-------
PRELIMINARY DRAFT
TABLE 1-13. SUMMARY TABLE: EFFECTS ON PULMONARY FUNCTION
OF LONG-TERM EXPOSURES TO OZONE
Effect/response
03 concentration, ppm
References
Increased lung volume
Increased pulmonary
resistance
Decreased lung
compliance
Decreased inspiratory
flow
Decreased forced
expiratory volume
(FEV,) and flow
(FEF)
[0.08], [0.12], 0.25
0.2
[0.2], 0.8
0.4
0.2, 0.8
0.5, 1.0
0.64
0.64
0.5, 0.8
0.64
[0.08], 0.12, 0.25
0.2, 0.8
0.64
Raub et al. (1983)
Bartlett et al. (1974)
Costa et al. (1983)
Martin et al. (1983)
Costa et al. (1983)
Yokoyama et al. , 1984
Wegner (1982)
Kotllkoff et al., 1984
Eustis et al. (1981)
Wegner (1982)
Raub et al. (1983)
Costa et al. (1983)
Wegner (1982)
Similar patterns of response for both antioxidant metabolism and oxygen
consumption are observed after exposure to ozone. A 7-day exposure to ozone
produces linear concentration-related increases in activities of glutathione
peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and
succinate oxidase (Mustafa and Lee, 1976; Chow et al., 1974; Schwartz et al.,
1976; Mustafa et al., 1973). Rats on a vitamin E-deficient diet experience an
increase in enzyme activities at 196 ug/m (0.1 ppm) ozone as compared to
392 ug/m (0.2 ppm) in animals on normal diets (Chow et al., 1981; Mustafa and
Lee, 1976; Mustafa, 1975). Research on these enzymes has shown that there is
no significant difference in effects from continuous versus intermittent
exposure; this, along with concentration-response data, suggests that the con-
centration of ozone is more important than duration of exposure in causing
these effects (Chow et al., 1974; Schwartz et al., 1976; Mustafa and Lee,
1976).
OZNORM/A
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PRELIMINARY DRAFT
Duration of exposure still plays a role, however. During exposures up to
1 or 4 weeks, antioxidant metabolism and 0~ consumption generally do not
change on the first day of exposure; by about day 2, increases are observed
and by about day 4 a plateau is reached (Mustafa and Lee, 1976; DeLucia et al.,
1975a). Recovery from these effects occurs by 6 days post-exposure (Chow
et al., 1976). This plateauing of effects in the presence of exposure does
not result in long-term tolerance. If rats are re-exposed after recovery is
observed, the increase in enzyme activities is equivalent to that observed in
animals exposed for the first time (Chow et al., 1976).
The influence of age on responsiveness is also similar for antioxidant
metabolism and oxygen consumption (Elsayed et al., 1982a; Tyson et al., 1982;
Lunan et al., 1977). Suckling neonates (5 to 20 days old) generally exhibited
a decrease in enzyme activities; as the animals grew older (up to about 180 days
old), enzyme activities generally increased with age. Species differences may
exist in this response (Mustafa and Lee, 1976; Mustafa et al., 1982; Chow
et al., 1975; DeLucia et al., 1975a). Studies in which monkeys have been
compared to rats did not include a description of appropriate statistical
considerations applied (if any); thus, no definitive conclusions about respon-
siveness of monkeys versus rats can be made.
The mechanism responsible for the increase in antioxidant metabolism and
oxygen consumption is not known. The response is typically attributed, however,
to concurrent morphological changes, principally the loss of type 1 cells and
an increase in type 2 cells that are richer in the enzymes measured.
Monooxygenases constitute another class of enzymes investigated after
ozone exposure. These enzymes function in the metabolism of both endogenous
(e.g., biogenic amines, hormones) and exogenous (xenobiotic) substances. The
substrates acted upon are either activated or detoxified, depending on the
substrate and the enzyme. Acute exposure to 1470 to 1960 |jg/m (0.75 to
1 ppm) ozone decreased cytochrome P-450 levels and enzyme activities related
to both cytochrome P-450 and P-448. The health impact of these changes is
uncertain since only a few elements of a complex metabolic system were measured.
The activity of lactate dehydrogenase is increased in lungs of vitamin E-
deficient rats receiving a short-term exposure to 196 ug/m (0.1 ppm) ozone
(Chow et al., 1981). Higher levels caused a similar response in rats, but not
in monkeys, on normal diets (Chow et al., 1974, 1977). This enzyme is frequent-
ly used as a marker of cellular damage because it is released upon cytotoxicity.
OZNORM/A 1-105 11/22/85
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PRELIMINARY DRAFT
It is not known, however, whether the increase in this enzyme is a direct
reflection of cytotoxicity or whether it is an indicator of an increased
number of type 2 cells and macrophages in the lungs.
An increase in a few of the measured activities of lysosomal enzymes has
3
been shown in the lungs of rats exposed to > 1372 (jg/m (0.7 ppm) ozone (Dillard
et al., 1972; Castleman et al., 1973a; Chow et al., 1974). This response is
most likely the result of an increase in inflammatory cells in the lungs
rather than an induction of enzymes, since lysosomal enzymes in alveolar
macrophages decrease after i_n vivo or i_n vitro exposure to ozone (Hurst et al.,
1970; Hurst and Coffin, 1971).
As discussed previously, long-term exposure to high 0, concentrations
causes mild lung fibrosis (i.e., local increase of collagen in centriacinar
interalveolar septa). This morphological change has been correlated with
biochemical changes in the activity of prolyl hydroxylase (an enzyme that
catalyzes the production of hydroxyproline) and in hydroxyproline content (a
component of collagen that is present in excess in fibrosis) (Last et al.,
1979; Bhatnagar et al., 1983). An increase in collagen synthesis has been
3
observed, with 980 ug/m (0.5 ppm) Cu being the minimally effective concentra-
tion tested (Hussain et al., 1976a,b; Last et al., 1979). During a prolonged
exposure, prolyl hydroxylase activity increases by day 7 and returns to control
levels by 60 days of exposure. When a short-term exposure ceases, prolyl
hydroxylase activity returns to normal by about 10 days post-exposure, but
hydroxyproline levels remain elevated 28 days post-exposure. Thus, the product
of the increased synthesis, collagen, remains relatively stable. One study
(Costa et al., 1983) observed a small decrease in collagen levels of rats at
392 and 1568 ug/m (0.2 and 0.8 ppm) 03 after an intermittent exposure for 62
days.
The effects of 0, on increasing collagen content may be progressive;
i.e., after a 6-week intermittent exposure of rats to 0.64 or 0.96 ppm 0,
ceased, collagen levels 6 week post-exposure were elevated over the levels
immediately after exposure (Last et al., 1984b). Also, there appears to be
little difference between continuous and intermittent exposure in increasing
collagen levels in rat lungs (Last et al, 1984b). Thus, the intermittent
clean air periods were not sufficient to permit recovery.
Although the ability of 03 to initiate peroxidation of unsaturated fatty
acids j_n vitro is well established, few jn vivo studies of lung lipids have
OZNORM/A 1-106 11/22/85
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PRELIMINARY DRAFT
been conducted. Generally, ozone decreases unsaturated fatty acid content of
the lungs (Roehm et al., 1972) and decreases incorporation of fatty acids into
lecithin (a saturated fatty acid) (Kyei-Aboagye et al., 1973). These altera-
tions, however, apparently do not alter the surface-tension-lowering properties
of lung lipids that are important to breathing (Gardner et al., 1971; Huber
et al., 1971).
One of the earliest demonstrated effects of ozone was that very high
concentrations caused mortality as a result of pulmonary edema. As more
sensitive techniques were developed, lower levels (510 ug/m , 0.26 ppm) were
observed to increase the protein content of the lung (Hu et al., 1982). Since
some of the excess protein could be attributed to serum proteins, the interpre-
tation was that edema had occurred. This effect was more pronounced several
hours after exposure ceased. At higher concentrations, a loss of carrier-
mediated transport from the air side of the lung to the blood side was observed
(Williams et al., 1980). These changes imply an effect on the barrier function
of the lung, which regulates fluxes of various substances with potential
physiological activities across the alveolar walls.
The biochemical effects observed in experimental animals exposed to 0,
are summarized in Figure 1-7 and Table 1-14 (see Section 1.8.1 for criteria
used in developing this summary).
1.8.3.4 Host Defense Mechanisms. Reports over the years have presented
substantial evidence that exposure to ozone impairs the antibacterial activity
of the lung, resulting in an impairment of the lung's ability to kill inhaled
microorganisms. Suppression of this biocidal defense of the lung can lead to
microbial proliferation within the lung, resulting in mortality. The mortality
response is concentration-related and is significant at concentrations as low
as 157 to 196 ug/m3 (0.08 to 0.1 ppm) (Coffin et al., 1967; Ehrlich et al.,
1977; Miller et al., 1978a; Aranyi et al., 1983). The biological basis for
this response appears to be that ozone or one of its reactive products can
impair or suppress the normal bactericidal functions of the pulmonary defenses,
which results in prolonging the life of the infectious agent, permitting its
multiplication and ultimately, in this animal model, resulting in death. Such
infections can occur because of 0., effects on a complex host defense system
involving alveolar macrophage functioning, lung fluids, and other immune
factors.
OZNORM/A 1-107 11/22/85
-------
rf-" ,<•<
*+•'
AH
o
CO
Cl . tl
0. 1 -
1 02-
a
> 0.3-
c
0
Z 04-
0
-^ 0.5-
c
0)
H 0.6-
0
u
0.7-
0)
C
N 0 8~
o
0.9-
1 R -
c
<
<
i
i
i
1
3
l 0 (.
l
l l
l O l
1
. i .
i
•> c
c
t
1 1
1
1
1 4
\
c
)
1
)
1 1
t 1
1
) O
1
1
1
(
1 0 1
1
• 1
1
1 <
4
1 (
1
1 {
1
^
t i
1 (
1 (
i 4
1 1
»
1
1 1
1
1
I
1
1 0
»
Figure 1-7. Summary of biochemical changes in experimental animals exposed to ozone.
See Table 1-14 for reference citations of studies summarized here.
-------
PRELIMINARY DRAFT
TABLE 1-14. SUMMARY TABLE: BIOCHEMICAL CHANGES
IN EXPERIMENTAL ANIMALS EXPOSED TO OZONE
Effect/response
Increased 02
consumption
03 concentration, ppm
[0.1], 0.2
[0.1], 0.2, 0.35, 0.5, 0.8
0.2, 0.5, 0.8
0.2, 0.5, 0.8
0.45
0.8
0.8 '
References
Mustafa (1975)
Mustafa and Lee (1976)
Mustafa et al. (1973)
Schwartz et al. (1976)
Mustafa et al. (1982)
Chow et al. (1976)
Elsayed et al. (1982a)
Increased lysosomal
enzyme activities
Increased lung
hydroxyproline
and prolyl
hydroxylase
activity
Altered mucus
glycoprotein
secretions
[0.2], [0.5], 0.8
0.7, 0.8
0.7, 0.8
[0.2], 0.5, 0.8
0.2, 0.8
0.45, 0.8
0.5, 0.64, 0.96
0.5
0.8
[0.2], [0.4], 0.5, 0.6, 0.8
0.5, 0.6, 0.8
0.6, 0.8
Increased alveolar
protein and
permeabi 1 ity
changes
Increased LDH
activity
[0.1],- 0.26, 0.51,
[0.25], 0.5, 1.0
0.6, 1.0
1.0
[0.1]
[0.5], 0.8
0.8
1.0
Increased NADPH
cytochrome c
reductase
activity
Increased GSH
metabolism
0.2, 0.35, 0.8
0.2, 0.5, 0.8
0.2, 0.5, 0.8
[0.1]
0.2
0.35
0.2,
0.32
0.45
0.5
0.5,
0.8
0.8
0.8
1.0
0.8
Chow et al. (1974)
Dillard et al. (1972)
Castleman et al. (1973a,b)
Hussain et al. (1976a,b)
Costa et al. (1983)
Bhatnagar et al. (1983)
Last et al. (1979, 1984b)
Last and Greenberg (1980)
Hesterberg and Last (1981)
Last and Kaizu (1980)
Last and Cross (1978)
Last et al. (1977)
Hu et al. (1982)
Alpert et al. (1971a)
Williams et al. (1980)
Reasor et al. (1979)
Chow et al. (1981)
Chow et al. (1977)
Chow and Tappel (1973)
Mustafa and Lee (1976)
Schwartz et al. (1976)
DeLucia et al. (1972, 1975a,b)
Chow et al. (1981)
Plopper et al. (1979)
Mustafa and Lee (1976)
Chow et al. (1974)
DeLucia et al. (1972, 1975a,b)
Schwartz et al. (1976)
Fukase et al. (1975)
Moore et al. (1980)
Mustafa et al. (1982)
Chow et al. (1975)
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PRELIMINARY DRAFT
TABLE 1-14 (continued). SUMMARY TABLE: BIOCHEMICAL CHANGES
IN EXPERIMENTAL ANIMALS EXPOSED TO OZONE
Effect/response
03 concentration, ppm
References
0.5, 1.0
0.7, 0.75, 0.8
0.8
Fukase et al. (1978)
Chow and Tappel (1972, 1973)
Elsayed et al. (1982a,b;
1983)
Increased NPSH
Decreased
unsaturated
fatty acids
0.8
0.9
0.9
0.1, 0.2
0.2, 0.5, 0.8
0.45
0.8
0.5
Chow et al. (1976b)
Tyson et al. (1982)
Lunan et al. (1977)
Plopper et al. (1979)
DeLucia et al. (1975b)
Mustafa et al. (1982)
Chow et al. (1976b)
Roehm et al. , 1972
The data obtained in various experimental animal studies indicate that
short-term ozone exposure can reduce the effectiveness of several vital defense
systems including (1) the ability of the lung to inactivate bacteria and
viruses (Coffin et al., 1968; Coffin and Gardner, 1972b; Goldstein et al.,
1974, 1977; Warshauer et al., 1974; Bergers et al; 1983. Schwartz and Christman,
1979; Ehrlich et al., 1979); (2) the mucociliary transport system (Phalen
et al., 1980; Frager et al., 1979; Kenoyer et al., 1981; (3) the immunological
system (Campbell and Hilsenroth, 1976; Fujimaki et al., 1984; Thomas et al.,
1981b; Aranyi et al., 1983; and (4) the pulmonary macrophage (Dowell et al.,
1970; Goldstein et al., 1971a,b, and 1977; Hadley et al., 1977; McAllen et al.,
1981; Witz et al. , 1983; Hurst et al., 1970; Hurst and Coffin, 1971; Amoruso
et al., 1981). Studies have also indicated that the activity level of the
test subject and the presence of other airborne chemicals are important vari-
ables that can influence the determination of the lowest effective concen-
tration of the pollutant. (Gardner et al., 1977; Aranyi et al., 1983; Ehrlich,
1980, 1983; Grose et al., 1980, 1982; Phalen et al., 1980; Goldstein et al. ,
1974; Illing et al., 1980).
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PRELIMINARY DRAFT
Ciliated cells are damaged by CL inhalation, as demonstrated by major
morphological changes in these cells including necrosis and sloughing or by
the shortening of the cilia in cells attached to the bronchi. Sufficient
ciliated cell damage should result in decreased transport of viable and non-
viable particles from the lung. Rats exposed to 784, 1568, 1960, or 2352
ug/m (0.4, 0.8, 1.0, or 1.2 ppm) for times as short as 4 hr have decreased
short-term clearance of particles from the lung (Phalen et al., 1980; Frager
et al., 1979; Kenoyer et al., 1981). Short-term clearance is mostly due to
mucus transport of particles, and the decreased short-term clearance is an
anticipated functional result predicted from morphological observations. The
mucous glycoprotein production of the trachea is also altered by 0, exposure.
Mucous glycoprotein biosynthesis, as measured ex vivo in cultured tracheal
explants from exposed rats, was inhibited by short-term continuous exposure to
1568 (jg/m3 (0.8 ppm) of 03 for 3 to 5 days (Last and Cross, 1978; Last and
Kaizu, 1980; Last et al., 1977). Glycoprotein synthesis and secretion recovered
to control values after 5 to 10 days of exposure and increased to greater than
control values after 10 days of exposure. With this increase in production of
mucus, investigators have found that the velocity of the tracheal mucus was
3
significantly reduced following a 2 hr exposure to 1960 ug/m (1.0 ppm) (Abraham
et al., 1980).
A problem remains in assessing the relevance of these animal data to
humans. Green (1984) reviewed the literature and compared the host antibacterial
defense systems of the rodent and man and found that these two species had
defenses that are very similar and thus provide a good basis for a qualitative
extrapolation. Both defenses consist of an aerodynamic filtration system, a
fluid layer lining the respiratory membranes, a transport mechanism for removing
foreign particles, microorganisms, and pulmonary cells, and immune secretions
of lymphocytes and plasma cells. In both rodents and humans, these components
act in concert to maintain the lung free of bacteria.
If the animal models are to be used to reflect the toxicological response
occurring in humans, then the endpoint for comparison of such studies should
be morbidity rather than mortality. A better index of 03 effect in humans
might be the increased prevalence of infectious respiratory illness in the
community. Such a comparison may be proper since both mortality from respira-
tory infections (animals) and morbidity from respiratory infections (humans)
can result from a loss in pulmonary defenses (Gardner, 1984). Whether the
OZNORM/A 1-111 11/22/85
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PRELIMINARY DRAFT
microorganisms used in the various animal studies are comparable to the organ-
isms responsible for the respiratory infections in a community still requires
further investigation.
Ideally, studies of pulmonary host defenses should be performed in man,
using epidemiological or volunteer methods of study. Unfortunately, such
studies have not been reported yet. Attention must therefore be paid to the
results of host-defense experiments conducted with animals.
