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A collection of articles regarding ETS or Second-hand smoke

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To the anti-smoking zealot, no argument is too extreme, no argument too far fetched if it can be employed to condemn smoking. Scientific method and statistical analysis have been replaced by the stretching of the truth and the spread of outright falsities in the name of defeating the evils of tobacco. It is permissible even to those trained in science and statistical analysis to abuse these tools if such abuse will lead to a smokeless society.

Nowhere is this more evident than in the debate over environmental tobacco smoke (ETS).

The fundamental question is whether science has proven a health risk to non-smokers. Anti-smoking advocates would have you believe the scientific debate over the dangers of ETS was settled long ago. They attempt to move their social /political movement forward under the camouflage of "science."

A review of studies on passive smoking was recently published in Consumers' Research. "Of the 30 studies, six reported a statistically significant association (between environmental tobacco smoke and lung cancer)...and 24 of the studies reported no statistically significant effect. " (If one uses studies only from the US to determine the risk of environmental tobacco smoke, you arrive at a statistically non-significant risk.)

Even attempts to enhance the significance of the individual studies by pooling them for so-called "meta-analysis" are not persuasive. These analyses show relative risks, according to Consumers' Research, of 1.08, or 1.34, or 1.42.

(Relative risk is expressed as a ratio; a risk ratio of 1.0 is, in real terms, a risk of zero.)

Some say even a risk ratio of 1.08 is too high to tolerate, much less a risk of 1.42. In that case, we should all stop drinking milk and impose mandatory exercise requirements on the populace.

One study showed the risk of lung cancer for those drinking pasteurized milk to be 2.1. A lack of physical activity produced a risk of 1.6.

There are significant difficulties with the "science" being used to make the case for "passive smoking."

"Confounding variables" is a fancy way of saying other factors may be at work in causing a disease. If confounders are not properly controlled, the study loses reliability.

The "passive smoking" studies have a spotty record, at best, in taking into account the 20 or so "confounding variables" associated with lung cancer. These variables range from nutrition, to genetic predisposition, to ethnicity, to diagnostic criteria. In many Asian studies, exposure to cooking fires and cooking oil vapor seem to be highly significant.

Recent work at EPA demonstrates how manipulation of data can give you different answers to the same question.

The EPA's draft risk assessment on ETS and lung cancer assigned a relative risk of roughly 1.3 to ETS. What is behind that number?

First, if one uses studies only from the United States to determine the risk, you arrive at a statistically non-significant risk. So studies from throughout the world were used to bring the calculation up to 1.3. Included in the international studies was a study done by Japanese researcher Hirayama which has been criticized for serious design flaws. Attempts to obtain the raw data from Hirayama for further analysis are not possible.

Why? The data of this research, published in 1981, have been destroyed. Coincidence or convenience? You decide. If one removes Hirayama from the calculations, the result is dramatically altered.

EPA has Guidelines for Carcinogenic Risk Assessment. These are guidelines to be followed by the Agency in the conduct of risk assessments. Yet in the case of ETS, the guidelines appear to have been applied inconsistently and incompletely.

For instance, the EPA Guidelines require that a risk assessment include not only human epidemiological evidence (fancy terminology for statistical studies usually derived from analyzing questionnaires) but actual animal exposure studies. Guess what? EPA chose not to include the results from animal inhalation studies. Why? The animal data is negative.

Before a casual interpretation is drawn from epidemiological data, it is generally a recognized principle that risk ratios must exceed 2 or 3. Part of the reason is that lower ratios can often be achieved merely on the basis of chance, bias, confounding, or, in the case of ETS, misclassification. In such cases, it is inappropriate under EPA's Guidelines to make a casual interpretation.

Misclassification is the term used to refer to individuals who are smokers but say they aren't. EPA's calculated risk is low enough that, according to some studies, it can be explained entirely on the basis of misclassification or the common lifestyle factors among spouses who live with smokers, such as diet, exercise, or alcohol consumption.

Some of the most illustrative evidence of what is going on here comes from the words of individuals involved in the process at EPA. When the EPA Science Advisory Board [SAB] Executive Committee reported on its review of EPA's draft risk assessment it noted that it had "difficulty in applying the Guidelines...as they are currently formulated to this complex and variable mixture."

The SAB report said "if Guidelines for Carcinogenic Risk Assessment can be used to cast doubt on a finding that the inhalation of tobacco smoke by humans causes an increased risk of lung cancer, the situation suggests a need to revise the Guidelines."

This prompted one member of the SAB Executive Committee to note that it sounded a little like they were saying "if the data doesn't fit the guidelines, the guidelines should be changed."

Following that meeting Dr. Morton Lippmann, who chaired EPA's review panel, was asked to quantify the risk of exposure to environmental tobacco smoke.

He indicated that most people had exposed themselves to greater risk driving across town in Washington traffic to EPA to attend the meeting. And the very next day when there was no press coverage of the SAB Executive Committee meeting Dr. Lippmann acknowledged that if the EPA guidelines were applied as written, or in his words "rigidly," there was "no clear mechanistic basis for calling [ETS] carcinogenic."

Dr. Jonathan Samet, another member of the EPA review panel, published an article in the Aug. 7, 1991 Journal of the American Medical Association [JAMA]. While Dr. Samet believes ETS is a carcinogen, he finally recognizes the numerous problems and uncertainties with the ETS epidemiological studies. Ironically, these criticisms would preclude a known human carcinogen classification for ETS under EPA's Guidelines.

He states that "because of the methodologic difficulties of assessing lifetime exposure to ETS and precisely describing risks that are not substantially elevated, these uncertainties in assessing the lung cancer risk of ETS may never be fully resolved though they remain a subject of research."

Despite the equivocal nature of the science, Dr. Samet very clearly articulated the "politically correct science" of ETS when he went on to say, "in the case of ETS it would be unfortunate if potentially irresolvable scientific uncertainties thwarted control."

