JOURNALOF
Vol.
APPLIED
38, No. 6, June
PHYSIOLOGY Printed
1975.
Exercise
in U.S.A.
responses following
ozone exposure
L. J. FOLINSBEE, F. SILVERMAN AND R. J. SHEPHARD Gage Research Institute and Department of Environmental Health, School of Hygiene, Uniuersity of Toronto, Toronto, Ontario, Canada
FOLINSBEE, L. J., F. SILVERMAN, AND R.J. SHEPHARD. Exercise responses following ozone exposure. J. Appl. Physiol. 38(6) : 996-l 001. 1975.-We have tested the response of 28 subjects to a threestage ergometer test, with loads adjusted to 45, 60, and 750/‘, of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W, sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure. VE, respiratory frequency (f& mixed expired were monitored conPea and Pco~, and electrocardiogram tinuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (7 = 0.98) and was accompanied by a decrease in tidal volume (7 = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.
respiratory maximal
frequency; exercise
tidal
volume;
oxidant
pollutant;
sub-
LEVELS OF OZONE that can develop (12, 32) in urban atmospheres and aircraft cabins cause changes of pulmonary function (including an increase of airway resistance and a decreased maximum static elastic recoil pressure (5, 10, 13). Failure of athletic performance to show anticipated seasonal gains has also been linked statistically to increases in ambient levels of oxidants (28). In man, performance changes could have a physiological or a psychological the discovery of a significant negative basis. However, correlation between oxidant levels and the track times of racehorses (Shephard, Hatcher, and Reid, unpublished data) supports a physiological explanation. A small increase in the oxygen cost of submaximal work might be anticipated from the rise of airway resistance, and some overall impairment of oxygen transport could arise from poor gas mixing and the decrease of pulmonary diffusing capacity (33). Accordingly, the present study was designed to study the effect of various ozone concentrations on submaximum exercise performance and certain resting measurements of pulmonary function ; a brief preliminary account of the work has been given elsewhere (9). METHODS
Subjects and experimental plan. The subjects were 28 young and healthy adults (20 M, 8 F). They were randomly as-
signed to one of six exposure groups (*! = 5). Two subjects each performed two test and two control experiments, with a 6-mo interval between the first and the second exposure. The remainder performed only one test and one control experiment. A physician performed a preliminary clinical examination with a view to excluding any patients with disease, or a history of sensitivity to inhaled allergens. Physical characteristics are summarized in Table 1; height, weight, and vital capacity were within normal limits. The endurance fitness (as judged from the maximurn oxygen intake predicted by Astrand (4) nomogram) ranged quite widely, but most values were somewhat above average; the mean for the men fell toward the upper end of the Swedish “average” range, while the mean for women reached the “good” category (4, 23). Ten of the subjects (7 M, 3 F) were ciga. rette smokers. Such subjects were asked not to smoke for 12 h prior to testing. In young subjects, this interval is suficient to reverse most of the acute effects of smoking on the cardiac and respiratory systems; any residual effects of the previous day’s smoking were encountered equally in test and control experiments. All subjects were given a preliminary familiarization visit to the laboratory; this included a submaximum bicycle ergometer test. Thereafter, they reported twice to the laboratory in a resting but nonbasal state. After prelirninarv pulmonary function testing, the subject spent a Z-h period in the exposure chamber, breathing (according to random sequence) either filtered air that was passed through activated charcoal and gauze filters (20 air changes per hour) or filtered air to which had been added 0.37, 0.50, or 0.75 ppm of ozone. In some experiments (rest), subjects rested throughout exposure, but in others intermittent exercise (IE) was performed. At 1 h and 55 min the pulmonary function tests were repeated. The ozone generator was then turned off and the subjects immediately performed a three-stage bicycle ergometer test while breathing room air. Exposure chamber. A plexiglass chamber similar to that described by Bates et al. (6) was used for all exposures. Ozone was generated by passing medical-grade oxygen (purity > 99.99 g;‘o) through a high intensity electrical field provided by a condenser discharge tube (20 W); this method of preparation essentially limits contamination by oxides of nitrogen to the minute quantities already present in filtered ambient air (27). The chamber ozone concentration was adjusted by varying the oxygen flow through the discharge tube and was recorded at 5-min intervals, using a coulometric ozone analyzer (Mast De-
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.
EXERCISE
FOLLOWING
TABLE
Sex
1.
