Using Criticial
Thinking to Better
Understand the
Health Concerns of Passive Smoking
Tommy Boone, PhD, MPH, FASEP,
EPC
Professor and Chair
Department of Exercise Physiology
The College of St. Scholastica
Duluth, MN
Introduction
The more one thinks about critical thinking,
the more it fits as an absolute necessity of an education. Students
simply can’t profit from the illusion of thinking. Professors,
in particular, can do something about the illusion. They have the
physical space and the opportunity to bring order to the random connection
of ideas. Thus, the structuring of real thinking begins with an understanding
of observations and possibilities. It is a matter of disconnecting from
the tradition of beliefs for the hope of furthering the existence and power
of the individual. Critical thinking is therefore a freeing process;
a step beyond the self-promoting ideas of yesterday or anyone with a reason
to benefit. Belief in something is powerful, but believing in the
right “something” is the difference between being right and being a failure.
Teaching students about belief is as difficult
as teaching students about the importance of critical thinking. The
wheels are already rolling; their thinking is already well captured.
How, then, can professors feel confident and/or right to alter the students’
course of events. Frankly, the lack of a good answer to this question
has probably kept some of my colleagues from trying. The problem
is that, even should they believe differently, the very act of not trying
is often interpreted as a confirmation of what they are doing as being
right. Students have no reason to understand the difference, and
thus the lack of disconfirming behavior masks the need for change.
Note that if the professors had pressed the issue of critical thinking,
it is logical that the illusion of learning would have been recognized.
Teaching is Just Teaching, Right?
In the grand scheme of things, “teaching
is teaching, right”. If so, then anyone can be a teacher and, frankly,
it just isn’t so! Even among teachers, those with the PhD, there
are many who can’t teach and many who care less about teaching. Merely
having the PhD, as a criterion for excellence in teaching, is as senseless
as having a key to a car means that the person can drive. We expect
more from professors and, especially the PhD prepared exercise physiologist.
All else being equal, the PhD should mean something. And, it should
mean more than a ticket to a college position or to validate the professor.
It is easy to get the big head, but it is much harder to split time with
what should be done on behalf of students and the profession and what is
typically done to benefit the professor. Increasingly, this difference
is becoming the target of distinction and thus the difference between the
extraordinary performance and the average performance. But, my professer
is different, I've heard. "I am happy about what I'm learning at
this college. What you’re saying doesn’t apply to my situation.”
What these statements have in common is that they are often cited in support
of a person’s beliefs. Students are convinced that the program offerings
are complete and justified. Such convictions are good, but only if
the evidence supports the beliefs. As an example, what if the distinction
between the student’s academics at one institution (say, exercise science)
is little more than “one” course from that of another student in a different
institution with an entirely different degree (e.g., physical education)?
Indeed, if only one course separates the exercise science concentration
from the physical education degree, the degree is then a physical education
degree.
The most likely reason for the lack of
confusion, that is, the lack of understanding of the differences between
exercise science and physical education is that the PhD exercise physiologists
are glad to have a college position. Why should they tell the students?
The layout, according to the past 50 years or so, is obviously beneficial
to traditional physical educators. Whether similar parallels exist
in academia is an interesting question. In view of what continues
to happen within the infrastructure of hundreds of university settings,
few college teachers with degrees in kinesiology, exercise science, physical
education, and/or exercise physiology appear interested in lending credibility
to a “pure” exercise physiology program. Similarly, the uninformed
remains convinced of what they are doing is right or they are afraid to
experiment with new ideas and/or possibilities. The problem is that
disconfirmation begins with critical thinking and, unless the PhD professors
have been taught how to think versus what to think, the likelihood
of confirming new ideas is very small. The end result is more professors
who are concerned with wanting to keep things as they are than with considering
hidden possibilities in change.
The important point here is that we cannot
forget the importance of teaching critical thinking. Those who do
so understand the importance of thinking straight. Those who don’t
often have to address the erroneous conclusions of unclear thinking.
If only our institutions were filled with critical thinkers, the hazards
of uncritical thinking would not be underestimated. This idea is illustrated
even more clearly by considering the relationship between low-density lipoprotein
cholesterol and coronary artery disease (CAD). If there is a strong
relationship, then the obvious strategy would be to lower cholesterol to
lower the probability of suffering from CAD. Left unchecked, high
cholesterol causes CAD, right? Unfortunately, on behalf of mankind,
the answer isn’t all that simple. There are many factors that appear
to associate with CAD and, therefore, angina pectoris or a myocardial infarction
(MI). As devastating as it is to have an MI, it is incorrect to believe
that it is caused solely by high cholesterol. There are simply
too many “risk” factors for CAD. Very likely, the loss of myocardial
integrity is a direct function of genetics; a scientific point of view
that is incalculable and will remain to be for decades.
