Select Committee on Health First Report

2  The health effects of secondhand smoke

9. Secondhand smoke (also known as environmental tobacco smoke, ETS, or 'passive smoking') is produced from two sources. The first is so-called 'mainstream smoke'; this is smoke which is puffed by the smoker, inhaled and then exhaled. The second is 'sidestream smoke', which is released into the ambient air from the smouldering tip of a lit cigarette between puffs. The constituents of mainstream and sidestream smoke are similar but their concentrations differ, in general being higher in sidestream smoke. The great majority of SHS consists of sidestream smoke.

10. Tobacco smoke contains more than 4,000 different chemicals, at least 50 of which are known carcinogens. These include benzo[a]pyrenes, aromatic amines and tobacco-specific nitrosamines. It also contains nicotine, toxins such as carbon monoxide and hydrogen cyanide and irritants such as acrolein. SHS consists of a gas phase and a particulate phase, the former including carbon monoxide, ammonia, dimethylnitrosamine, formaldehyde, hydrogen cyanide and acrolein, the latter, the complex of compounds collectively termed tar, including benzene and benzo[a]pyrene. Nicotine is present in both the gas phase and the particulate phase.[7]

11. High levels of particulates are found in tobacco smoke. Dr Richard Edwards, a Senior Lecturer in Public Health at the University of Manchester, told the Committee:

    When you are talking about exposure from particles which are known to affect health, and there are plenty of studies to show that particulate matter affects health, some of the places where you get the very greatest exposure is in the indoor environment in smoky pubs, much more than you do from traffic pollutants at the road side.[8]

12. The level of exposure to SHS can be measured in a number of ways. It is possible to measure directly the concentration of known constituents of SHS in the air. Surveys and questionnaires can collect information on a person's duration and frequency of exposure. Personal monitors can be used to measure exposure to nicotine or smoke particles. It is also possible to detect the constituents or metabolites of SHS in hair, blood, saliva or urine. In this way, the amount of SHS absorbed by a person can be assessed by levels of biomarkers such as nicotine (and, more usually, its breakdown product, cotinine) as well as by markers of DNA and protein damage.[9]

13. Since mainstream and sidestream smoke contain the same chemicals, exposure to SHS is likely to cause most, if not all, of the diseases caused by active smoking, but with a lower absolute level of risk.[10] Scientific studies have employed two main designs to investigate the effects of SHS on disease risk for non-smokers:

  • The case-control study, which compares exposure to SHS of people with and without a particular disease and thereby determines whether people with a disease are more likely to have been exposed;
  • The cohort study, which compares the incidence of disease in those with and without exposure to SHS prospectively over a period of time.

Many case-control studies have examined the effects of SHS by determining whether non-smoking women who have developed a smoking-related disease are more likely to have lived with a smoking partner than non-smoking women who do not have the disease. The focus has been predominantly on women because smoking has historically been much more common in men than in women.

14. A considerable body of evidence has accumulated over the last thirty years which has demonstrated with increasing certainty that exposure to SHS both causes illnesses and exacerbates existing ill health. In 1983, the Department of Social Services' Independent Committee on Smoking and Health affirmed a link between secondhand smoke and ill health, and, in 1988, went on to note that exposure to SHS could cause several hundred deaths from lung cancer in non-smokers in the UK each year. In 1986, the United States Surgeon-General had concluded that exposure to SHS presented a major risk to health.

15. More recently, the case that SHS is harmful to public health has been made by the Department of Health's Scientific Committee on Tobacco and Health. In 1998, it produced a report which concluded that exposure to SHS was a cause of lung cancer and heart disease in adults, as well as of a variety of diseases in children.[11] As a result, the report recommended restrictions on smoking in public places, and, where possible, a ban on smoking in the workplace. In 2004, SCOTH released Secondhand Smoke: Review of evidence since 1998, in which it concluded that:

  • There is an estimated 24% increased risk of lung cancer in non-smokers exposed to SHS;
  • There is an estimated 25% increased risk of heart disease in non-smokers exposed to SHS;
  • Exposure to SHS is strongly linked to an elevated risk of pneumonia, bronchitis, asthma, middle ear infection, decreased lung function and sudden infant death syndrome in children.[12]

16. In July 2005, the Royal College of Physicians (RCP) published Going smoke-free: The medical case for clean air in the home, at work and in public places, a report on secondhand smoke by the RCP Tobacco Advisory Group. This study presented a comprehensive survey of the available scientific data, as well as examining issues such as public response to potential smoke-free legislation and the likely health and economic effects of a ban on smoking in public places. It attempted to quantify the deaths attributable to SHS in the UK in 2003, and divided these deaths into those caused by exposure to SHS at home (the vast majority) and in the workplace.

17. The data were updated from those in a study by Professor Konrad Jamrozik, a public health specialist at the University of Queensland, which suggested that SHS caused approximately 12,200 deaths in the UK in 2003, of which a minimum of 500 were due to smoke in the workplace. Within that subsection, it was estimated that perhaps 50 deaths were due to smoke in hospitality industry workplaces. The Royal College of Physicians' report, in recording these figures, noted that the estimate of 12,200 deaths "is likely to be conservative".[13] The study also noted that a large proportion of the deaths occurred in those aged under 65.

