I’ve been meaning for some time to post up a fairly comprehensive list of secondhand smoking studies. H/T to Michael McFadden for a link to one such list at NYCClash. I’ve adapted the table below from that link. The Relative Risk (RR) is the relative probability of an SHS-exposed subject contracting lung cancer compared to an unexposed subject (RR=1). From the link:
It is well established in the field of epidemiology that a study producing a relative risk greater than 3.0 shows a strong association. A relative risk between 2.0 and 3.0 shows a weak association. A relative risk between 1.0 and 2.0 shows a very weak association and an even 1.0 means no association. Anything under 1.0 is considered to show a positive, rather than a negative, effect. Imagine that! To further underscore this standard, Marcia Angell of the prestigious New England Journal of Medicine has said, “As a general rule of thumb we are looking for a relative risk of 3 or more” before accepting a paper for publication. Robert Temple of the Food and Drug Administration said, “My basic rule is if the relative risk isn’t at least 3 or 4, forget it.” Even further, The National Cancer Institute explains, “Relative risks of less than 2 are considered small and are usually difficult to interpret. Such increases may be due to chance, statistical bias, or the effect of confounding factors [other possibilities] that are sometimes not evident.”
The Confidence Interval (CI) is an estimate of the reliability of the Relative Risk estimate, gives an range of values within which it is likely to be found. If the Confidence Interval includes a Relative Risk of 1.0 (no risk), then the result is deemed statistically insignificant. As can be seen from the table below, most of the Relative Risks are small, and most of the 110 or so studies are statistically insignificant, but I count 14 which show significant increased risk (red highlighted in yellow), and 2 which show significant decreased risk (blue highlighted in green).
| Name | Yr | Local | Type | Sex | RR | CI |
| Garfinkel 1 (+) | 81 | US | Spouse | F | 1.18 | .90-1.54 |
| Chan + | 82 | HK | Spouse | F | 0.80 | .43-1.30 |
| Correa(+!) | 83 | US | Spouse | F | 2.07 | .81-5.25 |
| Correa(+!) | 83 | US | Spouse | M | 1.97 | .38-10.32 |
| Trichopouls(+!) | 83 | Grk | Spouse | F | 2.08 | 1.20-3.59 |
| Buffler | 84 | US | Spouse | F | 0.80 | .34-1.90 |
| Buffler | 84 | US | Spouse | M | 0.51 | .14-1.79 |
| Hirayama (+)! | 84 | Jap | Spouse | F | 1.60 | 1.00-2.40 |
| Hirayama + | 84 | Jap | Spouse | M | 2.24 | 1.19-4.22 |
| Kabat 1(+) | 84 | US | Spouse | F | 0.79 | .25-2.45 |
| Kabat 1(+) | 84 | US | Spouse | M | NS | 0.20-5.07 |
| Garfinkel 2(+) | 85 | US | Spouse | F | 1.23 | 0.81-1.87 |
| Lam W | 85 | HK | Spouse | F | 2.01 | 1.09-3.72 |
| Wu(+!) | 85 | US | Spouse | F | 1.40 | 0.40-4.20 |
| Akiba(+) | 86 | Jap | Spouse | F | 1.50 | 0.90-2.80 |
| Akiba(+) | 86 | Jap | Spouse | M | 1.80 | 0.40-7.00 |
| Lee(+) | 86 | UK | Spouse | F | NS | 0.37-2.71 |
| Lee(+) | 86 | UK | Spouse | M | 1.30 | 0.38-4.39 |
| Bownson 1 | 87 | US | Spouse | F | 1.68 | 0.39-6.90 |
