In response to Mr. Lee’s comment1 which follows previous responses2,3
and my paper4, I offer further
explanation to resolve an apparent misunderstanding of the validity and
reliability of cotinine/creatinine ratio (CCR) measurement and his mishandling
of the formula of misclassification. I also express concerns about the lack of
scientific integrity in his reporting5 of the Japanese spousal study,
including his authorship.
As I demonstrated4, all indices of nicotine exposure (ambient
room,personal sampler monitors, and salivary
cotinine)
were well correlated but correlated poorly with CCR, raising doubts about the
validity of the CCR measurement.Yet
Lee maintains that CCR measurement in this study was the gold standard for
distinguishing true smokers from falsely reporting smokers.
There are several possibilities about why the CCR
measurement may have been invalid and unreliable in this study. In 1991 when I
sent the urine samples to the RJR laboratory (where the measurement was
performed), I was informed that all the dry ice sent with the sample had
sublimated before it reached the laboratory. This suggests that the sample was
not maintained at low temperature before analysis. Cotinine measurement is
temperature sensitive and measurement after the sample is exposed to high
temperature can make the measurement inaccurate6.
As I calculated4, the misclassification
and reverse misclassification were equally high suggesting inappropriateness of
the CCR measurements as the gold standard.Lee’s
neglect of reverse
misclassification, thusallows
him to claim an inflated false negative rate of smoking.Lee continues to justify his
misclassification formula by referring to his previous use of the formula.
However, this formulais dependent
on the prevalence of smoking among the study population and thereby artificially
inflates the misclassification rate
ofpopulations with low smoking
prevalence. By way of illustration, consider two hypothetical populations of
1000 people each with smoking rates of 10% (A) and 30% (B).Suppose that, due to the inaccurate CCR measurement, just 3% of true
smokers are classified as non-smokers by erroneously low CCRand3% of true non-smokers are classified as smokers by erroneously high CCR
(for the sake of simplification, I assume no false reports by the subjects). We
will get the following results.
A: If 10% smoke
Self report
Smoker
Nonsmoker
Total
CCR
High
(>100ng/mg)
97
27
124
Lee’s
Misclassification formula
Low(<100ng/mg)
3
873
876
=27/124=0.21
Total
100
900
1,000
B:
If 30% smoke
Self report
Smoker
Nonsmoker
Total
CCR
High
(>100ng/mg)
291
21
312
Lee’s
Misclassification formula
Low(<100ng/mg)
9
679
688
=21/312=0.06
Total
300
700
1,000
As
can be seen, Lee’s formula for misclassification is dependent on the
prevalence of smoking. With only a
slight (3%) inaccuracy in CCR measurement, he can thereby easily get more than
three times higher (0.21
vs.0.06) misclassification in a population with lower smoking prevalence, such as with Asian women.
After a long discussion between Proctor and me, Proctor finally
understood and accepted my point on the misclassification formula7.
Our final draft of the misclassification paper8, which Proctor sent
to me on November 9, 1992 with my name as a sole author, clearly mentioned the
high proportion of misclassification in both sides (self-reported non-smoking
subjects with high CCR and self-reported smokers with low CCR).
Lee
insists that reverse misclassification is relatively unimportant in his
abundant mathematical publications. However, I note that he seems to have
realized his mistake of using 28/106 as the misclassification rate of
self-reported smokers in his original study5 , having quietly
switched to 28/98 for this rate1 after I pointed out his confusion.
Despite his claim that reverse misclassification is implausible, it was observed
as a fact.
Lee
states that as
far as he is aware the
data never belonged to Yano. He should be aware that I developed the
questionnaire, and selected the study areas and subjects. I supervised the
survey at the study area (Shizuoka), erroneously referred to in Lee’s paper as Shizoka5. I planned and ordered the
data input, performed the data analysis and sent the disk to Proctor. On
learning from the experience of possible sample damage (from dry ice
sublimation) by the commercial shipment at the first phase study in 1991, I even
transported the second phase samples myself to the RJR laboratory, Winston
Salem, NC where CCR was measured. I discussed the scientific content of the
study with Proctor many times and he accepted my points7 and revised
the draft many times, always with my name as the author, and never with Lee’s.
As can be seen in the final draft8, Proctor and I reached a certain
agreement on the misclassification formula and the importance of the reverse
misclassification rate.
