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vM li' DIAGNOSIS AND SCREENING What Happens in Lead Poisoning? W.R. Lee. JR COLL PHYSICIANS LOND1981 Jan;15(1):48-54, j From author's discussion: This article deals with some of the features of clinical lead poisoning. The subject is confusing, because much has been written, particularly in the occupational medicine journals, about the effects ofincreased lead absorp tion without the development of clinical symp toms. Quite a small intake of lead may produce detectable biochemical or even neurophysiological changes, and it is difficult, if not impossible, to decide when these changes are simply an adapta tion to an increased intake of lead and when they indicate early poisoning. When a patient moves from symptomless "increased lead absorption" to lead poisoning, symptoms generally follow in a cer tain sequence. Lassitude is the first to appear, often followed by aching in joints and in limb mus cles and by abdominal colic. Among biochemical changes is an increased urinary excretion of amino levulinic acid and of coproporphyrin III. Motor nerve conduction velocity is often reduced, even since the neurologic syndrome has an insidious onset and then shows a sudden transition to overt and irreversible clinical intoxication. Additionally, the less obvious neuropsychological consequences that occur at lower levels of exposure can be pre vented only if excessive lead intake is detected and the child is removed from the source of lead. Care ful neurologic examination and the measurement of the blood lead level should allow early diagnosis. But the more subtle neurologic abnormalities are difficult to detect in any individual child, and, when the neurologic examination is clearly abnor mal, it is usually too late to prevent permanent damage. Blood lead level is difficult to determine, expensive, and available only in highly specialized laboratories; moreover, both day-to-day variations in analytical results and environmental contamina tion of samples may diminish the reliability of the method. For these reasons, the diagnosis of lead poisoning rests, at least at the screening level, on the detection of abnormalities of heme synthesis, for which precise and extremely sensitive micro chemical tests are available. in symptomless lead workers. The most frequently used diagnostic test for lead poisoning is the mea surement of blood lead, which is limited by its poor discriminatory value. The most useful hy pothesis for interpreting these results is to assume Lead Poisoning in Children A.H. Drummond, Jr. J SCH HEALTH 1981 Jan;51(l):43- 7. that the lead level in the circulating blood reflects not only the body burden of lead, but also the af finity for lead ofthe globin chains. The purpose of this article is to acquaint school health personnel with the dimensions of the lead poisoning problem. In a recent screening conduct ed by the Centers for Disease Control, some 7,950 Laboratory Diagnosis of Lead Poisoning of 116,668 children tested showed lead toxicity. In S, Piomelli and J. Graziano. PED1ATR CLIN addition to these unsuspected cases, from 12,000 NOR THAM 1980;2 7(4):843-53. to 16,000 children are treated each year nationwide for lead poisoning; about 200 of these children die. From authors' introduction: Because lead Nearly all the tissues of a child's body are affected poisoning :in childhood is almost jdways the result by lead poisoning, but the greatest effects are on of chronic exposure to lead, a laboratory,diagnosis the brain and nervous system. The early symptoms can usually be made long before overt clinical dis are often overlooked or misinterpreted. A correla ease develops. It is important to detect childhood tion has been reported between blood lead levels j lead poisoning before it becomes symptomatic. and behavior, progress in learning, and level of ac- 8 TEH 0531832 N33772 tivity in outwardly normal children. Recent re search suggests that there may be no safe threshold Sl f level of lead in a child's body below which there are no harmful effects. Several methods are recom' ! mended to detect children with lead toxicity and to reduce lead in the environment. i Riposte to "Environmental Lead and Young Children" (Editorial) F.J. Coodin, C. Dawes, G- W. Dean, P.R. Desjar dins, and J.B. Sutherland. CAN MED ASSOC J 1980 Sep 20;123(6):469- 71. In most environments it is difficult to determine the route of intake--inhalation or ingestion--of lead. Airborne lead may be inhaled or may settle pn food and he ingested; lead in dirt may be ingest ed or may be resuspended as dust and inhaled. Children are not only more susceptible than adults to the deleterious effects of lead; but also, because of their physical charact eristics and their tendency to put various objects in their mouths, children are likely to ingest more extraneous lead. A problem in the quantitation of lead pollution is the difficulty of accurately measuring blood lead levels. Because blood lead concentrations provide an indication of current or recent levels of exposure only, one in vestigator suggests measuring lead concentrations in bones or teeth to adequately assess the long term effects of environmental