| Gao | 87 | Chin | Spouse | F | 1.19 | 0.82-1.73 |
| Humble | 87 | US | Spouse | F | 2.20 | 0.80-6.60 |
| Humble | 87 | US | Spouse | M | 4.82 | 0.63-36.56 |
| Koo | 87 | HK | Spouse | F | 1.64 | 0.87-3.09 |
| Lam T | 87 | HK | Spouse | F | 1.65 | 1.16-2.35 |
| Pershagen(+) | 87 | Swed | Spouse | F | 1.20 | 0.70-2.10 |
| Butler | 88 | US | Spouse | F | 2.20 | 0.48-8.56 |
| Geng | 88 | Chin | Spouse | F | 2.16 | 1.08-4.29 |
| Inoue | 88 | Jap | Spouse | F | 2.25 | 0.80-8.80 |
| Shimizu | 88 | Jap | Spouse | F | 1.08 | 0.64-1.82 |
| Choi | 89 | Kor | Spouse | F | 1.63 | 0.92-2.87 |
| Choi | 89 | Kor | Spouse | M | 2.73 | 0.49-15.21 |
| Hole | 89 | Scot | Spouse | F | 1.89 | 0.22-16.12 |
| Hole | 89 | Scot | Spouse | M | 3.52 | 0.32-38.65 |
| Svensson | 89 | Swed | Spouse | F | 1.26 | 0.57-2.81 |
| Janerick | 90 | US | Spouse | M&F | 0.93 | 0.55-1.57 |
| Kalandidi | 90 | Grk | Spouse | F | 2.11 | 1.09-4.08 |
| Sobue | 90 | Jap | Spouse | F | 1.13 | 0.78-1.63 |
| Wu-Williams | 90 | Chin | Spouse | F | 0.70 | 0.60-0.90 |
| Liu Z | 91 | Chin | Spouse | F | 0.77 | 0.30-1.96 |
| Brownson 2 ^ | 92 | US | Spouse | F | NS | 0.80-1.20 |
| Stockwell ^ | 92 | US | Spouse | F | 1.60 | 0.80-3.00 |
| Liu Q ^ | 93 | Chin | Spouse | F | 1.66 | 0.73-3.78 |
| Wu | 93 | Chin | Spouse | F | 1.09 | 0.64-1.85 |
| Fontham ^ | 94 | US | Spouse | F | 1.29 | 1.04-1.60 |
| Layard | 94 | US | Spouse | F | 0.58 | 0.30-1.13 |
| Layard | 94 | US | Spouse | M | 1.47 | 0.55-3.94 |
| Zaridze | 94 | Russia | Spouse | F | 1.66 | 1.12-2.46 |
| Kabat 2 ^ | 95 | US | Spouse | F | 1.08 | 0.60-1.94 |
| Kabat 2 ^ | 95 | US | Spouse | M | 1.60 | 0.67-3.82 |
| Schwartz ^ | 96 | US | Spouse | F | 1.10 | 0.72-1.68 |
| Schwartz ^ | 96 | US | Spouse | M | 1.10 | 0.60-2.03 |
| Sun | 96 | Chin | Spouse | F | 1.16 | 0.80-1.69 |
| Want S-Y | 96 | Chin | Spouse | F | 2.53 | 1.26-5.10 |
| Wang T-J | 96 | Chin | Spouse | F | 1.11 | 0.67-1.84 |
| Cardenas ^ | 97 | US | Spouse | F | 1.20 | 0.80-1.60 |
| Cardenas ^ | 97 | US | Spouse | M | 1.10 | 0.60-1.80 |
| Jockel-BIPS | 97 | Ger | Spouse | F | 1.58 | 0.74-3.38 |
| Jockel-BIPS | 97 | Ger | Spouse | M | 1.58 | 0.52-4.81 |
| Jockel-GSF | 97 | Ger | Spouse | F | 0.93 | 0.66-1.31 |
| Jockel-GSF | 97 | Ger | Spouse | M | 0.93 | 0.52-1.67 |
| Ko ^ | 97 | Tai | Spouse | F | 1.30 | 0.70-2.50 |
| Nyberg | 97 | Swed | Spouse | F | 1.20 | 0.74-1.94 |
| Nyberg | 97 | Swed | Spouse | M | 1.20 | 0.57-2.55 |
| Boffetta (WHO) | 98 | Eur | Spouse | M&F | 1.16 | 0.93-1.44 |
| Kabat 1 ^ | 84 | US | Work | F | 0.70 | 0.30-1.50 |
| Kabat 1 ^ | 84 | US | Work | M | 3.30 | 1.10-10.40 |
| Garfinkel 2 ^ | 85 | US | Work | F | 0.93 | 0.70-1.20 |
| Wu ^ | 85 | US | Work | F | 1.30 | 0.50-3.30 |
| Lee ^ | 86 | UK | Work | F | 0.63 | 0.17-2.33 |
| Lee ^ | 86 | UK | Work | M | 1.61 | 0.39-6.60 |
| Koo ^ | 87 | HK | Work | F | 0.91 | 0.15-5.37 |
| Shimizu ^ | 88 | Jap | Work | F | 1.18 | 0.70-2.01 |
| Janerich ^ | 90 | US | Work | F&M | 0.91 | 0.80-1.04 |
| Kalandidi ^! | 90 | Grk | Work | F | 1.39 | 0.80-2.50 |
| Wu-Williams ^ | 90 | Chin | Work | F | 1.20 | 0.90-1.60 |
