EPA-600/1-76-001
March 1976
Environmental Health Effects Research Series
EFFECTS OF LOW LEVELS OF
OZONE AND TEMPERATURE STRESS
Health Effects Research Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711
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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environ-
mental Protection Agency, have been grouped into five series. These five broad
categories were established to facilitate further development and application
of environmental technology. Elimination of traditional grouping was con-
sciously planned to foster technology transfer and a maximum interface in
related fields. The five series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS
RESEARCH series. This series describes projects and studies relating to the
tolerances of man for unhealthful substances or conditions. This work is gener-
ally assessed from a medical viewpoint, including physiological or psycho-
logical studies. In addition to toxicology and other medical specialities, study
areas include biomedical instrumentation and health research techniques uti-
lizing animals—but always with intended application to human health measures.
This document is available to the public through the National Technical Informa-
tion Service, Springfield, Virginia 22161.
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EPA-600/1-76-001
March 1976
EFFECTS OF LOW LEVELS OF
OZONE AND TEMPERATURE STRESS
by
Steven M. Horvath
Lawrence J. Folinsbee
Institute of Environmental Stress
University of California
Santa Barbara, California 93106
Contract No. EPA 68-02-1723
Project Officer
George S. Malindzak
Health Effects Research Laboratory
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
HEALTH EFFECTS RESEARCH LABORATORY
RESEARCH TRIANGLE PARK, NORTH CAROLINA 27711
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DISCLAIMER
This report has been reviewed by the Health Effects Research
Laboratory, Environmental Protection Agency, and approved for publication.
Approval does not signify that the contents necessarily reflect the views
and policies of the U.S. Environmental Protection Agency, nor does mention
of trade names or commercial products constitute endorsement or recommendation
for use.
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ABSTRACT
Cardiopulmonary and metabolic responses of 20 adult males
(age 19-29) before, during and after a 2-hour exposure to either filtered
air or 0.50 ppm ozone under four ambient conditions (25°C, 45% rh;
31°C, 85% rh; 35°C, 40% rh; 40°C, 50% rh) were determined. Exercise
at 40% of the individual's VQ, was performed from 60-90 min of
<£ msjv
exposure. There were no cardiovascular changes due to ozone exposure
but heart rate increased and stroke volume decreased with increasing
heat stress. Rectal, mean body, and mean skin temperature also
increased in the heat and were significantly correlated (P < 0.05) with
WBGT. There was a decrease in vital capacity and total lung capacity
due primarily to a reduction of inspiratory capacity following ozone
exposure. Maximum expiratory flow (indicated by FEV, n _ n _ _, MEF50%,
1 • U 9^«UjO*U
MEF25%, and M4EF) was also reduced following ozone exposure but, as
with vital capacity, the greatest decrease occurred immediately
following the exercise period in ozone. The combination of heat stress
and ozone exposure resulted in significantly greater impairment of
pulmonary function and more numerous reported symptoms than in the room
temperature ozone exposure. The trachial-bronchial irritation caused
by ozone reduces the vital capacity and maximum expiratory flow and
this effect is more pronounced when the ozone exposure occurs in
a hot environment.
111
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CONTENTS
Page
Abstract iii
List of Figures vi
List of Tables ix
Acknowledgments x
Sections
I Conclusions 1
II Recommendations 2
III Introduction 3
IV Review of Literature 4
V General Objectives and Specific Aims 8
VI Research Methods 9
VII Results and Discussion 20
VIII References 47
IX Glossary of Terms, Abbreviations, and Symbols 54
X Appendices - 68
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LIST OF FIGURES
Figure . Page
Fig. la. Pre- and post-exposure values for FVC, RV, and TLC
for all eight ambient conditions. The histograms
represent the mean (±SE) for condition 1 (FA, 25°C),
while the numerals indicate the mean values for the
remaining seven conditions. Numbers 2, 3, and 4 on
the left of the SE bar are filtered air environments,
while 5, 6, 7, and 8 on the right of the SE bar are
equivalent ambient environments with 0.5 ppm ozone. 23
Fig. Ib. Pre- and post-exposure values for 1C, ERV, and FRC
for all eight ambient conditions. The histograms
represent the mean (±SE) for condition 1 (FA, 25°C),
while the numerals indicate the mean values for the
remaining seven conditions. Numbers 2, 3, and 4 on
the left of the SE bar are filtered air environments,
while 5, 6, 7, and 8 on the right of the SE bar are
equivalent ambient environments with 0.5 ppm ozone. 24
Fig. Ic. Pre- and post-exposure values for MW, Raw, and RV/TI£
for all eight ambient conditions. The histograms
represent the mean (±SE) for condition 1 (FA, 25°C),
while the numerals indicate the mean values for the
remaining seven conditions. Numbers 2, 3, and 4 on the
left of the SE bar are filtered air environments, while
5, 6, 7, and 8 on the right of the SE bar are equivalent
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LIST OF FIGURES (Con't)
Figure Page
ambient environments with 0.5 ppm ozone. 25
Fig. Id. Pre- and post-exposure values for MMEF, MEF50%, and
MEF25% for all eight ambient conditions. The histo-
grams represent the mean (±SE). for condition 1 (FA,
25°C), while the numerals indicate the mean values
for the remaining seven conditions. Numbers 2, 3,
and 4 on the left of the SE bar are filtered air
environments, while 5, 6, 7, and 8 on the right of
the SE bar are equivalent ambient environments with
0.5 ppm ozone. 26
Fig. le. Pre- and post-exposure values for FEV _, FEV ., and
FEV, n for all eight ambient conditions. The histograms
£« U
represent the mean (±SE) for condition 1 (FA, 25°C),
while the numerals indicate the mean values for the
remaining seven conditions. Numbers 2, 3, and 4 on
the left of the SE bar are filtered air environments,
while 5, 6, 7, and 8 on the right of the SE bar are
equivalent ambient environments with 0.5 ppm ozone. 27
Fig. 2a. Percent change in VC, MEF50%, and M4EF in all eight
ambient conditions as affected by a 30-min period of
exercise. There were no significant differences in the
first hour and these values were averaged for the
via
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LIST OF FIGURES (Con't)
Figure Page
comparisons after the exercise period. 31
Fig. 2b. Percent changes in FEV n, FEV- ., and FEV- n in
.1 • I/ A • I/ 3 • U
all eight ambient conditions as affected by a 30-rain
period of exercise. There were no significant differ-
ences in the first hour and these values were averaged
for the comparisons after the exercise period. 32
Fig. 3. Frequency of clinical symptoms observed consequent
to exposure to the eight conditions (four filtered air
and four 0.5 ppm ozone). 40
vin
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LIST OF TABLES
Subject Information 10
Exposure Conditions 11
Experimental Routine 11
Pulmonary Changes Prior to and After Exposure (2 Hours)
to Filtered Air or 0.5 ppm Ozone at Various Environmental
Conditions 21
5 Pulmonary Function Changes During 2-Hour Exposure
to Filtered Air or 0.5 ppm Ozorfe at Various Ambient
Environmental Conditions 29
6 Pulmonary Function Changes Following Exercise
and at End-Exposure 33
7 Peripheral Blood Flow (ml/100 ml/min) During Exposure
to Filtered Air or 0.5 ppm Ozone at Various Ambient
Environmental Temperatures 35
8 Metabolic and Cardiovascular Changes During Exposure
to Filtered Air or 0.5 ppm Ozone for 2 hours ^6
IX
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ACKNOWLEDGMENTS
The following were instrumental in conducting various phases of the
experimental program.
Dr. John F. Bedi
Dr. Nils W. Bolduan
Dr. Barbara L. Drinkwater
Dr. Lawrence J. Folinsbee
Dr. Jeffrey A. Gliner
Dr. Bernard Gutin
Dr. Steven M. Horvath
Dr. Alan R. Morton
Dr. Pierre M. Nizet
Dr. Peter Bt Raven
Dr. Jeames A. Wagner
Dr. James E. Wilkerson
Mr. James C. Delehunt
Mr. Robert S. Ebenstein
Mr. Michael B, Maron
Ms. Dorothy L. Batterton
Mr. David M. Brown
Mr. M. Fred Bush
Ms. Brigitte Hallier
Ms. Suzanne L. Hostetter
Mr. Richard R. Marcus
Mr. Douglas L. Marsh
Ms. Judy A. Matsen
Ms. Lovette Weir
We are especially appreciative of the unstinting efforts by our
office staff Ms. Patricia A. Boisvert and Ms. Darlene Clement to organize
our subjects and the typing of this report. To our many subjects we can
only say thanks. Their cooperation made these studies possible.
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SECTION I
CONCLUSIONS
Pulaonary dysfunction occurring consequent to exposure to
0.5 ppm 0_ is more pronounced following exercise and in hot
ambient environments. It is necessary to perform additional
studies utilizing different levels and durations of physical
activities as well as other concentrations of ozone in order
to determine threshold levels.
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SECTION II
RECOMMENDATIONS
1. Studies similar to the present program but which incorporate
a series of consecutive daily exposures to ozone should be
initiated immediately.
2. Other age groups both males and females should be evaluated
under conditions similar to those employed in the present study.
Smokers should also be included in any sample of the population
under consideration.
3. Studies should be initiated to evaluate the pulmonary effects of
multiple combinations of pollutants (0,, SO , NO etc.) at
O X X
different concentration levels.
4. Since exercise of a linited magnitude induced marked pulmonary
function changes, additional studies should be undertaken in
which the magnitude and duration of activity would differ
from the present investigation.
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SECTION III
INTRODUCTION
Many pollutant episodes occur during a temperature inversion
during which the ambient air pool has stagnated, therefore subjecting
the human organism not only to raised levels of environmental
contaminants but additionally to the stress of high ambient temperatures.
Dependent upon the constituent buildup during the alert, the resultant
"smog" can be generally designated: (a) reductive, consisting mainly
of carbon monoxide (CO), sulfur oxides (SO ), and particulates, usually
,A
in combination with high humidities and high or low temperatures (1-5);
or (b) oxidant or photochemical, consisting mainly of carbon monoxide
(CO), ozone (0_), nitric oxides (NO ), peroxyacetylnitrates (PAN), and
«j X
particulates, usually in combination with high temperatures and low
humidities (6-11).
The information available concerning CO and SO is generally
^v
regarded as adequate for the setting of realistic air quality standards
(AQS). However, new information, by Horvath and Raven at this Institute
(12-14) and Bates and Hazucha in Canada (15), regarding synergistic
actions of pollutants and other variables have led to the conclusion
that the simplistic view of "one pollutant, one effect" is unrealistic.
In contrast to CO and SO , the information concerning 0_ and NO as
X O A ^
single moieties is not available in a usable form for the setting
of AQS. The effects of the oxidant-type smog on man's ability to
work is unknown. Therefore, in this investigation we planned to study
the influence of 0_ on pulmonary, cardiac, and peripheral circulatory
function during rest and activity while exposed to a number of thermal
heat loads.
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SECTION IV
REVIEW OF LITERATURE
Early reports provided evidence for certain physiologic actions
of ozone (0_) (16-18). The primary targets of 0^ action are the lung
and the respiratory tract; however, interactions with the red blood
cell (RBC) and the central nervous system (CNS) have been noted (18, 19).
In 1953, Belknap (in reference 65) reported pulmonary congestion
consequent to exposure to high levels of ozone produced during helio-arc
welding. Levels of ozone (< 1 ppm) were also found to induce respiratory
tract irritation, headache, and shortness of breath (20, 21). The
prominent features of the response were rapidity of onset, marked dyspnea,
chest pain, and cough. Griswold et al. (22) reported that following
exposure to 1.5 ppm 0_ for 30 minutes and continuation of exposure with
2.0 ppm for 90 minutes, the subject experienced dry mouth and throat,
reduced ability to concentrate and think, altered taste sensation,
substemal pain, and paresthesia of the extremities. The long-term
sequelae were a loss of appetite, sleepless and uncomfortable nights,
cough developing two days after exposure and persisting for two weeks,
and expectoration of clear mucus. At the end of the acute exposure
subjects had an initial 17% reduction in 3-second vital capacity (VC)
which was still 7% below control levels 22 hours later. The maximum
breathing capacity was only 3% reduced.
Federal threshold limit values (TLV) and air quality standards
(AQS) have been based upon pulmonary data (23) and some industrial
observations (24). When 12 subjects were exposed to 0.6 to 0.8 ppm
03 for 2 hours, a significant reduction in pulmonary diffusing capacity
to CO (DLCO) occurred with only slight changes in VC and forced
expiratory volume (FEV), although diminution of FEV- __ x 40 estimated
\J • / O
maximal voluntary ventilation (MVV) and throat irritation occurred (25).
These findings suggested that 03 exerted its initial influence at the
level of the alveolar membrane. The changes were transient, persisting
for less than 24 hours after the subjects returned to clear air environ-
ments. Challen et al. (66) reported the presence of upper respiratory
symptoms in 11 of 14 welders exposed daily to 0, levels of 0.8 to 1.7 ppm.
-------
The symptoms disappeared following reduction of the levels to 0.2 ppm.
It was primarily from this data that the industrial TLV of 0.1 ppm
over 8 hours was obtained. Stokinger (26) reported that exposures
to 0.13 ppm maximum daily value of total oxidant caused an increased
number of asthmatic attacks in 5% of asthmatic subjects. By comparison,
exposures of nonasthmatic human volunteers to 0.3 ppm 0_ for 8 hours
resulted in nose and throat irritation and to 0.5 ppm for 3 hours
each day gave decreased FEV. Q after 8 weeks, but 0.2 ppm was without
effect after 12 weeks of 3-hour daily exposures. These were data that
served as the criteria for AQS for 0_ of 0.08 ppm for a 1-hour maximum (26)
Results of other experimental exposures of man (7, 23, 24, 27)
to low levels of ozone confirmed the findings outlined above. A
significant increase in airway resistance (R ) was observed when resting
£LW
subjects were exposed to 1.0 ppm for 1 hour (23, 24). However, few
investigations (27, 41, 42, 43) have considered the combined effect
of ozone and exercise. Bates et al. (27) studied the effects of 0.75
ppm 0, on 10 normal subjects during rest for 2 hours and on only 3
subjects during 15 minutes of light exercise followed by a rest for
15 minutes during a similar 2-hour exposure. The resting subjects
reported substemal soreness and cough, while a few had symptoms
of pharyngitis and dyspnea. Objectively, it was observed that the
subjects had a significant fall in maximum static elastic recoil
pressure of the lung, a significant increase in pulmonary resistance
with a decrease in flow rates measured at 50% vital capacity. However,
unlike a previous study (25) no significant reduction in CO uptake was
found. The investigators concluded that large and small airway effects
can be observed before changes in diffusion capacity (DLCQ) become
apparent. This conclusion was somewhat different from that obtained
in the previous study (25). The three subjects that exercised reported
symptoms far earlier during the exposure and all pulmonary effects were
more marked. Other studies have indicated that the effects of ozone
are not entirely restricted to the respiratory tract; however, the
mechanisms by which these extrapulmonary effects occur are unknown.
-------
The results of the above reported experiments suggested that
exposures to 0_ above 0.75 ppm for 2 hours or more caused physiological
impairment even if the subjects are resting quietly. The combination
of an exercise intensity sufficient to elevate ventilatory volumes to
20 liters/min significantly decreased the time of exposure at which
these effects were observed and suggested that the levels of ozone
now being found within urban environments (30, 31) might induce
significant physiologic impairment. It has also been reported that
during exposures to 1 ppm 0_ for 10 minutes the rate of oxyhemoglobin
desaturation was reduced (28), while Lagerwerff (29) reported that
visual acuity was significantly impaired at ozone levels from 0.2 to
0.5 ppm.
Following 30 minutes of exposure to 15 ppm 0_, rabbits showed a
50% reduction in oxygen uptake, which remained below normal for 2 days.
Repeated exposures resulted in similar responses, but, most interesting,
recovery was more rapid following each successive exposure. Ozone at
2 ppm for 3 hours produced similar responses in rats (32). The rabbits
were able to compensate to 1-hour exposures daily for 4 months; however,
with continued exposure a gradual deterioration in pulmonary performance
was found.
Other factors affect the inherent toxicity of 0_. Young mice
were found to be more susceptible to the acute toxic effects of 0,
than older animals (33), while a 15°F rise in ambient temperature
resulted in an increased susceptibility to 0_ in both mice and rats.