In the area of host defense of the lung against infection, present know-
ledge of the physiology, metabolism, and function have come primarily from the
study of various animal systems, but it is generally accepted that the basic
mechanisms of action of these defense cells and systems function similarly in
both animals and man. There are also human data to support this statement,
especially in such areas as immunosuppression, ciliostasis, and alveolar
macrophages. The effects seen in animals represent alterations in basic
biological systems. One can assume that similar alterations in basic defense
mechanisms could occur in humans since they possess equivalent pulmonary
defense systems. It is understood, however, that different exposure levels
may be required to produce similar responses in humans. The concentration of
0,, at which effects become evident can be influenced by a number of factors,
such as preexisting disease, virulence of the infectious agent, dietary factors,
concurrent exposure to other pollutants, exercise, or the presence of other
environmental stresses, or a combination of these. Thus, one could hypothesize
that humans exposed to CL could experience effects on host defense mechanisms.
At the present time, however, one cannot predict the exact concentration at
which effects may occur in man nor the severity of the effects.
The effects of 0, on host defense mechanisms in experimental animals are
summarized in Figure 1-8 and Table 1-15 (see Section 1.8.1 for criteria used
in developing this summary).
1.8.3.5 Tolerance. Examination of responses to short-term, repeated exposures
to 0, clearly indicates that with some of the parameters measured, animals
have an increased capacity to resist the effects of subsequent exposure. This
tolerance persists for varying times, depending on the degree of development
of the tolerance. Previous exposure to low concentrations of 0, will protect
against the effects of subsequent exposure to lethal doses and the development
of lung edema (Stokinger et al., 1956; Fairchild, 1967; Coffin and Gardner,
1972a; Chow, 1984). The prolongation of mucociliary clearance reported for CL
OZNORM/A 1-112 11/22/85
-------
\v*
~o°
0. 1 -
0.2-
£
a
a 0.3-
c
0
J: 0.5-
c
a
1 0.6-
0
0
o, 0-7-
c
0
£ 0.8-
0.9-
i PI -
^
c
<
(
i
«£$*
)
i i
) i
(
i
*
S >e
4
t
1 4
i
I
°° ^£
4
i <
(
1
^X*
)
} 4
1
1 1
4
1
I (
4
1 4f
^•"4"-
)
1
1 f
)
1
I
4
t
I
c
1
)
1
1
i 4
(3
S*rlff
I
i 4
1
1
1
i
1
1
1
i
1
:>j -
i
i
i
\
^
Figure 1-8. Summary of effects of ozone on host defense mechanisms in experimental
animals. See Table 1-15 for reference citations of studies summarized here.
-------
PRELIMINARY DRAFT
TABLE 1-15. SUMMARY TABLE: EFFECTS OF OZONE ON HOST DEFENSE
MECHANISMS IN EXPERIMENTAL ANIMALS
Effect/response
03 concentration, ppm
References
Delayed mucociliary
clearance; accelerated
alveolar clearance,
ciliary beating
frequency
Inhibited bactericidal
activity
Altered macrophage
membrane
Decreased macrophage
function
Altered no.
cells
of defense
[0.1]
0.4, 0.8, 1.0
[0.5]
1.0
0.8
0.5
0.99
0.62
0.4
0.4
1.0
0.1,
0.5
0.5
0.5, 1.0
0.25, 0.5
0.67
0.67
0.8
1.0
1.0
0.2
0.2, 0.35
0.2, 0.35
0.2, 0.5, 0.8
0.25
0.5
0.5, 0.88
0.5
0.54, 0.88
0.8
1.0
1.0
0.5, 0.88
0.5, 0.8
0.2
0.2
0.5, 0.8
Grose et al. (1980)
Kenoyer et al. (1981)
FHberg et al. (1972)
Abraham et al. (1980)
Phalen et al. (1980)
Friberg et al. (1972)
Goldstein et al. (1971a)
Goldstein et al. (1971b)
Bergers et al. (1983)
Warshauer et al. (1974)
Coffin and Gardner (1972b)
Goldstein et al. (1972)
Gardner et al. (1971)
Dowel 1 et al. (1970)
Hadley et al. (1977)
Goldstein et al. (1977)
Hurst et al. (1970;
Hurst and Coffin (1971)
Alpert et al. (1971b)
Coffin et al. (1968)
Coffin and Gardner (1972b)
Schwartz and Christman (1979)
Shingu et al. (1980)
McAllen et al. (1981)
Plopper et al. (1979)
Dungworth et al. (1975)
Castleman et al. (1977)
Boorman et al. (1977, 1980)
Barry et al. (1983)
Zitnik et al. (1978)
Stephens et al. (1974a)
Last et al. (1979)
Freeman et al. (1974)
Castleman et al. (1980)
Freeman et al. (1973)
Cavender et al. (1977)
Brummer et al. (1977)
Eustis et al. (1981)
Dungworth (1976)
Stephens et al. (1976)
OZNORM/A
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PRELIMINARY DRAFT
TABLE 1-15 (continued). SUMMARY TABLE: EFFECTS OF OZONE ON HOST DEFENSE
MECHANISMS IN EXPERIMENTAL ANIMALS
Effect/response
Increased suscepti-
bility to infection
Increased suscepti-
bility (cont'd)
Altered immune
activity
03 concentration, ppm
0.08
0.08, 0.1
0.1
0.1
0.1, 0.3
0.4, 0.7
[0.2]
0.5
[0.64]
0.3
0.7, 0.9
1.0
0.1
0.5, 0.8
0.5, 0.8
0.59
References
Coffin et al. (1968)
Miller et al. (1978a)
Ehrlich et al. (1977)
Aranyi et al. (1983)
Illing et al. (1980)
Bergers et al. (1983)
Bergers et al. (1983)
Wolcott et al. (1982)
[Sherwood et al. (1984)]
Abraham et al. (1982)
Coffin and Blommer (1970)
Thomas et al. (1981b)
Aranyi et al. (1983)
Osebold et al. (1979, 1980)
Gershwin et al. (1981)
Campbell and Hilsenroth
(1976)
can also be eliminated by pre-exposure to a lower concentration (Frager et
al., 1979). This effect is demonstrated for a short period of time and is
lost as soon as the mucus secretion rate returns to normal. However, not all
of the toxic effects of 0.,, such as reduced functioning activity of the pulmonary
defense system (Gardner et al., 1972); hyperplasia of the type 2 cells (Evans
et al., 1971, 1976a,b); increased susceptibility to respiratory disease (Gardner
and Graham, 1977); loss of pulmonary enzymatic activity (Chow, 1976, Chow
et al., 1976); and inflammatory response (Gardner et al., 1972) can be totally
prevented by prior treatment with low levels of 0.,. Dungworth et al. (1975)
and Castleman et al. (1980) have attempted to explain tolerance by careful
examination of the morphological changes that occur with repeated 03 exposures.
These investigators suggest that during continuous exposure to 03 the injured
cells attempt to initiate early repair of the specific lesion. The repair
phase results in a reduction of the effect first observed but lasts only for a
short time since the recovered cells are as sensitive to re-exposure to 03 as
the pre-exposed counterpart (Plopper et al., 1978). This information is an
important observation because it implies that the decrease in susceptibility
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PRELIMINARY DRAFT
to CL persists only as long as the exposure to 0., continues. The biochemical
studies of Chow et al. (1976) support this conclusion.
At this time, there are a number of hypotheses proposed to explain the
mechanism of this phenomenon (Mustafa and Tierney, 1978; Schwartz et al.,
1976; Mustafa et al., 1977; Berliner et al., 1978; Gertner et al., 1983b;
Bhatnagar et al. , 1983). Evidence by Nambu and Yokoyama (1983) indicates that
although the pulmonary antioxidant system (glutathione peroxidase, glutathione
reductase, and glucose-6-phosphate dehydrogenase) may play an active role in
defending the lung against ozone, it does not explain the mechanism of toler-
ance in that the development of tolerance does not coincide with the described
biochemical enhancement of the antioxidant system in the lungs of rats.
From this literature, it would appear that tolerance, as seen in animals,
may not be the result of any one single biological process, but instead may
result from a number of different events, depending on the specific response
measured. Tolerance does not imply complete or absolute protection, because
continuing injury does still occur, which could potentially lead to nonrever-
sible pulmonary changes.
Tolerance may not be long-lasting. During CL exposure, the increase in
antioxidant metabolism reaches a plateau and recovery occurs a few days after
exposure ceases. Upon re-exposure, effects observed are similar to those that
occurred during the primary exposure (Chow et al., 1976).
1.8.4 Extrapulmonary Effects of Ozone
It is still believed that 03, on contact with respiratory system tissue,
immediately reacts and thus is not absorbed or transported to extrapulmonary
sites to any significant degree. However, several studies suggest that possibly
products formed by the interaction of CL and respiratory system fluids or
tissue can produce effects in lymphocytes, erythrocytes, and serum, as well as
in the parathyroid gland, the heart, the liver, and the CNS. Ozone exposure
also produces effects on animal behavior that may be caused by pulmonary
consequences of 0^, or by nonpulmonary (CNS) mechanisms. The mechanism by
which 0, causes extrapulmonary changes is unknown. Mathematical models of 03
dosimetry predict that very little 03 penetrates to the blood of the alveolar
capillaries. Whether these effects result from 0., or a reaction product of 0,
which penetrates to the blood and is transported is the subject of speculation.
OZNORM/A 1-116 11/22/85
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PRELIMINARY DRAFT
1.8.4.1 Central Nervous System and Behavioral Effects. Ozone significantly
affects the behavior of rats during exposure to concentrations as low as
235 ug/m (0.12 ppm) for 6 hr. With increasing concentrations of 03, further
decreases in unspecified motor activity and in operant learned behaviors have
been observed (Konigsberg and Bachman, 1970; Tepper et al., 1982; Murphy
et al., 1964; and Weiss et al., 1981). Tolerance to the observed decrease in
motor activity may occur on repeated exposure. At low 0, exposure concentra-
3
tions (490 ug/m , 0.25 ppm), an increase in activity is observed after exposure
ends. Higher 0, concentrations (980 ug/m , 0.5 ppm) produce a decrease in
rodent activity that persists for several hours after the end of exposure
(Tepper et al., 1982, 1983).
The mechanism by which behavioral performance is reduced is unknown.
Physically active responses appear to enhance the effects of 0,, although this
may be the result of an enhanced minute volume that increases the effective
concentration delivered to the lung. Several reports indicate that it is
unlikely that animals have reduced physiological capacity to respond, prompt-
ing Weiss et al. (1981) to suggest that 0, impairs the inclination to respond.
Two studies indicate that mice will respond to remove themselves from an
atmosphere containing greater than 980 ug/m (0.5 ppm) (Peterson and Andrews,
1963, Tepper et al., 1983). These studies suggest that the aversive effects
of 03 may be due to lung irritation. It is unknown whether lung irritation,
odor, or a direct effect on the CNS causes change in rodent behavior at lower
0., concentrations.
1.8.4.2 Cardiovascular Effects. Studies on the effects of 0, on the cardio-
vascular system are few, and to date there are no reports of attempts to con-
firm these studies. The exposure of rats to 0, alone or in combination with
3
cadmium (1176 ug/m , 0.6 ppm 0.,) resulted in measurable increases in systolic
pressure and heart rate (Revis et al., 1981). No additive or antagonistic
response was observed with the combined exposure. Pulmonary capillary blood
flow and PaO? decreased 30 min following exposure of dogs to 588 ug/m (0.3
ppm) of On (Friedman et al., 1983). The decrease in pulmonary capillary blood
flow persisted for as long as 24 hr following exposure.
1.8.4.3 Hematological and Serum Chemistry Effects. The data base for the
effects of 03 on the hematological system is extensive and indicates that 0.,
or one of its reactive products can cross the blood-gas barrier, causing
changes in the circulating erythrocytes (RBC) as well as significant differ-
ences in various components of the serum.
OZNORM/A 1-117 11/22/85
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PRELIMINARY DRAFT
Effects of 0., on the circulating RBCs can be readily identified by exa-
mining either morphological and/or biochemical endpoints. These cells are
structually and metabolically well understood and are available through rela-
tively non-invasive methods, which makes them ideal candidates for both human
and animal studies. A wide range of structural effects have been reported in
a variety of species of animals, including an increase in the fragility of
RBCs isolated from monkeys exposed to 1470 |jg/m (0.75 ppm) of 0, 4 hr/day for
3
4 days (Clark et al., 1978). A single 4-hr exposure to 392 ug/m (0.2 ppm)
also caused increased fragility as well as sphering of RBCs of rabbits (Brinkman
et al., 1964). An increase in the number of RBCs with Heinz bodies was detected
following a 4-hr exposure to 1666 ug/m (0.85 ppm). The presence of such
inclusion bodies in RBCs is an indication of oxidant stress (Menzel et al.,
1975a).
These morphological changes are frequently accompanied by a wide range of
o
biochemical effects. RBCs of monkeys exposed to 1470 ug/m (0.75 ppm) of 0.,
for 4 days also had a decreased level of glutathione (GSH) and decreased
acetylcholinesterase (AChE) activity, an enzyme bound to the RBC membranes.
The RBC GSH activity remained significantly lower 4 days postexposure (Clark
et al., 1978).
Animals deficient in vitamin E are more sensitive to 0.,. The RBCs from
these animals, after being exposed to 0,, had a significant increase in the
activity of GSH peroxidase, pyruvate kinase, and lactic dehydrogenase, but had
a decrease in RBC GSH after exposure to 1568 ug/m (0.8 ppm) for 7 days (Chow
and Kaneko, 1979). Animals with a vitamin E-supplemented diet did not have
any changes in glucose-6-phosphate dehydrogenase (G-6-PD), superoxide dismutase,
or catalase activities. At a lower level (980 ug/m , 0.5 ppm), there were no
changes in GSH level or in the activities of GSH peroxidase or GSH reductase
(Chow et al., 1975). Menzel et al. (1972) also reported a significant increase
in lysis of RBCs from vitamin E-deficient animals after 23 days of exposure to
980 ug/m (0.5 ppm). These effects were not observed in vitamin E-supplemented
rats. Mice on a vitamin E-supplemented diet and those on a deficient diet
showed an increase in G-6-PD activity after an exposure of 627 ug/m (0.32 ppm)
of 03 for 6 hr. Decreases observed in AChE activity occurred in both groups
(Moore et al., 1980).
OZNORM/A 1-118 11/22/85
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PRELIMINARY DRAFT
Other blood changes are attributed to Ov Rabbits exposed for 1 hr to
3
392 |jg/m (0.2 ppm) of 0, showed a significant drop in total blood serotonin
3
(Veninga, 1967). Six- and 10-month exposures of rabbits to 784 |jg/m (0.4 ppm)
of 03 produced an increase in serum protein esterase and in serum trypsin
inhibitor. This latter effect may be a result of thickening of the small
pulmonary arteries. The same exposure caused a significant decrease in albumin
levels and an increase in alpha and gamma globulins (P'an and Jegier, 1971,
1976; P'an et al., 1972; Jegier, 1973). Chow et al. (1974) reported that the
serum lysozyme level of rats increased significantly after 3 days of continuous
exposure to 0, but was not affected when the exposure was intermittent (8 hr/day,
3
7 days). The 0., concentration in both studies was 1568 (jg/m (0.8 ppm) of 0.,.
Short-term exposure to low concentrations of 0, induced an immediate
change in the serum creatine phosphokinase level in mice. In this study, the
OT doses were expressed as the product of concentration and time. The C x T
value for this effect ranged from 0.4 to 4.0 (Veninga et al., 1981).
A few of the hematological effects observed in animals (i.e., decrease in
GSH and AChE activity and the formation of Heinz bodies) following exposure to
0, have also been seen following i_n vitro exposure of RBCs from humans (Freeman
and Mudd, 1981; Menzel et al., 1975b; Verweij and Van Steveninck, 1981). A
common effect observed by a number of investigators is that 0, inhibits the
membrane ATPase activity of RBCs (Koontz and Heath, 1979; Kesner et al., 1979;
Kindya and Chan, 1976; Freeman et al., 1979; Verweij and Van Steveninck,
1980). It has been postulated that this inhibition of ATPase could be related
to the spherocytosis and increased fragility of RBCs seen in animal and human
cells.
Although these j_n vitro data are useful in studying mechanisms of action,
it is difficult to extrapolate these data to any effects observed in man. Not
only is the method of exposure not physiological, but the actual concentration
of 0- reaching the RBC cannot be determined with any accuracy.
1.8.4.4 Cytogenetic and Teratogenic Effects. Uncertainty still exists regard-
ing possible reproductive, teratogenic, and mutational effects of exposure to
ozone. Based on various ijn vitro data, a number of chromosomal effects of
ozone have been described for isolated cultured cell lines, human lymphocytes,
and microorganisms (Fetner, 1962; Hamelin et al., 1977a,b, Hamelin and Chung,
1975a,b, 1978; Scott and Lesher, 1963; Erdman and Hernandez, 1982; Guerrero
etal., 1979; Dubeau and Chung, 1979, 1982). The interpretation, relevance,
OZNORM/A 1-119 11/22/85
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PRELIMINARY DRAFT
and predictive values of such studies to human health are questionable since
(1) the concentrations used were many-fold greater than what is found in the
ambient air (see Chapter 10); (2) extrapolation of i_n vitro exposure concentra-
tions to human exposure dose is not yet possible; and (3) direct exposure of
isolated cells to ozone is highly artifactual since it bypasses all the defenses
of the host that would normally be functioning in protecting the individual
from the inhaled gas. Furthermore, the direct exposure of isolated cells j_n
vitro to ozone may result in chemical reactions between ozone and culture
media that might not occur in vivo.