| Brownson 2 | 92 | US | Work | F | 0.79 | 0.61-1.03 |
| Stockwell ^ | 92 | US | Work | F | NS | NS |
| Fontham ^ | 94 | US | Work | F | 1.39 | 1.11-1.74 |
| Zaridze | 94 | Russia | Work | F | 1.23 | 0.74-2.06 |
| Kabat 2 ^ | 95 | US | Work | F | 1.15 | 0.62-2.13 |
| Kabat 2 ^ | 95 | US | Work | M | 1.02 | 0.50-2.09 |
| Schwartz ^ | 96 | US | Work | F&M | 1.50 | 1.00-2.20 |
| Sun | 96 | Chin | Work | F | 1.38 | 0.94-2.04 |
| Wang T-J | 96 | Chin | Work | F | 0.89 | 0.46-1.73 |
| Jockel-BIPS | 97 | Ger | Work | F&M | 2.37 | 1.02-5.48 |
| Jockel-GSF | 97 | Ger | Work | F&M | 1.51 | 0.95-2.40 |
| Ko ^ | 97 | Tai | Work | F | 1.10 | 0.40-3.00 |
| Nyberg | 97 | Swed | Work | F&M | 1.60 | 0.90-2.90 |
| Boffetta (WHO) | 98 | Eur | Work | F&M | 1.17 | 0.94-1.45 |
| Correa + | 83 | US | Childhd | F | NS | NS |
| Kabat & Wyn ^ | 84 | US | Childhd | F | 0.92 | 0.40-2.08 |
| Kabat & Wyn ^ | 84 | US | Childhd | M | 1.26 | 0.33-4.83 |
| Garfinkel 2 + | 85 | US | Childhd | F | 0.91 | 0.74-1.12 |
| Wu (+) | 85 | US | Childhd | F | 0.60 | 0.20-1.70 |
| Akiba + | 86 | Jap | Childhd | F&M | NS | NS |
| Gao ^ | 87 | Chin | Childhd | F | 1.10 | 0.70-1.70 |
| Koo ^! | 87 | HK | Childhd | F | 1.73 | 0.60-6.40 |
| Pershagen ^ | 87 | Swed | Childhd | F | NS | 0.40-2.30 |
| Svensson ^ | 89 | Swed | Childhd | F | 3.30 | 0.50-18.80 |
| Janerich ^ | 90 | US | Childhd | F&M | 1.09 | 0.68-1.73 |
| Sobue (^) | 90 | Jap | Childhd | F | 1.28 | 0.71-2.31 |
| Wu-Will(^)! | 90 | Chin | Childhd | F | NS | NS |
| Brownson 2 ^ | 92 | US | Childhd | F | 0.80 | 0.60-1.10 |
| Stockwell ^ | 92 | US | Childhd | F | 1.10 | 0.50-2.60 |
| Fontham ^ | 94 | US | Childhd | F | 0.89 | 0.72-1.10 |
| Zaridze | 94 | Russia | Childhd | F | 0.98 | 0.66-1.45 |
| Kabat 2 ^ | 95 | US | Childhd | M | 0.90 | 0.43-1.89 |
| Kabat 2 ^ | 95 | US | Childhd | F | 1.55 | 0.95-2.79 |
| Sun | 96 | Chin | Childhd | F | 2.29 | 1.56-3.37 |
| Wang T-J | 96 | Chin | Childhd | F | 0.91 | 0.56-1.48 |
| Jockel-BIPS | 97 | Ger | Childhd | F&M | 1.05 | 0.50-2.22 |
| Jockel-GSF | 97 | Ger | Childhd | F&M | 0.95 | 0.64-1.40 |
| Ko ^ | 97 | Tai | Childhd | F | 0.80 | 0.40-1.60 |
| Boffetta (WHO) | 98 | Eur | Childhd | F&M | 0.78 | 0.64-0.96 |
| Garfinkel 2 | 85 | US | Social | F | 1.42 | 0.75-2.70 |
| Lee | 86 | UK | Social | F | 0.61 | 0.29-1.28 |
| Lee | 86 | UK | Social | M | 1.55 | 0.40-6.02 |
| Janerich | 90 | US | Social | F&M | 0.59 | 0.43-0.81 |
| Stockwell | 92 | US | Social | F | NS | NS |
| Fontham | 94 | US | Social | F | 1.50 | 1.19-1.89 |
| Kabat 2 (^) | 95 | US | Social | F | 1.22 | 0.69-2.15 |
| Kabat 2 (^) | 95 | US | Social | M | 1.39 | 0.67-2.86 |
| Boffetta (WHO) | 98 | Eur | Social | M&F | 1.03 | 0.82-1.29 |
Column 1 codes:
^ = Figures from Final Report CA EPA 1997
! = Difference from Forces figures (usually slight, and not showing any consistent bias)
+ = 1986 Surgeon General’s Report
( ) = derived/approximate…
(WHO) = taken directly from WHO study
Column 6 codes:
NS = not significant
See also http://monographs.iarc.fr/ENG/Monographs/vol83/mono83-7.pdf for lists of studies.
