Respiratory Response of Humans Exposed to Low Levels of Ozone for 6.6 Hours

Abstract

Recent evidence suggests that prolonged exposures of exercising men to 0.08 ppm ozone (O3) result in significant decrements in lung function, induction of respiratory symptoms, and increases in nonspecific airway reactivity. The purpose of this study was to confirm or refute these findings by exposing 38 healthy young men to 0.08 ppm O3 for 6.6 h. During exposure, subjects performed exercise for a total of 5 h, which required a minute ventilation of 40 l/min. Significant O3-induced decrements were observed for forced vital capacity (FVC, -0.25 l), forced expiratory volume in 1 s (FEV1.0, -0.35 l), and mean expiratory flow rate between 25% and 75% of FVC (FEF25-75, -0.57 l/s), and significant increases were observed in airway reactivity (35%), specific airway resistance (0.77 cm H2O/s), and respiratory symptoms. These results essentially confirm previous findings. A large range in individual responses was noted (e.g., percentage change in FEV1.0; 4% increase to 38% decrease). Responses also appeared to be nonlinear in time under these experimental conditions.

Ozone dose–response effects of varied equivalent minute ventilation rates

“…In early 6.6 -h exposures to 0.08 ±0.12 ppm O 3 , individual subject's V E was varied as a function of 8 l/ min per liter of FVC (Folinsbee et al, 1988;Horstman et al, 1990 ) and 20 l min À1 m À2 of BSA (McDonnell et al, 1991 ). However, the effect of varied V E (l/min) on FEV 1.0 response was not examined in these studies.…”

Public health challenges posed by chemical mixtures.

“…Of particular health significance is the TSP component of air pollution, which is itself a complex mixture (54). Acute adverse respiratory effects of ozone exposure are also well documented in animal and human populations (55)(56)(57).…”

Overview of ozone human exposure and health risk analyses used in the U.S. EPA's review of the ozone air quality standard

“…Although all of the studies did not investigate all of these endpoints, it was possible to develop exposure-response relationships for 33 endpoints (i. e., each exposure-response relationship is associated with a specific endpoint and a specific study). Results for only four of these endpoints are presented in this paper: moderate-to-severe cough (for l-h exposures at heavy exertion, based on McDonnell et al 1983), moderate-to-severe chest pain on deep inspiration (for l-h exposures at moderate exertion, based on Seal et al 1993), and FEV1 decrements =15% and > 20% (for 8-h exposures at moderate exertion,based on Folinsbee et al 1988, Horstman et al 1990, and McDonnell et al 1991.…”

“…The basis for the development of health models for lung fhnction and symptoms endpoints is a number of controlled human exposure studies: q l-h exposures at heavy exertion2 studies by McDonnell et al (1983), Avol et al (1984), and Kulle et al (1985), s l-h exposures at moderate exertion3 studies by Seal et al ((1993), and 4 by Folinsbee et al (1988), q 6.6-h exposures at moderate exertion Horstman et al (1990), andMcDonnell et al (1991). Results of these studies were used to develop exposure-response relationships for 8-h exposures.…”

“…The heavy exertion effects are based on 1-to 3-h controlled human exposure studies by McDonnell et al (1983), Avol et al (1984), and Kulle et al (1985). The moderate exertion effects are based on results from 2-h controlled human studies by Seal et al (1993) and from 6.6-h controlled human studies by Folinsbee et al (1988), Horstman et al (1990), andMcDonnell et al (1991). The hospital admissions model is based on a multiyear study of air pollution and respiratory hospital admissions in New York City (Thurston et al 1992).…”