Important questions still exist regarding i_n vivo cytogenetic effects of
ozone in rodents and humans. Zelac et al. (1971a,b) reported chromosomal
abnormalities in peripheral leukocytes of hamsters exposed to 0, (0.2 ppm).
Combined exposures to ozone and radiation (227-233 rads) produced an additive
effect on the number of chromosome breaks in peripheral leukocytes. These
specific findings were not confirmed by Gooch et al. (1976) or by Tice et al.
(1978), but sufficient differences in the various experimental protocols make
a direct comparison difficult. The latter group did report significant increases
in the number of chromatid deletions and achromatic lesions resulting from
exposure to 0.43 ppm ozone.
Because the volume of air inspired during pregnancy is significantly
enhanced, the pregnant animal may be at greater risk to low levels of ozone
exposure. Early studies on the possible teratogenic effects of ozone have
suggested that exposures as low as 0.2 ppm can reduce infant survival rate and
cause unlimited incisor growth (Brinkman et al., 1964; Veninga, 1967). Kavlock
et al. (1979, 1980) found that pregnant rats exposed to 1.0 and 1.49 ppm ozone
showed a significant increase in embryo resorption rate, slower growth, slower
development of righting reflexes, and delayed grooming and rearing behavior,
but no increase in neonatal mortality was observed.
1.8.4.5 Other Extrapulmonary Effects. A series of studies was conducted to
show that 0, increases drug-induced sleeping time in a number of species of
animals (Gardner et al., 1974; Graham, 1979; Graham et al., 1981, 1982a,b,
1983, 1985). At 1960 |.ig/m3 (1.0 ppm), effects were observed after 1, 2, and 3
days of exposure. As the concentration of 0-> was reduced, increasing numbers
of daily 3-hr exposures were required to produce a significant effect. At the
lowest concentration studied (196 ug/m , 0.1 ppm), the increase was observed
at days 15 and 16 of exposure. It appears that this effect is not specific to
OZNORM/A 1-120 11/22/85
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PRELIMINARY DRAFT
the strain of mouse or to the three species of animals tested, but it is
sex-specific, with females being more susceptible. Recovery was complete
within 24 hr after exposure. Although a number of mechanistic studies have
been conducted, the reason for this effect on pentobarbital-induced sleeping
time is not known. It has been hypothesized that some common aspect related
to liver drug metabolism is quantitatively reduced (Graham et al., 1983).
Several investigators have attempted to elucidate the involvement of the
endocrine system in 0, toxicity. Most of these studies were designed to
investigate the hypothesis that the survival rate of mice and rats exposed to
lethal concentrations of 03 could be increased by use of various thyroid
blocking agents or by thyroidectomy. To follow up these findings, demons and
Garcia (1980a,b) and demons and Wei (1984) investigated the effects of a
3
24-hr exposure to 1960 ug/m (1.0 ppm) of 0., on the hypothalamo-pituitary-thyroid
system of rats. These three organs regulate the function of each other through
various hormonal feedback mechanisms. Ozone caused decreases in serum concen-
tration of thyroid stimulating hormone (TSH), in circulating thyroid hormones
(T, and T.) and in protein-bound iodine. No alterations were observed in many
other hormone levels measured. Thyroidectomy prevented the effect of 0, on
TSH and T. and hypophysectomy prevented effects on T., unless the animals were
supplemented with T. in their drinking water. The thyroid gland itself was
altered (e.g., edema) by 0.,. The authors hypothesyzed that 0, alters serum
binding of these hormones.
The extrapulmonary effects of ozone in experimental animals are summarized
in Figure 1-9 and Table 1-16. Criteria used in developing the summary were
presented in Section 1.8.1.
1.8.5 Interaction of Ozone With Other Pollutants
Combined exposure studies in laboratory animals have produced varied
results, depending upon the pollutant combination evaluated and the measured
variables. Additive and/or possibly synergistic effects of 03 exposure in
combination with NO, have been described for increased susceptibility to
bacterial infection (Ehrlich et al., 1977, 1979; Ehrlich, 1980, 1983), morpho-
logical lesions (Freeman et al., 1974), and increased antioxidant metabolism
(Mustafa et al., 1984). Additive or possibly synergistic effects from exposure
to 0, and HUSO, have also been reported for host defense mechanisms (Gardner
et al., 1977; Last and Cross, 1978; Grose et al., 1982), pulmonary sensitivity
OZNORM/A 1-121 11/22/85
-------
.a
0.
0.1-
E 0-2H
a
a
, 0.3H
c
0
~ 0.4-1
0
-2 e.sH
0
u
c 0.6H
u
« 0.7-
c
I 0 8H
0.9-
1 0
Figure 1-9. Summary of extrapulmonary effects of ozone in experimental animals.
See Table 1-16 for reference citations of studies summarized here.
-------
PRELIMINARY DRAFT
TABLE 1-16. SUMMARY TABLE: EXTRAPULMONARY EFFECTS OF OZONE
IN EXPERIMENTAL ANIMALS
Effect/response
CNS effects
Hematological effects
Chromosomal, reproduc-
tive, teratological
effects
Liver effects
Endocrine system
effects
03 concentration, ppm
0.05, 0.5
0.1 - 1.0
0.12 - 1.0
0.2, 0.3, 0.5, 0.7
0.5
0.5
0.5
0.6
1.0
1.0
0.06, 0.12, 0.48
0.2
0.2, 1.0
0.25, 0.32, 0.5
0.4
0.4
0.5
0.64
0.75
0.8
0.8
0.85
0.86
1.0
1.0
1.0
0.1
0.2
0.44
1.0
0.24, 0.3
0.43
0.1, 0.25, 0.5, 1.0
0.82
1.0
0.75
0.75
0.75
0.75
1.0
1.0
References
Konigsberg and Bachman (1970)
Weiss et al. (1981)
Tepper et al. (1982)
Murphy et al. (1964)
Tepper et al. (1983)
Reynolds and Chaffee (1970)
Xintaras et al. (1966)
Peterson and Andrews (1963)
Fletcher and Tappel (1973)
Trams et al. (1972)
Calabrese et al. (1983)
Brinkman et al. (1964)
Veninga (1967, 1970)
Veninga et al. (1981)
Moore et al. (1980; 1981a,b)
Jegier (1973)
P'an and Jegier (1972, 1976)
Menzel et al. Q972)
Larkin et al. (1983)
Clark et al. (1978)
Chow and Kaneko (1979)
Chow et al. (1974)
Menzel et al. (1975a)
Schlipkbter and Bruch (1973)
Dorsey et al. (1983)
Mizoguchi et al. (1973)
Christiansen and Giese (1954)
Brinkman et al. (1964)
Veninga (1967)
Kavlock et al. (1979)
Kavlock et al. (1980)
Zelac et al. (1971a)
Tice et al. (1978)
Graham (1979)
Graham et al. (1981, 1982a,b)
Veninga et al . (1981)
Gardner et al. (1974)
Atwal and Wilson (1974)
Atwal et al. (1975)
Atwal and Pemsingh (1981, 1984)
Pemsingh and Atwal (1983)
demons and Garcia (1980a,b)
demons and Wei (1984)
OZNORM/A
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PRELIMINARY DRAFT
(Osebold et al. 1980), and collagen synthesis (Last et al., 1983), but not
for morphology (Cavender et al., 1977; Moore and Schwartz, 1981). Mixtures of
Oj and (NH.)^ SO. had synergistic effects on collagen synthesis and morphometry,
including percentage of fibroblasts (Last et al., 1983, 1984a).
Combining 0.. with other particulate pollutants produces a variety of
responses, depending on the endpoint measured. Mixtures of 03> Fep(SO.)3,
HpSO., and (NH.KSO. produced the same effect on clearance rate as exposure to
Cu alone. However, when measuring changes in host defenses, the combination
of 03 with N02 and ZnSO. or 0., with SOp and (NH^SO^ produced enhanced effects
that can not be attributed to 0, only.
However, since these issues are complex, they must be addressed experi-
mentally using exposure regimens for combined pollutants that are more represen-
tative of ambient ratios of peak concentrations, frequency, duration, and time
intervals between events.
The interactive effects of 03 with other pollutants are summarized in
Figure 1-10 and Table 1-17.
1.8.6 Effects of Other Photochemical Oxidants
There have been far too few controlled toxicological studies with the
other oxidants to permit any sound scientific evaluation of their contribution
to the toxic action of photochemical oxidant mixtures. When the effects seen
after exposure to 0, and PAN are examined and compared, it is obvious that the
test animals must be exposed to concentrations of PAN much greater than those
needed with 0., to produce a similar effect on lethality, behavior modification,
morphology, or significant alterations in host pulmonary defense system (Campbell
et al., 1967; Dungworth et al., 1969; Thomas et al., 1979, 1981a). The concen-
trations of PAN required to produce these effects are many times greater than
what has been measured in the atmosphere (0.037 ppm).
Similarly, most of the investigations reporting HpO- toxicity have involved
concentrations much higher than those found in the ambient air (0.1 ppm), or
the investigations were conducted by using various j_n vitro techniques for
exposure. Very limited information is available on the health significance of
inhalation exposure to gaseous HpOp. Because HpO,, is highly soluble, it is
generally assumed that it does not penetrate into the alveolar regions of the
lung but is instead deposited on the surface of the upper airways (Last et al.,
1982). Unfortunately, there have not been studies designed to look for pos-
sible effects in this region of the respiratory tract.
OZNORM/A 1-124 11/22/85
-------
PO
Ul
0.2-
e
a
Q.
0.3-
c
•: 0 4~
0
i 05-
c
Q)
£ 0.6-
0
u
« 0 7-
c
0
£ 0 8-
Q 9-
1 C)
»' r»'
\° »" \-
,-S ,-H ^or r
0 or o^^ \-x
A V" 1 ?° A °C 09° a
_o CTo o ro* . <<*
c^° 0'" f.^0t NBf-*
V" "S.0 V ^a ^
1 1 1
0
•
O • • i
• '
(
l>
• <
<• •#>* o
0° BM° ^^
o&r o"r ?*- ^
,o9 & ,oNX ^^^ o°f
^ei A .r0 ^ o*>vc<
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Figure 1-10. Summary of effects in experimental animals exposed to ozone combined
with other pollutants. See Table 1-17 for reference citations of studies summarized here.
-------
PRELIMINARY DRAFT
TABLE 1-17. SUMMARY TABLE: INTERACTION OF OZONE WITH OTHER POLLUTANTS
Effect/response
Pollutant concentrations
References
Increased
pulmonary
lesions
Increased
pulmonary
sensitivity
Increased anti-
oxidant metabolism
and 02 consumption
Altered mucus
secretion
Increased collagen
synthesis
Increased
susceptibility to
respiratory
infections
[0.25 ppm 03
+2.5 ppm N02]
[0.5 ppm 03
+ 1 mg/m3 H2S04]
[0.5 ppm 03
+ 10 mg/m3 H2S04
0.64, 0.96 ppm 03
+ 5 mg/m3 (NH4)2 S04
0.9 ppm 03
+0.9 ppm N02
1.2 ppm 03
+ 5 mg/m3 (NH4)2S04
0.5 ppm 03
+ 1 mg/m3 H2S04
0.45 ppm 03
+4.8 ppm N02
0.5 ppm 03
+1.1 mg/m3 H2S04
[0.5], [0.8], 1.5 ppm 03
+ 5 mg/m3 (NH4)2S04
0.5 ppm 03
+ 1 mg/m3 H2S04
0.64, 0.96 ppm 03
+ 5 mg/m3 (NH4)2S04
0.05 ppm 03
+ 3760 |jg/m3 (NH4)2S04
0.05 ppm 03
+ 100-400 jjg/m3 N02
+1.5 mg/m3 ZnS04
0.1 ppm 03
+0.9 mg/m3 H2S04
(sequential exposure)
0.1 ppm 03
+4.8 mg/m3 H2S04
0.1 ppm 03
+ 940 pg/m3 N02
0.1 ppm 03
+13.2 mg/m3 S02
+1.0 mg/m3 (NH4)2S04
Freeman et al. (1974)
Moore and Schwartz (1981)
Cavender et al. (1978)
Last et al. (1984a)
Freeman et al. (1974)
Last et al. (1983)
Osebold et al. (1980)
Mustafa et al. (1984)
Last and Cross (1978);
Last and Kaizu (1980)
Last et al. (1983)
Last et al. (1983)
Last et al. (1984a)
Ehrlich et al. (1977, 1979);
Ehrlich (1980)
Ehrlich et al. (1983)
Gardner et al. (1977)
Grose et al. (1982)
Ehrlich (1980)
Aranyi et al. (1983)
OZNORM/A
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PRELIMINARY DRAFT
TABLE 1-17 (continued). SUMMARY TABLE:
WITH OTHER POLLUTANTS
INTERACTION OF OZONE
Effect/response
Pollutant concentrations
References
Altered upper
respiratory
clearance
mechanisms
[0.1 ppm 03
+1.1 mg/m3 H2S04]
(sequential exposure)
0.4 ppm 03
+7.0 ppm N02
0. 5- ppm 03
+ 3 mg/m3 H2S04
[0.8 ppm 03
+3.5 mg/m3
{Fe2(S04)3
+ H2S04
+ (NH4)2S04}]
Grose et al. (1980)
Goldstein et al. (1974)
Last and Cross (1978)
Phalen et al. (1980)
A few HI vitro studies have reported cytotoxic, genotoxic, and biochemical
effects of HpOp when using isolated cells or organs (Stewart et al., 1981;
Bradley et al., 1979; Bradley and Erickson, 1981; Speit et al., 1982; MacRae
and Stich, 1979). Although these studies can provide useful data for studying
possible mechanisms of action, it is not yet possible to extrapolate these
responses to those that might occur in the mammalian system.
Field and epidemiological studies have shown that human health effects
from exposure to ambient mixtures of oxidants and other airborne pollutants
can produce human health effects (Chapter 12). Few such studies have been
conducted with laboratory animals, because testing and measuring of such
mixtures is not only complicated, but extremely costly. In these studies, the
investigators attempted to simulate the photochemical reaction products pro-
duced under natural conditions and to define the cause-effect relationship.
Exposure to complex mixtures of oxidants plus the various components
found in UV-irradiated auto exhaust indicates that certain effects, such as
histopathological changes, increase in susceptibility to infection, a variety
of altered pulmonary functional activities were observed in this oxidant
atmosphere which was not reported in the nonirradiated exhaust (Murphy et al.,
1963; Murphy, 1964; Nakajima etal., 1972; Hueter etal., 1966). Certain
other biological responses were observed in both treatment groups, including a
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PRELIMINARY DRAFT
decrease in spontaneous activity, a decrease in infant survival rate, fertil-
ity, and certain pulmonary functional abnormalities (Hueter et al., 1966;
Boche and Quilligan, 1960; Lewis et al., 1967).
Dogs exposed to UV-irradiated auto exhaust containing oxidants either
with or without SO showed significant pulmonary functional abnormalities that
had relatively good correlation with structural changes (Hyde et al., 1978;
Gillespie, 1980; Lewis et al., 1974). There were no significant differences
in the magnitude of the response in these two treatment groups, indicating
that oxidant gases and SO did not interact in any synergistic or additive
manner.
1.9 CONTROLLED HUMAN STUDIES OF THE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL
OXIDANTS
A number of important controlled studies discussed in this chapter have
reported significant decrements in pulmonary function associated with 0-.
exposure (Table 1-18). In most of the studies reported, greatest attention
has been accorded decrements in FEV, „, as this variable represents a summation
of changes in both volume and resistance. While this is true, it must be
pointed out that for exposure concentrations critical to the standard-setting
process (i.e., <0.3 ppm 0,), the observed decrements in FEV, 0 primarily
reflect FVC decrements of similar magnitude, with little or no contribution
from changes in resistance.
Results from studies of at-rest exposures to 0, have demonstrated decre-
3
ments in forced expiratory volumes and flows occurring at and above 980 (jg/ra
(0.5 ppm) of 03 (Folinsbee et al., 1978; Horvath et al., 1979). Airway resis-
tance is not clearly affected at these 0, concentrations. At or below 588
3
|jg/m (0.3 ppm) of 0.,, changes in pulmonary function do not occur during at
rest exposure (Folinsbee et al., 1978), but the occurrence of some 0--induced
pulmonary symptoms has been suggested (Konig et al., 1980).
With moderate intermittent exercise at a Vp of 30 to 50 L/min, decrements
in forced expiratory volumes and flows have been observed at and above 588
ug/m (0.30 ppm) of 0 (Folinsbee et al., 1978). With heavy intermittent
exercise (VV = 65 L/min), pulmonary symptoms are present and decrements in
forced expiratory volumes and flows are suggested to occur following 2-hr
exposures to 235 (jg/m (0.12 ppm) of 03 (McDonnell et al., 1983). Symptoms
019END/A 1-128 11/22/85
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PRELIMINARY DRAFT
TABLE 1-18 SUMMARY TABLE: CONTROLLED HJMAN EXPOSURE TO OZONE
I
ro
Ozone b
concentration Measurement ' Exposure
ug/m3
HEALTHY
627
1960
980
980
1470
ppm method duration
ADULT SUBJECTS AT REST
0.32 HAST, NBKI 2 hr
1.0
0.5 CHEM, NBKI 2 hr
0.50 CHEM, NBKI 2 hr
0.75
Activity*1
level (VE) Observed effects(s)
R Specific airway resistance increased with
acetylcholine challenge; subjective symptoms
in 3/14 at 0.32 ppm and 8/14 at 1.0 ppm.
R (10) Decrement in forced expiratory volume and
flow.
R (8) Decrement in forced expiratory volume and
flow.
