EPA-600/1-78-006
January 1978 Environmental Health Effects Research Series
THE EFFECT OF NITROGEN DIOXIDE ON LUNG
FUNCTION IN NORMAL SUBJECTS
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. Environmental
Protection Agency, have been grouped into nine series. These nine broad cate-
gories were established to facilitate further development and application of en-
vironmental technology. Elimination of traditional grouping was consciously
planned to foster technology transfer and a maximum interface in related fields.
The nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environment Research and Development
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9. Miscellaneous Reports
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS RE-
SEARCH series. This series describes projects and studies relating to the toler-
ances of man for unhealthful substances or conditions. This work is generally
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clude biomedical instrumentation and health research techniques utilizing ani-
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This document is available to the public through the National Technical Informa-
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EPA-600/1-78-006
January 1978
THE EFFECT OF NITROGEN DIOXIDE ON LUNG FUNCTION
IN NORMAL SUBJECTS
by
Steven M. Horvath and Lawrence J. Folinsbee
Institute of Environmental Stress
University of California
Santa Barbara, California 93106
Contract No. 68-02-1757
Project Officer
Edward D. Haak, Jr.
Clinical Studies Division
Health Effects Research Laboratory
Research Triangle Park, N.C. 27711
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
HEALTH EFFECTS RESEARCH LABORATORY
RESEARCH TRIANGLE PARK, N.C. 27711
-------
DISCLAIMER
This report has been reviewed by the Health Effects Research
Laboratory, U.S. 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.
ii
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FOREWORD
The many benefits of our modern, developing, industrial society are
accompanied by certain hazards. Careful assessment of the relative risk
of existing and new man-made environmental hazards is necessary for the
establishment of sound regulatory policy. These regulations serve to
enhance the quality of our environment in order to promote the public
health and welfare and the productive capacity of our Nation's population.
The Health Effects Research Laboratory, Research Triangle Park,
conducts a coordinated environmental health research program in toxicology,
epidemiology, and clinical studies using human volunteer subjects. These
studies address problems in air pollution, non-ionizing radiation,
environmental carcinogenesis and the toxicology of pesticides as well as
other chemical pollutants. The Laboratory develops and revises air quality
criteria documents on pollutants for which national ambient air quality
standards exist or are proposed, provides the data for registration of new
pesticides or proposed suspension of those already in use, conducts research
on hazardous and toxic materials, and is preparing the health basis for
non-ionizing radiation standards. Direct support to the regulatory function
of the Agency is provided in the form of expert testimony and preparation of
affidavits as well as expert advice to the Administrator to assure the
adequacy of health care and surveillance of persons having suffered imminent
and substantial endangerment of their health.
The investigation described in this report is part of the Laboratory's
effort to provide a scientifically adequate health data base for refining
existing criteria for regulated pollutants.
'-John H. Knelsoh, M.D.
Director,
Health Effects Research Laboratory
iii
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ABSTRACT
Cardiopulmonary and metabolic responses of three groups, each
consisting of five adult males (age 19 - 29) were determined before,
during, and after a 2-h exposure to 0.62 ± 0.12 ppm NCL at 25°C and 45%
^ •
RH. The three groups exercised during exposure at 40% of VQ for
either 15, 30, or 60 min for groups C, A, and B, respectively. During
the exercise periods the ventilation was about 33 liters/min, a four-
fold increase over the resting level. There were no physiologically
significant cardiovascular, metabolic, or pulmonary function changes
which could be attributed to exposure to this level of N0? (0.62 ppm).
There were no differences between the groups in their response despite
the fact that groups A and B received more NO as a result of 28% and
84% greater ventilations, respectively.
IV
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CONTENTS
Page
Foreword iii
Abstract iv
List of Tables vi
Acknowledgments vii
SECTIONS
I Conclusions 1
II Recommendations 2
III Introduction 3
IV Review of Literature 4
V General Objectives and Specific Aims 7
VI Research Methods 8
VII Results and Discussion 22
VIII References 41
IX Glossary of Terms, Abbreviations, and
Symbols 47
X Appendix 62
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LIST OF TABLES
Table Page
1 Subject Information 9
2 Exposure Conditions 10
3 Experimental Routine 10
4 Pulmonary Function Changes Before and After Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group A) 23
5 Pulmonary Function Changes During 2-Hour Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group A) 24
6 Metabolic and Cardiovascular Changes During Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group A) 25
7 Comparison of Pulmonary Function Changes Before,
During, and After Exposure to 0.5 ppm Ozone or 0.6 ppm
Nitrogen Dioxide (Group A) 27
8 Pulmonary Function Changes Before and After Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group B) 29
9 Pulmonary Function Changes During 2-Hour Exposure
to Filtered Air or 0.6 ppra Nitrogen Dioxide (Group B) 30
10 Metabolic and Cardiovascular Changes During Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group B) 31
11 Pulmonary Function Changes Before and After Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group C) 34 .
12 Pulmonary Function Changes During 2-Hour Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group C) 35
13 Metabolic and Cardiovascular Changes During Exposure
to Filtered Air or 0.6 ppm Nitrogen Dioxide (Group C) 36
14 Pulmonary Function Changes Following N02 Exposure:
Pooled Data From Groups A, B, and C 38
vi
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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. James F. O'Hanlon
Dr. Peter B. Raven
Dr. Jeajnes A. Wagner
Mr. James C. Delehunt
Mr. Robert S. Ebenstein
Mr. Michael B. Maron
Ms. Dorothy L. Batterton
Mr. David M. Brown
Mr. M. Fred Bush
Mr. David A. D'Alfonso
Ms, Abby M. Evers
Ms. Janet A. Faith
Mr. Thomas Fuller
Mr. Zoltan Fuzessery
Ms. Brigitte Hallier
Ms. Suzanne L. Hostetter
Ms. K. Helen Luk
Mr. Richard R. Marcus
Mr. Douglas L. Marsh
Ms. Judy A. Matsen
Mr. Kazuya Mayeda
Ms. Janeen D. Robertson
Mr. Edwin A. Shaw
Ms. Lovette Weir
We are especially appreciative of the unstinting efforts by our
office staff, Ms. Patricia A. Boisvert and Ms. Margie Cho, 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.
vii
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SECTION I
CONCLUSIONS
No significant alterations in the multiple cardiovascular, pulmonary,
or metabolic measures occurred as a result of a 2-h exposure to 0.62
ppm NO- at variable levels of activity.
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SECTION II
RECOMMENDATIONS
1. The present air quality standards for N02 appear to be adequate to
protect young healthy adult males from acute cardiovascular or
pulmonary dysfunction. Long-term effects of ambient levels of N02
are uncertain especially if there remains a possibility of a
future increase in ambient N02 concentration.
2. ' The synergistic action of other air contaminants with N02 in relation
to the effect of various pollutant combinations on human health
is still in need of evaluation. Specifically, the presence of
sulfur dioxide and oxidants, notably ozone and peroxyacetylnitrate,
may in combination with N02 exaggerate effects induced by those
pollutants on the human respiratory system.
3. Individuals from other age groups, both male and female, and patients
with pulmonary disorders should be evaluated under similar conditions
to those employed in the present study.
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SECTION III
INTRODUCTION
Nitrogen dioxide is a reddish-brown colored gas with a characteristic
odor which is prevalent in areas where automobile use is heavy or where
other high temperature combustion processes are used. N0_ is important
in the formation of photochemical smog and is also an important constituent
of tobacco smoke. Concern over potential health effects from N0~ exposure,
either from the ambient atmosphere or from cigarettes, has produced a
number of studies in animals and man. These studies have been primarily
concerned with the role of N02 in acute and chronic pulmonary disease.
Unfortunately, the majority of investigations have dealt with concentrations
of NO- considerably in excess of those observed even on days of heavy
community air pollution. Although a few experimental studies have been
made on man, very little relevant data is available on the effects of
atmospheric levels of NO^ (< 1 ppm) on human subjects. Therefore, in
this investigation we planned to study the effects of acute exposure to
low levels of N02 (0.6 ppm) upon the pulmonary and circulatory function
of young adult male subjects.
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SECTION IV
REVIEW OF LITERATURE
In very high concentrations, N02 can produce edema (5] but manifestation
of this response takes several hours. Following a brief exposure (10 rain)
to 4 - 5 ppm NO- Abe (1) found a lag time of 30 rain before a maximum change
in airway resistance had occurred. In contrast, exposure to SO-
resulted in a rapid change in airway resistance which was reversed once the
S02 was withdrawn. Whereas ozone causes a decrease in both vital capacity
and forced expiratory flow (.2,3), NO- apparently causes only a reduction
in forced expiratory flow (1), an observation supported by epideraiological
data reported for Tokyo school children (4). It is suggested that the
acute response to N0_ may be related to increased histamine release from
the lung tissue although the evidence for this is not convincing (6).
In patients suffering from chronic non-specific lung disease, brief
exposure (2 min) to NO- concentration of > 2 ppm caused a significant
increase in airway resistance and the effects were correlated with the
concentration inhaled (7). In normal subjects a 15-min period of exposure
to a concentration of 2 - 5 ppm NO- caused a rise in airway resistance as
well as a decrease in diffusion capacity; no effect was seen following
a 15-min exposure to 0.5 - 1.5 ppm N02 (8,9).
Despite the epidemiologic data supporting a relationship between
N02 and respiratory dysfunction (4,10), clearcut evidence of changes in
pulmonary function due to reasonable ambient levels of NO- (0.20 - 1.0
ppm) is lacking. As Warner and Stevens (11) point out, it is difficult
to assess the contribution of other environmental factors (particulates,
high ambient temperatures, acid mists, SO-) in such epidemiological
studies.
There is some suggestion that elevated NO- levels may be related to
an increased frequency of respiratory illness (12) although these data
are not conclusive. An increased incidence of asthmatic attacks has also
been related to elevated pollutant levels (13) but weather changes may
-------
be more significant factors than NO- concentration in this relationship.
Makino (14), in Tokyo, demonstrated an increase in subjective symptoms
among school children (eye irritation, headache, respiratory difficulty)
when total oxidant levels exceeded 0.1 ppm, a relatively minor pollutant
episode. Interestingly, girls reported more symptoms than boys.
