Nicotine Addiction: Principles and Management

t

Nicotine Addiction : Principles and Management

EDITED BY

C . Tracy Orleans, Ph .D. Division of Behavioral Research Fox Chase Cancer Center

John Slade, M .D. Department of Medicine St. Peter's Medical Center University of Medicine and Dentistry of New Jersey

New York Oxford OXFORD UNIVERSITY PRESS 1993

Oxford University Press Oxford New York Toronto Delhi Bombay Calcutla Madras KaracM Kuala Lumpur Sinpqpore Hong Kong Tokyo Nairobi DaresSalaam GpeTown Melbourne Auckland Madrid

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and axsociated companiea in Berlin Ibadan

Copyright ©1993 by Oxford University Press, Inc . Published by Oxfonl University Presc, Inc ., 200 Madison Avenue, New Yorh, New York 10016

Oxford is a relQSleRd uademarkofOxfoni University Press All righu remved. No part ofthis publication mry be repmduoed, stored in a retrievat system, artrao .®itfcd, in any form or by any means, elatronic,mechanical,photooopyingretatding,orotherwise, wnhoutthe prior permisaon of Oxford University Pres . [tib'ary of Conge.st Gtaloging-in-Publication Data Nicotine addiction : principles and management / edited by C . Tracy Orleans,John,Slade. p. mn . ISBN 0-19•506441-0 l . Tobaxo habit. I . Orleans, C. Tracy . II. Slade, John D .), 1949RC567.N5235 1993 616 .5615--dc20 92-29443

987654321 Printed in the United States of America on acid-free paper

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OF NICOTINE ADDICTION ' Neialth . WHO Technica[ Re . o. 636 . Geneva : World Health 1979 . md Graham, E . A . Tobaxo a possible etiologic factor in = careinoma: A study of ax I eighty-four proved casa, 329-336, 1950 .

7 Tobacco Smoke Pollution James L . Repace

Inhaling the smoke from cigarettes, pipes, and cigars delivers nicotine to the brain more quickly and efficently than chewing tobacco leaf (Chapter 1) . However, the practice of burning tobacco leaves indoors exposes other people to indoor air pollution from tobacco combustion products containing many chemicals known to be harmful to human health. Although society, in the interest of public health, has long imposed quality standards for food, water, and indeed, for outdoor air, it has been slow to require that the indoor air be of a quality that will prevent morbidity and mortality . In general, the same amount of contaminant deposited on the lung surface from inhaled air that we breathe has greater potential for harm than an equal amount ingested in food or water, due to differences in absorption efficiency between the pulmonary and gastrointestinal membranes . For example, in a healthy adult, 5% of a gram of lead from a chip ofaccidentally ingested paint will be absorbed, while 95% of the same amount of lead inhaled as a fume from automobile exhaust will be absorbed. It is common for there to be strict controls on low-dose general population exposures to toxic agents which have only been proved to be harmful with long-term exposure at high doses. Pollutants such as asbestos, benzene, and radioactivity fall into this category. The 2 .5 million deaths per year worldwide caused by the cigarette qualifies tobacco smoke as extraordinarily harmful at high doses (Peto and Lopez 1990) . It is astonishing that this fact alone has not led to stringent controls on tobacco smoke pollution . Other environmental agents with the poten-

tial to cause far smaller amounts of harm have been banned from food, water, and air . For example, in 1988, Chilean grapes were banned from U .S. markets because cyanide contamination found on two grapes was of the order of a few percent of that delivered by smoking one cigarette . In estimating the magnitude of a public health risk from an environmental agent, a technique called risk assessment is typically employed by public health agencies . Risk assessment often relies on available data coupled with the use of models to estimate the expected magnitude of a public health risk . If the estimated risk is significant, risk management, generally in the form of regulation, is employed to control or eliminate the hazard. Risk assessment is also used to ascertain uncertainties in the estimated risk, as well as to point out directions for future research . Risk assessment has four main components: hazard assessment, exposure assessment, dose-response determination, and risk characterization . This chapter on the pollution of indoor air by tobacco smoke will follow this outline.