The Problem of Hidden Data
Moving away from the traditional way of
thinking requires a distinct discrimination. It is all about the
problem of hidden or absent data that influences the kinds of inferences
professors (and students) draw and, therefore, their beliefs about exercise
and heart disease. Often times, students are presented the obvious
views and the obvious relationships between disease and lifestyle issues
instead of the more complex and, frankly, the more mentally and emotionally
gratifying understanding of assumed beliefs.
Unfortunately, with the increased need
to find “the” cause for different diseases, there is an unfortunate (and
unscientific) movement to think very narrowly. The resulting problem
is one of a self-fulfilling prophecy. That is, although cholesterol
may be associated with CAD, the association as such doesn’t establish a
“cause and effect” relationship. This particular view, however outside
of mainstream thinking, is important to fully understanding the various
multi-faceted associations with CAD. Obviously, the exact cause or
causes remain to be determined.
This is but one example of hidden thinking;
the teaching of ideas without full disclosure of all the data. There
are many examples of uncritical thinking that result in the victimization
of the public. It is critical that the professor doesn’t neglect
the full set of data when lecturing on the relationship of one or more
variables to a disease and/or disorder. Making all the data available
to the student helps to prevent mis-understandings and the belief that
should the disease surface, “I did it to myself, there isn’t anyone else
to blame but me.” How can the student and/or individual in the community,
with similar coaching, not believe the self-fulfilling prophecy?
Hence, the absence of critical thinking and “critical lecturing” sets the
emotional circumstances for a premature understanding of the disease.
Beliefs are Difficult to Give Up
The tendency to make fast judgments by
exercise physiologists who have an obvious interest in the cardiovascular
system is “the” condition of today’s teaching. It is likely to be
full of errors and an over-reliance on the simplification of disease agents.
Professors are not deliberately driven to confuse or hide behind a common
belief. Instead, they believe certain things because they were taught
“X” causes “Y”. Beliefs are difficult to give up, especially
if they are associated with decades of thinking. Only by taking responsibility
to think clearly and objectively is it possible to dispel commonly accepted
views. As an example, take the assumed relationship between health
and negative mental imagery. Is it true that a person’s health is
susceptible to negative thinking? What if it isn’t true? Have
their been too many published books on mind-body issues, stress management
lectures, and psycho-self-help workshops? The short answer is that
it is likely that we have reached beyond the reality of the data.
Our hope in avoiding a specific disease is not consistent with the unknown
causes and occurrence of disease even in the most dedicated believer.
It is also possible that some individuals, including professionals in the
healthcare field, would not want to go through life thinking that their
emotions dictate the type of disease they may suffer from at some point
in life.
Indeed, the idea that our mental health
conforms to our mental images has always been problematic on several fronts.
One, it is very likely the general belief that thinking right will keep
the body’s physiology right is unfounded. Personally, I understand
that the human body isn’t so predictable, given its multi-complexity and
mystery. There is also the problem that if good thoughts and mental
pictures were to result in good health, then everyone who gets sick is
subject to blame him- or herself. Blaming the victim is too easy
and should be rejected. Physically disabled individuals either with
cancer or a chronic inflammatory disease should not have to live under
the false impression that they are responsible for their own misfortune.
While our knowledge of the power of the
mind in preventing or curing diseases is too uncertain to rely completely
on mental images, it is not illogical to understand how negative thoughts
can be self-defeating. If we are to succeed, we must make an effort
and, yes, we must believe in ourselves. There is a difference between
thinking positive to help us get moving in the right direction and “mental
phenomenon” that is scientifically without a guarantee of sound science.
At first glance, it could be argued that “the truth” will be known.
Meaning, surely, cancer is caused by a bad attitude. College students
and the general public are told that the mind influences the body.
Perhaps it does, but is influence the same as causing cancer?
The lesson that is important is the answer to the question, “What does
the evidence really show?” It may be best to begin an examination
of whether the evidence exists by using the skeptics approach to the problem
of passive smoking. Have scientists misplaced data, tampered with
the data, or made conclusions without considering all the facts.
If so, the net effect may be the validation of the researchers’ views.
How would the reader know that the paper
he/she is reading is a well-written product marketed for publication?
