Quantitative Urinary Coproporphyrin Excretion and Its Relation to Edathamil Calcium Disodium Administration in Children With Acute Lead Intoxication 12

Chisolm, J. Julian; Harrison, Harold E.

doi:10.1172/jci103367

Cited by 26 publications

(1 citation statement)

References 9 publications

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“…The haemoglobin level could not be correlated directly with the clinical grouping as it formed a part of it, but the haemoglobin level correlates significantly with the urinary coproporphyrin (r = 0o54) and ALA (r = o057) (P<0o05 in both cases). This agrees with the findings of Chisolm and Harrison (1956) and of Haeger-Aronsen (I960) that the urinary excretion of coproporphyrin and of ALA respectively are sensitive indices of 'metabolically active' and presumably toxic lead in the body.…”

Section: Resultssupporting

confidence: 92%

The Diagnosis of Industrial Lead Poisoning

Gibson

MacKenzie

Goldberg

1968

Occupational and Environmental Medicine

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A series of IOO lead workers from different industries, 9I at work and nine admitted to hospital with lead poisoning, was studied in order to define more clearly the clinical and biochemical criteria of lead poisoning in three stages-(A) a presymptomatic state of lead exposure (37 men), (B) a state of mild symptoms or mild anaemia (45 men), and (C) frank lead poisoning with severe symptoms and signs (i8 men).The tests used were haemoglobin, reticulocyte count, and blood lead, and urinary lead, coproporphyrin, In addition to the above tests, blood pressure, blood urea, and serum uric acid estimations were performed on all the men in order to elucidate the possible role of lead in the production of renal damage. Blood pressure and serum uric acid levels were similar for all three groups but the blood urea level was raised in group C. The reason for this finding was not established.It was found that scrap metal burning, battery manufacturing, and ship-breaking constituted the gravest lead hazards encountered in this survey whereas wire manufacture constituted the least. Workers in the most modern factory, a car-body pressing plant, gave average values just below the danger levels for the urinary coproporphyrin and ALA estimations despite apparently efficient protective measures. This finding underlines the importance of the medical supervision of lead workers.Lead and its compounds have been used by man for at least six thousand years (Brunton, I937) and today the demands of industry for lead rise steadily. Its toxic properties were first recognized by Hippocrates (Hunter, I962) and over the centuries more has been written about the causation and symptomatology of poisoning by lead than by any other toxic agent (Johnstone, i966).

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Section: Resultssupporting

confidence: 92%

The Diagnosis of Industrial Lead Poisoning

Gibson

MacKenzie

Goldberg

1968

Occupational and Environmental Medicine

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Comparative Tests for Diagnosis of Lead Poisoning

Morgan¹,

Burch²

1972

Arch Intern Med

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The level of erythrocyte enzyme delta-aminolevulinic acid dehydratase (ALA-D) has been determined in conjunction with other standard tests for lead poisoning. The mean for 53 healthy persons was previously shown to be 175 \m=+-\38units. Lead excretion rates above 1.0 mg/24 hr in response to 1 gm of edetate disodium calcium (Calcium Disodium Versenate) given intravenously were associated with depression of the enzyme activity to 60 units or less. Enzyme activity was maximally depressed when lead excretion exceeded 2 mg/24 hr. Activity of ALA-D was more sensitive and accurate in the diagnosis of lead poisoning than urinary ALA or coproporphyrin excretion and as good as blood or urine lead determinations. Activity of ALA-D is rapidly restored toward normal by treatment with edetate disodium calcium.The three most reliable tests used in the diagnosis of lead poi¬ soning have been blood lead, urine lead, and urinary delta aminolevulinic acid (ALA) excretion. Determination of blood lead levels has been notor¬ iously difficult and values are gener¬ ally unavailable or unreliable except in laboratories where large numbers of samples are regularly analyzed. Urinary lead determinations are awkward in that 24-hour urine vol¬ umes are required and excretion rates may be normal even in definite poi¬ soning, particularly if exposure has been remote or treatment previously given.1 The urinary excretion of ALA has been widely used in industry and in surveys of children exposed to lead paint.2·' Since 24-hour urine collec¬ tions are unavailable under those con¬ ditions, the concentration per 100 ml, with or without correction by the uri¬ nary creatinine concentration, has been utilized. Valid data depend largely upon the concentration of the urine specimen; if dilute specimens are obtained, false negatives may re¬ sult. Because of this intrinsic error and the difficulty in laboratory analy¬ sis of ALA, this test has not been completely satisfactory. The urinary lead excretion after administration of a chelating agent, such as calcium disodium ethylene-diaminetetracetic acid (Calcium Disodium Versenate), accurately reflects lead accumulation even in the chronic asymptomatic state.1·4 It is, however, awkward both by virtue of the necessity for admin¬ istration of the chelating agent and the collection of at least 12-hour urine specimens, as well as the difficult lab¬ oratory analysis for lead.More recently, the measurement of an erythrocyte enzyme, delta-aminolevulinic acid dehydratase (ALA-D), has been recommended for the diag¬ nosis of lead poisoning.50 This en¬ zyme is exquisitely sensitive to the effects of lead and decreases in activ¬ ity as blood lead values rise. Method¬ ology for determination of this en¬ zyme has not been uniform. The range of normal, the effects of small amounts of lead on enzyme activity, and the biologic significance of mod¬ erate depression of enzyme activity have not been well established. This laboratory has reevaluated the methods for ALA-D determination, establishing a recommended standard techniqu...

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