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SUMMARY
INTRODUCTION
This report reviews current knowledge about man-made
causes of changes in concentrations of stratospheric
ozone and the effects of those changes. Recent reports
of the National Research Council (NRC 1975, 1976a,b,
1978, 1979a,b) have treated the chemical and physical
aspects of potential reductions of stratospheric ozone in
detail. Part I of this report reviews recent develop-
ments on that subject. Part II deals with the effects of
reduction of stratospheric ozone on humans, other animals,
and plants, independently of what might cause the
reduction.
CHEMISTRY AND PHYSICS OF OZONE REDUCTION
s determined
The abundance of ozone in the stratosphere i_
by a dynamic balance among processes that produce and
destroy it and transport it to the troposphere. According
to current understanding, the most important photochemical
reactions regulating ozone involve molecular and atomic
oxygen and various radicals containing nitrogen, hydrogen,
and chlorine. All of these compounds have natural
sources, but their concentrations in the stratosphere can
be significantly altered by human activities. The human
activities that have thus far been identified as
potentially influencing stratospheric ozone are as
follows:
The release of gaseous chlorinated carbon
compounds, mainly chlorofluorocarbons (CFCs) and methyl
chloroform (CH3CC13). CFCs are used as foam-blowing
1
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2
agents, as working fluids in refrigeration systems, and
as propellants in aerosol sprays. Methyl chloroform is
an industrial solvent. These gases decompose in the
stratosphere providing a significant source of radicals
that contain chlorine.
· The release of nitrous oxide (N2O) from
combustion and its enhanced release from soils and waters
as a result of various agricultural and waste management
practices. Nitrous oxide decomposes in the stratosphere,
introducing radicals that contain nitrogen.
· The direct input of nitrogen radicals to the
stratosphere due to nitrogen oxides (NOx) in aircraft
engine exhausts.
· The increased abundance of carbon dioxide (CO2)
in the atmosphere due to combustion of fossil fuels and
deforestation. Increased carbon dioxide has a subtle
influence, causing the temperature of the stratosphere to
decrease, which leads to increased stratospheric ozone,
and changing stratospheric concentrations of water vapor.
Key Findings and Conclusions
Over the past several years, research, driven by
discrepancies between theory and observation, has led to
considerable improvement in our understanding of the
effects on stratospheric ozone of releases of CFCs and
oxides of nitrogen. As a result, previous discrepancies
between the estimates of models of stratospheric processes
and observed concentrations of certain important species
have been reduced. Important discrepancies still remain,
however, which means that there are still uncertainties
inherent in the results of modeling exercises.
Current scientific understanding, expressed in both 1-
and 2-dimensional models, indicates that if production of
two CFCs, CF2C12 and CFC13, were to continue into
the future at the rate prevalent in 1977, the steady
state reduction in total global ozone, in the absence of
other perturbations, could be between 5 percent and 9
percent. Comparable results from models prevalent in
1979 ranged from 15 percent to 18 percent. The
differences between current findings and those reported
in 1979 are attributed to refinements in values of
important reaction rates. Also, as an example, if the
atmospheric concentration of N2O were doubled in the
absence of other perturbations, total ozone would be
reduced by between 10 percent and 16 percent. Although
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atmospheric concentrations of N2O appear to be
increasing, we cannot reliably project the future course
of N2O emissions. Steady state reductions in both
these cases would be reached asymptotically in times on
the order of a century, although the assumption of doub-
ling N2O concentrations is unrealistic on such a time
scale. The effects of perturbations by CFCs and N2O
are not additive, so the estimates of effects of combined
perturbations require investigation of specific cases.
These results should be interpreted in light of the
uncertainties and insufficiencies of the models and
observations. For example, other chemicals released from
human activities are understood to have the potential for
affecting stratospheric ozone. Examples are methyl
chloride (CH3C1), carbon tetrachloride (CC14), and
particularly methyl chloroform. Observations of critical
species need to be extended and confirmed by a number of
measurements using independent techniques. Important
assumptions in the models about rate constants,
distributions of certain species, and the reactions
taking place need to be tested. Furthermore, three
important discrepancies between models and observations
remain to be resolved: More chlorine monoxide (C10) is
observed at altitudes above 35 km than is predicted, the
behavior of NOx in winter at high latitudes is
unexplained, and concentrations of CFCS in the lower
stratosphere are lower than the models suggest.
