Renal function 17 to 23 years after chelation therapy for childhood plumbism.

An elegant retrospective description of an epidemic of chronic renal failure occurring in patients with histories of untreated childhood lead poisoning in Queensland, Australia established beyond reasonable doubt the existence of lead nephropathy. However, a retrospective uncontrolled report from Boston in 1963 refuted the claim that there are serious renal consequences of untreated childhood lead poisoning. We conducted a controlled prospective, longitudinal study to examine the effects of childhood lead poisoning on renal function 17 to 23 years after chelation therapy. The present study reports the results of renal functional tests in a unique cohort of study subjects (N = 62) with significant lead poisoning (initial PbB > 100 micrograms/dl) diagnosed and treated between 1966 and 1972 and their age-matched control siblings (N = 19; initial PbB < 40 micrograms/dl). During the past nine years serial determinations of renal function on all study subjects and control siblings were obtained. Mean values of systolic and diastolic blood pressures, serum creatinine, serum beta 2-microglobulin, fractional excretion beta 2-microglobulin, urinary protein:creatinine ratio, serum phosphate, tubular reabsorption of phosphate, serum uric acid, and urinary specific gravity were similar in study subjects compared with sibling controls. The frequency of abnormal values for these tests was similar in the two groups. Multiple linear regression analyses failed to demonstrate a significant influence of the presence of plumbism or initial PbB on serum creatinine or systolic or diastolic blood pressure. A modest increase in serum creatinine values was observed over a nine year period in four of 62 study subjects (1.4, 1.4, 1.5, 1.6 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)

Height and weight following lead poisoning in childhood.

The effect of lead on growth was examined in 104 lead-poisoned subjects (Pb-B [blood lead concentration], 4.82 to 22.73 mumol/L) and 27 sib-controls (Pb-B, 0.48 to 1.88 mumol/L). Blood lead concentration, height, and weight are reported for 1974 (the year of their first posttreatment recall for evaluation) and for 1985 (the year of their sixth recall). In 1974, when their mean age was 8 years and their mean Pb-B was 1.68 mumol/L, about 70% of the patients and sib-controls were in the 50th to 95th percentiles for height and weight. In 1985, when their mean age was 18 years and all Pb-Bs were less than 1.20 mumol/L, height and weight percentiles were similar to those of 1974. Lead did not seem to affect the genetic predisposition for height attainment, at high or low blood lead levels.

Slow, natural reduction in blood lead level after chelation therapy for lead poisoning in childhood.

Lead poisoning is treated with chelating agents. We report the natural decline of blood lead (Pb-B) concentration after treatment(s) (1967 to 1972) in 74 patients whose maximal Pb-B level ranged from 100 to 471 micrograms/dL (4.83 to 22.73 mumol/L). These longitudinal data (range, nine to 17 years) disclose a predictable decrease in Pb-B levels after treatment that is independent of the maximal Pb-B level before therapy. The correlation between age in months and the logarithm of the Pb-B level was significant, and the equation defined by the regression line allows one to predict Pb-B levels at specific ages after chelation therapy. It is important to recognize the slow, natural decline of Pb-B levels after chelation therapy once the level is stable and below 70 micrograms/dL (3.38 mumol/L). Multiple repeated courses of calcium disodium edetate are unlikely to influence the natural decline of the Pb-B level in asymptomatic children.

Renal function 9 to 17 years after childhood lead poisoning.

Renal function was studied in 74 subjects who, between 1966 and 1972 (ages 1 to 6 years) had had blood lead levels (PbB) greater than or equal to 100 micrograms/dl (range 100 to 471 micrograms/dl, median 142 micrograms/dl) and in 21 sibling controls. PbB measured in 1983 in study subjects remained significantly higher than in sibling controls (mean +/- 1 SD 14.5 +/- 4.5 vs 11.6 +/- 2.6 micrograms/dl, P less than 0.01). The two groups did not differ in development of hematuria or leukocyturia. The frequency of elevated serum creatinine concentration, depressed creatinine clearance, elevated protein excretion, low urinary osmolality, elevated serum beta 2-microglobulin (beta 2-M), and elevated fractional excretion beta 2-M % X 100 was similar in the two groups. Mean values for these tests were similar in study subjects compared with sibling controls. Mean systolic blood pressure was significantly higher in study subjects compared with that in sibling controls (117 +/- 12 vs 109 +/- 10 mm Hg), but the control group contained a preponderance of females and the study group had more overweight females; mean diastolic blood pressure was similar in the two groups. We conclude that in our adolescent subjects who had had lead poisoning 9 to 17 years earlier, there is little if any evidence of chronic nephropathy.

The evolution of the radiologic lead line.

Serial radiographs of lead-poisoned children showed separation of lead lines from the zone of provisional calcification within four weeks at sites of rapid growth. Lead lines do not appear until blood lead attains a concentration of 70 to 80 micrograms/dl. They are not affected by treatment, but disappear spontaneously within four years. While they remain in the diaphysis, they provide a marker for the time of onset of lead toxicity and the subsequent rate of bone growth.

Lead poisoning without encephalopathy. Effect of early diagnosis on neurologic and psychologic salvage.

Medical and psychological status of 166 patients previously treated for lead poisoning and of 22 sibling controls were evaluated. Maximum blood lead levels ranged from 40 to 471 microgram/dL. Eighteen patients had definite symptoms, 32 had questionable symptoms, and 116 were asymptomatic. No patients developed seizures, other neurological sequelae, or abnormal nerve conduction velocity. No statistically significant relationship was found between blood lead concentration (PbB) and subsequent intellectual function. The mean IQ of the patient cohort was 87, approximately at the 50th percentile for inner-city schoolchildren in Chicago. Detection prior to encephalopathy and prompt detoxification were effective in preventing or minimizing sequelae despite high PbBs.

IQ following treatment of lead poisoning: a patient-sibling comparison.

Forty-seven children treated for lead poisoning (PbB 50 to 365 microgram/dl) were compared to siblings next in age (PbB less than 40 microgram/dl) by a battery of psychologic tests. Symptoms were present in 18 but none had frank encephalopathy. Physical and neurologic examinations revealed no residual damage. Mean psychologic test scores showed no significant difference between patients and controls except in the arithmetic subtest, in which patients' scores were not related to lead concentration. Intelligence tests failed to distinguish children successfully treated from their sibling controls.

Effect of a screening program on changing patterns of lead poisoning.

A biphase program of screening and treating high-risk children for lead poisoning resulted in a 30% fall in mean lead values in the target areas over a 5-year period. The mean and median for subjects under 6 years was 4-10 mug/100 ml higher than for those over 6. Median for a high incidence area was 42 mug/100 ml in 1967 and 30.0 in 1971; for a low incidence area, 33 and 20 mug/100 ml in the equivalent years. Ingestion of lead paint was observed or demonstrated by x-ray in 90% of 2200 patients treated in the Lead Clinic. Gross neurologic sequelae were limited to two cases of mild, persistent ataxia. Impaired intellectual performance was observed subsequently in several asymptomatic patients with initial blood lead levels (PbB) >/= 100 mug/100 ml.