Because
Lee never participated in the actual survey it may be that he was unaware of
details of the research such as the integrity of the sample which may have
seriously affected the interpretation of results. Nor did he participate in the
discussion which led Proctor and I to a deeper understanding of the analysis7.
Despite this, still Lee claims that because he proposed the research project, he
has aright to sole authorship
regardless of who actually conducted the research. This is a unique idea that
few scientists would accept.
Lee states: Had I not published the paper it seems that the findings
would never have appeared in the public domain at all.Did Yano also have sole rights to suppress the findings? Again, Iremind Lee thatProctor and I
agreed that the results did not indicate high misclassification in self-report
non-smokers but some failure in the study.7, 8 What both Proctor and
I prepared for publication, although Proctor ceased to contact me before we
could reach a final agreement, was totally different from what Lee eventually
published5. I consider that a description of a failed study
involving the inaccurate measurement of CCR was undeserving of publication.
Moreover, as a scientist committed to truth, I have a responsibility to be
critical of a report with erroneous interpretations based on invalid
measurements.
2.Yano E.Response
to P N Lee [Commentary].Tob
Control 2005;14:234-5.
3.Lee PN.Japanese spousal
study: a response to Professor Yano's claims [Commentary].Tob Control 2005;14:233-4.
4.Yano E. Japanese spousal smoking study
revisited: how a tobacco industry funded paper reached erroneous conclusions. Tob
Control 2005;14:227-35.
5.Lee PN. "Marriage to a smoker" may
not be a valid marker of exposure in studies relating
environmental
tobacco smoke to risk of lung cancer in Japanese non-smoking women.Int Arch Occup Environ Health 1995;67:287-94.
6.Hagan
RL, Ramos JM Jr, Jacob PM 3rd. Increasing urinary cotinine concentrations at
elevated temperatures: the role of conjugated metabolites. J Pharm Biomed
Anal. 1997;16:191-7.
7.Proctor
CJ. Fax to Dr E. Yano,
Teikyo
University
, October 26 1992.
I am the “WDE Irwin” quoted on page 67 as follows: “Years later
(1985), WDE Irwin, a technician with BAT in England, was asked how a
grooved filter could be made that would avoid criticism but also provide
good taste. He concluded: ‘Finally for cigarettes, I believe it to be a
self evident truth not only is there no smoke without fire, but also there
is no kick without smoke.’”
I am the “WDE Irwin” quoted on page 67 as follows: “Years later
(1985), WDE Irwin, a technician with BAT in England, was asked how a
grooved filter could be made that would avoid criticism but also provide
good taste. He concluded: ‘Finally for cigarettes, I believe it to be a
self evident truth not only is there no smoke without fire, but also there
is no kick without smoke.’”
“Technician” is not a correct identification of my status. At time
of the quote, I had 20 years experience in the tobacco industry and held
three quite separate primary degrees from British universities, majoring
in chemistry, economics and statistics. A quick search on Google would
have identified my status as “scientist”. My credibility as an iconoclast
could be compromised if I did not make this correction. Although no
longer in the tobacco industry, I may at some point seek to criticise a
report by the US Institute of Medicine, “Clearing the Smoke: The Science
Base for Tobacco Harm Reduction” published in 2001 and I shall need all
the credibility I can muster!
I read with great interest the article by Bjartveit and Tverdal
(2005), who investigated health consequences of smoking 1-4 cigarettes per
day. They found that in both sexes, smoking 1-4 cigarettes per day was
associated with a significantly higher risk of dying from ischaemic heart
disease and from all causes, and in women, from lung cancer [1].
Genetic studies suggest that all stages of tobacco...
I read with great interest the article by Bjartveit and Tverdal
(2005), who investigated health consequences of smoking 1-4 cigarettes per
day. They found that in both sexes, smoking 1-4 cigarettes per day was
associated with a significantly higher risk of dying from ischaemic heart
disease and from all causes, and in women, from lung cancer [1].
Genetic studies suggest that all stages of tobacco use and dependence,
maintenance of dependent smoking behavior and amount smoked are partially
under genetic control [2]. Many of cigarette smoke compounds and their
metabolites are substrates of phase I enzymes, represented by cytochrome
P450 enzymes, and glutathione S-transferases (GSTs). Although the study
investigating the association between smoking behavior and either
polymorphisms of GSTT1 or GSTM1, failed to show a significant association
[3], there are several reports indicating that genetic polymorphisms of
CYP2A6, CYP3E1, and CYP2D6 are associated with smoking behavior [4-6]. The
CYP2A6 poor-metabolizer genotypes result in altered nicotine kinetics [4].
