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SWimArtj " INCREASED LEAD ABSORPTION WITH ANEMIA AND SLOWED NERVE CONDUCTION IN CHILDREN NEAR A LEAD SMELTER Philip J. Landrigan, M.D. * Edward L, Baker, Jr.., M. D- ' Robert G. Feldman, M.D. 3 Dennis H. Cox, Ph.D, 4 Kenneth V, Eden, M.D- 3 Walter A. Orensteln, M.D-. 6 John A* Mather, M.D. ' Anthony J . Yarikel, M . 3 . 8 Ian H. Von Lindern, M,S. 9 J. Chief, Environmental Hazards .Activity, Cancer and Birth Defects Division, Bureau of Epidemiology, .Center for Disease Control, Atlanta, Georgia 30333 2. Medical Epidemiologist, Cancer and Birth Defects Division , Bureau of Epidemiology, Center for Disease Control, Atlanta, Georgia 30333 3. Professor of Neurology and Chairman .of the Department of Neurology, Boston University School of Medicine, 80 East Concord Street, Boston, Massachusetts 02118 4. Supervisory Research Chemist, Toxicology Branch, Clinical Chemistry Division, Bureau of Laboratories, Center for Disease Control, Atlanta-, Georgia 30333 5. Medical Epidemiologist, Field Services Division, Bureau of Epidem iology, Center.for Disease Control, Montana State Health Department, Helena, Montana 59601 6. Medical Epidemiologist, Vaccine Evaluation Section, Field Services Division, Bureau of Epidemiology, Center for Disease Control, Atlanta, Georgia 30333 7. State Epidemiologist, Division of Health, Idaho Department of Health and Welfare, Boise, Idaho 83720 8. Environmental Engineering Specialist, Division .of Environmental Ser vices, Idaho Department of Health and Welfare, Boise, Idaho .83720 9. Environmental Engineering Specialist, Division of Environmental Ser vices, Idaho Department pf Health and Welfare, Coeur d'Alene, Idaho 83814 From the Bureau of Epidemiology, U.S. Public Health Service, Center for Disease Control; The Department qf Neurology , Boston University School of Medicine; and the Idaho Department of Health and Welfare. Send requests for reprints to: Philip J. Landrigan, M.D., Bureau of Epidemiology, Center for Disease Control, Atlanta, Georgia 30333. -9:0- .t N 27645 cial status , or duration of inalysis was undertaken by ho had been selected for ie end pf medical screening sn, only 34 of the original excluded any pair in which r a change in his blood lead vice versa).. To augment this data, we therefore chose children who had no evident i not changed, but who had iad been dropped from the 21 such pairs were formed. i lead and .FEP levels, but isked whether their children .In, clumsiness, irritability. > or no on a pre-coded form. level of activity according h of six situations was y) to 4 {severely hyperactive), .y, parents were .asked to rage, above average, or below alate tapping tests similar .dre.n living near a smelter children In both groups. No .e groups in the results of conduction velocity in the 55 control children was 54.2 m/seC, while mean velocity in the lead absorption group was 51.6 m/sec (Table 6) .* This difference was statistically significant (t = 2.58, p< 0.01 by matched-pair one-tailed t-test), Sis.cussion increased absorption of lead, defined as a blood lead level 40 ug/lOOmli7 was found in 98.8% of children living within 1,6 kilometers of the north Idaho Smelter, To our knowledge, this is the highest prevalence of increased lead uptake ever recorded among children in a community. By contrast. only 1 of 89 children in the rural control area had levels h 40 ug/lOOml (mean 21.9 ug/lOOml). This latter distribution was almost identical to that noted in previous studies of children with no known abnormal exposures to