/ /







AIR QUALITY CRITERIA
FOR
NITROGEN OXIDES



\

SUMMARY AND
CONCLUSIONS









ENVIRONMENTAL PROTECTION AGENCY

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AIR QUALITY CRITERIA
FOR
NITROGEN OXIDES
SUMMARY AND
CONCLUSIONS
(Reproduced from original report AP-84)
ENVIRONMENTAL PROTECTION AGENCY
Air Pollution Control Office
Washington, D. C.
January 1971

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CHAPTER 11
SUMMARY AND CONCLUSIONS
A. INTRODUCTION
This document contains a consolidation
and an assessment of the current state of
knowledge regarding the group of air pollut-
ants known as the oxides of nitrogen. This
chapter provides a concise presentation of
that information, including reasonable con-
clusions for evaluating the concentrations of
nitrogen oxides (NOx) and the accompanying
situations that have an effect on either health
or welfare. The studies and data cited com-
prise the best available basis for developing
specific standards for NOx in the ambieftt air,
aimed at protecting public health and the
environment.
Although the essential role of NOx in the
production of photochemical oxidants is
treated from the physical-chemical standpoint
in this document, little research has been
done to demonstrate the significance of the
indirect effects of NOx on health, vegetation,
and materials through the photochemical
reaction mechanism; thus, only the direct
effects of NOx are treated here. A PCO pub-
lication AP-63, Air Quality Criteria for Photo-
chemical Oxidants, provides a comprehensive
review of photochemical oxidant effects.
Units of pollution concentration used in
this document are expressed as both mass per
unit volume (e.g., micrograms per cubic
meter, ng/m^) and as volume-ratios (e.g..
parts per million, ppm). Conversion between
these units requires a knowledge of the gas
density, which varies with temperature and
pressure measurement. In this document 25°C
(77° F) has been taken as standard tempera-
ture. and 760 mm Hg (atmospheric pressure
at sea level) as standard pressure. All refer-
ences to NOx are expressed in terms of NO2
mass per unit volume on the basis of the con-
version formula: ppm x 1880 =/jg/m^ at 25°
C, 760 mm Hg, unless otherwise specified.
Similarly, hydrocarbons and oxidant concen-
trations are expressed as mass of methane and
ozone per unit volume, respectively.
B. PROPERTIES OF NITROGEN OXIDES
AND PHYSICAL EFFECTS ON
LIGHT TRANSMISSION
Of the oxides of nitrogen known to exist,
only two, nitric oxide (NO) and nitrogen
dioxide (NO2) are emitted to the atmosphere
in significant quantities. Nitric oxide is
formed during all atmospheric combustion
processes in a spontaneous chemical reaction
between the nitrogen and oxygen in the air.
The amount formed depends on the combus-
tion temperature, the concentration of both
reactants and products, and the length of time
favorable conditions persist for the reaction.
Both NO and NOt are formed when com-
bustion temperatures exceed approximately
1093°C (2000° F), but usually less than 0.5
percent is NO^. More NO2 is formed when
atmospheric oxygen (O2) reacts with NO, but
at the dilute concentrations of NO charac-
teristically found in ambient atmospheres,this
reaction proceeds very slowly. During the
initial phases of exhaust gas dilution, how-
ever, the concentration of NO is high, and
forces the reaction to proceed more rapidly
until the exhaust has been sufficiently diluted
(to I ppm or less). At that time the major
process for converting NO to NO2 reverts to
the photochemical cycle.
Visibility reduction is common in polluted
atmospheres. Scattering and absorption of
light rays by particles and gases reduce the
11-

