Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98
BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7398.1057 (Published 15 May 2003) Cite this as: BMJ 2003;326:1057
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I must admit that, although I regard myself as reasonably
intelligent, I cannot be very clever because most of the statistical stuff
above is beyond me. I mean, I understand that if there are 10 horses in a
race, the probability is 9:1 that one of them will win the race. However,
it is fairly common for 'dead heats' to occur where 2 horses cross the
finishing line so closely together that no difference in position can be
seen. I would suppose that, if one found in reality that the occurrence of
'dead heats' was, say, 1 in 1000, the probability of a 9:1 ratio would
have to be reduced a little. I am not quite sure of my maths, but perhaps
8.999:1 would be correct? But one might go on to ask what is the
probability of a three way dead heat? It must happen occasionally - or
must it? Even if it has never happened in the past, it is still possible,
isn't it? In fact, it is always possible that all 10 horses could be
involved in a 'dead heat'.
As regards Passive Smoking, the statistical problem that arises in my
mind (and I very much stand to be corrected) is this. If we take the
probability of a smoker to be significantly affected by smoking to be
100%, do we see the probability of a passive smoker to be, say, 1%? Or
should that probability be 0.1%? Or even, 0.01%? Or even 0.001%?
Further, in the same way that it is always possible that 10 horses in
a race could possibly cross the finishing line at the same time, is it
right to project a minuscule possible percentage probability by virtue of
some sort of population multiplier to project an actual number of deaths
based on minuscule probabilities?
I must admit that Mr Atherton's sources bother me a little. If it is
true that the sources he quotes are funded by the tobacco industry, then
they may be suspect. But I did not see in Atherton's submission anything
self-contradictory.
In Repace's submission however, I did see a logical inconsistency.
Now, because I am afraid of what I might do to this response if I try
to go back, I will have to try to remember. Did Repace say that the the
incidence of harmful chemicals from tobacco smoke INSIDE enclosed premises
is 2 or 3 orders of magnitudes greater than the incidence OUTSIDE enclosed
premises? Words to that effect.
If we reasonably assume that, in most circumstances, the harmful
incidence (if I may reverse the logic a little) of tobacco smoke OUTSIDE
enclosed premises is unutterably minuscule for all intents and purposes
(bearing in mind the minuscule amount of carcinogenic chemicals in tobacco
smoke anyway), then '2 or 3 orders of magnitude' is still virtually zero.
It follows, therefore, that in Repace's opinion, the incidence of harmful
chemicals resulting from tobacco smoke INSIDE enclosed premises (in
normal, everyday circumstances) is zero, for all intents and purposes
(that is, as regards damage to health).
Repace is a very clever Professor. I am not.
Competing interests:
None declared
Competing interests: No competing interests
At soccer matches in the UK if it has reached an indistinct phase or
a team is losing a group of supporters often start singing/chanting, "its
all gone quiet over there." Or have the usual suspects asked you to stop
digging the hole?
I have 3 more posts to make but I have just come across this gem that
was published in The Lancet in July 2008 on lung cancer in non smokers, I
would be very grateful for your comments.
"Molecular genetics of lung cancer in people who have never smoked."
"Patients with lung cancer who have never smoked are more likely to
have mutations in epidermal growth factor receptor (EGFR) tyrosine kinase
and have better response to its inhibitors than do patients with tobacco-
associated lung cancer. Furthermore, the prevalences of mutations in KRAS
and P53 differ for patients with lung cancer who have never smoked and
those with tobacco-associated lung cancer. Genetic mutations seem to be
more common in patients with tobacco-associated lung cancer than in never
smokers. CURRENT EVIDENCE INDICATES THAT THE TWO TYPES OF LUNG CANCER ARE
BIOLOGICALLY DISTINCT."
http://www.ncbi.nlm.nih.gov/pubmed/18598932?ordinalpos=1&itool=PPMCLayou...
Competing interests:
Director, Freedom2Choose smokers rights organisation. Do I need to bang on about that I am not funded by pharmaceutical or tobacco comapnies?
Competing interests: No competing interests
Professor Repace may I take this opportunity to wish you a Happy New
Year.
I have had a quick review of your documentation (1)and frankly there
appear to be some serious deficiencies. You state reasonable fairly that
the accepted EPA figures are 15mg/m3. (2) Alas that is the annual figure.