lead27,28. proximity to the smelter was found here to explain 54.9% of the total variation in blood lead values. Close correlations were found between blood lead levels and childrens' exposure to lead in air, soil, and dust; the closest correlation was with air. That finding might suggest that inhalation was the principal pathway of lead uptake near the Idaho smelter, and air lead levels near the smelter were certainly sufficient to have produced transpulmonary absorption. However, air lead exposure was computed only as a function of distance from the smelter and thus variations in individual exposure may have been eclipsed, and the correlation artefactually strengthened. * Nerve conduction data were also analyzed in the 34 original pairs (ex cluding the 21 "recombinants"). Results were 54.8 m/sec in the control group (t S.E, 0.87) and 52.8 m/sec in the lead absorption group ( S .E. 0.85). In these original groups, the difference in results was of border line significance (t = 1.69, pZS0,05 by one-tailed, matched-pair, t-test), -102- DUP040009231 Also, inhalation alone cannot have accounted for the disproportionate elevations in lead levels seen among the younger, poorer, and more highly oral children. Thus, it must be inferred that ingestion of lead particulates, often perhaps inadvertently29 , was a second important pathway of lead intake.- In' sum, then, these data indicate that the emissions of the Idaho smelter were the principal source of lead contamination in Shoshone County, and that inhalation and ingestion of lead particulates emitted by .the smelter caused the widespread increased absorption of lead which was observed in children living in communities as far as 32 kilometers firpm the smelter. The studies into the health effects of lead absorption which were conducted among children living near the Idaho smelter showed that FEP elevations and anemia were the principal hematologic consequences of lead uptake (Figure 3). These findings did not differ from those reported previously in children with increased lead intake from other sources-. A clear dose-response relationship was found between the severity of the hematologic abnormalities and the degree of lead absorption. There was no evidence for a threshold of effect. The neurologic studies provided mild evidence for an association be tween lead intake and slowing of motor nerve conduction velocity. Al though none of the children included in this analysis had clinical neurologic disease or frankly pathologic conduction velocities, there was observed in them a statistically significant dose-effect relation between conduction velocity and blood lead level (Figure 4). No threshold was evident in this effect. Conduction velocities in the control children were similar to those seen in apparently healthy children from previous studies35. The findings here are consistent with those among adults in which abnormal. slowing of nerve conduction was found in relation to occupational lead exposure3*-33. They are consistent also with a growing body pf data -103- which Indicates that a var j psychologic function may | smelters'*'33 and from < | 1 inhibition of sulfhydryl-co I ceils was the common mac tologic changes noted here emitted by the. Smelter athe mercury, or antimony, may j children was not investigat TABLE 1. Airborne lead Levs Shoshone County, Year M. 1971 . 