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

Chapter: ASSESSING EXPOSURES TO ENVIRONMENTAL TOBACCO SMOKE

« Previous: PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE
Suggested Citation:"ASSESSING EXPOSURES TO 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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4
Introduction

Exposure to a variety of air contaminants has been shown to produce adverse health and discomfort responses in humans. In another report from the National Academy of Sciences (NRC, 1985), the methodological issues of studying exposures to air pollutants and subsequent health effects are discussed in detail. This part of the report considers issues relevant to assessing exposure to ETS. Ideally, evidence for health effects in humans should be demonstrated in epidemiologic studies that are consistent with a plausible hypothesis across a range of exposures or doses. However, many epidemiologic studies have substantial uncertainties associated with exposure variables. A framework for assessing exposures to environmental tobacco smoke (ETS) is discussed below. A variety of approaches to current and historic exposures to ETS, such as personal monitoring, locational monitoring, questionnaires, and biologic monitoring, are presented.

Concentrations of air contaminants exhibit pronounced spatial and temporal variations, regardless of the microenvironments in which they are found (outdoors, residential, industrial, etc.). Ideally, identifying the air contaminant or class of contaminants implicated in producing adverse health or comfort effects is essential in designing an air-monitoring program. In practice, however, it is often necessary to monitor a class of contaminants (for instance, total mass of respirable particles) or a proxy contaminant (for instance, nicotine), when the specific air contaminant producing the adverse impact can not be identified or easily measured. The air contaminants associated with ETS are comprised of a

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

broad range of many vapor- and particle-phase inorganic and organic chemicals noted in Chapter 2, some of which can undergo pronounced physicochemical changes. Assessing impact on human health and comfort requires the identification of proxy air contaminants for ETS that will permit a determination of exposure in a background of contaminants from other sources (see Chapter 5).

In epidemiologic studies of air contaminants, it is important to specify exposure to specific particulates or gases on a time scale corresponding to the health or comfort effect sought. The impact of exposure to an air contaminant should, ideally, be evaluated in terms of the biologic dose of the contaminant or its metabolites received by the target tissue. In most cases, this is not practical. The uptake, distribution, metabolism, and site and mode of action of the contaminant in humans is neither well understood nor easily measured. Moreover, dose cannot be directly assessed. Factors affecting the uptake of air contaminants include physical characteristics of the contaminant, as well as physiological characteristics and activity levels of the exposed person (see Chapter 7). In the absence of an ability to measure or specify the dose of a contaminant received, exposures to air contaminant(s) are assessed by either using biological markers, measured in the subject population, or by measuring the air-contaminant concentrations in the physical environment (Figure 4–1).

Exposures to airborne contaminants can be assessed by three basic approaches (Figure 4–1):

  • personal air-contaminant monitoring,

  • modeling, based on air sampling, time-activity patterns, and questionnaires, and

  • biological markers.

Personal monitoring employs samplers (worn by subjects) that record the integrated concentration individuals are exposed to in the course of their normal activity for time periods of several hours to several days (see Chapter 5).

The modeling approach employs the use of stationary monitors to measure the air-contaminant concentrations in a number of microenvironments. These measured concentrations are combined with time activity patterns (time budgets) to determine the average exposure of an individual as the sum of the concentrations in each environment weighed by the time spent in that environment.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

FIGURE 4–1 Flow diagram of components for assessing human exposures to air contaminants from environmental tobacco smoke.

Questionnaires are employed in two capacities: (1) to provide information on the physical properties of each environment, including source use parameters, in order to model the concentration of air contaminants in the microenvironment, thus permitting a prediction of air-contaminant concentrations in spaces not monitored; and (2) to provide a simple categorization of exposure levels, such as exposed versus unexposed or none versus low versus high.

Questionnaires have been used to categorize subjects’ exposure to ETS in all studies of risk of chronic lung disease reported to date. Chapter 6 discusses the use of questionnaires to categorize ETS exposures.

Chapter 7 reviews assumptions required to estimate exposure-dose relationships for ETS and gives an approximation to the dose received under a specific situation.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Chapter 8 examines the use of biological markers, such as urinary cotinine, as indices of exposure to ETS.

There are several factors (Figure 4–1) that determine the composition and level of ETS air contaminants in the indoor environments. Determining the range of values for each of these factors will lead to an understanding of their impact on ETS exposures. Efforts to modify or eliminate exposures to ETS must focus on the factors that control the concentrations in the physical environment, since these factors result in the exposure that relates to the adverse health or comfort effect.

REFERENCE

National Research Council, Committee on the Epidemiology of Air Pollutants. Epidemiology and Air Pollution. Washington, D.C.: National Academy Press, 1985. 224 pp.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

5
Assessing Exposures to Environmental Tobacco Smoke in the External Environment

Environmental tobacco smoke (ETS) is composed of more than 3,800 compounds. The emitted compounds are found in vapor or particulate phases, or in some cases both. Volatile material may evaporate from particles within seconds to minutes after emission (e.g., nicotine, see Chapter 2). ETS has not yet been adequately characterized such that its chemical and physical nature can be clearly defined. The concentration of any individual or group of ETS constituents in an enclosed space is a function of: (a) the generation rate of the contaminant(s) from the tobacco, (b) the source consumption rate, (c) the ventilation or infiltration rate, (d) the concentration of the contaminant(s) of interest in the ventilation or infiltration air, (e) the degree to which the air is mixed, (f) the removal of the contaminant(s) by surfaces or chemical transformations, and (g) the effectiveness of any air-cleaning devices that may be in use. Exposure to ETS takes place in many settings—such as public, industrial, nonindustrial occupational, and residential buildings—and is a function of the time an individual spends in a microenvironment and the concentration of the ETS constituents in that environment. ETS exposures can be determined either by extrapolation from fixed-location monitoring survey instruments that are portable or by direct personal monitoring, using lightweight pumps and filters worn by subjects.

This chapter will consider the methodology and data available for assessing human exposures to ETS in the physical (external) environment, including the suitability of proposed tracers or proxy air contaminants that would be representative of ETS, available data on ETS exposure from personal monitoring and monitoring of

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

indoor environments, and the application of modeling to assessing ETS exposures.

TRACERS FOR ENVIRONMENTAL TOBACCO SMOKE

It is difficult to assess the ETS contribution to exposures because it usually exists in a complex mix of air contaminants from other sources. It is not practical, or possible, to monitor the full range of air contaminants associated with ETS, even under laboratory conditions. Chamber and field studies of ETS have monitored proxy contaminants as indicators of ETS. Most studies to date have been less than ideal because the component that was measured did not meet all the following criteria for an ETS tracer. A marker or tracer for quantifying ETS concentrations should be:

  • unique or nearly unique to the tobacco smoke so that other sources are minor in comparison,

  • a constituent of the tobacco smoke present in sufficient quantity such that concentrations of it can be easily detected in air, even at low smoking rates,

  • similar in emission rates for a variety of tobacco products, and

  • in a fairly consistent ratio to the individual contaminant of interest or category of contaminants of interest (e.g., suspended particulates) under a range of environmental conditions encountered and for a variety of tobacco products.

While a variety of measures have been used as proxies or tracers of ETS, no single measure has met all the criteria outlined above, nor has any measure been universally accepted or recognized as representing ETS exposure.

Carbon monoxide (CO) has been measured extensively both in chamber studies (Bridge and Corn, 1972; Hoegg, 1972; Penkala and De Oliveira, 1975; Weber et al., 1976, 1979a,b; Weber and Fisher 1980; Weber, 1984; Muramatsu et al., 1983; Leaderer et al., 1984; Winneke et al., 1984; Clausen, et al., 1985) and in occupied public and nonindustrial occupational indoor spaces (see Table 2–4) to represent ETS levels. Under steady-state conditions in chamber studies, where outdoor CO levels are known and the tobacco brands and smoking protocols constant, CO can be a reasonably reproducible indicator of ETS exposure. The variability

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

of CO production from tobacco combustion is not well known and may vary considerably as a function of a number of variables (puff volume, puff duration, temperature, etc.). The ratio of CO, a nonreactive contaminant, to the more reactive gas-phase contaminants in ETS and to reactive suspended particulate mass is not well established, particularly in the dynamic phase of smoking, that is, the non-steady-state phase. Chamber and field studies have indicated that, under realistic smoking conditions that would be encountered in residences or offices, the typical smoking and ventilation rates would produce CO levels well within the levels observed in the outdoor air or in the indoor air generated from the indoor sources, such as kerosene heater, gas stove, etc. Consequently, it is difficult to factor out the contribution of CO from ETS in any specific, uncontrolled situation. In areas where heavy smoking is experienced, and where other sources of CO do not exist, CO may provide a rough measure of ETS exposure because the CO produced by the tobacco combustion will dominate.

Both chamber and field studies (Table 5–1) have demonstrated that tobacco combustion has a major impact on the mass of suspended particulate matter in occupied spaces in the size range <2.5 µm, defined in this report as respirable suspended particulates (RSP). Suspended particulate mass is a major component of environmentally emitted tobacco smoke. Even under conditions of low smoking rates, easily measurable increases in RSP have been recorded above background levels (Table 5–1). The term RSP, however, encompasses a broad range of particulates of varying chemical composition and size emanating from a number of sources (outdoors, cooking indoors, etc).

Smoking is not the only source of particulate matter suspended in the indoor air. The apportionment of the measured RSP to tobacco combustion in an occupied space will not be accurate unless the RSP emission rates for a variety of brands of tobacco are similar under a variety of conditions and source use information is obtained. The variability of RSP emissions into the environment for a variety of brands of tobacco needs to be investigated, as does the relationship between the vapor and particulate phases of tobacco-combustion emissions under a variety of environmental conditions, such as different humidities, and under a variety of smoking conditions, such as subject smokers versus smoking machines.

Suggested Citation:"ASSESSING EXPOSURES TO 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 5–1 Particulate Levels Measured in Indoor Environments, Including Smoking and Nonsmoking Occupancy

Study

Type of Premise

Occupancy

Volume, m3

Ventilation Type/Rate

Monitoring Type/Time

Concentrations Mean (range), µg/m3

Comments

Brunekreef and Boleij, 1982

4 residences

NS

N/—

G/2 mo

55 (20–90)

TSP, repeat measures 0.2 mg

7 residences

S=1

N/—

G/2 mo

125 (60–250)

TSP sensitivity

14 residences

S=2

N/—

G/2 mo

152 (60–340)

TSP sensitivity

1 residence

S=3

N/—

G/2 mo

335 (—)

TSP sensitivity

Outdoors

G/2 mo

—(41–73)

 

Cuddeback et al., 1976

2 taverns

S=5–40

NS=5–260

T=10–300

N,M/1–6 ach

G/9 h

446 (233–986)

TSP ventilation estimated

Elliot and Rowe, 1975

3 arenas

NS

G/24 h

55 (42–92)

TSP

3 arenas

S

T=2,000–14,277

M/—

G/0.3 h

350 (148–620)

TSP

First, 1984

1 school

NS

M/—

P/—

20 (—)

TSP

 

8 public buildings

S

N,M/—

P/—

260 (40–660)

TSP

Hawthorne et al., 1984

11 residences

NS

150–674

M/0.18–0.96

QCMI/5–15 min (over 6 h)

9–40 (—)

RSP, winter/summer—no sources

8 residences

NS

150–674

M/0.26–1.98

QCMI/5–15 min (over 6 h)

12–46

RSP, winter/summer—sourcese

2 residences

S

150–674

M/0.27–1.47

QCMI/5–15 min (over 6 h)

96–106

RSP, winter/summer—sourcese+cig.

Leaderer et al., personal communication

3 public buildings

NS

163–1,326

M/0.37–5.6d

G/4–21 h

17.8 (9.1–32.2)

TSP, repeat measures, all var.

7 public buildings

1.7–4.57b

T=2–6

168–600

M/0.77–7.53d

G/2–24 h

205.1 (58–452)

Measured (160.0 peak)

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Moschandreas et al., 1981

Outdoors

G/24 h

17.0 (—)

RSP, TSP also measured

2 offices

G/24 h

16.8–20.2 (53 peak)

RSP, TSP also measured

5 residences

NS

T=2–6

N/0.5–1.3 ach

G/24 h

19.4–4.01 (118.9 peak)

RSP, TSP also measured

5 residences

S

N/0.5–1.3 ach

G/24 h

36.9–99.9

RSP, TSP also measured

Nitschke et al., 1985

Outdoors

G/168 h

11.3±6.0 (1–28)

RSP

19 residences

NS

315–1,021

N/—

G/168 h

26.0±22.6 (6–88)

RSP, repeat measures, source mixe

11 residences

S

290–800

N/—

G/168 h

59.2±38.8 (10–144)

RSP, repeat measures, source mixe

Parker et al., 1984

1 residence

NS

T=3

N/0.2–1.9 ach

0/24 h

<10 (—)

TSP

2 residences

S=1–2

T=3–4

N/0.2–0.7 ach

0/24 h

10–46 (—)

TSP

Repace and Lowrey, 1980, 1982

Outdoors

P/2 min

42.9 (22–63)

RSP, average of 2-min samples

27 Public buildings

0.13–3.54f

M/—

P/2 min

278 (86–1,140)

RSP, average of 2-min samples

Sexton et al., 1984

Outdoors

19 homes

G/24 h

17.0±1.6 (6–23)

RSP, repeat samples

24 residences

NSc

N/—

G/24 h

25.0±1.0 (13–63)

Used fireplaces

Spengler et al., 1981

Outdoors

G/24 h

21.1±11.9 (—)

RSP, repeat measures

35 residences

NS

N/—

G/24 h

24.1±11.6 (—)

RSP, repeat measures

15 residences

S=1

N/—

G/24 h

36.5±14.5 (—)

RSP, repeat measures

5 residences

S=2

N/—

G/24 h

70.4±42.9 (—)

RSP, repeat measures

Spengler et al., 1985

Outdoors

N/—

G/24 h

18±2.1 (—)

RSP, repeat measures

73 residences

NS

G/24 h

28±1.1 (—)

RSP, repeat measures

28 residences

S

G/24 h

74±6.6 (—)

RSP, repeat measures

Sterling and Sterling, 1983

1 office

S restr.

G (?)/—

25.5 (15–36)

TSP

22 offices

S

G (?)/—

31.7 (—)

TSP

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Study

Type of Premise

Occupancy

Volume, m3

Ventilation Type/Rate

Monitoring Type/Time

Concentrations Mean (range), µg/m3

Comments

U.S. Department of Transportation, 1971

8 domestic planes

S

T=27–110

M/—

G/1–1/4, 2–1/2 h

Not given (—)

TSP

20 military planes

S

T=165–219

M/—

G/6–7 h

<10–120 (—)

TSP

Weber and Fischer, 1980

44 offices

S

N,M/—

P/2 min (30 ea)

133±130 (962 peak)

RSP, minus background level

aActive smokers per 100 m3.

bGrams of tobacco consumed.

cSome smoking was reported during 9 of the 280 samples.

dMeasured during 24-h periods by the perfluorocarbon tracer technique.

eSome residences had combinations of sources (kerosene heaters, wood stoves, etc.) and no cigarettes.

fActive smokers density per 100 m3.

ABBREVIATIONS:

ach=Air changes per hour

G=Gravimetric

M=Mechanical ventilation

N=Natural ventilation

NS=No smokers

O=Optical monitor

P=Piezoelectric balance

QCMI=Quality Crystal Microbalance Cosade Impactor

RSP=Respirable suspended particles

S=Smokers

T=Total occupants

TSP=Total suspended particles

restr.=building with smoking restrictions

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Nicotine exhibits many of the properties necessary to serve as a potential marker for ETS. It is unique to tobacco smoke, is a major constituent of the smoke, and occurs in environmental concentrations that are easily measurable. It has been used as a marker for ETS in several studies (Table 2–5). The major problems with using nicotine are: (a) the ratio of nicotine [recently found to be in vapor phase in ETS (Eudy et al, 1985)] to other ETS constituents (RSP, in particular) for a variety of brands of tobacco is not known, (b) the reactivity rate (removal rate) of nicotine relative to other ETS constituents is not known, (c) particulate-or vapor-phase nicotine once deposited on surfaces may be re-emitted, and (d) until recently sampling methods for nicotine have not been efficient in collecting total nicotine (both vapor and particulate phase). Two new air-sampling methods for nicotine (Muramatsu et al., 1984; Hammond et al., in press) hold promise for obtaining total nicotine concentrations with the sensitivity and accuracy required for environmental air monitoring.

A number of aromatic hydrocarbons (benzene, toluene, benzo[a]pyrene, pyrene, etc.) have been measured in field studies (Galuskinova, 1964; Just et al., 1972; Perry, 1973; Elliot and Rowe, 1975; Badre et al., 1978) investigating the impact of smoking on indoor air quality. Many of these air contaminants have other important sources, indoors and outdoors, that make measured levels difficult to interpret. Therefore, the aromatic hydrocarbons generally are poor indicators of ETS alone. Controlled chamber studies that elevate the variability of emission of the compounds from a variety of brands of tobacco have not been carried out, and the ratios of these compounds to categories of ETS contaminants (for instance, RSP) have not been established.

Tobacco-specific nitrosamines and nitrogen oxides (Tables 2–6 and 2–9), acrolein and acetone (Tables 2–7 and 2–8), and polonium-210 have been measured as indicators of ETS. The low environmental concentrations, existence of other sources, reactivity of the tracer contaminants, and lack of data on the ratios of these contaminants to ETS contaminants for a variety of brands of tobacco limit their usefulness as indicators of ETS in indoor spaces.

Research efforts need to be directed toward identifying a tracer or proxy air contaminant for ETS that meets the four criteria outlined above. At present, RSP is widely used as a general measure of ETS exposure indoors, particularly if the measurements are limited to locations where the levels of RSP from other sources

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

are known and present at a low background concentration. The variability of RSP emissions for a number of brands of cigarettes, however, has yet to be evaluated.

PERSONAL MONITORING

Measurements of concentrations of air contaminants in the immediate breathing zone of an individual provide information on personal exposure. Personal monitoring can be accomplished with active samplers that integrate concentrations across a variety of locations or conditions using filters or vapor traps with subsequent laboratory analysis. Continuous portable monitoring instruments are available but have not been widely used. Particles are measured by light-scattering principles or frequency change as mass is deposited on a vibrating quartz crystal. For the most part, gases are measured using IR absorption or electrochemical reactions. Continuous-recording instruments have been utilized more for characterizing microenvironments than for direct measurements of personal exposures. Passive personal monitoring utilizes diffusion and permeation to concentrate gases on a collection medium for subsequent laboratory analysis. Both active and passive monitors have been employed in assessing an individual’s total exposure to individual or general categories of air contaminants. A discussion of the type, application, and usefulness of passive monitors to assess air contaminant exposures can be found in Elliott and Rowe (1975) and Wallace and Ott (1982).

