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TABLE 1 – Relative risk of lung cancer among lifelong non-smoking women in relation to smoking by the husband
* indicates a prospective study, all others being case-control studies.
The list excludes studies which have been superseded by later results or included in other studies, or where data or size of study is generally regarded as being inadequate.
A variety of indices of ETS exposure were used in these studies. Nearly all considered smoking by the spouse (or partner) as a measure of exposure, with a number of studies considering ETS exposure by other household members, in the workplace, in childhood or in social situations.
Where necessary, relative risks and 95% confidence limits were estimated from data presented.
The above studies should not be interpreted as indicating a causal effect of ETS:
TABLE 2 - Relative risk of lung cancer among lifelong non-smoking men in relation to smoking by the wife
* indicates a prospective study, all others being case-control studies
The Notes at the foot of Table 1 are also relevant to this Table.
In these studies, the index of exposure is based on smoking by the spouse or, if not available, the nearest equivalent: otherwise exposed to ETS at home.
TABLE 3 - Relative risk of lung cancer among lifelong non-smokers reportedly exposed to ETS exposure in the work place
The Stockwell study (No 32) also reported finding no association but gave no detailed results.
TABLE 4 - Relative risk of lung cancer among lifelong non-smokers in relation to ETS exposure in childhood
Two other studies – Nos 3 and 11, reported finding no association but gave no detailed results.
TABLE 5 - Relative Risk of heart disease among lifelong non-smokers reportedly exposed to ETS in the work place
In study no. 21, the estimates were given by study No 32.
TABLE 6 – Meta - analysis : Lung Cancer
Fixed effects meta- analysis assumes all the individual study estimates derive from a common mean, with their contribution to the overall estimate depending only on within-study variability, with large studies carrying more weight than small ones.
Random effects meta-analysis assumes that the individual study estimates derive from a distribution of effects, with the weighting of the individual estimates depending both on the within-study and between-study variability.
This estimate is inflated by one study (No 14, Gao – China) reporting an extremely high estimate of 12.0 (4.30 – 32.0)
TABLE 7 – Meta-analysis: Lung Cancer
Of studies of smoking by the husband, by publication date
TABLE 8 – Meta-analysis: Heart disease
Meta-analysis, its difficulties and shortcomings, are explained at paragraph 17 et seq.
In this table, ‘spouse ever smoked‘ is used where a study also provides data for ‘spouse current smoker’, and estimates for ‘spouse current smoker’ are used where a study also provides data for ‘spouse ever smoked’.
As for lung cancer, heart disease studies published in recent years show a weaker relationship of risk to smoking by the spouse than previously published studies. It is notable that the relative risks from the two largest US studies, published in 1995 and 2003, were very close to 1.00 in each sex, and not statistically significant.
Again all the studies are subject to the same biases and confounding factors as are noted under Table 1.
Whilst completing this supplementary evidence for the Committee, two reports have been published upon which comment is relevant.
The first is a report by IARC1 , published only at the end of May but a short report of the findings were made and publicised earlier, in 2002. The 222-page section entitled ‘involuntary smoking’ reports the ETS studies and reviews that have been undertaken. It reaches no substantially different conclusions as to the findings of those studies and reviews than is reported here and as was reported in the findings of the IARC study published in 19982 .
IARC’s overall evaluation that exposure to ETS is carcinogenic to humans crucially depends on its evaluation that there is sufficient evidence that ETS causes lung cancer in humans, since IARC clearly considers the evidence that ETS causes other cancers in humans to be inconclusive. IARC considers that there is sufficient evidence of carcinogenicity of sidestream smoke condensates, but this finding on its own could not lead to ETS being classified as a Group 1 carcinogen. For the evidence that ETS causes lung cancer in humans to be considered sufficient, IARC requires that a positive association be observed for which “a causal interpretation is considered to be credible” and for which “chance, bias or confounding” can “be ruled out with reasonable confidence.”
