The Effects of Second Hand Smoke on the Long Term Health of Non Smokers


Read this and see whether you come to the same conclusion



CONTENTS:

  1. INTRODUCTION
  2. THE EVIDENCE DERIVED
  3. 1986 ENVIRONMENTAL TOBACCO SMOKE REPORT
  4. 2006 THE HEALTH CONSEQUENCES OF INVOLUNTARY EXPOSURE TO TOBACCO SMOKE
  5. DISCUSSION
  6. OVERALL CONCLUSIONS

1. INTRODUCTION

    If you want to find out the truth about smoking risks and those of second hand smoke (SHS) then you will need to put some considerable effort into the investigation.

    The enormous amount of data, information and propaganda produced by the anti-smoking movement cannot be scientifically dismissed in a couple of simple sentences - a fair case has to be built up and this will take time and effort, and the reading of many references, for anyone keen to understand the real facts.

    Hence I make no apology for the length of these pages. They only cover the principle arguments but if you get to the end of the pages then you will at least have a better perspective of the reality of risks of SHS and from there you can go on and investigate further.

    If you make the effort to go through these pages with an open mind then you will at first be shocked by the way the anti-smoking movement has been able to build up its "evidence" without significant dissent from society; then amazed at how this "evidence" has spread unchanged, or often embellished, across the world; and finally you will be alarmed at the arbitrary way our society's rules can be readily manipulated despite the two levels of supposedly rational government in Parliament.

    The possibility of other self interest groups adopting the anti-smoking movement's "business model" represents a real danger to our future freedoms.

    Read on if you are interested.....




2. THE EVIDENCE DERIVED

    To simplify and summarise a complex and detailed issue, the basic thrust of the anti-smoking and medical establishment case against second hand smoke is based on a large number of epidemiology and other studies investigating nonsmokers' historical exposure to second hand smoke (SHS) as a consequence of living with smokers. The bulk of the data relate to nonsmoking wives of smoking husbands, although other more direct case studies are also available. The level of exposure of the non-smoking wives to second hand smoke is then compared with their subsequent cancer rates and to the cancer rates of non-smokers married to non-smokers.

    Epidemiology Studies
    After much statistical manipulation of the data, each of the studies comes up with an estimate of whether there is a positive, negative or zero association with cancer in later life.

    This association is usually known as "relative risk" (RR) and has a value of 1 for no effect, greater than 1 for harmful effect, and less than 1 for a protective (beneficial) effect. For example, an RR of 1.2 represents a 20% increase in risk, an RR of 0.6 would represent a 40% decrease in risk (i.e a protective effect), an RR of 1 would imply no effect, and an RR of 3 a 200% increase in risk.

    However, because the calculations involve statistical methods, the results are normally qualified as being statistically significant or not significant at a certain level of "confidence". The standard level is usually taken to be 95%, but could be higher or lower. Also, the RR number should show a minimum and maximum that the number could take at the 95% confidence level. To see a more comprehensive (yet simple) explanation of the statistical methods used in epidemiology studies see here.

    If the result is "not significant" then it is unlikely that it has any real validity. However, a number of studies all pointing in the same direction could indicate that there is something interesting going on and provoke further investigation with improved and better targeted data collection.

    Also, adopting the Bradford Hill criteria, a "significant" result in itself does not necessarily imply a causal link, since a wide range of other factors in the data need to be considered as causes of the correlation.

    Also, because the data involved in this type of study contain so much uncertainty and variability, the normal rule of thumb adopted by the analysts requires that an RR needs to be defined as "significant" and to reach a risk threshold of RR=2 or 3 (100% to 200% increased risk) to get above the noise level of spurious correlations and have any scientific credibility.

    This list of results is taken from an Appendix in the book Velvet Glove, Iron Fist - A History of Anti-Smoking, by C. Snowdon which gives a very clear and rational explanation of 64 peer-reviewed studies. (You must read this book if you want a rational and balanced explanation of how we arrived at our current smoking ban - prepare to have your eyes opened!).

    Out of the 64 studies referenced (said to form the bulk of the epidemiology evidence), all have RR values around a factor of 10 less than this threshold value. So on this criteria alone they might justifiably be dismissed as irrelevant.

    Overall the results tend to fall very close to, on, and on either side of the null line. Statistical associations are also more reliable the larger the data set. So, taking the ten largest studies, the results for the RRs are :-

    1.29 (1.04-1.6)
    1.11 (0.88-1.39)
    0.70 (0.6-0.9)
    1.03 (0.6-1.7)
    1.53(1.06-2.21)
    1.10 (0.8-1.5)
    0.89 (0.42-1.92)
    1.1 (0.8-1.6)
    0.90 (0.6-1.4)
    0.96 (0.7-1.33)
    (The RRs underlined are statistically significant.)

