Jacobson M.Z. Atmospheric Pollution

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diameters and number concentrations of a Type I PSC are 1 m and 1 particle cm

3

respectively, although diameters vary from 0.01 to 3 m. Typical diameters and num-

ber concentrations of a Type II PSC are 20 m and 0.1 particle cm

3

, respectively,

although diameters vary from 1 to 100 m.

11.8.2. PSC Surface Reactions

Once PSC particles form in the polar winter stratosphere, chemical reactions take

place on their surfaces. Such reactions are called heterogeneous reactions and occur

after at least one gas has diffused to and adsorbed to a particle surface. Adsorption is

a process by which a gas collides with and bonds to a surface. The primary heteroge-

neous reactions that occur on Type I and II PSC surfaces are

ClONO

(g)  H

O(s) HOCl(g)  HNO

(a)

Chlorine Water-ice Hypochlorous Adsorbed

nitrate acid nitric

(11.34)

acid

298 ATMOSPHERIC POLLUTION: HISTORY, SCIENCE, AND REGULATION

ClONO

(g)  HCl(a) Cl

(g)  HNO

(a)

Chlorine Adsorbed Molecular Adsorbed

nitrate hydrochloric chlorine nitric

acid acid

(11.35)

(g)  H

O(s) 2HNO

(a)

Dinitrogen Water-ice Adsorbed

pentoxide nitric

(11.36)

acid

(g)  HCl(a) ClNO

(g)  HNO

(a)

Dinitrogen Adsorbed Chlorine Adsorbed

pentoxide hydrochloric nitrite nitric

acid acid

(11.37)

HOCl(g)  HCl(a) Cl

(g)  H

O(s)

Hypochlorous Adsorbed Molecular Water-ice

acid hydrochloric chlorine

(11.38)

acid

In these reactions, (g) denotes a gas, H

O(s) denotes a water–ice surface, HCl(a) denotes

HCl adsorbed to either a Type I or II PSC, and HNO

(a) denotes HNO

adsorbed to a

Type I or II PSC. Additional reactions exist for bromine. Laboratory studies show that

HCl(g) readily coats the surfaces of Types I and II PSCs. When ClONO

(g), N

(g), or

HOCl(g) impinges upon the surface of a Type I or II PSC, it can react with H

O(s) or

HCl(a) already on the surface. The products of these reactions are adsorbed species, some

of which stay adsorbed, whereas others desorb to the vapor phase.

In sum, heterogeneous reactions convert relatively inactive forms of chlorine in

the stratosphere, such as HCl(g) and ClONO

(g), to photochemically active forms,

such as Cl

(g), HOCl(g), and ClNO

(g). This conversion process is chlorine activa-

tion. The most important heterogeneous reaction is Reaction 11.35 (Solomon et al.,

1986; McElroy et al., 1986), which generates Cl

(g). Reaction 11.36 does not activate

chlorine. Its only effect is to remove nitric acid from the gas phase. When nitric acid

adsorbs to a Type II PSC, which is larger than a Type I PSC, the nitric acid can sediment

out along with the PSC to lower regions of the stratosphere. This removal process is

stratospheric denitriﬁcation. Denitriﬁcation is important because it removes nitrogen

that might otherwise reform Type I PSCs or tie up active chlorine as ClONO

(g).

11.8.3. Springtime Polar Chemistry

Chlorine activation occurs during the winter over the polar stratosphere. When the sun

rises in early spring, Cl-containing gases created by PSC reactions photolyze by

GLOBAL STRATOSPHERIC OZONE REDUCTION 299

(g)  h 2C

•

l(g)   450 nm

Molecular Atomic (11.39)

chlorine chlorine

2  (C

•

l(g)  O

(g) ClO

•

(g)  O

(g))

Atomic Ozone Chlorine Molecular (11.42)

chlorine monoxide oxygen

ClO

•

(g)  ClO

•

(g)

Chlorine Dichlorine (11.43)

monoxide dioxide

(g)  h ClOO

•

(g)  C

•

l(g)   360 nm

Dichlorine Chlorine Atomic

dioxide peroxy chlorine

radical

(11.44)

ClOO

•

(g)

•

(g)  O

(g)

Chlorine Atomic Molecular

peroxy chlorine oxygen

radical

(11.45)

(g) 3O

(g)