When rats rested in 1 ppm 0_, no acute effects were observed; however,
the concentration became lethal when the rats were exercised for a few
minutes each hour during exposure (18). Mice infected with Kleb&iella
pneumonias and then exposed to 0, showed shortened survival time and
increased mortality (34), and prior 0_ exposure decreased the resistance
to respiratory infection. More recent animal experiments have been
aimed primarily at the mechanism of action of '0, (35, 36, 37, 38) rather
than determination of critical levels. However, Yokoyama and Frank
(39) have evaluated the findings of Vaughan et al. (40), who observed
-------
that in muzzled dogs 100% of inhaled ozone was extracted by the upper
respiratory tract, indicating that Oj was not present in the alveoli.
Yokoyama and Frank demonstrated that, although nose breathing resulted
in removal of 0, from airstream more efficiently than the mouth at
low flow rates, when high flow rates and mouth breathing were utilized
the alveoli were exposed to significant amounts of ozone even though
the rate of "uptake" of 0, is reduced as the rate of flow increases.
O
These findings emphasized the need to determine the response of the
lung to low levels of ozone at raised levels of ventilatory exchange
as well as during periods of elevated ambient conditions.
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SECTION V
GENERAL OBJECTIVES AND SPECIFIC AIMS
This study was designed to determine the effects of 0.3 to
0.5 ppm ozone (0_) on the metabolic, thermoregulatory and cardio-
O
pulmonary systems of young men (18-30 years of age) while they were
exposed to different ambient temperature conditions. These conditions
ranged from normally cool (25°C and 45% rh) through warm wet (31°C and
85% rh) to hot dry (40°C and 50% rh). By including exercise levels
of approximately 40-45% of each subjects maximal capability it was
anticipated that it would be possible to evaluate the effect of these
conditions on man when he was at rest or at work. The findings obtained
from this investigation would enable regulatory agencies to evaluate
a level of 0.5 ppm 0, as a possible national level guideline to be
used for the health protection of the general population.
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SECTION VI
RESEARCH METHODS
SUBJECTS
Twenty-one young healthy males (ages 18-30 years) were selected
as subjects from some thirty volunteers. All volunteers were
nonsmokers [confirmed by blood carboxyhemoglobin (HbCO) analysis]
and were drawn from the student population of the University of California,
Santa Barbara campus. Subjects were completely informed as to the purpose
of the tests and signed University consent forms to act as human subjects.
Each volunteer was medically screened. A medical history questionnaire,
a resting 12-lead electrocardiogram, an exercise electrocardiogram (V.)
up to 160 beats each minute, determination of basal metabolic rate (BMR),
and a battery of clinical spirometric tests were used in evaluating
each subject. Following the screening the subjects performed a
•
maximal aerobic capacity (VQO ) test on a treadmill. Table 1 summarizes
& IllaJC
pertinent physical and physiological data of the participating subject.
Following the maximal performance test each subject was trained (two
1-hour sessions on separate days) in the procedures being utilized
for the determination of cardiovascular, pulmonary and peripheral
circulatory functions.
EXPERIMENTAL DESIGN
The following basic approach was used with all exposure conditions
being subject to random order presentation. Two groups of subjects
(designated A and B) were exposed to eight separate conditions. Exposure
to each condition was separated by a minimum of one week for each
individual subject. The exposure conditions for both the pollutant
and ambient environments are outlined in Table 2.
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Table 1. SUBJECT INFORMATION
——••—- • — - • •
Subj
No.
7495
7493
7496
7510
7505
7519a
7522
7504
7555a
7516*
7561
7659
7613a
7650
7658a
7674
7684
7822
7823
7887
7829 .
Age,
yr
19
22
24
20
21
22
21
21
21
19
21
21
22
20
20
20
20
23
23 ;
20
20 •
Ht,
cm
190.25
187.6
178.6
177.5
178.1
175.5
176.5
180.6
161.8
175.5
180.3
182.0
161.8
184.9
182.1
173.2
190.5
179.3
165.1
172.1
179.6 ,
Wt,
• kg
, 91.6
i 81.2
! 74.8
j 64.3
I 84.0
| 65.4
70.2
: 75.8
58.0
55.7
81.0
1 77.0
55.6
81.0
' 91.0
77.6
83.4
69.6
53.0
64.8
64.2 .
BSA,
m2
2.20
2.02
1.92
1.78
2.02
1.80
1.87
1.96
1.61
1.69
2.02
1.98
1.59
2.05
2.13
1.93
2.10
1.88
1.57
1.82
1.82
VC,
liters
8.45
6.60
6.09
5.12
5.72
5.94
5.25
5.40
4.28
5.75
5.61
7.36
4.47
6.42
6.24
6.36
6.22
5.77
4.31
5.20
. 4.34
FEV1 0,
A • W f
liters
6.99
5.30
4.76
4.77
4.23
4.66
4.37
4.38
3.72
4.87
4.21
4.37
3.84
5.31
5.12
4.93
4.75
4.23
3.96
4.49
4.16
FEV3 0,
** • V 9
liters
8.34
6.45
6.02
5.01
5.55
5.83
5.23
5.40
4.18
5.75
5.27
6.91
4.46
6.31
6.07
6.15
6.21
5.60
4.26
5.10
4.34
1C,
liters
6.13
4.02
4.44
3.34
3.59
3.35
3.32
3.29
2.51
4.44
4.08
4.66
3.02
4.47
4.65
4.23
3.60
3.62
2.97
2.99
2.67
ERV,
liters
2.32
2.58
1.65
1.17
2.14
2.60
1.93
2.11
1.77
1.31
1.53
2.70
1.45
1.95
1.59
2.12
2.62
2.09
1.33
2.07
1.66
RV/TLC,
%
20
15
24
26 !
22
32
23
20
22
32
23 j
23 j
32
26
23
25
31
30
31
26
; 23
MW,
liters
/rain
202
169
219
164
193
136
157
162
173
144
182
148
179
198
202
137
191
205
214
155
198
V02 max,
liters
/min
4.22
3.28
3.01
3.59
4.35
—
3.95
3.55
—
2.30
4.04
3.97
2.50
4.21
4.38
4.09
4.37
3.57
2.71
3.36
4.12
Subjects not completing the test series,
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Table 2. EXPOSURE CONDITIONS*
Exposure Temperature and relative humidity0
Set
Ambient air Bl B2 B3 B4
(Control exposures) 25°(45) 31°(85) 35° (40) 40°(50)
(Code 1) (Code 2) (Code 3) (Code 4)
Ozone (0.44 - 0.57 ppm) 25°(45) 31°(85) 35°(40) 40°(50)
(Experimental exposures) (Code 5) (Code 6) (Code 7) (Code 8)
a The equivalent WBGT temperatures for 1, 2, 3, and 4 conditions
are respectively 64.4, 85.2, 80.0 and 92.0°F and are respectively
similar for 5, 6, 7, and 8.
b
Exposure was for a 2-hour period.
All temperatures are Cels:
listed in parentheses (%).
c All temperatures are Celsius. Percentage relative humidity
EXPERIMENTAL PROTOCOL
Groups A and B underwent the routines outlined in Table 3.
Table 3. EXPERIMENTAL ROUTINE
Control Period Exposure Periodsa Recovery Period
Code Number 123 4567 8
Group A Pre-Exp. Tests
Group B Pre-Exp. Tests
R
R
W
R
W
W
W
R
R
Post-Exp. Tests
Post-Exp. Tests
a Each section = 15 minutes duration, R = sitting rest; W = work
« 45% *°2 «*•
Pre- and post-exposure tests lasted approximately 1-hour each.
During exposure, the group A subjects rested in the sitting position
for 1-hour then exercised for 30 minutes on a motor-driven treadmill at
•
approximately 45% VQ2 followed by a 30-minute seated rest. Group
B underwent a similar 2-hour exposure except that the exercise sessions
occurred in the second haIf-hour of exposure (Table 3).
Each subject was scheduled for eight experimental sessions.
Exposures occurred throughout the day although each individual was
always scheduled at the same time of day. On arrival at the Institute,
the subject was weighed nude and then connected to the appropriate
11
-------
monitoring leads for temperatures and electrocardiogram. Clothing
worn during the experiments consisted of tennis shoes, socks, shorts,
and supporter. Each subject was given a clinical chest examination
and seated for withdrawal of a 12-ml pre-exposure venous blood sample.
The subject then performed a battery of pulmonary tests on a 13. 5- liter
chain- compensated spirometer (W. E. Collins) and in a volume body
plethysmo graph (W. E. Collins). The subject then entered the exposure
chamber, set at the required ambient conditions, and was connected to
appropriate monitoring cables. The 2-hour exposure was divided for
convenience into eight 15-minute segments (numbered 1-8) (Table 3).
Each period for either group A or B was utilized as outlined in the
following summary:
SUMMARY OF PROTOCOL UTILIZED DURING EXPOSURES
PERIOD 1
GROUP A § B Minutes 0-2
Minutes 2-4
Minutes 4-6
Minutes 6-10
Minutes 10-15
Forearm blood flow.
-- Ventilatory volume OL), 0 and CO.
percentages , heart rate (HR) , tidal
volume (V ) , and respiratory frequency
(f_) . Temperatures : room (T ) , radiant
(Tr) , mean skin (Tgk) , and rectal (Tre) .
- Cardiac output (Q) , blood pressure (BP) ,
and HR.
- Steady-state diffusion capacity to
carbon monoxide (DL^,-).
- Pulmonary function tests: forced vital
capacity (FVC) ; forced expired volume at
1.0, 2.0, and 3.0 seconds (FEVj 0 2 0 3 0^'
flow at 50% and 25% vital capacity (MEF50%,
MEF25%) ; expiratory reserve volume (ERV) ;
and inspired capacity (1C). Closing volume
with slow vital capacity (VC) in duplicate.
Trm' V
' and T
re
12
-------
PERIOD 2
Group A & B Sitting rest
Minutes 5-6
Minutes 10-11
Minutes 11-14
PERIOD 3
Group A
PERIOD 4
Group A
Group B
PERIOD 5
Group A
Group B
— HR, BP, T , , T , T , T and forearm blood flow.
sk re rm r
-- HR, BP, T . , T
re-
V
FVC- FEV1.0,2.0,S.O- ERV- IC'
and MEF25%. Closing volume with slow
VC in duplicate.
Sitting rest — BP, HR, T . , T , T and T (each at
Six J7C A'Hi x
5, 10, and 15 min).
- BP, HR, Tsk, Tre, T^, and TT (each at
5, 10, and 15 min).
Exercise
Sitting rest
Minutes 0-2
Minutes 2-4
Minutes 4-6
Minutes 6-10
Minutes 10-15
Forearm blood flow.
VE, 02 and C02 percentages, HR, VT, fR,
Exercise
Minutes 2-4
Minutes 4-6
Minutes 6-10
Minutes 10-15
Exercise
Sitting
V V Tsk' re-
— Q, BP, and HR.
— Steady state DL^.
- FVC, FEV1 02030' MEF50%»
and 1C. Closing volume with slow VC in
duplicate. T^, TT, Tgk, Tre, and HR.
— VE, 02 and C02 percentages, VT, fR, T^
Q, BP, and HR.
Steady-state
- T
rad-
- T
re"
BP, HR, Tsk, Tre, T^, and Tr (each at
5, 10, and 15 min).
BP, HR, T_v, T. T , and T (each at
5K re rm r
10 and 15 min) . Forearm blood flow at 10 min.
13
-------
PERIOD 5 (Continued)
Minutes 3-10
PERIOD 6
Group A
Group B
Group B
Exercise
Minutes 2-4
Minutes 4-6
Minutes 6-10
Minutes 10-15
Sitting rest
Minutes 0-2
Minutes 2-4
Minutes 4-6
Minutes 6-10
Minutes 10-15
FVC, FEV. n , n , n, MEF50%, MEF25%, ERV,
1. U ,^. U , J. U
and 1C. Closing volume with slow VC in
duplicate.
VE, 02 and C02 percentages, VT, fR,
T , T . , T , and HR.
,r* sk* re*
Q, BP, and HR.
Steady-state
- Trm'Tr' Tsk' Tre' mA ™'
-- Forearm blood flow
-- VE, 02,and C02 percentages, VT, fR, HR,
T T T
>m' V sk'
~ Q and BP.
-- Steady-state
— FVC, FEVX 02030* MEF50%' MEF25%, ERV,
and 1C. Closing volume with slow VC in
duplicate. T , T , f., T , and HR.
rm T SK re
PERIOD 7
Group A Sitting rest
- BP, HR, T ., T , T , and T (each at
Siv TG TMU T
10 and 15 min). Forearm blood flow @ 10 min.
Minutes 3-10 — FVC, FEVj 0 2 o 3 0* MEF50%» MEF25%, ERV,
and 1C. Closing volume with slow VC in
duplicate.
Sitting rest — BP, HR, Tgk, Trg, T , and T (each at
5, 10, and 15 min). Forearm blood flow
@ 5 min.
PERIOD 8
Group A § B Sitting rest
Minutes 0-2
Minutes 2-4
-- Forearm blood flow.
VE, 02 and C02 percentages, VT, fR, HR,
Trm> Tre'
Tr'
14
-------
PERIOD 8 (Continued)
Minutes 4-6 — Q, BP, and HR.
Minutes 6-10 — Steady-state DLcQ.
Minutes 10-15 — FVC, FEV- , n, MEF50%, MEF25%,
X • U £ib«vfjO*l'
ERV, and 1C. Closing volume with slow
VC in duplicate. HR, BP, T , f"k,
Tre' ™d Trm-
At the end of the 2-hour exposure, the subject was allowed into
the FA atmosphere of the laboratory, disconnected from the monitoring
wires and seated on a chair. The attending physician immediately
gave a clinical chest examination, and 4 minutes after exposure
another 12-ml venous blood sample was obtained. The subject then
repeated the battery of spirometric tests. Following these post-
exposure tests, the subject completed a 33-item questionnaire,
was weighed nude, and then allowed to leave the laboratory on
permission of the examining physician.
15
-------
MEASUREMENT TECHNIQUES
Metabolic measurements were made using open-circuit indirect
calorimetric techniques (44). Ventilator/ volumes were monitored by
collecting timed volumes in a 120-liter chain-compensated spirometer.
Aliquot gas samples were analyzed for 0_% and CO-% in a Quintron gas
chromatograph calibrated against standard Haldane analyzed gases.
Accuracy of analysis was ±0.02% for CO- and ±0.05% for Q^. Incorporation
of appropriate temperature and barometric pressure corrections with
the raw metabolic data in the Institutes batch process computer
analysis resulted in the determination of all other metabolic parameters
(see Glossary).
Copper-constantan thermocouples were used to monitor rectal
temperature (T ) at the depth of 12 cm into the rectum. Mean skin
T&
temperature (T . ) was obtained from a weighted average of seven skin
surface temperatures (forehead, arm, finger, thigh, calf, chest and
abdomen). In addition, globe temperature and chamber air temperature
as well as a continuous monitor of relative humidity provided a
description of environmental conditions in terms of WBGT. The thermocouple
temperatures were recorded by a Honeywell multichannel digital recorder
and simultaneously recorded by a laboratory computer (PDP-12). Temperature
parameters were used in the calculation of thermoregulatory changes
as outlined in the Glossary section (45). All temperatures were measured
with an accuracy of ±0.1°C.
Cardiac output was determined using the carbon dioxide rebreathing
technique of Defares (46) as modified by Jenous et al. (47). Calculation
of mixed venous CCL (PVCQ7) was performed by the extrapolation method
(48) utilizing the laboratory computer display. This enabled the operator
to discard those points which obviously were not fitted to the general
rebreathing pattern and thereby obtain a better estimate of the point of
equilibrium. The coefficient of variation for repeated measurements
on one subject within a period of one hour was 10%. Tidal volume and
respiration rate were determined during the measurement of end tidal
carbon dioxide. Blood pressure was obtained by the indirect Riva Rocci
16
-------
method and heart rate from V. lead recorded on a Sanborn 500
Viso-Cardiette electrocardiograph. All electrocardiogram tracings
were read by the Institute's cardiologist. An oscilloscope display
of the electrocardiogram was continuously monitored. Estimation
of forearm blood flow was made using the strain-gauge plethysmographic
techniques of Whitney (49). The DI^Q was determined using the steady-
state technique of Filley et al. (50) as modified by Bates et al. (51).