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brightness and contrast of distant objects. The
degree of reduction depends on the concen-
tration and properties of the pollutants.
Nitrogen dioxide absorbs light energy over the
entire visible spectrum, although primarily in
the shorter, blue-wavelength regions; thus,
NOt can by itself reduce visibility. At pre-
sent, however, under most ambient condi-
tions, aerosols make the major contributions
to visibility reduction.
C.	SOURCES AND CONTROL OF
ATMOSPHERIC NITROGEN OXIDES
On a global basis, the total amount of
nitrogen oxides generated by natural sources
exceeds the amount from man-made, techno-
logical sources. Natural scavenging processes
keep background levels in nonurban areas
low. on the order of 8 pg/m^ (4 ppb) NOt
and 2 /ig/m^ (2 ppb) NO. In urban areas,
however, where 60 percent of the techno-
logical sources are located, the levels are fre-
quently higher because pollutants are added
faster than scavenging processes control them.
Fuel combustion is the major source of
technological NOx air pollution. Chemical
processing is responsible for high, but local-
ized emissions.
Control of NOx emissions has been di-
rected at both combustion sources and chemi-
cal processes. For stationary combustion
sources, the control principle has been based
on reducing either the flame temperature or
the availability of oxygen, to prevent NO
formation. Similar principles of control are
applicable to motor vehicles. Catalytic prin-
ciples, which have been applied to reduce
NOx emissions from chemical processes, are
also being investigated for possible use in
control of NOx in motor-vehicle exhaust.
D.	CHEMICAL INTERACTIONS
OF NITROGEN OXIDES
IN THE ATMOSPHERE
The role of NOx in the generation of pho-
tochemical oxidants is a complex function of
the interaction of certain hydrocarbons (HC)
with the NO2 photolytic cycle, which is dis-
cussed here as well as in the document AP-63.
Air Quality Criteria for Photochemical Oxi-
dants and the document AP-64, Air Quality
Criteria for Hydrocarbons,
In order to fully describe the HC-NOx-OX
interrelationship a comprehensive simulation
model that takes into account emission rates,
chemical reactions, and atmospheric disper-
sion factors, is required. In the absence of
such an applicable model an observation-
based model was developed and applied to
ambient aerometric data. This la** 1 model is
restricted to defining the maximum daily oxi-
dant that may be reached from a given early-
morning precursor level and, therefore, the
model results in definition of the upper-level
oxidant curve, as a function of precursor con-
centrations. The model for the NOx-OX rela-
tionship indicates that an NOx 6- to 9-a.m.
value of 80 /ig/m^ (0.04 ppm) is associated
with the reference concentration of 200
jug/m^ (0.1 ppm) maximum daily 1-hour-
average oxidant.
The reference concentration of 200 ^g/m^
OX used here was selected on the basis of
convenience and does not represent the
lowest health-related value (130 Mg/m^ OX)
expressed in APCO publication AP-63, Air
Quality Criteria for Photochemical Oxidants.
Application of the observation-based model
to ambient NOx, HC, and oxidant interrela-
tionships showed that the peak oxidant level
is dependent on the concentration of both
reactants. Analysis of data from three urban
areas indicates that a reference concentration
of 200	(0.1 ppm) maximum daily
1-hour-average oxidant is associated with an
HC range of 200 to 930	(0.3 to 1.4
ppm C) 6- to 9-a,m. nonmethane hydrocar-
bon, when the 6- to 9-a.m. average NOx,
expressed as N02, was below 80/ig/m^ (0.04
ppm). Similarly, observation of the 200
/ig/m^ (0.3 ppm C) nonmethane HC level
showed NOx in the range of 80 to 320pig/m^
(0.04 to 0.16 ppm), expressed as NO2. These
conclusions are supported by the predomi-
nance of weekend data near the low-concen-
tration end of the upper-limit oxidant curve,
which reflects the lower oxidant values from
lower emissions on weekends.
11-2

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E.	METHODS FOR MEASURING
NITROGEN OXIDES
Research.is still needed to develop and
thoroughly evaluate more sensitive, reliable,
and practical methods for measuring ambient
levels of NO, NOt, and NOx. All of the field
techniques in use at present can measure only
NO2 directly; NO must be oxidized to NO->,
then measured. NOx can be determined either
by summing NO and NO2 concentrations that
have been measured independently or by
oxidizing NO to NO^. then measuring the
total as NOt.
Any method used for measuring NO2 in
the ambient air should be calibrated against
atmospheres containing known amounts of
NO2. The use of permeation tubes to generate
the test atmospheres is recommended.
Two techniques are currently used in
atmospheric monitoring programs. For sam-
pling periods of 30 minutes or less, the most
suitable currently available method for meas-
uring NOt is the colorimetric Griess-Saltzman
method. This method can also be automated
for continuous measurement. The Jacobs-
Hochheiser method is the most suitable of the
available methods for long-term (up to 24
hours) sampling, or for situations requiring a
delay of the analysis for more than 4 hours
after sampling. The Griess-Saltzman and
Jacobs-Hochheiser methods are not inter-
changeable, can yield different results, and
must be chosen carefully, according to the
purposes of the sampling to be done.
When used in conjunction with an oxidiz-
ing prescrubber to convert NO to NO2, the
continuous Griess-Saltzman method can be
used to measure NO in ambient air in either a
series or parallel mode, with the same or
separate samples of air. Problems exist in
obtaining complete NO to NO2 oxidation,
and researchers disagree as to which of the
two modes is more satisfactory.
F.	ATMOSPHERIC LEVELS OF
NITROGEN OXIDES
Continuous measurement of the oxides of
nitrogen by various monitoring networks has
made it possible to compile tables of mean
concentrations averaged over different time
periods and to relate various temporal pat-
terns to photochemical and meteorological
parameters.
Both NO and NO2 concentrations display
distinct diurnal variations dependent on both
the intensity of the solar ultraviolet energy
and the amount of atmospheric mixing. In
many sampling areas, these variations are also
associated with the traffic patterns.
Nitric oxide shows an additional seasonal
variation, with higher values occurring during
the late fall and winter months. Nitrogen
dioxide, however, does not display any
distinct seasonal patterns.
The effect of meteorological parameters on
NO and NO2 concentrations has been reason-
ably well documented. As might be expected,
periods of stagnation and high traffic volume
in urban areas have resulted in high peak
levels of NOx.
Continuous measurement has indicated
that peak values of NO above 1.2 mg/m^ (1
ppm) are widespread, but NO2 concentrations
have rarely been measured at this level. Peak
concentrations of NO2 in urban areas rarely
exceed 0.94 mg/m^ (0.5 ppm).
Considerable differences were found among
NO2 data collected at the same site, at the
same time, but by different methods. The
methods of NO, NO2, and NOx measurement
are still in need of refining and must be
judged accordingly.
G. EFFECTS OF NITROGEN OXIDES
ON MATERIALS
Significant effects of NOx have been ob-
served and studied 011 three classes of ma-
terials: textile dyes and additives, natural and
synthetic textile fibers, and metals.
The most pronounced problem is associ-
ated with textile dyes and additives. Fading of
sensitive disperse dyes used on cellulose
acetate fibers has been attributed to NO2
levels below 188 mg/m^ (<100 ppm). Loss of
color, particularly in blue- and green-dyed
cotton and viscose rayon, has occurred in gas
dryers where NOx concentrations range from
1.1 to 3.7 mg/m^ (0.6 to 2 ppm). Yellow dis-
coloration in undyed white and pastel-colored
11-3