A relatively small number of studies have utilized personal monitors to determine total exposures to ETS (Muramatsu et al., 1984; Schenker et al., 1984; Sexton et al., 1984; Spengler et al., 1985; Hammond et al., in press). In one study (Spengler et al., 1985) indoor (residential), outdoor, and personal 24-hour concentrations of RSP (measured in this study as particles with a 50% cut point of 3.5 µm) were obtained for a sample of 101 nonsmoking individuals living in Roane County, Tennessee. In the sample, 28 of those monitored reported some exposure to ETS in either the home or workplace (nonindustrial), while 73 reported no such exposure. Each participant was sampled on 3 nonconsecutive days. Personal exposures to respirable particles for the subgroup exposed to ETS and the subgroup not exposed to ETS are shown in Figure 5–1. Personal exposures to RSP were dominated by indoor levels of ETS. Those reporting passive smoke exposure had

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

FIGURE 5–1 Cumulative frequency distributions of RSP concentrations from central site ambient and personal monitoring of smoke-exposed and nonsmoke-exposed individuals. Reprinted with permission from Spengler et al. (1985).

mean personal respirable participate levels 28 µg/m3 higher than those without passive smoke exposure. Particulate levels for those exposed to ETS showed a large variation, with approximately 25% of the personal samples having RSP levels in excess of the EPA ambient standard for outdoor total suspended particles. The EPA standard, however, includes particles up to approximately 50 µm and does not specify chemical composition. A direct comparison with the EPA standard requires a consideration of average time exposed as well as concentration.

Sexton et al. (1984) conducted 24-hour personal monitoring for RSP for 48 nonsmoking individuals for 24 different residences. Samples were collected every other day, for a 2-week period, during a heating season in Vermont. Those individuals reporting exposure to ETS for more than 2 hours per day had RSP levels 18.4 µg/m3 higher than those who reported no exposure (50.1 µg/m3 versus 31.7 µg/m3).

In demonstrating a new method for the collection and analysis of nicotine in air, one study (Muramatsu et al., 1984) obtained personal-monitoring samples of nicotine for one nonsmoker in 53 nonindustrial indoor microenvironments, including offices, houses, restaurants, cars, buses, etc. The samples were collected over a 1-hour to 8-hour time period in each space and were specific for nicotine. A wide range of nicotine concentrations were reported,

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

from 1.76 µg/m3 in a laboratory to 83.13 µg/m3 in a car. It is difficult to interpret these results in terms of an integrated exposure for a large segment of the population, since the sampling scheme did not explicitly provide population estimates of exposure—that is, personal samples were obtained on a microenvironment basis for only one individual. Lacking good data for the ratio of total nicotine to RSP in ETS, it is difficult to estimate the RSP exposure levels. The data, however, do demonstrate that the variability of nicotine concentrations and the occurrence of high concentrations of other ETS components can be found in various microenvironments.

In an epidemiologic study of the health effects of diesel exhaust on railroad workers (Schenker et al., 1984), which included a control group of railroad office workers who were not exposed to diesel exhaust but were exposed to ETS, ETS was recognized as an important component of the respirable particulate exposures. Hammond et al. (in press) used a newly developed air-sampling and analytical method for measuring total nicotine in collected RSP personal samples to determine the contribution of ETS to the RSP levels measured. Their results indicated that the major portion of the office workers’ RSP exposure is due to ETS. Ratios of nicotine to RSP for a variety of brands of tobacco need to be established before absolute ETS exposures can be assessed.

Personal monitoring can provide a useful measure of an individual’s exposure to an air contaminant or class of contaminants over a period of several hours to several days. The usefulness of personal monitors for assessing ETS exposure would be greatly enhanced if the personal monitor were passive in nature and inexpensive. Personal and portable monitors, however, need to be evaluated to determine their usefulness in establishing ETS exposures associated with long-term adverse health outcomes, such as cancer. They may be useful in establishing ETS exposures, in a background of confounding air contaminants, associated with short-term effects.

A variety of sample collection and analysis methods has been used to monitor individual constituents and categories of contaminants found in ETS for both personal monitoring and air monitoring of spaces. While this report does not offer a review and evaluation of the monitoring methods that have been employed and are available, it should be clearly noted that the specificity and sensitivity of the measurement method must be evaluated to

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

assess the uncertainties in the measured concentrations. The constituents of ETS will exhibit a pronounced spatial and temporal distribution in an indoor space and among indoor environments, due to variations in smoking rates and building characteristics. In interpreting measured concentrations of ETS constituents, one must recognize the potential for pronounced spatial and temporal variations.

CONCENTRATIONS OF ENVIRONMENTAL TOBACCO SMOKE IN INDOOR ENVIRONMENTS

Various Environmental Tobacco Smoke Constituents

There is a sizable body of literature reporting on measurements of various constituents (acrolein, aromatic hydrocarbons, carbon monoxide, nicotine, etc.) of ETS in a variety of microenvironments. These studies have reported a wide range of concentrations of ETS-related air contaminants under conditions of normal space use (Tables 2–4 to 2–9). However, the majority of the measurements are of very limited use in assessing actual human exposures to ETS for a large segment of the population for the following reasons:

  • the representativeness of the air contaminant measured to the total ETS in the space is unknown;

  • the proxy air contaminant measured may have a variety of other potential sources that were not accounted or controlled for;

  • data were not collected on smoking rates or numbers of smokers; and

  • important building characteristics such as infiltration or volume were not recorded.

While these studies have indicated the range of concentrations of several ETS-related air contaminants that can be found indoors, they do not provide a sufficient basis on which ETS indoor exposure estimates can be made.

Particulate Levels and Smoking Occupancy

The most extensive and suitable data base for modeling ETS is the RSP (<2.5 µm) associated with ETS. This RSP comprises

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

FIGURE 5–2 Monthly mean RSP concentrations in six U.S. cities. Reprinted with permission from Spengler (1981).

a major general category of ETS contaminants and is produced in concentrations that are easily measured in occupied spaces where smoking occurs.

In a survey of more than 80 homes in six U.S. cities (Spengler et al., 1981), 24-hour gravimetric samples of RSP were collected every sixth day for up to 2 years in stationary samplers in each home and outdoors. The resulting data (monthly RSP means) aggregated by the number of smokers are shown in Table 5–1 and Figure 5–2. Homes without smokers exhibited RSP levels roughly equal to outdoor levels and followed outdoor trends. The presence of just one smoker in a home had a pronounced impact on RSP levels. Using regression analysis, the authors estimated that the impact on overall average RSP levels in a residence of a pack-per-day smoker was approximately 20 µg/m3. The impact of smoking in a home with central air conditioning was effectively doubled, presumably due to reduced air exchange.

Table 5–1 presents the range of RSP levels measured in a variety of indoor microenvironments for smoking and nonsmoking occupancies. It also indicates whether direct measures of the variables necessary for the model outlined in Equation 5–1 below, or necessary to explain the RSP levels measured, were recorded. These variables include, among others, ventilation, mixing, removal by surfaces, and smoking occupancy. Outdoor levels of

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

RSP or total suspended participates are generally lower than or equal to indoor levels in homes without smoking.

Smoking occupancy is strongly associated with elevated levels of RSP in a variety of indoor microenvironments at levels well above outdoor concentrations and indoor concentrations where there is nonsmoking occupancy. However, few studies have directly recorded the data on the parameters that are necessary to validate models for predicting RSP levels due to smoking occupancy (see section below). Even so, using a number of assumptions, data in Table 5–1 have been used for model validation by some studies (Repace and Lowrey, 1980, 1982).

MODELING

The process of assessing exposure and attributing it to various microenvironments requires knowledge of the time individuals spend in such microenvironments and the typical air-contaminant levels (average and peak) occurring in them. The nature of the health or comfort effect under study determines the time-average concentration of concern. A number of microenvironments have been identified (Moschandreas, 1981), and time-budget surveys have shown that most individuals spend more than 90% of their time indoors, that is, in residential, industrial, and nonindustrial occupational environments (Szalai, 1972). The indoor residential and nonindustrial occupational environments represent the major microenvironments in which exposure to ETS takes place.

Tobacco combustion is a major source category that affects the quality of the air indoors. The air-contaminant concentrations in an enclosed space resulting from tobacco combustion, and hence human exposures, are the result of a complex interaction of several interrelated variables (Figure 4–1), including source air-contaminant emission characteristics and source use, building characteristics, infiltration or ventilation rates, air mixing, loss terms (removal by surfaces or chemical transformations), and the efficiency of air-cleaning equipment. The interaction of these variables in determining the resultant indoor concentrations of ETS has typically been evaluated in both controlled laboratory (chamber and test house) studies and field studies within the theoretical framework of the general mass-balance equation (Turk, 1963; Shair and Heitner, 1974; Esmen, 1978; Ishizu, 1980; Repace and Lowrey, 1980; Leaderer et al., 1984).

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

The mass-balance equation may be applied to tobacco smoke as either an equilibrium model (time-independent) or a dynamic model (time-dependent). Equilibrium models rely on the assumption that many of the input parameters—such as source rates, removal or loss rates, and ventilation rates—are constant, even though these parameters in actuality may vary considerably in time. These models are useful in developing air-contaminant emission factors for ETS in controlled laboratory studies and in assessing long-term average exposures in given indoor microenvironments. Dynamic models are usually more flexible than equilibrium models and can provide information on short-term concentrations. They may be used to compare the sensitivity of results to variations of input parameters. Equilibrium models, when applied to field studies of ETS, require average information on the impact variables, while dynamic models require a great amount of detailed information obtained as a function of time. Dynamic and equilibrium models are useful in laboratory studies; equilibrium models are best suited to evaluating and predicting ETS concentrations in field studies, particularly when average concentrations over a period of days or longer are of interest.

Equilibrium Models for RSP

Laboratory and field studies typically utilize some form of a single-compartment equilibrium model to evaluate the input parameters to the mass-balance equation, to evaluate field-study data, and to project RSP concentrations from ETS indoors. These studies have reduced the general single-compartment mass-balance equation to the following simplified form.

(5–1)

where Ceq is the equilibrium concentration of RSP in a space expressed as micrograms per cubic meter (µg/m3) due to ETS, G is the RSP generation rate from tobacco combustion into the space in micrograms per hour (µg/hour), nv is the ventilation or filtration rate in air changes per hour (ach), ns is the loss rate of RSP due to surface removal in a space in air changes per hour, V is the volume of the space in cubic meters (m3), and m is the mixing rate expressed as a fraction. The above model assumes no air-cleaning devices, either in the space or recirculated air.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Under laboratory conditions, the input parameters can be controlled and evaluated. In conducting field studies or in estimating past RSP levels indoors, the values on the right side of Equation 5–2 have to be determined from available data. It should be emphasized that this equation assumes equilibrium conditions, and, to the extent that any of the generation or removal terms are intermittent (e.g., smoking rate) or variable (e.g., ventilation rate), errors are introduced.

Generation Rate

The generation rate of RSP for ETS is a function of the number of cigarettes smoked and the emission rate of RSP per cigarette. Few studies have investigated the RSP emission rate for SS plus exhaled MS, i.e., contributions to ETS. One recent study (Rickert et al., 1984) examined sidestream and mainstream emissions of tar, nicotine, and carbon monoxide in 15 brands of Canadian cigarettes with a range of advertised mainstream tar deliveries (0.7 to 17.0 mg tar/cigarette). The experiments utilized a single-port smoking machine and collected mainstream emissions and sidestream emissions, from a small chamber, onto Cambridge filters. The subsequently measured sidestream emissions of tar were found to average 24.1 mg/cigarette with a range of 15.8 to 36.0 mg/cigarette. These emissions were independent of mainstream emissions, which averaged 11.4 mg of tar per cigarette with a range of 2.5 to 19.4 mg/cigarette. Sidestream emissions were higher for ventilated brands.

RSP emission rates were developed for 10 brands of U.S. cigarettes with rated tar deliveries from 1.0 to 23.0 mg and for one standard cigarette (University of Kentucky #1R3F). The study (B.P.Leaderer, S.K.Hammond, and T.Tosun, personal communication) utilized a 34-m3 chamber in which the cigarettes were smoked by occupants at a prescribed rate in an effort to create realistic environmental conditions. RSP measurements were made over a 4-hour period during equilibrium conditions via collection of well-mixed room air on filters with subsequent gravimetric analysis. RSP emission levels were found to range from 18.0 to 35.4 mg/cigarette, with an average of 26.9±4.8 mg/cigarette.

Three brands of British cigarettes (very low tar, 1.5 mg; low tar, 12 mg; and medium tar, 18 mg) were evaluated for both mainstream and sidestream emissions of tar (U.K. Government,

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

1980). The average RSP sidestream emission rate measured was 24.5 mg/cigarette, with a range of 23.0 to 26.4 mg. This study utilized a small test chamber and a smoking machine. The emission by-products were collected onto Cambridge filters.

Only one study (Hoegg, 1972) reports mainstream and sidestream RSP levels for cigarettes prior to 1970. This test chamber study reported a sidestream particle emission rate of 25.8 mg/cigarette and mainstream particle emission rate of 36.2 mg/cigarette for one brand of cigarette.

Current data would suggest an overall RSP emission rate from ETS in the range of approximately 20 to 36 mg tar/cigarette. An accurate estimate of an average emission rate for modeling purposes requires the weighing of the above emission data by the sales-weighted average cigarette brand sold. Data are not available to estimate the historical trend, if any, in the RSP emissions for ETS.

Equation 5–1 assumes a constant, or near constant, source emitting over a sufficiently long time period to reach and maintain equilibrium conditions. In controlled experiments a constant rate of tobacco combustion is easily obtained. In practice, however, tobacco combustion rates in terms of numbers of cigarettes consumed over some period of time in different indoor environments is variable. In the absence of detailed data on cigarette consumption in a space, such as number of cigarettes smoked, time smoked, total weight of tobacco consumed, etc., estimates are required. For example, one smoker in a household smoking at a national average rate of two cigarettes/hour and 10 minutes/cigarette constitutes an intermittent source [G(t)dt]. A continuous source would be the smoking of six cigarettes/hour. Using a 26-mg/cigarette emission rate, the estimated total RSP emissions from the intermittent source, i.e., 52 mg/hour, would be represented as being emitted uniformly over a 1-hour period for the full averaging time considered. In large occupied spaces where smoking is permitted, such as nonindustrial occupational environments, estimates (Bridge and Corn, 1972; Jaffe, 1978; Repace and Lowrey, 1980) would indicate that, at any given time, 11% of the population would be smoking (one-third of the U.S. population are smokers, who are smoking at the rate of two cigarettes/hour and 10 minutes/cigarette). This would constitute a continous source. In practice, the smoking rate is probably highly variable in time. The RSP emissions from this

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

example would also be averaged over time to produce uniform average emission rates per hour. For the estimation of equilibrium conditions in Equation 5–1, G=NE, where N is equal to the number of cigarettes consumed per hour in a space and E is the number of milligrams of RSP emitted into the environment per cigarette. The assumption of a continuous source introduces errors in the estimated RSP concentration.

It is also important to note that the equilibrium model assumes that the source will be emitting contaminants over a sufficiently long period of time to achieve balance with the removal mechanisms (ventilation, removal by surfaces, and air cleaning). If Ct is the concentration at time t (in hours) then:

(5–2)

where Ceq is the equilibrium concentration and N is the effective removal rate (N=nv+ns). If the total impact of the removal rate, i.e., ventilation plus loss to surfaces, is equivalent to one ach, 85% of the equilibrium concentration would be obtained in 2 hours. Thus, to the extent that the source emissions do not combine over long periods of time, the equilibrium concentration will not be reached and maintained, introducing errors into the estimated or modeled RSP.

Ventilation/Infiltration

The supply of fresh air to a space by ventilation (air supplied by mechanical systems) or by infiltration (uncontrolled movement of air through cracks and unintentional openings in the building envelope) serves to reduce the levels of air contaminants generated by an indoor source.

Building codes adopted and enforced by local, state, and federal government agencies generally specify minimal acceptable ventilation criteria to be maintained in buildings. These codes are usually derived from standards that have been promulgated by authoritative bodies (American National Standards Institute, American Society of Heating, Refrigerating and Air-Conditioning Engineers, etc.). These standards are usually developed by consensus and are generally voluntary until adopted by municipal or state governments. The studies of Yaglou et al. (1936) formed the basis of minimum required ventilation rates that persisted until 1979. These studies reported ventilation rates (fresh odor-free

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

air) in cubic feet per minute per person (cfm/person) necessary to provide an acceptable odor environment. They found that, as occupant density increased, so did the required cfm/person ventilation rate. Because of the odor level, smoking occupancy required significantly more ventilation air. A minimum ventilation rate of approximately 10 cfm/person for nonsmoking occupancy and an occupant density of 400 ft3/person was recommended. Prior to 1936, minimum recommended ventilation rates were as high as 30 cfm/person.

In 1973, the American Society of Heating, Refrigerating and Air-Conditioning Engineers (ASHRAE) adopted and published Standard 62–73 (Standards for Natural and Mechanical Ventilation). This standard recommended ventilation rates for various residential and commercial spaces on an occupancy-density basis. In 1981, ASHRAE adopted Standard 62–81 (Ventilation for Acceptable Indoor Air Quality), which also recommended ventilation rates for various residential and commercial spaces on an occupancy-density basis but distinguished between smoking and nonsmoking occupancy. Modal ventilation rates in this standard equaled 35 cfm/occupant for smoking occupancy and 7 cfm/occupant for nonsmoking occupancy.

As noted in Equation 5–1, ventilation rates are incorporated as ach. ASHRAE 62–73 recommended from 15 to 25 cfm/person for general office space with an estimated 10 persons/1,000 ft2 density, while ASHRAE 62–81 recommended 20 cfm/person when smoking is permitted and a 5-cfm/person minimum for nonsmoking occupancy with an estimated 7 persons/1,000 ft2 density occupancy. Assuming full occupancy and an 8-ft ceiling, ASHRAE 62–73 ventilation rate ranges are 1.13 and 1.9 ach, while ASHRAE 62–81 recommends a rate of 1.3 ach for smoking occupancy and 0.26 ach for nonsmoking occupancy. When considered on a space-by-space basis for commercial or residential environments as recommended by either ASHRAE 62–73 or ASHRAE 62–81, the ach rates vary considerably, depending on the use of the space and whether smoking is permitted.

In estimating ach’s for inputs into Equation 5–1, to assess either current or past RSP concentrations in occupied space due to ETS, the following points should be kept in mind:

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×
  • There are no data to indicate the current or past distribution of ach’s currently are or have been in a variety of commercial spaces in which smoking is or has been permitted.

  • Air-exchange rates are calculated from cfm/person rates specified in the standards for full occupancy. To the extent that occupancy is less than or greater than the designed figure, the cfm/person could be significantly different.

  • Ventilation codes are equivalent to design standards. In actual practice, the heating, ventilation, and air-conditioning (HVAC) system may not operate as designed. Interior alterations, modifications in occupancy, maintenance, and repair of equipment, and operator practice can significantly affect the performance of the HVAC system.

Air-infiltration values in housing are induced by differences in pressure across the structure envelope. Limited data exist to indicate what the current or past distribution of air-exchange rates in houses in the United States are or what the intra- or interseasonal variations are. One study of seasonal infiltration rates of 312 houses in North America (Grimrsud et al., 1982; Figure 5–3) found a median value of 0.5 ach. This study was based on new energy-efficient houses. Another study (Grot and Clark, 1979; Figure 5–3) of 266 low-income houses in North America found the median seasonal air-exchange rate to be 0.9 ach. Air-infiltration rates for both studies were taken without occupants in the houses. Normal activities of occupants would add an average 0.10 to 0.15 ach to the values reported in these two studies.

