Sources: World Health Organization (2001), European Center for Environment and Health (1999), Lvovsky (2001) (note: the study was not aimed at children, but the identified problems are strongly related to children's health), Pan American Center for Sanitary Engineering and Environmental Science (2001), G8 countries (1998), Commission for Environmental Cooperation (2000), U.S.A. - Cesses are vulnerable to disruption by toxicants, which cause irreversible adverse effects on body structure (birth defects, reduced growth rate) and function, (2) the potential for relatively high exposures related to diet, behavior and physiological/metabolic differences with adults, (3) immature detoxification systems, and (4) inadequate toxicity testing of chemicals for developmental, neurobehavioral, immunological, and reproductive system effects of perinatal exposures. Prenatal exposure of the male rat to androgen receptor antagonists (e.g. the pesticides vinclozolin, procymidone, linuron and dichlorodiphenyltrichloroethane [DDT]) causes decreased anogenital distance and induces areolas at relatively low doses, hypospadias, agenesis of reproductive accessory tissues and retained nipples at intermediate doses, and undescended testes and epididymal agenesis at high doses.
Polymorphisms involve two or more distinct alleles at a genetic locus at stable population frequencies too large (usually defined as ⱖ1%) to be explained by recurrent mutation alone—the average heterozygosity per nucleotide site in humans is about 1:1000. Exposure - the suspected causative agent persists in the environment or in vivo and can be measured, exposure levels vary in the target population or there is an opportunity to study several exposed and unexposed communities, people can recall their exposure accurately, or can be reconstructed from the data. Strength - The 16 studies that measured relative risk all found similarly high values (9-10 for moderate smokers, 20 or higher for heavy smokers).
Temporal relationship - the reported age of smoking onset fell long before any observable health effects. The latter, based on assumptions of low dose linearity and constant lifetime exposure, should include: (1) unit risk - the additional lifetime risk of cancer per unit dose of carcinogen, (2) dose at a given risk level - carcinogenic dose to come corresponds to a given risk, and (3) population risk - the additional lifetime risk of cancer at a specified dose of carcinogen in an exposed population. Percentage of children with elevated blood lead levels (ⱖ10g/dL), United States, NHANES II and III.
Knowledge gaps – the effectiveness of blood lead screening programs in reducing adverse health effects has not been tested in a randomized trial. Biomonitoring – monitoring the blood lead levels of the population in NHANES has enabled the evaluation of preventive interventions and the identification of ongoing needs. The contribution of lead-contaminated house dust and residential soil to the lead content in the blood of children.
MERCURY
Mercury levels in fish (10–30 g/g) and average fish consumption (300 g/day) in Minamata were much higher than current levels in the United States. A WHO expert panel reviewed dose-response data from Iraq and estimated the risk of fetal neurotoxicity to be 5% and 30%, respectively, at maternal hair mercury levels of 10–20 g/g and 70⫹g/g (World Health Organization , 1990 ). Given the high toxicity of mercury, it is surprising that only Germany and the United States have collected nationally representative data on mercury levels in children and women of childbearing age (Table 5–2) (Centers for Disease Control and Prevention 2001b, 2001c; Seifert et al., 2000).
Exposure to methylmercury from fish consumption is associated with mercury levels in maternal blood and hair, but not in breast milk. Women exposed during major poisonings had hair mercury levels of up to 700 g/g in Minamata (median 41 g/g) and over 400 g/g in Iraq. All mothers in longitudinal studies of fish-eating populations had hair mercury levels below 40 g/g.
Biomonitoring studies in the United States and Germany showed that mercury levels were generally low; in the United States, about 10% of women had mercury levels in their hair that were within one-tenth of potentially dangerous levels, indicating a relatively narrow margin of safety. Inuit communities that rely on a diet high in fish and marine mammals had the highest average levels of cord blood and adult mercury; Blood mercury levels varied significantly seasonally, consistent with the high consumption of fish and seafood in early fall and early winter.
Mercury levels in aquatic environments far from polluting industries and other forms of development are strongly related to air levels. Mercury levels in meat, liver and kidney from Swedish pigs declined during the 1980s, possibly due to reduced use of fish in pig feed. Among epidemiological studies, only the Faroe Islands study has shown adverse effects (reduced performance on tests of language, attention and memory at age 7) at maternal hair mercury levels of less than 10 g/g (Grandjean et al ., 1997).
The number of dental amalgam fillings in children and adults is related to the mercury content in the blood, breast milk and urine. Placental mercury levels are strongly correlated with maternal blood levels and the number of amalgam fillings (Ask et al., 2002). The study in the Faroe Islands showed that cord blood mercury levels were associated with significant deficits in language, attention and visual-spatial memory at age 7 years, independent of cord blood PCB levels.
OTHER METALS AND METALLOIDS
Exposure to airborne arsenic and other metals (lead, cadmium) from foundries was associated with a doubling of childhood cancer risk in an ecological study (Wulff et al., 1996). A cross-sectional study showed a borderline association between urinary cadmium and small proteins in children (Noonan et al., 2002). An epidemiologic study in Greece found an association between drinking water manganese levels and neurotoxicity outcomes in adults (Kondakis et al., 1989).
Knowledge gaps - the potential role of arsenic, cadmium and manganese in fetal and child health remains to be investigated. The most intensively studied PHAH is 2,3,7,8-tetrachloro--dibenzodioxin (TCDD), one of the most potent toxicants known (Schiestl et al., 1997). Body stature at age 10 years was not associated with blood PCB levels measured at age 8 years (Karmaus et al., 2002).
A recent German study, however, reported independent effects of prenatal and postnatal PCB exposure on cognitive deficits at 42 months of age (Walkowiak et al., 2001). Population-based epidemiological studies have shown associations between PCBs and cancers in adults, including non-Hodgkin's lymphoma (Rothman et al., 1997) and breast cancer. In Inuit infants, the risk of otitis media before 1 year of age was associated with prenatal exposure to DDE, hexachlorobenzene, and dieldrin, but not to PCBs (Dewailly et al., 2000).
Severe neurotoxicity, including coma, seizures, and death, has occurred following ingestion or excessive dermal exposure to N,N-diethyl-m-toluamide (DEET) (Briassoulis et al., 2001). Maternal but not paternal occupational exposure to PCP has been associated with IUGR (Dimich-Ward et al., 1996; Karmaus and Wolf, 1995). There was no association between birth weight and community exposure to malathion or parental occupation as farmers (Kristensen et al., 1997; Thomas et al., 1992).
Limb reduction defects—associated with maternal occupational and residential pesticide exposure (Engel et al., 2000; Shaw et al., 1999). Carcinogenic Risk Assessments - the EPA has concluded that pesticide active ingredients include 5 known, 71 probable, and 82 possible human carcinogens, many of which are still registered for use on food. In agricultural areas, children may be exposed to pesticides through various media, including significantly higher house dust concentrations from OPs compared to non-agricultural families (Lu et al., 2000).
Whole milk was the main source of DDE for persons in the upper decile of estimated daily intake (MacIntosh et al., 1996). Six million urban children living in poverty in the United States are at risk of exposure to pesticides widely used in schools, homes, and day care centers (Landrigan et al., 1999).