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fabrics has recently been attributed to NOx
by controlled laboratory experiments.
Laboratory and field observations have
shown that* cotton and Nylon textile fibers
can be deteriorated by the presence of NOx,
but specific reactants and threshold levels are
undetermined at this time.
Failure of nickel-brass wire springs on re-
lays has been related to high particulate
nitrate levels. This type of stress corrosion has
been observed when surface concentrations of
particulate nitrates have exceeded 2.4
jug/cm- and relative humidity was greater
than 50 percent. Another type of this corro-
sion has been associated with annual average
particulate nitrate concentrations of 3.0 and
3.4	pg/m3 with corresponding NOx levels of
124 and 158 #ig/m3 (0.066 and 0.084 ppm).
H. EFFECTS OF NITROGEN OXIDES
ON VEGETATION
The degree of injury occurring with the
lower concentrations of NO2 present in the
atmosphere remains to be determined. Expo-
sure of many kinds of plants to concentra-
tions of NCH above 47 mg/m^ (25 ppm) for
any extended period causes acute necrotic
leaf injury. Such lesions are usually charac-
teristic for each plant, but their nonspecific
character in relation to other toxicants
renders these symptoms of little value in diag-
nosing NO2 damage in the field.
The 1-hour visible-injury-threshold value
for NO2 can be achieved by exposing plants
to 18.8 to 28.2 mg/m^ (10 to 15 ppm). In-
creasing the exposure time, however, obviates
the threshold level; 4.3 to 6.6 mg/m^ (2.3 to
3.5	ppm) NO2 administered for 8 to 21 hours
and 1.9 mg/m^ (1 ppm) NO2 for 48 hours
cause equivalent leaf injury. Continuous fumi-
gation with 940 jug/m^ (0.5 ppm) NO2 for 35
days resulted in leaf drop and chlorosis in
citrus, but no actual necrotic lesions devel-
oped.
The effects of exposure to low levels of
NO2 for extended periods are less evident.
Recently completed studies suggested that
470 Mg/m^ (0.25 ppm) or less of NO2, sup-
plied continuously for 8 months will cause
11-4
increased leaf drop and reduced yield in navel
oranges.
The mechanism(s) by which NOx causes
direct injury to plants can only be postulated
at this time. Evidence of diurnal fluctuation
in sensitivity to NO-> has been presented, and
could indicate that the pollutant is reacting
with a particular plant metabolite, which only
accumulates at certain periods during the day.
The absence of a protective metabolite within
the plant at certain periods would also cause a
diurnal sensitivity.
Limited information regarding the effect of
nitric oxide 011 photosynthesis indicates that
NO would reduce the growth of plants if
concentrations in the range of 3.8 to 7.5
mg/m3 (2.0 to 4.0 ppm) persisted contin-
uously.
1. TOXICOLOGICAL EFFECTS OF
NITROGEN OXIDES
Both of the prominent oxides of nitrogen
present in ambient air are potential health
hazards. At ambient concentrations, NO pre-
sents no direct threat to general health; NO2
does, however. Effects of NO2 determined in
extensive studies are summarized in Table
11-1.
The toxicology of pitrous oxide (N20)and
other oxides of nitrogen does not appear to
be relevant to the problems of ambient air
pollution at the present time.
1.	Nitric Oxide
NO is not an irritant and is not considered
to have adverse health effects at concentra-
tions found in the atmosphere. Its greatest
toxic potential at ambient concentrations is
related to its tendency to undergo oxidation
to NO2. A 12-minute exposure to 3,075
mg/m^ (2,500 ppm) NO has proved lethal to
mice. In addition, NO has been observed to
inhibit bacterial hydrogenase activity at lower
concentrations—24.6 mg/m^ (20 ppm). This
inhibition was reversible, however, until the
exposure reached about 12,300 mg/m^
(10,000 ppm).
2.	Nitrogen Dioxide
NO2 exerts its primary toxic effect on the
lungs. High concentrations, greater than 188
mg/m^ (100 ppm), are lethal to most animal

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Table 11 — 1. SUMMARY OF REPRESENTATIVE N02 EFFECTS

NOt concentration.



Kffect
ppm
jug/111 -
Duration
Comment
Reference
Lowest level associated
with reference oxidant
production of 200 ng/m3
(0.1 ppm)
Increased incidence of
acute respiratory disease
in families
0.04
0.062
to
0.109
80
117 to
205
3 lu
(6 to 9 a.m.)
2 to 3 yr
Chattanooga study - 6-nio
mean concentration range
1
2
Increased incidence of
acute bronchitis in infants
and school children
0.063
to
0.083
118 to
156
2 to 3 yr
%
Chattanooga study ¦ 6-mo
mean concentration range
3
Human
olfactory threshold
0.12
225

Immediate perception
4
Rabbits -
structural changes in
lung collagen
0.25
470
4 hr/day
for 6 days
Still apparent 7 days after
final exposure
5
Navel orange -
leaf abscission;
decreased yield
0.25
470
8 mo.
continuously

