested what stuck on their ' league, but also pointed out that the cider was hands or accumulated under their fingernails. j shipped, stored and drunk from cheap lead-glazed It was about 1920 when clinicians in the United ' earthenware jugs which, he demonstrated, quickly States began linking paint, pica and the possi gave up their lead to acid cider [8], Hardy [9] de bility of unsuspected lead poisoning. Blackfan fended his hypothesis convincingly. "If the 30th [32] in 1917 described four children with lead ] part of a grain of iron taken daily for a few weeks poisoning. In one instance, a father stated that can produce the most salutary effects, is it diffi the patient, age two and a half years, and his I! ' cult to believe one half of that same quantity of a brother had recently ruined a set of parlor furni noxious mineral dissolved in wine taken occa ture by eating the paint off it--a striking example - I! i sionally for a number of years, should ultimately of what a patient may have to do to bring our at- | prove injurious?" The gradual disappearance of tention to a problem. Blackfan concluded, "I lead colic was largely due to cultural, economic would urge that energetic prophylactic measures and technologic changes in society without sig be taken with children who habitually eat painted nificant intervention by the medical profession. articles, in order to guard against the develop Exposure of the individual to lead has often ment of lead poisoning. Since my attention has been caused by an unusual set of circumstances, been directed to lead poisoning, I have found a such as a child swallowing a foreign body [10,11]. number of children who nibble the white pa,int It has been lead gone astray from its usual path, from enameled cribs." Strong [33] confirmed such as the lead poisoning that occurred in fami paint as a cause of lead poisoning in a nineteen lies which burned old battery cases to heat their month old boy. homes [12-14], Often it has been a flash-back to It was Ruddock [34] in 1924 who first pre bygone days--the use of inadequately glazed pot sented a strong case for the association of pica tery [15-17] or decorative pewter for food con and lead poisoning in children. He also recog tainers; the making of home-made wine [18--20] nized that there were many unsuspected mild or "moonshine whiskey" [21-23], and the use of cases of lead poisoning in children. By 1926, products, such as cosmetics [24,25], from coun McKhann [35] stated that lead poisoning was a tries with less stringent product regulation. relatively frequent occurrence in children: "In The child, at the turn of the century, lived in a our cases it has usually been associated with world of lead, as Ruddock remarked. There was pica . .. which causes ingestion of lead paint." lead paint on the walls, woodwork and window sills, Reports from hospitals and health departments porch railings, furniture, play-pens and cribs. Lead in the United States have documented the con chromate was used as a coloring for food [26]. tinuing occurrence of lead poisoning due to paint Toys were made of lead and painted with lead ingestion. More accurately documented than the paint. Even young infants were unprotected; lead cases themselves has been the variability of was used for nipple shields. Holt [27] described medical interest in this disease. In a Chicago an eight month old girl with no teeth whose source hospital, Tanis [36] attributed the finding of of lead was found to be a lead acetate ointment, thirteen children with plumbism in 1953 to in- 284 The American Journal of Medicine DUP050058688 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 an 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. [40] 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 /xg/100 ml or higher, a total of 3,935 cases. In smaller studies elevated 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 1959, 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 ^g/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 jtg/ 100 ml 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 Stood Level Oig/lOOml) xo 20 30 40 50 60 70-100 1104* 1969* No. % 157 5.9 552 20.8 738 27.8 556 21.0 319 12.0 156 5.9) 135 5.2>12.5 35 1.4) ` 1970 NO. 5,050 26,650 28,422 13,582 5,619 2,757 2,134 154 % 6,0 31.6 33.7 16.1 6.6 3.3) 2.5/6.0 0.2) Total Blood Samples 1/1-9/24/1971 No. 5,428 33,577 27,882 11,730 4,979 2,282 1,569 112 % 6.2 38.3 31.8 13.4 5.7 2.7) 1.8/4.6 0,1) 2,648 100.0 84,368 100.0 87,559 100.0 * Data available on 2,64$ of approximately 10,000 samples. 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) 81,626 100.0 . Volume $2, March 1972 DUP050058689 LEAD POISONING --QUINEE TABLE II Per Cent of Screened New York City Children with Lead Levels in First Blood Sample of 60 pS/100 ml or More, by Age and Race--January 1-September 30,1971 . Rate per 100 Children Screened Age <yr) <1 1 2 3 4 6 7 >7 Unknown Black '!2 5 6 4 3 !2 1 i i 0.5 Puerto Rican 1 1 2 1 1 1 1 1 1 0.1 Other Unknown Total i 12 223 Z13 Zl2 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 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 pg 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 number of first blood specimens obtained from in dividuals for the same period, the distribution of blood 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 TABLE III Lead Poisoning Casas (Blood Lead >60 /mg/100 ml) by Month In New York City-- 1969-1971 Year Month 1969 1970 1971 January February March April May June July August September October November December 71 58 50 59 85 84 77 72 55 43 33 40 29 103 44 119 85 177 112 124 177 146 325 232 375 251 471 234 383 188* 251 217 ... 179 ... Total * Provisional. 727 2,649 and above, the total number of tests was double 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 blood specimen repre sents the first sample obtained from an individual in 1971. ft 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 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 on white children are included in 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 found to have a lead level of 60 pg in his second or third blood sample would not be included in this calculation. Thus this eliminates a potential error which might arise if one group was more likely to be retested than another. The monthly incidence of lead poisoning re ported over the past three years in New York City is presented in Table III. The increase in cases be ginning in March 1970 reflects the initiation of a large scale community testing program. Whereas roughly 10,000 blood tests were performed in 1969, over 80,000 were performed in 1970. There was a steady testing program of approximately 10,000 blood samples a month in 1971. Although more cases become apparent in the summer 286 The American Journal of Medicine DUP050058690 LEAD POISONING -- GUINEE months, a significant number of cases can be un covered 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 2,500 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 New York City was the same except that more cases occurred in the two year old group than in the one year old age group. This age distribution of cases is similar to that found over the past twenty years in major U.S. cities. When apartments of children with lead poison ing (affected children) have been visited, lead paint and deteriorating surfaces have often been found [45]. It could be, however, that the home environments of these children and their "normal" young neighbors provide equal exposure to lead, but that the affected children have less parental Supervision or more pronounced pica. To investi gate this question, the Bureau of Lead Poisoning Control undertook a study in which apartments of the affected children were compared with apart ments of a control group. The affected group con sisted of one, two and three year old children with blood lead levels of 60 /xg or greater. The control group was matched by age and had blood lead levels of 10 or 20/g. TABLE IV Lead Poisoning Cases (Blood Lead Level >60 /xg/100 ml) in New York City, by Age and Race--January 1-September 30, 1971 Age (yr) <1 1 a 3 4 5 6 7 >7 Unknown Black 17 280 229 150 1U 79 43 22 12 5 Puerto Un Rican Other known 10 2 3 78 22 50 91 16 42 59 11 33 37 3 21 40 6 24 28 X 17 12 1 4 903 102 Total No. % 32 2.0 430 27.3 378 24.0 253 16.1 . 172 10.9 149 9.5 89 5.7 39 2.5 24 1.5 8 0.5 948 365 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 LM- p t' Volume 52, March 1972 287 DUP050058691 a LEAD 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 /x.g/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. 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Amer J Dis Child 32: 386, 1926. 36. Tanis AL: Lead poisoning in children including nine cases treated with edathamil calcium-disodiurn. Amer J Dis Child 89:325,1955. 37. Mellins RjB, 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 56:3711,1956. 40. Ingalls TH, Tiboni 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. Bfanksma 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. 288 The American Journal of Medicine DUP050058692