N
OZONE
997
EXPOSURE
p@sical characteristics of subjects
-
Age, yr
Ht,
cm
wt, kg
Predicted Aerobic Power, * ml 02/kg-min
Forced Vital C;raec:;tY, RTPS
STPD
M
F
20
8
24.6 (1929) 23.0 (ZO-
28)
177.6 (159192) 163 .O (157168)
69.8 (56.785.7) 56.4 (4964)
51.39 (33.266.9) 49.42 (42.9754.40)
5.28 (2.647.13) 3.98 (3.413.98)
Values are means with ranges in parentheses. Note jects each participated in two experiments, giving experimental and 30 control exposures. * Based obtained at control visit. 7 Predicted according of Goldman and Becklake (10). $ Predicted according tions of Anderson et al (3).
2. Comparison of ozone concentrations as methods
TABLE
y0 Predicted
VC
Calorimetric
Estimate,* pphm
t
$
100.4 (63120) 107.3 (96124)
98.6 (60117) 112.9 (9% 132) ~--
that two suba total of 30 on the data to equations to equa-
velopment Co.). Readings were checked periodically against the generally accepted standard chemical method (1) of analyzing total oxidants, the neutral buffered potassium iodide method (20). At or below 0.50 ppm, there correspondence between calorimetric and was good coulometric analysis. However, at 0.75 ppm, there were differences between the concentrations indicated by the two methods. Accordingly, both figures are reported (Table 2). Others also have noted discrepancies in analyzing less pure samples of ozone (8). Subsequent to completion of this study, preliminary comparisons of our analytical techniques with the more specific chemiluminescent analyzer suggest that the order of ozone exposures indicated was correct. Traces of NO, and SOZ, normally fairly low in the Toronto atmosphere and further reduced by the charcoal filter, do not seem to have distorted the reported concentrations significantly. In support of this, our observations have been that within the base-line noise of our instrument, the indicated concentration has been zero in the chamber before the addition of ozone; if significant levels of NO, or SO2 had been present, the meter would have indicated above or below zero, respectively. It is difhcult to carry out a true double-blind trial with a odor gas such as ozone, since it has a readily recognizable and can produce marked symptoms. Nevertheless, subjects were not told which day the ozone exposure would occur, and on control days the ozone concentration was raised to 0.05 ppm for approximately 5 min so that there was some smell of ozone on entering the chamber. was Pulmonary function tests. The forced vital capacity measured by a Collins spirometer and/or wedge spirometer (Med-Science Electronics). The maximum expiratory was derived from the flow and flow-volume curve (MEFV) volume outputs of the wedge spirometer; individual curves were displaved on a storage oscilloscope (Tektronix 5 103N) I and photographed by a Polaroid camera for subsequent analysis. Exercise protocol. During the IE exposures, subjects were 15-min periods of exercise on a required to alternate Monark bicycle ergometer with 15-min rest periods. The loading of the ergometer was adjusted to increase minute ventilation 2.5 times, as gauged from the preliminary familiarization test. The purpose was simply to simulate
37 37 50 50 75 75 * Values performed
rest IEt rest IEt rest IEt are means intermittent
37.2’ 37.0 50.4 49.7 71.7 63.1 =t SD. exercise.