Ozone Molecular (11.46)

oxygen

HOCl(g)  h C

•

l(g)  O

•

H(g)   375 nm

Hypochlorous Atomic Hydroxyl (11.40)

acid chlorine radical

ClNO

(g)  h C

•

l(g)  N

•

(g)   370 nm

Chlorine Atomic Nitrogen (11.41)

nitrite chlorine dioxide

Once Cl has been released, it attacks ozone. The catalytic cycle that destroys ozone in the

springtime polar stratosphere differs from that shown in Reactions 11.23 to 11.25, which

reduces ozone on a global scale. A polar stratosphere catalytic ozone destruction cycle is

This mechanism, called the dimer mechanism (Molina and Molina, 1986), is impor-

tant in the springtime polar stratosphere because at that location and time, the ClO(g)

required for Reaction 11.43 is concentrated enough for the reaction to proceed rapidly.

A second cycle is

•

l(g)  O

(g) ClO

•

(g)  O

(g)

Atomic Ozone Chlorine Molecular (11.47)

chlorine monoxide oxygen

•

r(g)  O

(g) BrO

•

(g)  O

(g)

Atomic Ozone Bromine Molecular (11.48)

bromine monoxide oxygen

BrO

•

(g)  ClO

•

(g) B

•

r(g)  C

•

l(g)  O

(g)

Bromine Chlorine Atomic Atomic Molecular (11.49)

monoxide monoxide bromine chlorine oxygen

(g) 3O

(g)

Ozone Molecular (11.50)

oxygen

(McElroy et al., 1986), which is important in the polar lower stratosphere. In sum,

chlorine activation and springtime photochemical reactions convert chlorine from

reservoir forms, such as HCl(g) and ClONO

(g), to active forms, such as Cl(g) and

ClO(g), as shown in Fig. 11.17. The active forms of chlorine destro

y ozone in catalytic

cycles.

Every November, the Antarctic warms up sufﬁciently for the polar vortex to break

down and PSCs to melt, evaporate, and sublimate. Ozone from outside the polar region

advects into the region. Ozone also regenerates chemically, and chlorine reservoirs of

ClONO

(g) and HCl(g) reestablish themselves. Thus, the Antarctic ozone hole is an

annual, regional phenomenon that is controlled primarily by the temperature of the polar

stratosphere and the presence of chlorine and bromine. The radial extent of the hole has

300 ATMOSPHERIC POLLUTION: HISTORY, SCIENCE, AND REGULATION

62%

HCl(g)

37%

ClONO

(g)

1% Cl(g), ClO(g)

Before PSC and photolysis

reactions

HCl(g)

ClONO

(g)

Cl(g), ClO(g)

After PSC and photolysis

reactions

Figure 11.17. Pie chart showing conversion of chlorine reservoirs to active chlorine. During

chlorine activation on PSCs, HCl(g) and ClONO

(g) are converted to potentially active forms of

chlorine that are broken down by sunlight in springtime to form Cl(g). Cl(g) forms ClO(g), both

of which react catalytically to destroy ozone.

grown and minimum ozone values have decreased steadily over the past several years.

The ozone dent over the Arctic is not nearly so large or regular as is that over the

Antarctic because the vortex around the Arctic is much weaker and temperatures over

the Arctic do not drop so low as they do over the Antarctic. Thus, PSC formation and

subsequent chemical reaction is less widespread over the Arctic than over the

Antarctic.

11.9. EFFECTS OF ENHANCED UV-B RADIATION ON LIFE

AND ECOSYSTEMS

In the absence of the stratospheric ozone layer, most UV-C radiation incidents at the

TOA would penetrate to the surface of the Earth, destroying bacteria, protozoa, algae,

fungi, plants, and animals in a short time. Fortunately, the ozone layer absorbs almost

all UV-C radiation. Ozone also absorbs most UV-B radiation, but some of this radiation

penetrates to the surface. UV

-B radiation affects human and animal health, terrestrial

ecosystems, aquatic ecosystems, biogeochemical cycles, air quality, and materials

(UNEP, 1998).

11.9.1. Effects on Humans

Increases in UV-B radiation have potential to affect the skin, eyes, and immune sys-

tem of humans. The layers of skin affected by UV-B are the epidermis (the outer,

nonvascular, protective layer of skin that covers the dermis) and the stratum corneum

(the top, horny layer of the epidermis, made mainly of peeling or dead cells). The lay-

ers of the eye affected by UV

-B are the cornea, the iris, and the lens. In the immune

system, the Langerhans cells, which migrate through the epidermis, are most susceptible

to damage.

11.9.1.1. Effects on Skin

The severity of effects of UV-B radiation on skin depends on skin pigmentation.

