EPA-AA-IMS/81-8
HEALTH EFFECTS OF CARBON MONOXIDE AND OZONE
July 1981
Inspection and Maintenance Staff
Emission Control Technology Division
Office of Mobile Source Air Pollution Control
Office of Air, Noise, and Radiation
United States Environmental Protection Agency
Ann Arbor, Michigan
Prepared With the Assistance Of:
ENERGY AND ENVIRONMENTAL ANALYSIS, INC.
1111 North 19th Street
Arlington, Virginia 22209
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INTRODUCTION
The purpose of this report is to summarize the information known about the
health effects of carbon monoxide (CO) and ozone (03), and how that
information is used by EPA to set National Ambient Air Quality Standards
(NAAQS's). An additional purpose of this report is to discuss the sources
most likely to contribute to high levels of CO and 03 and how EPA control
programs will reduce emissions from these sources in the future. For ease in
reading, all of the information in this report is presented in question and
answer format.
1. What are carbon monoxide and ozone?
Carbon monoxide (CO) and ozone (03) are two pollutants found in the air
which can have harmful impact on public health. Carbon monoxide is a
colorless, odorless, poisonous gas. Ozone is a pungent-smelling, faintly
bluish, toxic form of pure oxygen. Ozone differs from molecular oxygen (0£)
in that each molecule has an additional oxygen atom which makes it more
chemically and biologically reactive.
2. What are the man-made and natural sources of CO and 0^?
High concentrations of CO are largely the result of incomplete combustion of
fossil fuels, especially from highway vehicles. Processes such as forest
fires and the oxidation of atmospheric methane are natural sources of CO, but
together they make only a small contribution to atmospheric CO levels.
Ozone is formed by chemical reactions of volatile organic compounds (VOC) —
primarily hydrocarbons — and oxides of nitrogen (NOx) in the presence of
sunlight. Ozone originates mainly from VOC and NOx emissions produced by
motor vehicles, combustion of fossil fuels and industrial processes. However,
a small amount of 03 occurs naturally in the lower atmosphere from lightning
discharges and as the result of downward migration from the upper atmosphere.
In addition, there is evidence that vegetation emits organic vapors that may
react to form 03.
3. Why are these pollutants regulated by EPA?
Ambient levels (the concentration in the surrounding air) of CO and 03 can
be harmful to human health and the environment, especially in urban areas
where industry and/or automobiles are concentrated. Congress passed the Clean
Air Act to abate the growing air pollution problem. To protect the public's
health and welfare, the Clean Air Act and its 1970 and 1977 Amendments charge
the U.S. Environmental Protection Agency (EPA) with identifying harmful air
pollutants and setting ambient standards for each air pollutant that has
observed health effects. In addition, EPA is charged with the job of
enforcing these standards. Research has identified CO and 03 as air
pollutants which endanger public health at high concentrations; therefore,
raanmade CO and 03 are regulated by EPA.
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4. How does CO affect human health?
Carbon monoxide exposure can have harmful side effects, such as those
described below, depending on the concentration of ambient CO and the duration
of exposure. Carbon monoxide exposure affects human health by reducing the
oxygen level of the blood. Different parts of the body then suffer because
the blood cannot supply them with their normal amount of oxygen. Carbon
monoxide, like oxygen, can be transported by the blood from the lungs to body
tissues. Hemoglobin is the substance in the blood which normally carries
oxygen. If a person is exposed to CO, the hemoglobin will transport more CO
and less oxygen to body tissues than normal, since hemoglobin has a higher
affinity for CO than for oxygen. Hemoglobin carrying CO instead of oxygen is
known as carboxyhemoglobin (COHb). A deficiency of oxygen reaching the
tissues of the body, known as hypoxia, can result from elevated levels of COHb
in the blood. Hypoxia is considered to be one of the possible mechanisms of
CO toxicity. Another possible mechanism involves poisoning of the body's
cytochrome system by CO (the cytochrome system is the cellular pathway for
utilization of energy from food).
Table 1 presents the human health effects resulting from different exposures
to CO, and the corresponding COHb levels. For perspective, CO levels of 15
ppm to 30 ppm (eight-hour average) are typical on bad days in major U.S.
cities. Inhalation of sufficient amounts of CO can result in aggravation of
symptoms in individuals with cardiovascular diseases, central nervous system/
behavioral impairment, and possibly effects on fetal growth and development.
In addition, CO exposure may pose a greater health risk to persons at high
altitudes, particularly visitors who are accustomed to lower altitudes (EPA,
1979a).