    Of the total set of 64 studies, 9 found a statistically significant positive (harmful) link, 3 a statistically negative (beneficial) link, and 52 found no significant link either way. Of these 52 studies 65% showed a positive link and 35% a negative link.

    It is primarily from these data that the anti-smoking lobby controversially derived their adopted headline statement that "SHS causes lung cancer, increasing risk by 20% - 30%".

    In considering these results, we need to take into account the following facts.

    It has been shown that the reporting of scientific research results is biased towards positive and significant correlations, and that studies showing null or negative correlations are more likely to be abandoned unpublished. This is partly because scientists have to fight hard for research funds which allow them to pursue their careers, and good positive results will often attract more funding.

    This reporting bias is even more likely when dealing with smoking issues since scientists can face career limiting pressure when publishing results which can be seen to undermine the prevailing anti-smoking industry's "evidence" that second hand smoke causes cancer.
    The implication of this is that the results upon which the health effects of SHS are evaluated are likely to be a positive subset of a wider range of true results.

    In addition, the negative associations are mostly dismissed by the anti-smoking lobby as "implausible", since surely second hand smoke can only be harmful?

    Not necessarily so. There is scientific evidence that many toxic chemicals (even dioxin) exhibit beneficial effects at low dosage.The phenomenon is known as Hormesis. The mechanism is unclear, but it is suggested that the toxic element stimulates the body's immune response which then mops up other genetic damage in the process.

    Could this be the reason why many of the studies above, which include children exposed to second hand smoke, hint at a negative (protective) effect for subsequent lung cancer development? (e.g the WHO 1998 Report in which the only statistically significant result was that children raised by smokers were 22% less likely to get lung cancer. See here for a more readily digestible summary of the findings).

    You don't hear much discussion about this, but the medical establishments must be aware of it, since they go out of their way to head off any discussion by dismissing any cut-off point with such statements as "The scientific evidence indicates that there is no risk free level of exposure to second hand smoke". This statement is not scientifically justified.

    A further point is that research into lung cancer has shown that the type of lung cancer found in smokers lungs is mostly different to the type found in non-smokers, with the researchers stating that “Lung cancer in never-smokers should probably be regarded as a different disease-entity than smoking-induced lung cancer.” This information clearly undermines the hypothesis that second hand smoke is the primary causitive agent in non-smokers' lung cancers.

    Modern statistical analyses can be highly successful in finding relationships between variables, but at such low and variable correlations, the above results would be dismissed as meaningless for any topic other than the contentious issue of second hand smoke.

    However, with the conflicting issues and arguments just mentioned, it is possible that the true effects of low levels of second hand smoke are negligible or possibly even protective for non-smokers.

    Whatever the real truth, the cold evidence certainly comes nowhere near a ringing endorsement of the anti-smoking incantation that there is "overwhelming evidence" that "second hand smoke causes cancer".

    It is with this implausible level of evidence that the anti-smoking lobby set out to convince the world of the dangers of second hand smoke.

    But let's not dismiss it yet, let's give it a fair run and see whether there is any real justification for the imposition of the smoking bans in the leisure industry, with all the social distress and division, personal heartache, expense, unemployment and business closures they produced.

    To do this it is worth looking at two major reports, the first by the National Research Council USA in 1986 and the second, 20 years later, by the Surgeon General USA in 2006.





3. 1986 ENVIRONMENTAL TOBACCO SMOKE - Measuring Exposures and Assessing Health Effects. National Research Council

    In 1986 the very comprehensive study above was reported by the Committee on Passive Smoking.

    From the information provided in the science section of the Report, it does seem to have been carried out with a good degree of scientific rigour, and explains how it tries to deal with the problems of misclassification of data and other limitations. The tone of the conclusions is generally not strident and gives the impression of doing the best with the data that it realistically can. However, the executive summary tends to take a more partisan stance.

    This report covered the whole range of theoretically possible effects of SHS:- lung cancer, other cancers, cardiovascular disease, eye, nose and throat irritation, objectionable odour, allergic reactions, respiratory symptoms such as wheezing and coughing, respiratory infections and impacts on young children such as lung function, chronic ear infections, birth weight, growth and development.

    Other than for lung cancer, the study did not provide definitive or quantitative evidence for these effects :-

    Other Cancers: "There is no consistent evidence at this time of any increased risk of ETS exposure for cancers other than lung cancer." (ETS = environmental tobacco smoke)

    Cardiovascular:
    "No statistically significant effects of ETS exposure on heart rate or blood pressure were found in healthy men, women, and school-aged children during resting conditions. During exercise there is no difference in the cardiovascular changes for men and women between conditions of exposure to ETS and control conditions.

    With respect to chronic cardiovascular morbidity and mortality, although biologically plausible, there is no evidence of statistically significant effects due to ETS exposure, apart from the study by Hirayama in Japan."