6
Rats •
morphological changes
in lung mast cells
characterized by
degranulation
0.5
1.0
940
1880
4 hr
1 hr
Possibly precedes onset of
acute inflammatory reaction
7
Mice -
pneumonitis; alveolar
distension
0.5
940
6 to 24 hr/day
for 3 to 12 mo
Possibly emphysematous
condition
8
Mice -
increased susceptibility
to respiratory infection
0.5
940
6 to 24 hr/day
up to 12 mo
Based on mortality following
challenge with K. pneumoniae
9
Navel orange -
leaf abscission,
chlorosis
0.5
940
35 days,
continuously

6
Rats •
tachypnea, terminal
bionchiolar hypertrophy
0.8
1504
Lifetime,
continuously

10
11-5

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Table 11-1 (Continued). SUMMARY OF REPRESENTATIVE N02 EFFECTS

NO-> concentfation.



b-ffi'ct
ppm
jug /m-s
Duration
Comment
Reference
Rats -
bronchiolar epithelial
changes, loss of cilia,
reduced cytoplasmic blebbing
crystalloid inclusion bodies
0.8
to
2.0
1504
to
3760
Lifetime,
continuously
Possibly pre-cmphyscmatous
lesion
II
Rabbits -
structural changes in lung
collagen
1.0
1880
1 In
Denaturation of structural
protein suggested
12
Sensitive plants -
visible leaf damage
1.0
1880
21 to 48
hr

13
Rats, monkeys -
polycythemia
2.0
3760
3 wk.
continuously
Approximate doubling of red
cell number with lesser in-
creases in hematocrit and
hemoglobin
14
Man -
increase in airway
resistance
5
9,400
10 min
Transient
15
Monkeys -
tissue changes in lungs,
heart, liver, and kidneys
15
to
50
28.200
to
94,000
2 hr
Degree of damage directly
related to concentration
of NO 2
16
species; 90 percent of the deaths are caused
by pulmonary edema.
The concentration time product determines
nonlethal morbidity effects of NO2 expo-
sures. At 940 Mg/m^ (0.5 ppm) for 4 hours or
1.9 mg/m^ (1.0 ppm) for 1 hour, mast cells of
rat lungs became degranulated, possibly signi-
fying the onset of an acute inflammatory
reaction. These cells returned to normal 24
hours after exposure was terminated. Lung
proteins, collagen and elastin, were found to
be altered structurally in rabbits exposed to
1.9 mg/m^ (1 ppm) NO2 for 1 to 4 hours.
The condition was also reversible within 24
hours. Similar changes were observed in rab-
bits exposed to 470 Mg/m^ (0.25 ppm) NO2,
4 hours a day for 6 days, except that recovery
was delayed and some denaturation was still
apparent 7 days after the final exposure.
Denaturation of collagen and elastin associ-
ated with repeated exposure to NO2 has been
suggested as a possible factor in the patho-
genesis of pulmonary emphysema.
Lurly pulmonary emphysema-type lesions
have been observed in dogs exposed contin-
uously to 47.0 mg/m^ (25 ppm) for 6
months. In lung tissue from monkeys exposed
to 18.8 to 94.0 rng/m^ (10 to 50 ppm) NOi
for 2 hours, alveoli were expanded and had thin
septal walls. This response involved increas-
ing numbers of alveoli as the NCH concentra-
tion was increased. Hyperplasia has been ob-
served in respiratory bronchiolar epithelium
of hamsters exposed to 94.0 mg/m^ (50 ppm)
for 10 weeks, and a similar response was
noted in major bronchi and distal portions of
11-6