Healthy, non-smoking individuals commonly maintain a blood COHb level of
approximately 0.4 percent from natural body sources (EPA, 1979a). Research
has shown that COHb from the inhalation of CO increases the COHb level
additively (NAS, 1977). However, the COHb level of an individual which
results from inhalation of a given amount of CO varies somewhat according to
lung capacity and other factors that depend on the individual's age, amount of
exercise, and state of health. People with established cardiovascular disease
(e.g., angina pectoris) and/or pulmonary disorders are most likely to be
affected by CO because of reduced resistance to hypoxia. Anemic individuals
and fetuses may also be particularly sensitive to CO exposure.
Cardiovascular Systems
Experimental evidence indicates that low-level acute CO exposure (15-18 ppm
for 8 hours) may aggravate angina pectoris, a cardiovascular disease in which
mild exercise or excitement produces symptoms of pressure and pain in the
chest, by depriving cardiovascular tissue of oxygen. Angina may result in
cardiovascular damage, the degree of which is unknown, and it appears to be
the initial step in a series of progressively more serious symptoms that
accompany cardiovascular disease and irreversible heart damage.
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Increased COHb is known to dilate blood vessels of the coronary system,
permitting increased blood flow (EPA, 1979a). The additional blood flow that
occurs in response to the presence of COHb is apparently not sufficient to
provide normal tissue oxygenation even at COHb levels as low as four percent
(EPA, 1979a). Blood vessel dilation, though having some compensatory effects,
could result in coronary damage or other vascular effects as the cardio-
vascular system is forced to function beyond its capabilities.
Research has demonstrated that chronic exposure to CO levels that are typical
in many U.S. cities (15 to 30 ppm for 8 hours) aggravates angina pectoris and
dilates blood vessels, both of which may lead to more serious effects.
However, there are some conflicting data and more research is needed to
determine whether CO exposure from polluted air contributes to incidences of
heart attack or sudden deaths from coronary disease.
Fetal Abnormalities
Experimental studies of the effects of CO exposure during fetal development of
animals have shown harmful health effects such as reduced birth weight,
failure to gain weight at a normal rate after birth, reduced brain protein
levels at birth, and reduced levels of activity during the first year after
birth (EPA, 1979a). In many cases, the effects disappeared when the animals
reached adulthood. However, the implications of these findings in relation to
learning and social behavior of human children are clearly of concern.
Long-term exposure of pregnant animals to CO levels of 50 ppm has been shown
to result in COHb levels in the fetus that often exceed the mother's levels
(EPA, 1979a). Fetal hypoxia may interfere with important developmental
stages. Under normal conditions a fetus may be functioning at nearly critical
tissue oxygen levels, so that even moderate CO exposure could affect develop-
ment. The effect of CO on human fetuses is commonly measured by studying
babies born to smoking mothers, but it should be noted that cigarette smoke
contains substances other than CO that may affect fetal development.
Central Nervous System/Behavioral Effects
Experimentation on low-to-medium level CO exposures and their effects on the
human central nervous system show behavioral changes in sleep, alertness, and
muscular coordination (EPA, 1979a). Changes in sleep patterns may be caused
by reduced central nervous system activity. Alertness is an individual's
ability to detect small, unpredictable changes in his environment. Experi-
mental results have shown that COHb levels of 1.8 and 2.3 percent are
sufficient to reduce human perception of small changes in light and sound,
respectively. Such blood level changes may occur in persons exposed to CO
levels typical of bad days in major U.S. cities. These same experiments
indicated that, after a time, ability to detect small light and sound changes
is partially recovered even though COHb levels remain constant or increase.
In summary, exposure to carbon monoxide causes a reduction in the oxygen level
of the blood, and may hinder the cellular mechanism for conversion of food
energy into forms the body can use. Harmful side effects which can result
depend on the health of the person exposed and the level and duration of
exposure. CO exposure can be especially harmful for persons with cardio-
vascular disease or anemia, and for fetuses.
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TABLE 1. HEALTH EFFECTS OF VARIOUS LEVELS OF CARBOXYHEMOGLOBIN (COHb)
RESULTING FROM CARBON MONOXIDE EXPOSURE
% COHb
in the
Blood
Approximate Ambient CO
Level Required
to Produce
Given COHb *
1 hr (ppm)
8 hr (ppm)
Threshold
Effects
0.3-0.7
2.5-3.0
4.0-6.0
10.0-20.0
20.0-30.0
35
55-80
110-170
280-575
575-860
Physiologic norm for
non-smokers.
9 EPA National Primary
Ambient Air Quality
Standard.