1972 1973 1974 (Jan-Mar) * Arithmetic mean of 3 sam: DUP040009232 d for the disproportionate poorer , and more highly tion of lead particulates, ;taat pathway of lead emissions of the Idaho ition in Shoshone iarticulates emitted sorption of lead which far as 32 kilometers sorption which were slter showed that FEP ic consequences of !r from those reported am other sources1. sen the severity of the isorption. There was 5 for an association bection velocity. Als had clinical neurologic there was observed on between conduction aid was evident in Udren were similar svious studies2 3, iults in which abnormal occupational lead wing body of data which Indicates that a variety of subtle abnormalities in neurologic and psychologic function may be found in children with absorption of lead from smelters^'--'33 and from other sources3^ ~33. It may be suspected that inhibition of sulfhydryl-containing enzymes In neurons and in red blood cells vitas the common mechanism underlying the neurologic and hema- *57 tologic changes noted here" , The extent to which absorption of elements emitted by the smelter other than lead, such as cadmium, zinc, arsenic, mercury, or antimony, may have influenced these effects in the Idaho children was not investigated. TABLE 1, Airborne Lead Levels (ug/m3 air) by Distance from Smelter, Shoshone County, Idaho - 1971-1974 Year Within 3.2 Kilometers* 5S Kilometers 1971 19.72 1973 1974 (Jan-Mar) 3.9 8.6 16.1 13.2 < 1.0 <1.0 <1.0 < 1,0 ' * Arithmetic mean of 3 sampling sites at 1.4, 2,9, and 3.2 kilometers. -104- DUP040009233 I ! and experior p a in t. Shoshone County, Idaho - August, 1974 -SOl- cr p * P 5a*0 0o cr .0 to OL3Q CL to en AO CO p <4 is> to *. **-- o3 O CO to tAOO p n> orss o -P h> I 0 CO **J p o to 03 pp O CD AO to Ot O ot o> to -F* CO AO OO -O75 =5 O 5 CO -si AO *r*o0s0 JeO ft -s 73T -PJ *-* DUP04C009234 REFERENCES 1. Load: Airborne Lead in Perspective. Washington,D.C., National Academy of Sciences, Division of Medical Sciences, National .Research Council, Committee on Biologic Effects of Atmospheric Pollutants, 1972. 2. Helena Valley, Montana Area Environmental Pollution Study, U.S. Environmental Protection Agency, Office of .Air Programs, Research Triangle Park, North Carolina, Pub, No. AP-91, January, 1972. 3. Mclntire, M.S., and Angle, C.R.: Air Lead: Relation to Lead in Slgod of Black School Children Deficient in Giucose-6-Phosphate Dehydrogenase, Science 177:320-522, 1972. 4,, Roberts, T.M.; Hutchinson, T.C.; Paciga, j.; Chattopadhyay, A,; Jervis, R.E.; Van Loan, J.; Parkinson, D.K.: Lead Contamination around Secondary Smelters: Estimation of Dispersal and Accumulation by Humans. Science 186:1120-112.3, 1374. 5, Landrigan, P.J.; Gehlbach, S.H.; Rosenblum, B.F.; Shoults, J.M.," Candelaria, R,MBarthel, W.F-: Liddle, J.A.; Smrek, A.L.; Staehling, N.W; Sanders, J.F.: Epidemic Ldad Absorption near an Ore Smelter: The Role of Particulate Lead. New England Journal of Medicine, 232:123-129, i975. 6, Ordonez, B. R.; Ruiz, Romero LMora, R.: Investigaclon Epidemiologica .Sabre Niveies de Plpmp en la poblacion Infantil y en el Medio Ambiente Domiciliano de feuidad Juarez-, .Chihuahua, en Relacion con Una Fundidora de El Paso, Texas, Presented at the 33rd Annual Meeting, United States-Mexico Border Public Health Association, Los .Angeles,. ! April 6-10, 197S. 7, Oyanguren, H,, and Perez, E.: Poisoning of industrial Origin in a ' . - Community, ArOh Environ Health 13:18.5-189 1966. 8, Oliver, Sir T..: Lead Poisoning: from the Industrial, Medical, and Social Points of View. Lectures delivered at the Royal Institute of Public Health. P.B. .Hoeber, New York, 1914. 9, Dequidt, J.; Vaast, D., and Lespagnol, A.: Rlsques d'impregnation Saturnine ,au Vois inage d'uslnes de Traitement du Plomb. Pollut Atmos (Paris) 13:289-292, 1971. 