Plumbism from airborne lead in a firing range

An unusual exposure to a toxic heavy meta
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      Plumbism developed in a 17 year old boy while he was working in an indoor firing range. Diagnosis was delayed because a blood lead level was initially reported to be within normal limits and because acute intermittent porphyria was suspected. Subsequently, lead poisoning was clearly documented by characteristic abnormalities of the heme biosynthetic pathway in erythrocytes (inhibited δ-aminolevulinic acid dehydratase activity, increased protoporphyrin-IX), increased urinary excretion of δ-aminolevulinic acid and coproporphyrin, and elevated levels of lead in blood and urine. These abnormalities as well as decreased nerve conduction velocity and reduced hepatic cytochrome P-450 function, as assessed by metabolism of antipyrine, returned towards normal with chelation therapy. Investigation of the firing range showed airborne lead to be markedly increased during firing; a co-worker was also found to have asymptomatic lead poisoning. This experience shows that exposure to heavy metals can occur by mechanisms which are unusual and not widely recognized, and illustrates the importance of testing erythrocytes and urine for distinct biochemical abnormalities related to the heme synthetic pathway when differentiating hereditary hepatic porphyria from plumbism.
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      1. Criteria for a recommended standard—occupational exposure to lead. National Institute for Occupational Safety and Health, Washington, D.C1972
      2. Occupational Diseases. A Guide to Their Recognition. 3rd ed. Public Health Service Publication 1097. U.S. Government Printing Office, Washington, D.C1964
      3. Lead: Airborne lead in perspective. National Academy of Sciences, Division of Medical Sciences, National Research Council, Committee on Biological Effects of Atmospheric Pollutants, Washington, D.C1972
        • Alvares AP
        • Fischbein A
        • Sassa S
        • et al.
        Lead intoxication: effects on cytochrome P-450 mediated oxidations in liver.
        Clin Pharmacol Ther. 1976; 19: 183
        • Anania TL
        • Lucas JB
        • Seta JH
        Lead exposure at an indoor firing range.
        National Institute for Occupational Safety and Health, Technical Publication. 1974; (Cincinatti, Ohio)
        • Landrigan PJ
        • McKinney AS
        • Hopkins LC
        • et al.
        Chronic lead absorption. Result of poor ventilation in an indoor pistol range.
        JAMA. 1975; 234: 394
        • Wedeen RP
        • Maesaka JK
        • Weiner B
        • et al.
        Occupational lead nephropathy.
        Am J Med. 1975; 59: 630
        • Granick S
        • Sassa S
        • Granick JL
        • et al.
        Assays for porphyrins, δ-aminolevulinic acid dehydratase, and porphyrinogen synthetase in microliter samples of whole blood: applications to metabolic defects involving the heme pathway.
        in: 3rd ed. Proc Natl Acad Sci USA. 69. 1972: 2381
        • Sassa S
        • Granick JL
        • Granick S
        • et al.
        Studies in lead poisoning. I. Microanalysis of erythrocyte protoporphyrin levels by spectrofluorometry in the detection of chronic lead intoxication in the subclinical range.
        Biochem Med. 1973; 8: 135
        • Granick JL
        • Sassa S
        • Granick S
        • et al.
        Studies in lead poisoning. II. Correlation between the ratio of activated to inactivated δ-aminolevulinic acid dehydratase of whole blood and the blood lead level.
        Biochem Med. 1973; 8: 149
        • Mauzerall D
        • Granick S
        The occurrence and determination of δ-aminolevulinic acid and porphobilinogen in urine.
        J Biol Chem. 1956; 219: 435
        • Rimington C
        Quantitative determination of porphobilinogen and porphyrins in urine and porphyrins in faeces and erythrocytes.
        Association of Clinical Pathologists, Broadsheet. 1971; : 70
        • Sassa S
        • Granick S
        • Bickers DR
        • et al.