So 24 hours a day, 365 days a week that is an acceptable figure, you
however omit to mention is that the 24 hour acceptable level is 35mg/m3,
only recently reduced from 65mg/m3. In your example of the casino, are you
saying customers at a casino sit on their chairs 24 hours a day, 365 days
of the year? How did this omission come about?
Also, expecially if assume that tending to infinite exposure to
PM2.5, tending to zero time gives you the starting off point, a curve that
is heavily, inversely logarithmic would strongly suggest that the figures
for 12, 6, 4 and 1 hour would be well in excess of 90, 300, 600, and 2000
respectively. So there is every probabilty that 15 hours or less in that
casino would be perfectly safe at your quoted 75mg/m3 level.
On the WHO 25mg/m3 can you specify what is the time period, 1 year,
month, 2 seconds?
On "14,000 micrograms (ug) of SHS fine" could you explain to me where
are have said that, it seems words are coming out of my mouth
involuntarily.
Let us consider just one from Gori and Mantel.
Methylchloride 0.88 0.30 1,170
To get to a level of PM2.5 at the threshold level of 35mg for a 24
hour level you would need to be exposed to 116.67 smokers. And let me
remind you, the person would have to be there for 24 hours.
You said that "They (smoker's rights groups) quote pseudo-scientific
arguments." I guess you are just continuing the history of cheap ad
hominens that we have come to expect from pharmaceutical funded, tax free
pressure groups.
After this post I have an extensive Rapid Response which encapsulates
even more evidence of the harmlessness of SHS and points to where the
causes lie, much of it fresh research. All links can be referenced.
In conclusion I think Prof Repace has added nothing to the debate
except the ability to sail very close to the wind on scientific matters
and the .
The best summary of anti smoking movement is by Congressman Rick
Keller "I think we should have labelling on the people who bring these
lawsuits; a T-shirt that says 25% junk science, 50% greed and 25% seeking
publicity."
1. http://www.repace.com/factsheet.html
2. http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_index.html
3. http://velvetgloveironfist.blogspot.com/2009/11/john-banzhaf-ridiculed-
on-tv.html
Competing interests:
Director Freedom2Chose. We do not receive money or expenses from pharmaceutical or tobacco companies.
Competing interests: No competing interests
With the demise of the Tobacco Institute, the internet has become
infested with so-called Smokers' Rights groups. They quote pseudo-scientific arguments advanced by tobacco industry consultants to
convince the gullible that it is OK for smokers to liberate poisonous air
pollution inside buildings.
One of the most common specious arguments is the use of occupational
chemical Threshold Limit Values (TLVs) on carefully selected individual
components of secondhand smoke (SHS) to make the claim, as Mr. Atherton
does, "Not one comes close to any physically attainable danger level."
In the Gori-Mantel 100 cubic meter (m3) room hypothetical example Mr.
Atherton cites, 14,000 micrograms (ug) of SHS fine particles (PM2.5) would
be liberated per cigarette smoked. The WHO standard for PM2.5 is 25 ug/m3
and is the appropriate standard to use. This standard would be violated
by smoking less than 0.002 of a cigarette. Smoking a bit more than 3-1/2
packs of cigarettes would pollute the room to more than 10,000 ug/m3,
which would exceed the TLV for respirable dust. Thus, the example
Atherton cites actually refutes his argument.
More to the point, TLVs are limits intended for use in industrial
hygiene as guidelines, not as indoor air quality standards. Many TLVs
were set primarily for acute, not chronic, toxicity. TLVs do not take into
account synergistic effects with other chemicals in a mixture such as SHS,
and thus are even less valuable when considering complex mixtures in non-
industrial environments.
In fact the ACGIH committee that sets TLVs concedes that they do not
reflect long-term health effects such as cancer or reproductive damage or
illnesses such as fatigue, headaches, or decreased nerve conduction
response. TLVs exclude the sick, the elderly, asthmatics, and other
hypersensitive persons (Lippy and Turner, 1991). Finally, two potent
bladder carcinogens in SHS, 4-aminodiphenyl and 2-naphylamine, have no
permissible level of exposure (NIOSH, 1996).