HAZARD ASSESSMENT OF TOBACCO SMOKE POLLUTION Large-dose inhalation exposure to tobacco smoke (ordinary smoking) is a major cause ofcoronary heart disease, atherosclerotic peripheral vascular disease, lung and laryngeal cancer, oral cancer, esophageal cancer, emphysema, chronic bronchitis, intrauterine growth retardation, and low birth weight . In 129

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Table 7-1 43 Chemical Compounds Identified in Tobacco Smoke for which Then : is "Sufficient Evidence" of Carcinogenicity in Humans or Animals aoetaldehyde aerylonitrile arsenic benz(a)anthmcene benzene benzo(a)p}lene benzo(b)aumanthene benzo(k)Huoranthene cadmium chromium VI DDT

dibenzo(a,i)pyrene dibenzo(a,e)py :ene

dibenz(a,h)acridine dibeuz(a,j)acridine dibenz(a~h)anthnuxne

N'-nitmsodimethylamine N'nitmsonomipotine N-nitrosopipe'idine

dibenZo(a,l)pyrene

dibenzo(a,h)pyn :ne formaldehyde hydrazine indeno(1,2,3,cd)pyrene lead nickel N-nilrosodiethanolamine N-nitrosodiethylamine

N-nitrosdi-n-propylamine N-nitmsopyrtolidine N-niuosodi-nbutylamine mthatoluidine styrene unxbane vinylchlotide l,ldimethylhydmzine 2-nitropropane 2-napthylamine 4{mcthylnitrosamino}!{3-pytadyl)-l-bumnone 4aminobiphenyl 5-methychrysene 7H-0ibenzo(c,g)earbazole

9orm: GRC 1987.

addition, smoking has also been implicated as a probable cause of unsuccessful pregnancies, increased infant mortality, and peptic ulcer disease, as well as cancers of the bladder, pancreas, and kidney . Associations have been observed between smoking and cancer of the stomach (USDHHS 1989), cervical cancer (Slattery et al . 1989), and breast cancer (Horton 1988; Rohan and Baron 1989). Increased risks among smokers for hepatic cancer (Trichopoulos et al . 1987), leukemia (Kinlen and Rogot 1988), penile cancer (Hellberg et al . 1987), and anal cancer (Daling et al . 1987; USDHHS 1989) have also been reported . In short, scarcely an organ system of the human body remains undiseased from prolonged inhalation of large doses of tobacco smoke. As a result, there is a significant reduction in 6fe expectancy for smokers compared to nonsmokers (see Chapter 6) . Moreover, the lung cancer rate for males smoking as fewas one to nine cigarettes per day, as observed in the American Cancer Society's (ACS) 9 State and 25 State studies averaged sixfold times that of nonsmokers (whose annual lung cancer mortality rate was about 12 per 100,000), indicating large risks even at relatively low active smoking exposures, with no evidence ofa threshold for the effect (IARC 1986). In fact, ciganV tte smokers who do not inhale, as well as pipe and cigar smokers, have lung cancer risks which are severalfold that of nonsmokers. This suggests that the dose-response curve between exposure

to tobacco smoke and cancer risk rises steeply, and that even relatively small exposures, such as those encountered in passive smoking, might result in significant population risk . Because thresholds for effect have not been found for the many diseases of smoking, and because air pollution in general can cause human morbidity and mortality, the suspicion that tobacco smoke pollution (also called environmental tobacco smoke, or ETS) in buildings might increase nonsmokers'risk ofthese diseases has been raised (Repace and Lowrey 1980) . Experiments have shown that cigarettes, pipes, and cigars emit copious amounts of air pollution which grossly pollutes indoor atmospheres during smoking (Repace 1987b; Leaderer et al . 1987; USDHHS 1986; NRC 1986). In 1986, an estimated 424,000 metric tons of tobacco were burned indoors annually in the United States, contaminating indoor air with nearly 5,000 chemical substances, many of them toxic. In fact, 43 of these 5,000 meet the stringent criteria for listing as known carcinogens in humans or animals set forth by the International Agency for Research on Cancer (IARC), as shown in Table 7-1 (IARC 1987; Repace and Lowrey 1990) . Of the compounds that have been identified in tobacco smoke (Adams, O'Mara-Adams, Hoffman 1987 ; Guerin 1987 ; Sakuma et al . -1983,1984a,b), onlyabout 10% are found in the vapor phase, with the remainder in the particulate phase (Dube and Green 1982) .