No. and sex
of subjects Reference
13 male Konig et al. , 1980
1 female
40 male Folinsbee et al. ,
(divided into four 1978
exposure groups)
8 male Horvath et al. ,
7 female 1979
EXERCISING HEALTHY ADULTS
235
353
470
588
784
314
470
627
353
470
588
784
0.12 CHEM, UV 2.5 hr
0.18
0.24
0.30
0.40
0.16 UV, UV 1 hr
0.24
0.32
0.18 CHEM, UV 2.5 hr
0.24
0.30
0.40
IE (65) Decrement in forced expiratory volume and
@ 15-min Intervals flow suggested at 0.12 ppm with larger
decrements at > 0.18 ppm; respiratory
frequency and specific airway resistance
increased and tidal volume decreased at
> 0.24 ppm; coughing reported at all
concentrations, pain and shortness of
breath at J 0.24 ppm.
CE (57) Small decrements in forced expiratory
volume at 0.16 ppm with larger decrements
at >0.24 ppm; lower-respiratory symptoms
increased at >0. 16 ppm.
IE (65) Individual responses to 03 were highly
615-min intervals reproducible for periods as long as 10
months; large Intersubject variability
1n response due to intrinsic responsiveness
to 03.
135 male McDonnell et al. ,
(divided Into six 1983
exposure groups)
42 male Avol et al. . 1984
8 female
(competitive
bicyclists)
32 male McDonnell et al.,
1985a
-------
PRELIMINARY DRAFT
TABLE 1-18 (continued). SUMMARY TABLE: CONTROLLED HUMAN EXPOSURE TO OZONE
OJ
o
Ozone
concentration
ug/nr1
392
666
392
823
980
392
490
412
588
980
725
980
1470
784
784
ppm
0.20
0.35
0.2
0.42
0.50
0.20
0.25
0.21
0.3
0.5
0.37
0.50
0.75
0.4
0.4
Measurement >c Exposure Activity
method duration level (V_)
UV, UV 1 hr IE (77.5) @ vari-
(mouth- able competitive
piece) intervals
CE (77.5)
UV, UV 2 hr IE (30 for male,
18 for female
subjects)
@ 15-min intervals
UV, UV 2 hr IE (68)
(4) 14-min periods
UV, UV 1 hr CE (81)
CHEM, NBKI 2 hr R (10), IE (31,
50, 67)
@ 15-min intervals
MAST, NBKI 2 hr R (11) & IE (29)
@ 15-min intervals
UV, NBKI 2 hr IE (2xR)
@ 15-min intervals
CHEM, NBKI 4 3 hr IE (4-5xR)
MAST, NBKI
Observed effects(s)
Decrement in forced expiratory volume and
flow with IE and CE; subjective symptoms
increased with 03 concentration and may
limit performance; respiratory frequency
increased and tidal volume decreased with
CE.
Repeated daily exposure to 0.2 ppm did not
affect response at higher exposure concen-
trations (0.42 or 0.50 ppm); large inter-
subject variability but individual
pulmonary function responses were highly
reproducible.
Large intersubject variability in response;
significant concentration-response relation-
ships for pulmonary function and respiratory
symptoms.
Decrement in forced expiratory volume and
flow; subjective symptoms may limit per-
formance.
Decrement in forced expiratory volume and
flow; the magnitude of the change was
related to 03 concentration and V
Total lung capacity and inspiratory
capacity decreased with IE (50, 67); no
change in airway resistance or residual
volume even at highest IE (67). No
significant changes in pulmonary function
were observed at 0.1 ppm.
Good correlation between dose (concen-
tration x V_) and decrement in forced
expiratory volume and flow.
Specific airway resistance increased with
histamine challenge; no changes were
observed at concentrations of 0.2 ppm.
Decrement in forced expiratory volume and
SG was greatest on the 2nd of 5 exposure
days; attenuated response by the 4th day
of exposure.
No. and sex
of subjects Reference
10 male Adams and Schelegle,
(distance runners) 1983
8 male Gliner et al. , 1983
13 female
20 male Kulle et al. , 1985
6 male Folinsbee et al.,
1 female 1984
(distance cyclists)
40 male Folinsbee et al.,
(divided into four 1978
exposure groups)
20 male Silverman et al. .
8 female (divided into 1976
six exposure groups)
12 male Dimeo et al., 1981
7 female
(divided into three
exposure groups)
10 male Farrell et al. , 1979
4 female
-------
PRELIMINARY DRAFT
TABLE 1-18 (continued). SUMMARY TABLE: CONTROLLED HUMAN EXPOSURE TO OZONE
Ozone .
concentration Measurement ' Exposure
ug/m3 ppm method duration
784 0.4 CHEM, UV 3 hr
Ac t i v i ty
level (VE)
IE (4-5xR)
for 15 min
Observed effects(s)
Decrement in forced expiratory volume was
greatest on the 2nd of 5 exposure days;
attenuation of response occurred by the
5th day and persisted for 4 to 7 days.
Enhanced bronchoreactivHy with
methachol ine on the first 3 days;
attenuation of response occurred by
the 4th and 5th day and persisted
for > 7 days.
No. and sex
of subjects Reference
13 male Kulle et al. , 1982
11 female
(divided into two
exposure groups)
823 0.42
UV, UV
2 hr
IE (30)
Decrement In forced expiratory volume and
flow greatest on the 2nd of 5 exposure
days; attenuation of response occurred by
the 5th day and persisted for < 14 days with
considerable intersubject variability.
24 male
Horvath et al., 1981
921 0.47 UV, NBKI
980 0.5 MAST, NBKI
1176 0.6 UV, NBKI
1470 0.75 MAST, NBKI
2 hr IE (3xR)
6 hr IE (44) for two
15-min periods
2 hr IE (2xR)
(noseclip) ? 15-min Intervals
2 hr IE (2xR)
@ 15-min intervals
Decrement In forced expiratory volume and
flow greatest on the 2nd of 4 exposure
days; attenuation of response occurred by
the 4th day and persisted for 4 days.
Small decrements in forced expiratory
volume and specific airway conductance.
Specific airway resistance increased 1n 7
nonatopic subjects with histamine and
methachol ine and In 9 atoplc subjects
with histamine.
Decrements in spirometric variables
(20%-55%); residual volume and closing
capacity increased.
8 male
3 female
19 male
1 female
11 male
5 female (divided
by history of atopy)
12 male
Ltnn et al
Kerr et al
. , 1982b
. , 1975
Hoi tzman et al . ,
1979
Hazucha et
1973
al. ,
EXERCISING HEALTHY CHILORFN
235 0.12 CHEM, UV
2.5 hr IE (39)
015-min intervals
Small decrements in forced expiratory
volume, persisting for 24 hr. No subjec-
tive symptoms.
23 male
(8-11 yrs)
McDonnel 1
1985b.c
et al. ,
-------
PRELIMINARY DRAFT
TABLE 1-18. (continued) SUMMARY TABLE: CONTROLLED HUMAN EXPOSURE TO OZONE
Ozone .
concentration Measurement ' Exposure
Mg/nr* ppm method duration
Activity
level (V£)
Observed effects(s)
No. and sex
of subjects Reference
ADULT ASTHMATICS
392 0.2 CHEM, NBKI 2 hr
490 0.25 CHEM, NBKI 2 hr
IE (2xR)
@ 15-min intervals
R
No significant changes in pulmonary func-
tion. Small changes in blood biochemistry.
Increase in symptom frequency reported.
No significant changes in pulmonary func~
tion.
20 male Linn et al. , 1978
2 female
5 males Silverman, 1979
12 female
ADOLESCENT ASTHMATICS
235 0.12 UV 1 hr
(mouthpiece)
R
No significant changes in pulmonary function
or symptoms.
4 male Koenig et al. , 1985
6 female
(11-18 yrs)
SUBJECTS WITH CHRONIC OBSTRUCTIVE LUNG DISEASE
235 0.12 UV, NBKI 1 hr
i
'
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PRELIMINARY DRAFT
are present and decrements in forced expiratory volumes and flows definitely
occur at 314 to 470 pg/"1 (0.16 to 0.24 ppm) of 0., following 1 hr of continuous
heavy exercise at a V_ of 57 L/min (Avol et al., 1984) or very heavy exercise
at a VE of 80 to 90 L/min (Adams and Schelegle, 1983; Folinsbee et al., 1984)
and following 2 hr of intermittent heavy exercise at a VF of 65 L/min (McDonnell
et al., 1983). Airway resistance is only modestly affected with moderate
exercise (Kerr et al., 1975; Farrell et al., 1979) or even with heavy exercise
while exposed at levels as high as 980 (jg/rn (0.50 ppm) 0, (Folinsbee et al.,
1978; McDonnell et al., 1983). Increased fD and decreased VT) while maintain-
K I
ing the same VV, occur with prolonged heavy exercise when exposed at 392 to
•3 b
470 ug/m (0.20 to 0.24 ppm) of 0, (McDonnell et al., 1983; Adams and Schelegle,
•J
1983). While an increase in RV has been reported to result from exposure to
1470 ug/m (0.75 ppm) of 0., (Hazucha et al., 1973), changes in RV have not
3
been observed following exposures to 980 ug/m (0.50 ppm) of 0, or less, even
with heavy exercise (Folinsbee et al., 1978). Decreases in TLC and 1C have
been observed to result from exposures to 980 ug/m (0.50 ppm) of 0, or less,
with moderate and heavy exercise (Folinsbee et al., 1978).
Group mean decrements in pulmonary function can be predicted with some
degree of accuracy when expressed as a function of effective dose of 0.,, the
simple product of 0., concentration, V.-, and exposure duration (Silverman et
al. , 1976). The relative contribution of these variables to pulmonary decre-
ments is greater for 0, concentration than for Vp. A greater degree of predic-
tive accuracy is obtained if the contribution of these variables is appropri-
ately weighted (Folinsbee et al., 1978). However, several additional factors
make the interpretation of prediction equations more difficult. There is
considerable intersubject variability in the magnitude of individual pulmonary
function responses to 03 (Horvath et al., 1981; Gliner et al, 1983; McDonnell
et al., 1983; Kulle et al., 1985). Individual responses to a given 03 concen-
tration have been shown to be quite reproducible (Gliner et al., 1983; McDonnell
et al., 1985a), indicating that some individuals are consistently more respon-
sive to 0, than are others. No information is available to account for these
differences. Considering the great variability in individual pulmonary re-
sponses to 0^ exposure, prediction equations that only use some form of effec-
tive dose are not adequate for predicting individual responses to 0,.
In addition to overt changes in pulmonary function, enhanced nonspecific
bronchial reactivity has been observed following exposures to 03 concentrations
019END/A 1-133 11/22/85
-------
PRELIMINARY DRAFT
>588 \jg/m (0.3 ppm) (Holtzman et al., 1979; Kb'nig et al., 1980; Dimeo el al.,
1981). Exposure to 392 (jg/m (0.2 ppm) of 0, with intermittent light exercise
does not affect nonspecific bronchial reactivity (Dimeo et al., 1981).
Changes in forced expiratory volumes and flows resulting from CL exposure
reflect reduced maximal inspiratory position (inspiratory capacity) (Folinsbee
et al. , 1978). These changes, as well as altered ventilatory control and the
occurrence of respiratory symptoms, most likely result from sensitization or
stimulation of airway irritant receptors (Folinsbee et al., 1978; Holtzman et
al., 1979; McDonnell et al., 1983). The increased airways resistance observed
following 0, exposure is probably initiated by a similar mechanism. Different
efferent pathways have been proposed (Beckett et al., 1985) to account for the
lack of correlation between individual changes in SR and FVC (McDonnell
3W
et al. , 1983). The increased responsiveness of airways to histamine and
methacholine following 0, exposure most likely results from an 0.,-induced
increase in airways permeability or from an alteration of smooth muscle charac-
teristics.
Decrements in pulmonary function were not observed for adult asthmatics
exposed for 2 hours at rest (Silverman, 1979) or with intermittent light
exercise (Linn et al., 1978) to 0, concentrations of 490 |jg/m (0.25 ppm) and
less. Likewise, no significant changes in pulmonary function or symptoms were
found in adolescent asthmatics exposed for 1 hr at rest to 235 pg/m (0.12
ppm) of 03 (Koenig et al., 1985). Although these results indicate that asthma-
tics are not more sensitive to 0.. than are normal subjects, experimental-design
considerations in reported studies suggest that this issue is still unresolved.
For patients with COLD performing light to moderate intermittent exercise, no
decrements in pulmonary function are observed for 1- and 2-hr exposures to 0.,
concentrations of 588 ug/m3 (0.30 ppm) and less (Linn et al., 1982a, 1983;
Solic et al., 1982; Kehrl et al., 1983, 1985) and only small decreases in
forced expiratory volume are observed for 3-hr exposures of chronic bronchitics
to 804 ug/m3 (0.41 ppm) (Kulle et al., 1984). Small decreases in Sa02 have
also been observed in some of these studies but not in others; therefore,
interpretation of these decreases and their clinical significance is uncertain.
Many variables have not been adequately addressed in the available clini-
cal data. Information derived from 0., exposure of smokers and nonsmokers is
•J
sparse and somewhat inconsistent, perhaps partly because of undocumented
variability in smoking histories. Although some degree of attenuation appears
019END/A 1-134 11/22/85
-------
PRELIMINARY DRAFT
to occur in smokers, all current results should be interpreted with caution.
Further and more precise studies are required to answer the complex problems
associated with personal and ambient pollutant exposures. Possible age differ-
ences in response to (L have not been explored systematically. Young adults
usually provide the subject population, and where subjects of differing age
are combined, the groups studied are often too small in number to make adequate
statistical comparisons. Children (boys, aged 8 to 11 yr) have been the
subjects in only one study (McDonnell et al., 1985b) and nonstatistical compari-
son with adult males exposed under identical conditions has indicated that the
effects of 0- on lung spirometry were very similar (McDonnell et al., 1985c).
While a few studies have investigated sex differences, they have not conclu-
sively demonstrated that men and women respond differently to 0~, and consid-
eration of differences in pulmonary capacities have not been adequately taken
into account. Environmental conditions such as heat and relative humidity may
enhance subjective symptoms and physiological impairment following 07 exposure,
•J
but the results so far indicate that the effects are no more than additive.
In addition, there may be considerable interaction between these variables
that may result in modification of interpretations made based on available
information.
During repeated daily exposures to 0,, decrements in pulmonary function
are greatest on the second exposure day (Farrell et al., 1979; Horvath et al.,
1981; Kulle et al., 1982; Linn et al., 1982b); thereafter, pulmonary respon-
siveness to 0., is attenuated with smaller decrements on each successive day
than on the day before until the fourth or fifth exposure day when small
decrements or no changes are observed. Following a sequence of repeated daily
exposures, this attenuated pulmonary responsiveness persists for 3 (Kulle
et al., 1982; Linn et al., 1982b) to 7 (Horvath et al., 1981) days. Repeated
daily exposures to a given low effective dose of 0~ does not affect the magni-
tude of decrements in pulmonary function resulting from exposure at a higher
effective dose of 0, (Gliner et al., 1983).
There is some evidence suggesting that exercise performance may be limited
by exposure to 0,. Decrements in forced expiratory flow occurring with 0.,
exposure during prolonged heavy exercise (Vp = 65 to 81 L/min) along with
increased f0 and decreased VT might be expected to produce ventilatory limita-
ry I
tions at near maximal exercise. Results from exposure to ozone during high
019END/A 1-135 11/22/85
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PRELIMINARY DRAFT
exercise levels (68 to 75 percent of max VO-) indicate that discomfort associ-
ated with maximal ventilation may be an important factor in limiting perfor-
mance (Adams and Schelegle, 1983; Folinsbee et al., 1984). However, there is
not enough data available to adequately address this issue.
No consistent cytogenetic or functional changes have been demonstrated in
circulating cells from human subjects exposed to CL concentrations as high as
3
784 to 1176 ug/m (0.4 to 0.6 ppm). Chromosome or chromatid aberrations would
therefore be unlikely at lower 0, levels. Limited data have indicated that 0,
can interfere with biochemical mechanisms in blood erythrocytes and sera but
the physiological significance of these studies is questionable.
No significant enhancement of respiratory effects has been consistently
demonstrated for combined exposures of 0- with SO,,, N0?, and sulfuric acid or
particulate aerosols or with multiple combinations of these pollutants. Most
of the available studies with other photochemical oxidants have been limited
to studies on the effects of peroxyacetyl nitrate (PAN) on healthy young and
middle-aged males during intermittent moderate exercise. No significant
effects were observed at PAN concentrations of 0.25 to 0.30 ppm, which are
higher than the daily maximum concentrations of PAN reported for relatively
high oxidant areas (0.037 ppm). One study (Dreschler-Parks et al., 1984)
suggested a possible simultaneous effect of PAN and 0,; however, there are not
enough data to evaluate the significance of this effect. Further studies are
also required to evaluate the relationships between 0, and the more complex
mix of pollutants found in the natural environment.
1.10 FIELD AND EPIDEMIOLOGICAL STUDIES OF THE EFFECTS OF OZONE AND OTHER
PHOTOCHEMICAL OXIDANTS
Field and epidemiological studies offer a unique view of health effects
research because they involve the real world, i.e., the study of human popula-
tions in their natural setting. These studies have attendant limitations,
however, that must be considered in a critical evaluation of their results.
One major problem in singling out the effects of one air pollutant in field
studies of morbidity in populations has been the interference of other environ-
mental variables that are critical. Limitations of epidemiological research
on the health effects of oxidants include: interference by other air pollutants
or interactions between oxidants and other pollutants; meteorological factors
019END/A 1-136 11/22/85
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PRELIMINARY DRAFT
such as temperature and relative humidity; proper exposure assessments, including
determination of individual activity patterns and adequacy of number and
location of pollutant monitors; difficulty in identifying oxidant species
responsible for observed effects; and characteristics of the populations such
as hygiene practices, smoking habits, and socioeconomic status.
