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    Statement by
    Dr. Kenneth Olden
    Director, National Institute of Environmental Health Sciences, National Institutes of Health
    Health Effects of Air Pollution
    before the
    Senate Committee on Health, Education, Labor and Pensions, Subcommittee on Health

    September 3, 2002

    Mr. Chairman, I am pleased to appear before this Subcommittee to discuss the human health effects of air pollution that have been discovered by grantees of our Institute. My name is Ken Olden and I am the Director of the National Institute of Environmental Health Sciences (NIEHS) of the National Institutes of Health (NIH). The NIEHS has some of the longest-term epidemiologic studies on the health effects of air pollution in the country. Much of this research has been instrumental in identifying the more harmful aspects of air pollution and identifying groups who are more susceptible. I would also like to recognize the contributions in this effort of our sister Institutes and agencies both within and outside of the Department of Health and Human Services, especially the National Institute of Allergy and Infectious Diseases, the National Heart, Lung, and Blood Institute, the Centers for Disease Control and Prevention, and the Environmental Protection Agency. The NIEHS has developed a number of strong partnerships and collaborations with these and other agencies (for example, the Inner City Asthma Study and the Children's Environmental Health and Disease Prevention Centers). These collaborative efforts have been instrumental in supporting the research on which I will report today.

    Air pollution itself has a number of different components. Ozone, oxides, and sulfur dioxide are common gases found in polluted air. Additionally particulate matter such as soot is a byproduct of combustion that can appear concurrently with gases. Particulate matter comes in a variety of sizes, and the size, as well as other factors (i.e., respiration rate, oral or nasal breathing), affect deposition of particles in the lungs. Particulates are generally measured as microns or micro-meters ( m) in diameter. As a point of reference, the human hair is roughly 100 microns in diameter. What we are finding is that particles of 2.5 microns (PM2.5) and smaller may be more harmful than particles greater than PM2.5. Fine particulate pollution is usually a mixture of solid particles and liquid droplets that can include acid condensates as well as sulfates or nitrates. The solid components can include heavy metals such as mercury, cadmium, tin, vanadium or even lead. The health effects of other components of particulate matter and of ozone, on the other hand, have only recently begun to be understood and so will constitute the major part of my testimony.

    The earliest epidemiologic work on air pollution found that as air quality deteriorated, the number of hospitals admissions, asthma attacks, and deaths from all causes increased. These admittedly were crude measures of effect, but the evidence was sufficiently compelling to identify air pollution, particularly ozone, sulfur species and fine particulate air pollution, as being associated with these adverse effects. The elderly, asthmatics, and children were identified as particularly vulnerable subpopulations.

    Recent studies have refined this earlier work. These newer studies have been able to control for smoking, diet, occupation, and other lifestyle factors that were possible confounders in the earlier studies. Three of the major health effects associated with air pollution are: asthma attacks and other airway sensitivity disorders; lung cancer; and heart attacks. Given the prevalence and health costs of these diseases, it behooves us to try to prevent their occurrence.

    I will briefly mention some of these more recent findings. Peters, et al., 2001( Circulation, 103:2810-2815) examined several hundred patients with myocardial infarction (MI) and found that elevated concentrations of fine particles in the air were associated with an elevation in the risk of MIs within a few hours and 1 day after exposure. Further epidemiologic studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI in people. There have been, however, several small studies in people showing that particulate levels can increase biological products that enhance risk for coronary heart disease, which strengthens the possibility that particulates can trigger MIs. These products include C reactive protein (Peters, et al., 2001, Eur. Heart J., 22:1198-1204; Seaton, et al., 1999, Thorax, 54:1027-1032), plasma viscosity (Peters, et al., 1997, Lancet, 349:1582-1587), and blood fibrinogen (Ghio et al., 2000, Am. J. Respir. Crit. Care Med., 162:981-988). Further corroboration of the epidemiologic evidence can be found in animal studies of Godleski et al., 2002 (Res. Rep. Health Eff. Instit., 91:5-88), in which exposure to concentrated ambient particulate matter resulted in measurable electrocardiogram (EKG) changes.

