Ute T. Anzar

Respiratory effects of 0.75 ppm sulfur dioxide in exercising asthmatics: Influence of upper-respiratory defenses

To determine the influence of mouthpiece breathing on respiratory responses to sulfur dioxide (SO2), 23 young adult asthmatic volunteers were exposed in a chamber to 0.75 ppm SO2 during heavy exercise, once with breathing unencumbered and once while they wore noseclips and mouthpieces. These conditions (more severe than in typical ambient exposures) were deliberately chosen to produce significant physiological and clinical responses. Similar exposures to clean air served as controls. Exposure studies were separated by 1-week intervals and order was randomized. The protocol consisted of 10 min on a bicycle ergometer (mean load 650 kg-m/min, mean ventilation 40 liter/min), preceded and followed by response testing (body plethysmography, symptom questionnaires, and forced expiratory function tests; the last were performed only postexposure). During clean-air exposures, specific airway resistance (SRaw) and symptoms increased significantly, but no meaningful differences between mouthpiece breathing and unencumbered breathing were observed. Exposures to SO2 under these relatively severe conditions produced greater increases in SRaw than clean-air exposures regardless of the mode of breathing, but the excess increase was significantly greater with mouthpiece than with unencumbered breathing. Symptom changes and postexposure forced expiratory function showed qualitatively the same pattern of decrements with SO2 ad did SRaw, but the excess responses attributable to mouthpiece breathing did not attain statistical significance. Mouthpiece breathing can compromise upper-respiratory defenses against SO2 to the extent that responses are greater than with more natural breathing. The mode of breathing should be taken in account when applying laboratory human exposure data to air-quality risk assessment.

Response to ozone in volunteers with chronic obstructive pulmonary disease.

Twenty-eight volunteers with chronic obstructive pulmonary disease were exposed to 0.0, 0.18, and 0.25 ppm ozone in purified air for 1-hr periods with light intermittent exercise, with exposure conditions presented in random order at 1-month intervals. No statistically significant changes attributable to ozone were found in forced expiratory performance or percent oxyhemoglobin (measured near the beginning and end of each exposure). No ozone-related changes in clinical status were found by interviews that included the time for 1 wk before to 1 wk after each exposure, except that a moderate increase in lower respiratory symptoms was reported by nonsmokers in 0.18 ppm exposures only. Thus, a slight decrement in hemoglobin saturation with ozone exposure (reported in two previous studies of chronic obstructive pulmonary disease subjects) may not be a common occurrence under typical ambient exposure conditions.

Effect of high concentrations of oxygen on reparative regeneration of damaged alveolar epithelium in mice

Abstract The main purpose of the present study was to determine if high concentrations of oxygen (O 2 ) would inhibit cell division in alveoli undergoing reparative regeneration following injury by ozone (O 3 ). Mice were exposed to 2.5 ppm O 3 for 6 hr to injure the alveolar epithelium. Groups of animals were then allowed to recover in 20% O 2 with and without food, 40, 61, 80, and 95% O 2 with food. At daily intervals, the mice were injected with tritiated thymidine to label cells preparing to divide, and sacrificed 1 hr later. Lung tissue was prepared for light microscopic autoradiography and the proportion of labeled cells were determined. In mice exposed to O 3 , type 1 epithelium is injured and type 2 cells proliferate in order to repair the damage. Mice allowed to recover in 20% O 2 with and without food, and in 40% O 2 , had a maximum proliferation of type 2 cells (about eight times control) on the second day of recovery. By the fourth day repair seemed to be complete and labeling indexes had returned to normal. In mice allowed to recover in 61, 80, and 95% O 2 , type 2 cell proliferation was less than control on the second day and did not increase during 4 days of recovery. It was concluded that concentrations of O 2 at 61% and higher inhibit reparative cell division in O 3 -damaged alveoli of mice.

Controlled Exposure of Volunteers with Chronic Obstructive Pulmonary Disease to Nitrogen Dioxide

Twenty-two volunteers with chronic obstructive pulmonary disease were exposed to nitrogen dioxide at 0.0, 0.5, 1.0, and 2.0 ppm in a controlled environment chamber. Exposure lasted 1 hr and included two 15-min exercise periods, during which the mean ventilation rate was roughly 16 L/min. Pulmonary mechanical function was evaluated pre-exposure, after initial exercise, and at the end of exposure. Blood oxygenation was measured by ear oximetry pre-exposure and during the second exposure period. Symptoms were recorded during exposures and for 1-wk periods afterward. No statistically significant changes in symptom reporting could be attributed to nitrogen dioxide exposure at any concentration, compared to the 0.0 ppm control condition. Measures of pulmonary mechanics showed either no significant changes, or small and equivocal changes. Arterial oxygen saturation showed marginal improvement with exercise, regardless of nitrogen dioxide concentration.

Controlled exposures of volunteers with chronic obstructive pulmonary disease to sulfur dioxide.

Twenty-four volunteers with chronic obstructive pulmonary disease (COPD) were exposed to sulfur dioxide (SO2) at 0, 0.4, and 0.8 ppm in an environmental control chamber. Exposures lasted 1 hr and included two 15-min exercise periods (mean exercise ventilation rate 18 liter/min). Pulmonary mechanical function was evaluated before exposure, after initial exercise, and at the end of exposure. Blood oxygenation was measured by ear oximetry before exposure and during the second exercise period. Symptoms were recorded throughout exposure periods and for 1 week afterward. No statistically significant changes in physiology or symptoms could be attributed to SO2 exposure. Older adults with COPD seem less reactive to a given concentration of SO2 than heavily exercising young adult asthmatics. This may be due to lower ventilation rates (i.e., lower SO2 dose rates) and/or to lower airway reactivity in the COPD group.