During the evolution of Homo sapiens sapiens (the variant of Homo sapiens to which

every human belongs), humans who lived near equatorial Africa developed a dark pig-

ment, melanin, in their skin to protect the skin against UV radiation. As humans

migrated to higher latitudes, where temperatures were colder

, dark pigmentation pre-

vented what little sunlight was available from catalyzing essential chemical reactions

in the skin to produce vitamin D. Thus, the skin of people who migrated poleward

became lighter through natural selection (Leakey and Lewin, 1977). As populations

moved across Asia, into North America, and down toward equatorial South America,

the production of melanin again became an advantage. The fact that equatorial South

Americans have slightly lighter skin than do equatorial Africans suggests that the former

population has not been exposed to the intense equatorial UV radiation for nearly so

long as the latter population (Leakey and Lewin, 1977). In recent generations, segments

of light-skinned populations whose ancestors inhabited higher latitudes, such as 50 to

60N in Northern Europe, have migrated to lower latitudes, such as 15 to 35S in

South Africa, Australia, and New Zealand. Such migration has increased the susceptibil-

ity of these populations to the many effects of UV-B radiation on skin. Enhancements of

UV-B radiation due to reduced ozone further increase the susceptibility of light-skinned

populations to UV-B–related skin problems.

GLOBAL STRATOSPHERIC OZONE REDUCTION 301

UV-B effects on human skin include sunburn (erythema), photoaging of the skin,

and skin cancer. Symptoms of sunburn include reddening of the skin and, in severe

cases, blisters. Susceptibility to sunburn depends on skin type. People with the most

sensitive skin obtain a moderate to severe sunburn in less than an hour (Longstreth et

al., 1998). People who are most resistant to sunburn usually have dark-pigmented skin

and become more deeply pigmented with additional exposure to UV-B.

Photoaging is the accelerated aging of the skin due to long-term exposure to sunlight,

particularly UV-B radiation. Symptoms include loss of skin elasticity, wrinkles, altered

pigmentation, and a decrease in collagen, a ﬁbrous protein in connective tissue.

Skin cancer is the most common cancer among light-pigmented (skinned)

humans. Three types of skin cancers occur most frequently: basal cell carcinoma

(BCC), squamous cell carcinoma (SCC), and cutaneous melanoma (CM). Of all

skin cancers, about 79, 19, and 2 percent are BCC, SCC, and CM, respectively. BCC

is a tumor that develops in basal cells, which reside deep in the skin. As the tumor

evolves, it protrudes through the skin, growing to a large mass that scabs over. BCC

rarely spreads and can be removed by surgery or radiation treatment,

so it is rarely

fatal. SCC is a tumor that develops in squamous cells, which reside on the outside of

the skin. SCC tumors appear as red marks. SCC can spread, but it is readily removed

by surgery or radiation treatment and is rarely fatal. CM is a dark-pigmented and

often malignant tumor arising from a melanocyte, which is a cell that produces the

pigment melanin in the skin. CM tumors spread quickly and gro

w into dark, protrud-

ing masses that can appear anywhere on the skin. CM is fatal about one-third of the

time. In some locations, such as Northern Europe, CM is at least as common as is

SCC, the less common carcinoma. Susceptibility to skin cancer depends on a combi-

nation of skin pigmentation and exposure. For people with sensitive skin, it is not

necessary to be exposed to UV-B over a lifetime for a person to develop skin cancer.

Skin cancer rates usually increase from high latitudes (toward the poles) to lower lati-

tudes (toward the equator).

11.9.1.2. Effects on Eyes

With respect to the eye, the cornea, which covers the iris and the lens, is the tissue

most susceptible to UV-B damage. Little UV-B radiation penetrates past the lens to the

vitreous humor or the retina, the tissues behind the lens. The most common eye prob-

lem associated with UV-B exposure is photokeratitis or “snowblindness,” an

inﬂammation or reddening of the eyeball. Other symptoms include a feeling of severe

pain, tearing, avoidance of light, and twitching (Longstreth et al., 1998). These symp-

toms are prevalent not only among skiers, but also among people who spend time at

the beach or other outdoor locations with highly reﬂective surfaces. From a public cost

perspective, the most expensive eye-related disease associated with UV-B radiation is

cataract, a degenerative loss in the transparency of the lens that frequently results in

blindness unless the damaged lens is removed. Worldwide, cataract is the leading cause

of blindness. More severe, but less widespread, eye-related diseases are squamous cell

carcinoma, which affects the cornea, and ocular melanoma, which affects the iris and

related tissues.

