National Academies Press: OpenBook

Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects (1986)

Chapter: PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE

« Previous: INTRODUCTION
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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2
The Physicochemical Nature of Sidestream Smoke and Environmental Tobacco Smoke

INTRODUCTION

Mainstream smoke (MS) is the aerosol drawn into the mouth of a smoker from a cigarette, cigar, or pipe. Sidestream smoke (SS) is the aerosol emitted in the surrounding air from a smoldering tobacco product between puff-drawing. SS is a major source of environmental tobacco smoke (ETS), i.e., air pollution caused by the burning of tobacco products. Other contributors to ETS are the exhaled portion of MS and the smoke that escapes from the burning part of a tobacco product during puff-drawing. In addition, some volatile components (e.g., carbon monoxide) diffuse through cigarette paper and contribute to ETS.

Tobacco smoke aerosols are diluted with air by the time they are inhaled as ETS air pollutants. Furthermore, the physical characteristics and chemical composition of ETS change as the pollutants “age”: nicotine is volatilized; particle sizes decrease; nitrogen oxide gradually oxidizes to nitrogen dioxide; various components of the ambient air (e.g., radon daughters) can be adsorbed on the particles; and other physicochemical changes can occur.

In the scientific literature, the terms “passive smoke,” “passive smoking,” and “involuntary smoking” are used often. These terms do not adequately describe ETS and its inhalation, but they are used interchangeably with “ETS” in this report.

Most of the reported data on MS, SS, and ETS pertain to cigarette smoking. Few comparative data on smoke pollutants from other tobacco products are available.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

In the laboratory, cigarettes, cigars, and pipes are smoked by machines under standardized conditions (Wynder and Hoffmann, 1967) to obtain reproducible data for the determination of various individual constituents of undiluted MS and SS. Such data provide a scientific basis for comparing tobacco products and brands. The standardized machine-smoking conditions were developed 3 decades ago to simulate human smoking behavior (Wartman et al., 1959). However, these can differ substantially from those of today’s cigarette smokers, especially in the case of filter-tipped products that are designed to deliver low yields of tar and nicotine (Herning et al., 1981).

For cigarettes and cigarette-like cigars weighing up to 1.5 g, the most widely used machine-smoking conditions in the test laboratory are as follows: one 35-ml puff lasting 2 seconds taken once a minute. The butt length for nonfilter cigarettes is 23 mm. For filter-tipped cigarettes, the total length is increased 3 mm for filter tip plus overwrap (Pillsbury et al., 1969; Brunnemann et al., 1976). For cigars, the conditions are as follows: a 30-ml puff taken once every 40 seconds and a butt length of 33 mm (International Committee for Cigar Smoke Study, 1974). For pipe smoking the test calls for a bowl filled with 1 g of tobacco and for a 50-ml puff lasting 2 seconds to be taken every 12 seconds (Miller, 1964).

Several devices have been used for generating SS from cigarettes and cigars (Dube and Greene, 1982). Among them, the Neurath and Ehmke chamber or modification thereof have been used for chemical analytic work on SS (Neurath and Ehmke, 1964; Brunnemann and Hoffmann, 1974). When SS is generated, a stream of air is sent through a chamber at 25 ml/second. At this rate, the tar and nicotine yields in the MS of cigarettes and cigars smoked in the chamber are similar to those obtained by smoking cigarettes or cigars in the open air. However, the velocity of the airstream through the chamber has considerable influence on the yields of individual compounds in SS (Rühl et al., 1980; Klus and Kuhn, 1982). In order to collect the particulate matter of MS and SS, the aerosols are directed through a glass-fiber filter that traps more than 99% of all the particles with diameters of 0.1 µm or more (Wartman et al., 1959). The portion of the smoke that passes through the filter is designated as the vapor phase. This arbitrary separation into particulate phase and vapor phase does not necessarily reflect the physicochemical conditions prevailing in MS and

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

SS. However, it does reflect specific trapping systems and analytic methods that have been developed for the standardized determination of individual components or groups of components in MS or SS (Brunnemann and Hoffmann, 1982; Dube and Greene, 1982).

Standardized machine-smoking conditions do not exactly duplicate the smoking patterns of an individual, which depend on many factors. For example, low nicotine delivery in cigarette smoke generally induces a smoker to puff more frequently (up to 5 puffs/minute), to draw larger volumes (up to 55 ml/puff), and to inhale more deeply. Puffing more frequently increases the amount of tobacco consumed during generation of MS and thus diminishes the amount of tobacco burned between puffs. This, in turn, affects the release of combustion products in SS, so an increase in puff frequency diminishes the production of SS and ETS. Also, smoking behavior appears to depend strongly on the blood concentration of nicotine that the smoker desires to reach (Krasnegor, 1979; Grabowski and Bell, 1983).

The smoker, because of proximity to the source, usually inhales more of the SS and ETS originating from the burning of the tobacco product than a nonsmoker; however, we do not know the exact amount and we do not know the degree to which inhaled SS and ETS aerosols are retained in the smoker’s respiratory tract. Model studies with MS have shown that more than 90% of some hydrophilic volatile components (e.g., acetaldehyde) is retained after inhalation by the smoker (Dalham et al., 1968a). Therefore, one may assume that a large proportion of the hydrophilic agents in the vapor phase of SS and ETS is also retained when smoke-polluted ambient air is inhaled. In the case of hydrophobic components of the vapor phase of MS (e.g., carbon monoxide), the retained fraction depends on the depth of inhalation, but it hardly ever exceeds 50% (Dalham et al., 1968b). An active smoker generally retains 90% or more of MS particles (Dalham et al., 1968b; Hiller, 1984), whereas a nonsmoker exposed to ETS appears to retain a smaller percentage of ETS particles. It has been calculated that, depending on the degree of SS pollution, a nonsmoker exposed to ETS can retain 0.014 to 1.6 mg of particles per day from ETS (Hiller, 1984).

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

SIDESTREAM SMOKE

The SS generated between puffs originates from a strongly reducing atmosphere. Therefore, undiluted SS contains more combustion products that result from oxygen deficiency and thermal cracking of molecules than does MS. In addition, SS formation involves generation of higher amounts of compounds from nitrosation reactions. Consequently, SS differs substantially from MS.

Table 2–1 compares MS and SS from nonfilter cigarettes. During the consumption of one whole cigarette under standard smoking conditions, the formation of cigarette MS generated during 10 puffs (each 2 seconds) of a blended nonfilter cigarette requires 20 s and consumes 347 mg of tobacco. The formation of SS from the same cigarette smoldering requires 550 seconds and consumes 411 mg of tobacco. However, as shown with experimental cigarettes, the amounts of tobacco consumed during and between puffs depend greatly on the type of tobacco (Johnson et al., 1973a). In addition, MS and SS are generated at different temperatures. For example, under laminar atmospheric conditions, the SS of a smoldering cigarette enters the surrounding atmosphere about 3 mm in front of the paper burn line, at about 350°C (Baker, 1984).

The pH of the MS of a blended American cigarette ranges from 6.0 to 6.5, whereas the pH of SS is 6.7 to 7.5. Above a pH of 6.0, the proportion of unprotonated nicotine in undiluted smoke increases; therefore, SS contains more free nicotine in the gas phase than MS. The pH of SS of cigars is 7.5 to 8.7; pH values for pipe smoke have not been reported (Brunnemann and Hoffmann, 1974). Under conditions prevailing in MS, SS, and ETS, unprotonated nicotine is primarily present in the vapor phase; its absorption through the mucous membranes is faster; thus, its pharmacologic effect is different from that of unprotonated nicotine in the particulate matter (Armitage and Turner, 1970).