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The particulate phase of tains more than 40 knoi cinogens, including sub: tumor-initiators, tum( four classes of organ-s (lung, esophagus, pancn bladder (USDHHS 1981 the particulate mattersk the vapor phase (Pritch cause material from sm~ ited in the mucous/aqui veolar surface may inhalation oftobacco sm smokers may result in tI carcinogenic particulate to sites distal to the lung EXPOSURE ASSESSMEN SMOKE POLLUTION Exposure to an air pollut the product of three qual concentration in a given the individual's respirati tact .with the pollutant cl of time the person spen nated atmosphere . Toba trations in individual i may be assessed by mea ulation exposures, whic gate public health risk, assessed by a mathemati, In the case oftobacco sm ture consisting ofthousa stances, two constimen•, spirable suspended i (RSP), have been most as surrogates for th (USDHHS 1986) . Altho~ erated by other combus ing smoking in nonindu RSP from tobacco smo the other sources, includ fireplaces, dust reentraii pedestrian traffic, and d the outdoor air (Repace 1982; Meisner et al .1981 erer 1990; Lewtas 19. Hammond et al. (1988) exposures to RSP in se road workers . Mean calc RSP exposures for raili averaged over 90 vg/m' ;

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oke and cancer risk rises t even relatively small expohose encountered in passive result in significant populasholds for effect have not the many diseases of smok- air pollution in general can iorbidity and mortality, the )bacco smoke pollution (also mental tobacco smoke, or gs might increase nonsmakdiseases has been raised (Reyp 1980). Experiments have rettes, pipes, and cigars emit its of air pollution which indoor atmospheres during tce 1987b; Leaderer et al . i 1986; NRC 1986) . In 1986, 4,000 metric tons of tobacco loors annually in the United nating indoor air with nearly substances, many of them 43 of these 5,000 meet the a for listing as known carcinu or animals set forth by the gency for Research on Canshown in Table 7-1 (IARC and Lowrey 1990) . Of the t have been identified in toa (Adams, O'Mara-Adams, Guerin 1987 ; Sakuma et al . only about 10% are found in e, with the remainder in the se (Dube and Green 1982) .

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The particulate phase oftobacco smoke contains more than 40 known or suspected carcinogens, including substances described as tumor-initiatots, tumoo-promotors, and four classes of organ-specific carcinogens (lung, esophagus, pancreas, and kidney and bladder (USDHHS 1981) . Because much of the particulate matter slowly evaporates into the vapor phase (Pritchard 1988), and because material from smoke particles deposited in the mucous/aqueous layer of the alveolar surface may become dissolved, inhalation oftobacco smoke aerosol by nonsmokers may result in the dissemination of carcinogenic particulate phase components to sites distal to the lung. EXPOSURE ASSESSMENT OF TOBACCO SMOKE POLLUTION Exposure to an air pollutant is dependent on the product of three quantities: the pollutant concentration in a given microenvironment, the individual's respiration rate during contact with the pollutant cloud, and the length of time the person spends in the contaminated atmosphere . Tobacco smoke concentrations in individual microenvironments may be assessed by measurement, but pop ulation exposures, which determine aggregate public health risk, are more generally assessed by a mathematical exposure model . In the case oftobacco smoke, which is a mixture consisting ofthousands of different substances, two constituents, nicotine and respirable suspended particulate matter (RSP), have been most commonly selected as surrogates for the entire mixture (USDHHS 1986) . Although RSP may be liberated by other combustion processes, during smoking in nonindustrial indoor spaces, RSP from tobacco smoke generally dwarfs the other sources, including kerosene stoves, fireplaces, dust reentrained in room air by pedestrian traffic, and dust infiltrated from the outdoor air (Repace and Lowrey 1980, 1982 ; Meisner et al .1988 ; NRC 1986; Leaderer 1990; Lewtas 1989). For example, Hammond et al. (1988) measured personal exposures to RSP in several hundred rallroad workers. Mean calculated ETS-derived RSP exposures for railroad office workers averaged over 90 µg/m'; by comparison, all

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other sources of RSP for these dieselcxhaust exposed workers averaged less than 40 µg/ m3 .

RSP released indoors from tobacco combustion contributed an estimated 13,000 metric tons into the interiors of the nation's building stock in 1986 (Repace and Lowrey 1990). Surveys of respirable particulate air pollution have shown that, under typical conditions of ventilation and smoking occupancy in indoor microenvironments (i .e., homes, office buildings, sports arenas, bingo games, bowling alleys, waiting rooms, restaurants, and bars), air pollution levels due to tobacco smoke are far higher than those typically encountered indoors in the absence of smoking (Repace 1987b). The levels of RSP from ETS are even higher than levels of RSP observed in vehicles on busy commuter highways (Repace and Lowrey 1980) . In fact, whenever smoking occurs indoors, the short-term levels of air pollution generally far exceed the levels of RSP permitted by national outdoor air quality standards for inhalable particles (Figure 7-1) (Repace and Lowrey 1980 ; Repace 1987b). Personal and area monitoring studies of exposure have confirmed that human exposures to respirable particulate a'vpollution are dominated by indoor levels of ETS (Repace and Lowrey 1980; NRC 1986; USDHHS 1986 ; Spengler et al . 1985 ; Leaderer 1990) .fihis is possible because the population spends 90% of its time indoors-the bulk spent in just two microenvironments, home and work-and because there are few other strong sources of RSP (Leaderer 1990) . In addition, tobacco smoke is easily transmitted through mechanical ventilation systems in office buildings and aircraft, and by diffusion in naturally ventilated dwellings (Repace and Lowrey 1987b; Williams 1985 ; Vaughn and Hammond 1990; USDOT 1990) . Mathematical models have been developed to predict the concentration of RSP from tobacco smoke pollution as a function of the density of smokers in the building space and the rate of exchange of cleansing air between the building and the outdoors . The parameters of importance that determine the impact of tobacco smoke on indoor atmospheres are given in the following equation, which is used to estitnate the