Frank Davis 
I once analyzed those studies and categorized them in being statistically significant or prooving a negative or positive effect.
Although in Dutch, it must be clear what it shows. Especially the graph in the beginning is interesting.
Note that the above list only goes up to the year 1998. While I did not actually read and evaluate each of the studies listed, the coding indicates the sources the figures were taken from with unmarked studies being purely from the FORCES cited figures. Obviously some folks might feel that a source such as FORCES should not be taken at face value, but as can be seen in the figures coded with Cal EPA and SGR cross checking most of the FORCES figures cross-checked perfectly with those sources and I believe that in the cases of the few that didn’t ( eight of them, marked with exclamation points) the differences were usually quite minor. If I remember correctly I generally used the figures from the more “official” source in such conflicts (checking original publications where possible) or possibly occasionally averaged the differences.
I believe FORCES has a similar and more modern list done with a more intensive color-coding of the various results. I had no hand in that list and can’t vouch for it here, but I believe it was done by Gian and have always respected his dedication to accuracy in such things.
– MJM
It looks as if the latest studies are from 1998, is that correct? Not that I think they’d ever come up with any sort of conclusive evidence that second hand smoke was a risk to anyone, I just wonder if they even bother any more, or if the ‘debate is over’ based upon this field of evidence.
I think, in an absurd way, that the claims they make about smoking, be it active or passive, causing anything is humorous. A flame causes tinder (or tobacco) to ignite with some certainty. Smoking is no guarantee of any particular malady, regardless of some wanted statistical aberration or correlation.
Spiraling off topic, but maybe relevant given your previous posts, it seems as if good people such as you are trying to disprove a negative, which in the realm of flaccid debate the antis frame these days, is exactly what they want, like a cat chasing its tail. And maybe that’s been a part of the set up all along, removing things such as logic and reasoning years ago from classrooms, no one sees the impossibility of it. It’s like arguing with an insane person, where reality fluxes to fit whatever dream/fantasy state they’re in at the moment. Except in this case, it’s infected a majority of society as well.
Don’t know that I have an answer, but I deeply admire all you’re doing to fight it.
Post 1998, we’ve got Enstrom & Kabat:
Focusing on 35,561 never-smoking Californians married to smokers, who were followed by the Cancer Society for 39 years (1959 to 1998), the tabular results not only–and absolutely — showed no lung cancer risk whatsoever but actually showed a slightly lower risk than expected among the general never-smoker population.
These results held for both men (0.75 @ 95% confidence) and women (0.99 @ 95%), held both before and after the results were mathematically adjusted for seven relevant confounders, and further, showed no dose response trend (the risks did not grow with the amount of exposure.)
-“Environmental Tobacco Smoke And Tobacco-Related Mortality In A Prospective Study Of Californians, 1960-98,” Enstrom & Kabat, BMJ 5/17/03
The antis know that when it comes to ETS / Lung Cancer their argument is weak .Instead they focus on the combination of everything to justify their results and the consequent ‘public health interventions’ (i.e that ETS causes heart diseases,respiratory illnesses and Lung Cancer ).Even the official SCOTH Report of 2004 comes to an RR of just 1.24 !
We can raise two questions in here:
1) This level of ‘risk’ justifies a smoking ban? Or was it social engineering?
2) Did they act in a similar manner when it came to another risk ? Or is there a bias against smoking and anything related to it?
Also of interest is the number of people that were surveyed. Many of these studies were of a relatively small number of people and, as such, have limuited value or validity.
A large number of people, tho, does not insure validity if those people do not represent the public as a whole.
The American Cancer Society’s ACS-II was a study of over 1 million people; but, they were mostly white, middleclass, educated, and economically better off than the average group of people.