11.9.1.3. Effects on the Immune System

Human skin contains numerous cells to ﬁght infection that are produced by the

immune system. Enhanced UV-B radiation has been linked to suppression of these cells,

reducing resistance to certain tumors and infections. Suppressed immune responses to

302 ATMOSPHERIC POLLUTION: HISTORY, SCIENCE, AND REGULATION

UV-B have been reported for herpes, tuberculosis, leprosy, trichinella, candidiasis, leish-

maniasis, listeriosis, and Lyme disease (Longstreth et al., 1998).

11.9.2. Effects on Microorganisms, Animals, and Plants

Increases in UV-B radiation affect microorganisms, animals, and plants in a variety of

ways. Phytoplankton, which live on the surfaces of the oceans, are susceptible to slowed

growth, reproductive problems, and changes in photosynthetic energy harvesting enzymes

and pigment contents (Hader et al., 1998). Because these microorganisms are near the

bottom of the food chain, their deaths affect higher organisms. Algae and seagrasses,

which cannot avoid exposure to the sun, are also susceptible to damage by UV-B.

Animals are susceptible to several of the same UV-B hazards as are humans.

Squamous cell carcinomas have been found in cats, dogs, sheep, goats, horses, and

cattle, usually on unprotected skin, such as eyelids, noses, ears, and tails (Hargis,

1981, Mendez et al., 1997; Teifke and Lohr, 1996). Cataracts and skin lesions have

been found in ﬁsh (Mayer, 1992).

UV damage to crops varies with species and the crop’s ability to adapt. UV-B affects

the DNA of some crops and the rates of photosynthesis of others. For many crops, UV-B

changes life-cycle timing, plant form, and production of plant chemicals (Caldwell et al.,

1998). For others, it makes plants more susceptible to disease and attack by insects. Crop

yields of some plants are affected by enhanced UV-B, but those of others are not.

11.9.3. Effects on the Global Carbon and Nitrogen Cycles

Changes in UV-B radiation affect the global carbon and nitrogen cycles. UV-B dam-

ages phytoplankton, reducing their consumption of carbon dioxide gas [CO

(g)].

UV-B also enhances photodegradation (breakdown by light) of dead plant material,

increasing release of CO

(g) back to the air. UV-B enhances the release of carbon

monoxide gas [CO(g)] from charred vegetation (Zepp et al., 1998). With respect to the

nitrogen cycle, UV-B affects the rate of nitrogen ﬁxation by cyanobacteria (Hader et

al., 1998).

11.9.4. Effects on Tropospheric Ozone

Increases in UV-B radiation increase photolysis rates of UV

-B absorbing gases, such as

ozone, nitrogen dioxide, formaldehyde, hydrogen peroxide, acetaldehyde, and acetone.

Increases in photolysis rates of nitrogen dioxide, formaldehyde, and acetaldehdye

enhance rates of free-tropospheric ozone formation (Tang et al., 1998).

Whereas reductions in stratospheric ozone increase UV-B radiation reaching the

free troposphere, increases in aerosol loadings in urban air can either decrease or

increase UV-B radiation (Section 7.1.3.3). Reductions in UV-B in polluted air depress

ozone formation; increases in UV-B have the opposite effect.

11.10. REGULATION OF CFCs

The effects of CFCs on ozone were ﬁrst hypothesized by Molina and Rowland in

June 1974. As early as December 1974, legislation was introduced in the U.S.

Congress to study the problem further and give the U.S. EPA authority to regulate

GLOBAL STRATOSPHERIC OZONE REDUCTION 303

CFCs. This bill died before any action was taken. In 1975, the Congress set up a com-

mittee that ultimately recommended that spray cans, the primary sources of CFCs, be

labeled in such a way to identify whether they contained CFCs or an alternative

compound. In 1976, the U.S. National Academy of Sciences released a report sug-

gesting that CFC emissions were large enough to cause a long-term 6 to 7.5 percent

decrease in stratospheric ozone, potentially increasing surface UV-B radiation by 12

to 15 percent. On the basis of this report, the U.S. Food and Drug Administration

(U.S. FDA), the U.S. EPA, and the Consumer Product Safety Commission (CPSC)

issued a joint decision suggesting the phase-out of CFCs from spray cans. In October

1978, the manufacture and sale of CFCs for spray cans was banned in the United

States. At the time, the United States was responsible for half the global production

of CFCs used in spray cans.