Individuals lacking full function CYP2A6 alleles do not metabolize
nicotine and are less likely to become smokers and if they do, they smoke
fewer cigarettes per day in comparison with normal-nicotine metabolism
persons [4]. Therefore, slow inactivators may experience higher or longer
lasting levels of nicotine. This could increase effects of nicotine
toxicity. Also it is reported that the CYP2D6 ultra-rapid metabolizer
genotype may contribute to the probability of being addicted to smoking
[5]. Taken together, it is probable that the persons smoked 1-4 cigarettes
per day in the study of Bjartveit and Tverdal [1] belong to the slow
metabolizer genotypes. Therefore, the results of the study should be
interpreted with caution. Study with respect to polymorphisms of phase I
and II genes, might be find the threshold value for daily cigarette
consumption that must be exceeded before serious health consequences
occur.
REFERENCES
1 Bjartveit K, Tverdal A. Health consequences of smoking 1-4
cigarettes per day. Tob Control 2005;14:315-20.
2 Hall W, Madden P, Lynskey M. The genetics of tobacco use: methods,
findings and policy implications. Tob Control 2002;11:119-24.
3 Saadat M, Mohabatkar H. Polymorphisms of glutathione S-transferases
M1 and T1 do not account for interindividual differences for smoking
behavior. Pharmacol Biochem Behav 2004;77:793-5.
4 Tyndal RF, Sellers EM. Genetic variation in CYP2A6-mediated
nicotine metabolism alters smoking behavior. Ther Drug Monit 2002;24:153-
60.
5 Saarikoski ST, Sata F, Husgafvel-Pursianen K, et al. CYP2D6 ultra-
rapid metabolizer genotype as a potential modifier of smoking behaviour.
Pharmacogenetics 2000;10:5-10.
6 Yang M, Kunugita N, Kitagawa K, et al. Individual differences in
urinary cotinine levels in Japanease smokers: relation to genetic
polymorphism of drug-metabolizing enzymes. Cancer Epidemiol Biomarkers
Prev 2001;10:589-93.
We thank Dr Graham F Cope for his valuable remarks, and agree that
underreporting of daily cigarette consumption might be of importance when
assessing the risk in light smokers.[1]
Dr Cope refers to two papers: a cross-sectional randomised study on
smoking reduction in pregnant women, and an assessment of smoking status
in patients with peripheral arterial disease.[2][3] Our study did not
conc...
We thank Dr Graham F Cope for his valuable remarks, and agree that
underreporting of daily cigarette consumption might be of importance when
assessing the risk in light smokers.[1]
Dr Cope refers to two papers: a cross-sectional randomised study on
smoking reduction in pregnant women, and an assessment of smoking status
in patients with peripheral arterial disease.[2][3] Our study did not
concentrate on subgroups in need of regular medical attention; it covered
all residents aged 35-49, except people with a history or symptoms
indicating cardiovascular diseases (among them peripheral arterial
disease) and diabetes.[4] A general population in the 1970s may be less
inclined to underreport consumption, than present-day pregnant women and
sick people, who do not want to incur the disapproval of the healthcare
professionals.
Based on a review and meta analysis Patrick and co-workers found that
interviewer-administered questionnaires, observational studies, reports by
adults, and biochemical validation with cotinine plasma were associated
with higher estimates of sensitivity and specificity. Our study compares
favourably with these points: The study includes only adults, all
questionnaires were checked by a nurse in an interviewer situation, and in
one of the three counties, biochemical validation was carried out in all
participants by determination of serum thiocyanate.[5] Certainly, levels
of thiocyanate may be influenced by factors other than smoking;
nevertheless, the dose-response between mean levels of thiocyanate and
reported number of cigarettes is remarkable:
Number of cigarettes per day
MALES
FEMALES
No.
Mean (SD)
No.
Mean (SD)
0
6212
33.9 (14.0)
7908
33.5 (14.2)
1-4
169
45.3 (18.4)
515
52.0 (22.0)
5-9
855
59.6 (20.7)
1661
70.9 (24.5)
10-14
1570
69.6 (22.2)
1800
81.5 (24.0)
15-19
1056
76.3 (23.1)
569
90.8 (25.5)
20-24
699
81.5 (26.4)
247
96.1 (25.6)
25+
235
87.3 (27.9)
36
99.7 (28.3)
Finally, the attending persons reported their actual number of
cigarettes per day in a special box in the questionnaire. Here they were
allowed to give a range of daily consumption, for example, 10-15
cigarettes. In our analyses, however, we used the highest figure stated by
the participant. Hence, a report of 3-6 cigarettes per day was categorized
in the 5-9 cigarettes group.