The issue is control. It is a desire by anti-tobacco activists to eliminate tobacco from the landscape. Clearly, they have no interest in allowing objective scientific evidence to POST in the way of achieving that goal. To do so would be politically incorrect.

Proving dangers to non-smokers from "environmental tobacco smoke" (ETS, or "passive smoke") has not been easy for anti-smoking activists. While every nag in every airport waiting room complains about her "smoke allergy," no study has ever established allergenic properties in tobacco smoke. While children have been shown to be sensitive to ETS, it has long been known that children are more sensitive to anything in the air, from ragweed to dust, and most people would grant to parents, not the state, the responsibility to keep them away from pollutants. Attempts to link heart disease to ETS have not borne fruit. And in 1986, a Yale University medical school study of asthmatics exposed to ETS showed that not only did the smoke not cause any acute respiratory risk-- it actually decreased bronchial constriction.

"Even with the 'rigged jury' of standard statistical procedures," wrote Dr. Kevin Dowd in the June 1991 issue of the British journal Economic Affairs, "it turns out, contrary to popular myth, that there is still no convincing evidence in favour of the adverse effects of passive smoking." Yet, a year previous to that, the EPA, having failed in its attempts to establish clear-cut and readily confirmable proof of the harms of ETS, had used a complicated and irregular scientific route to claim a minimal link. Patching toPOSTher spousal studies, the EPA claimed that women married to smokers were 1.28 times as likely to contract lung cancer--and that ETS was to blame. The EPA leaked a draft risk assessment describing environmental tobacco smoke as a "known human carcinogen." The months since have seen anti-smoking activists calling for more legislation in public places, and tobacco interests and libertarians pointing out gaps in what they say is dishonest and politicized science.

Exposure to environmental tobacco smoke is difficult to measure by increments. First of all, although irresponsible scientists have tried, one can't extrapolate lung cancer risk from the dosages active smokers take into their lungs. For one, the substances are chemically and quantitatively different: "active" tobacco smoke is made up of smoke particles--and plenty of them--while "passive" smoke is highly diluted, with a partially vaporous content. In addition, "active" smokers take deep breaths through their mouths and hold the smoke in their lungs. "Passive" smokers breathe largely through the nose, which filters out impurities.

While blood tests and urine samples do show that non-smokers absorb nicotine from the smokers around them, it is in such small doses that this can be seen as a triumph more for modern scientific calibration than for any cause-and-effect relationship. It's rather like remarking that every cubic foot of ocean water contains ash from Mount Pinatubo, or that almost all of the paper money in Miami contains traces of cocaine--it's true, impressive, and meaningless. In real-life settings, the dangers of particulates are even less impressive. A 1978 study in the International Archives of Occupational Environmental Health claimed that it would take 11 to 50 hours in an extremely smoke-polluted environment to absorb as much nicotine as a smoker takes in from one cigarette. In Britain, where smoking was legal on subway trains until the mid-1980s and was until recently permitted on buses, the Freedom Organization for the Right to Enjoy Smoking Tobacco estimated that one would have to ride in the smoking section of a bus for four - and-a-half weeks to be exposed to one cigarette's worth of nicotine. It's possible to measure the "respirable suspended particles" that surround a smoker, but very difficult to distinguish them from other particles that may be in the air from cooking, rug fibers, car exhaust, air-conditioning, etc. Pro-smoking activists like to mention "sick building syndrome" as an major contributor. At first glance, calling poor ventilation a "syndrome" and a health threat appears as hysterical as using the word "choc-a-holic" to claim that the science-fictionesque terrors that afflict the true addict apply to someone who is basically a glutton. But the 1976 Legionnaires' disease outbreak is a sick-building incident that cost twenty-nine lives, and occupational studies tend to bear the pro-smokers out: in only 2 to 4 percent of indoor air quality problems is tobacco smoke the major culprit.

How much particulate matter enters the air due to smoking? Anti-smoking activists would have us believe a tremendous amount. Dr. David Burns, testifying before the Los Angeles City Council Health Committee, argued that particulates, "when smoking is allowed, [increase] about ten-fold from the background levels." This is simply falsehood in the service of anti-smoking propaganda--a 1990 study of smoking sections in forty-one restaurants showed that only half of the particulates were from smoke; another study, from 1988, put the figure at 28 percent. As far as eating in restaurants is concerned, the cuisine might be as much of a risk as the smoke: a 1987 Shanghai study by Dr. YT. Gao and three researchers from the National Cancer Institute found that nonsmoking women who cooked with rapeseed oil had an incidence of lung cancer 2.5 times as high as those who cooked with soybean oil. Given the ineffectiveness of exposure measurements, researchers have sought a link in epidemiological studies, i.e. studies based on the incidence of affliction across large populations. Here is what the thirty studies that have been conducted to date report: twenty-four show no statistically significant link at all; six show a weak link; nine show that being married to a smoker actually decreases one's chance of contracting lung cancer.

One would think that a combined study--showing ETS exposure from all sources, including the work environment and including other smoking family members--would show a clearer relationship. Yet no combined study has ever shown a statistically significant association. Even shoddier is the failure of most of the lung cancer tests to probe cancers histologically--that is, by sampling for oncogens in cells of the infected organs. Only limited histology was done even in the large and influential 1981 Hirayama study from Japan, which is the cornerstone of the ETS/cancer scare. As everyone knows, cancer metastasizes, and failure to distinguish between cancers that originated in the lungs and those that moved there from another organ makes the figures considerably "softer." The Hirayama study also relied on questionnaires, which made no attempt to determine which non-smokers were ex-smokers.