Although IARC presents its own up-dated meta-analysis of the evidence relating ETS exposure to lung cancer risk in non-smokers, these analyses are not adjusted for bias or confounding. Instead, the conclusion that the excess risk “remains after controlling for some potential sources of bias and confounding” relies heavily on previously published meta-analyses of the evidence. The majority of the latter are old and based on limited data; of the only two citations by IARC in the last 10 years, IARC fails to address even adequately the substantial issues concerning misclassification, other biases and confounding that those citations raise, and fails to address the claim that the association of spousal smoking with lung cancer risk in non-smokers essentially disappears if proper adjustments are made. In this regard, the views of the eminent authorities quoted in paragraph 47 of this evidence to the Committee are also pertinent.
The second publication is that of a study3 examining levels of cotinine, a biomarker of exposure to ETS, with the risk of coronary heart disease and stroke. This study took data from the British regional heart study, which is a prospective study of cardiovascular disease in men aged 40-59 years that began in 1978-80. In 1978-80, research nurses administered a questionnaire on present and previous smoking habits – but not asking about ETS exposure - and blood samples were taken and frozen. In 2001-02, those samples were thawed and cotinine concentration (a nicotine metabolite and crude marker for ETS exposure) was measured. The cotinine values for each person were then compared with heart disease events over the period 1980 to 2000.
The study found no increase in risk of stroke associated with ETS exposure as measured by cotinine, a finding which contradicts results from an earlier retrospective case-control study4 . It found no increase in risks for coronary heart disease when measured after 15 to 20 years. For life-time non-smokers, the study reports increases in risk that are not statistically significant for all adjustments apart from one.
As the study states, it was “modest in size with limited precision”. It also expressed concern as to possible misclassification arising from men in the higher cotinine groups smoking cigarettes on an intermittent basis. Such misclassification might account for the otherwise puzzling finding of a relative risk for non-smokers exposed to ETS being almost the same as that for active smokers of 1 to 9 cigarettes a day.
Contrary to the sensationalist headlines reporting the study in the popular press, the researchers’ conclusions were appropriately modest and prompt further questions about the nature of the association, if any, between ETS and heart disease, rather than provide any definitive answers.
Studies referred to in Tables 1 to 5
1 Garfinkel L. Time trends in lung cancer mortality among nonsmokers and a note on passive smoking. J Natl Cancer Inst 1981;66:1061-6.
2 Chan WC, Fung SC. Lung cancer in non-smokers in Hong Kong. In: Grundmann E, editor. Cancer Epidemiology, Volume 6. Stuttgart, New York: Gustav Fischer Verlag, 1982;199-202. (Cancer Campaign.)
3 Correa P, Pickle LW, Fontham E, Lin Y, Haenszel W. Passive smoking and lung cancer. Lancet 1983;2:595-7.
4 Trichopoulos D, Kalandidi A, Sparros L. Lung cancer and passive smoking: conclusion of Greek study [Letter]. Lancet 1983;2:677-8.
5 Buffler PA, Pickle LW, Mason TJ, Contant C. The causes of lung cancer in Texas. In: Mizell M, Correa P, editors. Lung cancer: causes and prevention, Proceedings of the International Lung CancerUpdate Conference, New Orleans, Louisiana, March 3-5, 1983. Deerfield Beach, Florida: Verlag Chemie International, Inc, 1984;83-99.
6 Hirayama T. Lung cancer in Japan: effects of nutrition and passive smoking. In: Mizell M, Correa P, editors. Lung cancer: causes and prevention, Proceedings of the International Lung Cancer UpdateConference, New Orleans, Louisiana, March 3-5, 1983. Deerfield Beach, Florida: Verlag Chemie International, Inc, 1984;175-95.
7 Kabat GC, Wynder EL. Lung cancer in nonsmokers. Cancer 1984;53:1214-21.
8 Garfinkel L, Auerbach O, Joubert L. Involuntary smoking and lung cancer: a case-control study. J Natl Cancer Inst 1985;75:463-9.
9 Lam WK. A clinical and epidemiological study of carcinoma of lung in Hong Kong [Thesis]. University of Hong Kong; 1985.
10 Wu AH, Henderson BE, Pike MC, Yu MC. Smoking and other risk factors for lung cancer in women. J Natl Cancer Inst 1985;74:747-51.