    Effects on children:
    "Evidence has accumulated indicating that nonsmoking pregnant women exposed to ETS on a daily basis for several hours are at increased risk for producing low-birth weight babies, through mechanisms which are, as yet, unknown. Recent studies show a dose-response relationship between the number of cigarettes smoked by the father and birth weight of the children of nonsmoking pregnant women.

    A few studies have reported that children of smokers have reduced growth and development. These require further corroboration to differentiate in utero exposure from subsequent childhood exposures.

    Household exposure to ETS is linked with increased rates of chronic ear infections and middle-ear effusions in young children. For children with nasal allergies and recurrent otitis media, ETS exposure may synergistically increase their risk of persistent middle-ear effusions."


    However, having regard to these possible risk associations for children the report recommended:-

    ... it is prudent to eliminate smoking and the resultant ETS from the environments of small children.

    Using the word "eliminate" seems a rather extreme recommendation, given the tentative nature of the evidence - "minimise" may have been more appropriate.

    This is the only really blatant bias observed in the science chapters of the report, but the fact that it is there does make one question whether all the data have really been analysed in a truly even-handed way. Only the analysts can answer that question. As the report was requested by the Office of Air and Radiation of the Environmental Protection Agency (EPA) and the Office of Smoking and Health of the Department of Health and Human Services, and was being driven by the Committee on Passive Smoking, then realistically one must ask what pressure the analysts were under.

    For the conclusions above, the report also recommended a range of further investigations and data gathering designed specifically to clarify the questions left unanswered.


    The main thrust of the report related to the links with lung cancer.

    Lung Cancer:
    The group's findings were analysed through a meta-analysis based on 13 studies, split into male and female where possible, and you can see the variability of the results in this graph on page 234 of the report.

    They summarised their findings as :- (the italics are mine...)

    "A summary estimate from epidemiologic studies places the increased risk of lung cancer in nonsmokers married to smokers compared with nonsmokers married to nonsmokers at about 34%."

    However, accounting for some misclassification could lower this and they stated that:-
    " a true relative risk of 1.15 or more could, by a reasonable set of misclassification biases, be elevated to 1.30 in an epidemiologic study. Stated differently, this implies that reasonable misclassification does not account for the total increased risks reported by the epidemiologic studies, leaving the conclusion that the risk of lung cancer following exposure to other people‘s smoke, as judged by whether a nonsmoker has a smoking spouse, would be increased by a minimum of 15%, and most probably increased by 25% (i.e., 1.25). (If the percentage of women smokers were as high as 50%, it would be 1.20.)."

    and then qualified the estimate with

    "To some extent, misclassification (bias) may have contributed to the results reported in the epidemiologic literature. However, bias is not likely to account for all of the increased risk. The best estimate, allowing for reasonable misclassification, is that the adjusted risk of lung cancer is increased about 25% (i.e., RR =1.25) in nonsmokers married to smokers compared with nonsmokers married to nonsmokers. When one allows for exposure to nonsmokers who report themselves as unexposed, the adjusted increased risk is at least 24%.

    The adjusted increased risk to a group of nonsmokers married to nonsmokers is at least 8% (i.e., RR=1.08) compared with truly unexposed subjects. This excess risk may come about from exposures in the workplace or other public places."


    Surely such low figures of risk are becoming meaningless?

    Subsequent reports take the value of RR=1.25 (ie. 25% increase in risk) as being the outcome of the study, although it seems it could be around a minimum of RR=1.15 (15% increase).

    These results are about a factor of 10 below the normally accepted threshold of 200% to 300% required to demonstrate credibility of the result. One must realistically ask whether such low level results can be valid.

    Also, even if valid, the result refers to the risk of a non-smoking wife married to a smoking husband, exposed to second hand smoke fairly continuously, and clearly at a much greater exposure (probably over 100 times) than a non-smoker married to a non-smoker in an environment where "No Smoking" areas were prevalent and workplace smoking was effectively non-existent. This will be discussed in more detail later.



    Biological Marker Studies
    The report also looked at "biological marker" studies, which measured levels of a non-carcinogenic substance called cotinine in the urine of non-smokers. As nicotine is the only source of cotinine, when other nicotine sources are avoided (e.g. nicotine gum, chewing tobacco and nicotine patches), this substance gives a measure of exposure to SHS.

    With the lack of any definitive information the researchers assumed a linear relationship between cotinine and any carcinogenic components of SHS.

    (Again, this is an assumption in favour of "causing harm at vanishingly low levels" of second hand smoke. Hormesis implies there could be a cut-off where harmful effects give way to beneficial effects, but the researches do not model this scenario - just the continuing harm one.)

