Renal Dysfunction Indicators in Lead Exposed Workers

Kap-Yeol JUNG; Sang-Ju LEE; Joon-Youn KIM; Young-Seoub HONG; Sung-Ryul KIM; Dong-Il KIM; Jue-Bok SONG

doi:10.1539/joh.40.103

Kap-Yeol JUNG, Sang-Ju LEE, Joon-Youn KIM, Young-Seoub HONG, Sung-Ryul KIM, Dong-Il KIM, Jue-Bok SONG

著者情報

キーワード: Renal function indicators, Lead exposure

ジャーナルフリー

1998 年 40 巻 2 号 p. 103-109

DOI https://doi.org/10.1539/joh.40.103

詳細

Published: 1998 Received: 1997/05/12 Available on J-STAGE: 2006/04/07 Accepted: 1997/09/18 Advance online publication: - Revised: -
訂正情報
訂正日: 2006/04/07 訂正理由: - 訂正箇所: 論文抄録訂正内容: Wrong : Real Dysfunction Indicators in Lead Exposed Workers: Kap-Yeol JUNG, et al. Department of Preventive Medicine and Industrial Medicine Research Institute, Dong-A University School of Medicine-This study was undertaken to find out which indicators were most valuable as markers of renal dysfunction related to lead exposure. We selected 75 male workers from the secondary lead smelter, plastic stabilizer and radiator manufacturing industries (the “exposed” group) and 64 male office workers (the “control” group). Blood lead, blood zinc protoporphyrin, urine lead, urine coproporphyrin, δ-aminolevulinic acid dehydratase activity, and urine δ-aminolevulinic acid were chosen as indicators of lead exposure. Blood urea nitrogen, serum creatinine, serum uric acid, urine N-acetyl-β-D-lucosaminidase, urine albumin, urine α₁-microglobulin and urine β₂-microglobulin were used as indicators of renal dysfunction. The urine α₁-microglobulin level was significantly associated with the lead exposure level. Blood urea nitrogen, urine N-acetyl-β-D-glucosaminidase and urine al-microglobulin levels were highly correlated with indicators of lead exposure. Urine α₁-microglobulin had the highest correlation with other indicators of renal function. Conclusively, blood urea nitrogen, urine N-acetyl-β-D-glucosaminidase and urine α₁-microglobulin are useful indicators, but urine α₁-microglobulin is the earliest and the most valuable indicator of renal dysfunction due to lead exposure.
Right : Real Dysfunction Indicators in Lead Exposed Workers: Kap-Yeol JUNG, et al. Department of Preventive Medicine and Industrial Medicine Research Institute, Dong-A University School of Medicine—This study was undertaken to find out which indicators were most valuable as markers of renal dysfunction related to lead exposure. We selected 75 male workers from the secondary lead smelter, plastic stabilizer and radiator manufacturing industries (the “exposed” group) and 64 male office workers (the “control” group). Blood lead, blood zinc protoporphyrin, urine lead, urine coproporphyrin, δ-aminolevulinic acid dehydratase activity, and urine δ-aminolevulinic acid were chosen as indicators of lead exposure. Blood urea nitrogen, serum creatinine, serum uric acid, urine N-acetyl-β-D-lucosaminidase, urine albumin, urine α₁-microglobulin and urine β₂-microglobulin were used as indicators of renal dysfunction. The urine α₁-microglobulin level was significantly associated with the lead exposure level. Blood urea nitrogen, urine N-acetyl-β-D-glucosaminidase and urine al-microglobulin levels were highly correlated with indicators of lead exposure. Urine α₁-microglobulin had the highest correlation with other indicators of renal function. Conclusively, blood urea nitrogen, urine N-acetyl-β-D-glucosaminidase and urine α₁-microglobulin are useful indicators, but urine α₁-microglobulin is the earliest and the most valuable indicator of renal dysfunction due to lead exposure.

