Monitoring Environmental Exposures: Now It’s Personal

Abstract

Most diseases are thought to arise from the combined effects of genes and the environment. While great strides have been made in our understanding of human genetics, the contribution of environmental exposures to disease remains poorly understood. This lack of understanding impedes real progress in identifying genetically susceptible people whose responses to environmental agents are severe or unique relative to the general population. If identified, targeted prevention and treatment strategies might be applied to these groups, with potentially lifesaving results. Without more personal exposure information, however, scientists have a limited ability to identify pollution-susceptibility genes that elevate disease risk. This mismatch between exposure and genetic research slows the identification of environmental factors that—if altered or removed—could even prevent some diseases from occurring in the first place. “Genes aren’t modifiable,” explains Frederica Perera, a professor of environmental health sciences at the Mailman School of Public Health of Columbia University. “So, these environmental components in diet, food, water, and air are the only ones we can act on for disease prevention.” Exposure is, at a core level, the instance of environmental stimuli such as chemicals, infectious agents, diet, and lifestyle factors interacting with the human body. But studying human exposures poses difficult challenges. Scientists studying the effects of chemical pollutants can’t ethically dose people, so they often base their dose–response estimates on animal models. Further, they base their estimates of human exposure on indirect measures taken from a person’s home or work environment, along with assumptions about individual behaviors that influence the risk of coming into contact with a given pollutant. In a typical study, epidemiologists might use census figures, questionnaires, and general environmental monitoring data (such as samples of water from a household tap or soil in a schoolyard) to estimate how much of a given chemical an individual has come into contact with, and for how long. But while these studies approximate population-level exposures, they provide little information about real exposures to individual people. And because of this, scientists know little about how specific pollutants—particularly in combination with each other, with diet, and with physical activity—affect any individual’s response to the pollutant. With a clear need for progress, exposure assessment has recently come under the spotlight. This year, the NIEHS launched the Exposure Biology Program (EBP), a four-year effort with two overarching goals: to improve exposure assessment technology, and to identify biomarkers for common pathogenic mechanisms that reflect the human response to environmental agents. Such biomarkers could include changes in metabolites, proteins, or DNA that reflect the individual’s genetic susceptibility to environmental harm. “Right now we don’t really understand how exposure levels translate to human health risk, so our goal is to fill that gap,” says EBP coordinator Brenda Weis, a senior scientific advisor at NIEHS. “We need to get a better measure of exposure at the point of human contact, and we need to integrate those measures with biological response measures derived from samples taken directly from exposed people. So, this is a more ‘medical’ approach to exposure assessment—in the sense that measures are taken on a personal level—rather than the broader, ecological approaches we’ve been using so far.”