Current Evidence On The Health Impact Of SHS

Cancers

In 2002, the International Agency for Research on Cancer (IARC) reviewed more than 50 studies of passive smoking and lung cancer and concluded that the excess risk of lung cancer from exposure to a spouse’s smoking was 20% for women and 30% for men. In Britain, with a population of around 58 million people, this would amount to several hundred extra lung cancer deaths per year. Daily exposure to SHS for many hours during childhood was found by Vineis and colleagues (2005) to be associated with an excess risk of lung cancer in adulthood of 263%. The Californian EPA has carefully reviewed available evidence up to 2005 in an attempt to determine which health impacts can be causally associated with SHS exposure. They concluded that, as well as lung cancer, exposure to SHS is causally associated with nasal cancer and with breast cancer in younger, premenopausal women. They found evidence suggestive of a causal impact on cervical and nasopharyngeal cancer in adults and brain cancer and lymphoma in children.

Heart Disease And Stroke

The chemicals in SHS have an immediate impact on body tissues and give rise to damage that can culminate in heart disease and stroke. In the UK, the excess risk of coronary heart disease (CHD) among nonsmoking men was 45% to 57% over 20 years, according to their cotinine levels at baseline (Whincup et al., 2004). Barnoya and Glantz (2005) point out that the excess risk of CHD in passive smokers (30%) appears high when compared with the excess risk of CHD in smokers (78%) and may be due to sensitivity of body tissues to the chemicals in tobacco smoke such that even a small concentration can effect a fairly large response. It is widely accepted that SHS exposure is causally related to heart disease mortality, acute and chronic CHD morbidity, and altered vascular properties of the circulatory system.

In contrast to the evidence for an impact of SHS on CHD, the evidence for an impact on stroke is mixed. For example, the UK study mentioned above did not find an association with stroke but other studies have done so. In a retrospective case-control study using a population-based stroke register in New Zealand, exposure to secondhand smoke was associated with an excess risk of stroke of 74% (Bonita et al., 1999). In another case control study of hospital patients with acute ischemic stroke and neighborhood controls in Australia, there was an excess risk of stroke of 103% for exposure from a spouse with a dose–response relationship according to the number of cigarettes smoked by the spouse (You et al., 1999). In a 16-year follow-up of 27 698 never-smoking subjects aged 30 to 85 years in the Kaiser Permanente Medical Care Program in the United States, there was an age and sex-adjusted excess risk of ischemic stroke of 51% for more than 20 hours exposure to SHS per week at home but no effect for workplace exposure (Iribarren et al., 2004). Finally, in a case-control study of deaths in Hong Kong, exposure to SHS at home was implicated in fatal stroke with an excess risk of dying from stroke of up to 108% for those with two or more smokers at home (McGhee et al., 2005). Thus, the evidence on stroke appears to be mounting, leading the California EPA to conclude that the evidence at present is suggestive of a causal impact of SHS on risk of stroke in adults.

Other Adult Conditions

There are substantial data on self-reported respiratory symptoms associated with workplace exposure to SHS and in places where smoke-free workplace policies have been implemented surveys have shown reductions in symptoms. The current evidence supports a causal relationship with asthma, both induction and exacerbation, and with eye and nasal irritation, and it is suggestive of a causal relationship with chronic respiratory symptoms and exacerbation of cystic fibrosis. SHS exposure may also impact on fertility and menstrual disorders.

Childhood Conditions

In children, it is accepted that there is a causal relationship between exposure to SHS and a variety of respiratory disorders such as asthma, acute lower respiratory infections such as bronchitis and pneumonia, chronic respiratory symptoms, and middle ear infections. Both active and passive smoking by the mother during pregnancy as well as exposure of the baby to SHS after birth may have an impact on the child’s lung function. There is also evidence of a causal relationship between SHS exposure and lowbirthweight babies, pre-term delivery, and sudden infant death syndrome (SIDS), while there is suggestive evidence of a causal link with spontaneous abortion, decreased pulmonary function, and allergic sensitization in newborns, as well as developmental disorders in children, leading to impaired cognition and behavioral problems.

