We are grateful that the eLetter from Ms Cunnison provides an
opportunity for us to clarify some aspects of our work [1].
In the past there has been no authoritative guidance on the
protection of public health from risks from particulate matter (PM) in
indoor air. It is therefore a welcome development that the recent WHO Air
Quality Guidelines for Indoor Air [2] concluded that there is no...
We are grateful that the eLetter from Ms Cunnison provides an
opportunity for us to clarify some aspects of our work [1].
In the past there has been no authoritative guidance on the
protection of public health from risks from particulate matter (PM) in
indoor air. It is therefore a welcome development that the recent WHO Air
Quality Guidelines for Indoor Air [2] concluded that there is no
convincing evidence for a difference in the hazardous nature of PM from
indoor sources as compared with those from outdoors, and the document thus
goes on to recommend that the 2005 WHO outdoor air quality guidance for PM
should be applied to indoor environments [3]. Therefore, regardless of the
location of the sources, PM2.5 concentrations should be kept at levels
below 25 ?g/m3 averaged over a 24-h period and less than 10 ?g/m3
averaged over a year.
We acknowledge that car journeys are always much less than 24 hours
and in our paper we clearly stated that comparison of measurements with
the WHO PM2.5 guidance level should be done with some caution as this
health-based value is based on a 24-hour average. However, we also say it
is "important to consider that children who are exposed to SHS in cars may
also be exposed to SHS within their home setting and so, while we do not
have data here on 24 h average levels, it is reasonable to assume that the
time spent in the car will only be one of several micro-environments where
children may be exposed to SHS and hence elevated PM2.5 levels over the
course of the day."
To add to this point our group have also recently reported 24-hour
PM2.5 levels measured in over 100 homes in Scotland and Ireland [4]. It is
interesting to note that the concentrations in the 20 smoking homes in
that study averaged over 140 ?g/m3 compared to average of 10 ?g/m3 in the
80 non-smoking homes, both values averaged over 24-hours.
We consider that our data highlight that smoking in cars exposes
children to high levels of second-hand cigarette smoke. Steps to
discourage smoking in these semi-public spaces will, in our opinion,
increase public awareness of the dangers of exposing children to SHS
within indoor settings and encourage smokers to stop exposing children to
cigarette smoke in all situations.
Dr Sean Semple, Mr Andrew Apsley, Dr Karen Galea, Dr Laura MacCalman,
Mrs Brenda Friel, Ms Vicki Snelgrove.
References
1. Semple S, Apsley A, Galea KS, Maccalman L, Friel B, Snelgrove V.
Secondhand smoke in cars: assessing children's potential exposure during
typical journey conditions. Tob Control. 2012;21:578-83.
2. World Health Organisation. (2010). WHO Guidelines for Indoor Air
Quality. Selected Pollutants. ISBN 978 92 890 0213 4. Copenhagen,
Denmark,WHO. Available at
http://www.euro.who.int/__data/assets/pdf_file/0009/128169/e94535.pdf
[accessed 19th October 2012]
3. World Health Organisation. (2005) WHO Air Quality Guidelines.
Global update. Available at
http://www.who.int/phe/health_topics/outdoorair_aqg/en/ [accessed 19th
October 2012].
4. Semple S, Garden C, Coggins M, Galea KS, Whelan P, Cowie H,
S?nchez-Jim?nez A, Thorne PS, Hurley JF, Ayres JG. Contribution of solid
fuel, gas combustion, or tobacco smoke to indoor air pollutant
concentrations in Irish and Scottish homes. Indoor Air. 2012;22:212-23.
NOT PEER REVIEWED In this interesting study by Cheah et al,1 the authors have raised
several safety issues concerning electronic cigarettes. The majority of
them were based either on the finding that nicotine content was
inconsistent or that chemical constitution (for example glycols) may be
hazardous to health.
There is some inconsistency in characterizing polypropylene glycol as
"a known irritant when inhaled o...
NOT PEER REVIEWED In this interesting study by Cheah et al,1 the authors have raised
several safety issues concerning electronic cigarettes. The majority of
them were based either on the finding that nicotine content was
inconsistent or that chemical constitution (for example glycols) may be
hazardous to health.
There is some inconsistency in characterizing polypropylene glycol as
"a known irritant when inhaled or ingested" in introduction section and as
"a non-toxic chemical" in discussion section. This substance has been
"generally recognized as safe" (GRAS) by FDA for ingestion, however, only
few studies have evaluated the long term inhalation risk. A study by
Robertson et al2 found that in experimental animals inhaling large
quantities of propylene glycol for 12-18 months no lung, kidney, liver,
spleen or bone marrow irritation or disease was observed, while others
have used it on a daily basis as a vehicle for drug administration without
finding any significant irritant effects on the respiratory tract. There
are also no reports from electronic cigarette users that propylene glycol
has caused any significant irreversible damage besides some throat
irritation and cough, that has been resolved by using liquids not
containing propylene glycol.
