Student Research: Katia Harb
, , 2002
Faculty Advisor: Jane Q. Koenig
Cardiopulmonary Effects of 300 ppb Nitrogen Dioxide in Chronic Obstructive Pulmonary Disease and Asthma Patients
Nitrogen dioxide (NO2) is a highly reactive gas emitted from the burning of fossil fuels at high temperatures. The primary sources in outdoor air are motor vehicles and coal-fired power plants. Oxidant injury is the primary mechanism in which NO2 damages the lung but the biological mechanisms in which it affects the cardiac system are largely unknown. Previous studies have linked short-term exposures to changes in airway responsiveness and lung function in individuals with pre-existing respiratory illnesses. However, the results of these studies show mixed findings.
The purpose of this study was to determine if exposure to 300 ppb NO2 (the concentration that may be experienced at a bus stop), could cause short-term sub-clinical cardiovascular and pulmonary effects in chronic obstructive pulmonary disease (COPD) and asthma patients. This was a double-blind crossover study where 6 subjects, at least 50 years of age, were exposed to filtered air and 300 ppb NO2 for 30 minutes while resting. Pulmonary system measurements included arterial oxygen saturation, exhaled nitric oxide and carbon monoxide, 8-Isoprostane levels in exhaled breath condensate, and lung function. Cardiovascular measurements included blood pressure and heart rate. These measurements and symptom ratings were collected before exposure, 30 minutes after exposure, and 18 hours after exposure. Paired T-tests and bootstrap analyses were used to compare differences in post-exposure measurements with baseline measurements for both sessions.
The results of this study showed no significant changes in cardiopulmonary function attributable to nitrogen dioxide exposure; however some patterns were observed. Arterial oxygen saturation decreased in three subjects after exposure to NO2 . This was not observed after exposure to air.