We anticipate that research on these problems in the
field, in the laboratory, and in theory currently under
way, planned, and proposed will lead to continued
improvement in understanding, resulting in further
reduction of the remaining discrepancies between theory
and observation. In particular, simultaneous measurement
of the important chemical species as a function of
altitude and latitude by various methods should prove
critical to improving understanding during the next
several years.
Examination of the historical record of measurements
of ozone does not reveal a significant trend in total
ozone that can be ascribed to human activities. This
observational result is consistent with those of current
models, since no detectable trend would be expected on
the basis of current theory.
Because data on total global ozone cannot be analyzed
to distinguish among causes of ozone changes, total ozone
data alone cannot be relied upon for early detection of
an anthropogenic change. Measurement of the spatial and
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4
temporal distribution of critical trace species and
ozone, together with theoretical modeling taking into
account all the major influences on stratospheric ozone,
offers promise of understanding the causes of ozone
changes and the consequences of alternative actions in
response.
Recommendations
1. The national research program, including
atmospheric observation, laboratory measurements, and
theoretical modeling, should maintain a broad perspective
with emphasis on areas of disagreement between theory and
observation. Highest priority in research should be
given to a coordinated program to understand the spatial
and temporal distributions of important species, such as
C10 and the hydroxyl radical (OH).
2. The global monitoring effort should include both
ground-based and satellite observations of total ozone
and concentrations of ozone above 35 km, where theory
indicates the largest reductions might occur. Sound,
satellite-based systems for stratospheric observations
are essential.
3. Potential emissions of N2O, CO2, CH3CC13,
and other relevant gases should be assessed and their
consequences for stratospheric ozone evaluated. Models
should be developed to describe the consequences for
stratospheric ozone of future emissions of these gases.
BIOLOGICAL EFFECTS OF INCREASED
SOLAR ULTRAVIOLET RADIATION
Stratospheric ozone acts as a shield to screen out much
of the short-wavelength ultraviolet (W) in sunlight.
Slight changes in this ozone layer may result in large
changes in the amount of damaging UV striking the surface
of the earth. Living creatures have adapted to the
present level of UV and to its fluctuations from season
to season and during the day. Part II of this report
gives the current state of knowledge about the effects on
biological systems of an increase in W resulting from a
decrease in stratospheric ozone concentration.
Each of the findings and conclusions summarized below
has important implications for future research--either in
efforts to decrease the uncertainty in concepts or in
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5
efforts to increase quantitative knowledge. These
research implications are spelled out in our list of
major recommendations. Recent advances in knowledge
since the last NRC report on the subject (NRC 1979a) have
clarified our view of the problem but have also pointed
out scientific areas not emphasized in earlier reports
that confound the simple prediction of the effects of
ozone depletion on biological systems. The unraveling of
these difficulties will be accomplished only by a
research effort directed by knowledgeable scientists,
especially photobiologists. In many instances, we are
still not sure of the scientific questions to be asked.
Similar comments were made in earlier NRC reports (NRC
1975). The fact that they have not been acted on with
any reasonable financial commitment accounts for a large
part of our inability to make better predictions.
It seems certain that more than 90 percent of skin
cancer other than melanoma in the United States is
associated with sunlight exposure and that the damaging
we nabs are in the UV-B region (290 nm to 320 nm) of
the spectrum. A decrease in ozone will be accompanied by
a well-predicted increase in W -B. We estimate that
there will be a 2 percent to 5 percent increase in basal
cell skin cancer incidence per 1 percent decrease in
stratospheric ozone. The increase in squamous cell skin
cancer incidence will be about double that. Where
this range the value falls depends on which theory
used to make the estimate and on the appropriate
dosimetric data used. The predicted increases are
appreciably greater at lower latitudes than at higher.
Although the incidence of malignant melanoma increases
with a decrease in latitude, the degree to which sunlight
in
is
is responsible Is not apparent, and there are few data
implicating UV-B as the only responsible wavelength
region. Therefore it is not appropriate to make
quantitative predictions about the increase in the
incidence of this disease associated with a decrease in
ozone.