11 Akiba S, Kato H, Blot WJ. Passive smoking and lung cancer among Japanese women. Cancer Res 1986;46:4804-7.
12 Lee PN, Chamberlain J, Alderson MR. Relationship of passive smoking to risk of lung cancer and other smoking-associated diseases. Br J Cancer 1986;54:97-105.
13 Brownson RC, Reif JS, Keefe TJ, Ferguson SW, Pritzl JA. Risk factors for adenocarcinoma of the lung. Am J Epidemiol 1987;125:25-34.
14 Gao Y-T, Blot WJ, Zheng W, Ershow AG, Hsu CW, Levin LI, et al. Lung cancer among Chinese women. Int J Cancer 1987;40:604-9.
15 Humble CG, Samet JM, Pathak DR. Marriage to a smoker and lung cancer risk. Am J Public Health 1987;77:598-602.
16a Koo LC, Ho JH-C, Saw D, Ho C-Y. Measurements of passive smoking and estimates of lung cancer risk among non-smoking Chinese females. Int J Cancer 1987;39:162-9.
16b Koo LC, Ho JH-C, Saw D. Is passive smoking an added risk factor for lung cancer in Chinese women? J Exp Clin Cancer Res 1984;3:277-83.
17 Lam TH, Kung ITM, Wong CM, Lam WK, Kleevens JWL, Saw D, et al. Smoking, passive smoking and histological types in lung cancer in Hong Kong Chinese women. Br J Cancer 1987;56:673-8.
18 Pershagen G, Hrubec Z, Svensson C. Passive smoking and lung cancer in Swedish women. Am J Epidemiol 1987;125:17-24.
19 Butler TL. The relationship of passive smoking to various health outcomes among Seventh day Adventists in California [Thesis]. Los Angeles: University of California; 1988.
20 Geng G-Y, Liang ZH, Zhang AY, Wu GL. On the relationship between cigarette smoking and female lung cancer. In: Aoki M, Hisamichi S, Tominaga S, editors. Smoking and health 1987, Proceedings ofthe 6th World Conference on Smoking and Health, Tokyo, 9-12 November 1987. Amsterdam: Elsevier Science Publishers B.V. (Biomedical Division), 1988;483-6. International Congress Series No. 780.
21 Inoue R, Hirayama T. Passive smoking and lung cancer in women. In: Aoki M, Hisamichi S, Tominaga S, editors. Smoking and health 1987, Proceedings of the 6th World Conference on Smokingand Health, Tokyo, 9-12 November 1987. Amsterdam: Elsevier Science Publishers B.V. (Biomedical Division), 1988;283-5. International Congress Series No. 780.
22 Shimizu H, Morishita M, Mizuno K, Masuda T, Ogura Y, Santo M, et al. A case-control study of lung cancer in nonsmoking women. Tohoku J Exp Med 1988;154:389-97.
23 Choi S-Y, Lee K-H, Lee T-O. A case-control study on risk factors in lung cancer. Korean J Epidemiol 1989;11:66-80.
24 Hole DJ, Gillis CR, Chopra C, Hawthorne VM. Passive smoking and cardiorespiratory health in a general population in the west of Scotland. BMJ 1989;299:423-7.
25 Svensson C, Pershagen G, Klominek J. Smoking and passive smoking in relation to lung cancer in women. Acta Oncol 1989;28:623-9.
26 Janerich DT, Thompson WD, Varela LR, Greenwald P, Chorost S, Tucci C, et al. Lung cancer and exposure to tobacco smoke in the household. N Engl J Med 1990;323:632-6.
27 Kalandidi A, Katsouyanni K, Voropoulou N, Bastas G, Saracci R, Trichopoulos D. Passive smoking and diet in the etiology of lung cancer among non-smokers. Cancer Causes Control 1990; 1:15-21.
28 Sobue T. Association of indoor air pollution and lifestyle with lung cancer in Osaka, Japan. Int J Epidemiol 1990;19(Suppl 1):S62-S66.
29 Wu-Williams AH, Dai XD, Blot W, Xu ZY, Sun XW, Xiao HP, et al. Lung cancer among women in north-east China. Br J Cancer 1990;62:982-7.
