Lead poisoning in children was first discovered in 1890 in Queensland, Australia. The lead source was not identified until 1904, when a researcher traced it to the paint used on railings and verandahs. The first discovery of lead poisoning in the United States (with a traceable source) was in 1914; the child had chewed the paint off of his crib. At this time they linked lead poisoning as a cause of convulsions in children. As research progressed and more children were found with high lead levels, symptoms caused by lead were expanded to include lead meningitis, acute encephalopathy, intellectual dullness, reduced consciousness, seizures, comas, and death (Chisholm, 1982).

Lead is a metal found virtually everywhere even today. Sources of lead include auto body shops, electric storage batteries, glazes for china dishes, crockery, insecticides, electric cable insulation, hose, pipe, sheet and floor coverings. Lead is associated with stain glass work, jewelry making and antique ceramic doll painting. Although lead in paint was outlawed, there are still many homes that have lead paint (White et al, 1990). Lead found in gasoline was found in one study to account for 23--27% of the lead blood levels in the people tested (Wagner, 1991). This exposure to lead sources is more of a concern for children due to the characteristic habit of children to taste everything they touch; this characteristic is known as pica. Children are also in closer contact with their lead polluted environment during play. They are more active and exposed to outdoor contaminates and they inhale dust and dirt that are lead contaminated. Furthermore, the adsorption rate of lead in the digestive tract is up to 10 times greater in children that in adults (Wagner, 1991). Lead toxicity may also occur transplacentally and be detrimental to the neurological development of the fetus.

In the 1950’s and 1960’s, lead poisoning was found to be prevalent in the slums of the inner cities. These areas were referred to as the "lead belt" because these run down houses were havens for lead exposure. The flaking paint on walls, the chipping plaster ceilings, and the old furniture exposed these children to a real hazard. Pica was an important contributing factor and children, ages 1 to 3 were at the greatest risk. Siblings in these situations were often affected and recurrence was common because the lead paint was not removed. The prognosis for these children became worse with each recurrence (Chisholm, 1982).

This lead poisoning problem finally received the attention it deserved in 1971 when the Lead-Based Paint Poisoning Prevention Act was put into effect. This act provided Federal assistance to help communities carry out screening and treatment programs (Chisholm, 1982).

The improved screening and treatment of lead poisoning decreased the severity of symptoms usually seen. However, the level of lead in the blood does not establish what symptoms are seen, since lead in blood only establishes current exposure. Recently, studies have shown that a long exposure to low amounts of lead may have severe neurobehavioral effects that are not diagnosed until the child enters school (Singhal et. al., 1980).

In the most extreme cases of lead poisoning, which were seen due to lack of testing, children exhibited neuropathy and encephalopathy. The symptoms may begin with intractable seizures and proceed to coma and death within a short period of time. Other cases showed signs of drowsiness, altered consciousness, frequent episodes of vomiting and profound ataxia leading to coma. There are many nonspecific symptoms such as muscle weakness or tremor, numbness, paralysis, persistent headache, or depression that are common before the more severe symptoms. These symptoms present clinically very similarly to cerebral edema and increased intracranial pressure of unknown origin. Lead poisoning is easily overlooked as a cause for these symptoms (Singhal, 1980).

Of the children that present with lead caused chronic encephalopathy 82% suffer from recurrent seizures and mental retardation. The symptoms may resemble many degenerative diseases of the central nervous system. Children with high levels of blood lead may exhibit steady loss of motor control or speech followed by convulsive disorder. Lead poisoning in adults more often presents as peripheral neuropathy involving motor function and usually little sensory involvement (Singhal,1980).

