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Testimony on National Institute of Environmental Health Sciences' FY 1998 Budget by Dr. Kenneth Olden
Director, National Institute of Environmental Health Sciences National Institutes of Health
Accompanied by
Dr. Samuel H. Wilson, Deputy Director, NIEHS
Mr. Charles E. Leasure, Jr., Associate Director for Management, NIEHS
Ms. Laurie Johnson, Budget Officer, NIEHS
Dr. Harold Varmus, Director, NIH
Mr. Dennis P. Williams, Deputy Assistant Secretary, Budget, DHHS

U.S. Department of Health and Human Services

Before the House Appropriations Committee, Subcommittee on Labor, Health and Human Services, Education and Related Agencies
February 27, 1997

Mr. Chairman and Members of the Committee, I am pleased to appear before you today to discuss the important work of the National Institute of Environmental Health Sciences.

Virtually all diseases have both a genetic and an environmental component. Thus both environmental health research and human genome research are vital for fulfilling the public health mission of this Nation.

The opportunity to make a difference in the environmental health sciences has never been greater. The discipline has undergone a rapid transition and, coupled with advances made in genetic research, we are nearing a breakthrough in the "bottleneck" currently encountered when we try to identify environmental hazards that contribute to human illness. We are now poised to make enormous progress to prevent, diagnose, and treat the environmental components of diseases. Although we cannot yet say which environmental or genetic factor is the most important contributor to a specific disease, nor which individual is most likely to develop a particular disease, that day is not far off. When that day arrives, policy makers can more rationally determine the best, most cost-efficient ways to protect public health without unnecessarily sacrificing economic vitality.

Efforts to control environmentally-caused illness must be based on the understanding of human-environment interaction at the molecular level. Many of the common diseases such as cancer, Alzheimer's, Parkinson's, osteoporosis, and asthma appear to arise from the complex interplay between inherited genetic alterations and the environment. So, before we can prevent or improve the treatment of such diseases, we need a better understanding of the individual function of genes involved in the growth and development of humans and the ability of environmental agents to interact with, and damage, these genes.

In considering future research needs and opportunities, we have focused on areas of fundamental knowledge and practical issues relevant to understanding the role of the environment in the etiology of human illness. The areas of emphasis represent issues where major information gaps exist, where reasonable research questions can be formulated, where technologies are available, and where understanding offers the potential to significantly improve public health and regulatory policy.

Today, I would like to talk about some of the critical research needs and plans for the upcoming year.

First, we need to continue our effort to develop new and better carcinogenicity and toxicity test systems. While we have greatly improved test methods, they are still too costly and too time consuming for use in screening the thousands of natural and synthetic environmental chemicals requiring toxicity assessment. Opportunities now exist to develop alternative testing methods by incorporating knowledge of molecular and cellular mechanisms associated with the toxic or carcinogenic process.

Second, environmental health research can also capitalize on recent developments in molecular and cell biology to develop a mechanistic understanding of the toxic action of environmental agents. Under this scheme the actual biological events that lead to toxicity will be determined. Insights into molecular mechanisms of diseases will: 1) provide a more rational basis for assessing human risk based on data obtained in animals; 2) suggest new laboratory procedures for use in epidemiologic studies to more precisely identify the causes of human illnesses; 3) increase understanding of the wide person-to-person variation in risk to disease; and 4) provide the basis to develop molecular medicine strategies to prevent, detect, and treat various diseases.

Third, knowledge of mechanisms is also a prerequisite for prevention/ intervention using molecular medicine approaches. The field of environmental toxicology has historically limited its prevention efforts to eliminating or reducing environmental exposures. While this remains the most pragmatic approach, behavioral intervention is not possible in some cases because the causative agent cannot be readily controlled. Although much progress is being made in the laboratory in defining the environmental basis of disease and dysfunctions, this knowledge and technology is not being effectively translated into the practice of medicine. The recent creation of the clinical program within the NIEHS underscored the importance of translating discoveries made in the laboratory to benefit individuals and populations in terms of improved health status and reduced health care costs.

Fourth, research is needed to determine the genetic, behavioral, and developmental basis for the wide variation in individual responsiveness to exposures to environmental toxicants. There are indications that differences in responsiveness can be related to age, gender, lifestyle, or genetic predisposition. These differences could be important for human risk assessment.

NIEHS proposes to greatly expand its molecular genetics research on susceptibility genes for environmentally-induced diseases through a new Environmental Genome Project. This genome project, which makes use of technology developed by the human genome research efforts, will acquire a population database on the sequence diversity for the environmental disease susceptibility genes.