About 300–400 of the more than 3,800 compounds identified in tobacco smoke have been measured in MS and SS. Table 2–2 lists the amounts of selected substances reported to occur in the MS and in SS from the burning of a whole nonfilter cigarette and the range of the ratio of their amounts in SS/MS. A ratio greater than unity means that more of a substance is released in SS than in MS. The separation of the compounds in Table 2–2 into vapor phase and particulate phase constituents reflects the conditions

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–1 Some Physiocochemical Characteristics of Fresh, Undiluted Mainstream and Sidestream Smoke from a Nonfilter Cigarettea

Characteristics

MS

SS

Reference

Duration of smoke production, s

20

550

Neurath and Horstmann, 1973

Tobacco burned, mg

347

411

Neurath and Horstmann, 1973

Peak temperature during formation, °C

900

600

Wynder and Hoffmann, 1967

pH

6.0–6.2

6.4–6.6

Brunnemann and Hoffmann, 1974

Number of particles per cigarette

10.5×1012

3.5×1012

Scassellatti-Sforzoline and Savino, 1968

Particle size, µm

0.1–1.0

0.01–0.8

Carter and Hasegawa, 1975; Hiller et al., 1982

Particle mean diameter, µm

0.4

0.32

Carter and Hasegawa, 1975; Hiller et al., 1982

Gas concentration, vol.%

 

Carbon monoxide

3–5

2–3

Keith and Derrick, 1960

Carbon dioxide

8–11

4–6

Wynder and Hoffmann, 1967

Oxygen

12–16

1.5–2

Baker, 1984

Hydrogen

3–15

0.8–1.0

Hoffmann et al., 1984a,b

aData were obtained under standard laboratory smoking conditions of one puff per minute, lasting 2 s, and having volume of 35 ml. Mainstream smoke collected directly from end of cigarette. Sidestream smoke was measured 4 mm from burning cone (gas temperature, 350°C).

prevailing in MS and does not apply to the distribution of these compounds in the vapor phase and particulate phase of SS.

The ratio of the amount of tobacco burned during SS generation to that burned during MS generation is 1.2:1 to 1.5:1 (see Table 2–1 for data on nonfilter cigarettes). Therefore, if one assumed that the combustion process is the same during the generation of the two kinds of smoke, the ratios of their various constituents would also be between 1.2:1 and 1.5:1. That is not the case, as indicated by the higher SS/MS values in Table 2–2. For instance, in the first part of Table 2–2, which lists volatile compounds, the ratios for carbon monoxide range from 2.5 to 4.7, for carbon dioxide from 8 to 11, for acrolein from 8 to 15, and for benzene about 10.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–2 Distribution of Constituents in Fresh, Undiluted Mainstream Smoke and Diluted Sidestream Smoke from Nonfilter Cigarettesa

Constituent

Amount in MS

Range in SS/MS

Vapor phaseb

 

Carbon monoxide

10–23 mg

2.5–4.7

Carbon dioxide

20–40 mg

8–11

Carbonyl sulfide

18–42 µg

0.03–0.13

Benzenec

12–48 µg

5–10

Toluene

100–200 µg

5.6–8.3

Formaldehyde

70–100 µg

Acrolein

60–100 µg

8–15

Acetone

100–250 µg

2–5

Pyridine

16–40 µg

6.5–20

3-Methylpyridine

12–36 µg

3–13

3-Vinylpyridine

11–30 µg

20–40

Hydrogen cyanide

400–500 µg

0.1–0.25

Hydrazined

32 ng

3

Ammonia

50–130 µg

40–170

Methylamine

11.5–28.7 µg

4.2–6.4

Dimethylamine

7.8–10 µg

3.7–5.1

Nitrogen oxides

100–600 µg

4–10

N-Nitrosodimethylaminee

10–40 ng

20–100

N-Nitrosodiethylaminee

ND-25 ng

<40

N-Nitrosopyrrolidinee

6–30 ng

6–30

Formic acid

210–490 µg

1.4–1.6

Acetic acid

330–810 µg

1.9–3.6

Methyl chloride

150–600 µg

1.7–3.3

Particulate phaseb

 

 

Particulate matterc

15–40 mg

1.3–1.9

Nicotine

1–2.5 mg

2.6–3.3

Anatabine

2–20 µg

<0.1–0.5

Phenol

60–140 µg

1.6–3.0

Catechol

100–360 µg

0.6–0.9

Hydroquinone

110–300 µg

0.7–0.9

Aniline

360 ng

30

2-Toluidine

160 ng

19

2-Naphthylaminec

1.7 ng

30

4-Aminobiphenylc

4.6 ng

31

Benz[a]anthracenee

20–70 ng

2–4

Benzo[a]pyrened

20–40 ng

2.5–3.5

Cholesterol

22 µg

0.9

γ-Butyrolactonee

10–22 µg

3.6–5.0

Quinoline

0.5–2 µg

8–11

Harmanf

1.7–3.1 µg

0.7–1.7

N′-Nitrosonornicotinee

200–3,000 ng

0.5–3

NNKg

100–1,000 ng

1–4

N-Nitrosodiethanolaminee

20–70 ng

1.2

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Constituent

Amount in MS

Range of SS/MS

Cadmium

100 ng

7.2

Nickeld

20–80 ng

13–30

Zinc

60 ng

6.7

Polonium-210c

0.04–0.1 pCi

1.0–4.0

Benzoic acid

14–28 µg

0.67–0.95

Lactic acid

63–174 µg

0.5–0.7

Glycolic acid

37–126 µg

0.6–0.95

Succinic acid

1 10–140 µg

0.43–0.62

aData from Elliot and Rowe (1975); Schmeltz et al. (1979); Hoffmann et al. (1983); Klus and Kuhn (1982); Sakuma et al. (1983, 1984a,b); Hiller et al. (1982). Diluted SS is collected with airflow of 25 ml/s, which is passed over the burning cone.

bSeparation into vapor and paniculate phases reflects conditions prevailing in MS and does not necessarily imply same separation in SS.

cHuman carcinogen (U.S. Department of Health and Human Services, 1983).

dSuspected human carcinogen (U.S. Department of Health and Human Services, 1983).

eAnimal carcinogen (Vainio et al., 1985).

fl-methyl-9H-pyrido[3,4-b]-indole.

gNNK=4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone.

The high SS/MS values of carbon monoxide and carbon dioxide show that more of each of these constituents is generated in the oxygen-deficient cone during smoldering than during puff-drawing. After passing briefly through the hot cone, most of the carbon monoxide is oxidized to carbon dioxide, probably because of the high temperature gradient and sudden exposure to air.

The high SS/MS values of volatile pyridines are thought to be due to the fact that these compounds are formed from the alkaloids during smoldering (Schmeltz et al., 1979). Hydrogen cyanide is formed primarily from protein at temperatures above 700°C (Johnson and Karg, 1971). Thus, smoldering of tobacco at 600°C does not favor the pyrosynthesis of hydrogen cyanide to the extent that it occurs during MS generation.