Hackney et al. (15,16), in studying the response of normal and
"sensitive" subjects to ozone (0.25 ppm) found no physiologically important
effect of adding NO (0.3 ppm) to their ozone atmosphere. Pengelly (17),
reported that one of three subjects exposed to 0.9 - 1.4 ppra of NO for
two hours showed an increased pulmonary resistance for the duration of
exposure. This same subject had previously shown a marked sensitivity
to ozone. After 180 days of continuous exposure to 1 ppm NO-, Kosmider
and Miscewicz (18) found an increase in blood cholesterol, lipids, and
lipoproteins in normal males and suggested that NO- may have arterio-
sclerotic actions. Busey (19), found no physiological effects in
monkeys after 87 weeks of continuous exposure to 0.51 ppm of NO-."
However, at 6.8 ppm NO., rapid shallow breathing occurred as well as
bronchiolar thickening and focal emphysema.
The association of NO- exposure with increased respiratory tract
infections and the emphysomogenic action of NO- have been studied
more carefully in non-primates. Loss of cilia, damage to bronchiolar
epithelial lining (20), reduced surfactant synthesis (21), increased
evidence of infection and emphysema (22,23), depression of mucociliary
transport (24,25), have all been observed in animals exposed to varying
concentrations of NO- from 0.9 - 20.0 ppm for periods of from one week
to more than a year. However, these and other rodent studies have a
questionable relationship to responses which may be expected from
environmental exposure to NO- because of the high concentrations of NO-
used and the continuous rather than intermittent nature of the exposure.
Furthermore, because of its relative insolubility, N0_ tends to penetrate
further towards the peripheral airways than either SO- or 0, and thus
in long term exposures appears to have a greater effect on small airways
and alveolar septa (23,26). Prolonged exposure to lower NO- levels
-------
(lifetime exposure to 0.8 ppm NO-) did not increase the incidence of
emphysema in rats. The only symptom observed was an increase (20%) in
respiratory rate (27).
At present ambient levels (0.0 - 1.0 ppm) nitrogen dioxide is not
associated with the marked effect on respiratory function that has been
observed with exposure to ozone. Although some increase in respiratory
infection may be expected with repeated N0_ exposure, acute decrease in
lung volume or forced expiratory flow would not be anticipated at the
present ambient levels. The cumulative effect of several years of
exposure to low levels of NO- on humans cannot be determined although
some acceleration of the aging process of the lung is possible (28,29).
Morrow (30) in a review of recent NO- literature concluded that
"injurious effects and important predisposing actions of N0? are more
3
likely to occur at levels between 1 and 3 ppm (2000 - 6000 ug/m )."
He also stated that the current air quality standard (0.05 ppm N02) is
not conservative and may represent a. level where the probability of
deleterious health effects is unacceptable. Goldstein (31), however,
feels that the present N0_ standard is adequate and furthermore
suggests that a transient increase in airway resistance as a result of
NO- exposure is inconsequential as a health hazard. This view is
definitely open to question, since any detrimental physiological
response, however small, represents a deterioration in the quality
of life.
-------
SECTION V
GENERAL OBJECTIVES AND SPECIFIC AIMS
This study was designed to determine the effects of acute exposure
to 0.6 ppm nitrogen dioxide (N02) on the metabolic and cardiopulmonary
systems of young men (18 - 30 years of age) under normal ambient temperature
conditions (25°C, 45% RH).
Since studies on resting subjects do not adequately represent the
normal state of man in his environment, the subjects of this study
exercised for variable periods of time at levels equivalent to 35 - 45%
of their maximal capability. The effect of exposure to NO- at different
levels of intake could then be evaluated when man was either at rest or
at work as well as the factor of differing absolute levels of inhaled N02-
The findings obtained from this investigation may be used by regulatory
agencies to evaluate a level of 0.5 ppm N07 as a possible guideline for
the health protection of the general population.
-------
SECTION VI
RESEARCH METHODS
SUBJECTS
Eighteen young healthy males (ages 18 - 30 years) were selected as
subjects from some 20 volunteers (Table 1). All volunteers were
non-smokers (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
£ max
treadmill. Each subject was then trained (1-hour sessions) in the
procedures being utilized for the determination of cardiovascular and
pulmonary functions.
EXPERIMENTAL DESIGN
The following basic approach was used with all exposure conditions
presented in random order. Three groups of subjects (designated A, B,
and C) were randomly exposed to two 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
environment are outlined in Table 2.
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Table 1. SUBJECT INFORMATION
Subject
No.
7816
7834
7970
7966
7942
7915
7940
7986
7993
8088
8063
7996
8086
8080
8034
8071
Age,
yr
25
21
22
20
20
20
2C
23
21
20
20
20
21
21
22
23
Ht,
cm
180
178
181
191
185
191
177
165
173
172
189
173
178
185
176
188
Wt,
kg
75.2
79.0
78.0
89.5
78 . 5
83.0
78.0
52.2
57.6
65.0
84.8
77.0
67.8
73.0
71.1
64.6
TLC,
ml
7778
7377
8442
10,434
8074
8435
8002
6529
7333
6450
7906
7515
6636
8488
6944
7294
FRC,
ml
3729
3743
4734
4974
3947
4758
3596
3751
4044
3423
3964
3833
3064
4785
2907
4263
VC,
ml
6129
5942
6766
83C4
6420
6499
6604
4250
5729
4969
6302
5699
5343
6522
5626
5093
FFV
cvi.o ,
ml
4486
4921
5012
6615
5174
5028
5056
3846
5080
4247
4148
4360
4763
5860
4524
4860
^2 max ,
liters/min
2.97
4.39
3.32
4.22
4.23
4.38
4.26
2.68
3.36
3.33
3.92
3.70
3.74
3.98
3.68
3.39
Workload,
°2 max
FA
34
23
41
37
40
40
43
44
36
40
38
46
42
44
40
44
N02
36
25°
40
34
36
42
41
36
32
39
45
30
38
43
41
30
Workload was set too low in ozone study and was not changed in order
to permit ozone-nitrogen dioxide comparison.
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TABLE 2. EXPOSURE CONDITIONS
Temperature and relative humidity.
WBGT = 64.4°F
Exposure
Ambient air
(Control exposures)
(Experimental exposure)
txposure was for a 2-h period.
EXPERIMENTAL PROTOCOL
Groups A,. B, and C underwent the routines outlined in Table 3.
25°C 45% RH
(Code 1)
25°C 45% RH
(Code 2)
TABLE 3. EXPERIMENTAL ROUTINE
Group A
Group B
Group C
Control Period
Code Number
Pre-Exp. Tests
Pre-Exp. Tests
Pre-Exp. Tests
Exposure Periods'
1
R
W
R
2
R
R
R
3
R
W
R
4
R
R
W
5
W
W
R
6
W
R
R
7
R
W
R
8
R
R
R
Recovery Period
Post-Exp. Tests
Post-Exp. Tests
Post-Exp. Tests
45%
section = 15 min duration; R = sitting rest; W = work at 35 -
max-
Pre- and post-exposure tests lasted approximately 1 h each. During
exposure, the group A subjects rested in the sitting position for 1 h
then exercised for 30 min on a motor-driven treadmill at approximately
•
35 - 45% VQ_ followed by a 30 min seated rest. Group B underwent a
£» nlcuC
10
-------
similar 2-h exposure except that the exercise sessions occurred inter-
mittently during the exposure each 15-min period of exercise being followed
by a 15-min rest period. Group C exercised in the fourth period only.
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 monitoring leads for electrocardiogram and rectal temperature
for Group B. Clothing worn during the experiments consisted of tennis
shoes, socks, and shorts. Each subject was given a clinical chest
examination. The subject performed a battery of pulmonary tests on a
13.5-liter chain-compensated spirometer (W. E. Collins) and in a body
plethysmograph (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-h exposure was divided for convenience
of analysis into eight 15-min segments (numbered 1-8) (Table 3). Each
period for either group A, B, or C was utilized as outlined in the following
protocol.
s PROTOCOL DURING EXPOSURES
PERIOD 1
GROUP A
Minutes 2-4
Minutes 4-6
Minutes 6-10
•- Ventilatory volume (V_), 0^ and (XL
percentages, heart rate (HR), tidal volume
(VT), and respiratory frequency (fD) .
- 1 K »
Temperatures: Room (T ) , radiant (R ).
•- Cardiac output (OJ , blood pressure (BP), and
HR.
-- Steady-state diffusion capacity to carbon
monoxide (DLCQ)•
Minutes 10-15 -- Pulmonary function tests: forced vital
capacity (FVC), forced expired volume at
1.0. 2.0, and 3.0 sees (FEV^^ ^ 3
-------
mean forced expiratory flow (FEF 25 -
75%) in duplicate. Closing volume (CV),
with slow vital capacity (VC) in duplicate.
T , T .
rra* r
PERIOD 2
GROUP A
Minutes 5-6
Minutes 10-11 --
Minutes 11-14 -
HR, BP, T , T i
HR, BP, T , T .
FVC, FEV 2 Q 3 Q, FEF 50%, FEF 75%, and
FEF 25 - 75%, in duplicate. CV with slow VC
in duplicate.
PERIOD 3
GROUP A
-- BP, HR, T , T (each at 5, 10, and 15 rain).
PERIOD 4
GROUP A
•
Minutes 2-4 -- V , 0_ and CO- percentages, HR, V , f , T ,
c £ fc IK rffl
T .
Minutes 4-6
Minutes 6-10
Minutes 10-15
- Q, BP, HR.
-- Steady-state DLCQ.
- FVC, FEV^Q^ 2>Qj 3>(), FEF 50%, F£F 75%,
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. T , T , HR.
r rra r
PERIOD 5
GROUP A
— BP, HR, T m, Tr (each at 5, 10, and 15 min).
PERIOD 6
GROUP A
Minutes 2-4 — V_, 0 and C0_ percentages, V , f , T , T , HR.
t i £. i R rm r '
12
-------
Minutes 4-6
Minutes 6-10
Minutes 10-15
Q, BP, HR.
Steady-state
Trm' V HR'
PERIOD 7
GROUP A
-- BP, HR, T
rm
T (each at 10 and 15 rain) .
r
Minutes 3-10
FVC' FEV1.0, 2.0, 3.0' FEF 50%' FEF 75%>
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate.
PERIOD 8
GROUP A
Minutes 2-4 — V , 0, and (XL percentages, V^,, fn, HR, T ,
c t. z IK nn
T .
.r
•- Q, BP, HR.