Anyway, most studies only look at the comparative risk of getting a disease and an equally important question is the comparative risk for not getting the disaease in question.
For instance, it is never mentioned and is a figure that we should shout out, current smokers have 99.95% of never-smokers chances of not getting lung cancer.
A never-smoker exposed to SHS/ETS has a 1/40,000 chance of lung cancer and 99.998% of a non-exposed never-smokers chance of not getting lung cancer.
Gary K.
“The National Cancer Institute explains, “Relative risks of less than 2 are considered small and are usually difficult to interpret.”
In case someone is wondering why.
‘1’ is caused by other things and ‘2’ is 1 + 1; or, a 50% chance of causation by ‘1’ and a 50% chance of causation by the second ‘1’.
Thus, a RR=2 implies only a 50% chance of causation by whatever is being considered.
A RR=1.25(SHS/ETS and lung cancer/heart attack) means there is an 80% chance/probability of causation by something other than SHS/ETS.
There a five .25’s in 1.25 and SHS/ETS is only 1 out of 5.
By the same reasoning, there has to be a RR=.49 or less for there to a chance of a ‘protective’ effect.
Antis claim that a 25% increase, in many studies, means more than just an individual 20% possibility of causation. They claim that if there are 1,000 such people, there will be 200 with 100% probability of causation.
But; if you flip a coin 5 times and come up heads all 5 times, you do not have a 100% chance of a tails coming up on your 6th flip. The chances are still 50-50!!
This has been poorly stated; but, a RR=1.25 means nothing more than that whatever causes the .25 has only a 20% chance of causation and an 80% chance/probability of non-causation. A RR=2 is like flipping a coin as to causation.
It’s interesting that most of the studies don’t show a significant effect. Most scientist would concede that there at most a mild effect of second-hand smoke on people, but from a political standpoint and a public health standpoint, even a mild effect is something that can be lessened with regulation.
Outside of the possible direct effects on kids and adults exposed to second-hand smoke, there are some studies that suggest that more smokers quit and less kids pick up smoking when bans are enacted. Only time will tell if smoking bans improve the health of the population as a whole in terms of smoking rates and smoking-related disease prevalence.
Except that smoking rates were on the way down, year on year, pre ban and cures and/or containments for illness/diseases had been found to increase life expectancy for the past 100 years, somewhat confusing any projected claims for the ‘success’ of any ban.
We will never know but it would be claimed.
“smoking rates were on the way down, year on year”
Rates are down; but, only because there are the same number of current smokers to compare to a rising total population.
In the USA, in 1990, there were about 45 million current smokers and about 44 million ex-smokers for a total of 89 million ever-smokers.
As of late, there are about 46 million current smokers and about 48 million ex-smokers for a total of 94 million ever-smokers.
This brings us to a curious question about ASH’s claim that half of the smokers will die from a disease caused by their having smoked.
The USA CDC tells us that there are about 400,000 smokers deaths per year due to diseases caused by smoking.
Half of the 94 million is 47 million and at 400,000 deaths per year, it will take about 117 years for that half of the smokers to die.
Since there are no smoking related deaths below the age of 35, the average smoker must live to be about 152 years of age.
This fact should be pointed out to ASH’s Debrah A. the next time she makes such a stupid claim. ;)
from a political standpoint and a public health standpoint, even a mild effect is something that can be lessened with regulation.
As if health was the only thing that mattered. Which, of course, it is not. There are other things, such as friendship and community and freedom, which matter far more. All of these, of course, are lessened with regulation.
Considering that most (if not all) of these studies were “policy-based, evidence making” research, the results are even less convincing.
Thanks to Wiel for the extra information. It seems the list is a little out of date. The Enstrom and Kabat study of 2003 is one obvious missing study.
Walt
“Post 1998, we’ve got Enstrom & Kabat:”
Warning: the health police can seriously addle your brain
“The demise of a supposed major risk to public health might be expected to prompt celebration among medical experts and campaigners. Instead, they scrambled to condemn the study, its authors, its conclusions, and the journal that published them. The reaction came as no surprise to those who have tried to uncover the facts about passive smoking. More than any other health debate, the question of whether smokers kill others as well as themselves is engulfed in a smog of political correctness and dubious science.
Researchers who dissent from the party line face character assassination and the termination of grants. Those who report their findings are vilified as lackeys of the tobacco industry, and accused of professional misconduct (in 1998, campaigners tried to have this newspaper censured by the Press Complaints Commission for our reports on passive smoking. They failed.).