Ventilation or infiltration rates in commercial and residential buildings can vary by an order of magnitude among and within buildings, season to season and within a season. Unfortunately, there are few data available that would allow for an accurate estimate of the distribution of air-exchange rates in commercial and residential spaces currently or over the past several years. A range of 0.4 to 1.5 ach would seem reasonable.

Removal by Surfaces

Next to ventilation, the major mechanism for removal of suspended particulate matter is surface deposition. Surface deposition of particles indoors is a function of several variables, including particle size and composition, temperature, humidity, type and quantity of surface material in a room, surface-to-volume rates,

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

FIGURE 5–3 Histograms of infiltration values in two different samples of North American housing, (a) Average seasonal infilitration of 312 recently constructed houses; the median value is 0.5 air changes per hour (ach). Reprinted with permission from Grimsrud et al. (1982). (b) Average seasonal infiltration of 266 older low-income houses; the median is 0.9 ach. Reprinted with permission of Grot and Clark (1979).

and turbulence. In laboratory studies under conditions of ideal mixing, surface-deposition rates (h−1) for ETS were found to vary from an equivalent 0.1 h−1 to 1.8 h−1 (Leaderer et al., 1986). The greater the degree of turbulence introduced into the chamber and the higher the surface-to-volume ratio, the higher the surface deposition.

One recent chamber study evaluated the importance of materials (rugs, wall paper, and painted wall board), surface area of

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

materials, temperature, humidity, and turbulence on the deposition rate of RSP generated by tobacco combustion under conditions of ideal mixing (Leaderer et al., 1986). In these experiments, the deposition rate of RSP was determined by monitoring the decay of RSP and carbon dioxide (injected into the chamber) under the experimental conditions examined. The difference between the RSP and carbon dioxide (nonreactive tracer gas) represented the RSP deposition rate. This study found the most pronounced impact on deposition in this chamber to be the air-recirculation rate (fresh-air-ventilation rate held constant) or turbulence. The type and quantity of material, temperature, and humidity were also found to impact particle deposition in a significant way. The results of this study indicate that a particle deposition rate of 0.2 to 0.8 h−1 for ideal mixing might typically be encountered in occupied spaces.

Mixing

Once released into an enclosed space, air contaminants move through it by dispersion. Dispersion determines where the high and low concentrations of the contaminant will occur. Dispersion is controlled by diffusion, which is the movement from areas of high to low concentrations, and by mixing, which is the movement of air in the space. When ideal mixing occurs in a space, i.e., m=1 in Equation 5–1, no spatial gradient of an air contaminant like RSP exists, and the full effectiveness of ventilation and sink rates in removing the contaminant is seen. In controlled laboratory studies, ideal mixing is easily obtained through the use of mixing fans or the rapid recirculation of the air. In occupied spaces, however, ideal mixing is hardly ever obtained unless a great deal of turbulence is introduced to the space and the supply- and exhaust-air system is carefully designed. Less than ideal mixing can result in a pronounced concentration gradient of a contaminant in the space. The ventilation rates and removal by surfaces under those conditions are not as effective in lowering air-contaminant levels. The mixing term is usually defined as the ratio of effective ventilation to theoretical ventilation.

In an occupied space, the value of the mixing factor is affected by the source and its use, room geometry, air supply and exhaust design, air-flow rates, obstacles in a room, and activity of the occupants. In addition, the mixing factor is specific for a precise

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

location. No data exist that would indicate the distribution of the values for the mixing factor in occupied spaces. A limited number of studies show a range of mixing factors from 0.1 to near 1.0 (Brief, 1960; Kasuda, 1976).

Volume

The volume of the space in which smoking occurs is highly variable. It can range from a few cubic meters in a car to several thousand cubic meters in large auditoriums or sports arenas. The highest RSP levels from ETS will tend to occur in smaller spaces with high smoking rates.

Predicting Environmental Tobacco Smoke Exposures from Tobacco Combustion

Utilizing Equation 5–1, expected RSP concentrations indoors from ETS can be estimated for a range of the input parameters that realistically can be expected under normal smoking occupancy. Figures 5–4 and 5–5 allow for the easy calculation of RSP levels due to ETS as a function of Smoking rate, ventilation, sink rate, mixing, and volume of the space (see the example outlined in the legends of these figures). The calculations treat the spaces of concern (e.g., multiroom home or a single room in a house) as a single compartment with no air-cleaning devices. The total amount of RSP (in milligrams) from ETS can be determined in Figure 5–5 as a function of the smoking rate and effective removal rate (N). The removal rate is equal to the sum of ventilation plus removal by surfaces times the mixing factor. The total amount of RSP calculated from Figure 5–4 is then entered into Figure 5–5 to determine the RSP concentrations (in micrograms per cubic meter) expected for a given volume of space. The calculations used to generate these figures assume that:

  • an average total RSP emission rate is 26 mg/cigarette,

  • the emissions are nearly consistent and averaged over a 1-h period,

  • near steady-state or equilibrium conditions are reached quickly,

  • no air-cleaning devices are in use,

  • background levels of RSP in a space are zero, and

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

FIGURE 5–4 Diagram for calculating the RPS mass from ETS emitted into any occupied space as a function of the smoking rate and removal rate (N). The removal rate is equal to the sum of the ventilation or infiltration rate (nv) and removal rate by surfaces (ns) times the mixing factor m. The calculated ETS RSP mass determined from this figure serves as an input to Figure 5–5 to determine the ETS respirable suspended particulate mass concentration in any space in µg/m3. Smoking rates (diagonal lines) are given as cigarettes smoked per hour. Mixing is determined as a fraction and nv and ns are in air changes per hour (ach). All three parameters have to be estimated or measured. Calculations were made using the equilibrium form of the mass-balance equation (Equation 5–3) and assume a fixed emission rate of 26 mg/cigarette of RSP.

Shaded area shows the range of RSP emissions that could be expected for a residence with one smoker smoking at a rate of either 1 or 2 cigarettes per hour for the range of mixing, ventilation, and removal rates occurring in residences under steady-state conditions.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

FIGURE 5–5 Diagram to calculate the ETS RSP concentration in a space as a function of the total mass of ETS RSP emitted (determined from Figure 5–4) and the volume of a space (diagonal lines). The concentrations shown assume a background level in the space of zero. The particulate concentrations shown are estimates during smoking occupancy. The dashed horizontal lines (A, B, C, and D) refer to National Ambient Air Quality Standards (health-related) for total suspended particulates established by the U.S. Environmental Protection Agency. A is the annual geometric mean. B is the 24-hour value not to be exceeded more than once a year. C is the 24-hour air pollution emergency level. D is the 24-hour significant harm level. Shaded area shows the range of concentrations expected (from Figure 5–4) for a range of typical volumes of U.S. residences and rooms in these residences.

  • a one-chamber model is appropriate.

In these figures, the RSP-emission rate is assumed constant. If, in fact, this rate is variable, then the predicted RSP level will also vary. As already discussed, the input parameters to Equation 5–1 are known to vary greatly under realistic occupancy conditions, with few or no data available on the distribution of the values of those input parameters. Figures 5–4 and 5–5 highlight the large effect that small variations in the input parameters can have on the predicted RSP concentration.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

For example, for a range of conditions that can be expected to be encountered in private residences with one smoker (shaded areas in Figures 5–4 and 5–5), RSP levels in residences or public places during smoking occupancy can vary by more than two orders of magnitude from approximately 17 to 5,000 µg/m3. This example assumes one smoking resident smoking at a rate of either one or two cigarettes/hour. Relatively easy-to-obtain information on some of the input parameters, such as building volume or typical smoking densities, obtained through questionnaires or observation, can serve to significantly reduce the range of estimated exposures. It is also clear from Figures 5–4 and 5–5 that, for the vast majority of conditions, RSP levels due solely to ETS can be expected to equal or exceed levels specified in National Ambient Air Quality Standards for the total suspended particulates (Code of Federal Regulations, 1985). These standards are health-based and reflect different averaging times as well as levels of exposure. Direct comparison of exposures with the standards requires consideration of particle size, concentration, and time. The physical and chemical nature of the particulate matter resulting from tobacco smoke is different from particulate matter observed outdoors in ambient air. These different particulate matters no doubt have different biological effects. Therefore, direct comparisons of exposures to outdoor standards should be made with caution.

Application of Respirable Suspended Particulates Model

The most extensive use of the mass-balance equation for assessing RSP levels due to ETS in occupied spaces has been by Repace and Lowrey (1980). Drawing upon the best available data from several sources, including both measured and estimated parameters, they proposed and applied in field observations a condensed version of the mass-balance equation for estimating RSP exposures due to ETS in a variety of indoor microenvironments. Their model is

(5–3)

where Ceq is the equilibrium of concentration of RSP due to ETS expressed in micrograms per cubic meter, Ds is the density of active smokers expressed as units of burning cigarettes observed in a space per 100 m3 over the sampling time frames, and nv is the

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

ventilation or infiltration rate in ach. The constant term (650) is calculated from a standard set of assumed conditions for smoking rates, RSP emission rates, mixing factors, ventilation rates, and sink rates. These standard sets of conditions are derived largely from experimental data and building standards.

Although many of the input parameters were estimated from the literature, which is based on limited experimental data, Repace and Lowrey (1980, 1982) applied Equation 5–3, or similar equations, to a variety of situations and found that they produced reasonably accurate estimates in a limited number of occupied spaces with smoking occupancy. Apparently, easy-to-obtain data on building volumes, design occupancy, smoking occupancy, type of ventilation systems, and building standards can improve the prediction of RSP concentrations. In using Equation 5–3, the major assumptions deal with mixing, ventilation rates, and sink rates. Additional field testing of the Repace and Lowrey model, as well as a better understanding of the variability of the input parameters, either estimated or measured for use in Equation 5–3, is needed.

SUMMARY AND RECOMMENDATIONS

In investigating the adverse health and comfort impact of air contaminants, it is important to specify the exposure to a specific air contaminant or a class of air contaminants on the time scale corresponding to the health or comfort effect being evaluated. Accurate data on exposure is essential to minimize misclassification of exposure in epidemiologic studies of air contaminants. In the absence of an indicator of the dose of the contaminant, target tissue exposures may be estimated by use of biological markers, by personal monitors, or by the air monitoring of microenvironments in which people spend time combined with time activity patterns.

ETS is comprised of several thousand chemicals in both the gas and particulate phases. While several individual constituents of ETS have been measured in a number of microenvironments as a proxy for ETS (nicotine, CO, acrolein, etc.), none have met all of the criteria necessary for a suitable proxy, nor has an individual contaminant been uniformly accepted or recognized as representing ETS exposure. New methods of measuring nicotine in air hold promise for using nicotine as a suitable proxy for ETS, but considerable development and testing need to be done. The single largest component of ETS by weight is the RSP, which refers to particles

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

less than 2.5 µm and is highly variable in chemical composition. The RSP fraction of ETS is currently the best and most-utilized general category of air contaminants to represent ETS exposure.

A limited number of studies that employed personal monitors to measure total RSP found that individuals who reported being exposed to ETS were exposed to RSP concentrations consistently greater than those who reported no exposure. Furthermore, the distribution of RSP concentrations varied widely (from 10 µg/m3 to more than 200 µg/m3). The limited number of samples, lack of data on the environments where the exposure took place, and lack of a specific proxy for ETS do not permit accurate estimation of the ETS exposure or extension of the data to a larger population. They do indicate, however, that individuals who report exposure to ETS will have greater RSP exposures than those who do not.

Measurements of RSP levels in various indoor environments (residences, offices, restaurants, bars, bowling alleys, airplanes, arenas, etc.) have clearly shown that RSP levels will be considerably above background levels (outdoor levels or nonsmoking levels) when smoking is reported in the space.

Modeling of RSP concentrations due to ETS in any indoor environment usually utilizes a simplified form of the mass-balance equation. These models are typically single-chamber models that assume steady-state or equilibrium conditions to estimate RSP levels and require as input parameters an RSP-emission rate for tobacco combustion, number of cigarettes consumed, ventilation or infiltration rates, removal rates by surfaces, air mixing in the space, and volume of the space. Information on the current or past distribution of these input parameters in the range of microenvironments in which individuals spend the majority of their time (residences, offices, etc.) is not available. The variability of one or more of the input parameters can make a difference of as much as an order of magnitude in the estimated RSP concentration. Additional variability in the estimated RSP levels is introduced to the extent that the equilibrium assumptions do not hold (i.e., an intermittent rather than continuous source).

Gathering data on easily measured input parameters such as smoking rates or volume can substantially reduce the variability of the estimated RSP levels. Limited field tests of the general equilibrium model, in which some of the input parameters were measured and others were estimated either from chamber studies or building codes, have predicted RSP levels reasonably well over a

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

wide range of values of input parameters. While the predicted level of RSP exposure due to ETS may be highly variable using models, it is clear from the models that, even using the most conservative estimates for the input parameters, RSP levels when smoking is allowed will result in substantial increases over nonsmoking occupancy RSP levels. This is consistent with the concentrations measured through personal monitoring or area monitors in various microenvironments.

What Is Known
  1. Various individual chemical constituents of ETS have been measured in indoor spaces as proxies for ETS, but their suitability as proxies for ETS exposures has not been well established.

  2. The total RSP, measured by personal monitors, has been found to be elevated for individuals who reported being exposed to ETS as compared with those who reported no exposure.

  3. The distributions of RSP measured by personal monitors and by portable monitors vary widely. However, levels of RSP measured in various indoor environments have clearly shown that RSP levels will be considerably above background levels when smoking is reported in the space.

  4. Limited field tests of the mass-balance, general-equilibrium model in which some of the input parameters are measured and others are estimated have predicted RSP levels reasonably well over a wide range of values of input parameters.

What Scientific Information Is Missing
  1. There is a lack of data on the environments where measurements have been taken. Consequently, an accurate estimate of the ETS exposure or extension of the data to a large population based upon present data may not be possible.

  2. A suitable proxy or tracer air contaminant is not available for total ETS exposure. Nicotine may be a good indicator for exposure to the vapor phase. However, the relative proportions of various constituents of ETS in the particulate and vapor phases need further study to determine the extent to which a tracer for one phase can be used to infer exposure to the other phase.

  3. Information on current or past distributions of the input parameters for the mass-balance models of RSP concentrations is

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

not available for a range of microenvironments in which individuals spend the majority of their time.

  1. When levels of various constituents of ETS are measured in field situations, data should be gathered on input parameters such as smoking rates or volume so that a detailed field evaluation of the equilibrium model can be made.

  2. ETS exposure in epidemiologic studies needs to be improved. Questionnaires must be validated. Personal and microenvironmental monitoring studies should be conducted to determine the predictive value of various exposure assessment methodologies. This might be achieved as part of a nested design in a larger epidemiologic study.

  3. The variability of RSP emissions into the environment and the relationship between vapor and particulate phases need to be investigated for a variety of brands of tobacco.

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Leaderer, B.P., W.S.Cain, and R.Isseroff, and L.G.Berglund. Ventilation requirements in buildings. II. Particulate matter and carbon monoxide from cigarette smoking. Atmos. Environ. 18:99–106, 1984.

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Moschandreas, D.J., D.J.Pelton, and J.Zabransky. Comparison of indoor and outdoor air quality. EPRI EA-1733. Electric Power Research Institute, 1981.

Suggested Citation:"ASSESSING EXPOSURES TO 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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Moschandreas, D.J. Exposure to pollutants and daily time budgets of people. Bull. N.Y. Acad. Med. 57:845–859, 1981.

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Suggested Citation:"ASSESSING EXPOSURES TO 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:"ASSESSING EXPOSURES TO 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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6
Assessing Exposures to Environmental Tobacco Smoke Using Questionnaires

The active component(s) of environmental tobacco smoke (ETS) associated with various health effects may be different for acute and chronic outcomes. Also, the mechanisms of action differ. Furthermore, as discussed in Chapter 2, the relative concentrations of various components of ETS change over time, i.e., as the smoke ages. Therefore, the use of a single proxy pollutant, such as respirable particulates, or an indirect measure of ETS limits the ability to assess responses to ETS exposure. For some investigations, indirect assessment is probably not adequate to evaluate health effects for at least two reasons. First, the tobacco smoke components that affect the health outcome may not be related to the indirect assessment in a simple way, e.g., vapor-phase-component concentrations cannot be adequately measured by particulate-phase components. Secondly, a variety of host factors affect the actual dose received so that assessment of exposure does not accurately (or completely) represent dose (see Chapter 7).

A variety of methods is used to estimate individual exposures associated with human health effects in industrial and nonindustrial settings. These exposure indicators may be direct—such as the use of personal-monitoring data or biochemical measures obtained by testing body fluids for the compound or its metabolites—or indirect—such as the use of data from interview responses of family members regarding activities of the subject and modeling based on environmental monitoring of the ambient or industrial setting. The resulting data from direct and indirect indicators of exposure can be expressed in quantitative or qualitative terms.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

The advantages and disadvantages of the various exposure measures used in industrial and nonindustrial settings are summarized in Table 6–1. The issues raised in this table are directly relevant to assessing ETS exposure. The use of surrogate measures derived from questionnaire responses and the issues resulting from use of these measures are discussed in this chapter.

EXPOSURE HISTORIES DERIVED FROM QUESTIONNAIRES

Questionnaire responses of study subjects or family/household members are used for two purposes. First, questionnaires are used to obtain data on the physical characteristics of each environment and the time-activity patterns of the individual in each environment. These data can be used with individual monitoring data to estimate (usually by modeling) the air-contaminant levels in the microenvironment and to estimate time-weighted, integrated individual exposures. Second, questionnaire responses provide a basis for classification of individuals into broad categories of exposure based on self (or proxy) reports of exposure to individuals who smoke. Questionnaires of the latter type have provided the bases for associating ETS to the increased risk of nonmalignant and malignant disease.

There are several major issues in epidemiologic studies of health effects of exposure to ETS that rely on indirect measures of exposure as derived from questionnaire data.

First, the assessment of ETS exposures associated with acute health effects requires a different approach than that for chronic health effects. Acute health effects, such as respiratory infections, are manifested shortly after exposure and are of short duration. By inference, these health outcomes depend only on exposures in the recent past. In contrast, chronic health effects are conditions that are associated with long-term exposure to ETS, that is, they are manifested after some prolonged period of time and are of long duration. In evaluating the association of ETS with chronic diseases, knowledge about the duration of exposure and the duration of time from initial exposure to disease onset is more important than the duration of the disease.