We find it reasonable to conclude that the results presented in our paper
reflect a marked increased risk in light smokers.
References
1. Cope GF. Health consequences of smoking 1-4 cigarettes per day. Letter
to journal. Tob Cont 2005 http://tc.bmjjournals.com/cgi/eletters/14/5/315.
2. Cope GF, Nayyar P, Holder R. Feedback from a point of care test for
nicotine intake to reduce smoking during pregnancy. Ann Clin Bioch
2003;40:674-679.
3. Hobbs SD, Wilmink ABM, Adam DJ, Bradbury AW. Assessment of smoking
status in patients with peripheral arterial disease. J Vasc Surg
2005;41:451-456
4. Bjartveit K, Tverdal A. Health consequences of smoking 1-4 cigarettes
per day. Tob Cont 2005;14:315-320.
5. Patrick DL, Cheadle A, Thompson DC, Diehr P, Koepsell S, Kinne S. The
validity of self-reported smoking: a review and meta-analysis. Am J Public
Health 1994;84:1086-1093.
6. Foss OP, Lund-Larsen PG. Serum thiocyanate and smoking: interpretation
of serum thiocyanate levels observed in a large health study. Scan J Clin
Lab Invest 1986;46:245-251.
I read the paper by Bjartveit and Tverdal with a great deal of
interest(1). I welcome the fact that highlighting smoking, even a small
number of cigarettes has a significant effect on ischaemic heart disease.
However, these findings should be considered with a certain amount of
scepticism, as the findings are based entirely on self-reported smoking
habit. Biochemically validated research, both by ourselves(2), and
other...
I read the paper by Bjartveit and Tverdal with a great deal of
interest(1). I welcome the fact that highlighting smoking, even a small
number of cigarettes has a significant effect on ischaemic heart disease.
However, these findings should be considered with a certain amount of
scepticism, as the findings are based entirely on self-reported smoking
habit. Biochemically validated research, both by ourselves(2), and
others(3) have found that many smokers will admit to their habit, but will
significantly under-report their cigarette consumption; believing that
reporting a low number of cigarettes a day, say 1-4, will not incur the
disapproval of the healthcare professional. Also to be taken into account
is that biochemical analysis shows that the intake of nicotine and other
tobacco products is extremely variable within categories of cigarette
consumption, and is dependent on a number of variables such as smoke
topography (number, frequency and volume of puffs from a cigarette), depth
of inhalation, age, gender, yield of nicotine, etc. So some individuals
who consume a small number of cigarettes a day will ingest the same level
of tobacco products as other smokers with a higher daily intake.
Compensation, when a smoker cuts down on cigarette consumption, but smokes
more efficiently, is a factor mentioned in the text of the paper, is an
example whereby cigarette consumption does not reflect nicotine intake.
So, although the paper and ensuing publicity has brought to the attention
of the public the dangers of any level of smoking, using self-reported
information should be used with a certain degree of caution.
References
1. Bjartveit K, Tverdal A. Health consequences of smoking 1-4
cigarettes per day. Tob Cont 2005; 14: 315-320.
2. Cope GF, Nayyar P, Holder R. Feedback from a point of care test for
nicotine intake to reduce smoking during pregnancy. Ann Clin Bioch 2003;
40 : 674-679
3. Hobbs SD, Wilmink ABM, Adam DJ, Bradbury AW. Assessment of smoking
status in patients with peripheral arterial disease. J Vasc Surg 2005; 41:
451-456.
British American Tobacco (Nigeria) Limited (BAT) and their cohorts
the world over should come to terms with the fact that the truth cannot be
hidden forever even from the man on the streets.
Mr Kehinde Johnson did not need to comment at all because there was
nothing to comment about! He should have apologised for being a part of
this systematic elimination of defenceless people the world over.
British American Tobacco (Nigeria) Limited (BAT) and their cohorts
the world over should come to terms with the fact that the truth cannot be
hidden forever even from the man on the streets.
Mr Kehinde Johnson did not need to comment at all because there was
nothing to comment about! He should have apologised for being a part of
this systematic elimination of defenceless people the world over.