15-18 Cardiac function
decrements in impaired
individuals; increased
blood flow.
30-45 Visual impairments,
decreased alertness,
reduced maximal work
capacity.
75-155 Slight headache,
weakness, dilation of
veins, central nervous
system changes,
general coordination
problems.
155-235 Severe headaches,
nausea.
* For perspective, CO levels of 15 ppm to 30 ppm (8-hour average) are typical
on bad days in major U.S. cities.
SOURCE: Air Quality Criteria for Carbon Monoxide (Preprint). 1979.
Environmental Criteria and Assessment Office, Office of Research and
Development, U.S. EPA, Research Triangle Park, NC. EPA-600/8-79-002.
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5. How does Ch affect human health?
Ozone can impair lung function, change the cellular composition of the lungs,
increase susceptibility to infectious disease, and disturb the biochemical
balance of the lungs and other organs. Ozone is an irritant which causes
cough, chest discomfort, and irritation of mucous membranes of the nose,
throat and trachea (windpipe) at 03 levels that are often observed in urban
environments. Exercise requiring greater air volume intake also increases
irritation. Table. 2 lists the health effects that may occur at various levels
of ozone concentration and exposure time.
Short-term exposure (one hour) to approximately 0.30 ppm of 03 has been
shown to impair lung function in healthy persons. In the majority of
experimental studies in which 03 exposure has caused changes in lung
function in healthy individuals, function has returned to normal within a few
hours after exposure ended. Similar 03 exposure for individuals with
respiratory illnesses such as asthma, chronic bronchitis, or emphysema may
result in moderate to severe interference with normal activities. Approxi-
mately 4.0 to 5.5 million asthmatics live in urban areas within the United
States (EPA, 1978a). More than 80 percent of the 500 03 monitoring sites
measured values greater than the 0.12 ppm EPA standard during 1977 (U.S. EPA,
1978). Therefore, it is probably safe to say that 3 to 4 million people who
are particularly sensitive to 03 pollution live in areas with high 63
levels.
Ozone inhalation can increase the probability of infectious lung disease. The
exact mechanism of this effect is not well understood. Research on rabbits
has shown that 03 damages the cells responsible for destroying infectious
bacteria in the lungs. Such a finding strongly suggests the extent to which
03 can impair the body's defenses and, thus, increase the incidence of acute
and chronic respiratory disease. However, similar human responses may not
occur at exactly the same doses at which effects have been demonstrated in
experimental animals.
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TABLE 2. SUMMARY OF HUMAN HEALTH EFFECTS OF OZONE
Ozone
Concentration* Exposure
(ppm)
Effect
Reference
0.02-0.05
0.10
0.12
0.15-0.25
0.30
0.37
0.50
0.50
0.75
1 hour
1 hour
1 hour
1-2 hours
1-2 hours
2.75 hours
6-10 hours
1-2 hours
Detectable odor
Minor breathing difficulties
Decreased lung function in school children, increased
asthmatic attacks, irritation of respiratory tract
for persons with respiratory illnesses
Impaired lung function in those exercising rigorously,
cough and chest discomfort
Reduction in lung function, impaired lung function
in lightly-exercising individuals
Increased fragility of red blood cells, deleterious
effect on cellular enzymes
Increased frequency of chromosomal aberrations
Decreased lung function (effect enhanced by exercise),
dryness of nose and throat, chest discomfort, nausea,
decreased work performance.
Stupfel, 1976
I
U.S. Bureau of National
Affairs, 1978
EPA National Primary Ambient
Air Quality Standard
FR, 44:8202, 1979
Ferris, 1978; U.S. Bureau of
National Affairs, 1978;
Casarett and Doull, 1975
Ferris, 1978; U.S. Bureau of
National Affairs, 1978
Ferris, 1978
Ferris, 1978
Ferris, 1978
* For perspective, ozone levels of 0.1 ppm to 0.3 ppm (1-hour average) are
typical on bad summer days in many major U.S. cities.
SOURCE: Compiled by Energy and Environmental Analysis, Inc.; Arlington, VA, 1979.
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6. What are EPA'9 air quality standards for CO and 0^ and how do these
standards protect public health?
