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Research to develop better biomarkers of exposure and effects must be stimulated so that better epidemiology of possibly exposed populations can be done. With better biomarkers, the occurrence and extent of exposure can be established, and better prediction of possible adverse effects from such exposures can be made.

With better biomarker-based epidemiology we can also document the occurrence, extent and nature of groups of people who are highly susceptible to specific hazards in both the workplace and as a result of their living space, for example, near waste dumps, substandard housing, and so forth. Without more basic and long-supported research, none of these objectives can be net in the near future.

INFANT MORTALITY

Mr. Stokes: We have heard much about Infant mortality. In the justification (page 123), it is stated that: "The period of growth and development from fertilization to the time of weaning is particularly susceptible to harmful effects fron natural and nannade hazards." To what degree are environmental hazards contributing to the incidence of infant mortality?

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Dr. Hoel: Even though infant mortality is intensively studied, we still have little understanding of what its underlying causes are. Rates of infant death have been falling in the U.S. since at least the turn of the century. Much of this decline is attributed to improved medical care, but better nutrition and hygiene could also be playing a large role.

Against the background of declining rates, there could easily be subgroups of the population in which environmental exposures are causing Infant deaths. We know that mothers' smoking increases the risk of infant mortality, and we suspect that other pollutants in air, or other exposures in the workplace or general environment can do likewise. However, the contribution of such factors to total infant mortality is unknown at this time.

Mr. Stokes: Is the Institute supporting any studies in this area, and considering the relationship between the environment and infant development, should we be doing more in this area?

Dr. Hoel: The Institute has had a long-standing commitment to improving the health of infants. One of our first epidemiologic studies was polychlorinated biphenols, or PCBs, and their effects on infant development. This study has shown that babies with higher PCB exposures are delayed in their motor development. In another study we have developed an improved measure of early human pregnancy that has launched a new generation of studies of early fetal death and its causes.

We are also paying close attention to more Indirect ways that environmental exposures might affect infant health. For example, the recent report that radiation exposure of fathers might cause cancer in their children has led us to give new attention to fathers' exposures and infant health. Finally, there may be ways that environmental factors interact with genetic

characteristics to injure the fetus. We are heavily committed to these studies and believe even more could be done as resources become available.

INDOOR AIR AND ASTHMA

Mr. Stokes: Children who live in households with tobacco smokers have more respiratory illness and compromised lung functions, as measured by NIEHS studies. Research suggests that irreversible lung damage in the child may be associated with the mother's smoking during pregnancy and with newborn exposure to tobacco smoke while the lungs are still developing. elaborate further as to what your studies have found in this area?

Would you

Dr. Hoel: The NIEHS has and continues to support a number of studies relating indoor air pollution to adverse human health effects. One study, the 6-Cities Survey, reported that children had higher rates of respiratory illness and lower lung function measurements associated with environmental tobacco smoke due to parental smoking. This association was shown to be significant with current maternal smoking and smoking during pregnancy. These epidemiological findings suggest that irreversible damage to the lungs may be associated with maternal smoking during pregnancy or during the neonatal period, when the lungs are still developing.

This association indicates the need to further explore the biological basis of fetal/neonatal damage through basic research.

Mr. Stokes: We have heard a lot during these hearings about the rising incidence of asthma amongst blacks, particularly with black children. What is the correlation between smoking, or other indoor air concerns (11ke nitrogen dioxide), and asthma in the black community.

Dr. Hoel: Much of the increase in hospitalization rates in blacks has been correlated with poverty conditions, but specific causes have not been identified Factors which may play a role include indoor and outdoor environmental pollutants, as well as inadequate medical care.

We know that children whose mothers smoke cigarettes have increased respiratory problems, including asthma. Both prenatal and postnatal exposures may be important. Smoking during pregnancy may increase the risk of asthma even more than smoking during infancy and childhood. We are looking into this possibility with data from California.

NIEHS has long supported many studies of various kinds of lung damage associated with differing types of air pollution. Our "6 Cities" and now "24 Cities Studies" supported at Harvard University are among the best known, largest and longest continuing studies in this research area. Because of this "Cities' research, now stretching back over 17 years, and many other smaller grants, scientists have begun to understand the many variables and "actors" anong pollutants affecting lung functions, especially in children.

Most of these NIEHS supported studies have also pointed to interactions of several air pollutants. Recently identified pollutant synergisms resulting in lung damage include those between ozone, acids, and small particles. The nitrogen oxides, including nitrogen dioxide, are newer candidates for serious

consideration as lung damaging pollutants. Nitrogen oxides are produced in the burning of most hydrocarbons, including all oil derived fuels, but especially gasoline and diesel fuel, kerosene and natural gas.

Indoor air concentrations of all air pollutants are frequently higher than outdoors, but are often derived in part from outdoor air pollution. This is certainly true for air borne acids, particles/aerosols and most oxidants and cigarette smoke.

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Almost all air pollutants produce more lung damage when combined with cigarette smoke. This has been previously studied with things like asbestos and radon combined with smoking, but also in our "Cities" and other studies we see evidence for synergism when air borne acids and ozone are combined with smoking. Thus, nitrogen oxides are good candidates for synergism in their adverse health effects by cigarette smoke and this needs more careful study.