k 3.z It * zt zt
0.9 0.3 0.4 0.5 5.6 2.7 t Experiments
39.8 37.2 49.6 48.4 74.8 76.6
zt rk rf= zt zk xt
in
which
0.9 3.3 6.3 4.8 1.8 1.4 subject
the periodic i ncremen .ts of respiratory minute volume encountered during normal daily activity. Exercise during exposure should not be confused with the definitive exercise test completed immediately after exposure. The definitive test required three stages of submaximal bicycle ergometer exercise, with loads adjusted to 45, 60, and 75 % of predicted aerobic power. The first two loads were sustained for 3 min each and the last load for 4 min. Data collection continued for 6 min after cessation of effort. Subjects pedaled at 50 rpm throughout. The heart rate was measured from 6-s recordings of the electrocardiogram (lead CM,) at the end of each minute. Subjects respired from a modified Otis-McKerrow valve, connected on the inspiratory side to a Parkinson-Cowan dry gasmeter and on the expiratory side to a lo-liter mixing box. Part of the mixed expired gas was drawn continuously through a Beckman LB-2 infrared CO2 analyzer and a Beckman E-2 paramagnetic oxygen analvzer. Recordings of expired air composition were corrected for the response time of these two instruments as well as the lag imposed by the mixing box (15 s for 90 % washout at expired flow of 60 limin). The CO 2 concentration, electrocardiogram, and respiratory minute volume were recorded continuously on a Honeywell Visicorder. The oxygen concentrations were determined and noted at 30-s intervals. Statistical analysis. The significance of differences in response between ozone and control exposures at any given concentration was examined by a standard paired t-test. The correlation between the effective ozone exposure (see RESULTS) and the percent change of selected variables was tested by linear regression analysis. RESULTS
Symptoms. Ma “Y subjects beta me aware that thev had been exposed to an oxious gas as symptoms developed. The pattern of symptoms was much as described previously by Bates et al. (5), including throat irritation, tracheal soreness or pain, and coughing (pa rticularly on attempting to maneuve rs). There was a perform max imum respiratory gradation of complaints with the intensitv of ozone exposure, and at 0.75 ppm intermittent exercise (IE), symptoms were moderately severe. There were no changes in heart rate, respiratory frequency, or tidal volume while the subjects were at rest. The subject group was rather small for subdivisions, but as wi th the physiological measurements, we could show no significant differences in symptomatology either between males and females or be-
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.
998
FOLINSBEE,
tween smokers and nonsmokers. Neither was there any effect of the order in which the control and exposure procedures were implemented. Exercise response. The mean heart rates over the 30 control experiments were 118, 140, and 164/min for the final minute at the first, second, and third stages of the standard submaximal exercise test. Details of responses to the final loading are shown in Table 3. There was no significant change of oxygen consumption or of respiratory minute volume at anv of the ozone concentrations examined. On the basis of t-testing, the heart rate was apparently decreased in one comparison (0.37 ppm IE, r) < 0.05), but no great practical significance can be attached to this, since the change was not confirmed by regression analysis, and in anv event the heart rate was increased in another comparison (0.50 ppm rest, P < 0.05). The main change was in respiratory pattern. Respiratory rates varied considerably from one control series to another (averages ranged from 24.4 to 36.0/ min) ; nevertheless, these differences were not statistically significant, and did not vitiate the analysis of respiratory patterns since each subject served as his own control. Respiratory frequency was elevated at the higher levels of ozone exposure (0.37 ppm IE, 0.50 ppm IE, 0.75 ppm rest, and 0.75 ppm IE), while there was a coincident decrease of tidal volume at 0.50 ppm IE and 0.75 ppm IE. There was a tendency for the ventilatory equivalent for oxygen to increase, but this was only significant (P < 0.01) in one of the six series of exposures (0.50 ppm rest). TABLE 3. 0 xygen consumption, heart rate, ventila tion, tidal volume, respiratory frequerq, and uen tila tory equivalent at 7.5 5% of aerobic power after a Z-h exposure to jiltered air or to ozone
SILVERMAN,
AND
SHEPHARD
The relationships between ozone exposure and the changes of respiratory pattern are explored further in Figs. 1 and 2. Respiratory frequency (fIl) increased with ozone concentration, and at any given concentration was greater following exposures where the subject had exercised intermittently. Over the range studied, the percentage change was apparently close to a linear function of concentration. The tidal volume (VT) generally showed a decrease with a rise of ozone concentration, the effect being more marked in experiments where subjects exercised during exposure. To present rest and IE data on the same graphs, an equivalent exposure was calculated for the IE data; this makes the simplifying assumption (3 1) that the dose of ozone received is directly proportional to the average respiratory minute volume (that is, the effective concentration is increased by (1 + 2.5)/Z = 1.75 in IE experiments). On this basis, there was a closely linear relationship (r = 0.98, P < 0.01) between the dose of ozone and the percentage change of fR in the postexposure exercise tests, with a somewhat less precise correlation for VT (r = 0.9 1, P < 0.02). Figure 2 illustrates data obtained at 75 % of predicted VOW max. The same pattern of ventilatory response was observed at the two lower work loads. Lung function changes. The change in the ventilatory pattern during exercise was accompanied by alterations of resting pulmonary function. There was a trend for the forced vital capacity to diminish (Fig. 3), statistically significant at 0.75 ppm (rest), 0.50 ppm (IE) and 0.75 ppm (IE). Maximum expiratory flow rate at 50 o/o of vital capacity (Fig. 4) was significantly reduced in all three series of IE exposures. DISCUSSION
Breathing pattern. Our subjects showed a marked and rather consistent alteration in the pattern of respiration
______
.L
TjOZ, l/min
Ozone Exposure Condition
f &min
STPD
VE
VT,
]imih
liters
RTPS
I
f R/min
B
BTPS
VT
---
C 0.37
ppm
rest
E C
0.37
ppm
IE
E C
0.50
ppm
rest
E C
0.50
ppm
IE
E C
0.75
ppm
rest
E C
0.75
ppm
IE
Values are during exposure; paired t-test.