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the respiratory tract of hamsters exposed to
18.8 mg/m^ (100 ppm) for 6 hours.
Long-teum exposures to NCH concentra-
tions that do not produce acute inflammatory
responses have a cumulative, sustained effect,
suggestive of a pre-emphysematous condition.
Examination of lung tissue from rats ex-
posed to 3.8 mg/m3 (2 ppm) for their natural
lifetimes showed loss of cilia; decreased bron-
chiolar blebbing;and intercellular, crystalloid,
rod-shaped, inclusion bodies. Similar effects
have been seen in lungs of rats continuously
exposed to 1.5 mg/m3 (0.8 ppm). Alveoli in
lungs of mice exposed to 940 ng/m-* (0.5
ppm) for 3 to 12 months on 6-. 18-. and
24-hour daily schedules have shown increase
in size from distension rather than from septal
breakage. The accompanying inflammation of
the bronchiolar epithelium and reduction in
distal airway size suggested the development
of early focal emphysema.
Rats chronically exposed to 18.8 to 47,0
mg/m^ (10 to 25 ppm) NO 2 developed com-
pensatory changes, such as polycythemia and
thoracic kyphosis, with lateral flaring of the
ribs.
Since certain pathological changes seen in
animals after experimental NOt exposure are
similar to changes that occur in the patho-
genesis of chronic obstructive pulmonary
disease in man, it is suggested that long-term,
low-level exposures to NC>2 may play a signifi-
cant role in the development of chronic lung
disease.
Exposure of mice, hamsters, and squirrel
monkeys to NO2 increased susceptibility to
bacterial pneumonia and influenza infection.
The susceptibility has been demonstrated by a
significantly increased mortality, decreased
survival time, and a reduction in ability to
clear infectious agents from the lungs. In
mice, threshold for increased susceptibility to
Klebsiella pneumoniae occurred after expo-
sure to 6.6 mg/m^ (3.5 ppm) NCb for 2
hours, if the infectious challenge was given
within 1 hour after the NO2 exposure. Squir-
rel monkeys exposed to 18.8 nig/m^ (10
ppm) NO2 for 2 hours and then challenged
with K. pneumonia aerosol retained the in-
fectious agent in their lungs for extended
periods of time.
In long-term studies of mice, significantly
increased susceptibility to infection occurred
after continuous daily exposure to 940^ig/m^
(0.5 ppm) NO2 for 3 months, and after 6- and
18-hour daily exposures for 6 months. A
significant increase in susceptibility to influ-
enza virus or K. pneumoniae was also seen in
squirrel monkeys continuously exposed to
18.8 and 9.4 mg/m^ (10 and 5 ppm) NO2 for
1 and 2 months, respectively. In addition,
interferon formation has been impaired and
resistance lo viral infection has decreased
following exposure of rabbits to 47.0 mg/m^
(25 ppm) NO2 for 3 hours. Researchers con-
jecture thai such increased susceptibility to
infection may also be significant in the patho-
genesis of human lung disease.
Inhalation of NOi can produce other
systemic effects, although these are generally
secondary to the effects on the lungs. In
monkeys exposed to 28.2 to 94.0 mg/rn^ (15
to 50 ppm) NO2 for 2 hours, cellular changes
appeared in heart, liver, and kidney tissue. A
circulating substance, possibly a lung anti-
body, has been detected in the blood of
guinea pigs exposed to 9.4 mg/m^ (5,0 ppm)
for 4 hours daily. 5 days per week for 5.5
months. Rats and monkeys continuously
exposed to 3.8 mg/m^ (2.0 ppm) NCH for 3
weeks developed marked polycythemia.
Methemoglobin has been detected in the
blood of several species exposed to NCH con-
centrations greater than 122 mg/m^ (70 ppm)
for I hour.
The small amount of information available
concerning the toxicologieal effects of the
oxides of nitrogen in man pertains to levels
higher than those found in ambient air.
Experimental exposure of volunteer subjects
to 9.4 mg/m^ (5 ppm) NCM for 10 minutes
has produced a substantial, but transient, in-
crease in airway resistance. Other data, de-
rived from occupational exposure to high-con-
centration mixtures of NO and NOi.are com-
plicated by the presence of other pollutants.
11-7

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Impaired pulmonary function, evidenced
by reduced maximal breathing capacity, in-
creased expiratory resistance, and occasional
decreased vital capacity, has been observed in
patients accidentally exposed to high concen-
trations of nitrous fumes for a few minutes.
Such evidence has persisted for more than 2
years after the exposure, in some cases. In one
case, occupational exposure to 169 mg/m^
(90 ppm) NOi for 30 minutes produced
pulmonary edema and a vital capacity 50
percent lower than expected 18 hours later.
Exposure to very high concentrations for
about 5 minutes has produced death within 2
days to 5 weeks.
The threshold for odor perception of NO->
is about 225 /jg/m^ (0.12 ppm).
J. EPIDEMIOLOGICAL APPRAISAL OF
NITROGEN OXIDES
Nitrogen dioxide, the only oxide of nitro-
gen examined in epidemiological surveys, can
be significantly correlated with increased
respiratory disease at mean 24-hour concen-
trations between 117 and 205	(0.062
and 0.109 ppm).
Effects of community exposure to NOt
were studied in four residential areas of
greater Chattanooga. The ventilatory per-
formance (FEVq 75) °f children in a high-
NC>2 area was significantly reduced, when
compared to the performance of children in
control areas. In addition, an 18.8 percent
relative excess of respiratory illness occurred
among families exposed to high NO2 concen-
trations. A 10.4 percent excess occurred
among families in an elevated-particulate area.
The increased incidence of acute respiratory
disease was observed when the mean 24-hour
NO2 concentration, measured over a 6-month
period, was between 117 and 205 Mg/m-*
(0.062 and 0.109 ppm) and the mean sus-
pended nitrate level was 3.8 fig/m^ or greater.
In a retrospective study of the same Chatta-
nooga area, exposure to intermediate and high
levels of NO2 in ambient air was associated
with a significant increase in the frequency of
acute bronchitis among infants exposed for 3
years and school children exposed for 2 and 3
years. When increase was observed, the mean
24-hour NOi concentration, measured over a
6-month period, had ranged between 118 and
156 jug/m-^ (0.063 and 0.083 ppm) and the
mean suspended nitrate level had been 2.6
/ig/rn-^ or greater.
A report from Czechoslovakia indicates
that NOx has produced several alterations in
the peripheral blood. Increased levels of
methemoglobin were observed in school chil-
dren residing in a town that had relatively
high ambient levels of nitrogen oxides. The
findings in that report require further clari-
fying investigation, however, before conclu-
sions can be drawn.
The Chattanooga studies have several impli-
cations in regard to respiratory illness-implica-
tions that can be extended to other cities.
Since NOt does not exhibit marked seasonal
variations (See discussion chapter 6, Section
B,2), direct comparison of the NASN yearly
averages with the lower limit at which health
effects were noted in the Chattanooga studies
is. therefore, possible. Any site that exhibits a
concentration of 11 3 ng/m^ (0.06 ppm) or
greater exceeds the Chattanooga health-
effect-related NOt value. Ten percent of cities
with populations of less than 50,000 show a
yearly average equal to or exceeding 113
fig/m3 (0.06 ppm). In the population range
from 50,000 to 500,000, 54 percent of the
cities in the United States equal or exceed a
yearly average of 113 jug/m^ (0.06 ppm)
NO2. In the over-500,000 population class,
85 percent of the cities equal or exceed 113
jug/m^ (0.06 ppm) NO2 on a yearly average.
K. AREAS FOR FUTURE RESEARCH
1. Environmental Aspects of Oxides of
Nitrogen
The fate of as much as 50 percent of the
nitrogen oxides that become incorporated
into the photochemical complex is still unde-
termined, for many of the nitrogen oxide
end products remain unidentified.
Even for the identified nitrogen oxides the
relationship between emissions and air quality
11-8