lead exposure. Impact of Community Screening on Diagnosis, Treatment, and Medical Findings of Lead Poison ing in Children J. Schneider, B. Aurori, L. Amend, and D. Soltanoff. PUBLIC HEALTH REP 1981 Mar-Apr; 96(2):143- 9. From authors' conclusion: Review of the medi cal records of 525 children diagnosed as lead poi soned during 5 years indicates that a citywide lead poisoning prevention program has resulted in a de crease in the number of children with lead-induced seizures and with central nervous system involve ment, as well as a decrease in the mean whole blood lead concentrations (PbB's) in symptomatic children. However, the large number of multiple treatment episodes suggests a serious problem of re-poisoning because lead was not eradicated from the children's environments. The high proportion of children with PbB's of 40 jxg/dl or greater indi cates that the program has had a limited impact on the incidence of elevated blood lead levels. Find ings of this study indicate that, although extensive screening and clinical follow up are effective in pre venting the more serious aspects of lead poisoning, they do not address the issue ofprevention. Pica Patterns, Toxocariasis, and Elevated Blood Lead in Children L.T. Qlickman, I.U. Chaudry, J. Costantino, F.B. Clack, R.H. Cypess, and L. Winslow. AM J TROPMED HYG1981 Jan;30(l):77-80, Authors' abstract: Blood samples were obtained during a lead screening program from 100 children aged 1-6 years in Allegheny County, Pennsylvania, to determine whether there was any association be tween specific forms of pica and infection with Toxocara canis, the principal Cause of visceral larva migrans in the United States, or elevated blood lead levels. Significant associations were found be tween: (1) feces, soil, or grass pica and Thxocara in fection; (2) paint or plaster pica and elevated blood lead; and (3) dog ownership and Toxocara infection. These findings suggest that an accurate pica history may be useful in identifying potential health problems in children. The Relationship between Zinc Protoporphyrin (ZPP) and "Free" Erythrocyte Protoporphyrin (FEP) in Lead-Exposed Individuals V. Karacic, D. Prpic-Majic, and S. Telisman. INT ARCH OCCUR ENVIRON HEALTH 1980; 47(2):165- 77. Authors' abstract: The relationship between zinc protoporphyrin (ZPP) and total erythrocyte protoporphyrin, measured as "free" erythrocyte protoporphyrin (FEP), was determined in 194 adult subjects with different occupational and nonoccupational lead exposures. Furthermore, the ZPP-FEP comparison was considered with respect to the dose-effect relationship of ZPP and FEP with blood lead (PbB) for males and females, re spectively. Bilirubin (Bil.) interferences in ZPP analysis were taken into account. A very dose and highly significant relationship (r=0.962, p < 0.001) was established between ZPP and FEP values. A significant correlation (p < 0.001) be tween log ZPP or log FEP and PbB (males, r = 0.767 and 0.718; females, r = 0.525 and 0.405) was also found. It was established, by both in vitro and in vivo studies, that Bil. interferes with the ZPP fluorescence readings; the relationship be tween "false" positive ZPP concentrations and Bil. concentrations (in vitro, r ** 0.987; in vivo, r -- 0.903) was highly significant (p < 0.001). A small but highly significant (r = 0.948, p < 0.001) in fluence of increased carboxyhemoglobin (COHb) concentrations on the decrease in hematofluorometer ZPP readings, due to inadequate oxygena tion of the blood, was found. The results obtained confirm the usefulness of ZPP determinations using hematofluorometers for surveillance of in- 9 TEH 0531833 DUP050032330 employed. The standard addition method was used to minimize the matrix effects of whole blood. The ASV results correlated well with those obtained by flameless atomic absorption analysis. The methods are simple, reliable, and suitable for applications in the clinical field. The procedure "** using the Charge Transfer Analyzer is recommend ed because of its sensitivity and rapidity. Screening for Lead Absorption C.R. Comm, L. Garcia, Jr., and J.D. Repko. OCCURHEALTHSAF1981 Mar;5Q(3):8-12. Recent attention in occupational medicine to the neurological consequences of industrial lead exposure has led to the development of a method of partial antidromic blocking to determine the conduction velocity of the slower nerve fibers of the ulnar nerve. Since the slower conducting fibers of peripheral motor nerves are thought to be sus ceptible first to damage in neuropathies induced by absorption of lead, this technique appears to be ap propriate for detecting subclinical nerve damage in individuals without clinical neurological symptoms. The described technique and equipment for neu rological surveillance of workers could provide re sults conclusive enough to warrant removing an employee from ajob. University Conducts Lead Exposure Study Anonymous. OCCUR HEALTH SAF 1981 Feb; 50(2):36-7. The nervous system is particularly vulnerable to the toxic effects of certain heavy metals. In some industries, workers are unwittingly exposed for long periods of time before clinical manifestations are noted. Chronic low-level exposures may go