The coefficient of variation of DL™ determination for repeat measurements
on one subject at rest was 12% and at moderate exercise (40% VQO v)
£ IIicLX
was 6%. Combinations of the cardiovascular and metabolic data enabled
the calculations of various cardiorespiratory parameters, i.e. diffusion/
perfusion ratio and ventilation/perfusion ratio (see Appendix A for
a sample printout of measured and calculated data).
The procedures outlined by Kory et al. (52) were used for pulmonary
function tests. A 13.5-liter chain-compensated spirometer (W. E. Collins
Co.) was used for pre- and post-exposure pulmonary measures and a
Wedge spirometer (Med Science Electric Co.) connected via appropriate
pre amplifiers to a multichannel pen recorder was used during the
exposure period for the determination of FVC, FEV n , n _ _, 1C, ERV,
1 *\J y £• • U ) O • U
MEF50%, MEF25% and mid portion of the FVC (M1EF). The helium dilution
technique was used for the measurement of residual volume (RV) before
and after exposure and total lung capacity (TLC) was calculated using
this value. MW was determined prior to and following exposure. All
volumes and flow rates measured in these tests were corrected to BTPS.
During exposure duplicate determinations of closing volume (CV) and
slow vital capacity (SVC) using a helium bolus technique (53, 54) were
made. Calculation of other pulmonary function parameters were performed
by computer (see Appendix B). Comparison of volumes measured on numerous
subjects at the same time of day on the chain-compensated spirometer
and the Wedge spirometer indicated that at volumes between 3 and 6 liters
the wedge spirometer was consistently higher by 200 ml — a difference
ranging from 3-7%. However, as comparisons between values obtained
by the two methods were not made, corrected values were not utilized.
The coefficients of variation of repeat measurements of vital capacity
17
-------
on one subject made at hourly intervals during one day ranged from
0.9% to 5.0%, whereas the coefficient of variation of repeated
measurements of closing volume would range from 10% to 30%, which
is consistent with recently reported results (55, 56).
CHAMBER DESIGN AND CONTROL
A 1.8 m wide by 2.4 m long by 2.6 m high double-walled flow-
through acrylic environmental chamber was utilized for chamber exposures.
Inlet air was filtered through activated charcoal, Baralyme, soda lime,
Drierite, and gauze before entering the chamber. Air was forced into
the chamber at flow rates ranging from 200 liters/min to 500 liters/min
resulting in exchange turnover in the chamber ranging from once every
56 min to once every 22 min. Minimal air movement across the subject
occurred due to the dispersive design of the inflow air. Automatic
regulated heating dehumidifier and air conditioner allowed for
appropriate temperature control. When needed for humidification steam
was piped directly into the air inflow. However ozone was put directly
into the chamber and mixed with the chamber air by blow fans. The
chamber was equipped with a small motor-driven treadmill, chair and
appropriate equipment for the subject to perform the tests without
experimenter assistance. All rubber components were protected from
ozone attack by a weekly coating of anti-oxidant (Armor-all).
Ozone was generated (Ozone Research Inc.) outside the chamber
utilizing pure oxygen to remove the possibility of nitrogen oxide
production. Ozone concentration was continuously monitored utilizing
the chemiluminescence technique. The monitor (McMillan Corp.) was
calibrated prior to each ozone exposure using a standard calibrated
ozone generator (Monitor Labs Inc.). In addition, an aliquot sample
was drawn through midget impingers once each exposure for the
determination of ozone concentration by the neutral buffered potasium
iodide method (57). The mean 2-hour exposure ozone concentration measured
by the chemiluminescence technique was 0.507 ±0.04 and that obtained
utilizing aliquot samples and chemically analyzed was 0.498 ± 0.07 ppm.
The ozone sampling inlet was placed near to an average position of
18
-------
the subject's head during exposure (always withing 24 inches). Exposure
incorporating combinations of high temperatures and humidities
resulted in a rapid breakdown of ambient ozone. In order to maintain
the ozone levels during the cyclic operation of the dehumidifiers and
air conditioners a second ozone generator was built by Institute
personel using the design outlined by Hazucha (58). This backup
generator consisted of two 12,000-volt transformers connected in
series discharging through pure oxygen. The ozone output of this
generator was in excess of 100 ppm.
STATISTICAL EVALUATION OF DATA
Data were analyzed by a series of analyses of variance. For
pre- and post-test measurements, a three-factor factorial analysis
of variance with repeated measures across time, environment and
ambient air was used; for the pre-exercise and post-exercise periods,
a two-factor analysis of variance with repeated measures across
environment and ambient air. In all cases where a significant
interaction was observed, a test was made of the simple main effects
followed by a Newman-Keuls test of ordered means where appropriate.
Prior to the collection of data, it was decided to make an a priori
comparison of responses at codes 4 and 8 regardless of the outcome
of the F test (59), since code 8 was the most extreme condition in
0- and code 4 was the FA equivalent. All hypotheses were tested
for significance at an alpha level of 0.05.
19
-------
SECTION VII
RESULTS AND DISCUSSION
RESULTS
The mean values of pulmonary function measurements made before
and after exposure under four environmental conditions to filtered
air (codes 1-4) as well as to 0.50 ppm ozone (codes 5-8) are summarized
in Table 4 and Figs, la through le. VC declined an average of 350 ml
following ozone exposure (P < 0.05) regardless of the environment
when compared with the measurement made before exposure. There was
no change in VC following exposure to filtered air in any environment
except in condition B4 (see Table 2), where the VC declined whether
ozone was breathed or not. However, the decrease in VC in condition
B4 was less with FA than in comparable exposure with 0-. The decline
in vital capacity was primarily due to a decline in inspiratory
capacity. 1C was reduced an average of 300 ml (P < 0.01) following
ozone exposure but did not change following filtered air. There were
no significant changes in ERV in any condition. The resting
expiratory position of the lungs (FRC) tended to increase following
the exposure regardless of the conditions. The change was small
(average 109 ml) and the physiological significance is questionable
as neither ERV or RV, whose sum comprises the FRC, showed significant
changes. The total lung capacity was reduced an average of 250 ml
(P < 0.05) primarily due to the decrease in inspiratory capacity.
However, the ratio RV/TLC increased regardless of the exposure
conditions.
The flow-related pulmonary function measurements all showed
significant decreases following the ozone exposure regardless of
the thermal conditions. The forced expired volume was reduced
following ozone exposure whether measured at 1, 2, or 3 sec. The
greatest reduction (500 ml) (P < 0.01) occurred at 1 sec (FEV ).
.1 • U
The decrease in FEV, n (450 ml) and FEV, n (350 ml) was smaller.
fi • \J *J • U
The average decline in FEV _ is of the same magnitude as the
decrease in FVC (350 ml) and can probably be accounted for on this
20
-------
Table 4. PULMONARY CHANGES PRIOR TO AND AFTER EXPOSURE (2 HOURS)
TO FILTERED AIR OR 0.5 ppm OZONE
AT VARIOUS ENVIRONMENTAL CONDITIONS*,b
tsi
VC, ml
FEV1>{), ml
FEV2t(), ml
FEV3 Q, ml
1C, ml
ERV, ml
FRC, ml
RV, ml
TLC, ml
RV/TLC, %
MMEF, liters/sec
MEF50%, liters/sec
MEF25%, liters/sec
R , cm R-0/ liters -sec
£LW &
MW, liters/min
Filtered Air
Code 1 Code 2 Code 3 Code 4
Pre
60811410
47821165
57141338
60161433
38431303
2238+190
39511229
1713+159
7794+502
22.0+1.6
5.0910.29
5.1110.54
2.5910.32
1.68+0.20
219+13
Post
60961415
47141329
57611308
60531393
38241265
22721223
4080+180
18081146
7904+405
23.212.2
4.8010.40
5.3710.55
2.3910.33
1.8210.17
208115
Pre
60961356
51151290
59071385
60861391
3855+214
22411179
39931160
17521103
78491337
22.611.6
5.3510.43
5.5110.43
2.6210.26
1.76+0.20
22219
Post
61061426
50291322
5878+426
61001470
3848+230
2300+215
40811134
1781+134
78881350
23.012.3
5.2810.34
5.1010.46
2.3710.27
1.94+0.24
21919
Pre
61811386
5020+406
58141397
6034+393
38981231
22831243
39691328
1687+188
78671509
21.311.6
5.1210.69
5.7610.67
2.6810.47
1.7310.17
219+12
Post
61211404
48631376
5659+390
59691409
37501191
23701246
41651276
17951138
79161433
22.911.8
4.9410.52
5.2410.54
2.33+0.27
1.8510.19
212+11
1
Pre
60911405
5043+248
58901416
60961434
38121221
2273+219
4092+224
18201139
79111429
23.211.8
5.2810.44
5.9210.45
2.88+0.44
1.86+0.25
226110
Post
5943+371
4920+152
57211253
59711333
37441243
21991168
42931238
20941144
8037+433
26.2+1.6
5.44+0.39
5.66+0.55
2.51+0.35
1.8310.08
210+7
.
a
Subjects walked at approximately 40% VQ, _ from 60-90 minutes of exposure.
£• IQcLX
CM
Q>
W
rf
o
•u
§
b P<0.05 for underlined data; see Notes in righ£ column and STATISTICAL EVALUATION OF DATA subsection.
-------
Table 4. (Continued)
K)
8
FA > 03
FA > 03
FA > 03
FA > 03
No change
Pre < Post
No change
FA > 03
Pre < Post
FA > 03
FA > 03
FA > 03
Pre > Post
-------
•00
LP
00
N
(C
in
o
re
CO
o
0.
UJ
cr
Q.
q
d
v
o.
in
CJ
CO
o
Q.
IT
Cl
If
o:
a.
o
O
o
o
en
O
o
o
oo
o
o
o
o
o
-------
00
to
CO
(O
i^%
CO
N- -— 1 {J
Q.
O
N
' CM
I I I 1
UJ
1 a.
10
ill III
O
H
X.
(T
O
ro
l
to
CM
CO
O
Q.
">
CM
U
(T
Q.
in
csi
o
CM
10
C>
O
00
CM
O
0
V
o.
n
O
I 1 1 1
o o o
^r CM o °
CM CM CM 2
CO
o
Q.
UJ
Q.
1 1
0 0
<£ *
FIGURE Ib.
Pre- and post-exposure values for 1C, ERV, and FRC for all eight
ambient conditions. The histograms represent the mean (±SE) for
condition 1 (FA, 25°C), while the numerals indicate the mean values
for the remaining seven conditions. Numbers 2, 3, and 4 on the
left of the SE bar are filtered air environments, while 5, 6, 7,
and 8 on the right of the SE bar are equivalent ambient environments
with 0.5 ppm ozone.
24
-------
00
(O
|O_
I
to
-------
0
d
v
o.
II
*
W
O
CL
10
Cl
CO
UJ
Cg
O.
10
CM
CO
O
O.
00
10
10
CM
UJ
o:
o.
CM
CO
fO
(O
2
CM
111
or
Q.
55
10
CM
u.
UJ
o
10
u_
UJ
U-
UJ
2
§
o
5t'
'03S/H
3
q
CM
FIGURE Id.
Pre- and post-exposure values for MMEF, MEF50%, and MEF25%
for all eight ambient conditions. The histograms represent
the mean (±SE) for condition 1 (FA, 25°C), while the numerals
indicate the mean values for the remaining seven conditions.
Numbers 2, 3, and 4 on the left of the SE bar are filtered
air environments, while 5, 6, 7, and 8 on the right of the
SE bar are equivalent ambient environments with 0.5 ppm ozone.
26
-------
CM
ro
"CM-
V
in
CO
in
CM
IO
O
6
V
Q.
U
CM
"
tJrtO
to
(0
IO
-T»
O
O
O
co
0
Q-
o
o>
CO
fO
UJ
o:
£L
CO
2
o
o>
CO
CM
LJ
o:
Q.
CO
o
a.
O
o
CO
UJ
a:
a.
8
o
o
o
CO
o
o
o
ID
FIGURE le,
"1W
FIGURE le.
Pre- and post-exposure values for FEVi.o, FEV2.0» and FEV3.0
all eight ambient conditions. The histograms represent the mean
(±SE) for condition 1 (FA, 25°C), while the numerals indicate the
mean values for the remaining seven conditions. Numbers 2,3,
and 4 on the left of the SE bar are filtered air environments,
while 5, 6, 7, and 8 on the right of the SE bar are equivalent
ambient environments with 0.5 ppm ozone.
27
-------
basis alone. The decrease in FEV2 Q and FEV^ Q must be attributed
to reduced maximum flow. MMEF was reduced by 0.7 liter/s from the
pre-exposure value (P < 0.05). Similarly, the MEF50% was reduced
by an average of 0.85 liter/s following ozone exposure. The
decrease in flow was greater than the change following exposure to
filtered air and was not dependent on the thermal conditions. The
MEF25% was reduced after ozone exposure but the change was less
dramatic (0.16 liter/s).
Changes which occurred during the exposure are summarized in
Table 5* and Figs. 2a and 2b. The time (in min from the beginning
of exposure) at which the measurement is made is indicated.
Measurements made immediately following the exercise period
(100 min) - VC, FEV. n, FEV, n, and FEV_ n -were reduced when
J. • U fc • U o • U
ozone was present in the exposure chamber (Table 6). MEF25% was
higher in code 4 and code 8 (the most severe thermal conditions).
This effect may be due to a decrease of the ERV because of faintness
felt by some subjects; a prolonged expiratory maneuver (a Valsalva
maneuver) would tend to aggravate any problems of hypotension due
to venous pooling in the legs caused by heat exposure.
Cardiovascular Function-
Cardiovascular and metabolic alterations during the 2-h exposure
to filtered air or ozone under the four thermal conditions are
summarized in Tables 7 and 8.
The primary change in cardiovascular function was a rise in
exercise heart rate at higher ambient temperatures (B4 > B2, B3 > Bl).
This was accompanied by a decline in stroke volume (Bl > B4) as cardiac
output in the heat was not significantly altered by temperature or
ozone exposure. Stroke index, cardiac index, or (a - v)0~ difference
were neither affected by temperature nor ozone exposure.
*See Appendix C for a discussion of closing volume data for this time
period.
Cardiac output and stroke volume values are not presented but can be
calculated from the mean BSA (1.97) and mean heart rate (Table 8)
using the value given for cardiac index (CI = CO/BSA).
28
-------
Table 5.
PULMONARY FUNCTION CHANGES DURING 2-HOUR EXPOSURE
TO FILTERED AIR OR 0.5 ppm OZONE
AT VARIOUS AMBIENT ENVIRONMENTAL CONDITIONS
a,b
CODE 1
CODE 2
CODE 3
CODE 4
Time,0
min
12.5
27.5
57.5
100.0
117.5
12.5
27.5
57.5
100.0
117.5
12.5
27.5
57.5
100.0
117.5
12.5
27.5
57.5
100.0
117.5
FVC,
ml
6035±376
62521416
6166±369
61271391
62021410
62871396
62141414
61881422
60641400
62431411
63931441
63081433
62271442
62171413
64741438
61451411
61431391
60331411
54781405
58761408
FEV1.0'
ml
44781239
46221185
45581183
46131195
47531136
51401203
47971153
49871147
47411138
50081214
47821109
50691363
48701133
48881144
5068161
48651242
48021236
48491235
46911232
46081229
FEV2.0'
ml
53591252
56421244
56241219
56121259
57401352
59601342
57591264
5912+365
57661258
60061339
57731246
60231466
57731398
57921328
61671336
55931291
55431330
56651371
52611377
51911348
FEV3.0'
ml
5555+276
60351340
59951306
59361349
6010+451
62441408
60981347
62121442
59921332
6225+410
61801419
6242+485
60661548
61241419
64821391
57761326
57351345
59481440
54251433
54721408
MMEF,
liters/sec
4.5510.61
4.7110.53
4.1910.53
4.3910.46
4.63+0.47
5.3510.26
5.0910.46
5.0310.32
4.5610.34
5.0910.22
4.3910.35
5.4010.52
4.79+0.58
4.8410.34
4.7410.38
5.0110.56
5.18+0.49
5.1110.58
5.6410.69
5.2510.53
MEF50%,
liters/sec
5.5210.75
5.1910.56
5.23+0.48
5.09+0.65
5.3310.49
6.6810.34
6.1710.47
5.8610.35
5.1110.46
5.4610.60
5.9910.47
6.1710.67
5.60+0.64
5.6310.43
5.6810.60
6.46+0.72
6.12+0.48
6.45+0.68
6.4810.81
6.0510.57
MEF25%
liters/sec
2.7410.42
2.4610.35
2.2210.32
2.29+0.26
2.47+0.33
2.79+0.32
2.7910.18
2.75+0.30
2.48+0.31
2.68+0.31
2.6310.40
3.0210.31
2.89+0.42
2.56+0.26
2.8010.29
2.9310.50 ]
3.1610.60
3.0810.77 d
3.10+0.54
2.9910.57 J
y
a Subjects walked at approximately 40% Vg2 max from 60-90 minutes.
b Underlined values are significantly reduced (P<0.10) in ozone exposures at this time
(immediately post-exercise).
c Time is elapsed time in minutes from the beginning of ozone exposure.