EPA National Ambient Air Quality Standards (NAAQS) for CO and 03 are as
follows:
03 Primary Standards
CO Primary Standards (not be exceeded, on
Averaging . (second highest value average, more than once
Time in the year) per year)
8 hour 9 ppm No Standard
1 hour 35 ppm 0.12 ppm (on a
daily maximum
basis)
For CO, compliance with the NAAQS means that the standard is not exceeded more
than one day per year in an air quality region. For ozone, compliance means
that the average number of days per year above the standard, computed over a
three year period, is less than or equal to one. These standards were set and
are periodically reexamined according to the results of scientific and medical
studies that reflect the most recent understanding of the toxicological
effects of each pollutant and the potential of each pollutant to effect the
health of the general public. An independent Science Advisory Board advises
EPA on the standards. Each primary standard provides an adequate margin of
safety because of the uncertainty in evaluating human health problems
associated with low concentrations of these pollutants, and to protect
especially sensitive individuals from harmful health effects.
EPA established the NAAQS for CO in 1971 and, after recently reviewing the
scientific basis for the standard, proposed revisions to the primary one-hour
CO standard in August 1980. EPA established the NAAQS for photochemical
oxidants in 1971 and replaced it with a revised ozone standard in 1979.
The standards shown above are known as "primary" air quality standards. For
ozone, there is also a "secondary" standard. The difference between the two
is that the primary standard is intended to protect human health, while the
secondary standard protects trees, crops and inanimate materials, which are
important contributors to human welfare.
The primary and secondary standards for ozone happen to be the same. No
secondary standard is required for CO because effects on trees, crops, and
inanimate materials from CO have been observed only at relatively high ambient
concentrations beyond those likely to occur in urban areas.
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7. What are the major sources of high concentrations of CO and
Carbon monoxide from manmade sources is produced- almost totally by the
incomplete combustion of fossil fuels. In 1977, an estimated 102.7 million
metric tons (113.2 million U.S. tons) of CO were emitted to the atmosphere
from manmade sources in the United States (EPA, 1979a). Of this total, 75.2
percent can be attributed to highway transportation sources, with approximate-
ly 8 percent, or 8.3 million metric tons of CO, emitted from industrial
processes. Three industries — chemicals manufacturing, petroleum refining,
and metal refining — are the most significant industrial sources of CO
emissions, a combined 7.3 million metric tons. The remaining 17 percent of
nationwide CO emissions is attributable to non-highway vehicles (construction
equipment, vessels, etc.), stationary source fuel combustion, solid waste, and
open burning.
Ozone is not emitted directly into the air. It is a secondary pollutant, that
is, a product of atmospheric chemical reactions between two precursors —
volatile organic compounds (VOC) and oxides of nitrogen (NOx) — which, in the
presence of sunlight, react to form 03. Volatile organic compounds and NOx
are emitted from both natural and manmade sources. Over the entire U.S., VOC
emissions from natural sources exceed those from manmade sources. However,
manmade sources tend to be geographically concentrated in urban centers so
they are by far the primary cause of high concentrations .of VOC and NOx. The
natural sources of VOC are spread out over a much larger area and their VOC
emissions are very diluted with fresh air. In addition, urban areas with
ozone problems usually have ambient VOC to NOx ratios of about 10:1, which is
close to the optimum ratio for ozone formation. Rural areas typically have
much higher VOC to NOx ratios, due to the fact that NOX emissions are low in
these areas. Therefore, there is insufficient NOX in rural areas to drive
the photochemical reactions necessary for substantial ozone production (EPA,
1980a).
Approximately 28 million metric tons (30.8 million U.S. tons) of VOC are
emitted from man-made sources in the United States each year. Most of the
hydrocarbon load, estimated to make up at least two-thirds of the VOC
emissions (EPA, 1980b), occurs from gasoline evaporation and motor vehicle
tailpipe exhaust emissions. Other major sources of VOC, including HC, are
gasoline distribution systems, chemical processing industries, and industries
that use organic solvents, such as paint.
Nationwide estimates of NOx emissions attribute 21.7 million metric tons (23.9
million U.S. tons) per year (or 95 percent) to fuel combustion (EPA, 1978a).
The major sources of fuel combustion and the respective NOx emissions are:
highway fuels, 7.4 million metric tons per year; non-highway fuels, 2.2
million metric tons per year; non-industrial sources, 5.8 million metric tons
per year.
In summary, then, while both CO and the precursors of 03 are emitted from a
variety of source types, it should be noted that the major source of both 03
precursors and CO is motor vehicle tailpipe emissions.
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8. In what areas are concentrations of CO and 0-3 greatest?