30 Liu Z, He X, Chapman RS. Smoking and other risk factors for lung cancer in Xuanwei, China. Int J Epidemiol 1991; 20:26-31.
31 Brownson RC, Alavanja MCR, Hock ET, Loy TS. Passive smoking and lung cancer in non-smoking women. Am J Public Health 1992;82:1525-30.
32 Stockwell HG, Goldman AL, Lyman GH, Noss CI, Armstrong AW, Pinkham PA, et al. Environmental tobacco smoke and lung cancer risk in nonsmoking women. J Natl Cancer Inst 1992;84:1417-22.
33 Du YX, Cha Q, Chen YZ, Wu JM. Exposure to environmental tobacco smoke and female lung cancer in Guangzhou, China. In: Proceedings of Indoor Air '93, Volume 1. 1993;511-6.
34 Liu Q, Sasco AJ, Riboli E, Hu MX. Indoor air pollution and lung cancer in Guangzhou, People's Republic of China. Am J Epidemiol 1993;137:145-54.
35a Fontham ETH, Correa P, Reynolds P, Wu-Williams A, Buffler PA, Greenberg RS, et al. Environmental tobacco smoke and lung cancer in nonsmoking women. A multicenter study. JAMA 1994;271:1752-9.
35b Reynolds P, Fontham ETH, Wu A, Buffler PA, Greenberg RS. Occupational exposure to environmental tobacco smoke [Letter]. JAMA 1996;275:441-2.
36 Layard MW. Ischemic heart disease, lung cancer, and spousal smoking in the National Mortality Followback Survey. 1994. Submitted to OSHA re Proposed Rules, Federal Register Vol 59, No 65, Docket No H-122
37 de Waard F, Kemmeren JM, van Ginkel LA, Stolker AAM. Urinary cotinine and lung cancer risk in a female cohort. Br J Cancer 1995;72:784-7.
38 Kabat GC, Stellman SD, Wynder EL. Relation between exposure to environmental tobacco smoke and lung cancer in lifetime nonsmokers. Am J Epidemiol 1995;142:141-8. Erratum 1996;143:527.
39 Schwartz AG, Yang P, Swanson GM. Familial risk of lung cancer among nonsmokers and their relatives. Am J Epidemiol 1996;144:554-62.
40 Sun X-W, Dai X-D, Lin C-Y, Shi Y-B, Ma Y-Y, Li W. Environmental tobacco smoke (ETS) and lung cancer among nonsmoking women in Harbin, China [Abstract]. International symposium on lifestyle factors and human lung cancer, Guangzhou, China, 12-16 December 1994. Lung Cancer 1996;14(Suppl 1):S237.
41 Wang S, Hu Y, Wu Y, Li X, Chi G, Chen Y, et al. A comparative study of the risk factors for lung cancer in Guangdong, China. International symposium on lifestyle factors and human lung cancer, Guangzhou, China, 12-16 December 1994. Lung Cancer 1996;14(Suppl 1):S99-S105.
42 Wang T, Zhou B, Shi J. Lung cancer in nonsmoking Chinese women: a case-control study. International symposium on lifestyle factors and human lung cancer, Guangzhou, China, 12-16 December 1994. Lung Cancer 1996;14(Suppl 1):S93-S98.
43a Cardenas VM, Thun MJ, Austin H, Lally CA, Clark WS, Greenberg RS, et al. Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study II. Cancer Causes Control 1997; 8:57-64. Erratum 1997;8:675.
43b Cardenas VM. Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study II [Thesis]. Atlanta, Georgia: Emory University; 1994.
44 Zheng S, Fen R, Wu Z, Cao L, Ling Y, Li M, et al. Studies on relationship between passive smoking and lung cancer in non-smoking women. Zhonghua Yu Fang Yi Xue Za Zhi 1997;31:163-5.
45 Auvinen A, Makelainen I, Hakama M, Castren O, Pukkala E, Reisbacka H, et al. Indoor radon exposure and risk of lung cancer: a nested case-control study in Finland [Erratum letter]. J NatlCancer Inst 1998;90:401-2.
46 Boffetta P, Agudo A, Ahrens W, Benhamou E, Benhamou S, Darby SC, et al. Multicenter casecontrol study of exposure to environmental tobacco smoke and lung cancer in Europe. J Natl CancerInst 1998;90:1440-50.