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Fig.7-1 . RESPIRABLE PARTICLE DENSITY vs ACTIVE SMOKER DENSITY

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smoke pollution constiti levels. (Compare the va1 those shown in Figure , H,K,L,M,andNaret• and V are reception halh ing room ; I is a bowlin( are bingo games; while [smoking discouraged, I is a lodge hall dinner-c bars; F is a nightclub; home during a party.) T the calculated air excha Given the nature oftc ulate matter shown in such exposure be consit servers or patrons? If t decides to save money exchange rate to 5 cu makeup air per minutt air changes/h, a level many "energy-efticien tion codes), the RSP 1ev is 319 µg/m', and after near steady-state value pare this calculation tc ure 7-l, taken at a dim comparison, the nation standard for inhalable in diameter) is 50 µg/ 7-1). Pollution of air in smoke is so pervasive unaware that they are probably due to the f believe that because 1 the'u immediate envir being exposed to tobw ple, Jarvis and Russell that among 100 U .K . had undetectable cot nearly half reported' 1987). Tobacco smol central air systems of may expose workers c ing for this result 4 19876). Similar resuh United States by Cur (1989,I990):of663r nary cntinine levels v reported exposure tc had detectable leveL level in the nonsmc (0.7% of the mean %

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quantity of tobacco smoke pollution in indoor spaces . The total concentration of RSP from cigarette smoke plus background sounxs, in units of micrograms per cubic meter (pgJm3), as a function of time, t, in units of hours, in a space is given by the following expression (Repace 1987a) ; RSP -6 21,7001 ~ l[1 - e'Qj + B, where N is the num\\\ber/of smokers (who are assumed to smoke cigarettes at the rate of 2 per hour), V is the space volume in cubic meters, N/V is called the habitual smoker density. C is the air exchange rate, in air changes per hour, e isthe base of natural logarithms, and B isthe baekground concentration of RSP in the space (Repace 1987a). To understand the enormous impact of smoking on the indoor air, consider, as an illushative example, the realistic numbers for a typical restaurant, under full occupancy and code-specified ventilation (which is often observed in the breach) for this equation. A typical indoor background RSP level in the absence ofsmoking is B= 20 µg/m' (Repace and Lowrey 1980, 1982, 1987a,b) . A typical restaurant's maximum occupancy is of the

order of 70 persons per 1,000 square feet (about 100 m') of floor area (ASHRAE 1989), and assuming that the restaurant is filled to capacity, at a smoking prevalence of 29%, 20 patrons per 1,000 square feet will be smokers. Assuming a 12-foot ceiling, this yields a volume V= 12,000 cubic feet, or 340 cubic meters (a volume approximately the same as a typical single family house) . The smoker density is 5 .9 X 10-' habitual smokers per cubic meter, equivalent to a burning cigarette density of about 1 .8 burning cigarettes per 100 cubic metets (compare with Figure 7-1) (Repace and Lowrey 1980, 1982, 1987a) . Tbe American Society of Heating, Refri6eratmg, and Air Conditioning Engineers (ASHRAE), the design ventilation code-recommending organization, recommends 20 cubic feet of outdoor makeup air per minute per occupant (10 Lps/occ) fora well-ventilated restaurant dining room (ASHRAE 1989), equivalent to an air exchange rate of C = 7 air ehanges per hour (20 cfm/ocs X 70 occ/12,000 cf X 60 min/hr). Applying these numbers to our equation, it is seen that at the end of a half hour, the RSP level increases 10-fold, from 20 pg/m' to a near steady-state level of 197 ug/m', and, while smoking persists, tobacco O T W O t7 03 O CJ7 GS