訂正日: 2006/04/07 訂正理由: - 訂正箇所: 引用文献情報訂正内容: Wrong : l) Baker EL, Landrigan PJ, Barbour AG. Occupational lead poisoning in the United States: Clinical and biochemical findings related to blood levels. Br J Ind Med 1979; 36: 311-322.
2) Seppalainen AM, Hernberg S, Vesanto R, Kock B. Early neurotoxic effects of occupational lead exposure. Neurotoxicology 1983; 4: 181-192.
3) Rom WN. Environmental and Occupational Medicine, 2nd ed. Little Brown and Company, Boston 1983; 831-841.
4) Forni A, Camiagh G, Sechi GC. Initial occupational exposure to lead: chromosome and biochemical finding. Arch Environ Health 1976; 31: 73-78.
5) Forni A, Sciame A, Bertazzi PA, Allesio L. Chromosome and biochemical studies in women occupationally exposed to lead. Arch Environ Health 1980; 35: 139-146.
6) Assennato G, Paci C, Baser ME. Sperm count suppression without endocrine dysfunction in lead exposed men. Arch Environ Health 1987; 42: 12l-l27.
7) Cullen MR, Kayne RD, Robins JM. Endocrine and reproductive dysfunction in men associated with occupational inorganic lead intoxication. Arch Environ Health 1984; 39: 431-440.
8) Lanceraux E. N6phrite et arthrite saturnines: coincidence de ces affections: paeallele avec la néphrite et l''arthrite gouteusses. Arch de Générales Médicines 1881; 6: 641-647.
9) Aub JC, Fairhall LT, Minot AS, Reznikoff P. Lead poisoning. Medicine 1925; 4: 1.
10) Oliver T. Disease due to metallic poisons, dust, fumes etc., Disease of occupation. Metheun and Co, London 1914: 137-215.
11) Goyer RA, May P, Cates MM, Krigman MR. Lead and protein content of isolated inclusion bodies from kidneys of lead poisoned rats. Lab Invest 1970; 22: 245-251.
12) Goyer RA, Rhyne BC. Pathological effects of lead. Ind Rev Exp Patho 1973; 12: 1-77.
l3) Cramer K, Goyer RA, Jagenburg R, Wilson MH. Renal ultrastructure renal function and parameters of lead toxicity in workers with different period of lead exposure. Br J Ind Med 1974; 31: 113-127.
l4) WHO. Environmental health criteria 119 principles and method for the assessment of nephrotoxicity associated with exposure to chemicals. WHO 1991: 159-194.
15) Verschoor M, Wibowo A, Herber R, Hemmen JV, Zielhuis R. Influence of occupational low level lead exposure on renal parameters. Am J Ind Med 1987; 12: 341-351.
l6) Endo G, Horiguchi S, Kiyota I. Urinary N-acetyl-β-D-glucosaminidase actibity in lead exposed workers. J Appl Toxicol 1990; 10: 235-247.
17) Endo G, Konishi Y, Kiyota A, Horiguchi S. Increase of urinary albumin in workers exposed to lead. J Sci Labour 1993; 69: 3-12.
18) Shihabi ZK, Konen JC, O''Coner ML. Albuminuria vs urinary total protein for detecting chronic renal disorder. Clin-Chem 1991; 37: 621-625.
19) Endo G, Konishi Y, Kiyota A, Horiguchi S. Urinary β₁-microglobulin in lead workers. Bull Environ Contam Toxicol 1993; 50: 744-752.
20) Kusano E, Suzuki M, Asano Y, Itoh Y, Takagi K, Kawai T. Human α₁-microglobulin and its relationship to renal function. Nephron 1983; 41: 320-326.
21) Itoh Y, Enomoto H, Kawai T. α₁-microglobulin in cadmium poisoning. Nephron 1983; 35: 211-218.