The most quantitatively useful information of the effects of acute exposure
to photochemical oxidants presented in this chapter comes from the field
studies of symptoms and pulmonary function. These studies offer the advantage
of studying the effects of naturally-occurring, ambient air on a local subject
population using the methods and better experimental control typical of
controlled-exposure studies. In addition, the measured responses in ambient
air can be compared to clean, filtered air without pollutants or to filtered
air containing artificially-generated concentrations of 0., that are comparable
to those found in the ambient environment. As shown in Table 1-19, studies by
Linn et al. (1980, 1983) and Avol et al. (1983, 1984, 1985a,b) have demonstrated
that respiratory effects in Los Angeles area residents are related to CL
concentration and level of exercise. Such effects include: pulmonary function
3
decrements seen at 0~ concentrations of 282 |jg/m (0.144 ppm) in exercising
healthy adolescents; and increased respiratory symptoms and pulmonary function
decrements seen at 0- concentrations of 300 |jg/m (0.153 ppm) in heavily exer-
3
cising athletes and at 0, concentrations of 341 ug/m (0.174 ppm) in lightly
exercising normal and asthmatic subjects. The light exercise level is probably
the type most likely to occur in the exposed population of Los Angeles. The
observed effects are typically mild, and generally no substantial differences
were seen in asthmatics versus persons with normal respiratory health, although
symptoms lasted for a few hours longer in asthmatics. Many of the normal
subjects, however, had a history of allergy and appeared to be more sensitive
to 0,. than "non-allergic" normal subjects. Concerns raised about the relative
contribution to untoward effects in these field studies by pollutants other
than 0, have been diminished by direct comparative findings in exercising
athletes (Avol et al., 1984) showing no differences in response between chamber
exposures to oxidant-polluted ambient air with a mean 0, concentration of
3
294 |.ig/m (0.15 ppm) and purified air containing a controlled concentration of
generated 0^ at 314 ug/m (0.16 ppm). The relative importance of exercise
level, duration of exposure, and individual variations in sensitivity in
producing the observed effects remains to be more fully investigated, although
019END/A 1-137 11/22/85
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PRELIMINARY DRAFT
TABLE 1-19. SUMMARY TABLE: ACUTE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IN FIELD STUDIES WITH A MOBILE LABORATORY
CO
Mean ozone ^
concentration Measurement '
ug/ro3 ppro method
2152 0.144 UV,
UV
i'"300 0.153 UV,
UV
306 0.156 UV,
NBKI
323 0.165 UV,
NBKI
341 0.174 UV,
NBKI
Exposure Activity
duration level (V£)
1 hr CE(32)
1 hr CE(53)
1 hr CE(38)
1 hr CE(42)
2 hr IE(2 x R)
9 15-min
interval s
Observed effect(s)
Small significant decreases in FVC (-2.1*), FEV0 75
(-4.0%), FEV, o (-3.7%), and PEFR (-4.4%) relative
to control with no recovery during a 1-hr post-
exposure rest; no significant increases in
symptoms.
Mild increases in lower respiratory symptom scores
and significant decreases in FEV, (-5.3%) and
FVC; mean changes in ambient air were not statisti-
cally different from those in purified air contain-
ing 0. 16 ppm 03.
No significant changes for total symptom score or
forced expiratory performance in normals or
asthmatics; however, FEV, remained low or
decreased further (-3%) 3 hr after ambient air
exposure in asthmatics.
Small significant decreases in FEV, (-3.3%) and
FVC with no recovery during a 1-hr postexposure
rest; TLC decreased and AN2 increased slightly.
Increased symptom scores and small significant
decreases in FEV, (-2.4%), FVC, PEFR, and TLC
in both asthmatic and healthy subjects however,
25/34 healthy subjects were allergic and "atypi-
cally" reactive to 03.
No.
of subjects Reference
59 healthy Avol et al., 1985a,b
adolescents
(12-15 yr)
50 healthy Avol et al . , 1984
adults (compe-
titive bicy-
clists)
48 healthy Linn et al., 1983;
adults Avol et al. , 1983
50 asthmatic
adults
60 "healthy" Linn et al., 1983;
adults Avol et al. , 1983
(7 were
asthmatic)
34 "healthy" Linn et al., 1980, 1983
adults
30 asthmatic
adults
Ranked by lowest observed effect level for 03 in ambient air.
Measurement method: UV = ultraviolet photometry.
""Calibration method: UV = ultraviolet photometry standard; NBKI = neutral buffered potassium iodide.
Minute ventilation reported in L/min or as a multiple of resting ventilation. CE = continuous exercise, IE = intermittent exercise.
-------
PRELIMINARY DRAFT
the results from field studies relative to those factors are consistent with
results from controlled human exposure studies (Chapter 11).
Studies of the effects of both acute and chronic exposures have been
reported in the epidemiological literature on photochemical oxidants. Investi-
gative approaches comparing communities with high CL concentrations and communi-
ties with low 0, concentrations have usually been unsuccessful, often because
actual pollutant levels have not differed enough during the study, or other
important variables have not been adequately controlled. The terms "oxidant"
and "ozone" and their respective association with health effects are often
unclear. Moreover, information about the measurement and calibration methods
used is often lacking. Also, as epidemiological methods improve, the incorpor-
ation of new key variables into the analyses is desirable, such as the use of
individual exposure data (e.g., from the home and workplace). Analyses employing
these variables are lacking for most of the community studies evaluated.
Studies of effects associated with acute exposure that are considered to
be qualitatively useful for standard-setting purposes include those on irritative
symptoms, pulmonary function, and aggravation of existing respiratory disease.
Reported effects on the incidence of acute respiratory illness and on physician,
emergency room, and hospital visits are not clearly related with acute exposure
to ambient 0., or oxidants and, therefore, are not useful for deriving health
effects criteria. Likewise, no convincing association has been demonstrated
between daily mortality and daily oxidant concentrations; rather, the effect
correlates most closely with elevated temperature.
Studies on the irritative effects of 0, have been complicated by the
presence of other photochemical pollutants and their precursors in the ambient
environment and by the lack of adequate control for other pollutants, meteoro-
logical variables, and non-environmental factors in the analysis. Although 0,
does not cause the eye irritation normally associated with smog, several studies
in the Los Angeles basin have indicated that eye irritation is likely to occur
in ambient air when oxidant levels are about 0.10 ppm. Qualitative associations
between oxidant levels in the ambient air and symptoms such as eye and throat
irritation, chest discomfort, cough, and headache have been reported at >0.10 ppm
in both children and young adults (Hammer et al., 1974; Makino and Mizoguchi,
1975; Okawada et al., 1979). Discomfort caused by irritative symptoms may be
responsible for the impairment of athletic performance reported in high school
students during cross-country track meets in Los Angeles (Wayne et al., 1967;
019END/A 1-139 11/22/85
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PRELIMINARY DRAFT
Herman, 1972) and is consistent with the evidence from controlled human exposure
studies indicating that exercise performance may be limited by exposure to CL
O
(Chapter 11). Although several additional studies have shown respiratory
irritation apparently related to exposure to ambient CL or oxidants in community
populations, none of these epidemiological studies provide satisfactory quanti-
tative data on acute respiratory illnesses.
Epidemiological studies in children and young adults suggest an association
of decreased peak flow and increased airway resistance with acute ambient air
exposures to daily maximum 1-hr 0., concentrations ranging from 20 to 294 |.ig/m
(0.01 to 0.15 ppm) over the entire study period (Kagawa and Toyama, 1975;
Kagawa et al., 1976; Lippmann et al., 1983; Lebowitz et al., 1982, 1983;
Lebowitz, 1984; Bock et al., 1985; Lioy et al., 1985). None of these studies
by themselves can provide satisfactory quantitative data on acute effects of
0,, because of methodological problems along with the confounding influence of
other pollutants and environmental conditions in the ambient air. The aggrega-
tion of individual studies, however, provides reasonably good qualitative
evidence for an association between ambient 0, exposure and acute pulmonary
function effects. This qualitative association is strengthened by the consis-
tency between the findings from the epidemiological studies and the results
from the field studies in exercising adolescents (Avol et al., 1985a,b) which
have shown small decreases in forced expiratory volume and flow at 282 |jg/m
(0.144 ppm) of 0, in the ambient air; and with the results from the controlled
»}
human exposure studies in exercising children which have shown small decrements
in forced expiratory volume at 235 ug/m (0.12 ppm) of 0, (Section 11.2.9.2).
In studies of exacerbation of asthma and chronic lung diseases, the major
problems have been the lack of information on the possible effects of medica-
tions, the absence of records for all days on which symptoms could have occurred,
and the possible concurrence of symptomatic attacks resulting from the presence
of other environmental conditions in ambient air. For example, Whittemoro and
Korn (1980) and Holguin et al. (1985) found small increases in the probability
of asthma attacks associated with previous attacks, decreased temperature, and
with incremental increases in oxidant and 0., concentrations, respectively.
Lebowitz et al. (1982, 1983) and Lebowitz (1984) showed effects in asthmatics,
such as decreased peak expiratory flow and increased respiratory symptoms,
that were related to the interaction of 03 and temperature. All of these
studies have questionable effects from other pollutants, particularly inhalable
019END/A 1-140 11/22/85
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PRELIMINARY DRAFT
particles. There have been no consistent findings of symptom aggravation or
changes in lung function in patients with chronic lung diseases other than
asthma.
Only a few prospective studies have been reported on morbidity, mortality,
and chromosomal effects from chronic exposure to 0.. or other photochemical
oxidants. The lack of quantitative measures of oxidant exposures seriously
limits the usefulness of many population studies of morbidity and mortality
for standards-setting purposes. Most of these long-term studies have employed
average annual levels of photochemical oxidants or have involved broad ranges
of pollutants; others have used a simple high-oxidant/low-oxidant dichotomy.
In addition, these population studies are also limited by their inability to
control for the effects of other factors that can potentially contribute to
the development and progression of respiratory disease over long periods of
time. Thus, insufficient information is available in the epidemiological
literature on possible exposure-response relationships between ambient CL or
other photochemical oxidants and the prevalence of chronic lung disease or the
rates of chronic disease mortality. None of the epidemiological studies
investigating chromosomal changes have found any evidence that ambient CL or
oxidants affect the peripheral lymphocytes of the exposed population.
1.11 EVALUATION OF HEALTH EFFECTS DATA FOR OZONE AND OTHER PHOTOCHEMICAL
OXIDANTS
1.11.1 Health Effects in the General Human Population
Controlled human studies of at-rest exposures to 0^ lasting 2 to 4 hr
have demonstrated decrements in forced expiratory volume and flow occurring at
and above 0.5 ppm of 0.. (Chapter 11). Airway resistance was not significantly
changed at these 03 concentrations. Breathing 0., at rest at concentrations
< 0.5 ppm did not significantly impair pulmonary function although the occur-
rence of some 0--related pulmonary symptoms has been suggested in a number of
studies.
One of the principal modifiers of the magnitude of response to 0., is
minute ventilation (V_), which increases proportionately with increases in
exercise work load. Adjustment by the respiratory system to an increased work
load is characterized by increased frequency and depth of breathing. Consequent
increases in Vp not only increase the overall volume of inhaled pollutant, but
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the increased tidal volume may lead to a higher concentration of ozone in the
lung regions most sensitive to ozone. These processes are further enhanced at
high work loads (VV > 35 L/min), since the mode of breathing changes at that
V.- from nasal to oronasal.
Even in well-controlled experiments on an apparently homogeneous group of
healthy subjects, physiological responses to the same work and pollutant loads
will vary widely among individuals. Despite large interindividual variability,
the magnitude of group mean lung function changes is positively associated
with the level of exercise and ozone concentration. Based on reported studies
of 1 to 3 hr duration (Chapter 11 and references therein), significant pulmo-
nary function impairment (decrement) occurs when exercise is combined with
exposure to ozone:
1. Light exercise (V£ < 23 L/min) - Effects at > 0.37 ppm 0"3;
2. Moderate exercise (V£ = 24 to 43 L/min) - Effects at > 0.30 ppm 03;
3. Heavy exercise (V£ = 44 to 63 L/min) - Effects at > 0.24 ppm 0.,; and
4. Very heavy exercise (V_ > 64 L/min) - Effects at > 0.18 ppm 0,, with
suggestions of decrements at 0.12 ppm 0,.
For the majority of the controlled studies, 15-min intermittent exercise
alternated with 15-min rest was employed for the duration of the exposure.
The maximum response to 0, exposure can be observed within 5 to 10 min follow-
ing the end of each exercise period. Functional recovery, at least from a
single exposure with exercise, appears to progress in two phases: during the
initial rapid phase, lasting between 1 and 3 hr, pulmonary function improves
more than 50 percent; this is followed by a much slower recovery that is
usually completed within 24 hr. In some individuals, despite apparent func-
tional recovery, other regulatory systems may still exhibit abnormal responses
when stimulated; e.g., airway hyperreactivity might persist for days.
Continuous exercise equivalent in duration to the sum of intermittent
exercise periods at comparable ozone concentrations (0.2 to 0.4 ppm) and
minute ventilation (60 to 80 L/min) seems to elicit greater changes in pulmonary
function but the differences between intermittent and continuous exercise are
not clearly established. More experimental data are needed to make any quanti-
tative evaluation of the differences in effects induced by these two modes of
exercise.
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A close association has been observed between the occurrence of respiratory
symptoms and changes in pulmonary function in adults acutely exposed in environ-
mental chambers to CL (Chapter 11) or to ambient air containing 0., as the
predominant pollutant (Chapter 12). This association holds for both the
time-course and magnitude of effects. Studies on children and adolescents
exposed to 03 or ambient air containing 03 under similar conditions have found
no significant increases in symptoms despite significant changes in pulmonary
function (Avol et al. , 1985a,b; McDonnell et al., 1985a,b). Epidemiological
studies of exposure to ambient photochemical pollution are of limited use for
quantifying exposure-response relationships for 0, because they have not
adequately controlled for other pollutants, meteorological variables, and
non-environmental factors in the data analysis. Eye irritation, for example,
one of the most common complaints associated with photochemical pollution, is
not characteristic of clinical exposures to 0,, even at concentrations several
times higher than any likely to be encountered in ambient air. There is
limited qualitative evidence to suggest that at low concentrations of 0.,,
other respiratory and nonrespiratory symptoms, as well, are more likely to
occur in populations exposed to ambient air pollution than in subjects exposed
in chamber studies (Chapter 12).
Discomfort caused by irritative symptoms may be responsible for the
impairment of athletic performance reported in high school students during
cross-country track meets in Los Angeles (Chapter 12). Only a few controlled-
exposure studies, however, have been designed to examine the effects of CL on
exercise performance (Chapter 11). In one study, light intermittent exercise
(Vr = 20-25 L/min) at a high 0, concentration (0.75 ppm) reduced postexposure
maximal exercise capacity by limiting maximal oxygen consumption; submaximal
oxygen consumption changes were not significant. The extent of ventilatory
and respiratory metabolic changes observed during or following the exposure
appears to have been related to the magnitude of pulmonary function impairment.
Whether such changes are consequent to respiratory discomfort (i.e., symptomatic
effects) or are the result of changes in lung mechanics or both is still
unclear and needs to be elucidated.
Environmental conditions such as heat and relative humidity may alter
subjective symptoms and physiological impairment associated with On exposure.
Modification of the effects of 03 by these factors may be attributed to in-
creased ventilation associated with elevated body temperature but there may
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also be an independent effect of elevated body temperature on pulmonary function
(VC).
Numerous additional factors have the potential for altering responsiveness
to ozone. For example, children and older individuals may be more responsive
than young adults. Other factors such as gender differences (at any age),
personal habits such as smoking, nutritional deficiencies, or differences in
immunologic status may predispose individuals to susceptibility to ozone. In
addition, social, cultural, or economic factors may be involved. Those actually
known to alter sensitivity, however, are few, largely because they have not
been examined adequately to determine definitively their effects on sensitivity
to 0_. The following briefly summarizes what is actually known from the data
regarding the importance of these factors (see Section 13.3.3 for details):
1. Age. Although changes in growth and development of the lung with
age have been postulated as one of many factors capable of modifying responsive-
ness to 0.,, sufficient numbers of studies have not been performed to provide
any sound conclusions for effects of u\ in different age groups.
2. Sex. Sex differences in responsiveness to ozone have not been
adequately studied. Lung function of women, as assessed by changes in FEV, 0,
might be affected more than that of men under similar exercise and exposure
conditions, but the possible differences have not been tested systematically.
Further research is needed to determine whether there are systematic differences
in response that are related to sex.
3. Smoking Status. Differences between smokers and nonsmokers have
been studied often, but the smoking histories are not documented well. There
is some evidence, however, to suggest that smokers may be less sensitive to 03
than nonsmokers.
4. Nutritional Status. Antioxidant properties of vitamin E in preventing
ozone-initiated peroxidation i_n vitro are well demonstrated and their protective
effects _i_n vivo are clearly demonstrated in rats and mice. No evidence indi-
cates, however, that man would benefit from increased vitamin E intake relative
to ambient ozone exposures.
5. Red Blood Cell Enzyme Deficiencies. There have been too few studies
performed to document reliably that individuals with a hereditary deficiency
of glucose-6-phosphate dehydrogenase may be at-risk to significant hematolog-
ical effects from 0., exposure. Even if 0., or a reactive product of 0.,-tissue
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interaction were to penetrate the red blood cell after rn vivo exposure, it is
unlikely that any depletion of glutathione or other reducing compounds would
be of functional significance for the affected individual.
