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.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL031429-05
Application #
3342542
Study Section
Toxicology Study Section (TOX)
Project Start
1984-03-01
Project End
1992-02-29
Budget Start
1989-03-01
Budget End
1990-02-28
Support Year
5
Fiscal Year
1989
Total Cost
Indirect Cost
Name
State University New York Stony Brook
Department
Type
Schools of Medicine
DUNS #
804878247
City
Stony Brook
State
NY
Country
United States
Zip Code
11794
Foster, W M; Stetkiewicz, P T; Freed, A N (1997) Retention of soluble 99mTc-DTPA in the human lung: 24-h postdeposition. J Appl Physiol 82:1378-82
Groeben, H; Foster, W M; Brown, R H (1996) Intravenous lidocaine and oral mexiletine block reflex bronchoconstriction in asthmatic subjects. Am J Respir Crit Care Med 154:885-8
Foster, W M; Jiang, L; Stetkiewicz, P T et al. (1996) Breath isoprene: temporal changes in respiratory output after exposure to ozone. J Appl Physiol 80:706-10
Foster, W M; Stetkiewicz, P T (1996) Regional clearance of solute from the respiratory epithelia: 18-20 h postexposure to ozone. J Appl Physiol 81:1143-9
Foster, W M; Wills-Karp, M; Tankersley, C G et al. (1996) Bloodborne markers in humans during multiday exposure to ozone. J Appl Physiol 81:794-800
Wagner, E M; Foster, W M (1996) Importance of airway blood flow on particle clearance from the lung. J Appl Physiol 81:1878-83
Weinmann, G G; Weidenbach-Gerbase, M; Foster, W M et al. (1995) Evidence for ozone-induced small-airway dysfunction: lack of menstrual-cycle and gender effects. Am J Respir Crit Care Med 152:988-96
Smaldone, G C; Foster, W M; O'Riordan, T G et al. (1993) Regional impairment of mucociliary clearance in chronic obstructive pulmonary disease. Chest 103:1390-6
Foster, W M; Silver, J A; Groth, M L (1993) Exposure to ozone alters regional function and particle dosimetry in the human lung. J Appl Physiol 75:1938-45
Emmons, K M; Weidner, G; Foster, W M et al. (1992) Improvement in pulmonary function following smoking cessation. Addict Behav 17:301-6

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