JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. University of California Press and American Institute of Biological Sciences are collaborating with JSTOR to digitize, preserve and extend access to BioScience. Laboratory bioassays provide a first step in testing for chemical effects on ecosystems but are inadequate for predicting effects on natural populations and on ecosystem-level features. For these purposes we need microcosm studies, controlled experimental manipulations of whole ecosystems, and a sound theoretical basis for extrapolation.In its responsibility to evaluate the potential effects of chemical substances proposed for release into the environment, the Environmental Protection Agency (EPA) faces profound challenges. The American Chemical Society's Chemical Abstract Service lists some 6 million chemicals, with an estimated 63,000 in common use today (Maugh 1983). Passage during the 1970s of the Toxic Substances Control Act (TSCA) as well as major amendments to the Clean Water Act (CWA); Federal Insecticide, Fungicide and Rodenticide Act (FIFRA); and Resource Conservation and Recovery Act (RCRA) meant that EPA had to evaluate data supplied by regulatees on the potential deleterious health and environmental effects of numerous chemical substances or mixtures (Bedford 1984). Even before this legislation, EPA and its predecessor agencies were required to establish criteria to protect human health and the environment against pollutants. Yet little was known about the range of sensitivity of organisms to various anthropogenic chemicals, and the basic concepts of ecosystem structure and function were not well established. Earlier researchers (Forbes 1887, Forbes and Richardson Kimball is with the Research Department, Appalachian Mountain Club, Gorham, NH 03851, and Levin (to whom all correspondence should be directed) is with the

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This study evaluated the acute effects of ambient ozone (O3), fine particulate matter (PM2.5), and strong aerosol acidity on the pulmonary function of exercising adults. During the summers of 1991 and 1992, volunteers (18-64 years of age) were solicited from hikers on Mt. Washington, New Hampshire. Volunteer nonsmokers with complete covariates (n = 530) had pulmonary function measured before and after their hikes. We calculated each hiker's posthike percentage change in forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), the ratio of these two (FEV1/FVC), forced expiratory flow between 25 and 75% of FVC(FEF25-75%), and peak expiratory flow rate (PEFR). Average O3 exposures ranged from 21 to 74 ppb. After adjustment for age,sex, smoking status (former versus never), history of asthma or wheeze, hours hiked, ambient temperature, and other covariates, there was a 2.6% decline in FEV1 [95% confidence interval (CI), 0.4-4.7; p = 0.02] and a 2.2% decline in FVC (CI, 0.8-3.5; p =0.003) for each 50 ppb increment in mean O3. There were consistent associations of decrements in both FVC (0.4% decline; CI,0.2-0.6, p = 0.001) and PEFR (0.8% decline; CI, 0.01-1.6; p = 0.05) with PM2.5 and of decrements in PEFR (0.4% decline; CI, 0.1-0.7; p = 0.02) with strong aerosol acidity across the interquartile range of these exposures. Hikers with asthma or a history of wheeze (n = 40) had fourfold greater responsiveness to ozone than others. With prolonged outdoor exercise, low-level exposures to O3, PM2.5, and strong aerosol acidity were associated with significant effects on pulmonary function among adults. Hikers with a history of asthma or wheeze had significantly greater air pollution-related changes in pulmonary function.ImagesFigure 1Figure 2