Document YG9bNRBmQqdDxmNgKgO50gXbN

LEAD AND INORGANIC LEAD RESPIRATOR SELECTION RECOMMENDATIONS National Institute for Occupational Safety and Health 5600 Fishers Lane Rockville, Maryland 20857 March 15, 1977 m N 30682 "/ DUP040013654 HIOSH Lead and Inorganic Lead Respirator Selection Recommendations, Karch 15, 1977 Airborne Particulate Concentration of Lead Fire-Fighting in excess of 200 mg/M^ or entry and escape from unknown concentrations Required Respirator t Self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positivepressure mode. Self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positivepressure mode. Sot in excess of 200 mg/H3 Sot in excess of 100 mg/M^ A combination respirator which includes a type C supplied-air respirator with a full facepiece operated in pressure-demand or other positive-pressure or continuous-flow mode and an auxiliary self-contained breathing apparatus operated in pressure-demand or other positive-pressure mode. A Type C supplied-air respirator with a full facepiece Operated in pressure-demand or other positive-pressure mode or with a full facepiece, helmet or hood operated in continuous-flow mode. A powered air-purifying respirator with a high efficiency particulate filter. Hot in excess of 5 mg/Jp !i A Type C supplied-air respirator operated in pressure' demand or other positive-pressure or continuousflow mode. a high efficiency particulate filter respirator with a full facepiece* Any supplied-air respirator with a full facepiece. Bot in excess of 1 mg/M^ Any self-contained breathing apparatus with a full facepiece. Any dust and mist respirator, except single-use respirator or quarter mask. Any fume respirator or high efficiency particulate filter respirator. Any supplied-air respirator. Any self-contaii'-ed breathing apparatus. Kot in excess of 0.5 mg/M^ Any dust and mist respirator, except single-use. FOLLOWUP OF HEALTH HAZARD EVALUATION (76-36) EAGLE PTCHER INDUSTRIES JOPLIN, MISSOURI Background: During a NIOSH Health Hazard Evaluation (76-36) of lead exposure at the Eagle Richer Industries, Lead Chemicals Plant in Joplin, Mo., 17 . of 53 workers examined were found to have elevated blood urea nitrogen (BUN) levels on at least one of two determinations; 2 workers had borderline results. Levels ranged from 21 to 44 mg/lOOml. Ten of these workers had been treated with oral calcium disodium EDTA on at least one occasion. Symptoms and signs of lead toxicity in this group included periperipheral neuropathy, anemia, and gastrointestinal and neuromuscular symptoms. Serum creatinine levels were within normal limits on all workers tested. Since elevated BUN levels are associated with renal disease, a wellrecognized sequela of chronic lead exposure, further medical evaluations were deemed necessary to determine: 1) the extent of renal functional impairment in these workers; 2) the role of occupational lead exposure in the etiology of this disease. Accordingly, these 19 workers (2 workers with borderline results were Included) were referred to a board-certified nephrologist in Tulsa, Oklahoma for outpatient diagnostic studies which were performed in July. Methods: Following complete history and physical examination, blood and urine tests were performed on specimens from each worker. In evaluating renal concentrating ability, the osmolality of a urine sample collected after * **,*. DUP040013656 a 12-hour water fast was determined (1). Creatinine and lead clearances were determined using 1 hour timed urine collections and simultaneously collected blood samples. Lead levels were determined by atomic absorption spectrophotometry. Beta^microglohulin levels were determined using a radioimmunoassay procedure.