22) Gatell JM, SanMiguel JG, Zamora L. Tobramycin and amikacin nephrotoxicity. Value of serum creatinine versus urinary concentration of β_{223) Department of Labor, Korea, Korean Occupational Safety and Health Act 1994 (in Korean).
24) Tomokuni K. Comparison of the activity values of erythrocyte δ-aminolevulinic acid dehydratase as measures by two different methods. Ind Health 1975; 13: 191-194.
25) Tomokuni K, Ogata M. Simple method for detennination of urinary δ-aminolevulinic acid as an index of lead exposure. Clin Chem 1972; 18: 1534-1536.
26) Soulsby J, Smith RLA. Simplified method for the quantitative determination of urinary coproporphyrin in lead workers. Br J Ind Med 1974; 31: 72-74.
27) Lee SY, Jung YS. Clinicopathological analysis. Yonsei University Press, 1981.
28) Shionogi Company. A method of U-NAG measurement. 1991.
29) Metzman E. Protein quantification on both branches of the Heidelberger curve by monitoring the kinetic of immunoprecipitation. Boehring Institute Mitteilungen 1985; 78: 167-172.
30) Edward LC, Heiderman JH. Noninvasive monitoring of renal transplant function by analysis of beta 2-microglobulin. Kidney transplantation 1983; 23: 767-775.
31) Selander S, Cramer K. Interrelationships between lead in blood, lead in urine and ALA in urine during lead work. Br J Ind Med 1970; 27: 28-32.
32) Kim JY, Kim JM. Blood zinc protoporphyrin level as a biological indicator of lead exposure. The Dong-A J Medicine 1989; l: 37-46.
33) Kim JM, Kim HA, Lee GM, Lee EY, Kang JB. Astudy of hemoglobin, blood lead and blood zinc protoporhyrin in lead smelter workers. Kor J Occupational Health 1986; 25: 69-75.
34) Lee BK, Kim JM, Lee GM, Lee EY, Cho YS. The relationship among biological exposure indices in the lead smelter workers. Kor J Occup Health 1984; 23: l-7.
35) Goyer RA, Wilson MH. Lead-induced inclusion bodies: Results of ethylene diamine tetraacetic acid treatment. Lab Invest 1975; 32: 149-156.
36) Valciukas JA, Lilis R. A composite index of lead effects: Comparative study of four occupational groups with different levels of lead absorption. Int Arch Occup Environ Health 1982; 51: 14.
37) Lilis R, Anderson H, Blumberg W, Eisinger J. Lead effects among secondary smelter workers with blood lead levels below 80μg/dl. Arch Environ Health 1977; 32: 256-285.
38) Hammond PB, Lerner SI, Gartside PS. Hanenson IB, Roda SB, Foulkes ES. The relationship of biological indices of lead exposure to the health status of workers in a secondary lead smelter. J Occup Med 1980; 22: 475-484.
39) Hernberg S. Biochemical, subclinical and clinical responses to lead and their relation to different exposure level. Nordberg, NY, 1976.
40) Marga V, Anton W, Robert H, Hemmen JV, Zielhuis R. Influence of occuptional low-level lead exposure on renal parameters. Am J Ind Med 1987; 12: 341-35l.
41) Omae K, Sakurai H, Higashi T, Muto T. Ichigawa M, Sasaki N. No adverse effects of lead to renal function in lead-exposed workers. Ind Health 1990; 28: 77-83.
42) Ahn KD, Lee SS, Lee BK, Kim DH. Relationship between lead exposure indices and renal function in lead exposed workers. Kor J Occup Med 1993; 5: 58-75.

