many instances, the benefit of human epidemiology is not available to resolve discrepant animal studies. In such circumstances, a false positive can lead to the limitation or ban of a particular useful chemical. However, public health scientists are perhaps more concerned about false negatives, such as the case with arsenic. In this example, animal bioassays for carcinogenicity generally have failed to identify the potent carcinogenic effects of arsenic that are known to occur in humans. Animal toxicology or human epidemiology alone does not address all of the challenges in regulating chemicals, and thus the science behind regulatory decisions requires a multidisciplinary approach.
In recent years, tremendous advances have been made in molecular biology to elucidate cellular pathways and mechanisms that contribute to the understanding of how chemicals might contribute to human disease, but these advances are not a panacea for regulatory policy. Many cellular and molecular pathways have been highly conserved throughout evolution, and thus fundamental biological knowledge learned from simple organisms may be quite relevant to human biology. However, the evolutionary processes that dictate how humans respond to their environment select against other pathways, giving rise to large species differences in how organisms respond to their immediate environment, including chemical exposures. This is a challenge in the “omics” technology, in which scientists can measure changes in the expression of 10,000–20,000 different genes in response to a chemical exposure, but they are not always able to interpret the significance of such changes in terms of human health. Similar to advances in science, advances in technology have resulted in the vanishing zero: Environmental health scientists are able to measure chemicals in the body at lower and lower concentrations. However, scientists are not yet at a point at which they can make biological sense of the low-level presence of these chemicals.