Because fuel combustion in highway vehicles is the -single largest source of
0 precursors and of CO, pollution levels tend to be greatest in urban areas
with high traffic volumes. Also, basin-like geography and meteorological
conditions that reduce ventilation decrease the rate at which air mixes and
disperses pollutants. Table 3 presents major U.S. cities (population greater
than 200,000) with the ten worst CO and 03 levels based on the design values
used in 1979 State Implementation Plans. (Design values are the pollutant
measurements that are compared to the air quality standards to determine
whether the standards are being met or not. Thus, they are an indicator of a
city's level of a pollutant over a recent period of time.) In 1982, 39 major
cities are projected not to attain the CO standard and 36 major cities are
projected not to attain the ©3 standard.
TABLE 3. MAJOR U.S. CITIES (POPULATION GREATER THAN 200,000)
WITH THE TEN HIGHEST CO AND 03 DESIGN VALUES*
Cities with Highest CO Values
1. Bridgeport (Fairfield), CT
2. Los Angeles (South Coast Air
Basin), CA
3. Phoenix, AZ
4. Denver, CO
5. Cleveland, OH
6. Albuquerque, NM
7. New York, metropolitan
8. Pittsburgh, PA
9. Chicago, IL
10. Fresno, CA
Cities with Highest 0-^ Values
1. Los Angeles (South Coast Air
Basin), CA
2. Houston, TX
3. Milwaukee, WI
4. New York, metropolitan
5. Chicago, IL
6. Detroit, MI tied
6. Cleveland, OH
7. Philadelphia, PA
7. Wilmington, DE
7. Pittsburgh, PA tied
7. Cincinnati, OH
7. San Diego, CA
8. Ventura-Oxnard-Thousand Oaks, CA
9. St. Louis, MO
10. Allentown-Bethlehem-Easton, PA
* In 1982, 39 major cities (population greater than 200,000) are projected to
exceed the national ambient air quality standard for CO and 36 are projected
to exceed the 03 standard.
SOURCE: EPA Internal Memorandum; March 26, 1980; from G.T. Helms, Chief,
Control Programs Operations Branch, CPDD, to all Air Branch Chiefs,
Regions I-X.
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9. Under what weather conditions and at what times of day are concentrations
highest?
In generali concentrations reach the highest levels when temperature
inversions occur or when stagnant air masses lie over urban areas for extended
periods. Inversions (which limit vertical mixing) can occur when a layer of
cool, heavy air falls and is warmed through compression. When this air layer
comes to rest, it is frequently of a higher temperature than the surface air
layer, so that the surface air layer is trapped. This phenomenon is known as
a subsidence inversion and occurs most frequently during summer months.
Ground-based inversions also may trap surface air and inhibit pollutant
dispersion. They occur during cold fall and winter months when the ground
cools faster than the air column, creating a cool surface air layer that will
not rise, mix with upper air layers, and disperse pollutants. Finally,
large-scale air masses associated with high pressure weather systems may
occasionally stall for several days, leading to the buildup of high pollutant
concentrations.
Ozone formation requires sunlight and high temperatures (greater than 70°F).
Therefore, concentrations of 63 are higher on sunny days, especially in the
summer in the early afternoon when sunlight is more direct than it is in the
winter. Subsidence inversions, which are common during summer months, further
aggravate the problem by preventing the normal dispersion of 63. In the
absence of an inversion, 03 generated during daylight hours is lost by
atmospheric mixing, the natural movement of air masses, and by chemical
reaction, especially on ground surfaces. Nighttime levels are consequently
greatly reduced. Urban 03 levels rise again the next day as automobiles and
stationary sources emit ozone precursors and sunlight promotes the 63
producing reaction.
Carbon monoxide concentrations often follow predictable trends. In most
cities, CO levels peak at seven to nine a.m., four to seven p.m., and ten p.m.
to midnight. The first two peaks are due to emissions from rush-hour
traffic. The midnight peak can be attributed primarily to undispersed
emissions, as a result of calm wind conditions or the reversal of wind flow
patterns from the daytime norm. The highest CO levels tend to occur in the
fall and winter when colder ambient temperatures result in increased
production of CO emissions from cars, in addition to CO emitted from other
fuel-burning sources. Also, low wind speeds and ground-based inversions which
occur during winter and fall result in decreased dispersion of CO emissions
and contribute substantially to the occurrence of high ground-level CO
concentrations.
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10. What is the air quality index given on radio and TV?
The air quality index, also known as the Pollutant Standards Index (PSI), is a
health-related index designed to inform the public about harmful air pollution
levels (see Table 4). The PSI is based generally on the primary short-term
National Ambient Air Quality Standards (NAAQS) and Federally established
levels for categorizing the severity of pollution episodes. Each day, the
highest pollutant level in relation to the ambient standard for that pollutant
measured at any .one monitoring area is reported as the PSI index. As
described in Table 4, a PSI value of 100 or above signifies that health risks
are . present for certain segments of the population. The proportion of the
population for which health risks are present increases as the PSI value rises.