Moreover, Castleman and Ziem (1988) found serious conflicts of
interest in the setting of Threshold Limit Values (TLVs). Corporate
representatives listed officially as “consultants” were given primary
responsibility for developing TLVs on proprietary chemicals of the
companies that employed them.
Finally, the cigarette-equivalent arguments quoted uncritically by
Atherton and attributed to Gori and Mantel make an unstated and
unjustifiable assumption of a linear dose-response relationship. There is
demonstrable evidence that the dose-response relationship between tobacco
smoke exposure and cardiovascular or lung cancer mortality is highly non-
linear, rising steeply at small doses and saturating at the doses inhaled
by smokers (Repace, 1992; Pope et al., 2009).
The National Academy of Sciences (2009) report - the latest
scientific report on SHS in a long line dating back to 1986 - concluded:
"there is a causal association between smoking bans and decreases in heart
attacks." The time for debate is long gone. Governments contemplating
smoking bans are taking heed.
Castleman BI, and Ziem GE (1988) Corporate Influence on Threshold
Limit ValuesAmerican Journal of Industrial Medicine 13531-559.
Lippy BE, Turner RW (1991). Complex Mixtures in Industrial
Workspaces: Lessons for Indoor Air Quality Evaluations. Environmental
Health Perspectives 95: 81-83.
NIOSH (1996). NIOSH Pocket Guide to Chemical Hazards. U.S. Centers
for Disease Control and Prevention, DHHS Publication No. 94-116.
Pope CA 3rd, Burnett RT, Krewski D, Jerrett M, Shi Y, Calle EE, Thun
MJ (2009). Cardiovascular mortality and exposure to airborne fine
particulate matter and cigarette smoke: shape of the exposure-response
relationship. Circulation 120:924-927.
Repace JL. Is the dose -response curve between tobacco smoke
exposure and lung cancer really linear from active smoking to passive
smoking?" ENVIRONMENT INTERNATIONAL 18: 427-429 (1992).
Competing interests:
The author is a secondhand smoke consultant.
Competing interests: No competing interests
Professor Repace I thank you for your reply.
As we all know the dose makes the poison. Let me ask you what would
you prefer, to be in a garage for a hour with a smoker or a car with its
engine running?
So let us consider the evidence that exists for SHS for PM2.5 and
other poisons and carcinogens.
In 1991 Drs. Gori and Mantel conducted an experiment on some of the
carcinogens in tobacco smoke and assumed the person was in a 100m3 room
sealed and unventilated.
"Estimated number of cigarettes required to reach TLV
levels from sidestream smoke emission of selected chemicals
in a sealed and unventilated 100 m3 enclosure (Gori and Mantel, 1991) (1)
(Please note: 100 m3 are equivalent to a room 22' x 21' x 8' ceiling,
or 3,696 cubic feet)
SSS = Side Stream Smoke (Worse than passive smoke, as it is measured
by holding the electronic sniffer right on top of the burning end of a
cigarette, thus prior to any environmental dilution) TLV = Threshold Legal
Value
The first nimber is SSS Component mg/cigarette
The second is SSS output mg/m3
The third is Cigarettes required
Methylchloride 0.88 0.30 1,170
Acetaldehyde 1.26 180.00 1,430
Nitrogen oxides 2.80 50.00 1,780
Phenol 0.25 19.00 7,600
Benzene 0.24 32.00 13,300
Dimetylamine 0.036 18.00 50,000
Benzo(a)pyrene 0.00009 0.20 222,000
Polonium 0.4pCi 3pCi/l 750,000
Toluene 0.000035 375.00 1,000,000
Not one comes close to any physically attainable danger level.
You mention heart attacks, again since smoking bans have come in
where are the reductions? A meta analysis of heart attacks in America
conducted by the universities of Stanford and Wisconsin "examined a total
of 217,023 heart attack admissions and 2.0 million heart attack deaths in
468 counties in all 50 states over an eight-year period." Its conclusions
were:
"1. "In contrast with smaller regional studies, we find that
workplace bans are not associated with statistically significant short-
term declines in mortality or hospital admissions for myocardial
infarction or other diseases."
2. "An analysis simulating smaller studies using subsamples reveals
that large short-term increases in myocardial infarction incidence
following a workplace ban are as common as the large decreases reported in
the published literature."