Then there is the question of confounding factors, like Dr. Gao's rapeseed oil. Confounding factors in smoking are so numerous and unpredictable that it is almost impossible to unravel smoking as a cause from a welter of non-smoking behaviors that smokers engage in with shocking disproportion. Stanley Coren, a Canadian expert on "handedness," writes that a study in Michigan has shown that left-handers smoke considerably more than right-handers. (They also die nine years earlier--and not due to smoking.) In 1990, two papers published in the Journal of the American Medical Association by stop smoking researchers Alexander Glassman and Robert Anda showed that smokers were six times as likely a nonsmokers to suffer from major depression and twice as likely to suffer from chronic depression. David Kroglt, an anti-smoker, remarked on the smoking personality in one of the most fascinating books of 1991*:
It is easy to see how a study such as Hitayama's could be drastically wrong if his subjects came disproportionately from working-class industrial areas (they did), and if smoking is more prevalent among the Japanese working classes (it is), Hirayama's wives of smokers would have a higher rate of lung cancer than wives of non-smokers, regardless of smoking behavior. Finally, rates of lung cancer infection vary drastically according to race and nationality: British epidemiologist PRJ Burch showed in the 1970s that Finns, who smoke only half as much as Americans, are twice as likely to develop lung cancer. Using foreign studies to arrive at cancer links is like using African numbers to measure the threat of AIDS in North America--the entire mechanism of infection may be different. It's significant that the EPA did not cite a single U.S. study showing an ETS/cancer link in its risk assessment--in fact, no U.S. study has ever found such a link. A particularly weak aspect of the 1990 EPA report is that it relied on meta-analysis, or weighting different studies to arrive at an aggregate figure...i.e., not analyzing data but analyzing analyses. It's very useful in narrowing down conclusions from a battery of similar experiments with similar controls, but irresponsible when used--as it is here--to draw common assumptions about disparate populations, especially when those populations have been established as having vastly varying rates of affliction. There was obvious selective bias at work in the 1990 EPA risk assessment. Three of the most comprehensive studies of passive smoke ever undertaken were inexplicably excluded from the risk assessment: the so-called Shimizu and Sobue studies from Japan, and the largest American case-control study ever conducted, by Luis Varcla of Yale University, which was later published in the New England Journal of Medicine. None of the three studies showed any statistical link between spousal smoking and lung cancer. Publication bias, though not the EPA's fault, is also a factor--studies showing no link between ETS and lung cancer have tended not to be published, as they were non-news until the Hirayama study. As Michael Fumento has written of AIDs in these pages, "Occasional heterosexual cases will make news for the same reason that planes that crash make news while planes that land safely do not."

The EPA went out on a limb to classify passive smoke as "Group A: Known Human Carcinogen," even though most of the studies showed no significant risk, some showed a negative risk, and the final risk ratio, after meta-analysis, was a slim 1.28. (The highest ever recorded for ETS was another Hirayama study, the so-called "Inouye/Hirayama," at 2.55.) When a similar assessment was made of diesel emissions in 1989, the risk ration was 2.6 and all the animal laboratory tests came out positive (all were negative for ETS). Despite the seemingly graver threat, the EPA rated diesel only as "Group B: Probable Human Carcinogen." An EPA review of the carcinogenic properties of electromagnetic fields in 1990 found several risk ratios over 3.0, as well as a "consistently repeated pattern of lymphoma, leukemia, nervous system cancer and lymphoma in childhood studies." But electromagnetic fields were not deemed sufficiently perilous even to classify. The ETS risk assessment is the only one the EPA has ever based solely on epidemiological evidence. The fact that it failed to meet the EPA's own seven-point guidelines for epidemiological studies of potential carcinogens (issued in 1989) makes it seem even more like advocacy.

Radical anti-smokers claim they have to act as advocates to counter the advocacy of tobacco companies, and tobacco interests do indeed have major budPOSTs for their own independent research into smoking hazards. But the industry has no monopoly on the profit motive. The EPA even commissioned anti-smoking activist Stanton Glantz to write a chapter in its draft report on ETS hazards. Glantz, who runs cigarette-quitting seminars and develops anti-smoking regulations for profit, had this to say, at the 1990 World Conference on Tobacco and Health in Australia, about his motives for opposing environmental smoke:

The main thing the science has done on the issue of ETS, in addition to help people like me pay mortgages, is it has legitimized the concerns that people have that they don't like cigarette smoke. And that is a strong emotional force that needs to be harnessed and used. We're on a roll, and the bastards are on the run.

Others may be motivated to push bad science not out of avarice but ignorance. There are even those who muddy the water out of a genuine social concern. Michael Gough, program manager of the Biological Applications Program of the Office of Technology Assessment, chooses to ignore the science of ETS in the interest of reducing smoking, as he indicated in an October 29, 1990 letter to Thomas Botelli, manager for scientific issues at Philip Morris.

Without careful reading of the thesis [by Luis Varela, finding no link between ETS and lung cancer] or careful attention to the ETS issue, I tend to agree with the thesis and the general conclusions of your letter. On the other hand, I probably profoundly disagree with any use that might be made of those conclusions by Philip Morris or any other tobacco company. Anything that reduces smoking has substantial health benefits, and making smokers into pariahs, for whatever reasons, does just that.

Who loses from willingness to accept bad science as a basic policy? Citizens wishing to exercise their liberties, of course, and not just smokers. As Dr. James Le Fanu put it in Britain's Sunday Telegraph last May, "We could reach a situation where health activists, using dubious scientific evidence, will be in a position to blackmail us into behaving the way they think we should. It is not an attractive prospect."

Second, on a more personal level, the smoking widower who has lost his wife to lung cancer--and whose being further stigmatized as a murderer and a "pariah" is the goal of the EPA report--loses again. For a closer examination of the grounds on which the husband is made a pariah, let's take the highest available estimate of a non-smoking woman's annual risk of contracting lung cancer--48 per 100,000--and see what danger he poses to her. If we accept, arguendo, the 1.28 risk ratio, the smoker's wife's risk rises to 61 per 100,000. That's 13 extra cases per 100,000. Put simply, maximizing in every way possible the most estreme scenario painted by the EPA study, a smoking husband has a 1- in-7,700 chance of giving his wife lung cancer in a given year in the future. How reasonable is it to torture him with the prospect that he is slowly knocking off his loved ones?