E
2.07 so.59 2.30 ztO.48 2.45 ho.64 2.32 Ito. 2.58 zto.90 2.56 ztO.88 2.76 zto.95 2.70 zkO.88 2.11 SO.60 2.16 x110.64 2.39 ho.48 2.50 zto.50
means C,
167.8 zt12.13 168.8 zk11.71 161.0 +12.90* 153.8 M2.83 165.2 h7.12' 168.8 zlz4.92 159.8 zt9.20 159.4 M7.14 158.6 zt3.13 158.2 zt6.57 171 M6.48 174.2 Ml.73
=t SD. filtered
IE air;
70.18 ZJZ21.39 73.96 zt21.30 66.56 ~16.83 62.56 zt11.23 79.75 h41.96 85.17 zk40.29 79.70 zt32.83 82.47 zt31.61 61.63 zt14.22 67.00 rfi18.68 60.35 zt14.22 67.80 zt12.83 indicates E, ozone.
1.91 sfo.41 2.19 ztO.52 2.31 ~0.65 1.98 ~0.25 2.35 ztO.61 2.46 ho.61 2.20 &0.69* 1.98 zto.70 2 .Ol ~0.63 1.92 zto.53 2.74 rt1.03* 2.05 so.59
35.6 st10.16 33.0 zt5.5 29.2 zk4.32' 31.8 zk4.71 33.0 HO.37 34.2 j.Ao.71 36.0 *7.14* 42.8 Ik9.52 31.4 *4.93* 35.2 zt5.36 24.4 rt8.38" 34.0 zk8.06
intermittent * P
Vol.
APPLIED
38, No. 6, June
PHYSIOLOGY Printed
1975.
Exercise
in U.S.A.
responses following
ozone exposure
L. J. FOLINSBEE, F. SILVERMAN AND R. J. SHEPHARD Gage Research Institute and Department of Environmental Health, School of Hygiene, Uniuersity of Toronto, Toronto, Ontario, Canada
FOLINSBEE, L. J., F. SILVERMAN, AND R.J. SHEPHARD. Exercise responses following ozone exposure. J. Appl. Physiol. 38(6) : 996-l 001. 1975.-We have tested the response of 28 subjects to a threestage ergometer test, with loads adjusted to 45, 60, and 750/‘, of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W, sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure. VE, respiratory frequency (f& mixed expired were monitored conPea and Pco~, and electrocardiogram tinuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (7 = 0.98) and was accompanied by a decrease in tidal volume (7 = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.