The furore over last week’s negative findings, reported in the respected British Medical Journal, has its origins in research published in the same journal in October 1997. ”
After reviewing the evidence from dozens of studies, researchers at the Wolfson Institute of Preventive Medicine, London, concluded that being married to a smoker increases the “risk” of lung cancer and heart disease by around 25 per cent.
The results were seized on by health campaigners as final proof of what they had known all along: that smokers are not just killing themselves – they are also killing innocent bystanders, and must be stopped.
The same issue of the BMJ carried an editorial by Dr Ronald Davis, the editor of the journal Tobacco Control, declaring: “Health advocates should pursue all strategies that would help accomplish that goal, including education, legislation, regulation and litigation.”
http://www.telegraph.co.uk/science/science-news/4769409/Warning-the-health-police-can-seriously-addle-your-brain.html
But it was already too late.
Anti-tobacco had got what it wanted.
January 1999
WHO LAUNCHES PARTNERSHIP WITH THE PHARMACEUTICAL INDUSTRY TO HELP SMOKERS QUIT
“The strength of the Partnership Project lies in the fact that it has brought together three major pharmaceutical companies, Glaxo Wellcome, Novartis Consumer Health and Pharmacia & Upjohn, all manufacturers of treatment products for tobacco dependence, to support a common goal that will have a significant impact on public health. The Project provides a model which can provide a basis for future partnerships with the private sector in other important health areas.”
http://www.who.int/inf-pr-1999/en/pr99-04.html
Sunday 8 March 1998
Passive smoking doesn’t cause cancer – official
“THE world’s leading health organisation has withheld from publication a study which shows that not only might there be no link between passive smoking and lung cancer but that it could even have a protective effect”
“Despite repeated approaches, nobody at the WHO headquarters in Geneva would comment on the findings last week. At its International Agency for Research on Cancer in Lyon, France, which coordinated the study, a spokesman would say only that the full report had been submitted to a science journal and no publication date had been set.
The findings are certain to be an embarrassment to the WHO, which has spent years and vast sums on anti-smoking and anti-tobacco campaigns.”
http://web.archive.org/web/20021128202555/http://www.telegraph.co.uk/htmlContent.jhtml?html=/archive/1998/03/08/wtob08.html
The WHO responded with
PASSIVE SMOKING DOES CAUSE LUNG CANCER, DO NOT LET THEM FOOL YOU
http://www.who.int/inf-pr-1998/en/pr98-29.html
Less than a year before they announced their partnership with the drugs companies.
“The WHO responded with
PASSIVE SMOKING DOES CAUSE LUNG CANCER, DO NOT LET THEM FOOL YOU”
The only problem they have is that they can not tell who it is that has the lung cancer ’caused’ by SHS/ETS.
The 1993 EPA Report stated that never-smokers have a lung cancer death rate of 1/10,000 and we know they claim a 25% increased risk or a 1.25/10,000 rate for those exposed to SHS/ETS.
That gives a rate of 5/40,000 with 1 caused by SHS/ETS and the other 4 by something else.
There is just no way to tell which of the 5 is the 1 and they have an 80% probability of being wrong if they pick one.
Sooo, they don’t, they just say that they KNOW 1 of the 5 is caused by SHS/ETS without proof that 1 actually exists.
This is rather like believing in the existence of Fairies, or Poseidon, or Thor.
That is rather like believing that air that is smoke-free is clean,pure air.
But, the monies from the drug companies and govt’s is real enough for them.
“That gives a rate of 5/40,000 with 1 caused by SHS/ETS and the other 4 by something else.”
Never-smokers not exposed to SHS/ETS have a 39,996/40,000 chance of not getting lung cancer.
Never-smokers exposed to SHS/ETS have 39,995/40,000 chance of not getting lung cancer and that is 99.998% of the non-exposed never-smokers chances.
136 million never-smokers divided by 40,000 gives us the 3,400 lung cancer deaths claimed to be caused by SHS/ETS exposure.
Passive smokers inhale six cigarettes a year – Telegraph
Sunday 16 August 1998
“PASSIVE smokers inhale the equivalent of just six cigarettes a year from other people’s smoke, according to the largest ever study of actual exposure levels of non-smokers.
The figure, which undermines previous warnings about the dangers of passive smoking, is a thousand times lower than that faced by direct smokers, and so tiny that it could not be measured statistically. Results from personal air monitors carried by more that 1,000 people in cities across Europe reveal that even the most highly-exposed passive smoker inhales the equivalent of 0.02 of a cigarette a day – 10 times lower than Government-backed estimates.