10. Nordman, C.H.; "Hernberg, S,; Nikkanen, J.; Ryhanen, A.: Blood Lead Levels and Erythrocyte Delta-Aminolevulinic Acid Dehydratase Activity in People Living around a Secondary Lead Smelter. Work Environ Health 10:19-25, 1973. 11, DeRosa , E,, and Gobbato, F,: Epidemia di Saturnismo Non Professionale per Inquinamento da Effluent! Industriale. Igiene Moderns (Parma) 63:472-484, 1970. f j 12. Graovac-Leppsavic, j Senicar, L,; .Milic, |. tamiiiation of Meza ' In Proceedings of t j Health Aspects Of ! j CommJss.idn of the .E j DissemiHatibn:.of Kh | tion, pp. 685-703, j i j13. Martin, A.E.; Eairw Recent epidemiologi | origin, . .Presented a f Environment and Hee 1 14. Landrigan, P.J. ; W: Barthel, W.F.; Rose Children'With chroni ! 1975. 15. Lansdown, R.G,;.C1 H.T.; Turner, W. C ' a population study. 16. McNeil , J. L., and : ; elevated! blood lead sented alt CDC-EPAHealth. Paris, June . 17, Medical aspects of : 1971, IS. Yankel, A,J., and w ; of lead in dust, seal ; Meeting of the Pact Control Association 19, Water Quality Crite . of Sciences, Natior . Board, Committee o 20, Barthel, W.F.; Smrt i P.J.; Gehlbach, S.i i absorption determir. cial Analytical Che: , 21, Granick. S.; Sassa aminpleyuiinic acid microliter samples -involving the heme 2.2, Searle, B,; Chan, and urine by anodic 23. Klein, M.; Namer, as a source of fatal siderations , N Eng -103- DUP040009235 sn, D .C. National nces, National Research 'Spheric Pollutants, 1972, lutlon Study, U.S. Programs, Research , January, 1972, Relation to Lead in icose-6-Phosphate Chattopadhyay, A.; Lead Contamination ersal and Accumulation B.F.; Shoults, Smrek, A.L.; Staehling, on:near an Ore Smelter: irnal of Medicine, ivestigacion 'Epide.mfologica 1 y en el Medio Ambiente Relacfon con Tina Punrd Annual Meeting, sociation, Los Angeles, hduslrial Origin in a 966. striai, Medical, and he Royal Institute of iisques d'impregnation du Plomb. Poilut Atmcs Ryhanen, A,? Blood Lead old Dehydratase Activity Iter, Work- Environ itumismo Non Prpfes.sio.nale ene Modems (Parma) 12. Graovae-Leposavic, L,; Djuric, D.; Valjarevic, V.; Senicar, H.; Senicar, L.; Miiic, S.; and Delic, V.: Environmental Lead Con tamination of Meza Valley: Study on Lead Exposure of Population. In Proceedings of the international Symposium on Environmental Health Aspects of Lead, Amsterdam, Oct. 2-6, 1962 , Luxembourg, Commission of the European Communities Directorate General for Dissemination of Knowledge, Centre for Information and Documents- tion, pp, 685-703, 1973. 13. Martin, A.E.; Fairweather, F.A.; Buxton, R. St. J.; Roots, L.M,: Recent epidemiological studies of environmental lead of industrial origin. Presented at the CDC-EPA-WHO International Symposium-- Environment ar.d Healtn. Paris, June, 1974, 14. Landrigan, P.J. ; Whitworth, R.H.; Balph, R.W.; Staehling, N.W.; Barthel, W.F.;' Rosenblum, B.F.: . Neuropsychologic dysfunction in children with chronic low-level lead absorption, lancet 1:708-713, 1975. 15. tansdown, R.G.; Clayton, B.,; Graham, P.J.; Shepherd, J.; Delves, H.J.; Turner, W. p.t Blood lead levels, behavior, and intelligence, .a population study. Lancet I: 339-541, 1974. 