Concerning the production of carbonyls, it should be mentioned that
electronically heated cigarettes that are mentioned in the study are in no
way similar to electronic cigarettes. The temperature in electrically
heated cigarettes is 600oC.3 Glycerol has a boiling point of 290oC, and
diluting it with 10% water (usually, for electronic cigarette liquids
glycerol is diluted with 15-20% water) the boiling point is 138oC,4
significantly lower than the 250oC needed to produce acrolein. These
theoretical concepts have been backed up by data provided by Schripp et
al,5 who found traces of formaldehyde not attributed to electronic
cigarette use, and Romagna et al,6 who found no acrolein or formaldehyde
in the air after electronic cigarette use for several hours.
An important finding of the study was the absence of nitrosamines.
This has been somewhat underestimated by the authors. Nicotine in
electronic cigarette liquids (and in other products, including
pharmaceutical products) is derived from tobacco. Therefore, there is a
possibility that nitrosamines may be present; in fact, they have been
detected in approved nicotine gum and patch products.7 We think that the
absence of nitrosamines is an important finding of this study and should
have been further discussed, since they are major causes of lung disease
including cancer.
Quality control during the production process is a major issue in
electronic cigarette industry. Unfortunately, the fact that no regulation
has been implemented by public health authorities allows low-quality
products to be available to the market. This may raise safety issues like
the presence of nitrosamines mentioned above. In addition, this is also
the reason for the inadequate labeling of these products. We think that
regulation standards should include proper labeling not only about the
contents but also about the risks of accidental exposure to the liquids,
similarly to other consumer products used daily in every home. However, we
believe that the nicotine content discrepancies that the authors have
found do not represent a major health risk, since it is well known that
smoking is a dynamic process and changes in response to the yield
characteristics of the cigarette.8 Most probably, the users would have
adjusted their smoking pattern to the nicotine levels obtained by the use
of these liquids. In fact, this has been a problem of tobacco cigarettes,
with FTC protocol levels of nicotine significantly underestimating
nicotine doses to smokers.8 This is accompanied by an underestimation of
doses of carcinogens obtained by smokers, like nitrosamines, which were
not found in electronic cigarettes tested in this study. Thus, it is not
the nicotine that poses a health risk but other chemicals that are
released during the smoking process.
References
1. Cheah NP, Chong NWL, Tan J, Morsed FA, Yee SK. Electronic nicotine
delivery systems: regulatory and safety challenges: Singapore perspective.
Tob Control, 2012. Dec 1 [Epub ahead of print]
2. Robertson OH, Loosli CG, Puck TT, Wise H, Lemon WM, Lester W Jr.
Tests for the chronic toxicity of propylene glycol and triethylene glycol
on monkeys and rats by vapor inhalation and oral administration. J
Pharmacol Exper Ther 1947;91:52-76.
3. Patskan G, Reininghaus W. Toxicological evaluation of an
electrically heated cigarette. Part 1: overview of technical concepts and
summary of findings. J Appl Toxicol 2003;23:323-8
4. Flick EW. Industrial solvents handbook, 5th edition, 1998. ISBN 0-
8155-1413-1 Noyes Data Co, 1998
5. Schripp T, Markewitz D, Uhde E, Salthammer T. Does e-cigarette
consumption cause passive vaping? Indoor Air 2012. Jun 2 [Epub ahead of
print]
6. Romagna G, Allifranchini E, Bocchieto E, Todeshi S, Esposito M,
Farsalinos K. Cytotoxicity of electronic cigarette vapor extract on
cultured mammalian fibroblasts (ClearStream-Life project): comparison with
tobacco smoke extract [abstract].
[http://www.srnteurope.org/assets/Abstract-Book-Final.pdf] Poster RRP17.
14th Annual Meeting of the Society for Research on Nicotine and Tobacco
Europe, Helsinki, 2012. (accessed December 2012).
7. Cahn Z, Siegel M. Electronic cigarettes as a harm reduction
strategy for tobacco control: a step forward of a repeat of past mistakes?
J Public Health Policy 2011;32:16-31.
8. Djordjevic MV, Stellman SD, Zang E. Doses of nicotine and lung
carcinogens delivered to cigarette smokers. J Natl Cancer Inst 2000;92:106
-11.
I am a lay person, but curious as to how these conclusions are reached. How is it possible to describe 25 ug/m3 as a WHO _indoor_ air quality standard, when it seems to have been designed as an outdoor standard?
More importantly how is it possible to apply the standard to journeys lasting under half an hour, when the standard specifically directs how to deal with short exposure times (http://www.epa.gov/ttn/caaa/t1/memoranda/pmf...
I am a lay person, but curious as to how these conclusions are reached. How is it possible to describe 25 ug/m3 as a WHO _indoor_ air quality standard, when it seems to have been designed as an outdoor standard?
More importantly how is it possible to apply the standard to journeys lasting under half an hour, when the standard specifically directs how to deal with short exposure times (http://www.epa.gov/ttn/caaa/t1/memoranda/pmfinal.pdf), and in all cases described in this study they would have been discounted. The statement, 'PM2.5 concentrations in cars where smoking takes place are high and greatly exceed international indoor air quality guidance values', in this context is false: according to the guidance, peaks that rise well above the standard are not in themselves considered hazardous to health. The authors declare that opening windows produced high values 'at some point in the measurement during all the smoking journeys': this does not indicate a health risk either.
Are we to understand that non-smoking journeys never measured above 25 ug/m3?
This study seems to reinvent the guidance for EPA guidelines.
