Document 15EvVZnQE80zR0LZzDgLaxY1E

RESEARCH AND EVALUATION Toxicity, Mutagenicity, and Teratogenicity of Lead (7.2?. Gerber, A. Leonard, and P. Jacquet. MUTATRES 1980Sep;76(2):ll$-41. Authors' summary: Environmental contamina tion by lead has greatly increased as more and more lead is used for gasoline and in various indus trial products, although severe cases of lead intoxi cation, as often seen in former times, have become rare owing to better health care. These facts have drawn attention to effects of lead which may arise, possibly without a threshold, at low exposure levels. Among the classical manifesta tions of lead intoxication are anemia and gastroin testinal, renal, and nervous symptoms. Those in the nervous system and perhaps also in the kidney may have consequences even at subclinical levels of lead exposure. Thus, the possibility that such exposure may cause mental alterations in children, induce late renal damage, or affect nerve conduc tion is now much debated. The mechanisms of action of lead on the developing central nervous system are still uncertain, They may be related to a composition between lead and calcium on the syn aptosomal level. Among the typical stochastic risks, tumors have been found in lead-intoxicated rodents, but do not seem to occur in man, and the situation with respect to genetic risks is not entirely clear. Certain effects of lead on genetic material have been observed in simple organisms, and it ap pears that lead exposure in vivo or in vitro can induce light chromosomal aberrations such as gaps and fragments. Under conditions of calcium deficiency, severe aberrations such as dicentrics may also arise; but the data, on man are controver sial because lead is almost never the only potential ly mutagenic agent to which people are exposed in an industrial environment. Nevertheless, the effi ciency of lead in causing such aberrations appears low compared with that of other mutagenic agents so that genetic effects of lead do not appear of pri mary concern for human health. Lead can prevent implantation of the embryo, delay its growth during later stages of pregnancy and, when injected during organogenesis particularly under conditions of calcium deficiency, cause malformations. The risks to the developing human organism are diffi cult to evaluate owing to the large differences in lead metabolism between man and rodent, so stud ies on species resembling man are desirable. Prenatal and Neonatal Toxicology and Pathology of Heavy Metals L. W. Chang, P.R. Wade, J.G. Pounds, and K.R. Reuhl ADV PHARMACOL CHEMOTHER 1980;17:195-231. The adverse effects of lead on the reproductive system have been well documented. The develop ing organism is especially sensitive to lead poison ing. The harmful effects of lead on the fertility and reproduction of humans as a result of occupational exposure have long been recognized. Lead readily crosses the placenta, producing an increase in blood lead levels in the fetus. Mammary transfer may pose a significant source of lead to newborns; in addition, the intestinal absorption of lead may be greatly enhanced by milk. The importance of lead as a human teratogen has not been estab lished, although spontaneous abortion in human patients as a result of high lead exposure has been reported. Evidence for these effects has been borne out by studies in rats, mice, hamsters, and other animal models. Similar results and studies are discussed for mercury and cadmium. The phe nomena of metal-metal interaction and metalelement interaction within maternal and fetal sys tems make the overall understanding of metal toxicology more complex. Metal-induced teratolo gy represents one of the most important areas in toxicology. Immunotoxicology of Heavy Metals L.D. Koller. INT J IMMUNOPHARMACOL 1980;2(4):269- 79. 