Document 6bVjkX32NE3LYDdpqdRmkvzQm

A REPORT OF RECENT HELICAL STUDIES OF FIVE U.S. LEAD PLANTS National laattoTfU %$& I"? v Department pf Health, Education, and Keifaxe l March 1977 L Vrtto.ia'ia^'affetWf \ V \ N 30680 ?C DUP040013312 _ 04-0005-0471 ssaa . 2 Epidemiologic studies conducted in l75-76 in 5 different lead plants across the XJ.S. have shown unacceptably high blood lead levels and symptoms of lead poisoning in every plant studied. Hema tologic, neurologic, and renal damage due to lead were also encountered, inappropriate medical practices were noted including the misuse of oral chelating drugs and allowing lead-poisoned workers to continue to be ex posed to lead during chelation therapy. The usefulness of monitoring blood lead and/or protoporphyrin levels as indicators of lead toxicity was clearly shown by the high degree of correlation between these measurements and the. signs and symptoms of lead toxicity. The newly developed portable method of zinc protoporphyrin (Z.P?) "J determination was shown to be a promising method of screening lead-exposed worker s. In several locations, home contamination with lead dust from lead plants resulted in lead absorption and in one location lead poisoning among workers' children. These studies illustrate the importance of good work practices which*in addition to minimising worker exposure,will minimize exposure to his family. Chronic neurologic and renal effects of lead exposure were demonstrated in this study, neuropathy was noted at a relatively low blood lead level (8;lug/100ml) and after only 2 months of exposure. Abnormal glomerular function (elevated blood urea nitrogen and creatinine levels and de creased glomerular filtration rates) and abnormal tubular function (im paired urinary concentrating ability and reduced lead clearance rates) were noted in lead workers. u- ?i DUP040013313 04-0005-0472 J These findings emphasize the need for improved industrial hygiene measures in the lead industry and the importance of biological monitoring in preventing lead toxicity. Based on the data contained in this report, a standard of 60pg/100ml is recommended as the "biologic threshold limit value" for lead. i 99 j DUP040013314 04-0005-0473 4 A. Introduction Occupational lead poisoning has been recognized since the 19th century'*' and methods for its prevention were well developed in Greet 7 Britain in the early 20th century , Nevertheless, eradication or even control of this disease is far froa a reality in the United States in 1976, The current report summarizes the results of 5 recent lead plant investigations (Table 1) conducted by the National institute for Occu pational Safety and Health and the Bureau of Epidemiology, Center for Disease Control, which clearly demonstrate that lead* poisoning is occur ring with an alarming frequency in lead plants across the country. (Detailed reports of these investigations are included as appendices.) Investigations of 6 other similar plants are currently in progress; data from these studies will be added to the current report as they become available. In the current report, special attention is given to studies which relate blood lead levels to signs and symptoms of lead toxicity and to studies of the chronic effects of lead exposure. DUP040013315 04-0005-0474 5 B. Summary of Investigations: 1. Memphis, Tennessee: Secondary lead smelter* Following reports of excessive blood lead levels and clinical lead poisoning at this plant, 77 (92%) of 84 current employees and 1 former employee were examined in November 1975 . Concurrently, community lead exposure and exposure of workers' families to lead 4 carried home on work clothing was evaluated. Workers blood levels ranged up to 184 vg/100 ml with 67% >60 yg/100 ml (Table 2). Highest blood lead levels were seen in production area workers. Classical symptoms of lead poisoning were evident* abdominal pain (17%), gastrointestinal dysfunction (22%), joint pain (28%), neuromuscular symptoms (27%), and anorexia (23%)* Ten workers were found to have lead neuropathy, with weakness of wrist extensor muscles. Anemia 5 (hemoglobin concentration <lAga/lOO ml ) was noted in 11 workers and correlated with elevated blood lead levels and erythrocyte protopor phyrin concentrations. Elevated blood urea nitrogen (BUN) levels (greater than 20 mg/100 ml) were seen in 6 workers. These asotemic workers had worked at the plant longer and were older than workers with normal BUN levels. Increased arsenic absorption was noted in 10 (14%) of 72 employees. A survey oi 228 children living neat the smelter shoved no excessive lead absorption. In January 1976, manage ment temporarily closed the smelter and initiated efforts to redesign the production process. Young children of smelter workers were found to have elevated blood lead levels and 8 were hospitalized and treated for lead poisoning. (Details of that investigation are discussed below.) * Complete report - Appendix 1 6* Complete report - Appendix l DUP040013316 04-0005-0475 3. Joplin, Missouri; Lead chemicals plant* V In March and May 1976, medical evaluations of 53 production workers at this plant revealed blood lead levels from 39 to 135 ug/100 ml, with 83% > 60ug/100 ml. Comparable levels of erythrocyte protoporphyrin were noted. Three workers were anemic; wrist weakness was noted on physical examination of 1 worker; ankle drop in 1 worker; and tremor of the out stretched hands in 2 workers. Symptoms compatible with lead intoxication were noted in 20 workers (Table 3). The most notable finding of this study involved renal disease among these workers: 17 had elevated blood urea nitrogen (BUN) levels (>.20 mg/ 100 ml) further studies revealed significant impairment of renal tubular and/or glomerular function in 7 workers which may represent lead nephropathy, (A more detailed discussion' is given below.) 3, Salt Lake City, Utah: Secondary lead smelter** A medical evaluation 6 of 36 (862) of the plant's 42 employees was conducted in January 1976 following the hospitalization of 7 workers for lead poisoning. Two of those hospitalized had blood lead levels over 250 ug/100 ml and evidence of possible lead encephalopathy. Niretoen employees had unequivocal lead poisoning*** within the previous 4 months; * Complete report - Appendix 3 ** Complete report - Appendix 4 ***Lead poisoning was defined in this study as a blood lead level >80ug/ 100ml and/or urine lead levels >250ug/100ml plus symptoms compatible with lead toxicity vhlch could not be otherwise explained. As discussed below, manifestations of lead toxicity are seen at blood lead levels < 8Oug/10Qml and, therefore, this definition uses criteria which may exclude persons suffering from the toxic effects of lead. I 1 10/ l DUP040013317 04-0005-0476 t 7 13 workers were anemic. These cases of acute lead poisoning were related to a change in plant processes: two small rotary furnaces, previously used for antimony production, were used to process lead in December 1975, Inadequate ven tilation of these furnaces was felt to be responsible for the elevaced air lead levels in the plant. One case of lead poisoning occurred in the company president who was apparently exposed outside the production area: the air intake for the ventilation system for his office was adjacent to the furnace room. j The smelter was closed by the local and tote health departments on January 16, 1976, and the plant was ordered to reduce lead exposure to an acceptable level. The plant was reopened in February 1976 after engineering controls were instituted and personal industrial hygiene stressed, but was closed again in June 1976 after blood lead levels of employees were noted to be rising, 4, Eagan, Minnesota: Secondary lead smelter* Two cases of chronic lead poisoning in employees at this plant were reported to the state health department and medical studies of employees and their families were conducted in Hay 1976, The median blood lead level of the 38 workers was 72.5 eg/100 ml; 762 had levels >60 eg/100 ml. Workers on the night shift had the highest average blood level. Four workers had weakness of wrist and/or ankle extensor muscles; 10 workers had tremor of the outstretched hands. There was no consistent relation ship between lead poisoning symptoms and blood lead levels. Five (162) of Complete report - Appendix 5 j /02 DUP040013318 04-0005-0477 8 31 children (ages 1-9) of plant employees had blood lead levels >30 Ug/ 100 ml, indicating increased lead absorption. ! 5. Atlanta, Georgia: Secondary lead smelter A brief visit to this plant was performed in March 1976 as a follow-up to an earlier KIOSK study performed in 1971, Five workers were interviewed and plant blood testing records reviewed. Seventy percent of the plants' 39 employees had blood lead levels >60 yg/100 ml In February 1976, as compared with 74% over 60 ug/100 ml in January 1975. The percentage of workers with blood lead levels over 8{f pg/100 ml had fallen during this period from 43t to 26%. Workers at this plant who were treated for lead poisoning with intravenous chelation were allowed to remain on the Job during therapy. ISmft of ? The Tennessee and Utah investigations represent studies of rela tively acute exposure to lead ; the average duration of exposure to lead Was 4 months and 2 months, respectively. In all the other locations, exposures were more chronic, lasting up to 30 years in some instances. This difference in exposure duration was associated with differences in the prevalence of symptoms and signs of lead toxicity. These effects are discussed separately below, III, Relationship of blood lead and protoporphyrin levels to manifestations of lead toxicity. The usefulness of blood lead testing in evaluating workers exposed to lead has been extensively debated. Some workers feel that blood lead 103 DUP040013319 04-0005-0478 yr j .j.".niinp / gg>;iyi^-5 8i '^gp^-y^gy'tyW*'t.a^jgg-:?."f \I y } and erythrocyte protoporphyrin (EP) levels hear no relationship to symptoms or signs of lead toxicity and, therefore, these tests have no value in screening lead-exposed workers. However, in the currently reported group of studies, blood lead and EP levels were well correlated with the manifestations of lead toxicity. 1. Symptoms.; Elood lead and EP levels were correlated with the classical symptoms con sistent with lead intoxication (Table 3). Persons reporting symptoms during the previous year had significantly higher blood lead levels than workers without symptoms (Table 4) . Sixty to seventy percent of *workers with symptoms during the past year were currently symptomatic at the time of the interview. Furthermore, the higher the blood lead or erythrocyte protopor phyrin level the greater was the proportion of symptomatic workers. The relationship between blo'>d lead levels and symptoms was clearest in a plant (Tennessee) where workers had been employed for a relatively short period (average duration of employment * 5 months). In plants (Minnesota, Missouri) where the average duration of employment was greater (4 and 20 years, respectively) symptoms correlated less clearly with EP and lead levels (Table 5). Forty-nine percent of workers with blood lead levels from 60 to 79yg/ 100ml reported symptoms during the past year consistent with lead poisoning. Within this blood lead range, workers with higher EP levels had higher symptom rates (Table 6). Lower symptom rates were noted for each blood lead category when we considered only workers Symptomatic at the time of the interview and blood testing (Table 7). Twenty-three percent of workers with blood lead levels from 60 to 79yg/iOOml were currently experiencing symptoms ! ^ i j IO<{ DUP040013320 04-0005-0479 compatible with lead c-oisoaing when tested. Most of those with blood lead levels below 60pg/100ml who had reported symptoms dufing the previous year were not symptomatic at the time of testing. Since the symptoms of lead poisoning are nonspecific and 'may be re lated to other disease processes, the same questionnaire used to evaluate symptoms in lead workers in Missouri was administered to an age-matched control group without occupational lead exposure, The prevalence of symptoms consistent with lead toxicity was much lower in unexposed worker* than in lead workers living in the same town (Table 8). 