With regard to the carcinogenic potential of SS, it is important to consider the SS/MS ratio of NOx—4 to 10. More than 95% of the NOx inhaled by the smoker is in the form of nitric oxide, and only a small portion is oxidized to the powerful nitrosating agent, nitrogen dioxide. Only a small fraction of nitric oxide is expected to be retained in the respiratory system by being bound to hemoglobin. NOx released into the environment in SS

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

is partially oxidized to nitrogen dioxide (Vilicins and Lephardt, 1975). Thus, environments polluted with SS are expected to contain increased concentrations of the hydrophilic nitrosating agent, nitrogen dioxide.

Perhaps the most remarkable data in this portion of Table 2–2 are the very high SS/MS values of ammonia, nitrogen oxide, and the volatile N-nitrosamines. Studies with [15N]nitrate have shown that, during burning of tobacco, nitrate is reduced to ammonia, which is released to a greater extent in SS than in MS during puff-drawing (Just et al., 1972). An extreme example is the case of a cigarette made exclusively from burley tobacco, a variety generally rich in nitrate (2.0–5.0% in U.S. survey); ammonia is released in SS at 8,500 µg/cigarette (SS/MS 170, according to Johnson et al., 1973b). (In the case of a blended cigarette, the greater generation of ammonia in SS causes an increased pH, which can be above 7, whereas the pH of MS is about 6.)

The ranges of high SS/MS ratios of the highly carcinogenic volatile N-nitrosamines (such as N-nitrosodimethylamine—20 to 100) have been well established (Brunnemann et al., 1977, 1980; Rühl et al., 1980).

The second part of Table 2–2 lists some constituents of particulate matter, their amounts reported to occur in MS during the burning of one cigarette, and ranges of the relative amounts in SS/MS. The increases in SS of tobacco-specific N-nitrosamines, such as 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), N-nitrosodiethanolamine, and N′-nitrosonornicotine, are up to fourfold. Presently we do not know whether the tobacco-specific N-nitrosamines are present in the particulate phase or in the vapor phase of ETS (Hoffmann and Hecht, 1985).

Constituents of the vapor phase would be less likely to settle with the smoke particles, but would remain in the ambient air for longer spans of time. Research is needed to evaluate this distribution, which is important with respect to the carcinogenic potential of SS. The meaning of the abundant release of amines in SS (SS/MS, to 30-fold)—as indicated by the data in aniline, 2-toluidine, and the alkaloids—should also be examined. Some amines are readily nitrosated to N-nitrosamines, but analytic data on secondary reactions of amines in polluted environments are lacking.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–3 Relative Concentrations (SS/MS) of Selected Components in Fresh, Undiluted Smoke of Four 85-mm Commercial American Cigarettesa

Constituentc

Constituent Concentrations in Smokeb

Cigarette A, NF

Cigarette B, F

Cigarette C, F

Cigarette D, PF

SS

SS/MS

SS

SS/MS

SS

SS/MS

SS

SS/MS

Tar, mg/g

22.6

1.1

24.4

1.6

20.0

2.9

14.1

15.6

Nicotine, mg/g

4.6

2.2

4.0

2.7

3.4

4.2

3.0

20.0

CO, mg/g

28.3

2.1

36.6

2.7

33.2

3.5

26.8

14.9

NH3, mg/g

524

7.0

893

46

213.1

6.3

236

5.8

Catechol, µg/g

58.2

1.4

89.8

1.3

69.5

2.6

117

12.9

BaP, ng/g

67

2.6

45.7

2.6

51.7

4.2

448

20.4

NDMA, ng/g

735

23.6

597

139

611

50.4

685

167

NPYR, ng/g

177

2.7

139

13.6

233

7.1

234

17.7

NNN, ng/g

857

0.85

307

0.63

185

0.68

338

5.1

aData from Adams et al. (1985). Tar values for MS: cigarette A, 20.1 mg; cigarette B, 15.6 mg; cigarette C, 6.8 mg; cigarette D, 0.9 mg.

bNF=nonfilter cigarette; F=filter cigarette; PF=cigarette with perforated filter tip; BaP=benzo[a]pyrene.

cNDMA=N-nitrosodimethylamine; NPYR=N-nitrosopyrrolidine; NNN=N′-nitrosonornicotine.

To comprehend the data in Table 2–2 fully, some aspects should be emphasized. First, the data are based on analyses of nonfilter cigarettes that were smoked under standard laboratory conditions. Second, those conditions, established according to smoking patterns observed 3 decades ago, have been shown not to reflect today’s smoking behavior. The difference is especially evident in the case of filter cigarettes designed for low smoke yields. Most consumers inhale the smoke of such cigarettes more intensely than the smoke of nonfilter cigarettes (Hill and Marquardt, 1980; Herning et al., 1981). This difference affects the yield of SS. Conventional cigarette filter tips primarily influence the yield of MS, but have little impact on SS yield. However, highly active filter tips, especially those with perforations, also affect the yield of SS (Adams et al., 1985). It is apparent in Table 2–3 that for all cigarettes studied the SS/MS values are greater than 1 for many toxic and carcinogenic constituents.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–4 Measured Concentrations of Carbon Monoxide in ETSa

Location

Tobacco Burned

Ventilation

Carbon Monoxide Concentrations, ppm

References

 

Nonsmoke Controls

Mean

Range

Mean

Range

Rooms

4.3–9

2.2±0.98

0.4–4.5

Coburn et al., 1965

Train

1–18 smokers

Natural

0–40

Harmsen and Effenberger, 1957

Submarines (66 m3)

157 cigarettes/day

94–103 cigarettes/day

Yes Yes

<40 <40

Cano et al., 1970

18 military aircraft

Yes

<2–5

U.S. Department of Transportation, 1971

8 commercial aircraft

Yes

<2

U.S. Department of Transportation, 1971

Rooms

5–25

Porthein, 1971

14 public places

<10

Perry, 1973

Ferry boat

18.4±8.7

3.0±2.4

Godin et al., 1972

Theater foyer

3.4±0.8

1.4±0.8

Godin et al., 1972

Intercity bus

23 cigarettes

3 cigarettes

15 changes/h

15 changes/h

32

18

Seiff, 1973

2 conference rooms

8 changes/h

8 (peak)

1–2

Slavin and Hertz, 1975

Office

236 m3/h

Natural

<2.5–4.6

< 2.9–9.0

Harke, 1974

Automobile

2 smokers (4 cigarettes)

Natural

Mechanical

42 (peak)

32 (peak)

13.5 (peak)

15.0 (peak)

Harke and Peters, 1974

9 night clubs

Varied

13.4

6.5–41.9

Sebben et al., 1977

14 restaurants

9.9±5.5

9.2 (outdoor)

3.0–35

Sebben et al., 1977

45 restaurants

8.2±2.2

7.1±1.7

Sebben et al., 1977

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

33 stores

10.0±4.2

11.5±6.5

11.5±6.5

Sebben et al., 1977

3 hospital lobbies

4.8

Sebben et al., 1977

6 coffee houses

Varied

2–23

Badre et al., 1978

Room

18 smokers

50

Badre et al., 1978

Hospital lobby

12–30 smokers

5

Badre et al., 1978

2 train compartments

2–3 smokers

4–5

Badre et al., 1978

Automobile

3 smokers

2 smokers

Natural, open

Natural, closed

14

20

Badre et al., 1978

10 offices

2.5±10

1.5–1.0

2.5±1.0

1.5±4.5

Chappell and Parker, 1977

15 restaurants

4.0±2.5

1.0–9.5

2.5±1.5

1.0–5.0

Chappell and Parker, 1977

14 night clubs and taverns

13.0±7.0

3.0–29.0

3.0±2.0

1.0–5.0

Chappell and Parker, 1977

Tavern

Artificial

None

8.5

35 (peak)