19 Ts TEH 0531843 N33774 From author's conclusions: From data which have been accumulated, lead appears to consistent ly suppress most of the segments of the immune system, while cadmium has produced mixed reac tions. Mercury suppresses the primary humoral immune response, while selenium enhances humoral immunity. Zinc deficiency results in atro phy of the thymus with subsequent reduction in the humoral immune capacity. Nickel deters many segments of the immune response. Many of the other metals also compromise various parts of the immune system. This review is certainly not complete, but fit] has compiled considerable data to document the adverse effects of metals on the immune response of experimental animals. Many of these immuno suppressive features are unaccompanied by clinical signs of disease. Therefore, it is apparent that many metals are detrimental to health by mecha nisms other than direct toxicity. A chemical that impairs or destroys any portion of the immune system usually limits the defense mechanism of a host to infectious agents, thereby potentiating pathogenicity of that organism. A host that is ren dered increasingly susceptible to an infectious agent is likely to develop complications or succumb to what normally would be a nonfatal condition. Behavioral Effects of Moderate Lead Exposure in Children and Animal Models; Part 1, Clinical Studies R. Bomschein, D. Pearson, and L. Reiter. CRC CRITREV TOXICOL 1980;8(1):43- 99. From authors' conclusions and recommenda tions: A total of 22 studies were reviewed which addressed the question of the effects of moderate lead exposure on the behavioral development of children. There was no clear trend indicating that moderate lead exposure caused any abnormalities in behavioral development in children, nor was there any compelling evidence which suggested that this was not the case. A further complication with respect to these studies is that many of them had methodological deficiencies which undermined the credibility of their results. The. findings from all 22 studies appear to be contradictory and do not offer any resolution to the question of whether moderate lead exposure is a significant health hazard. The data reviewed do not permit une quivocal determination of die level at which lead exposure begins to constitute a significant health hazard, as reflected in impaired neurobehayioral development. The ideal course that needs to be taken in this area of research is to prospectively monitor lead exposure arid behavioral develop ment in large samples of children. Careful and per sistent monitoring of lead exposure should enable the investigators to more appropriately approach the controversial question of whether moderate lead exposure affects behav? ral development in children. Careful attention needs to be paid to de veloping and using a number oftests to tap discrete behavioral functions that mediate intellectual and social behavior. A rigorous neuropsychological ap proach to assessing behavioral functions should be adopted in studies as the best way of ensuring mea surement of areas of skill where deficits due to moderate lead exposure are likely to occur. A final recommendation would be for investigators to adopt multivariate research designs in approaching the study ofthis problem. Behavioral Effects of Moderate Lead Exposure in Children and Animal Models: Part 2, Animal Studies R. Bomschein, D. Pearson, and L. Reiter. CRC CRITREVTOXICOL 1980:8(2)Ml-52. From authors' critique: Clarification of the nature of the interaction between lead and behav ior has been sought through the use of animal models. Unfortunately, much of the data generated by these animal studies are of little use due to inap propriate exposure levels or the lack of control over, and systematic variation of, critical indepen dent variables known or suspected to interact with lead. However, one of the most damaging aspects of these animal studies has been a lack of a clinical perspective, both in the definition of the critical issues and in the design of studies to deal with these issues. Few animal studies adequately simu late the lead exposure conditions found in young children, either with respect to the levels of expo sure or the timing of the exposure. There is often an inadequate or nonexistent history of lead expo sure with respect to both the external and internal dose. Correlative measures of lead toxicity in other target systems, e.g., hematopoietic or renal indices, are generally absent. This makes it im possible to assess accurately the relative sensitivity of the major target organ systems in the leadexposed animal. The present data do not permit us to distinguish clearly between the effects of lead exposure