    The report looked at levels of cotinine in non-smokers and estimated that the exposure of non-smokers to SHS would be about 1% of the smokers' direct dose, although this could be overestimated by 50%, since cotinine degrades half as fast in a non-smoker compared to a smoker. This would give an estimate of 0.5% of smokers direct dose. This was discussed but didn't seem to be taken into account in the final figures.

    Given this fact the report states :-

    Based on the above dosimetric considerations, the risk of lung cancer from ETS exposure among nonsmokers in the United Kingdom and United States would be small. Assuming linearity in the dose-response relationships, the risk would be about 1% of the excess risk in active smokers. This is equivalent to a relative risk of 1.14 in males, given that the relative risk in average male active smokers is 10 to 15 times greater than in nonsmokers (Hammond, 1966; Doll and Peto, 1978). For ETS-exposed women, the average relative risk may be less.(Taking into account the 50% variation in degradation time of cotinine in a non-smoker, the relative risk could actually be around 1.07).

    Hence, this method gives a potential risk increase of around 7% - 14% for male non-smokers and a "lower" figure for females.

    On the validity of the proposed relative risk the report fairly recognised the dependence on there being no cut-off level of second hand smoke below which it was deemed harmless :-

    "In part, this depends on whether there is a threshold dose of cigarette smoke exposure below which there is no increase in risk. Biological theory and current evidence on low-dose exposure to carcinogens do not provide evidence for such a threshold, and it is generally thought that one is unlikely (Office of Science and Technology Policy, 1985). If there is no threshold, it follows that exposure to tobacco smoke at low concentrations, such as that experienced by nonsmokers exposed to ETS, will cause an increased risk of lung cancer. The risk, of course, will be expected to be very much smaller than that associated with active smoking because of the much lower exposure of the bronchial epithelium to tobacco smoke".

    In other words, the suggestion is that if you are exposed to SHS at a level of 1000th of a smoker, then you will have 1000th of his/her risk of developing cancer.

    This principle is fundamental to the anti-smoking lobby's claim that "there is no risk free level of exposure to second hand smoke".

    As mentioned before, recent research into the effect of Hormesis suggests that this hypothesis could be wrong, and at low concentrations second hand smoke could even offer a protective effect.

    This is the background of evidence with which the anti-smoking lobby set out to convince the world that second hand smoke was highly dangerous for the non-smoking public.

    .
    .
    .
    20 Years Later .....



4. 2006 THE HEALTH CONSEQUENCES OF INVOLUNTARY EXPOSURE TO TOBACCO SMOKE - A Report of the Surgeon General. (Executive Summary here)

    In the intervening 20 years, the scientific literature had become flooded with the results of research on the health effects of second hand smoke, defining new "associations" with disease intending to bolster up the relatively insignificant risk ratio of 1.25 for lung cancer. Most of this was funded by the anti-smoking lobby, governments and medical establishments readily supported by the pharmaceutical industry.

    This report is a compilation of all the key research papers rather than doing any direct analysis of raw data itself. Full Report here. It also brings together the varying nomenclature of earlier research papers under a new "revised standard language of causality" to express the validity or otherwise of reported risks. In future the results would be expressed as falling into one of four standard categories :-

      LEVEL 1 - Evidence is sufficient to infer a causal relationship
      LEVEL 2 - Evidence is suggestive but not sufficient to infer a causal relationship
      LEVEL 3 - Evidence is inadequate to infer the presence or absence of a causal relationship (which encompasses evidence that is sparse, of poor quality, or conflicting)
      LEVEL 4 - Evidence is suggestive of no causal relationship.

    These categories seem to muddy the waters somewhat, since they look like value judgments and not mathematically valid associations? Also, they don't seem to allow "evidence shows no causal relationship".

    What exactly does "infer" mean? The Oxford dictionary says "deduce from evidence and reasoning, rather than from explicit statements".

    I think we can begin to see where this is going.

    Why is there no negative association, such as "The report found no causal link for..."??

    Reading the Report it becomes clear that the Surgeon General seeks to move the anti-smoking agenda forward to the next phase of control by talking of "deadly involuntary smoking diseases" and the "contamination of outdoor spaces as well as indoor spaces" by the "combustion at high temperatures of tobacco, paper and additives".

    The report is of a completely different character to the National Research Council Report of 1986. It is clearly highly political in its objectives. From the outset it demonstrates its intention to produce a definitive catalogue of the "overwhelming evidence" of the dangers of second hand smoke. It signals its intention that despite the progress to date "second hand smoke remains a serious public health hazard that can be prevented by making homes, work places, and public places completely smoke free".

    Interestingly, in coming to its conclusions on whether to classify a health risk as Level 1, 2, 3, or 4, the report says "The quantitative results of the meta-analyses, however, were not determinate in making causal inferences in this Surgeon Generalís report. In particular the level of statistical significance of estimates from the meta-analyses was not a predominate factor in making a causal conclusion."

