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Write a short paper, 500-700 words in length, analyzing Hueper’s (1955) article. In your essay, respond to the following questions:What methodology did Hueper (1955) use to reach his conclusions?What epistemology seems to inform Hueper’s (1955) approach to his subject?Based on his line of thinking, to what ontology does Hueper (1955) seem to subscribe?What flaws in Hueper’s (1955) paradigm led to such a faulty conclusion?Your paper should be properly formatted per APA guidelines. Robustly support your points with appropriate sources. Cite these sources and provide a correctly formatted reference list.
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1.4/2.3 Assignment (40 points)
Course: 3WI2024 Found of Doctoral Research (BADM-702-01B)
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demonstrates
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a basic
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addresses the
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addresses only
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addresses or
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address the
prompt(s).
citations and
references).
citations and
references).
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evidence of
critical
thinking.
Provides some
evidence of
critical
thinking.
Demonstrates
a limited
understanding
of relevant
course
concepts using
course
materials and
additional
resources (with
citations and
references).
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limited
evidence of
critical
thinking.
Does not
adequately
demonstrate
an
understanding
of relevant
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concepts or
provide
evidence of
critical
thinking.
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Written
Communicati
on and
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ng
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communication
is easy to read
and
understand.
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or written
communication
is not as clear
due to many
issues with the
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spelling.
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clearly through effective
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grammar and
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only minimal
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robustly
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follow the key
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33 points minimum
29 points minimum
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Lung Cancers
and Their Causes
W. C. Hueper,
The recent forceful propagation of the
cigarette theory of lung cancer has greatly
stimulated interest in the causes of these
tumors. The present controversy
related
to the etiology of pulmonary
cancers is
not so much concerned with the question
whether or not cigarette smoking may
cause cancer of the lung as with the de
termination of the relative role that ciga
rette smoking in relation to the other
known and still unknown environmental
factors may assume in the production of
these neoplasms and in their increase dur
ing recent decades. Since it has been
claimed on the basis of restricted statis
tical and experimental evidence that ciga
rette smoking is the principal cause of
lung cancer and has been mainly respon
sible for its marked and progressive in
crease, a critical evaluation of the evi
dence available that does not support this
contention
and that indicates that other
environmental
factors play a more im
portant part may be in order so as to
obtain a balanced assessment of the causal
aspects of the lung cancer problem.
Defects in the Evidence Supporting
the Cigarette Theory of Lung Cancer
Although the statistical data collected
by the majority
of investigators
have
shown the existence of positive and al
legedly causal associations between ciga
rette smoking and lung cancer, the fol
lowing observations
militate against the
claim of a predominant
role of cigarette
smoking.
1. Several recent statistical
analyses
failed to confirm any consistent correla
tion between cigarette smoking and lung
canoer.
2. The liability to error in correlating
conditions that are very common, such as
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lung cancer, cigarette smoking, pulmonary
tuberculosis, exposure to silica, arsenicals,
soot, and engine exhaust, may be con
siderable, since such common conditions
must often be concomitant
without im
plying a causal relationship,
unless addi
tional epidemiological,
medical, and ex
perimental evidence supports such a con
clusion. The coincidental
nature of such
statistical correlations is, for instance, well
established for exposure to silica and pul
monary cancer and for the frequent co
existence of pulmonary tuberculosis and
lung cancer. Similarly fallacious from a
scientific-medical
viewpoint is the repeat
edly expressed contention that trauma to
the breast is a significant causal factor in
the development of cancer of this organ
because of the existence of significant sta
tistical relations between the two events.
3. A distinct increase in lung cancer
started around the turn of the century,
i.e., well before the cigarette-smoking
habit became widespread and two decades
before even the minimal latent period of
any large number of potential cigarette
smoke cancers of the lung had elapsed.
4. This increase in frequency of lung
cancer was, moreover,
not a uniform
phenomenon
but was first observed in
some highly industrialized
regions and
communities
mainly located in Central
Europe. It extended from such foci in
irregular fashion to other areas and coun
tries during the following decades, becom
ing demonstrable
in the Scandinavian
countries and Italy only after 1930 and
involving rural population groups of the
same country much later and to a lower
degree than urban populations.
Lung
cancer rates have preserved this irregular
epidemiological pattern into present times.
The highest rates are in general found in
large, industrialized
communities.
They
drop gradually with the size of the com
munity and the density of population to
the lowest rates present in the rural,
agricultural
areas. However,
even here
95
96
rates of different countries.
