期刊
RISK ANALYSIS
卷 28, 期 4, 页码 877-890出版社
WILEY
DOI: 10.1111/j.1539-6924.2008.01084.x
关键词
asthma; Clean Air Act; decision analysis; gene-environment interaction; genetics; particulate matter; risk analysis
类别
资金
- NIEHS NIH HHS [ES07033, ES-09601] Funding Source: Medline
In 2002, the U.S. Environmental Protection Agency (EPA) released an Interim Policy on Genomics, stating a commitment to developing guidance on the inclusion of genetic information in regulatory decision making. This statement was followed in 2004 by a document exploring the potential implications. Genetic information can play a key role in understanding and quantifying human susceptibility, an essential step in many of the risk assessments used to shape policy. For example, the federal Clean Air Act (CAA) requires EPA to set National Ambient Air Quality Standards (NAAQS) for criteria pollutants at levels to protect even sensitive populations from adverse health effects with an adequate margin of safety. Asthmatics are generally regarded as a sensitive population, yet substantial research gaps in understanding genetic susceptibility and disease have hindered quantitative risk analysis. This case study assesses the potential role of genomic information regarding susceptible populations in the NAAQS process for fine particulate matter (PM2.5) under the CAA. In this initial assessment, we model the contribution of a single polymorphism to asthma risk and mortality risk; however, multiple polymorphisms and interactions (gene-gene and gene-environment) are known to play key roles in the disease process. We show that the impact of new information about susceptibility on estimates of population risk or average risk derived from large epidemiological studies depends on the circumstances. We also suggest that analysis of a single polymorphism, or other risk factor such as health status, may or may not change estimates of individual risk enough to alter a particular regulatory decision, but this depends on specific characteristics of the decision and risk information. We also show how new information about susceptibility in the context of the NAAQS for PM2.5 could have a large impact on the estimated distribution of individual risk. This would occur if a group were consequently identified (based on genetic and/or disease status), that accounted for a disproportionate share of observed effects. Our results highlight certain conditions under which genetic information is likely to have an impact on risk estimates and the balance of costs and benefits within groups, and highlight critical research needs. As future studies explore more fully the relationship between exposure, genetic makeup, and disease status, the opportunity for genetic information and disease status to play pivotal roles in regulation can only increase.
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