    Err, 'scuse me, just run that by me again.....!

    Further, it states that the making of a causal link "involved judgments based on an array of quantitative and qualitative considerations that included the degree of heterogeneity in the designs of the studies that were examined".

    Oh! right then.......uummmm...interesting approach.....



    So let's look at what the Executive Summary Report comes up with.

    The Executive Summary provides major conclusions on the health risks associated with second hand smoke under Chapters 5 to 9.

    Looking at cancer risks first:


Chapter 7. Cancer among adults from exposure to second hand smoke
    Disease = Lung Cancer
    Risk Found = Level 1 risk - "sufficient to infer a causal relationship"

    This is one of only two quantified results (the other being coronary heart disease) in the whole set of conclusions and states:-
    "The evidence is sufficient to infer a causal relationship between secondhand smoke exposure and lung cancer among lifetime nonsmokers. This conclusion extends to all secondhand smoke exposure, regardless of location. The pooled evidence indicates a 20 to 30 percent increase in the risk of lung cancer from secondhand smoke exposure associated with living with a smoker".
    There is no discussion in arriving at this conclusion about the probable under-reporting of null or negative effects. To assume that the results of research used in the study are the only results ever achieved is probably misleading, since, for a number of factors, as discussed in "Scientific integrity - where has it gone?" it is highly likely that some results showing a null or beneficial effect will have been quietly abandoned unpublished.
    The report on "Systematic Review of the Empirical Evidence of Study Publication Bias and Outcome Reporting Bias" states in its conclusions that
    "Recent work provides direct empirical evidence for the existence of study publication bias and outcome reporting bias. There is strong evidence of an association between significant results and publication; studies that report positive or significant results are more likely to be published and outcomes that are statistically significant have higher odds of being fully reported. Publications have been found to be inconsistent with their protocols. Researchers need to be aware of the problems of both types of bias and efforts should be concentrated on improving the reporting of trials." Further evidence here.

    Interestingly, no mention is made here of the many results which showed a protective effect for children exposed to parents' SHS. Surely these results would warrant mention and some explanation in a genuinely unbiased scientific report?


    Diseases = Breast cancer; and nasal sinus cancer
    Risk Found = Level 2 risk - "suggestive but not sufficient"

    Diseases = Nasopharyngeal carcinoma; and cervical cancer.
    Risk Found = Level 3 risk - "inadequate to infer"


    So there we have it. If we accept the way the risk figure for lung cancer has been derived (which many don't), after 20 years of intense and targeted effort in examining the link with cancer, the best the researchers can come up with is a supposed risk of 20%-30%, based on a probably biased subset of the true data, in line with the 1986 NRC result and still a factor of 10 below the accepted threshold of 200% or 300% for this type of study.


Chapter 8. Cardiovascular Diseases from Exposure to Secondhand Smoke

    Disease = Coronary heart disease
    Risk Found = Level 1 risk - "sufficient to infer a causal relationship"

    This is the only other quantified risk in the whole report. It states :-
    "The evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and increased risks of coronary heart disease morbidity and mortality among both men and women. Pooled relative risks from meta-analyses indicate a 25 to 30 percent increase in the risk of coronary heart disease from exposure to secondhand smoke."


    Diseases = stroke; and atherosclerosis
    Risk Found = Level 2 risk - "suggestive but not sufficient"


    The remaining associations in the other chapters are all dealt with in qualitative terms using the new revised standard language. In summary form these are:-


Chapter 5. Reproductive and Developmental Effects from Exposure to Secondhand Smoke

    Out of 17 potential disease types investigated the following links were established:-

    Diseases = Sudden infant death syndrome; and a small reduction in birth weight
    Risk Found = Level 1 risk - "sufficient to infer a causal relationship"

    Diseases = maternal exposure during pregnancy and preterm delivery; prenatal and postnatal exposure and childhood cancer; childhood leukemias; and childhood lymphomas; and childhood brain tumours
    Risk Found = Level 2 risk - "suggestive but not sufficient"

    Diseases = female fertility or fecundability, spontaneous abortion; neonatal mortality; congenital malformations; cognitive functioning among children; behavioural problems among children; children's height/growth; maternal exposure during pregnancy and childhood cancer; exposure during infancy and childhood cancer; prenatal and postnatal exposure and other childhood cancer types
    Risk Found = Level 3 risk - "inadequate to infer"

Chapter 6. Respiratory Effects in Children from Exposure to Secondhand Smoke

    Diseases = parental smoking and lower respiratory illnesses in infants and children; parental smoking and middle ear disease including recurrent otitis media and chronic middle ear effusion; cough, phlegm, wheeze and breathlessness; parental smoking and children ever having asthma; parental smoking and onset of wheeze illnesses in early childhood; maternal exposure during pregnancy and persistent adverse effects on lung function; exposure after birth and lower level of lung function during childhood
    Risk Found = Level 1 risk - "sufficient to infer a causal relationship"