The lung
cancer—death rate in England,
for in
stance, is twice as high as that in the
United States although Americans smoke
30 per cent more cigarettes than English
men. Such discrepancies
cannot intelli
gently be explained by the bold assertion
that Englishmen
smoke cigarettes,
for
economical reasons, to their very tip and
therefore
inhale more tar fumes than
Americans
who often throw cigarettes
away when half smoked.
6. In view of the considerable
varia
tions in the male-female sex ratio at dif
ferent times, in different localities, and in
different
demographic
groups
ranging
even during recent years from 1:1 to 50:1,
it is most unlikely that such discrepancies
and changes are attributable to variations
in the intensity of one single factor such
as cigarette smoking. They appear rather
to be due to alterations and variations in
the type and extent of action of a broad
spectrum of environmental
carcinogenic
agents affecting the members of the two
sexes to different degrees.
7. The various known or suspected
lung-cancer—causing agents or exposure
conditions encountered
in industry have
been shown to be associated with the de
velopment of pulmonary cancers of dif
ferent histological
types. In fact, two
different histological types, such as squa
mous-cell carcinoma and adenocarcinoma,
were occasionally found to coexist in the
same pulmonary
cancer. Squamous-cell
carcinoma
of the bronchi, therefore,
is
neither pathognomonic
for any specific
respiratory carcinogen nor is it the only
histological type found in lung cancers
of occupational
origin. Long before the
cigarette era squamous-cell carcinomas of
the bronchi represented
an appreciable
fraction of the total lung cancers ob
served. They are not pathognomonic
of a
cigarette-smoke
etiology. Therefore
it is
scientifically incorrect to claim that this
histological type of cancer was rare befdre
1920 and appeared only with the adoption
of the cigarette-smoking
habit.
8. It is definitely surprising that there
does not exist a positive statistical corre
lation between cigarette
smoking
and
15424863, 1955, 3, Downloaded from https://acsjournals.onlinelibrary.wiley.com/doi/10.3322/canjclin.5.3.95, Wiley Online Library on [06/01/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
marked variations exist in the lung-cancer
rates observed among metropolitan
areas
of the same country (U.S.A.) and even
the same State (Ohio). It is, moreover, re
markable that the annual progression rates
of lung-cancer deaths in the U.S.A. were
higher during the first three decades of
this century than during the subsequent
fifteen years and that the progression rates
of lung-cancer
morbidity in the popula
tions of ten metropolitan
areas in the
United States are highly irregular accord
ing to the results of surveys made in 1937
and 1947.
Such local variations
in lung-cancer
frequency ranging up to several hundred
per cent, as well as the graduated inci
dence pattern in urban-rural respects, are
not in harmony with the concept that one
single habit factor has been operative in
the production
of lung cancer. Rather
these observations indicate that several or
many factors acting in different intensity
and combinations
and at different times
have been active in bringing about this
highly characteristic
and significant epi
demiological pattern, which conforms well
with the occupational
and environmental
air-pollution pattern related to the devel
opment, spread, and types of modern in
dustry through
the various
countries,
regions, and towns.
Such marked fluctuations in lung-can
cer frequency of regional and particularly
rural-urban
type can not conveniently
be
disposed of by the explanation that they
reflect differences in the cigarette-smok
ing habits of different population groups.
There is likewise no acceptable scientific
evidence supporting
the claim that the
paradoxical
behavior of the progression
rates of lung cancer during the last four
decades is attributable
to the fact that
many cigarette smokers did not live long
enough in recent decades to develop lung
cancer because of their precocious death
from coronary thrombosis—also allegedly
elicited in the majority of cases by ciga
rette smoking.
5. It is remarkable,
moreover,
that
there does not exist any parallelism be
tween the rate of cigarette consumption
per capita and the lung-cancer-death
mors in mice that are histological and his
togenetic equivalents of the human bron
chogenic variety of cancer.
The development of pulmonary tumors
observed in certain strains of inbred mice,
moreover, depends upon the action of a
primary hereditary factor that, according
to our present knowledge, is totally ab
sent in the causation of the great majority
of bronchogenic
cancers in man. Consti
tutional
hereditary,
congenital,
or ac
quired factors may influence cancer de
velopment in man by their possible effects
upon susceptibility
to exogenous or en
dogenous specific agents but they are not
truly causative in their action.