Other studies around the world have also confirmed that smoking bans
do not lead to less heart attacks, including the ill fated Scottish study.
Triumphed throughout the world as proof positive, the study was just
another example of the SHS junk science of publication bias. The project
leader Professor Jill Pell conveniently left out January and February
months, of course, which see the highest number of heart attacks. The
author Chris Snowdon under a Freedom Of Information Act request has
obtained the figures. They dropped by 7.2% and the next year by 7.8,
establishing a constant non correlation with smoking bans. "Scotland
enacted its smoking ban (April 2005 to March 2006), there were 16,199
admissions for acute coronary syndrome. In the second year of the smoking
ban (April 2007 to March 2008) there were 16,212 admissions – slightly
more than there had been before the legislation was enacted." (4&5)
The same is true for England, Wales, Australia and New Zealand. (5&6)
Infact heart attacks rose after the implementation of the smoking ban in
Australia.
The Professor Glantz's Helena study has been widely criticised as
publication bias. (7)
Time prevents me giving a broader answer but I will return tomorrow
with some more comments. But suffice as to say there is precious little
evidence of any increased mortality from SHS.
1. http://www.forces.org/articles/art-fc11.htm
2. http://www.nber.org/papers/w14790.pdf
3. http://tobaccoanalysis.blogspot.com/2009/04/new-study-of-national-
heart-attack.html
4. http://www.spiked-online.com/index.php/site/article/7451/
5. http://www.spiked-online.com/index.php/site/article/5988/
6. http://velvetgloveironfist.blogspot.com/2009/10/no-heart-miracle-
in-any-australian.html
7.http://www.bmj.com/cgi/eletters/bmj.38055.715683.55v1#560
Competing interests:
Director: Freedom2Choose a smokers rights group. We are not funded or expensed by pharmaceutical or tobacco companies
Competing interests: No competing interests
Dr. Kabat continues to insist that the world is "hyping health risks"
of secondhand smoke, but his outlying view has never been supported by the
science. Secondhand smoke contains in excess of 170 hazardous substances,
including many regulated in the U.S.: 3 regulated outdoor air pollutants
and 33 hazardous air pollutants regulated under the Clean Air Act, 47
pollutants classified as hazardous wastes whose disposal in solid or
liquid form is regulated by the Resource Conservation and Recovery Act, 67
known human or animal carcinogens, and 3 industrial chemicals regulated
under the Occupational Health and Safety Act (Repace, 2007).
Moreover, secondhand smoke is a major source of fine particle
exposure (PM2.5). Long-term exposure to PM2.5 is associated with
increased cardiovascular mortality, various blood markers of
cardiovascular risk, histopathological markers of subclinical chronic
inflammatory lung injury, and subclinical atherosclerosis. Short-term
exposure is associated with cardiovascular mortality and hospital
admissions, stroke mortality and hospital admissions, myocardial
infarction, pulmonary and systemic inflammation and oxidative stress,
altered cardiac autonomic function, and arterial vasoconstriction. The
cardiopulmonary response to PM2.5 on both daily and long-term time scales
appears to be linear across the range of outdoor air PM concentrations as
measured by local monitoring stations (Pope et al., 2001, 2006, 2009).
Concentrations of secondhand smoke PM2.5 indoors exceed PM2.5 from
outdoor air pollution in developed countries by 1 to 3 orders of
magnitude, as dozens of peer-reviewed exposure science publications
confirm (e.g., Repace, 2006). Therefore, to attempt to prevent control of
exposure to secondhand smoke by referring to epidemiological studies with
no measurement of exposure other than a questionnaire concocted by persons
with little or no experience in air pollution exposure assessment would be
the height of imprudence if taken seriously.
James Repace
Pope CA, Dockery DW (2006). Health Effects of Fine Particulate Air
Pollution: Lines that Connect. Journal of the Air & Waste Management
Association 56:709–742.
Pope C.A., Eatough D.J., Gold D.R., Pang Y., Nielsen K.R., Nath P.,
et al. Acute exposure to environmental tobacco smoke and heart rate
variability. Environ Health Perspect 2001: 109: 711-716.