on cognitive function (learning/memory) and effects on sensory-motor function, arousal, or motivation, which in turn can produce perform ance differences. Relevance of these animal data to the clinical situation and ease of interpretation of data can be increased in future studies by consider ation of the following: (1) Better documentation of internal dosage levels is needed. Blood and tissue lead levels during exposure and at the time of test ing are necessary. (2) Use of exposure protocols 20 TEH 0531844 DUP050032340 which do not produce growth retardation or the use of experimental designs which permit an evalu ation of the nature of the interaction between level of lead exposure and degree of growth retardation should be encouraged. (3) Increased numbers of litters should be included in each treatment group in order to reduce the contribution made by "litter effects," A second alternative would be to use a genetically more homogeneous test population, (4) Standard reference compounds (positive con trols) or environmental manipulations which permit an evaluation of test sensitivity should be incorporated into the experimental design. (5) In clusion of correlative indices of lead toxicity, e.g.> free erythrocyte protoporphyrin levels in blood or ALA in the urine, would aid in the extrapolation of animal data to humans. Concentrations of Lead in the Tissues of Children P.S. Barry, BR J IND MED 1981 Feb-,38 (1):61- 71. Author's abstract: T,wenty-four different tissues from 73 children and infants, including still births, were analyzed for lead content. In the youn gest group of 49 infants aged under 1 year, includ ing 14 stillbirths, the mean, concentrations of lead in their soft tissues were all less than 0.3 ppm and nearly all were less than the concentrations found in the soft tissues of older children or of adults. The mean concentrations of lead in the bones in the infant group were greater than in their soft tissues, but still less than 1 ppm, and were 10-40 times less than in bones of adults and about 3 times less than in the bones of older children, Lower concentrations of lead were observed in the tissues of stillbirths than in those of neonatal live births, at a 95% level of significance by analysis of variance. In 24 children aged 1-16 there was no clear evidence of increase oflead concentrations in the bones with increasing age; neither Was there evidence of a difference in the concentrations of lead in types of bone. Although the mean concen trations in the bones were greater in the children aged 1-16 than in those of infants aged under 1 year, the data did not suggest that a progressive ac cumulation of lead occurred in the bones, [until] probably [at about] the end of the second decade of life, by winch time the growing phase will be nearing completion. In 18 children aged 1-9 and in 6 children aged 11-16 the concentrations oflead in the soft tissues were similar, and comparable with those observed in women. The ratio differences between ash-weight and wet-weight measurement in the different types of bone in children did not differ proportionately from the adult ratios, sug gesting a similarity in the patterns of deposition of lead in bone, irrespective of age. No differences in tissue lead concentrations by sex were observed in the infant group of children. Or when the concen trations in the tissues were related to the years in which the samples were obtained. Individual tissues showed different concentrations and pat terns of distribution of lead, which were skewed more towards low values in the infant group than in older children. The results of other studies, of which there have not been many, were found to be in general agreement with those reported here. The exposure of infants to lead appeared to be less than in older children or in adults, probably for rea sons associated with lack of availability and paren tal care. In Vivo Determination of bead in the Skeleton after Occupational Exposure to Lead L. Ahlgren, B, Haeger-Aronsen, S, Mattsson, and A. Schutz. BR J IND MED 1980 May;37(2): 109-13. Authors' abstract: The concentrations of lead in the phalanges and in the blood were determined in 22 subjects who had formerly been exposed to lead in a storage battery plant, which had