2. Hematologic Effects: "P Blood lead and erythrocyte protoporphyrin levels were closely correlated (r0.76) especially in the range of blood lead concentrations from AO to SO iig/100 ml (Figure 1). Erythrocyte protoporphyrin levels were closely correlated with levels of zinc protoporphyrin (ZPP) measured g directly by a new technique using a dedicated portable hematofluoro- meter (r" ,9A) and when measured by the standard method of Laraola et al9 (Figure 2). Thus, the above-mentioned relationships between symptoms, blood lead levels and EP levels would also hold for ZPP determinations as well. Anemia, defined as a hemoglobin level < 1A gm/100 ml , were noted in IAS of workers at the Tennessee plant and in 31S in Utah. Both of these outbreaks represented relatively acute exposure to lead and the rates were higher than in those plants where chronic exposure to lead was occurring (no anemia was noted in Minnesota and US of Missouri workers were anemic). i or DUP040013321 04-0005-0480 ' 'A ' .... . XI Comparison of blood lead and EP levels with hemoglobin levels shows a pattern similar to that noted previously for symptom rates. The higher the lead or EP level the lower the hemoglobin level (Tables 8 and 9). Leadrelated anemia is associated with elevated EP levels and elevated blood lead levels10; therefore, to differentiate anemia related to lead toxicity from anemia of other causes, EP levels in anemic and non-anesnic workers were com pared. Anemic workers had significantly higher EP levels and blood lead than noa-anemic workers. The clinical significance of anemia varies with the degree of hemoglo`* bin depression. Symptoms classically associated with anemia (i.e., tiredness, fatigue, etc.) are not generally encountered at hemoglobin levels above 8 gra/100 rol^\ Decrements in work performance as measured by standard techniques hap been noted at hemoglobin levels of 11 to 13 gm/ 100 ml . A dose-response effect between hemoglobin level and work per formance was noted throughout the range of hemoglobin levels from 3 to 17 gm/100 ml; a threshold effect was not seen, hesistance to infection may also be impaired in anemic persons 13, out the relationship between the degree of anemia and the degree of decreased resistance has not bee*, established. Therefore, the definition of anemia cannot be based on clinical abnormalities but must be related to the concentration of hemo globin in the blood of in normal persons. The lower limit of normal for U.S. adult males living at sea level has been consistently reported as 14 gm/100 ml * ' and this level has been used in defining anemia throughout this report. "7"^- s' 4> 4- DUP040013322 04-0005-0481 12 -- IV. ^ Relationships of duration of exposure to manifestations of lead toxicity In the Tennocsee study, blood lead levels rose during the first month pi employment and reached a plateau 2 to 3 months after beginning work (Figure 3). At that same plant, symptoms did not develop until 2 to 3 months of employment were completed (Table 10). The predominant symptoms varied with duration of exposure; after brief exposure (2 to 3 months), gastrointestinal Symptoms predominated whereas constitutional symptoms and joint pains were relatively more common after prolonged exposure (over 1 year). if Tn other locations, workers acutely exposed to lead experienced relatively more gastrointestinal symptoms than chronically exposed workers. The highest relative rate of gastrointestinal symptoms was noted in lead poisoning cases in Utah (Table 11) where exposures were very brief (3-4 months duration). Workers in the Minnesota plant were chronically exposed and noted more nonspecific, constitutional symptoms (e.g,, tiredness, irritability, joint pains, muscle weakness)(Table 12). Anemia was noted only after 2 months of work with 1 exception (one worker who had completed 1 month of work, was anemic (Hgb; 13,0 gm/ 100 ml, lead level; 79 vg/100 ml, E? level; 299 yg/100 ml)). "2 \\ 1| XJ /I / .07 i DUP040013323 04-0005-0482 13 Wrist extensor weakness was noted in 2 workers who had completed only 2 months of employment at the Tennessee plant. They had blood lead levels of 81 and 130 vg/100 ml and EP levels of 281 and 258 vg/ 100ml. One worker at the Minnesota plant with 2 months of exposure had a blood lead level of 78 vg/100 ml and an EP level of 250ug/100 ml and mild asymmetrical ankle extensor weakness. Thirteen other workers from Tennessee had evidence of either wrist or ankle weakness; all had worked for at least 7 months and had'blood leaf, levels above 80 vg/ 100 ml and EP levels above 250 vg/100 ml. One former worker in Tennessee who had worked for 3 months and terminated employment 2 months prior to our testing had mild asymmetrical wrist extensor weakness with a blood lead level of 41 and an EP level of 49 vg/100 mi. Although no definite relationships were noted between duration of exposure and development of overt lead nephropathy, some abnormalities of renal function were correlated with duration of lead exposure. The highest prevalence of abnormal renal function tests was noted in Missouri where 17 (322) of 53 workers tested had elevated blood urea nitrogen (BUN) levels; workers with abnormal results had worked at the plant for 4.5 to 31 years. Six (82) of 78 workers in Tennessee had elevated SUN levels; 3 (82) of 38 workers in Minnesota had elevated senna creatinine levels (> 1,5 mg/100 ml). Except for 3 workers with less than 2 months of lead exposure, no worker with less than 3*s years of exposure had abnormal renal function tests. Thus, no azotemia was noted prior to approximately 4 years of lead exposure. (Of DUP040013324 04-0005-0483 14 V. Renal Function Testing - Missouri Specific ranctional abnormalicies Included decreased glomerular filtration rate {<91 rnl/min^) in 8 of 19 workers tested, decreased urinary concentrating ability (inability to concentrate the urine oelow 800 mosn/liter after a 12hour water fast^) in 8 workers, and elevated urinary beta^nicrogiobulin levels (> 37Dug/liter ) in 2 workers (Table 34), A significant negative correlation was noted between duration of lead exposure and rate of lead clearance** {Figure 4), Since a modest age effect was noted in relation to lead clearance (i.e., ' si? impaired lead clearance in older workers), data from workers aged 45-55 'va analyzed and a significant negative relationship was again noted between dotation of exposure and lead clearance rate (Figure 55, Decrease in lead clearance was associated in most workers with impaired urinary concentrating ability and decreased glomerular filtration rate. Blood lead levels increased with de creasing le3d clearance rate. y *Lead clearance was calculated by determining tf.a lead concentration in a timed, measured urine sample and the lead concentration of a whole blood sample drawn during the urine collection period; clearance was computed by the standard formula: UV C *= ----- P where C" clearance of the substar.ee U urine concentration, of the substance P* bit J concentration of the substance X6 V- urine flow rate over collection period i '3, ft ': j * - 1- 1 DUP040013325 04-0005-0484 ' \ r\ > . / t .. / '/ i wr IS Although this observation must be confirmed on a larger series of workers with varyii'g exposure periods, those data suggest that the measurement of lead clearance may be a useful tool in evaluating renal function in lead workers. VI. Chelation Theranv In the Missouri plant, oral EDTA was administerfed to workers with evidence of lead toxicity (anemia) or to workers with elevated blood lead levels, intravenous chelation therapy was also used. During therapy, workers were removed from exposure to lead. In the Georgia plant, intra venous chelation was used but the workers were allowed to continue working at the plant during therapy. In Tennessee, intravenous chelation was reserved for workers with evidence of lead toxicity; no oral therapy was prescribed, In Missouri, chelated workers had slightly higher BUM levels than non-chelated workers (Table 15); these workers were also older than those without a ..chelation history and had longer lead exposure. VII. Illness in Children of Lead Workers Health effects of occupational lead exposure are not limited to the workers themselves but extend to involve workers' families, especially their children. Lead dust carried hone on work clothing has apparently resulted in contamination of the home environment in several locations. Studies in Tennessee, Minnesota, and Vermont have shown elevated lead content in household dust taken from homes of lead workers. Young children living in these hones have been shown to have elevated blood lend levels, so-e high enough to require hospitaliza. Jon and chelation therapy. t(0 DUP040013326 04-0005-0485 A study (4) of lead workers' children, 1-6 years of age, and age- matched neighborhood controls showed elevated " blood lead and EP levels in the lead workers' children. Thirty-eight (42%) of 91 children tested had blood lead levels >30 yg/100 ml, indicating increased lead absorption. Fight children had levels _> 80 ^ig/100 ml and were hospitalized and chelated. Blood . levels of workers' children increased as the fatheis duration of employment at the smelter increased (Table 16) in a manner similar to that previously noted (Figure 3) in the workers themselves. '* The children's blood levels were modestly correlated with their fathers' blood lead levels (Table 17) and closely correlated with the level of lead in household dust (r * .50, p <.0025) (Table 18). The hypothesized mechanism of exposure was through ingestion of lead-rich household dust through normal hand-to-mouth activity common in young children. This mechanism has been shown to be responsible for lead absorption in children exposed to lead in inner cities (17) and in children living near primary lead smelters (18,19). J I I I jf | | I 1 | f I I "| VIII.Performance of Blood Lead Analyses In the Missouri plant, periodic blood lead testing was performed as part of an ongoing medical surveillance program* The blood tests were analyzed in a laboru.ary which appears to be providing results which are consistently lower than the actual lead content of the sample. A study using blind. split sample analyses showed this laboratory to be approximately 30" lower than the target value determined by the 'oxicoiogy laboratory of the Center for Disease Control (Table 19). f | J i I DUP040013327 04-0005-0486 IX. Biologic Monitoring System 17 If lead toxicity is to be prevented, a biologic monitoring system should be instituted which removes a worker from exposure prior to the development of Illness. Since overt toxicity (i.e., wrist weakness nr.d lead-related anemia) was noted at a lea-: level of about S') uc/100 r.l. ard since anemia and lead-related symptomatology were noted at blood level:: below SO ug/lOO ml, this value should not be used as the ''biologically safe" value. In our studies, we encountered no workers with evidence of lead-related aneaia, wrist weakness, or lead-related renal disease, with a blood lead level <60 eg/100 ml, Very few workers with blood lead levels <60 ug/lOOal had syr.ytoas consistent with lead intoxication. Since the primary reason for biologic monitoring is to prevent the occurrence of overt illness and chronic disability in workers exposed to hazardous materials, a level should be set which provides a margin of safety which will insure that the cost sus ceptible workers will not develop lead toxicity, the data in this report clcariy support the setting of a blolonlc threshold limit value of 60 ng/lOOal for occupationally-exposed populations* Deleterious health effects nay occur at lower bipod levels and, if these are conclusively demonstrated in the future, this standard should be revised downward. C. History of Plant Inspections and Citations Every plant studied had been inspected by 0S!tA daring the 12 month peri prior tc our medical studies. The Missouri plant had beer, cited by OSHA in 1975 alleging a situation that CvUld cause serious physical harm. Our medical studies were performed during the 1 year abatement period If D : DUP040013328 04-0005-0487 IB which expired September 10, 1976. During the abatement period, workers were required to wear respirators and a program of improved engineering controls and medical and environmental surveillance were instituted. The Tennessee plant had been inspected by the State of Tennessee's Occupational and Radiological Health Division and found to be in violation of existing standards on numerous occasions since 1951 (Table 19). the company had been cited twice (1972 and 1974) for excessive exposure to airborne lead and once for an inadequate respiratory protection program (1575). Our studies there were performed during an. abatement period. The Minnesota plant had been found to have excessive airborne lead exposure on numerous occasions since 1949 (Table 20), The most recent inspection in November 1975 had documented air lead levels up to 14 times the standard (0.2 ng/n*). Despite these numerous inspections and citations, significant health problems were noted in workers employed at each oi these plants. evaluation of -the Usefulness of the Protooornhvrin Test i;> Screening Lead Workers; Determination of the protoporphyrin