-- Steady-state DLCQ.
" ^ FEV1.0, 2.0, 3.0' FEF 50%> FEF 75%'
FEF 25 - 75% in duplicate. . CV with slow VC
in duplicate. HR, BP, T , T .
Minutes 4-6
Minutes 6-10
Minutes 10-15
PROTOCOL DURING EXPOSURES
PERIOD 1
GROUP B
Exercise
Minutes 6-8
Minutes 8-10
Minutes 10-14
Minutes 14-15
- VE, 02 and C02 percentages, VT, fR,
T , T , HR.
.r re'
-- Q, BP, HR.
-- Steady-state DL-.Q.
-- T , T ,, T , HR.
rm rad re
PERIOD 2
GROUP B
Minutes 5-6
Minutes 6-14
BP and HR, T^, T., T^.
FVC' FEV1.0, 2.0, 3.0' FEF
13
-------
FEF 25 - 75% in duplicate. CV with slow
VC in duplicate.
Minutes 14-15 — BP and HR.
, ?r,
PERIOD 3
GROUP B
Exercise
Minutes 6-8 — V
E,
and C02 percentages, V?, £R,
T , T , HR.
.r re'
Minutes 8-10
Minutes 10-14
Minutes 14-15 -- T
•- Q, BP, HR.
•- Steady-state D^ .
rra
, T ,,
rad re
T , HR.
PERIOD 4
GROUP B
Minutes 5-6
Minutes 6-14
-- BP and HR, T , T , T .
rra T re
— FVC,
Q
, FEF 50%, FEF 75%,
FEF 25 - 75% in duplicate. CV with slow
VC in duplicate.
r , T ,
rm' r'
re
PERIOD 5
GROUP B
Exercise
Minutes 6-8
Minutes 8-10
Minutes 10-14
Minutes 14-15
•
VE, 02 and C02 percentages, Vy, £R, Tre, HR.
Q, BP, HR.
Steady-state DLCQ.
T , T ,, T , HR.
rm rad' re'
PERIOD 6
GROUP B
Minutes 5-6
Minutes 6-14
BP and HR, T^, Tr» T^,
FEV1.0, 2.0. 3.0> FEF 50%« FEF 75%'
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. T , T , T .
r rm r' re
Minutes 14-15 — BP and HR.
14
-------
PERIOD 7
GROUP B
Exercise
Minutes 6-8
Minutes 8-10
Minutes 10-14
Minutes 14-15
-- V£, 02 and C02 percentages, V?, fR,
T , T , HR.
.r' re'
Q, BP, HR.
- Steady-state
- T , T ,, T , HR.
rra' rad* re'
PERIOD 8
GROUP B
Minutes 5-6
Minutes 6-14
- BP and HR, T^,
- FVC» FEV1.0, 2.0, 3.0' FEF 50%' FEF 75%>
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. T , T , T .
Minutes 14-15 — BP and HR.
PROTOCOL DURING EXPOSURES
PERIOD 1
GROUP C
Minutes 2-4 — V , 02 and C02 percentages, HR, V , f ,
Minutes 4-6
Minutes 6-10
Minutes 10-15
T , T .
.rm r
- Q, BP, HR.
— Steady-state
< FEV
1.0, 2.0, 3.0' FEF 50%' FEF 75%'
FEF 25 - 75% in duplicate. Of with slow VC
in duplicate. T , T , and HR.
PERIOD 2
GROUP C
— BP, HR, T , T (each at 5, 10, and 15 min).
PERIOD 3
GROUP C
Minutes 2-4 -- V , 0- and CO percentages, HR, V , £ ,
t Z i. IK
T , T .
rm r
15
-------
Minutes 4-6
Minutes 8-15
- Q, BP, HR.
- FVC, FEV1 Q 2 0 3 Q, FEF 50%, FEF 75%,
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. T , T , HR.
r rm r
PERIOD 4
GROUP C
Exercise
Minutes 6-8
Minutes 8-10
Minutes 10-14
Minutes 14-15
— VE, 02 and C02 percentages, V?, fR, T
rm'
T .
•- Q, BP, HR.
-- Steady-state
- v vHR-
PERIOD 5
GROUP C
Minutes 2-4
Minutes 4-6
Minutes 8-15
-- V_, 0 and CO percentages, HR, V_, fD, T ,
t z z IK nn
Tr'
- Q, BP, HR.
-- FVf FFV FFF ^0% FFF 7^%
hVL' htV1.0, 2.0, 3.0' hbh bUo> hth 7be>
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. T , T , HR.
r rm' r'
PERIOD 6
GROUP C
Minutes 2-4
Minutes 4-6
Minutes 8-15
•
-- VE, 02 and C02 percentages, HR, VT, £R, T^,
T .
.r
--'Q, BP, HR.
" ™- FEV1.0, 2.0, 3.0' FEF 50%' FEF 75%'
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. T , T , HR.
r nn' r
16
-------
PERIOD 7
GROUP C
Minutes 2-4 — V_, 00 and CO. percentages, HR, V_,, f_, T ,
c f. f- IK nn
Minutes 4-6
Minutes 8-15
T .
.r
-- Q, BP, HR.
-- FVC, FEVX 2 Q 3 Q, FEF 50%, FEF 75%,
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. T , T , HR.
r mr r'
PERIOD 8
GROUP C
Minutes 2-4 -- V , 0_ and C00 percentages, V •, fD, HR,
fc i. £• i K
Minutes 4-6
Minutes 6-10
Minutes 10-15
T , T .
.rm' r
-- Q, BP, HR.
-- Steady-state
FEV
DLCO'
1.0. 2.0, 3.0' FEF 50%> FEF 75%'
FEF 25 - 75% in duplicate. CV with slow VC
in duplicate. HR, BP, T , T .
rm r
At the end of the 2-h exposure, the subject was disconnected from the
monitoring wires, returned to the filtered air atmosphere of the laboratory,
and seated on a chair. The attending physician immediately undertook a
clinical chest examination. 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.
17
-------
MEASUREMENT TECHNIQUES
Metabolic measurements were made using open-circuit indirect
calorimetric techniques (32). Ventilator/ volumes were monitored by
collecting timed volumes in a 120-liter chain-compensated spirometer.
Gas samples were analyzed for 0?% and C0_% in a Quintron gas chromatograph,
A, £
calibrated against standard Haldane analyzed gases. Accuracy of analysis
was ±0.02% for CO, and ±0.05% for 09» All metabolic parameters (see
•A £3
Glossary) were calculated.
Copper-constantan thermocouples were used to monitor rectal
temperature (T ) at the depth of 12 cm into the rectum. 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 (approximately 64 for groups A, B, and C)„ The thermocouple temperatures
•
were recorded by a Honeywell multichannel digital recorder and simultaneously
recorded by a laboratory computer (PDF-12). All temperatures were
measured with an accuracy of ±0.1°C.
Cardiac output was determined using the carbon dioxide rebreathing
technique of Defares (33) as modified by Jenous et al. (34). Calculation
of mixed venous C0_ (PvCCL) was performed by the extrapolation method (35)
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
method and heart rate from V, lead recorded on a Sanborn 500 Viso-Cardiette
Q
electrocardiograph. All electrocardiogram tracing were read by the
Institute's cardiologist. An oscilloscope display of the electrocardiogram
was continuously monitored. The DLrn was determined using the steady-
L»vJ
state technique of Filley et al. (36) as modified by Bates et al. (37).
The coefficient of variation of DL™ determination for repeat measurements
of one subject at rest was 12% and at moderate exercise (40% VQ, ) was
£» IDcLJC
18
-------
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 for a
sample printout of measured and calculated data).
The procedures outlined by Kory et al. (38) 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 , 1C, ERV, FEF 50%,
x • U j £ • (J j o.U
FEF 75%, and FEF 25 - 75%. The helium dilution technique was used for
the measurement of functional residual capacity. Before and after exposure
the 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 (39,40) were made. Thoracic gas
volume (TGV) and airway resistance were measured in a body plethysmograph
(Collins) using the method of DuBois (41,42). Calculation of other
pulmonary function parameters were performed by computer (see Appendix).
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 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 (43,44).
19
-------
CHAMBER DESIGN AND CONTROL
A 1.8 ra 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 rain to once every 22 min. Minimal air movement across the subject
occurred due to the dispersive design of the inflow air. A regulated
heating dehumidifier and air conditioner allowed for appropriate temperature
control. When needed for humidification steam was piped directly into
the air inflow. Nitrogen dioxide was added directly to chamber air inlet
via a proportional system from a gas cylinder containing 1% NO. in
nitrogen. 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 possible effects of air pollutants by a weekly coating of anti-oxidant
(Armor-all).
NO- concentration was continuously monitored by the chemiluminescence
technique. An aliquot sample was drawn through fritted glass bubblers,
once each exposure for the determination of NO- concentration by the
Saltzman (45) method. The mean 2-h exposure N0~ concentration measured
by the cherailuminescence technique and that checked by aliquot samples
chemically analyzed was 0.62 ± 0.12 ppm. The NO- sampling inlet was placed
near to an average position of the subject's head during exposure (always
within 24 inches).
STATISTICAL EVALUATION OF DATA
Data were analyzed by a series of analyses of variance. For pre-
and post-test measurements, a two-factor factorial analysis of variance
with repeated measures across time and ambient air was used; for the pre-
exercise and post-exercise periods, a one-factor analysis of variance
with repeated measures across ambient air. In all cases where a significant
20
-------
interaction was observed, a test was made of the simple main effects
followed by a Newman-Keuls test of ordered means where appropriate. All
hypotheses were tested for significance at an alpha level of 0.05.
21
-------
SECTION VII
RESULTS AND DISCUSSION
RESULTS
Group A
The protocol for this group was identical to that in a previously
completed study of the effects of ozone on cardiorespiratory performance
(46). All subjects in this group had participated in our earlier
ozone experiments.
