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Based upon the information reviewed, lead is the primary contaminant of concern. Preschool-age children and fetuses are usually the most vulnerable segments of the population for exposure to this contaminant. Infants and children are exposed to lead mainly through diet and ingestion of non-food materials associated with normal early hand-to-mouth behavior. Chronic exposure to low lead levels has been shown to cause subtle effects on the central nervous system which can result in deficits in intelligence, behavior, and school performance. Recent information indicates that children with blood lead levels as low as 10 g/dL can develop neurological and cognitive deficits. In addition, lead has been found to lower intelligence quotient (I.Q.) scores, slow growth, and cause hearing problems in children. Available evidence is not sufficient to determine whether lead-associated deficits are irreversible. Lead is especially harmful to unborn children. Exposure to lead during pregnancy has been correlated with premature births, low birth weight infants, and spontaneous abortions [1].

Anemia is the most serious effect of lead on the hematologic system. Lead-induced anemia occurs primarily by the lead-induced inhibition of several enzymes involved in the production of hemoglobin. Exposure to lead has been associated with hypertension, renal failure, and gout. Lead has not been shown to be carcinogenic in humans; however, high doses of lead have been found to produce kidney tumors in laboratory studies of rats and mice. The extremely high cumulative doses of lead used in animal studies are difficult to extrapolate to low-level exposure in humans, and do not provide a sufficient basis for quantitative risk assessment. Based on animal data, EPA currently classifies lead as a B2 carcinogen (probable human carcinogen) [1].

Although no threshold level for adverse health effects has been established, evidence suggests that adverse effects occur at blood lead levels at least as low as 10 g/dL. The Centers for Disease Control and Prevention (CDC) has determined that a blood lead level greater than or equal to 10 g/dL in children indicates excessive lead absorption and constitutes the grounds for intervention. The 10 g/dL level is based on observations of enzymatic abnormalities in the red blood cells at blood levels below 25 g/dL and observations of neurologic and cognitive dysfunction in children with blood lead levels between 10 and 15 g/dL [2].

A number of studies are available relating blood lead levels in children to levels of lead in the environment. In general, blood lead levels rise 3-7 g/dL for every 1,000 ppm increase in soil or dust lead concentration. Regression models for the correlation between blood lead levels and soil lead levels predict that soil lead concentrations between approximately 500 and 1000 ppm would result in blood lead levels below 10 g/dL [3]. The concentration of lead in soil from the ash pile near the Hunter residence was 544 mg/kg, slightly above the maximum concentration generally deemed appropriate for residential yards. The public health significance of the lead in the soil from the ash pile depends upon the size of the contaminated area and whether young children play in the contaminated soil. Under most normal exposure scenarios, lead confined to soil from one small area would not be expected to present a public health threat unless children frequently played in that area.

It is difficult to determine with any degree of certainty the risks associated with the lead found in the residential well west of the site. In 1996, the EPA reported a lead concentration of 93 g/L in water from this well. In 1997, the TNRCC did not find lead in water from this same well. Based on available information we cannot determine the reason for the differences in these results; however, in the absence of additional data and in the interest of public health it would be prudent to determine the public health implications based on the EPA results. A lead concentration of 93g/dL could present a threat to public health particularly if children are using this water. Children absorb a greater proportion of ingested lead and as mentioned previously are more susceptible to the subtle effects of ingesting lead. Using EPAs Integrated Exposure Uptake Biokinetic (IEUBK) model, the probability is high (approximately 45%) that a child chronically ingesting water containing 93 g-lead per liter of water would have a blood lead level greater than 10 g/dL (Figure1b). Lead (43 g/L) also was found in water from the domestic well 1,000 feet south of the site entrance. Although this was a background sample chonic ingestion of water from this well also could result in elevated blood lead levels in children (15% probability of exceeding 10 g/dL).

Figure 1a

Figure 1b

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