Genetic approaches used in the past have identified many susceptibility genes for environmental diseases. An individual with a defect in such a gene has an elevated risk of becoming ill after an environmental exposure. The molecular mechanisms of susceptibility are not well understood; however, we are now able to categorize many of the susceptibility genes into five broad classes: Genes controlling the distribution and metabolism of toxicants; genes for the DNA repair pathways; genes for the cell cycle control system; genes for metabolism of nucleic acid precursors; and genes for signal transduction systems controlling expression of the genes in the other classes. The NIEHS Environmental Genome Project will be a broad, multi-center effort to obtain information about DNA sequence diversity for the U.S. population on all of the environmental disease susceptibility genes now recognized, which number greater than 200. The Project will be expanded as additional susceptibility genes are discovered.

The availability of a population database on environmental disease gene diversity will allow us to conduct more focused molecular epidemiology that relates environmental exposures and disease to individual susceptibility genotype. Ultimately, information from such medical genetic epidemiology will allow us to greatly enhance public health through better prevention strategies for environmental diseases.

The Environmental Genome Project will provide information for future research on molecular mechanisms of susceptibility gene products. The project will also foster development of new high, through-put technology for the application of genetics in medical epidemiology as a function of environmental exposure.

Fifth, investigation of the mechanisms and health effects of mixtures is another area where lack of information is a serious problem. The data on exposure and toxicology of mixtures is inadequate for assessing health risk. The current toxicologic databases were developed using single chemicals in animal bioassays, whereas humans are exposed at a variety of levels to large numbers of chemicals either concurrently or sequentially via multiple pathways. Mixtures of chemicals are ubiquitous in ground and surface water, and in air, food and soil. For example, 700 organic chemicals have been identified in the drinking water supply of the U.S., 40 of which are possible carcinogens; 320 toxic industrial chemicals are released into ambient air, of which 60 are possible carcinogens; and approximately 380 pesticides are applied to food sources, 66 of which have been identified as actual or potential carcinogens. Furthermore, the problem of mixtures is not limited to chemical interactions since health outcome may also be influenced by physical or biological agents. For example, risk of radon-induced lung cancer is increased in cigarette smokers and people infected with hepatitis B virus are more susceptible to aflatoxin-induced liver cancer. Thus, our inability to say whether agents act in an additive, synergistic, or antagonistic fashion creates real problems in health risk assessment.

Sixth, research is needed to develop methods for screening environmental pollutants and natural products for endocrine-disrupting effects and for assessing the health effects of these exposures. Although the possibility for human health effects of these hormonally-active agents remains hypothetical, their pervasiveness and persistence in the environment make this an area of significant public health concern. These chemicals can potentially alter the balance of physiological systems whose coordination is controlled by delicately balanced neuroendocrine mechanisms.

Animal studies have demonstrated that exposure of the fetus to endocrine-disrupting chemicals can profoundly disturb organ development. Field studies have shown an association between exposure to endocrine-disrupting chemicals in the environment and developmental anomalies in fish, birds, reptiles and other wildlife species. These anomalies include feminization of male fish, birds and mammals; decrease in reproductive potential, and under-developed genitalia. Human exposure to synthetic estrogen (e.g., diethylstilbestrol) during early development caused reproductive organ dysfunction, abnormal pregnancies, cancers of the reproductive tract, and decreased fertility in females.

Given the large numbers of hormonally-active chemicals released into the environment over the past 50 years, more research is needed concerning the health consequences associated with chronic exposure to low doses of mixtures of endocrine-disrupting chemicals during the various stages of development. Exposure during the development of the embryo, fetus, and neonates is of particular concern because the consequences may be both more striking and permanent.

Lastly, a major challenge is to strengthen the links between fundamental science, toxicology, epidemiology, and risk assessment. To make environmental health research findings more applicable to human risk assessment, monitoring of human exposure to specific chemicals must be undertaken using improved and highly sensitive analytical procedures. NIEHS-supported scientists continue to generate novel and innovative biomarkers of environmental exposure that could be incorporated into a national survey to assess to what extent people absorb or retain the chemicals in their environment. This more "real world" assessment would greatly strengthen our capability to conduct risk assessment policy that reflects actual, rather than putative, exposures. To be most useful, this survey would include information concerning the nature of the exposure, estimated numbers of persons exposed, and demographic information such as age, gender, socioeconomic status, race or ethnicity, and geographic region.

In summary, environmental health policy decisions are only as good as the scientific foundation upon which they are founded; that is, the data and models used in assessing the risk, and the assumptions made in the absence of facts. The guiding principal should be good science for good decisions. Health risk assessment policy decisions affect millions of lives and involve hundreds of billions of dollars. Such an investment is worth doing and worth doing well.

The budget request for FY1998 is $313,583,00. I would be pleased to answer any questions.

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