11. What effects do CO and 0-^ pollution have on plant life?^
Carbon monoxide and 63 both are capable of affecting plant growth. In
general, 03 is much more harmful to plant life than CO because plants are
capable of absorbing and metabolizing small amounts of CO. Effects of 03
usually are measured as changes in plant growth (stem and root), coloration,
vigor, photosynthesis, respiration, or leaf injury.
Ozone is highly toxic to plant life. It has been shown to affect the
permeability of cell membranes which, depending on the 03 concentration and
length of exposure, can result in effects to the entire plant. Research has
determined that chronic exposure to 03 in concentrations at or below those
often found in urban areas (0.05 ppm to 0.20 ppm) causes leaf injury and
reduces root and top weight in trees, shrubs, and agricultural crops (EPA,
1978a).
Botanical experimentation has found that chronic exposure to CO I.-vels as low
as 20 ppm and 24 ppm may suppress the nitrogen-fixing bacteria in :oot nodules
of legumes or produce abnormal leaf formation in pea and bear, seedlings.
However, these concentrations should not be considered threshold levels for
plants in general due to the lack of supporting research findings and because
plants vary widely in their sensitivity to CO (EPA, 1979a). Also, food crops
and forests are not generally located near areas of dense traffic, which is
where these levels of CO can occur.
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TABLE 4. DEFINITION OF POLLUTANT STANDARD INDEX (PSI) VALUES
Pollutant Level
PSI
Index
Value
Air Quality
Level
TSP
(24-hour)
ug/m3
S02
(24-hour)
ug/m3
CO
(8-hour)
mg/m3
°3
(1-hour)
ug/m3
N02
(1-hour)
ug/n3
Health Effect
General Health
Effect*
Cautionary
Statements
500
Significant
Harm
1000
2620
57.5
1200
3750
400
Emergency
857
2100 46.0 1000 3000 Hazardous Premature death of ill and
elderly. Healthy people will
experience adverse symptoms
that affect their normal
activity.
All persons should remain
indoors, keeping windows
and doors closed. All
persons should minimize
physical exertion and avoid
traffic.
300 Warning 625
200 Alert 375
100 NAAQS 260
50 501 of NAAQS 75"
0 0
1600 34.0 800 2260 Hazardous Premature onset of certain
diseases in addition to signi-
cant aggravation of symptoms
and decreased exercise toler-
ance in healthy persons.
800 17.0 400C 1130 Very Significant aggravation of
Unhealthfi/1 symptoms and decreased exer-
cise tolerance in persons with
heart or lung disease, with
widespread symptoms in the
healthy population.
365 10.0 240 Unhealthful" Mild aggravation of symptoms
in susceptible persons, with
•irritation symptoms in the
healthy population.'
80° 5.0 120 Moderate8
0 0.0 0 . Good3
Elderly and persona with
existing diseases should
stay indoors and avoid
outdoor activity.
Elderly and persons with
existing heart or lung
disease should stay indoors
and reduce physical
activity.
Persona with existing heart
or respiratory ailments
should reduce physical
exertion and outdoor
activity. '
D Annual primary NAAQS.
c 400 ug/m3 was used instead of the 0-j Alert Level of 200 ug/m3.
SOURCE: U.S. Environmental Protection Agency, "Guidelines for Public Reporting of Daily Air Quality
Pollutant Standard Index."
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12. How prevalent are these effects on plant life?
The environmental-effects on plants of 03 pollution are more prevalent than
the effects of CO pollution. Many cases of regional vegetational effects of
03 have been documented. Similar reports of CO toxicity do not appear to be
available.
Ozone pollution has been recognized as a chronic pollution problem only during
the last 20 to 25 years. It was first noted in Southern California, where the
impact appears to be most severe. Studies were made to determine the economic
losses incurred in citrus groves and vineyards as a result of 03 in the
Southern California atmosphere. It was found that 03 was responsible for
reduced plant water use, reduced photosynthesis, increased leaf and fruit
drop, and severe reduction of marketable fruit yield. Lemon trees and orange
trees exposed to at least 0.10 ppm of 03 over a growing season produced 32
percent and 54 percent less fruit, respectively, than an atmosphere with no
0 . Vineyards in areas where the ambient 03 concentration often exceeded
0.25 ppm over the May through September growing season reported a 12 percent
yield reduction the first year and a 61 percent yield reduction the second
year (U.S. EPA, 1978a). And from 1972 through 1976, ozone-induced damage to
Southern California vegetable and field crops resulted in an estimated $14.8
million per year in consumer losses (EPA, 1979b).