^ MEF25% higher in codes 4 and 8 than in all others.
(Continued on next page.)
-------
Table 5 (continued).
PULMONARY FUNCTION CHANGES DURING 2-HOUR EXPOSURE
TO FILTERED AIR OR 0.5 ppm OZONE .
AT VARIOUS AMBIENT ENVIRONMENTAL CONDITIONS '
CODE 5
CODE 6
CODE 7
CODE 8
Time,0
min
12.5
27.5
57.5
100.0
117.5
12.5
27.5
57.5
100.0
117.5
12.5
27.5
57.5
100.0
117.5
12.5
27.5
57.5
100.0
117.5
FVC,
ml
62121366
61301416
62151401
59911392
59451386
59551274
59851316
59771302
57561355
58961411
62221396
61461472
61671430
55641443
58381414
61581385
61871369
62291395
54741354
57821275
FEV1.0'
ml
48491246
47341241
47051202
45411215
44371277
46391236
45971202
45991231
42071165
43491162
47701290
44641214
45031223
42701329
43251256
46041236
48461216
45551381
41741244
43961205
FEV2.0'
ml
57631306
57031333
57621320
54591318
53831349
55391239
55331260
55271268
51501277
53541301
57251402
56741426
54221235
50561417
52441307
55771312
55681391
56981374
50361289
52891270
FEV
htV3.0'
ml
59971351
59591414
60161387
57401382
57081394
57761248
57681291
57301292
54941332
56751383
60041400
59551467
56321246
52911454
55281350
59031403
56961358
60041399
54801285
55761287
MMEF,
liters/sec
4.9210.36
4.4810.37
4.6110.43
4.3010.32
4.1110.44
4.7110.41
4.6710.40
4.6610-40
3.9910.38
4.2510.34
4.88+0.52
4.4910.44
4.4410.44
4.3510.68
4.1010.54
4.7910.53
5.2910.51
4.6610.47
4.1110.43
4.2610.36
MEF50%,
liters/sec
5.5910.48
5.36+0.46
5.2910.48
4.9310.32
4.7910.51
5.4010.48
5.6110.51
5.3510.49
4.5010.39
4.7510.34
5.5910.47
5.43+0.54
5.2110.51
4.9010.61
4.5510.33
5.4010.66
5.46+0.63
5.19+0.54
4.5210.53
5.34+0.56
MEF25%
liters/sec
2.5510.24
2.4110.35
2.6510.40
2.36+0.42
2.45+0.40
2.40+0.25
2.84+0.55
2.4910.28
2.07+0.27
2.2710.26
2.70+0.48
2.4010.24
2.5610.32
2.32+0.51
1.9110.30
2.3410.42 ]
2.7010.41
2.8310.40 d
2.5710.50
2.5410.41 J
CM
o
Subjects walked at approximately 40% VQ
from 60-90 minutes.
Underlined values are significantly reduced (P<0.10) in ozone exposures at this time
(immediately post-exercise) .
Time is elapsed time in minutes from the beginning of ozone exposure.
MEF25% higher in codes 4 and 8 than in all others.
-------
O P. P "0
O H- W ft
W 3 O
O O rt O
3 » O 3*
(/) (A O. p
P H- O*OQ
H> 3 X »
<6 ft P H-
43* 3
ft"
jf H-p,
<0 w 3 2
x ft tn
4 3* (o 01
O O H O
H- C H- dP
"S."
0 <
' n
(D
P P
303
(D p.
a
rt (P g
3* X S
(0 (D rfl
w H n
(/>
H- O
S1^ §
H H« O.
Hj H-
rt H- rt
3* O H-
(0 p O
m
NJ
P
% CHANGE
20
10
0
-10
-20 H
20
10
0
-10
-20 H
CODES:
1-5
3-7
1-5 3-7
1-5 3-7
2-6 4-8
2-6 4-8
2-6 4-8
v^ v\
50% FLOW MMEF
MEAN OF 3 PERIODS, FIRST 60 MIN.
POST EXERCISE (at 5 MIN.)
•
POST EXERCISE (at 30 MIN.)
VITAL CAPACITY
FILTERED AIR (CODES 1-4)
0.5 ppm. 03 (CODES 5-8)
-------
P 3 O *O
(B°|8
P H- H- (ft
OQ W rt 3
(ft 3 H- rt
(X H- O
h^. *«4 ^\
rt) P O
H> H- W ST
on P
^ 0) pj y
p H-
H- H> 3
O H> (ft
O H> O TJ
HJ 3 !~*
H- O CTO
O W
3 P Tl
w H- ra
P ON) l-H
htj r+ 1 • O
rt 3* SO C
(ft (ft (•"<• 53
H 3 tn
H) P
rt H-'rt 3 M
3* HJ (D (X O4
(ft W H •
rt H- Ti
(D o m
x af o. <
(ft O W
Hj C O •
O H rt>O
H'
w p: (B H-
(ft 3 X 3
D. (ft
*T3 HP
(ft rt O i-1
H- (ft W .
O W) (ft (ft
CL (ft • h"
. OP
< 3*
H-3^ ^
C (ft P
(» H g
W (ft O*
H*
£ * (ft
(6 (ft 3
H H rt
(0 (ft
% CHANGE
20 -
10 -
0
^S
-10 -
-20 -
20 -
10 -
0 -
-10 -
-20 -
CODES:
1-5 3-7 1-5 3-7
» A
^^^^^ jfe ^^^^^ ^^
^^^f 9^^^^^ ^^^^ ^*^m
^^^™ ^^^^^ ^^^^« ^^^^^
^ »-* ^ vr>
2-6 4-8 2-6 4-8
\^ \>* V4 v*-*4
v v w^*
FEV 1 SEC. FEV 2 SEC.
• MEAN OF 3 PERIODS, FIRST 60 MIN.
^••••••H
• POST EXERCISE (at 5 MIN.)
A POST EXERCISE (at 30 MIN.)
1-5 3-7
^^
^^^^A f
^^^^^ ^^ii
^^•_ ^\. ^L
v
2-6 4-8
*** ^
FEV 3 SEC.
- FILTERED AIR (CODES 1-4)
- 0.5 ppm. 03 (CODES 5-8)
-------
Table 6. PULMONARY FUNCTION CHANGES
FOLLOWING EXERCISE AND AT END-EXPOSURE
CM
CM
a X indicates mean value for periods 1-4.
/
b Percent change is indicated for post-exercise period (P. 16) and end-exposure period (P. 18).
(Continued on'next page.)
CODE 1
CODE 2
CODE 3
CODE 4
VC, ml
FEVi.Q, ml
FEV2.o, ml
FEV3.o, ml
MEF50%, liters/ sec
MMEF, liters/ sec
VC, ml
FEVi.o, ml
FEV2.o, ml
FEVs.o, ml
MEF50%, liters/sec
MMEF, liters/sec
VC, ml
FEVi.o, ml
FEVo.O. ml
FEVs.o, ml
MEF50%, liters/sec
MMEF, liters/sec
VC, ml
FEVi.o, ml
FEV2.0, ml
FEVs.o, ml
MEF50%, liters/sec
MMEF, liters/ sec
Period
1
6034
4478
5359
5555
5.52
4.55
6287
5140
5960
6244
6.68
5.35
6393
4782
5773
6180
5.99
4.39
6144
4865
5593
5776
6.46
5.01
Period
4
^
6252
4622
5641
6035
5.19
4.71
6214
4797
5759
6098
6.17
5.09
6308
5069
6023
6242
6.17
5.40
6142
4802
5543
5735
6.12
5.18
Period
8
\j
6166
4558
5625
5995
5.23
4.19
6188
4987
5912
6212
5.86
5.03
6226
4870
5773
6066
5.60
4.79
6034
4849
5665
5948
6.45
5.11
X*
6143
4552
5542
5795
5.31
4.48
6230
4975
5877
6185
6.24
5.16
6309
4907
5856
6163
5.92
4.86
6107
4839
5600
5820
6.34
5.10
Period
16
A \J
6127
4613
5612
5937
5.09
4.39
6064
4741
5766
5992
5.11
4.56
6216
4888
5792
6124
5.63
4.84
5478
4691
5261
5470
6.48
5.64
% b
change
(P. 16)
-0.26
+1.33
+ 1.27
+2.45
-2.32
-2.08
-2.66
-4.70
-1.89
-3.12
-18.1
-11.6
-1.47
-0.39
-1.09
-0.63
-4.90
-0.41
-10.30
-3.06
-6.05
-6.01
+ 2.21
+10.59
Period
18
AW
6202
4752
5740
6010
5.33
4.63
6242
5008
6006
6225
5.46
5.09
6474
5068
6167
6482 i
5.68
4.74
i
5876
4608
5191
5963
6.05
5.25 !
1
change
(P. 18)
+0.96
+4.39
+3.57
+3.71
+0.38
+3.35
+0.19
+0.66
+2.19
+0.65
-12.5
-1.36
+2.62
+3.28
+5.31
+5.18
-4.05
-2.47
-3.78
-4.77
-7.30
+2.46
-4.57
+2.94
-------
Table 6 (continued).
PULMONARY FUNCTION CHANGES
FOLLOWING EXERCISE AND AT END-EXPOSURE
CODE 5
CODE 6
«
CODE 7
CODE 8
VC, ml
FEVi.o, ml
FEV2.0, ml
FEVs.O, ml
MEF50%, liters/ sec
MMEF, liters/ sec
VC, ml
FEV1>0, ml
FEV2.0, ml
FEV3.o, ml
MEF50%, liters/sec
MMEF, liters/ sec
VC, ml
FEVi.o, ml
FEV2.0, ml
FEV3 D, ml
MEF50%, liters/sec
MMEF, liters/sec
VC, ml
FEVi.o, ml
FEV2.0, ml
FEV3.o, ml
MEF50%, liters/sec
MMEF, liters/sec
Period
•j
6212
4849
5763
5997
5.59
4.92
5955
4639
5539
5776
5.40
4.71
6222
4770
5725
6004
5.59
4.88
6158
4604
5577
5903
5.40
4.79
Period
A
6130
4734
5703
5959
5.36
4.48
5985
4597
5533
5768
5.61
4.67
6146
4464
5674
5955
5.43
4.49
6187
4846
5568
5696
5.46
5.29
Period
6215
4705
5762
6016
5.29
4.61
5977
4599
5527
5730
5.35
4.66
6167
4503
5422
5632
5.21
4.44
6229
4555
5698
6004
5.19
4.66
X*
6186
4763
5743
5991
5.41
4.67
5972
4612
5533
5758
5.45
4.68
6178
4579
5607
5864
5.41
4.60
6191
4668
5614
5868
5.35
4.91
Period
i &
5991
4541
5459
5740
4.93
4.30
5756
4207
5150
5494
4.50
3.99
5564
4270
5056
5291
4.90
4.35
5474
4174
5036
5480
4.52
4.11
% b
change
(P. 16)
-3.15
-4.66
-4.94
-4.19
-8.87
-7.92
-3.62
-8.78
-6.92
-4.58
-17.43
-14.74
-9.94
-6.75
-9.83
-9.77
-9.43
-5.43
-11.58
-10.58
-10.30
-6.61
-15.51
-16.29
Period
18
5945
4437
5384
5708
4.79
4.11
5896
4349
% b
change
(P. 18)
-3.90
-6.84
-6.25
-4.72
-11.46
-11.99
-1.27
-5.70
5354 -3.24
5675
4.75
4.25
5838
4325
5244
5660
4.55
4.10
5782
4396
5289
5576
5.34
4.26
-1.44
-12.84
-9.19
-5.50
-5.55
-6.47
-3.48
-15.90
-10.87
-6.61
-5.83
-5.79
-4.98
-0.19
-13.24
a v~
indicates mean value for periods 1-4.
Percent change is indicated for post-exercise period (P. 16) and end-exposure period (P. 18).
-------
CM
VI
Table 7. PERIPHERAL BLOOD FLOW (ml/100 ml/min) DURING EXPOSURE
TO FILTERED AIR OR 0.5 ppm OZONE
AT VARIOUS AMBIENT ENVIRONMENTAL TEMPERATURES
Period
1
3
5
8
15a
18
1
3
5
8
15a
18
Code 1
(FA)
1.81
2.34
1.61
1.75
1.91
2.19
1.37
1.74
1.77
1.71
3.50
1.43
Code 5
(O3)
1.88
2.46
2.72
2.27
2.48
2.30
1.97
1.56
1.15
2.44
2.67
2.12
MEAN
Code
(FA)
3.92
3.20
3.21
3.68
4.74
4.64
MEAN HAND
3.72
4.59
3.53
4.35
5.61
3.97
FOREARM FLOW
2 Code 6
(03)
3.60
2.59
3.10
2.65
4.43
3.42
AND FOREARM
2.63
3.65
3.38
3.31
4.57
4.76
Code 3
(FA)
2.50
2.72
2.68
3.83
5.58
4.35
FLOW
2.51
3.19
4.19
4.41
3.53
7.15
Code 7
(03)
2.15
2.46
2.19
2.37
3.32
2.34
2.11
2.79
3.90
3.25
2.97
4.03
Code 4
(FA)
3.29
3.43
4.56
4.02
5.89
7.51
3.77
4.08
5.46
3.67
5.30
5.61
Code 8
(03)
3.76
4.53
3.88
4.56
7.79
7.57
2.49
2.93
4.58
3.86
--
3.82
a
Post-exercise (exercise period 30 minutes duration).
-------
Table 8. METABOLIC AND CARDIOVASCULAR CHANGES
DURING EXPOSURE TO FILTERED AIR OR O.S ppm OZONE
FOR 2 HOURS
U)
CODE 1
CODE 2
CODE 3
1*
ICODE 4
1
;CODE s
j
CODE 6
I
<
CODE 7
CODE 8
1
Time,
min
3
48
83*
108
3
48
83a
108
3
48
83*
108
3
48
83a
108
3
48
83»
108
3
48
83a
108
3
48
83a
108
3
48
83a
108
•
w
VBTPS'
liters/min
9.7410.74
9.32±1.23
3S.95±1.19
9.50±0.88
9.75±0.5S
9.28±0.66
36.58±0.98
9.87±0.63
10.13±0.91
9.4910.84
36.1711.15
10.3010.52
10.2711.41
11.3511.70
40.3212.72
15.1314.03
8.4810.62
8.8710.78
33.3311.68
8.7410.53
9.7210.86
10.4811.15
35.2112.11
11.48+1.14
9.4911.10
10.43+1.35
34.1912.12
9.7810.77
9.7410.96
9.9511.50
39.1211.40
14. 7811.69
v
alveol.'
liters/min
6.1610.53
5.67+0.93
27.6611.21
6.0510.67
6.1010.48
6.0310.64
30.21+1.22
6.6410.64
6.56+0.71
6.2810.68
30.3311.40
6.6910.43
6.85+1.45
7.5711.56
32.40+3.23
11.3813.47
5.2410.59
5.6010.66
27.8211.79
5.3910.40
5.8210.59
6.7111.17
29.4512.21
7.71±0.37
6.1510.96
6.7011.17
28.77+2.25
6.66+0.82
6.27+0.73
6.60+1.34
32.01+1.43
9.95+1.59
RR,
breaths/rain
16.611.1
15.5±1.6
21.411.8
16.411.7
16.611.1
15.511.7
24.612.8
16.611.6 .