Most would not know that published papers are a collection of calculated
assumptions to astonish the reviewers in hopes of being acceptable for
publication. Because publishing is so important for tenure, promotion,
and financial gain, it is unfortunately the case that some professors write
either knowingly or unknowingly in a manner that confirms their bias.
The challenge of course is to write as objectively as possible and, thus
avoid the errors and biases of human judgment. The following information
about passive smoking is presented to encourage the reader to take a step
back and ask, “Does the information put closure on the belief that passive
smoking causes a variety of healthcare problems or is there sufficient
doubt to conclude that passive smoking is not the cause of certain pathologies?”
Passive Smoking: Is it Dangerous?
While the mainstream smoke inhaled into
the larger airways of the lungs leaves particles that are considered harmful
[1], the involuntary exposure to the smoke that circulates
into the air between puffs may also be harmful and, perhaps, deadly to
non-smokers [2]. This smoke is called sidestream
smoke, and presently there is a major debate in the scientific literature
as to whether it is harmful [3,4]. This paper identifies
the medical and research issues in the debate on passive smoke and lung
cancer.
The Concerns
The dangers associated with passive smoke
have been debated for more than 20 years. However, only recently
has the exposure to sidestream smoke, as a health concern, been identified
and concluded as a major cause of indoor air pollution. In fact,
according to the Environmental Protection Agency, passive smoking is classified
as a class A carcinogenic environmental condition with more than 40 carcinogenic
compounds. The conclusion, if there is no safe threshold for carcinogens,
is that sidestream smoke carries with it sufficient reason to question
the exposure [5],
Unfortunately, the non-smoker is generally
unaware of the contents of sidestream smoke, particularly N-nitrosamine,
benzo-[a]-pyrene, carbon monoxide, and heavy metals that may cause cancer
[6,7]. The non-smoker may also be poorly informed
about various irritations induced by sidestream smoke, particularly symptoms
from irritation of the eyes and throat to headache and coughing.
The otherwise healthy non-smoker who is allergic to cigarette smoke may
experience wheezing, sneezing, and nausea [8,9].
The unhealthy person with coronary artery disease may experience increased
episodes of chest pain (angina pectoris) and/or electrical irregularities
of the myocardium when exposed to passive smoke [10].
Aside from passive smoke being a source
of irritation and a nuisance, it may increase the risk of lung cancer.
The results of numerous studies have supported this notion [11-14].
However, these studies have been criticized for the small number of subjects
with differing designs, for subject participation from different hospitals,
and for lack of histological confirmation [14].
As to the latter concern, the 1983 study by Correa et al. [15],
however, demonstrated histological confirmation for 97% of the cases.
Their work, that agrees with Trichopolous et al. [11].
strengthens the suspicion that passive smoke may contribute to lung cancer.
Both studies support earlier contention [12] that heavy
smoking by one member of the spouse pair increases the lung cancer risk
of the non-smoking partner.
Most of the cases of lung cancer in the
non-smoking partner are found in women [16,17].
The reason for the female's increased incidence of lung cancer when exposed
to secondhand smoke is unclear. First, sidestream cigarette smoke,
although containing toxic components [18], is diluted
in the ambient air and, second, the bronchial epithelial changes in the
smoker are rarely found in the non-smoker [19].
This latter point is important since results associated with passive smoke
must differ with reports of different types of lung cancer [20].
For example, Trichopoulos et al. [11] reported a histologically
confirmed diagnoses of 35%; whereas, Chan and Fung [21]
reported 82%. Some studies [14] excluded adenocarcinoma
while it predominated in others [12,20,21].
There is also the question of previous
studies focusing just on the spouse's smoking. Kabat and Wynder [20]
pointed out that the measure of exposure to passive smoke is influenced
by the time the non-smoking spouse is in the presence of the smoker and
whether the smoker is a light or heavy smoker. There is also the
additive factor of previous exposure to smoke by earlier marriages, relatives,
and at restaurants and at work, or by travel via trains and buses.
The Mechanisms
The question remains, "By what mechanism
does passive smoke cause lung cancer?" Theoretically, the volatile
components of cigarette smoke cause lesions [22].
Nitrosamine content, in particular, in passive smoke is reported by Stock
[23] to be some 50 times greater than in mainstream
smoke. Other reports [24,25] indicate that sidestream
smoke has 52 times as much dimethylnitrosamine, 16 times as much naphthalene,
28 times as much methylnophtholene, 3.4 times as much benzo-[a]-pyrene,
and 5.6 times as much toluene as mainstream smoke.