level in bipod has been proposed as a method of screening workers for excess lead absorption. The newlydeveloped portable henatofluorineter, which measures mine protoporphyrin directly from a drop of blood, provides a rapid and inexpensive method of performing this analysis. DUP040013329 04-0005-0488 Measurement of the sensitivity and specificty of a screening test Is essential in evaluating its usefulness. "Sensitivity is the extent to which persons Who truly manifest a characteristic are so classified; specificity is the extent to which persons who do not manifest a character istic are correctly classified" (20)(Example, table 22). Using dats from 152 workers from 3 plants (Tennessee, Missouri, and Minnesota), the sensi tivity and specificity of the EP test was calculated using different levels of acceptability for EP and blood lead (Table 23). Ninety-six percent of the workers with blood lead levels MSOug/lOOml had EP levels >10Dug/ lOQal (sensitivity); 602 of workers with blood lead levels less than 60ug/ 100ml had EP levels <lOQug/lOOml (specificity). The usefulness of a screening test varies vit-h the prevalence of the characteristic for which screening is performed. As the characteristic becomes less common, the number of "false positives" (e.g>, workers with "abnormal" EP tests but "normal" blood lead levels) will increase. The predictive value positive (PVP) measurement is a useful indicator of the applicability of screening tests to a given situation, since it incorporates specificity and prevalence into its calculations (21). PVP number with positive EP test & elevated lead level number with positive EP test In a plant with a high prevalence of elevated lead levels (plant ATable 24), the EP test, using lOOug/lOOml as the cut off value, would be more useful (i.e., have a higher predictive value) than in plants (Tables 25 & 26) with lower prevalence of elevated lead levels. As seen in Ar... nv DUP040013330 04-0005-0489 m*4^v%.ijyRrt.i**|ip ***. aw**!*:,vy**}*w*fcy < 20 ' Tables 24-26, as the prevalence of elevated blood lead levels decreases ' the number of false positives {workers with "abnormal" EP test but "normal" blood lead level) Increases, X a? i -- DUP040013331 04-0005-0490 fa b le 1, Lead P la n t In v e s tig a tio n s .1975-1976 *o rt u 0) 0 .-1 CU T3 o Q> (6 W -a c bo un 3 O o u c: o 04 A. X C o H 6 <n 1 cNl t O O Co oo rl V"| H <N H H O1 e o p H r a <630 63 (i* -<WH3 *- c* 1e3 Ou W At w o ii *5 *4 o<oOr\ r*4 ti CO -0S-*4f in r* P *4 ft C H Pe W4 o ao. * H Mfil r*"a4> ftos Ha *C5 uoo CO tCa A. H9 .rUuV-4 (O3 W E *wv <uC o * *ouCeol 4 IP 4uo3 &aE >Uv ouca3 Cl CO u fij H4-1 a gS >ht* *s Coul CO S3 > u< a 0 as X 0P > io C 43 R: ,J2 A. *-4 3* c t!S 4-1 <3 43 c 13 a E a. 60 H *4 o V b 5 3 14 .-4: 2: W CO < >N iO. nj r- sO 3J o> !> u r< lO 0 CO f- e-4 r- It Cl UD 0* l H fn H O os M 6 JS H <9 JS Cl 43 2 > O *4 5n a O R O 0 as S' <3 0 2 ! . r'*"' j: // ! DUP040013332 04-0005-0491 Table 2: Bipod lead levels In lead plant workers Blood lead level (MR/lOOml) < AO 40-59 60-79 80 Total tested Memphis, TO 14 (18Z) 12 (15%) 26 (33%) 26 (33%) 7$ Joplin, M0 1 (2%) 7 (17%) 21 (50%) 13 (31%) 42 Blood lead level (u r /IOGs iI) Atlanta, GA A Oo 6 (15%) 40-59 6 (15%) 60-79 17 (44%) > 80 30 (26%) Total tested 39 Salt Lake City, i (3%) 5 (17%) 2 (7%) 21 (72%) - 29 V Blood lead level (u k /IOOs I) 40-59 60-79 > 80 Total tested Eaean, MS 3 (8%) 6 (16%) 17 (45%) 12 (32%) 38 TOTAL 25 (11%) 36 (16%) 83 (37%) 82 (36%) 226 I 117 1 d DUP040013333 04-0005-0492 Table 3. Symptoms of Lead Poisoning 1, Gastrointestinal symptoms (Nausea, vomiting, diarrhea, and/or constipation} 2, Abdominal pain 3* Neuromuscular symptoms (muscular weakness and/or tremor) 4. Anorexia 5. Joint pains 6. Constitution complaints (fatigue, insomnia, irritability, and/or headache). in DUP040013334 04-0005-0493 fable 4. Distribution of symptoms and blood lead levels of employees, Memphis, Tennessee, November 1S75 Symptom Gas trointeetinal symptoms Abdomina' pain Neuromus cular symptoms Anorexia Joint pains Constitutional complaints Present/ Present Absent Present Absent Present Absent Present Absent Present Absent Present Absent Number Employees (%) 17 (22%) 61 13 (17%) 65 21 (27%) 57 18 (232) 60 22 (28%) 60 31 (40%) 47 Blood Lead Level Kean (un/lOOml). 101.24* 65.98 100.77* 68.25 94.52* 65.98 93.89* j 67.60 92.59* 66.23 89.68* 63.11 Significantly greater than level of those without symptoms (? < .01, 1-tailed t test) // ? DUP04001333S 04-0005-0494 table 5 Percentage of Workers with Symptoms* of bead Poisoning by Blood Lead and Erythrocyte Protoporphyrin Level at Three Lead Plants Location Tennessee Missouri Minnesota Ratio, (%) of Symptomatic Workers by Blood Lead Level (ug/iOOral) <40 40-59 60-79 1/13 cer) ro/1 <o%)jt f0/2 (or)j 2/12 17%) 6/7 (57%) 2/6 (33t) 7/26 (27::) 7/21 (67%) 9/14 (64%) > 80 18/26 (69%) 7/13 (54%) 5/12 (62%) Tennessee Missouri Minnesota Erythrocyte Protoporphyrin Level (ug/lOOml) <100 100-199 200-299 > 300 2/26 (6%) [1/1 (100Z)) 0/2 (0t)] 2/1.3 (15%) 4/10 (40%) 1/5 (20%) 11/16 (69%) 10/15 (62%) [0/4 (OS)] 13/21 (62%) 9/15 (60%) 15/23 (65%) *Twp or more of symptoms in Table 3 during past year ^Brackets around ceils with 5 nsembers or leas ii Po DUP040013336 04-0005-0495 Table 6 Percentage of Symptomatic* Vorkuta by Blood Load and Erythrocyte Protoporphyrin (E?) Level Ratio (I) of Lead Workers With Symptoms By Blood Lead Level (up/lOOml) Erythrocyte protoporphyrin (jjg/lOOal blood) o V 40-59 60-79 > so Total <100 100-199 200-299 300-399 > 400 1/15 (7%) 2/9 (22%) {0/5 (0%)] t0/I (0t)}+ 2/10 (20*) 5/15 (33%) -" {3/3 (100%)] 10/19 (53%) - t1/2 (502)] 10/14 (71%) - - 5/8 (63%) - 3/29 i(107) [0/2 (0%)] 7/28 i(25%) 8/13 (62%) 21/35 (60%) 7/14 (50%) 18/20 (60%) 15/22 (68%) 20/30 (67%) Total 1/16 (ST.) 8/24 (33%) 30/61 (49%) 30/51 (59%) *Two or more of the syisptosm or symptom categories in Table 3 during past year +BracV.ets around cells where 5 or less persons represented. )3t : DUP040013337 04-0005-0496 / Table 7 -.................... --1 i L j Percentage of Workers CurrentlySymptomatic* by Blood Lead and EP Level Erythrocyte Protoporphvrln < 100 100-199 200-299 300-399 >.400 Ratio (2) of Symptomatic Workers by Blood Lend Level ( pg/lOOml) < 40 40-59 60-79 > 80 0/13 (02) 0/8 (02) [0/5 (02)) - [0/1 (0%)} [0/4 COX)J 3/14 (212) [0/2 (02)J - [2/3 (672)] 3/15 (202) 5/12 (422) - [0/1 (02)'] [2/5 (402)1 3/10 (302) - - [2/5 (402)] 8/15 (53?) 'r j * . Total 0/26 (02) 3/21 (142) 10/30 (332) 5/16 (312) 10/20 (502) Total 0/14 (02) 2/16 (132) 10/44 (232) 16/39 (412) 1! T i i 3 5 ' Workers reporting 2 or more symptoms in Table 3 at time of blood sampling. i 12 2 j ; -! DUP040013338 04-0005-0497 Table & Current symptoms of lead toxicity in lead workers and controls Missouri, 1976 Symptoms Insomnia Excessive Fatigue Dizziness Muscle Weakness Joint Pain Abdominal Cramps Nausea Constipation Lead Workers (43) 5 (12%) 19 (44%) 8 (19%) 6 (14%) 10 (23%) 1 f.z?> 1 (2%) 0 Controls (15) 1 (7%) l (7%) 0 o 4 (26%) 0 0 i 0 : ' ! i i i J DUP040013339 04-0005-0498 table 10. Mean Hemoglobin Level by Erythrocyte Protoporphyrin Range Missouri 1976 Eryth'ocyte Protoporphyrin Levelj(ug/lOOal) Humber tested Perce itage Anesnic+ Mean Hemoglobin Level <200 11 OX 15.89 200 - 399 21 19X 15.03* > 400 mv--... li 18X 14.70** ' Standard Deviation 0.91 1.03 \ 0,78 Significantly less than mean level for EP < 200 C t - 2.26, p < .025, one tailed, t) irk Significantly less than mean level for EP levels < 200 (t - 3.14, df - 20) (p < .005, one tailed t ) + Anemia defined as hemoglobin level< 14.0 gras/100ml DUP040013341 04-0005-0500 Table 11. Percentage of production workers with symptoms by duration of employment, Tennessee 1976 Symptoms Nausea MONTHS OF EMPLOYMENT COMPLETED 0-1 2-3 4-12 > 12 utm (N12) (N-S) (H-20) OX 331 632 252 Total Number Reporting Symptoms 14 Constipation OX 8X 132 302 8 Anorexia 62 42? 632 352 18 Abdominal pain Muscular weabness Joint pains OX OX OX 251 502 252 502 172 882 252 352 452 11 14 19 Fatigue ox 252 75% 302 15 Insomnia ox 252 25% 252 10 Irritability ox 252 632 152 11 ; 12 DUP040013342 04-0005-0501 TABLE IS. Occurrence of Symptoms in Lead Smelting Plant Employees--Hinnesota 1976 Symptoms Number with Symptom Percent with Symptom Tiredness Loose bowel movements Irritability Joint pains Muscle weakness Loss of appetite Headache Leg cramps Constipation Nausea* Trouble sleeping Throwing up* Abdominal pain* Weight loss** Shakes 17 11 9 9 9 7 6 6 6 5 4 4 3 2 2 52 33 27 27 r ti 21 18 18 18 16 12 13 9 6 6 * Excluding 1 employee with symptom due to ulcers. ** Excluding 2 employees with symptom due to diet* Of the 2 with weight loss not related to diet, 1 lost 20 pounds in 15 months and 1 lost 22 pounds in 7 months. + 13 of these 14 smoke. mI DUP040013343 04-0005-0502 . . . . ' ''V 36 ' Table 12, Frequency of syaptpns among 22 cases of lead poisoning, Utah 1976 Symptom Abdominal cramps Nausea Diarrhea Headache Dizziness Anorexia Vomiting Paresthesias Constipation Fatiguabillty Myalgias Height loss Irritability Chest pain Muscle veakness Tremor Joint pains Number 19 18 12 12 12 12 9 9 8 8 7 6 5 5 4 4 4 Percent 86 82 55 55 55 55 41 41 36 36 32 27 23 - 23 18 18 13 1I *\s DUP040013344 04-0005-0503 J p * l* N O 6 ri N O O 'O O (O H ^^ O N O CO 4 ,H >0 N os m n o H H O N O O CO ^ r-l 0 O P 9 O O O jr4 9 r-l >-l 9 O <M HOJOlOOtOCO O O ID U1M vO CM CM -IT Or~in00OCOM cSm OinsOCr-HCoHCWM OIsOsolCr-llfototO-)iNS>Pr> it--ll --X ^ --U --4 Oo en ? .o.O CD to rO^k u p 001 inNCiiNoo rt ifi o mo >ora o >., oo io n sr,ooivPiqiMPNOyOBlOC'r-QsO<H H H r-i H H H H Ch A 03 00 G V H C 4oHJ U G Mi-4rt-iioCcinvrKtNWH'rOm' '!fmflmlNtvON0s0o'Os'rOi'iinn*-o4 s<oSsOo>in''(iOo >oo 03 55 w ft? 44 o HV Owt- c tDwa wG <3; CP o ^4 1o1 ^4 ofxi 2 w<in No on co n^ o^ HNd'fn m o CM 6* <M N <N CH W CM -4 H <M CM *h >t CO 3 oCO pi vvC^.OcVNh*TW`*T1ufOvvNoCcOo!sOPCsMr^h.CnO<*,PA,>MGOu{'vtOAHinC*A|ICON\J S<y H *-4 c m a <r in-*o r> coO'OHNcOiitin'P^fl&O' fH tH r*l rl H t-4 r-l r-J ?H rH H o, Sg ss H cm 00 0) 3rM *fii Jt o +1 wn 5 rt w M 'Z r-i 3 g II O r-4 4J a u0) <u u0U1 01 o >* t o uai *SJ r*rt 3H .3x ^2 -o<n 4to4 O <u -o jS H(pQ aiP3 So H CM o <3 " jss 5i 4r4t 0m) aj wO (3 3o 44 ao aa o >0) M r-4 O 44 44 TaQO) 44 a a ` 5.5 Mp M* P* 3 DUP040013345 04-0005-05(74 Table 15. Blood Urea Nitrogen (BUN) Levels and Serum Creatinine by Treatment History, March 1976, Missouri* No. of Courses** of Oral EDTA None 1-3 4-13 Total Number 28 10 5 Mean BUN 17.28 19.30 21.00 Mean Creatinine 1.01 1.08 1.12 Number (%) Elevated * G (21) 3 (30) 2 (40) Greater than 20 mg/109 ml Courses consisted of 4 gms EDTA orally for 5-7 days no \ DUP040013346 04-0005-0505 Table 16, Relationship of children's blood lead level to duration of father's employment at smelter--Memphis, November 1975, Months of Employment Completed bv Esther 0-2 3-4 5 - 12 Children"'s Blood lead Level (ur/lO0al) Rusher 5 Mean 26.4 * + S,D. 5.0 8 43.7 Hr 21.1 4 59.5 + 13,4 f 4 ? DUP040013347 04-0005-0506 Table 17 Blood lead levels of current workers* children by parental blood lead level--Memphis, November 1975 Father's blood lead level < 60pg/100ml Total No. of Children 12 No. (%) of Children with blood lead levels 30-79u?,/100ol > 80u r /100ml 1 C 8.3%) 0 60-79pg/100nl 35 15 <45.7%) 0 80-142pg/100ml 25 12 (48.0%) "1 4 (16%) I' 1 DUP040013348 04-0005-0507 Table 18. Comparison of lead concentrations in household dust with children's blood lead level--Memphis, November 1975 Dust Lead Concent ration (PPP> 0 - 1000 1000-2000 2000-3000 5000-6000 7000-80,000 Children's Blood lead Level (ua/lOOal) Number He - '. S.D, 18 21. .J + 7.' 8 5 .41,6*+11.1 5 46.2* + 21.1 4 65.0* + 10.4 6 73.3* +>34.0 Significantly greater than mesa level of children exposed to 0 - 1000 ppm level of lead in duet (p < .001). /3 3 | DUP040013349 04-0005-0508 Tabic 19, Lead Concentration in Split Blood Samples, May 1976 ab c Lub CDC NIOSH Contract Lab Private Lab Sample $ 1 2 3 4 5 6 7 8 9 10 11 12 13 1A 15 16 17 18 19 20 21 22 23 2A ! 25 i 26 27 28 29 30 112 95 98 68 71 62 88 92 88 73 212 72 78 83 79 64 71 82 176 54 56 76 96 130 74 82 78 72 96 84 112 88 110 69 72 62 85 92 92 70 115 80 81 76 91 66 87 80 157 77 5A 76 96 144 74 85 82 77 101 91 80.1 58.3 74.5 49.3 46.2 42.9 63.1 63.9 64.8 47,8 80.9 i 53.4 i 61.5 51.8 64.8 46.1 57,5 50.2 103.6 50.2 34.8 51,0 68.8 87.4 48,6 57.5 56.7 52.6 66.4 60.7 \ Mean Percent difference from CDC result:: HIOSK Contract Lab + 4.0% Private Lab - 29.2% Number (Percent) With acceptable result*: NIOSR Contract Lab 27/30 (90%) Private Lab 1/30 (3.3%) Acceptable result: + 15% for blood level JA* + 6 ug/lOOtel for blood level < AO. j .. __[JYJ > it \.................... .. .............. -'r-'1 -............................... DUP040013350 04-0005-0509 Table 20. History of Inspections and Citations at a Secondary'Lead Smelter, Tennessee Excessive Airborne Lead Concentration Koted Year 1952 1953 1955 1956 1958 1962 1965 1972 1974 Enforcement Letter or Citation Issued Year Humber of Letters/ Citations 1951 1953 1955 1958 1961 1962 > 1965 1967 1970 1971 1972 1974 1975 1 1 1 2 1 4 1 3 1 1 1 1 1 / J?3~ DUP040013351 ' 04-0005-0510 Table 21. Minnesota Secondary Lead Smelter: Record of Inspections and Citations by State and Federal Agencies Excessive air lead concentrations noted Compliance order or citation issued 1549 1950 1955 1955 195? 