been closed for 7 years. The bone lead concentration was mea sured in vivo by using an X-ray fluorescence tech nique in which two 57Co y-ray sources were used for generating the characteristic X-rays of lead, which were measured with a Ge(Li) detector. In three subjects the variation of the lead concentra tion along the forefinger was measured together with the lead concentration in the tibia. The mea sured lead concentrations in the phalanges were between 20 pg/g (our detection limit) and 118 jug/g. The lead concentration in the phalanges was found to increase with the length of employment, but no simple relation was found between the lead concentrations in the blood and in the phalanges. The decrease in the blood lead concentration after the cessation of exposure was followed in four sub jects. Seven years after exposure had ended, the blood lead concentration was found to be more dependent on the daily intake of lead than on the release of lead from the skeleton. These experi mental results could be explained by a twocompartment model using exchange rates given in publications. This model has also been used to cal culate the blood lead concentration that could be achieved after a sudden release of lead from the skeleton. The Distribution of Lead in Human Teeth, Using Charged Particle Activation'Analysis T. Al-Naimi, M-I- Edmonds, and J.H. Eremlin. PHYS MED BIOL 1980 Jul;23(4):719-26. 21 TEH 0531845 DUP050032341 Authors' abstract: A technique has been devel oped to measure lead content in teeth by using 3He*+ activation analysis. The -activity produced in the teeth is recorded on plastic film alpha-track detectors (LR-I15) and compared with the activity produced by the lead contained in standard glass. The concentration in teeth from three areas of the United Kingdom has been determined as a func tion of age. The lead content is found to increase with age in dentine and pulpal dentine, but not in enamel. A Nuclear Microprobe Investigation of Heavy Metal Distribution in Individual Osteons of Human Femur ULindh. INTJAPPL RADIAT1SOT1980 Dec; 31(12):737-46. Author's abstract: The analytical capacity of charged-particle induced interactions for assess ment ofmulti-element distributions in mineralized tissue was explored in autopsy sections of human femur. The PIXE {particle-induced X-ray emission spectroscopy] technique was employed in a nuclear microprobe with 2.5 MeV protons. Comparison of the standard method approach and the direct utili zation of analytical formulae was performed. De tection limits of a few ppm were attained for some elements, and the positional resolution was 20 fim. The analytical errors did not exceed 15%. Concentration gradients of lead and zinc resulting from occupational exposure were dearly estab lished within individual osteons ofthe femur. Role of Altered Herne Synthesis in Lead Neurotoxicity E.K. Silbergeld and J.M. Lamon. JOM 1980 Oct;22(10):680-4. Authors' conclusions: The effects of lead on heme synthesis can be assodated with the accumu lation of possibly neuroactive precursors or deple tion of heme for nonhemoglobin metabolism, or both. These consequences provide support for the following conclusions: (1) increased aminolevulin ic add (ALA) associated with lead exposure may represent not only an accessible indicator of lead exposure, but also the presence of increased pro duction of a potential neurotoxin; (2) The inhibi tion of heme synthesis produced by lead may have functional significance for heme-dependent pro cesses (hemoproteins) other than red cell hemoglobin; (3) The relationship of lead absorp tion, or of tissue lead concentrations, to these phe nomena is unclear and requires further research; (4) The possibility that altered heme metabolism may be responsible for the neurotoxic manifesta tions of lead poisoning may provide an explanation of the well-described neurological similarities be tween lead poisoning and the acute attack forms of porphyria. High Affinity of Lead for Fetal Hemoglobin C.N. Ong and W.R. Lee. BR JIND MED 1980 Aug;37(3):292-8. Authors' abstract: In vitro experiments using ^Pb were performed to identify lead-binding components in human hemoglobin. Sephadex A-50 ion-exchange chromatography of hemolysate showed that different types of hemoglobin