16. McNeil, J.L,, and Ptasnik, J,A>.: Evaluation of long-term effects of elevated blood lead concentrations in asymptomatic children. Pre sented at CDG-EpA-WTlO .International Symposium--Environment and Health. Paris, June, 1974, 17. Medical aspects Of childhood lead poisoning. Pediatrics 48:464-46.8, 1971, 18. Yankel, A .J., and von Lindern, I.: Procedures employed fora study of lead in dust, soil, and the ambient ,air. Presented at the Annual ' Meeting of the Pacific Northwest International Section, Air Pollution Control Association. Boise, Nov, 1.7-19, .1974, 19. Water Quality Cxiteria-1972. Washington, D.G., National Academy of Sciences, National Academy of Engineering, Environmental Studies Board, Committee on Water Quality Criteria, 1972. 20. Barthel, W.FSmrek, A.F.; Angel, G.P.; Liddle, J.A.; Landrigan, P.J.; Gehlbach, S.H.; Chisolm, J.j,: Modified Delves' cup atomic absorption determination of lead in blood. Journal of American OffiCial Analytical Chemists 56:1252-1256, 1973. 21. Granick, S.; Sassa, S., Granick, J.L.: Assays for porphyrins, delta aminolevulinic acid dehydratase, and prophyrinogen synthetase in microliter Samples of whole Bloo^: applications to metabolic defects involving the heme pathway. Prop Nat Acad Sci USA 6,9:238.1-2385, 1972. 22. Searle, B.:; Chan, W.; Davidow, B.: Determinations of lead in blood and urine by anodic stripping voltammetry. Clin Chem 19:76-80, 1973, 23. Klein, M.; Namer, R.; Harpur, .; Corbin, R.: Earthenware containers as a source of fatal lead poisoning: case study and public health con siderations, N Engl J Med 283-669-672, 1970. / -110- Si : s 1II1 1I iI I -I ii I: I I; *? DUP040009236 Fig.I Airborne Lead Concentrations Suspended{ Particulates) by Distance and Direction from Smelter, Shoshone County, Idaho, July 1974 24. Hollingshead, A.B., and RecUlch, F.C.; Social Class andMental Illness. New York:: Jqhn Wiley and Sons, 19 58. 25. Feldman, R.G.; Haddow, J,; Kopito, L.; Schwachman, Ei.: Altered peripheral nerve conduction velocity, chronic lead intoxication in children. Am J Dis Child 125:39-41, 1973. 26. Werry, J.S.: Developmental hyperactivity. Pediatr Clin North Am, 15:581-599, 1968. 2.7. Robinson, M.J.; Karpinski, F.E., Brieger, H.: The concentration of lead in plasma, whole blood and erythrocytes of infants and children. Pediatrics 21:793-797, 1958. 28. Moncrieff, A.A.: Koumides, O.P.; Clayton, B,E.; Patrick, A.D.; Renwick, A. G. C,; Roberts, G. E.: Lead poisoning in children. Arch Dis Child 39:1-13, 1964. 29. Sayre, J.W.; Charney, E.; Vostal, J.; Pless, I.B.: House and hand dust- as a potential source of childhood lead exposure. Am J ..Dis Child 127:167-170, 1974, 30. Catton, M.J.; Harrison, M.J.G.; Fullerton, P.M.; Kazantzis, <3.: Subclinicai neuropathy in lead workers. Br Med J 2:80-82, 1970. 31. ..Seppala.inen, A.M.; Hembe.rg,'S.: Sensitive technique for detecting subclinicai neuropathy in lead workers. Br J Ind Med 29:443 , 1972. 32, Seppalainen, A.M.; Tola, S.; Bernberg, S.; KOck, B.: Subclinicai neuropathy of "s.afe" levels of lead exposure. Arch Environ Health .30:180-183, 1975. 33, Carnow, B.W., and Carnow, V.: Unsuspected community lead intoxi cation and emissions from a Smelter: The El Paso Story. Presented at the 66th Annual Meeting, Air Pollution Control.Association, Chicago, June 26, 1973. 34, Perino, j., and Ernhart, C.B.: The relation of subclinicai lead levels to cognitive and sensorimotor impairment in black pre-schoolers. J Learn Disabilities 7:26-30, 1974, 35, de la Burde, B., Choate, M.S., Jr.: Early .asymptomatic lead exposure and development at school age. J Pediatrics 87:638-642, ,1975. 36, Pueschel, S.M.; Kopito, L.; Schwachman, H.: Children with an increased lead burden, a screening and follow-up study. JAMA 222:462-466, 1972, ' 37, Millar, J.A.; Battistini, V-; Gumming, R.L.C.; Carswell, F.; Goldberg, A.: Lead and d-aminolevulinic acid dehydratase levels in mentally retarded children and in lead-poisoned suckling rats . Lancet 2:695698, 1970. f \ | 1 { I -111- DUP040009237 Si5 DUP040009238 8 8 , DO 68.80 T.T.Bjl Fig. 4 PERONEAL. NERVE CONDUCTION VELOCITY VERSUS BLOOD LEAD LEVEL, IDAHO, 1974 YfCONOUCTION VELOCITY) 64.8 ~.0X (BLOOOLEADl ir*-0.38J (n-202) i: x x ? 