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needs further definition through improved
instrumentation, expansion of the number of
monitoring stations, and more accurate deter-
mination of the location and distribution of
sources.
A model for predicting upper limits of
photochemical oxidant pollutants from ob-
served HC and NOx levels has been presented,
but needs further definition, sophistication,
and revision before it can be applied on a
practical basis.
2.	Effects on Vegetation and Materials
a.	Materials
Further research is needed to define reli-
able dose-response relationships for vulnerable
materials. The effects of variables such as
temperature, relative humidity, sunlight, and
other pollutants on the damage potential of
the nitrogen oxides must also be determined.
b.	Vegetation
The biochemical, enzymatic, and other
metabolic responses of plants to ambient
levels of the nitrogen oxides are in need of
research-based delineation. Evidence of diur-
nal variations in sensitivity suggests the exist-
ence of either extra-sensitive or protective
metabolites in some plants. Evidence of syner-
gistic effects of NOx in mixtures containing
other air pollutants should be investigated
further.
3.	Toxicity of Oxides of Nitrogen
In order to ascribe toxicity to a specific
concentration range of NOx, the relation of
metabolic tissue changes to NCH concentra-
tion-time responses and the relative impor-
tance of low-concentration, long-time expo-
sures versus short-time, peak ambient concen-
trations should be studied. The interactions of
the oxides of nitrogen with particulate pollut-
ants in relation to biochemical, biophysical,
infectious, immunological, and ultrastructural
response parameters require further research
aimed at elucidating possible synergistic
damage or protection. Tolerance to NO2 in
the presence of oxidant pollutants has been
suggested as a result of exploratory studies.
but the biologic importance of such protec-
tion needs to be defined.
Further examination of w vivo biochemical
and biophysical effects of exposure to typical
ambient concentrations of the oxides of nitro-
gen relative to: (1) oxidation of fatty acid
double bonds in lung surfactants; and (2)
denaturation or alteration of lung proteins
(collagen and elastin, enzymes, and cellular
membranes) is needed before optimal treat-
ment for. or protection from exposures can
be developed.
4. Epidemiology of Oxides of Nitrogen
In order to determine the effect of NOx on
the health of the general population, epidemi-
ological research must be expanded to in-
clude: (I) studies to determine which seg-
ments of the population are most susceptible
to the oxides of nitrogen; (2) studies to pre-
cisely delineate the relationship between
niethemoglobin levels, peripheral blood altera-
tions, and nitrogen oxide concentrations; (3)
replication of studies of the enhanced suscep-
tibility to respiratory infection that occurs
with exposure to ambient levels of NOx: and
(4) studies to determine the relationship
between other pollutants and the oxides of
nitrogen and their material effect on human
health.
L. CONCLUSIONS
Derived from a careful evaluation of the
studies cited in this document, the conclu-
sions given below represent the best judgment
of the scientific staff of the Air Pollution
Control Office of EPA regarding the ef-
fects that may occur when various levels
of nitrogen oxides are reached in the ambient
air. More detailed information from which
the conclusions were derived, and the qual-
ifications that entered into the considera-
tions of these data, can be found in appro-
priate chapters of this document.
1. Nitric Oxide
a. Effects on Humans
No evidence shows that NO produces sig-
nificant adverse health effects at the ambient
11-9