Finally, it goes without saying that science suffers for the cause of smoking prevention. But what if the cause itself suffers? It is not uncommon that when bad science is introduced into the structure of social policy, the entire edifice of prescription and caution collapses. In 1985 the British government sent a hysterical mailing on AIDS to every household in the country. Making dire predictions of an epidemic, it warned that AIDS was an equal opportunity disease from which no one was safe, and urged extreme caution for all. The result? Old ladies in provincial towns were petrified. Non- monogamous homosexuals and intravenous drug users, if convinced by the packet that their risk was no different from that of the rest of the country, now saw less reason than ever to modify their behavior. Within a year, the London Spectator was suggesting that this "public service" was actually spreading AIDS.

Closer to home, paranoid anti-drug organizations like Partnership for a Drug-Free America may be exacerbating the drug problem by demonizing drugs like marijuana-- mild compared to the President's Halcion, and quite innocuous compared to alcohol. It is a point starkly made by Dr. Lester Grinspoon, a Harvard psychiatrist and drug specialist, as written up by Richard Blow in an excellent expose of Partnership that appeared in Washington's City Paper last December:

Partnership ads about marijuana "scare the hell" out of a high school senior. This student then goes off to college, where his roommate smokes marijuana, with no apparent adverse effects and without going on to shoot heroin. He begins to wonder if he's been lied to, and winds up trying pot for himself. He lives. Having rejected Partnership warnings about marijuana, he might subsequently reject more important warnings about riskier drugs such as cocaine or heroin.

Such a backlash could result if people consider the questionable science of environmental tobacco smoke reason to ignore the surgeon general's and other warnings on the hazards of tobacco smoking itself. If so, the EPA's hasty risk assessment could create more than inconvenience, rancor, and diminished personal liberty--it could create smokers.

Composition of Cigarette Smoke

Cigarette smoke is a heterogeneous mixture of gases, uncondensed vapors, and liquid particulate matter (32). As it enters the mouth, the smoke is a concentrated aerosol with millions or billions of particles per cubic centimeter (25,30). The median size of the particles is about 0.5 micron (1). For purposes of investigating chemical composition and biological properties, smoke is separated into a particulate phase and a gas phase, and the gas phase is frequently subdivided into materials which condense at liquid-air temperature and those which do not. The large quantities of material required for investigation of the chemical components are prepared on smoking machines (25) in which large numbers of cigarettes are smoked simultaneously in a fashion designed to simulate average smoking habits, and a yellow brown condensate known as tobacco tar is collected in traps cooled to the temperature of dry ice ( 70) C or liquid nitrogen (-196 C.). The tar thus contains all of the particulate phase of smoke as well as condensable components of the gas phase. The amount of tar from the smoke of one cigarette is between 8 and 10 mg., the quantity varying according to the burning and condensing conditions, the length of the cigarette, the use of a filter, porosity of paper, content of tobacco, weight and kind of tobacco.

An important factor determining the composition of cigarette smoke is the temperature in the burning zone. While air is being drawn through the cigarette the temperature of the burning zone reaches approximately 884 C. and when the cigarette is burning without air being drawn through it the temperature is approximately 835 C. (42). The smoke generated during puffing, when air is being drawn through the cigarette, is called main- stream smoke; that generated when the cigarette is burning at rest is called side-stream smoke. At the temperatures cited extensive pyrolytic reactions occur. Some of the many constituents of tobacco are stable enough to distil unchanged, but many others suffer extensive reactions involving oxidation, dehydrogenation, cracking, rearrangement, and condensation. The large number and variety of compounds in tobacco smoke tar is reminiscent of the composition of the tar formed on carbonization of coal, which in many cases is conducted at temperatures lower than those of a burning cigarette. It is thus not surprising that some 500 different compounds have been identified in either the particulate phase of cigarette smoke or in the gas phase.

In one study 5 regular cigarettes (70 mm, long, about 1 g, each) without filter tips produced 17-40 mg. of tar per cigarette. In another investigation 43 174,000 regular size American cigarettes afforded a total of 4 kg. of tar, an average of 2 mg. per cigarette. In still another study (31) 34,000 70-mm. cigarettes were smoked mechanically on a constant puff-volume type machine with which 45-ml. puffs, each of two seconds duration, were taken at one minute intervals from each cigarette. Eight puffs were required to smoke each cigarette to an average butt length of 30 mm. The smoke was condensed in a series of three glass traps cooled in liquid air. The condensate was rinsed out of the traps with ether, water, and hexane. The yield of condensate nonvolatile at 25 C. and 25 mm. of mercury was 20.9 mg. per cigarette.

Procedures for gross separation into basic, acidic, phenolic, and neutral fractions and for further processing of these fractions vary from laboratory to laboratory. The criteria upon which identification is based also vary. The most reliable identifications are based upon an ultraviolet absorption spectrum and/or a fluorescence spectrum in good agreement over the entire range with that of an authentic sample and include one or more of the following: Rf value observed in a paper chromatogran ( 11); order of elution from alumina; mass spectrometry.

Compounds of the Particulate Phase Other Than Higher Polycyclics

This brief summary is based largely on the comprehensive review by Johnstone and Plimmer of the Medical Research Council at Exeter University, England (24). It should be noted that water constitutes 27 percent of the particulate phase. The major groups of compounds included are shown in Table 1.

Aliphatic and Alicyclic Hydrocarbons

Almost all of the possible hydrocarbons, C, through C, saturated and unsaturated, straight-chain and branched-chain, have been reported to be present in tobacco smoke. Intermediate, normally liquid paraffins are present. All the C26 through C33 n-alkanes have been identified, as well as the C21 and C20-C33 isoparaffins.