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smoke pollution constitutes 83% of the RSP levels . (Compare the value just calculated to those shown in Figure 7-1 . Data points, E, H, K, L, M, and N are typical restaurants ; B and V are reception halls ; J is a hospital waiting mom; I is a bowling alley; D, G, and T are bingo games ; while 0 is a sports arena [smoking discouraged, but not enforced] ; B is a lodge hall dinner-dance; C and Q are bars; F is a nightclub ; and A is a private home during a party.) The dashed lines show the calculated air exchange rates . Given the nature oftobacco smoke particulate matter shown in Table 7-1, should such exposure be considered healthy for the servers or patrons? If the restaurant owner decides to save money by decreasing the air exchange rate to 5 cubic feet of outdoor makeup air per minute per occupant (1,75 air changes/h, a level still common under many "energy-efficient" building ventilation codes), the RSP level afterone-halfhour is 319 µg/m', and after 3 hours increases to a near steady-state value of 742 µg/m'! (Compare this calculation to data point B in Figure 7-1, taken at a dinner-dance .) By way of comparison, the national outdoor air quality standard for inhalable particles (< 10 µm in diameter) is 50 yg/m' (shown in Figure 7-1). Pollution of air in buildings by tobacco smoke is so pervasive that many people are unaware that they are even exposed . This is probably due to the fact that many people believe that because no one is smoking in their immediate environment, they are not being exposed to tobacco smoke . For example, Jarvis and Russell (1984, 1987) showed that among 100 U.K. nonsmokers, only 12 had undetectable cotinine levels, although nearly half reported "no exposure" (IARC 1987). Tobacco smoke recirculated in the central air systems of commercial buildings may expose workers unknowingly, accounting for this result (Repace and Lowrey 1987b). Similar results were reported in the United States by Cummings and associates (1989, 1990): of 663 nonsmokers whose urinary cotinine levels were studied, only 76% reported exposure to ETS ; however, 91% had detectable levels . The mean cotinine level in the nonsmokers was 8.84 ng/ml (0.7% of the mean value reported for 130

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s per 1,000 square feet ' Qoor area (ASHRAE C that the restaurant is asmoking prevalence of 1,000 square feet will be a 12-foot ceiling, this = 12,000 cubic feet, or volume approximately al single family house). ' is 5.9 X 10-Z habitual meter, equivalent to a asity of about 1 .8 bumlcubic meters (compare apace and Lowrey 1980, - American Society of :ug, and Air ConditionRAE), the design ventimending organization, vbic feet of outdoor mute per occupant (10 entilated restaurant din:1989), equivalent to an ' C= 7 air changes per 70 occ/12,000 cf X 60 these numbers to our that at the end of a half increases JO-fold, from steady-state level of 197 noking persists, tobacco

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smokers in the same study), and the range was 0-85 ng/ml ; 92% of cotinine values were less than 20 ng/ml. Cotinine levels tended to increase with the number of reported exposun•.s to ETS . Based on time-budget studies, most people spend the bulk of their time in just two microenvironments : home and work . Since many persons exposed at home are also exposed at work, those exposed both at home and at work represent a most-exposed group of passive smokers (Repace and Lowrey 1985b). Moreover, exposure probabilities are high at work: for example, in the Cummings study (1990), 77%were exposed in the workplace, and 22% were exposed while at home. Similar conclusions about the importance of these two microenvironments were reported by Riboli and colleagues (1990) . Cummings et al . (1990) reported that 84% of subjects who did not live with a smoker had detectable cotinine levels . This finding has important implications for epidemiological studies of passive smoking and disease . Most such studies use domestic exposure as a surrogate for total exposure to passive smoking, and unaccounted for exposures outside the home may confound an actual association, since this exposure misclassification tends to bias the mortality ratio toward unity . Insofar as public health measures are concerned, the two most important sites for interventions to control tobacco smoke pollution are the home and the workplace: the former by public information, the latter by public information and regulation . DOSE-RESPONSE DETERMINATION Heart Disease .Wells (1988), Glantz and Parmley (1991),

and Steenland (1992) have reviewed the evidence that passive smoking increases the

risk of death from heart disease . In 10 epidemiological studies on the risk of death

from ischemic heart disease or myocardial infarction among nonsmokers living with smokers, the exposed groups experienced an overall 20-30% higher risk than the unexposed groups . Glantz and Pannley (1991)

note that these epidemiological studies are complemented by a variety of physiological