1960 1963 1964 1966 1972 1973 1974 1975 1963 1970 1973 1974 1975 ' l 2 > j 3 t J i in DUP040013352 \ 04-0005-0511 o At A O Table 22 Calculation of Sensitivity and Specificity Blood Lead Level Number of Workers with Erythrocyte Protoporphyrin Levels & <50 Total 130 7 137 TOTAL 2 13 132 20 15 152 Sensitivity ** Number correctly Identified as positive* Total number positive 130/137 952 Specificity Number correctly identified as negative** Total number negative 13/15 872 y# * positive * blood lead level >40pg/l00ml ^negative * blood lead level <40ug/100ral ,1' si , Vi i 13 yj DUP040013353 ' 04-0005-0512 Table 23 Sensitivity and Specificity of Erythrocyte Protoporphyrin (EP) Screening Test in Selecting Workers with Elevated Lead Levels-. Sensitivity Acceptable blood lead level 40 yg/100ml 60 yg/lOOml 80 yg/100ral Acceptable EP Levels 50yR/100al blood 100 ii s/100ml 95% 90% 99% 96% 100% 100% 200u r /100ml 70% 78% 9,8% Acceptable blood lead level 40yg/100al 60yg/100tnl 80yg/100ml Specificity Acceptable EP Levels '1 SOUR/lOOnl blood 100 lig/lOOnl 200pg/l0Qml 87% 94% 100% 50% 60% 88% 21% 29% 55% :! 132 | DUP040013354 04-0005-0513 - />V \ VSr- /f .#.7!.V/4jf. Ssf :*!* * Table 24 Effect of Screening Hypothetical Plant A Using Different Levels of EP Acceptability 1) Assume plant with 100 workers; 2) 75 with blood lead levels >60ug/lOOml 3) 25 with blood lead levels < 60vig/100al 5 < Using EP cut off of 100 pg/100 ml whole blood (sensitivity 962, specificity 602)^ 1) Correctly positive*: 72 workers 2) Fail to identify 3 workers with elevated blood lead levels 3) Correctly identify 15 workers with ''normal" blood lead levels 4) Incorrectly label 10 workers with "normal" levels as having increased lead absorption Using EP cut off of 200 Ug/IGO ml blood (sensitivity 782, specificity 882) 10 Correctly positive: 58 workers 2) Fail to identify 17 workers with elevated blood ldad levels 3) Correctly identify 22 workers with "normal" blood lead levels 4) Incorrectly label 3 workers with "normal" levels as having increased lead absorption Workers with elevated EP who in fact have elevated blood lead level (>60ug/100ml). 13? DUP040013355 04-0005-0514 / / ', A<ww table 25 Effect of Screening Hypothetical Plant B Using Different Levels of EP Acceptability k1} Assume plant with 100 workers; 2) 50 with blood lead >60ug/100nl 3) 50 with blood lead < 60Mg/l00ml Using EP put off of IQOug/lOOml 1) Correctly identify 48 workers wtih elevated blood lead levels 2) Fail to identify 2 workers with elevated blood lead levels 3) Correctly identify 30 workers with "normal" blood lead levels A) Incorrectly label 20 workers with "normal" blood lead levels as having increased lead absorption Using EP cut off of 200ug/100ml 1) Correctly identify 39 workers with elevated blood lead levels 2) Fail to identify 11 workers with elevated lead levels 3) Correctly identify 44 workers with "normal" blood lead levels 4) Incorrectly label 6 workers with "normal" blood lead*levels as having increased lead absorption /Yd ii DUP040013356 04-0005-0515 Table 26 Effect of Screening Hypothetical Plant C Using Different Levels of EP Acceptability 1) Assume plant with 100 workers 2) 20 with blood lead level >_60ug/100ml 3) 80 with blood lead level < 60ug/10pml Using EP cut off of 100 yg/lOOml: 1) Correctly identify 19 workers with elevated blood lead levels 2) Fail to identify 1 worker with elevated blood lead levels 3) Correctly identify 48 workers with "normal" blood lead levels 4) Incorrectly label 32 workers with "normal" blood lead levels as having increased lead absorption Using EP cut off of 200 pg/lOOmi: 1) Correctly identify 16 workers with elevated blood lead levels 2) Fail to identify 4 workers with elevated lead levels 3) Correctly identify 70 workers with "normal" blood lead levels 4) Incorrectly label 10 workers with "normal" blood lead levels as having Increased lead absorption -i / // Y DUP040013357 ! 04-0005-0516 . Table 27 Predictive Value Positive of F.P Test Using Different Levels of Acceptability in Plants with Varying Prevalence of Elevated Blood Leaa Levels. Plant A B C Prevalence of El<vated Lead* Levels 751 50% 202 Using EP Cut Off of 100ug/100ml blood 882 712 372 Using EP Cut Off of 200pg/100ml 9:52 872 622 / *> 60up,/100ml I IV2 .1 // DUP040013358 i 04-0005-0517 EP C O N C E N T R A T IO N p q /lO O m l W HO LE BLOOD)( Fig, y. BLOOD LEAD AMO ERYTHROCYTE PROTOPORPHYRIN LEVELS IN WORKERS, MEMPHIS, TENNESSEE, 1975 i Ns DUP040013359 04-0005-0518 DUP040013360 i 04-0005-0519 PROTOPORPHYRI N CONCENTRRTI D N S /M 15 5 D U R I/ Z IN C PROTOPORPHYRIN CONCENTRATION CMCG/100 K L ) Ffa 3 LEAD LEVEL IN PRODUCTION WORKERS; BY LENGTH OF EMPLOYMENT \ /Yjf DUP040013361 I 04-0005-0520 uO ft LEAD CLEARANCE RATE BY DURATION OF LEAD YERRS OF LERO EXPOSURE V i. -' DUP040013362 04-0005-0521 F ig. 5 ' LERD CLEARANCE RATE BY DURATION OF LERD E CNIM/TH) 31BH 3mmmT> <JH31 m - - is - is wi DUP040013363 04-0005-0522 YEARS D r LEHD EXPOSURE REFERENCES 1. Tanqueral des Plai.ches L: Lead Diseases: A treatise, with notes and additions on the use of lead pipe and its substitutes. Lowell, toss.: Daniel Bixby and Co., 1848 2. Legge TM: Thirty years' experience of industrial maladies (Shaw Lectures). J Roy Soc Arts 77:1023-1039, 1929 3. Center for Disease Control: Lead poisoning--Tennessee. Morbidity and Mortality Weekly Report 25:86, 1976 4. Baker EL, Folland DS, Taylor TA, et al: Lead poisoning in children of lead workers: home contamination with industrial di*st. New Engl J Med, in press, 1977 5. Wintrobe MM, Lee GR: Pallor and Anemia,in Wintrobe MM, Thorn GW, Adams RO, et el: Harrison's Principles of Internal Medicine, 7th Edition, New York: HcGraw Hill Co. 1974, pgs. 288-289, 2043,^ 6. Center for Disease Control: Occupational lead poisoning-Utah. Mor bidity and Mortality Weekly Report 25:1*1-182, 1076 7. Pioaelli S, Davidow B, Guinea UF, et al: The FEP (free erythrocyte porphyrins) test: a screening micromethod for lead poisoning. 8. Bluaberg WE, Eislnger J> Lamola AA, Zuckerman DM: A new quick test for lead poisoning: a dedicated portable hematofluorometer. J Lab Clin Med, In press 9. Lamola AA, Joselow M, Yamane T: Zinc protoporphyrin (ZPP): a simple, i sensitive, fluorometric screening test for lead poisoning. Clin , Chea 21:93-97, 1975 10. Elwood PC, Waters WE, Greene WJW, Sweetnam P: Symptoms and circulating haemoglobin level. J Chron Dis 21:615-628, 1969 11. Viteri FE, Torua B: Anaemia and physical work capacity. Clin Haematol 3:609-626, 1974 12. World Health Organisation Technical Report Series No, 580, WHO, Geneva, 1975 13, Wintrobe MM, Thorn GW, Adams RO, et al: op clt pg. 2042 14. Hamburger J, Richet C, Crosnier J, et al: Nephrology. Philadelphia, W.B. Saunders Co,, 1968 ins / DUP040013364 04-0005-0523 15. Berggard I, Bearn AG: Ieolation and properties of a low molecular weight B,,-globulin occurring in human biologic fluids. J Biol Chem 243:40957 1968 16. Pitts RF: Physiology of the kidney and body fluids; an introductory text. Chicago: Year Book Medical Publ, 1968 17. Lepow ML, Bruckman L, Rubion RA, et al: Role of airborne lead in internal body burden of lead in Hartford children. Environ Health Perspectives 7:99-102, 1974 18. Landrigan PJ, Baker EL, Feldman RG, et al: Increased lead absorption with anemia and slowed nerve conduction in children near a lead smelter. J Pediat 89:904-910,1976 19. Landrigan PJ, Gehlbach SG, Rosenblum BP, et al: Epidemic lead absorp tion near an ore smelter: the role of particulate lead. N Engl J Med 292:123-129, 1975 20. HacMahon B, Pugh TP: Epidemiology, Principles and Methods. Boston: Little, Brown andcol, 1970, pg 261-262 21. Vecchio TJ: Predictive value of a single diagnostic test in uneelected populations. N Engl J Med 274:1171-1173. i - s' / t m] DUP040013365 04-0005-0524 Appendix 1 FOR ADMINISTRATIVE USE LIMITED DISTRIBUTION HOT FOR PUBLICATION PUBLIC HEALTH SERVICE-CDC-A*.lanta EPI-76-33-2 Kirch 5, .1976 TO : Director, Center for Disease Control FROM : Cancer end Birch Defects Division Bureau of Epideaioipgy SUBJECT: Occupational Lead Poisoning in Tennessee SUMMARY Following reports of excessive blood lead levels and illness in workers at a secondary lead smelter in Memphis, Tennessee, 77 (921) of 84 current employees and 1 former employee were examined in November 1975. Blood lead levels ranged to ISBpg/ 100ml. with 332 >SDlig/100ml, Elevated blood lead levels were seen in all areas of the plant, especially in production workers. Classic"! symptoms of lead poisoning were evident; abdominal pain (173!), gastrointestinal dysfunction (222), joint pain (281), neuromuscular symptoms (271), and anorexia (232). Ten workers were found to have lead neuropathy, with weakness of wrist extensor muscles. Anemia was noted in 11 workers and correlated With elevated blood lead levels and erythrocyte protoporphyrin concentrations. There w s b also suggestive evidence of lead-related renal disease. Increased arsenic absorption was noted in 10 (142) of 72 employees. Thirty-two (682) of 47 children of smelter workers had blood lead levels >30ug/100nl; 4 of these children with levels >80Ug/ :100ml were hospitalized and treated for lead poisoning. A survey of 228 children living near the enel". r showed no exces sive lead absorption. In January 1976, management temporarily closed the smelter and initiated efforts to redesign the pro duction process. INTRODUCTION On November 14, 1975, Philip J. Landrlgan, H.D., Chief, Environmental Hazards Activity, Cancer and Birth Efects Division, Bureau of Epidemiology, was notified by David S. Tolland, M.D., EIS Officer located in Tennessee, of a problem of lead poisoning in workers at a secondary lead smelter In Memphis. Preliminary evaluation of the plant by Myron Frank, H.P.H., Staff Epidemiologist, Division of Communicable Disease Control, Tennessee Department of Public Health, had indicated that blood lead levels were ele vated to >60ug/1.00ml iii 46 of 67 employees tested in early November 1975: 4 had levels >200ug/100al, 16 between 100 and 199ug/100ml, and 26 between 60 and 9Sug/100nl. An industrial hygiene evaluation by the Department of Public Health's Division of Occupa tional end Radiological Health in November 1974 had noted excessive exposure to air borne lead within the plant, and a visit In October 1975 revealed an inadequate res piratory protective program. In discussions with Dr. Foiland and Robert H. Hutcheson, Jr., M.P., Tennessee State Epidemiologist; George Lovejoy, M.D,, Director, Shelby County Health Department, Memphis * * ,, v^ Gordon D. Nifong, Ph.D., HEW Region IV, Division of Prevention; Robert Llgo, M.D., Chief, Medical Services Branch, Division of technical Services, NIOSH; Eduard L. Baker, Jr., H.T., BIS Officer; and Dr. Lcndriean, it was decided chat further studies were indi cated. A preliminary visit on November 21 by Dr. Baker; T.A, Taylor, Memphis-Shelby Cwnty Health Department; Myron Frank; and Ken Kronoveter, Industrial Hygienist, tlvision of Technical Services, NIOSH, revealed that in view of the excessive blood lead levels in the workers, extensive medical evaluations should begin without delay. Dr. Baker and Wendy A. Peterson, epidemiology-elective student. Bureau of Epidemiology, left for Memphis on No amber 24 to Join Dr. Holland and begin the investigation. j BACRPTJOUHD The secondary smelter in southwest Memphis, Tennessee, recovers lead from scrap storage batteries and combines the purified metal with other substances (such as Iron, tin, arsenic, or antimony) for resale. The smelter was opened in 1948 and has under gone several structural modifications, including most recently the installation, in 1974, of bag houses designed to control atmospheric lead emissions. In the 11 months preceeding this investigation (December 1974-October 1975), 25.5 million pounds of lead were smelted. Flow of materials through the plant begins in the battery wrecking area, where plates and terminals a -e removed and conveyed to the reverberatory furnace. The reverbera-ory furnace yields pure "soft" lead, which is transported to the casting and refining ares, an4 slag, which is ref ined in the blast furnace along with iron to make "hard" lead. In the casting and refining department, the lead ip melted, combined with other sub stances, and uast into "pigs" for delivery to the customer. The arei surrounding the furnaces and casting department, called the yard. Is used for storing and transporting raw and processed metal. Bag houses are used to collect emissions from the reverbera tory furnace, thus reducing environmental contamination and permitting recy:ling. of lead contained in the effluent. Malfunctioning of this system in late 1974 and 1975 resulted in the accumulation of several tons of finely divided particulate ..ead which is scored in an open area of the yard. Maintenance men circulate throughout the work areas to repair malfunctioning equipment, the office and laboratory are separated from Che production area in a cleaner section of the company's property. This plant has been monitored by the State of Tennessee since shortly after operlng and has been found to be in violation of standards on many occasions (Table 1). Over the past 4 years, the company has bee.