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Health Evidence Bulletins - Wales (logo)
Team Leaders: Dr Meirion Evans. Mr Alan Bennett

Literature searches completed on 10 May 1998

5: Environmental Tobacco Smoke (Passive smoking)

This document is a supplement to, not a substitute for, professional skills and experience. Users are advised to consult the supporting evidence for a consideration of all the implications of a recommendation.

The Statements The Evidence
5.1 The carcinogenic potential of ETS
5.1a. Environmental tobacco smoke (ETS, passive smoking) is a Group A human carcinogen as defined by the United States Environment Protection Agency i.
See also Cancers bulletin in this series ii.
i. Environmental Protection Agency Respiratory health effects of passive smoking: lung cancer and other disorders. Washington DC: Office of Air & Radiation, 1992 (EPA/600/6-90/006F)
(Type IV evidence - systematic review & meta-analysis of observational studies)
ii. In preparation
5.2 Effects of ETS in adults
5.2a. Exposure to ETS is a cause of lung cancer in never-smoking spouses (especially women ),i,ii and in non-smoking work colleagues (especially women ) iii,iv. The estimated excess risk of lung cancer in women non-smokers who live with smokers is 26% (95% confidence interval 7-47%)ii. This represents an extra 2-3 lung cancer deaths per year per 100,000 non-smokers exposed to ETSv. There is also a dose-response between cancer risk and number of cigarettes smoked by a person’s partnerii. i. Environmental Protection Agency Respiratory health effects of passive smoking: lung cancer and other disorders. Washington DC: Office of Air & Radiation, 1992 (EPA/600/6-90/006F)
(Type IV evidence - systematic review & meta-analysis of observational studies)
ii. Halshaw AK, Law M, Wald NJ. The accumulated evidence on lung cancer and environmental tobacco smoke. British Medical Journal 1997; 315: 980 – 988.
http://www.bmj.com/cgi/content/full/315/7114/980
(Type IV evidence - systematic review & meta-analysis of observational studies)
iii. Reynolds P, Fontham E. Passive smoking and lung cancer. Annals of Medicine. 1995; 27: 633 - 640
(Type IV evidence - systematic review & meta-analysis of observational studies)
iv. Siegal M. A review of employee exposure and health effects. Journal of the American Medical Association 1993; 270: 490 - 493
(Type IV evidence - systematic review & meta-analysis of observational studies)
v. UK Health Departments. Report of the Scientific Committee on Tobacco and Health. London: HMSO, 1998
(Type V evidence – expert opinion)

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5.2b. Exposure to ETS is a cause of ischaemic heart disease (IHD) in never-smoking spousesi. Enhanced platelet aggregation is a plausible mechanism for the association. The best estimate of excess risk of IHD in non-smokers exposed to ETS compared with those not exposed is 23% (relative risk, RR = 1.23)i.
See also Cardiovascular Diseases bulletin in this seriesii.
i. Law MR, Morris JK, Wald NJ. Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence. British Medical Journal 1997; 315: 973 – 980
http://www.bmj.com/cgi/content/full/315/7114/973
(Type IV evidence - systematic review & meta-analysis of observational studies)
ii. Health Evidence Bulletins Wales: Cardiovascular Diseases. Cardiff: Welsh Office, 1998
http://hebw.cardiff.ac.uk/cardio/chapter1.html
(Summaries of evidence classified according to type)
5.2c. ETS also has subtle but significant effects on respiratory health including coughing, phlegm production, chest discomfort and reduced lung functioni. i. Environmental Protection Agency Respiratory health effects of passive smoking: lung cancer and other disorders. Washington DC: Office of Air & Radiation, 1992 (EPA/600/6-90/006F)
(Type IV evidence - systematic review & meta-analysis of observational studies)
5.3 Effects of ETS in infants
5.3a. The risk of Sudden Infant Death Syndrome (SIDS) is doubled in infants of mothers who smoke. The pooled odds ratio for maternal smoking is 2.08 (95%CI 1.90 to 2.21)i.
See also Maternal & Early Child Health bulletin in this seriesii.
i. Anderson RH, Cook DG. Passive smoking and sudden infant death syndrome: review of the epidemiological evidence. Thorax 1997; 52: 1003 - 1009
(Type IV evidence - systematic review & meta-analysis of observational studies)
ii. Health Evidence Bulletins Wales: Maternal & Early Child Health. Cardiff: Welsh Office, 1998
http://hebw.cardiff.ac.uk/maternal/chapter23.html
(Summaries of evidence classified according to type)
5.3b. Parental smoking also increases risk of lower respiratory tract illness in infants. The pooled odds ratio for either parent smoking is 1.48 (95%CI 1.40 to 1.57) and for maternal smoking is 1.64 (95%CI 1.54 to 1.73)I.
See also Respiratory Diseases bulletin in this seriesii.
i. Strachan DP, Cook DG. Parental smoking and lower respiratory illness in infancy and early childhood. Thorax 1997; 52: 905 - 914
(Type IV evidence - systematic review & meta-analysis of observational studies)
ii. Health Evidence Bulletins Wales: Respiratory Diseases. Cardiff: Welsh Office, 1998
http://hebw.cardiff.ac.uk/respdis/chapter4.html
(Summaries of evidence classified according to type)

