As to the levels that pose a danger to the child, there is still some uncertainty. Rutter, who reviewed all of the evidence up to 1980, concluded that persistent blood levels above 40 mcg/dL may cause slight cognitive impairment and, less certainly, an increased risk of behavioral difficulties. More recently, Canfield and colleagues reported, from a prospective study of 172 children, that even lower levels may induce a decline in IQ at 3 and 5 years of age. These data require confirmation before general acceptance. Further compounding the problem of interpreting low-level lead exposure in children with blood lead concentrations below 45 mcg/dL is the observation by Rogan and colleagues that treatment with succimer, while successful in reducing lead levels, did not improve cognitive or behavioral function.
The oral lead chelator succimer is approved for outpatient treatment of asymptomatic children with blood lead levels higher than 45 mcg/dL. A 3-week course of treatment is given, with weekly monitoring of blood lead levels to identify lead mobilization from bones and soft tissues (Jorgensen).
In 1988, on the basis of epidemiologic and experimental studies in the United States, Europe, and Australia, the Agency for Toxic Substances and Disease Registry set a much lower threshold for neurobehavioral toxicity (10 to 15 mcg/dL). It estimated that 3 to 4 million American children have blood levels in excess of this amount. Needleman and colleagues studied the long-term effects of low doses of lead in asymptomatic children, 132 of whom had had demonstrable levels of lead in the dentin of shed teeth (average 24 mg/dL). Eleven years later, the children were found to have behavioral abnormalities proportionate to their early lead levels. In comparison to a normal population, more had dropped out of school and more had lower vocabulary and grammatical reasoning scores, more reading difficulty, poorer hand-eye coordination performance, slower finger-tapping rates, and longer reaction times. The authors claimed to have eliminated other confounding variables such as lower social class and genetic factors. These findings are similar to those of the long-term studies of Baghurst and colleagues (see also Mahaffey). There are no adequate pathologic or MRI studies of such cases.
Lead intoxication in adults is much less common than in children. The hazards to adults are the result of inhaling the dust of inorganic lead salts and the fumes from the burning of objects containing lead or involvement in processes that require the remelting of lead. Painting, printing, pottery glazing, lead smelting, welding, and storage battery manufacturing are the industries in which these hazards are likeliest to occur. In the past, miners and brass foundry and garage workers (during automobile radiator repair, when soldered joints are being heated; see Goldman et al) were the ones most at risk. Currently, other, sometimes idiosyncratic, sources are more common. For example, the authors have encountered a striking case of lead encephalopathy in a man of Indian origin who was taking large amounts of an Ayurvedic herbal remedy for arthritis. The first manifestation was a series of generalized seizures followed by a fluctuating encephalopathy. His serum lead level was 70 mcg/dL, and 24-h urine collection contained 1,550 mg of lead (normal being less than 400 mg). There was a T2-weighted hyperintensity in the cerebral cortex. Whitfield and colleagues reviewed 23 instances of lead encephalopathy in adults. At the time of their report most cases were caused by moonshine (homemade whiskey from lead-lined stills). More recently, most cases have been from various herbal medications, as already mentioned. Combined lead and arsenic poisoning from herbal compounds is also known.