As more has been discovered of the effects of lead toxicity the levels of acceptable lead in the blood have been decreased. The main focus had been on work related exposure rather than the general population. In addition, the only overt signs of lead toxicity ware originally the encephalopathy and neuropathy associated with severe and long-term exposure. Since the discovery of "subclinical and subtle health effects" the levels of lead in the blood have been re-evaluated. Blood lead levels must reach 80 g/dL or more to elicit the most severe symptoms, but lead levels as low as 10 g/dL in children can cause cognitive and behavioral effects. However, the Center for Disease Control considers the 25 g/dL level to be the action level. As detection methods become more advanced and tests for the effects more accurate, it is suggested that this level will be lowered (Goyer, 1990).

Although neurological effects of lead are considered the most severe, lead can cause many other problems. It has been shown that lead can be associated with immunodeficiency. Lead can interfere with the natural chemical balance of the body required for proper immunity by effecting the action of CD4+ T lymphocytes. This action allows for greater opportunity of pathogens to infect. The opposite side of the lead toxicity effect, is that it may also cause autoimmunity and cancers by activating B cell differentiation (McCabe et. al., 1991).

The detection of lead in the blood can only be done when moderate lead levels are reached. Children with estimated blood levels of 25 g/dL or greater are suggested by the Center for Disease Control to undergo the lead mobilization test. Children with lead levels above 55 g/dL must undergo immediate treatment to reduce their load burden. This is carried out most successfully by hospital administration of one or more chelating agents, and lead diuresis. Lead diuresis is achieved by administering CaNa²EDTA which allows mobilization of lead and clearance by the kidneys.

In a study conducted to determine the efficiency of chelation therapy of 178 lead poisoned children, 112 were less than 3 years of age; 62 were African-American, 103 were Hispanic and 13 were of other racial or ethnic background. The lead levels detected originally by the lead mobilization test were 13 to 60 g/dL. The children with lead levels above 40 g/dL were chosen for chelation therapy. There were 32 children treated. The skeleton is the primary site effected by chelation therapy, therefore the older children were benefited more quickly by the treatment. The chelation therapy resulted in 88 +/- 9% reduction in lead levels. Unfortunately, this treatment is not overly effective when lead levels are below 40 g/dL (Markowitz et. al., 1991).

Lead toxicity has been around for centuries, and it is impossible to completely eradicate it. Lead is a heavy metal that is readily available in many environmental forms, including the air, water, and food. The objective is to limit the exposure to dangerous amounts of lead. This is essential for the proper development of children. The first major steps have been taken to reduce lead exposure of children by eliminating lead from household paints, and reducing the amount in gasoline. The key to preventing serious neurological and behavioral deficiencies in children, is detecting lead when it is initially introduced to the child’s surroundings and when it is first detected in the blood. Very low levels of lead in the blood can cause slow learning and motor skill impairment. Parents and pregnant women should be advised as to the risks and educated as to the possible sources of lead in their environment.

BIBLIOGRAPHY:

Chisolm, J., and O’Hara, D. Lead Absorption in Children. Urban and Schwarzenberg, Baltimore-Munich, 1982.

Goyer, R. A. Lead Toxicity: From Overt to Subclinical to Subtle Health Effects. Environmental Health Perspectives, Vol. 86, 1990, pp.177-181.

Markowitz, M. and Rosen, J. Need for the Lead Mobilization Test in Children with Lead Poisoning. The Journal of Pediatrics. Vol. 119, No. 2, August 1991, pp. 305-310.

McCabe Jr., M. and Lawrence, D. Lead, A Major Environmental Pollutant, Is Immunomodulatory by Its Differential Effects on CD4+ T Cell Subsets. Toxicology and Applied Pharmacology, Vol. 111, 1991, pp. 13-23.

Singhal, R. L., and Thomas, J. A. Lead Toxicity. Urban and Schwarzenberg, Baltimore-Munich, 1980.

Wagner, H. M. Recent Trends In Human Lead Exposure. New Horizons in Biological Dosimetry, 1991, pp. 179-186.

White, R., Feldman, R., and Travers, P. Neurobehavioral Effects of Toxicity Due to Metals, Solvents, and Insecticides. Clinical Neuropharmacology, Vol. 13, No. 5, 1990, pp. 392-412.