It is evident from this critical analysis
of the evidence related to the cigarette
theory of lung cancer that it contains a
number of serious defects and inconsist
encies and that for these reasons alone
an acceptance of the broad claims made
for it should be withheld.
Etiological Importance of
Environmental Factors of
Nontobacco Nature
The wisdom of this just-stated conclu
sion becomes strikingly obvious when due
consideration is given to the large amount
of data incriminating other environmental
air pollutants with which, for occupational
and environmental
reasons,
industrial
worker groups as well as the general popu
lation have effective, frequent, and pro
longed contact.
It is often asserted by the protagonists
of the cigarette theory that there does not
exist any alternative
theory of general
validity that might account for the causa
[ion of most lung cancers and that would
explain the increase in lung cancer and its
sex distribution. The facts are as follows:
1. The evidence on specific occupa
tional lung-cancer
hazards affecting al
most exclusively
males in restricted
worker groups provides in many respects
conclusive proof of the existence of car
cinogenic air pollutants.
2. The available information indicates
that similar or identical, while often miti
97
15424863, 1955, 3, Downloaded from https://acsjournals.onlinelibrary.wiley.com/doi/10.3322/canjclin.5.3.95, Wiley Online Library on [06/01/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
cancers of the lip and mouth, although
without doubt tarry liquid oozing from the
tip and tarry fumes have direct and in
tense contact with these parts, since sta
tistical evidence supports the claim that
cigar and pipe smoking conveys an ex
cessive liability to labial and oral cancer.
One must wonder also about the total
absence of cancer of the skin of the fingers
holding cigarettes in view of their often
intensely
dark-brown—stained
skin im
pregnated with tobacco tar. The assertion
that the first three fingers are immune to
tobacco tar, while they are not immune
to coal tar, is an evasive explanation lack
ing any scientific value and manufactured
ad hoc.
9. The claimed absence of a positive
statistical association between lung can
cer and the habit of inhaling cigarette
smoke is inconsistent with the rule that the
incidence rate of occupational cancers in
creases with the intensity of exposure to
a carcinogen.
It is also disconcerting
to
note that there is no significant statistical
relation
between chronic tracheal
and
bronchial diseases and cancer of the lung,
although cigarette cough is a characteristic
symptom of chain smokers and despite
the fact that such respiratory diseases are
excessive in several worker groups suf
fering from certain types of occupational
lung cancer.
10. Although, after many failures to
demonstrate
known carcinogenic
hydro
carbons in cigarette
tar and cigarette
paper tar, English investigators
recently
succeeded in obtaining very small amounts
of 3,4-benzpyrene from artificially smoked
cigarettes,
it should be noted that this
polycyclic hydrocarbon
can be obtained
during the incomplete combustion of any
carbonaceous
matter under suitable con
ditions of temperature and oxygen supply.
11. The inconsistent
results obtained
by various investigators when tobacco or
cigarette tar was applied to the skin of, or
inhaled by, experimental animals indicate
that tobacco tar is apparently at best a
weak carcinogen to the skin of mice and
perhaps also to the skin of rabbits, while
the inhalation of cigarette smoke even
when successful failed to elicit lung tu
98
nous-dial
painters
inhaling
radioactive
dust and/or gases.
The lung-cancer-attack
rates for mem
bers of these occupational
groups are
many times those found for the general
population of the same age and sex. Fe
males were affected by occupational
re
spiratory
cancers through contact with
only two of the agents listed (asbestos
lung; radioactive
gases [luminous-dial
painters]—paranasal
sinus) because males
are exclusively employed in the other haz
ardous operations.
Whenever in a haz
ardous industry, such as the asbestos in
dustry, both males and females were
employed and sustained the same type and
a similar degree of exposure, there was a
trend toward an equalization of the lung
cancer—attack rate.
Exposures to occupational
respiratory
carcinogens
are sometimes characterized
by a typical symptom complex involving
not only the respiratory organs but also
other tissues and organ systems. The
symptom complex associated with coal-tar
cancer provides a striking illustration of
this diagnostically
and etiologically
im
portant phenomenon.
Respiratory
expo
sure to coal-tar fumes always entails also
cutaneous contact with this material and
accounts for the occurrence of the various
manifestations
of chronic coal-tar derma
titis: warts, cutaneous horns, papillomas,
and carcinomas of the skin among mem
bers of such worker groups. Such a char
acteristic cutaneous symptom complex is,
on the other hand, totally absent for ciga
rette chain smokers, while the chronic in
flammatory
manifestations
of laryngitis
and tracheitis seen in chain smokers still
have a debatable significance. Cancers of
the trachea are uncommon and cancers of
the larynx have not only shown a minor
increase during recent decades but also
displayed a sex-related distribution
pat
tern different from that of lung cancers.