Although overall CFC emissions decreased as a result of the ban of CFCs in spray

cans, tropospheric mixing ratios of CFCs continued to increase due to the fact that

emission of CFCs from other sources still occurred. Through the late 1970s and much

of the 1980s, the use of CFCs for refrigeration and foam production and as solv

ents

increased. To limit damage due to CFCs, it was necessary to reduce their emission

from all sources. In 1980, the U.S. EPA proposed limiting emission of CFCs from

refrigeration to current levels at the time, but the proposed regulations were thwarted

by the new presidential administration.

On the international front, the Vienna Convention for the Protection of the Ozone

Layer was convened in March 1985 to discuss CFCs. The result of this convention was

an agreement, signed initially by twenty countries, stating that signatory countries had an

obligation to reduce CFC emissions and to study further the effect of CFCs on ozone. In

September 1987, a second international agreement, the Montreal Protocol, was signed

initially by twenty-seven countries,

limiting the production of CFCs and Halons. The

Montreal Protocol has since been modiﬁed by the London Amendments (1990),

the Copenhagen Amendments (1992), and the Montreal Amendments (1997). The

purpose of the amendments was to accelerate the phase-out of CFCs. Table 11.4 shows

304 ATMOSPHERIC POLLUTION: HISTORY, SCIENCE, AND REGULATION

Source: AFEAS (2001).

Table 11.4. Percentage of 1990 CFC Production Allowed in Developed Countries

under Different Agreements/Laws

1990 100

1991 100 100 85

1992 100 100 80

1993 80 80 75 50

1994 80 80 25 25 15

1995 80 50 25 25 0

1996 80 50 0 0

1997 80 15

1998 80 15

1999 50 15

2000 50 0

European

Montreal London U.S. Clean Air Copenhagen Union

Protocol Amendments Act Amendments Amendments Schedule

Year (1987) (1990) (1990) (1992) (1994)

the phaseout schedule of CFCs resulting from the Montreal Protocol, the London

Amendments, and the Copenhagen Amendments. Also shown in the table are phaseout

schedules under the U.S. Clean Air Act Amendments of 1990 and the European Union

Schedule of 1994. The Copenhagen Amendments of 1992 also called for the complete

phase out of Halons by 1994, the complete phase out of carbon tetrachloride and

methyl chloroform by 1996, and the freeze in HCFC production to speciﬁed values by

1996.

The major effect of the Montreal Protocol, later amendments,

and earlier regula-

tions to ban the use of CFCs in spray cans has been a dramatic decrease in the

emission of CFCs and a corresponding increase in the emission of HCFCs and HFCs,

as illustrated in Fig. 11.18. The ﬁgure shows emissions from CFCs produced by

reporting companies between 1931 and 1998. Reporting companies include eleven

major manufacturers who are estimated to account for 40 percent of worldwide pro-

duction of CFCs, 90 percent of worldwide production of HCFC-22, and 100 percent of

worldwide production of other HCFCs and all HFCs. Most remaining CFCs and

HCFC-22 are produced in Russia and China.

Figure 11.18 shows that HCFC and HFC emissions increased in the 1990s.

Although HCFCs break down more readily in the troposphere than do CFCs, HCFCs

still contain chlorine, some of which can reach the stratosphere and damage the ozone

layer. Because of their potential to destroy ozone, HCFC production rates were frozen

under the Copenhagen amendments. HFCs, however, contain no chlorine and do not

pose a known threat to the ozone layer. Unfortunately, they are strong absorbers of

thermal-IR radiation and contribute to global warming.

Because CFC emissions have declined due to the Montreal Protocol, tropospher-

ic mixing ratios of CFC-11 have also begun to decrease and those of CFC-12 have

begun to level off, as shown in Fig. 11.19(a). More substantial decreases in carbon

tetrachloride [CCl

(g)] and dramatic decreases in methyl chloroform [CH

CCl

(g)]

have been measured, as shown in Fig. 11.19(b). Figures 11.19(b) and (c) show that

HCFC-22, HCFC-141b, HCFC-142b, and HFC-134a mixing ratios increased in the

1990s, as expected, because the emissions of these species increased during this

period.

GLOBAL STRATOSPHERIC OZONE REDUCTION 305

100

200

300

400

500

1930 1940 1950 1960 1970 1980 1990 2000

Release (1,000 metric tons/yr)

Year

CFC-12

CFC-11

CFC-113

HCFC-22

HCFC-141b

HFC-134a

Figure 11.18. Changes in the emissions of selected CFCs, HCFCs, and HFCs, produced by

reporting companies only, between 1931 and 1998.