Naturally, the actual exposure to these
chemicals depends on factors mentioned earlier [20]
plus the volume of smoke generated, the volume of air, room ventilation,
and the differences in which the cigarette is smoked. There are also
other confounding influences. Auerback and Garfinkel [26]
stated that radiation treatment (with exposure to ionizing radiation) may
lead to lung cancer. There is also the possibility of lung cancer
developing in the non-smoker subsequent to healed tuberculosis scars [27]
or, in the female non-smoker, as an estrogen-related tumor (adenocarcinoma)
[26].
The reports of mutagens in the urine of
passive smokers [29] suggest the possibility of increased
cancer risk for specific non-respiratory sites. This point is supported
by the data from Sandler et al. [30] who found a significant
association between passive smoke and lung cancer [odds ratio (OR) of 1.9].
They reported OR for other sites (such as cancer of the cervix) that were
statistically significant. In agreement, Buckley et al. [31]
found a 4-fold risk of cervical cancer among passive smokers. However,
following statistical adjustment for the husbands' number of sexual partners,
the risk decreased to 2-fold that was not significant. Although similar
findings have been reported by Brown and associates [32].
Hirayama [12] reported that the risk for cervical cancer
was not increased.
Wald et al. [7] reported
a 35% increase in the risk of lung cancer among non-smokers living with
smokers compared with non-smokers living with non-smokers. They concluded
that about a third of the cases of lung cancer in non-smokers who lived
with smokers may be attributed to passive smoke. This view is supported
by the earlier study by Wald and Ritchie [33] in which
the average urinary cotinine concentration among non-smokers married to
smokers was about three times that among non-smokers married to non-smokers.
If urinary cotinine levels reflect exposure
to carcinogens in passive smoke, then the findings of increased lung cancer
risk among non-smokers might be expected. Cotinine levels among non-smokers
living with 2-pack-a-day smokers have been reported to be roughly the same
in smokers of less than 3 cigarettes per day [34].
If there is a relationship between urinary cotinine levels, carcinogens,
and passive smoke, it is not an easy one to duplicate. Hence, even
though researchers have concluded that passive smoke may increase the non-smokers'
risk of lung cancer, they have stated as well that not all studies have
shown significant associations [20,35].
Moveover, even with the pooling of data on non-smokers from three case-control
studies, Dalager et al. [36] concluded that the small
number of cases precluded a definitive answer on the carcinogenic effects
of passive smoke.
The Problems
The problem with the statement that passive
smoking causes lung cancer is the omission of other factors as risk factors
for lung cancer. Take, for example, the study by Alvanja and associates
[37] in which the authors found a significant 2.2-fold
age-adjusted risk of lung cancer in non-smoking women who had not smoked
for at least 15 years compared with lifetime non-smokers. Here is
an indication that non-smokers are subject to lung cancer, but rather than
passive smoke as the cause -- it was the residual effects of having smoked
earlier in one's lifetime!
Alvanga et al. [37]
also reported that 41% of the women with lung cancer reported having at
least one previous lung disease. They found that the risk of lung
cancer following previous lung disease was similar among lifetime non-smokers
(OR = 1.4) and former smokers (OR = 1.5). Asthma and pneumonia were
significantly related to lung cancer (OR = 2.7 and 1.5, respectively) among
lifetime non-smokers, and that previous lung disorders were significantly
related to both adenocarcinomas (OR = 1.4) and all other cell types combined
(OR = 1.8).
The mechanism by which pre-existing lung
diseases may increase the risk of lung cancer in lifelong non-smokers is
not known. Asthma may increase the time within the lung for carcinogenic
exposure to contact the epithelial cells [37].
Pneumonia may increase lung cancer risk (adenocarcinomas, in particular)
if it results in lung scars [26]. These findings
support the contention of some researchers [38] that
chronic obstructive pulmonary disease may be associated with increased
risk of lung cancer.
What is strikingly important in the work
by Alvanja et al. [37] is that they concluded approximately
13% of the lung cancer among lifelong non-smokers is attributable to previous
lung disease! This point is not considered in most studies.
Also, many articles fail to adequately address the role domestic radon
exposure, diet, occupation, and familiar factors may account for lung cancer
among non-smokers.
Instead, the growing awareness that passive
smoke is said to cause lung cancer [5,39-42]
is witnessed by the increased restrictions on where people can smoke [43].