- cited 3 times by the Tennessee Department of Public Health Occupational and Radiological Health Division--twice for excessive exposure to airborne lead (1972 and October 1974) and once (October 1975) for an inadequate res piratory protection program. In October 1974, airborne lead levels ranged from 0.32,0 rag/n' calculated as an 8-hour time-weighted average* (twa). The inspections which resulted in the last 2 of these citations were prompted by reports of lead poisoning in workers at Che plant. Com;any records of blood lead testing of 12 long-term workers showed a rise in their average blood lead levels over the 12 months proceeding this investigation. PRELDUN.Y INVESTIGATIONS On October 31, Myron Frank, H.P.H., Staff Epidemiologist, Epidemiology Section, Tennes see Department of Public Health (TDPH), visited the smelter at She request of the Occupational and Radiological Division, TDPH. He interviewed .and obtained venous blood samples on 67 workers. Of these, 53.72 were found to have blood lead levels above HOug/lOOml, a level indicative of excessive absorption of lead requiring immediate medical evaluation (1). Fifty-four and one-half percent had significantly elevated levels (>lS0yg/100ml blood) of erythrocyte protoporphyrin, indicative of toxic inhi- * *The Occupational Saxety and Health Administration has established 0.2mg/m as the 0-hour average allowable exposure for lead in air in the workplace. 2 I S~f j' jii i i j' I 4 i i DUP040013367 04-0005-0526 r * '* ' * I l* * - >. 1f. . 9, -i A -- _ bition of hemoglobin metabolism by lead (2). Accordingly, more comprehensive examina tions were planned to assess the health consequences of these elevated blood levels. TABLE 1 History of Lead Exposure At A Secondary Lead Smelter Excessive Airborne Lead Concentration Noted Enforcement Letter or Citation Issued s .- Year Number of Letters/ Year Citations 1952 1953 1955 1956 1958 1962 1965 1972 1974 .1951 1953 1955 1958 1961 1962 1965 1967 1970 1971 1972 1974 1975 1 1 1 2 1 4 1 3 1' > 1 1 1 1 METHODS On November 24 and 25, workers were requested to participate in a comprehensive medical examination designed to evaluate the health effects of lead exposure at the plant. Participation was voluntary, and workers were advised of the provisions of the Privacy Act of 1974. Attempts were made to contact former workers who had terminated employ ment within the past 3 months. Those agreeing to participate were interviewed by 2 ; representatives of the Memphis-Shelby County Health Department regarding their work : histories, symptoms during ,he past year consistent with lead poisoning, and certain demographic information. Two physicians who were not aware of the workers' exposure histories performed brief physical examinations, with special attention given to the ! nervous system (Appendix 15. Blood pressure was measured by an automated system. Laboratory tests included blood sampling for determinations of lead, erythrocyte pro toporphyrin (EP), hemoglobin, urea nitrogen, glucose, cholesterol, and uric acid con centrations; urine sampling for arsenic concentration; chest x-ray; and, on selected individuals (those examined on the second day and those with elevated blood lead levels on earlier testing), measurement of conduction velocity of the right ulnar nerve, ~"""Blood sampling, chest x-ray, and physical exams were performed in a mobile unit supplied by the Memphis-Shelby County Health Department with the assistance of county health department personnel. Nerve conduction tests were performed by Richard Cilmartin, M.D., staff neurologist, LeBonheur Children's Hospital, who used cutaneous electrodes with out sedation. Blood and urine analyses were performed in the laboratories of the Memphis-Shtlby County Health Department; the Clinical Chemistry Division, Bureau of Laboratories, CDC; and the National Institute for Occupational Safety and Health. A concurrent Industrial hygiene evaluation was conducted by John Baker, Industrial Hygienist, Occupational and Cadiologlc&l Health Division, TDPH. This evaluation in cluded sampling of personnel in each area of -he plant to determine individual levels of exposure to airborne lead. t IS* I .4 'v x DUP040013368 04-0005-0527 'S ^ -- b -s-; > - Children of workers end of families living near the plant were tested for lead absorp tion by the Childhood Lead Poisoning Prevention Program, Hemphis-Shelby County Health Department, under the leadership of T.A. Taylor, Director. Seventy-seven current employees'-and 1 former employee participated in these evaluations representing 92? of the work force eaployed on November 24, 1975. All workers were in terviewed and tested for blood lead and CP concentration and urine arsenic level* Com'* plete physical examinations, blood chcnistry testing, and chest -x-rays were performed on all except 7 workers, who were not tested because of a shortage of personnel on the second afternoon. Ulnae nerve conduction velocities were measured on 41 workers, RESULTS Blood Lead. Testing - Blood lead levels ranged from 16 to 184pg/100al, with .2.6 workers (322) having levels >80ug/i00l, 52 (67?) having levels >60ug/100ml, and 64 (822) haying levels >40vg/100nl,e Elevated blood lead levels were seen in all areas of the plant, especially in production workers (Table 2), Elevated levels in men in battery wrecking and the yard (considered by the company to be relatively low exposure areas) were re lated in part to transfer of personnel to these areas from high exposure jobs after high lead levels or illness had occurred. These areas of the plant also exceeded the OSHA standard for lead in air. Significantly elevated lead levels were noted in workers who had worked less than 1 month (mean * Slug/lOOal). Blood lead levels >60tig/100ml were noted only in those working store than 2 months (Figure 14). Svmotoms - Classical symptoms of lead poisoning were closely related to elevated blood levels. The percentage of workers with 2 or more of these symptoms increased with increasing lead levels (Table 3). Workers with symptoms had significantly higher lead levels than those without symptoms (Table 4). TABLE 2 dob Category of Employees and Associated Findings, Memphis, Tennessee, Koves&er 1975 Job Category Blood Lead Levels Humber of (iig/100ml) Employees Mean (+ S.E.M.) Battery wrecking 10 104.00 (+ 14,66) Maintenance 9 87.22 ( 9.14) Yard 7 85.86 ( 16.26) Furnaces 24 77.29 (+ 5.35) Truck driver 1 72,00 Casting 8 70.00 (+ 9.55) All Production 59 89.35 ( *.1.5) Supervisor 5 49.60 (+ 5.67) laboratory 2 47.50 (+ 12.50) Cf flee 12 40.83 (+ 5.12) Honproduction 19 43.84 (i 3,71) Median Months of Employment 2 11 2 5.5 70 3.5 4 1 10 17.5 12 Race (Percent Black) 90 11 71 88 100 100 76 0 0 0 0 *A blood lead level >60us/100ml is currently felt to represent excessive absorption of lead requiring immediate medical attention, A level >40ug/100al indicates increased lead absorption (JL). V , IS3 \ DUP040013369 04-0005-0528 / - -- .5 .40 N Fig. / LEAD LEVEL IN PRODUCTION WORKERS BY LENSTH OF EMPLOYMENT 9 l V-. TABLE 3 Blood Lead Levels of Employees in a Secondary Lead Smelter, Memphis, Tennessee, November 1975 < AOus/lOOml Number of Employees 14 (181) Number with 2 or more symptoms of lead poisoning* 2 (142) 40-79uR/10Qal 38 (492) 11 (292) > SOug/lOOal 26 (332) 17 (652) *1, CaBerointestlnal symptoms (nausea, vomiting, diarrhea, and/or constipation) 2. Abdominal pain 3. Muscular weakness and/or tremor 4. Anorexia 5. Joint pains. 6. Consttutlonal complaints (fatigue, insomnia, irritability, and/ Or headache) 5 lsv x DUP040013370 04-0005-0529 TABLE 4 Distribution of Symptoms and Blood Bead Bevels of Employees, Memphis, Tennessee November 1975 Symptom Present/ Absent Number Employees (2) Blood Lead Level Mean (lie/100ml) . Gastrointestinal symptoms Present Absent 17 (222) 61 101.24* 65.98 Abdominal pain Present Absent 13 (172) 65 100.77* 68.25 Neuromus cular symptoms Present Absent 21 (272) 57 94.52* 65.98 Anorexia Present Absent 18 (232) 60, 93.89* 67.60 Joint pains Present Absent 22 (282) 60 92.59* 1 66.23 Constitutional complaints Present Absent 31 (402) 47 89.68* 63.11 `Significantly greater than level of those without symptoms (p < .01, 1-talled t test) Hematologic Effects - Inhibition of hemoglobin synthesis by lead was demonstrated by a close relationship (r * .76) between blood lead levels end blood levels of erythro cyte protoporphyrin (EP), a hemoglobin precursor which accumulates because of enzym atic Inhibition of lead (Figure 7). Anemia, defined as a hemoglobin concentration less than 14 g/lOOml (3), was seen in 11 workers. Anemic workers had significantly higher blood lead end EP levels than non-anemic workers (lead: 108,2 vs 86.0ug/ 100ml, p < .01; EP: 309.4 vs 182.3Ug/100ml blood, p< .01). Neurological Effects - Peripheral neuropathy was seen in 10 workers, manifested by weakness of wrist extensor muscles tested by physical examination. Workers with weakness had significantly higher lead and EP levels than those not effected (lead: 97.2 vs 69.8ug/100ml, p< .025; EP: 326.5 vs 176.9ug/100mi blood, p< ,01), Nerve conduction velocity did not correlate with the presence of wrist weakness or with lead or EP levels. Renal Effects - Elevated blood urea nitrogen (BUN) levels (greater than 20mg/100ml) were seen in 6 workers (range 22-40mg/100ml). Mean lead levels for azotemic and nonazotemic workers were 95.00 and 71.89i:g/100ml, respectively; these means are not signif icantly different. Azotemic patients had worked at the plant for a longer time and were older than those with normal BUN levels. 6 iss DUP040013371 04-0005-0530 Fig 2 BLOOD LEAD AND ERYTHROCYTE PROTOPORPHYRIN LEVELS IN WORKERS. MEMPHIS, TENNESSEE. 1975 Arsenic Analyse* - Elevated urine arsenic concentrations (greater than lOOwg/liter, when corrected to a specific gravity of 1.024) were noted in 10 of 72 (14Z) workers tested. Uigaest levels were seen in the casting area, where arsenic is added to mol ten lead (Table 5). Other Resales - Abnormalities other than wrist weakness which were detected on physical examination and were suggestive of lead toxicity included tremor of the hands (2 workers), diminished or asytsaetrlcal deep tendon reflexes (4), and possible lead lines on the gums (2). Hypertension was noted in 3 workers. Serum uric acid levels were normal in all workers tested. Slood glucose and cholesterol levels bore no relation ship to lead or arsenic levels. Chase X-rays were normal in all but 2 workers--1 with pleural scarring and the other with a nonspecific process requiring repeat studies. .........