Most of us know the people who control Hollywood. Well, the Movie
Industry is controlled in a similar manner, by their Cousins. They assist
in the production of the films by, having their cancer causing product
portrayed as a natural thing that your favorite stars do, so why aren't
you?
Films should have NO tobacco products in them whatsoever!!!
If I had my way, I'd stop all tobacco production. If You want to smoke,
grow...
Most of us know the people who control Hollywood. Well, the Movie
Industry is controlled in a similar manner, by their Cousins. They assist
in the production of the films by, having their cancer causing product
portrayed as a natural thing that your favorite stars do, so why aren't
you?
Films should have NO tobacco products in them whatsoever!!!
If I had my way, I'd stop all tobacco production. If You want to smoke,
grow it, cut it & wrap it, & you don't sell it to anyone!!
Smith et al provides us with a remarkable review of tobacco industry
efforts to influence tobacco tax which deserves several comments.(1)
First, such efforts can be quite successful as in France: From
February 2004 to September 2012 there was no increase in tobacco taxes,
accordingly cigarette sales remained unchanged and smoking prevalence of
the youngest increased during Sarkozy's presidency, an exception amon...
Smith et al provides us with a remarkable review of tobacco industry
efforts to influence tobacco tax which deserves several comments.(1)
First, such efforts can be quite successful as in France: From
February 2004 to September 2012 there was no increase in tobacco taxes,
accordingly cigarette sales remained unchanged and smoking prevalence of
the youngest increased during Sarkozy's presidency, an exception among
developed countries.(2) The WHO must scrutinize the implementation of
Article 5.3 of the Framework Convention on Tobacco Control which requires
protecting public health policies from the influence of the tobacco
industry. Indeed, the French example of the influence of the tobacco
industry on a government is not unique.(3)
Second, the 16th point of industry tactics (Table 2 in 1) which is
"trying to undermine tobacco control experts" can be harder and damaging,
eg. slapping and sacking.(4) In November 2009, one of us (GD) was sued for
libel by the French tobacconists' Union, because he stated on television that cigarettes kill two smokers each
year for every tobacconist. In December 2009 as a tenured senior
consultant in GD's unit, I (AB) was sacked by the Ministry of Health, even
against the advice of the National Statutory Committee. Both of us won in
court, the tobacconists' claim was rejected in 2011 by the Appeal Court
and the sacking was cancelled in 2012 by the Administrative Court of Paris
on the grounds that it was illegal.(5) However, none of us received
compensation for the damages.
Third, even low and middle income countries can successfully resist
tobacco industry efforts to influence tobacco control. Uruguay's tobacco-
control campaign is associated with a substantial, unprecedented decrease
in tobacco use of 4*3% per year during 2005-11.(6) We must keep in mind
that the little Uruguay (GDP $31 billion) has been even sued in 2009 by
the giant Philip Morris ($25 billion in total revenues for a market
capitalization of $95 billion) before the World Bank's International
Center for Settlement of Investment Disputes.(7)
Integrity, courage and mainly enduring efforts are needed against the
tobacco industry.
References
1 Smith KE, Savell E, Gilmore AB. What is known about tobacco
industry efforts to influence tobacco tax? A systematic review of
empirical studies. Tob Control 2012, Online First August 12. DOI:
10.1136/tobaccocontrol-2011-050098
2 Braillon A, Mereau AS, Dubois G. [Tobacco control in France:
effects of public policy on mortality].Presse Med. 2012;41:679-81.
3 Arnott D, Berteletti F, Britton J et al. Can the Dutch Government
really be abandoning smokers to their fate? Lancet 2012;379:121-2.
4 Dubois G. Abuse of libel laws and a sacking: The gagging of public
health experts in France. Tobacco Control Blog November 8th, 2010.
Available at http://blogs.bmj.com/tc/2010/11/08/
5 Witton J and O'Reilly J. Tobacco scientist win against illegal
sacking. Addiction 2012;107:1714-5
6 Abascal W, Esteves E, Goja B et al. Tobacco control campaign in
Uruguay: a population-based trend analysis. Lancet 2012, Early Online
Publication, 14 September. doi:10.1016/S0140-6736(12)60826-5
7 Lencucha R. Philip Morris versus Uruguay: health governance
challenged. Lancet. 2010;376:852-3.