Costs

In the face of mounting evidence of health effects and the possibility of legislative measures to reduce exposure, there have been attempts to assess the costs of passive smoking to communities in both summary health impacts and dollar costs. One of the most important impacts is on mortality. In the United States, it has been estimated that SHS causes between 35 000 and 62 000 deaths a year from cardiovascular disease, compared with an estimate of around 143 000 from active smoking, and about 3000 deaths due to lung cancer compared with 85 000 for active smoking (U.S. Department of Health and Human Services, 2004). In the UK, Jamrozik (2005) estimated that passive smoking at work causes over 600 deaths per year while passive smoking at home accounts for almost 11 000 deaths per year, most of these in people over 65 years old. The Society of Actuaries carried out a partial costing of the economic impacts of SHS in the United States using available data and concluded that the annual costs of excess medical care, mortality, and morbidity were over US$10 billion (Behan et al., 2005). In Hong Kong, the cost of health-related impacts of passive smoking was estimated to be around a quarter of the equivalent costs of active smoking (McGhee et al., 2006).

Smoke-Free Policies

The World Health Organization Framework Convention on Tobacco Control (FCTC) has as its objective

‘to protect present and future generations from the devastating health, social, environmental and economic consequences of tobacco consumption and exposure to tobacco smoke.’

Among its guiding principles is the statement that

‘effective legislative, executive, administrative or other measures should be contemplated at the appropriate governmental level to protect all persons from exposure to tobacco smoke.’

With the support of the FCTC, the move toward smoke-free policies around the world has gathered pace. Several countries now have smoke-free workplaces, including restaurants and bars. Initial findings on impacts of these policies are encouraging with reduced exposures to SHS among staff, customers, and other visitors. A smoke-free policy temporarily enacted in Helena, Montana, in the United States was associated with an immediate downturn in hospital admission rates for acute myocardial infarction (Sargent et al., 2004). After the law was repealed 6 months later, the admission rates rose again. Further data on the impact of smoke free legislation on outcomes, such as acute admissions to hospitals, should become available as smoke-free legislation is enacted in more places.

Even outdoors, a dense plume of tobacco smoke poses a potential hazard to those who cannot avoid it. Hence parks, beaches, the entrances to smoke-free buildings, and transport interchanges are being considered in various jurisdictions for designation as smoke-free areas. Another incentive toward such restrictions is the littering of areas in which smoking is permitted by dropped cigarette butts, which is apparently increasing as smokers are forced out of buildings. In some countries, smoking inside a car is being considered as a road safety issue and smoking inside the home as potential child abuse. Thus, smoke-free policies are increasingly seen as important public health measures by a variety of agencies.

In health policy terms, passive smoking is often seen as a more serious problem than active smoking because of the harm done to lifelong nonsmokers, to children in their most vulnerable years, and to a large proportion of the population due to the ubiquitous presence of smokers in many countries. The effects of passive smoking have long been denied by the tobacco industry. However, the overall weight of evidence indicates that exposure to secondhand smoke is a major and wholly preventable public health hazard.

Bibliography:

  1. Barnoya J and Glantz SA (2005) Cardiovascular effects of secondhand smoke: Nearly as large as smoking. Circulation 111: 2684–2698.
  2. Behan DF, Eriksen MP, and Lin Y (2005) Economic Effects of Environmental Tobacco Smoke. Society of Actuaries (SOA) http://www.soa.org/.
  3. Bonita R, Duncan J, Truelsen T, Jackson RT, and Beaglehole R (1999) Passive smoking as well as active smoking increases the risk of acute stroke. British Medical Journal 8: 156–160.
  4. Gilpin EA, Farkas AJ, Emery SL, Ake CF, and Pierce JP (2002) Clean indoor air: Advances in California, 1990–1999. American Journal of Public Health 92: 785–791.
  5. Iribarren C, Darbinian J, Klatsky AL, and Friedman GD (2004) Cohort study of exposure to environmental tobacco smoke and risk of first ischemic stroke and transient ischemic attack. Neuroepidemiology 23: 38–44.
  6. Jamrozik K (2005) Estimate of deaths attributable to passive smoking among U.K. adults: Database analysis. British Medical Journal 330: 812–815.
  7. Janson C, Kunzli N, de Marco R, et al. (2006) Changes in active and passive smoking in the European Community Respiratory Health Survey. European Respiratory Journal 27: 517–524.
  8. McGhee SM, Ho LM, Lapsley HM, et al. (2006) Cost of tobacco-related diseases, including passive smoking, in Hong Kong. Tobacco Control 15: 125–130.
  9. McGhee SM, Ho SY, Schooling M, et al. (2005) Mortality associated with passive smoking in Hong Kong. British Medical Journal 330: 287–288.