15.611.5
15.811.9
22.9+2.4
17.611.8
17.8+1.7
18.611.0
27.6+4.8
19.512.3
13.6+1.5
14.411.9
22.6+2.4
16.4+1.4
14.911.1
15.812.1
23.9+3.4
18.6+3.0
15.913.4
19.113.1
29.518.0
20.6±4.8
14.9+0.9
13.4±1.6
28.916.0
18.011.7
0, uptake,
liters/min
STPD
0.3010.02
0.2810.04
1.4410.06
0.3010.03
0.3110.01
0.2910.02
1.4510.02
0.3010.02
0.3210.02
0.28+0.02
1.4210.03
0.3010.02
0.3110.03
0.3210.04
1.5510.08
0.3910.06
0.2610.02
0.26+0.02
1.3210.04
0.26+0.02
0.2810.02
0.2910.02
1.4310.07
0.33+0.03
0.26+0.02
0.2810.03
1.3110.09
0.30+0.03
0.29+0.02
0.29±0.02
1.4510.06
0.3910.04
%
V02 max
0.08+0.01
0.0710.01
0.3810.02
0.08+0.01
0.0810.01
0.08+0.01
0.3910.02
0.08+0.01
0.0910.01
0.0710.00
0.3810.02
0.0810.01
0.08+0.01
0.09+0.01
0.42+0.02
0.1010.02
0.07+0.01
0.07+0.01
0.3510.02
0.0710.01
0.0710.00
0.0810.01
0.3810.02
0.0910.01
0.0710.00
0.0810.01
0.3510.02
0.0810.01
0.0810.01
0.0810.01
0.39+0.02
0.1010.01
R
0.8310.02
0.8010.02
0.8810.02
0.8010.02
0.80+0.02
0.8010.03
0.9010.02
0.8310.04
0.8110.03
0.8710.04
0.9210.02
0.86+0.03
0.8210.02
0.8110.04
0.8810.02
0.8410.03
0.7910.03
0.8510.03
0.9210.03
0.8310.03
0.8110.03
0.83+0.03
0.8910.03
0.85+0.04
0.89+0.04
0.89+0.05
0.9210.03
0.83+0.03
0.8310.04
0.81+0.05
0.92+0.01
0.8610.04
0. pulse
4.0610.27
3.8410.40
12.2210.80
3.97i0.24
4.1210.21
3.6710.29
11.19+0.36
3.6210.28
3.8610.31
3.32+0.36
11.0010.48
3.5510.38
3.55+0.33
3.64+0.42
10.5310.73
3.4410.47
3.83+0.25
3.7310.22
11.43+0.68
3.0540.29
3.54+0.35
3.51+0.29
10.49+0.82
3.55+0.44
3.48+0.37
3.4910.32
10.36+0.79
3.53+0.33
3.68+0.38
3.27+0.20
9.62+0.69
3.4910.43
CI,
liters/
min-m
2.93+0.31
2.0310.11
8.07+0.84
2.7510.30
2.9810.21
2.6610.28
8.7810.48
2.8110.24
3.5110.33
2.82+0.27
8.85+0.58
3.38+0.38
2.7610.26
2.9410.36
9.4310.45
2.8910.28
2.7610.33
2.9610.51
8.3310.79
2.7910.17
2.6410.25
2.72+0.33
8.2910.53
2.8710.30
2.48+0.19
2.58+0.25
7.6410.54
2.78+0.19
2.7310.23
3.08+0.23
8.57+0.60
3.7910.44
HR,
beats/min
74.213.7
73.615.2
119.014.4
74.413.7
75.5+3.2
79.913.1
130.413.2
85.214.1
84.615.9
86.115.2
130.415.4
89.417.5
86.2+4.1
88.9+4.6
149.618.0
111.215.8
69.214.4
69.1+4.0
116.514.2
83.9+4.9
80.014.0
83.2+5.0
137.914.3
94.8+5.5
77.4+4.7
80.414.2
127.4+4.4
86.4±2.9
82.817.8
88.616.2
153.4+7.2
113.7+9.2
to
-------
Table 8. (Continued)
Blood pressure, torr
Systolic
120±5
120±4
133+6
12013
117±4
122±4
131 ±3
119±4
119±2
119±3
138±6
118±3
116±3
116±4
13S+S
112±4
115±2
11614
134±4
117±4
113±3
114±4
134±5
114±3
121±3
116i3
127+2
114+3
119+4
119+4
* A ^«— ^
135*8
J» «/J— W
113i6
Oiastolic
81.013.2
85.214.4
71.2±1.7
80.0±3.2
81.212.3
85.6±2.4
78.1±2.7
83.3+2.9
79.212.2
82.113.5
70.714.3
82.712.1
81.112.8
83.212.0
78.219.5
77.312.3
78.813.0
79.812.0
77.313.3
77.812.3
83.212.5
84.015.1
74.418.6
81.914.4
82.212.3
81.212.0
70.0+6.0
78.912.6
84.6+3.8
84.913.2
79.615.9
76.313.4
TPR,
-5
dyn-sec cm
13861145
19371178
4961117
14261191
13371152
1492+180
463116
13741169
11531134
14361129
455+45
12311174
1474+214
1459+196
434+63
135S1204
14441198
13511136
4801111
1356+83
15191150
15221191
427118
13431139
16021148
1540+122
461+69
1354171
1482+162
1313+99
483157
10121125
cwf
kg>m/min
9.5211.75
6.5610.25
29.9117.59
9.0611.31
9.2810.69
9.2811.19
29.6811.65
9.4711.05
10.8610.94
8.8710.80
31.4711.51
10.6511.26
8.02+0.82
9.0311.12
34.6911.21
8.71+1.12
8.3010.99
9.17+1.04
30.6415.06
8.80+0.79
8.0010.85
8.1610.90
32.0610.71
9.0511.05
8.2110.81
7.9510.71
28.0012.37
8.6910.69
8.84ld.91
9. 77+0. 85
30.56+2.06
11*. 6211. 67
Index of left
ventricular
function
(SPxHRxlflS)
9.3211.03
8.7311.13
1.68+0.68
8.9210.61
9.3510.78
9.8910.59
17.3210.88
10.6210.76
9.5810.46
9.8210.42
17.9011.18
10.8510.88
9.9010.47
10.7610.65
21.0710.87
12.0910.56
8.44+0.75
8.0210.60
16.5410.64
9.3510.95
8.9410.64
9.3210.82
17.9111.01
11.0811.10
9.46+0.55
9.5010.57
15.6310.78
9.84+0.50
10.61+0.87
11.1511.09
20.8711.88
12.5911.07
Dk:o
18.011.5
22.713.3
51.1+3.7
19.612.6
19.712.7
22.213.2
52.015.7
24.415.4
20.911.5
22.212.2
48.612.5
21.311.4
22.312.6
22.812.3
53.216.1
30.913.4
22.211.6
20.411.7
49.412.6
22.211.7
19.513.2
16.112.0
48.415.9
18.413.5
20.913.5
22.2+2.8
52.715.0
19.812.9
21.112.5
18.6+1.7
52.214.3
22.314.9
V4
1.1310.14
1.37+0.43
1.77+0.15
1.15+0.16
1.09+0.16
1.2410.18
1.8010.18
1.2610.18
0.9510.11
1.17+0.12
1.80+0.15
1.1310.13
1.4310.50
1.52+0.40
1.8110.24
2.1610.69
1.10+0.27
1.0410.20
1.8510.26
1.0110.10
1.2610.25
1.2910.30
1.8210.23
1.4810.26
1.32+0.23
1.37+0.25
1.94+0.28
1.32+0.22
1.17+0.08
1.16+0.30
1.9810.18
1.4010.25
Diff.
Perf.
3.1610.33
4.79+0.93
3.25+0.32
3.77+0.46
3.1710.41
4.3010.64
2.9710.41
4.59+0.85
3.1110.32
4.08+0.36
2.88+0.22
3.5510.47
4.4210.54
4.2610.55
3.0410.54
6.11+1.13
4.1710.52
3.4010.39
2.8510.29
4.0610.42
3.98+0.97
2.8810.57
3.0210.47
3.5710.76
4.5810.94
4.5410.59
3.37+0.43
3.85+0.71
4.07+0.56
3.12+0.24
3.2810.45
2.9610.48
T
re'
°C
37.3+0.1
37.2+0.1
37.610.1
37.6+0.1
37.310.2
37.2+0.2
37.710.1
37.810.1
37.210.1
37.210.1
37.710.1
37.8+0.1
37.1+0.1
37.210.1
37.810.1
38.0±0.1
37.2+0.2
37.110.1
37.510.1
37.5+0,1
37.2+0.1
37.210.1
37.7+0.1
37.8+0.1
37.1+0.1
37.1+0.1
37.5+0.1
37.6+0.1
37.2+0.2
37.210.2
37.810.2
38.210.1
V
°C
35.4+0.1
35.410.1
35.7+0.2
36.0+0.1
35.9+0.2
36.210.2
36.5+0.1
36.610.1
36.210.1
36.4+0.1
36.8+0.1
36.710.1
36.210.2
36.610.1
37.110.2
37.210.2
35.410.2
35.5+0.1
35.810.1
36.010.1
36.010.1
36.210.1
36.610.1
36.710.1
36.0+0.1
36.210.1
36.6+0.1
36.610.1
36.3+0.2
36.6+0.1
37.2+0.2
37.510.2
Tissue
conductance ,
kcal/
ra2.h-l.oc-l
8.210.5
8.310.9
41.312.5
9.911.2
12.0+0.5
15.3H.7
68.614.4
13.3+1.3
16.4+1.4
19.111.6
82.8+5.9
16.212.0
19.4+2.9
28.315.8
141.8134.1
29.8+7.9
7.8+0.7
8.511.0
42.4+3.2
9.1+0.8
11.2+0.8
14.7+1.1
68.8+3.6
15.511.2
12.3+1.1
17.0+1.9
77.7+6.8
14.8+1.3
17.8+1.6
24.8+2.6
136.3115.8
30.4+4.8
to
0)
60
O)
6
O
1
in
-------
Temperature Effects
Several significant changes occurred as a result of heat stress
and were found irrespective of the presence of ozone. Ventilation
(VE BTPS) was higher in condition B4 (the most severe heat stress as
judged by WBGT index) than in all other conditions. This was accompanied
by a higher oxygen consumption in B4 than in Bl or B3, the less severe
•
thermal stress conditions. Despite the compensating increase in Vg2
in the hot environment, the oxygen consumed per heart beat (oxygen
pulse) was higher in the coolest environment, Bl. As expected, the
rectal temperature (T ), mean body temperature (Tfe), and mean skin
temperature (T ,)were higher in the hotter environment. The Trg was
significantly higher in B4 than in Bl. However, Tgk showed a progressive
rise with increasing heat stress, B4 > B3 > B2 > Bl. Mean body
temperature showed a similar progressive rise except that B2 and B3
were not significantly different, B4 > B3, B2 > Bl. The increased
heat stress is reflected in a higher tissue conductance. The combination
of increased body temperature and increased ventilation resulted in
a significantly higher respiratory heat loss in condition B4. When
correlated with web bulb globe temperature index (WBGT), rectal
temperature showed a significant linear correlation (P < 0.01)
(r = 1.00). Oxygen pulse (r = -0.96) and mean body temperature
(r = 0.97) were also significantly correlated with WBGT. These
findings are supported by an analysis of variance which indicated
a rise of rectal, mean skin, and mean body temperature with increasing
thermal stress, as anticipated.
Clinical Observations
Effects of the environment on the normal human are manifested
frequently as signs and symptoms referable to the particular
physiological system affected. When young adult males are exposed
for two hours to an environment containing 0.5 ppm of 0_ and made to
work at varying levels of ambient heat and humidity, they develop
symptoms and signs mainly in the mid-respiratory tract. These
consist of substemal discomfort, dryness of the throat, difficulty
in deep inspiration, tenderness of the trachea, occasionally chest
38
-------
pain, cough and auscultatory rales. General symptoms also may
occur and consist of slight nausea, dizziness, headache, and syncope,
Fifty-eight observations on eight subjects exposed to all
ambient temperatures and ozone led to a meaningful deduction that
exposure as described produces one or more of the above clinical
symptoms. A chi-square analysis gave x = 25.5; P < 0.01. The
following summarization presents this data:
Filtered
Air
0.5 ppra
0,
No symptoms
Symptoms
25
23
When we look at the data relating the various ambient conditions
to symptoms singly or in combination, it is apparent that at condition 8
[ambient temperature (T ) = 40°C, relative humidity (rh) = 80%,
A
0.5 ppm 0-] symptoms occurred 20 times in eight runs, whereas at
code 4 (T = 40°C, rh = 80%, FA) symptoms appeared twice and neither
cl
time were they referable to the respiratory tract (Fig. 3). Also to
be noted is the high number of subjects (7) with general symptoms on
exposure to ozone with high heat and humidity. Thus it would appear
that a hot, humid environment containing 0.5 ppm 0_ produces distinct
signs and symptoms of respiratory tract dysfunction, in combination
with evidence of general stress response. The presence of 0_ seems
to contribute to the latter by its specific effects on the respiratory
tract.
The nature of the respiratory symptoms suggests that the ozone
affects mainly the components of the mid-respiratory tract
(laryngotracheal and bronchial). Somewhat surprising is the absence
of symptoms in the conjunctivae, the nasal passages, and the oropharynx.
This contrasts with effects produced by peroxyacetylnitrate (PAN),
where eye symptoms and nasal congestion are seen early in exposure.
When general symptoms occurred (nausea, syncope, weakness, dizziness),
39
-------
rt 11
O H
n>
H-X
OQ
3- O
rt HI
O O
O I—
3 M.
CL 3
M- H-
rt O
H- (a
O !-•
3
(A (A
O rt
C O
H 3
_
H- O
H- cr
rt w
(D (D
CX (D
P.
P>
H- O
H O
P U)
3 (D
O-X)
81!
rt
O O
•
tn »
O H
N 0)
O
(D
25-
(0
m
10-
IW
(O
„
z
0
20
16
13
10
234
FA
5678
0*
-------
they subsided on terminating exposure in the chamber, or very soon
afterward. Headache persisted up to 12 hours in two subjects. Two
other subjects noted persistence of substernal tightness.
The following protocol abstracts provide examples of runs under
the most stressful conditions:
EXPERIMENT NO. 7707
Code 8 (T = 40°C, rh = 80%, 0.5 ppm 0_)
cL O
Time: 1230 -- Pre-exposure blood drawn. No symptoms. Chest clear.
Tre = 37.4°C, HR = 72.
1315 — Into chamber. HR = 90.
1400 — Tre = 37.6°C, HR = 113. Sweating on torso.
1432 — Start walk. Trg = 37.6°C, HR = 93.
1450 — T = 37.8°C, HR = 150.
1500 -- Face flushed. Sweating = 2 plus. T = 38.0°C,
HR = 170.
1502 — End walk. Feels ok but "hot."
1510 -- Occasional cough. Breathing "hot" (in chamber).
Tre = 38.4°C, HR = 120.
1520 — Sweating = 3 plus. Flushed. Tre = 38.5°C, HR = 120.
1530 — Deep breath hurts. Out of chamber. Feels tired and hot.
No other respiratory symptoms. Exam normal except for
flushed face.
1540 — Post-exposure blood drawn. Follow-up normal.
EXPERIMENT NO. 7700
Code 7 (T = 35°C, rh = 40%, 0.5 ppm 0,)
a ^
Time: 1315 — No symptoms. No cold. Chest clear. Pre-exposure
blood drawn.
1342 -- Into chamber. T = 37.0°C. Orone exposure at 1352.
376
1440 — T = 37.2°C, HR = 87.
1455 - Start walk. HR = 90, T = 37.4°C.
r c
1500 -- HR = 118, Tre = 37.8°C.
1525 — End walk. HR = 150, Tr£j = 38.0°C. Coughing moderately.
Tight chest.
41
-------
EXPERIMENT NO. 7700
(CONTINUED)
Time: 1530 -- Frequent cough during pulmonary function tests.
1532 — Slight nausea. Slight pallor. Coughing. BP = 108/65,
HR = 140.
1535 — Frequent yawning.
1540 — Final period. Slight recovery from symptoms. Less
coughing. Feels better but still pale.
1555 — Out of chamber. Much improved. Chest clear. No rales
after cough but breath sounds exaggerated.
1600 -- Post-exposure blood drawn.
FOLLOW-UP NOTE: 2/26/75 — Felt chest tightness till 6 p.m. that night.