Second, quality of information obtained by interview or self-administered questionnaires may vary among studies and may vary for different disease outcomes. For example, the assessment

Suggested Citation:"ASSESSING EXPOSURES TO 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 6–1 Indicators of Individual Exposure in Industrial and Nonindustrial Settings—Advantages and Disadvantages

Indicator

Advantages

Disadvantages

1. DIRECT

  1. Biologic monitoring of body fluids for the compound and/or its metabolites—quantitative (e.g., blood level)

  1. Identifies exposed individuals

  2. Provides measure of body burden for some agents (e.g., metals)

  3. Measures absorption of compound from all routes of entry—respiratory, cutaneous, and oral

  4. Gives information about prior exposure

  1. Many methods still in developmental stages and lack validation

  2. May be expensive due to need for specially trained personnel and sophisticated equipment

  3. May require concurrent air sampling if exposures are not constant

  4. Interpretation may be influenced by variation in uptake with physical exertion and interference from diet and drugs

  5. Requires careful timing of specimen collection, especially for blood samples

  6. Subject consent required to obtain specimens

  7. Lack of population reference values

  1. Personal industrial hygiene or ambient monitoring, single and multiple—quantitative

  1. Estimates exposure for individual employees

  2. Can be performed easily by the employer

  3. Exposure to multiple compounds can be assessed simultaneously

  1. Requires cooperation of worker or study subjects to wear monitoring equipment

  2. Does not measure body burden

  3. Limited ability to assess multiple routes of exposure

  4. Gives no information about prior exposures

  5. May not correspond with results of area sampling

  6. Samples may not reflect “average” work day; taking of measurements should consider shifts, production, seasons, etc.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Indicator

Advantages

Disadvantages

  1. Employer or other reports of exposure to compound—qualitative

  1. Provides details of accidental releases

  2. Can indicate safety procedures/protective measures

  1. Data may be incomplete (unreported)

  2. Exposure quantified subjectively

  3. Episodic measurement of unusual occurrences rather than “average” workday exposure

  1. Self-reports of exposure to compound—qualitative

  1. Provides details of accidental releases

  2. Can indicate personal hygiene and safety habits

  3. Can obtain chronology of work experience with multiple agent exposures

  1. Potential for recall bias

  2. Employees may be unaware of exposure

  3. Potential for falsification of exposure for personal gain

  4. Potential for lost to follow-up (missing information) in retrospective studies

2. INDIRECT

  1. Biological monitoring

(1) with chromosome studies—quantitative or qualitative

  1. Identified changes in the genetic material

  2. Indicates systemic exposure to a mutagen

  1. Expensive, due to need for specially trained personnel and sophisticated equipment

  2. Relationship between changes in mutation rates and reproductive outcomes is unknown

  3. Results may be confounded by smoking and environmental factors (e.g., effect of smoking on sister chromatid exchanges in lymphocytes; radiation effects)

  4. Individual variability in baseline rates

  5. Most chromosomal aberrations are nonspecific

(2) by measuring changes in biochemical responses (e.g., elevated rate of thiocyanate production in

  1. Identifies alterations in normal constituents of body fluids and changes in rate of normal biochemical processes

  1. Does not quantify body burden

  2. Results may be confounded by drugs, nutrition, and disease

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

response to cyanide exposure)—quantitative or qualitative

  1. Requires understanding of compound’s metabolism in body

  1. Area industrial hygiene or ambient monitoring—quantitative

  1. Documents concentration of agent in work environment

  2. Variety of measurement techniques available

  3. Can be performed easily by the employer

  1. May not correspond with results of personal sampling

  2. Measurements have multiple sources of variation

  3. Does not indicate specific exposure level for individual employees

  4. No information about previous exposures

  5. Type of sample taken may be inappropriate for health effects being studied

  1. Employer work area assignment records (work histories)—qualitative (specific estimates may be made using job-exposure linkage) or quantitative (may be developed by using duration of time spent in different environments)

  1. Can provide chronologic work experience for duration of exposure

  2. Can indicate exposure to multiple agents

  3. May provide supplementary information

  1. May be incomplete or may be unavailable

  2. Records not designed for research purposes

  3. Presumed exposure by work assignment may be based on subjective criteria

  4. Record review is time-consuming

Activity diaries of study subjects, recording time spent in different microenvironments

  1. Surrogate (next of kin) interview responses regarding work history and activity history of study subject—qualitative (specific estimates made using a job-exposure linkage) or quantitative (estimates developed using duration of time spent in environments)

  1. Can obtain information about confounding factors

  2. Identifies major agents to which exposed

  3. May provide supplementary demographic information about employees

  1. Limited by knowledge of employee’s work

  2. May produce overestimate or underestimate of exposure

  3. Time-consuming to locate and interview

  4. Lack of validation of data

  5. Differential quality of information by degree of kinship

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

of maternal smoking during the first year of life of a child may be a much more accurate measure of exposure to ETS related to respiratory illness than a summary history of ETS exposure related to lung cancer. Data quality for ETS exposures can be affected in major ways by differential and nondifferential misclassification of exposure. In Chapter 12, the impact of misclassifying exposed subjects as nonsmokers, when they are in fact current smokers or exsmokers, is discussed. Therefore, it is important to determine whether nonsmoking subjects are, in fact, never smokers or currently nonsmokers, i.e., exsmokers. Another source of bias is the misclassification of exposure among nonsmokers. That is, nonsmokers who say they have not been exposed may in fact have had significant exposures. In both cases, detailed probes are needed.

Third, the role of major confounding exposures needs to be assessed. For instance, occupational exposures to other air contaminants may cause pulmonary disorders.

Fourth, the evaluation of ETS exposures should attempt to assess all such exposures rather than focus solely on exposures from smoking by family members (spouse, mother, or father) or focus solely on the home environment. An adequate assessment of total ETS exposure will necessitate a consideration of exposure levels in specific microenvironments—such as home, school, work, vehicle, and recreation—and the duration of time an individual is exposed in these environments. Developing such a measure is complex even for relatively acute health outcomes, such as acute cardiovascular, respiratory, or neurotoxic symptoms, for which it may be sufficient to estimate recent exposures. Developing a comprehensive measure to ETS exposures is far more complex for diseases with long induction times, such as cancer and chronic obstructive pulmonary disease. The data required for modeling a long-term integrated ETS exposure may be far more detailed than are available or can be reliably obtained. Further, when a surrogate informant is used, that person most likely will be able to report on exposures in only some of the microenvironments. In this case, it may be impossible to develop a comprehensive index.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

ENVIRONMENTAL TOBACCO SMOKE EXPOSURE DATA FOR STUDIES OF ACUTE AND CHRONIC HEALTH EFFECTS

The acute health effects of ETS in children, such as respiratory illnesses, have been assessed in the National Health Interview Survey (NHIS) by determining smoking status of one or both parents or smoking status of adults in the household (Bonham and Wilson, 1981). In this national probability sample of households, parental smoking histories and reports of respiratory illness among children were obtained at one point in time. By contrast, in the Harvard Air Pollution Respiratory Health Study (Six Cities Study), information on current smoking habits for parents and all household members who smoke regularly in the home is obtained annually to determine amount of cigarette smoking in the home environment to which the children aged 6–13 years are exposed (Ware et al., 1984). (In Chapter 11 the assessment of exposure to parental smoking in studies of respiratory illness in children is discussed in more detail.)

In studies of chronic health effects in adults, such as cancer, exposure of nonsmokers to ETS has been largely determined by smoking status of the spouse. Most studies of lung cancer among nonsmoking women have relied solely or principally on information regarding smoking status of the spouse to assess ETS exposures, with little attempt to corroborate self-reports of exposure to ETS.

The difficulties in assessing ETS exposure are similar to difficulties of assessing occupational exposures (Axelson, 1985). Both exposures are complex and variable. The problem of obtaining adequate information about ETS exposure might be overcome by obtaining data from multiple respondents and by using corroborating procedures. However, the conceptual difficulty concerning the determination of exposure is unresolved or unaddressed in most studies. Exposure to a substance involves a varying intensity over some period of time prior to the development of disease. These factors may influence the absorption and distribution of an agent in the body as well as the biotransformation and excretion of the agent. Therefore, these factors probably influence the risk of the health outcome of interest. For exposures extending over long periods of time, a simple “cumulative dose” usually is calculated by a time integration of the intensity. The estimate of

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

exposure over long periods of time is expressed as average number of cigarettes per day or the calculation of “pack years.” This type of measure does not provide for an independent consideration of latency, does not consider variability in exposure over the time period, and represents two components of exposure, one of which may be more precisely measured (duration) than the other (intensity) (Doll and Peto, 1978). Axelson (1985) describes some sophisticated adjustments that have been proposed for weighting time periods of exposure to estimate cumulative-dose measures.

These proposed methods have not been widely adopted, probably due to both the complexity of the method as well as the recognized limitations of exposure data typically available. The more common, simplified procedure is to apply an appropriate induction/latency period in the analysis of studies of cancer or other chronic diseases. This practice suggests, however, that more attention be given to identifying the separate effects of late (recent) exposures versus early (remote) exposures on development of various diseases. These effects may also be mediated by the age at which the exposures occurred.

The proposal described by Johnson and Letzel (1984) advocates a method of assessing exposures to ETS experienced over an entire lifetime. The major limitation of this approach is that it has not been validated. Johnson and Letzel (1984) argue that since no objective criteria for lifetime exposure to ETS exists, a direct validation of an instrument to assess lifelong ETS exposure cannot be obtained. They propose that the instrument be validated on a recent time frame, such as 24-hour data. From these data the investigators argue by analogy that the method, when expanded to a longer time frame, can be regarded as valid. While this approach may seem less than ideal, the constraints due to data availability and quality emphasize the importance of the type of methods development and corroboration illustrated by the work of Johnson and Letzel (1984).

DATA QUALITY

Misclassification of individual ETS exposure may be differential (biased) or nondifferential (random). Differential misclassification would result in a distortion of the estimate of risk in either direction, depending on the direction of the misclassification. Nondifferential misclassification would result in a reduction

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

of power in a study, thus making it more difficult to detect a true association of exposure with risk of disease.

One form of differential misclassification that is a major concern in studies of ETS exposures is the active smoking status of study subjects. This misclassification may be considered differential because spouses and children of smokers are more likely to be smokers (or have smoked) themselves, even though they are reported as “nonsmokers.” The effects of this differential misclassification are discussed in Chapters 11 and 12. One way to minimize this problem is to have multiple questions that probe for previous cigarette usage, even if the subject has defined himself or herself as a nonsmoker.

Another form of differential misclassification is that resulting from the biased reporting of exposure to ETS by individuals with existing respiratory diseases, such as asthma or chronic bronchitis. One might conjecture that individuals with existing respiratory diseases may be more or may be less likely to report exposure to ETS than individuals without such existing conditions.

In studies of ETS exposures, information about the smoking habits of the subject, family, and household members is obtained by interviews with the study subject when available, or by interview with a family member when the study subject is deceased or unavailable. That is, surrogate respondents may be used to collect information regarding personal exposures of the study subject.

The validity of surrogate information in most studies is uncertain, and the direction of any potential bias is rarely known (Gordis, 1982). The feasibility of this approach for a variety of exposures and habits has been examined (Pickle et al., 1983). Also, several studies have assessed the reliability and validity of surrogate respondents for various kinds of exposures (Rogot and Reid, 1975; Kolonel et al., 1977; Marshall et al., 1980; Baumgarten et al., 1983; Humble et al., 1984; Greenberg et al., 1985; Herrmann, 1985; Lerchen and Samet, 1986). In all of these studies, agreement between self and surrogate responses improves when the amount of detail required for the response is decreased. This observation was first reported by Rogot and Reid (1975) and subsequently observed in studies comparing self versus spouse/surrogate responses.

Lerchen and Samet (1986) reported perfect agreement of cigarette-smoking status (ever/never) as reported by lung cancer cases and their wives, but only 66 (86%) of the 77 wives married to smokers were able to supply complete details about

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

their husbands’ cigarette-smoking habits. In this study, agreement (expressed as correlation coefficients) was quite good for all smoking-related variables, such as age at which the subject started to smoke (0.48), total years of smoking (0.91), and average number of cigarettes smoked per day (0.44). The mean values reported by cases and their wives were not significantly different for any variable. Overall, the agreement observed for self- and surrogate-reported smoking-related information was better than the agreement for education, occupation, and dietary information.

Pershagen and Axelson (1982) also reported perfect agreement for smoking status information obtained by interview with a close relative (parent, wife, or child) for 14 lung cancer cases when information was compared with that obtained previously by the plant physician. Their inquiry was limited to smoker/nonsmoker status. Damber (1986) and Pershagen (1984) reported 99% agreement between reports of close relatives and hospital records for ever/never smoking studies in a sample of 86 patients admitted for respiratory disease. The agreement for number of years smoked (±5 years) was 74%.

Other studies have noted additional features of the responses from surrogates. The report by Pickle et al. (1983) indicates that respondents other than spouse and direct next-of-kin (siblings, parents, and children) are more likely to not know relevant information. Marshall et al. (1980) demonstrated the increase in sensitivity obtained by combining information from two or more surrogate respondents, and Herrmann (1985) showed that husbands reported data for wives as reliably as wives reported exposures of husbands.

Recent data from the NCHS Epidemiologic Followup Study (NHEFS) in 1982–1984 of participants in the National Health and Nutrition Examination Survey (NHANES I) in 1971–1975 provides a strong confirmation of these earlier reports (S.R.Machlin, J.C. Kleinman, J.H.Madans, National Center for Health Statistics, personal communication). This analysis is based on a subsample of 5,669 individuals with data regarding baseline smoking status available from both NHANES I and NHEFS. Agreement rates between NHANES I and NHEFS for the 5,029 subject responses versus the 640 proxy responses at follow-up are compared (Tables 6–2 and 6–3). When smoking status is broadly defined as ever/never, the 91% agreement rate for proxy responses compares quite favorably with the 95% agreement rate of subject responses

Suggested Citation:"ASSESSING EXPOSURES TO 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 6–2). Similar high agreement is observed for proxy and subject responses at follow-up when smoking status is considered as current/not current (Table 6–3). Additional analyses of these data to assess the factors associated with agreement between baseline and follow-up responses considered age, race, gender of subject, type of respondent at follow-up, and smoking status at baseline. Estimates of the relative odds of disagreement indicated that only the effect of race did not interact with any of the other variables included in the multiple logistic model. Significant two-way interactions were observed for type of informant and age of subject, baseline smoking status and gender of subject, and baseline smoking status and age of subject. These results suggested that proxy respondents were more than twice as likely to misclassify smoking status for subjects less than 65 years of age, but not for subjects age 65 years and over. When amount smoked (current amount at baseline versus usual amount at follow-up) is compared for smokers only, the agreement rates are substantially affected by type of respondent; 55% agreement for subject responses versus 35% agreement for proxy responses. When this comparison is made with nonsmokers included, a much higher rate of agreement for both subject (80%) and proxy (74%) responses is observed. This comparison is strongly influenced by the substantial proportion of nonsmokers (over 60%). Of concern, however, is the high proportion of self-reported current and former smokers at baseline who are reported as never smokers at follow-up; 5.6% by self respondents and 12.9% by proxy respondents. These results are discussed later in the section concerned with confounding.

Another large cohort study in England and Wales provides information regarding the proportion of people who say that they have never smoked but, in fact, have done so in the past (N. Britten, University of Bristol, England, personal communication). A large longitudinal study of children born in 1 week in England and Wales in 1946 has included several follow-up visits, the most recent of which was done in 1982 when the subjects were 36 years of age. Table 6–4 presents some results. A portion (4.9%) of the subjects said they had never smoked as much as one cigarette a day in 1982 when in fact they had previously reported that they smoked. These subjects had reported smoking at a rate of about half the current smokers. Nearly all of exsmokers (93%) had smoked 10 or more years earlier.

Suggested Citation:"ASSESSING EXPOSURES TO 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 6–2 Percent Distribution of Smoking Status at Baseline Exam (NHANES I, 1971–75), According to Smoking Status at Follow-up (NHEFS, 1982–84) by Type of Respondent at Follow-up

Baseline Smoking Status (NHANES I)

Smoking Status Reported at Follow-up

Ever No.

Percent

Never No.

Percent

Total No.

 

Type of Follow-up Respondent: Self

Ever

2,675

95.6

125

5.6

2,800

Never

122

4.6

2,107

94.4

2,229

Total

2,797

100.0

2,232

100.0

5,029

 

Type of Follow-up Respondent: Proxy

Ever

329

95.1

38

12.9

367

Never

17

4.9

256

87.1

273

Total

346

100.0

294

100.0

640

SOURCE: Information obtained from National Center for Health Statistics (S.R.Machlin, J.C.Kleinman, J.H.Madans, personal communications).

TABLE 6–3 Percent Distribution of Smoking Status at Baseline Exam (NHANES I, 1971–75), According to Smoking Status at Follow-up (NHEFS, 1982–84) by Type of Respondent at Follow-up

Baseline Smoking Status (NHANES I)

Smoking Status Reported at Follow-up

Current No.

Percent

Not Current No.

Percent

Total No.

 

Type of Follow-up Respondent: Self

Current

1,722

89.5

124

4.0

1,846

Not Current

202

10.5

2,981

96.0

3,183

Total

1,924

100.0

3,105

100.0

5,029

 

Type of Follow-up Respondent: Proxy

Current

186

83.4

24

5.8

210

Not Current

37

16.6

393

94.2

430

Total

223

100.0

417

100.0

640

SOURCE: Information obtained from National Center for Health Statistics (S.R.Machlin, J.C.Kleinman, and J.H.Madans, personal communication).

Suggested Citation:"ASSESSING EXPOSURES TO 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 6–4 Smoking Habits of Cohort Members at Age 36 Who Previously Reported That They Had Smoked at Least One Cigarette a Day

Smoking Status Reported in 1982

Most Recent Age at Which Smoking Was Reported

Number of Subjects

Percentage of All Reported Ever-Smokers (No.=2,080)

Mean No., cig./day

Interval Between Age Started Smoking and Age 36

Nonsmokers who had previously reported smoking (No.=102)

31 yr (1977)

7

0.34

12.7

25 yr (1971)

18

0.87

5.1

9.5

20 yr (1966)

49

2.36

4.2

5.4

<20 yr (before 1966)

28

1.35

5.8

1.8

Total

102

4.90

 

 

Percent of Current Smokers (No.=1,127)

 

 

Current smokers who had previously reported smoking (No.=1,048)

31 yr (1977)

819

72.67

20.6

 

25 yr (1971)

136

12.07

12.7

20 yr (1966)

84

7.45

11.4

<20 yr (before 1966)

9

0.80

16.1

SOURCE: Based on data from the MRC National Survey of Health and Development (N.Britten, personal communication, University of Bristol, England).

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Therefore, both longitudinal studies indicate that about 5% of self-reported lifelong nonsmokers may, in fact, have smoked. Rogot and Reid (1975) observed that there was a tendency of surrogate informants to report a higher tobacco consumption than previously reported by the study subjects. However, Lerchen and Samet (1986) observed no such differential in the reporting by wives of amount smoked by their husbands as compared with that reported by husbands.

The body of evidence on surrogate responses to questions about smoking status suggests that the validity of such data may be limited and that spouses and, perhaps, other close family members can provide an accurate, but simple, smoking history (ever/never, smoker/nonsmoker). However, detailed information about amount and number of years smoked may be inaccurate and may result in substantial misclassification of study subjects by exposure status. These findings, although from a limited number of studies, have direct implications for the studies of ETS exposures where ETS exposure information is derived from surrogate reports. It should be noted that in the special instance where the spouse surrogate is reporting on his personal smoking history, the information regarding ETS exposure of the nonsmoking study subject may be more accurate with regard to home exposures than the report by the study subject.