* I \ 7 /5"C_ | DUP040013372 04-0005-0531 r^.rf*****, \ TABLE 5 Arsenic Levels of Employees, by Job Category, Memphis, Tennessee, November 1975 Category Number Urine Arsenic Levels* (ug/liter) Mean (+ S.E.M.) Casting Maintenance Battery Wrecking Yard Furnaces Supervisor Office and Lab 8 8 9 6 '21 5 14 107,0 74.5 58.9 31.1 39.7 (+ 22.7) (+ 20.7) (+ ie.3) 7.2) <+ 6.2) 67.7 (+ 36.8) 16.7 (+ 1.6) Corrected to a specific gravity of 1.024 "by the formulas _ . ,_ ,__(1.024 -r 1.0) _______ ..Measured epor one n a on (sample epccific gravity - 1,-0) Concentration Community end Fgaily Testing - The Hemphts-Shelby County Health Department's Childhood Lead Screening Program tooted 228 children under 6 years of age in census tract 55, which borders the'smelter end extends 1 mile to the north and east. Thirteen children (6X) bad positive tests, i.e., a blood lead level greater than 30yg/100al and an EP level over 59ug/100l bipod. The homes of these children were located throughout the census tract. In a census tract of comparable socioeconomic composition located in an industrial area without a lead smelter, 29 of 307 (92) children tested had positive tests. Children of smelter workers were also tested in November and December .1975. Prelimi nary results on 4.7 children revealed 32 (682) with lead levels >_30yg/100al, 20 (43Z) over 39ug/100al, end 5 (112) with a lead level over 80ug/i0dal or an EP over 190ug/10Ctal blood,* Four children were hospitalised and chelated during the week of January 5, 1976. Two infants were found to have elevated levels: a 4-month-old boy with a lead level of SO and an EP of 185, and another 4-onth-old hoy with a lead level of .52 and an EP of 92. Correlation of Exposure with Signs and Symptoms - Manifestations of lead poisoning are proportional to the exposure to lead, 2 Important determinants of which are duration of exposure and dose. These parameters can be roughly evaluated by relating length of employment and blood lead level to the presence of signs or symptoms of lead poisoning. None of the workers who had worked at the plant less than 2 months had experienced gastrointestinal symptoms (or abdominal pain) or were found to have wrist drop (Figure 3), One worker, who had completed 1 month of work, was anemic (Hgb 13.0 gm/ 100ml with a lead level of 79yg/100ml and an EP of 299ug/i00al). *A lead level >30yg/100al in children is Indicative of excessive absorption; a lead level >80yg/100ml or an EP level >_190yg/ 100ml blood represents excessive absorption which necessitates immediate medical attention (4). 8 ' ................................. _ _____ ................................ . . ; j / 5~7 i 1 1t i 1 DUP040013373 04-0005-0532 Fig. 3 PERCENTAGE OF PRODUCTION WORKERS WITH SYMPTOMS AND SIGNS, 8Y LENGTH OF EMPLOYMENT 40 WRISTDROP Much higher rates of symptoms end signs Appeared in those working for 2-3 months and for 4-12 months. For 5 of 6 symptom categories, those working over a year re ported fewer symptoms than chose working for 4-12 months. 1 O1-- i --r 40l ANEMIA BOv GASTROINTESTINAL SYMPTOMS Gastrointestinal symptoms, wrist drop, and anemia tended to occur at comparable blood lead levels (Figure 4). Virtually no workers had these manifestations with a blood level below SOug/100ml. Approxi mately 202-251 of workers with either gestrolntestlonal symptoms, anemia, or wrist drop had blood lead levels less than 80ug/100ml. A cumulative percentage of 502 with a given sign or symptom was reached at approximately 90ug/100ml. PERCENTAGE rtg 4 HiassEn a n o c u mu l a t iv e p e r c e n t a g e o f w o r k e r s WITH SYMPTOMS AMO SIGNS, 6Y SLOOP LEAD LEVEL Relationship of Air Levels to Blood LevclsThere were S individuals who had both blood testing and air sampling performed on November 25; all of these individuals had worked for at lehst 2 months in the job which they held on that day. There was a correlation (r .56, n " 8) between individual blood and air levels. Mean area alt lead concentrations, however, were poorly correlated with mean blood levels of employees working In that area (Table 6). In the battery wrecking area, where air lead levels averaged .12 ng/m worker blood levels ranged from 66 to l$4wg/lDQal, with the lowest levels being in those working for less than 2 months (66, 75, and 79bg/10Qml). DISCUSSION Employment *t this lead smelter poses a significant risk to the health of pro duction workers and their children. Ane mia, peripheral neuropathy, and possible kidney damage occurred in workers as prob able Sequelae of occupational exposures to lead. Hospitalization of smelter workers' children for treatment of lead poisoning Occurred as an apparent result of their exposure to dust from their fathers' con taminated work clothing. Moderately ele vated blood lead levels have been noted previously (5,'6) in children of lead smelter workers, but none of the levels were high enough to require hospitaliza tion or treatment. In December 1975, 12 plant workers received outpatient chelation with intramuscular injections of calcium EffTA as treatment for signs and symptoms of lead poisoning. 9 / 17$ DUP040013374 04-0005-0533 TABLE 6 Mean Air Lead Concentrations and Blood Lead Levels of Employees, by Job Category, Memphis, Tennessee, November 1975 Job Category Mean Air Lead Concentrations (mg/nr, 8-hr. TWA) Number of Workers Sampled Kean Blood Levels for Workers (ng/lOOniV _ _ . . I Number Yard .39 2 69,7 5 Smelter .35 5 72.4 20 Casting .35 4 88.9 8 Maintenance ,27 2 89.5 U battery Wrecking .12 3 110.1 7 Only workers who had not been transferred f ro another job category during the previous 2 months. The most alarming finding of this investigation is the occurrence of lead poisoning in children of lead workers. Preliminary data from a study of these children revealed elevated concentrations of lead (up to .60,000 ppm) in household duet in their hemes, most of which did not contain lead paint. This finding underscores the importance of personal hygiene in preventing family members' exposure to lead originating In the workplace and of surveillance of family members. This plant is hot unique among secondary lead smelters. An investigation by GDC (?) of a similar smelter in Troy, Alabama, revealed that SIS of workers had blood lead levels over 80ug/10Qml, and 8 had been hospitalised for lead poisoning. Since the Initial investigation, 21 addi tional employees of the Alabama smelter have been diagnosed as having lead poisoning, and 6 have been hospitalised. Environmental contminstlon that has caused human and animal illness has been documented around other secondary lead smelters (6,8). One of the most significant findings in this study was that approximately 252 of workers with signs and/or symptoms of lead poisoning had lead levels in a range pre viously presumed to be safe (below 80ug/100al). While there was good evidence for a dose-response relation in these symptoms, there was no evidence of a threshold of effect. Other recent work has also demonstrated the presence of neurologic (10) and renal (11) toxicity in lead workers with blood lead levels below 80tg/100a. Inhibition of heme biosynthesis has likewise been shown in this and in previous studies to occur at blood lead levels well below 80ug/100ml. Such findings support the current ini tiative to revise the acceptable level for lead in the blood of workers downward to 60ug/100nl. An unresolved issue is whether or not the pathologic processes caused by lead absorp tion are reversible. Anemia, when related to lead-induced enzymatic inhibition, is reversible upon cessation of lead exposure. Levels of protoporphyrin in the blood and urine also tend to return to normal, though more slowly than the blood lead level. Neurotoxicity of lead may be irreversible if the extent or severity of exposure is great encugh (12)t however, peripheral neuropathies with wrist drop are often reversible 10 I IS In their early stages - The status of renal toxicity is more controversial: an early_ effect of lead on the kidney Is a reversible tubular dysfunction (Fanconi's syndrome) with little glomerular involvement. Chronic "end-stage'' renal disease due to lead is - - felt by some to follow prolonged severe exposures. Furthermore! recent studies have shown increased rates of lung cancer in workers with prolonged exposure to arsenic (13) and lead (14). RECOMMENDATIONS 1. Occupational exposure to lead at this plant must be terminated itnnedlately to ' prevent further disease among this seriously affected group of workers.. Temporary Closure of the plant is the only way to assure cessation of exposure. Interim measures! such as respirator use and improved personal hygiene should reduce lead exposures hut may delay meaningful irprovements. Specific hygiene procedures are discussed in the HIOSH Criteria Document on Occupational Exposure to inorganic Lead (1). Engineering controls are the only way in which a permanent reduction in exposure cao be assured. The plant was closed temporarily on January 19, 1976; it reopened 1 week later at a reduced level of production. Improved personal hygiene and respiratory protective measures have been instituted. 2. Workers with symptoms of lead poisoning, evidence of systemic ^ffects of lead, or elevated blood lead levels should be removed from exposure and should be referred immediately to a physician for evaluation. Maury Bronstein, M.D., internist, examined all referred workers December 1975-January 1976, treating several of them. 3. A controlled study of children of lead workers should be performed to evaluate sources of lead in the home and to relate these sources to blood lead level elevations. The study is currently being.conducted in cooperation with the Memphis Childhood Lead Screening Program. 4. A more comprehensive evaluation of neurologic and renal toxicity of lead exposure in these workers should be undertaken by specialists in the Memphis area. Workers could be referred through the county health department for such studies, Richard Gilmartln, M.D., Staff Neurologist, LeBonhaur Children's Hospital, and Fred Hatch, M.D., Chief, Division of Nephrology, University of Tennessee Medical Center, began seeing referred patients in mid-January 1976. REFERENCES 1. Criteria for a recommended standard--occupational .exposure to inorganic lead. Washington, DC., U.S. Department of Health, Education, and Welfare, National Institute for Occupational Safety and Health, 1976 2. Fiomelli S, Davidow B, Guinea JJF, et al: The FEP (free erythrocyte porphyrins) test: a screening micromethod for lead poisoning. Pediatrics 51:254-259, 197:3 3. Wintrobe MM, Thorn GW, Adams RD, et al: Harrison's principals of internal medi cine, 6th edition, ricCraw-Uill, Mew York, pg 2015, 1970 4. Increased lead absorption and lead poisoning in young children. U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, Atlanta, GA 1975 ^ 11 /CO DUP040013376 04-0005-0535  5. Landrigan PJ, Baker EL, Feldman K5, et al: Increased lead absorption with subclinical poisoning among children near a smelter. Proceedings of the Inter national Conference on Heavy Metals in the Environment. Toronto, 27-31 October 1975 6. Martin AE, Falrweather FA, Buxton R St. J, et al: Recent epidemiological studies of environmental lead of industrial origin. Proceedings of the CDC-EPA-WKO Inter national Symposiurr--Environment and Health, Parts, June 1974 7. Levine RJ, Moore RH Jr., McLaren CD, ct air Occupational lead poisoning, animal deaths, and environmental contamination at a scrap smelter. AJI'H (in press) 8. Hammond PB, Aronson AL; Lead poisoning in cattle and horses in the vicinity of a smelter. Ann NY Acad Sci 111: 595-611, 1964 9. Roberts TM, Hutchinson TC, Paciga J, et al: Lead contamination around Secondary smelters; estimation of dispersal and accumulation by humans. Science 186:11201123, 1974 10. Seppalalnen AM, Tola S, Hernberg S, et al: Subclinical neuropathy at "safe" levels of lead exposure. Arch Environ HIth 30:180-183, 1975 ' J' 11. Weeden RP, Maesaka JK, Weiner B, et al: Occupational lead nephropathy. AHJ 59; 630-640, 1975 12. Coyer RA, Rhyne BE: Pathological effects of lead. International review of experi mental pathology 12:1-77, 1973 13. Ott CM, Holder BB, Cordon HL: Respiratory cancer end occupational exposure to arsenicals. Arch Environ Hlth 29:250-255, 1974 14. Cooper WC, Caffey WR; Mortality of lead workers. J Oce Med 17:100-107 Edward L, Baker, Jr., M.D. Environmental Hazards Activity Cancer and Birth Defects Division Burejau of Epidemiology Bobby F. Craft, Ph.D. Acting Director Division of Surveillance, Hazard Evaluation $ and Field Studies Rational Institute for Occupational Safety and Health David S. FolfamrTM.D. SIS Officer Assistant State Epidemiologist Tennessee Department of Public Health Philip J. Landrigan, M.D. Chief, Environmental Hazards Activity Cancer and Birth Defects Division Bureau of Epidemiology John Liddle, P.i.D. Assistant Chief Toxicology Breach Clinical Chemistry Division Bureau of Laboratories i- f; Clark V. Heath, Jr,, M.D. 'I rector Cancer and Birth Defects Division Bureau of Epidemiology 12 !(,( DUP040013377 04-0005-0536 I.D. i APPENDIX 31 - . ^..- - Form Approved OMB No. 68-R1009 NAME AGS SEX MAILING ADDRESS RACE: PHONE # DATE HIRED JOB DESCRIPTIONS AT SMELTER (MOST RECENT FIRST) INCLUSIVE DATES SYMPTOMS DURING THE PAST YEAR; Loss of appetite Headcche Muscular Weakness Nausea Vomiting Diarrhea Constipation Cough YES NO DURATION YES NO DURATION Tremora Insomnia Irritability j. Joint Pains Fatigue \ Leg Cramps Abdominal Pain ONSET DATE OF 1st SYMPTOM HAVE YOU SEEN A PHYSICIAN ABOUT ANY OF THESE SYMPTOMS? RECEIVED TREATMENT FOR THESE SYMPTOMS? . .... HOSPITALIZED? __________________ . . . ... ....... ALCOHOLIC BEVERAGE CONSUMPTION? ... _________' NOEOCCUPATIONAL ACTIVITIES WITH POSSIBLE EXPOSURE TO LEAD OR TO DUST OR FUMES? '. . ......................... j PHYSICAL EXAM: SKIN CHEST NEUROLOGICAL CRANIAL (INCLUDING FUND!) MOTOR (WRIST OR ANKLE DROP) (GRIP STRENGTH) SENSORY .CEREBELLAR TREMOR ' _________ .. _________ .. .' - . . . .