Pope CA 3rd, Burnett RT, Krewski D, Jerrett M, Shi Y, Calle EE, Thun
MJ (2009). Cardiovascular mortality and exposure to airborne fine
particulate matter and cigarette smoke: shape of the exposure-response
relationship. Circulation 120:924-927.
Repace JL (2004). Respirable Particles and Carcinogens in the Air of
Delaware Hospitality Venues Before and After a Smoking Ban. Journal of
Occupational and Environmental Medicine, 46:887-905.
Competing interests:
The author is a secondhand smoke consultant, and has testified in litigation involving injury from secondhand smoke exposure.
Competing interests: No competing interests
I will do my usual disclaimer that I accept most of the evidence on
active smoking, after all that it is one of the conclusions of the
Enstrom/Kabat paper, or is it another "flaw" in the report Professor
Glantz and Dr. Michael Thun? (1)
Climate-Gate has come at an opportune moment when the Climate
Research Unit (CRU) at the University of East Anglia has been caught with
its hands in the cookie jar, manipulating and cherry picking data for its
own agenda, for funding and influence purposes. We I guess have had this
from 1975 when Sir George Godber the British Chief Medical Officer
(Surgeon General) said at the World Health Organization "...{to} foster an
atmosphere where it was perceived that active smokers would injure those
around them, especially their family and infants or young children who
would be exposed involuntarily to the smoke in the air." (2)
One fact that has recently come to my attention is the November 1994
Congressional Health Sub-Committee report into SHS/ETS. It was headed up
by Henry Waxman an anti smoker and its conclusions were:
"•the statistical evidence does not appear to support a conclusion
that there are substantial health effects of passive smoking;
•it is possible that very few or even no deaths can be attributed to ETS;
•if there are any lung cancer deaths from ETS exposure, they are likely to
be concentrated among those subjected to the highest exposure levels...
primarily among those nonsmokers subjected to significant spousal ETS.
•‘Even when overall risk is considered, it is a very small risk and is not
statistically significant at a conventional 95% level." (3)
This comes on the heels of Judge William Osteen destroying the 1993
EPA report, best summed up here.(4)
“Yes, it's rotten science, but it's in a worthy cause. It will help
us to get rid of cigarettes and become a smoke-free society" so said Alvan
Feinstein, Yale University epidemiologist writing in Toxological Pathology
in 1999 on passive smoking."
I have also recently discovered this paper published in the NEJM on
how much non smokers consume exposed to smokers. (5)
In the paper attached, exposed non smokers, "smoke" the equivalent of
between 0.009 of a cigarette an hour in a packed bar, to 0.001 if at a bus
stop.
The bar worker, working 40 hours a week, takes 111.11 hours or nearly
3 weeks to have one cigarette. The person at the bus stop would assuming
they were sat there 24 hours a day would be there for 41.67 days to
consume one cigarette.
BTW if a room had air conditioning the bar worker would need to be
exposed to an infinite number of smokers, i.e all the smoke is taken out.
Sir Richard Doll who in the 1950s made the link between lung cancer
and active smoking also those who smoked </= 3 cigarettes a day had no
raised risks in lung cancer and heart disease. Therefore passive smoking
cannot cause lung cancer or heart disease. (6) Page 8
In Historian Chris Snowdon's book, Velvet Glove Iron Fist a History
Of Anti Smoking the 2006 Neuberger paper on "Factors For Lung Cancer in
Iowa Women" was included an the paper says "A significant inverse
association was found for those with some college education (OR=0.63, 95%
CI=0.48-0.81) and for those with adult passive smoke exposure at home
(OR=0.37, 95% CI=0.26-0.54). (7)
It actually suggests it is protective, and statistically
significantly too.
I would suggest too that anti smokers look at the "Reference Guide on
Epidemiology" and I quote "The threshold for concluding that an agent was
more likely than not the cause of an individual’s disease is a relative
risk greater than 2.0. Recall that a relative risk of 1.0 means that the
agent has no effect on the incidence of disease. When the relative risk
reaches 2.0, the agent is responsible for an equal number of cases of
disease as all other background causes. Thus, a relative risk of 2.0 (with
certain qualifications noted below) implies a 50% likelihood that an
exposed individual’s disease was caused by the agent." Hence an RR of 1.25
implies that there is an 80% chance is was not ETS in lung cancer for
example that caused the disease. (8, page 384)
As well as the science I particularly object to the way the anti
smoking movement has strived to demonise, denormalise and marginalise
smokers. If we were an identifiable group of people like African-
Americans, Latinos, Jews or gays there would be a justifiable world wide
outcry at the way we have been treated.