    Diseases = parental smoking and the natural history of middle ear effusion; parental smoking and the onset of childhood asthma
    Risk Found = Level 2 risk - "suggestive but not sufficient"

    Diseases = parental smoking and an increase in the risk of adenoidectomy or tonsillectomy among children; parental smoking and the risk of immunoglobulin E-mediated allergy in their children
    Risk Found = Level 3 risk - "inadequate to infer"


Chapter 9. Respiratory Effects in Adults from Exposure to Secondhand Smoke

    Diseases = odor annoyance; and nasal irritation
    Risk Found = Level 1 risk - "sufficient to infer a causal relationship"

    Diseases = persons with nasal allergies more susceptible to developing nasal irritation; acute respiratory symptoms including cough, wheeze, chest lightness, and difficulty breathing; chronic respiratory symptoms; acute decline in lung function in persons with asthma; a small decrement in lung function in the general population; adult-onset asthma; worsening of asthma control; risk for chronic obstructive pulmonary disease
    Risk Found = Level 2 risk - "suggestive but not sufficient"

    Diseases = acute decline in lung function in healthy persons; an accelerated decline in lung function; morbidity in persons with chronic obstructive pulmonary disease
    Risk Found = Level 3 risk - "inadequate to infer"




5. DISCUSSION

    The above results show that for 20 years after the first report the anti-smoking lobby and medical establishment trawled just about every ailment possible to try and obtain further evidence of the "deadly" danger of second hand smoke. The fact that, other than for lung cancer and cardiovascular disease, there is no quantification for the risk demonstrates that the information (even the most tentative) just wasn't there - otherwise it would have been widely publicised.

    In the early 2000s the writing must have been on the wall for the anti-smoking movement that unequivocal and quantitative evidence against second hand smoke was not likely to be forthcoming, hence their move to more qualitative "standard language of causality", designed to provide the press and other less rigorous thinkers with the ammunition to further stoke their propaganda campaign and anti-smoking crusade.

    The WHO (Word Health Organisation) Study of 1998 on "Exposure to Environmental Tobacco Smoke and Lung Cancer in Europe" (The full report was never formally reported by the WHO) could have been part of this writing on the wall, since it famously came up research results showing "no statistically significant link between passive smoking and lung cancer". It did come up with a non-significant 16% risk increase, which was half their currently recognised headline risk, and a 22% statistically significant protective effect for children whose parent(s) smoked. Its attempts to bury the embarrassing news led the "Economist" to comment that "The World Health Organisation is showing signs of allowing politics to get in the way of the truth". This provoked a typically political and incensed response from ASH who had the temerity to accuse the article of an "outrageous misinterpretation" of the results, while continuing to do exactly that themselves by reiterating all the misleading headline mantras of the anti-smoking movement. They did not mention the significant protective effect the results showed for children of smokers. A WHO press release, though less overwrought, also just repeated the traditional mantras and again failed to comment on the significant protective effect on children with smoking parents.

    How do they get away with it? Where were the rest of the press - didn't they see the irony? One can only conclude that they themselves are effectively part of the anti-smoking movement or, worse, politically and/or financially controlled by them.

    Lung Cancer
    Overall, it is evident that with respect to lung cancer and second hand smoke, after over 40 years of detailed scrutiny, the highest possible rate the anti-smoking establishment could come up with is an increased risk of 20%-30%. There are many who feel, with good reason, that this figure is suspect and that it just reflects an inherent uncertainty in the highly variable and probably incomplete and biased data sets. It also ignores the possibility of a cut-off point for harm from second hand smoke. (These issues were discussed in Section 1 above).

    It should also be made clear, and often it is not, that this figure is derived from data relating to non-smoking wives living with a smoker. Thus, the intensity of exposure will be relatively high, since it will occur not only in the home, but also in all social activities which they would tend to be involved in together, and with like minded smoking friends/family.

    In addition, the data from which this estimate is derived relate mainly to an era before the advent of separate "No-Smoking" areas in both the workplace and leisure industry. Hence, exposure levels at that time were substantially higher than the levels experienced during the early 2000s, prior to the ban coming in, when the prevalence of "Non-Smoking Areas" was almost universal and smoking in the workplace was a thing of the past.

    Hence, prior to the ban, neversmokers who wished to avoid second hand smoke could already lead a virtually smoke-free life.