Asthma is often made worse by air pollutants. NIEHS supports a number of studies of this problem. The University of Rochester, the University of Washington, Seattle, and of course, Harvard University are all places where several NIEHS grantees are studying the effects of various air pollutants on asthma. Air borne oxidants are especially damaging to lung tissue and seem most likely to make asthma much worse. Common air borne oxidants include the nitrogen oxides and ozone. Air borne oxidants and particles are now the subject of several studies seeking to decipher the puzzle of which are the major concerns for serious lung damage like asthma. Some research by NIEHS grantees has suggested that air borne oxidants cause aging of the lung which resembles very closely the lung changes seen in asthma.

Thus air pollutants such as cigarette smoke, nitrogen and sulfur oxides, ozone, small particles of all kinds, not only can make asthma worse and trigger asthma attacks, but they might even be parts of the cause of asthma in some people not otherwise prone to this disease.

Air pollution of all kinds is much more likely in congested cities and in substandard/crowded housing. The use of space heaters, which contribute both particles and nitrogen oxides, and attempts to conserve energy by "tightening up" on air exchange in living quarters, are only some of the ways by which minority communities may contribute to the higher incidence of lung disease, including asthma, for which they are known. In all studies made so far, it is children who have suffered the most from all the causes of lung disease.

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CHARACTERIZATION OF BUDGET

Mr. Early: Doctor, how would you characterize your budget request; would you say that it is a growth budget or a status quo budget?

Dr. Hoel: The FY 1992 request is an increase of 5.6% over FY 1991. I wouldn't call it a growth budget. However, within the budget we will be able to begin some new projects.

CLEAN AIR ACT

Mr. Early: Doctor, would you briefly summarize for us NIEHS' responsibilities under the Clean Air Act Amendments of 1990?

Dr. Hoel: Our responsibilities under the Clean Air Act Amendments fall into three general categories. First, NIEHS is to offer advice and consultation to the Administrator of EPA as a member of an Interagency task force on research and as a member of a science advisory panel for the Mickey Lealand Urban Air Toxics Research Center, soon to be established in a major university.

Second, NIEHS is to conduct a study to determine the threshold level of mercury exposure, below which adverse human health effects are not expected to

We are to submit a report to Congress by November 15, 1993, on this subject.

occur.

Third, NIEHS is authorized to conduct a program of basic research to identify, characterize, and quantify risks to human health from air pollutants. This final responsibility is to be primarily achieved through grants to medical schools and universities but may also include research done in our own Institute. We are to expand the education and training of physicians in environmental health in addition to the program of basic research.

In addition to these statutory responsibilities, NIEHS staff have been discussing with EPA staff the need for additional toxicologic data necessary for conducting risk assessments of 189 air toxics listed in the law.

Mr. Early: How do you plan to proceed in implementing these provisions?

Dr. Hoel: With respect to our responsibilities for providing advice and consultation, we are participating on the EPA Administrator's interagency research task force. We have been meeting with EPA staff to assure that our research plans are coordinated and that there will not be any unnecessary duplication of effort.

Determining a threshold level, or levels, of mercury as mandated in the law presents a significant scientific challenge. We know that high levels of mercury exposure can cause acute illness and death. We also know that lower exposures can cause illness in children and sensitive adults. We are currently conducting and supporting a wide range of studies aimed at identifying the effects of low level exposures on the nervous system and on reproduction. NIEHS scientists recently assisted the Agency for Toxic

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Substances and Disease Registry and the EPA in a review of all available scientific literature on mercury. We intend to convene a group of experts to review all this inforaation on mercury and to seek their guidance on determining threshold levels. An interia report will be prepared outlining the findings and recomendations of the experts sone time next year.

NIEHS basic research into the health effects of air pollutants will provide the broad base of knowledge needed by EPA and state air pollution control prograz zanagers to efficiently and effectively achieve the ambitious goals of the Clean Air Act established by Congress last year. It is our intention to solicit applications for grants for such research both fron those institutions with long and distinguished histories of advancing the understanding of the effects of air pollution on human health and from scientists and research physicians with new and innovative Ideas for studies.

Mr. Early: What are your prograx plans in this area for FY 1991 and Fy 19922

Dr. Hoel: In FY 1991, ve vill take a final look at the review ve conducted last year to determine research needs and information gaps in current understanding of the health effects of air pollutants. We will summarize that review and sake it available to the university-based biomedical research community and our Institute Advisory Council. We vill continue to work with EPA to assure that our research plans are well coordinated. In FY 1992, NIEHS will be prepared to award grants for the most important and scientifically sound research studies needed to fill critical inforzation gaps.

Mr. Early: Does your FY 1992 budget request include new funds for this purpose?

Dr. Hoel: No, it does not. Last year while we were preparing our budget request for FY 1992, we were aware that Congress vas likely to pass the Clean Air Act Amendments and that there were proposals for an expanded role for NIEHS. We had developed several planning documents identifying health research needs in the basic biomedical sciences, in toxicology, and in epidemiology consistent with the drafts of the proposed legislation which were publicly available. The bill was passed in October and signed into law on November 15, 1990. Consequently, it was not until late November that we knew exactly what was expected of us. By that time, it was too late to make any major revisions in our budget request.

RESEARCH MANPOWER Mr. Early: Doctor, what is your assessment of the current research manpower situation in the area of environmental health?

Dr. Hoel: There are needs for training in both clinical and basic areas of environmental health. On the basic side of the research aanpower situation, continued and expanded training efforts are critical since exciting advances are being made in understanding the nature of deleterious interactions between hunan systems and environmental agents. The field of molecular biology has opened up new routes of Investigation from biomarkers

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