Deborah M. Drechsler-Parks

Pulmonary function responses of older men and women to ozone exposure

The pulmonary function of 8 men and 8 women (51 to 76 years of age), all nonsmokers, was measured before and after 2-h exposures to filtered air (FA) and 0.45 ppm ozone (O3). The subjects alternated 20-min periods of rest and 20-min periods of cycle ergometer exercise at a workload predetermined to elicit a ventilatory minute ventilation (VE) of approximately 25 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, and 5 min after each exercise period. Ventilatory minute volume (VE) was measured during the last 2 min of each exercise period, and heart rate was monitored throughout each exposure. The pulmonary function data were evaluated as the percentage change from pre- to post-exposure to partially remove the effect of differences between men and women in absolute lung volume. There were no statistically significant (p greater than 0.05) differences between the responses of men and women to FA or O3 exposure. There were no significant (p greater than 0.05) changes in any variable consequent to FA exposure. Exposure to O3 induced significant (p less than 0.01) decrements in FVC, FEV1.0, and FEV3.0 at post-exposure compared to pre-exposure. Ozone exposure induced no significant (p greater than 0.05) effect on FEF25-75% or FEF75%. Men had a significantly (p less than 0.05) higher mean exercise VE than women (27.9 +/- 0.29 L vs. 25.4 +/- 0.8 L; mean +/- SD). Since the men and women had similar decrements in pulmonary function, even though the women inhaled less O3, the data suggest that women may be somewhat more responsive to O3 than men. We also compared the responses of our older subjects with those of young men and women that we studied with the same protocol, and with published results of other investigators who have studied young men and women. This comparison suggests that older individuals may be less responsive to O3 than young individuals.

Effects of peroxyacetyl nitrate alone and in combination with ozone in healthy young women

Metabolic and pulmonary functions were investigated in 10 nonsmoking, young adult women who were exposed for 2 h (21 °C WBGT) to four conditions: 1) filtered air (FA), 2) 0.27 ppm peroxyacetyl nitrate (PAN), 3) 0.48 ppm ozone (O3), and 4) 0.48 ppm O3 + 0.27 ppm PAN (PAN/O3). The subjects alternated 15-min periods of rest and 20-min periods of bicycle ergometer exercise eliciting a of 25 L. Functional residual capacity (FRC) was determined preand post-exposure. Forced vital capacity (FVC) was determined before and after exposure, as well as 5 min after each exercise period. Heart rate was monitored throughout the exposure, and metabolic functions were measured during the last 2 min of each exercise period. There were no changes in any variable consequent to FA or PAN exposure. During O3 and PAN/O3 exposures, a decrease in V T, a concomitant increase in f R, and no change in occurred. Both O3 and PAN/O3 induced significant (p < 0.05) decrements in FVC, FEV1.0, FEV2.0, FEV3.0, FEF25-75%, IC, ERV, and TLC, bu...

Cardiac Output Effects of 03 and No2 Exposure in Healthy Older Adults

Eight healthy adults (56-85 yrs) were exposed in an environmental chamber to filtered air (FA), 0.60 ppm NO2, 0.45 ppm 03, and 0.60 ppm NO2 + 0.45 ppm 03 to investigate the effects of NO2 and 03 exposure on cardiac output. The subjects were exposed to each condition for two hours, while they exercised and rested in alternating 20-min periods. Minute ventilation averaged 26-29 l/min among the four exposures. Cardiac output was measured by the noninvasive impedance cardiography method, and was recorded prior to each exposure with the subject at rest, and during the last five minutes of each exercise period. There were no differences in cardiac output at preexposure among the four exposures. The exercise-induced increase in cardiac output with NO2/O 3 exposure was significantly smaller (P < 0.05) than with the FA or 03 alone exposures. Reaction products of inhaled NO 2 are known to cross the lung membranes, probably as a nitrate or nitrite. N02 and 03 are also known to react together to form nitrate and nitrite. We hypothesize that a nitrate or nitrite reaction product of inhaled 03 and NO2 crosses the lung membrane into the general circulation, where it functions as a vasodilator, thereby reducing cardiac output.