Table 1.--Major classes of compounds in the particulate phase of cigarette smoke

Terpenes and Isoprenoid Hydrocarbons

Isoprene, the basis unit of the terpenes and of higher terpenoids has been identified in cigarette smoke (34) as have its dimers, dipentene and 1.8-p-menthadiene. The triterpene squalene, consisting of six isoprene units and shown to be present in smoke (47) is of interest because of the possibility of its being cyclized to polycyclic compounds and because of its ready

Passive Smoking: How Great A Hazard? By Gary L. Huber, MD, Robert E. Brockie, MD, and Vijay K. Mahajan, MD

Reports from medical journals, the popular media, and federal regulatory agencies about the adverse health effects of passive smoking have convinced many jurisdictions to ban smoking in public places. What is often missing from such discussions is the scientific basis for the health-related claims. The following article examines the scientific data concerning the ascertainable risk from inhalation of environmental tobacco smoke. One of its authors, Dr. Gary Huber, spoke at a recent CR symposium on "Science and Regulation" (see article on page 35).--Ed.

About 50 million or so Americans are active smokers, consuming well over 500 billion tobacco cigarettes each year. The "secondhand" smoke--usually called "environmental tobacco smoke," or more simply "ETS"--that is generated is released into their surroundings, where it potentially is inhaled passively and retained by nonsmokers. Or is it?

Literally thousands of ETS-related statements now have appeared in the lay press or in the scientific literature. Many of these have been published, and accepted as fact, without adequate critical questioning. Based on the belief that these publications are accurate, numerous public policies, regulations, and laws have been implemented to segregate or restrict active smokers, on the assertion that ETS is a health hazard to those who do not smoke.

What quantity of smoke really is released into the environment of the nonsmoker? What is the chemical and physical quality, or nature, of ETS remnants in our environment? Is there a health risk to the nonsmoker? In concentrations as low as one part in a billion or even in a trillion parts of clean air, some of the highly-diluted constituents in ETS are irritating to the membranes of the eyes and nose of the non-smoker. Cigarette smoking is offensive to many nonsmokers and some of these highly-diluted constituents can trigger adverse emotional responses, but do these levels of exposure really represent a legitimate health hazard?

Clear answers to these questions are difficult to find. The generation, interpretation, and use of scientific and medical information about ETS has been influenced, and probably distorted, by a "social movement" to shift the emphasis on the adverse health effects of smoking in the active smoker to an implied health risk for the nonsmoker. The focus of this movement, initiated by Sir George Godber of the World Health Organization 15 years ago, was and is to emphasize that active cigarette smokers injure those around them, including their families and, especially, any infants that might be exposed involuntarily to ETS.

By fostering the perception that secondhand smoke is unhealthy for nonsmokers, active smoking has become an undesirable and an antisocial behavior. The cigarette smoker has become ever more segregated and isolated. This ETS social movement has been successful in producing tobacco cigarette consumption, perhaps more than other measures, including mandatory health warnings, advertising bans on radio and television, and innumerable other efforts instituted by public health and medical professional organizations. But, has the ETS social movement been based on scientific truth and on reproducible data and sound scientific principles?

At times, not surprisingly, the ETS social movement and scientific objectivity have been in conflict. To start with, much of the research on ETS has been shoddy and poorly conceived. Editorial boards of scientific journals have selectively accepted or excluded contributions not always on the basis of inherent scientific merit but, in part, because of these social pressures and that, in turn, has affected and biased the data that are available for further analyses by professional organizations and governmental agencies. In addition, "negative" studies, even if valid, usually are not published, expecially if they involve tobacco smoke, and thus they do not become part of the whole body of literature ultimately available for analysis. Negative results on ETS and health can be found in the scientific literature, but only with great difficulty in that they are mentioned in passing as a secondary variable in a "positive" study reporting some other finding unrelated to ETS.

To evaluate critically any potential adverse health effects of ETS, it must first be appreciated that not all tobacco smoke is the same, and thus the risk for exposure to the different kinds of tobacco smoke must be considered independently.

What Is ETS?

The three most important forms of tobacco smoke are depicted in Figure 1. Mainstream smoke is the tobacco smoke that is drawn through the butt end of a cigarette during active smoking; this is the tobacco smoke that the active smoker inhales into his or her lungs. The distribution of mainstream smoke is summarized in Table 1 (page 12). Sidestream smoke is the tobacco smoke that is released in the surrounding environment of the burning cigarette from its smoldering tip between active puffs. Many publications have treated sidestream smoke and ETS as if they were one and the same, but sidestream smoke and ETS are clearly not the same thing. Sidestream smoke and ETS have different physical properties and they have different chemical properties. Environmental tobacco smoke is usually defined as a combination of highly diluted sidestream smoke plus a smaller amount of that residual mainstream smoke that is exhaled and not retained by the active smoker. What really is ETS? In comparison to mainstream smoke and sidestream smoke, ETS is so highly diluted that it is not even appropriate to call it smoke, in the conventional sense. Indeed, the term 'environmental tobacco smoke" is a misnomer.

Why is ETS a misnomer? Several reports on smoking and health from the Surgeon General's Office, a National Research Council review of ETS in 1986, the more recent Environmental Protection Agency's risk assessment of ETS, and several review articles all have provided a long list of chemical constituents derived from analyses of mainstream smoke and sidestream smoke, with the implication that because they are demonstrable in mainstream smoke and sidestream smoke these same constituents must, by inference, also be present in ETS. No one really knows if they are present or not. In fact, most are not so present or, if they are, they are present only in very dilute concentrations that are well below the level of detection by conventional technologies available today.

Only 14 of the 50 biologically active "probable constituents" of ETS listed by the Surgeon General, for instance, actually have been measured or demonstrated at any level in ETS. The others are there essentially by inference, not by actual detection or measurement. Thus, there are 36 constituents in these lists that are inferred to be present in ETS, but their presence has not been confirmed by actual detection or measurement. In this sense, then, ETS is really not smoke in the conventional sense of its definition, but rather consists of only a limited number of "remnants" or residual constituents present in highly dilute concentrations.