    Assuming that there is no cut-off point for exposure to second hand smoke below which it has no effect (disputed and probably wrong), then, for neversmokers prior to the ban, exposure must have realistically been around 1% or less of the relatively intense exposure of the non-smoking wives during the period to which the data relate. (Even then it is difficult to envisage how those who want to lead a smokefree life could end up being relatively continuously exposed to SHS). This brings the effective increase in risk of 20%-30% down to around 0.2% to 0.3%.

    The risk of a neversmoker dying of lung cancer in their 60th year is around 13 per 100,000 (see Absolute risks - Putting risk into perspective). So the maximum increased supposed risk due to second hand smoke exposure will be around 13 x 0.003 = 0.039 per 100,000, or 3.9 per 10 million, or substantially less than 1 in 2 million. This risk is that experienced in their 60th year after a lifetime of exposure to low level SHS.

    The lifetime risk of dying of lung cancer for a smoker is quoted as being about 16% (males-17.2%, Females-11.6%), whereas for a neversmoker it is around 1.4% (males-1.3%, females-1.4%). The risks are often quoted as deaths per 1000, so in this case would be 172 per 1000 for male smokers and 13 per 1000 for male neversmokers, and for females would be 116 per 1000 for female smokers and 14 per 1000 for female never smokers.

    So smoking cigarettes directly over a lifetime increases the risk of developing lung cancer by about 13 times for males and 8 times for females. However, some estimates put the lifetime relative risk factor at around 15%, whereas looking directly at WHO data a lifetime risk factor of less than 10% seems possible.
    These figures logically put into perspective the minimal risk that SHS must cause to non-smokers who avoid SHS wherever they can.

    The supposed lifetime increase in risk due to SHS for neversmokers during the period in the early 2000s before the ban was brought in would be (as calculated above) around 0.2% - 0.3% on top of the baseline lung cancer rate for neversmokers (say 1.4%) - this would give an max. increased risk of 1.4x0.3% or about 0.0042% or 0.042 per 1000. However, this would only be valid for a lifetime of relatively continuous exposure to recreational SHS and it becomes almost impossible to envisage how this could arise for someone who wished to lead a smokefree life.

    The position of non-smoking employees is slightly different, in that they may have to work in smoking areas. So, non-smoking employees working in smoking areas may have a similar risk increase to the non-smoking wives married to smoking husbands, i.e. max increased risk of 1.4x30%= 0.4% or 4 per 1000.

    Imposing proper ventilation and other more specific measures, such as air curtains to shield the main working area from smoke, would be able to reduce exposure to 10%, 1% or even less for properly designed systems. This would give a residual risk of around 0.4 - 0.04 per 1000 respectively. So, employees could have been readily protected from the (still supposed) risks from second hand smoke. Again, to suffer this level of risk would require a lifetime of working under these conditions.

    Clearly, these levels of risk are meaningless from any practical viewpoint, particularly as the increased lung cancer risk of 20%-30% for SHS is a dubious and disputed upper limit. The figures certainly don't warrant the harsh punitive actions being taken against those who wish to smoke socially.

    Overall, the discussion above has demonstrated that for non-smokers, in the leisure environment prevalent before the smoking ban came into force, the lung cancer risk from exposure to second hand smoke must have been negligible. For non-smoking employees, any small supposed risk could have been effectively removed by appropriate ventilation.

    Also, if the medical profession is seriously concerned about the health risks of smoking, it should encourage tobacco manufacturers to increase organic production and remove additives to at least create a healthier cigarette. It should also publicise the case for the health benefits of reducing cigarette consumption, making it more of a social activity, and something to look forward to outside the home, rather than allowing it to become a continuous and automatic habit.


    Cardiovascular Disease
    The other quantitative association of risk with second hand smoke was for coronary heart disease (CHD). Here the study found a positive association with an increased risk of 25%-30% in contradiction to the earlier 1986 National Research Council Report discussed earlier which could find no link.

    Research into the causes of CHD have been carried out extensively over the past 40 years and the links with diet and lack of exercise and direct smoking well established.

    Long term smoking has been associated with an increased risk of CHD for smokers of around 2 to 4 times that of a non-smoker, nowhere near the 10 to 15 times risk associated with lung cancer. If direct smoking has only this reduced impact, then intermittent and very limited exposure to second hand smoke, particularly in a "No Smoking Area" environment of the recent past, and following the same arguments as above, must logically be minimal or non-existent.

    Also, the fact that a diet high in fruit and vegetables, undertaking moderate exercise and consuming only modest amounts of alcohol can EACH offset the effect of direct smoking would seem to mitigate against second hand smoke being any sort of serious risk for CHD.

    The Surgeon General's report doesn't provide any absolute risks, and the credibility of the reported link has been somewhat damaged by the "definitive" reports of a reduction in the general public's heart attacks directly associated with the imposition of the smoking ban. These have since been shown to be scientifically invalid - basically, just cynical propaganda.

