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As part of the Voluntary Children's Chemical Evaluation Program (VCCEP) program, a risk assessment was performed to evaluate the risks to children from environmental benzene exposures. This paper summarizes this risk assessment. Risk was characterized using two distinct methods: USEPA's default type of risk assessment, which used the Reference Dose (RfD) and Cancer Slope Factor (CSF) to characterize non-cancer and cancer risks, as well as a Margin of Safety (MOS) approach that utilized a point of departure (POD). The exposures for most scenarios evaluated in this VCCEP risk assessment are lower than both the cancer and non-cancer PODs by several orders of magnitude, indicating a large MOS and corresponding low potential for toxicity at these exposures. The highest benzene exposures likely experienced by children, associated with the lowest MOS, are from cigarette smoke. In addition, the potential for age-related differences in the sensitivity towards benzene-induced toxicity was investigated. In general, this risk assessment does not indicate that children are likely to be at a elevated risk of AML or hematopoietic toxicity associated with environmental exposures to benzene.

Negative effects of perinatal exposure to background levels of dioxins and PCBs in Europe and the USA have been documented. Four facets of development are reviewed in this paper: 1. Brain development and thyroid hormone metabolism. 2. Hepatic effects. 3. Hematopoietic system effects. 4. Lung function. Effects on IQ and behaviour have been documented in children on both sides of the Atlantic Ocean. Non-dioxin-like PCBs, measured in maternal and cord blood and current plasma samples have been implicated. Interference with thyroid hormone metabolism in the mother, in the foetus and in the newborn baby could be responsible for these effects on brain development. During early gestation the foetus is completely dependent on maternal thyroxine (T4). Lower T4 levels in the mother, caused by dioxins and PCBs, might negatively influence (early) brain development. It is plausible that the intrauterine dependency on maternal T4 and the high T4 need shortly after birth makes both these periods vulnerable for environmental influences. Effects of dioxin exposure on thyroid hormone metabolism have been described in the period shortly after birth. These effects are no longer found after two years of age indicating a transient effect. In animal studies, in utero exposure has led to effects on brain development due to abnormal induction of liver enzymes. This induction resulted in lower testosterone and estrogen levels, interfering with brain development in the vulnerable period of language development and the development of visuo-spatial abilities. In humans this developmental period occurs around the thirtieth week of pregnancy. Follow-up studies in puberty and adolescence of the different cohorts studied is necessary to evaluate these negative influences. Damaging effects on the liver found shortly after birth have proven to be transient. Effects on the haematopoietic system are clear immediately after birth, for instance on white blood cells and thrombocytes. An increase in middle ear infections (otitis media) in relation to current levels of PCBs at the age of 4 years was described in the Rotterdam study. Negative effects on lung function in the sense of increased obstruction was found after 8 years in relation to perinatal exposure to dioxins in the Zaandam study. This rather new finding might explain the sharp increase in lung problems in children in the Western world.

Biological indicators of lead effects on the central nervous system (as measured by performance tests), hematogenous bone marrow (hemoglobin levels) and kidney function (BUN Levels) can be combined in an integrative index (INDEX). This integrative index can be in turn related to indicators of lead exposure and absorption. Such an index was calculated by removing age effects in measures of performance and kidney function and then transforming all the variables to Z (standard) units. Secondary lead smelter workers and a control group were studied. In secondary lead smelter workers this INDEX was found to be significantly correlated with ZPP, blood lead levels, and duration of lead exposure. In this population the magnitude of the correlation coefficients with ZPP levels was much higher than than for blood lead levels. INDEX had a higher correlation with ZPP than with each of its components: performance test scores, hemoglobin, and BUN levels. Although performance test scores, hemoglobin, and BUN levels were shown to discriminate between the control, non-lead-exposed population, and the lead-exposed group, INDEX (and particularly one pair of its components, CNS and hemoglobin levels) achieved the best discrimination between groups. The concept of an integrative index of biological effects of lead may be especially useful in defining populations at high risk for developing chronic, potentially irreversible neurologic and kidney dysfunction, and in assessing the severity of lead effects in individual cases.