Chappell and Parker, 1977

Office

Natural, open

1.0

10.0 (peak)

Chappell and Parker, 1977

Restaurant

Mechanical

5.1

2.1–9.9

4.8 (outdoors)

Fischer et al., 1978

Restaurant

Natural

2.6

1.4–3.4

1.5 (outdoors)

Fischer et al., 1978

Bar

Natural, open

4.8

2.4–9.6

1.7 (outdoors)

Weber et al., 1976

Cafeteria

11 changes/h

1.2

0.7–1.7

0.4 (outdoors)

Weber et al., 1976

44 offices

1.1

6.5 (max)

Weber, 1984

25 offices

2.78±1.42

2.59±2.33

Szadkowski et al., 1976

Tavern

6 changes/h

11.5

10–12

2 (outdoors)

Cuddeback et al., 1976

Tavern

1–2 changes/h

12.0

3–22

Cuddeback et al., 1976

aTime-weighted average (TWA) of carbon monoxide, 50 ppm (55 mg/m3). TWA=average concentration to which worker may be exposed continuously for 8 h without damage to health (National Institute for Occupational Safety and Health, 1971).

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

PRINCIPAL CHEMICAL CONSTITUENTS OF ENVIRONMENTAL TOBACCO SMOKE

Air dilution physicochemically changes SS and other contributors to ETS. Depending on the degree of air dilution of SS, the concentration of particles in ETS can range from a few micrograms to 300–500 mg/m3. A high degree of air dilution can reduce this yield to a few micrograms per cubic meter. At the same time, the median diameter of the particles will decrease from 0.32 µm to 0.14 or 0.098 µm (Keith and Derrick, 1960; Wynder and Hoffmann, 1967; Ingebrethsen and Sears, 1985). Another change caused by air dilution of SS is the volatilization of nicotine. In ETS, nicotine is present almost exclusively in the vapor phase (Eudy et al., 1985). In addition, redistributions of other constituents in SS due to air dilution might account for the presence of other semivolatile chemicals in the vapor phase of ETS, but we lack data on such effects.

The scientific literature contains an abundance of data on indoor air pollution by ETS (U.S. Public Health Service, 1979; National Research Council, 1981). We limit our review here to measurements made under field conditions and have excluded data from experimental studies. Most of the published data, summarized in Tables 2–4 through 2–9, do not exclude the possibility that, even though the respiratory environments analyzed were polluted largely by ETS, some other sources of pollution contributed to the reported concentrations of individual agents. (Many studies have dealt with the measurement of particulate matter in environments polluted by tobacco smoke. Chapter 5 discusses the measurement of particulate matter, and the results of the studies are summarized in Table 5–1.)

Table 2–4 shows concentrations of carbon monoxide measured in a variety of indoor spaces with and without occupancy by smokers. Carbon monoxide concentrations were generally higher in spaces where smoke was present. They were highly variable, however, and collected data on each space were insufficient (e.g., number of cigarettes smoked and volume of space) to show a consistent relationship.

Tobacco is the only known source of nicotine, so the Nicotiana alkaloid is a specific indicator for tobacco smoke pollution. Nicotine concentrations in smoke-polluted rooms were generally found to be 5–50 µg/m3 and much higher (up to 500 µg/m3) in

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

heavily polluted environments (Table 2–5). In small interior compartments, such as automobiles, occupants who smoke tobacco have generated nicotine concentrations of 1,010 µg/m3 (Badre et al., 1978).

Freshly generated tobacco smoke contains nitric oxide, but not nitrogen dioxide. On release into the environment, nitric oxide is gradually oxidized to nitrogen dioxide. The estimated half-life of nitric oxide is 10–20 minutes, depending on the degree of air dilution. Table 2–6 shows concentrations of nitric oxide and nitrogen dioxide in smoke-polluted environments and indicates means ranging from 9 to 195 ppb for nitric oxide and 21 to 76 ppb for nitrogen dioxide. Generally, the nitrogen oxide values reported in Table 2–6 are significantly in excess of those observed for outdoor atmospheres. However, some severe air pollution episodes in industrial areas have reportedly caused levels of 100 ppb, which persisted over several hours or even for several days (Goldsmith and Friberg, 1977). As a constituent of the respiratory environment, nitrogen dioxide conceivably contributes to endogenous nitrosation, which leads to the presence of nitrosamines in exposed subjects. Whereas it has been clearly demonstrated that inhaled cigarette smoke increases the endogenous formation of N-nitrosamines (Hoffmann and Brunnemann, 1983; Ladd et al., 1984; Lu et al., 1986; Tsuda et al., 1986), the endogenous formation of N-nitrosamines in nonsmokers exposed to ETS has so far not been demonstrated (Brunnemann et al., 1984).

Tables 2–7 and 2–8 show concentrations of acrolein and acetone in ETS. These volatile carbonyl compounds are known to affect mucociliary function and thus inhibit the clearance of smoke particles from the lung (Wynder and Hoffmann, 1967).

Table 2–9 shows concentrations of some additional toxic agents in ETS. Benzene, N-nitrosodimethylamine, N-nitrosodiethylamine, and the polynuclear aromatic hydrocarbons, represented by benzo[a]pyrene, are of concern, because they are known carcinogens (Vainio et al., 1985).

RADIOACTIVITY OF ENVIRONMENTAL TOBACCO SMOKE

The radioactive isotopes of lead (Pb-210), bismuth (Bi-210), and polonium (Po-210), known as long-lived radon daughters in the decay chain of uranium via radium and radon (Radford and

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–5 Measured Concentrations of Nicotine in ETSa

Location

Tobacco Burned

Ventilation

Nicotine Concentrations, µg/m3

References

Mean

Range

Train

Natural, closed

0.7–3.1

Harmsen and Effenberger, 1957

6 coffee houses

Smokers varied

25–52

Badre et al., 1978

Room

18 smokers

500

Badre et al., 1978

Hospital lobby

12–30 smokers

37

Badre et al., 1978

2 train compartments

2–3 smokers

36–50

Badre et al., 1978

Automobile

3 smokers

Natural, open

Natural, closed

65

1,010

Badre et al., 1978

Submarines (66 m3)

157 cigarettes/day

94–103 cigarettes/day

Yes

Yes

32

15–35

Cano et al., 1970

Train

4.9

Hinds and First, 1975

Bus

6.7

Hinds and First, 1975

Bus waiting room

1.0

Hinds and First, 1975

Airline waiting room

3.1

Hinds and First, 1975

Restaurant

5.2

Hinds and First, 1975

Cocktail lounge

10.3

Hinds and First, 1975

Student lounge

2.8

Hinds and First, 1975

44 offices

0.9±1.9

13.8 (peak)

Weber and Fischer, 1980

aTime-weighted average (TWA) of nicotine, 500 µg/m3. TWA=average concentration to which worker may be exposed continuously for 8 h without damage to health (National Institute for Occupational Safety and Health, 1971).