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and biochemical data from human studies that show that exposure to tobacco smoke pollution adversely affects platelet function and damages arterial endothelium in a way that increasesthe risk of heart disease. These observations have recently been experimentaliy confirmed in rabbits exposed to passive smoking by Zhu and colleagues (1992) . Glantz and Parmley (1991) also reviewed evidence that exposure exerts significant effects on exercise capability of both normal persons and those with heart disease by affecting the body's ability to deliver and utilize oxygen . Further, they report that in animal experiments, exposure to ETS also depresses cellular respiration at the mitochondrial level, and that polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Lung Cancer Several official bodies have addressed the question of whether passive smoking causes lung cancer. In 1986, the U .S . Surgeon General concluded that "involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers" (USDHHS 1986 p 7) . Also in 1986, the National Research Council (NRC) concluded that "exposure to ETS increases the incidence of lung cancer in nonsmokera" (NRC 1986 p 10) . The NRC estimated that the risk of lung cancer was increased by roughly 30% for nonsmoking spouses of smokers relative to nonsmoking spouses. The following year, the International Agency for Research on Cancer (IARC) stated that "exposure to tobacco smoke gives rise to some risk of cancer" (IARC 1987). In 1992, the U .S. Environmental Protection Agency (EPA) reviewed the original 13 epidemiological studies which had been the basis for these initial findings plus 17 more, for a total of 30 studies of passive smoking and lung cancer, and concluded that ETS is a "class A," or "known human carcinogen" (USEPA 1992) . Finally, in 1991, the National Institute for Occupational Safety and Health issued a report which concluded that ETS meets the criteria for classification asan "occupational carcinogen," and called atten-

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tion to the "possible association between exposure to ETS and increased risk of heart disease in nonsmokers" (NIOSH 1991) . With respect to quantitation of lung cancer risk, EPA used actual epidemiological data and vital statistics to estimate the number of nonsmokers affected . The EPA report concluded that passive smoking is causally associated with lung cancer in adults . This report concluded that, following the EPA guidelines for carcinogen risk assessment, ETS causes approximately 3,000 (+_2,000) lung cancer deaths annually in the United States in never-smokers and ex-smokers . Pediatric Diseases

Tobacco smoke pollution causes the children of parents who smoke to have up to 300,000 cases annually of bronchitis and pneumonia, increased prevalence of asthma, cough, sputum production, wheeze, and middle ear effusions, as well as up to 1,000,000 exacerbated cases of existing asthma annually. (NRC 1986 ; USDHHS 1986; USEPA 1992). Further, a recent study (Janerich et al . 1990) concluded that exposure to tobacco smoke pollution during childhood was associated with increased susceptibility to lung cancer in adulthood . Dose-Response Relationship Suppose it were possible to measure exactly the dose of all lung carcinogens breathed in during passive smoking . Suppose further that the number of lung cancer deaths induced could be precisely measured . A pop• ulation-based dose-response function could then be defined, yieldingthe number of lung cancer deaths per year in the population at risk, peraverage number of milligrams oftobacco smoke carcinogens inhaled per day . Although it is not possible to actually measure the total dose of lung carcinogens from tobacco smoke polluted atmospheres to the nonsmoking population, from measured RSP levels and mathematical models, it is possible to estimate the exposure the nonsmoking population has to the particulate phase of tobacco smoke. Also, although it is also not possible to precisely measure the population response, that is, the number of

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lung cancer deaths (or points) per year from pa magnitude can be estima ological cohort studies . I dose-response model ca; based on observed physi, logical phenomena . This timate of the true dose-i By comparing the pred mathematical model witl dependent cohort studie mortality, the accuracy < tion can thereby be est proach permits the pred'u passive-smoking disease given level of exposure . T the designation of contr procedures which will yiel level of public health prot Repace and Lowrey [ l! 1993 (in press)] have deve response model . This has! estimation of the risks ofl the workplace [Repace al 1993 (in press)], and in a pace 1988; USDOT 1990 wrey (1985a) estimated t age population risk from 1 five lung cancer deaths pE years at risk, per millign inhaled per day, for population aged 35 years plications for public hea scribed in the next sectior RISK CHARACTERIZATP TOBACCO SMOKE POL : How significant is the i smoke? An answer is Pro ing U .S . federal approachvironmental carcinogens . cer risk triggers regulat consistency among variot Travis and co-workers (1~ the use of cancer risk estit federal standards and in tory initiatives to determi between risk level and fet tion. They find definite p, tency in the federal n Travis et al . (1987) consid of risk, lifetime cancer ri