Literature searches completed 10.5.98
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5.4 Effects of ETS in children
5.4a. Parental smoking increases risk of asthma and respiratory symptoms in schoolchildreni,ii,iii. ETS is associated with increased prevalence of cough, sputum and wheeze and a small but significant reduction in lung functioni. It exacerbates symptoms in asthmatics,i,iii and is also associated with increased risk in children under 5 of pneumonia, bronchitis and bronchiolitis i,ii. There is evidence of a dose-response relationship between risk and number of smokers in the homeiii. The pooled odds ratios for either parent smoking are 1.21 (95%CI 1.10 to 1.34) for asthma; 1.24 (95%CI 1.17 to 1.31) for wheeze; and 1.40 (95%CI 1.27 to 1.53) for coughiii. Maternal smoking is associated with an increased risk of wheeze up to age 6 (pooled odds ratio 1.31, 95%CI 1.22 to 1.41) but less strongly thereafter (pooled odds ratio 1.13, 95%CI 1.04 to 1.22)iv. No consistent relationship has been found between parental smoking and either allergic sensitisation or bronchial hyper-reactivity. Evidence that exposure to ETS causes asthma is therefore inconclusiveiii.
See also Respiratory Diseases bulletin in this seriesiv.
i. Environmental Protection Agency Respiratory health effects of passive smoking: lung cancer and other disorders. Washington DC: Office of Air & Radiation, 1992 (EPA/600/6-90/006F)
(Type IV evidence - systematic review & meta-analysis of observational studies)
ii.
DiFranza JR, Lew RA. Morbidity and mortality associated with use of tobacco products by other people. Pediatrics 1996; 97: 560 - 568
(Type IV evidence - systematic review & meta-analysis of observational studies)
iii.
Cook DG, Strachan DP. Parental smoking and prevalence of respiratory symptoms and asthma in school age children. Thorax 1997; 52: 1081 - 1094
(Type IV evidence - systematic review & meta-analysis of observational studies)
iv. Strachan DP, Cook DG. Parental smoking and childhood asthma: longitudinal and case-control studies. Thorax 1998; 53: 204 - 212
(Type IV evidence - systematic review & meta-analysis of observational studies)
v. Health Evidence Bulletins Wales: Respiratory Diseases. Cardiff: Welsh Office, 1998
http://hebw.cardiff.ac.uk/respdis/chapter4.html
(Summaries of evidence classified according to type)
5.4b. Middle ear disease in children is linked with parental smoking and this association is likely to be causali,ii. The pooled odds ratio for recurrent otitis media if either parent smokes is 1.41 (95%CI 1.19 to 1.65), and for middle ear effusion is 1.38 (95%CI 1.23 to 1.55)i.
See also Respiratory Diseases bulletin in this series.
i. DiFranza JR, Lew RA. Morbidity and mortality associated with use of tobacco products by other people. Pediatrics 1996; 97: 560 - 568
(Type IV evidence - systematic review & meta-analysis of observational studies)
ii. Strachan DP, Cook DG. Passive smoking, middle ear disease and adenotonsillectomy in children. Thorax 1998; 53: 50 - 56
(Type IV evidence - systematic review & meta-analysis of observational studies)
5.5 ETS and blood cotinine
5.5a. There appears to be a strong link between self reported ETS exposure levels and blood cotinine levels and diagnosed disease i.
Further research to link cotinine with exposure and morbidity, such that cotinine could be used as a useful screening tool, would be helpful.
i. Tunstall-Pedoe H, Brown CA, et al. Passive smoking by self report and serum cotinine and the prevalence of respiratory and coronary heart disease in the Scottish Heart Health Study. Journal of Epidemiology and Community Health 1995; 49: 139 – 143
(Type IV evidence – observational study

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Health Evidence Bulletins: Wales, Duthie Library, UWCM, Cardiff CF14 4XN. e-mail: weightmanal@cardiff.ac.uk