had dif ferent affinities for lead. For the hemolysate from adults, lead was present in both Hb A (a2 /82)and HB Ag Oxg S2). In the hemolysate from newborn infants, the hemoglobin of fetal origin, Hb F (a y2), showed a much greater affinity for ^Pb than the adult hemoglobin, Hb A (<x2 02), obtained from maternal blood. Analysis ofthe 203Pb-labelled hemoglobin suggested that about 82% of M3Pb was in the globin polypeptide. Further analysis with carboxylmethyi (CM) cellulose chromatography in dicated that the y globin of fetal origin had a higher affinity for a3Pb than the fi globin, whereas a globin appeared to be unimportant in lead bind ing. The results of the different affinities for lead of different Hb types are discussed with regard to the effect oflead upon hemoglobin synthesis. Simultaneous Quantitation of Zinc Protoporphy rin and Free Protoporphyrin in Erythrocytes by Acetone Extraction D. Hart and S. PiomeUi. CLIN CHEM 1981 Eeb;27(2):220-2. Authors' abstract: Erythrocyte protoporphyrin content is increased in several human and veteri nary disorders in which heme synthesis is disrupt ed. The nature of the defect determines whether zinc protoporphyrin, or unchelated (free) proto porphyrin, or both, are present in the erythrocytes. Extraction of the protoporphyrin into acetone/wa ter (80/20 by vol) is a simple, rapid technique by which each protoporphyrin species is delivered into solution without zinc being removed from zinc protoporphyrin. The ratio ofzinc protoporphy rin to total protoporphyrin concentration correlat ed significantly with the ratio of fluorescence emis sion intensities at the zinc protoporphyrin peak and at an isosbestic point. This concentration ratio may be used with a quantitative measure of total erythrocyte protoporphyrin to define the absolute zinc protoporphyrin and free protoporphyrin con tent of erythrocytes. 22 TEH 0531846 Quantitative Assay of Erythrocyte "Free" and Zinc-Protoporphyrin: Clinical and Genetic Stud ies S. Schwartz, B. Stephenson, D. Sarkar, H. Freyholtz, and G, Ruth. INT J B10CHEM 1980; 12(5-6);!053-7, Authors' summary: An improved extraction procedure and two flcorimetric techniques have been developed for the quantitative assay of "free" and Zn-protoporphyrin in circulating ery throcytes. Sources of error (including nonspecific fluorescence and diminished fluorescence due to absorbance of exciting light) can be essentially eliminated, especially through analysis of second derivative fluorescence spectra. As an alternative, the content of the two forms of protoporphyrin can be determined by noting the magnitude and relative intensity of fluorescence before and after acidification to remove any bound zinc. The con centration of "free" protoporphyrin was elevated specifically in acute Pb poisoning, in bovine (heter ozygous) carriers of the protoporphyria trait , and in groups of renal patients undergoing dialysis. Many of the latter also showed appreciable amounts of Zn-coproporphyrin. Though the "free" protoporphyrin comprised an average of only 7%-10% of file total in normal humans, it usu ally constituted 25% or more of the total in normal cows, rats, rabbits, and dogs. New Method for Liquid-Chromatographic Mea surement of Erythrocyte Protoporphyrin and Coproporphyrin M. Salmi and R. Tenhmen. CLIN CHEM 1980 Dec;26(13):1832-5. Authors' abstract: We describe a "highpressure" liquid-chromatographic method for separating all the porphyrins in the heme bi osynthetic pathway. The preliminary extraction and purification method is such that only eryth rocyte porphyrins with fewer than five carboxyl groups, which include protoporphyrin and the much smaller amount of coproporphyrin present, are measured. The porphyrins extracted from erythrocytes are chromatographically separated by use of a simple eluent system and fluorometrically detected. "Ultra-Clean" isotope Dilution/Mass Spectrometric Analyses for Lead in Human Blood Plasma indicate That Most Reported Values Are Artificially High /. Everson and C.C. Patterson. CLIN CHEM 1980 Oct;26(11);1603- 7 Authors' abstract: We measured lead concen trations in venous blood plasma from two subjects, one having a typical exposure and the other a high exposure to lead. Our preliminary data, obtained by isotope