        A microassay for uroporphyrinogen I synthase: one of three abnormal enzyme activities in acute intermittent porphyria, and its application to the study of the genetics of this disease.
        in: 3rd ed. Proc Natl Acad Sci USA. 71. 1974: 732
        • Watson CJ
        • Taddeini L
        • Bossenmaier I
        Present status of the Ehrlich aldehyde reaction for urinary porphobilinogen.
        JAMA. 1964; 190: 501
        • Baloh RW
        Laboratory diagnosis of increased lead absorption.
        Arch Environ Health. 1974; 28: 198
        • Teisinger J
        Biochemical responses to provocative chelation by edetate disodium calcium.
        Arch Environ Health. 1971; 23: 280
        • Emmerson BT
        Chronic lead nephropathy: the diagnostic use of calcium EDTA and the association with gout.
        Aust Ann Med. 1963; 12: 310
        • Brodie B
        • Axelrod J
        • Soberman R
        • et al.
        The estimation of antipyrine in biological materials.
        J Biol Chem. 1949; 179: 25
        • Anderson KE
        • Alvares AP
        • Sassa S
        • et al.
        Studies in porphyria. V. Drug oxidation rates in hereditary hepatic porphyria.
        Clin Pharmacol Ther. 1976; 19: 47
        • Alvares AP
        • Kapelner S
        • Sassa S
        • et al.
        Drug metabolism in normal children, lead poisoned children and normal adults.
        Clin Pharmacol Ther. 1975; 17: 179
        • Fromke VL
        • Lee MY
        • Watson CJ
        Porphyrin metabolism during versenate therapy in lead poisoning. Intoxication from an unusual source.
        Ann Intern Med. 1969; 70: 1007
        • Dickinson L
        • Reichert EL
        • Ho RCS
        • et al.
        Lead poisoning in a family due to cocktail glasses.
        Am J Med. 1972; 52: 391
        • Berk PD
        • Tschudy DP
        • Shepley LA
        • et al.
        Hematologic and biochemical studies in a case of lead poisoning.
        Am J Med. 1970; 48: 137
        • Lambie JA
        Lead poisoning in missile-silo workers.
        JAMA. 1967; 200: 137
      4. J Pediatr. 1975; 87: 824
        • Haeger-Aronsen B
        An assessment of the laboratory tests used to monitor the exposure of lead workers.
        Br J Ind Med. 1971; 28: 52
        • Goyer RA
        • Rhyne BC
        Pathological effects of lead.
        Int Rev Exp Pathol. 1973; 12: 1
        • Dagg JH
        • Goldberg A
        • Lochhead A
        • et al.
        The relationship of lead poisoning to acute intermittent porphyria.
        Q J Med. 1965; 34: 163
        • Catton MJ
        • Harrison MJG
        • Fullerton PM
        • et al.
        Subclinical neuropathy in lead workers.
        Br Med J. 1970; 2: 80
        • Mustajoki P
        • Seppalainen AM
        Neuropathy in latent hereditary hepatic porphyria.
        Br Med J. 1975; 2: 310
        • Lamola AA
        • Piomelli S
        • Poh-Fitzpatrick MB
        • et al.
        Erythropoietic protoporphyria and lead intoxication: the molecular basis for difference in cutaneous photosensitivity. II.
        J Clin Invest. 1975; 56: 1528
        • Conney AH
        Pharmacological implications of microsomal enzyme induction.
        Pharmacol Rev. 1967; 19: 317
        • Vesell ES
        • Page JG
        Genetic control of the phenobarbital-induced shortening of plasma antipyrine half-lives in man.
        J Clin Invest. 1969; 48: 2202
        • Marver HS
        • Schmid R
        The porphyrias.
        (chap 45)in: Stanbury JB Wyngaarden JB Fredrickson DS The Metabolic Basis of Inherited Disease. 3rd ed. McGraw-Hill Book Co, New York1972