18. Recent evidence has also demonstrated a disturbing aspect of the epidemiology concerning exposure to SHS, namely that even low levels of exposure can cause a significant increase in the risk of heart disease. A cohort study published in the British Medical Journal in 2004 suggested that the risk of ischaemic heart disease[14] in non-smokers who were exposed to SHS was comparable to that in regular smokers who smoked between one and nine cigarettes per day. Giving evidence to the Committee, Dr Allan Hackshaw, Deputy Director of the Cancer Research UK and University College London Cancer Trials Centre and a specialist in epidemiology and medical statistics, summed up the issue:

    The relationship between passive smoking and lung cancer is linear, but for heart disease it is not. You only need a small amount of exposure and that gives you your big risk of heart disease. That has been shown in lots of studies of active smokers, as in passive smokers as well.[15]

19. The tobacco industry does not accept the weight of scientific evidence that SHS is a substantial hazard to the health of non-smokers. Dr Steve Stotesbury, Industry Affairs Manager and Chief Scientist for Imperial Tobacco Ltd, told the Committee that "the scientific evidence, if you take it as a whole—and that includes the lung cancer, heart disease and chronic bronchitis—is currently insufficient to establish that other people's tobacco smoke is a cause of any disease".[16] He went on to cast doubt on the effect of SHS on the health of children, saying that there was "insufficient evidence" to demonstrate a link.[17]

20. Dr Stotesbury drew attention to a study carried out by Professors James Enstrom and Geoffrey Kabat which was published in the British Medical Journal in 2003. The study was an analysis of data collected by the American Cancer Society's Cancer Prevention Study, which monitored 118,094 Californian adults from 1959 to 1998. In particular, Enstrom and Kabat concentrated on the 35,561 non-smokers who were married to smokers, on the grounds that they would be exposed to SHS on a regular basis. The study concluded that exposure to SHS had no significant association with an increased risk of death from lung cancer or coronary heart disease.[18]

21. However, the study by Enstrom and Kabat has also been widely criticised. It was funded by the tobacco industry and supported by the Centre for Indoor Air Research (CIAR), a now-defunct group founded by, and financially dependent on, tobacco manufacturers. The methodology has also been questioned, on the grounds that it does not distinguish sufficiently clearly between people who were exposed to SHS and those who were not, and that it was based on a small subset of the American Cancer Society's data. The Chief Medical Officer, Professor Sir Liam Donaldson, concluded that Enstrom and Kabat "carried out a study with a flawed methodology which led them to the wrong conclusions".[19]

22. The central issue, as the Royal College of Physicians' report stressed, is the importance of examining and analysing all of the evidence rather than focusing on a single study. It noted that individual studies are susceptible to bias, but that systematic overviews and quantitative meta-analysis could address the problems inherent in the individual studies. Finally, it reported that "for studies of ETS effects on health there is an overall consistency within the published literature, derived from diverse locations and a variety of study designs, which is impressive".[20]

23. Dr Hackshaw went on to summarise the scientific evidence:

    Passive smoking you can think of as a mild form of active smoking, so it must be associated with some risk. There are many studies on active smoking. There have also been many studies in passive smoking in non-smokers. There are over 50 on lung cancer and they consistently show that the increase in risk is of the order of 25%. Similarly for the studies of heart attacks: they consistently show that the risk is of the order of about 25% […] Estimates of the number of deaths were published in the BMJ [British Medical Journal] recently by Professor Jamrozik. That was a simple analysis based on various estimates of the prevalence of exposure, people who are exposed to passive smoke, the increase in risk associated with four specific disorders and the number of people who get lung cancer, heart disease, stroke and chronic lung disease each year, and if those estimates are put together in a formula you get a rough idea of how many deaths per year you can expect […] The figure quoted in the report is about 12,000.[21]

The Chief Medical Officer told the Committee that "any doubts or scepticism about the health impact of secondhand smoke are resolved scientifically in my view".[22] He went on:

    There have been syntheses of the research evidence by major international bodies and expert committees that have reviewed the validity of the research and essentially the risks to non-smokers of inhaling a smoker's smoke through being exposed to 50 carcinogens, which is roughly the number of cancer causing chemicals in cigarette smoke, and to carbon monoxide. There are both short-term risks of an increased risk of clotting of the blood and therefore of a heart attack and longer-term risks such as cancer, coronary heart disease, chronic bronchitis and promoting asthma attacks in children.[23]

24. We are convinced by the evidence of experts, including the Chief Medical Officer, the Royal College of Physicians, SCOTH, the US Surgeon General and the World Health Organisation, that secondhand smoke is a serious and preventable cause of death and ill-health.

7   Royal College of Physicians, Going smoke-free: The medical case for clean air in the home, at work and in public places, July 2005, ISBN 1 86016 246 0. Back

8   Q 72 Back

9   See, for example, Report of the British Medical Association Board of Science and Education and Tobacco Control Resources Centre, Towards smoke-free public places, November 2002, p. 1. Back

10   See Ev 4, 6, 9, 17 and 23, Volume II Back

11   First Report of the Scientific Committee on Tobacco and Health, March 1998. Back

12   Report of the Scientific Committee on Tobacco and Health, Secondhand Smoke: Review of evidence since 1998, November 2004; see also World Health Organisation International Agency for Research on Cancer, Tobacco Smoke and Involuntary Smoking, IARC Monographs Volume 83, 2004. Back

13   Royal College of Physicians, Going smoke-free: The medical case for clean air in the home, at work and in public places, July 2005, ISBN 1 86016 246 0. Back

14   Also known as coronary artery disease; the accumulation of fatty deposits on the walls of the coronary arteries, limiting the supply of oxygen to the heart muscle. Back

15   Q 83 [Dr Hackshaw] Back

16   Q 136 Back

17   Q 147 Back

18   James E. Enstrom and Geoffrey C. Kabat, Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98, British Medical Journal, vol 326 (May 2003), p 1057. Back

19   Q 442 Back

20   Going smoke-free, p 26. Back

21   Qq 65-66 Back

22   Q 433 Back

23   Q 434 Back

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Prepared 19 December 2005