Personalized exposure assessment: promising approaches for human environmental health research

Abstract

New technologies and methods for assessing human exposure to chemicals, dietary and lifestyle factors, infectious agents, and other stressors provide an opportunity to extend the range of human health investigations and advance our understanding of the relationship between environmental exposure and disease. An ad hoc Committee on Environmental Exposure Technology Development was convened to identify new technologies and methods for deriving personalized exposure measurements for application to environmental health studies. The committee identified a "toolbox" of methods for measuring external (environmental) and internal (biologic) exposure and assessing human behaviors that influence the likelihood of exposure to environmental agents. The methods use environmental sensors, geographic information systems, biologic sensors, toxicogenomics, and body burden (biologic) measurements. We discuss each of the methods in relation to current use in human health research; specific gaps in the development, validation, and application of the methods are highlighted. We also present a conceptual framework for moving these technologies into use and acceptance by the scientific community. The framework focuses on understanding complex human diseases using an integrated approach to exposure assessment to define particular exposure-disease relationships and the interaction of genetic and environmental factors in disease occurrence. Improved methods for exposure assessment will result in better means of monitoring and targeting intervention and prevention programs.

Figure 1. A schematic representation of markers of exposure, response, and susceptibility in the exposure–disease continuum: an example for PAHs and cancer. CYP2A6, cytochrome P4502A6 gene; ETS, environmental tobacco smoke; GSTM1, glutathione S-transferase M1 gene; PAHs, polycyclic aromatic hydrocarbons; Arrows indicate predictability of each marker for exposure or disease in the exposure–disease continuum. Adapted from NRC (1987). PAHs in ETS and urban air are a marker for exposure source. GSTM1 null genotype and blood PAH–DNA adducts are independent markers of cancer case status (disease) but have a multiplicative effect in combination (Perera et al. 2002; Tang et al. 1995). GSTM1 null genotype is a predictor of tissue PAH–DNA adducts, which are a marker for altered function (Perera et al. 2002; Rundle et al. 2000; Tang et al. 1995). CYP2A6 variant is a marker for increased internal dose of nicotine and protective effect on cancer development (Spitz et al. 2005). Plasma cotinine is a marker for internal exposure to ETS but is not correlated with blood PAH–DNA adducts (Mooney et al. 2005). Blood PAH adducts are a marker for PAH/ETS exposure, internal dose, biologically effective dose, early biologic response, and cancer (Mooney et al. 2005; Perera et al. 2002, 2004; Poirier and Beland 1992; Veglia et al. 2003; Whyatt et al. 1998). Tissue PAH–DNA adducts are a marker for altered function and cancer (Rundle et al. 2000).

Figure 2. Conceptual strategy for integration of new exposure assessment technologies in human environmental health research.