Cotinine, the major metabolite of nicotine, can be detected in blood, urine, and saliva of active cigarette smokers and of those passively exposed to ETS. Coultas et al. (1986) demonstrated that nonsmokers exposed to cigarette smoke in their homes have detectable levels of salivary cotinine that increase as the number of smokers in the home increases from 1 to 2 or more (Table 6–5). Biochemical corroboration is not as promising for remote exposures to ETS. Corroboration of historical exposures, therefore, must rely on other methods, such as review of historical records. Results of recent biochemical measures may be used to corroborate self-reports of recent exposures for individuals for whom reports of both recent and remote exposures are available. The quality of historical data for an individual can be inferred from data using results from biochemical corroboration. This approach has been proposed by Johnson and Letzel (1984).

The true validity of retrospective ETS exposures is impossible to establish. Wherever possible, other methods to corroborate exposure estimates should be used to assess and confirm the quality

Suggested Citation:"ASSESSING EXPOSURES TO 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 6–5 Salivary Cotinine Concentration (ng/ml) in Nonsmokers by Age and Number of Active Smokers in Household

Age, yr

Number of Household Smokers

None

One

Two or More

Younger than 6

0;1.7;68a

3.8;4.1;41

5.4;5.6;21

6–17

0;1.3;200

1.8;2.4;96

5.3;5.6;25

Older than 17

0;1.5;316

0.65;2.8;60

0;3.7;12

aMedian; mean; number of subjects.

SOURCE: Coultas et al. (1986).

of self- and proxy reports of ETS exposure as well as active smoking status of study subjects. Other methods currently available for comparison with questionnaire and interview responses include biochemical measures, environmental modeling, review of existing records, and reports of additional respondents.

OTHER VARIABLES

Confounding factors that should be considered in the design, collection, and use of questionnaire data are other risk factors associated with the disease that may or may not be correlated with exposures to ETS. In the case of lung cancer, such risk factors include, but are not limited to:

  • occupation and industry of employment,

  • exposure to specific respiratory carcinogens, such as asbestos, arsenic, radon, etc., in occupational or nonoccupational settings,

  • dietary factors,

  • family history of cancer (Ooi et al., 1986),

  • residential history,

  • housing characteristics,

  • years of education, and

  • socioeconomic status.

Confounding factors relevant to the assessment of pulmonary function and respiratory illness are listed in Table 11–1. In addition, exsmokers and current smokers have been (or are) exposed to active smoking for some period of time. Therefore, these individuals may have been exposed to higher concentrations and longer

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

duration of ETS, due to their own smoking patterns. Thus, an evaluation of the increased risk associated with exposure to ETS for any disease that is strongly associated with active smoking will need to control for smoking status of the individual study subjects. The confounding effects of active smoking were not adequately controlled in several investigations of lung cancer (discussed in Chapter 12). This concern is particularly relevant in studies of acute respiratory illness in children and adolescents where the study subjects may be disinclined to report their smoking behavior accurately or the parents may be unaware of their child’s active smoking (described in Chapter 11).

A history of exposure to all other known or suspected confounding factors should be obtained in a comparable manner for cases and comparison subjects by interview and corroborated whenever possible by comparison with existing records or self-reports obtained before development of the disease. The exposure data collected should strive to be as detailed as possible with respect to intensity, duration, and calendar time for all exposures, including ETS exposures. However, one should be cognizant of the limitations imposed on data quality, especially when the investigation relies on surrogate responses. Such quantification at best provides an approximation of exposure, whether the information is obtained from the individual himself or from a surrogate.

SUMMARY AND RECOMMENDATIONS

There are problems with self- and proxy reports of ETS exposure inferred from questionnaire responses that limit the utility of these data. The best method by which to estimate individual ETS exposures is not known, and this lack of information hampers all efforts at assessing data quality, including data validity. At present all methods used and proposed are indirect, although some provide quantitative measures and some qualitative measures (smoker/nonsmoker). However, information on exposure from monitoring and detailed environmental-modeling studies of RSP indicate that only 30–40% of the variation in exposure can be explained using this approach (see Chapter 5). Further, biochemical methods to assess ETS exposure are extremely limited in the assessment of historical exposures that are most important with regards to chronic health effects. Therefore, exposure data derived

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

from questionnaire responses have an extremely important role in existing and future studies of ETS exposures.

What Is Known
  1. Surrogate responses from spouses or close family members can provide data as accurate as self-reports for simple ever/never smoker status and current amount smoked. However, with such simple classifications, an error rate of about 5% is observed whereby ever smokers are misclassified as lifelong nonsmokers. This error is present for self-respondents as well as proxies.

What Scientific Information Is Missing
  1. Differences in exposure levels between home and work environments have not been described in existing studies. In addition to the amount of time that an individual may spend in a work setting, the actual exposure may vary within the setting due to physical characteristics of the work environment as well as the number of active smokers present.

  2. Future investigations should be concerned with detailed characterization of ETS that would provide a more precise estimation of individual exposures and include additional considerations of physical characteristics of the environment, activity patterns of the study subject, and ages at which exposures occurred. These data could be entered into a model, from which exposure estimates can be made.

  3. Because of the importance of misclassification of active smoking status, repeated and complementary efforts to determine and corroborate smoking status should be made in the collection of exposure data. Specific probes regarding former smoking status might be included in the questionnaire, even if the study subject has defined himself or herself as a nonsmoker.

  4. Confounding factors should be considered in the design, collection, and use of questionnaire data. These will vary with the health effect being assessed. The evaluation of ETS exposures should attempt to assess all such exposures, including both the home and work environment rather than focus solely on the smoking status of one family member, e.g., spouse.

  5. The comparability of questionnaires used to assess ETS has not been established, and this would be desirable.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

REFERENCES

Axelson, O. Dealing with the exposure variable in occupational and environmental epidemiology. Scand. J. Soc. Med. 13:147–152, 1985.


Baumgarten, M., J.Siemiatycki, and G.W.Gibbs. Validity of work histories obtained by interview for epidemiologic purposes. Am. J. Epidemiol. 118:583–591, 1983.

Bonham, G.S., and R.W.Wilson. Children’s health in families with cigarette smokers. Am. J. Public Health 71:290–293, 1981.


Coultas, D.B., J.M.Samet, C.A.Howard, G.T.Peake, and B.J.Skipper. Salivary cotinine levels and passive tobacco smoke exposure in the home. Am. Rev. Respir. Dis. 133:A157, 1986.


Damber, L. Lung cancer in males: An epidemiological study in northern Sweden with special regard to smoking and occupation. Umeä University Medical Dissertations, Umeä, Sweden, 1986. 135 pp.

Doll, R., and R.Peto. Cigarette smoking and brochial carcinoma: Dose and time relationships among regular smokers and lifelong non-smokers. J. Epidemiol. Comm. Health 32:303–313, 1978.


Gordis, L. Should dead cases be matched to dead controls? Am. J. Epidemiol. 115:1–5, 1982.

Greenberg, E.R., B.Rosner, C.H.Hennekens, R.Rinsky, and T.Colton. An investigation of bias in a study of nuclear shipyard workers. Am. J. Epidemiol. 121:301–308, 1985.


Herrmann, N. Retrospective information from questionnaires. I. Comparability of primary respondents and their next-of-kin. Am. J. Epidemiol. 121:937–947, 1985.

Humble, C.G., J.M.Samet, and B.E.Skipper. Comparison of self- and surrogate-reported dietary information. Am. J. Epidemiol. 119:86–98, 1984.


Johnson, L.C., and H.W Letzel. Measuring passive smoking: Methods, problems and perspectives. Prev. Med. 13:705–716, 1984.


Kolonel, L.N., T.Hirohata, and A.M.Y.Nomura. Adequancy of survey data collected from substitute respondents. Am. J. Epidemiol. 106:476–484, 1977.


Lerchen, M.L, and J.M.Samet. An assessment of the validity of questionnaire responses provided by a surviving spouse. Am. J. Epidemiol. 123(3):481–489, 1986.


Marshall, J., R.Priore, B.Haughey, T.Rzepka, and S.Graham. Spouse-subject interviews and the reliability of diet studies. Am. J. Epidemiol. 112:675–683, 1980.


Ooi, W.L., R.C.Elston, V.W.Chen, J.E.Bailey-Wilson, and H.Rothschild. Increased familial risk for lung cancer. J. Natl. Cancer Inst. 72:217–222, 1986.


Pershagen, G. Validity of questionnaires data on smoking and other exposures, with special reference to environmental tobacco smoke. The Respir. Dis. 133(Suppl.):76–80, 1984.

Pershagen, G., and O.Axelson. A validation of questionnaire information on occupational exposure and smoking. Scand. J. Work Environ. Health 8:24–28, 1982.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Pickle, L.W., L.M.Brown, and W.J.Blot. Information available from surrogate respondents in case-control interview studies. Am. J. Epidemiol. 118:99–108, 1983.


Rogot, E., and D.D.Reid. The validity of data from next-of-kin in studies of mortality among immigrants. Int. J. Epidemiol. 4:51–54, 1975.


Ware, J.H., D.W.Dockery, A.Spiro III, F.E.Speizer, and B.G.Ferris, Jr. Passive smoking, gas cooking, and repiratory health of children living in six cities. Am. Rev. Respir. Dis. 129:366–374, 1984.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

7
Exposure-Dose Relationships for Environmental Tobacco Smoke

ESTIMATING DOSE

When considering the risks of exposure to environmental tobacco smoke (ETS) by nonsmokers, it is not enough to evaluate exposure and response. The actual dose received should be considered. Typically, for smokers, the exposure is given in terms of number of cigarettes smoked per day or cumulative pack-years. For nonsmokers, the exposure is usually characterized in terms of particle or gas concentration in micrograms per cubic meter. But what is known about the total integrated dose to the respiratory tract resulting from exposure to ETS by nonsmokers? What fraction of inspired particles and gases is deposited and fails to exit with the expired air? Moreover, what is the fate of the deposited smoke?

Although highly variable in concentration, ETS includes many of the same constituents as the smoke entering the active smoker’s lungs. Both particulate and gaseous phases are present, as described in Chapter 2. In principle, the retained dose for either inhaled particles or gases can be approximated in a straightforward manner:

(7–1)

The deposited dose, in micrograms per hour, equals the ventilation rate in cubic meters per hour times the concentration of particle or gas in the inspired air in milligrams per cubic meter ([C]), times the collection efficiency (CE). CE has no dimensions; it is the fraction of the inhaled particle or gas that deposits and thus

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

fails to exit with the expired air. Thus, the dose is directly proportional to three variables: ventilation, pollutant concentration, and the fraction deposited.

First, consider ventilation . The standard 70-kg adult at rest breathes about 7.5 L/min (International Commission on Radiological Protection, 1975). However, a value of 20 L/min would be more appropriate for adults in indoor environments who periodically stand, walk, type, or perform other modest tasks. During heavy exercise, ventilation can increase by a factor of as much as 10, to exceed 100 L/min (International Commission on Radiological Protection, 1975).

The concentration of various constituents in ETS ([C]) that might be encountered in various situations has been discussed in Chapters 2 and 5.

PARTICLE SIZE

For particles, collection efficiency (CE) is determined primarily by two factors: particle size and breathing pattern. If the geometric size, shape, and density of the individual particles or droplets are known, then the distribution of particle diameters can be described. Because it is a better predictor of the behavior of the particle in the respiratory tract, aerodynamic diameter rather than optical measurement is used to express the range of particle sizes. Aerodynamic diameter is defined as the diameter of a sphere of unit density that has the same settling velocity as the particle being measured. It may be expressed as the count median aerodynamic diameter (CMAD) or mass median aerodynamic diameter (MMAD). These are, respectively, the diameters for which half of the number (or mass) of the particles are less than that diameter and for which half exceed it.

The particles in mainstream cigarette smoke have been measured by several investigators using a variety of analytical devices. Because of the different apparatus and methods of smoke generation and dilution, results vary. However, to an order of magnitude, the findings are reasonably consistent. McCusker et al. (1983) used a device called the single particle aerodynamic relaxation time (SPART) analyzer to size mainstream particles from several brands of cigarettes, with and without filters. The MMAD for all brands averaged approximately 0.46 mm and was not markedly

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

different when the filters were removed. Particulate concentrations per milliliter ranged from 0.3×109 to 3.3×109, depending on whether the cigarettes were rated ultralow, low, or medium in tax content.

Hinds (1978) compared the particulate size distribution in cigarette smoke using an aerosol centrifuge and a cascade impactor. Although these devices are based on different physical principles, the MMAD values were comparable to those measured by McCusker et al. (1983), ranging from 0.37 to 0.52 µm. Variations depend primarily on the dilution of the smoke. Keith and Derrick (1960) used a specially modified centrifuge, termed a conifuge, to analyze cigarette smoke and reported MMAD and concentration values similar to Hinds (1978) and McCusker et al. (1983). Particulate analysis by a light-scattering photometer yielded a MMAD of 0.29 µm and particulate concentrations of 3×1010/ml.

Time and concentration can modify tobacco smoke. Cigarette smoke aerosols contain volatile components, and evaporation gradually reduces particle diameters. It is also true that when the particle concentrations are extremely high, like those encountered in mainstream smoke, the aerosol can agglomerate rapidly because nearby particles collide with each other and coalesce. If smoke is cooled (reducing the vapor pressure of volatile components) and diluted in room air (reducing the probability of particle collisions), the size of the particles will become more stable. Particle size may also change within the human respiratory tract. After air containing smoke is drawn into the mouth and upper respiratory tract, it becomes humidified. Smoke particles can grow in size because of their affinity for water, termed hygroscopicity (Hiller, 1982a).

BREATHING PATTERN

Particle size is a critical factor in determining the collection efficiency, but breathing pattern is also important For example, large slow tidal volumes will favor alveolar deposition, while high inspiratory flows will promote deposition at bifurcations in the airways. Breath-holding is also important. The greater the elapsed time before the next expiration, the higher the fraction of inspired particles deposited, since there is more time for particles to sediment or diffuse. Individual anatomic differences may influence the amount and distribution of deposited particles. The cross section of airways will influence the linear velocity of the inspired air.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Increasing alveolar size decreases alveolar deposition. Preexisting disease can also modify the deposition of smoke. For environmental tobacco smoke (diameters of particles ranging from 0.1 µm to 1 µm) the sedimentation and diffusion mechanisms will be the primary mechanisms of deposition.

Changes in the rate and pattern of breathing associated with exercise can also affect the total dose of cigarette participates deposited in the lungs. Bennett et al. (1985) reported that exercise increased the percent deposition of experimentally generated aerosols (MMAD of 2.6 µm) in human subjects. The reason for this observation was that during exercise, breathing patterns change so that flow rates are increased. Increasing the flow rates also increases the inertial impaction. Also, exercise is frequently associated with a shift from nose to mouth breathing. Consequently, the filtration of large particles that takes place in the upper respiratory tract no longer occurs. Increased deposition was also measured in exercising hamsters that inhaled a radiolabelled aerosol (activity median diameter of 3 µm) (Harbison and Brain, 1983). These results are relevant to those who breathe air containing ETS when their minute ventilation is increased while working or during periods of exercise.

DEPOSITION OF CIGARETTE SMOKE PARTICLES

The factors discussed in the previous sections indicate that experimental measurements of the concentration of smoke aerosols in indoor environments, i.e., exposure concentrations, are insufficient for predictions of smoke deposition. ETS smoke is constantly changing, thereby complicating the collection of accurate and reproducible data regarding its particulate size. In addition, alterations in respiratory structure and respiratory rate can affect deposition of particulates. These complexities stress the importance of actual measurement of regional deposition of cigarette smoke particles in human lungs. However, little is published on this important area, despite the prevalence of passive smoking and concerns about its impact on human health. The majority of the available information on deposition of particles present in cigarette smoke is based on theoretical or physical models of the lungs and measurements of differences between the concentrations of tobacco smoke aerosol or model aerosols in inhaled and exhaled air.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

A model to predict the percent of deposition of particles based on MMAD was developed by the Task Group on Lung Dynamics (1966) of the International Commission on Radiological Protection. The respiratory tract was divided into three main regions: nasopharynx, trachea and bronchi, and the alveolar. In conjunction with estimates of particle clearance, deposition calculations were made for these regions at three different inhalation volumes. This model suggests that about 30% of the particles within the size range present in cigarette smoke will deposit in the alveolar region and 5–10% in the tracheobronchial region. This model also emphasizes the impact of particle solubility on the total integrated dose with time. Brain and Valberg (1974) developed convenient nomograms and a computer program to calculate how particle solubility and particle size significantly affect the net amount of particulates retained in the lungs. Although the basic outline of the model is generally correct, more recent measurements suggest that values for alveolar deposition of particles 0.1–1.0 µm are too high by a factor of at least 2 (Heyder, 1982). The extent to which ETS particles are hygroscopic and increase in size within the respiratory tract is an important and unresolved issue that adds further uncertainty.

Aerosol deposition has also been studied in airway casts. Physical models of the upper airways of human lungs have been made by a double-casting technique to study particulate deposition at several airway generations (Schlesinger and Lippman 1972). Different flow rates and particle sizes were used to study deposition patterns. Schlesinger and Lippman (1978) reported a correlation between the deposition sites of test aerosols in their lung casts and the most common sites of origin of bronchogenic carcinoma in smoking humans. Both occurred preferentially at bifurcations. Martonen et al. (1983) added an oropharyngeal compartment and a replica cast of the larynx to the tracheobronchial casts in order to better simulate airflow patterns in the upper respiratory tract. They used these models to evaluate the amount of cigarette smoke condensate deposited in the airways at different flow rates. More condensate was present in areas where airways branched and especially at the bifurcation points, indicating increased levels of impaction. Aerosol was also deposited preferentially along posterior airway walls of the branching regions.

Hiller et al. (1982a) measured the collection efficiency in adults of an aerosol containing three different sizes of polystyrene latex

Suggested Citation:"ASSESSING EXPOSURES TO 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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spheres in nonsmoking humans. They measured a 10% deposition for 0.6-µm (MMAD) spheres, which is similar to the results of Davies et al. (1972) and Muir and Davies (1967) using 0.5-µm aerosols and Heyder (1982) using aerosols that were 0.2 to 1.0 µm in size. The size ranges of these aerosols are comparable to those experimentally measured in cigarette smoke, as previously discussed.

In contrast to passive smoking, the estimates of the collection efficiency of smoke particles during active smoking are substantially higher (about 70%) for at least two reasons (Hiller et al., 1982b). First, the much higher particulate concentrations in mainstream smoke may give rise to more agglomeration and greater hydroscopic growth in the respiratory tract. Both processes produce larger particles with higher collection efficiencies. Second, and more important, the breathing pattern used by the active smoker is markedly different than normal breathing. It is characterized by a slow deep inspiration followed by breath-holding. This increases the average residence time of the smoke particles and thus increases the fraction of inhaled particles that deposit in the lung.