__________ ,. TF 4.240 (CDC) 11-75 13 IU j DUP040013378 04-0005-05.37 . ,r:i V.i. '? : * ' DISTRIBUTION: Hailing keys 53-1,2,3 John F. Finklea, M.D., Director, NIOSH, Room 3-30 Park Building, 5600 Fishers Lane, Rockville, Md 20852 Lawrence A. Plumles, M.D., Medical Science Advisor, EPA (RD-678), *01 M Street, Washington DC 20460 Roscoe M. Moore, Jr., D.V.M., Chief, Priorities Evaluation Branch, Office of Occupa- ttonal Health Surveillance and Biometrics, NIOSH, Room 3-32 Parkiavn Building, 5600 Fishers Lane, Rockville, Md 20852 Robert Citron, Director, Smithsonian Institution, Center for Short-Lived Phenomena, 60 Garden Street, Cambridge, Ha 02138 Kenneth Bridbord, M.D., Acting Associate Director, Extramural Coordination and Special Projects, Room 3-50 Park Building, NIOSH, 5600 Fishers Lane, Rockville, Md 20852 Vernon Houk, M.D., Director, Environmental Health Services Division, Bureau of State Services, COG, Buckhcad Room 511, Atlanta, Ga 30333 John Liddle, Ph.D., Assistant Chief, Toxicology Branch, Clinical Chemistry Division, Bureau of Laboratories, Chamblee 32 rm 19, Atlanta, Ga 30333 Dennis Co k , Ph.D., Toxicology Branch, Clinical Cnemistry Division, Bureau of Labora tories, CDC, Chamblee 32, Atlanta, GA 30333 Renate Kimbrough, M.D., Medical Research Officer, Toxicology Branch, Clinical Chemistry Division, Bureau of Laboratories, CDC, Chamblee 31 rm 5, Atlanta, Ga 30333 David S. Foiland, M.D., EIS Officer Tennessee Department of Public Health, Cordall Hull Building, 6th Avenue If, Nashville, Tn 37219 1 Robert H. Hutcheson, Jr. , M.D., 109 Capital Towers, Nashville, Tn 37219 Myron Prank, M.P.H., Staff Epidemiologist, Division of Communicable Disease Control, Tennessee Department of Public Health, Cordell Hull Building, 6th Avenue N, Nashville, Tn 37219 Robert Ligo, M.D., Chief, Medical Services Branch, NIOSH, DSKEFS, Robert A. Taft Laboratory, 4676 Columbia Parkway, Cincinnati, Ohio 45226 George Lcrvejoy, M.D., Director, Shelby County Health Department, Memphis, Tn 38103 Gordon D. Nlfong, Ph.D., HEW Region IV, Division of Prevention, Room 836, 50 Seventh Street NE, Atlanta, GA 30323 Ken Kronoveter, Industrial Hygienist, Division of Technical Services, NIOSH, Post Office and Courthouse, Cincinnati, Oh -45202 T.A. Taylor, Director, Childhood Lead Poisoning Prevention Program, Men^his-Shelby County Health Department, Menphis, Tn 38103 I | | 5f 14 11 -5_! DUP040013379 04-0005-0538 April 29, 1976 APPendix 4 MEMORANDUM TO: Harry L. Gibbons, M.D., M.P.H., Director Salt Lake City-County Health Department FROM: Alan C. Barbour, M.D., E.I.S. Officer Dan Peterson, Occupational Health, Salt Lake City-County Health Department Jeff Throckmorton, Radiation-Occupational Health, Bureau of Environmental Health SUBJECT; Epidemic of Lead Poisoning at a Secondary Swelter IKTRODUCT10!> In late December 1975 the Salt Lake City-County^Health Department was notified by 3 local physician of 2 recently hospitalised cases of lead poisoning. Investigation revealed another 3 men who had been admitted in December and January to the same hospital and who had been diagnosed as having The 5 men worked at a small secondary smelter in Salt Lake City. Members of the Salt lake City-County Health Department, and of tie Bureaus of Environmental Health, of Disease Prevention and of Laboratories of the Utah State Division of Health began an investigation of this outbreak of lead poisoning among the smelter workers. BACKGROUND The secondary smelter is located in an industrial area of Salt Lake City but there are clusters of private residences within 1,000 meters of the smelter stack <See Map I). The work force usually consists of 20 people: a manager and one part-time secretary in the office, two chemists, two supervisors, two general cleanup and maintenance men, one part-time custodian and 11 furnace workers on three, 3-man shifts per 24 hours. Employee turnover is greatest A among Che furnace workers; 36 men filled those 11 positions between September 1975 and .January 1976. I <7<T DUP040013452 i Harry 1.. Gibbons, M.D., M.P.H. April 29, 1976 Page 2 Prior to 1971 the sodter processed lead. When it changed ownership in 1971, antimony was smelted. Proa January 1 to August 6, 1975 they produced '92,000 pounds of antimony. On August 6 the smelter operation wps A again changed to produce lead using the process of direct reduction of ; oxide material. Into the stationary reverbatory furnace, the furnace V / workers shovel lead dross shipped in from primary smelters in the Los Angeles, California and Portland, Oregon, The charging material has average concentrations of 73% lead (Pb), 4.5% sulfur, 1.32 antimony (Sb), 1,1% tin, 0,7% copper, 9.8% iron, 0.3% arsenic (As), and 0.2% zinc. The final product averages 87% lead and 13% antimony with traces of tin and copper. The exhaust of the furnace is to a bag house and then through the stack. (See Map 2) The smelter has a changing room with showers and a small lunch room for employees. METHODS Case definitions of lead poisoning and probable lead poisoning ate listed in Table 1. Questionnaires eliciting information on length of employment, job duties, work and social habits, symptoms and onsets were administered to available workers who were both employed at the secondary smelter at some time in period September 1975 - January 1976 and had blood and/or urine lead levels performed between September and January. Whole blood lead and urine lead and arsenic levels were performed at the Bureau of Laboratories, Utah State Division of Health. Blood samples were drawn into 15- ml heparinized tubes; these tubes had a back ground of 0.25 yug of lead per tube at maximum. If 10 ml of blood had /8Gr DUP040013453 Harry t. Cibbons, H.D., M.P.H. April 29, 1976 Page 3 been drawn Into one tube, the background of the blank tube would contribute at most 2.5 jig to the test result. The colorimetric method of j(ccnan was used for blood lead determination. Fifteen duplicate blood samples were also tested at the Western Area Occupational Health Laboratory, National Institute for Occupational Safety and Health for whole blood lead, arsenic, and antimony by atomic absorption. Unless otherwise indicated all lead levels used are those reported by the State laboratory. Air samples were taken from both personal and stationary samplers on - -'T* three days during different activities. They were analyzed for lead, arsenic, and antimony using a O.kSj* rdllipore filter on a M.S.A. permissible portable pump. Ceiling deposits, settled dust, and floor dirt in the furnace room and other locations were also analyzed. Hospital and physician records of the workers were reviewed after obtaining appropriate releases, INVESTIGATION Forty-two persons (41 males, 1 female} both worked at the smelter in the period September to January and had had a lead determination performed. Eleven asymptomatic men had worked only in September but had not been tested. Of the 42, 36 (86%) were interviewed. Six had either left the state or gave no forwarding address when they moved. Nineteen cases of definite lead poisoning and 3 cases of probable lead poisoning occurred among the 36. The distribution in time of the definite and probable cases by date of onset pf symptoms is shown in Figure 1A, Seven men were hospitalized; their admission dates are shown in Figure IB. The mean duration of hospitalization was 9 days with range of 4 to 14 days. i , >>. * s'- s wi DUP040013454~ Harry L. Gibbons, M.D., M.P.U. April 29, 1976 Pnge 4 The incidence of lead poisoning when adjusted for exposure (worker-months) was 75 per 100 worker-months during December and 3 per 100 worker-months for the period of August to November (Table 2), CLINICAL The frequency of symptoms Of the 22 cases are listed in Table 3. Specific muscle weakness was not a prominent symptom in this outbreak; no worker had wrist drop cither subjectively or t.hen examined at time of first treatment. Two hospitalized cases who were tested had ^mild peroneal nerve slowing On r.erve conduction velocity. Mean duration of symptoms was 20.5 days. One worker was ill for 90 days before diagnosis and chelation therapy started. He had been treated for "peptic ulcer". Two workers may have had encephalopathy; one presented with a history of periodic confusion; another had a grand cal seizure after being seizure-free on medication for 3 years, A total of 19 of the cases received chelation therapy. In Figure 2 are the distribution of blood lead levels (State Laboratory values) for asymptomatic and symptomatic workers. The symptomatic worker who had a blood lead of 20had at the same time a urine concentration of 0,44 rag/L, elevated urine coproporphyrins (0.9 mg/L> and AALA (22 rag/L), and anemia (Hemoglobin 13.0 Gms). Twenty-one workers who had blood lead determinations also had hemo globins performed. Figure 3 shows these hemoglobin levels by blood lead level (50-79, 80-120, and >120 yugZ). Twelve of IS men with blood Pb2:80^i.g% had hemoglobins less than 14.5 Gms. When blood lead levels were adjusted for a hemoglobin of 15.0 Gms, the mean values for the 50-79, 80-120, and >120j u l gZ groups were respectively 15,2, 13.5, and 13.5 Gms hemoglobin. The worker with a 10.9 Gms hemoglobin, highest determined blood lead level Mat Harry L. Gibbon, H.D,, M.P.il. April .29,. 1976 Page 5 was 80 yigZ (110 ^g% when corrected to 15.0 Cm llgb), His urine A ALA was 59 mg/L (normal<6 mg/L), his erythrocyte protoporphyrin was 100 MgZ/lOO ml, urine coproporphyrin was 607^.g/24 hrs, (normal<2Q0), and his bone marrow showed increased iron stores, increased sideroblasts, and ringed sideroblasts. Of those workers with blood Pb levels ofrS0^tgZ, 7 of 12 with more than 6 months employment at the smelter had hemoglobins Of less than 14.5 Gmn. Only i of 7 workers with 6 or less months of smelter employment and blood Pb levels of 2:80yj.g% had hemoglobins below that level. Serum transaminase (SCOT) levels were elevated in 4 of 8 workers with 'P Pb levels sJSOy.sgZ (mean 105 units, range 66-156, with normal;40 units); six workers with Pb levels of 50-79^.gZ all had normal SCOT levels. Alkaline phosphatase, LDH, and bilirubin levels were normal in all 12, Four definite cases had Blip's oyer 20 but the highest was only 28 and creatinine levels were normal. Tests for reducing substances in the urine or to cases were negative. Duplicate samples tested for blood lead at N.I.O.S.U. laboratory had higher levels than the state laboratory in 13 of the 15 samples. Agreement was closest in the range of values 55 to 168; the mean difference between the two laboratories was 10.3y-gZ (Table 6), Whole bleed arsenic levels of 15 samples all were below the detectable level by atomic absorption. Arsenic levels on 20 workers' urine samples, 14 (702) of which had elevated concentrations of lead (>150^g/L), were in normal range (10-60ycg/L). Blood antimony levels in 7 of the 15 workers were above the limit p detection (Table 6). Five of these 7 had the highest blood lead levels among all the cases, A 24 hour urine for antimony was less than 200y^-g/L in hospitalized case whose urine lead on the same sample was 480yicg/L, Urine antimony levels p*1000yig/L indicate significant absorption. DUP040013456 Harry L. Gibbons, M.D., M.P.H. April 29, 1975 Page 6 EPIDEMIOLOGY The cluster of 20 cases with onset in or around December suggested au intense exposure of limited duration. Among these 20 cases were two refractory repairmen on contract to maintain the equipment. These 2 plus A other repairmen from the same contractor worked at the smelter for short periods in December. Blood lead levels were drawn on the 6 repair men on December 23. Work logs were examined to determine the timing and amount of exposure. Table 4 shows that it was not the total hours of 'm exposure in.December but specifically the hours worked during the week of December B-1A that best identified cases and elevated lead levels. We then looked at all those employed at the smelter in December. Because only 7 workers (controls) were not cases during this time, the those with levels >120 ^tg2 for stratified comparisons of types and amounts of exposure. Table 5 summarizes these comparisons. Among the 22 cases there was greater exposure to the furnace room than controls. The cases (both^and>120 ^g%) tended to have a higher percentage of smokers and to spend more of their day at smelter (full-time vs. part-time) than controls. The 9 workers with level >120^.gZ all worked full-time. The sub-group with levels >120 when compared with other sub-group of cases and controls tended to be older, to have worked at the smelter for more tha>. 