OZONE EFFECT ON RESPIRATORY TRACT MUCUS AND PERMEABILITY

将研究人类的呼吸道粘膜 非侵入性地与放射性气溶胶，以确定影响 环境污染物臭氧对气道黏膜纤毛功能的影响。 将研究重复暴露于0.2和0.4 PPM臭氧的情况， 确定是否发生粘膜功能的适应，以及 是否气道功能和主观适应 症状与臭氧对 粘液纤毛功能 功能异常的吸烟者， 在纵向研究中进行评价，以确定粘膜纤毛 功能，已知这些受试者在习惯性 香烟，是受臭氧暴露;在后续行动中，后 戒烟6个月，粘膜纤毛对臭氧的反应 将重新评估暴露。 改变臭氧对 将用利多卡因研究粘膜生理学 气溶胶，麻醉对臭氧敏感的气道受体， 与抗坏血酸（口服），以减少组织介质释放 吸入臭氧的过程中 最后，臭氧暴露对 呼吸气溶胶的沉积分数将评估为3 颗粒尺寸，2、4和6微米直径， 粗颗粒污染 这些粒子将 放射性标记，因此将提供有关 肺内的局部沉积。 我们的技术利用伽马射线 照相机成像和室暴露于臭氧。 的 获得的信息将支持我们的假设， 膜生理学是肺的主要决定因素 对刺激性刺激的反应，并更好地定义 环境污染物在气道的诱导或进展 异常

In man the respiratory mucous membranes will be investigated non-invasively with radio-aerosols to determine the effects of ambient pollutant, ozone, on airway mucociliary function. Repetitive exposure to 0.2 and 0.4 PPM ozone will be studied to determine if adaptation of mucus membrane function occurs, and whether the adaptation of airway function and subjective symptoms are causally related to the effects of ozone on mucociliary function. Smokers, with abnormal function, will be evaluated in longitudinal study to determine if mucociliary function, known to be depressed in these subjects while habituated to cigarettes, is influenced by ozone exposure; at follow-up, after 6 months of smoking cessation, mucociliary response to ozone exposure will be re-evaluated. Modification of ozone effects on mucous membrane physiology will be studied with lidocaine aerosol, to anesthetize airway receptors sensitive to ozone, and with ascorbic acid (orally), to reduce tissue mediators released during ozone inhalation. Lastly, the effect of ozone exposure on the deposition fraction of respired aerosol will be evaluated for 3 particle sizes, 2, 4 and 6 micron m diameters, representatives of coarse mode particulate pollution. These particles will be radiolabeled and thus will provide additional information on regional deposition within the lung. Our technique utilizes gamma camera imaging and chamber exposures to ozone. The information obtained will support our hypothesis that mucus membrane physiology is a primary determinant of the lung response to irritant stimuli, and better define the role of environmental pollutants in the induction or progression of airway abnormalities.