Clinical Manifestations

For many decades the appellation "lead poisoning" has referred to the clinically apparent symptoms manifested by this metal's toxic effects on the intestine, brain, and nerves. Before dealing with them in detail, however, the less obvious effects of lead poisoning are noted briefly.

Lead can interfere with the physiology of almost every body function. At "low" blood concentration (less than 40 micrograms [¡xg] lead/100 ml blood [dl]), there is some evidence that it can impair intellectual capacity development in children, an effect of potentially greater significance for a population than the more overt symptoms usually associated with the concept of lead poisoning. In the mouth, lead may combine with sulfur produced by local bacteria, producing a linear, black precipitate on the gums sufficiently apparent and unique to be of diagnostic value. Episodes of intense lead exposure may cause temporary arrest of long bone growth visible as a horizontal band of radiodensity ("bone lead line").

Lead produces moderate anemia with resulting facial pallor by poisoning enzymes necessary for the formation of hemoglobin, the blood's principal oxygen carrier. Lead excreted through the kidneys can poison the renal cells, eventually terminating in fatal renal failure. Effects well documented in animals, though less convincingly in humans, include suppression of gonadal function (with consequent decreased fertility or sterility) as well as carcinogenic and teratogenic activity associated with increased rates of abortion, stillbirth, and neonatal mortality.

The symptom of lead poisoning most commonly encountered in the historical literature is abdominal pain. Its cause is usually attributed to intestinal spasm, though the abdominal muscles may participate in the painful, uncontrolled contractions usually termed "colic." When they are severe and prolonged, such affected individuals may be driven to desperate measures for relief. Similar pain may be seen in the common forms of diarrhea, but that asso ciated with lead poisoning is accompanied by constipation, and hence the common reference to the abdominal pain of lead intoxication as "dry bellyache." In individual cases such a state could be simulated by inflammation of the gallbladder, pancreas, or stomach, and by stones in the kidney or bile passages, but these conditions neither would be accompanied by other symptoms or signs of lead toxicity, nor would they affect large segments of a population or occupation.

Lead also has a destructive effect on nerves (peripheral neuropathy), whose ability to transmit the electrical impulses to the muscle is then reduced or completely blocked, producing muscle paralysis. Peculiarly (and diagnostically) the nerves supplying those muscles (extensors), which normally raise the wrist or foot, are especially commonly affected, causing the unique affliction of "wrist drop" (often termed "the dangles" in the past) and "foot drop."

Serious disturbances of behavior leading to convulsions, coma, and death are the most severe and feared of lead's effects. Children are notoriously more susceptible to such brain toxicity, and even a single episode of convulsions, when not fatal, often causes permanent, residual cerebral damage. Meningitis, tumors, trauma, and other diseases may result in identical convulsive seizures, and their lead etiology may be recognizable in the literature only through their association with other features of lead toxicity.

Finally it should be noted that lead poisoning may cause gout. This condition is due to the reduced ability of the lead-poisoned kidney to excrete uric acid, a product of normal protein metabolism. The retained uric acid is frequently deposited in the soft tissue, often near joints, resulting in exquisitely tender inflammation. The etiology of the renal toxicity underlying most cases of gout is unknown, but when the kidney injury is caused by lead, it is known as "saturnine gout," in reference to the association of lead with that planetary god by the ancients.

A rough correlation exists between the amount of lead in the blood and the presence of these various signs and symptoms. At lead levels below 40 ¿u.g/dl, clinically evident effects are uncommon, but with progressively increasing concentrations above 80 /xg/dl, symptoms become more probable. Many modifying and influencing factors, however, give rise to diagnostic difficulties.

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