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atmospheric concentrations thus far meas-
ured (chapter 9, section B.).
b.	Effects on Materials and Vegetation
Damaging effects to materials at ambient
pollutant levels of nitrogen oxides have been
observed; however, concentrations of NO
producing these effects have not been pre-
cisely determined (chapter 7. sections C and
D).
When beans were exposed to concentra-
tions of 12.3 mg/m^ (10 ppm). apparent
photosynthesis was reduced 50 to 70 percent;
when exposed to 4.9 mg/m-1 (4 ppm), a 10
percent reduction occurred (chapter 8, sec-
tion B).
c.	Effects on Laboratory Animals
A concentration of 3,075 mg/m^ (2,500
ppm) is lethal to mice after a 12-minute expo-
sure. Fully reversible inhibition of bacterial
hydrogenase activity occurs jit a concen-
tration of 24.6 mg/m^ (20 ppm) (chapter 9,
section B).
2. Nitrogen Dioxide
a. Effects on Humans
(1)	Short-Term Exposure. Limited studies
show that exposure to NO2 for less than 24
hours continuously can have several concen-
tration-dependent effects.
1.	The olfactory threshold value of NO? is
about 225 ^g/m^ (0.12 ppm) (chapter 9,
section C.2.a.l).
2.	Exposure to 9.4 mg/m^ (5 ppm) for 10
minutes has produced transient increase
in airway resistance (chapter 9, section
C.2.a.2).
3.	Occupational exposure to 162.2 mg/m^
(90 ppm) for 30 minutes has produced
pulmonary edema 18 hours later, accom-
panied by an observed vital capacity that
was 50 percent of the value predicted for
normal function (chapter 9, section
C.2.b).
(2)	Long-Term Exposure. An increased inci-
dence of acute respiratory disease was observed
in family groups when the mean range of 24-
hour NO? concentrations, measured over a 6-
month period, was between 117 and 205 pg/m^
(0.062 and 0.109 ppm) and the mean sus-
pended nitrate level during the same period
was 3.8 /ig/111^ or greater.
The frequency of acute bronchitis in-
creased among infants and school children
when the range of mean 24-hour NOt concen-
trations, measured over a 6-month period, was
between 118 and 156 /ig/m^ (0.063 and
0.083 ppm) and the mean suspended nitrate
level during the same period was 2.6 jug/m^ or
greater (chapter 10, section C. 1).
Yearly average NOi concentrations exceed
the Chattanooga health-effect-related value of
113 #ig/m3 (0.06 ppm) in 10 percent of cities
in the United States with populations of less
than 50,000, 54 percent of cities with popula-
tions between 50,000 and 500,000, and 85
percent of cities with populations over
500,000 (chapter 10, section d.).
b. Effects on Materials and Vegetation
Although damage to materials has been
attributed to the oxides of nitrogen in ambient
atmospheres, the precise air-concentrations
producing these effects have not been deter-
mined (chapter 7, sections C and D).
Crops and ornamental plants can be classi-
fied into three groups with respect to NOx
sensitivity: sensitive, low sensitive, and resist-
ant. Several characteristic effects have been
observed among the sensitive plants studied
with regard to direct NO2 exposure.
1.	Exposure to 470 pg/m^ (0.25 ppm) of
NO2 for 8 months caused leaf abscission
and decreased yield among navel oranges
(chapter 8. section G).
2.	Exposure to NO? concentrations of 940
Aig/m^ (0.5 ppm) for 35 days resulted in
leaf abscission and chlorosis on citrus
fruit trees (chapter 8, section G).
3.	Exposure to NO2 concentrations of 1.9
mg/ni^ (1 ppm) for 1 day can cause
overt leaf injury to sensitive plants
(chapter 8, section G).
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c. Effects on Laboratory Animals
(1)	Short-Term Exposure. Short-term effects
of NC>2 on anfrnals can be summarized by the
analyses of five salient experiments.
1.	Exposure of rats to either 940 A»g/m^
(0.5 ppm) for 4 hours, or 1.9 mg/m^
(1.0 ppm) for 1 hour has produced
degranulation of lung mast cells (chapter
9, section C.l .b.3).
2.	Structural changes in collagen were ob-
served in rabbits exposed to 1.9 mg/m-3
(1.0 ppm) for I hour (chapter 9, section
C.l.b.2).
3.	The threshold for increased suscepti-
bility of mice to respiratory infection by
K. pneumoniae is 6.6 mg/m3 (3.5 ppm)
for 2 hours (chapter 9, section C. I.d).
4.	Exposure of monkeys to 28.2 to 94.0
nig/m-^ (15 to 50 ppm) for 2 hours has
produced damage to their lungs, heart,
liver, and kidneys and pulmonary
changes that resemble those seen in
human emphysema (chapter 9, sections
C.l.b.3 and C.l.c.l).
5.	In rabbits exposed to 47.0 mg/m^ (25
ppm) for 3 hours interferon formation
and resistance to viral infection de-
creased (chapter 9, section C. 1 .d).
(2)	Long-Term Exposure. Long-term expo-
sure to NO2 altered several functions in animal
circulatory and respiratory systems.
1.	Structural changes were found in lung
tissue collagen from rabbits exposed to
470 #ig/m3 (0.25 ppm) 4 hours a day for
6 days (chapter 9, section C.l.b.2).
2.	Enhanced susceptibility of mice to
respiratory infection by K. pneumoniae
was observed after 3 months of contin-
uous exposure to 940 Mg/m3 (0.5 ppm)
(chapter 9, section C. 1 d).
3.	Polycythemia has been reported in rats
and monkeys exposed continuously to
3.8 mg/m^ (2.0 ppm) for 3 weeks
(chapter 9, section C.l.c.3).
4.	Changes resembling those seen in human
emphysema were reported in the follow-
ing: mice exposed 6 to 24 hours daily,
for a period of 3 to 12 months to 940
(ig/m3 (0.5 ppm) (chapter 9. section
C.l.b.3); rats continuously exposed to
18.8 to 47.0 ing/m^ (10 to 25 ppm) for
4 to 12 months (chapter 9, section
C. l..b.3); and dogs continuously ex-
posed to 47.0 mg/m^ (25 ppin) for 6
months (chapter 9, section C. 1 .b.3).
3. Other Nitrogen Oxide Effects
a.	Photochemical Relationships
An observation-based model applied to
ambient NOx, HC. and oxidant interrelation-
ships showed that peak oxidant yield was
dependent on the concentration of both reac-
tants. Analysis of data from three urban areas
indicated that a reference concentration of
200 jug/m^ (0.1 ppm) maximum daily
1 -hour-average OX could be associated with a
hydrocarbon range of 200 to 930 //g/m^ (0.3
to 1.4 ppm C) 6- to 9-a.m. nonmethane
hydrocarbon, expressed as methane, when the
6- to 9-a.m. average NOx. expressed as NO2,
was below 80 ng/m^ (0.04 ppm). A similar
observation related an NOx range of 80 to
320 ng/m^ (0.04 to 0.16 ppm). expressed as
NO2. with 200 iiglm$ (0.3 ppm C) nonmeth-
ane hydrocarbon.
b.	Stress Corrosion
Nitrogen oxide reaction products have been
associated with corrosion and failure of elec-
trical components. In two cities where this
problem has been observed, the 1965 average
airborne particulate nitrate concentration
were 3.0 and 3.4 j/g/m3 with associated
average NOx levels of 124 and 158 pg/m3
(0.066 to 0.084 ppm).
M. RESUME
Adverse health effects, as evidenced by a
greater incidence of acute bronchitis among
infants and school children, have been ob-
served, under the conditions prevailing in the
areas where studies were conducted, when the
mean 24-hour N02 concentration, measured
by the Jacobs-Hochheiser method, over a
6-month period, varied from 118 to 156
Mg/m3 (0.063 to 0.083 ppm). On an annual
basis, a maximum 24-hour average as low as
284 ngfm3 (0.15 ppm) would be expected to
be associated with a 6-month mean of 118
11-11