They are, according to English statistics,
more common among females in rural
areas than among
those residing
in
Greater London.
Epidemiological
studies on lung can
cer for larger industrial groups have dem
onstrated
not only marked differences
15424863, 1955, 3, Downloaded from https://acsjournals.onlinelibrary.wiley.com/doi/10.3322/canjclin.5.3.95, Wiley Online Library on [06/01/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
gated, exposures exist not only for much
larger groups of industrial workers com
posed of several millions of persons but
also for the general population through
the medium of industrial effluents, gaso
line and diesel engine exhaust, and dusts
from asphalted
and oiled roads and
abraded rubber tires.
3. The epidemiological
evidence in
criminating exposures from these sources
in the production of lung cancer and its
increased frequency among large indus
trial worker groups and the general popu
lation is almost as good as that available
for cigarette smoking.
4. The experimental
evidence in re
gard to the carcinogenic
action and po
tency of these industrial and industry
related factors, especially as far as coal
tar and atmospheric
soot and other car
bonaceous and metallic pollutants are con
cerned, is a great deal more conclusive
than that supporting carcinogenic
prop
erties of tobacco tar and strikingly demon
strates their far-greater carcinogenic
po
tency over that experimentally
displayed
by tobacco tar.
The existence
of respiratory-cancer
hazards involving the lung and/or
the
nasal cavity, paranasal sinuses, and larynx
has reliably been demonstrated for:
(1) retort workers of gas-manufactur
ing plants and coke ovens because of the
inhalation of hot coal-tar fumes;
(2) workers exposed to the inhalation
of certain petroleum-oil mists and fogs en
countered in some operations of oil re
fineries, in metallurgical
manufacturing
plants, and textile works;
(3) isopropyl – alcohol
manufacturers
exposed to inhalation of vapors from the
crude liquor (isopropyl oil);
(4) nickel refinery
workers
having
contact with nickel dust and nickel car
bonyl vapors;
(5) chromate
manufacturers
and
chrome-pigment
handlers inhaling chro
mium-containing
compounds;
(6) arsenical insecticide producers and
users;
(7) asbestos workers with pulmonary
asbestosis;
(8) radioactive-ore
miners and lumi
99
15424863, 1955, 3, Downloaded from https://acsjournals.onlinelibrary.wiley.com/doi/10.3322/canjclin.5.3.95, Wiley Online Library on [06/01/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
servations suggest that industry-related
air
of lung cancer frequency among members
of various groups but also have shown ex
pollutants
may representa distinct
lung
cessive frequency rates for industrial pop
cancer hazard for considerable portions of
thegeneralpopulation,
especially
thosere
ulations exposed to known occupational
sidingand workinginindustrialized
urban
respiratory carcinogens, such as coal-tar
communities. This conclusion is supported
and pitch fumes and dust; mist, fumes,
and vapors of various petroleum deriva
by the fact that during recent decades the
rise in lung-cancer frequency was not only
tives; metal dusts; and fumes and exhaust
associated with an increased consumption
fumes from gasoline and diesel engines.
Excessive liabilities to lung cancer have
of cigarettes, but by a remarkable, and in
pant even more pronounced, risein the
been recorded for transportation
workers,
rubber and plastic workers, employees of
construction
of asphalted roads, in the
consumption
of motor fuel, and in the
the nonferrous-metal
industry, operating
production of industrial
and domestic
railroad
workers,
boiler scalers, metal
fuel oils,patent fuel,crude petroleum,
grinders, polishers, welders, lathe work
petroleumasphalt,
coal tar,isopropanol,
ers, foundry workers, engineers, mechan
asbestos,arsenicand chromium com
ics, machinists, crane operators in smel
pounds,and nickel;
i.e.,
of conditions
and
ters, painters, coal-tar workers, asphalters,
materials having proved or suspected re
chimney
sweeps,
stokers,
patent-fuel
lations
to respiratory
cancers.