Some of the difficulty in making quantitative
predictions about humans comes from uncertainties (even
in simple cellular systems) about the effects of inter-
=~ ; an c amine ~ i nays wavelengths in a broad band, such as
an ~ ~ w~= ALVIN -_~ _~ ,, 7 _
in the ultraviolet of sunlight, in producing antagonistic
or synergistic effects. Moreover, it has been learned
only recently that rapid repair of sunlight damage to
human skin takes place during irradiation. An appreciable
fraction is photorepair mediated by visible light, and a
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6
similar phenomenon seems to take place in anchovy
populations. The quantitative magnitudes of such effects
are not known.
The effects of ozone depletion on other animals and
plants in the biosphere are as important as the direct
effects on human health. However, scientists are still
not able to predict quantitative effects on crop plants
or ecosystems.
The details of our findings and recommendations are
spelled out in Chapters 3, 4, and 5. Key findings and
conclusions and major research recommendations have been
extracted from the chapters and are listed below.
Estimates are given, where possible, of how long the
recommended research might take under ideal circumstances
Key Findings and Conclusions
Molecular and Cellular Studies (Chapter 3)
1. Deoxyribonucleic acid (DNA) is probably the primary
target in animal cells for most deleterious effects of
UV-B, especially effects involving mutagenesis and
neoplastic transformation. Other targets of possible
biological significance for UV-B effects include
membranes, ribonucleic acid (RNA), and proteins.
2. The spectrum for absorption of energy by DNA for
wavelengths in the W-B region and the spectra for
biological damage to DNA as a function of wavelength
(action spectra) are known. The absorption spectrum and
the action spectra are similar but not identical,
probably because long-wavelength light is absorbed in
some components of this genetic material that are not
effective in changing the structure of DNA. The action
spectra in the UV-B region for affecting mammalian cells
(killing, mutation, and neoplastic transformation) are
similar to those for damaging DNA.
3. The formation of pyrimidine dimers (bonds between
pyrimidine residues in one of the two strands of DNA that
distort the normal DNA helical structure) appears to be
the major injury to DNA from W-B irradiation.
4. There are major interactions between the effects
of UV-A (320 nm to 400 nm) and those of W -B on DNA in
cells. Some of these are antagonisms, whereby W -A
effects significantly reduce or repair the W -B damage.
Except for photoreactivation, which involves enzymic
splitting of pyrimidine dimers back to normal single
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7
residues mediated by W-A and visible light, these
interactions are still poorly understood.
5. In excision repair, dimers are removed from one
strand of a DNA double helix by enzymes that work in the
dark, leaving the unaltered strand as a template for
reconstitution of a new normal strand. Photoreactivation
and excision repair of pyrimidine dimers occurs rapidly
in human skin.
Ecosystems and Their Components (Chapter 4)
6. Both W -A and W-B have been reported to be
detrimental to plant growth and development and to a
number of physiological processes of plants, when
examined under non-field conditions. The adaptability of
plant species appears to be sufficient, under current
ambient levels of UV-B, to maintain food crop yields.
The potential for further adaptation to predicted
increases in ambient W-B is not known.
7. Ambient W -B at present levels or similar levels
in the laboratory can damage sensitive aquatic organisms
or stares in their lifecycles that occur at the water's
_
surface. Natural populations of aquatic organisms have
adapted to current W-B levels so as co Relax ~ ~. ~=
reproduction potential. In the case of anchovy larvae,
it has been demonstrated that photorepair of W -B damage
is effective even at UV-B levels significantly higher
-
than those that would result from predicted ozone
depletions. Photorepair may be a general adaptive
mechanism of organisms evolving in the presence of W -B.
Currently, there is no information from which to predict
the magnitude of adverse effects of enhanced W-B on
. .
aquatic organisms.
8. From limited field experiments on terrestrial
plants and laboratory experiments with captured or
cultured aquatic organisms, it appears that different
species of both plants and animals have different
sensitivities to increases in UV-B above current levels.
Changes in species compositions and abundances of
organisms have been observed In s~mu~acea aquatic
ecosystems subjected to enhanced W-B. Mathematical
models show that in systems subject to large natural
oscillations in the size of the Copulation, there are
severe limitations on the minimum population density
needed to maintain a species. However, the data
currently available on food chains in the natural
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8
ecosystem are not precise enough or complete enough to be
used to predict population dynamics or the displacement
of an individual species under current environmental
conditions. It is doubtful therefore that a statistically
significant causal relationship between increased W -B
levels and food chain success can be predicted in the
near future.