* Urinary amino add screen was performed using thin layer chromatography. Urine aminolevulinic acid (ALA) was measured by standard techniques. Blood chemistry tests (including creatinine,BUN, and 'trie acid) were performed using an automated clinical analyzer. Hemogram, differential, routine urinalysis, and VDRL were performed by standard methods. Participants were informed prior to testing of the voluntary nature Of the studies and that medical information would be treated in a confidential manner in compliance with the provisions of the Privacy Act. Results: History: Six of the 19 workers were hypertensive (blood pressure greater than 140/90 by history or when examined during this evaluation). Two workers were on treatment for hypertension at the time of examination. One hypertensive worker gave a history of a cerebrovascular accident in 1975, Eleven workers reported histories of musculoskeletal symptoms (wrist, elbow, back, or shoulders). Three men complained of recurrent abdominal colic and two men noted chronic easy fatiguability. *Kits produced by Pharmacia Diagnostics, Inc,, Upsala, Sweden. V^r DUP040013657 - 3Physical Examination: Physical examinations were generally within normal limits. No wrist drop or lead lines were noted. Laboratory Examinations: 1. Renal Function Testing Only five of the 19 workers tested had elevated BUN levels (722 mg/IOOml) and only one had an elevated serum creatinine concentration (>1.5 mg/IOOml) (Table 1). However, 8 (422) had decreased creatinine clearance (<91 ml/ min/1.73 sq m BSA) (Table 2). Impaired urine concentrating ability (i.e., Inability to concentrate the urine below 800 mosm/liter after an overnight water fast) was noted in 8 of 15 workers tested (Table 2). Lead clearance* calculated by the standard formula* (V), tended to decrease with increasing duration of exposure to lead (Figure 1). This inability to clear lead was independent of the age of the worker: analysis -of data from 45-55 year old men shows the same negative relationship between duration of exposure and clearance rate (Figure 2). Routine urinalyses were essentially within normal limits. Lead Tests: Fifteen (792) workers had blood lead levels >60ug/100ml, 7 (372) had levels >80ug/100ml. Erythrocyte protoporphyrin (EP) and urinary ALA levels showed comparable elevations (Table 3). EP and ALA-U levels were not correlated with lead clearance' rate (r = .05 and .17 respectively). UV * C = P where C = clearance; U * urine lead concentration; P = blood lead concentration; V = urine flow rate over collection period y/6 T DUP040013658 . -4- , Hematologic Tests; Five workers were anemic (hemoglobin less than 14 gm/100ml) (Table 3). Hemoglobin levels were not correlated with blood lead or EP levels or with lead clearance rate. Other Tests: Serum chemistry tests were generally within normal limits. Urinary betag microglobulin levels were strikingly elevated in two workers (993 and 4890 ug/liter) and normal in all others tested. Urinary amino acid screen was normal in all. ^ Discussion: These studies clearly demonstrate a significantly increased prevalence of mildly to moderately severe kidney disease in employees at the Eagle Picher plant in Joplin, Missouri. Although further studies are needed to clarify the cause of these disorders, lead nephropathy is a likely etiology for several reasons. These workers have been heavily exposed to lead for prolonged periods (5-30 years) and manifest other toxic sequelae of lead exposure including anemia, recurrent colic and joint symptoms. Both renal glomerular and tubular dysfunction were noted in these men, a pattern previously noted (2*3) in other studies of lead nephropathy. A positive relationship exists between the degree of renal dysfunction (impaired lead clearance) and duration of exposure to lead; an effect which is independent of age. In view of these findings, other etiologies of renal disease seem unlikely but must be ruled out with further testing. DUP040013659 -5 This study illustrates the insensitivity of blood urea nitrogen and serum creatinine determinations and routine urinalysis in detecting renal disease; this finding has been well documented in the medical literature (1). More sensitive measures should be used in screening for lead nephropathy in exposed populations; such tests could include measurement of lead clearance, creatinine clearance, and urine concentrating ability as were done in the current report. All testing was performed over several hours in a doctor's offit- and could be adapted to in-plant screening. In view of the impaired lead clearance noted in some of these workers, they would be expected to demonstrate greater toxicity from lead exposure than coworkers without such impairment. However, we did not find any relationship between hematologic toxicity and impaired renal function. Of