Slept ok. No cough.
Four of these subjects had spent their childhood and youth in a
smoggy area of California (Pomona, Pasadena, or Century City); the
others in various parts of the United States. All the subjects were
nonsmokers.
Subjective Analysis of Ozone Exposures
All subjects answered a questionnaire at the end of each exposure.
The questionnaire contained 33 questions concerning the subject's
physical and psychological feelings following the experiment. The
questionnaire was divided into three distinctive areas. The first
dealt with physical factors (dryness of the throat or irritation of
the eyes, etc.), the second was concerned with central nervous
system changes (fatigue, lack of energy, etc.), while the third
related to psychological states (pleasure, happiness, anxiety, or
depression.
The data obtained from this questionnaire was analyzed by a
two-factor analysis of variance (pollutants x ambient air condition).
The results demonstrated several significant changes in subjective
responses as a function of ozone, but not as a function of ambient
temperature; nor were there any interactions between the two. The
significant changes found as a function of ozone were for the most
42
-------
part in the physical portion of the scale which showed an overall
difference at the 0.05 level of significance. More specifically,
subjects felt significantly more chest tightness, throat irritation,
headaches, heart pounding and, overall, less comfortable. There was
a lack of complaints of eye irritation as a function of the ozone
exposures.
Subjects felt significantly less vigorous, less refreshed, less
energetic and reported greater dizziness as a function of the ozone
treatments as compared to filtered air (P < 0.05). There were no
significant changes in psychological state accompanying ozone
exposure. This was evident on questions concerning pleasure, happiness,
anxiety, and depression, which failed to differentiate any of the
treatment conditions.
Overall it appeared that the subjects' feeling about his physical
state correlated rather well with the pulmonary changes as a function
of ozone exposure. On the other hand, the subjects' complaints of
fatigue and lack of energy appear to be of a CNS origin, as the
metabolic data do not corroborate a higher level of work performed
under exposure to ozone.
DISCUSSION
Pulmonary Function
N
Overall, ozone had a marked effect on the lung, causing a reduction
in vital capacity, primarily a result of a decreased inspiratory capacity,
as well as a decline in maximum expiratory flow throughout the full range
of vital capacity.
A decline in vital capacity could occur as a result of a decreased
maximum inspiration or a rise in residual volume. A decrease of
inspiratory capacity does not rule out the latter, as this could be a
result of an increase in mean chest position as suggested by Silverman
et al. (unpublished). However, the lack of a significant increase in
residual volume would seem to confirm that the decrease in inspiratory
capacity was the result of a decreased maximal inspiration despite a
43
-------
small (100 ml) but significant increase in functional residual capacity.
A decline in TLC is consistent with the findings of Clamann and Bancroft
(60) as well as some of the subjects studied by Silverman et al. (61).
However, Hazucha et al. (43) found the decline in vital capacity in
their subjects was due to an increase of residual volume with no
significant change in the total lung capacity. It is not clear whether
this change is dependent on the type of ozone exposure; more specifically
could it depend on the amount and type of exercise performed, the
temperature and humidity conditions during exposure, or the concentration
of ozone present in the chamber atmosphere? The evidence from this study
and others (27, 60, 61) would support the view that a decrease of vital
capacity can occur as a result of a limitation of maximum inspiration.
The difficulty noted in taking a deep breath would suggest that the
decreased maximum inspiration may result from voluntary limitation of
inspiratory effort due to discomfort caused by ozone stimulating the
tracheo-bronchial irritant receptors. Whether or not this limitation
may be overridden in exceptionally well motivated subjects is open to
question. We made every effort to ensure that our subjects performed
the vital capacity maneuvers to the best of their ability, however it
could not be determined whether their effort was voluntarily or
physiologically limited.
The influence of the environmental conditions during exposure on
the ozone-induced decrease in vital capacity is partially clarified in
this study. When ozone exposure was combined with heat stress, the
greatest decline in VC occurred, suggesting that ambient temperature
and humidity are important in the degree of effect experienced during
ozone exposure. Whether the thermal effect is synergistic with ozone
or whether the effects of temperature and humidity are merely additive
is not clear. A decline in VC was also observed in condition B4
when no ozone was present, which indicates that increased heat and
humidity alone can result in a decrease in vital capacity. The cause
of this change is unclear. There is some possibility of a rise in
central blood volume as a result of heat stress but if such a blood
volume increase occurred, an increase in residual volume would be
expected, and this was not found. The lack of a decline in inspiratory
44
-------
capacity or in total lung capacity makes this decline in vital capacity
more difficult to explain - possibly a nonsignificant change in both
measures contributed to a significant change in VC.
The maximum expiratory flow is similar to that found in other
studies (27, 42, 61). It may be significant, however, that the largest
change occurred after the exercise period. A decline in FEV, n, MMEF,
JL • w
or MEF50% is generally attributed to an increase in large airways
resistance. This is most likely a result of a reflex bronchoconstriction
secondary to stimulation of tracheo-bronchial irritant receptors. An
increase in Raw measured at FRC would support this view. The decline in
FEV1 Q (5.8%) and in MEF50% (14.6%) is of the same order of magnitude
that would be expected when an effective dose is calculated using the
formula of Silverman et al. (61) (i.e. in this study effective dose =1.5
rest dose). That the subjects did not voluntarily limit their expiratory
effort is confirmed by the lack of change in FEV/VC ratio. However, a
decline in MW regardless of exposure conditions may suggest a lack of
motivation following 2 hours of test procedures despite the encouragement
given for this effort.
It is interesting that the greatest change in pulmonary function
occurred immediately after the exercise period (Table 6). The results
of other studies would suggest a slight improvement in some pulmonary
function measures (notably FEV, Q) immediately following exercise (62).
In the control condition (code 1), there was either no change (VCT or
a slight increase (FEV, Q - 0 ? 0) in the measured function. With
ozone exposure, there was a more marked decrease in vital capacity and
FEV, _ immediately after exposure. In the subsequent measurement
J. • U
period (-25 rain post exercise) many of the changes had begun to show
improvement despite continued exposure to ozone. There is some
similarity between the observed decline in FVC and FEV\ _ following
exercise and that observed in exercise-induced asthma (63). With
this affliction, the greatest decline in FVC and FEVj Q occurs within
5-10 min following exercise and then begins to return towards "normal."
The significant decrease in work \Q during all ozone exposures
•
could be a real occurrence or an error due to calculation of Vg2 by
45
-------
the Haldane transform, which would not account for an increased
inspired 0- due to possible excess 02 entering the room consequent
to generation of 0- from 100% 00. If the latter were true, then
•j 2
inspired 0. would have to be 21.34-21.44% rather than the ambient
value of 20.93%. Such differences in inspired oxygen concentration
could not be demonstrated by analysis of the oxygen content of the
room by either Haldane or gas chromatographic analysis. The highest
value so obtained was 20.99% 02 — insufficient to explain the
•
differences observed. If such 0 changes had occurred, Vo2 at
rest and post-exercise should have shown a decline in 0_ atmosphere.
Although occasionally the 0_ values were lower, they were also the
<3
same or higher. No statistical differences were noted at these
rest periods in contrast to the significant difference (P < 0.05)
during exercise.
The lack of a significant change in any cardiovascular
parameters as a result of ozone exposure is not surprising in
light of the instability of ozone and the probability that it does
not reach the circulation as molecular 0_. Despite suggestive
changes in red cell enzymes (64) which demonstrate some extrapulmonary
effect of ozone, there is no significant effect on the cardiac output
or heart rate either at rest or during exercise. It should be noted
that the cardiac output and heart rate are fairly crude indices of
function or control in the cardiovascular system and we are unable
to rule out more subtle changes in the cardiovascular system which
may occur over longer periods of exposure to ozone.
46
-------
SECTION VIII
REFERENCES
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health of the 1966 Eastern seaboard ai-r pollution episode. Arch.
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47
-------
11. Stokinger, H. E. Toxicological interactions of mixtures of air
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48
-------
21. Wikka, S. Ozone: Its physiologic effects and analytic determination
in air. Acta Chem. Soand. 5: 1359-1367, 1951.
22. Griswold, S. S., L. A. Chambers, and H. L. Motley. Report of a
case of exposure to high ozone concentrations for 2 hours. A.M.A.
Arch. Ind. Health 15: 108-118, 1957.
23. Goldsmith, J. R., and J. A. Nadel. Experimental exposure of
human subjects to ozone. J. Air Pollut. Control Ass. 19: 329-330,
1969.
24. Hallett, W. Y. Effect of ozone and cigarette smoke on lung function.
Arch. Environ. Health 10: 295-302, 1965.
25. Young, W. A., D. B. Shaw, and D. V. Bates. Effect of low
concentrations of ozone on pulmonary function. J. Appl. Phyeiol.
19: 765-768, 1964.
26. Stockinger, H. E. Toxicity of airborne chemicals: Air quality
standards - a national and international view. Annu. Rev.
Pharmacol. 12: 407-422, 1972.
27. Bates, D. -V., G. M. Bell, C. D. Burham, M. Hazucha, J. Mantha,
L. D. Pengelly, and F. Silverman. Short-term effects of ozone on
the lung. J. Appl. Physiol. 32: 176-181, 1972.
28. Brinkman, R., and H. B. Lamberts. Ozone as a possible radiomimetic
gas. Nature 181: 1202-1203, 1958.
29. Lagerwerff, J. M. Prolonged ozone inhalation and its effects on
visual parameters. Aeroepace Med. 34: 479-486, 1963.
30. Mosher, J. C., W. G. Macbeth, M. J. Leonard, T. P. Mullins, and
M. F. Brunelle. The distribution of contaminants in the Los
Angeles basin resulting from atmospheric reactions and transport.
J. Air Pollut. Control Ass. 20: 35-42, 1970.
31. National Air Pollution Control Administration. Air Quality Criteria
for Photochemical Oxidante. Publication AP-63. March 1970,
Department of Health, Education, and Welfare.
49
-------
32. Scheel, L. D., J. Dobrogorski, J. T. Mountain, J. L. Svirbely, and
H. E. Stokinger. Physiologic, biochemical, immunologic and
*
pathologic changes following ozone exposure. J. Appl. Fhysiol.
14: 67-80, 1959.
33. Stokinger, H. E. Evaluation of acute hazards of ozone and oxides
of nitrogen. A.M.A. Arch. Ind. Health 15: 181-190, 1957.
34. Purvis, M. R., S. Miller, and R. Ehrlich. Effect of atmospheric
pollutants on susceptibility to respiratory infection. J.
Infect. Vis. 109: 238-242, 1961.
35. Chow, C. K., and A. L. Tappel. Activities of pentose shunt and
glycolytic enzymes in lungs of ozone-exposed rats. Arch. Environ.
Health 26: 209-216, 1973.
36. Freeman, G., R. Stephens, D. L. Coffin, and J. F. Stara. Changes
in dogs' lungs after long-term exposure to ozone. Arch. Environ.
Health 26: 209-216, 1973.
37. Heuter, F. G., and M. Fritzhand. Oxidants and lung biochemistry.
Arch. Int. Med. 128: 48-53, 1971.
38. Matsumura, Y., K. Mizuno, T. Miyamoto, T. Suzuki, and Y. Ashima.
The effects of ozone, nitrogen dioxide and sulphur dioxide on
experimentally induced allergic respiratory disorders in guinea
pigs. Amer. Rev. Eespir. Die. 105: 262-267, 1972.
39. Yokoyama, E., and R. Frank. Respiratory uptake of ozone in dogs.
Arch. Environ. Health 25: 132-138, 1972.
40. Vaughan, T. R., L. F. Jennelle, and T. R. Lewis. Long-term
exposure to low levels of air pollutants. Arch. Environ. Health
19: 45-50, 1969.
41. Stokinger, A., W. Wagner, and P. Wright. Studies of ozone
toxicity I. A.M.A. Archives Ind. Health 14: 158-162, 1956.
42. Folinsbee, L. J., F. Silverman, and R. J. Shephard. Exercise
responses following ozone exposure. J. Appl. Physiol. 38: 996-1001,
1975.
50
-------
43. Hazucha, M., F. Silverman, C. Parent, S. Field, and D. V. Bates.
Pulmonary function in man after short-term exposure to ozone.
Arch. Environ. Health 27: 183-188, 1973.
44. Consolazio, C. F., R. E. Johnson, and L. J. Pecora. Physiological
Measurements of Metabolic Functions in Man. McGraw-Hill Book Co.
Inc., New York, 1963, pp. 1-98.
45. Brickwedde, F. G. Temperature: Its Measurement and Control in
Science and Industry. Vol. Ill, Parts 1 and 2. Rhienhold Publishing
Corp., New York, 1962.
46. Defares, J. G. Determination of PVCOo from the exponential rise
during rebreathing. J. Appl. Physiol. 13: 159-164, 1958.
47. Jenous, R., G. Lundin, and D. Thomson. Cardiac output in healthy
subjects determined with a CO- rebreathing method. Acta Fhysiol.
Scand. 59: 390-399, 1963.
48. Klaus en, K. Comparison of C02 rebreathing and acetylene methods
of cardiac output. J. Appl. Fhysiol. 20: 763-766, 1965.
49. Whitney, R. J. The measurement of volume changes in human limbs.
J. Physiol. 121: 1-27, 1953.
50. Filley, G. F., D. J. Macintosh, and G. W. Wright. Carbon monoxide
uptake and pulmonary diffusing capacity in normal subjects at "
rest and during exercise. J. Clin. Invest. 33: 530-539, 1954.
51. Bates, D. V., N. G. Boucot, and A. E. Dormer. The pulmonary
diffusing capacity in normal subjects. J. Physiol. (Lond.)
129: 237-244, 1955.
52. Kory, R. C., R. Callahan, H. G. Basen, and J. C. Synes. The
Veterans Administration. - Army cooperative study of pulmonary
function. Amer. J. Med. 30: 243-258, 1961.
53. Travis, D. M., M. Greens, and H. Dan. Simultaneous comparison of
helium and nitrogen expiratory "closing volumes". J. Appl. Physiol.
34: 304-308, 1973.
51
-------
54. Linn, W. S., and J. D. Hackney. Nitrogen and helium "closing
volumes" simultaneous measurement and reproducibility. J. Appl.
Physiol. 34: 396-399, 1973.
55. Becklake, M., M. Leclerc, H. Strobach, and J. Swift. The NZ
closing volume test in population studies: sources of variation
and reproducibility. Am. Rev. Respir. Dis. Ill: 141-147, 1975.
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volume measurements in normal man. Am. Rev. Respir. Die. Ill:
135-140, 1975.
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Air Pollutants. USPHS #999-AP-ll, May, 1965.
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Function in Man (Ph.D. thesis). Montreal: McGill University, 1973.
59. Winer, B. J. Statistical Principles in Experimental Design.
2nd. ed. New York: McGraw-Hill, 1971.
60. Clamann, H. and R. Bancroft. Toxicity of ozone in high altitude
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changes in ozone: Interaction of concentration and ventilation.
Submitted August 1975.
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1969.
63. Fitch, K. and A. Morton. Specificity of exercise in exercise-
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64. Buckley, R., J. Hackney, K. Clark, and C. Posin. Ozone and human
blood. Arch. Environ. Health 30: 40-43, 1975.
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Cited by Stokinger, H., Ozone toxicology. Arch. Env. Health 10:
719-731, 1965.
52
-------
66. Challan, R. J., D. Hickish, and J. Bedford. Investigation of
some health hazard in inert gas tungsten-arc welding shop. Brit.
J. Indust. Med. 15: 276-282, 1958.
67. Siegel, S. Nonparametric Statistics for the Behavioral Sciences.
McGraw-Hill, New York, 1956, p. 166.
53
-------
SECTION IX
GLOSSARY OF TERMS, ABBREVIATIONS, AND SYMBOLS
(1) RESPIRATORY MEASUREMENTS
Parameter and Formula
1. Ventilatory Volume
(a) V (uncorrected volume)
310
,., „,,„_
Cb) V BTPS =
(c) VE STPD = V£ x
h gas
P
- w
Abbreviation
Units
BP - WVP
BP - 47
273
273 + gas temp. E
BTPS
STPD
liters/min
liters/min
liters/min
2. Respiratory Rate
3. Tidal Volume
V£
RR
4. Ventilatory Equivalence Ratio
V,. BTPS
P, = barometric
bar
pressure
P = water vapor
w pressure at
the gas temp.