Right : l) Baker EL, Landrigan PJ, Barbour AG. Occupational lead poisoning in the United States: Clinical and biochemical findings related to blood levels. Br J Ind Med 1979; 36: 311-322.
2) Seppalainen AM, Hernberg S, Vesanto R, Kock B. Early neurotoxic effects of occupational lead exposure. Neurotoxicology 1983; 4: 181-192.
3) Rom WN. Environmental and Occupational Medicine, 2nd ed. Little Brown and Company, Boston 1983; 831-841.
4) Forni A, Camiagh G, Sechi GC. Initial occupational exposure to lead: chromosome and biochemical finding. Arch Environ Health 1976; 31: 73-78.
5) Forni A, Sciame A, Bertazzi PA, Allesio L. Chromosome and biochemical studies in women occupationally exposed to lead. Arch Environ Health 1980; 35: 139-146.
6) Assennato G, Paci C, Baser ME. Sperm count suppression without endocrine dysfunction in lead exposed men. Arch Environ Health 1987; 42: 12l-l27.
7) Cullen MR, Kayne RD, Robins JM. Endocrine and reproductive dysfunction in men associated with occupational inorganic lead intoxication. Arch Environ Health 1984; 39: 431-440.
8) Lanceraux E. N6phrite et arthrite saturnines: coincidence de ces affections: paeallele avec la néphrite et l'arthrite gouteusses. Arch de Générales Médicines 1881; 6: 641-647.
9) Aub JC, Fairhall LT, Minot AS, Reznikoff P. Lead poisoning. Medicine 1925; 4: 1.
10) Oliver T. Disease due to metallic poisons, dust, fumes etc., Disease of occupation. Metheun and Co, London 1914: 137-215.
11) Goyer RA, May P, Cates MM, Krigman MR. Lead and protein content of isolated inclusion bodies from kidneys of lead poisoned rats. Lab Invest 1970; 22: 245-251.
12) Goyer RA, Rhyne BC. Pathological effects of lead. Ind Rev Exp Patho 1973; 12: 1-77.
l3) Cramer K, Goyer RA, Jagenburg R, Wilson MH. Renal ultrastructure renal function and parameters of lead toxicity in workers with different period of lead exposure. Br J Ind Med 1974; 31: 113-127.
l4) WHO. Environmental health criteria 119 principles and method for the assessment of nephrotoxicity associated with exposure to chemicals. WHO 1991: 159-194.
15) Verschoor M, Wibowo A, Herber R, Hemmen JV, Zielhuis R. Influence of occupational low level lead exposure on renal parameters. Am J Ind Med 1987; 12: 341-351.
l6) Endo G, Horiguchi S, Kiyota I. Urinary N-acetyl-β-D-glucosaminidase actibity in lead exposed workers. J Appl Toxicol 1990; 10: 235-247.
17) Endo G, Konishi Y, Kiyota A, Horiguchi S. Increase of urinary albumin in workers exposed to lead. J Sci Labour 1993; 69: 3-12.
18) Shihabi ZK, Konen JC, O'Coner ML. Albuminuria vs urinary total protein for detecting chronic renal disorder. Clin-Chem 1991; 37: 621-625.
19) Endo G, Konishi Y, Kiyota A, Horiguchi S. Urinary β₁-microglobulin in lead workers. Bull Environ Contam Toxicol 1993; 50: 744-752.
20) Kusano E, Suzuki M, Asano Y, Itoh Y, Takagi K, Kawai T. Human α₁-microglobulin and its relationship to renal function. Nephron 1983; 41: 320-326.
21) Itoh Y, Enomoto H, Kawai T. α₁-microglobulin in cadmium poisoning. Nephron 1983; 35: 211-218.
22) Gatell JM, SanMiguel JG, Zamora L. Tobramycin and amikacin nephrotoxicity. Value of serum creatinine versus urinary concentration of β₂-microglobulin. Nephron 1985; 41: 337-345.
23) Department of Labor, Korea, Korean Occupational Safety and Health Act 1994 (in Korean).
24) Tomokuni K. Comparison of the activity values of erythrocyte δ-aminolevulinic acid dehydratase as measures by two different methods. Ind Health 1975; 13: 191-194.
25) Tomokuni K, Ogata M. Simple method for detennination of urinary δ-aminolevulinic acid as an index of lead exposure. Clin Chem 1972; 18: 1534-1536.
26) Soulsby J, Smith RLA. Simplified method for the quantitative determination of urinary coproporphyrin in lead workers. Br J Ind Med 1974; 31: 72-74.
27) Lee SY, Jung YS. Clinicopathological analysis. Yonsei University Press, 1981.
28) Shionogi Company. A method of U-NAG measurement. 1991.
29) Metzman E. Protein quantification on both branches of the Heidelberger curve by monitoring the kinetic of immunoprecipitation. Boehring Institute Mitteilungen 1985; 78: 167-172.
30) Edward LC, Heiderman JH. Noninvasive monitoring of renal transplant function by analysis of beta 2-microglobulin. Kidney transplantation 1983; 23: 767-775.
31) Selander S, Cramer K. Interrelationships between lead in blood, lead in urine and ALA in urine during lead work. Br J Ind Med 1970; 27: 28-32.
32) Kim JY, Kim JM. Blood zinc protoporphyrin level as a biological indicator of lead exposure. The Dong-A J Medicine 1989; l: 37-46.
33) Kim JM, Kim HA, Lee GM, Lee EY, Kang JB. Astudy of hemoglobin, blood lead and blood zinc protoporhyrin in lead smelter workers. Kor J Occupational Health 1986; 25: 69-75.
34) Lee BK, Kim JM, Lee GM, Lee EY, Cho YS. The relationship among biological exposure indices in the lead smelter workers. Kor J Occup Health 1984; 23: l-7.
35) Goyer RA, Wilson MH. Lead-induced inclusion bodies: Results of ethylene diamine tetraacetic acid treatment. Lab Invest 1975; 32: 149-156.
36) Valciukas JA, Lilis R. A composite index of lead effects: Comparative study of four occupational groups with different levels of lead absorption. Int Arch Occup Environ Health 1982; 51: 14.
37) Lilis R, Anderson H, Blumberg W, Eisinger J. Lead effects among secondary smelter workers with blood lead levels below 80μg/dl. Arch Environ Health 1977; 32: 256-285.
38) Hammond PB, Lerner SI, Gartside PS. Hanenson IB, Roda SB, Foulkes ES. The relationship of biological indices of lead exposure to the health status of workers in a secondary lead smelter. J Occup Med 1980; 22: 475-484.
39) Hernberg S. Biochemical, subclinical and clinical responses to lead and their relation to different exposure level. Nordberg, NY, 1976.
40) Marga V, Anton W, Robert H, Hemmen JV, Zielhuis R. Influence of occuptional low-level lead exposure on renal parameters. Am J Ind Med 1987; 12: 341-35l.
41) Omae K, Sakurai H, Higashi T, Muto T. Ichigawa M, Sasaki N. No adverse effects of lead to renal function in lead-exposed workers. Ind Health 1990; 28: 77-83.
42) Ahn KD, Lee SS, Lee BK, Kim DH. Relationship between lead exposure indices and renal function in lead exposed workers. Kor J Occup Med 1993; 5: 58-75.}