6 months, and to eat more than 3 meals a week at the smelter. There was no significant difference or trend when the following parameters were examined: frequency of respirator use, frequency of shower and change of clothes after work, alcohol consumption, timing of 8 hour shift, possession of earthenware pottery at home, or milk consumption. The no / DUP040013457 Harry L, Cibbons, M.D., M.P.H. April 29, 1976 Page 7 workers denied caking any lead metal home with them. Only 3 of the 22 cases had any children less than 8 years old at home; the majority of workers were cither single or had grown children. One symptomatic case with onset in December was the company president; his highest blood level was 167yrg*. He spent less than 102 of his time in the furnace room, did mostly office work, and ate all of his meals outside of the plant. A female Secretary worked 3-4 hours a day in an 4)U ' T* adjacent office (see cap). She never went into the furnace room. The secretary was asymptomatic but had a blood lead level of 42^tgZ. What was their exposure? We found that the intake for the ventilation-heating system supplying their offices was located in the warehouse room nest to the furnace room. The question of why 20 workers became ill in December remained. When the amount of lead smelted by month was tabulated (Figure ^f) we saw that no lead was processed in November and relatively little in December. The two cases with onsets in early October followed a month when 249,000 pounds were processed. In November the furnace was closed down for cleaning; the workers did maintenance work around tbs smelter. In December, although little lead was actually processed, an attempt was made to increase output. Two smaller capacity rotary furnaces were utilized for two weeks (December 2-15) in addition to the large stationary furnace. These rotary furnaces were not adequately ventilated, and fumes accumulated in the furnace room. Several workers described the air inside of the furnace room as being like a "thick fog" for one week. I V ----- JV____ DUP040013458 Harry L. Gibbons, M.D., M.P.H, April 29, 1976 Page 8 ENVInON'MENTAL SAMPLING Both personal and stationary air sampling showed excessive air lead concentrations especially during charging activitfs (Table 7). The sampling was done when only the reverbatory furnace was being used; the 2 rotatory furnaces were not in operation. Breathing z$nc samples showed thac employees were being exposed to up to 21 times the O.S.H.A. B-hour time weighted average for lead and 64 times the O.S.H.A. exposure limit for a 2-hour 38 minute sample. t Although all employees said that they used their respirators "frequently" or ".always", several were observed to be inconsistent in their use. However, one full-time employee^who spent less than 50? of time in the furnace room^had antimony hypersensitivity reactions and wore his respirator religiously; his blood icaa ievel was 143yj.g?> Area samples of the smelter revealed the following: (1) Ceiling deposits in the furnace room were 17? lead, 1Z antimony, and 0.5? arsenic; (2) Dust on the furnace room floor was 13% lead, 0.25% antimony, and 1% arsenic; (3) A wipe sample off 2.5 sq. feet of the lunch room table yielded 0.46 mg lead, 1.45 mg antimony, end 0.25 mg arsenic; and (4) 2,5 sq. feet wipe sample off the secretary's desk contained 0.41 mg lead, 1.25 mg antimony, and 0.35 mg arsenic. DISCUSSION We found that the outbreak was in major part due co the operation of the rotatory furnaces without adequate ventilation in early December, Two part-time workers, became ill after only 2 days exposure in the furnace room. The distribution in time and clinical presentation of the cases j^_ was more consistent with a high intensity exposure than chronic lead poisoning. / J i DUP040013459'. Harry L. Gibbons, M.D., M.P.li, April 79, 1976 Page 9 i. There is, though, some evidence of excessive lead exposures before and since the limited operation of the rotatory furnaces: (1) Two of the cases had onsets of illness in October; (2) Air lead concentrations were excessively high during normal operation of the reverbatery furnaces; and (3) long term employees tended to have lower hcraoglobjns than employees of shorter duration. Vhiie, the main route of intoxication was undoubtedly inhalation of the inorganic lead fumes and particles from the furnaces, the considerable environmental contamination of work and eating areas could hxve contributed to the worker's lead burdens., Arsenic (As) and antimony (Sb) were present in excessive concentr-cious in some of the air samples and in substantial amounts in dust and deposits. But there was no evidence of a significant contribution of either of these metals to the illnesses occr.. Arsenic urine levels were never elevated and while blood arsenic levels do not correlate as well with clinical status as urine As concentrations, blood As levels were not elevated in specimens from patients at their most symptomatic times. The blood Sb levels seem to vary directly with blood Fb levels but they were 1 to 2 orders of inagnitude less than the corresponding Pb concentrations. This was an epidemic of inhalation lead poisoning in an industrial setting. Such occurrences were common in the earlier part of this century and before, but at frimeri-lju, lead poisoning is primarily an endemic problem in roost industries. Most attention has been focused on settinc exact tolerable limits of exposutc-both air concentrations and blood concentrations.. In this dramatic outbreak such subtleties are less relevant, A small industry operated with little comprehension of the toxicity of lead and with excessive exposures of lead for all its employees. Such an industry should not n i 5 /" s. \ ' .v / A. *< DUP040013460 Harry L. Gibbons, M.D., H.P.H. April 29, 1976 Page 10 have even begun their lead smelting without prior consultation on proposed process, engineering and safety programs. CONTROL MEASURES ' (1) After initial evaluation imminent danger notices were posted, and the management was advised to inform their employees as to the danger cited by this notice. (2) When air sampling should excessive lead concentrations during normal operation and when the deficiencies were not corrected, the onto)ter was closed. (3) v.en more adequate furnace ventilation systems were installed for exhaust of fumes, when methods of charging that minimized dust emissions were instituted, and when housekeeping had improved, the smelter was re-opened. (4) Surveillance by air sampling and periodic blood lead levels of workers will continue. We wish to acknowledge the laboratory assistance of Dick Issacs and Jack Omar.at the Bureau of Laboratories, Utah State Division of Health. f. /9y s s DUP040013461  i'h I-/ i " "<& . -! >' -w -r,*\ -`- 'w " ****' . .V''1 :ttr :;* ft? ' T^.vy >u. *' . 'ey. :; ~ \\) -': ftift*' ` ft, ft i 'Hr ' r-ftft- ft 5C ft r Hi r -f tr::: ft','"* -ft>s:. 'f 't'. ' , C) j s- s: ft''ftftftftft-'" : .r vr-ft-ft'"' - ' ;_ ?!:_! . * . i' ! J, . iu* - ft rft,- : i' i -1 < j TT'! - . - t < ' -ft >- v;- ~1 i ! : Sft . - ,.-ft ~-l ' - v';: :1 -ft ft: I;- r "s***~r iV 4w. .. : -ft * . . .. \v.l-' ,ft:,Cft ftKftft `r; u'i . *4 if/>,f U! r !R ?*!; ft.v-wft-'ft l ; " ! : _ - I -v> -ft 'Ms ft); ; \. * * `\ V. '*>!'** * . . '-'.-A. .. .. ^'"v Ki_, ' 't ' \!f t.jj- r-- v, I 'll.: *-!_ -i I . 8 -A - `14. '.r../i': mu' - jt 1;!:i-i : U- '-r. ? ' ~-vxy;v.- =-- ' -- ,> ! " v:/i i - > . . . -U 1 /? . . i! j .j .j : - r~f' 1 - si-., --v-v r/ : ; n' i:.. .. ,,i._ '`1 ........... : * v-.' r' ft;; ..... J / H-l. vv ft ft ? vv ,\ . .. -v--:----- 1.-' "-''ft ' ' . ' : ______ ASL. . \ ' ' r - ' .. (-! \ .V . * * . i - Reproduced from best available copy I 1b ; ! i DUP040013462 1Hd cms IM Smtmd 140-KS 3s/ of oM$r 10 | ] vcfm o\i< ViI'k AZl C* d\<g m // izi <\[j z lc[5 \x r*--i------1 !/[a <=} \b 1$ ?o ej? 14 il h ij4 u ig WOK Of O/US-CT f\6m IB \\oipmy.mt> o&65 BV U&C of frDMSS'OAj 5- -T------ 1-----~l 4tftofaa \<\ 10 Ilk n Up 3 5) tt/7rt .21 3S ij'l )l wr'i'u- nr .T7V# .1/V-rr,v/ im -#- DUP040013463 5w- M- f\6-ot6 AL BwtfD UAv UQL- o mo *c Dit t o s 2^ /fcJ0>- Eo - bO ~ %' Ab - * 4 o0 o $ S .5. T--l----- ------ 1---- ------ ~----------r--r t t CUM I<rm^ ST/4T05 4* /??J DUP040013464 no lb'0- no- / criviQ i 13,0 - tii. If llA : .j A'W/vlj - SntflZiZ- C\)Cfcl'c: S' 8/ %U&> UAD ^{7<T6< l',Al . 9,0 i?d DUP040013465 ___________________ ____ }?f "i\ f .................. *>.* ^ i DUP040013466 TABLE X CASE DEFINITIONS A. Definite Lead Poisoning: Requited either: (1) Two of the following criteria plus blood lead level of >\?,0y<g/100 ml Gg%); (2) The presence of three of the following criteria plus blood lead of 1: SO^g/lOQ ml g'A) blood or urine lead of > 200^ug/L. B. Probable Lead Poisoning: This diagnosis required either; (1) The presence of one of the following criteria plus blood lead of it.80^/^g/100 ml blood or ur ine lead of >200ytg/L; or (2) the presence of two of the following criteria plus blood lead of 50-79 zig/100 ml o urine lead of 150- 200y,g/L. 1 CRITERIA 1. Abdominal pain or cramps, 2. Cctistitvt'ionai symptoms (at least two of the following: headache, general weakness, myalgias, dizziness, fatigueaoiiicy, in Liability 3 and/or insomnia) . 3. Gastrointestinal dysfunction (nausea, anorexia, Vomiting, diarrhea, . and/or constipation), 4. Neuromuscular symptoms (specific muscular weakness, tremor, and/or paresthesias), 5. Joint pains and/or chest pains. 6. Anemia (hemoglobin 14.5 Gms for adult male at 4500 feet above sea level). 7. Elevated free erythrocyte protoporphyrin (PEP) level (ar 110 ^.g/100 ml blood) and/or elevated urinary delta amino levulinic acid (ALA) level of>20 mg/L. \ l t Poo e.\. DUP040013467 i > A ik mis t-November December TABLE 2 Incidence of Lead Poisoning at Secondary Smelter August - December 1975 Number of Worker-Months Exposure-' 78 24 Number Of Cases* 2 18 Cases/100 Worker-Months 3 75 * Excludes 6 refractory repairmen . who worked <7 days in December. ! j Pot DUP040013468 TABLE 3 Frequency of Symptoms Among 22 Cases of Lead Poisoning* Symptom Abdominal cramps Nausea Diarrhea Headache Dizziness Anorexia Vomiting Tl--o .* C* Constipation Fatigueability General weakness Myalgias Weight loss (> 2 Kg) Irritability Chest pain Specific muscle weakness Tremor Insomnia Joint pains* Number Reporting 19 18 12 12 12 12 9 9 8 8 8 7 6 5 c 4 4 4 .4 Percent 86 82 . 55 5$ 55 55 41 41 36 36 36 32 27 23 23 18 18 18 18 * 19 definite and 3 probable cases. /\ II Jo? * DUP040013469 Exposure o f R e fra c to ry Repairmen to S m elter December 1975 23 1 38 1 b u 3 woa. X a a\ C\ CO st 0u) H w H eg b r-4 04 1 tn H <y O o 3 pQJ b w >3* ? t-4 V) 1 o CO a. ku w po V) k P r*oi o <y Q tu 0) oc O uu ea o. V) C >. p so rS G) > 0 a /* > CO J3 <vj P**s. 04 *0 r4 OV o pa 0- . o O' 00 CO o r*H w \D Ov H o Q o H O o 00 o r> Oo o oH f-4 >*S V. Ws w sa m w js 04 CM O p r-* >s 2a H CM o o o CO CO \ Mf <r O is M CO CM H m <o a> CO CO CO CO CO CO jtf M O ts 1 ) j' , ; J i \ \ i i. s i i , 1 oj DUP040013470 TABLE 5 Characteristics of Controls and Cases Mean Age (range) Control W-l 35 (17-60) Case (Blood Pb^lZO/ig) K12 7 27 (18-48) Case (Blood Pb >120 g) N=9 / 41 (20-61) Length of employment 5=6 months >-6 months 4 3 7 *3 56 Dally work Part-time Full-time 4 3 5 7 0 9 Cigarette smoking Yes Ho 1 6 8 4 7 2 Alcohol consumption Never or occasional Moderate to heavy i Futfnace room exposure* ! 50% of day 50% of day 5 2 5 0 8 4 2 8 5 4 4 5 Meals at smelter* 0-2/week 3-5+/veek 2 3 6 4 2 4 * Excludes 6 Refractory Repairmen. s I X I ? I | 71 i ri i i ! 1 1 1 .i i i DUP040013471 L a b o ra to rie s Mi / s' Bureau of L a b o ra to rie s *aoc oCH *C4O <5 *.cCo4O rO-o4 so .j1 0 i || Jo 4> i ii i t}c i ! DUP040013472 TABLE 7 Activity for Day General cleanup AIR SAMPLE COKCEMTUATLOXS OX THREE DAYS Location furnace worker office welder 81 welder 82 furnace room chemist lunch room Sample Result s {nu;/nj3) Dura tion if pb Sb As 242 > 330 214 339 317 244 261 ,060 .0318 .564 ,262 .096$ .168 .152 .586 .000 ,915 . 454 .107 ,223 .487 ,0025 .0021 ,0169 .006 .0043 .0034 .0043 Tapping furnace furnace worker $1 furnace worker 82 furnace room office welder 164 165 182 170 180 1,61 ,586 1.21 .0-96 , 729 2.93 .909 1.65 .000 .912 Charging furnace furnace worker furnace room welder 81 welder 82 office lunch room 197 8.40 380 2.65 357 1.39 188 .574 344 ,121 322 .029 DUP040013473 Harry L. Gibbons, M.D. April 29, 1976 Page 11 Distribution: 'Jeff Throckmorton. Radiation-Occupational Health Dan Peterson, Salt Lake City-County Health Department Rieh Uauck, Salt Lake City-County Health Uepartstnt Lynn Thatcher. Bureau of Environmental Health Dennis Dally, Bureau of Environmental Health Dick Isaacs Taira Fukushima, M.D. Lyman J. Olsen, M.D. Edward Baker, M.D., Environmental Hazards Activity Cancer and Birth Defects Division, Bureau of Epidemiology, Philip Landrigan, M.D., Environmental Hazards Activity Cancer and Birth Defects Division, Bureau of Epidemiology, CPC CDC DUP040013474