    The results of recent analysis (Jan 2012) by the British Heart Foundation indicate that deaths from strokes and heart attacks has halved over the period 2002 to 2010. As there has only been a limited reduction in smoking of around 6% from 2002 to 2010, then this must surely demonstrate the lack of credibility of the anti-smoking lobby's claim that smoking is a key component of such deaths, and must really put to bed any notion that SHS is a factor.

    Again, as for lung cancer, the risk, if valid, is very low, and the introduction of properly ventilated smoking rooms would prevent any risk whatsoever to the general non-smoking public who wish to avoid second hand smoke. The risk to employees working in smoking areas could, as for lung cancer, be effectively removed by properly designed extraction and air quality protection measures in the workplace.



    Other Disease and Irritations
    With regard to the other long list of "suggestive but not sufficient causal links", the lack of quantitative associations with serious disease must detract from their credibility.

    Having said that, it is clear that many people are adversely affected by tobacco smoke in terms of eyes, nose, throat and odour, and some suffer considerable irritation, sometimes extreme.

    This is no reason to completely ban tobacco smoke, it just requires public venues to have completely smoke free areas where such people can choose to go.

    Providing enclosed and properly ventilated smoking rooms for the use of smokers would effectively remove any irritation while maintaining the civil liberties of those who wish to continue, and enjoy, smoking.

    With regard to the effect of second hand smoke on young children, many studies relating to a cancer risk seem to show a negative risk (i.e protective effect). For example, the infamous WHO 1998 Report on Passive Smoking and Cancer showed that children growing up with smoking parents had a 22% (statistically significant) less chance of getting lung cancer.
    On the other hand there may potentially be some association with ear, nose, throat and other health problems. Whether these are entirely down to second hand smoke or other associated lifestyle factors is no doubt difficult to establish exactly.

    However, young children are a special category, since they do not have the option, in general, to avoid second hand smoke. For these reasons, it would be best to be cautious and educate families about the potential health risks, and provide incentives for smoking parents to minimise smoking in the home, and lower the concentration of second hand smoke in rooms where children are. Providing ventilated smoking rooms in public venues would go a long way to reducing smoking in the home.





6. OVERALL CONCLUSIONS
  1. From all the above evidence, it seems clear that although there are real risks associated with direct smoking, the risks associated with second hand smoking have been, broadly speaking, fabricated. The claims made by the anti smoking movement have not been scientifically justified.

  2. For direct smokers, it is not widely understood that out of 100 male smokers who have smoked 20 cigarettes a day from the age of 18, 83 of these do not die of lung cancer by age ~75 even after lifetime of smoking. For female smokers the figure is higher - 88 out of 100 will not die of lung cancer. (There are some who believe that because of the way the data are collected even this level of risk is overestimated.)

  3. With the ability to minimise one's exposure to second hand smoke, as during the "No Smoking Area" era prior to the 2007 ban, it has been shown that even before the ban, non-smokers (not married to smokers) had a negligible risk of contracting lung cancer from tobacco smoke, and even less risk regarding coronary heart disease.

  4. A key argument for the blanket ban put forward by the anti-smoking lobby was that employees working in smoking areas would be subject to "highly dangerous" second hand smoke.
    However, in looking at the absolute risks involved, it is clear that properly ventilated smoking rooms, with special air curtains (or other methods of maintaining clean air in the primary working area of the non-smoking employee) would bring even any potential risk down to negligible levels.


  5. For children, the risk of contracting lung cancer through SHS has not been scientifically established, indeed there is some evidence that low level exposure has a protective effect. The main concerns relate to potential respiratory problems.
    As children often cannot choose whether to be in the presence of SHS, parents should be educated as to any possible risks, particularly for those children with sensitive respiratory systems or who suffer specific respiratory ailments. It would be wise for Government to seek to encourage smoking outside the home in public ventilated smoking venues, rather than to force smoking onto the street or back into the home in full view of children .


  6. It is accepted that for some adults with sensitive respiratory systems, SHS can cause irritation. However, the provision of smoke free venues would allow them to avoid any contact with SHS.

  7. It is clear that the leaders of the anti-smoking movement have stretched and bent the science beyond recognition to produce propaganda "facts" for promoting their objectives.

    Unfortunately, the general public, including most politicians, take the information promoted by the anti-smoking industry at face value, no doubt believing that such an august body of assumed professionals would not try to deceive them. Unfortunately this is not so, and anyone who attempts to get at and understand the facts will also see that it is not so.


The above facts put into perspective the lack of any practical impact that occasional exposure to second hand smoke must have on the absolute risk of cancer for non-smokers.

With separate ventilated smoking rooms for smokers, all non-smokers who don't like the smell of smoke can remain smoke free and effectively eliminate second hand smoke from their lives.



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** Page last updated January 2012 **