The activity of δ-aminolaevulinic acid dehydratase (ALA-D; porphobilinogen synthase) was measured in whole blood from a group of workers with acute exposure to lead and with low blood lead levels, a group of workers with chronic lead exposure and high blood lead levels, and a group of people without undue environmental lead exposure. The activity of ALA-D was reduced significantly at low blood lead levels only if undue exposure to lead had occurred, and was thus a reflection of low level lead poisoning. In chronic lead exposure the enzyme was not invariably reactivated fully with dithiothreitol, indicating more severe enzyme poisoning. The one lead worker with symptomatic lead poisoning had the most marked enzyme suppression. Measurement of both ALA-D activity and blood lead levels was more useful than the measurement of blood lead levels alone in the diagnosis and assessment of the severity of lead poisoning.
References
1.
NeedlemanHL. The health effects of low level exposure to lead. Ann Rev Public Health1981; 2: 277–98.
2.
AshbyJAS. A neurological and biochemical study of early lead poisoning. Br J Ind Med.1980; 37: 133–40.
3.
BakerELWhiteRFPothierLJOccupational lead neurotoxicity—improvement in behavioural effects after reduction of exposure. Br J Ind Med.1985; 42: 507–17.
4.
WilliamsBJGriffithsWHAlbrechtCMCardiac effects of chronic lead poisoning. In: BrownSS, ed. Clinical Chemistry and Chemical Toxicology of Metals. Elsevier/North-Holland Press1977; 127–30.
5.
ShaperAGPocockSJ. Blood lead and blood pressure. Br Med J1985; 291: 1147–9.
6.
EmmersomBT. Chronic lead nephropathy. Kidney International1973; 4: 1–5.
7.
WedeenRPMaesakaJKWeinerBOccupational lead nephropathy. Am J Med.1975; 59: 630–41.
8.
CooperWCGaffeyWR. Mortality of lead workers. J Occup Med.1975; 17: 100–107.
9.
MahaffeyKRAnnestJLRobertsJMurphyRS. National estimates of blood lead levels: United States, 1976–1980. N Engl J Med.1982; 307: 573–9.
10.
FellGS. Lead toxicity: problems of definition and laboratory evaluation. Ann Clin BioChem.1984; 21: 453–60.
11.
BarltropD. Laboratory indices of exposure to lead. In: BrownSS, ed. Clinical Chemistry and Chemical Toxicology of Metals. Elsevier/North Holland Press1977; 167–77.
12.
ValentineJLBalohRWBrowdyBLSubclinical effects of chronic increased lead absorption—a prospective study. Part 4. Evaluation of heme synthesis effects. J Occup Med.1982; 24: 120–5.
13.
TelišmanSKeršancAPrpić-MajićD. The relevance of arguments for excluding ALAD from the recommended biological limit values in occupational exposure to inorganic lead (WHO 1980). Int Arch Occup Environ Health1982; 50: 397–412.
14.
BerlinASchallerKH. European standardized method for the determination of aminolevulinic acid dehydratase activity in blood. J Clin Chem Clin BioChem.1974; 12: 389–90.
15.
SassaSGranickJLGranickSStudies 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: 135–48.
16.
GranickJLSassaSGranickSStudies 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: 149–59.
17.
FujitaHYamamotoRSatoKIkedaM. In vivo regulation of Δ-aminolevulinate dehydratase activity. Toxicol Appl Pharm1985; 77: 66–75.
18.
GeisseSBrullerHJDossM. Porphobilinogen synthase (Δ-aminolevulinic acid dehydratase) activity in human erythrocytes: reactivation by zinc and dithiothreitol depending on influence of storage. Clin Chim Acta1983; 135: 239–45.
19.
ChisolmJJThomasDJHamillTG. Erythrocyte porphobilinogen synthase activity as an indicator of lead exposure in children. Clin Chem.1985; 31: 601–5.
20.
WigfieldDCFarrantJP. Assay of Δ-aminolaevulinate dehydratase in 10 μl of blood. Clin Chem.1981; 27: 100–3.
21.
MitchellRADrakeJEWittlinLARejentTA. Erythrocyte porphobilinogen synthase (delta-aminolaevulinate dehydratase) activity: a reliable and quantitative indicator of lead exposure in humans. Clin Chem.1977; 23: 105–11.
22.
MarksGS. Exposure to toxic agents: The heme biosynthetic pathway and hemoproteins as indicators. CRC Critical Reviews in Toxicology1985; 15: 151–79.
23.
WadaOTakeoKYanoYΔ-aminolevulinic acid dehydratase in low level lead exposure. Arch Environ Health1976; 31: 211–5.
24.
BarltropDSmithAM. Kinetics of lead interaction with human erythrocytes. Post Grad Med J1985; 51: 770–3.
25.
BruengerFWStevensWStoverBJ. The association of 210Pb with constituents of erythrocytes. Health Physics1973; 25: 37–42.
26.
RaghavanSRVCulverBDGonickHC. Erythrocyte lead-binding protein after occupational exposure. I. Relationship to lead toxicity. Environ Research1980; 22: 264–70.
27.
RaghavanSRVCulverBDGonickHC. Erythrocyte lead-binding protein after occupational exposure. II. Influence on lead inhibition of membrane Na+, K+-adenosinetriphosphatase. J Toxicol and Environ Health1981; 7: 561–8.
28.
AlbaharyC. Lead and hemopoiesis: The mechanism and consequences of the erythropathy of occupational lead poisoning. Am J Med.1972; 52: 367–78.
29.
RaghavanSRVGonickHC. Isolation of low-molecular-weight-lead-binding protein from human erythrocytes. Proc Soc Exp Biol Med.1977; 155: 164–7.