To compare the amount of smoke deposited in the lungs of an active smoker with an individual exposed to ETS, first consider a pack-a-day smoker (about 20 cigarettes during an 8-hour period). The average tar rating in mainstream smoke (MS) over the past couple of decades has been about 14 mg/cigarette. Therefore, the total amount of tax inspired is 280 mg/8 h. Assuming a collection efficiency of 70%, the amount of tar deposited is 196 mg/8 h.

As pointed out in Chapter 5, smoke particles can range from 50 to 500 µg/m3 in public places where smoking occurs and from 20 to 150 µg/m3 in homes with smokers. Consider a nonsmoker who breathes at 10 L/min, or 4,800 L/8 h. With modest exercise, this could increase to 20 L/min, or 9,600 L/8 h. Based on estimates by Hiller et al. (1982a,b), the collection efficiency of particles in ETS is about 10%. Therefore, the total amount of smoke particles deposited in a nonsmoker in these environments for 8 h could range from approximately 0.0096 mg/8 h=20 µg/m3×4.8 m3/8 h×0.1 to an extreme of 0.5 mg/8 h=500 µg/m3×10 m3/8 h×0.1. This would be approximately 0.005% to 0.26% of that amount of tar deposited in the active smoker’s lungs after smoking 20 cigarettes. The active smoker, of course, also breathes the ETS, so that the total dose received by the active smoker is the mainstream smoke plus a passive smoking dose equivalent to that received by the

Suggested Citation:"ASSESSING EXPOSURES TO 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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nonsmoker exposed to ETS. However, since the dose received due to breathing ETS-contaminated air is so small, this additional contribution to the total dose is negligible.

Benzo[a]pyrene (BaP) is one of the primary constituents of particles in mainstream smoke. From Table 2–10 one can estimate that a nonsmoker exposed to ETS receives a higher relative dose of BaP than of RSP. However, the ambient measurements, which are used to estimate the dose for the nonsmoker, may be elevated in view of the high outdoor concentrations that are reported in these studies. More data on the fate of BaP in ETS and on ambient concentrations are needed before estimates of the relative doses can be made meaningfully.

Although the amount of smoke deposited in the lungs of nonsmokers during exposure to ETS is small compared with that encountered by the active smoker regarding mainstream smoke, it may differ in composition and toxicity. For example, as discussed in Chapter 2, certain constituents are present in much higher concentrations in sidestream smoke as compared with mainstream smoke (Weiss et al., 1983). These possible differences in composition must be explored.

PARTICLE RETENTION IN THE LUNGS

The amount of particles present at different sites in the lungs is not only dependent on deposition. Retention of smoke depends on the balance between the amount of each constituent that deposits in the respiratory tract and the efficiency of the lung clearance mechanisms in the airways and alveoli. Clearance mechanisms are a dynamic component of normal lung function and operate to keep the lung clean and sterile. Particles depositing in the airways are entrained in the mucus layer that lines the airway. This layer is swept toward the mouth by the action of ciliated cells and eventually swallowed. Mucus transport is approximately 1–2 cm per minute in the trachea, but is slower in smaller airways. In addition, macrophages present in the airways may phagocytose deposited particulates and be carried towards the mouth by the mucociliary transport system. Particulates reaching the alveolar region—those that are usually less than several micrometers—are soon engulfed by alveolar macrophages. Some of these cells gradually migrate towards the airways and exit the lung via the

Suggested Citation:"ASSESSING EXPOSURES TO 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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mucociliary escalator. Dissolution of particles is an additional important clearance mechanism.

Lung disease and cigarette smoking itself can affect particle clearance and retention in smokers’ lungs. Previous studies have shown that smokers have different aerosol deposition patterns and slower clearance rates than nonsmokers (Albert et al., 1969; Sanchis et al., 1971; Cohen et al., 1979). These alterations in clearance are, in part, caused by components within cigarette smoke that affect the quantity and rheological properties of the mucous. Components of cigarette smoke, also, can impair phagocytosis by alveolar macrophages (Ferin et al., 1965). Clearance mechanisms in smokers may be further compromised by lung diseases, such an emphysema and fibrosis, and by exposure to other air pollutants.

Measurements of the long-term retention of compounds associated with cigarette particulates in the lungs are difficult to estimate from data obtained with airway casts or from differences between inhaled and exhaled aerosol concentration, since these methods do not take into account clearance mechanisms. Unfortunately, few data are available regarding the actual retention and sites of deposition of cigarette smoke particles in either nonsmoking humans or animals exposed to ETS. The most accurate method that could be used is quantification of particulate deposits in individual pieces of tissue dissected from the lung. Impossible in living animals, this is a tedious procedure in animal lungs or human material obtained at surgery or autopsy and is especially difficult for large lungs. One can also attempt to quantify dose by examining saliva, serum, or urine. These possibilities are discussed in Chapter 8.

GASES IN ENVIRONMENTAL TOBACCO SMOKE

In addition to the particulate phase, we must also consider exposure-dose relationships for gases in ETS. As before, breathing pattern influences gas uptake. Of particular importance is the difference between oral and nasal breathing. Breathing by mouth increases the exposure of the airways, while breathing by nose (as would be true for nonsmokers exposed to ETS most of the time) offers some protection for the lower respiratory tract.

The most important variable determining the amount and site of uptake is the water solubility of the gas in question. Gases that are highly soluble in water, such as formaldehyde or acrolein, will

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

be almost completely removed by the upper respiratory tract, especially during nasal breathing. The concentration of other gases, such as the oxides of nitrogen, which have an intermediate solubility, will decrease as the inspired bolus penetrates deeper and deeper into the lungs. There will be uptake of gas in the upper airways, but significant amounts will also penetrate to respiratory bronchioles and alveoli. Finally, there are gases of low solubility, such as carbon monoxide. No significant uptake of CO occurs in the upper airways, and it is only slowly absorbed across the air-blood barrier. In the absence of heavy exercise and very high ventilation rates, many hours are required to establish an equilibrium between inspired GO and carboxyhemoglobin in the blood.

As was true for particles, we can estimate the gas uptake for active smokers and for passive smokers. As reviewed in Chapter 2, CO from ETS can range from less than 1 to 8 ppm. If the background air has little or no CO, even the upper estimates of 8 ppm will have a negligible effect on carboxyhemoglobin levels. Almost 2 hours would be required to reach 1% carboxyhemoglobin (Peterson and Stewart, 1975). This is approximately the same as background levels of carboxyhemoglobin, which are associated with endogenous production of carbon monoxide. Even after 15 hours, when the equilibrium value of 1.7% COHb is finally reached, the effect should be insignificant. However, if air pollution from mobile and stationary sources produces higher background levels of CO, then an incremental exposure of 1 to 8 ppm could produce some added burden of carboxyhemoglobin.

Reactive or highly soluble gases such as formaldehyde, acrolein, or oxides of nitrogen present a different situation. Acrolein has a very high water solubility (40 g/100 ml). Because of this high solubility in the airway lining fluids, one would anticipate a collection efficiency approaching 100%. Moreover, this would occur rapidly, so that acrolein is classified as an upper respiratory tract irritant. According to Table 2–10, there are between 60 and 100 µg of acrolein generated per cigarette. Thus, from 20 cigarettes, 1.2 to 2.0 mg of acrolein would be deposited in the respiratory tract of the active smoker.

Chapter 2 suggests that levels of acrolein in public places where smoking is permitted could range from 10 to 50 µg/m3. Using similar assumptions to that made for particles, we estimate that the nonsmoker would inhale 4.8 to 10 m3 of air per 8 hours. Assuming a collection efficiency of 100%, the total amount of

Suggested Citation:"ASSESSING EXPOSURES TO 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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acrolein deposited in the passive smoker would be approximately 0.048 to 0.5 mg. We select 1.6 mg/8 hours as the mid-range dose for the active smokers, which assumes 20 cigarettes smoked per 8 hours with 80 µg acrolein per cigarette. Using this value, the nonsmoker exposed to ETS for 8 hours would then receive approximately 3 to 31% of that received by the active smoker. When the contribution of ETS is included for the active smoker, the nonsmoker exposed to ETS for 8 hours would receive between 5 and 24% of that of an active smoker. The relatively high dose of acrolein received by the nonsmoker reflects the high collection efficiency for this hydrophilic component and the persistence of vapor-phase components in the air even when filtration is used. Table 2–10 gives comparisons of the amount of other materials inspired for both active smokers and individuals exposed to ETS over shorter periods of time.

SUMMARY AND RECOMMENDATIONS

A number of studies have measured the levels of specific constituents of ETS under natural conditions (reviewed in Chapters 2 and 5). The extrapolation from relative exposures to relative doses received is difficult. Variation in the percent of time individuals spend in particular environments such as home, workplace, and so forth, and the variations in uptake and clearance, discussed in this chapter, will affect the actual dose received.

Using a simple, first-approximation model for exposure and retention, the relative daily dose received for a nonsmoker exposed to ETS can be compared with the dose received by an active smoker. For RSP, the estimates were up to 0.26%. For acrolein, a hydrophillic, vapor-phase constituent, the relative dose is estimated to be much higher, 3 to 31%, whether or not the ETS exposure of the active smoker is considered. Nicotine, another constituent that appears primarily in the vapor phase of ETS, has an estimated relative dose of up to 1% (see Chapter 8).

The extent to which these are indicative of the relative exposures to specific constituents that are important for particular health effects in active smokers or in nonsmokers exposed to ETS cannot be determined for any of the health effects reviewed later in this report. Nevertheless, the estimated relative exposures give

Suggested Citation:"ASSESSING EXPOSURES TO 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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some idea of the potential range of relative exposures, for constitutents that are found both in the vapor phase and in the particulate phase.

Because of the range of estimated relative doses, it would be ideal to make estimates of the relative dose based on the specific constituent(s) that are most relevant to the health effect being assessed. However, many of these specific constituents, for instance the carcinogenic constituents such as benzo[a]pyrene, N-nitrosodimethylamine, and N-nitrosodiethylamine, are difficult to measure; therefore, there are not enough data available to make meaningful estimates of the relative doses of these constituents. Also, biological markers might be potentially informative indicators of the relative doses. However, as reviewed in Chapter 8, to date only carbon monoxide, nicotine, and cotinine have been measured extensively in humans.

What Is Known
  1. Particle size and breathing pattern are critical factors in the deposition of ETS in humans.

  2. Theoretical models predict that 30 to 40% of the particles with the size range present in cigarette smoke will deposit in the alveolar region and 5 to 10% in the tracheobronchial region.

  3. The collection efficiency of smoke particles during active smoking has been measured to be about 70%. On the other hand, the collection efficiency is estimated to be only 10% for nonsmokers exposed to ETS.

What Scientific Information Is Missing
  1. Actual measurement of regional deposition of cigarette smoke particulates in human lungs is not available.

  2. There are little data regarding the actual retention and sites of deposition of ETS particulates in either humans or animals.

  3. The concentrations of various components in vapor and particulate phases of MS and ETS differ. Consequently, research is needed, particularly for vapor-phase components, to see how these differences affect dose.

Suggested Citation:"ASSESSING EXPOSURES TO 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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REFERENCES

Albert, R.E., M.Lippmann, and W.Briscoe. The characteristics of bronchial clearance in humans and the effect of cigarette smoking. Arch. Environ. Health 18:738–755, 1969.


Bennett, W.D., M.S.Messina, and G.C.Smaldone. Effect of exercise on deposition and subsequent retention of inhaled particles. J. Appl. Physiol. 59:1046–1054, 1985.

Brain, J.D., and P.A.Valberg. Models of lung retention based on ICRP Task Group report. Arch. Environ. Health 28:1–11, 1974.


Cohen, D., S.F.Arai, and J.D.Brain. Smoking impairs long-term dust clearance from the lung. Science 204:514–517, 1979.


Davies, C.N., J.Heyder, and M.C.Subba Rama. The breathing of half-micron aerosols. I. Experimental. J. Appl. Physiol. 32:591–600, 1972.


Ferin, J., G.Urbankova, and A.Vlokova. Influence of tobacco smoke on the elimination of particles from the lungs. Nature 206:515–516, 1965.


Harbison, M.L., and J.D.Brain. Effects on exercise of particle deposition in Syrian golden hamsters. Am. Rev. Respir. Dis. 128:904–908, 1983.

Heyder, J. Particle transport onto human airway surfaces. Eur. J. Respir. Dis. 63(Suppl. 119):29–50, 1982.

Hiller, F.C., M.K.Mazumder, J.D.Wilson, P.C.McLeod, and R.C.Bone. Human respiratory tract deposition using multimodal aerosols. J. Aerosol. Sci. 13:337–343, 1982a.

Hiller, F.C., K.T.McCusker, M.K.Mazumder, J.D.Wilson, and R.C.Bone. Deposition of sidestream cigarette smoke in the human respiratory tract. Am. Rev. Respir. Dis. 125:406–408, 1982b.

Hinds, W.C. Size characteristics of cigarette smoke. Am. Ind. Hyg. Assoc. J. 39:48–54, 1978.


International Commission on Radiological Protection (ICRP), Task Group of Committee 2 of the International Commission on Radiological Protection. Physiological data for reference man, pp. 346–347. In ICRP. Report of the Task Group on Reference Man (ICRP 23). New York: Pergamon, 1975.


Keith, C.H., and J.C.Derrick. Measurement of the particle size distribution and concentration of cigarette smoke by the “conifuge.” J. Colloid Sci. 15:340–356, 1960.


Martonen T.B., and J.E.owe. Cigarette smoke pattern in a human respiratory tract model. Proc. Ann. Conf. Eng. Med. Biol. 25:171, 1983 (abstract).

McCusker K., F.C.Hiller, J.D.Wilson, M.K.Mazumder, and R.Bone. Aerodynamic sizing of tobacco smoke particulate from commercial cigarettes. Arch. Environ. Health 38:215–218, 1983.

Muir D.C.F., and C.N.Davies. The deposition of 0.5 µm diameter aerosols in the lungs of man. Ann. Occup. Hyg. 10:161–174, 1967.


Peterson, J.E., and R.D.Stewart. Predicting the carboxyhemoglobin levels resulting from carbon monoxide exposures. J. Appl. Physiol. 39:633–638, 1975.


Sanchis J., M.Dolovich, R.Chalmers, and M.T.Newhouse. Regional distribution and lung clearance mechanisms in smokers and non-smokers, pp. 183–191. In E.H.Walton, Ed. Inhaled Particles, Part III. Surrey, England: Unwin Brothers Ltd., 1971.

Suggested Citation:"ASSESSING EXPOSURES TO 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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Schlesinger R.B., and M.Lippmann. Particle deposition in casts of the human upper tracheobronchial tree. Am. Ind. Hyg. Assoc. J. 33:237–251, 1972.

Schlesinger R.B., and M.Lippmann. Selective particle deposition and bronchogenic carcinoma. Environ. Res. 15:424–431, 1978.


Task Group on Lung Dynamics. Deposition and retention models for internal dosimetry of the human respiratory tract. Health Phys. 12:173–207, 1966.


Weiss S.T., I.B.Tager, M.Schenker, and F.E.Speizer. The health effects of involuntary smoking. Am. Rev. Respir. Dis. 128:933–942, 1983.

Suggested Citation:"ASSESSING EXPOSURES TO 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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8
Assessing Exposures to Environmental Tobacco Smoke Using Biological Markers

Previous chapters have dealt with the formation and composition of tobacco sidestream smoke, its contribution to environmental tobacco smoke (ETS), and the conditions that govern the physicochemistry and toxicity of ETS. Personal monitoring of exposure and analysis of the respiratory environment enable us to estimate the level of toxic agents for individuals exposed to ETS. Studies on the uptake of smoke constituents by individuals and on the metabolic fate of such constituents can provide information relative to epidemiologic observations and the actual exposure levels of different populations.

Exposure to ETS may depend on several factors, including the number of smokers in an enclosed area, the size and nature of the area, and the degree of ventilation. Thus, optimal assessment of exposure should be done by analysis of the physiological fluids of exposed persons rather than by analysis of respiratory environment. The development of new biochemical methods enables us to obtain measurements of exposure to ETS by determining the uptake of specific agents in body fluids and calculating the risk relative to that of the exposure of active smokers. The uptake of individual agents from ETS can be determined by biochemical measures that have been developed for assessment of active smoking behavior, as long as these measures are sensitive and specific enough for quantitating exposure to such agents by nonsmokers.

Suggested Citation:"ASSESSING EXPOSURES TO 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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BIOLOGICAL MARKERS IN PHYSIOLOGICAL FLUIDS

Thiocyanate

The hydrogen cyanide (HCN) absorbed from tobacco smoke is detoxified in the liver, yielding thiocyanate (SCN). However, SCN in serum and other biological fluids does not exclusively originate from inhaled tobacco smoke. Thiocyanate also can be derived from the diet (Haley et al., 1983; Jarvis, 1985).

Before 1975, primarily two colorimetric methods were used for the manual determination of thiocyanate in biological fluids (Aldridge, 1944; Bowler, 1944). Subsequently, the automatic method by Butts et al. (1974) has found wide application in comparing physiological fluids from smokers and nonsmokers. It entails determination of thiocyanate by its reaction with ferric ions, which yield a color complex with maximal absorbance at 460 nm, the intensity of which can be measured in an autoanalyzer. In sera of nonsmokers, Butts et al. (1974) determined up to 95 µmol/L of SCN. The critical value in differentiating between smokers and nonsmokers was 85 µmol/L of SCN. In other investigations, 100 µmol/L of SCN was found to be the critical level for serum (Junge et al., 1978) and for saliva (Luepker et al., 1981). This fact and the low concentrations of HCN in ETS (Hoffmann et al., 1984) explain why some investigators were unable to distinguish between nonsmokers exposed to ETS and those without any exposure to tobacco smoke (Hoffmann et al., 1984; Jarvis, 1985).

Similarly, the mean serum level of SCN in healthy pregnant women at term who were exposed to ETS (35.9 µmol/L) was not distinctly different from that in those without ETS exposure (32.3 µmol/L), nor was there a measureable difference in SCN levels in the umbilical cords of the neonates (26 versus 23 µmol/L) (Hauth et al., 1984).

In one study, it appeared that there was a trend toward higher thiocyanate levels in the saliva of nonsmoking children residing with smokers compared to the SCN levels in saliva of children without ETS exposure, yet this trend was insignificant (Gillies et al., 1982). In a study of six volunteer nonsmokers exposed to a smoke-filled room for 4 hours, there was a significant increase in salivary SCN. However, the SCN values of the nonsmokers

Suggested Citation:"ASSESSING EXPOSURES TO 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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exposed to ETS were not distinguishable from those nonsmokers free of tobacco smoke exposure (Pekkanen et al., 1976).

In another study, mean serum thiocyanate levels were reported to be significantly higher (p<0.002) for children and adolescents with exposure to cigarette smoke at home (n=14; SCN=97.3±45.4 µmol/L) than for those not exposed (n=10; SCN=54.2±11.3 µmol/L). The authors of the latter study also reported a weak correlation between thiocyanate concentration and number of cigarettes smoked per family (Poulton et al., 1984). This study was criticized because some of the determined thiocyanate levels were within the range reported for heavy cigarette smokers. It is likely that there was deceptive reporting of adolescent smoking status (Jarvis, 1985). Based on the observations to date, the level of thiocyanate in saliva, serum, and/or urine is not useful as an indicator for the uptake of ETS by a nonsmoker.