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–6 Measured Concentrations of Nitrogen Oxides in ETSa

Location

Tobacco Burned

Ventilation

Nitrogen Oxides Concentrations, ppb

References

Mean

Range

Nonsmoke Control, Mean

Restaurant

Mechanical

NO2 76

NO 120

59–105

36–218

63 (outdoors)

115 (outdoors)

Fischer et al., 1978

Restaurant

Natural

NO2 63

NO 80

24–99

14–121

50 (outdoors)

11 (outdoors)

Weber, 1984

Bar

Natural, open

NO2 21

NO 195

1–61

66–414

48 (outdoors)

44 (outdoors)

Weber et al., 1979

Cafeteria

11 changes/h

NO2 58

NO 9

35–103

2–38

27

5

Weber et al., 1979

44 offices

Varied

Varied

NO2 24±22

NO 32±60

115 (peak)

200 (peak)

Weber and Fischer, 1980

aTime-weighted averages (TWAs): nitric oxide, 25 ppm; nitrogen dioxide, 1 ppm. TWA=average concentration to which worker may be exposed continuously for 8 h without damage to health (National Institute for Occupational Safety and Health, 1971).

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–7 Measured Concentrations of Acrolein in ETSa

Location

Tobacco Burned

Ventilation

Acrolein Concentrations

References

Mean

Range

Coffee houses

Varied

0.03–0.10 mg/m3

Badre et al., 1978

Room

18 smokers

0.185 mg/m3

Badre et al., 1978

Hospital lobby

12–30 smokers

0.02 mg/m3

Badre et al., 1978

2 train compartments

2–3 smokers

0.02–0.12 mg/m3

Badre et al., 1978

Automobile

3 smokers

2 smokers

Natural, open

Natural, closed

0.03 mg/m3

0.3 mg/m3

Badre et al., 1978

Restaurant

Mechanical

Natural

7 ppb

8 ppb

Fischer et al., 1978

Bar

Natural, open

10 ppb

Weber et al., 1976

Cafeteria

11 changes/h

6 ppb

Weber et al., 1976

aTime-weighted average (TWA) of acrolein, 0.1 ppm. TWA=average concentration to which worker may be exposed continuously for 8 h without damage to health (National Institute for Occupational Safety and Health, 1971).

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–8 Measured Concentrations of Acetone in ETSa

Location

Tobacco Burned

Ventilation

Acetone Concentrations, mg/m3

References

Mean

Range

6 coffee houses

Varied

0.91–5.88

Badre et al., 1978

Room

18 smokers

0.51

Badre et al., 1978

Hospital lobby

12–30 smokers

1.16

Badre et al., 1978

2 train compartments

2–3 smokers

0.36–0.75

Badre et al., 1978

Automobile

3 smokers

2 smokers

Natural, open

Natural, closed

0.32

1.20

Badre et al., 1978

aTime-weighted average (TWA) of acetone, 250 ppm. TWA=average concentration to which worker may be exposed continuously for 8 h without damage to health (National Institute for Occupational Safety and Health, 1971).

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–9 Measured Concentrations of Various Toxic Agents in Rooms Polluted with ETS

Pollutant

Location

Concentration

Nonsmoke Control Concentration

References

Benzene

Public places

20–317 µg/m3

Badre et al., 1978

N-Nitrosodimethylamine

Restaurant, public places

0.01–0.24 µg/m3

0.005 µg/m3 (inside)

Brunnemann et al., 1977; Stehlik et al., 1982

N-Nitrosodiethylamine

Restaurant, public places

<0.01–0.2 µg/m3

Stehlik et al., 1982

Anthanthrene

Coffee houses

4.1–9.4 ng/m3

2.8–7.0 ng/m3 (outdoors)

Just et al., 1972

Benzo[a]fluorene

Indoors

39 ng/m3

Grimmer et al., 1977

Benzo[a]pyrene

Restaurant, public

2.8–760 ng/m3

4.0–9.3 ng/m3 (outdoors)

Galuskinova, 1964; Just et al., 1972; Perry, 1973; Grimmer et al., 1977

Benzo[-]pyrene

Coffee houses

3.3–23.4 ng/m3

3.0–5.1 ng/m3 (outdoors)

Just et al., 1972

Coronene

Coffee houses

0.5–1.2 ng/m3

1.0–2.8 ng/m3 (outdoors)

Just et al., 1972

Perylene

Coffee houses

0.7–1.3 ng/m3

0.1–1.7 ng/m3 (outdoors)

Just et al., 1972

Pyrene

Coffee houses

4.1–9.4 ng/m3

0.1–1.7 ng/m3 (outdoors)

Just et al., 1972

Phenols (volatile)

Coffee houses

7.4–11.5 ng/m3

Just et al., 1972

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Hunt, 1964; Martell, 1975; Hill, 1982), are present in tobacco and therefore appear in tobacco smoke. Furthermore, when radon is present in the air, aerosol particles, including those of tobacco smoke, tend to adsorb the earlier decay products of radon, namely the so-called short-lived daughters (Po-218, Pb-214, Bi-214, and Po-214), i.e, those preceding the long-lived daughters in the decay chain (Raabe, 1969; Kruger and Nothing, 1979; Bergman and Axelson, 1983).

The presence of Pb-210 and subsequent decay products in tobacco might derive from uptake of Pb-210 from the soil, especially if radium-rich phosphate fertilizers have been used (Tso et al., 1966). It may also result from adsorption of short-lived radon daughters on the leaves of the tobacco plant when phosphate fertilizers are used and the leakage of radon from the ground is therefore increased. This adsorption applies to short-lived daughters, which then decay to the long-lived Pb-210, and subsequent nuclides found in the tobacco when phosphate fertilizers, containing radium-226, are used (Fleischer and Parungo, 1974; Martell, 1975). The origin of these decay products could also be due to the general occurrence of radon in the atmosphere (Hill, 1982).

In recent years, relatively high concentrations of radon and short-lived radon daughters have been found in indoor air in homes in several countries (Nero et al., 1985). In clean air, the short-lived radon daughters tend to be more unattached to aerosol particles and therefore are more easily deposited on walls, furniture, etc., especially through electrostatic forces. In the presence of an aerosol like tobacco smoke, some of the short-lived radon daughters are attached to particles, and therefore remain available for inhalation to a much greater extent than would otherwise be the case. Indoor radon-daughter concentration can more than double in the presence of tobacco smoke (Bergman and Axelson, 1983). Since radon daughter exposure is a well-known cause of lung cancer in miners, the described attachment of radon daughters to cigarette smoke would contribute to the carcinogenic potential of ETS (Little et al., 1965; Rajewsky and Stahlhofen, 1966; Radford and Martell, 1978). Given the presence of appreciable amounts of radon in indoor air, irradiation of the bronchial tract from radon daughters attached to smoke aerosol could be more important than the irradiation from the long-lived daughters in the tobacco itself. This subject needs further research, especially in light of recent reports on the widespread prevalence of indoor radon throughout the world.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TOXIC AND CARCINOGENIC AGENTS IN TOBACCO SMOKE

Combustion products of cigarettes are the main contributors of ETS. Therefore, comparisons of concentrations of specific toxins and carcinogens in ETS (Tables 2–4 through 2–9) with corresponding concentrations in MS are relevant.

However, comparisons of MS and ETS can be appropriate only if one considers the important differences in chemical composition (including pH) and physicochemical nature (e.g., particle size, air dilution factors, and distribution of agents between vapor and particulate phases) between the two aerosols. Furthermore, ETS in indoor environments is often accompanied by pollutants in the work environment or derived from other sources, such as cooking stoves and space heaters. There are also important differences between inhaling ambient air and inhaling a concentrated smoke aerosol during puff-drawing. Finally, chemical and physicochemical characteristics based on analysis of smoke generated by machine smoking are not fully comparable with those of compounds generated when a smoker inhales cigarette smoke. Especially in the case of low-yield cigarettes, the yields of constituents appear to be different between machine smoking and human smoking (Herning et al., 1981).