dilution/mass spectrometric techniques in an ultra-clean laboratory, show lead concentra tions of 0:02 fig/l and 2 pgj\, respectively, in their blood plasma, and 110 pgR and 800 pgh, respec tively, in samples of whole blood. These results in dicate that plasma lead concentrations previously reported have been overestimated by a large factor and that further improvements in analytical proce dures are needed in most laboratories before data on lead concentrations in blood plasma can be properly interpreted. Our preliminary data indicate a positive correlation between lead intake and lead concentrations in blood plasma. Lead in Bone. I. Direct Analysis for Lead In Milli gram Quantities of Bone Ash by Graphite Fur nace Atomic Absorption Spectroscopy L.E. Wittmers, Jr., A. Alich, and A.C. Avfderheide. AM J CLIN PATHOL 1981 Jan;75(l):80-5. Authors' abstract: A method for direct lead content analysis of milligram quantities of bone ash by flameless atomic absorption spectroscopy is described. Bone ash (25 mg) is dissolved with HNO* and diluted with HaO and La^ (1,000 pg/ml) solution. Lanthanum ion is used to sup press matrix interferences possibly arising in part from sulfate components of the bone ash. Two bulk bone samples (about 14 and 60 pg Pb/g ash, respectively) were used to determine daily, witbinday, and overall variability of the method. Values for "low lead" bone samples were 14.08 1.74 (SD) pg Pb/g ash and for "high lead" bone sam ples were 60.85 5.24 (SD) pg Pb/g ash. The overall value of 58 lead recovery determinations from bone ash analysis was 103.5% 12.9% (SD). These values compare favorably with results pre viously reported for gram amounts ofsample. Abnormal Distribution of Lead in Amyotrophic Lateral Sclerosis--Reestimation of Lead in the Cerebrospinal Fluid S. Conradi, L.O. Ronnevi, G. Nise, and O. Vesterberg. JNEUROL SCI 1980 Dec;48(3):413-8. Authors' abstract: The lead concentration in CSF [cerebrospinal fluid] was determined by flameless atomic absorption spectrophotometry in 16 ALS [amyotrophic lateral sclerosis] patients and 22 control cases. The mean values were 0.69 23 TEH 0531847 < -v-r j:;-: V:: ' :r:r::':v:;: : DUP050032343  0,55 (ALS) and 0*41 0.37 (controls), p < 0.01. This confirms our earlier findings of raised CSF lead levels in ALS, but the present values are lower than previously reported for both ALS pa tients and controls. The Percutaneous Absorption of Lead-203 in Humans from Cosmetic Preparations Containing Lead Acetate, as Assessed by Whole-Body Counting and Other Techniques M.R. Moore, P.A. Meredith, W.S. Watson, D.J. Sumner, M.K. Taylor, and A. Goldberg. FOOD COSMET TOXICOL 1980 Aug;18(4):399-405. Authors' abstract: The percutaneous absorption of lead from two hair-darkening cosmetic prepara tions containing lead acetate has been measured by radioisotopic tracer techniques, using lead-203 ace tate, in eight normal human male subjects. Spiked preparations were applied in fluid and dried forms to each subject's forehead (with periods of 1 month between each-application). The quantity of lead absorbed was calculated from blood counts, whole-body Counts, and urine radioactivity. Re sults were normalized for each subject by adminis tration of an IV tracer dose of lead-203 chloride, from which absorption was calculated. It was found that absorption of lead through the skin was essentially zero, with results ranging between 0 and 0,3% of the dose applied to whole skin. Slight absorption was found when the skin was broken. The potential hazard of the use of such cosmetic preparations is therefore considered to be insignificant. i" r i!': 24 DUP050032344 SELECTED BIBLIOGRAPHY "Ahlgren L, Haeger-Aronsen B, Mattsson S, Schutz A: In vivo determination oflead in the skeleton after oc cupational exposure to lead. BR J IND MED 1980 May;37(2):109-13. "Ai-Naimi T, Edmonds MI, Fremlin JH: The distribu tion of lead in human teeth, using charged particle activation analysis. PHYS MED BIOL 1980 Jul; 25(4):7l9-26. Arutjunov VD, Batsura ID, Gribova IA, Kruglikov GG: Scanning electron-microscopic and light-optics investigations of erythrocytes in toxic anemia. BR I IND MED 198.1 Feb;38(l):72-5. "Barry PS: Concentrations oflead in the tissues of child ren. BR JIND MED 1981 Feb;38(l):61-71. Bernard