un recognized. The Department of Neurology at Boston University School of Medicine has detected subclinical damage among industrial workers and schoolchildren exposed to lead and other neuro- toxins by using sensitive neurophysiological tephniques that measure the speed at which an impulse travels along a nerve. A research team is conduct ing a case-control study among 112 workers at a lead foundry and a valve manufacturing company, which are located on the same grounds. Previous studies have found adverse physiologic, neurologi cal, and psychological reactions among children and adults who had been exposed to even low doses of lead over a period of time in their homes or industrial environments. For example, behavioral disturbances were eight times more fre quent in children exposed to lead than in children in a control group. These studies will contribute to the development of a protocol that codld have broad application in the evaluation of occupational exposure to all neurotoxins. Subclinical Effects of Chronic Increased Lead Absorption -- A Prospective Study. III. Neurolog ic Findings at Followup Examination G.H. Spivey, R.W. Baloh, C.P. Brown, B.L. Brody, D.S. Campion, J.L. Valentine, D.E. Morgan, and B.D, Culver. JOM 1980 Sep;22(9):607-12. Authors' abstract: Neurologic examination, nerve conduction testing, and electrO-oculographic testing have been performed at a baseline examina tion and a followup examination in a group of lead workers with blood lead levels predominantly be tween 60 and 80 /ng/dl and in a group of control workers. A statistically significant decreased saccade accuracy measurement in the lead workers compared with the controls was found at both examinations. No other simple test or pattern of findings differentiated between the lead workers and the controls, and the biological significance of the lower saccade accuracy is not clear. Nerve con duction measurements do not appear to be a satis factory method of detecting subclinical neurologic effects oflead exposure. 11 TEH 0531835 ,"iiv. t -1*? ,.i*iy`pr jg1r. ~ -wTM DUP050032331 v.5 SELECTED BIBLIOGRAPHY Anonymous-. Occupational lead poisoning (editorial). 'Lee SW, Meranger JC: Direct methods for the determi MED J AUST 1980 Sep 20;2(6):297-8. nation of lead in whole blood by anodic stripping vol tammetry. AM J MED TECHNOL 1980 Dec;46 'Anonymous: University conducts lead exposure study. (12):8S3-7. OCCUP HEALTH SAF1981 Feb;50(2):36-7. 'Lee WR: What happens in lead poisoning? J R COLL Batuman V, Maesaka JK, Haddad B, Tepper E, Landy PHYSICIANS LOND 1981 Jan;15(l):48-54. E, Wedeen RP: The role of lead in gout nephropathy. N ENGL J MED 1981 Feb 26;304(9):520-3. 'Piomelli S, Graziano J: Laboratory diagnosis of lead poisoning. PEDIATR CLIN NORTH AM 1980; Chopra A, Handa F, Sidhu KS: A spectrophotometric 27(4):843-53. assay of blood porphyrins in Punjabis--a pilot study. INDIAN J MED RES 1980 Jun;71:970-4. Reif MC, Constantiner A, Levitt MF: Chronic gouty nephropathy: a vanishing syndrome? (editorial). N 'Coodin FJ, Dawes C, Dean GW, Desjardins PR, Su ENGL J MED 1981 Feb 26;304(9):535-6. > : therland JB: Riposte to "Environmental lead and young children" (editorial). CAN MED ASSOC J Sachs HK: The evolution of the radiologic lead line. 1980 Sep 20;123(6):469-71. RADIOLOGY 1981 Apr; 139(l):81-5, 'Corum CR, Garcia L Jr, Repko ID: Screening for lead 'Schifman RB, Finley PR: Measurement of near-normal absorption. OCCUP HEALTH SAF 1981 Mar; concentrations of erythrocyte protoporphyrin with the 50(3):8-12. hematofluorometer: influence of plasma on "front- surface illumination" assay, CLIN CHEM 1981 Jan; de Silva PE, Donnan MB: Blood lead levels in Victorian 27(0:153-6, children. MED J AUST 1980 Sep 20;2(6):315-8. 'Schneider J, Aurori B, Armenti L, Soltanoff D: Impact 'Drummond AH Jr: Lead poisoning in children. J SCH of community screening on diagnosis, treatment, and HEALTH 1981 jan;51(l):43-7. medical findings of lead poisoning in children. PUBLIC HEALTH REP 1981 Mar-Apr;96(2):143-9. 'Glickman LT, Chaudry IU, Costanfipo J, Clack FB, Cypess RH, Winslow L: Pica patterns, toxocariasis, 'Spivey GH, Baloh RW, Brown CP, et al: Subclinical ef 1),. ! and elevated blood lead in children. AM J TROP fects of chronic increased lead absorption--a prospec MEDHYG 1981 Jan;30(l):77-80. tive study. EOt. Neurologic findings at followup exami nation. JOM 1980 Sep; 22(9) :607-l 2. 'Karacic V, Prpic-Majic D, Telisman S: The relationship between zinc protoporphyrin (ZPP) and "free'' eryth Zuniga-Charles MA, Gonzales-Ramirez JD, Molina- rocyte protoporphyrin (FEP) in lead-exposed indi Ballesteros G: Erythrocyte protoporphyrin IX as a diag viduals. INT ARCH OCCUP ENVIRON HEALTH nostic and therapy evaluating tool in lead poisoning. 1980;47(2):165-77.* ARCH ENVIRON HEALTH 1981 Jan-Feb;36(l): 40-3. *La Brecque JJ: The determination of free erythrocyte porphyrins (FEP) by a semi-automated fluorometric 'Zygowicz ER, Hollebone BR, Perkins HM: Use of technique, ACTA CIENT VENEZ 1978;29(6): magnetic circular dichroism spectroscopy for biologic 479-81. monitoring of occupational exposures to toxicants. CLIN CHEM 1980 Sep;26(10):1413-8. 'Abstracted gfffgggp- 12 TEH 0531836 DUP050032332