The findings, published by an internationally respected UK-based team of air monitoring experts, are the biggest blow yet to the credibility of the Government’s insistence that passive smoking causes fatal diseases.”
“A team led by Dr Keith Phillips of Covance Laboratories, an independent consultancy in Harrogate, has found that even passive smokers who live and work with smokers are typically exposed to just 0.1 per cent of the dangerous components of cigarette smoke inhaled by smokers”
http://www.forces.org/evidence/files/passmok2.htm
the Covance laboratories study into non-smokers’ exposure to ETS
Dear friends,
This is in response to Mike Daube and Fenton Howell’s request for background on the Covance laboratories study into non-smokers’ exposure to ETS. This was reported in the Sunday Telegraph of 16 August 1998 and picked up around the world. The study used personal air quality monitors mounted on volunteers to measure their exposure to ETS as they went about their normal business. The newspaper report suggests that exposure is one thousandth of that of a smoker – equivalent to 6 cigarettes per year – 10 times lower than Government backed estimates.”
“These are the fingerprints of tobacco industry propoganda.”
Staying open-minded
Finally, we should not have closed minds and assume that all that challenges the consensus is wrong or misguided. It just may be that cotinine measurements are wrong at low ETS exposures. It may be that exposure is declining. Let’s hope it is! It is just that a serious challenge to the consensus should be mounted using the established scientific approach, not through the tell-tale approach of tobacco industry PR.”
Clive Bates
http://www.globalink.org/tobacco/docs/ets/Covence.shtml
“10 times lower than Government-backed estimates.”
Tony Blair’s 10 Years Of Tobacco Control
1997 – 2007
http://www.medicalnewstoday.com/releases/75557.php
So whose estimates were the new government backing and for how long had they backed them?
Labour Government’s tobacco spin spins them off track
The Lancet
“Smoking is the greatest single cause of preventable illness and premature death in the UK. We will therefore ban tobacco advertising”—Labour Party manifesto, 1997
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2897%2921046-9/fulltext
And why was such reassuring new evidence not a great relief to the government?
If the correct method of protecting public health had been used, there would never have been a ban in the UK, as the HSE could not produce epidemiological evidence that second hand smoke was harmful (see HSE OC255/15 the OHSA in America came to a similar conclusion) as this ban was brought in under the guise of protecting employees from SHS, under normal circumstances the HSE would have been given the power to require that ventilation was up to an adequate standards as with any other related perceived danger in the air such as welding smoke etc.
The HSE were called twice to speak pre-ban in Hansard on both occasions they stated that as this law was not being brought in by the HSE, they could not comment.
The reason the ban was brought in under the Health act 2006 was that no evidence was needed that SHS is significantly harmful, how our MP’s managed to be conned by the anti-smoking establishment, shows that the MP’s were either ignorant of the truth or were willing to go along with this ban for social engineering purposes, (I believe they were ignorant) as the then health Minister Patricia Hewitt and others were engineering a full ban, as she had stated in Hansard as far back as 2002, that a partial ban was not the aim, a full ban was the aim of the legislation.
This legislation was brought about by people who were not interested in the truth, and proceeded to lie about the benefits of a ban, Patricia Hewitt and Caroline Flint being the main culprits and we cannot forget Liam Donaldson input.
Frank,
One minor problem with your list (and many others that I have seen) is that some of the studies you list actually report an ‘Odds Ratio’ rather than a ‘Relative Risk’. I haven’t worked out how many do but one example is the Fontham study of 1994. The odds ratio will always be a little higher than the relative risk figure.
I can’t work out a precise figure for the Fontham study because I don’t have raw data and adjustment info but it is approx RR 1.19 as opposed the reported OR of 1.29. It makes no difference in terms of statistical significance though.
On a far more important note, I can generate studies like these SHS ones and then produce meta-analyses with high levels of significance from purely random numbers where there is no correlation whatsoever. And I can do it every time just using a little judicious publication bias. I have knocked up a programme to demonstrate this and am toying with buying some web space so people can play around with it themselves.
Of course, in the real world, there are far more biases available to assist researchers in their crusade. e.g. misclassification bias.
Tony
“The reason the ban was brought in under the Health act 2006 was that no evidence was needed that SHS is significantly harmful,”
Because they had already signed in 2004 this statement of belief on behalf of the country that the government –
“Recognize that scientific evidence has unequivocally established that exposure to tobacco smoke causes death, disease and disability, and that there is a time lag between exposure to smoking and the other uses of tobacco products and the onset of tobacco-related diseases.”