There were no demonstrable cardiovascular or pulmonary effects due
to the pollutant, nitrogen dioxide. The pulmonary function measurements
taken before and after N02 exposure are presented in Table 4. The
MW was lower (P < 0.05) after NO- exposure than in the pre-exposure
period. However, this was not accompanied by any other significant
changes in pulmonary function which would suggest that this change was
produced by N0_. The pulmonary function measurements made during the
exposure period are summarized in Table 5. When the pre-exercise
pulmonary function measurements were compared with the post-exercise
measurements, there was a tendency for the measures of maximum expiratory
flow (FEVj^ Q, FEV2 Q, FEF 50% - P < 0.10, FEF 25 - 75% - P < 0.05) to
decrease slightly. However, these changes were small and within the
variability of similar measurements made throughout the exposure and
therefore we believe they are of minimal importance. Cardiorespiratory
data collected during the exposure is presented in Table 6. There were
no significant changes attributable to nitrogen dioxide exposure. During
the exercise period, as expected, there was an increased metabolic rate
and the consequent increase in ventilation, cardiac output, blood pressure,
and associated variables.
The pulmonary function changes occurring with ozone were compared
to the values obtained during NO exposure (Table 7). Significant
decreases in VC, FEV FEF 25 - 75%, FEF 50%, and FEF 75% had occurred
22
-------
Table 4. PULMONARY FUNCTION CHANGES BEFORE AND AFTER EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP A)
(NOTE: Values are mean 1 SD; n = 5.)
FVC, ml
FOV1.0' ml
FEF25-75%, liters/sec
FEF50%, liters/sec
FEF75%, liters/sec
1C, ml
DRV, ml
FRC, ml
RV, ml
TLC, ml
R , cm H00/ liters -sec
3W £.
MW, liters/min
Filtered Air
(Code 1)
Pre
6686±478
52151322
5.57±0.72
5.1210.47
1.9510.16
42371363
24491205
42921375
18431202
85291675
1.8210.10
225.34116.3
Post
66981446
52941424
5.0710.71
5.2310.61
2.3510.56
42011397
24971127
44931456
19961379
86941824
1.9010.24
219.2120.2
Nitrogen Dioxide
(Code 2)
Pre
67381465
52681499
4.8410.93
4.8510.31
2.2310.48
41541376
25841212
4158+224
15741123
83121527
1.8610.22
231119
Post
67201490
52271367
4.6010.58
4.9110.41
2.2510.28
41641406
25561151
42741229
17181182
84381616
1.8710.19
210126"
P < 0.05.
-------
Table 5. PULMONARY FUNCTION CHANGES DURING 2-HOUR EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP A)
(NOTE: Exercise at 45% VQ, during minutes 60-90.)
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
12
27
57
100
117
12
27
57
100
117
FVC,
ml
69411475
6812±407
6727±452
6718±379
6936±546
69521462
7152+579
6977±437
68111421
68881449
FEV1.0,
ml
5438±563
53121345
52721533
52221481
53441607
48751740
50601338
• 53051435
507013546
52081394
FPV
KV2.0,
ml
64921580
63431470
62301572
62471493
6255+715
62301355
64791580
63921515
62511511"
63971557
FFV •
hhV3.0,
ml
67141S39
65851442
65521514
64861445
67851588
66521475
69271668 '
:
66971514 !
65331494
66771518
FEF25-75%,
liters/sec
5.5710.90
5.3110.69
4.6910.67
4.7310.77
5.3810.91
4.2910.26
4.3210.36
4.9610.48
4.5410.49°
4.7510.54
FEF50%,
liters/sec
6.54H.26
6.2010.88
5.6711.00
5.7110.80
5.6611.12
4.8710.28
4.9210.16
S. 70 10. 61
5.2410.51"
5.7410.65
FEF7S%,
liters/sec
2.7210.55
2.4910.32
2.5410.75
2.5010.68
2.4810.57
2.1510.20
2.0310.29
2.2210.26
2.2410.37
2.2H0.23
" P < O.OS.
t>
' < O.OS. ~\
< 0.10. J
100 min < 57 min.
-------
Table 6. METABOLIC AND CARDIOVASCULAR CHANGES DURING EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP A)
N>
Ln
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
5
50
80
no
5
50
80
110
VBTPS ,
liters/rain
8.53±1.23
8. 61+1. IS
33.1314.14'
9.2±0.77
10.33±1.17
8.60±0.48
32.89+3.01
9.21±0.91
V
liters/min
5.53±0.99
5.65±1.18
26.8±3.58
6.13+0.49
6.96±1.24
5.61±0.51
27.03±2.85
6.14+0.70
RR,
breaths/min
13.6+1.8
12.8+1.7
23.2±2.7
13.8+1.3
13.8±1.4
13.4±2.0
21.4±3.5
14.4±1.4
*°2.
liters/min
0.29+0.04
0.29±O.OS
1.33±0.16
0.31+0.02
0.34±0.03
0.27+0.02
1.28±0.10
0.31±0.04
% % max
7+1
8±1
35+4
8+1
9 + 1
7+1
34+3
8+1
R
0.82+0.03
0.80 ±0.03
0.89±0.02
0.80+0.04
0.81±0.01
0.8310.02
0.9010.02
0.78+0.03
02 Pulse,
ml/beat
3.93+0.49
3.9510.50
11.83+1.58
3.97+0.27
4.65+0.40
3.72+0.41
10.61+1.03
3.80±0.44
01,
liters/min-m
3.0310.24
2.3910.23
7.810.73
3.18+0.36
2.92+0.40
2.3710.35
7.84+0.63
3.64+0.44
60
rt
p.
a
o
1
c
a
o
u
FA < NO .
-------
Table 6. (Continued)
1
1 Time,
' min
i
i
! 5
Code 1
50
(Filtered Air) j 80
Code 2
(Nitrogen Dioxide)
110
5
50
80
110
IIR,
beats/min
72.4+5.0
76.212.7
111.8±3.2
78.6±2.0
72.G12.2
71.4*2.7
122. 413. Z1
80.4+2.8
BP, torr
SP
11712
11813
13014
12212
12013
12114
13113
11813
DP
8212
8315
7113
79+6
8313
7913
7711
8213
TPR,
dyn-sec cm
1262+120
16141160
473+69
12351190
14041222
16651230
494147
10811146
CW,
kg- m/rain
9.79+1.07
7.7210.75
27.83+3.37
10.63+1.23
9.53+1.33
7.75+0.96
28.0912.65
11.8611.78
DLCO,
ml/min • torr
24.915.1
20.4+3.6
52.617.8
26.2+5.2
25.214.3
25.4+2.9
56.4+6.3
26.9+2.6
Y
-------
Table 7. COMPARISON OF PULMONARY FUNCTION CHANGES BEFORE, DURING, AND AFTER
EXPOSURE TO 0.5 ppm OZONE OR 0.6 ppm NITROGEN DIOXIDE (GROUP A)
Code 1 Pre- exposure
(Filtered Air) Post-exercise
n=8 Post-exposure
Code 5 Pre- exposure
(0.5 ppm Ozone) Post-exercise
n=8 Post-exposure
Code 1 Pre- exposure
(Filtered Air) Post-exercise
n=5 Post-exposure
Code 2 Pre- expo sure
(0.6 ppm N02) Post-exercise
n=5 Post-exposure
FVC,
ml
6081±410
6127±391
6096+415
61231395
59911392b
59381407°
6686±478
67181379
66981446
67381465
68111421
67201490
PEV
hbvi.o ,
ml
47821165
46131195
47141329
50521329
454112156
46491282°
52151322
52221481
52941424
52681499
50701354
52271367
FEF25-75%,
liters/sec
5.0910.29
4.3910.46
4.8010.40
5.2910.56
4.3010.32
4.5710.44°
4.9910.72
4.7310.77
5.0710.71
4.8410.93
4.5410.49
4.6010.58
FEF50%,
liters/sec
5.1110.54
5.0910.65
5.3710.55
5.8610.66
4.9310.32
5.3810.36°
5.1210.47
5.7U0.80
5.2310.61
4.8510.31
5.2410.51
4.9110.41
FEF75%,
liters/sec
2.5910.32
2.2910.26
2.3910.33
2.6710.34
2.3610.42
2.1810.15°
1.9510.16
2.5010.68
2.3510.56
2.2310.48
2.2410.37
2.2510.28
Significantly reduced after 0- exposure.
Significantly less than other measurements made during exposure at other times.
-------
in all eight subjects following ozone exposure (46). No such changes
were observed during or consequent to N02 exposure in the subsample
of five subjects.
Group B
The subjects in Group B exercised during the first, third, fifth,
and seventh 15-min periods of the exposure, a total of 60 min of
increased ventilation. The pulmonary function measurements made before
and after exposure in filtered air (Code 1) and nitrogen dioxide -
0.60 ppm (Code 2) are presented in Table 8. No striking alterations in
pulmonary function occurred as a result of nitrogen dioxide exposure.
The vital capacity decreased slightly following exposure in both the
filtered air and nitrogen dioxide experiments. This change in VC was
accompanied by a slight decrease in expiratory reserve volume. None
of the measures of forced expiratory flow showed significant changes
or trends indicative of a decrement in pulmonary performance. The
pulmonary function measures made during the exposure in the rest
period after each exercise period are summarized in Table 9. No
significant changes were observed either with time of exposure or with
NO- exposure.
Cardiovascular and metabolic measurements made during the four
exercise periods are summarized in Table 10. Several changes were noted
with repetition of the exercise period. Respiratory exchange ratio
diminished (P < 0.01) as did end tidal Pco2 (p < 0.05). and rectal
temperature was increased (P < 0.01) with each subsequent exercise period.
In addition, steady state exercise heart rate increased (P < O.OS), as
did pulse pressure (P < 0.01), systolic pressure (P < 0.05), and cardiac
work (P < 0.05). The total peripheral resistance was lower (P < 0.01)
during NO- exposure than during filtered air exposure although neither
cardiac output nor mean blood pressure (the data used to calculate TPR)
we're significantly different during NO- exposure. Other cardiovascular
and metabolic measurements showed no variation with NO- exposure.
28
-------
Table 8. PULMONARY FUNCTION CHANGES BEFORE AND AFTER EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP B)
to
FVC, ml
FEVj Q, ml
FEF25-75%, liters/sec
FEFSO%, liters/sec
FEF75%, liters/sec
1C, ml
ERV, ml
FRC, ml
RV, ml
TLC, ml
R , cm H-0/ liters -sec
clVf £.
