Document JvNDx90Zqw4No4nNyKBR1K3r

'% Wh m i';* Ja me s R. To b ix , M.D>. Cenessee Hospital Health Service 220 Alexander Street Rochester, Neu? York 14607 Re f e r en c e s 1. Mellins, R. B., and Jenkins, C. D.: Epidemio logical and psychological study of lead poisoning in children. J.A.M.A., 158:16, ms: * 2. Bradley, j. E., Powell, A. E., Niermann, W., McGrady, K. R., and Kaplan, E.: The incidence of abnormal blood levels pf lead in a metro politan clinic. J. Pediat. 49:1,1956. 3. Chisolm, J. J., and Harrison, H. E.: The expo sure of children to lead. Ped iat r ic s , 18:943, 1956. 4. McLaughlin, M- D.: Lead poisoning in New York City, 1950-1954. New York J. Med., 50:3711, 1956. 5. Jenkins, C. D., and Mellins, R. B.: Lead poi soning in children. Arch. Neurol. Psychiat, 77:70,1957* 6. Byers, R. K.: Lead poisoning. Ped iat r ic s , 23: 585, 1959. 7. Ingalls, T. H., Tiboni, E. A:, and Werrin, M.: Lead poisoning in Philadelphia, 1955-1960. Arch. Environ. Health, 3:575, 1961. 8. Schucker, G. W., Vail, E, H., Kelly, E. B., et at.: Prevention of lead paint poisoning among Baltimore children. Public Health Rep., 80:969,1965* 9. Barltrop, D., and Killala, R.: Factors influenc ing exposure of children to lead. Arch. Dis. Child., 44:476, 1969, 10. Sorkin, N.: Stippling of the retina in lead poi soning. New Eng. J. Med., 269:779, 1963. 11. Smith, H. D.: Pediatric lead poisoning. Arch. Environ. Health., 8:256,1964. 12. Jacobziner, H.: Lead poisoning in children. Clin. Pediat, 5:277, 1966. 13. Greengard, J.: Lead poisoning in childhood: Signs, symptoms, current therapy and clinical expression. Clin. Pediat, 5:269, 1966* 14. Kopito, L., Byers, R. K., and Shwachman, H.: Lead in hair of children with chronic lead poisoning. New Eng. J* Med., 276:949, 1967. 15. Sayre, J. W., and Wilson, D. J.: Spot test for lead in paint. Pe d ia t r ic s , 46:783,1970, 16. Tobin, K.: Economic conditions confronting migrant families: Wayne County--1967. (unpublished) 17. Sanitary Code of New York State* Section XV. Lead Levels in Cord Blood Lead is not a natural body element and hence it is important to establish "normal" lev els.1 There have been many attempts to quanta tate and define the meaning of "normai'' with regard to human blood lead determinations. These attempts measure blood from varied populations: adults working in industrial situa tions, hospitalized children of varying ages, and urban ghetto dwellers.1-4 It is well known that lead in high concentrations in the human body produces disease and permanent brain damage.3'7 However, the effects of chronic ex posure to lower levels of blood lead (below 60. /.ig/100 ml) are largely unknown* Speculations have ranged from the supposition that there are no measureabie effects, to fears that low lead levels may produce subtle forms of minimal brain damage including learning disorders and personality disturbances. Recent work by Hemberg and Nikkanen in Finland,8 Millar, et al, in Hie United Kingdoma-and Weissberg, et shows a demonstrable inverse relationship between low blood lead levels (in the range of 5 to 40 \xg) and the activity of the enzyme 8aminolevulinie acid dehydrogenase as mea sured in vitro in heraolysates of human red blood cells. This suggests that these "nprmaT levels may indeed be subdinically toxic. The toxicity of lead at these low levels must be de fined. Then, suspected lead poisoned patients may be compared against these "normaF' vah ues. Since previous studies in this regard have concerned themselves with children with vary ing degrees of exposure to environmental lead,1-4*11:13 it was felt that there might be value in measuring cord blood lead levels in new born infants to approximate more closely the rinexposed subject arid to increase our base line information. Me t h o d Twenty-four mothers were included in tills study which was conducted over a period of 1 year to rule out seasonal variation. All were followed and delivered by the same obstetri cian in the same hospital. Of these 24,11 were from suburban middle class backgrounds and 13 were from an urban ghetto known as the "Hir in New Haven. Specimens were ob tained as follows: (1) venous maternal blood during labor (2) fetal cord blood at the time of delivery