Omid Fotuhi,1 Geoffrey T Fong,1,2 Mark P Zanna,1 Ron Borland,3 Hua-
Hie Yong,3 K Michael Cummings4
1. Department of Psychology, University of Waterloo, Waterloo,
Ontario, Canada
2. Ontario Institute for Cancer Research, Toronto, Ontario, Canada
3. The Cancer Council Victoria, Melbourne, Victoria, Australia
4. Department of Health Behavior, Roswell Park Cancer Institute, Buffalo,
New York, USA
Omid Fotuhi,1 Geoffrey T Fong,1,2 Mark P Zanna,1 Ron Borland,3 Hua-
Hie Yong,3 K Michael Cummings4
1. Department of Psychology, University of Waterloo, Waterloo,
Ontario, Canada
2. Ontario Institute for Cancer Research, Toronto, Ontario, Canada
3. The Cancer Council Victoria, Melbourne, Victoria, Australia
4. Department of Health Behavior, Roswell Park Cancer Institute, Buffalo,
New York, USA
Email for lead author, Omid Fotuhi: ofotuhi@uwaterloo.ca
NOT PEER REVIEWED
Response to letter:
In our recent study--using a large set of nationally representative
samples of smokers from Canada, the US, the UK, and Australia--we reported
on the longitudinal patterns of smoking-related beliefs and how these
beliefs vary with changes in smoking status. We found a consistent pattern
of attitude-behaviour congruence: smokers highly endorsed risk-minimizing
beliefs (e.g., "I have the genetic make-up that allows me to smoke without
any health problems") and functional beliefs (e.g., "Smoking helps me
concentrate"). But the most interesting finding was the longitudinal
pattern of how these justifications for smoking changed over time as their
smoking status changed: smokers endorsed these beliefs the least when they
had quit; and again endorsed these beliefs to their pre-quit levels if
they relapsed back to smoking, whereas the levels of endorsement of these
beliefs stayed low among those smokers who had quit smoking and were able
to stay quit in the long-term. We proposed that the waxing and waning of
these smoking-related beliefs as a function of smoking status were driven
by motivations to reduce cognitive dissonance (Festinger, 1957)--a
fundamental human motivation to maintain consistency between one's
attitudes and one's behaviours.
In response to these findings, Gould, Clough, and McEwen have offered
a thoughtful commentary. In addition to writing about the importance for
public health measures to target smokers' erroneous beliefs that smoking
reduces stress, they agreed with our view that smokers are driven to
modify their risk-minimizing beliefs because of their motivation to reduce
dissonance.
However, Gould et al. suggest that an alternate mechanism is
responsible for the longitudinal pattern of functional beliefs that we
report in our study. Rather than being driven by dissonance-reducing
motivations, they suggest that higher endorsements of functional beliefs
among smokers are "representations of smokers' genuine experiences of
nicotine withdrawal 'in between' cigarettes or on quitting."
We, on the other hand, do not see a contradiction between their
interpretation and ours. Rather, we suggest that the physiological
reactions to withdrawal and dependence are the starting point for the
cognitive dissonance process. This is a view that has long been shared by
dissonance researchers (e.g., Zanna, Cooper, & Taves, 1978; Croyle
& Cooper, 1983).
So the Gould et al. account does not, at the core, differ from our
account. They are pointing out the nature of the reasons for the
justifications, which is the whole point of our argument: the fact that
smokers are addicted and that they suffer withdrawal symptoms leads to the
search for justifications for their smoking (rather than saying that "I am
addicted"). The physiological symptoms of dependence and withdrawal can,
therefore, lead to effects far outside the realm of the physiology of the
smoker.
Thus, their account is not an alternative explanation--it may well be
the starting point for what then become biases in cognitions to justify
smoking.
In addition, when looking at the data from our study, we note that
non-quitters endorsed both risk-minimising and functional beliefs more,
compared to successful and failed quitters, at all three waves--even at
times when all three groups were smoking (wave 1). Because it is unlikely
that the pattern of risk-minimizing beliefs (e.g., "You've got to die
someday, so why not enjoy yourself and smoke") is driven primarily by
withdrawal symptoms--and given the strikingly similar pattern for both
functional and risk-minimizing beliefs--we suggest that, at least in part,
similar dissonance-reducing processes may also be responsible for the
shifting of functional beliefs as smokers vacillate between smoking and
having quit.
Furthermore, let us be clear that we do not claim that all smokers'
smoking-related beliefs are distortions that serve only to reduce
dissonance. We fully acknowledge that there may, in fact, be unique and
genuine physiological experiences of nicotine consumption and withdrawal.
We propose, however, that these experiences can more effectively be
captured by specific measures that tap into the visceral aspects of
nicotine addiction. For instance, the Hughes (1992) article cited by Gould
and colleagues nicely captures these physiological experiences among
quitters at various time points (e.g., increased irritability, hunger,
restlessness, and cravings to smoke). These items are more directly
representative of physiological responses to nicotine consumption and
withdrawal than some of our functional beliefs measure (e.g., "Smoking is
an important part of your life" or "Smoking makes it easier to
socialize").
In fact, we would even argue that in comparison to risk-minimizing
beliefs, functional beliefs are more readily employed in the service of
dissonance reduction because they are less likely to be countered by
reality constraints (Kunda, 1990). Specifically, we think that the
functional beliefs in our study [(1) "You enjoy smoking too much to give
it up"; (2) "Smoking calms you down when you are stressed or upset"; (3)
"Smoking helps you concentrate better"; (4) "Smoking is an important part
of your life"; and (5) "Smoking makes it easier for you to socialize"] are
exactly the kind of malleable beliefs that smokers commonly employ--more
so than the risk-minimizing beliefs which may be countered by rational
thought (e.g., "The medical evidence that smoking is harmful is
exaggerated")--to rationalize a behaviour that they know is harmful to
their health.
Nonetheless, we appreciated the comments by Gould et al. because they
encouraged us to take a closer look at our data and, consequently, to
further think about our original interpretation of the findings.
We hope that further research continues to explore the role of
attitudes in the domain of health behaviour, and specifically addictive
behaviours, such as smoking. Experimental studies that more clearly
determine causality and studies that examine the taxonomy of
rationalizations commonly used by smokers would be especially useful for
the advancement of this research topic. These findings would also have the
important potential of informing policies to more effectively help save
lives.