Source: AFEAS (2001). Nonreported emissions are estimated to account for 60 percent of CFC production, 10

percent of HCFC-22 production,

and 0 percent of HCFC-141b and HFC-134a production.

Because stratospheric mixing ratios of CFCs lag behind those in the troposphere,

the stratospheric ozone layer is not expected to recover fully until 2050 (WMO, 1998).

The annual occurrence of the Antarctic ozone hole is not expected to disappear for

several decades as well.

11.11. SUMMARY

In this chapter the stratospheric ozone layer was discussed, with an emphasis on long-

term global ozone reduction and seasonal Antarctic ozone depletion, both caused by

enhanced levels of chlorine and bromine in the stratosphere. Damage to the ozone layer

is of concern because decreases in ozone permit solar UV-B radiation to penetrate to the

Earth’s surface, where it harms humans, animals, microorganisms, and plants. The story

of environmental damage to the ozone layer may have a positive ending.

Chloroﬂuorocarbons, emitted since the 1930s, slowly diffused into the middle strato-

sphere with an overall transport time of 50 to 100 years. Most CFCs emitted in the

1930s did not reach the middle stratosphere until the 1970s, and those emitted today

will not reach the middle stratosphere for another 50 to 100 years. In 1974, a relation-

ship between CFCs and ozone loss was hypothesized. Between the 1970s and today,

measurements have shown a global ozone reduction and a seasonal Antarctic depletion.

306 ATMOSPHERIC POLLUTION: HISTORY, SCIENCE, AND REGULATION

200

250

300

350

400

450

500

550

600

19861988199019921994199619982000

Mixing ratio (pptv)

Year

CFC-12

CFC-11

100

150

200

1988 1990 1992 1994 1996 1998 2000

Mixing ratio (pptv)

Year

CCl

(g)

CCl

(g)

HCFC-22

(a) (b)

(c)

1993 1994 1995 1996 1997 1998 1999 2000

Mixing ratio (pptv)

Year

HCFC-142b

HCFC-141b

HFC-134a

Figure 11.19. Change in mixing ratio of several (a,b) chlorinated gases at Mauna Loa Observatory, Hawaii,

since 1987 and (c) ﬂuorinated gases at Mace Head, Ireland, since 1994. Data for (a) and (b) from Mauna

Loa Data Center (2001); for (c) from Prinn et al. (2000).

In 1978, regulations banning the use of CFCs in spray cans were implemented in the

United States. Concerned that the ban on CFCs from spray cans was not enough, the

international community agreed to regulate all CFC emissions through the Montreal

Protocol. In 2000, reported CFC emissions were less than one-tenth those in 1976, and

global ozone levels are expected to be replenished to their original levels by the year

2050 as CFCs currently in the atmosphere are slowly removed.

11.12. PROBLEMS

11.1. Explain why an ozone maximum occurs immediately outside the polar v

ortex

during the same season that the ozone hole occurs over the Antarctic.

11.2. Brieﬂy summarize the steps resulting in the Antarctic ozone hole and its recov-

ery. Explain why the ozone dent is never so severe as the ozone hole.

11.3. Write down the chlorine catalytic cycles responsible for ozone reduction

(a) over the Antarctic

(b) in the global stratosphere

Why is the Antarctic mechanism unimportant on a global scale?

11.4. What effect do you think volcanic aerosol particles that penetrate into the strat-

osphere have on stratospheric ozone during the daytime when chlorine

reservoirs are present? How about during the nighttime?

11.5. If the entire global stratospheric ozone layer takes only a year to form from

scratch chemically in the presence of oxygen, why will today’s ozone layer,

which has deteriorated a few percent since 1979, take up to 50 years to regen-

erate to its 1979 level?

11.6. Why does bromine destroy ozone more efﬁciently than does chlorine?

11.7. Why do CFCs not cause damage to ozone in the troposphere?

11.8. Some people argue that natural chlorine from volcanic eruptions and the ocean

is responsible for global ozone reduction and Antarctic ozone depletion. What

argument contradicts this contention?

11.9. Explain why the ratio of UV-B to total solar radiation reaching the top of the

atmosphere is greater than that reaching the ground, as seen in Table 11.1.

11.10. Explain how UV-B levels at the ground in polluted air can be less than those in

unpolluted air, if both the polluted air and clean air are situated under an ozone

layer that is partially depleted by the same amount.

GLOBAL STRATOSPHERIC OZONE REDUCTION 307