Because the levels of ETS cannot be quantified accurately as such in the environment, some investigators have attempted to measure one or more constituent parts of ETS as a "substitute marker" for ETS as a whole. The most frequently employed such "marker" has been nicotine or its first metabolically stable breakdown product, cotinine. Nicotine was considered an "ideal marker" because it is more or less unique to tobacco, although small amounts can be found in some tomatoes and in other food sources. In the mainstream tobacco smoke that is inhaled by the active smoker, nicotine starts out almost exclusively in the tiny liquid droplets of the particulate phase of the smoke. Because the smoke particles of ETS become so quickly and so highly diluted, however, nicotine very rapidly vaporizes from the liquid suspended particulates and enters the surrounding gas. In technical terms, the process by which nicotine leaves the suspended aerosol particle to enter the surrounding gas phase is called "denudation."

As a vapor or gas, nicotine reacts with or absorbs onto almost everything in the environment with which it comes into contact. Thus, nicotine is not a representative or even a good surrogate marker for the particulate phase, or even the gas-vapor phase, of ETS. In fact, there are no reliable or established markers for ETS. The remnant or residual constituents of ETS each have their own chemical and physical behavior characteristics in the environment and none is present in a concentration in our environment that reaches an established threshold for toxicity.

Measuring Health Risks

Because the level of exposure to ETS or the dose of ETS retained cannot be quantified under every-day, real-life conditions, the health effects following exposure to residual constituents of ETS have been impossible to evaluate directly. In broad terms, two different approaches have been employed in an attempt to assess indirectly the health risks for exposure of the nonsmoker to the environmental remnants of ETS. The first of these involves a theoretical concept that is called "linear risk extrapolation." Linear risk extrapolation has been employed extensively in attempts to determine the risk for lung cancer in nonsmokers exposed to ETS.

This concept of linear risk assumes that if there is a definable health risk for the active smoker, then there also must be a projected lower health risk for the nonsmoker exposed to ETS. This is represented schematically in Figure 2. The risk has been presumed to be linear from the active smoker to the nonsmoker exposed to ETS, based proportionately on the relative exposure levels and retained doses of smoke; it thus requires some measurement of tobacco smoke exposure for both groups. This is fairly easy to achieve in the active smoker, in part because mainstream smoke has been so well-characterized and it is delivered directly from the butt-end of tghe cigarette into the smoker. Such is obviously not the case, however for the nonsmoker exposed to ETS.

Most projections of linear risk for ETS-exposure have been based on the use of nicotine as a representative marker of exposure. A few projections have been based on carbon monoxide levels or amounts of respirable suspended particulates in the environment, but these approaches are fraught with even greater error. Since nicotine initially is in the particulate phase of the mainstream smoke inhaled by the active smoker and it is present primarily as a highly diluted gas-phase remnant or residual vapor-phase constituent in the nonsmoker's environment, the concept of a linear health risk from the active smoker to the nonsmoker is based on rather shaky scientific-reasoning.

That is to say, it is not valid to estimate a health risk for exposure to the particulate phase in the active smoker and then compare it with the health risk for exposures to the gas phase in the ETS exposed nonsmoker. Simply stated, "like" is not being compared to "like." Mainstream smoke and the residual constituents of ETS represent very different exposure conditions. Whether present in mainstream smoke or in ETS, particulate phase and gas phase constituents have very different biological properties, as well as different physical and chemical characteristics, and any associated health risks are also very different. The concept of linear risk extrapolation for ETS is based on a theory that when applied to ETS incorporates unsound assumtions that are not valid. There is no way, as yet, to evaluate or compare the levels of exposure in active smokers and nonsmokers exposed to ETS.

The second approach used to evaluate health risks for nonsmokers exposed to ETS has employed epidemiologic studies. Epidemiology is a branch of medical science that studies the distribution of disease in human populations and the factors determining that distribution, chiefly by the use of statistics. The chief function of epidemiology is the identification of populations at high risk for a given disease, so that the cause may be identified and preventative measures implemented.

Epidemiologic studies are most effective when they can assess a well-defined risk. Because ETS-exposure levels cannot be measured or in any other way quantified directly, even by representative markers, epidemiologists have had to use indirect estimates, or surrogates, of ETS exposure. For nonsmoking adults, the number of active smokers that are present in the household has been used as a surrogate for ETS exposure. Usually the active smoking household member has been th non-smoker's spouse. With a few limited exceptions, disease rates in nonsmokers exposed to a spouse who smokes have been the basis for all epidemiologic assessments.

Almost all of these studies have evaluated nonsmoking females married to a husband who smokes. For childre, the surrogate for ETS exposure has been the number of parents in the household who smoke. Estimates of ETS exposure based on spousal or parental surrogates have been derived by various questionnaires; no study employs any direct quantification of ETS or of ETS remnant constituents in the actual environment of the nonsmoker. Questionnaires of smoking habits are notoriously limited and often inaccurate, in part because of the "social taboo" that smoking has become and, in part, for other reasons related to the ETS social movement. Nevertheless, data from questionnaires about smoking behavior in spouses or in parents are the only estimates of ETS exposure available. Rates for three diseases in nonsmokers exposed (via surrogates) to ETS have been assessed: lung cancer, coronary heart disease, and respiratory illness in infants and small children. Only lung cancer will be discussed in this article.

ETS and Lung Cancer

What is the state of evidence on ETS and lung cancer? Almost all of the epidemiologic studies that are available to answer that question are based on the concept of some measurement of relative risk. None of the studies actually has measured exposure to ETS or to any of its residual constituents directly. Relative risk is a relationship of the rate of the development of a disease (such as lung cancer) within a group of individuals exposed to some variable in the population studied (such as ETS) divided by the rate of the same disease in those not exposed to this variable.

