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Many of the physical differences in children compared to adults put them at increased risk from toxicants in their environments. Because children are growing, they have a higher metabolic rate relative to their size compared to adults. For this reason, children consume relatively more of all the things needed to sustain life and growth; they eat more food, drink more water, and breathe more air. Children thus get a higher exposure per kilogram of body weight to many pollutants. Moreover, children have a higher surface area to body mass ratio, so their potential for dermal absorption is also higher. Children are also at risk in utero. Toxicants which are either small molecules or fat-soluble cross the placenta easily, as do some metals. Children also have longer remaining life expectancy, meaning that exposures with long lead times before disease (such as many carcinogens) can be more problematic for children, who are more likely to live long enough to experience an adverse effect. Finally, crawling on the floor and children’s short stature can increase their exposure to heavy airborne toxicants, such as mercury, which will be concentrated closer to the ground, in children’s breathing zone. Metabolism of many pharmaceuticals and environmental contaminants differ by age. Cytochrome P450 (phase 1) and conjugating (phase 2) enzyme development during early life can result in slower detoxification and clearance of many chemicals in neonates and young children. For example, while conjugation by some UGT enzymes is mature by 2 months, for others adult activity is not reached until puberty. For some chemicals the metabolic pathways are age dependent; for example, acetaminophen is metabolized by sulfation rather than glucuronidation in the neonate.

Young children are in a period of rapid growth. In addition to implying a higher metabolic rate for their size, this means that they have many cells rapidly dividing, further increasing their susceptibility to environmental insults. As a result, though adults can generally be expected to have a predictable pattern of insults with exposure to toxicants, regardless of the timing of exposure, the same cannot be said for children. In children there are specific developmental windows of susceptibility. For example, it is well described that alcohol exposure in utero has differential effects based on the timing of that exposure. Lead exposure during childhood can result in long-term cognitive deficits at lower levels than in adults because the exposure affects children during a period of substantial learning. Adolescence represents another time period of rapid growth concentrated around the development of sexual organs. As in younger children, adolescents are uniquely susceptible to toxicants during this period of growth and differentiation.

Many childhood behaviors also contribute to an increased risk of environmental exposures. Young children go through an exploratory phase which involves mouthing behaviors, meaning that they may have significantly higher exposure via ingestion of toxicants that adults would not ingest. Similarly, by crawling (in young infants) or ...

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