47 Shen XB, Wang GX, Zhou BS. Relation of exposure to environmental tobacco smoke and pulmonary adenocarcinoma in non-smoking women: A case control study in Nanjing. Oncol Rep 1998;5:1221-3.
48 Zaridze D, Maximovitch D, Zemlyanaya G, Aitakov ZN, Boffetta P. Exposure to environmental tobacco smoke and risk of lung cancer in non-smoking women from Moscow, Russia. Int J Cancer 1998;75:335-8.
49 Boffetta P, Ahrens W, Nyberg F, Mukeria A, Brüske-Hohlfeld I, Fortes C, et al. Exposure to environmental tobacco smoke and risk of adenocarcinoma of the lung. Int J Cancer 1999;83:635-9.
50 Jee SH, Ohrr H, Kim IS. Effects of husbands' smoking on the incidence of lung cancer in Korean women. Int J Epidemiol 1999;28:824-8.
51 Rapiti E, Jindal SK, Gupta D, Boffetta P. Passive smoking and lung cancer in Chandigarh, India. Lung Cancer 1999;23:183-9.
52 Speizer FE, Colditz GA, Hunter DJ, Rosner B, Hennekens C. Prospective study of smoking, antioxidant intake, and lung cancer in middle-aged women (USA). Cancer Causes Control 1999;10:475-82.
53 Zhong L, Goldberg MS, Gao Y-T, Jin F. A case-control study of lung cancer and environmental tobacco smoke among nonsmoking women living in Shanghai, China. Cancer Causes Control 1999;10:607-16.
54 Lee C-H, Ko Y-C, Goggins W, Huang J-J, Huang M-S, Kao E-L, et al. Lifetime environmental exposure to tobacco smoke and primary lung cancer of non-smoking Taiwanese women. Int J Epidemiol 2000;29:224-31.
55 Malats N, Camus-Radon A-M, Nyberg F, Ahrens W, Constantinescu V, Mukeria A, et al. Lung cancer risk in nonsmokers and GSTM1 and GSTT1 genetic polymorphism. Cancer EpidemiolBiomarkers Prev 2000;9:827-33.
56 Wang L, Lubin JH, Zhang SR, Metayer C, Xia Y, Brenner A, et al. Lung cancer and environmental tobacco smoke in a non-industrial area of China. Int J Cancer 2000;88:139-45.
57 Johnson KC, Hu J, Mao Y. Lifetime residential and workplace exposure to environmental tobacco smoke and lung cancer in never-smoking women, Canada 1994-97. Int J Cancer 2001;93:902-6.
58 Lagarde F, Axelsson G, Damber L, Mellander H, Nyberg F, Pershagen G. Residential radon and lung cancer among never-smokers in Sweden. Epidemiology 2001;12:396-404.
59 Nishino Y, Tsubono Y, Tsuji I, Komatsu S, Kanemura S, Nakatsuka H, et al. Passive smoking at home and cancer risk: a population-based prospective study in Japanese nonsmoking women. CancerCauses Control 2001;12:797-802.
60 Ohno Y, Wakai K, Ando M, Shimokata K, Saka H, Yamamoto M, et al. 151: Studies on health effects of passive smoking - multicancer case-control study of the relationship between passive smoking and lung cancer in lifetime nonsmokers. In: SRF Annual Report 2001. 2002;857-61.
61 Rachtan J. Smoking, passive smoking and lung cancer cell types among women in Poland. Lung Cancer 2002;35:129-36.
62 Seow A, Poh W-T, Teh M, Eng P, Wang Y-T, Tan W-C, et al. Diet, reproductive factors and lung cancer risk among Chinese women in Singapore: evidence for a protective effect of soy in nonsmokers. Int J Cancer 2002;97:365-71.
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64 Zatloukal P, Kubík A, Pauk N, Tomášek L, Petruzelka L. Adenocarcinoma of the lung among women: risk associated with smoking, prior lung disease, diet and menstrual and pregnancy history. LungCancer 2003;41:283-93.