References
Croyle, R. T., & Cooper, J. Dissonance arousal: Physiological
evidence. J Pers Soc Psychol. 1983;45:782-791.
Festinger L. A Theory of Cognitive Dissonance. Evanston, IL: Row,
Peterson, 1957.
Hughes JR. Tobacco withdrawal in self-quitters. J Consult Clin
Psychol. 1992;60(5):689-97.
Kunda Z. The case for motivated reasoning. Psychol Bull.
1990;108:480e98.
Zanna, M. P., & Cooper, J. Dissonance and the pill: An
attribution approach to studying the arousal properties of dissonance. J
Pers Soc Psychol 1974;29:703-709.
NOT PEER REVIEWED This study violates basic ethical principles of research conduct
because it exposes children to unreasonable and unnecessary risks,
intentionally encourages parents to put their children at risk, and fails
to incorporate alternative methods that would reduce these risks.
The Helsinki declaration states that:
"The benefits, risks, burdens and effectiveness of a new intervention
must be...
NOT PEER REVIEWED This study violates basic ethical principles of research conduct
because it exposes children to unreasonable and unnecessary risks,
intentionally encourages parents to put their children at risk, and fails
to incorporate alternative methods that would reduce these risks.
The Helsinki declaration states that:
"The benefits, risks, burdens and effectiveness of a new intervention
must be tested against those of the best current proven intervention,
except in the following circumstances:
1. The use of placebo, or no treatment, is acceptable in studies
where no current proven intervention exists; or
2. Where for compelling and scientifically sound methodological
reasons the use of placebo is necessary to determine the efficacy or
safety of an intervention and the patients who receive placebo or no
treatment will not be subject to any risk of serious or irreversible harm.
Extreme care must be taken to avoid abuse of this option."
In the present study, children in group 1 were provided with an
intervention to reduce their exposure to secondhand smoke: parents were
asked not to smoke in the presence of their children. Children in group 2
were not provided with any treatment. According to the Helsinki
declaration, this would have been acceptable only if: (1) there was no
treatment available; or (2) children receiving no treatment would not be
subject to any risk of serious harm. Neither of these conditions are met.
Furthermore, this study goes beyond simply providing no treatment to
the children in group 2. Instead of simply observing these children over
time, the study protocol called for "asking" the parents not to change
their smoking habits.
In other words, the investigators knowingly and intentionally placed
the children in group 2 at significant risk of health damage.
In the United States, the federal regulations on the protection of
human subjects (section 46.406a) would have allowed this research to be
conducted on minors only if: "The risk represents a minor increase over
minimal risk." This condition is clearly not met, as the risks of
pneumonia, bronchitis, respiratory illness, and cardiovascular damage are
a major increase over minimal risk.
Moreover, there was an alternative procedure available that would
have provided the same scientific knowledge without putting children at
substantially more than minimal risk. The investigators could have
encouraged all parents not to smoke around their children and then
followed all the children over time as a single group. Then, they could
have assessed changes in secondhand smoke exposure and related those
changes (or lack of changes) to the persistence or disappearance of sleep
bruxism.
There is no justification for the investigators asking parents to
continue to smoke in the presence of their children.
Rather than acknowledge that they made a mistake, the instead defend
the study. But in defending the study, they deliver a definitive knock-out
blow to their argument that the study was ethical. They point out that
after being randomized to group 2, a number of the families dropped out of
the study, refusing to participate because: "aware of the risks of SHS,
[they] decided to reduce it and therefore did not participate."
If the subjects themselves realized that they were being put at undue
risk by agreeing to participate in the study, then it is quite clear that
this research was unethical. In fact, after a number of families refused
to participate because of the risks to which they were being asked to be
exposed, the IRB should have been informed and the study should have been
halted.
The authors go on to justify their research by noting that "all of
the parents of group 2 remaining in the trial were those who reported not
being able to reduce children's exposure to SHS." This is an unacceptable
argument. A feeling that one is not able to take a particular action is no
justification for investigators putting the children of those subjects at
risk and failing to deliver any intervention to encourage those parents to
quit, reduce their smoking, or not smoke in the presence of their
children.
NOT PEER REVIEWED We wish to comment on the findings of Smerecnik et al.1 with respect
to significant advances in genetic testing , which are highly relevant to
their review. Unlike the early single genetic marker tests analysed by
Smerecnik et al.,1 where subjects are dichotomised to positive or negative
results, genetic susceptibility tests for lung cancer are now multivariate
risk tests.2 These new risk tests incorpora...
NOT PEER REVIEWED We wish to comment on the findings of Smerecnik et al.1 with respect
to significant advances in genetic testing , which are highly relevant to
their review. Unlike the early single genetic marker tests analysed by
Smerecnik et al.,1 where subjects are dichotomised to positive or negative
results, genetic susceptibility tests for lung cancer are now multivariate
risk tests.2 These new risk tests incorporate clinical and genetic data
to derive a composite gene-based risk score. In doing so they recognise
that (1) environmental factors, like how much you smoked, are important
and (2) genetic data alone is not sufficiently accurate to assess a
person's risk. These distinguishing features of the recently developed
lung cancer susceptibility tests are very important in assessing how
patients respond for two reasons. First, this approach acknowledges that
environment is important and that regardless of level of risk, all smokers
can significantly mitigate that risk by quitting smoking (a unique feature
of smoking-related lung diseases). This means there is no concern about
genetic determinism (or nihilism), risk reduction is always possible.