Carbon Monoxide and Carboxyhemoglobin

Carbon monoxide (CO) in the body originates from endogenous processes as well as environmental sources. The endogenous production of CO is primarily a consequence of the breakdown of hemoglobin and of other heme-containing pigments. Healthy adults produce about 0.4 ml of CO per hour (0.5 mg/h; Coburn et al., 1964). This provides the major portion of CO that is found as carboxyhemoglobin (COHb) in nonsmokers. In nonsmokers without occupational exposure to CO, COHb ranges from 0.5 to 1.5% (National Research Council, 1981; Wald et al., 1981).

The inhalation of CO from the environment is followed by an increase of the CO concentration in the alveolar gas and by diffusion from the gas phase through the pulmonary membrane into the blood. CO is complexed with blood to form COHb and, as such, is transported throughout the body. Complexing it with hemoglobin occurs with a strong coordination bond with the iron of heme, a bond that is about 200 times stronger than that with molecular oxygen. CO is only slowly released from the blood in the process of exhaling. In the case of nonsmokers who have been exposed to elevated levels of CO in the air for a few hours, the half-life of COHb lasts 2–4 hours (National Research Council, 1981).

Monitoring of absorbed CO in the blood is done primarily by the analysis of CO in alveolar gas and by the analysis of COHb

Suggested Citation:"ASSESSING EXPOSURES TO 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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in blood. The most widely used technique in the clinical laboratory is the determination of COHb with automated differential spectrophotometry (National Research Council, 1977). The determination of CO in exhaled air by standardized gas analyzers has been used less frequently. However, the portable “Ecolyzer” and other similar instruments have proved to be reliable instruments for the recent validations of the reported smoking habits among populations in field studies (Vogt et al., 1979). The data from both measurements, amount of CO in the alveolar gas and the concentration of COHb in blood, are well correlated. Theoretically, the slope of the graph relating the percent of concentration of COHb to alveolar CO should be about 0.155 at CO concentrations of 0–50 ppm. Most laboratory studies have confirmed this correlation experimentally (National Research Council, 1981). In the case of cigarette smokers who have inhaled puffs of smoke containing 20,000–50,000 ppm of CO, the correlation between exhaled CO and COHb is also in good agreement (r=0.97; Heinemann et al., 1984).

The COHb levels are of value for comparing degrees of smoke inhalation. In a study of men aged 34–64 years, cigarette smokers had on the average 4.7% of COHb; cigar smokers, 2.9%; pipe smokers, 2.2%; and nonsmokers, 0.9% (Wald et al., 1981, 1984). However, measurements of exhaled CO or COHb are not valid indicators of chronic exposure to ETS. A study of 100 self-reported nonsmokers who were divided into four groups—without exposure to ETS, with little, with some, and with a lot—revealed no significant differences in measurements of expired CO (5.0–5.7 ppm; mean, 5.61±2.70 ppm) or COHb (0.80–0.94%; mean, 0.87± 0.67%) (Jarvis and Russell, 1984). This observation is also supported by a study of six nonsmoking flight attendants who served in the smokers’ section of a trans-Pacific aircraft. Preflight COHb levels were 1.0±0.2% and postflight levels (after serving round-trip) were 0.7±0.2% (Foliart et al., 1983).

Heavily smoke-polluted environments can lead to elevated absorption of CO. This was shown for seven nonsmokers exposed for 2 hours in a pub, whose exhaled air revealed an average of 5.9 ppm of CO, a level that corresponds to the alveolar gas of a smoker after smoking one cigarette (Jarvis et al., 1983). Another study showed that twelve nonsmokers, sharing the nonairconditioned environment of a room with four smokers who smoked four cigarettes each within 30 minutes, had an COHb increase of the

Suggested Citation:"ASSESSING EXPOSURES TO 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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same magnitude as that measured in a smoker after consuming one cigarette (Huch et al., 1980).

Even though tobacco smoke is a major source for indoor air pollution, additional sources may contribute to increased CO concentrations in air and, consequently, to higher COHb levels in exposed subjects. Such sources include gas stoves, faulty furnaces, and space heaters (National Research Council, 1981). For example, kerosene heaters can be a major source for indoor pollution. Depending on the model and flame setting, kerosene space heaters generate up to 6.5 mg of CO per minute of operation (Leaderer, 1982).

In summary, CO in alveolar air and as COHb in nonsmokers originates from endogenous processes as well as from environmental sources. ETS is an important pollutant of indoor environments; however, except for highly polluted settings, CO levels in exhaled air and COHb levels in the blood are not statisically significantly elevated following exposure to ETS, although acute short-term exposures from 3–4 hours may be detected if blood or expired air is sampled within 30 minutes of the end of exposure. In sum, however, measurements of exhaled CO and of COHb are not useful indicators of exposure to ambient ETS except in acute exposure studies in the laboratory. CO measures are a marker of gas-phase exposure to ETS.

Nicotine and Cotinine

Disregarding nicotine-containing chewing gum and nicotine aerosol rods as aids for smoking cessation, the presence of nicotine and that of its major metabolite, cotinine, in biological fluids is entirely due to the exposure to tobacco, tobacco smoke, or environmental tobacco smoke. The determination of nicotine and cotinine in saliva, blood, or urine of active and passive smokers is done primarily by gas chromatography (GC) with a nitrogen-sensitive detector and by radioimmunoassay (RIA).

The GC method requires great precaution in order to avoid contamination by traces of nicotine from the environment or from solvents and/or equipment. This is of major importance for samples containing nicotine at levels <20 ng/ml of fluid, as is the case in nonsmokers exposed to ETS (Feyeraband and Russell, 1980). The GC method can be used to measure concentrations of nicotine as low as 1 ng/ml and concentrations of cotinine as low as 5 ng/ml

Suggested Citation:"ASSESSING EXPOSURES TO 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 samples of physiological fluids (Jacob et al., 1981). An experienced chemist can analyze up to 25 samples per day for nicotine and cotinine.

The radioimmunoassays for nicotine and cotinine represent probably the most direct technique available. These assays have only low cross-reactivities with other naturally occurring metabolites of nicotine. The sensitivity of these assays is about 0.5 ng/ml for both nicotine and cotinine and has inter- and intra-assay variations of ±5% (Langone et al., 1973; Hill et al., 1983). An experienced biochemist with automated equipment can analyze up to 80 samples (plus 20 control samples) per day. So far, the RIA method has been used by a limited number of laboratories because it requires the synthesis of specific nicotine and cotinine derivatives for the generation of serum albumin conjugates and the raising of antibodies to these conjugates (Langone et al., 1973). In addition, the RIA method also requires careful drawing and handling of samples to avoid contamination.

Table 8–1 presents results from the major studies on the uptake of nicotine by nonsmokers under acute exposure conditions. These data show that exposure to high levels of ETS in laboratories can lead to a significant uptake of nicotine. This uptake is clearly reflected in the concentrations of nicotine in plasma (up to 0.9 µg/ml for nonsmokers compared with a mean value of 14.8 µg/ml for smokers, an increase of 15-fold) and in urine (84 ng/ml for nonsmokers, compared with 1,750 ng/ml, a increase of 20-fold) (Russell and Feyeraband, 1975; Hoffmann et al., 1984). The significantly higher values for nicotine in the plasma compared to urine may be explained by the short initial half-life in smokers of 9 minutes and relatively short terminal half-life in smokers of 2 hours (Benowitz et al., 1982).

Table 8–2 presents data for nicotine and cotinine uptake as measured in physiological fluids of nonsmokers exposed, to ETS under daily life conditions. With the exception of the report by Matsukura et al. (1984), the data demonstrate that the involuntary exposure of the passive smoker amounts to a few percent or less of the amount of nicotine that is inhaled by a cigarette smoker. Table 8–3 compares nicotine and cotinine levels as determined in one laboratory in plasma, saliva, and urine of nonsmokers with and without ETS exposure and of active smokers. This comparison shows that, generally, concentrations of nicotine and cotinine in plasma, saliva, and urine of nonsmokers exposed to ETS amount

Suggested Citation:"ASSESSING EXPOSURES TO 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 8–1 Nicotine Uptake by Nonsmokers Exposed to ETS Under Laboratory Conditions

Authors

ETS—Conditions

No. of Nonsmokers

Results

Harke, 1970

Room—170 m3

7

Excretion in the urine (6 h after exposure)

 

(1) 11 smokers consumed 100 cigarettes during 2 h; no ventilation (30 ppm CO)

 

Nicotine: 10±6.8 µg/6 h

Cotinine: 35±34.5 µg/6 h

 

 

(2) as (1)—but with regular ventilation (5 ppm CO)

7

Nicotine: 18±7 µg/6 h

Cotinine: 19±9.4 µg/6 h

 

Cano et al., 1970

Room—66 m3

 

 

 

 

4 smokers and 2 nonsmokers

 

Excretion in the urine

Nicotine, µg/24 h

 

(a) lived together for 5 days

 

Day 1—no smoking

0

 

 

 

Day 2—98 cigarettes smoked

35–44

 

 

 

Day 3—121 cigarettes smoked

50–61

 

 

 

Day 4—98 cigarettes smoked

62.5–70

 

 

 

Day 5—88 cigarettes smoked

47–50

 

(b) lived together for 4 days

2

Day 1—97 cigarettes; 15 µg nic./m3

23–34

 

 

 

Day 2—96 cigarettes; 22 µg nic./m3

22.5–58

 

 

 

Day 3—94 cigarettes; 35 µg nic./m3

47.5–69

 

 

 

Day 4—103 cigarettes; 33 µg nic./m3

32–65

Russell and Feyerabend, 1975

(1) Room—43 m3

12

Nicotine

9 smokers consumed 80 cigarettes and 2 cigars; no ventilation (38 ppm CO)

 

Before exposure: 0.73±1.6 µg/ml plasma

After 78 min exposure: 0.90±0.29 µg/ml plasma

15 min after ending exposure: 80.0±58.7 ng/ml urine

No experimental ETS exposure: 12.4 ng/ml urine

8.9 ng/ml urine

 

(2) Two groups measured after lunch

14

13

No experimental ETS exposure: 12.4±16.9 ng/ml urine

8.9±9.1 ng/ml urine

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

Authors

ETS—Conditions

No. of Nonsmokers

Results

Hoffmann et al., 1984

Room—16 m3

6

Time during exposure

Nicotine

Cotinine

4 cigarettes concurrently and continuously machine smoked for 80 min; 6 air exchanges/h (200 g nic./m3 20 ppm CO)

 

0

Saliva:

Plasma:

Urine:

3 ng/ml

0.2 ng/ml

17 ng/mg creat.

1.0 ng/ml

0.9 ng/ml

14 ng/mg creat.

80 min

Saliva:

Plasma:

Urine:

730 ng/ml

0.5 ng/ml

84 ng/mg creat.

1.4 ng/ml

1.3 ng/ml

28 ng/mg creat.

 

Time following exposure

 

30 min

Saliva:

Plasma:

148 ng/ml

0.4 ng/ml

1.7 ng/ml

1.8 ng/ml

150 min

Saliva:

Plasma:

Urine:

17 ng/ml

0.7 ng/ml

100 ng/mg creat.

3.1 ng/ml

2.9 ng/ml

45 ng/mg creat.

300 min

Saliva:

Plasma:

Urine:

7 ng/ml

0.6 ng/ml

48 ng/mg creat.

3.5 ng/ml

3.2 ng/ml

55 ng/mg creat.

aAbbreviations: creat., creatinine; nic., nicotine.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

to less than 1% of the mean values observed in physiological fluids of active smokers, even though some nicotine measurements in plasma give a higher reading (Jarvis et al., 1984).

In a large-scale study of 839 nonsmokers (identified by their questionnaire response and also having a cotinine concentration of <20 ng/ml of saliva), cotinine levels increased with the number of smokers in the home for each of three age groups examined independently (<5, 6–17, and >18 years). The cotinine levels in saliva were found to be significantly associated with increasing number of smokers per household within each age group. The median salivary cotinine levels in adult smokers was 287 ng cotinine/ml (Coultas et al., 1986).

Matsukura et al. (1984) report that cotinine in the urine of ETS-exposed nonsmokers reaches an average of 1.56±0.57 µg/mg of creatinine when 40 or more cigarettes per day have been smoked in the home of the exposed subjects. In the case of cigarette smokers, they found cotinine levels of 8.57±0.39 µg/mg of creatinine in urine. This study has been questioned because its findings of cotinine in urine of both active and passive smokers indicate levels substantially higher than those reported in other studies (Adlkofer et al., 1985; Pittenger, 1985) (see Chapter 12).

Nicotine uptake by infants of cigarette-smoking mothers appears to be higher than is generally observed for the adult nonsmoker. The amount of cotinine excreted in the infant’s urine has been found to be correlated with the number of cigarettes smoked by the mother in the 24 hours preceding the measurement (Greenberg et al., 1984).

The analysis of nicotine and cotinine in physiologic fluids can be misleading if made on very light smokers or nonsmokers who either sniff tobacco or are tobacco chewers or snuff-dippers. In the case of the very light smoker, nicotine and cotinine values may be similar to those of nonsmokers who had exposure to high levels of ETS (Russell and Feyerabend, 1975; Wald et al., 1984). In the case of individuals who use tobacco nasally, or orally, on a regular basis, the nicotine and cotinine values may approach those of heavy cigarette smokers (Russell et al., 1980; Russell et al., 1981; Palladino et al., in press). In both groups, the analysis of COHb will reveal that these subjects are light smokers or nonsmokers, respectively. However, nicotine and cotinine levels for such persons are clearly not valid for the determination of their exposure to ETS.

Suggested Citation:"ASSESSING EXPOSURES TO 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 8–2 Nicotine Uptake by Nonsmokers Exposed to ETS Under Daily Life Conditionsa

Authors

Group of Nonsmokers

No. of Nonsmokers Examined

Results

Russell and Feyerabend, 1975

Hospital employees

 

 

(urine collection 1 h after lunch)

 

 

ng/ml

 

(a) Group 1

14

Nicotine in urine:

12.4±16.9

 

(b) Group 2

13

Nicotine in urine:

8.9±9.1

Feyerabend et al., 1982

Hospital employees and outpatients

 

 

ng/ml

 

(a) nonexposed to ETS during the morning (self report)

30

Nicotine in the urine:

7.5±8.5

 

 

Nicotine in saliva:

5.9±4.4

 

(b) exposed to ETS during the morning (self report)

 

Nicotine in urine:

21.6±28.9

 

 

Nicotine in saliva:

10.1±9.7

Foliart et al., 1983

Flight attendants

6

Nicotine in serum:

ng/ml

 

(San Francisco-Tokyo-San Francisco)

 

(a) before flight

1.6±0.8

 

(b) after flight

3.2±1.0

Wald et al., 1984

Hospital staff and outpatients

 

 

ng/ml

 

(a) nonexposed to ETS

22

Cotinine in urine:

2.0 (0.0–9.3)

 

(b) exposed to ETS (self report)

199

Cotinine in urine:

6.0 (1.4–22.0)

 

ng/ml

Wald and Ritchie, 1984

(a) husbands of nonsmokers

101

Cotinine in urine:

8.5±1.3

 

(b) husbands of smokers

20

Cotinine in urine:

25.2±14.8

Jarvis et al., 1983

Employees in an office, sample collection at 11:30 a.m. (I) and 7:45 p.m. (II) (time between collections including 2-h stay in smoking “pub”)

7

ng/ml

Before

After

 

 

I

II

 

Nicotine in plasma:

0.76

2.49

 

Nicotine in saliva:

1.90

43.63

 

Nicotine in urine:

10.51

92.63

Cotinine in plasma:

1.07

7.33

Cotinine in saliva:

1.50

8.04

Cotinine in urine:

4.80

12.94

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

 

(Differences between I and II are statistically highly significant; p values range from <0.01 to <0.001)

Jarvis et al., 1985

Nonsmoking school children (11–16-yr-old)

 

ng/ml

 

I. Neither parent smoked

269

Cotinine in saliva:

0.44±0.68

II. Only father smoked

96

Cotinine in saliva:

1.31±1.21

III. Only mother smoked

76

Cotinine in saliva:

1.95±1.71

IV. Both parents smoked

128

Cotinine in saliva:

3.38±2.45

Matsukura et al., 1984

472 nonsmokers

 

 

Urine collection in the morning

(a) smokers in home

272

µg cot./mg creat.

0.79±0.1

(b) nonsmokers in home

200

 

0.51±0.09

Cigarettes smoked per day in home of nonsmokers

 

1–9

25

µg cot./mg creat.

0.31±0.08

10–19

57

 

0.42±0.10

20–29

99

0.87±0.19

30–39

38

1.03±0.25

>40

28

1.56±0.57

Unspecified

25

0.56±0.16

Greenberg et al., 1984

Infants under 10 months of age (not breastfed)

 

 

(a) not exposed to ETS

18

Urine ng nic./mg creat.

0 (0–59)

 

Urine ng nic./mg creat.

4 (0–145)

Saliva ng nic./mg creat.

0 (0–3)

 

(b) exposed to ETS

28

Urine ng nic./mg creat.

53 (0–370)

 

Urine ng cot./mg creat.

351 (41–1,885)

Saliva ng nic./mg creat.

12.7 (0–166)

Saliva ng cot./mg creat.

9 (0–25)

aAbbreviations: cot., cotinine; creat., creatinine; nic., nicotine.

Suggested Citation:"ASSESSING EXPOSURES TO 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 8–3 Approximate Relations of Nicotine as a Parameter Between Nonsmokers, Passive Smokers, and Active Smokersa

Nicotine/Cotinine

Nonsmokers without ETS Exposure No.=46

Nonsmokers with ETS Exposure No.=54

Active Smokers No.=94

Mean Value

% of Active Smokers’ Value

Mean Value

% of Active Smokers’ Value

Mean Value

Nicotine (ng/ml)

 

in plasma

1.0

7

0.8

5.5

14.8

in saliva

3.8

0.6

5.5

0.8

673

in urine

3.9

0.2

12.1*

0.7

1,750

Cotinine (ng/ml)

 

in plasma

0.8

0.3

2.0*

0.7

275

in saliva

0.7

0.2

2.5**

0.8

310

in urine

1.6

0.1

7.7**

0.6

1,390

aDifferences between nonsmokers exposed to ETS compared with nonsmokers without exposure: *p<0.01; **p<0.001.

SOURCE: Jarvis et al., 1984.

Cotinine elimination in the plasma of nonsmokers exposed to ETS was reported to be slower than cotinine elimination in the plasma of active smokers. Cotinine elimination from urine was also significantly slower. In a study of 10 chronic smokers and 4 nonsmokers experimentally exposed to ETS, the half-life of elimination of cotinine from plasma was 49.7 hours in nonsmokers and 18.5 hours in smokers (Sepkovic et al., 1986). Disappearance of cotinine from urine was also significantly slower in nonsmokers than in chronic smokers (32.7 hours versus 21.9 hours). These preliminary data need to be considered when using cotinine to quantify the dose in nonsmokers exposed to ETS.