Dr. Chris Proctor's statement typifies the message that British
American Tobacco (Nigeria) Limited has tried to pass across to
unsuspecting people, that their tobacco is "safer" than smuggled
brands.This is most unfortunate because it is not based on any scientific
evidence. In fact, the scientific findings in this area are to the
contrary. A time will come in our developmental process in Nigeria that
such misrepresentation of facts will attract severe punishment!
Another trick which is employed by the company is the use of Nigerian
symbols of success and national pride such as historical materials as a
means of advertisement for their products. Advertising cigarretes under
the guise of promoting national pride is another slap in the face of the
Nigerian people by BAT (Nigeria) Limited. Nigerians know when to be
proudly Nigerian. Certainly, our national pride is not baased on tobacco
but on the legacy of our fore-fathers.
I take succour in the Yoruba saying that "If a lie goes on for twenty
years, the truth catches it in a day". This lies have gone on for more
than twenty years and the truth has caught up with them.
It is time for all those who know the truth to speak up. We need a
critical mass of determined and committed folks to finish this work and
make our world truly tobacco free!
Professor Eiji Yano raises a number of issues in his letter(1) which
responded to my commentary(2) on his article(3) about the Japanese spousal
study, as does Chapman in his editorial(4). Here I reply to the main
points raised.
INTERPRETATION OF THE DATA
Studies of environmental tobacco smoke (ETS) exposure and lung cancer
commonly identify a...
Professor Eiji Yano raises a number of issues in his letter(1) which
responded to my commentary(2) on his article(3) about the Japanese spousal
study, as does Chapman in his editorial(4). Here I reply to the main
points raised.
INTERPRETATION OF THE DATA
Studies of environmental tobacco smoke (ETS) exposure and lung cancer
commonly identify a group of self-reported non-smoking women and then
compare risk according to the smoking habits of the husband. If some true
smokers are erroneously included among the female subjects, an apparent
relationship of spousal smoking with lung cancer may be seen even when no
true effect of ETS exists. This has been mathematically demonstrated
(e.g.5), with attempts to correct for it made by major independent
authoritative reviews of the evidence on passive smoking and lung
cancer.(6-8) The magnitude of the bias depends (among other things) on
the extent to which women who smoke are misclassified as non-smokers. It
can also be shown mathematically(5) that a given rate of misclassification
of smokers as non-smokers is a much more important cause of bias than is
the same rate of the reverse misclassification, of non-smokers as smokers.
Since such reverse misclassification is also implausible, adult women
having little reason to claim erroneously to be smokers, the major
reviews(6-8) have all ignored its minor effects.
Given that in the Japanese spousal study (using a urinary
cotinine/creatinine ratio, CCR, above 100 ng/mg as an index of true
smoking), the reverse misclassification rate (8/298 = 2.7%) was anyway
much lower than the misclassification rate itself (28/98 = 28.6%), it
becomes abundantly clear that reverse misclassification is not relevant to
the passive smoking/lung cancer issue. It is difficult to understand why
Yano places such emphasis on it.
Yano(1) states that I am "confused with the calculation formula" and
that my "definition of misclassification was obtained by dividing those
with >100 ng/mg CCR (n = 28) by self-reported non-smokers (n = 318)."
It appears that Yano himself is confused. I had previously made it
clear(2) that the denominator should not be 318, but 98, the number of
women with a CCR value indicative of smoking (or perhaps 106, if one also
includes those women who claimed to smoke but had a CCR <100 ng/ml).
The misclassification rate calculation is clearly based on CCR
>100 ng/mg validly indicating smoking. Such an assumption is widely
used(9), though may be subject to some error, and was the best technique
available at the time. Most smokers admit to smoking, so that self-report
has some validity as an indicator of true smoking status, but this does
not help us estimate the magnitude of the misclassification bias. The
observed lack of correlation in the Japanese spousal study between CCR in
non-smokers (with CCR <100 ng/mg) and other indices of ETS exposure
suggests that inaccuracy in CCR measurement at low levels may be
important. However, such inaccuracy may not be relevant to the
misclassification rate calculation, which merely attempts to use CCR to
distinguish smokers from non-smokers. Over half the self-reported non-
smokers with values over 100 ng/mg actually had values of 1000 ng/mg, and
it would be very surprising indeed if errors in CCR measurement were so
huge that these women were really non-smokers.