The “effective dose” concept in older adults exposed to ozone

Previous research on young adults has indicated that the magnitude of pulmonary function decrements induced by exposure to ambient ozone (O3) is related to the effective dose of O3 inhaled. The effective dose is defined as the product of O3 concentration (in ppm), mean minute ventilation (VE) and duration of exposure (min). The relative contributions of the three components of effective dose to the development of pulmonary function decrements in older adults are unknown. Twelve healthy, nonsmoking men and women (60-79 years) participated in each of four experiments: (1) a 1-h continuous exercise protocol, and (2) a 2-h intermittent exercise protocol, each performed while exposed to filtered air (FA), and to 0.45 ppm O3, resulting in different effective doses of O3. Pulmonary function (forced vital capacity, FVC, functional residual capacity, FRC, and associated calculated parameters) was measured pre- and postexposure. Ozone exposure induced significant decrements in forced expiratory volume in 0.5, 1.0 and 3.0 seconds (FEV0.5, 1.0, 3.0), regardless of the exercise protocol. There were no changes in FVC with any exposure protocol. There were significant decrements in forced expiratory flow rate at 25% and 50% of FVC (FEF25%, FEF50%) and in forced expiratory flow rate between 25% and 75% of FVC (FEF25-75%) with all four exposures, suggesting a fatigue effect. There were no differences between the decrements induced in FEV1.0 by O3 exposure under the two exercise protocols. The mean exercise VE was 25.3 l/min for the continuous exercise protocol, and was 25.2 l/min for the three exercise periods of the intermittent exercise protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation by older individuals repeatedly exposed to 0.45 parts per million ozone for two hours.

To test for an increased reaction to ozone (O3) in older individuals following an initial exposure, and to test for adaptation and its duration, we exposed 10 men and 6 women (60-89 years old) in an environmental chamber to filtered air and 3 consecutive days of O3 exposure (0.45 ppm), followed by a fourth O3 exposure day after a two day hiatus. Subjects alternated 20-min exercise (minute ventilation = 27 L) and rest periods for 2 hours during each exposure. Subjects rated from one to five, 16 possible respiratory/exercise symptoms prior to and following the exposure. Pulmonary function tests were performed before, and during each rest period and following the exposure. Metabolic measurements were obtained during each exercise period. No significant changes in any symptom question occurred, in spite of a threefold increase in the total number of reported symptoms during O3 exposure. Small but significant pre-to-post decrements on the first and second O3 days in forced vital capacity (FVC-111 and 104 mL), forced expiratory volume in 1 (FEV1-171 and 164 mL) and 3 seconds (FEV3-185 and 172 mL) occurred without concomitant changes in any flow parameter of the forced expiratory maneuver. No differences in the group mean response in FVC, FEV1 or FEV3 on the third or fourth day of O3 exposure and the filtered air exposure were found. The observed changes were due to significant physiological changes in eight of the subjects. Unlike young subjects, no evidence of an increased pulmonary function response to a second consecutive O3 exposure was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Duration of increased pulmonary function sensitivity to an initial ozone exposure

The metabolic and pulmonary function effects were investigated in six non-smoking young adults who were exposed for 2 hours (22 degrees C WBGT) to: filtered air (FA) 0.45 ppm ozone (DAY1); and two days later to a second exposure to 0.45 ppm ozone (DAY2). The subjects alternated 20-minute periods of rest and 20-minute periods of bicycle ergometer exercise at a workload predetermined to elicit a ventilatory minute volume (VE) of 27 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, as well as 5 minutes after each exercise period. Heart rate was monitored throughout the exposure, and VE, oxygen uptake (VO2), respiratory rate (fR), and tidal volume (VT) were measured during the last 2 minutes of each exercise period. There were no changes in any variable consequent to FA exposure. Both ozone exposures induced significant (P less than 0.05) decrements in FVC; FEV1.0 (forced expiratory volume in 1 second); FEV3.0 (forced expiratory volume in 3 seconds); FEF25-75% (average flow rate between 25% and 75% of FVC); and total lung capacity (TLC). The decrements following the DAY2 ozone exposure were significantly greater than following DAY1, and averaged 7.2 percentage points greater than those following the DAY1 exposure.

