Asthma and respiratory irritants (ozone).

Abstract

Asthmatics appear to be more susceptible to the effects of air pollutants than nonasthmatics. The present studies were undertaken to examine the effects of exposing asthmatics to ozone concentrations that occur in the environment. Seventeen well-documented male and female asthmatics have been exposed for 2 hr in an environmental chamber to 0.25 ppm of ozone on one occasion (ozone) and to air on another occasion (air). Effects were assessed by measurements of pulmonary function obtained prior to (0 hr), every half-hour during and at the end of all exposures (2 hr). Paired t-test analysis of lung volumes, forced expiratory volume in 1 sec (FEV1.0), and maximum expiratory flow rates at 50% of vital capacity (V50%VC) showed no significant changes (p greater than 0.05) when the following comparisons were made: 0 hr air vs 0 hr ozone, 0 hr air vs. 2 hr air, 0 hr ozone vs. 2 hr ozone, 2 hr air vs. 2 hr ozone. There was variability in severity of asthma and pulmonary function status; most subjects were taking some form of medication at the time of study. Some asthmatics showed no change or improvement with both air and ozone and others developed greater reductions in pulmonary function with ozone than with air. Approximately one-third of the asthmatics demonstrated greater changes in V50%VC with exposure to 0.25 ppm of ozone relative to air exposure. These studies indicate that acute exposures to ozone at realistic concentrations in the environment can produce adverse responses in some asthmatics.

Spatial Enablement to Support Environmental, Demographic, Socioeconomics, and Health Data Integration and Analysis for Big Cities: A Case Study With Asthma Hospitalizations in New York City

“…Several variables, listed and described in Table 1, have been chosen for this study. For air pollution, we chose the PM2.5 and ozone concentrations, as among all the pollutants they appear to be particularly relevant in asthma exacerbation (14, 15) and open data about their monitoring in NYC is easily available. We then chose a set of other environmental data related to asthma (e.g., industrial land use) and some socioeconomic factors that appeared to be relevant in previous research (8, 12).…”

Pulmonary Inflammation Induced by Subacute Ozone Is Augmented in Adiponectin-Deficient Mice: Role of IL-17A

“…In the lung, ozone induces epithelial injury and an inflammatory response that includes a neutrophilic influx and induction of acute phase cytokines including IL(interleukin)-1, IL-6, TNF-α (tumor necrosis factor alpha), as well as the neutrophil chemotactic factors KC (keratinocyte-derived chemokine), MIP-2 (macrophage inflammatory protein), and LIX (LPS induced CXC chemokine) (3–12). Ozone is a trigger for asthma attacks and significantly decreases pulmonary function in asthmatic subjects (13–15). Importantly, responses to ozone are augmented in obese and overweight individuals (16, 17).…”

ROCK insufficiency attenuates ozone-induced airway hyperresponsiveness in mice

“…O 3 causes airway and pulmonary epithelial injury that results in a robust inflammatory response that includes generation of numerous cytokines, chemokines, and other inflammatory moieties, as well as recruitment of neutrophils and macrophages to the lungs (29,51,65). O 3 also causes AHR both in humans and in animals (12,16,55,57). The ability of O 3 to induce both AHR and inflammation may contribute to the role of O 3 as an asthma trigger.…”