Table 2–10 compares concentrations of some smoke constituents in the MS generated in the laboratory from one cigarette to those inhaled by a nonsmoker exposed to ETS for 1 hour.* The physical and chemical changes that occur in reactive smoke constituents during aging of the compounds after their emission into the environment must also be considered. For example, nitric oxide is generated in a cigarette during smoking and is chemically

*  

The computations for exposures to nonsmokers for 1 hour in Table 2–10 are made using the equation:

assuming an average respiratory rate of 10 L/minute. To convert from ppm (or ppb) to mg/m3, the following equation is used:

where RT at 20°C is 24.45.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

intact when it leaves the cigarette in MS about 2 seconds later. However, once emitted into SS and diluted to become an ETS component, nitric oxide is partially oxidized to nitrogen dioxide and progressively more oxidized as more time elapses, producing a potent hydrophilic nitrosating agent.

SUMMARY AND RECOMMENDATIONS

The smoldering of tobacco between puffs generates SS. Undiluted SS contains some toxic compounds in much higher concentrations than MS, especially ammonia, volatile amines, volatile nitrosamines, some nicotine decomposition products, and aromatic amines. Furthermore, decay products of radon from the tobacco and from other sources adsorbed on some particles in indoor air might contribute to the carcinogenic potential of ETS.

SS is a major contributor to ETS. Respiratory environments that are polluted with SS contain measurable amounts of nicotine and other toxic agents, including carcinogens. We lack data on the presence and concentrations of many of the known SS components in polluted, enclosed environments. The concentrations of toxic agents of ETS are governed primarily by the amount of tobacco smoked, the degree of ventilation, and the volatility of the agents. Future studies should concentrate on the analysis of toxic and carcinogenic agents in smoke-polluted environments.

What Is Known
  1. SS is the aerosol that is freely emitted into the air from the smoldering tobacco products between puffs.

  2. ETS consists of diluted SS, exhaled MS, smoke that escapes from the burning cone during puff-drawing, and vapor-phase components (such as carbon monoxide) that diffuse through cigarette paper into the environment. However, secondary reactions can occur before a nonsmoker inhales ETS, such as aging, volatilization of nicotine, and adsorption of radon daughters on particles.

  3. Undiluted SS contains higher concentrations of some toxic compounds than undiluted MS, including ammonia, volatile amines, volatile nitrosamines, nicotine decomposition products, and aromatic amines.

  4. Conventional cigarette filter tips primarily influence the yield of MS, but have little impact on the yield of SS. Highly

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 2–10 Concentrations of Toxic and Carcinogenic Agents in Cigarette Mainstream Smoke and ETS in Indoor Environmentsa

Agentc

Mainstream Smoke from Nonfilter Cigarette

Inhaled as ETS Constituent During 1 Hour: Range

Exceptionally High Valuesb

Weight

Concentration

Weight

Concentration

Weight

Concentration

CO

10–23 mg

24,900–57,400 ppm

0.6–13 mg

1–18.5 ppm

22 mg

32 ppm

NO

100–600 µg

230,000–1,380,000 ppb

7–88 µg

9–120 ppb

144 µg

195 ppb

NO2

<5 µg

<7,600 ppb

24–86 µg

21–76 ppb

119 µg

105 ppb

Acrolein

60–100 µg

750,000–125,000 ppb

80–69 µg

6–50 ppb

110 µg

80 ppb

Acetone

100–250 µg

120,000–300,000 ppb

210–710 µg

150–500 ppb

3,400 µg

2,400 ppb

Benzened

12–48 µg

11,000–43,000 ppb

12–190 µg

6–98 ppb

190 µg

98 ppb

NDMAe

10–40 ng

9–38 ppb

6–140 ng

0.003–0.077 ppb

140 ng

0.072 ppb

NDEAe

4–25 ng

3–17 ppb

<6–120 ng

<0.002–0.05 ppb

120 ng

0.05 ppb

Nicotine

1,000–2,500 µg

430,000–1,080,000 ppb

0.6–30 µg

0.15–7.5 ppb

300 µg

75 ppb

BaPf

20–40 ng

5–11 ppb

1.7–460 ng

0.00027–0.074 ppb

460 ng

0.074 ppb

aValues for inhaled ETS components calculated from values in Tables 2–4 through 2–9 and respiratory rate of 10 L/min. Data from unventilated interiors of automobiles excluded (Badre et al., 1978). Concentrations for MS are calculated by diluting weights given in volume of 350 ml, that is 10 puffs at 35 ml/puff.

bChosen to classify reported data that require confirmation.

cNDMA=N-nitrosodimethylamine; NDEA=N-nitrosodiethylamine; BaP=benzo[a]pyrene.

dHuman carcinogen, according to International Agency for Research on Cancer (Vainio et al., 1985); suspected carcinogen, according to American Conference of Governmental Industrial Hygienists (1985).

eAnimal carcinogen according to the International Agency for Research on Cancer (Vainio et al., 1985).

fSuspected human carcinogen according to the International Agency for Research on Cancer (Vainio et al., 1985) and according to the American Conference of Governmental Industrial Hygienists (1985).

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

active filter tips, especially perforated ones, also affect the yield of components in SS.

  1. Radioactive decay products in tobacco itself, for instance, Pb-210 and Po-210, and short-lived radon daughters adsorbed on smoke particles in indoor air can contribute to the carcinogenic potential of ETS.

  2. ETS in indoor environments is accompanied by pollutants, such as nitrogen oxides and carbon monoxide, derived from other sources, including cooking stoves and space heaters. ETS contains measurable amounts of nicotine and other toxic agents, including carcinogens. The concentrations of toxic agents of ETS are governed primarily by the amount of tobacco smoked, the degree of ventilation, and the volatility of the agents.

  3. Nicotine, found in MS primarily in the particulate phase, occurs in ETS primarily in the vapor phase. Therefore, filters designed to reduce particles in the air will not substantially alter the nicotine concentration.

What Scientific Information Is Missing
  1. We lack data on the presence and concentrations of toxic and carcinogenic components in tobacco-smoke-polluted enclosed environments.

  2. The distributions of various agents in vapor and particulate phases of ETS are not well characterized. Further, the effect of air-cleaning systems on these distributions has not been studied. Distributions are important with respect to the carcinogenic potential of ETS.

  3. We need to examine the importance of the abundant release of amines into ETS. We lack analytic data on secondary reactions of amines in polluted air, such as N-nitrosation and condensation with other ETS components.

  4. The transfer of constituents other than nicotine from the particulate phase of SS to the vapor phase of ETS could be important with respect to the retention of ETS in the respiratory tract of nonsmokers.

  5. We do not know the extent to which nitrogen dioxide can contribute to endogenous nitrosation in nonsmokers as a constituent of the respiratory environment. Endogenous nitrosation leads to nitrosamines in exposed subjects.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
  1. We need studies to determine the extent to which ETS differs from MS in ways related to health and their relative toxicities.

  2. We should analyze toxic and carcinogenic agents in smoke-polluted environments, especially enclosed natural environments, and their uptake by nonsmokers.

  3. Research should be conducted on interactions between ETS and radon daughters, especially as radon daughters can adhere to RSP, and can thereby enter the lung.