8 ,H 0 5 7 . CD 68.00 CONDUCTION' VELOCITY (M /i k ) 5 6 .6 0 S I.B O -16,10 30.DQ < t . i0 O.OB 15.00 30.00 45.00 60.00 ?S.00 BLOOD LEAD 30.00 105.00 - '120.00 135.00 Ao.00 | -115- A Discus sic j for Chi: | P. S. Gartside, Dept, of Environment; f Technical , Numerous data h 1childre n who were test i} ] we wish to review the -i intelligence testing by { | The data compile } proper contexts will ad I is important for the rea } pair technique in such sex differences and SEf : could, in fact, explain j gan data. As shown in | analyses have been per \ little or no difference w j In particular, we ; velocities using Gregor j and no Statistical slghi: | tailed t-test). Furthers | of all the children meas | Children had nerve cond I duction velocity range - > Aug,, *74 -- 47 mg% - 7i f duction velocity measur ; were retested using stm ; DUP040009239 EAD LEVEL, IDAHO, 1974 0.00 135.00 ?50.00 A Discussion Concerning the Significance of Results for Children Tested in The Shoshone Project P. S. Gartside, Asst. Professor, Division of .Biostatistics, Dept, of Environmental Health, University of Cincinnati Medical Center R. K. Panke, M.D., Member, Technical Steering Committee, Shoshone Project Numerous data have been accumulated on a statistical sample of children who were tested in the Shoshone Lead Project. In particular, we wish to review the neurological studies by Landrigan, et al, and the Intelligence testing by Gregory, et al. The data compiled by the Landrigan and Gregory groups, if put in proper context, will add useful knowledge to the literature. However, it is important for the reader of this material to be aware that the matched pair technique in such a situation is not without pitfalls. Age differences, sex differences and SES point discrepancies in favor of the high Pb group could, in fact, explain many of the small differences found In the Landri gan data. As shown in Table I, other matched pairing and statistical analyses have been performed on these same two groups of children and little or no difference was found. In particular, we would like to point out that nerve conduction velocities using Gregory's 50 more closely matched pairs were analyzed and no statistical significance was found (see Table II; p = 0.11 by onetailed t-test). Furthermore, examination of nerve conduction velocities of all ihe chlldren measured by Landrigan, et al, revealed that only six children had nerve conduction velocities below 45 meter/sec (nerve con duction velocity range - 37.5 m/sec - 43.0 m/sec, blood Pb range In Aug., '74 ?= 47 mg% - 74 mg%), Eight months after the initial nerve con duction velocity measurements, all six children who tested below 45 m/sec were retested using similar but different techniques at the Department of -116- i \ { I : DUP040009240 Child Neurology., University of Washington School of Medicine. All slit children were found to have nerve conduction velocities within the normal range* (NCV range = 45.1 m/sec - 72.0 m/sec, blood lead range 35 mg% 62 mg%), thereby indicating reversible nerve conduction velocity depression, or possibly technique differences or recording error in data collection. Further collection of data is planned by the Department of Health and Welfare, State of Idaho, Data are difficult to collect