respiratory maximal
frequency; exercise
tidal
volume;
oxidant
pollutant;
sub-
LEVELS OF OZONE that can develop (12, 32) in urban atmospheres and aircraft cabins cause changes of pulmonary function (including an increase of airway resistance and a decreased maximum static elastic recoil pressure (5, 10, 13). Failure of athletic performance to show anticipated seasonal gains has also been linked statistically to increases in ambient levels of oxidants (28). In man, performance changes could have a physiological or a psychological the discovery of a significant negative basis. However, correlation between oxidant levels and the track times of racehorses (Shephard, Hatcher, and Reid, unpublished data) supports a physiological explanation. A small increase in the oxygen cost of submaximal work might be anticipated from the rise of airway resistance, and some overall impairment of oxygen transport could arise from poor gas mixing and the decrease of pulmonary diffusing capacity (33). Accordingly, the present study was designed to study the effect of various ozone concentrations on submaximum exercise performance and certain resting measurements of pulmonary function ; a brief preliminary account of the work has been given elsewhere (9). METHODS
Subjects and experimental plan. The subjects were 28 young and healthy adults (20 M, 8 F). They were randomly as-
signed to one of six exposure groups (*! = 5). Two subjects each performed two test and two control experiments, with a 6-mo interval between the first and the second exposure. The remainder performed only one test and one control experiment. A physician performed a preliminary clinical examination with a view to excluding any patients with disease, or a history of sensitivity to inhaled allergens. Physical characteristics are summarized in Table 1; height, weight, and vital capacity were within normal limits. The endurance fitness (as judged from the maximurn oxygen intake predicted by Astrand (4) nomogram) ranged quite widely, but most values were somewhat above average; the mean for the men fell toward the upper end of the Swedish “average” range, while the mean for women reached the “good” category (4, 23). Ten of the subjects (7 M, 3 F) were ciga. rette smokers. Such subjects were asked not to smoke for 12 h prior to testing. In young subjects, this interval is suficient to reverse most of the acute effects of smoking on the cardiac and respiratory systems; any residual effects of the previous day’s smoking were encountered equally in test and control experiments. All subjects were given a preliminary familiarization visit to the laboratory; this included a submaximum bicycle ergometer test. Thereafter, they reported twice to the laboratory in a resting but nonbasal state. After prelirninarv pulmonary function testing, the subject spent a Z-h period in the exposure chamber, breathing (according to random sequence) either filtered air that was passed through activated charcoal and gauze filters (20 air changes per hour) or filtered air to which had been added 0.37, 0.50, or 0.75 ppm of ozone. In some experiments (rest), subjects rested throughout exposure, but in others intermittent exercise (IE) was performed. At 1 h and 55 min the pulmonary function tests were repeated. The ozone generator was then turned off and the subjects immediately performed a three-stage bicycle ergometer test while breathing room air. Exposure chamber. A plexiglass chamber similar to that described by Bates et al. (6) was used for all exposures. Ozone was generated by passing medical-grade oxygen (purity > 99.99 g;‘o) through a high intensity electrical field provided by a condenser discharge tube (20 W); this method of preparation essentially limits contamination by oxides of nitrogen to the minute quantities already present in filtered ambient air (27). The chamber ozone concentration was adjusted by varying the oxygen flow through the discharge tube and was recorded at 5-min intervals, using a coulometric ozone analyzer (Mast De-
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.
EXERCISE
FOLLOWING
TABLE
Sex
1.
N
OZONE
997
EXPOSURE
p@sical characteristics of subjects
-
Age, yr
Ht,
cm
wt, kg
Predicted Aerobic Power, * ml 02/kg-min
Forced Vital C;raec:;tY, RTPS
STPD
M
F
20
8
24.6 (1929) 23.0 (ZO-
28)
177.6 (159192) 163 .O (157168)
69.8 (56.785.7) 56.4 (4964)
51.39 (33.266.9) 49.42 (42.9754.40)
5.28 (2.647.13) 3.98 (3.413.98)
Values are means with ranges in parentheses. Note jects each participated in two experiments, giving experimental and 30 control exposures. * Based obtained at control visit. 7 Predicted according of Goldman and Becklake (10). $ Predicted according tions of Anderson et al (3).
2. Comparison of ozone concentrations as methods
TABLE
y0 Predicted
VC
Calorimetric
Estimate,* pphm
t
$
100.4 (63120) 107.3 (96124)
98.6 (60117) 112.9 (9% 132) ~--
that two suba total of 30 on the data to equations to equa-
velopment Co.). Readings were checked periodically against the generally accepted standard chemical method (1) of analyzing total oxidants, the neutral buffered potassium iodide method (20). At or below 0.50 ppm, there correspondence between calorimetric and was good coulometric analysis. However, at 0.75 ppm, there were differences between the concentrations indicated by the two methods. Accordingly, both figures are reported (Table 2). Others also have noted discrepancies in analyzing less pure samples of ozone (8). Subsequent to completion of this study, preliminary comparisons of our analytical techniques with the more specific chemiluminescent analyzer suggest that the order of ozone exposures indicated was correct. Traces of NO, and SOZ, normally fairly low in the Toronto atmosphere and further reduced by the charcoal filter, do not seem to have distorted the reported concentrations significantly. In support of this, our observations have been that within the base-line noise of our instrument, the indicated concentration has been zero in the chamber before the addition of ozone; if significant levels of NO, or SO2 had been present, the meter would have indicated above or below zero, respectively. It is difhcult to carry out a true double-blind trial with a odor gas such as ozone, since it has a readily recognizable and can produce marked symptoms. Nevertheless, subjects were not told which day the ozone exposure would occur, and on control days the ozone concentration was raised to 0.05 ppm for approximately 5 min so that there was some smell of ozone on entering the chamber. was Pulmonary function tests. The forced vital capacity measured by a Collins spirometer and/or wedge spirometer (Med-Science Electronics). The maximum expiratory was derived from the flow and flow-volume curve (MEFV) volume outputs of the wedge spirometer; individual curves were displaved on a storage oscilloscope (Tektronix 5 103N) I and photographed by a Polaroid camera for subsequent analysis. Exercise protocol. During the IE exposures, subjects were 15-min periods of exercise on a required to alternate Monark bicycle ergometer with 15-min rest periods. The loading of the ergometer was adjusted to increase minute ventilation 2.5 times, as gauged from the preliminary familiarization test. The purpose was simply to simulate
37 37 50 50 75 75 * Values performed
rest IEt rest IEt rest IEt are means intermittent
37.2’ 37.0 50.4 49.7 71.7 63.1 =t SD. exercise.