Though I would be happy to see results of further studies using up-to
-date state-of-the-art chemical methods to detect nicotine metabolites in
self-reported non-smokers, the conclusion I reached in 1995 that
misclassification rates are much higher in Japanese than in Western
populations(10) seems to be correct. I note that the existence of high
misclassification rates in Asian women has in fact been independently
confirmed.(11)
RIGHTS TO PUBLICATION OF THE FINDINGS
Yano states(1) that I used his data without his consent. As far as I
am aware, the data never belonged to Yano. The study had been funded by
the industry who had carried out the cotinine analyses (blind of self-
reported smoking status). I had originally proposed that the study be
done, following conduct of a similar study in England, which the industry
supported at my request, and which I reported the results of.(12) The
original intention had been for Yano to be a major author, but problems
arose because his interpretation of the findings differed materially from
mine, due to his misunderstanding of the complexities of
misclassification. Discussions took place between Yano and Proctor, who
played an important role in planning and organisation of the study on
behalf of the tobacco companies who funded it, and I was told that these
discussions led to Yano deciding not to be an author, and to his
understanding that the work would be published by others.
I had assumed that Proctor would keep Yano informed about the status
of the publication and was surprised Yano did not find out about the
paper, published in 1995, until some 7 or 8 years later. Clearly, one of
us should have kept him informed, and for this I apologise. In his
original article,(3) Yano states that "at no stage in my interactions with
Proctor was Lee's name or role ever mentioned." This is surprising
inasmuch as the study proposal stated that I would assist in reviewing the
study design and in interpreting the data. Was Yano really unaware of the
previous literature on misclassification of smoking, in which I figured
prominently (see 2) when conducting a study, a major aim of which
concerned the determination of misclassification rates?
GHOST AUTHORSHIP
Chapman(4) considers that "it is hard to imagine a more flagrant example
of attempted ghost authorship". It is difficult to see why Chapman sees
the publication as ghost authorship at all, when I proposed the study,
helped in its design and then published it. The study was a joint
enterprise, as I saw it, and it is perfectly normal for some of the
scientists involved in a study to write a draft for others to agree to.
It would clearly have been better had a version acceptable to all, with
Yano in the author list, been published. However, Yano's failure to
understand the mathematics of misclassification made this impossible.
There was no agreement I am aware of that Yano had sole rights to
authorship. Had I not published the paper(10) it seems that the findings
would never have appeared in the public domain at all. Did Yano also
have sole rights to suppress the findings?
POSTSCRIPT
At the end of the day it is interesting that, though the evidence of high
misclassification rates in Japanese women has been independently
confirmed,(11) the relevance of this to the ETS/lung cancer relationship
has been ignored in recent major reviews of ETS and lung cancer
(e.g.8,13). I have demonstrated the major biasing effect of this finding
in detail elsewhere(14).
References
1. Yano E. Response to P N Lee [Commentary]. Tob Control
2005;14:234-5.
2. Lee PN. Japanese spousal study: a response to Professor Yano's
claims [Commentary]. Tob Control 2005;14:233-4.
3. Yano E. Japanese spousal smoking study revisited: how a tobacco
industry funded paper reached erroneous conclusions. Tob Control
2005;14:227-35.
4. Chapman S. Research from tobacco industry affiliated authors:
need for particular vigilance [Editorial]. Tob Control 2005;14:217-9.
5. Lee PN, Forey BA. Misclassification of smoking habits as a
source of bias in the study of environmental tobacco smoke and lung
cancer. Stat Med 1996;15:581-605.
6. Committee on Passive Smoking, Board on Environmental Studies and
Toxicology, National Research Council. Environmental tobacco smoke.
Measuring exposures and assessing health effects. Washington D.C.:
National Academy Press; 1986.
7. National Cancer Institute. Shopland DR, editor. Respiratory
health effects of passive smoking: lung cancer and other disorders. The
report of the US Environmental Protection Agency. USA: US Department of
Health and Human Services, Public Health Service, National Institutes of
Health; 1993. (Smoking and Tobacco Control. Monograph 4.) NIH Publication
No 93-3605.
8. Hackshaw AK, Law MR, Wald NJ. The accumulated evidence on lung
cancer and environmental tobacco smoke. BMJ 1997;315:980-8.
9. Lee PN, Forey BA. Misclassification of smoking habits as
determined by cotinine or by repeated self-report - a summary of evidence
from 42 studies. J Smoking-Related Dis 1995;6:109-29.
10. Lee PN. "Marriage to a smoker" may not be a valid marker of
exposure in studies relating environmental tobacco smoke to risk of lung
cancer in Japanese non-smoking women. Int Arch Occup Environ Health
1995;67:287-94.