and analyze in a clinical Industrial setting because of the large number of cpncpmitant variables. Multiple regression analysis should be used wherever possible in future studies of this population in order to make adjustments for the effect of signifi cant concomitant variables such as age; sex; cleanliness of the home; location of residence; and Occupation, education, and intelligence status of the parents. Finally, because of the inconsistent results of data anlysis as shown above, we feel that a significant relationship between bipod lead and nerve conduction velocity has not been established. It should also be reiterated that there were no clinically anemic children. While Landrigan, et al, might correctly consider a hematocrit of less than 33% to be abnormal, many clinicians feel that a definite threshold value cannot be defined. It is more important clinically to consider changes or depression of hematocrit, since individual differences often show values below 33% in completely healthy children. The subjective and objective impressions of local medical practitioners in the Kellogg area reveal that there does not appear to be Wide-spread anemia or hematocrit depression; however, these impressions should be confirmed by further prospective studies, * Gamstorp , 1. Normal conduction velocity of ulnar, median, and peroneal nerves in Infants, children and adolescents. Acta Fed, Sunni., 146; 68, 1963, -117- jaX-a. >vo-tw- a. tu w m r-- m xn > O a vR-) Hdj -fSlpj rd-l 0 44' <T -- cr Jo** X^:'3s o <U _aa. im .01 *vVr>-) oAcS XI 3 >>W- v -.OQ-rS(0- <Q S_ > go in. *n\ <n\ S li 00{>-f SS Sf3' oiz! sc.o! *eSii SSi i== 1 2jfci oinf. S! Sf Z VOM X 3.r- i-- J3 r-- VI JA C5_ nj Vi >, T3 ` S- ttl 0;0. &i SZ QCa- <uc . uT X 3-OiX, j 3 *-- BJ . a. ior-- -a CO --. 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Cl .a 3 ST <j sa cl rs (9 .O 3 3* or Q 3 5" .<tQo CL 3a. : *3 3 <Q & TA81E X COMPARISON OF MATCHED PAIRS AND REGRiSSION_AHALYSIS SUBJECTS - - - - --'---- -j n Jh QSHONE COUNTY Matched Pairs 34 l.andrigan Maximum Age Subjects Difference for Detween Pb Regression Study Group Analysis & Control Group 11+ months Mean Age Difference Between Pb Se t Of 5iubjects Study Group Study G fdu^TControl Group & Control " M F ~ TT F' Group 7.50 vs. 18 16 18 16 7.42 ..Maximum Point Iilood Pb/NCV ilood Pb/NCV Difference on on SocioEconomic P Value p Value 1 Tailed t Regression latched Pairs Analysis Index t * 1.69 p =x o.gs Landrigan P . 0.05 Gartside Blood Pb/IQ P Value 2 Way Analysis of Variance F = .397 df * 1/66 P> .538 Gregory 1 it 20 Gregory (Recombinant) 11+ months 2l LandriganJ (Recombinant; S4 Gregory 11+ months : 11+ months 7.32 vs, 25 29 25 29 7.28 P = 0,05 Gartside F " .213 d?s.1/106 T = .650 Greqory 55 Landrigan 50 Gregory 11+ months 6.65(1.32) vs. 26 6 62(*1.37) 29 26 16 pt. oil a t 2,58 29 0-66 pt. continuum P < 0.0) Landrioan 8 pt. on a 52.4 vs. 53.S 4 months 7,29 vs.' 24 26 7.37 .24 26 11-77 pt. continuum P = 0.11 Gartside approx..5 IQ pt lower than con trols - P<.001 P=.Q38; P=.040; P=.037 Greqory 202 Landrigan 168 Graaorv 1 r 5 -0.38 t * -2.12 P 0.02 Landri qatij.IUP040009242" I...' ! Gregory -8XI-- 1t I i 1 15mco ,* ,o 1M 1 jS r!3 Jarjo iiOM te m |o!m ii *-<JCO S j! ia js ' |2m *9H ' 'iaans ' pa** 23: j XTeauojgd pua^ueTpatu 'j bi '/ | saxprqs p a t io * asaqj ' jaASMOg 'uoissaid XOU saop aiaqj jet# luaAai | 1 suofss.aiduiT QArtoafqo | U| % MO{3q sanxsA Moqs | UOTSsajdap j o saBuuqo japjsx 1 30.UUBO anjeA pjoqssjq; 931 ij %ZZ usqx ssat jo j u o q j t . 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