k 3.z It * zt zt
0.9 0.3 0.4 0.5 5.6 2.7 t Experiments
39.8 37.2 49.6 48.4 74.8 76.6
zt rk rf= zt zk xt
in
which
0.9 3.3 6.3 4.8 1.8 1.4 subject
the periodic i ncremen .ts of respiratory minute volume encountered during normal daily activity. Exercise during exposure should not be confused with the definitive exercise test completed immediately after exposure. The definitive test required three stages of submaximal bicycle ergometer exercise, with loads adjusted to 45, 60, and 75 % of predicted aerobic power. The first two loads were sustained for 3 min each and the last load for 4 min. Data collection continued for 6 min after cessation of effort. Subjects pedaled at 50 rpm throughout. The heart rate was measured from 6-s recordings of the electrocardiogram (lead CM,) at the end of each minute. Subjects respired from a modified Otis-McKerrow valve, connected on the inspiratory side to a Parkinson-Cowan dry gasmeter and on the expiratory side to a lo-liter mixing box. Part of the mixed expired gas was drawn continuously through a Beckman LB-2 infrared CO2 analyzer and a Beckman E-2 paramagnetic oxygen analvzer. Recordings of expired air composition were corrected for the response time of these two instruments as well as the lag imposed by the mixing box (15 s for 90 % washout at expired flow of 60 limin). The CO 2 concentration, electrocardiogram, and respiratory minute volume were recorded continuously on a Honeywell Visicorder. The oxygen concentrations were determined and noted at 30-s intervals. Statistical analysis. The significance of differences in response between ozone and control exposures at any given concentration was examined by a standard paired t-test. The correlation between the effective ozone exposure (see RESULTS) and the percent change of selected variables was tested by linear regression analysis. RESULTS
Symptoms. Ma “Y subjects beta me aware that thev had been exposed to an oxious gas as symptoms developed. The pattern of symptoms was much as described previously by Bates et al. (5), including throat irritation, tracheal soreness or pain, and coughing (pa rticularly on attempting to maneuve rs). There was a perform max imum respiratory gradation of complaints with the intensitv of ozone exposure, and at 0.75 ppm intermittent exercise (IE), symptoms were moderately severe. There were no changes in heart rate, respiratory frequency, or tidal volume while the subjects were at rest. The subject group was rather small for subdivisions, but as wi th the physiological measurements, we could show no significant differences in symptomatology either between males and females or be-
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (129.186.138.035) on January 16, 2019.