Successive daily brief exposures of healthy human subjects to 07 (<0.7 ppm
O
for approximately 2 hr) induce a typical temporal pattern of response (Chap-
ter 11, Section 11.3). Maximum functional changes that occur after the first
or second exposure day become progressively attenuated on each of the subsequent
days. By the fourth day of exposure, the average effects are not different
from those observed following control (air) exposure. Individuals need between
3 and 7 days to develop full attenuation, with more sensitive subjects requiring
more time. The magnitude of a peak response to 0- appears to be directly
related to 0., concentration. It is not known how variations in the length or
•3
frequency of exposure will modify the time course of this altered responsive-
ness. In addition, concentrations of 0- that have no detectable effect appear
not to invoke changes in response to subsequent exposures at higher CL concen-
trations. Full attenuation, even in ozone-sensitive subjects, does not persist
for more than 3 to 7 days in most individuals, while partial attenuation might
persist for up to 2 weeks. Although the severity of symptoms is generally
related to the magnitude of the functional response, partial attenuation of
symptoms appears to persist longer, for up to 4 weeks.
Whether populations exposed to photochemical air pollution develop at
least partial attenuation is unknown. No epidemiological studies have been
designed to test this hypothesis and additional information is required from
controlled laboratory studies before any sound conclusions can be made.
Ozone toxicity, in both humans and laboratory animals, may be mitigated
through altered responses at the cellular and/or subcellular level. At present,
the mechanisms underlying altered responses are unclear and the effectiveness
of such mitigating factors in protecting the long-term health of the individual
against ozone is still uncertain. A growing body of experimental evidence
suggests the involvement of vagal sensory receptors in modulating the acute
responsiveness to ozone. It is highly probable that most of the decrements in
lung volume reported to result from exposures of greatest relevance to standard-
setting (<0.3 ppm CL) are due to inhibition of maximal inspiration rather than
changes in airway diameter. None of the experimental evidence, however, is
definitive and additional research is needed to elucidate the precise mechanism(s)
associated with ozone exposure.
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1.11.2 Health Effects in Individuals with Pre-Existing Disease
Currently available evidence indicates that individuals with preexisting
disease respond to CL exposure to a similar degree as normal subjects. Patients
with chronic obstructive lung disease and/or asthma have not shown increased
sensitivity to 0, in controlled human exposure studies, but there is some
indication from epidemiological studies that asthmatics may be symptomatically
and possibly functionally more sensitive than healthy individuals to ambient
air exposures. Appropriate inclusion and exclusion criteria for selection of
these subjects, however, especially better clinical diagnoses validated by
pulmonary function, must be considered before their sensitivity to 0, can be
adequately determined. None of these factors has been sufficiently studied in
relation to CL exposures to give definitive answers.
1.11.3 Extrapolation of Effects Observed in Animals to Human Populations
Animal experiments on a variety of species have demonstrated increased
susceptibility to bacterial respiratory infections following 0, exposure.
Thus, it could be hypothesized that humans exposed to 03 could experience
decrements in their host defenses against infection. At the present time,
however, these effects have not been described in humans exposed to 0^, so
that concentrations at which effects might occur in man or the severity of
such effects are unknown and difficult to predict.
Animal studies have also reported a number of extrapulmonary responses to
0.,, including cardiovascular, reproductive, and teratological effects, along
with changes in endocrine and metabolic function. The implications of these
findings for human health are difficult to judge at the present time. In
addition, central nervous system effects, alterations in red blood cell morpho-
logy and enzymatic activity, as well as cytogenetic effects on circulating
lymphocytes, have been observed in laboratory animals following exposure to
0,. While similar effects have been described in circulating cells from human
0
subjects exposed to high concentrations of 0.,, the results were either incon-
sistent or of questionable physiological significance (Section 13.3.8). It is
not known, therefore, if extrapulmonary responses would be likely to occur in
humans when exposure schedules are used that are representative of exposures
that the population at large might actually experience.
Despite wide variations in study techniques and experimental designs,
acute and subchronic exposures of animals to levels of ozone < 0.5 ppm produce
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similar types of responses in all species examined. A characteristic ozone
lesion occurs at the junction of the conducting airways and the gas-exchange
regions of the lung after acute 0., exposure. Dosimetry model simulations
predict that the maximal tissue dose of CL occurs in this region of the lung.
Continuation of the inflammatory process during longer 0. exposures is espe-
cially important since it appears to be correlated with increased airway
resistance, increased lung collagen content, and remodeling of the centriacinar
airways, suggesting the development of distal airway narrowing. No convincing
evidence of emphysema in animals chronically exposed to CL has yet been pub-
lished, but centriacinar inflammation has been shown to occur.
Since substantial animal data exist for 0,-induced changes in lung struc-
ture and function, biochemistry, and host defenses, it is conceivable that man
may experience more types of effects than have been established in human
clinical studies. It is important to note, however, that this is a qualitative
probability; it does not permit assessment of the ozone concen-trations at
which man might experience similar effects.
1.11.4 Health Effects of Other Photochemical Oxidants and Pollutant Mixtures
Controlled human studies have not consistently demonstrated any modifica-
tion of respiratory effects for combined exposures of 0., with S0?, N0?, CO, or
H?S(L and other particulate aerosols. Ozone alone is considered to be respon-
sible for the observed effects of those combinations or of multiple mixtures
of these pollutants. Combined exposure studies in laboratory animals have
produced varied results, depending upon the pollutant combination evaluated,
the exposure design, and the measured variables (Section 13.6.3). Thus, no
definitive conclusions can be drawn from animal studies of pollutant interac-
tions. There have been far too few controlled toxicological studies with
other oxidants, such as peroxyacetyl nitrate or hydrogen peroxide, to permit a
sound scientific evaluation of their contribution to the toxic action of
photochemical oxidant mixtures. There is still some concern, however, that
combinations of oxidant pollutants with other pollutants may contribute to the
symptom aggravation and decreased lung function described in epidemiological
studies on individuals with asthma and in children and young adults. For this
reason, the effects of interaction between inhaled oxidant gases and other
environmental pollutants on the lung need to be systematically studied using
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exposure regimens that are more closely representative of ambient air ratios
of peak concentrations, frequency, duration, and time intervals between events.
1.11.5 Identification of Potentially At-Risk Groups
Despite uncertainties that may exist in the data, it is possible to
identify the groups that may be at particular risk from exposure to ozone,
based on known health effects, activity patterns, personal habits, and actual
or potential exposures to ozone.
The first group that appears to be at particular risk from exposure to
ozone is that subgroup of the general population characterized as having
preexisting respiratory disease. Available data on actual differences in
sensitivity between these and healthy members of the general population indicate
that under the exposure regime used to date, individuals with preexisting
disease may not be more sensitive to ozone than healthy individuals. Neverthe-
less, two considerations place these individuals among groups at potential
risk from exposure to ozone. First, it must be noted that concern with trigger-
ing untoward reactions has necessitated the use of low concentrations and low
exercise levels in most studies on subjects with mild preexisting disease.
Therefore, few or no data on responses at higher concentrations and higher
exercise levels are available for comparison with responses in healthy subjects.
Thus, definitive data on responses in individuals with preexisting disease are
not available. Second, however, it must be emphasized that in individuals
with already compromised pulmonary function, the decrements in function produced
by exposure to ozone, while similar to or even the same as those experienced
by normal subjects, represent a further decline in volumes and flows that are
already diminished. Such declines may be expected to impair further the
ability to perform normal activities. In individuals with preexisting diseases
such as asthma or allergies, increases in symptoms upon exposure to ozone,
above and beyond symptoms seen in the general population, may also impair or
further curtail the ability to function normally.
The second group at apparent special risk from exposure to ozone consists
of individuals ("responders"), not yet characterized medically except by their
response to ozone, who experience greater decrements in lung function from
exposure to ozone than the average response of the groups studied. It is not
known if "responders" are a specific population subgroup or simply represent
the upper 5 to 20 percent of the ozone response distribution. As yet no means
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of determining in advance those members of the general population who are
"responders" has been devised.
Data presented in this chapter underscore the importance of exercise in
the potentiation of effects from exposure to ozone. Thus, a third group
potentially at risk from exposure to ozone is composed of those individuals
(healthy and otherwise) whose activities out of doors, whether vocational or
avocational, result in increases in minute ventilation. Although many individ-
uals with preexisting respiratory disease would not be expected to exercise at
the same levels one would expect in healthy individuals, any increase in
activity level would bring about a commensurate increase in minute ventilation.
To the extent that the aged, the young, males, or females participate in
activities out of doors that raise their minute ventilations, all of these
groups may be considered to be potentially at risk, depending upon other
determinants of total ozone dose, CL concentration, and exposure duration.
Other biological and nonbiological factors have the potential for influenc-
ing responses to ozone. Data remain inconclusive at the present, however,
regarding the importance of age, gender, and other factors in influencing
response to ozone. Thus, at the present time, no other groups are thought to
be biologically predisposed to increased sensitivity to ozone. It must be
emphasized, however, that the final identification of those effects that are
considered "adverse" and the final identification of "at-risk" groups are both
the domain of the Administrator.
1.12 REFERENCES
1.12.1 Introduction
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1.12.2 References for Properties, Chemistry and Transport of Ozone and
Other Photochemical Oxidants and Their Precursors
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Atkinson, R. ; Aschmann, S. M. (1984) Rate constants for the reactions of 0.,
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(1984a) Rate constants for the gas-phase reactions of NO, radicals with a
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1584-1587. J
Atkinson, R.; Aschmann, S. M.; Winer, A. M.; Pitts, J. N., Jr. (1984c)
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dialkenes, cycloalkenes, and monoterpenes at 295 ± 1 K. Environ. Sci.
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References for Properties, Chemistry, Transport (cont'd.)
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References for Properties, Chemistry, Transport (cont'd.)
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References for Properties. Chemistry. Transport (conl1d.)
Derwent, R. G. ; Hb'v, 0. (1980) Computer modeling studies of the impact of
vehicle exhaust emission controls on photochemical air pollution forma-
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Dimitriades, B. (1972) Effects of hydrocarbon and nitrogen oxides on photo-
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the nature of ozone, oxides of nitrogen, and nonmethane hydrocarbons in
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019END/A 1-153 11/22/85
-------
PRELIMINARY DRAFT
References for Properties, Chemistry, Transport (cont'd.)
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019END/A
1-154
11/22/85
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References for Properties, Chemistry, Transport (cont'd.)
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019END/A 1-155 11/22/85
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PRELIMINARY DRAFT
References for Properties, Chemistry, Transport (cont'd.)
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019END/A
1-156
11/22/85
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PRELIMINARY DRAFT
References for Properties, Chemistry, Transport, (cont'd.)
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019END/A 1-157 11/22/85
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PRELIMINARY DRAFT
References for Properties, Chemistry, Transport (conl'd.)
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019END/A 1-158 11/22/85
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PRELIMINARY DRAFT
References for Properties, Chemistry, Transport (cont'd.)
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019END/A 1-159 11/22/85
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PRELIMINARY DRAFT
1.12.3 References for Sampling and Measurement of Ozone and Other Photochemical
Oxiclants and Their Precursors
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Bufalini, J. J.; Gay, B. W. , Jr.; Brubaker, K. L. (1972) Hydrogen peroxide
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019END/A 1-160 11/22/85
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PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)
California Air Resources Board. (1978) California air quality data: July-
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Chameides, W.L.; Tan, A. (1981). The two-demensional diagnostic model for
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Cohen, I. R.; Purcell, T. C.; Altshuller, A. P. (1967) Analysis of the oxidant
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DeMore, W. B. ; Romanovsky, J. C. ; Feldstein, M.; Hamming, W. J.; Mueller, P.
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019END/A 1-161 11/22/85
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PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)
Dietz, W. A. (1967) Response factors for gas chromatographic analyses. J. Gas
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F. R. (1971, April 30) 36: 8186-8201. National primary and secondary air
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F.R. (1975, February 18) 40: 7042-7070. Ambient air monitoring reference and
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F.R. (1976, December 1) 41: 52686-52692. National primary and secondary ambient
air quality standards: nitrogen dioxide measurement principle and calibra-
tion procedure.
F.R. (1979, February 8) 44: 8221-8233. Calibration of ozone reference methods.
Flamm, D. L. (1977) Analysis of ozone at low concentrations with boric acid
buffered KI. Environ. Sci. Techno!. 11: 978-983.
Fontijn, A.; Sabadell, A. J.; Ronco, R. J. (1970) Homogeneous chemiluminescent
measurement of nitric oxide with ozone: implications for continuous
selective monitoring of gaseous air pollutants. Anal. Chem. 42: 575-579.
Fried, A. ; Hodgeson, J. (1982) Laser photoacoustic detection of nitrogen dio-
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Gay, B. W., Jr.; Bufalini, J. J. (1972a) Hydrogen peroxide in the urban atmos-
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chemistry series: 113.)
Gay, B. W., Jr.; Bufalini, J. J. (1972b) Hydrogen peroxide in the urban atmos-
phere. Environ. Lett. 3: 21-24.
Gay, B. W.; Noonan, R. C. ; Bufalini, J. J.; Hanst, P. L. (1976) Photochemical
synthesis of peroxyacyl nitrates in gas phase via chlorine-aldehyde
reaction. Environ. Sci. Techno!. 10: 82-85.
Grosjean, D. (1983) Distribution of atmospheric nitrogenous pollutants at a
Los Angeles area smog receptor site. Environ. Sci. Techno!. 17: 13-19.
Grosjean, D.; Fung, K.; Collins, J.; Harrison, J.; Breitung, E. (1984) Portable
generator for on-site calibration of peroxyacetyl nitrate analyzers.
Anal. Chem. 56: 569-573.
Hanst, P. L. ; Wong, N. W.; Bragin, J. (1982) A long-path infrared study of Los
Angeles smog. Atmos. Environ. 16: 969-981.
Hauser, T. R.; Cummins, R. L. (1964) Increasing sensitivity of 3-methyl-2~benzo-
thiazolone hydrazone test for analysis of aliphatic aldehydes in air.
Anal. Chem. 36: 679-681.
019END/A 1-162 11/22/85
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PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)
Heikes, B.C. (1984) Aqueous H202 production from 03 in glass impingers.
Atmos. Environ. 18: 1433-1445.
Heikes, B. G.; Lazrus, A. L.; Kok, G. L.; Kunen, S. M. ; Gandrud, B. W. ; Gitlin,
S. N. ; Sperry, P. D. (1982) Evidence for aqueous phase hydrogen peroxide
synthesis in the troposphere. JGR J. Geophys. Res. 87: 3045-3051.
Hendry, D. G. ; Kenley, R. A. (1977) Generation of peroxy radicals from peroxy
nitrates (R02N02). Decomposition of peroxyacyl nitrates. Atmos. Environ.
99: 3198-3199.
Hodgeson, J. A.; Krost, K. J. ; O'Keeffe, A. E. ; Stevens, R. K. (1970) Chemi-
luminescent measurement of atmospheric ozone: response characteristics
and operating variables. Anal. Chem. 42: 1795-1802.
Hodgeson, J. A.; Stevens, R. K. ; Martin, B. E. (1972) A stable ozone source
applicable as a secondary standard for calibration of atmospheric monitors.
ISA Trans. 11: 161-167.
Hodgeson, J. A.; Hughes, E. E.; Schmidt, W. P.; Bass, A. M. (1977) Methodology
for standardization of atmospheric ozone measurements. In: Dimitriades,
B. , ed. International conference on photochemical oxidant pollution and
its control; September 1976; Raleigh, NC. Proceedings: v. I. Research
Triangle Park, NC: U.S. Environmental Protection Agency; pp. 3-12; EPA
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019VEE/A 1-172 11/22/85
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PRELIMINARY DRAFT
1.12.5 References for Effects of Ozone and Other Photochemical Oxidants on
Vegetation
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019VEE/A 1-173 11/22/85
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PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)
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019VEE/A 1-174 11/22/85
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References for Vegetation Effects (cont'd.)
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019VEE/A 1-175 11/22/85
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PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)
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019VEE/A 1-176 11/22/85
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PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)
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References for Vegetation Effects (cont'd.)
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References for Vegetation Effects (cont'd.)
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References for Vegetation Effects (cont'd.)
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References for Vegetation Effects (cont'd.)
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Thompson, C. R. ; Kats, G.; Cameron, J. W. (1976) Effects of photochemical air
pollutants on growth, yield, and ear characteristics of two sweet corn
hybrids. J. Environ. Qual. 5: 410-412.
019VEE/A 1-181 11/22/85
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PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)
Tingey, D. T. (1977). (To be supplied).
Tingey, D. T. ; Reinert, R. A. (1975) The effect of ozone and sulfur dioxide
singly and in combination on plant growth. Environ. Pollut. 9: 117-125.
Tingey, D. T.; Taylor, G. E. , Jr. (1982) Variation in plant response to
ozone: a conceptual model of physiological events. In: Unsworth, M. H. ;
Ormrod, D. P., eds. Effects of gaseous air pollution in agriculture and
horticulture. London, United Kingdom: Butterworth Scientific; pp. 113-138.
Tingey, D. T. ; Thutt, G. L. ; Gumpertz, M. L. ; Hogsett, W. E. (1982) Plant
water status influences ozone sensitivity of bean plants. Agric. Environ.
7: 243-254.
Tonneijck, A. E. G. (1984) Effects of peroxyacetyl nitrate (PAN) and ozone on
some plant species. In: Proceedings of the OECD workshop on ozone;
Gothenburg, Sweden.
U.S. Environmental Protection Agency. (1978) Air quality criteria for ozone
and other photochemical oxidants. Research Triangle Park, NC: U.S.
Environmental Protection Agency, Environmental Criteria and Assessment
Office; EPA report no. EPA-600/8-78-004. Available from: NTIS, Spring-
field, VA; PB80-124753.
Walmsley, L.; Ashmore, M. L.; Bell, J. N. B. (1980) Adaptation of radish Raphanus
sativus L. in response to continuous exposure to ozone. Environ. Pollut.