11. Lee PN. Passive smoking and lung cancer: Strength of evidence
on passive smoking and lung cancer is overstated [Letter]. BMJ
1998;317:346-7.
12. Lee PN. Lung cancer and passive smoking: association an
artefact due to misclassification of smoking habits? Toxicol Lett
1987;35:157-62.
13. International Agency for Research on Cancer. Tobacco smoke and
involuntary smoking, Volume 83. Lyon, France: IARC; 2004. (IARC Monographs
on the evaluation of carcinogenic risks to humans.)
14. Lee PN, Forey BA, Fry JS. Revisiting the association between
environmental tobacco smoke exposure and lung cancer risk. III. Adjustment
for the biasing effect of misclassification of smoking habits. Indoor
Built Environ 2001;10:384-98.
Allowing the tobacco industry to define "reasonable regulation," an
industry whose economic survival will always depend upon finding new and
creative ways to entice children and teens into permanent chemical
enslavement, is like allowing Hitler to write health standards for dead
camps.
While awaiting fine-tuning of FDA regulatory bills, it's time for the
U....
Allowing the tobacco industry to define "reasonable regulation," an
industry whose economic survival will always depend upon finding new and
creative ways to entice children and teens into permanent chemical
enslavement, is like allowing Hitler to write health standards for dead
camps.
While awaiting fine-tuning of FDA regulatory bills, it's time for the
U.S. Congress to expressly allow cities and states to take immediate steps
to insulate youth from all corporate image, newspaper, magazine,
sponsorship, and point of sale tobacco industry marketing.
Two decades of selective binding technology could immediately allow
entire zip codes to be free of all magazine and newspaper tobacco ads, if
local governments were only granted authority to protect their youth.
Modern dependency science has taught us that history is a ridiculous
excuse for demanding that high grade ethanol products be sold in stand
alone liquor stores, while high grade nicotine delivery devices are
marketed inside a child's neighborhood candy, chip and soda store.
With almost a half a million annual U.S. deaths, it's beyond time
that point of sale marketing was no long visible from sidewalks or school
buses. It's beyond time to grant local government express authority to
exclude youth from all tobacco sales locations.
Inside adult only sales locations, allow the industry to advertise
and market to its heart's content. But no pictures in ads or displays,
other than the product, and grant local government authority to demand
premises dependency warning signs.
I enjoyed Derek Yach’s editorial. I believe that the FCTC and new
research that will support its transnational aspects can make a big
difference. But will they?
I would warn against over optimism and for an understanding of the
commitment and sustained action that will be required. First, one must
face the fact that the primary governance of tobacco issues has been and
continues to be located in the tobacco...
I enjoyed Derek Yach’s editorial. I believe that the FCTC and new
research that will support its transnational aspects can make a big
difference. But will they?
I would warn against over optimism and for an understanding of the
commitment and sustained action that will be required. First, one must
face the fact that the primary governance of tobacco issues has been and
continues to be located in the tobacco business. This has been and could
continue to be the case for many years since the tobacco industry spends
more money than national and supranational bodies on controlling tobacco
governance. They also spend it using both legal and illegal means
necessary to their objectives. They also spend it with monopolistic focus
and agreement on core issues.
In contrast, to believe that there is some kind of international, or
even focused national governance of tobacco control is just not supported
by the evidence. Many countries have no central organization to forward
national tobacco control planning and policy, no plan for research, no
systematic monitoring of even the most basic indicators of importance to
tobacco control, and little or no money to fund tobacco control. And
while the fact that the FCTC requires more from these nations, without
adequate funding and sustained commitment, the lack of national governance
is likely to continue and the chance of global governance to be only a
remote dream.
How does a country get the necessary money and the necessary
commitment? Suppose you are from a poor country with a population of 25
million. What if you convinced society, including politicians and
scientists that they need to immediately bring tobacco use to a very
limited level? What if you could get $3 per person per year dedicated to
this job through taxing the tobacco industry? If you had the money and
the commitment, you could possibly make rapid progress through a
comprehensive approach to governing tobacco supply and demand.
Some countries have done so already. So where is the worldwide push
and coordination for all countries to generate funding and political will?
Until there is more effort in this direction, I doubt there will ever be a
global governance system for tobacco control. Urgency is appropriate, but
considering the historical record and present lack of money and
commitment, I believe slow progress is more likely. I wish I were wrong.
