FEBRUARY 5, 1997

Mister Chairman and members of the Subcommittee, I am George D. Thurston, a tenured Associate Professor of Environmental Medicine at the New York University (NYU) School of Medicine. My scientific research involves investigations of the human health effects of air pollution.

I am also the Director of the National Institute of Environmental Health Sciences' (NIEHS) Community Outreach and Education Program at NYU. A goal of this program is to provide an impartial scientific resource on environmental health issues to decision-makers, and that is my purpose in speaking to you here today.

Ozone (03) is a highly irritant gas which is formed in our atmosphere in the presence of sunlight from other air pollutants, including nitrogen oxides and hydrocarbons. These "precursor" pollutants, which cause the formation of ozone, are emitted by pollution sources including automobiles, electric power plants, and industry.

The adverse health consequences of breathing ozone at levels below the current U.S. National Ambient Air Quality Standard (NAAQS) of 120 parts per billion (ppb) are serious and well documented. This documentation includes impacts demonstrated in controlled chamber exposures of humans and animals, and observational epidemiology showing consistent associations between ozone and adverse impacts across a wide range of human health outcomes. The noxious nature of ozone is also evidenced by the way it visibly 1,eats away" at materials such as rubber, an elastic substance sharing characteristics with human lungs.

Observational epidemiology studies have shown compelling and consistent evidence of adverse effects by ozone below the current U.S. standard. These studies follow people as they undergo varying real-life exposures to pollution over time, or from one place to another, and then statistically intercompare the health impacts that occur in these populations when higher (versus lower) exposures to pollution are experienced. These epidemiologic studies are of two types: l) population-based studies, in which an entire city's population might be' considered in the analysis; and, 2) cohort studies, in which selected individuals, such as a group of asthmatics, are considered. Both of these types of epidemiologic studies have shown confirmatory associations between ozone air pollution exposures and increasing numbers of adverse impacts, including:

- decreased lung function (a measure of our ability to breathe freely);
- more frequent asthma symptoms;
- increased numbers of asthma attacks;
- more frequent emergency department visits;
- additional hospital admissions, and;
- increased numbers of daily deaths.

In my own research, I have found that ozone air pollution is associated with increased numbers of respiratory hospital admissions in New York City, Buffalo, NY, and Toronto, Ontario, even at levels below the current standard of 120 ppb. My ozone-hospital admissions results have been confirmed by other researchers considering locales elsewhere in the world. The U.S. EPA used my New York City asthma results in their "Staff Paper" when estimating the health benefits of lowering the ozone standard. However, they failed to consider other respiratory admissions affected, such as for pneumonia or bronchitis. Thus, considering the published results from various cities, the EPA analysis underpredicts the respiratory hospital admission benefits of their proposed regulations by about a factor of two.

This month, the results of a study I conducted on the effects of air pollution on children at a summer "asthma" camp in Connecticut will be published. This study of a group of about 50 moderate to severely asthmatic children shows that these children experience diminished lung function, increased asthma symptoms, and increased use of unscheduled asthma medications as ozone pollution levels rise. On the highest ozone days, the risk of a child having an asthma attack was found to be approximately 40 percent greater than on an average study day, with these adverse effects extending to below 120 ppb O3.

More recently, I have found that daily mortality also rises after high ozone days in the U.S. cities of New York City, Atlanta, Detroit, Chicago, St. Louis, Minneapolis, San Francisco, Los Angeles, and Houston, even after accounting for other factors such as season and weather, and at ozone levels below the current NAAQS standard. I find that the risk of death rises by about 6 percent on ozone days having a 1-hour maximum of ozone that is 100 ppb above the average. While not yet published, these U.S. results are supported by previously published results, and by a recent spate of new papers by other researchers showing similar associations between ozone an4 human mortality around the globe. Recently published studies have shown this relationship in: London, Amsterdam, and Belgium. In addition, papers recently submitted for publication have also shown similar associations between ozone exposure and human mortality in both Rotterdam, the Netherlands, and Brisbane, Australia.