9. Only minor effects of increased W-B levels are
predicted for animals used for human food.
Direct Human Health Hazards (Chapter 5)
10. A reduction in the concentration of stratospheric
ozone will not create new health hazards, but will
· · .
Increase existing ones.
Effects Other Than Cancer
11. There is evidence that direct acute effects of UV
on humans, such as sunburn (acute erythema) and corneal
inflammation (photokeratitis), are linked more strongly
to W -B than to W -A.
12. Acute erythema and photokeratitis can be
predicted accurately for a given dose and spectrum of
UV-B, since the action spectra, dose-response curves, and
intensity-time reciprocity relationships are known.
13. Ultraviolet radiation affects many aspects of the
immune system of animals and humans. Allergic contact
dermatitis, skin graft rejection, tumor susceptibility,
and function and viability of individual circulating and
noncirculating cells of the immune system can be altered,
primarily by W-B.
Skin Cancer Other Than Melanoma
14. Data on the relative incidence rates of basal and
squamous cell cancers in highly pigmented (black) versus
lightly pigmented (white) persons indicate that more than
90 percent of skin cancers other than melanoma in U.S.
whites are attributable to sunlight.
15. Molecular, cellular, and whole animal data all
implicate UV-B as the major carcinogenic component of
sunlight for skin cancers other than melanoma. The
evidence is stronger for squamous than basal cell cancers
because animals rarely get basal cell cancers. In
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9
humans, basal cell cancers are virtually all related to
sunlight.
16. Based on animal studies, UV-B is implicated not
only as an initiator of carcinogenesis but also as a
promoter (in the general sense and via indirect effects)
of chemical carcinogenesis. With the current state of
knowledge, it is not possible to assess the extent to
which increasing exposures to chemicals would result in
increases in skin cancers due to synergism, over and
above any increase because of increased UV-B exposure
alone.
17. A 1 percent reduction in the amount of strato-
spheric ozone is predicted to give an approximate 2
percent increase in biologically effective UV-B.
Epidemiological data suggest that a 2 percent increase in
UV-B would give a 2 percent to 5 percent increase in
basal cell skin cancers. For squamous cell skin cancers
the increase would be about twice these values (4 percent
to 10 percent).
18. The risk of developing skin cancers other than
melanoma and the increased risk due to increased exposure
to UV-B could be mitigated by individuals through changes
in lifestyle that would reduce exposure.
Melanoma
19. The incidence of skin melanoma appears to depend
on latitude, an indication that sunlight is a contributing
factor. Circumstantial evidence such as occupational
differences and location of the cancers on the body
suggests, however, that exposure to sunlight is only one
of several factors. The association between sunlight and
melanoma is not strong enough to make a prediction of
increased incidence due to increased exposure to UV based
on epidemiological data.
20. The only evidence that suggests UV-B causes
melanoma in humans comes from studies of people with the
inherited disease xeroderma pigmentosum. These people
have a known defect in the mechanism that would repair
UV-B damage to DNA, and they also have a very high
incidence of skin cancers, including melanoma.
21. There are no reliable animal models for
light-induced melanoma. The only models currently
available are animals with chemically induced,
preexisting pigmented lesions that can be made to look
like melanoma after UV irradiation.
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10
Major Research Recommendations
The estimates following each recommendation of how long
the research might take are educated guesses based on the
experience of individual committee members. The estimates
provide only a rough idea of how long the research might
take under ideal circumstances.
Molecular and Cellular Studies (Chapter 3)
1. An understanding is needed of why broad bands of
UV (heterochromatic radiation) often do not act on DNA in
viva and on in vitro cell systems as a simple sum of
monochromatic wavelengths.
(a) Studies of interactive effects between UV-A and
W -B are fundamental to understanding the mechanisms
of cancer induction by sunlight. Such studies r
employing bacteria or cultured mammalian cells, would
take about two to five years.
(b) An understanding is needed of W -A-induced repair
systems in bacteria, as a first step in understanding
possible similar systems in higher organisms. This
would take about two to five years.
(c) Experiments should be conducted to determine the
rate and extent of photoreactivation in humans in
sunlight. Data are needed on how the level of dimers
depends on the relative amounts of W -A and visible
light compared with the amount of dimer-producing
UV-B. These experiments would take about two to five
years.