MVV, liters /rain
Filtered Air
(Code 1)
Pre
5649±399
45121232
4.6410.58
4.7510.59
2.3810.33
34561294
21941161
39631283
17691285
74181388
1.810.21
17518
Post
55551428°
46161258
4.6910.47
5.2210.73
2.4810.33
36251288
19301204"
38441340
19131328
74681396
1.9310.22
16519
Nitrogen Dioxide
(Code 2)
Pre
57181414
46221266
4.5610.55
4.910.61
2.4510.25
35841255
21341218
38821218
17481131
74661391
1.4510.21
167111
Post
55411415°
47461307
4.2910.63
4.8810.68
2.5410.41
34701248
20701198°
38321301
17621194
73021484
1.6510.27
16619
P < 0.05.
-------
Table 9. PULMONARY FUNCTION CHANGES DURING 2-HOUR EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP B)
(NOTE: Exercise at 45% VQ
during minutes 0-15, 30-45, 60-75, and 90-105.)
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
27
57
87
110
27
57
87
110
FVC,
ml
5606±381
5591±465
5506±479
5579±435
5708±457
55751470
5600±459
54981437
FEV1.0.
ml
41851263
41991356
41041322
41421324
44721315
43041364
43341447
43221362
FEV2.0 ,
ml
50201290
49491416
48501418
49981399
53291393
50721379
51031434
51001368
FEV3.0 .
ml
52421351
51811456
51231486
52411451
55711461
54691523
53661418
53401389
FEF25-75%,
liters/sec
4.8810.48
4.5110.96
4.2910.88
4.0110.85
4.2210.68
4.2710.61
4.0710.63
4.0110.57
FEF50%,
liters/sec
4.6710.65
4.4510.88
4.4110.67
4.56*0.78
4.7610.72
4.4910.81
4.69±0.73
4.2510.71
FEF75%,
liters/sec
2.3310.34
2.4710.73
2.1510.34
2.3610.31
2.3810.44
2.3310.42
2.3510.52
2.4310.37
U)
o
-------
Table 10. METABOLIC AND CARDIOVASCULAR CHANGES DURING EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP B)
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
5
35
65
95
5
35
65
95
VBTPS ,
liters/min
33.3513.45
32.3313.10
33.77+3.51
33.7313.65
32.4713.94
32.2413.45
31.5013.55
32.5513.34
V
liters/rain
27.15+3.02
26.87+2.56
28.22+3.03
27.39+2.78
27.83+2.98
•27.31+2.92
26.43+2.95
27.5913.04
RR,
breaths/min
18.2+2.0
19.211.9
21.211.8
19.711.7
17.811.7
19.2+1.2
18.S+1.6
18.211.7
liters/min
.
1.42+0.14
1.4310.12
1.4710.12
1.48+0.14
1.4510.17
1.4510.17
1.3910.17
1.4910.18
* V02 max
3912
3912
4012
4011
3912
39 12,
38+2
4012
R
0.910.03
0.87+0.01
0.8510.02
0.83+0.01
0.90+0.01
0.8710.02
0.86+0.02
0.84+0.02
0- Pulse.
ml /beat
13.01 + 1.40
12.4411.42
12.76+1.29
12.87+1.60
13.2311.70
13.04+1.51
12.12+1.36
12.7011.44
CI,
liters/min-m
8.3410.37
8.16+0.47
8.37+0.53
8.21+0.29
8.9910.94
9.2811.10
8.51+0.55
9.0910.74
a
ex
u
I
d
o
a
o
CJ
P < 0.01 (N02 < FA).
-------
Table 10. (Continued)
OJ
NJ
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
5
35'
65
95
5
35
65
95
HR,
beats/min
108.6+4.0
112.5+4.6
112.0+4.4
115.2+4.7
110.2+4.6
109.2+5.0
112.215.7
113.7+5.6
BP,
SP
123+3
135+4
131+4
13012
114±5
128+5
12914
13213
torr v
DP
7213
7514
7213
7114
7414
75+6
7414
7514
TPR
, -5
dyn-sec cm
465+31
508+41
478+35
478+32
406133°
432+23°
466+41°
442+23°
CW
kg-m/min
25.9411.35
27.90+2.24
27.85+2.56
27.06+1.26
27.14+2.46
30.5113.57
28.50+3. 15
30.88+2.59
Di
LCO ,
ml/min- torr
46.4+2.5 -
50.0+4.1
51.913.9
50.014.1
49.8+5.2
51.914.9
50.6+5.3
50.1+3.9
VA/Q
1.75+0.17
1.78+0.17
1.80+0.13
1.79+0.15
1.70+0.25
1.64+0.26
1.6610.22
1 .65+0.25
DifC. Port.
3.02+0.14
3.3110.29
J.3810. 30
3.26+0.20
3.07+0.22
3.10+0.41
3.13+0.18
2.95+0.24
P < 0.01 (NO < FA).
-------
Group C
The subjects in this group performed exercise only in the fourth
of the eight 15-min periods and measurements were repeated at IS-min
intervals following exercise. The pulmonary function measurements made
in the pre-exposure and post-exposure periods are shown in Table 11.
No pulmonary function change occurred which could be attributed to
nitrogen dioxide exposure. The FEF 50% was greater before than after
the exposure on the filtered air day. There is no apparent reason
for this and it is probably due to random variation. None of
cardiovascular or metabolic parameters measured during exposure Showed
any significant variation due to nitrogen dioxide exposure (Table 12).
Similarly, pulmonary function tests made during the chamber exposure
were not affected by nitrogen dioxide (Table 13).
All Groups
The pre- and post-exposure pulmonary function data of the three
groups of subjects (n = 16) were analyzed collectively for the effect
of 0.62 ppm N02 (Table 14). Overall, there was a trend (P < 0.10) for vital
capacity to decrease slightly following NO- exposure but this change
was small (approximately 80 ml) and is of doubtful physiological
importance. Expiratory reserve volume was smaller (P < 0.05) following
exposure to either filtered air or N02 apparently as a result of a
decrease in end expiratory position due to a larger tidal volume (P < 0.05).
This may reflect some anticipation on the part of the subject as a
result of the large number of respiratory maneuvers already performed.
Closing volumes were too variable and erratic preventing us from
performing any statistical analysis. There was a fall in maximum
voluntary ventilation post-exposure apparently reflecting the fatigue
and perhaps decreased motivation in the subjects.
Symptomatology
Individual subjective responses to nitrogen dioxide exposure were
determined from reported symptoms and answers to our questionnaire.
33
-------
Table 11. PULMONARY FUNCTION CHANGES BEFORE AND AFTER EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP C)
FVC, ml
FEVj Q, ml
FEF2S-75%, liters/sec
FEF50%, liters/sec
FEF75%, liters/sec
1C, ml
ERV, ml
FRC, ml
RV, ml
TLC, ml
R , cm H00/ liters -sec
aw 2
MVV, liters/min
Filtered Air
(Code 1)
Pre
56801239
47831332
5.5910.73
6.3810.79
2.9510.64
36371222
20431262
38401421
17971203
74771323
1.7810.24
204114
Post
57181195
47711232
5.4710.65
5.3610.30°
2.6110.50
36881126
20291167
36881462
16591387
73781377
1.6410.11
21019
Nitrogen Dioxide
(Code 2)
Pre
57181317
49641260
5.8810.55
5.8010.64
3.1710.52
35741160
21451209
37001421
15551317
72731410
1.9310.36
213113
Post
56751299
49351288
5.7810.57
5.9410.36
2.8610.54
36571203
20171232
37551489
17381340
74121389
2.1610.53
221119
P < 0.05.
-------
Table 12. PULMONARY FUNCTION CHANGES DURING 2-HOUR EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP C)
(NOTE: Exercise at 45%
during minutes 45-60.)
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
12
43
72
87
100
117
12
43
72
87
100
117
FVC,
ml
57674312
5670±242
5642±257
5712+219
5605+278
55504234
5698+284
57221244
5679±273
5761+279
56711273
5646+304
FEVi.o,
ml
4732+290
4803+214
4776±282
45401254
45551246
4547+337
4683+326
4747+285
4616+241
4738+324
46921425
4597+358
FEV2.0 ,
ml
5443+281
54531202
53331207
5423+183
52851203
51911229
54821287
55021247
53921210
55021227
5384+291
53311300
FEV3.0,
ml
5638+276
56071231
55671229
56011196
55151251
54571220°
5651+275
56661246
5587+252
56921254
56051268
5477+271
FEF25-75%,
liters/sec
5.3910.67
5.53+0.57
4.96+0.69
4.6110.57
5.04+0.61
4.30+0.38
5.19+0.51
4.99+0.68
5.25+0.55
5.26+0.75
4.74+0.72
4.82+0.62
FEF50%,
liters/sec
5.65+0.45
6.0110.25
5.53+0.76
5.2510.62
5.7210.36
5.16+0.61
5.7910.73
5.3910.87
5.60+0.36
5.28+0.58
5.66+0.81
5.4810.70
FEF75%,
liters/sec
2.98+0.30
3.41+0.40
2.65+0.52
2.63+0.26
2.37+0.32
2.27+0.38
2.93+0.53
2.74+0.75
2.79+0.30
3.26+0.56
2.82+0.56
3.07+0.59
CO
Ul
P6 and P13 > P18 (87 and 100 min > 117 Bin).