A, Reels HA, Buchet JP, Lauwerys RR: Com parison, by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, of urinary'proteins excreted by workers exposed to cadmium, mercury or lead. TOXICOL LETT 1980Mar;S(3-4):219-22. "Bomschein R, Pearson D, Reiter L: Behavioral effects of moderate lead exposure in children and animal models: part 1, clinical studies. CRC CRIT REV TOXICOL 1980;8(l):43-99. "Bomschein ft, Pearson D, Reiter L: Behavioral effects of moderate lead exposure in children and animal models: part 2, animal studies. CRC CRIT REV TOXICOL l980;8(2):101-52. "Chang LW, Wade PR, Pounds JG, Reuhl KR: Prenatal and neonatal toxicology and pathology of heavy metals. ADV PHARMACOL CHEMOTHER 1980; 17:195-231. Chiba M, Ogihara K, Kikuchi M: Effect of a lead on leu cine aminopeptiadase activity in human blood. IND HEALTH 1980;18(l):S5-7. "Conradi S, Ronnevi LO, Nise G, Vesterberg O: Abnor mal distribution of lead in amyotrophic lateral sclero sis--reestimation of lead iln the cerebrospinal fluid. J NEUROL SCI 1980 Dec;48 (3) :413-8. "Everson J, Patterson CC: "Ultra-clean" isotope dilu tion/mass spectrometric analyses for lead in human blood plasma indicate that most reported values are ar tificially high. CLIN CHEM 1980 Oct;26 00:1 <503-7. Fischer AB, Skreb Y: Cytotoxicity of manganese for mammalian cells in vitro--comparisons with lead, mercury and cadmium. ZENTRALBL BAKTERIOL (B) 1980;171 (6)525-37. Form A: Chromosomal effects of lead: a critical review. REV ENVIRON HEALTH 1980; 3 (2) :113-29. "Gerber GB, Leonard A, Jacquet P: Toxicity, mutagen icity and teratogenicity of lead. MUTAT RES 1980 Sep;76(2):115-41. "Hart D, Piomelli S: Simultaneous quantitation of zinc protoporphyrin and free protoporphyrin in eryth rocytes by acetone extraction. CLIN CHEM 1981 Feb;27(2);220-2. "Roller LD: Immunotoxicology of heavy metals. INT J IMMUNOPHARMACOL 1980,2(4) :269-79. Lalit BY, Ramacbandran TV, Rajan S: Lead-210 content of food samples in India. RADIAT ENVIRON BIOPHYS I980;18(l):13-7. "Lindh U: A nuclear microprobe investigation of heavy metal distribution in individual osteons of human femur. INT J APPL RADIAT ISOT 1980 Dec; 3l(l2):737-46. Moore MR, Graham DJ: Monopyrroles in porphyria, psychosis and lead exposure. INT J BIOCHEM 1980; 12 (5-6) :8 "Moore MR, Meredith PA, Watson WS, Sumner Dj, Taylor MK, Goldberg A: The percutaneous absorption, oflead-203 in humans from cosmetic preparations con taining lead acetate, as assessed by whole-body count ing and other techniques. FOOD COSMET TOXICOL 1980 Aug; 1:8 (4) :399-405. ' Morava E, Gergely A: Recent problems with lead and cadmium. BIBLNUTR DIETA 1980;29:39-47. 25 "Abstracted TEH 0531849 ffRllllllllll!IlP DUP050032345 1 :igif O'Flaherty EJ, Hammond PB, Lemer SI, Hanenson IB, *Schwartz S, Stephenson B, Sarkar D, Freyholtz H, fitt Roda SM: The renal handling of delta-aminolevulinic Ruth G: Quantitative assay of erythrocyte "free" and acid in the rat and in the human. TOXICOL APPL zinc-protoporphyrin: clinical and genetic studies. PHARMACOL 1980 Sep 30;55(3):423-32. ij INTJBIOCHEM 1980; 12(5-6) :10S3-7. if *Ong CN, Lee WR: High affinity of lead for fetal hemoglobin. BR j IND MED 1980 Aug;37(3) :292-8. Silbergeld EK, Lamon JM: Role of altered heme synthesis in lead neurotoxicity, JOM 1980 Oct;22(10):680-4. Pleban PA, Kerkay J, Pearson KH: Polarized Zeeman- effect flameless atomic absorption spectrometry of cadmium, copper, lead, and manganese in human kidney cortex. CLINCHEM 1981 Jan;27(l);68-72. Valentine WN, Paglia DE: Erythrocyte disorders of purine and pyrimidine metabolism. HEMOGLOBIN 1980;4(5-6);669-81. i J'ii Rockley MG, Davis DM, Richardson HH: Fourier- transformed infrared photoacoustic spectroscopy of Wittmers LE Jr, Alich A, Aufderheide AC: Lead in biological materials. SCIENCE 1980 Nov 21; bone. I. Direct analysis for lead in milligram quanti 210 (4472) :918-20. ties ofbone ash by graphite furnace atomic absorption spectroscopy. AM j CLIN PATHOL 1981 Jan; *Salmi M, Tenhunen R: New method for liquid- 75(l):80-5 chromatographic measurement of erythrocyte proto Yunis AA, Salem Z: Drug-induced mitochondrial porphyrin and coproporphyrin. CLIN CHEM 1980 damage and sideroblastic change. CLIN Dec;26(13):1832-5. HAEMATOL 1980 Oct;9(3):607-19. I DUP050032346