workers, furnace men, rollers, and as
phalters. While the epidemiological
evi
In contrastto theinconsistent
and con
dence supporting
such correlations
be
troversial
observations
on the experi
tween certain occupational
activities and
mental productionof cancersby tobacco
lung cancer has only circumstantial value,
tar, there is available a large array of ob
the observations
are in good agreement
servations on the appearance of cancers
with those made in connection with the
in various organs and tissues and different
recognized occupational
respiratory can
species following the cutaneous,
subcu
cers of the lung, as well as in harmony
taneous,intrapulmonary,
intraosseous,
re
with the factthatlung-cancerrateshave spiratory, and intravenous administration
been found to be up to severalhundred of coal tar, pitch and asphalt, soot, creo
per cent higher in industrial states than in
sote oil, anthracene oil, shale oils, petro
agricultural
states, and in industrialized
leum derivatives and carbon blacks and
communities
than in rural areas of the
theirbenzolic
extracts.
Earlyand frequent
same state (Connecticut,
New York,
cancersof theskinor subcutaneoustissue
Ohio, Colorado,Montana) or the same have consistently
been obtainedwithben
country (England, Germany, Austria).
zol extracts of the particulate phase of air
Their apparentetiological
significancepollutants even in a strain of mice that
naturally
isratherresistant
tospontaneou.@
is, moreover, indicated by the fact that
and experimentalcancerformation.Con
appreciable
amounts of 3 ,4-benzpyrene
siderable
amounts of 3,4-benzpyrene,
sur
have been demonstrated
not only in the
passing many times those tentatively
particulate phase of the air pollutants of
found in cigarette tar, have been isolated
the mainly coal-burning
industrial cities
from coaltar,shaleoil,and soot.
of England but also in that of the atmos
phere of Los Angeles where industry and
Since practically
all known or sus
transportation
depend upon petroleum
pectedenvironmentalcausesof lung can
cerwerediscoveredduringthelast
twenty
fuels.
thatthereexist
Itismoreover noteworthythatduring fiveyears,itismost likely
other,still
unknown, respiratory
carcino
smog conditions the benzpyrene content
evidence,
of the airmay riseseveralfold,
and that gens. Appreciable experimental
as well as a few observations on environ
in Austria the lung-cancer rate was about
mental lung cancer, suggests that the de
twice as high in communities located on
velopmentof pulmonary cancersmay not
main traffic arteries as in those situated
be entirely
attributable
to agentsthatare
remote from main highways.These ob
that cigarette smoking is not a major fac
tor in the causation of lung cancer nor
had it a predominant
role in the remark
able increase of these tumors during re
cent decades.
Conclusions
3. In view of the fact that not only a
1. The total
epidemiological,
clinical,
great deal of the existing circumstantial
pathological,
and experimental
evidence
epidemiological
evidence but also prati
on hand clearly indicates that not a single
cally the entire factual and conclusive evi
but several if not numerous industrial or
dence available on exogenous respiratory
industry-related
atmospheric
pollutants
carcinogens
are either of occupational
are to a great part responsible
for the
origin or point to industry-related
factors,
causation of lung cancer.
it would be most unwise at this time to
2. While the available data do not per
base future preventive measures of lung
mit any definite statement as to the relative
cancer hazards mainly on the cigarette
importance of the various recognized re
theory and to concentrate the immediate
spiratory carcinogens
in the production
epidemiological
and experimental
efforts
of lung cancers in the general population,
on this evidently overpropagandized
and
they nevertheless
unmistakingly
suggest
insufficiently documented concept.
What’s That Again?
In the busy search for other-than-cigarette-smoke
causes of lung cancer two odd
ones were suggested at a recent smoke-cancer-heart
conference:
1. Absence from our modern, ultrahygienic, highly public-healthed
environment of
some unidentified, previously existing, anti-cancer, protective agent—a microorganism
annihilated
by sulfonamides
or antibiotics, a food constituent
removed by refining
processes, or some other entirely unknown, eliminated environmental
factor or custom
of civilization.
2. Drugs, like Fowler’s solution, formerly much esteemed by the physician. This
idea was said to be consistent with the known long latent period of lung cancer.
These two nebulous, hypothetical
factors—one negative, the other iatrogenic
show imagination but they seem, at this point, to have a good deal less to support them
than cigarette smoke and dirty air of cities.
100
15424863, 1955, 3, Downloaded from https://acsjournals.onlinelibrary.wiley.com/doi/10.3322/canjclin.5.3.95, Wiley Online Library on [06/01/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
inhaled, but perhaps also may be to agents
entering the human body by other routes
(alimentary-tract,
skin, parenteral).
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