-------
Table 13. METABOLIC AND CARDIOVASCULAR CHANGES DURING EXPOSURE
TO FILTERED AIR OR 0.6 ppm NITROGEN DIOXIDE (GROUP C)
to
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
5
35
SO
65
80
95
110
5
35
50
65
80
95
110
VBTPS ,
liters/rain
9.1±1.34
9.14+0.82
36.9611.93
11. 91±1.07
10.7710.89
9.5510.66
9.7310.58
9.7910.79
9.2810.94
34.5114.33
10.7210.64
9.3910.61
8.5210.50
7.9310.26
V
liters/min
5.8211.17
5.6110.69
31.2411.22
9.0110.78
7.3411.14
6.2710.89
6.4111.0
6.5910.64
5.9510.74
27.7813.67
8.2010.63
6.1310.29
5.2610.36
4.6710.19
1
RR,
breaths/rain
13.611.4
15.612.5
21.212.9
14.212.3
14.011.4
14.211.8
14.012.4
13.611.6
15.411.9
21.213.3
IS. 612. 4
14.211.8
14.811.8
14.811.8
*°2.
liters/rain
0.3110.04
0.310.04
1.6010.06
0.3810.02
0.3710.03
0.3410.03
0.3210.02
0.2910.03
0.2810.03
1.3510.15
0.3410.02
0.3010.01
0.2710.01
0.2610.01
* *02 ^x
8H
811
43H
1011
ion
911
911
8H
811
3613
9H
811
711
711
R
0.7310.04
0.7710.05
0.8810.03
0.8810.04
0.7410.06
0.7310.06
0.7410.05
0.8710.05
0.8310.04
0.9210.03
0.9410.05
0.8U0.05
0.8010.06
0.7310.03
02 Pulse,
ml/beat
4.1710.57
4.3810.38
14.2310.96
4.7310.16
5.1910.16
5.0310.25
4.7410.33
4.1410.30
4.2710.47
13.1712.13
4.0610.41
4.1710.29
3.7410.30
3.6810.12
CI,
liters/min-m
2.9510.16
2.8510.24
10.07H.01
3.7010.28
3.2210.20
2.9310.16
3.0710.37
2.8010.18
2.8210.05
10.8410.91
4.0810.51
3.1310.38
2.9310.29
2.8710.39
01
to
10
o.
u
9
C
g
•8
a
o
-------
Table 13. (Continued)
Code 1
(Filtered Air)
Code 2
(Nitrogen Dioxide)
Time,
min
5
35
50
65
80
95
110
5
35
50
65
80
95
110
HR,
bed ts/ nun
| 72.814.2
1 67.8±3.3
112.013.2
81.212.8
72.214.0
67.614.2
67.812.8
70.8H. 6
66.612.3
116.216.7
84.215.8
; 73.613.0
69.012.7
70.013.2
BP, torr
SP
11817
12U6
13419
124+6
11917
121+5
11817
12U5
11816
133±7
12616
123±5
117±5
11915
DP
80+6
82+5
82+4
81+3
7714
8517
8U6
81+4
8017
8118
79+7
82+6
79+6
8017
TPR,
j..n sec CTri-S
1326194
1440+17
427+48
1100175
1196168
1406+96
1349+19
1437110
1387197
395154
1041+17
1359121
1365116
1421115
CW,
kg-ra/min
8.95+0.61
8.9110.68
34.81+3.51
11.86+1.19
9.97+0.96
9.1710.49
9.2810.76
8.7010.54
8.57+0.45
36.7711.36
13.0711.10
9.8410.99
8.8210.85
8.8411.22
Di
ml/rain • torr
25.4+2.5
50.013.6
—
25.4+3.0
27.014.8
....
54.512.3
---
26.212.7
1
Diff. Perf.
i
1.02+0.16 j 4.5210.33
1.0410.14 ',
1.70+0.21 i 2.6710.25
1.28+0.19
1.18+0.14
1.1310.15
1.1610.22
1.2710.16
1.1110.17
1.38+0.24
1.0610.15
1.09+0.18
0.95+0.13
0.91+0.. 12
---
4.4610.58
5.23H.12
---
2.7210.28
---
5.4310.66
-------
Table 14. PULMONARY FUNCTION CHANGES FOLLOWING N02 EXPOSURE:
POOLED DATA FROM GROUPS A, B, AND C (n = 16).
00
FVC, ml
FEV1.0> ml
FEF25-75%, liters/sec
FEF50%, liters/sec
FEF75%, liters/sec
1C, ml
ERV, ml
FRC, ml
VT, ml
TLC, ml
R , cm H_0/liters-sec
3.W ,£
MVV, liters/min
Filtered Air
Pre
5983±900
4816+639
5.05+1.36
5.37±1.41
2.42±0.90
3756±674
2226±435
4028±715
868±304
7784+1057
1.80+0.38
200±33
Post
5963±908
4876±670
5. 05H.21
5.27±1.18
2.4810.89
38241626
21381425°
39981875
9641317°
782311227
1.8310.42
1961366
Nitrogen Dioxide
Pre
60371928
4931+729
5.06H.45
5.1711.16
2.6110.95
3759+602
22781468
3911+598
8591252
76701968
1.7310.55
201140
Post
59511963"
49551656
4.8511.34
5.2211.16
2.5510.86
37451643
22061455°
39461717
8941274°
7691+1108
1.88+0.72
195+4 26
< 0.05. ")
< 0.10. J
(See text.)
-------
No significantly different responses were reported between NO- and
filtered air exposure. Occasionally symptoms were noted primarily
associated with the exercise stress and included fatigue and slight
dizziness. The subjects reported that they were "more tired" after
the Grovip B exposures which was anticipated since this group exercised
for a greater amount of time during the 2 h than in the other two
experimental sessions. No physical signs related to N02 exposures
were detected by the physician's examination.
DISCUSSION
A 2-h exposure to nitrogen dioxide at a concentration of
0.62 ppm had no profound effects on either the cardiovascular or
pulmonary function of young men. The few and unrelated changes which
did occur following NO- exposure showed no consistent pattern. The
few instances where statistically significant changes were found
should, therefore, be regarded with some skepticism since they
could not be related to concomitant changes in associated parameters.
In Group A, the decrease in MW following N0£ exposure was not
accompanied by any change in vital capacity or maximum expiratory
flow. Such a change in MW could possibly occur if there was a marked
increase in laryngeal resistance but this is unlikely as the subjects
reported no symptoms indicative of this increased resistance. In
Group B, the slight decrease in total peripheral resistance during
ozone exposure was not accompanied by other alterations in circulatory
function. When data from all subjects was pooled, the only overall trend
was for a small decrease in vital capacity. This was surprising
because most studies evaluating the effect of higher concentrations of
NO- on pulmonary function (1,4,9,10,17) have suggested that following
exposure to NO- there was an increase of airway resistance or a decrease
of maximum expiratory flow but that there was usually no effect on lung
volumes. These effects have been shown with concentrations of NO- greater
than 1 ppm and the lack of a change in maximum expiratory flow in our
subjects was not unexpected.
39 •
-------
In a study of exercising subjects, Rokaw (47) found an increased
airway resistance at 1.5 and 3.0 ppm NCL. They found no change at
^*
0.5 ppm N02 which is in agreement with our results. Although the
toxicity of N02 has been demonstrated when humans (1,5,8) or animals
(19,22,24) have been exposed to concentrations which exceed present
ambient levels (> 1.0 ppm), the effect of exposure to ambient
levels (0.20 - 0.50 ppm) is minimal (4,10,14,15,16,17). These limited
effects of ambient levels of NCL are in striking contrast to the effects
of ozone on pulmonary function at present ambient concentrations that
we (46) and others (2,3,15,16) have observed.
Several factors in these present experiments differ from those
usually employed in studies on the effects of NO- on man. None of
£f
our subjects were smokers and thus they had not been previously exposed
to the NO- arising from cigarette smoking. It has been suggested that
the potential ill effects from NO exposure would be greater in smokers.
The ambient exposure concentrations were relatively low, being at levels
which occur primarily during heavy smog days where hourly averages
of about 0.6 ppm have been reported,, However, some of the exposed
subjects exercised for up to one-half of their exposure time to
N02. Consequently since their alveolar ventilations had been increased
by four to five fold by the exercise, they would have been exposed
to relatively higher levels of inhaled NO.. Nonetheless, only minimal
alterations in pulmonary functions were observed and these did not
show a consistent pattern indicative of an overall effect of the
nitrogen dioxide exposure.
40
-------
SECTION VIII
REFERENCES
1. Abe, Matsuo. Effects of mixed NO- - SO- gas on human pulmonary '
functions. Bull. Tokyo Med. Dent. Univ. 14: 415-433, 1967.
2. Bates, D., G. Bell, C. Burnham, M. Hazucha, J. Mantha, L. Pengelly,
and F. Silverman. Short-term effects of ozone on the lung.
J. Appl. Physiol. 32: 176-181, 1972.
3. Silverman, F., L. Folinsbee, and R. J. Shephard. Pulmonary function
changes in ozone - Interaction of concentration and ventilation.
J. Appl. Physiol. (in press.)
4. Kagawa, J., and T. Toyama. Photochemical air pollution. Arch.
Environ. Health 30: 117-122, 1975.
5. Kleinfeld, M. Acute pulmonary edema of chemical origin. Arch.
Environ. Health 10: 942-946, 1965.
6. Thomas, H., R. Stanley, S. Twiss, and P. Mueller. Sputum histaraine
and inhalation toxicity. Environ. Lett. 3: 33-52, 1972.
7. Smidt, V.:, and G. von Nieding. Arrway resistance after inhalation
of 1 - 10 ppm NO- and 20 - 30 ppm NO with and without previous
treatment with broncholytic drugs. Bull. Physio-Pathol. Resp.
10: 594, 1974.
8. Nieding, G. von, G. Krekeler, H. Fuchs, M. Wagner, and K. Koppenhagen.
Studies of the acute effects of NO- on lung function: Influence of
diffusion, perfusion, and ventilation in the lungs. Int. Arch.
Arbeitsmed. 31: 61-72, 1973.
41
-------
9. Nieding, G. von, M. Wagner, H. Krekeler, V. Smidt, and K. Muysers.
Minimum concentrations of NO- causing acute effects on the
respiratory gas exchange and airway resistance in patients with
chronic bronchitis. Int. Arch. Arbeitsmed. 27: 338-348, 1971.
10. Shy, C., J. Creason, M. Pearlman, K. McClain, F. Benson, and
M. Young. The Chattanooga school children study: Effects of
community exposure to nitrogen dioxide. I. Pulmonary Function.
J. Air Poll. Control Assoc. 20: 539-545, 1970.
11. Warner, P., and I. Stevens. Revaluation of the "Chattanooga
school children study", in light of other contemporary government
studies. J. Air Poll. Control Assoc. 23: 769-772, 1973.
12. Shy, C., J. Creason, M. Pearlman^, K. McClain,, F. Benson, and
M. Young. The Chattanooga school children study: Effects of
community exposure to nitrogen dioxide. II. Respiratory Illness.
J. Air Poll. Control Asspc. 20: 582-588, 1970.
13. Girsh, L. Air pollutants. Chap. 24 in: Allergy and Irrmunology
In Children. F. Speer, and R. Dodchom (eds.) Springfield, Thomas,
1973.
14. Makino, K. Photochemical smogs and conscious symptoms. Tokyo
Metropolitan Government Institute of Hygiene. Progress Report #2
on Public Nuisance Researches: 42-46, 1973.
15. Hackney, J., W. Linn, J. Mohler, E. Pedersen, P. Bressacher, and
A. Russo, Experimental studies on human health effects of air
polluntants II. Arch. Environ. Health 30: 379-384, 1975.