Second, in contrast to these early single marker tests, there are no
"positive" and "negative" tests, all smokers tested have some level of
risk and importantly, only lifelong non-smokers are "low risk" (more
accurately reflecting the real-world situation).
We have developed a gene-based lung cancer risk score based on a persons
smoking, age, COPD, family history and genetic markers, where these
previously validated variables are combined to derive a composite score.2
This score has been prospectively verified and assigns smokers to
elevated, high and very high risk according to their total risk profile.3
We have assessed the potential clinical utility of this lung cancer risk
score in a feasibility study where randomly selected smokers underwent
brief counselling and were offered smoking cessation treatment. We found
84% of the smokers offered the test took the test, of which 52% took NRT
and 28% had quit smoking 6 months after testing (2 fold and 5 fold greater
than controls respectively).4 We conclude that our lung cancer
susceptibility test improved the outcome of brief intervention, by
facilitating the use of smoking cessation products (NRT) and subsequent
quit rate. Such a finding concurs with the tension-trigger-treatment model
proposed by Robert West where our gene-based test increased motivational
tension, undermined optimistic bias and, for 30-50% of smokers, triggered
a favourable outcome (NRT uptake and/or quitting smoking).
References
1. Smerecnik C, Grispen JE, Quaak M. Effectiveness of testing for genetic
susceptibility to smoking-related diseases on smoking cessation outcomes:
a systematic review and meta-analysis. Tob Control 2012; 21: 347-354.
2. Young RP, Hopkins RJ, Whittington CF, et al. Individual and cumulative
effects of GWAS susceptibility loci in lung cancer: associations after sub
-phenotyping for COPD. Plos One 2011; 6: e16467.
3. Young RP, Hopkins RJ, Hay B, Gamble GD. GWAS and candidate SNPs for
COPD and lung cancer combine to identify lung cancer susceptibility:
validation in a prospective study. Am J Respir Crit Care Med 2010; 181:
A3738.
4. Hopkins RJ, Young RP, Hay B, et al. Lung cancer risk testing enhances
NRT uptake and quit rates in randomly recruited smokers offered a gene-
based risk test. Am J Respir Crit Med 2012; 185: A2590.
Conflict of Interest:
Dr Young has helped to develop a gene-based risk test for lung cancer susceptibility. Patents related to this test are held by Synergenz Bioscience Ltd who helped fund the research underlying the develeopment of this test.
NOT PEER REVIEWED Fotuhi et al concluded in their interesting study of patterns in
smokers' cognitive dissonance-reducing beliefs that rationalisations about
smoking change systematically with changes in smoking behaviour(1).
Moreover, they argue that: i) changes in attitude on quitting are higher
for 'functional' beliefs rather than 'risk-minimising' beliefs and ii) if
smokers relapse these functional beliefs return to p...
NOT PEER REVIEWED Fotuhi et al concluded in their interesting study of patterns in
smokers' cognitive dissonance-reducing beliefs that rationalisations about
smoking change systematically with changes in smoking behaviour(1).
Moreover, they argue that: i) changes in attitude on quitting are higher
for 'functional' beliefs rather than 'risk-minimising' beliefs and ii) if
smokers relapse these functional beliefs return to pre-quit levels, iii)
that changes in beliefs follow the changes in behaviour (quitting),
suggesting that iv) these changes are rationalisations invoked in the
service of motivation to reduce cognitive dissonance and that v) smokers
are able to reduce dissonance by modifying their beliefs in ways that help
to rationalise their continued smoking.
We wish to suggest an alternative understanding. The functional belief
items include questions such as "smoking calms you down when you are
stressed or upset" and "smoking helps you concentrate better". We propose
that these items are not examples of dissonance-reducing attitudes but are
representations of smokers' genuine experiences of nicotine withdrawal 'in
between' cigarettes or on quitting, i.e. 'stress' and 'poor
concentration'(2). In this way they are more a proxy for the physiological
states induced by nicotine deprivation rather than attitudes and beliefs
per se. Therefore 'risk-minimising beliefs' such as 'the medical evidence
that smoking is harmful is exaggerated' and 'you've got to die of
something, so why not enjoy yourself and smoke' may more truly represent
cognitive dissonance, as they do not overlap with experiences indicating
withdrawal symptoms.
A misinterpretation of these withdrawal symptoms by smokers and a
commonly held belief that smoking reduces stress will undoubtedly result
in the kind of results that the authors report - but should these results
really be interpretated as supporting their hypothesis? Once smokers stop
smoking, withdrawal symptoms subside over ensuing weeks (3), with
'functional' justifications for smoking naturally receding. They would
return when the smoker then recommences to a physiological state of
dependency and nicotine deprivation.
The theory of reasoned action holds that attitude changes precede
behavioural change (4). The authors conclude that their study shows
conversely, for smokers that their changes in attitudes are likely to be a
result of their changes in smoking behaviour. This interpretation does not
prove causation if these 'cognitive-dissonance' measures are more an
indication of the presence of physiological symptoms rather than attitudes
and beliefs per se.