It is important to keep in mind that the above described epidemiology is supported by a large body of knowledge from controlled exposure studies that give consistent and/or supportive results, and that have demonstrated pathways by which ozone can damage the human body when it is breathed. Clinical studies have demonstrated decreases in lung function, increased frequencies of respiratory symptoms, heightened airway hyper-responsiveness, and cellular and biochemical evidence of lung inflammation in healthy exercising adults exposed to ozone concentrations as low as 80 parts per billion for 6.6 hours.

Airway inflammation in the lung is among the serious effects that have been demonstrated by controlled human studies of ozone at levels typically experienced by most Americans. Airway inflammation is especially a problem for children and adults with asthma, as it makes them more susceptible to having asthma attacks. For example, recent controlled human studies have shown that prior exposure to ozone enhances the reactivity of asthmatics to aeroallergens such as pollens, which can trigger asthma attacks.

In addition, increased inflammation in the lungs can make the elderly more susceptible to pneumonia, a major cause of illness and death in this age group.

It has been argued that, since the prevalence of asthma has risen over the last decade while air pollution levels have not, air pollution cannot be affecting asthma. However, this is not correct. This trend merely indicates that air pollution probably does not cause' people to become asthmatic, but it does not contradict the fact that air pollution adversely affects those who already have asthma. Indeed, as the asthma "epidemic" causes the number of persons with asthma to rise, whatever the cause of this "epidemic" turns out to be, there is a bigger and bigger percentage of the U.S. public who can be severely affected by air pollution.

The EPA has proposed a standard of 80 ppb averaged over an 8-hour period, rather than the existing 120 ppb limit for the highest hour of each day. The switch to an 8-hour average is clearly appropriate, based on the scientific evidence that the cumulative effects of multiple hours of exposure are worse for people than a single peak hour of exposure. However, since significant adverse effects are well documented down to the 80 ppb level, the EPA proposal provides no margin of safety. This is especially true since the proposed law will allow several exceedances of this level before a violation is cited. Thus, the health evidence would indicate that a standard set at 70 ppb ozone averaged over an 8 hour period is needed, if any margin of safety is to be provided to she public, rather than the 80 ppb recommended by the EPA.

On this subject, it is interesting to note what levels other deliberative bodies have recommended regarding permissible ozone levels. In Canada, the daily 1-hr maximum allowed is 80 ppb of ozone, which is roughly equivalent to an 8 hour limit of about 60 ppb ozone. In addition, The World Health Organization (WHO) recently released their "Update and Revision of the Air Quality Guidelines for Europe", and they similarly recommended an 8-hour average guideline of 60 ppb for ozone. Also, the American Conference of Governmental Industrial Hygienists (ACGIH) has recently proposed lowering the widely' employed workplace Threshold Limit Value - Time Weighted Average (TLV-TWA) limit for ozone to 50 ppb over an eight hour work day for workers under heavy exertion. This would indicate that healthy American workers need to be protected from levels that would be perfectly legal for the rest of us to breathe under the US EPA's proposals. The EPA's new proposed ozone limit is weak when compared to standards set or recommended by others.

It is also important to remember that the EPA proposed ozone standard is less' stringent than the O3 limit that prevailed in the U.S. during the 1970's, before the EPA decided to relax the limit to 120 ppb in February, 1979. Until that time, our standard was the same as the Canadians: 80 ppb ozone as a daily one hour maximum, or equivalent to about a limit of 60 ppb when averaged over 8 hours. Thus, while the EPA proposal is more stringent than the existing law, it is far less restrictive than the law of the land in the U.S. during the 1970's.

In conclusion, I would like to reiterate the key messages contained in the letter that I and 26 other air pollution researchers and physicians sent' to President Clinton last month:

- Please listen to the medical and scientific community on this issue.
- Exposures to O3 and PM air pollution have been linked to medically significant adverse health effects.
- The current NAAQS for these pollutants are not sufficiently protective of public health.

Thank you for the opportunity to speak to you on this important issue.