RR or £T
breaths/min
ml/breath
V BTPS/VO, liters breathed
C £• ^ « M_ ^\
Oxygen Uptake
liters 0,
54
-------
(2) METABOLIC MEASUREMENTS
Parameter and Formula
Abbreviation
Units
1. Oxygen Uptake
(a)
VE STPD x True
100
VE STPD x True OJ& x 1000
100 x Pre Wt
VE STPD x True 02% x 1000
100 x Lean Body Mass
Vo2 liters 02/min
ml
)2 ml Oj/LBM-min"1
2. True Oxygen
(%N2 x 0.265) - %02 in expired air
True 0,
3. Respiratory Exchange Ratio
% Expired C02 C02 Production
or
% Expired 02 Oxygen Uptake
VEC02
no units
4. Excess Carbon Dioxide
V£ STPD x
(%C02 Expired - 0.03) .
100
- VQ2 * 0.75
Excess CO- liters
5. Maximal Aerobic Power
and/or
Maximal Aerobic Capacity
(The largest value of oxygen uptake obtained
when a subject performs maximal exhaustive
work.)
55
•
V02 max
liters/min
ml 02/kg'min"1
V
ml O^/LBM-min"1
-------
Parameter and Formula
6. Percent of Maximal Oxygen Uptake
Abbreviation Units
%Vo
2 max
x 100
'2 max
7. Energy Production
cal/liter 02 = 1.27604 x R + 3.82041
(a) = cal/liter 02 x 60 x liter 02/min
(b) =
Pre Wt, in kg
BSA
(d) = c x 1.163
(3) CARDIOVASCULAR
1. Cardiac Output = Stroke Volume x HR
vo.
cao2 - cvo2
2. Cardiac Index
Body Surface Area, in m2
M
M
M
M
kcal/h
kcal/kg-h"1
kcal/m2^"1
watts/m2
liters/min
CI liters/min-m"2
Body Surface
Area = BSA
56
-------
Parameter and Formula
Abbrevi ati on Units
3. Cardiac Work
CW kg'm/min
SP x 13.6 x
1000
4. Heart Rate
HR, f_ beats/min
5. Stroke Volume
SV
ml/beat
Q
I^^^B^M
HR
6. Stroke Index
SI ml/beat-m~2
SV
^^•^^^^
BSA
7. Stroke Work
SW g-in/beat
SP x 13.6 x SV
1000
8. Oxygen Pulse
0, Pulse ml 02/beat
1000
HR
57
-------
Parameter and Formula
Abbreviation
Units
9. Arteriovenous Oxygen Difference (a - v)02 diff. ml 02/liter blood
1000
10. Systolic Pressure (Arterial)
SP, P
sys
torr
11. Diastolie Pressure (Arterial)
DP- Pdias
torr
12. Mean Blood Pressure (Arterial) MBP, P.
bl
torr
SP - DP
DP
13. Pulse Pressure
PP
torr
SP - DP
14. Total Peripheral Resistance
TPR
dyn'sec cm~5
1.333 x 60 x MBP
(4) PULMONARY
1. Forced Vital Capacity
FVC (ml, ml/kg) ml/m2
58
-------
Parameter and Formula
Abbreviation
Units
2. Timed Forced Expired Volumes
(1.0, 2.0, and 3.0 seconds)
FEV
1.0
FEV.
2.0
FEV
3.0
ml
3. Forced Expired Volumes as a FEV. _/%FVC
percentage of Forced Vital Capacity
FEV Q/%FVC
FEV
1.0
x 100
FVC
FEV3>0/%FVC
4. Inspired Capacity
1C
ml
5. Expiratory Reserve Volume
ERV
ml
6. Functional Residual Capacity
FRC
ml
7. Residual Volume
RV
ml, ml/kg, ml/in2
8. Total Lung Capacity
VC + RV
TLC
ml, ml/kg, ml/m2
9. Residual Volume/Percent Total
Lung Capacity
RV
TLC
x 100
RV/%TLC
10. Maximal Mid-Expiratory Flow
MMEF
liters/sec
59
-------
Parameter and Formula
Abbreviation
Units
11. Maximal Voluntary Ventilation
12. Maximal Expiratory Flow
50% of Vital Capacity
13. Maximal Expiratory Flow
25% of Vital Capacity
MW
MEF50%
MEF25%
(5) HEMATOLOGIC
1. Hemoglobin
2. Hematocrit
3. Plasma Proteins
4. Lactate
5. Carboxyhemoglobin
HbCO (vol%)
Hb
Hct
Hla
HbCO
x 100
Hb (g%) x 1.39
(6) TEMPERATURE REGULATORY
1. Rectal Temperature
2. Forehead Temperature
3. Arm Temperature
4. Finger Temperature
5. Thigh Temperature
liters/min
liters/sec
liters/sec
mMoles/liter,
%
mEq/liter
%, vol%
T
re
T
'hd
T
arm
Tfing
T
'thi
°C
°c
°c
°c
°c
60
-------
Parameter and Formula
6. Calf Temperature
7. Chest Temperature
8. Toe Temperature
9. Room Temperature
10. Air Temperature
11. Radiant Temperature
12. Globe Black Temperature
13. Wall Temperature
14. Wet Bulb Temperature
15. Mean Skin Temperature
Tsk=0-07Thd+0-36Tch+0-05Tfing
Abbreviation
calf
lch
toe
rm
g
wall
wb
sk
Units^
°C
°C
°C
°C
°C
+ 0.20 T...
tni
16. Mean Body Temperature
0.65 Tre + 0.35 T~sk
17. Body Heat Content
Pre Wt x 0.83 f.
BSA
18. Wet Bulb Globe Temperature Index
0.3Tg+0.7Twb
61
BHC
WBGT
kcal/m2
O/-i ft
C(°F)
-------
Parameter and Formula
19. Tissue Conductance
kcal/m2^"1 Energy Prod
Abbreviation
Units
kcal/m2^"1-^"1
T - T
're sk
Tre - Tsk
BSA
22. Skin Evaporative Heat Loss
g/h
20. Respiratory Evaporative Water Loss Resp.
V BTPS x factor x 60 L°SS
c
(The factor is determined from density
steam tables and is dependent on temp.
of expired gases.)
21. Respiratory Evaporative Heat Loss Resp. Heat Loss kcal/m2'h
Resp. H20 Loss x 0.58
Evap. Heat Loss kcal/m2^"1
[Pre Wt - Post Wt - Resp. HO Loss - Excess CO- (g)] x 0.580
BSA
62
-------
ALPHABETICAL LIST OF ABBREVIATIONS AND SYMBOLS USED
(a - v)02 diff. arteriovenous oxygen difference
alveol. (A) alveolar
AQS air quality standards
BHC body heat content
BMR basal metabolic rate
BP blood pressure
BSA body surface area
BTPS body temperature and pressure,
saturated with water vapor
cal calorie (s)
C 0- arterial oxygen content
CI cardiac index
cm centimeter (s)
CNS central nervous system
CO carbon monoxide
C02 carbon dioxide
CV closing volume
C 0- venous oxygen content
CW cardiac work
°C degree (s) Celsius
°F degree (s) Fahrenheit
diff. difference
D diffusion capacity to carbon monoxide
LCO
DP diastolic pressure
dyn dyne(s)
ERV expiratory reserve volume
63
-------
evap. evaporative
FA filtered air
fc cardiac frequency (same as HR)
FEV forced expired volume
FEV, 0 forced expired volume (1.0 second)
FEV, n forced expired volume (2.0 seconds)
-------
maximal expiratory flow
MEF25% maximal expiratory flow
at 25% of vital capacity
MEF50% maximal expiratory flow
at 50% of vital capacity
milliequivalent(s)
min minute (s)
ml milliliter(s)
MMEF maximal mid expiratory flow
mMoles millimoles
MW maximum voluntary ventilation
N£ nitrogen
NO oxides of nitrogen
^^
02 oxygen
0, ozone
P probability of wrongfully rejecting the
null hypothesis (level of significance)
P. barometric pressure
P water vapor pressure
W
PAN peroxyacetylnitrate
% percent
perf. perfusion
PP pulse pressure
ppm parts per million
press . pressure
prod. production
Q cardiac output
65
-------
R respiratory exchange ratio
R airway resistance
aw
RBC red blood cell
resp. respiratory
rh relative humidity
RR respiratory rate (same as fR)
RV residual volume
s, sec second(s)
SE standard error
SI stroke index
SO sulfur oxides
A
SP systolic pressure
STPD standard temperature and pressure, dry
SV stroke volume
SVC slow vital capacity
SW stroke work
syst. systolic
T ambient air temperature
fl
T arm temperature
arm r
T. mean body temperature
T .£ calf temperature
T , chest temperature
Tf. finger temperature
T globe temperature
T,, forehead temperature
66
-------
TT radiant temperature
Tre rectal temperature
Tfro room temperature
Tgk mean skin temperature
Ttni thigh temperature
T toe temperature
T.. wall temperature
TV wet bulb temperature
temp. temperature
TLC total lung capacity
TLV threshold limit values
TPR total peripheral resistance
V volume
V timed ventilator/ volume
V. alveolar ventilation
A
V./Q ventilation perfusion ratio
V_ ventilator/ volume, expired
o
VO- ox/gen uptake
V02 maximal aerobic capacity
max (maximal aerobic power)
\/. tidal volume
T
VC vital capacity
W, wt weight
WBGT wet bulb globe temperature index
yr year(s)
•£ statistical datum derived in the
chi-square test
67
-------
SECTION X
APPENDICES
A. Printout of Metabolic, Temperature,
and Cardiovascular Data 69
B. Printout of Pulmonary Function Data 77
C. Closing Volumes and Closing Capacities 82
68
-------
APPENDIX A
COMPLETE MEAN DATA WAS FORWARDED EARLIER.
INDIVIDUAL DATA ARE STORED IN OUR DATA BANK.
69
-------
EX.NO. STUDY DATE A6E SEX ORE •!. POST «T. MT.CM t»>A 8* PBE TEMP POST TEMP MRS. PA RM TEMP BEL.MUM UP TIME
7706 POLUTO <<-26-7S 20 M 63.20 *2.9l» I ff.S 1.01 .00 37.50 37.60 I Z5.O »S 764 1300
PERIOD EVENT v/m» RR » 02 > CO2 CAS TE«P ET cj^ v STPO * BTPS T 02 L/OZ/MIN ML OZ/KC 02 » »r » «AX MR
i PI z-« 10.6 is ir.se 2.as i».o s.oi w.rs 11.73 3.si 0.3* s.4i «.OT 3«.33 o.io e«
• p* 2-« io.» 20 ir.aa z.ss i«.i «.a> a.«i ii.a* 3.21 0.32 ••v* 3.30 37.5* o.o» «o
13 P6 2-4 31.2 17 16.34 4.17 19.1 6.2* 26.68 34.32 4.72 1.33 21.44 II.OX 23.47 0.38 123
la pa 2-4 a.9 22 17.69 2.71 t«.i 3.37 n.ia 9.as 3.40 o.za 4.41 3.er 33.36 o.oa 72
MAXIMUM OXVtoE^ JO TAKE « 3.39
-------
METABOLIC OAT*: EX. N3. 77O8
R EXCESS COZ KCAL/KG>HR KCAL/HR KCAL/NZ-HR ML O2/LBM KATTS/M2 TIDAL VOL* ML
I O.80 0.0166 1.56 99.50 »*«r> 0.00 A3.676 651.78
• 0.79 0.0114 l.«3 90.51 50.2* O.OO 5O.477 591.S6
II 0.88 O.I7IO 6.30 J97.91 2Z1.0k 0.00 257.096 203O.3*
IS 0.79 O.OI04 1.27 79.95 «4.^2 0.00 5I.66O 447.54
-------
TEKPERATUKEi: 7708
EVENT RECTAL
PI
PI
Pi
P2
P3
P3
P3
P4
P«
a
PS
PS
P6
P6
P7
P7
P7
PS
pa
2-4
14-13
b-6
10-11
4-5
9-10
14-IS
2-4
14-15
4-5
•-10
14-13
2-4
14-15
4-5
9-10
14-IS
2-4
14-IS
37.4
37.3
37.2
37.2
37.2
37.1
37.1
37.1
37.1
37.4
37.5
37.6
37.6
37.7
37.7
37.6
37.7
37.6
37.6
FODtHEAD ARM
3S.6
35.6
35. 7
35.7
33.7
35.6
35.8
35.9
35.7
3S.5
35.4
35.3
35.2
35.1
35.0
34.7
34.S
34.3
35.1
ROOM
30.6
31.1
31.2
31.1
31.0
31.0
31.1
31.1
31.3
31.4
31.3
31.6
31.7
31.8
31.8
31.7
31.8
31.7
31.9
TEMP. MEAN
FINGER
32.9
32.3
32. O
32.6
32.6
32.6
32.1
32.1
32.3
32.3
32.3
32.3
32.3
32.3
32.3
32.3
32.3
32.3
32.3
24.49
THIGH
30.*
30.6
30.2
30.2
30.2
30.9
30.1
JO.I
30.9
31.2
31 .4
31.8
32.4
32.9
33.5
33.3
33.1
33.1
32.8
RADIANT
CAL* CHEST
30.4
30.1*
30.9
3U.9
31.1
30. »
3..0
30. fc
31.0
31. S
92.0
32.4
39. J
93.5
34.9
34.7
34.5
94.1
93. H
TEMP. MtAN
31.2
31.4
31.0
31.}
30. r
31.3
3J.J
31.7
31. S
32. »
32.8
33.*
33.4
91.7
34.8
1».7
33.6
34.4
32.1
24.41
ABDOMEN
31 .2
31.4
31.0
31 .O
30.7
31.5
31.4
31.2
31.6
31.7
31.8
31.9
92.0
92.1
92.2
32.3
92.8
33.1
30.9
_____ _
0.0
o.o
o.o
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
o.o
0.0
0.0
0.0
0.0
0.0
RADIANT
23.4
23.9
23.3
24. O
23.6
23.9
24.1
24.2
.3.9
24.0
24.5
24.6
24.7
24.8
25.1
25.0
24.9
24.8
24.8
• ALL
0.0
0.0
0.0
o.o
o.o
0.0
0.0
•.•
0.0
o.o
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
0.0
KM. A
23.4
24.0
24.6
23.9
23.9
24.0
24.0
24.6
24.0
24.6
24.6
24.7
24.8
24.9
25.1
24.9
24.8
24.7
24.7
-------
GJ
EVENT
PI
PI
P2
P2
P3
P»
PI
P4
P4
PS
P5
PS
P6
P6
P7
P7
P7
pa
P8
2-4
14-15
5-6
10-11
4-5
9-10
• 4-15
2-4
14-15
4-5
9-10
14-15
2-4
14-15
4-5
9-10
14-15
2-4
14-15
MEAN SKIN
TEMP.
31.4
31. 5
31.3
31.3
31.2
31. »
31.2
31.2
31.8
32.O
32.2
32.4
32.7
32.9
33.2
33.3
33.1
J3.2
32.4
MEAN BOOT
TEMP.
35.3
35.3
35.1
35.1
35.1
35.2
35.0
35.0
35.2
35.5
35.6
35.8
35.9
36.0
36.1
36.1
36.1
36.1
35.8
BOO* HEAT
KCAL/M2
1028.9
1028.1
1023.7
1024.3
1023.2
IO2S.*
1021.0
1021.4
1026.6
1034.7
1038. S
1043.0
IO45.6
1O49.6
1052.5
1051.4
1051.5
1051.4
1042.7
RADIATION
KCAL/M2-HR
3J.5
J2.0
25.2
30.7
31.1
32.5
29.8
29.5
33.0
3.1.6
32.4
33.1
33.6
34.3
34.3
35.1
34.7
35.9
32.1
Tl SSU£
9•^
0.0
3.0
0.0
0.0
O.O
0.0
H.6
0.0
0.0
».u
II. 0
.s.o
0.0
0.0
0.0
0.0
13.2
O.O
RESP.EVAP.
KCAL/N2-HR
6.8
0.0
0.0
0.0
0.0
0.0
0.0
6.9
0.0
0.0
0.0
0.0
20.1
0.0
0.0
O.O
0.0
5.7
0.0
SKIN EVAP.