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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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3
In Vivo and In Vitro Assays to Assess the Health Effects of Environmental Tobacco Smoke

INTRODUCTION

Suitable methods for assessing the potential for adverse health effects resulting from exposure to environmental tobacco smoke (ETS) are limited by the complexity of the composition of the mixture. In vivo and in vitro assays are commonly used to establish carcinogenicity and in some cases to extrapolate risks to humans. For complex mixtures such as ETS, these assays may be done on the mixture itself or on individual chemical constituents. Many properties of ETS change as the smoke “ages” after its initial generation. Aging probably affects the bioavailability, as well as physicochemical characteristics, of the smoke.

As inhalation is the primary route by which humans are exposed to tobacco smoke, it is obviously the preferred method of administration in animal models for evaluating the toxicological properties of both cigarette smoke and ETS. While extensive inhalation studies have been performed on the toxicological properties of mainstream cigarette smoke (MS), far fewer studies have been performed on sidestream smoke (SS) and ETS. The selection of appropriate animal models requires familiarity with exposure systems, as well as with basic anatomical differences between the model and human respiratory tracts.

Methods other than inhalation, such as in vitro assays, have been developed for the evaluation of MS. A few of these methods have been applied to the assessment of the relative toxicological properties of SS versus MS. These methods are frequently criticized because of differences in the way the smoke constituents

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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are presented to the test system as compared with that which occurs in the human situation. Despite these limitations, the use of cigarette smoke condensate (CSC) from MS has provided insight into the relative carcinogenic potential of various constituents in the MS of cigarettes. Similar studies using suitable condensates from SS and aged ETS could provide additional data on the effects of ETS.

IN VIVO ASSAYS ON ENVIRONMENTAL TOBACCO SMOKE

Exposure Methods in Laboratory Research

Several methods are available to evaluate the potential health effects of inhaled pollutants. Some common ones are whole-body exposure, head-only exposure, nose- or mouth-only exposure, lung-only exposure, or partial-lung exposure. Since the primary objective of an inhalation experiment is to determine the effects of the test substances or mixture on the respiratory system, it is preferable to eliminate or limit exposure through the skin or through ingestion (such as through contact with materials deposited on the fur or contaminated food and water).

Three methods have been used to determine the amount of material deposited in the respiratory tract (Phalen, 1984): direct measurement, calculations using airborne concentrations and uptake models, and calibration of the exposure apparatus using tracer substances. Direct measurement requires analysis of major components and their metabolites in tissues as well as in urine and feces or measurement of the amounts of material in the inspired and expired air. Aside from calculating dose based upon particle aerodynamic size and physiological data on lung function of experimental animals, tracers can provide reasonable estimates of exposure.

Inhalation exposure chambers are used for those studies in which whole-body exposure is desired. The ability to expose a large number of animals at one time and the absence of a need to restrain or anesthetize the animals are among the advantages in using this approach. There are, however, several major disadvantages. The animals are exposed through skin absorption and mouth ingestion and, in prolonged instances, by food and possibly water contamination. Animals tend to avoid exposure in such

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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chambers by huddling together or covering their noses with their own fur. Losses of particulate aerosols to the interior walls of the chambers are also frequently a problem.

Head-only exposure systems eliminate many of these problems. The disadvantages of these systems are that the animal must be restrained and is stressed or anesthetized, and there is difficulty in forming an adequate seal.

Nose- or mouth-only exposure systems further limit exposure to the oral cavity and the respiratory tract. Masks or the use of catheters in the nose are generally used with larger animals. Lung and partial-lung-only exposure systems such as endotracheal tubes are employed to bypass the upper respiratory tract and to directly expose the lung. Most of these methods require that the animal be anesthetized, which may alter normal respiration. Other disadvantages include disruption of normal airflow by the presence of tubes in the airways and the loss of normal humidification and thermal regulation of the inspired air caused by bypassing the upper respiratory tract.

Intratracheal instillation is an alternative to inhalation for evaluating the effects of individual compounds on the respiratory system. While there are several advantages in employing this bioassay technique, it is also known that the distribution of test material to respiratory tissue may differ from that which would be obtained by actual inhalation exposures. Instillation of an aqueous suspension of radiolabeled particles resulted in a less uniform deposition than inhalation (Brain et al., 1976).

Animal Models in Inhalation Studies

The selection of an appropriate animal model for inhalation studies with potentially toxic agents is compounded by the fact that one of the major functions of the mammalian sensory apparatus is to limit the exposure to toxic agents either by altering breathing or by producing avoidance behavior (Alarie, 1973; Wood, 1978). Also, the selection of animal species and strains for inhalation exposure studies requires thorough evaluation. The use of several (at least three) animal species, several dose levels, and animals that metabolize the suspect toxin in a similar manner to humans is recommended for those studies that attempt to evaluate human hazards (Stuart, 1976). The appropriate animal model should have (1) a similarity to the human respiratory tract with

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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respect to anatomy, physiology, and susceptibility; (2) a life span appropriate for the proposed study; (3) a sensitivity to certain classes of toxic agents; (4) anatomical or physiological properties that could lead to increased precision in empirical measurements; (5) an existing data base; (6) a documented history of appropriate procedures; and (7) an adaptability for generating data that might be used for mathematically modeling the animal system and its responses to airborne particulates.

Results of Inhalation Studies

Inhalation studies on the carcinogenicity of MS have been performed on a variety of laboratory animals. The early studies with rodents have been previously reviewed (Wynder and Hoffmann, 1967; Mohr and Resnik, 1978). More recent studies verify these findings for several animal species exposed to whole smoke or MS. A few studies have exposed mice to the vapor phase of fresh MS, and one (see below) exposed mice to the vapor phase of flue-cured MS. Because commonly utilized filter systems do not remove many of the vapor-phase constituents, studies contrasting the effects of exposure to whole smoke with the effects of exposure to the gas phase should throw some light on the possible health effects of ETS.

Male and female C57Bl mice (100 in each group) were exposed nose only for 12 minutes daily to the gas phase of smoke of cigarettes prepared from flue-cured tobaccos (Harris et al., 1974). The treated mice had lung tumors and emphysema, independent of the tumors, which were not found in control mice.

A total of 219 C57Bl and 186 BLH mice were exposed to the gas phase of cigarette MS. The particulate matter was removed by passing the smoke through a Cambridge filter. The animals were exposed to the gas phase of 12 cigarettes for 90 minutes daily over 27 months. The percentages of mice with lung adenomas were 5.5% and 32% in the smoke-exposed C57Bl and BLH mice, as compared with 3.4% and 22% for their respective controls (Otto and Elmenhorst, 1967). Therefore, it appears that there are carcinogenic constituents in the vapor phase of the smoke.

Using Snell’s mice, similar studies evaluated the toxicological properties of whole MS and the gas phase of MS. In these studies, the animals were housed in individual chambers during the exposure (Leuchtenberger and Leuchtenberger, 1970). There was

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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a significant difference (p<0.1) in the incidence of pulmonary tumors between the animals exposed to whole smoke and control animals. The difference was greater (p=0.005) for animals exposed to only the gas phase of cigarette smoke as compared with the same controls, so that the rate of tumors among the gas-phase-exposed animals was greater than among the whole-smoke exposed animals.