42
-------
16. Hackney, J., W. Linn, D. Law, S. Kawza, H. Greenberg, R. Buckley,
and E. Pederson. Experimental studies on human health effect of
air pollutants.III. Arch. Environ. Health 30: 385-390, 1975.
17. Pengelly, D. Acute respiratory effects of NCL at ambient levels.
Proc. Can. Conf. on Atmos. Pollution Gravenhurst, 1974 (Abst.).
18. Kosmider, S., and A. Misiewicz. Experimental and epidemiclogical
investivations on the effect of nitrogen oxides on lipid metabolism.
Int. Arch,, Arbeitsmed. 31: 249-256, 1973.
19. Busey, W. Chronic exposure of cynomolgus monkeys to nitrogen
dioxide singly and in binary combination with certain air borne
pollutants. Project Report. CAPM 6-68-2. Feb., 1972, NTIS
PB 212 797.
20. Stephens, R. J., G. Freeman, and M. Evans. Early response of
lungs to low levels of nitrogen dioxide. Arch. Environ. Health
24: 160-179, 1972.
21. Seto, K., M. Kawakami, K. Sugita, M. Shishido, M. Yamaji, and
T. Tsuda. Influence of inhalation of ozone and nitrogen dioxide
on the formation of phospholipids on the lung. Igaku to
Seibutsugaku. 86: 317-320, 1973.
22. Kosmider, S., M. Luciak, K. Zajusz, A. Misiewicz, and J. Szygula.
Studi.es on emphysemogenic action of nitrogen oxides. Patol. Pol.
24: 107-125, 1973.
23. Kleinermart, J. Reparative processes of the lung in: Aging of the
Lung. L. Gander (ed.) Grune and Stratton, New York, 1964.
43
-------
24. Giordano, A., and P. Morrow. Chronic low level nitrogen dioxide
exposure and mucociliary clearance. Arch. Environ. Health 25:
443-449, 1972.
25. Arrier, E., and R. Rhoades. Long-term nitrogen dioxide exposure.
Arch. Environ. Health 26: 156-160, 1973.
26. Ichioka, M. Model experiments on absorbability of the airway
mucous membrane of S02 and NCL gases. Bull. Tokyo Med. Dent.
Univ. 19: 361-375, 1972.
27. Freeman, G., N. Furiosi, and G. Haydon. Effects of continuous
exposure of 0.8 ppm NCL on respiratory in rats. Arch. Environ.
Health 13: 454-456, 1966.
28. Mueller, P., and M. Hitchcock. Air quality criteria - toxicological
appraisal for oxidants, nitrogen oxides, and hydrocarbons. J. Air
Poll. Control Assoo. 19: 670-676, 1969.
29. Gross, P. The pulmonary effects of air pollution in: Aging of the
Lung. L. Gander, and J. Meyer (eds.) New York: Grune, 1964.
30. Morrow, P. E.' An evaluation of recent NO toxicity data and an
attempt to derive an ambient air standard for NO by established
toxicological procedures. Environ. Res. 10: 92-112, 1975.
31. Goldstein, E. Reevaluation of the air quality standard for nitrogen
dioxide. Calif. Air Environment 4: (2) 3-5, 1974.
32. Consolazio, C., R. Johnson, and L. Pecora. Physiological measurements
of metabolic functions in man. New York: McGraw Hill, 1-98,
1963.
44
-------
33. Defares, J. G. Determination of PvC02 from the exponential rise
during rebreathing. J. Appl. Fhysiol. 13: 159-164, 1958.
34. Jenous, R., G. Lundin, and D. Thomson. Cardiac output in healthy
subjects determined with a CQ- rebreathing method. Acta Physiol.
Soand, 59: 390-399, 1963.
35. Wise, M. E., and J. G. Defares. Correspondence: Venous PCO? and
cardiac output obtained from rebreathing curves: By extrapolation
or by a plateau method. Clin. Soi. 43: 303-305, 1972.
36. Filley, G. F., D. J. Macintosh, and G. IV. Wright. Carbon monoxide
uptake and pulmonary diffusing capacity in normal subjects at
rest and during exercise. J. Clin. Invest. 33: 530-539, 1954.
37. Bates, D. V., N. G. Boucot, and A. E. Dormer. The pulmonary
diffusing capacity in normal subjects. J. Physiol (Land.)
129: 237-244, 1955.
38. Kory, R. C., R. Callahan, H. G. Basen, and J. C. Synes. The
Veterans Administration - Army cooperative study of pulmonary
function. Am. J. Med. 30: 243-258, 1961.
39. Travis, D. M., M. Greens, and H. Dan. Simultaneous comparison of
helium and nitrogen expiratory "closing volumes". J. Appl. Physiol.
34: 304-308, 1973.
40. Linn., W. S., and J. D. Hackney. Nitrogen and helium "closing
volumes" simultaneous measurement and reproducibility. J. Appl.
Fhysiol. 34: 396-399, 1973.
41. DuBois, A. B., S. Botelho, G. Bedell, R. Marchall, and J. Coraroe. A
rapid plethysmographic method for measuring thoracic gas volume. J.
Clin. Invest. 35: 322-326, 1956.
45
-------
42. DuBois, A., S. Botelho, and J. Comroe. A new method for measuring
airway resistance in man using a body plethysmograph. J. Clin.
Invest. 327-335, 1956.
43. Becklake, M., M. Leclerc, H. Strobach, and J. Swift. The N2
closing volume test in population studies: Sources of variation
and reproducibility. Am. Rev. Respir. Dis. Ill: 141-147, 1975.
44. McFadden, E., B. Holmes, and R. Kiker. Variability of closing volume
measurements in normal man. Am. Rev. Respir. Dis. Ill: 135-140,
1975.
t
45. Saltzman, B. Selected methods for the measurement of air pollutants.
U. S. Public Health Service #999-AP-ll, pp. C1-C7, 1965.
46. Folinsbee, L. J., and S. M. Horvath. Effects of low levels of
ozone and temperature stress on cardiac pulmonary and peripheral
circulatory functions of men during submaximal work. Report on
EPA Contract #68-02-1723, 1975.
47. Rokaw, S. N., H. Swann, R. Keenan, and J. Phillips. Human exposures
to single pollutants - N02 in a controlled environment facility.
Paper presented at AMA Air Pollution Medical Research Conference,
Denver, Colorado, 1968.
-------
SECTION IX
GLOSSARY OF TERMS, ABBREVIATIONS, AND SYMBOLS
(1) RESPIRATORY MEASUREMENTS
Parameter and Formula
Abbreviation
Units
1. Ventilatory Volume
•
Ca) Vp (mn corrected volume)
310 BP * W*
fbl V DTPS - V x x
\.uj »E */!*« »E -- 273 + g^ temp. BP - 47
,.„, 'E "'*" 'E 760 273 + gas temp.
•
•
VE liters/min
•
VE BTPS liters/min
•
VB STPD liters/min
C
P. = barometric
pressure
w
water vapor
pressure at
the gas temp.
2. Respiratory Rate
RR or
breaths/min
3. Tidal Volume
VE
RR
ml/breath
4. Ventilator/ Equivalence Ratio
V£ BTI'S
Oxygen Uptake
V BTPS/Vo7 liters breathed
C £f ^^f^^^^^^f^^^^mmy^^^f^^^^t^fm^^
liters 0,
47
-------
(2) METABOLIC MEASUREMENTS
Parameter and Formula
Abbreviation
Units
1. Oxygen Uptake
•
VE STPD x True 02%
(a)
(c)
100
V STPD x True 02% x 1000
100 x Pre Wt
•
V STPD x True 02% x 1000
100 x Lean Body Mass
V02
V02
liters 02/min
ml
-1
ml Oj/LBM-min"1
2. True Oxygen
(%N2 x 0.265) - %02 in expired air
True 0,
3. Respiratory Exchange Ratio
no units
% Expired C02 C02 Production
% Expired 02 °r Oxygen Uptake
4. Excess Carbon Dioxide Excess CO,
i
(%C02 Expired - 0.03)
VE STPD x fL__ V02 x 0.75
liters
5. Maximal Aerobic Power VQ
and/or
Maximal Aerobic Capacity
(The largest value of oxygen uptake obtained
when a subject performs maximal exhaustive work.)
2 max
liters/min
ml 02/kg-min"
ml 02/IBM-min"
48
-------
Parameter and Formula
Abbreviation
Units
6. Percent of Maximal Oxygen Uptake
VOr
x 100
V<3
2 max
%V0
2 max
7. Energy Production
cal/liter 02 = 1.27604 x R + 3.82041
(a) = cail/liter
a
60 x liter 02/min
Cb) -K
(c)
Pre Wt, in kg
a
BSA
(d) = c x 1.163
(3) CARDIOVASCULAR
1. Cardiac Output = Stroke Volume x HR
VQ2
Ca°2 - Cv°2
2. Cardiac Index
•
Q
M
M
M
M
Body Surface Area, in m
CI
Body Surface
Area = BSA
kcal/h
-1
kcal/kg'h
kcal/m2^"1
watts/m
liters/min
liters/min-m
-2
49
-------
Parameter and Formula
3. Cardiac Work
SP x 13.6 x Q
1000
4. Heart Rate
5. Stroke Volume
JL
HR
6. Stroke Index
SV
BSA
7. Stroke Work
SP x 13.6 x SV
1000
8. Oxygen Pulse
VQ2 x 1000
HR
Abbreviation Units
CW kg-m/min
HR, fr beats/rain
L
SV
SI
sw
ml/beat
ml/beat-m
-2
g-in/beat
CL Pulse ml 02/beat
50
-------
Parameter and Formula
Abbreviation
Units
9. Arterio-Mixed Venous
Oxygen Difference
(a - v)02 diff. ml 0,/liter blood
V02 x 1000
10. Systolic Pressure (Arterial)
SP, P
sys
torr
11. Diastolic Pressure (Arterial)
DP, P.. torr
' dias
12. Mean Blood Pressure (Arterial)
MBP, F.
bl
torr
SP - DP
DP
13. Pulse Pressure
PP
torr
SP - DP
14. Total Peripheral Resistance
TPR
dyn-sec on
-5
1.333 x 60 x MBP
(4) PULMONARY
1. Forced Vital Capacity
FVC (ml, ml/kg) ml/in''
51
-------
Parameter and Formula
Abbreviation
Units
2. Timed Forced Expired Volumes
(1.0, 2.0, and 3.0 seconds)
3.