Note on judgments in employment cases involving ETS
The only cases of which the TMA is aware are those which there is an official court record, or where there has been a news report in the columns of the press.
The only case in which there has been full adjudication of the facts is the English case of Silvia Sparrow v St Andrew’s Homes Limited that was heard in the Manchester High Court in 1998. In this case, the Plaintiff, who was a state-enrolled nurse in a nursing home, claimed that ETS had caused or aggravated her asthma. In May 1998, her claim was dismissed and the Judge found that her employers had done all that was reasonably practicable to take reasonable care of Mrs Sparrow’s safety at work. In particular, the Judge concluded that there was insufficient scientific evidence relating to the causation of asthma in adults to be able to conclude that ETS caused her asthma. He said that what science there was, was “small in compass and speculative in weight”. The onus was on Mrs Sparrow to find other work, given that simple adjustments to the work place could not resolve the issue to her satisfaction.
In 1990, a case was heard by the Social Security Commission, Clay v Adjudication Officer. It is understood that Miss Clay worked as a social security officer and claimed that her asthma was aggravated by exposure to ETS. The Social Security Commissioner who decided her case, found that she had extreme sensitivity to the chemicals in tobacco smoke and that the case turned on its own special facts. He specifically stated that his decision was “no precedent for other cases where it may be alleged that there has been a deleterious effect from the gradual day-by-day process of employees being obliged to inhale other employees’ tobacco smoke.”
There may be other cases which have been brought in the UK, but these are the only two of which we are aware and for which we have any information.
The website of ASH makes reference to an award made in May 2000 in relation to Matthew Comstive, whose mother, Collette Comstive, was apparently exposed to ETS while working at Great Universal Stores during her pregnancy. ASH reported that a judge in chambers awarded the sum of £5,000. However, this may have been as a result of a settlement, rather than a court adjudication.
We are also aware that over the past 10 years there have been some 10 cases in respect of which legal proceedings were commenced but then settled, with the settlement details generally remaining confidential:
In England and Wales
Veronica Bland v Stockport Borough Council (1993) (reported settlement - £15,000)
Beryl Roe v Stockport Borough Council (1995) (reported settlement - £25,000)
Walmsley v Scottish & Newcastle (1997)
Michael Dunn v Napoleons Casino (2000)
In Northern Ireland
McGuirk v Southern Health & Social Services Board (1993)
McCalmont v Eastern Health & Social Services Board (1995)
Megarry v Police Authority for Northern Ireland (1998)
McClusky v Groby ex-Servicemen’s Social Club (2001)
Agnes Rae v Strathclyde Joint Police Board (1995)
Margaret Pacetta v Clydesdale Bank (1996)
We are also aware of several cases brought to the Employment Tribunal and Employment Appeals Tribunal in the context of constructive unfair dismissal claims:
In Waltons & Morse v Dorrington (1997), Mrs Dorrington lodged a claim for constructive and unfair dismissal on the grounds that she was forced to resign as a result of her employer’s failure to provide a smoke-free environment in which she could work. On appeal the Employment Appeals Tribunal held that:
“[I]t is an implied term of every contract of employment that the employer will provide and monitor for employees, so far as is reasonably practicable, a working environment which is reasonably suitable for the performance by them of their contractual duties. The starting point for the implication of such a term is the duty on an employer under s.2(2)(e) of the Health and Safety at Work Act to provide and maintain a working environment for employees that is reasonably safe and without risk to health and is adequate as regards facilities and arrangements for their welfare at work. The right of an employee not to be required to sit in a smoke-filled atmosphere affects the welfare of employees at work, even if it is not something which directly is concerned with their health or can be proved to be a risk to health.”
The Employment Appeals Tribunal concluded that it would have been reasonably practicable for the employers to have solved the problem by telling those who smoked that they would not be permitted to smoke in the building because it rendered the working conditions of other employees unacceptable. It was therefore reasonably practicable for the employers to have provided the employee with a working environment that was suitable for the performance by her of her contractual duties. The conditions in which they were requiring Mrs Dorrington to work therefore rendered them in breach of the implied term to provide a reasonably suitable working environment.