998
FOLINSBEE,
tween smokers and nonsmokers. Neither was there any effect of the order in which the control and exposure procedures were implemented. Exercise response. The mean heart rates over the 30 control experiments were 118, 140, and 164/min for the final minute at the first, second, and third stages of the standard submaximal exercise test. Details of responses to the final loading are shown in Table 3. There was no significant change of oxygen consumption or of respiratory minute volume at anv of the ozone concentrations examined. On the basis of t-testing, the heart rate was apparently decreased in one comparison (0.37 ppm IE, r) < 0.05), but no great practical significance can be attached to this, since the change was not confirmed by regression analysis, and in anv event the heart rate was increased in another comparison (0.50 ppm rest, P < 0.05). The main change was in respiratory pattern. Respiratory rates varied considerably from one control series to another (averages ranged from 24.4 to 36.0/ min) ; nevertheless, these differences were not statistically significant, and did not vitiate the analysis of respiratory patterns since each subject served as his own control. Respiratory frequency was elevated at the higher levels of ozone exposure (0.37 ppm IE, 0.50 ppm IE, 0.75 ppm rest, and 0.75 ppm IE), while there was a coincident decrease of tidal volume at 0.50 ppm IE and 0.75 ppm IE. There was a tendency for the ventilatory equivalent for oxygen to increase, but this was only significant (P < 0.01) in one of the six series of exposures (0.50 ppm rest). TABLE 3. 0 xygen consumption, heart rate, ventila tion, tidal volume, respiratory frequerq, and uen tila tory equivalent at 7.5 5% of aerobic power after a Z-h exposure to jiltered air or to ozone
SILVERMAN,
AND
SHEPHARD
The relationships between ozone exposure and the changes of respiratory pattern are explored further in Figs. 1 and 2. Respiratory frequency (fIl) increased with ozone concentration, and at any given concentration was greater following exposures where the subject had exercised intermittently. Over the range studied, the percentage change was apparently close to a linear function of concentration. The tidal volume (VT) generally showed a decrease with a rise of ozone concentration, the effect being more marked in experiments where subjects exercised during exposure. To present rest and IE data on the same graphs, an equivalent exposure was calculated for the IE data; this makes the simplifying assumption (3 1) that the dose of ozone received is directly proportional to the average respiratory minute volume (that is, the effective concentration is increased by (1 + 2.5)/Z = 1.75 in IE experiments). On this basis, there was a closely linear relationship (r = 0.98, P < 0.01) between the dose of ozone and the percentage change of fR in the postexposure exercise tests, with a somewhat less precise correlation for VT (r = 0.9 1, P < 0.02). Figure 2 illustrates data obtained at 75 % of predicted VOW max. The same pattern of ventilatory response was observed at the two lower work loads. Lung function changes. The change in the ventilatory pattern during exercise was accompanied by alterations of resting pulmonary function. There was a trend for the forced vital capacity to diminish (Fig. 3), statistically significant at 0.75 ppm (rest), 0.50 ppm (IE) and 0.75 ppm (IE). Maximum expiratory flow rate at 50 o/o of vital capacity (Fig. 4) was significantly reduced in all three series of IE exposures. DISCUSSION
Breathing pattern. Our subjects showed a marked and rather consistent alteration in the pattern of respiration
______
.L
TjOZ, l/min
Ozone Exposure Condition
f &min
STPD
VE
VT,
]imih
liters
RTPS
I
f R/min
B
BTPS
VT
---
C 0.37
ppm
rest
E C
0.37
ppm
IE
E C
0.50
ppm
rest
E C
0.50
ppm
IE
E C
0.75
ppm
rest
E C
0.75
ppm
IE
Values are during exposure; paired t-test.
E
2.07 so.59 2.30 ztO.48 2.45 ho.64 2.32 Ito. 2.58 zto.90 2.56 ztO.88 2.76 zto.95 2.70 zkO.88 2.11 SO.60 2.16 x110.64 2.39 ho.48 2.50 zto.50
means C,
167.8 zt12.13 168.8 zk11.71 161.0 +12.90* 153.8 M2.83 165.2 h7.12' 168.8 zlz4.92 159.8 zt9.20 159.4 M7.14 158.6 zt3.13 158.2 zt6.57 171 M6.48 174.2 Ml.73
=t SD. filtered
IE air;
70.18 ZJZ21.39 73.96 zt21.30 66.56 ~16.83 62.56 zt11.23 79.75 h41.96 85.17 zk40.29 79.70 zt32.83 82.47 zt31.61 61.63 zt14.22 67.00 rfi18.68 60.35 zt14.22 67.80 zt12.83 indicates E, ozone.
1.91 sfo.41 2.19 ztO.52 2.31 ~0.65 1.98 ~0.25 2.35 ztO.61 2.46 ho.61 2.20 &0.69* 1.98 zto.70 2 .Ol ~0.63 1.92 zto.53 2.74 rt1.03* 2.05 so.59
35.6 st10.16 33.0 zt5.5 29.2 zk4.32' 31.8 zk4.71 33.0 HO.37 34.2 j.Ao.71 36.0 *7.14* 42.8 Ik9.52 31.4 *4.93* 35.2 zt5.36 24.4 rt8.38" 34.0 zk8.06
intermittent * P