Click to access 9241591013.pdf
I choose to believe in the Loch Ness monster but I wouldn’t sign a binding treaty to confirm that it was real.
The figure of a “passive smoker’s exposure” being 1/1,000th of the exposure of a smoker on average was the one I finally settled on in Brains after looking at a number of different studies using different approaches and arriving at figures from 1/100th to about 1/10,000th or less.
I still wasn’t comfortable with it however because of the wide range of estimation and so I worked on developing a model of my own that I called the “bio-physical model.” Basically I took a reasonable estimate of the total concentration of the smoke in the air of a “model pub” of a reasonable size and with a reasonable number of smoking customers and a reasonable level of air exchange rates per hour. I outlined exactly how I arrived at the “reasonable” figures and pointed out that any of them could be raised or lowered for different circumstances or under different assumptions but that overall the midrange result would be in that ballpark based upon Surgeon Generals’ figures for sidestream and mainstream smoke output of most components of concern. I then took that concentration and using a standard breathing rate for mild to mid activity levels (I think it was 1/liter per minute or somesuch) and computed how it would work out compared to the claimed FTC and SGR figures for mainstream smoke exposure for a primary smoker.
The figure I came up with by that method ALSO came out in the general 1/1,000th range. A very crowded, smok-filled poorly ventilated pub might be more like 1/100th or 1/50th, while a nice restaurant with few actively smoking smokers and a high level of ventilation might be 1/100,000th.
But I think the 1/1,000th figure is the most reasonable.
– MJM
The latest such study that I know of was conducted in 2010 and states this result:
A case-control study in the greater Toronto area to evaluate potential lung cancer risk factors including environmental tobacco smoke (ETS) exposure, family history of cancer, indoor air pollution, workplace exposures and history of previous respiratory diseases with special consideration given to never smokers, found no association between either exposure to ETS at home or at the workplace and lung cancer risk.
Click to access 1471-2407-10-285.pdf
Have you all seen this page that a group of us put up sometime last year and we ran ad words linking to it for a whole year? http://fightingback.homestead.com/ We ran out of ”funding” and we stopped running the ad as of mid-may. If anyone has anything to add to this webpage, pertaining to SHS and only SHS, please forward it to me at votrevoix@cagecanada.ca and I’ll make sure I put it up.
We alternated different ads to be printed into google searches of selective keywords and in different websites when the same keywords showed up and this throughout the globe.
The 1st ad read this:
Second hand smoke
Is not a significant health risk
Bans are based on pseudoscience
http://www.fightingback.homestead.com
The 2nd read:
2nd hand smoke is not a significant
health risk.Dont let them fool you!
http://www.fightingback.homestead.com
The 3rd read:
Smoking Bans
Are based on political & corporate
corruption. Find out why at
http://www.fightingback.homestead.com
We got millions of impressions and thousands of hits. We could have done a lot better with more financial help but not too many people or organizations came through unfortunately and eventually we had to stop but the webpage is there for all to refer to and spread around. :-(
These are very good ads, Iro – and the website content is quite good, but the site layout is too ugly.
I would very much like to contribute to a new round of ads, but the website needs layout work. Doen’t anyone know a web-layouter, we can pay to do this?
I am sure someone can rework it with a more sophisticated software and probably for free. Why doesn’t each one of us ask around?
Klaus, Beauty is in the eye of the Beholder. :> Yeah, black on grey isn’t sampling the rainbow, but the layout is ideal for conveying the amount of information it conveys quite clearly and in a “businesslike” no-frills format. There are times when that’s the best approach — e.g. when you want to impress your audience that you’re a serious concern and not just a web-kid flashing your skills with a bunch of half-baked links.
Seriously: I like the layout. And the mild impression that it might be a low-budget act that doesn’t know how to do better is dispelled as one goes down through it and sees the layout for the books and links near the bottom.
:)
Michael
I believe also that the confidence levels are important for the level of RR. The standard level in statistics is 95%, but I believe some of the studues into SHS have a level of 90%. This enables the RR to edge over the 2 and significance can be claimed. There is alot about this over at Velvet Glove Iron fist and at numberwatch
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Since when tobacco smoke is more lethal than the fumes of millions of cars rooming on
planet earth ??? specially the DIESEL cars !! the more of those cars the more Cancer
will be spread around, politician & scientist of today they are all corrupted not worth an
ONION…… The one with BRAIN.
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