Sir Liam Donaldson the current Chief Medical Officer in the UK who
said, "But if we want to go further we have got to reinforce all these
other tobacco measures and denormalise smoking completely." (9)
"I feel free to go anywhere I want. My self-esteem has also improved.
I no longer feel like a "second-class citizen" because I'm a smoker. I
don't get dirty looks from non-smokers anymore." (10)
"Now we know it’s a dirty, smelly habit that only really weak people
indulge in and nobody in the entire state you’re in has a right to do it
in that state. Shame on smokers! Dirty, dirty smokers! Now here they are
getting all this free time to go along with their emphysema and lung
cancer." (11)
On civil liberties dictating legal past times on private property I
find an abomination as a libertarian. I see the bullying tactics of the
anti smoking lobby a disgrace for those scientists who are prepared to
debate the truth. You only see how Seffrin and Thun tried to get Professor
Enstom removed from UCLA on the basis of "Scientific Misconduct." (12)
In conclusion I will be in words of Sir Winston Churchill, fighting
the anti smoking movement on the landing grounds, the beaches, the hills
et al. When you have misled millions on the science, feel democracy and
free speech is an add on to society, and try to bulldoze all dissent in
your way, the world must know.
1.
http://www.actuaries.org.uk/__data/assets/pdf_file/0003/101892/fac_sm200...
2. http://iarnuocon.newsvine.com/_news/2007/10/17/1028570-secondhand-
smoke-mirrors
3. http://www.legacy.library.ucsf.edu/tid/oio50c00/pdf?search="crs
report for congress redhead rowberg"
4. http://www.lcolby.com/colby.htm
5.
http://www.legacy.library.ucsf.edu/tid/hmf16b00/pdf?search="concentrations
of nicotine tobacco smoke in public places
6. http://www.forcesitaly.org/italy/download/gori-mantel.pdf
7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876736/
8.
http://www.fjc.gov/public/pdf.nsf/lookup/sciman06.pdf/$file/sciman06.pdf
9. http://www.guardian.co.uk/society/2007/jun/24/health.smoking
10. http://www.quitsmoking.com/info/articles/whatitmeans.htm
11. http://blogs.bnet.com/stanley-bing/?p=440
12.http://www.scientificintegrityinstitute.org/SeffrinThunACS032907.pdf
Competing interests:
Director: Freedom2Choose a smoker's rights group. We receive no funding or expenses from pharmaceutical or tobacco companies.
Competing interests: No competing interests
Having spent a lot of interesting time studying the scientific litterature on passive smoking - thanks to Legacy - it seems to me as if cause and effect has been turned upside down in regard to the the question of industry affiliation in this research area.
Studies and articles written by authors with affiliation to the tobacco industry do not reach their conclusions as a "result" of their affiliation with the industry, as the Bero & Barnes paper suggests (1). This suggestion, which is a widespread belief in the anti-tobacco establishment, probably rests on small knowledge about how private, free-enterprise businesses operate.
In fact the truth seems to lie in the reverse direction: It is not possible for these authors to have a scientific paper funded by government bodies or health agencies, since a serious anti-tobacco dogma exists in these offices. Thus, authors with differing opinions only have the tobacco industry to turn to, if they want their papers funded.
This explains the outcome of the Bero & Barnes paper quite nicely. The mechanism is explained in depth in papers by several authors, among them psychology professor Bernhardt Liebermann (2), professor of economics, Michael L. Marlow (3), and Enstrom & Kabat themselves (4, 5).
It would be interesting if someone did the exact opposite study, than that of Bero & Barnes: - A review of all the passive smoking studies, where the reviewers were blinded to the introductions and the conclusions of the study papers - leaving the reviewers only with the study methods and the results - the tables.
Such a review would finally make clear - no matter what funding source - that more than 80% of the passive smoking studies do not show any significant risk. And that almost all of the studies show no dose-respond trends.
