GB House Pipes
The Pipe Cam
Tools & Accessories
A collection of articles regarding ETS or Second-hand smoke
Back One Step
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been replaced by the stretching of the truth and the spread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
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
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
"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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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.
Back One Step
95% of our orders are shipped the day they are received.
- You MUST be at least 18 years of age to purchase tobacco products in Tennessee!
- We do not sell tobacco products in Maine or Arizona.
- All Packages are shipped US Post Office unless you specify UPS.
- All Customers will be Charged for Shipping & Return Postage on any Refused or Returned package(s).
- International Customers: You are to check with your local customs & duty officials to see if there are additional duties or fees required, or if there are prohibitions on tobacco or amounts of tobacco which can be shipped to your country.
- Charge card customers may order by calling
- To check on an order call 865-436-4412, 9am-3pm Eastern Time Monday-Friday.
- Visit our showroom on D-Level of the Mountain Mall, on the corner of Parkway and River Road in Gatlinburg!
- We are open 7 days a week.
- Prices subject to change without prior notice.
- No Cash Refunds. Merchandise credit ONLY on returns.
- We DO NOT ship cigarettes.
603 Skyline Dr.
Gatlinburg, TN 37738
24hr Fax: 1-865-430-7476
© 2009 Gatlinburlier, Inc. All Rights Reserved.
THE GATLINBURLIER DOES NOT SHIP CIGARETTES.
WARNING: This product contains nicotine. Nicotine is an addictive chemical.
OUR NEW OLD BLEND
As with any avalanche of lemons into one's life, survivors attempt to make lemonade and so it is with the Gatlinburlier Tobacconist. G&B Tobaccos new licensing and stature as a Tobacco Manufacturer now presents many opportunities for our loyal long-time customers. Not only does this new status make the Gatlinburlier the only truly legal tobacco retailer in the country, but it opens opportunities for us to expand our lines, since our access to specialty tobaccos has been vastly expanded. We plan to offer special deals on our new products as we produce new blends and attempt to improve some of our existing blends.
Tobacco being a natural product varies in characteristics year to year. It takes constant adjusting to keep blends consistent in taste, color, and burning qualities. In many cases blenders keep several years worth of tobaccos on hand so as to phase out one years product while phasing in another years crop to minimize the changes in the qualities of the blends. Over the 37 years that we have blended tobaccos some of our suppliers have left the business and other tobacco components have changed so much that we think we need to make adjustments to a few of our blends.
Gatlin-Burley our Americanized English once contained a very special Green River Valley tobacco which became unavailable. Given our new contacts within the industry we now have access to this rare tobacco, and have re blended this great blend, with just a touch of Latakia to meet its original qualities.
Gatlin-Burley was a blend created to keep the smoker's interest and encourage the maturation of the smoker's own tastes. Thirty-seven years ago it was our flag ship. It was an Americanized English that seemed to change taste as the smoker's pallet change over the course of one day and over the course of many weeks.
As a special short term offer we will send you a two ounce bag of this fabulous rebirth of greatness for only $5.95.
This extraordinary blend mixes fabulously with our Cades Cove Cavendish and our Chimney Smoke to make it even more tame for the American taste. For those looking to find a slightly more mature taste than is offered by our "natural aromatics" - Gatlin-Burley is the tobacco blend they are seeking, but "Made Even Better®".
2oz for only $5.95