N40761 X /f 7 V' 608 ADRENAL HYPERPLASIA mercury, strontium 90, chromium, selenium, and others becomes more prevalent, it will be come increasingly important to assess the effects of these substances on human beings more accurately. Standards for their control wilt become increasingly crucial. Su mma r y Blood lead levels were determined on 24 mothers during labor and on the blood of their newborn offspring. The mean value for the mother's blood lead was 13.2 jAg/100 gm (range 10 to 20) and for the Cord blood 12.3 (range 10 to 20) p.g/100 gm whole blood. These levels are lower than "normal" blood lead standards usually accepted in the diagno sis and treatment of childhood lead poisoning. Pa u l Ha r r is , M.D. - Department of Pediatrics Ma r s h a l l R. Ho l l e y , M.D. Department of Obstetrics and Gynecology Yale University School of Medicine 333 Cednr Street New Haven, Connecticut 06510* 1 2 3 4 5 6 7 Supported in part by Children and Youth Project 651, Children's Bureau, HSMHA, Department of H.E.W.; and NIMH Grant MH1736-02. Re f e r e n c es 1. JfCehoe, R, A.: The metabolism of lead in man in health and disease. The Harben lectures 1960. J. Roy. Inst. Public Health, 24:177, 1981. 2. Robinson, M. J* Karpinski, F. E., and Brieger, H.: The concentration of lead in plasma, * ; whole blood and erythrocytes of infants and children. Ped iat r ic s , 21:793,1958. 3. Moncrieff, A. A., Koumides,. O. P., Clayton, B. E., Patrick, A. D., Renwick, A. G. C., and Roberts, G. E.: Lead poisoning in children.. Arch. Dis. Child., 39:1,1984, 4. Goldwater, L. L, and Hoover, L. J.: An inter national study of "normal" levels of lead in blood and urine. Arch. Environ. Health, 15: 50,1907. 5. Perlstein, M. A., and Attala, R.: Neurologic se- quellae of pJuxnblsm in children. Clin. Pediat, 5:292, 1900. 6. Byers, R. K., and Lord, E. E,: Late effects of lead poisoning on mental development Amer. J. Pis. Child., 66:471, 1943. 7. Thurston, D. R., Middlekamp, J. N., and Ma son, E.: The late effects of lead poisoning. J. Pediat., 47:413, 1955. 8. Hernberg, S., and Nikkanen, J.: Enzyme inhibi tion by lead under normal urban conditions.. Lancet, 1:63,1970. 9. Millar, J. A., Gumming, R. L. C-, Battistini, V., Carswell, F., and Goldberg, A.: Lead and 5- aminolaevulinic acid dehydratase* levels in mentally retarded children and in lead poi soned suckling rats, Lancet, 2:695, 1970. 10. Weissberg, J. B., Lipschutz, F., and Oski, Frank A.: 5-aminolevuIinic acid dehydra tase activity in circulating blood cells; Test for lead poisoning. New Eng J. hied., 284: 565,1971. 11. Bradley, J. E., Powell, A. E., Nieramn, W., McGrady, K. R., and Kaplan, E.: The inci dence of abnormal blood levels of lead in a metropolitan pediatric clinic with observa tion on value of coproporphyrinuria as a screening test. J. Pediat., 49:1, 1956. 12. Blanksma, L. A.. Sachs, H. K., Murray, E. F., and O'Connell, M. J.: Incidence of high blood lead levels in Chicago children. Ped i at r ic s , 44:661, I960. , 13. Griggs, R. C., Sunshine, L, Newill, V. A., Newton, B. W., Buchanan, S,, and Reisch, C. A.: Environmental factors in childhood lead poisoning. J.A.M.A., 187:703, 1964. 14. Cholak, J., Hubbard, P. M.. and Buskey, K. A.: The determination of lead in freshly Voided urine. J. Ind. Hyg. Tox., 30:59,1947.- 15. Woessner, W. W., and Cholak, j. A.: Improve- . ments In the rapid screening method for lead in urine. Arch. Ind. Hyg. Occ. Med., 7: 249,1953. 16. Scanlon, J.: Umbilical cord blood lead concen tration. Amer. J. Pis. Child., 121:325, 1971. The Incidence of Associated Anomalies in 105 Patients with Congenita! Adrenal Hyperplasia A survey of 105 patients with defective adrenal steroid 21-hydroxylation, the most com mon defect in congenital adrenal hyperplasia, has been carried out to determine the presence of additional congenital or developmental anom-. alies. The following is a report of this survey. The diagnosis of congenital adrenal hyper plasia was suspected in infants who presented with ambiguous genitalia or with defect in electrolyte metabolism manifested by failure to thrive, vomiting and dehydration with hypona tremia and hyperkalemia. Measurement of ele vated levels of urinary 17-ketosteroids, 11-keto DUP050058751