2. Data are needed on the rates of repair, in the
dark and in laboratory light, of W -irradiated human skin
cells as a function of UV dose. The differences, if any,
between acute and chronic irradiations should be deter-
mined. One might be able (with informed consent) to
study individuals who are exposed to high levels of UV-B
as part of phototherapy for psoriasis. The aim of such
experiments would be to determine whether the kinetics of
dark repair of damage from pyrimidine dimers in human
skin show two components, a slow one and a fast one, as
is true for human cells irradiated in vitro. The two
components represent repair of DNA in different regions
of the DNA strands. Equally important questions are,
what other types of biologically important damages occur
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11
in skin, what are their lifetimes, and are any of them
persistent? These data could be obtained in about four
or five years.
Ecosystems and Their Components (Chapter 4)
3.
Techniques must be developed for simulating
changes in W -B under natural ambient conditions. Only
in this way can dose-response relationships be obtained.
If these techniques cannot be developed for studies at
temperate latitudes, they might best be achieved in a low-
latitude (subtropical), minimal-cloud-cover, multiuser
facility, which would provide W -B radiation corresponding
. . .
-^ r=~ scone concentrations at more northern 1acz
tudes. Priority should be given to screening representa
~__= ~ ~ _,-~ ~ Imp ~ ; ~-i By \?_
tlve species 01 1mpoLCant 1~" Flails ayes ~ v- Gus.._._,`
ing possible adverse effects on crop productivity.
Dosimetry and environmental regulation techniques must be
developed to ensure optimum experimental conditions--
conditions equivalent to the higher latitude ambient
field conditions of the plants being tested. Without
strict attention to these control conditions, studies
will have limited potential for extrapolation or
prediction. It would take about three years to develop
the facility and another three years to conduct the
species screening experiments.
4.
The effects of W dose on elements of aquatic food
chains cannot be determined unless (a) the underwater
spectral irradiances are integrated over the varying
positions of organisms in water columns to obtain the
exposures that simulate spectral intensities in the
natural systems, and (b) damage to individuals can be
related to population dynamics in the natural ecosystem.
This would require an integrated research approach
involving physical hydrography, physical optics, and
organism physiology. It would take about five years to
develop this approach and obtain results. Unless W-B
studies are made as a part of an ecosystem study, effects
on populations and interactions among populations cannot
be predicted. (Testing for whole ecosystem effects is
addressed in another NRC report, Testing for Effects of
Chemicals ~ ~c~L~c~ (NRC 1981).)
war made for anchovy larvae
An attempt to incorporate such an integrated approach
~ . The interdisciplinary
approach used in the anchovy study to assess W -B damage
to food chains, together with the specific laboratory
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12
measurements, should serve as a model for future research
proposals.
Direct Human Health Hazards (Chapter 5)
5. Studies (animal and human) should be conducted in
the developing field of photoimmunology to determine the
magnitude of UV effects on the human immune system, the
effective wavelengths, and the dose-response relationship.
Results may increase understanding of skin cancer
mechanisms, other effects of UV on skin, and certain
other diseases.
five years.
6. Animal studies of UV-induced skin cancers other
than melanoma are needed to understand interactions among
parameters such as intermittent exposures, different
wavelengths, dose rates, chemical carcinogens and
promoters, and agents that modify cellular responses to
irradiation. These studies would take about two to five
These studies would take about two to
years.
7. The Surveillance, Epidemiology, and End Results
program of the National Cancer Institute routinely
collects data on incidence of melanoma. The incidence of
skin cancers other than melanoma should be surveyed every
decade at a time coinciding with the population census,
so as to determine trends in time. Only a few locations
are necessary, but these should be the same as past
survey locations. Data should be collected in a way that
permits cohort as well as cross-sectional analysis.
8. Animal models for W - or light-induced melanomas
are needed. They would allow studies of action spectra,
dose-response curves, waveband interactions, and other
parameters. It is not possible to predict how long it
would take to develop such models.
9. To determine the association between W and
melanoma, it would be useful to determine the incidence
of the various subtypes of melanoma and their dependence
on latitude. Although this will be difficult because the
majority of melanomas are of the superficial spreading
type, the methodology is available. Careful epidemio-
logical studies that are based on reliable clinical and
histological studies of subtypes of melanoma are needed.
Representative terms from entire chapter:
skin cancers