Various species of pine trees also are experiencing effects from 03
pollution, especially in certain regions of the country. In the Appalachian
Mountains, a disease known as emergence tipburn (which mainly affects the
eastern white pine) has been attributed to 03 levels as low as 0.12 ppm
(U.S. EPA, 1978a). Emergence tipburn appears to affect only genetically
sensitive trees within the species and gradually destroys them. The eastern
white pine is an important pioneer tree (i.e., it often is one of the first to
grow in a previously unfcrested area), which starts the natural ecological
progression toward a fully established forest ecosystem. The destruction of
these trees, then, may disrupt the balance of some forest ecosystems in the
eastern United States.
Mixed pine forests in the San Bernardino Mountains east of Los Angeles and
ponderosa pine in the Sequoia National Park also have sustained serious injury
from chronic 03 exposure. Mixed pine forests located on the western slopes
of the southern Sierra Nevadas appear to be affected by 03 transported from
the San Joaquin Valley of California (U.S. EPA, 1978a). These trees are an
important part of California's lumber industry.
It is evident, then, that secondary 03 standards are needed to protect the
quality of forest ecosystems and food crops in the U.S. and that primary CO
and 03 standards are needed to protect the health of the U.S. population.
13. What is EPA doing to help reduce levels of these pollutants?
EPA is working to carry out the Clean Air Act as amended in 1970 and 1977 to
reduce air pollution and improve air quality. In response to these amend-
ments, EPA promulgated National Ambient Air Quality Standards (NAAQS). These
standards defined the principal types of air pollutants and the levels of each
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that should not be exceeded for the protection of public health and welfare.
Carbon monoxide and 63 are two of the six regulated air pollutants (the
others are sulfur dioxide, particulate matter, nitrogen dioxide, and lead).
According to the provisions of the 1977 Amendments to the Clean Air Act, each
State is required to develop specific State Implementation Plans (SIP's) for
improving air quality in areas not meeting the NAAQS and for maintaining the
purity of the air in areas as clean as or cleaner than that specified by the
NAAQS. EPA is assisting the States in the technical work of pollution
measurement, planning, and control so that they may develop and carry out
their implementation plans. EPA also distributes Federal funds appropriated
by Congress to the States for use in achieving air quality goals.
Besides setting and enforcing air quality standards, EPA also is responsible
for establishing pollution emission limits for automobiles. To enforce these
emission standards, EPA tests prototype models of all new cars and trucks to
ensure that they comply with the legal standards, performs assembly line tests
and orders recalls when defective emission control components are identified
through in-use testing. And under EPA's guidance, state are implementing
inspection and maintenance (I/M) programs to reduce levels of in-use emissions
from motor vehicles.
Another EPA program mandated by the Clean Air Act is the New Source
Performance Standards (NSPS) for stationary sources, which are emission limits
for certain source categories (e.g., power plants) determined to contribute
significantly to air pollution levels.
14. How much progress has been made?
Progress has been made both in the development of programs to clean the air
(planning) and in actual reductions in ambient pollutant concentrations
(implementation). For example, State Implementation Plans (SIP's) have been
developed by all States. These plans include a definite timetable for a
step-by-step attainment of National Ambient Air Quality Standards (NAAQS).
Also included in the SIP's of those States granted extensions from 1982 to
1987 for demonstrating attainment with 03 and/or CO standards are plans for
motor vehicle inspection and maintenance, and programs to improve mass
transportation and reduce personal vehicle use in urban areas, in order to
reduce automobile exhaust emissions.
In general, ambient levels of CO are lower now than in the recent past and are
continuing to decline. Between 1972 and 1977, approximately 80 percent of the
monitoring sites in the United States showed long-term improvements in CO
levels (EPA, 1978b). This trend is fairly consistent throughout the United
States. On the other hand, 03 trends are not as encouraging. About
one-third of all monitoring sites throughout the country have noted increasing
03 levels from 1972 to 1977 (EPA, 1978b). And in the period from 1974 to
1978, there were no substantial changes in the yearly average of daily maximum
ozone levels for a collection of 51 sites studied by the President's Council
on Environmental Quality (CEQ, 1980). However, ozone monitoring in Los
Angeles, where the problem is most severe, has indicated substantial long-term
reductions in ambient levels.
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15. What are the legal deadlines for attainment of the standards?