In summary, the determination of nicotine and, especially, of cotinine in saliva, blood, and/or urine of nonsmokers exposed to ETS represents at present the most appropriate assay for estimating long-term (average daily) exposure. However, venipuncture needed to get serum samples is often impractical, if not impossible. The use of saliva for nicotine and cotinine assays, despite some advantages, also has certain inherent weaknesses, such as uncharacteristically high readings immediately after heavy ETS exposure and the need to wait several hours after exposure for the

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

cotinine concentration to stabilize (Hoffmann et al., 1984). Saliva is a particularly erratic source on which to make nicotine measures. Urinalysis for cotinine is the preferred method for assessment of long-term ETS exposure, because the sampling is noninvasive, the excretion rate of cotinine is only slightly dependent on the pH of urine, and assessment of the average daily exposure on the basis of cotinine levels is independent of the restrictions posed by variations of the half-life of nicotine in smokers and nonsmokers (Beckett et al., 1971; Klein and Gorrod, 1978).

Creatinine—Reference Compound for Urine Analysis

Urine sampling does have some associated problems. Often it is impractical to collect 24-hour urine samples for the analysis of biological markers of direct exposure to tobacco smoke or to ETS unless undertaken under strict medical supervision, such as in a metabolic ward. In this case, the ratio of biological markers to creatinine is often used to allow for variations in fluid intake (and excretion) (see Table 8–1).

Creatinine excretion varies from person to person, but the daily output for each individual is almost constant from day to day. Urinary creatinine bears a direct relation to the muscle mass of the individual. The milligram amount of creatinine excreted during 24 hours per kilogram of body weight is often expressed as the creatinine coefficient. The coefficient varies from 18 to 32 in men (total excretion 1.1–3.2 g/day) and from 10 to 25 in women (total excretion 0.9–2.5 g/day). The coefficient is largely independent of variations in diet, since creatinine in healthy persons is of endogenous origin. In older people, the daily output of creatinine may decrease to 0.5 g/day. In cigarette smokers, urinary output of creatinine in men appears to decrease with greater number of cigarettes smoked per day (Adlkofer et al., 1984). However, this finding needs to be confirmed.

Based on the variations in daily creatinine excretions in the urine, one has to be aware of the limitation of the factor “amount of biological marker per milligram of creatinine.” In a study with 15 adult male cigarette smokers, the daily creatinine excretion varied between 1.0 and 2.5 g and the cotinine excretion between 1.3 and 13.1 mg (Hoffmann and Brunnemann, 1983). However, in certain cases, such as with healthy infants, the daily variations in urinary excretion are rather small. Thus, the measured nanograms of

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

cotinine per milligram of creatinine in urine reflect the inhalation of environmental nicotine from ETS rather well (Greenberg et al., 1984).

For the determination in urine, creatinine is complexed with picric acid and the resulting red color is measured spectrophotometrically, a task now predominately done with an autoanalyzer (Faulkner et al., 1976).

Although the determination of cotinine in urine without reference to creatinine has resulted in meaningful data in some studies, the standardized cotinine levels per unit of creatinine may give a more stable measure of ETS exposure—particularly when limited urine samples must be used.

Hydroxyproline

Inhalation of nitrogen dioxide causes degradation of lung collagen and elastin (Kosmidar et al., 1972; Hatton et al., 1977). This degradation results in elevated urinary excretion of hydroxyproline (Lewis, 1980). It is thus possible that the NO2 in tobacco smoke, and even NO2 in ETS, has the same lung-damaging effect as pure NO2.

Kasuga et al. (1981) reported two studies in which healthy cigarette smokers excreted significantly more hydroxyproline than healthy nonsmokers and exsmokers. In the case of 6- to 11-year-old children of smoking parents, Kausga et al. (1981) found elevated hydroxyproline levels in the urine. Because of the relatively low concentration of NO2 in ETS (see Chapter 2), this finding was unexpected. Adlkofer et al. (1984) were unable to confirm this finding in a study of 23 nonsmokers exposed to ETS.

At present, the question of quantitative aspects of urinary hydroxyproline excretion in nonsmokers exposed to ETS is not settled. It will require additional studies before this compound and its ratio to creatinine can be used as indicators for the degree of ETS exposure.

N-Nitrosoproline

N-nitrosoproline (NPRO) in urine reflects endogenous formation of nitrosamines, many of which are known animal carcinogens (Preussmann and Steward, 1984; Vainio et al., 1985). NPRO appears neither to undergo metabolism in mammals nor to alkylate

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

cellular macromolecules. NPRO is considered to be nonmutagenic and noncarcinogenic and is excreted nearly quantitatively in urine. It has been shown that endogenous formation of NPRO is significantly increased in cigarette smokers (Hoffmann and Brunnemann, 1983; Ladd et al., 1984; Scherer and Adlkofer, in press). The increase is probably due to the high concentrations of nitrogen oxides in tobacco smoke that serve as nitrosating agents and the elevated concentration of thiocyanate in smokers that catalytically enhance the endogenous formation of nitrosamines such as NPRO. These effects are absent in nonsmokers without ETS exposure.

In one 5-day study, four male nonsmokers with controlled diets were exposed to known degrees of ETS for three periods of 80 minutes each on day 3 and day 4. Their 24-hour urine voids were analyzed for NPRO and for cotinine. While the cotinine levels in the urine of these nonsmokers increased from 5–7 ng/ml to 215–360 ng/ml, the NPRO excretion did not significantly change (Brunnemann et al., 1984). In another controlled study with 10 nonsmokers exposed to ETS containing 45 ppb of NO2, 400 ppb of NO, and 22 ppm of CO, urinary output of NPRO was also not elevated while COHb had increased significantly (Scherer and Adlkofer, in press). Although these two studies require confirmation and should include analytical assessment of nitrosothioproline (NTPRO) (Tsuda et al., 1986), another endogenously formed nitrosamine, at present neither NPRO nor NTPRO measurement in urine can be used to indicate exposure to ETS.

Aromatic Amines

During the burning of cigarettes, 20–30 times more aromatic amines are released into the sidestream smoke than are present in the mainstream smoke (see Chapter 2). Although at this time there is a lack of analytical data, it may be assumed that indoor environments that are strongly polluted with ETS contain measurably higher amounts of aromatic amines than ambient air without tobacco smoke pollution.

Preliminary data indicate that free aniline and o-toluidine, serving as surrogates for aromatic amines, are increased, although not significantly, in the 24-hour urine voids of cigarette smokers (3.1±2.6 µg and 6.3±3.7 µg) compared with nonsmokers (2.8 ±2.5 µg and 4.1±3.2 µg) (El-Bayoumy et al., in press). The

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

next step requires the assay of the metabolites of aniline and o-toluidine in the urine of both smokers and nonsmokers. A study of the urinary excretion of aromatic amines in passive smokers would be indicated only if the total amounts of individual amines and their metabolites in smokers’ urine are found to be significantly increased.

GENOTOXICITY OF THE URINE

The evaluation of the genotoxicity of urine in nonsmokers with ETS exposure must consider the possibility of confounding effects, because DNA modifiers may be present in urine as a consequence of dietary intake or as a secondary result of the activity of infectious agents in the urine of the host. Nevertheless, urinary constituents may be DNA modifiers, because the inhaled agents are known or suspected mutagens or because the inhaled agents lead to the formation of such biologically active compounds.

Since 1975, the most widely used assay for genotoxicity of human urine is the determination of mutagenicity in bacterial-tested strains with and without activation by enzyme-induced liver homogenate.

In 1977, Yamasaki and Ames reported the presence of mutagens in the urine of cigarette smokers, thus suggesting a correlation between mutagens in smokers’ urine and increased risk for bladder cancer. Since publication of these data, other studies have reported an association of urinary mutagens that are active in bacterial tester strains with cigarette smoking (International Agency for Research on Cancer, 1986), but not all results from these studies have been consistent. One reason for the divergent findings could be the influence of dietary factors on the mutagens in the urine of smokers (Sasson et al., 1985) and, perhaps also, nonsmokers exposed to ETS.

Three studies have attempted to explain the possible mutagenic activity of the urine of nonsmokers exposed to ETS. In one study, fractions and subfractions were isolated by high-pressure liquid chromatography (HPLC) from the urine of five passive smokers. Upon metabolic activation by S9 liver homogenates from rats pretreated with 3-methylcholanthrene, these materials were mutagenic in TA-bacterial tester strains (Putzrath et al., 1981). It appeared that these mutagens are a complex mixture of urinary

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

components in the polar lipophilic subfractions. Due to a lack of diet control, these results are ambiguous.

In a second assay of urine for bacterial mutagenicity, 8 male nonsmokers (25 and 35 years of age) were placed in a poorly ventilated room (10 m3) with 10 smokers for an 8-hour period (Bos et al., 1983). The 12-hour urine samples of the nonsmokers were collected before, during, and after exposure to ETS. Metabolically activated concentrates of the urine samples were analyzed for mutagenic activity in the tester strain, TA 1538. Urine samples collected directly after exposure to ETS were significantly more mutagenic (relative activity: 3.9±1.0) than urine samples of the same nonsmokers prior to (3.1±0.7) or long after ETS exposure (2.5±0.5).

In the third study, six women who were medical students were exposed to ETS in a 10-m3 exposure chamber on 2 consecutive days for one 3-hour session in the mornings and a 2-hour session in the afternoons. During these sessions, three of the women smoked a total of 30 cigarettes per day of a low-yield filter-tipped brand (5.4 mg tar, 0.4 nicotine, 4.6 mg CO); the other three women did not smoke. After 3 days without exposure and without cigarette smoking by any of the women, the exposure was repeated with reversal of the roles, so that those who had previously been nonsmokers now were smokers, and vice versa. The CO concentration in the chamber averaged 3.0 ± 0.9 ppm. The uptake of smoke was assessed by determination of COHb, cotinine, and thiocyanate in the plasma. Urine samples were collected at the end of the daily smoking periods. Urine was concentrated according to Yamasaki and Ames (1977) and tested for mutagenicity with tested strain TB98 using rat liver homogenate for metabolic activation (Sorsa et al., 1985). As is evident from the data in Table 8–4, COHb values for nonsmokers and passive smokers were indistinguishable, while there was a trend for higher plasma cotinine values in the passive smokers. The authors observed an increase in the mutagenicity of the urine of passive smokers during the period of study. The differences observed were not significant.

On the basis of presently available data, it is likely that the exposure of nonsmokers to heavy ETS increases the potential for metabolically activated genotoxic activity of their urine above and beyond the mutagenic activity that is observed in urine of the same nonsmokers before and long after exposure to ETS. However, before validating the Ames bacterial assay for mutagenicity as an

Suggested Citation:"ASSESSING EXPOSURES TO 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 8–4 Pooled Data of Various Biological Parameters Measured in Blood and Urine of Six Subjects After Periods of Nonsmoking, Passive Smoking, and Active Smoking

Exposure

COHb

Plasma Cotinine

Plasma Thiocyanate

Mutagenicity in Urine

Number of samples

Mean±SE, %

Number of samples

Mean±SE, ng/ml

Number of samples

Mean±SE, µmol/L

Number of samples

Mean±SE, number of induced revertants/ml

No smoking

12

0.57±0.04a

12

1.4±0.2

12

70.8±9.9

12

4.2±1.2

Passive smoking

12

0.55±0.05a

12

2.1±0.4b

12

71.8±9.9

24

5.8±1.0

Active smoking

12

3.38±0.54

12

54.4±11.4

12

70.7±10.2

24

6.4±0.8

aValues below the detection limit (0.5%) included as 0.4%.

bDifference between nonsmoking and passive smoking values not significant but suggestive (p<0.10; t-test).

SOURCE: Sorsa et al., 1985.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×

appropriate method for estimating the genotoxic effect of the urine of ETS-exposed nonsmokers, the method itself and the diet of test subjects have to be standardized. Research in this area is needed, as are studies on the isolation and identification of the active agents in the urine of ETS-exposed nonsmokers.

Adducts Formed in Passive Smokers upon Exposure to ETS

Since about 1975, highly sensitive methods have been developed for the determination of protein- or DNA-adducts of environmental carcinogens and toxic agents in circulating blood. Methods probing these reactions for the toxic agents known to occur in tobacco smoke and ETS include determination of hemoglobin adducts of nitrosodimethylamine, methyl chloride, vinyl chloride, and benzene (National Institute of Environmental Health Sciences, 1984), as well as 4-aminobiphenyl (Green et al., 1984). DNA adducts with the smoke carcinogen, benzo[a]pyrene (BaP), have been described (Santella et al., 1985), and the tobacco-specific 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) leads to O6-methylguanine in DNA (Hoffmann and Hecht, 1985). RIA’s have been developed for quantitative determination of both the BaP-DNA adduct and O6-methylguanine (Perera et al., 1982; Foiles et al., 1985). So far, the method for the determination of the DNA adducts has been applied to the analysis of benzo[a]pyrene in smokers (Shamsuddin et al., 1985). In addition, the hemoglobin-4-aminobiphenyl assay has been used for the analysis of the blood of smokers (Tannenbaum et al., in press). In both cases, only a limited number of samples have been analyzed for these adducts. Nevertheless, the data appear encouraging. Another sensitive method for quantifying DNA adducts is the P32-postlabelling technique, which has been applied to human tissues (Gupta et al., 1982; Everson et al., 1986).

Validation and quantitative determination of the uptake of tobacco smoke carcinogens is urgently needed. Assays of adducts of BaP, aromatic amines, and tobacco-specific nitrosamines with protein or DNA in the circulating blood are the most promising tests of exposure to tobacco smoke. Once such assays have been advanced to yield reproducible, informative methods in smokers, they may be subsequently refined to such sensitivities that they

Suggested Citation:"ASSESSING EXPOSURES TO 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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will also furnish reliable data on such adducts in the blood of passive smokers.

FUTURE NEEDS

At present, the best method for quantifying human exposure to ETS is the assay of nicotine and cotinine in urine and possibly saliva. Nicotine and cotinine can also be determined in serum samples, but these samples require invasive techniques. In smoke-polluted environments, nicotine is present in the vapor phase as a free base, thus its uptake by the passive smoker may not be representative of the uptake of acidic and neutral smoke components from the vapor phase nor of any component in the particulate phase. Thus, future studies should be concerned with developing techniques to measure the uptake by the nonsmoker of various other types of tobacco-specific ETS components. This may include assays for the vapor-phase 3-vinylpyridine or flavor components that are indigenous to tobacco. Particulate-phase agents to be traced could include solanesol, tobacco-specific nitrosamines, and polyphenols such as chlorogenic acid or rutin. These components are likely to be found only in trace amounts in ETS, and, thus, only minute quantities would be found in the circulating blood of passive smokers, making the development of assays difficult. The development of new trace methods for quantifying the levels of some tobacco-specific materials in nonsmokers may require the identification of adducts formed between the ETS components and the proteins in blood. This approach would require the development of highly sensitive methods such as immunoassays (e.g., RIA, ELISA) or postlabelling with radioisotopes or other markers.

The epidemiological studies on the effects of exposure to ETS by nonsmokers have to consider a number of non-ETS-related factors. This fact underlines the urgent need for the development of highly sensitive dosimetric methods for ETS-specific carcinogens that can be applied in field studies.

SUMMARY AND RECOMMENDATIONS

Passive smokers are exposed to trace amounts of toxic agents including tumor initiators, tumor promoters, carcinogens, and organ-specific carcinogens when inhaling ETS. The determination of thiocyanate, nicotine, and cotinine in body fluids such as saliva,

Suggested Citation:"ASSESSING EXPOSURES TO 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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serum, and urine, as well as quantitication of CO in alveolar air and COHb in blood, has been useful for the assessment of the habits of individuals and groups of smokers of cigarettes, cigars, and pipes. Currently, for measuring the exposure to ETS by nonsmokers, nicotine and cotinine appear useful. In acute exposure studies, COHb can be a useful marker.

Nicotine and cotinine, however, may not be directly related to the carcinogenic potential of the smoke. Indicators that are related to the carcinogenic risk are needed. To assess the risks involved in the exposure to carcinogenic agents from ETS, sensitive dosimetry methods for tobacco-specific compounds are urgently needed. During the last decade, immunoassays and postlabelling methods have been developed for tracing toxic and carcinogenic agents in circulating blood. These methodologies should be used for the development of dosimetry studies in nonsmokers exposed to ETS. Protein and DNA adducts may provide exposure measures that could be effectively used in epidemiologic studies.

What Is Known
  1. Determinations of thiocyanate, nicotine, and cotinine in saliva, serum, and urine, as well as quantification of CO in alveolar air and carboxyhemoglobin in blood, have been shown to be useful parameters for the assessment of the habits of individuals and groups of active smokers of cigarettes, cigars, and pipes. However, in general, only nicotine and its metabolite cotinine have proven useful for measuring the exposure to ETS of nonsmokers.

  2. Assessment of average daily exposure on the basis of cotinine levels in saliva and urine is independent of the restrictions posed by variations of the half-life of nicotine in smokers and nonsmokers.

  3. The determination in urine of the amount of cotinine per milligram of creatinine should provide a more stable measure of recent environmental exposure to nicotine from ETS than cotinine without reference to creatinine, particularly when limited volumes of urine are available.

  4. It is likely that the exposure of nonsmokers to ETS increases the mutagenic activity of their urine over the activity observed in urine of the same nonsmokers when not exposed to ETS.

Suggested Citation:"ASSESSING EXPOSURES TO 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.
×
What Scientific Information Is Missing
  1. The question of urinary hydroxyproline excretion in nonsmokers exposed to ETS is not settled.

  2. A study on the urinary excretion of aromatic amines in nonsmokers exposed to ETS is needed in order to correlate the total amounts of individual amines and their metabolites in the urine of nonsmokers exposed to ETS.

  3. Where exposure histories can be specified clearly, validation of the use of adduct assays to determine and quantify uptake of tobacco smoke carcinogens is needed.

  4. Information is needed on certain tobacco-specific constituents and their fate in the ETS-exposed nonsmoker, including solanesol, tobacco-specific nitrosamines, and polyphenols such as chlorogenic acid or rutin.

  5. Knowledge of the levels of nitrosothioproline following exposure to ETS as well as nitrosoproline is needed.

  6. Knowledge of the effects of diet is needed when interpreting results of the Ames bacterial assay for mutagenicity of the urine of ETS-exposed nonsmokers.

  7. Identification of the mutagenic agents in the urine of ETS-exposed nonsmokers needs to be made.

  8. Future studies should be concerned with methodologies that enable us to assay the uptake by the nonsmoker of various other types of ETS components that are tobacco-specific.

  9. New trace methods will have to be developed for dosimetry studies of carcinogens involving adducts (DNA and protein) and the development of highly sensitive methods such as immunoassays or postlabelling for other products.

  10. The epidemiological studies on the effects of ETS exposure in nonsmokers should consider a number of non-ETS-related factors. This fact underlines the urgent need for the development of highly sensitive dosimetric methods for ETS-specific carcinogens that can be applied in field studies.

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Suggested Citation:"ASSESSING EXPOSURES TO 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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III
HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS

Suggested Citation:"ASSESSING EXPOSURES TO 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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Next: HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS »
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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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