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Controlled human laboratory studies have shown that there is a disproportionately greater pulmonary function response from higher hourly average ozone (O3) concentrations than from lower hourly average values and thus, a nonlinear relationship exists between O3 dose and pulmonary function (FEV1) response. The nonlinear dose-response relationship affects the efficacy of the current 8-h O3 standard to describe adequately the observed spirometric response to typical diurnal O3 exposure patterns. We have reanalyzed data from five controlled human response to O3 health laboratory experiments as reported by Hazucha et al. (1992), Adams (2003, 2006a, 2006b), and Schelegle et al. (2009). These investigators exposed subjects to multi-hour variable/stepwise O3 concentration profiles that mimicked typical diurnal patterns of ambient O3 concentrations. Our findings indicate a common response pattern across most of the studies that provides valuable information for the development of a lung function (FEV1)-based alternate form for the O3 standard. Based on our reanalysis of the realistic exposure profiles used in these experiments, we suggest that an alternative form of the human health standard, similar to the proposed secondary (i.e., vegetation) standard form, be considered. The suggested form is an adjusted 5-h cumulative concentration weighted O3 exposure index, which addresses both the delay associated with the onset of response (FEV1 decrement) and the nonlinearity of response (i.e., the greater effect of higher concentrations over the mid- and low-range values) on an hourly basis. [ABSTRACT FROM AUTHOR]

Recent studies have shown enhanced responsiveness to ozone in obese mice. Adiposity has not been examined as a possible modulator of ozone response in humans. We therefore examined the relationship between body mass index and the acute spirometric response to ozone (O3) exposure among 197 nonasthmatic young adults (aged 18-35 yr) studied in our human exposure facility from 1992 to 1998. Each subject had been exposed to 0.42 ppm O3 for 1.5 h with intermittent exercise designed to produce a minute ventilation of 20 L/min/m2 body surface area (BSA). Spirometry (pulmonary function) was measured pre- and immediately postexposure to determine acute ozone-induced changes. The decrement in forced expiratory volume in 1s (ΔFEV1) as percent of baseline was significantly correlated with BMI, r = -0.16, p = .03, with a slightly stronger correlation in women (n = 75), r = -0.22, p = .05, and no significant correlation in men. BMI had a greater range in women than in men in our study. In women greater ozone-induced decrements were seen in overweight (BMI > 25 kg/m2) than in normal weight (BMI 18.5 to 25 kg/m2), and in normal weight than in underweight (BMI < 18.5 kg/m2) for all spirometric variables considered (p trend ≤ .022). Although our population studied was predominantly normal weight, we found that higher body mass index may be a modest risk factor for adverse pulmonary effects associated with ozone exposure, especially for women. [ABSTRACT FROM AUTHOR]

ABSTRACT. Waste incinerators are an increasingly common means of solid waste disposal. However, little is documented about the physical health of community members who live close to incinerators. During a 3-yr epidemiological study, spirometric lung function was tested once annually among residents from 3 communities surrounding a hazardous waste, biomedical, or municipal incinerator and among residents in 3 comparison communities. A total of 1,016 nonsmoking individuals, aged 8-80 yr, participated during at least 1 of the 3 yr of the study; 358 individuals participated all 3 yr. Daily air-quality sampling was done for 1 mo/yr in all 6 communities. The average monthly concentrations of particulate matter with diameters of 2.5 μm and less (PM[sub 2.5] [range = 14.6-31.5 μg/m³]) in all communities were similar during the 3 yr of study. The mean daily PM[sub 2.5] concentrations were significantly less than the U.S. Environmental Protection Agency's allowable 24-hr standard of 65 μg/m³. Individual incinerators contributed less than 2.5% of the areas' total PM[sub 2.5] levels. There was no difference in percent predicted forced vital capacity, forced expiratory volume in 1 sec, or forced expiratory flow rate over the middle 50% of the forced vital capacity among members of the incinerator communities, compared with nonincinerator communities, and there were no significant differences in lung function within the 3 sets of communities. There was no evidence from this study that an association existed between residence in these 3 waste incinerator areas, which met state and federal emissions regulations, and average spirometric pulmonary function of nonsmoking community members. [ABSTRACT FROM AUTHOR]

Ozone exposure causes acute decrements in pulmonary function, increases airway responsiveness, and changes the breathing pattern. We examined these responses in 19 ozone-responsive (D FEV1 > 5%) young females exposed to both air and 0.35 ppm ozone. The randomized 75-min exposures included two 30-min exercise periods at V E 40 L/min. Responses were measured before, during, and after exposure and at 18 and 42 h postexposure. FVC, FEV1, and FIV0.5 decreased (p < .01) immediately postexposure by 13.2%, 19.9%, and 20.8%, respectively, and the airway responsiveness was significantly increased. Raw increased (p < .05), while TGV remained essentially unchanged. At 18 h postexposure, the airways were still hyperresponsive and FEV1 and FIV0.5 were still 5% below the preexposure levels. There were no residual effects in any of the variables at 42 h postexposure. During exercise in ozone the tidal volume was decreased (-14%) and respiratory frequency increased (+15%). The changes in airway responsiveness were not related to changes in spirometric measurements. We found no significant differences between postair and postozone mouth occlusion pressure (Pm0.1) and the hypercapnic response to CO2 rebreathing. We conclude that ozone induced typical acute changes in airway responsiveness and that ventilatory (exercise), spirometric (inspiratory and expiratory), and plethysmographic pulmonary function may show some residual effects for up to 18 h after exposure. The ozoneinduced alteration in breathing pattern during exercise does not appear to be related to a change in ventilatory drive. [ABSTRACT FROM AUTHOR]