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Atg/m3. Adverse health effects, as evidenced
by an increased incidence of acute respiratory
disease, have been observed in family groups
when the mean 24-hour N02 concentration
measured over a 6-month period was between
117 and 205 ng/m3 (0.062 and 0.109 ppm)
and the mean suspended nitrate level was 3.8
/Lig/m3 or greater.
An analysis of 3 years of data collected in
three American cities shows that on those
several days a year when meteorological con-
ditions are most conducive to the formation
of photochemical oxidant, and the 6- to 9-u.m.
nonmethane hydrocarbon concentration is
200 fig/m3 (0.3 ppm C), a 6- to 9-a.m. NOx
concentration (measured by the continuous
Saltzman Method and expressed as N02) that
ranges between 80 and 320 /ig/m1 (0.04 and
0.16 ppm) would be expected to produce a
1-hour photochemical oxidant level of 200
fig/nr1 (0.1 ppm) 2 to 4 hours later. If this
same functional relationship exists at the low-
est levels at which photochemical oxidant has
been observed to adversely affect human
health, the corresponding nonmethane hydro-
carbon concentration would be approx-
imately 130 /ig/m3 (0.2 ppm C) and the 6- to
9-a.m. NOx level would be as high as 214
jug/m3 (0.11 ppm).
Adverse effects on vegetation such as leaf
abscission and decreased yield of navel
oranges have been observed during fumigation
studies when the N02 concentration (mea-
sured by the continuous Saltzman Method)
was 470 /ig/m3 (0.25 ppm) during an
8-month period.
Nitrate compounds have been identified
with corrosion and failure of electrical com-
ponents. In two cities where these effects
were observed, the average airborne nitrate
particulate concentrations were 3.0 and 3.4
/ig/m3 with associated average NOx levels of
124 and 158 jug/m3 (0.066 and 0.084 ppm).
It is reasonable and prudent to conclude
that, when promulgating ambient air quality
standards, consideration should be given to
requirements for margins of safety that would
take into account possible effects on health,
vegetation, and materials that might occur
below the lowest of the above levels.
IN. RKFKRKNCKS
1. Air Quality Criteria for Photochemical Oxidants.
National Air Pollution Control Administration.
Washington. D C. Publication No. AP-63. March
1970.
2.	Shy. et al. The Chattanooga School Study:
Effects of Community Exposure to Nitrogen
Dioxide. Incidence of Acute Respiratory Illness.
To be published in J. Air Pollut. Contr. Ass,,
1970.
3.	Pearlman. M. E.. et al. Nitrogen Dioxide and
Lower Respiratory Illness. Submitted to
Pediatrics, 1970.
4.	Henschler, P, et al. Olfactory Threshold of Some
Important Irritant Gases and Manifestations in
Man by Low Concentrations. Arch.
Gewerbepathol. Gewerbehgy., Berlin. 17:
547-570. llJ60.
5.	Mueller, P. K. and M. Hitchcock. Air Quality
Criteria-Toxicological Appraisal for Oxidants.
Nitrogen Oxides, and Hydrocarbons. J. Air
Pollut. Control Ass., 19: 670-676. 1969.
6.	Thompson, C. R., et al. Effects of Continuous
Exposure of Navel Oranges to NO2. Atmos.
Environ. In Press, 1970.
7.	Thomas, H. V.. P. K. Mueller, and G. Wright.
Response of Rat Lung Mast Cells to Nitrogen
Dioxide Inhalation. J. Air Pollut. Contr. Ass.. 17:
33-35, 1967.
8.	Blair, W. H,, M, C. Henry, and R. Ehrlich.
Chronic Toxicity of Nitrogen Dioxide: II. Effects
on Histopathology of Lung Tissue, Arch,
Environ. Health, IS: 186-192, 1969.
9.	Ehrlich, R. and M. C. Henry. Chronic Toxicity of
Nitrogen Dioxide: I. Effects on Resistance to
Bacterial Pneumonia. Arch. Environ. Health, 17:
860-865, 1968.
10. Freeman, G., N. J. Furiosi and G. B. Haydon.
Effects of Continuous Exposure to 0.8 ppm NOi
on Respiration of Rats. Arch. Environ. Health.
13: 454-456, 1966.
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11. Freeman. G. and ('¦. B. lla>don. Fmphysema
After. L».».w-Lev*sl Fxposure lo NIC) v Arch.
Hnvii'on. Health. 
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