23: 165-177.
Wilhour, R. G. ; Neely, G. E. (1977) Growth response of conifer seedlings to
low ozone concentrations. In: Dimitriades, B. , ed. International
conference on photochemical oxidant pollution and its control: proceedings,
vol. II; January; Research Triangle Park, NC. Research Triangle Park, NC:
U.S. Environmental Protection Agency; pp. 635-645; EPA report no.
EPA-600/3-77-001b. Available from: NTIS, Springfield, VA; PB-264233.
Wukasch, R. T. ; Hofstra, G. (1977a) Ozone and Botrytis interactions in onion-
leaf dieback: open-top chamber studies. Phytopathology 67: 1080-1084.
Wukasch, R. T. ; Hofstra, G. (1977b) Ozone and Botrytis spp. interaction in
onion-leaf dieback: field studies. J. Am. Soc. Hortic. Sci. 102: 543-546.
Yang, Y.-S.; Skelly, J. M.; Chevone, B. I.; Birch, J. B. (1983) Effects of
long-term ozone exposure on photosynthesis and dark respiration of eastern
white pine. Environ. Sci. Technol. 17: 371-373.
019VEE/A
1-182
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PRELIMINARY DRAFT
1.12.6 References for Effects of Ozone on Natural Ecosystems and Their Components
Barnes, R. L. (1972) Effects of chronic exposure to ozone on photosynthesis
and respiration of pines. Environ. Pollut. 3: 133-138.
Benoit, L. F. ; Skelly, J. M. ; Moore, L. D. ; Dochinger, L. S. (1982) Radial
growth reductions of Pinus strobus L. correlated with foliar ozone sensi-
tivity as an indicator of ozone-induced losses in eastern forests. Can.
J. For. Res. 12: 673-678.
Bormann, F. H. (1985) Air pollution and forests: an ecosystem perspective.
BioScience 35: 434-441.
Botkin, D. B. ; Smith, W. H. ; Carlson, R. W. ; Smith, T. L. (1972) Effects of
ozone on white pine saplings: variation in inhibition and recovery of net
photosynthesis. Environ. Pollut. 3: 273-289.
Carlson, R. W. (1979) Reduction in the photosynthetic rate of Acer, Quercus,
and Fraxinus species caused by sulfur dioxide and ozone. Environ. Pollut.
18: 159-170.
Cowling, E. B. (1985) Effects of air pollution on forests: Critical review
discussion papers. J. Air Pollut. Control Assoc. 35: 916-919.
Coyne, P. E. ; Bingham, G. E. (1981) Comparative ozone dose response of gas
exchange in a ponderosa pine stand exposed to long-term fumigations. J.
Air Pollut. Control Assoc. 31: 38-41.
Dochinger, L. S. ; Townsend, A. M. (1979) Effects of roadside deicer salts and
ozone on red maple progenies. Environ. Pollut. 19: 229-237.
Duchelle, S. F. ; Skelly, J. M. ; Sharick, T. L.; Chevone, B. I.; Yang, Y.-S.;
Nellessen, J. E. (1983) Effects of ozone on the productivity of natural
vegetation in a high meadow of the Shenandoah National Park of Virginia.
J. Environ. Manage. 17: 299-308.
Ehrlich, P. R. ; Mooney, H. A. (1983) Extinction, substitution, and ecosystem
services. BioScience 33: 248-254.
Farnworth, E. G. ; Tidrick, T. H. ; Jordan, C. F. ; Smathers, W. M., Jr. (1981)
The value of natural ecosystems: an economic and ecological framework.
Environ. Conserv. 8: 275-282.
Hacskaylo, E. (1972) Mycorrhizae: the ultimate in reciprocal parasitism?
BioScience 22: 577-583.
Hogsett, W. E. ; Plocher, M.; Wildman, V.; Tingey, D. T.; Bennett, I. P. (1985)
Growth response of two varieties of slash pine seedlings to chronic ozone
exposures. Can. J. Bot. (In press).
019VEE/A 1-183 11/22/85
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PRELIMINARY DRAFT
References for Ecosystem Effects (cont'd.)
Krause, G. H. M.; Prinz, B.; Jung, K. D. (1984) Forest effects in West Germany.
In: Davis, D. D. ; Millen, A. A.; Dochinger, L., eds. Air pollution and
the productivity of the forest: proceedings of the symposium; October
1983; Washington, DC. Arlington, VA: Izaak Walton League of America; pp.
297-332.
Kress, L. W. ; Skelly, J. M. (1982) Response of several eastern forest tree
species to chronic doses of ozone and nitrogen dioxide. Plant Dis. 66:
1149-1152.
Kress, L. W.; Skelly, J. M.; Hinkelmann, K.H. (1982) Growth impact of 03, N02,
and/or S02 on Platanus occidental's. Agric. Environ. 7: 265-274.
Laurence, J. A.; Weinstein, L. H. (1981) Effects of air pollutants on plant
productivity. Annu. Rev. Phytopathol. 19: 257-271.
Mahoney, M. J. (1982) An analysis of the potential effects of air pollutants
emitted during coal combustion on yellow poplar and loblolly pine and
influences on mycorrhizal associations of loblolly pine. Unpublished.
Blacksburg, VA: Virginia Polytechnical Institute and State University;
Ph.D. Thesis.
Manion, P. D. (1985) Effects of air pollution on forests: Critical review dis-
cussion papers. J. Air Pollut. Control Assoc. 35: 919-922.
Mann, L. K. ; McLaughlin, S. B.; Shriner, D. S. (1980) Seasonal physiological
responses of white pine under chronic air pollution stress. Environ. Exp.
Bot. 20: 99-105.
McBride, J. R. ; Semion, V.; Miller, P. R. (1975) Impact of air pollution on
the growth of ponderosa pine. Calif. Agric. 29: 8-10.
McCool, P. M. ; Menge, J. A. (1983) Influence of ozone on carbon partitioning
in tomato: potential role of carbon flow in regulation of the mycorrhizal
symbiosis under conditions of stress. New Phytol. 94: 241-247.
McCool, P. M.; Menge, J. A.; Taylor, 0. C. (1979) Effects of ozone and HC1 gas on
the development of the mycorrhizal fungus Glomus faciculatus and growth of
'Troyer' citrange. J. Amer. Soc. Hort. Sci. 104: 151-154.
McLaughlin, S. B. (1985) Effects of air pollution on forests: A critical review.
J. Air Pollut. Control Assoc. 35: 512-534.
McLaughlin, S. B.; McConathy, R. K.; Duvick, D.; Mann, L. K. (1982) Effects of
chronic air pollution stress on photosynthesis, carbon allocation, and
growth of white pine trees. For. Sci. 28: 60-70.
Miller, P. L. (1973) Oxidant-induced community change in a mixed conifer
forest. In: Naegele, J. A., ed. Air pollution damage to vegetation.
Washington, DC: American Chemical Society; pp. 101-117. (Advances in
chemistry series: no. 122.)
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PRELIMINARY DRAFT
References for Ecosystem Effects (cont'd.)
Miller, P. R. ; Elder-man, M. J. , eds. (1977) Photochemical oxidant air pollu-
tant effects on a mixed conifer forest ecosystem: a progress report,
1976. Corvallis, OR: U.S. Environmental Protection Agency; EPA report no.
EPA-600/3-77-104. Available from: NTIS, Springfield, VA; PB-274531.
Miller, P. R. ; Parmeter, J. R., Jr.; Taylor, 0. C.; Cardiff, E. A. (1963)
Ozone injury to the foliage of Pinus ponderosa. Phytopathology 53: 1072-
1076.
Miller, P. R. ; Parmeter, J. R., Jr.; Flick, B. H. ; Martinez, C. W. (1969)
Ozone dosage response of ponderosa pine seedlings. J. Air Pollut. Control
Assoc. 19: 435-438.
Miller, P. R. ; Taylor, 0. C. ; Wilhour, R. G. (1982) Oxidant air pollution
effects on a western coniferous forest ecosystem. Corvallis, OR: Corvallis
Environmental Research Laboratory; EPA report no. EPA-600/D-82-276.
Available from: NTIS, Springfield, VA; PB83-189308.
Mooi, J. (1980) Influence of ozone on the growth of two poplar cultivars.
Plant Dis. 64: 772-773.
National Park Service. (1985) Testimony of the National Park Service before the
Subcommittee on Parks and Recreation. Washington, D.C.: U.S. House of
Representatives, Committee on Interior and Insular Affairs; 99th Congress,
1st session.
National Research Council. (1977) Ozone and other photochemical oxidants.
Washington, D.C.: National Academy of Sciences; pp. 437-585.
Odum, E. P. (1985) Trends expected in stressed ecosystems. BioScience. 35: 419-422.
Parmeter, J. R. , Jr.; Bega, R. V.; Neff, T. (1962) A chlorotic decline of
ponderosa pine in southern California. Plant Dis. Rep. 46: 269-273.
Patton, R. L. (1981) Effects of ozone and sulfur dioxide on height and stem
specific gravity of Populus hybrids. For. Sci. Res. Pop. NE-471.
Price, H. ; Treshow, M. (1972) Effects of ozone on the growth and reproduction
of grasses. In: Proceedings of the international air pollution conference;
Melbourne, Australia, pp. 275-280.
Reich, P. B. ; Amundson, R. G. (1985) Ambient levels of ozone reduce net photo-
synthesis in tree and crop species. Science. 230: 566-570.
Risser, P. G. (1985) Toward a holistic management perspective. BioScience.
35: 414-418.
Stark, R. W. ; Cobb, F. W. , Jr. (1969) Smog injury, root diseases and bark
beetle damage in ponderosa pine. Calif. Agric. 23: 13-15.
019VEE/A 1-185 11/22/85
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PRELIMINARY DRAFT
References for Ecosystem Effects (cont'd.)
Tingey, D. T.; Wilhour, R. G.; Standley, E. (1976) The effect of chronic ozone
exposures on the metabolite content of ponderosa pine seedlings. For.
Sci. 22: 234-241.
Treshow, M.; Stewart, D. (1973) Ozone sensitivity of plants in natural commun-
ities. Biol. Conserv. 5: 205-214.
U.S. Environmental Protection Agency. (1978) Air quality criteria for ozone
and other photochemical oxidants. Research Triangle Park, NC: U.S. Environ-
mental Protection Agency, Environmental Criteria and Assessment Office;
EPA report no. EPA-600/8-78-004. Available from: NTIS, Springfield, VA;
PB83-163337.
Woodwell, G. M. (1970) Effects of pollution on the structure and physiology of
ecosystems. Science (Washington, DC) 168: 429-433.
Yang, Y.-S.; Skelly, J. M. ; Chevone, B. I.; Birch, J. B. (1983) Effects of
long-term ozone exposure on photosynthesis and dark respiration of eastern
white pine. Environ. Sci. Technol. 17: 371-373.
1.12.7 References for Other Welfare Effects of Ozone and Other Photochemical
Oxidants
Beloin, N. J. (1972) Fading of dyed fabrics by air pollution: a field study.
Text. Chem. Color. 4: 77-78.
Bogaty, H. ; Campbell, K. S.; Appel, W. D. (1952) The oxidation of cellulose by
ozone in small concentrations. Text. Res. J. 22: 81-83.
Bradley, C. E. ; Haagen-Smit, A. J. (1951) The application of rubber in the
quantitative determination of ozone. Rubber Chem. Technol. 24: 750-775.
Edwards, D. C. ; Storey, E. B. (1959) A quantitative ozone test for small
specimens. Chem. Can. 11: 34-38.
Haylock, J. C.; Rush, J. L. (1976) Studies on the ozone fading of anthraquinone
dyes on nylon fibers. Text. Res. J. 46: 1-8.
Haylock, J. C.; Rush, J. L. (1978) Studies on the ozone fading of anthraquinone
dyes on nylon fibers; part II: in-service performance. Text. Res. J. 48:
143-149.
Haynie, F. H.; Spence, J. W.; Upham, J. B. (1976) Effects of gaseous pollutants
on materials—a chamber study. Research Triangle Park, NC: U.S. Environ-
mental Protection Agency, Environmental Sciences Research Laboratory; EPA
report no. EPA-600/3-76-015. Available from: NTIS, Springfield, VA;
PB-251580.
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PRELIMINARY DRAFT
References for Other Welfare Effects (cont'd.)
Heuvel, H. M. ; Huisman, R. ; Schmidt, H. M. (1978) Ozone fading of disperse
blue 3 on nylon 6 fibers. The influence of physical fiber properties.
Text. Res. J. 48: 376-384.
Kamath, Y. K. ; Ruetsch, S. B. ; Weigmann, H.-D. (1982) Microspectrophotontetric
study of ozone fading of disperse dyes in nylon. Text. Res. J.:
53: 391-402.
Kerr, N. ; Morris, M. A.; Zeronian, S. H. (1969) The effect of ozone and laun-
dering on a vat-dyed cotton fabric. Am. Dyest. Rep. 58: 34-36.
McCarthy, E. F. ; Stankunas, A. R. ; Yocom, J. E. ; Rae, D. (1983) Damage cost
models for pollution effects on material. Research Triangle Park, NC:
U.S. Environmental Protection Agency, Environmental Sciences Research
Laboratory; EPA report no. EPA-600/3-84-012. Available from: NTIS,
Springfield, VA; PB-140342.
Nipe, M. R. (1981) Atmospheric contaminant fading. Text. Chem. Color.
13: 18-28.
Salvin, V. S. (1969) Ozone fading of dyes. Text. Chem. Color. 1: 245-251.
Salvin, V. S. ; Walker, R. A. (1955) Service fading of disperse dyestuffs by
chemical agents other than the oxides of nitrogen. Text. Res. J. 25:
571-585.
Schmitt, C. H. A. (1960) Lightfastness of dyestuffs on textiles. Am. Dyest.
Rep. 49: 974-980.
Schmitt, C. H. A. (1962) Daylight fastness testing by the Langley system. Am.
Dyest. Rep. 51: 664-675.
Upham, J. B. ; Haynie, F. H. ; Spence, J. W. (1976) Fading of selected drapery
fabrics by air pollutants. J. Air Pollut. Control Assoc. 26: 790-792.
Veith, A. G. ; Evans, R. L. (1980) Effect of atmospheric pressure on ozone
cracking of rubber. Polym. Testing 1: 27-38.
Wenghoefer, H. M. (1974) Environmental effects on RFL adhesion. Rubber Chem.
Technol. 47: 1066-1073.
Yocom, J. E. ; Kawicki, J. M. ; Hoffnagle, G. F. (1985) Estimating materials
damage from oxidant pollutants. In: Proceedings of the APCA Specialty
Conference: evaluation of the scientific Basis for Ozone/Oxidants Stan-
dards, Houston, TX, November 28-30, 1984. Pittsburgh, PA: Air Pollution
Control Association.
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PRELIMINARY DRAFT
1.12.8 References for Toxicological Effects of Ozone and Other Photochemical
Oxidants
Abraham, W. M. ; Januszkiewicz, A. J.; Mingle, M.; Welker, M.; Wanner, A.;
Sackner, M. A. (1980) Sensitivity of bronchoprovocation and tracheal
mucous velocity in detecting airway responses to 03. J. Appl. Physiol.:
Respir. Environ. Exercise Physiol. 48: 789-793.
Abraham, W. M.; Lauredo, I.; Sielczak, M.; Yerger, L.; King, M. M.; Ratzan, K.
(1982) Enhancement of bacterial pneumonia in sheep by ozone exposure. Am.
Rev. Respir. Dis. Suppl. 125(4 pt. 2): 148.
Abraham, W.; Chapman, G. A.; Marchette, B. (1984a) Differences between inhaled
and intravenous carbacnol in detecting 03-1nduced airway effects. Environ.
Res. 35: 430-438.
Abraham, W. M. ; Delehunt, J. C. ; Yerger, L. ; Marchette, B. ; Oliver, W. , Jr.
(1984b) Changes in airway permeability and responsiveness after exposure
to ozone. Environ. Res. 34: 110-119.
Aharonson, E. F. ; Menkes, H.; Gurtner, G.; Swift, D. L. ; Proctor, D. F. (1974)
Effect of respiratory airflow rate on removal of soluble vapors by the
nose. J. Appl. Physiol. 37: 654-657.
Alpert, S. M. ; Schwartz, B. B. ; Lee, S. D. ; Lewis, T. R. (1971a) Alveolar
protein accumulation: a sensitive indicator of low level oxidant toxi-
city. Arch. Intern. Med. 128: 69-73.
Alpert, S. M. ; Gardner, D. E.; Hurst, D. J.; Lewis, T. R.; Coffin, D. L.
(1971b) Effects of exposure to ozone on defensive mechanisms of the lung.
J. Appl. Physiol. 31: 247-252.
Amdur, M. 0.; Ugro, V.; Underbill, D. W. (1978) Respiratory response of guinea
pigs to ozone alone and with sulfur dioxide. Am. Ind. Hyg. Assoc. J. 39:
958-961.
Amoruso, M. A.; Witz, G. ; Goldstein, B. D. (1981) Decreased superoxide anion
radical production by rat alveolar macrophages following inhalation of
ozone or nitrogen dioxide. Life Sci. 28: 2215-2221.
Aranyi, C.; Vana, S. C. ; Thomas, P. T. ; Bradof, J. N. ; Fenters, J. D. ; Graham,
J. A. ; Miller, F. J. (1983) Effects of subchronic exposure to a mixture
of 03, S02, and (NH4)2S04 on host defenses of mice. J. Toxicol. Environ.
Health 12: 55-71.
Atwal, 0. S. ; Pemsingh, R. S. (1981) Morphology of microvascular changes and
endothelial regeneration in experimental ozone-induced parathyroiditis.