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de association between exid increased risk of heart nokers" (NIOSH 1991) . jantitation of lung cancer tual epidemiological data to estimate the number of ted . The EPA report cone smoking is causally as; cancer in adults . This rethat, following the EPA rcinogen risk assessment, wimately 3,000 (+_ 2,000) is annually in the United iokers and ex-smokecs. s pollution causes the chilwho smoke to have up s annually of bronchitis increased prevalence of ,utum production, wheeze, :ffusions, as well as up to rbated cases of existing . (NRC 1986; USDHHS 92) . Further, a recent study 990) concluded that exposmoke pollution during ;ociated with increased sus; cancer in adulthood . Relationship jossible to measure exactly ng carcinogens breathed in smoking. Suppose further - of lung cancer deaths in:necisely measured . A popso-response function could yielding the number of lung :r year in the population at number of milligrams oftorcinogens inhaled per day . Yt possible to actually mease of lung carcinogens from 3olluted atmospheres to the )pulation, from measured mathematical models, it is nate the exposure the nonttion has to the particulate ) smoke. Also, although it is e to precisely measure the onse, that is, the number of

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lung cancer deaths (or other disease end points) per year from passive smoking, its magnitude can be estimated from epidemiological cohort studies . In this manner, a dose-response model can be constructed, based on observed physical and epidemiological phenomena . This model yields an estimate of the true dose-response function . By comparing the predictions of such a mathematical model with the results of independent cohort studies of lung cancer mortality, the accuracy of the approximation can thereby be estimated. This ap• proach permits the prediction of the risk of passive-smoking disease associated with a given level of exposure. This in turn permits the designation of control and abatement procedures which will yield a predetermined level of public health protection . Repace and Lowrey [ 1985a, 1986, 1987a, 1993 (in press)] have developed such a doseresponse model . This has been utilized in the estimation of the risks of passive smoking in the workplace [Repace and Lowrey 1985b, 1993 (in press)], and in airliner cabins (Repace 1988; USDOT 1990). Repace and Lowrey (1985a) estimated the aggregate average population risk from passive smoking as five lung cancer deaths per 100,000 personyears at risk, per milligram of tobacco tar inhaled per day, for the non-smoking population aged 35 years or older . The implications for public health policy are described in the next section . RISK CHARACTERIZATION OF TOBACCO SMOKE POLLUTION How significant is the risk from tobacco smoke? An answer is provided by considering U .S. federal approaches to regulating environmental carcinogens. What level ofcancer risk triggers regulation, and is there consistency among various federal agencies? Travis and co-workecs (1987) have reviewed the use of cancer risk estimates in prevailing federal standards and in withdrawn regulatory initiatives to determine the relationship between risk level and federal regulatory aotion . They find definite patterns and consistency in the federal regulatory process. Travis et al . (1987) considered two measures of risk, lifetime cancer risk to the most ex-

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posed individual and aggregate or average population risk, which incorporates population size. One-third of the time, federal agencies calculated aggregate risks by multiplying the risk to the most exposed by the population at risk, and two-thirds of the time, risks were calculated by taking into account variations in exposure level . The latter approach is the preferred method . The regulatory actions considered in the analysis were performed by the Consumer Product Safety Commission, the Environmental Protection Agency, the Food and Drug Administration, and the Occupational Safety and Health Administration . Travis et al. (1987) describe two technical terms current in risk assessment circles: de manijestis risk and de minimis risk . A de manifestis risk is literally a risk ofobvious or evident concern, and has its roots in the legal definition of an "obvious risk," one recognized instantly by a person of ordinary intelligence . De minimis risk has been used for a number of years by regulators to define an acceptable level of risk that is below regulatory concern . This term stems from the legal princi¢le, de minimis non curat lex, "the law does not concern itselfwith trifles ." Demanifestis risks are so high that agencies almost always acted to reduce them, and de minimis risks are so low that agencies almost never act to reduce them . The risks falling in between these extremes were regulated in some cases, but not in others . Two categories were described : small populations and large populations. For low aggregate risk, the de man ijest is level for individual risk was found to be about 4 X 10-' (a lifetime probability of four deaths per 1,000 persons at risk), and the de minimis level was 1 X 10'` . For example, the EPA, in declining to regulate natural radionuclide emissions from elemental phosphorus plants with an individual lifetime risk of l X 10-', weighed the maximum risk to the most exposed individuals against the low aggregate risk (0 .06 cancer deaths per year), and against other factors such as cost . However, when the aggregate population risk level was large, that is, above 250 cancer deaths per year, the de manifestis risk dropped to about 3 X 10-', and the de minimis risk dropped to 1 X 10-6 . For example, if the lifetime risks of harm from ex-