Forced Expired Volumes as a
percentage of Forced Vital Capacity
FEV
1.0
FVC
x 100
4. Inspirator/ Capacity
5. Expiratory Reserve Volume
FEV
1.0
FEV
2.0
FEV
3.0
FEV n/FVC%
x * U
FEV2 Q/FVC%
FEV. n/FVC%
o • u
1C
ERV
ml
ml
ml
6. Functional Residual Capacity
FRC
ml
7. Residual Volume
RV
ml, ml/kg, ml/m"
8. Total Lung Capacity
VC + RV
TLC
ml, ml/kg, ml/m^
9.
Residual Volume/Percent Total
Lung Capacity
RV
TLC
x 100
10.
Maximal Mid-Expiratory Flow
or
Mean Forced Expiratory Flow
during middle half of FVC
RV/%TLC
MMEF
FEF 25 - 75%
FEF 25 - 75%
liters/sec
52
-------
Parameter and Formula
Abbreviation
Units
11. Maximal Voluntary Ventilation
MW
liters/min
12. Maximal Expiratory Flow
50% of Vital Capacity
MEF50%
liters/sec
or
Forced Expiratory Flow @
50% of FVC exhaled
FEF 50%
13. Maximal Expiratory Flow
25% of Vital Capacity
or
Forced Expiratory Flow @
75% of FVC exhaled
MEF25%
FEF 75%
liters/sec
(5) TEMPERATURE REGULATORY
1. Rectal Temperature
re
2. Forehead Temperature
3. Arm Temperature
4. Finger Temperature
Thd -
T
arm
T
fing
°C
°C
°C
5. Thi{jh Temperature
Tthi
53
-------
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
Abbreviation
T
calf
T v
ch
T
toe
T
rm
T
a
T
r
T
g
T
wall
T
wb
T
Units
°C
°C
°C
•c
°C
°C
°C
°C
°C
8C
Tsk a °'07 Thd + °'36 Tch + °-05 Tfing
0.20 t
16. Mean Body Temperature
0.65 T + 0.35 T .
re SK
°c
17. Body Heat Content
Pre Wt x 0.83 T",
BSA
BHC
kcal/ni
54
-------
Parameter and Formula
Abbreviation
Units
18. Wet Bulb Globe Temperature Index
0.3 T * 0.7 T .
g wb
19. Tissue Conductance
kcal/m2-h"1
T _ T
sk
= Energy Prod
T - T .
re sk
WBGT
°C(°F)
kcal/m2-h"1 'C'1
20. Respiratory Evaporative Water Loss
V_ BTPS x factor x 60
(The factor is determined from density
steam tables and is dependent on temp.
of expired gases.)
Resp. H_0
Loss
g/h
21. Respiratory Evaporative Heat Loss
Resp. H(>0 Loss x 0.58
2 _
Resp. Heat Loss kcal/m -h
C-V
22. Skin Evaporative Heat Loss
Evap. Heat toss kcal/m -h"
[Pa-e Wt - Post Wt - Resp. HO Loss - Excess CO (g)] x 0.580
£ £•
BSA
55
-------
ALPHABETICAL LIST OF ABBREVIATIONS AND SYMBOLS USED
(a - v)0- diff. arterio-mixed venous 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
CO- % carbon dioxide
CV closing volume
C 02 venous oxygen content
CW cardiac work
°C degree(s) Celsius
°F degree(s) Fahrenheit
diff. difference
diff. perf. diffusion perfusion
diffusion capacity to carbon monoxide
56
-------
DP
dyn
ERV
evap.
FA
fc
FEF 50%
FEF 75%
FEF 25 - 75%
AFEF .75%
FEV
FEV
FEV
FEV
.0
2.0
3.0
FRC
FVC
g
h
H, ht
Hb
HbCO
Hct
HLa
diastolic pressure
dyne(s)
expiratory reserve volume
evaporative
filtered air
cardiac frequency (same as HR)
forced expiratory flow after 50% of FVC exhaled
forced expiratory flow after 75% of FVC exhaled
forced expiratory flow during middle half of FVC
difference between FEF 75% on helium and
air flow volume curve
forced expired volume
forced expired volume (1.0 second)
forced expired volume (2.0 seconds)
forced expired volume (3.0 seconds)
respiratory frequency
functional residual capacity
forced vital capacity
gram(s)
hour(s)
height
hemoglobin
carboxyhemog1obin
hematocrit
lactate
57
-------
HR
1C
K
*g
IBM
m
M
max
MBP
MEF
MEF25%
MEF50%
mEq
min
ml
MMEF
mMoles
MW
N2
NO
water
heart rate (same as fr)
C
inspirator/ capacity
tissue conductance
kilogram(s)
lean body mass
meter(s)
energy production
maximal, maximum
mean blood pressure
maximal expiratory flow
maximal expiratory flow
at 25% of vital capacity
maximal expiratory flow
at 50% of vital capacity
milliequivalent(s)
minute(s)
mi Hi liter Cs)
maximal mid expiratory flow
millimoles
maximum voluntary ventilation
nitrogen
oxides of nitrogen
oxygen
ozone
probability of wrongfully rejecting the
null hypothesis (level of significance)
-------
barometric pressure
p water vapor pressure
PvCO. mixed venous carbon dioxide partial pressure
PAN peroxyacetylnitrate
% percent
perf. perfusion
PIF point of identical flow on helium and air
flow volume curves
PP pulse pressure
ppm parts per million
press. pressure
prod. production
•
Q cardiac output
R respiratory exchange ratio
R airway resistance
RBC red blood cell
resp. respiratory
RH relative humidity
RR respiratory rate (same as fR)
RV residual volume
s, sec second(s)
SD standard deviation
SE standard error
SI stroke index
SO sulfur oxides
x
i
SP systolic pressure
59
-------
STPD standard temperature and pressure, dry
SV stroke volume
SVC slow vital capacity
SW stroke work
syst. systolic
T ambient air temperature
a
T arm temperature
arm *
T. mean body temperature
T .- calf temperature
T . chest temperature
T-. finger temperature
T globe temperature
T. ,. forehead temperature
T radiant temperature
T rectal temperature
rc
T room temperature
7 , mean skin temperature
SK ,
T . . thigh temperature
T toe temperature
toe
T wall temperature
T . wet bulb temperature
temp. temperature
TGV thoracic gas volume
TLC total lung capacity
TLV threshold limit values
TPR total peripheral resistance
60
-------
V volume
•
V timed ventilator/ volume
•
VA alveolar ventilation
A , -
• •
V./Q ventilation perfusion ratio
t\
•
Vn ventilator/ volume, expired
c
•
Vo oxygen
max
maximal aerobic capacity
(maximal aerobic power)
V- tidal volume
VC vital capacity
H, wt weight
WBGT wet bulb globe temperature index
yr year(s)
2
X statistical datum derived in the
chi -square test
61
-------
SECTION X
APPENDIX
PRINTOUT OF METABOLIC, CARDIOVASCULAR
AND PULMONARY FUNCTION DATA
62
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91.02 6370
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90.63 6300
0.03 0
0.00 0
09.74 6441
0.00 0
90.67 6581
92.8U 6348
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96.01
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96.33
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90.01
0.00
95.62
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96.67
97.45
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0.00
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4.18
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1.54
4.20
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73.52
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1C
ML
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0.0
0.0
0.0
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190.0
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0.00
37. Oi
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33.00
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33.16
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33.57
36.90
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0.00
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98.21
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86.01
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86.36
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87.28
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56.50
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0.000
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0.000
0.000
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0.00
0.00
O.oO
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0.00
0.00
0.00
0.00
0.00
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2.42
0.00
2.10
0.00
2.31 .
. 0.00 .
0.00
DIFF.PfcRF
O.uO
0.00
0.00
0.00
3.42
0.00
3.92
0.00
0.00
V ALV
L/M1N
O.UO
0.00
33.53
0.00
34.69
0.00
35.3d
0.00
0.00
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CO
/"•
tVtNl ft., .1) SfAttil 1C ofANJ fcKV ilANU KV
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IT" j»osT EX?
-------
TECHNICAL REPORT DATA
I'lcosf reuJ liiuriit-iiuns on the reverse before completing)
1. REPORT NO.
EPA-600/1-78-006
4. TITLE AND SUBTITLE
THE EFFECT OF NITROGEN DIOXIDE ON LUNG FUNCTION IN
NORMAL SUBJECTS
3. RECIPIENT'S ACCESSION* NO.
5 REPORT DATE
January 1978
6. PERFORMING ORGANIZATION CODE
7. 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, California 93106
10. PROGRAM ELEMENT NO.
1AA601
11. CONTRACT/GRANT NO.
68-02-1757
12. SPONSORING AGENCY NAME AND ADDRESS
Health Effects Research Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
T-Hanolp Park. N.C. 2771]
13. TYPE OF REPORT AND PERIOD COVERED
RTP,NC
4. SPONS
14. SPONSORING AGENCY CODE
EPA 600/11
15. SUPPLEMENTARY NOTES
16. ABSTRACT
Cardiopulmonary and metabolic responses of three groups, each consisting of
five adult males (age 19 - 29) were determined before, during, and after a
2 hour exposure to 0.0.62 + 0.12 ppm N02 at 25°C and 45% RH. The three groups
exercised during exposure at 40% of Vn« for either 12, 30, or 60 min. for groups
4* Ul&A
C, A, and B, respectively. During the exercise periods the ventilation was about
33 liters/min, a four-fold increase over the resting level. There were no
physiologically significant cardiovascular, metabolic, or pulmonary function
changes which could be attributed to exposure to this level of N02 (0.62 ppm).
There were no differences between the groups in their response despite the fact
that groups A and B received more N02 as a result of 28% and 84% greater
ventilations, respectively.
7.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
lung
nitrogen dioxide
air pollution
b.lOENTIFIERS/OPEN ENDED TERMS
c. COSATI Field/Group
06 F, P, T
8. DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
19. SECURITY CLASS .'This Kepnrtj
UNCLASSIFIED
21. NO. OF PAGES
81
20. SECURITY CLASS /Tliis papa)
UNCLASSIFIED
22. PRICE
EPA Form 2220-1 (9-73)
74
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