Citing a great, late epidemiologist, Dr. Alvan Feinstein, who died in 2001: "Passive smoking is a rotten science ..." (6)
Disclaimer: I run a private business not related to tobacco. My private blog is tobacco related, though: Klaus K blog
----------
1. Deborah Barnes & Lisa Bero: Why Review Articles on the Health Effects of Passive Smoking Reach Different Conclusions JAMA, 1998.
2. Bernhardt Liebermann: The social construction of a health menace. A cautionary tale. 1993
3. Michael L. Marlow: Honestly, Who Else Would Fund Such Research? Econ Journal Watch, 2008
5. Geoffrey C. Kabat: Hyping Health Risks, 2008
6. Alvan Feinstein: Critique - Justice, Science, and the Bad Guys. Toxicologic Pathology, 1992
Competing interests:
None declared
Competing interests: No competing interests
I've seen only one comment reference Diesel Exhaust. Admittedly, one
breathes deeper while walking or exercising out of doors and exposed to
random amounts of diesel exhaust. Diesel exhaust is just as carcinogenic as
tobacco smoke, primary or secondary.
Competing interests:
None declared
Competing interests: No competing interests
More scepticism for your review.
"Environmental tobacco smoke revisited: the reliability of the data
used for risk assessment."
Nilsson R.
Department of Genetic and Cellular Toxicology, Stockholm University,
Sweden. robertn@kemi.se
Several epidemiological studies have found a weak, but consistent
association between lung cancer in nonsmokers and exposure to
environmental tobacco smoke (ETS). In addition, a purported link between
such exposure and coronary heart disease (CHD) has been of major concern.
Although it is biologically plausible that ETS has a contributory role in
the induction of lung cancer in nonsmoking individuals, dose-response
extrapolation-supported by the more solid database for active smokers-
gives an additional risk for lung cancer risk that is more than one order
of magnitude lower than that indicated by major positive epidemiological
studies. The discrepancy between available epidemiological data and
dosimetric estimates seems, to a major part, to reflect certain systematic
biases in the former that are difficult to control by statistical analysis
when dealing with risks of such low magnitudes. These include, most
importantly, misclassification of smoking status, followed by
inappropriate selection of controls, as well as certain confounding
factors mainly related to lifestyle, and possibly also hereditary
disposition.
A significant part of an association between lung cancer and exposure
to ETS would disappear, if, on the average, 1 patient out of 20 nonsmoking
cases had failed to tell the interviewer that he had, in fact, recently
stopped smoking. In the large International Agency for Research on Cancer
(IARC) multicenter study even lower misclassification rates would abolish
the weak, statistically nonsignificant associations that were found. In
the former study an apparent significant protective effect from exposure
to ETS in childhood with respect to lung cancer later in life was
reported, a most surprising finding. The fact that the mutation spectrum
of the p53 tumor suppressor gene in lung tumors of ETS-exposed nonsmokers
generally differs from that found in tumors of active smokers lends
additional support to the notion that the majority of tumors found in ETS-
exposed nonsmokers have nothing to do with tobacco smoke. The one-sided
preoccupation with ETS as a causative factor of lung cancer in nonsmokers
may seriously hinder the elucidation of the multifactorial etiology of
these tumors. Due to the high prevalence of cardiovascular disease in the
population, even a modest causal association with ETS would, if valid,
constitute a serious public health problem. By pooling data from 20
published studies on ETS and heart disease, some of which reported higher
risks than is known to be caused by active smoking, a statistically
significant association with spousal smoking is obtained. However, in most
of these studies, many of the most common confounding risk factors were
ignored and there appears to be insufficient evidence to support an
association between exposure to ETS and CHD. Further, it seems highly
improbable that exposure to a concentration of tobacco smoke at a level
that is generally much less than 1% of that inhaled by a smoker could
result in an excess risk for CHD that-as has been claimed-is some 30% to
50% of that found in active smokers.
There are certainly valid reasons to limit exposure to ETS as well as
to other air pollutants in places such as offices and homes in order to
improve indoor air quality. This goal can be achieved, however, without
the introduction of an extremist legislation based on a negligible risk of
lung cancer as well as an unsupported and highly hypothetical risk for
CHD.
PMID: 11726024 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/11726024
Competing interests:
David Atherton. Director Freedom2Choose.info
See previous posts.
Competing interests: No competing interests