In Vivo Bioassays Other Than Inhalation

Alternative methods have been used to assess the relative chronic toxicity of cigarette MS in an attempt to reduce the cost and technical difficulties associated with inhalation experiments. The most common approach has been to use the CSC in bioassay procedures. In preparing the condensate, many of the volatile and semivolatile components are lost. In addition, it is not known how the aging of the CSC may affect chemical composition and biological activity.

To date, only one study has examined the carcinogenic potential of the condensate of SS of cigarettes (Wynder and Hoffmann, 1967; International Agency for Research on Cancer, 1986). Cigarette “tar” from the SS of nonfilter cigarettes, which had settled on the funnel covering a multiple-unit smoking machine, was suspended in acetone and applied to mouse skin for 15 months. Fourteen of 30 Swiss-ICR mice developed benign skin tumors, and 3 had carcinomas. In a parallel assay of MS from the same source, a 50% CSC:acetone suspension applied to deliver a comparable dose of CSC to 100 Swiss-ICR female mice led to benign skin tumors in 24 mice and malignant skin tumors in 6. This indicates that the smoke condensate of SS has greater tumorigenicity per equivalent dose on mouse skin than MS “tar” (p<0.05; Wynder and Hoffmann, 1967).

IN VITRO ASSAYS ON ENVIRONMENTAL TOBACCO SMOKE

Several short-term bioassays have been performed to evaluate the genotoxicity of cigarette MS. These studies have been the subject of two recent reviews (DeMarini, 1981; Obe et al., 1984). While most of them have evaluated the effects of CSC, some have attempted to evaluate either the gas phase or the whole smoke.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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The most commonly employed assay for mutagenic activity employs various strains of Salmonella typhimurium. Whole smoke as well as CSC from four types of tobacco were found to be mutagenic in S. typhimurium TA1538 (Basrur et al., 1977). Recent studies have shown that SS is also mutagenic in a system where the smoke was tested directly on the bacterial plates (Ong et al., 1984). They support extensive assays performed on CSC that indicate that tobacco smoke has significant mutagenic potential and show that the particulate matter of SS is likely to be a significant contributor to the mutagenic activity of indoor air particulate matter (Bos et al., 1983; Lofröth et al., 1983). Thus, similar mutagenic activity for the CSC of SS would be expected.

In another study (Lewtas et al., in press), condensate from air polluted with ETS for 10 hours was used in an assay employing S. typhimurium. The average indoor air mutagenicity per cubic meter was significantly correlated with the number of cigarettes smoked.

Another in vitro assay measures the number of sister-chromatid exchanges (SCEs) in human lymphocytes. Valadand-Barrieu and Izard (1979) used a solution of the gas phase from cigarette MS. They showed that this solution induced a significant dose-related increase in SCEs.

SUMMARY AND RECOMMENDATIONS

Sufficient data are not available to assess the relative genotoxicity and toxicity of whole ETS. A few isolated reports have dealt with the genotoxicity of SS and ETS, and the relative toxicity of MS and SS. In order to evaluate ETS, it is suggested that in vitro genotoxicity assays in at least two systems should be done with ETS per se as well as with its particulate matter. These assays under controlled and, subsequently, under field conditions should not be limited to freshly generated ETS, but should also attempt to determine effects of various degrees of air dilution and aging. In a comprehensive analytical approach, data should be generated to determine systematically the concentrations of toxic and tumorigenic agents in various milieus with ETS. At the same time, it may be useful to examine the uptake of tobacco-specific agents as well as the mutagenicity of the urine of nonsmokers exposed to ETS. All of these measures should be considered in the context of detailed exposure histories.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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What Is Known
  1. The lungs of various species have different physiological properties, making each of them the experimental species of choice only for certain situations, depending on the objective of the research study.

  2. ETS and SS have been shown to be mutagenic in a system where the smoke was tested directly on bacterial plates.

  3. The extensive studies of MS can serve as a guideline for the evaluation of ETS. Many of the constituents in the smokes are similar. Despite the limitations of extrapolating from various bioassays to man, the use of CSC from MS has provided insight as to the contribution of various components to the carcinogenic potential of MS from cigarettes.

  4. In the only study reported to date using SS condensate, SS condensate was shown to be more carcinogenic than MS condensate.

What Scientific Information Is Missing
  1. Only a few laboratory methods have been applied toward the assessment of the relative toxicological and genotoxic properties of SS generated from cigarettes and, more importantly, of ETS. Research is needed to clarify the appropriate methods for estimating genotoxicity and to isolate and identify the active agents in body fluids of ETS-exposed nonsmokers.

  2. Comparative inhalation studies with MS, SS, and ETS are still needed. Such assays, while not duplicating human exposure patterns, would provide more definitive information about the relative carcinogenic potential of SS in comparison to the MS of the same cigarettes.

  3. The aging of the atmosphere in which ETS occurs can have a profound effect on its chemical composition, physical characteristics, and overall biological effects. Therefore, studies of aged ETS are needed.

  4. Where exposure histories can be specified clearly, validation and quantitative determination of genotoxic markers for substances in ETS that also occur in the environment would be of value for measuring dose of ETS.

  5. In examining the effects of MS, many research workers have used condensates of the smoke painted on the shaved skin of mice.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Similar work with skin painting has not been done with ETS and would be of value for assessing the differential toxicity of ETS and MS.

  1. In vitro assays are needed for estimation of the tumor promotion and cocarcinogenic effect of ETS. In vitro tests are quicker than in vivo tests, and enough material can not be collected to do in vivo tests.

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Leuchtenberger, C., and R.Leuchtenberger. Effects of chronic inhalation of whole fresh cigarette smoke and of its gas phase on pulmonary tumorigenesis in Snell’s mice, pp. 329–346. In P.Nettesheim, M.G. Hanna, Jr., and J.W.Deatherage, Jr., Eds. Morphology of Experimental Respiratory Carcinogenesis. Proceedings of a Biology Division, Oak Ridge National Laboratory, Conference, Gatlinburg, Tenn., May 13–16, 1970. Washington, D.C.: U.S. Atomic Energy Commission, 1970.

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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Mohr, U., and G.Resnick. Tobacco carcinogenesis, pp. 263–367. In C.C. Harris, Ed. Pathogenesis and Therapy of Lung Cancer. New York: Marcel Dekker, 1978.


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Valadaud-Barrieu, D., and C.Izard. Action de la phase gazeuse de fumée de cigarette sur le taux d’echanges des chromatides-soeurs du lymphocyte humain in vitro. C.R. Acad. Sci. (Paris) 288:899–901, 1979.


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Wynder, E.L., and D.Hoffmann. Tobacco and Tobacco Smoke: Studies in Experimental Carcinogenesis. New York: Academic Press, 1967. 730 pp.

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

II
ASSESSING EXPOSURES TO ENVIRONMENTAL TOBACCO SMOKE

Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 36
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 37
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 38
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 40
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 41
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 42
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 44
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 45
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 46
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 47
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 48
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 49
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 50
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 51
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 52
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 53
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 55
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 56
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 57
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 58
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 59
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
Page 61
Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
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Suggested Citation:"PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Page 64
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This comprehensive book examines the recent research investigating the characteristics and composition of different types of environmental tobacco smoke (ETS) and discusses possible health effects of ETS. The volume presents an overview of methods used to determine exposures to environmental smoke and reviews both chronic and acute health effects. Many recommendations are made for areas of further research, including the differences between smokers and nonsmokers in absorbing, metabolizing, and excreting the components of ETS, and the possible effects of ETS exposure during childhood and fetal life.

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