Provisions of the'Clean Air Act Amendments of 1970 originally established July
1975 as the deadline for compliance with the National Ambient Air Quality
Standards (NAAQS). This deadline was found to be unachievable and was
extended to 1982 by the 1977 Amendments to the Clean Air Act. For some
States, the deadline was further extended to 1987 for CO and 03 because of
the demonstrated difficulty in reducing current emission levels, especially of
motor vehicles, within a relatively short time frame.
16. What is EPA doing to help ensure attainment of the standards?
EPA has a number of continuing programs to ensure that CO and 03 NAAQS"s are
attained and maintained. For mobile sources, the Federal Motor Vehicle
Control Program provides for an increasingly stringent set of emission
standards designed to control emissions from cars, trucks, buses, and motor-
cycles. As new vehicles with low emission levels replace older vehicles with
high emissions, the total pollutant burden from motor vehicles should be
lessened. However, emissions will continue to deteriorate as individual
vehicles age. In addition, total miles traveled by passenger vehicles
increased during the decade from 891 billion miles per year in 1970 to 1.1
trillion miles per year in 1978 (MVMA, 1980); this meant that emission
reductions in the 1970's were at least partially offset by increased vehicle
usage and this could also happen in the 1980's. Population and economic
growth have also led to increases in emissions from sources other than motor
vehicles. Therefore, in order to further reduce motor vehicle emissions,
Congress required in the Clean Air Act Amendments of 1977 that inspection and
maintenance programs be implemented if State Implementation Plans for 03
and/or CO cannot demonstrate attainment of the NAAQS by 1982. I/M programs
will help maintain the efficiency of automotive emission control systems by
requiring repair of vehicles which do not pass a tailpipe emission test.
Transportation control measures are another option available to States and
local areas for reducing mobile source pollution. Examples of transportation
control measures include carpool/vanpools, express bus lanes, park-and-ride
lots, and parking surcharges.
Controls on stationary sources are dependent on whether the source is in an
attainment or a nonattainment area and whether the source is to be constructed
or already exists. Some new sources have emission limits dictated by New
Source Performance Standards (NSPS's) if they are in a category of sources
determined to contribute significantly to air pollution levels. New sources
in nonattainment areas are required to control to the lowest achievable
emission rate, while new sources in attainment areas must use the best
available control technology. Existing sources in nonattainment areas are
required to reduce emissions by adopting at a minimum reasonably available
control technology.
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REFERENCES
Casarett, L.J., and Doull, J. 1975. Toxicology. The Basic Science of Poisons.
New York: MacMillian.
Ferris, B.J. 1978. "Health Effects of Exposure to Low Levels of Regulated Air
Pollutants," Journal of Air Pollution Control Association 28(5):482-497.
National Academy of Sciences (NAS). 1977. Carbon Monoxide. Prepared by the
Committee on Medical and Biologic Effects of Environmental Pollutants,
National Research Council.
Stupfel, M. 1976. "Recent Advances in Investigations of Toxicity of
Automotive Exhaust." Environmental Health Perspectives 17:253-285.
U.S. Bureau of National Affairs. 1978. "Criteria for Ozone and Other
Photochemical Oxidants," Environmental Reporter, Federal Laws Index
BNA:31:2151-31:2162.
U.S. Environmental Protection Agency (EPA). 1978a. Air Quality Criteria for
Ozone and Other Photochemical Oxidants. EPA-600/8-78-004.
U.S. EPA. 1978b. National Air Quality, Monitoring and Emissions Trends •
Report. 1977. EPA-450/2-79-022.
U.S. EPA. 1979a. Air Quality Criteria for Carbon Monoxide (Preprint).
EPA-600/8-79-022.
U.S. EPA. 1979b. Methods Development for Assessing Air Pollution Control
Benefits. Vol. III. EPA-600/5-79-001c.
U.S. Government Printing Office. 1979. Federal Register 44:8202.
U.S. EPA. 1980a. Natural Sources of Ozone: Their Origin and Their Effect on
Air Quality. EPA-AA-IMS/AQ-80-2.
U.S. EPA. 1980b. Review of Criteria for Vapor-Phase Hydrocarbons.
EPA-600/8-80-045. RTF, N.C.
EPA Internal Memorandum; March 26, 1980, from G.T. Helms, Chief, Control
Programs Operations Branch, CPDD, to all Air Branch Chiefs, Regions I-X.
Council on Environmental Quality. 1980. Environmental Quality -'1980. The
Eleventh Annual Report of the Council on Environmental Quality.
Motor Vehicle Manufacturers Association of the U.S. Inc. (MVMA). MVMA Motor
Vehicle Facts and Figures '80. Detroit, Michigan.
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