Relative risk is most frequently expressed as a "risk ratio," which is a calculated comparison of the rate of the disease studied in the exposed population divided by the rate of that disease in some control population not exposed to the variable studied. The terms "risk ratio" and "relative risk" are often used synonymously. Thus, the relative risk in all epidemiologic ETS studies on lung cancer is expressed as the rate of lung cancer in the ETS-exposed group (individuals married to a household smoker) divided by the rate of lung cancer where there was no ETS exposure (no household smokers). If the disease rates were exactly the same in these two groups, the risk ratio would be 1.0.

There have been 30 epidemiologic studies on spousal smoking and lung cancer published in the scientific literature. Twenty-seven of these epidemiological studies were case control studies, where the effect of exposure to spousal smoking was evaluated retrospectively on data that had already been available for review. The "cases" were compared, by the derived risk ratio, to the rate of lung cancer in "control" or nonsmoking individuals who were married to nonsmokers.

Three of the studies followed cohort populations of individuals exposed to spousal smoking prospectively over the course of time. A "cohort" is any designated group of people. A "cohort study" identifies a group of people that will be exposed to a risk and a group that will not be exposed to that risk, and then follows these groups over time to compare the rate of disease development as a function of exposure or no exposure.

The first studies were published in 1982 and the last studies were published in 1990. The studies originate broadly from different parts of the world and, for the most part, involve evaluations of lung cancer in nonsmoking females married to a smoking male partner; eight of the studies have limited data on nonsmoking males married to smoking females. Some of the studies are quite small, listing fewer than 20 subjects; others are based on larger populations, with four studies reporting between 129 and 189 cancer cases. Of the 30 studies, six reported a statistically significant association (identified by a positive relative risk ratio in the spousally-exposed to the non-exposed population) and 24 of the studies reported no statistically significant effect. The average estimated relative risk ratio for each study and each sex is listed in Table 2, as are the confidence intervals reported by the authors or, where not reported, calculated by others in published review articles.

Some of the negative studies--that is, some of the 24 studies that did not show a statistically significant association between the development of lung cancer and exposure to spousal smoking--contained data that suggested to the authors or to other reviewers a "positive trend." In most of science, "trends" do not count; data stand as either statistically significant or not statistically significant, with significance determined by specific accepted rules of biostatistics. New rules should not be "made to fit" an otherwise unproved hypotheses, just because the subject is tobacco and the observed results do not support the hypothesis investigated.

ETS Risk Weak

A relative risk is called strong or it is called weak, depending on the degree of association, or the magnitude of the risk ratio. A strong relative risk would be reflected by a risk ratio of 5 to 20 or greater. Weak relative risks, by conventional definition, have risk ratios in the range of 1 to 3 or so. Within the 30 epidemiologic studies on ETS and lung cancer, there are 37 different total reported sets of risk ratios for male or female nonsmokers.

Nine of the studies report risk ratios of less than 1.0. Thus, the results from all epidemiologic studies consistently reveal only weak lung cancer risks for nonsmokers exposed to spousal smoking, with only six of the studies reaching statistical significance; 24 epidemiologic studies report no statistically significant effect for ETS exposure.

Weak relative risks, however, do not exclude casual relationships. When the relative risks are weak it is very difficult to determine if the effect is artifactual or if it is real. Weak associations are close in magnitude to a level of risk that is sometimes called "background noise," and at this level of risk there are variables other than the one studied that can influence the statistical association.

When a series of epidemiologic studies reveals consistently weak associations that sometimes individually reach statistical significance and sometimes do not, all of the data can be pooled into a more comprehensive assessment to enhance the confidence of the assessment. This is called a "meta-analysis." There are specific rules, however, for combining data and not every published study lends itself to this kind of assessment. The National Research Council concluded, in 1986, that 13 of the then available studies met criteria that would permit a combined meta-analysis risk assessment. When the data from these 13 studies were combined, the net relative risk from all available studies was represented by a risk ratio of 1.34. The risk ratios as the result of other adjusted meta- analyses available for review vary from 1.08 to 1.42, with generally lower values derived from population studies in the United States and with somewhat higher levels of risk derived on populations outside of the United States.

No matter how the data from all of the epidemiological studies are manipulated, recalculated, "cooked," or "massaged," the risk from exposure to spousal smoking and lung cancer remains weak. It may be 1.08 or it may be 1.34 or it may be 1.42, but all of those still represent a weak relative risk. No matter how these data are analyzed, no one has reported a strong risk relationship for exposure to spousal smoking and lung cancer. Combining all the data from all epidemiological studies does not result in an enhancement of the relative risk--the risk for lung cacer with exposure to spousal smoking is weak.

In addressing this problem, Ernst Wynder, of the American Health Foundation, stated that when an assessment of relative risk is weak (that is, when the odds risk ratios are in the range of 2 to 1 or less) the possibility exists that the finding is artificial and a consequence of problems in the case control selection or is due to the presence of confounders (or confounding variables) and interpretation biases which need to be carefully considered. Confounding variables must be controlled in order to obtain an undistorted estimate of the effect of a study factor, such as spousal smoking, on risk. This is especially true when the studied risk factor has a weak association.

At least 20 confounding factors have been identified as important to the development of lung cancer. These include nutrition and dietary prevention, exposure to occupational carcinogens, exposure to various air pollution contaminants, genetic predisposition and family prevalence, circulating beta-carotene levels (as well as vitamin E and vitamin A levels), history of alcohol consumption, exposure to alpha emitting radiation (such as radon daughters), geographical residence and country of origin, presence or absence of selenium and other trace metals, healthy versus unhealthy lifestyles, age, gender, housing conditions, race, marital status, ethnicity, socio-economic status, diagnostic criteria, and perhaps most importantly of all, an enhanced clustering of risk factors. Thus, a large number of confounding variables are important to any consideration of spousal smoking and lung cancer, and no reported study comes anywhere close to controlling, or even mentioning, half of these.

Is ETS a Health Hazard?