We do agree, however, with Fotuhi et al's proposal that public health
measures should target smokers' beliefs that smoking reduces stress. This
would promote greater understanding about the withdrawal process and link
it to why pharmacotherapy can be a useful adjunct to quitting and thereby
increase their sense of response and self-efficacy (5).
We have been working in Australia with Indigenous smokers who have a
high prevalence of smoking. One of the teaching tools we have developed is
a simple visual model to explain to the lay public in the context of a
group or personal intervention why smoking increases stress levels, how
withdrawal symptoms make smokers more stressed and how nicotine
replacement therapy can be efficacious (6).
Resistance to anti-tobacco messages, and cognitive dissonance will
most likely continue to plague smokers who do not feel able to quit.
Although for Indigenous smokers, knowledge acquisition alone may not be
enough to support successful cessation (7), we believe smokers'
justifications for smoking may also represent the truth for them of their
experiences of withdrawal, and a lack of understanding about nicotine
deprivation.
References
1. Fotuhi O, Fong GT, Zanna MP, Borland R, Yong H-H, Cummings KM.
Patterns of cognitive dissonance-reducing beliefs among smokers: a
longitudinal analysis from the International Tobacco Control (ITC) Four
Country Survey. Tobacco Control. January 3, 2012. doi:
10.1136/tobaccocontrol-2011-050139
2. Parrott AC, Garnham NJ, Wesnes K, Pincock C. Cigarette Smoking and
Abstinence: Comparative Effects Upon Cognitive Task Performance and Mood
State over 24 Hours. Human Psychopharmacology: Clinical and Experimental.
1996;11(5):391-400.
3. Hughes JR. Tobacco withdrawal in self-quitters. J Consult Clin Psychol.
1992;60(5):689-97.
4. Fishbein M, Ajzen, I. Belief, attitude, attention and behaviour: An
introduction to theory and research. Reading, MA: Addison-Wesley; 1975.
5. Witte K, Meyer G., Martell, D. Effective health risk messages: a step-
by-step guide. Thousand Oaks, CA: Sage Publications; 2001.
6. Baker F, Gould, GS. Blow Away The Smokes DVD: Quit Cafe Scene starts
13.00min. 2011 [4 July 2012]; Available from:
http://www.blowawaythesmokes.com.au
7. Gould G, Munn, J, Watters, T, McEwen, A, Clough, A. Knowledge and views
about maternal tobacco smoking and barriers for cessation in Aboriginal
and Torres Strait Islanders: a systematic review and meta-ethnography. Nic
Tob Res. 2012;under review
The author seeks to analyze the interference of the International
Tobacco Growers Association (ITGA) in the decisions of the 4th Conference
of the Parties (COP 4) on the Framework Convention on Tobacco Control
(FCTC) regarding Guidelines recommending the prohibition of additives in
cigarettes and includes Brazil as one of the countries influenced by this
organization.
As members of the Brazilian del...
The author seeks to analyze the interference of the International
Tobacco Growers Association (ITGA) in the decisions of the 4th Conference
of the Parties (COP 4) on the Framework Convention on Tobacco Control
(FCTC) regarding Guidelines recommending the prohibition of additives in
cigarettes and includes Brazil as one of the countries influenced by this
organization.
As members of the Brazilian delegation to COP4, we are deeply concerned
with the conclusions drawn by the author, that were based mainly on the
size and composition of the delegation as an indicator of the possible
interference of ITGA.
We are aware that the Association of Brazilian Tobacco Growers (AFUBRA), a
member of ITGA, pressed government officials and legislators to work
against the approval of the Guidelines and related recommendations. Their
arguments were recently published in the Journal in the News Analysis
session(a).
However this misinformation was challenged publicly ( b) and their
pressure has not influenced Brazil's government position as can be
demonstrated in the records of COP4 plenary discussions and confirmed by a
recent regulation that positioned Brazil as the first country in the world
to adopt a total ban on cigarette additives.
In Brazil, a National Inter Ministerial Commission for the Implementation
of the WHO FCTC (CONICQ), created by Presidential Decree, has proven to be
very successful in the implementation of an inter sectorial agenda for
tobacco control, aligning all sectors of the government with the FCTC
objectives and neutralizing the tobacco industry interference on tobacco
control policies. Currently, eighteen different sectors of the government
are part of CONICQ and most of its representatives attended COP4 due to
the priority assigned to the theme and the opportunity the proximity of
Uruguay has provided for Brazil's delegates' participation.
As a major tobacco producer, apart from implementing the core FCTC
provisions, Brazil has the additional duty to safeguard 180,000 tobacco
growers and their families from sanitary, social and economic
vulnerabilities related to this activity in view of FCTC Articles 17 and
18. For this reason the Ministry of Agrarian Development and the Ministry
of Agriculture are part of CONICQ and Brazil has joined the article 17 and
18 FCTC Working Group as a key facilitator Party.
However, the author highlighted the number of representatives of the
Brazilian delegation as suspiciously higher than usual and drew
attention to the fact that it had six representatives from the Ministry of
Agriculture, a sector of the government claimed by the author to be an
ally of the tobacco industry. Apart from not being true (the delegation
had only one representative from this Ministry of Agriculture, the
other five being representatives from the Ministry of Agrarian Development, which
is responsible for the National Program for Diversification in Tobacco
Cultivated Areas), this statement raises an unfair suspicion of conflict
of interests and violation of Article 5.3 by the country, a theme that has
been treated with utmost importance by CONICQ, which has recently published
ethical guidelines for its membership.
