Figure 5-3 shows reported effects of lead at various concentrations in the blood. Effects that have been clearly established and are well accepted by the scientific community are indicated by solid lines, effects with less certainty are indicated by dashed lines, and more controversial effects are indicated by dotted lines. For example, frank anemia occurs at blood concentrations of 80 µg/dL or above; reduced hemoglobin synthesis occurs in adults at 50 µg/dL and above, although this effect might occur in children at lower concentrations; loss of hearing acuity occurs above 30 µg/dL, but hearing loss has been measured down to 10 µg/dL; and while the effect of lead on diastolic blood pressure is clear above 50 µg/dL, some studies indicate effects on systolic blood pressure above 30 µg/dL, and effects below 10 µg/dL are seen in some studies. Several effects have no apparent threshold (for example, the effects on children's cognitive function, on blood pressure, and on heme synthesis), and other effects might not demonstrably affect health.

The bottom of Figure 5-3 presents the most recent information on the distribution of blood lead concentrations in the United States, from NHANES III, phase I, 1988-1991 (JAMA 1994). There has been a remarkable reduction in blood lead concentrations in the United States over the last 15 years. There has been a 78% drop in the average, from 12.8 to 2.8 µg/dL, primarily it is believed, because of the removal of lead from gasoline. But a distribution of blood lead exists in the population, and the data indicate that a small portion of the population has blood lead over 10 µg/dL, as do 9% of children aged 1-5; and 0.2% of the population (over 0.5 million people) have blood lead over 30 µg/dL. Any added lead in the environment might make those people more likely to experience the adverse effects of lead.

The lead emissions of incinerators are highly variable (see Chapter 4, Table 4-8 and Table 4-10, and this is reflected in the facts that the mean value of lead emissions from hazardous-waste incinerators is 100 times the median value and that the estimated range of air concentrations due to emissions varies by more than 8 orders of magnitude (from 2.0 × 10-8 to 7 µg/m3). Although maximal lead air concentrations due to emissions is 7 µg/m3, which exceeds the ambient-air standards of the EPA, over 95% of the incinerators were estimated to produce ambient concentration increments everywhere less than 0.5 µg/m3; similarly, maximal lead air concentrations due to emissions from cement kilns was 7 µg/m3, but 95% would be less than 1.2 µg/m3. Translating airborne lead to blood lead is complex but has been well studied: for young children and accounting for both the direct route (inhalation) and the indirect route (ingestion of soil, dust, and food contaminated by airborne lead) of exposure, each microgram of airborne lead per cubic meter could increase blood lead by about 4 µg/dL (EPA 1989; CalEPA 1996).

Although the average hazardous-waste incinerator and the average cement kiln would contribute less than 1 µg/dL to the blood lead burden of children around the facilities, there is the potential for the worst-case emitters to add about 20 µg/dL to the lead burden of nearby children. Thus, while the effect of

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