Does exposure to the remnants or residual constituents of ETS represent a legitimate health hazard to the nonsmoker? In considering spousal smoking, lung cancer, and the confounding factors, Linda Koo, at the University of Hong Kong, cautioned that it may not be the hazards of tobacco smoke that are being evaluated, but a whole range of behaviors that result from having a smoking husband, which may, in turn, increase the risk for certain diseases among the wives and children. Indeed, confounding variables are always present and they are so numerous and so complex that they may make it impossible ever to know the true risk for lung cancer in nonsmokers exposed to spousal smoking.

Are the studies on the projections of levels of ETS residual constituents in our environment, and the studies on the spousal smoking and lung cancer, a reflection of "bad science?" Not necessarily, for they are the best science that is available today. Sir Bradford Hill of Oxford University cautioned years ago that it is important to remember that all science is subject to being reinterpreted or to being changed and modified by advancing knowledge. As newer technologies are applied to the assessment of environmental tobacco smoke, clearer understandings will evolve.

Has there been a "misrepresentation of science" in the common perception of ETS today? Active tobacco smoking and environmental tobacco smoke are controversial, very emotional, and highly politicized subjects. In the quagmire of ETS forces operative in politics, emotion, and science, it has been difficult to sort out scientific fact from unsound conjecture. Unfortunately, scientific data have not always been utilized objectively by governmental agencies or regulatory bodies that have their own inherent public health or political agenda. Good science ultimately must rest on established proven scientific methods, and the full results generated by these scientific methods. When these methods are compromised, scientific integrity is lost and society pays the price. Interpretations and judgements may vary, as a function of an investigator's bias or to expedite one or another political, social or emotional objective.

Richard Lindzen, of the Massachusetts Institute of Technology, has emphasized that problems will arise where we will need to depend on scientific judgement, and by ruining our credibility now we leave society with a resource of some importance diminished. The implementation of public policies must be based on good science, to the degree that it is available, and not on emotion or on political needs. Those who develop such policies must not stray from sound scientific investigations, based only on accepted scientific methodologies. Such has not always been the case with environmental tobacco smoke.

Lifestyle - Poison at Home and at Work

A new report calls secondhand smoke a killer

The logic is simple: if the chemicals in tobacco smoke can kill 4000,000 American smokers every year, couldn't those same chemicals affect the nonsmokers who live and work around burning cigarettes? Studies consistently support that inference, yet environmental tobacco smoke (ETS) is still widely treated as an annoyance, while lesser hazards, such as the Alaron apples, are regulated or banned. Those days may now be numbered. Last week, scientists at the U.S. Environmental Protection Agency released, in draft form, the most sweeping analysis yet of how passive smoking affects people's respiratory health. The report links ETS to a range of childhood ilnesses and terms it a "known human carcinogen." If the agency adopts that designation, cigarette smoke could soon enjoy the same status as arsenic, asbestos and coke-oven emissions.

Few of the EPA's findings are new; both the National Research Council and the surgeon General's office sounded similar warnings in 1986, and the EPA released an earlier draft of the current report in 1990. But the new document includes more data than any of its predecessors, and its conclusions are generally stronger. The surgeon general reported, for example, that ETS may exacerbate symptoms in asthmatic kids. Drawing on 50 recent studies the new EPA report concludes that passive smoking not only aggravates up to 1 million existing cases of childhood asthma each year but causes 8,000 to 26,000 new cases. The report also links ETS to pneumonia, bronchitis and reduced lung function and labels it a known cause of middle-ear effusion, a leading source of childhood surgery.

To gauge the association between passive smoking and adult lung cancer, the EPA researchers compiled the results of 30 studies from different parts of the world. Each study compared lung-cancer rates for two classes of nonsmoking women--those living with smokers and those living with nonsmokers. Most carcinogens work too subtly to show measurable effects at the doses people receive in daily life (that's one reason researchers are always pumping megadoses into lab animals). Yet in each of the eight countries the surveys examined, smokers' spouses suffered significantly more than their share of lung cancer. And the women breathing the most smoke suffered the greatest increase in risk. The EPA researchers estimate that Americans who live or work among smokers experience a 20 to 30 percent increase in lung-cancer risk and that ETS causes 3,000 U.S. lung-cancer deaths each year.

Though the report deals only with respiratory diseases, many researchers now believe that passive smoking causes a similar increase in heart-disease risk, triggering another 35,000 deaths each year. Alarmed by those figures, the American Heart Association is now asking the EPA to mount a separate review of passive smoking and cardiovascular illness. But if the agency declares secondhand smoke a carcinogen, further study may be redundant. Though EPA risk assessments don't dictate policy, they weigh heavily on the agencies that do. If secondhand smoke were listed as a known carcinogen, the General Services Administration would likely ban smoking in all federal buildings. OSHA (the Occupational Safety and Health Administration) could force private employers to follow suit.

To become official, the EPA's draft report still needs to pass muster with a scientific advisory board (SAB) and with the agency's administrator, William Reilly. But staffers don't anticipate major problems. Two years ago, after taking public testimony on the earlier draft, the SAB endorsed the report's basic conclusions but asked for more data and analysis. Those revisions are now in place. The cigarette industry, which has lobbied for years to soften the findings, isn't pleased to see them strengthened. In a press statement issued last week, the Washington based Tobacco Institute accused the EPA of an antismoking bias and questioned the new findings on children and secondhand smoke. "Children are exposed to many different things that could potentially impact their respiratory health," the institute said. "The children's ETS-exposure studies ... are not remotely adequate in controlling for the many potential factors."

The industry has ample resources, but it's fighting a powerful current. As recently as 1990, only three American towns had banned smoking in restaurants or workplaces. Today, says Julia Carol of the Berkeley-based Americans for Nonsmokers' Rights, 24 municipalities mandate smoke-free workplaces, 26 have banned smoking in restaurants and a few even boast smoke-free bars or prisons. Separate seating was a nice thought, Carol says, but "sitting in the nonsmoking section of a building is like swimming in the nonchlorinated section of a pool." The difference, of course, is that a little chlorine won't kill you. Other people's cigarettes may.

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