    Pope, et al., 2002 (JAMA, 287:1132-1141) recently published the results of a study that followed 500,000 adults over 16 years. This study found that fine particulate and sulfur oxide-related pollution was associated with several fatal diseases. These findings provide evidence that long-term exposure to fine particulate air pollution common to many metropolitan areas is an important risk factor for deaths from heart and lung diseases. Interestingly, they also showed a protective effect of education level There is no real reason to assume that people with lower education have a greater susceptibility to effects of particulate matter. If, however, you accept that education level is a surrogate for income level, then this study also suggests that adverse health effects of air pollution may also exhibit a socioeconomic disparity component.

    The studies I have mentioned so far have focused on adults, but children are another vulnerable population that can be affected by air pollution. Asthma is a serious lung disorder that has been increasing in children. A number of factors seem to be implicated in asthma, particularly exposure to indoor allergens such as mold spores, cockroaches, dust, and second-hand smoke. Other studies are focussing on a possible link of asthma to decreased rates of breast feeding and an increase in childhood obesity. Outdoor air might play a role, too. It has been demonstrated repeatedly in industrialized cities in the United States and the world that ozone and other lung irritants can trigger asthma attacks, accounting for the increased hospitalizations observed during episodes of high air pollution, particularly of ozone (Peden, 2002, Environ. Health. Perspect., 110 (suppl 4):565-568). New evidence suggests that ozone might actually be involved in causing asthma. A recent study (McConnell, et al., 2002, Lancet, 359:386-391) found that children in communities with high average ozone levels who compete in three or more team sports have a three-to-four times higher risk of developing respiratory illness than do non-athletic children. The more sports children participate in, the greater the effect. Most of the children who were diagnosed with asthma had no history of wheezing, suggesting that they may not have previously undiagnosed asthma made worse by ozone. Rather, these children apparently developed new cases of asthma. This study did not exclude the possibility that other pollutants also might play a role in asthma development. These pollutants would include particulates, and active and passive tobacco smoke. Despite these limitations, the results from this study merit further investigation.

    Even in children who do not develop serious lung diseases, air pollutants have been shown to adversely affect normal lung development. Children followed from ages 10 to 14 years were found to have a 10 percent lower lung function growth rate if they lived in polluted areas compared to less polluted areas (Gauderman, et al., 2000, Am. J. Respir. Crit. Care Med., 162:1383-1390). These studies indicate that high levels of air pollution might be robbing our children of optimal lung growth and development. The effects of these early decrements in function, factored over their lifetimes, are of serious concern.

    Air pollution can also act synergistically with other adverse environmental conditions. For example, heat waves cause increased mortality in human populations. If a heat wave occurs in the presence of poor air quality, the effect is enhanced. The synergy between high temperatures and poor air quality has been observed around the world, including Japan (Piver et al., 1999, Env. Health Perspec., 107:911-916), Belgium (Sartor, et al., 1995, Environ. Res., 70:105-113), and Greece (Katsouyanni, et al., 1993, Arch. Env. Health, 48:235-242). These results give another layer of complexity to understanding the human health effects of air pollution. In fact, dissecting the health consequences of air pollution must account for the types of pollutants, the accompanying exposure conditions, the age of individuals, and the health and genetic susceptibilities of these individuals.

    To achieve a greater control of exposure conditions than is possible with human subjects, Federally-supported scientists are taking advantage of animal models. The NIEHS Inhalation Toxicology Branch and our intramural and extramural scientists are working with rodent models of lung injury/ inflammation/dysfunction to examine the effects of exposure to particulates and ozone. Some of these studies include investigations with knockout and transgenic mice that can begin to examine the interrelationships between environmental exposures and genetics. These and other state-of-the-art studies enhance and expand upon the associations found in human epidemiologic studies.

    Health effects of air pollution will continue to be an important component of the Federal environmental health research portfolio. In my testimony I have highlighted some of the more important findings recently made by researchers supported by the Federal Government. I would be happy to answer any questions you might have.

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Last revised: May 13, 2003