In other words, according to some experts, the opinion is that biological
plausibility of the epidemiological findings has been established and,
thus causality has been established as well. Consider, for example,
the conclusion by Glantz and Parmley [3] that "...passive
smoking causes...lung cancer...." However, simply concluding the
issue in a scientific manner via various scientific journals does not mean
that passive smoke causes lung cancer. Equally true is the notion
that just because some people find active and/or passive smoking "genuinely
distasteful" [44-46] does not make either type of smoking
"the" cause of lung cancer.
Overall, however, it is hard to overlook
the role of various mutagenic substances in cigarette smoke, especially
since greater than 80% of all cases of lung cancer in the United States
is believed to be due to cigarette smoke [47].
Nitrosamine and polycyclic aromatic hydrocarbons may contribute to an early
carcinogenic process [37], particularly with regard
to mutations in the p53 tumor suppressor gene [48].
Other contributors may be the role various promotional exposures to phenols,
diet, and numerous other lifestyle factors in the development of lung cancer.
The likelihood of individuals with inherited predispositions to smoking-related
carcinomas cannot be discounted either, and may become a major issue in
the future with new research in molecular genetics [47].
Until then, there is still the recognized
association between cigarette smoke and renal cancer [49],
myeloid leukemia [50], and cancer of the pancreas [51]
to mention a few. These observations are consistent with the magnitude
of the risk of lung cancer from passive smoke. But, given these findings,
one would expect that the particulates, which are reported to be 10 times
greater in mainstream smoke than in passive smoke, would result in even
more lung cancer than cited in the literature. Moreover, in that
the cigarette smoker inhales about 420 mg of tar per day (14 mg per cigarette)
versus the non-smoker's exposure to 1.43 mg of tar per day [52],
active smoking should be significantly more damaging to the lungs with
a greater predisposition to significantly more lung cancer but is it?
Lung cancer appears to be associated with
a multitude of factors in some subjects while relative few in others.
The debate whether cigarette smoke causes lung cancer is confounded since
lung cancer is associated with numerous conditions. Consider, for
example, in Utah where the per capita cigarette consumption was 1,500 in
1976, the death rate from lung cancer among males for 1950 through 1969
was 22/100,000 -- the lowest in the United States according to Rawson [53].
The author stated that in Idaho, where the per capita cigarette consumption
was 2,500, (1,000 more than in Utah), the male death rate from lung cancer
was 23/100,000, and in Wyoming, where the male death rate from lung cancer
was 27/100,000, the 1976 per capita consumption of cigarettes was 3,200
or twice that of Utah. Colorado had a 1976 per capita cigarette consumption
of 2,700 and a male death rate from lung cancer of 28/100,000. Rawson
[53] stated that the relatively low lung cancer death
rates in states adjacent to Utah are not too different from the low death
rate among Utahans in spite of significantly greater cigarette consumption
rates.
In addition, although urinary cotinine
is reported to be correlated with exposure to passive smoke, there is the
question of biologic significance of the exposure. Wald and colleagues
[54] reported median urinary cotinine levels of 1,655
ng/ml in cigarette smokers, 6 ng/ml in passive smokers, and about 2 ng/ml
in non-smokers not exposed to passive smoke. Given these values,
it is difficult to understand that if smokers with reported urinary cotinine
levels as high as 1,655 versus 6 ng/ml (and passive smoking is said to
cause lung cancer), then all smokers should have lung cancer. Yet
the reality of the research findings is such that it is impossible to conclude
that all smokers will develop lung cancer. About all one can say
is that "...passive smoking may result in an increased morbidity
and mortality among non-smokers" [55]. The link
between passive smoke and lung cancer is not as straightforward as frequently
reported [56].
The Questions
An interesting question is "Why the fuss
over lung cancer from passive smoke?" When, according to Wells [57]
and Kawachi et al. [58], the number of heart disease
deaths due to passive smoke is an order of magnitude greater (37,000) than
the number of lung cancer deaths due to passive smoke (3,700). The
problem with passive smoke would appear to be heart disease deaths not
lung cancer deaths! Deaths from other cancers (12,000) increase the
total to 15,700, which is still less than one-half of the deaths due to
heart disease even though the relative risks for heart disease and lung
cancer in association with passive smoke were similar, that is, 1.3 for
both diseases [59,60].
Regardless of the impression one may get
from various news sources and scientific journals, there is also the question
of whether it is right and, if so, to what degree to regulate the presence
of cigarette smoke in the workplace and to ban cigarettes entirely if it
seems warranted? There is the very real possibility that despite
the regulatory measures, the rate of lung cancer will be maintained since
there are so many carcinogens affecting the general population. In
fact, it is highly probable that no one potent carcinogen is the culprit.