KCAL/M7-HR
52.4
O.O
0.0
0.0
O.O
0.0
0.0
52.6
O.O
O.O
0.0
8.0
31.9
0.0
O.O
0.0
0.0
53.9
0.0
EXCESS C02
GRAMS/H4
3.6V
o.oo
0.00
0.00
0.00
0.00
0.00
2.75
O.OO
o.oo
0.00
o.oo
25.83
0.00
o.oo
0.00
0.00
2.45
0.00
RESP. M20
CM /MR
21.3
0.0
O.O
0.0
O.O
O.O
O.O
21.5
0.0
0.0
O.O
O.O
62.8
0.0
0.0
O.O
0.0
17.9
0.0
-------
EX.NO. STUDY DATE AGE SEX PRE »T. POST ft, Hf.CM U»A d1 »RE TE**P POST TEMP MRS.PA MM TEMP REL.MUM 6P THE
7*32 PIM.UTO 01-I4-T5 24 M 7«. I 73.6 177.4 l.»2 .JJ 37.* 37.6 2 25.0 45 763 IZ30
100 EVENT CARDIAC OUTPUT
LSMIN.
1
2
3
4
5
6
1
a
9
IO
11
12
13
14
15
16
17
ia
19
PI 4-6
14-15
P2 5-6
10-11
P3 5-6
10-11
14-15
P4 «- 6
14-15
P5 5-6
10-11
14-15
P6 5-6
14-15
P7 5-6
tO-ll
14-13
PB 5-6
14-15
5.900
O.OOO
0.000
0.000
0.000
O.OOO
0.000
4.100
0.000
0.000
O.OOO
0.000
15.300
0.000
O.OOO
O.OOO
O.OOO
7.600
0.000
HEART RATE
BEATS/HIM.
67.0
0.0
84.0
78.0
77.0
ao.o
75.0
ai.o
0.0
113.0
117.0
125.0
134.0
134.0
90.0
91.0
0.0
79.0
0.0
L Q2XNM.
0.29
0.00
0.00
O.OO
O.OO
0.00
0.00
O.I6
0.00
O.OO
0.00
0.00
1.J1
0.00
0.00
0.00
0.00
0.22
0.00
srsrouic
PRESSURE
113.0
0.3
110.0
na.o
3.0
117.0
lit.)
124.0
0.0
124.0
1J3.0
0.9
12ft. 0
134.}
126.0
0.0
9.0
114.0
0.9
DIASTOLIC
PRESSURE
80.0
0.0
ao.o
70.0
O.O
83.0
ao.o
ao.o
o.o
ao.o
64.0
o.o
74.0
74.0
7B.O
0.0
0.0
72.0
0.0
STROKE VOL.
ML/BEAT
67.82
0.00
O.OO
O.OO
O.OO
O.OO
O.OO
50.62
O.OO
0.00
0.00
O.OO
1 1 4. i a
O.OO
O.OO
O.OO
O.OO
96.20
0.00
STROKE INDEX
MU/BEAT-M2
35.32
0.00
0.00
0.00
0.00
0.00
0.00
26.36
0.00
0.00
0.00
0.00
59.47
0.00
0.00
O.OO
0.00
SO.lt
0.00
-------
Et.NO. 7»3Z
PE4IOD
1
2
3
•
S
A
7
•
-J
t/1 ,
10
It
12
13
14
IS
1ft
17
ia
19
EVENT CARDIAC INDEX
L/NIN-M2
PI 4-6
»«-15
P2 5-6
10-11
P3 5-6
10-11
14-15
P4 5-6
14-15
PS 5-6
10-11
14-13
P» 5-6
14-1S
P7 5-6
10-11
14-13
PO 5-6
14-19
3.O7
o.oo
o.oo
0.00
o.oo
0.00
0.00
2*14
0.00
0.00
0.00
0.00
7.97
O.OO
0.00
0.00
0.00
3.96
0.00
A-V 02 DIFF.
ML O2/L
48.56
0.00
0.00
0.00
0.00
0.00
0.00
39.49
0.00
0.00
o.oo
0.00
as. 39
0.00
o.oo
0.00
0.00
28.83
o.oo
TOT.PEBIPH.RES. PULSE P1ESS.
UVNES.ScC.CN-S
1220.03
0.00
0.00
0.00
O.OO
0.00
O.OO
1 646.69
0.00
0.00
o.oo
0.00
477.44
0.00
0.00
0.00
0.00
90S. 04
0.00
30.00
0.00
30. OO
4a.oo
0.00
34.00
38.00
44.00
0.00
44.00
66.01
o.»
52.00
60.UO
48.40
0.84
0.09
42.00
0.00
MEAN BLOOD
PRESSURE
90. OO
0.00
90.00
86.00
0.00
94.33
92.67
94.67
0.00
94.67
•6.00
0.00
• 1.33
94.00
94.00
0.00
0.00
• 6.00
0.00
STROKE WORK
GRAMS-MS BE AT
IOI. 453
O.OOO
o.ooo
0.000
o.ooo
o.ooo
0.000
•5.361
O.OOO
o.ooo
0.000
o.ooo
145.657
O.OOO
o.ooo
0.000
0.000
149.152
O.OOO
C AMD I AC •OMK
KC-MSNIN.
8.826
O.OOO
0.000
O.OOO
O.OOO
O.OOO
O.OOO
6.914
0.000
••000
o.ooo
0.000
26.218
0.000
0.000
0.000
0.000
11.783
O.OOO
srsr.
INDEX
9S70
0
9240
9204
O
9360
aaso
10044
0
14012
IS2IO
0
168*4
17956
11340
0
0
9006
0
-------
ON
EX. NO. STUOV DATE AGE SEX PRE »T. POST «T. MT.CH
7747 POLUTO 03-20-75 20 N 78.90 78.70 184.9
EVENT PERIOD F lift E ARM BLDOOFUOM * CHANGE HAND SUOODFLOW
ML/100ML..MIN M./100NL.MIN
PI 4-6
P2 6-8
P3C Al 6-8
P4CAI4-6
P 5(8)6-8
P6IBI6-8
P7 ft-8
Pa 4-6
1
3
S
a
10
13
IS
18
1.750
2.480
1*860
2.620
O.OOO
O.OOO
2.790
2.990
O.O
41.7
6.3
49.7
0.0
0.0
59.4
70.9
o.««
1.730
1*000
o.aeo
o.uoo
0.000
8.530
2.130
BS4 8= PRE TEMP POST TEMP HRS.
2.03 .30 37.70 37.70 I
« CHANGE TOTAL. 8LOOOFLOW * CHANGE
Ml/lOONL.MIN
0.0
94.4
12.4
-1.1
O.O
0.0
Bt>H.«
149.3
2.640
4.210
2.860
3.500
0.000
0*000
11.320
5.120
0.0
59.5
8.3
32.6
0.0
O.O
328.8
•3.9
-------
APPENDIX B
PRINTOUT OF PULMONARY FUNCTION DATA
77
-------
00
PERIOD EVENT
I PRE EXP
2 PI REST
4 P2 REST
8 P4
II PS IBI
13 P6
16 P7 IO
IB P8
19 POST EXP 7401
TE
4-75
TLV
ML
7*97
0
O
0
0
0
0
0
7401
*ce SEX
24 M
FVC
ML
6O7I
5997
6330
6197
0
0
6330
6364
6I3B
PRE «T. POST »T.
T4.I 73.6
1 SEC
ML
4662
4265
4665
4598
0
O
4531
4731
4667
• HT.CM BiA
177. a 1.91
1 itC
* »*t
76.79
71. IZ
73.70
74.20
0.00
0.00
71.58
74.34
76.03
a«
.00
2 Stt
ML
5476
54 Jl
5664
5611
0
0
5507
5697
5530
»RE TEMP POST
37.4 37
2 SEC
* FVC
90.23
90.5*
89.48
90.87
0.00
0. OO
88.42
89.52
90.09
TEMP HRS.PA
.6 2
3 SEC
ML
5758
5731
6031
5997
8
0
5931
•064
5773
RM TEMP
25.0
3 SEC
% FVC
94.84
95.56
95.28
96.77
0.00
0.00
• 3. TO
95.29
94.05
REL.HUM BP
45 763
SOX
L/SEC
• .10
4.4ft
6.53
5.86
o.oo
8.80
4.00
4.56
4.11
TIME
1230
25*
L/SEC
1.79
1.86
2.10
1.67
0.00
0.80
1.80
1.96
1.57
-------
R100
1
2
4
8
11
13
16
18
19
EVENT
PRE EXP
PI REST
P2 REST
P4
PS (81
P6
P7 CAI
P6
POST CXP
1C
ML
4058
0
0
0
0
0
a
•
3705
ERV
ML
2012
0
0
a
0
0
0
0
2443
FRC
ML
3638
0
0
O
o
0
•
0
3696
RV
ML
1626
0
0
0
o
0
o
0
1263
RV/TLV
*
*l.l
0.0
0.0
0.0
o.o
0.0
tt.O
0.0
17.1
MNF
L/SEC
4.8*
3.70
3.90
3.67
0.00
0.00
J.7J
3.82
3.76
MUC
L'HIM
229.0
J.O
0.0
a. u
0.0
9.0
0.0
0.0
206. O
m
3/111
11
16
IS
IS
0
0
17
16
,
TV
N ML
1300
0
0
0
O
0
0
O
1120
: LV/MT
NL/CM
43.29
0*00
0.00
0.00
0*00
0.00
0.00
0.00
41.63
VC/MT
ML/CM
34.15
33.73
35.60
34.85
0.00
0.00
35. 6O
39.79
34.82
TLV/KG
ML/KG
103.87
O.OO
0.00
0.00
0.00
O.OO
0*00
O.OO
99.88
VC/K6
OL/KG
81.99
90.93
85.43
S3. 63
O.OO
O.OO
68.43
69.86
62.63
OLCO
ML/MIM.
0.00
17.20
0.00
31.60
O.OO
50.20
0.00
34.2O
8.6O
-------
PEftlOP
1
2
4
a
it
13
16
18
19
00
O
EVENT
PHE EXP
PI NEST
P2 REST
P4
PS 181
P6
P7 r*»
pa
POST S.KP
SVC 1
ML
0
5997
5997
5«64
0
6
arsT
5997
O
C«C 1
ML
0
«66
828
560
0
0
soo
617
O
PIF
i.
o. ao
o.oo
o.oo
0.00
0.00
0.00
o.ao
o.oo
o.oo
SVC 2
ML
0
5*64
6l3i>
5797
0
0
9997
61 JO
0
;v 2
ML
0
5JJ
66*
S«
a
0
?»>
76ft
«
L/SEC
0.00
o.oo
0.00
0.00
0.00
0.90
0.00
0.00
o.oo
CLOS.CAPI
ML
o
2292
2454
2186
0
0
2126
2249
0
CC «TLV
0.0
29.8
31.9
28.4
0.0
0.0
27.6
29*1
0.0
CLOS.CAP2
ML
0
21 59
2292
2186
0
0
2406
2392
fl
CC *TL\
0.0
28.0
29.0
28.4
O.O
0.0
31.3
31.1
6.0
-------
RIOO EVENT SIT ERV
ML
1
2
*
8
II
13
16
18
19
PRE EXP
PI REST
P2 flESr
P4
PS
-------
APPENDIX C
CLOSING VOLUMES AND CLOSING CAPACITIES
In the present series closing volumes were determined at
frequent intervals with a minimum of two and up to four measurements
at each time. Although most of our subjects had closing volumes
during the preliminary testing, a few did not. It was anticipated
that these latter would demonstrate a closing volume change
consequent to ozone exposure. However, it became obvious that
in these young subjects closing volumes were only randomly obtained
and furthermore these tended to disappear more frequently following
exercise. The following tabulation presents a frequency distribution
of closing volumes obtained across codes and periods.
PERIOD
1
2
4
7
8
Z
CODE
1
3
4
4
3
3
17
2
5
4
5
4
4
22
3
3
2
5
3
5
18
4
4
3
3
2
2
14
5
4
5
6
2
3
20
6
4
4
4
3
3
18
7
4
4
3
3
3
17
8
4
4
3
1
2
14
1
V
31
30 j
33
21
25
140
A Friedman (67) two-way analysis of variance (not quite the
appropriate method of analysis but the best available for this
purpose) indicated that there should be no reason to anticipate
differences in codes or differences in periods. Disappearance of
CV following exercise (periods 7 and 8) was significant at the
0.05 level, suggesting the need for further investigation of this
alteration. Only two of our subjects had closing volumes present
82
-------
during all of their tests in the eight conditions. Data (closing
volume in miHiliters measured from residual volume) from one of these
subjects follows. No significant changes related to any of the
conditions was noted.
PERIOD
1
2
4
7
8
X
CODE
1
600
747
560
640
692
647.8
2
520
748
536
422
455
536.2
3
552
582
889
522
552
619.4
4
772
960
754
822
822
826
5
697
523
726
697
639
656.4
6
911
607
886
728
683
763
7
716
690
562
600
780
669.6
8
567
634
667
400
600
573.6
666.9
686.4
697.5
603.9
652.9
661.5
Data from another subject, who had apparently normal closing
volumes during the periods preceding exercise and disappearance after
exercise, are given below.
PFBTnn
rCKlULF
1
2
4
7
8
CODE
1 2
534
— 534,
430
771
— 504
3
442
883
204
136
340
4 5
675 —
427 410
673 547
6
591
830
576
589
814
7
771
136
640
484
8
398
451
531
The validity of closing volumes as a measure of small airway
closure is questioned for these young normal subjects (55, 56). Other
measures may have to be employed to obtain this information.
83
-------
TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
REPORT NO.
EPA-600/1-76-001
3. RECIPIENT'S ACCESSIOWNO.
4. TITLE AND SUBTITLE
EFFECTS OF LOW LEVELS OF OZONE AND TEMPERATURE STRESS
5. REPORT DATE
March 1976 (Issuing Date)
6. PERFORMING ORGANIZATION CODE
'. AUTHOR(S)
Steven M. Horvath and Lawrence J. Folinsbee
8. PERFORMING ORGANIZATION REPORT NO.
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Institute of Environmental Stress
University of California
Santa Barbara, CA 93106
10. PROGRAM ELEMENT NO.
1AA601
11.
EPA 68-02-1723
12. SPONSORING AGENCY NAME AND ADDRESS
Health Effects Research Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
13. TYPE OF REPORT AND PERIOD COVERED
7/1/1971* through 6/30/1975
14. SPONSORING AGENCY CODE
EPA-ORD
15. SUPPLEMENTARY NOTES
16. ABSTRACT
Cardiopulmonary and metabolic responses of 20 adult males (age 19-29) before,
during and after a 2-hour exposure to either filtered air or 0.50 ppm ozone under
four ambient conditions (25°C, h^% rh; 31°C, &5% rh; 35°C, Uojf rh; UO°C, 50$ rh)
were determined. Exercise at kO% of the individual's Vn/, was performed from
, . U2 max *
bO-90 mm of exposure. There were no cardiovascular changes due to ozone
exposure but heart rate increased and stroke volume decreased with increasing
heat stress. Rectal, mean body, and mean skin temperature also increased in the
heat and were significantly correlated (P 0.05) with WBGT. There was a decrease
in vital capacity and total lung capacity due primarily to a reduction of inspiratory
capacity following ozone exposure. Maximum expiratory flow (indicated by
FEV1.0, 2.0 3.0' MEF50*. MEF25/5, and MMEF) was also reduced following ozone
exposure bu£, as with vital capacity, the greatest decrease occurred immediately
following the exercise period in ozone. The combination of heat stress and ozone
exposure resulted in significantly greater impairment of pulmonary function and
more numerous reported symptoms than in the room temperature ozone exposure.
The trachial-bronchial irritation caused by ozone reduces the vital capacity and
maximum expiratory flow and this effect is more pronounced when the ozone exposure
occurs in a hot environment.
17.
KEY WORDS AND DOCUMENT ANALYSIS
a.
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS
c. cos AT i Field/Group
Ozone
Heat Stress
Cardiovascular system
Respiratory System
06 F
13. DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
19. SECURITY CLASS (ThisReport/
UNCLASSIFIED
21. NO. OF PAGES
20. SECURITY CLASS (This page)
UNCLASSIFIED
22. PRICE
EPA Form 2220-1 (9-73)
84
ft U. 5. GOVERNMENT PRINTING OFFICE: 1976-657-695/5390 Region No. 5-11
------- |