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Real Dysfunction Indicators in Lead Exposed Workers: Kap-Yeol JUNG, et al. Department of Preventive Medicine and Industrial Medicine Research Institute, Dong-A University School of Medicine—This study was undertaken to find out which indicators were most valuable as markers of renal dysfunction related to lead exposure. We selected 75 male workers from the secondary lead smelter, plastic stabilizer and radiator manufacturing industries (the “exposed” group) and 64 male office workers (the “control” group). Blood lead, blood zinc protoporphyrin, urine lead, urine coproporphyrin, δ-aminolevulinic acid dehydratase activity, and urine δ-aminolevulinic acid were chosen as indicators of lead exposure. Blood urea nitrogen, serum creatinine, serum uric acid, urine N-acetyl-β-D-lucosaminidase, urine albumin, urine α₁-microglobulin and urine β₂-microglobulin were used as indicators of renal dysfunction. The urine α₁-microglobulin level was significantly associated with the lead exposure level. Blood urea nitrogen, urine N-acetyl-β-D-glucosaminidase and urine al-microglobulin levels were highly correlated with indicators of lead exposure. Urine α₁-microglobulin had the highest correlation with other indicators of renal function. Conclusively, blood urea nitrogen, urine N-acetyl-β-D-glucosaminidase and urine α₁-microglobulin are useful indicators, but urine α₁-microglobulin is the earliest and the most valuable indicator of renal dysfunction due to lead exposure.

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