The likelihood of significant synergistic
effects of numerous carcinogens should be considered when "the" cause,
such as passive smoke, is discussed in association with a specific cancer
(such as lung cancer). Who knows how many of the non-smoking wives
of the published studies were at some point exposed to asbestos?
Who has studied the role high attitudes (such as Denver) and flying at
high altitudes may have on the incidence of lung cancer from cosmic radiation?
Have the authors of the various studies considered the geographic influence
on their subjects' cancer? Do immunosuppressive drugs contribute
to an increased risk of lung cancer?
In men with Klinefelter's syndrome, the
risk of developing breast cancer is 66 times that in normal men [61].
Is it possible that lung cancer, for example, whether in the presence of
passive smoke or not is associated with abnormal chromosomes? Is
a certain genetic factor associated with the eventual development of lung
cancer? Do susceptible individuals in affected families develop the
same type of cancer [62], and have the epidemiologists
carefully examined this factor in their research? Very likely only
a small proportion of the individuals exposed to passive smoke will manifest
lung cancer. These individuals probably have a constitutional predisposition
that increases their individual susceptibility to the cigarette smoke.
The problem of latency, that is, the period
between first exposure and onset of disease may vary between 5 and 50 years,
[63] has not been thoroughly investigated. Is it
possible that passive smoke may serve to influence the latency period of
lung cancer that may have been initiated by some other known or unknown
occupational agent? If the answer is "maybe" or "yes" then, if researchers
fail to address the type, strength, and interaction of exposure to other
chemicals, their findings may be correctly interpreted as premature and/or
misleading.
Unfortunately, given the complexity of
the
multi-dimensional nature of risk factors affecting human beings, crucial
retrospective dose data are often not available. Also, diagnostic
criteria and methods not only change over time but may be interpreted differently
as well. The subject's perceived exposure or lack of exposure to
a particular chemical may be subject to a variety of biased views.
The task of identifying and documenting past exposures is a researcher's
nightmare, which is often incomplete without careful consideration of what
it means to the outcome of the study.
Aside from these concerns, the official
position of the National Institute for Occupational Safety and Health is
"...exposure to any known or suspected carcinogen must be reduced to the
lowest level possible by whatever means available" [64-65].
Obviously, one way to do this, regarding passive smoke, is to eliminate
active smoke. This decision would seem appropriate since it is difficult
to determine the "safe" level of human exposure to passive smoke with any
degree of confidence. Some authorities [64] would
still argue that passive smoke has not been proven to be a carcinogen.
Summary
Experimental epidemiological studies face
many problems, and whether they are retrospective or prospective studies
does not matter that much. What matters is the accuracy of the measurement
of all possible confounding influences. Because it is practically
impossible to measure everything, the studies are at best crude estimates
of associations that may or may not be statistically and/or biologically
significant.
What would be refreshing in many of these
reports is the authors' attempt at being fair and reasonable with their
conclusions. Too often the only hint of their trustworthiness, as
scientific thinkers, is the relatively frequent use of the word "may."
By concluding that passive smoke may or seems to cause lung cancer, the
researchers leave the door open to the reader that the published manuscript
attempts to allow for both sides of a controversial topic. But, is
this approach and its apparent inadequate covering of alternative views
of the same topic a fair and critical (straight thinking) analysis?
Probably not! The truth about lung cancer and passive smoke, as defined
by epidemiological studies, is that the findings apply to whole populations
and not individuals. Dickman [66] points out that,
"Although the conclusion may be interesting scientifically, it has little
practical value." Hence, unfortunately, risk factors cannot be used
to predict which individual will get lung cancer from passive smoke if
in fact passive smoke causes lung cancer.
Is it possible that much of the literature
on passive smoke and lung cancer has made the typical individual on the
street less concerned about lung cancer if he/she does not smoke or does
not associate with smokers? The answer is "yes" but does this individual
have all the facts? The answer is "no" and, therefore, by not educating
the students (and the public at large) to take full responsibility for
health matters, including the interpretation of research findings, both
have become more comfortable in certainty than with probabilities. The
probability is, regardless of individual similarities, individuals differ
in ways little understood by most researchers. The difficulty in
extrapolating from rodents to humans is easy enough to understand, but
there is also the problem (although more difficult to understand by most
researchers) of extrapolation from many humans to just one human.
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