greater importance is the potentiation of lead neurotoxicity by lead nephropathy which has been previously reported but was not evaluated in this study. Further work is indicated to clarify the significance cf impaired lead clearance ability. The current report of mildly to moderately severe renal disease which may relate to lead exposure at Eagle Richer i dustries, Lead Chemicals Plant in Joplin, Missouri, further illustrates the importance of reducing lead exposure at this plant. The recommendations made in the previous HHE report should receive further attention as well as those noted below. Recommendations: 1) Seven workers identified by the nephrologist (Dr, Browning) as having impaired renal function should be removed from lead exposure. These individuals should be reassigned by the company to a lead free area of employment. Any Vvi DUP040013660 -6- lead exposure, even at air levels below the OSHA standards, may exacerbate existing renal disease. This recommendation applies even to individuals \ with renal impairment which is felt to be unrelated to lead exposure,' 2) Further medical studies are indicated to determine the etiology and reversibility of renal functional impairment. These studies should be performed as soon as possible to avoid further deterioration in renal function. NIOSH will pay for the medical expenses of those wishing to have further tests. 3) Periodic screening of other lead exposed workers is indicated to detect early lead-related renal disease. This could best be accomplished by measuring creatinine clearance and urinary concentrating ability every six months on workers with more than 20 years of lead exposure. Since these indicators become abnormal rather late in the course of renal disease, more sensitive methods should be sought to detect lead nephropathy in its early, reversible stage. Report prepared by: Edward L. Baker, Jr., M.D, Acting Chief Environmental Hazards Activity Cancer and Birth Defects Division Bureau of Epidemiology Center for Disease Control, Atlanta, Ga. Medical Evaluations Performed by: . David Browning, Jr., M.D. 6565 South Yale Tulsa, Oklahoma 74136 NIOSH Project Officer: Robert N, Ligo, M.D. Medical Section Industry-Wide Studies Br. Division of Surveillance, Hazard Evaluation, and Field Studies Cincinnati, Ohio 9v? DUP040013661 TABLE 1. Routine Renal Function Tests, Eagle Picher Industries, 4k ' July 1976 Sul. 'ct 1 2 3 4 5 6 7 8 > 10 11 12 13 14 15 16 17 18 19 BUR Level (lag/100ml) 18 15 25 26 17 24 15 18 18 19 15 18 15 18 15 13 27 23 16 Creatinine Level (mg/100ml) 1.1 0.9 1.2 1,2 0.9 0,8 0.8 0.9 1.0 1.0 1.0 1.0 1.0 ' 1.2 1,0 0.7 1.9 1.4 0.8 Routine Urinalysis Normal normal hyaline casts, 5-6 wbc/hpf granular casts normal normal normal normal normal normal normal normal normal normal normal normal normal normal normal Konaal range <22 <1.5 ys"o\ DUP040013662 TABLE 3. Hematologic Testing, Eagle Picher Industries, July 197$ Sublect 1 2 3 4 5 6 7 8 9 10 U 12 13 14 15 16 17 18 19 ; ,1 Hemoglobin Level (ga/lOOml) 15.5 15.2 14.8 12.6 15.1 14,8 14.2 12.3 14,7 15,4 13.8 15.3 15.0 13.0 14.0 14.8 13.2 14.9 14.3 Hematocrit (vol. %) 44.1 44.9 42.7 36.7 44.2 43.1 41.8 36,1 43.5 45,0 39.9 44.3 43.1 43.1 41.1 42.2 40,1 44,1 42,5 Erythrocyte Protoporphyrin (yg/lOOml rbc) 502 361 260 468 464 142 449 426 548 351 174. * 237' 164 164 200 278 401 ... 532 244 Urinary Delta ALA (mg/lOOml) 1.46 0.35 0,51 0.18 0,89 1.82 *..59 0.85 0.37 0.33 1.14 0.62 1.60 1.60 0,92 1.92 1.27 0.78 0,91 DUP040013664 . LERD CUERRRNCE RRTE BY 0URRT10N DF LERD' EXPPSUR1 YERK5 OF EERO EXPOSURE r BI a a uj X fmB to z o--n mtn rw* av 1/1 B Q n a ts h o. 3S 33 2S 23 "- * '5 j 2 -m / -s "T T U 14 CNIW/IW) 3XHa 3^NHHH313 <JH31 TB Vf3 1 DUP040013665 LEH!> CLERRRNCE RRTE BY DURRTIDN OF LERO E ,S 1 WORKERS HE-SS YERR5 OF REE YERR5 OF LERD EXPOSURE \ r-" -jr *3.- .t REFERE3CES 1. Pitts RF: Physiology of the kidney and body fluids; an introductory text. Chicago: Year Book Medical Publ, 1968 2. Crasser K, Coyer RA, Iagenburg R, et al: Renal ultrastructure, renal function, and parameters of lead toxicity in workers with different periods of lead exposure. Brit J Indus Med .'1:113-127, 1974 3. Weeded RP, Kaesaka JK, Weiner B, et al: Occupational lead nephro pathy. Amer J Med 59:630-641, 1975 as -- x /S'f