Pulmonary function responses of older men and women to NO2

The pulmonary function of eight men and eight women (51 to 76 years of age), all non-smokers, was measured before and after 2-hr exposures to filtered air (FA) and 0.60 ppm nitrogen dioxide (NO2). The subjects alternated 20-min periods of rest and 20-min periods of cycle ergometer exercise at a work load predetermined to elicit a ventilatory minute volume (VE) of approximately 25 liter/min. Functional residual capacity was determined pre- and postexposure. Forced vital capacity was determined preexposure and 5 min after each exercise period. VE was measured during the last 2 min of each exercise period, and heart rate was monitored throughout each exposure. The pulmonary function data were evaluated as the percentage change from pre- to postexposure to partially remove the effect of differences between men and women in absolute lung volume. There were no statistically significant (P greater than 0.05) differences between the responses of men and women to FA or NO2 exposure. There were no significant (P greater than 0.05) changes in any variable consequent to FA or NO2 exposure. Our older subjects had responses to NO2 exposure similar to those of young adults, suggesting that, at least for healthy people, exposure to 0.60 ppm NO2 has little effect.

Reproducibility of the pulmonary function response of older men and women to a 2-hour ozone exposure.

To test the reproducibility of the pulmonary function response to ozone exposure in older individuals, eight men and eight women, average age 62.8 years, participated in three 2-hour exposures to 0.45 ppm ozone at 23.3 C and 62.5 percent relative humidity. The first and second exposures were separated by an average time of 17.2 days, and 27.3 days separated the second and third exposures. Subjects alternated riding a bicycle ergometer for 20 minutes at an average minute ventilation of 26 liters BTPS (body temperature pressure, saturated), with 20-minute rest periods. Forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV-1), and forced expiratory flow between 25 and 75% of FVC (FEF 25-75%) were measured pre and post exposure. The reproducibility of individual pre-post changes were assessed by calculation of the best linear fit and correlation coefficients between exposures. For FVC and FEV-1, the slopes were significantly different from 1, and correlation coefficients not significantly different from zero, implying that older individuals may not respond consistently to similar ozone exposures.

The dose-response relationship in older men exposed to ozone

Nine male subjects (56-71 years) were exposed to filtered air (FA) or 0.45 ppm O3 with inhaled dose altered by varying ventilation volume (VE = 25, 40, or 55 L/min (BTPS)) to evaluate pulmonary function dose-responses in older men. The subjects walked on a motor-driven treadmill and rested in alternating 20-min periods during the 2-h exposures. Functional residual capacity and maximal voluntary ventilation (MVV) were measured pre- and postexposure. Forced expiratory volume in 1 s (FEV1.0) and forced expiratory flow rate between 25% and 75% of vital capacity (FEF25-75%) were calculated from FVC. Residual volume (RV) was calculated from FRC. VE was measured during the last 4 min of each exercise period, and the electrocardiogram was monitored throughout each exposure. There were no significant changes in any measured parameter with FA exposure. All three O3 exposures induced small, statistically significant decrements in FVC and FEV1.0, but no significant changes in FEF25-75%. There were no significant differences among responses to the three O3 exposures. The decrements in measured pulmonary functions were smaller than typically observed in young males exposed to similar inhaled doses of O3. The data suggest possible saturation of the pulmonary response mechanism at a low degree of functional impairment in older men. Reflex-mediated impairment of inspiration, with concomitant reduction in all dependent pulmonary functions has been suggested as the mechanism of pulmonary dysfunction with O3 exposure in young adults. The results suggest that this reflex may be less active in older adults.