Erratum to Mandel, L; BC Alamar; and SA Glantz, “Smokefree Law did not affect revenue from
gaming in Delaware” Tobacco Control 14 (2005), 10-12.
The results in the original publication reflect a data entry error. The revised table in
this erratum present the results with this error corrected. Using the corrected data, White's test
for heteroskedasticity rejected homoskedasticity (p = 0.016) in t...
Erratum to Mandel, L; BC Alamar; and SA Glantz, “Smokefree Law did not affect revenue from
gaming in Delaware” Tobacco Control 14 (2005), 10-12.
The results in the original publication reflect a data entry error. The revised table in
this erratum present the results with this error corrected. Using the corrected data, White's test
for heteroskedasticity rejected homoskedasticity (p = 0.016) in the case of total revenues. We
corrected for the heteroskedasticity in total revenues by using a weighted least squares analysis
using the inverse of the number of video lottery machines as the weight. White's test of the
residuals from the weighted regression did not reject homoskedasticity (p=0.293). Average
revenues were homoskedastic (p=0.13) so we continued to use an unweighted regression, as in
the original paper. The analysis based on the corrected data confirms the results of the published
paper, that the smokefree law had no effect on revenue from gaming in Delaware.
...
I am the “WDE Irwin” quoted on page 67 as follows: “Years later (1985), WDE Irwin, a technician with BAT in England, was asked how a grooved filter could be made that would avoid criticism but also provide good taste. He concluded: ‘Finally for cigarettes, I believe it to be a self evident truth not only is there no smoke without fire, but also there is no kick without smoke.’”
“Technician” is not a correct id...
To the Editor,
I read with great interest the article by Bjartveit and Tverdal (2005), who investigated health consequences of smoking 1-4 cigarettes per day. They found that in both sexes, smoking 1-4 cigarettes per day was associated with a significantly higher risk of dying from ischaemic heart disease and from all causes, and in women, from lung cancer [1]. Genetic studies suggest that all stages of tobacco...
Dear Editor,
We thank Dr Graham F Cope for his valuable remarks, and agree that underreporting of daily cigarette consumption might be of importance when assessing the risk in light smokers.[1]
Dr Cope refers to two papers: a cross-sectional randomised study on smoking reduction in pregnant women, and an assessment of smoking status in patients with peripheral arterial disease.[2][3] Our study did not conc...
I read the paper by Bjartveit and Tverdal with a great deal of interest(1). I welcome the fact that highlighting smoking, even a small number of cigarettes has a significant effect on ischaemic heart disease. However, these findings should be considered with a certain amount of scepticism, as the findings are based entirely on self-reported smoking habit. Biochemically validated research, both by ourselves(2), and other...
British American Tobacco (Nigeria) Limited (BAT) and their cohorts the world over should come to terms with the fact that the truth cannot be hidden forever even from the man on the streets.
Mr Kehinde Johnson did not need to comment at all because there was nothing to comment about! He should have apologised for being a part of this systematic elimination of defenceless people the world over.
Dr. Chri...
Response to E Yano and S Chapman
P N Lee
Professor Eiji Yano raises a number of issues in his letter(1) which responded to my commentary(2) on his article(3) about the Japanese spousal study, as does Chapman in his editorial(4). Here I reply to the main points raised.
INTERPRETATION OF THE DATA
Studies of environmental tobacco smoke (ETS) exposure and lung cancer commonly identify a...
An excellent PM documents review! Thanks!
Allowing the tobacco industry to define "reasonable regulation," an industry whose economic survival will always depend upon finding new and creative ways to entice children and teens into permanent chemical enslavement, is like allowing Hitler to write health standards for dead camps.
While awaiting fine-tuning of FDA regulatory bills, it's time for the U....
I enjoyed Derek Yach’s editorial. I believe that the FCTC and new research that will support its transnational aspects can make a big difference. But will they?
I would warn against over optimism and for an understanding of the commitment and sustained action that will be required. First, one must face the fact that the primary governance of tobacco issues has been and continues to be located in the tobacco...
Erratum to Mandel, L; BC Alamar; and SA Glantz, “Smokefree Law did not affect revenue from gaming in Delaware” Tobacco Control 14 (2005), 10-12.
The results in the original publication reflect a data entry error. The revised table in this erratum present the results with this error corrected. Using the corrected data, White's test for heteroskedasticity rejected homoskedasticity (p = 0.016) in t...
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