III. Some pathologic considerations. Am. J. Pathol. 102: 297-307.
Atwal, 0. S.; Pemsingh, R. S. (1984) Occurrence of mallory body-like inclusions
in parathyroid chief cells of ozone-treated dogs. J. Pathol. 142: 169-174.
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PRELIMINARY DRAFT
References for Toxlcological Effects (cont'd.)
Atwal, 0. S. ; Wilson, T. (1974) Parathyroid gland changes following ozone
inhalation: a morphologic study. Arch. Environ. Health 28: 91-100.
Atwal, 0. S. ; Samagh, B. S. ; Bhatnagar, M. K. (1975) A possible autoimmune
parathyroiditis following ozone inhalation. II. A histopathologic, ultra-
structural, and immunofluorescent study. Am. J. Pathol. 80: 53-68.
Barry, B. E. ; Miller, F. J. ; Crapo, J. D. (1983) Alveolar epithelial injury
caused by inhalation of 0.25 ppm of ozone. In: Lee, S. D. ; Mustafa,
M. G. ; Mehlman, M. A., eds. International symposium on the biomedical
effects of ozone and related photochemical oxidants; March 1982; Pinehurst,
NC. Princeton, NJ: Princeton Scientific Publishers, Inc; pp. 299-309.
(Advances in modern environmental toxicology: v. 5).
Bartlett, D., Jr.; Faulkner, C. S. II; Cook, K. (1974) Effect of chronic ozone
exposure on lung elasticity in young rats. J. Appl. Physiol. 37: 92-96.
Bergers, W. W. A.; Gerbrandy, J. L. F.; Stap, J. G. M. M.; Dura, E. A. (1983)
Influence of air polluting components viz ozone and the open air factor
on host-resistance towards respiratory infection. In: Lee, S. D. ; Mustafa,
M. G. ; Mehlman, M. A., eds. International symposium on the biomedical ef-
fects of ozone and related photochemical oxidants; March 1982; Pinehurst,
NC. Princeton, NJ: Princeton Scientific Publishers, Inc.; pp. 459-467.
(Advances 1n modern environmental toxicology: v. 5).
Berliner, J. A.; Kuda, A.; Mustafa, M. G. ; Tlerney, T. F. (1978) Pulmonary
morphologic studies of ozone tolerance in the rat (a possible mechanism
for tolerance). Scanning Electron Microsc. 2: 879-884.
Bhatnagar, R. S.; Hussain, M. Z.; Sorensen, K. R.; Mustafa, M. G.; von Dohlen,
F. M.; Lee, S. D. (1983) Effect of ozone on lung collagen biosynthesis.
In: Lee, S. D. ; Mustafa, M. G. ; Mehlman, M. A., eds. International
symposium on the biomedical effects of ozone and related photochemical
oxidants; March 1982; Pinehurst, NC. Princeton, NJ: Princeton
Scientific Publishers, Inc.; pp. 311-321. (Advances in modern environ-
mental toxicology: v. 5).
Boatman, E. S. ; Sato, S. ; Frank, R. (1974) Acute effects of ozone on cat
lungs. II. Structural. Am. Rev. Respir. Dis. 110: 157-169.
Boche, R. D. ; QuilUgan, J. J. , Jr. (1960) Effects of synthetic smog on spon-
taneous activity of mice. Science (Washington, DC) 131: 1733-1734.
Boorman, G. A.; Schwartz, L. W. ; McQuillen, N. K. ; Brummer, M. E. G. (1977)
Pulmonary response following long-term intermittent exposure to ozone:
structural and morphometric changes. Am. Rev. Respir. Dis. 115: 201.
Boorman, G. A.; Schwartz, L. W.; Dungworth, D. L. (1980) Pulmonary effects of
prolonged ozone insult in rats: morphometric evaluation of the central
acinus. Lab. Invest. 43: 108-115.
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PRELIMINARY DRAFT
References for Toxicological Effects (cont'd.)
Bradley, M. 0.; Erickson, L. C. (1981) Comparison of the effects of hydrogen
peroxide and X-ray irradiation on toxicity, mutation, and DNA damage/
repair in mammalian cells (V-79). Biochim. Biophys. Acta 654: 135-141.
Bradley, M. 0.; Hsu, I. C.; Harris, C. C. (1979) Relationships between sister
chromatid exchange and mutagenicity, toxicity, and DNA damage. Nature
(London) 282: 318-320.
Brinkman, R.; Lamberts, H. B.; Veninga, T. S. (1964) Radiomimetic toxicity of
ozonised air. Lancet (7325): 133-136.
Brummer, M. E. G. ; Schwartz, L. W. ; McQuillen, N. K. (1977) A quantitative
study of lung damage by scanning electron microscopy: inflammatory cell
response to high-ambient levels of ozone. Scanning Electron Microsc. 2:
513-518.
Calabrese, E. J. ; Moore, G. S.; Grunwald, E. L. (1983) Ozone-induced decrease
of erythrocyte survival in adult rabbits. In: Lee, S. D.; Mustafa, M. G.;
Mehlman, M. A., eds. International symposium on the biomedical effects of
ozone and related photochemical oxidants; March 1982; Pinehurst, NC.
Princeton, NJ: Princeton Scientific Publishers, Inc.; pp. 103-117. (Ad-
vances in modern environmental toxicology: v. 5).
Campbell, K. I.; Hilsenroth, R. H. (1976) Impaired resistance to toxin in
toxoid-immunized mice exposed to ozone or nitrogen dioxide. Clin. Toxicol.
9: 943-954.
Campbell, K. I.; Clarke, G. L. ; Emik, L. 0.; Plata, R. L. (1967) The atmos-
pheric contaminant peroxyacetyl nitrate. Arch. Environ. Health 15: 739-744.
Castleman, W. L.; Dungworth, D. L.; Tyler, W. S. (1973a) Cytochemically detec-
ted alterations of lung acid phosphatase reactivity following ozone
exposure. Lab. Invest. 29: 310-319.
Castleman, W. L. ; Dungworth, D. L. ; Tyler, W. S. (1973b) Histochemically
detected enzymatic alterations in rat lung exposed to ozone. Exp. Mol.
Pathol. 19: 402-421.
Castleman, W. L.; Tyler, W. S.; Dungworth, D. L. (1977) Lesions in respiratory
bronchioles and conducting airways of monkeys exposed to ambient levels
of ozone. Exp. Mol. Pathol. 26: 384-400.
Castleman, W. L.; Dungworth, D. L.; Schwartz, L. W.; Tyler, W. S. (1980) Acute
respiratory bronchiolitis: an ultrastructural and autoradiographic study
of epithelial cell injury and renewal in rhesus monkeys exposed to ozone.
Am. J. Pathol. 98: 811-840.
Cavender, F. L. ; Steinhagen, W. H.; Ulrich, C. E.; Busey, W. M.; Cockrell, B.
Y. ; Haseman, J. K. ; Hogan, M. D. ; Drew, R. T. (1977) Effects in rats and
guinea pigs of short-term exposures to sulfuric acid mist, ozone, and
their combination. J. Toxicol. Environ. Health 3: 521-533.
019VEE/A 1-190 11/22/85
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PRELIMINARY DRAFT
References for Toxicological Effects (cont'd.)
Cavender, F. L. ; Singh, B. ; Cockrell, B. Y. (1978) Effects in rats and guinea
pigs of six-month exposures to sulfuric acid mist, ozone, and their
combination. J. Toxicol. Environ. Health 4: 845-852.
Chow, C. K. (1976) Biochemical responses in lungs of ozone-tolerant rats.
Nature (London) 260: 721-722.
Chow, C. K. (1984) Glutathione peroxidase system in the lungs of ozone-tolerant
and non-tolerant rats. In: Bors, W. ; Saran, M. ; Tait, D. , eds. Oxygen
radicals in chemistry and biology; proceedings of the third international
conference; July 1983; Neuherberg, West Germany. Berlin, West Germany:
Walter de Gruyter & Co.; pp. 707-712.
Chow, C. K. ; Kaneko, J. J. (1979) Influence of dietary vitamin E on the red
cells of ozone-exposed rats. Environ. Res. 19: 49-55.
Chow, C. K. ; Tappel, A. L. (1972) An enzymatic protective mechanism against
lipid peroxidation damage to lungs of ozone-exposed rats. Lipids 7:
518-524.
Chow, C. K. ; Tappel, A. L. (1973) Activities of pentose shunt and glycolytic
enzymes in lungs of ozone-exposed rats. Arch. Environ. Health 26: 205-208.
Chow, C. K. ; Dlllard, C. J. ; Tappel, A. L. (1974) Glutathione peroxidase
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1.12.9 References for Controlled Human Studies of the Effects of Ozone and
Other Photochemical Oxidants
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PRELIMINARY DRAF1
References for Controlled Human Studies (cont'd.)
Avol, E. L. ; Linn, W. S. ; Venet, T. G.; Shamoo, D. A.; Hackney, J. D. (1984)
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PRELIMINARY DRAFT
References for Controlled Human Studies (cont'd.)
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Valencia, L. M. ; Venct, T. G. ; Hackney, J. D. (1982a) Short-term respira-
tory effects of 0.12 ppm ozone exposure in volunteers with chronic ob-
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Dis. 125: 491-495.
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PRELIMINARY DRAFT
References for Controlled Human Studies (cont'd.)
Linn, W. S. ; Shamoo, D. A.; Venet, T. G. ; Spier, C. E.; Valencia, L. M. ;
Anzar, U. T. ; Hackney, J. D. (1983) Response to ozone in volunteers with
chronic obstructive pulmonary disease. Arch. Environ. Health 38: 278-283.
McDonnell, W. F. ; Horstmann, D. H. ; Hazucha, M. J. ; Seal, E. , Jr.; Haak, E.
D. ; Salaam, S. ; House, D. E. (1983) Pulmonary effects of ozone exposure
during exercise: dose-response characteristics. J. Appl. Physiol.: Respir.
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McDonnell, W. F., III; Hortsman, D. H. ; Abdul-Salaam, S.; House, D. E. (1985a)
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Respir. Dis. 131: 36-40.
McDonnell, W. F. , III; Chapman, R. S. ; Leigh, M. W.; Strope, G. L.; Collier,
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0.12 ppm ozone exposure. Am. Rev. Respir. Dis.: in press.
McDonnell, W. F.; Chapman, R. S.; Horstman, D. H.; Leigh, M. W.; Abdul-Salaam,
S. (1985c) A comparison of the responses of children and adults to acute
ozone exposure. In: Proceedings of an international specialty conference
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1.12.10 References for Field and Epidemiological Studies of the Effects of
Ozone and Other Photochemical Oxidants
Avol, E. L. ; Linn, W. S. ; Shamoo, D. A.; Venet, T. G.; Hackney, J. D. (1983)
Acute respiratory effects of Los Angeles smog incontinuously exercising
adults. J. Air Pollut. Control Assoc. 33: 1055-1060.
Avol, E. L.; Linn, W. S. ; Venet, T. G.; Shamoo, D. A.; Hackney, J. D. (1984)
Comparative respiratory effects of ozone and ambient oxidant pollution
exposure during heavy exercise. J. Air Pollut. Control Assoc. 34: 804-809.
Avol, E. L.; Linn, W. S. ; Shamoo, D. A.; Valencia, L. M.; Anzar, U. T. ; Hackney,
J. D. (1985a) Respiratory effects of photochemical oxidant air pollution
in exercising adolescents. Am. Rev. Respir. Dis. 132: 619-622.
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PRELIMINARY DRAFT
References for Field and Epidemiological Studies (cont'd.)
Avol , E. L. ; Linn, W. S. ; Shamoo, D. A.; Valencia, L. M., Anzar, U. T.;
Hackney, J. D. (1985b) Short-term health effects of ambient air pollution
in adolescents. In: Proceedings of an international specialty conference
on the evaluation of the scientific basis for an ozone/oxidant standard;
November 1984; Houston, TX. Pittsburgh, PA: Air Pollution Control Assoc-
iation; in press. (APCA transactions: v. 4).
Bock, N. ; Lippmann, M.; Lioy, P.; Munoz, A.; Speizer, F. (1985) The effects of
ozone on the pulmonary function of children. In: Proceedings of an inter-
national specialty conference on the evaluation of the scientific basis
for an ozone/oxidant standard; November 1984; Houston, TX. Pittsburgh, PA:
Air Pollution Control Association; in press. (APCA transactions: v. 4).
Hammer, D. I.; Hasselblad, V.; Portnoy, B.; Wehrle, P. F. (1974) Los Angeles
student nurse study: daily symptom reporting and photochemical oxidants.
Arch. Environ. Health 28: 255-260.
Herman, D. R. (1972) The effect of oxidant air pollution on athletic perfor-
mance [master's thesis]. Chapel Hill, NC: University of North Carolina.
Holguin, A. H. ; Buffler, P. A.; Contant, C. F., Jr.; Stock, T. H.; Kotchmar,
D. J.; Hsi, B. P.; Jenkins, D. E.; Gehan, B. M.; Noel, L. M. ; Mei, M.
(1985) The effects of ozone on asthmatics in the Houston area. In:
Proceedings of an international specialty conference on the evaluation of
the scientific basis for an ozone/oxidant standard; November 1984;
Houston, TX. Pittsburgh, PA: Air Pollution Control Association; in press.
(APCA transactions: v. 4).
Kagawa, J. ; Toyama, T. (1975) Photochemical air pollution: its effects on
respiratory function of elementary school children. Arch. Environ. Health
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Kagawa, J. ; Toyama, T.; Nakaza, M. (1976) Pulmonary function test in children
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implications of air pollution research: proceedings of the 1974 air
pollution medical research conference; December 1974; San Francisco, CA.
Acton, MA: Publishing Sciences Group, Inc.; pp. 305-320.
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gas stoves on daily peak flow rates in asthmatic and non-asthmatic families.
Eur. J. Respir. Dis. 65 (suppl. 133): 90-97.
Lebowitz, M. D. ; O'Rourke, M. K. ; Dodge, R. ; Holberg, C. J. ; Gorman, G. ;
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adverse health effects of biological aerosols, other aerosols, and indoor
microclimate on asthmatics and nonasthmatics. Environ. Int. 8: 375-380.
Lebowitz, M. D. ; Holberg, C. J. ; Dodge, R. R. (1983) Respiratory effects on
populations from low level exposures to ozone. Presented at: 76th annual
meeting of the Air Pollution Control Association; June; Atlanta, GA.
Pittsburgh, PA: Air Pollution Control Association; paper no. 83-12.5.
019VEE/A 1-213 11/22/85
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PRELIMINARY DRAFT
References for Field and Epidemiological Studies (cont'd.)
Linn, W. S. ; Jones, M. P.; Bachmayer, E. A.; Spier, C. E. ; Mazur, S. F. ; Avol,
E. L. ; Hackney, J. D. (1980) Short-term respiratory effects of polluted
ambient air: a laboratory study of volunteers in a high-oxidant community.
Am. Rev. Respir. Dis. 121: 243-252.
Linn, W. S. ; Avol, E. L. ; Hackney, J. D. (1983) Effects of ambient oxidant
pollutants on humans: a movable environmental chamber study. In: Lee, S.
D. ; Mustafa, M. G. ; Mehlman, M. A., eds. International symposium on the
biomedical effects of ozone and related photochemical oxidants; March
1982; Pinehurst, NC. Princeton, NJ: Princeton Scientific Publishers,
Inc.; pp. 125-137. (Advances in modern toxicology: v. 5).
Lioy, P. J. ; Vollmuth, T. A.; Lippman, M. (1985) Persistance of peak flow
decrement in children following ozone exposures exceeding the National
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Lippmann, M.; Lioy, P. J. ; Leikauf, G.; Green, K. B.; Baxter, D.; Morandi, M.;
Pasternack, B. S. (1983) Effects of ozone on the pulmonary function of
children. In: Lee, S. D. ; Mustafa, M. G.; Mehlman, M. A., eds. Interna-
tional symposium on the biomedical effects of ozone and related photo-
chemical oxidants; March 1982; Pinehurst, NC. Princeton, NJ: Princeton
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v. 5).
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1.12.11 References for Evaluation of Health Effects Data for Data for Ozone and
Other Photochemical Oxidants
Avol, E. L. ; Linn, W. S.; Shamoo, D. A.; Valencia, L. M.; Anzar, U. T.;
Hackney, J. D. (1985a) Respiratory effects of photochemical oxidant air
pollution in exercising adolescents. Am. Rev. Respir. Dis.: in press.
Avol, E. L. ; Linn, W. S. ; Shamoo, D. A.; Valencia, L. M.; Anzar, U. T.;
Hackney, J. D. (1985b) Short-term health effects of ambient air pollution
on the evaluation ofthe scientific basis for an ozone/oxidant standard;
November 1984; Houston, TX. Pittsburgh, PA: Air Pollution Control Asso-
ciation; in press. (APCA transactions: v. 4).
019VEE/A 1-214 11/22/85
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PRELIMINARY DRAFT
References for Evaluation of Health Effects Data (cont'd.)
McDonnell, W. F. , III; Chapan,
A. M. (1985a) Respiratory
to 0.12 ppm ozone exposure.
R. S. ; Leigh, M. W. ; Strope, G. L. ; Collier,
responses of vigorously exercising children
Am. Rev. Respir. Dis.: in press.
McDonnell, W. F.; Champan, R. S. ; Horstman, D. H.; Leigh, M. W. ; Abdul-Salaam,
S. (19855) A comparison of the responses of children and adults to acute
in the evaluation of the scientific basis for an ozone/oxidant standard;
November 1984; Houston, IX. Pittsburgh, PA: Air Pol'lution Control
Association; in press. (APCA transaction v. 4).
019VEE./A
US GOVEI1NUENI F'HINIIWC OFKCt. 6 46-0 J 4/200 ?5
.1-215
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