The Employment Appeal Tribunal has also considered the issue of ETS from the perspective of a smoker. In Dryden v Greater Glasgow Health Board (1992), Mrs Dryden, a nurse employed at the Western Infirmary in Glasgow, lodged a complaint of constructive dismissal following a ban on smoking on the employer’s premises. The Tribunal dismissed the complaint holding that there was no implied term to the effect that Mrs Dryden was entitled to be provided with a place to smoke at work. There was no basis for holding that there was any implied term to the effect that failure to provide such facilities was a breach of the implied term of trust and confidence.
Thank you for the opportunity to submit supplementary evidence to the Committee for consideration. I hope the points outlined below help clarify our position and will aid the Committee’s consideration of the Prohibition of Smoking in Regulated Areas (Scotland) Bill (‘the Bill’).
In the oral evidence session the Committee questioned the British Hospitality Association Scotland’s (BHA) position. The BHA supports the Voluntary Charter as long as it continues to have industry and government support. If the Voluntary Charter is no longer supported in this way a total ban on smoking in places of employment is viewed by the BHA as the only logical step open to government. A partial ban on smoking in certain public areas or a ban that is introduced at a local authority level are viewed by our organisation as the worst possible policy or legislative options.
If legislation is to be brought forward it must deliver clear health benefits, be Scotland-wide or in the case of Health and Safety legislation UK-wide. The legislation must also be straight forward to implement and enforce. Penalties must be focussed on those individuals who smoke in areas of employment rather than penalising operators for the offences of others. Legislation must be applied equitably across all areas to which the public have access and not just where food is served. The Bill as currently drafted does not meet this criterion.
The BHA believes that the Voluntary Charter has delivered tangible results; indeed, as the Committee has already heard it has met or exceeded almost all of its original targets. The Voluntary Charter provides consumer choice while extending the number of smoke free areas. However, we are fully aware that for the Charter to succeed it must have political, public and industry support. If the situation arises where the Voluntary Charter no longer has support, we would then support legislation in this area.
The BHA has a number of concerns with the Bill as currently drafted. These include:
The Committee inquired whether the Voluntary Charter Group had discussed ‘ratcheting’ up the Voluntary Charter in response to concerns that it was not delivering improvements at a rate which satisfied stakeholders. In a meeting with Tom McCabe MSP, Deputy Minister for Health on 20 May 2004, the Charter Group comprising the Scottish Licensed Trade Association, Scottish Beer and Pub Association and the BHA made a number of proposals which would ‘ratchet’ up the Voluntary Charter. These proposals would extend the Charter to include registered clubs within the Charter and that:
The Charter Group also suggested that under a revamped Voluntary Charter all licensed premises would be required to have a designated (but not segregated) non-smoking area in areas where food is not served and that the size of that area will be increased yearly as follows:
Year 1 – minimum of 30% of public floor space
Year 2 – minimum of 40% of public floor space
Year 3 – minimum of 50% of public floor space
It was the view of the Voluntary Group that the three year period will allow the Scottish Executive to monitor the impact of the new regulations and gauge public opinion as to whether the percentages should be increased. However, the position of the Deputy Health Minister was that the Voluntary Charter Group should put these proposals forward during the Scottish Executive consultation on smoking in public.
The Committee requested further information on the BHA’s position on the economic impact of the Bill. Our position is that the Scottish Executive research (commissioned as part of the Scottish Executive consultation) on the economic impact of similar bans on smoking should be carried out and published before legislation in this area is considered.
I hope this additional clarification and information will be helpful and does not leave the Committee in doubt of our position that the only options are a continuation of the Voluntary Charter or a total ban on smoking in public.
1 IARC Monograph on the Evaluation of Carcinogenic Risks to Humans, Volume 83, Tobacco Smoke and Involuntary Smoking. 2004
2 Boffetta, P et al, Multi-centre case-control study of exposure to environmental tobacco smoke in Europe, Journal of the National Cancer Institute, 1998;90: 1440-1450 and IARC Technical Report No 33, IARC 1998
3 Whincup, P H et al, Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ Online First,30 June2004
4 Bonita, R et al, Passive smoking as well as active smoking increases the risk of acute stroke. Tobacco Control 1999;8:156-160