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Rationale: Identification of the minimal ozone (O^sub 3^) concentration and/or dose that induces measurable lung function decrements in humans is considered in the risk assessment leading to establishing an appropriate National Ambient Air Quality Standard for O^sub 3^ that protects public health.
Objectives: To identify and/or predict the minimal mean O^sub 3^ concentration that produces a decrement in FEV^sub 1^ and symptoms in healthy individuals completing 6.6-hour exposure protocols.
Methods: Pulmonary function and subjective symptoms were measured in 31 healthy adults (18-25 yr, male and female, nonsmokers) who completed five 6.6-hour chamber exposures: filtered air and four variable hourly patterns with mean O^sub 3^ concentrations of 60, 70, 80, and 87 parts per billion (ppb).
Measurements and Main Results: Compared with filtered air, statistically significant decrements in FEV^sub 1^ and increases in total subjective symptoms scores (P < 0.05) were measured after exposure to mean concentrations of 70, 80,and87ppbO^sub 3^. Themeanpercentchange in FEV^sub 1^ (±standard error) at the end of each protocol was 0.80 ± 0.90, -2.72 ± 1.48, 25.34 ± 1.42, 27.02 ± 1.60, and 211.42 ± 2.20% for exposure to filtered air and 60, 70, 80, and 87 ppb O^sub 3^, respectively.
Conclusions: Inhalation of 70 ppb O^sub 3^ for 6.6 hours, a concentration below the current 8-hour National Ambient Air Quality Standard of 75 ppb, is sufficient to induce statistically significant decrements in FEV^sub 1^ in healthy young adults.
Keywords: ozone; clinical study; exposure assessment; human
Ozone is the primary oxidant found in photochemical air pollution and is one of the six criteria air pollutants identified in the 1971 United States Clean Air Act as adversely affecting public health. Human clinical exposure studies have played an important role in the risk assessment required to set the National Ambient Air Quality Standard (NAAQS) for ozone. These clinical exposure studies have been designed to expose defined subpopulations of individuals while varying ozone concentrations, exposure duration, and minute ventilations. A central question inherent in these studies has been as follows: What is the minimal mean ozone concentration that produces a statistically significant decrement in FEV^sub 1^ and other markers of response?
Early clinical studies focused on manipulating ozone concentration and/or minute ventilation (VE) by adjusting exercise workloads, while limiting the duration of exposure to...