The author also stated that the majority of tobacco producers grow other agricultural products. This is not the reality in Brazil where
most tobacco growers do not rely on other agricultural products for income
generation. They are fully dependent on the tobacco supply chain
articulated by major transnational tobacco companies that attract them
through the deceptive calls that growing tobacco generates wealth and
prosperity. What they actually find is an endless cycle of debt, economic
dependency and health risks inherent to this activity. In this context
they do need support to shift to other livelihoods. Thereby, FCTC articles
17 and 18 deserves special attention from FCTC Member States as they
represent not only an important tool for rescuing tobacco growers from
this risky economic dependence but a way to reduce the power of
tobacco companies to interfere with the FCTC implementation.
Finally, it's worth noting that even considering its status as a major
tobacco producer and exporter, Brazil is a country that has proven to be
capable to reduce smoking prevalence by 50% in the last 20 years by
implementing sound tobacco control measures.
We would appreciate if this letter is published in order to correct erroneous and unacceptable
conclusions mentioned in the article that reflect on the credibility of Brazil's
delegation.
On behalf of the Brazilian delegation that attended COP4
Dr Tania Maria Cavalcante
Coordinator of the Executive Secretariat of the National Commission for
the Implementation of the FCTC (CONICQ)/ National Cancer Institute/
Ministry of Health/Brazil
Mrs Adriana Gregolin
Coordinator, National Program for Diversification in Tobacco Cultivated
Areas /Family Farming Secretariat / Ministry of Agricultural
Development/Brazil
Prof Dr Vera Luiza da Costa e Silva
Coordinator, Center for Studies on Tobacco
Control Policies, National Public Health School, Oswaldo Cruz Foundation,
Ministry of Health/Brazil
(a) News analysis - Brazil: industry fury at new proposals September
2011 Volume 20 Issue 5. Available at
http://tobaccocontrol.bmj.com/content/20/5/323.full
(b) Aditivos em cigarros / Instituto Nacional de Cancer Jose Alencar
Gomes da Silva, Comissao Nacional para a Implementacao da Convencao-Quadro
para o Controle do Tabaco e de seus Protocolos. -- Rio de Janeiro : Inca,
2011. Available at
http://bvsms.saude.gov.br/bvs/publicacoes/aditivos_cigarros_notas_tecnicas.pdf
Dear Editor,
We are grateful that the eLetter from Ms Cunnison provides an opportunity for us to clarify some aspects of our work [1].
In the past there has been no authoritative guidance on the protection of public health from risks from particulate matter (PM) in indoor air. It is therefore a welcome development that the recent WHO Air Quality Guidelines for Indoor Air [2] concluded that there is no...
NOT PEER REVIEWED In this interesting study by Cheah et al,1 the authors have raised several safety issues concerning electronic cigarettes. The majority of them were based either on the finding that nicotine content was inconsistent or that chemical constitution (for example glycols) may be hazardous to health.
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Smith et al provides us with a remarkable review of tobacco industry efforts to influence tobacco tax which deserves several comments.(1)
First, such efforts can be quite successful as in France: From February 2004 to September 2012 there was no increase in tobacco taxes, accordingly cigarette sales remained unchanged and smoking prevalence of the youngest increased during Sarkozy's presidency, an exception amon...
Omid Fotuhi,1 Geoffrey T Fong,1,2 Mark P Zanna,1 Ron Borland,3 Hua- Hie Yong,3 K Michael Cummings4
1. Department of Psychology, University of Waterloo, Waterloo, Ontario, Canada 2. Ontario Institute for Cancer Research, Toronto, Ontario, Canada 3. The Cancer Council Victoria, Melbourne, Victoria, Australia 4. Department of Health Behavior, Roswell Park Cancer Institute, Buffalo, New York, USA
Email for l...
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NOT PEER REVIEWED We wish to comment on the findings of Smerecnik et al.1 with respect to significant advances in genetic testing , which are highly relevant to their review. Unlike the early single genetic marker tests analysed by Smerecnik et al.,1 where subjects are dichotomised to positive or negative results, genetic susceptibility tests for lung cancer are now multivariate risk tests.2 These new risk tests incorpora...
NOT PEER REVIEWED Fotuhi et al concluded in their interesting study of patterns in smokers' cognitive dissonance-reducing beliefs that rationalisations about smoking change systematically with changes in smoking behaviour(1). Moreover, they argue that: i) changes in attitude on quitting are higher for 'functional' beliefs rather than 'risk-minimising' beliefs and ii) if smokers relapse these functional beliefs return to p...
The author seeks to analyze the interference of the International Tobacco Growers Association (ITGA) in the decisions of the 4th Conference of the Parties (COP 4) on the Framework Convention on Tobacco Control (FCTC) regarding Guidelines recommending the prohibition of additives in cigarettes and includes Brazil as one of the countries influenced by this organization. As members of the Brazilian del...
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