N

0

w ~ 10

0

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10

136

THE

DISEASE

OF

NICOTINE

ADDICTION

TOBACCO SMOKE P

Table 7-2 Summary of Risk Assessments of Lung Cancer Deaths (LCDs) in U .S . Nonsmokers from Environmental T6bacoo Smoke (ETS) Exposure (Adjusted to 1988)

Study

Range ofEstima[es (LCDSperyear)

Fong(1982Y Repace and Lowrey (1985-87) RusseB et al. (I986Y

960"-4,800` 6851-6,850'

Rubins (1986)

4314t-8,625"

Weas(1988) Wakletal .(1986) KulleretaL (1986)9 Wigleet al . (1987) Amodel et aL (1987) Mean, all 9 studies: Mean, 8 studies, excluding Amadel et al .

(female LCDs only) (83%workplace)# 19-97

Table 7-4 Total Annua fmm Passive Smoking (al

Mean or Best Estimate (LCDs per year) 2,900 6,700 ± 340 1 .107j 6,470 3,320' 8,124J >6,035t 5,6911 .58° 4,500 ± 2,800 5 .000 ± 2,400

Estimatec Deaths

Heart disease

35,000

Lungeancer

5,000

Othereancer

10,000

Total

Saonr. Rep.oe .nd Luany 1990. •Fatimate ouu. iauryolated 6om au0mfr ovesa0 mt euimue . 6Baed on mb8nnrityssumptioo 4lowdoses 'Hned on Soerity .vumption at low doax 4lnaer Ipund bued on rmukes• mwrahk suspended prtitulate mana (a8% ewpmum erlnWalatioe (adjmted to iudude earmoken} •Beu mtimate b ued an epidemioloay (adjuued tn bMude ee-uookes) . f6tf ed on liunr e.MpoLtion fmm niaocoe in ®okcs. +Sved on u,im.y cetiniae aod ETS epidemiolop . haaf cd on Gmr multiwge from smoken .ad unmry eoenine . 'Basd on EIS epidemiologyaud nuaunokae LCD nles( .djunedm hidudeeximokms). Aaxdon minecotiniae in U.K nemmotrqs, E[S epidemiology(adjuned to include examokan) . t8attd an uumttialiulap,padonofqualita6rejudgnenG 'Based an extrapnlaf icn of C .mdi .n results m Us . uummokera "Baudon Saearecn.polation homrn.inam RSP in emokenc

posure to a pollutant were of the order of I X 10'6, and 75 million persons were at risk, then this would produce about 75 deaths per lifetime. If 75 years is used as an exposure lifetime, this is l estimated death per year . How does the estimated annual mortality of various regulated carcinogenic air pollutants and tobacco smoke pollution compare with the de minimis risk level? Nine workers have estimated the lung cancer mortality risk of tobacco smoke pollution. Table 7-2 reproduces the nine estimates. In some cases, the lung cancer deaths are interpolated from an overall estimate that includes estimated tobacco smoke pollution-caused deaths from diseases other than lung cancer, and additionally includes ex-smokers in those cases where the authors did not include them in the original estimate. This facilitates intercomparison of studies . The mean of all estimates is 4,500 ± 2,800, and with the estimates of Arundel et al . (which differ by more than two standard deviations from the remainder) removed, about 5,000 ± 2,400 .

Cause

50,000

involuntary airborne public health combini TOTAL MORTALITY SMOKE POLLUTION Irmally, four group : (1982), Glantz and F (1988) and Taylor, ec mated the total numlr deaths from all cause' cancer) at around 5C United States . This ra7 smoking as the thirc cause of death, beh caused by smoking it by alcohol . Table 7-4 breakdown of the deat

Table 7-3 characterizes this estimated risk by comparison with the estimated risks for other indoor and outdoor airborne carcinogens (Repace and Lowrey 1990) . It is seen that tobacco smoke pollution poses a far more serious public health risk than all other

RISK MANAGEMENT SMOKE POLLUTION

Table 7-3 Comparison ofE'stimated Annual

Given the seriousne&k bacco smoke pollutior health be protected? 7 for Occupational t (NIOSH) has recomm to ETS in the workpl prohibiting smoking use can be completelk recommends that exp4 the lowest feasible cot 1991). What are the r forts to control toba . short of completely el the building? Repace 1993 (in press)] have a for lung cancer risk .

Cancer Deaths from Various Airborne Carcinogens in the U.S. 7ndoorPa!lutaus No. Environmental tobacco smoke 5,0011' (homes & workplaces) Radon gas in homes 4,000` OutdaorPollumnt.a No. Asbestos t5 Vinylohloride