Secondhand Smoke Research Paper

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Definition And Composition

Secondhand smoke (SHS) is a mixture of the smoke emanating from the lighted tip of a cigarette (sidestream smoke) and that exhaled by the smoker (mainstream smoke). It is also referred to by the tobacco industry’s preferred term, environmental tobacco smoke (ETS). The International Agency for Research on Cancer has defined those who are exposed to SHS from others’ smoking as passive smokers, highlighting the nonvoluntary nature of the exposure. SHS is a complex mixture of over 4000 chemicals, most of them formed during the combustion process, and includes nicotine as well as carcinogens and toxins. From biomarker data it is clear that nonsmokers absorb these chemicals in sufficient quantities to be measurable. The actual composition of SHS varies depending on what is being smoked and the smoking pattern of those producing the smoke, but most, typically around 90%, of SHS is composed of sidestream smoke. Both sidestream and mainstream smoke contain many of the same contaminants but sidestream smoke emissions of many of the known carcinogens and toxins are considerably higher than the mainstream emissions due to lower combustion temperatures in a smoldering cigarette. In previously secret research conducted by the tobacco industry it was shown that the sidestream component of SHS is about four times more toxic by weight than mainstream smoke. SHS contains particulate matter and a single smoker can push the indoor levels of particulates way beyond the levels acceptable for outdoor air pollution in most countries.

Biology

Since SHS contains known carcinogens, it would be expected that exposure of, for example, lung tissue to SHS would lead to the development of tumors and we do find an association between SHS exposure and lung cancers. There is also strong evidence that SHS is involved in the development of cardiovascular disease in passive smokers through impacts on the blood and circulatory system. Exposure to SHS has been shown to activate blood platelets and damage the cells that line the walls of blood vessels. This increases the risk of a blood clot forming within the blood vessel. Within 30 minutes of breathing SHS, there is impairment of the normal dilation response of blood vessels to an increased demand for blood flow, although partial recovery may occur after the long-term cessation of exposure in healthy individuals. A number of studies have shown associations between exposure to SHS and stiffness of blood vessels, lower blood serum levels of high-density lipoproteins and antioxidants, and higher levels of inflammatory markers. All of these effects are similar and in some cases, not very different in magnitude, to the kind of effects seen in active smokers and are physiologically related to the development of heart disease.

Measuring Exposure

Biomarkers

The ability to quantify the level of exposure to SHS in an objective fashion is important in establishing the association of exposure with health effects. This has led to the use of a number of biomarkers of exposure based on tobacco products and their metabolites. When using biomarkers, it must be kept in mind that their concentrations are the end product of a process of absorption, distribution, storage, metabolism, and excretion whose mechanisms we do not always fully understand.

One biomarker that is commonly used for the measurement of exposure to SHS is cotinine, a metabolite of nicotine that is relatively stable with a longer half-life. Cotinine levels can be measured in serum, saliva, urine, and hair; the measured cotinine levels of nonsmokers who are exposed to SHS are usually 2 to 3 times lower than those of active smokers. In one large, multicenter study on health impacts of exposure to SHS, Vineis and others (2005) found that while self-reported exposure was associated with cotinine levels and with the risk of respiratory disease and lung cancer, the presence of detectable cotinine in blood plasma was not associated with the health impacts. This highlights one of the main limitations of biomarkers, that they reflect relatively recent exposure to SHS while disease pathogenesis is often a longer process happening over months or years of exposure. However, other studies have shown relationships between cotinine levels and respiratory symptoms and Whincup and colleagues (2004) found an association between serum cotinine levels at the start of follow-up and coronary heart disease 20 years later.

Environmental Monitoring Of SHS Levels

Several constituents of SHS can be measured in air including nicotine, particulates, carbon monoxide, and other chemicals. The levels of these pollutants in the air of specific venues, when combined with information on frequency and duration of visits to those venues, allows estimation of an individual’s overall exposure to SHS. Concentrations of tobacco-derived pollutants in indoor workplaces where smoking is allowed can equal or exceed the levels in homes of smokers, and the highest workplace levels have been found in bars and smoking sections of aeroplanes. The California Environmental Protection Agency (EPA) has estimated that indoor levels of particulates in entertainment venues such as casinos can range from less than 15 mg/m3 in venues where smoking is prohibited to 350 mg/m3 in those in which smoking is allowed. Inside a closed vehicle, levels of over 1000 mg/m3 have been recorded.

Self-Reported Exposure To SHS

Because of the limitations of biomarkers as indicators of longer-term exposure, self-reports of exposure are used in many studies on health impacts of SHS, sometimes supplemented by measurement of biomarkers. The principal difficulty in self-reporting is in estimating the dose of SHS that an individual is exposed to. This has usually been estimated for indoor exposure by asking about the number of smokers nearby, the number of cigarettes consumed, and the number of hours of exposure. However, this neglects issues such as the size of the room and does not cover outdoor exposure such as at a bus stop. Many of the studies on health impact are based on reports of having a smoking spouse or, for children, whether the parents smoke or used to smoke. This imprecision hinders quantification of impacts and reduces the statistical power of epidemiological studies. Another source of error that may lead to underestimates of health impacts is that even those who consider themselves not exposed to SHS are often found to have measurable levels of biomarkers, which demonstrates how difficult it can be to avoid exposure to SHS.

Epidemiology

Prevalence Of Exposure

Although the magnitude of the risks for many of the chronic and fatal diseases associated with passive smoking are relatively small compared with those for active smoking, the potential exposure of nonsmokers is large. Such exposure can take place in the home, workplaces, leisure venues such as restaurants, bars, and bowling alleys, and public places such as shopping malls, streets, and bus stops, or anywhere that smoking is allowed. Even smokers are exposed to the SHS from other smokers and some recent studies have indicated an impact of SHS over and above that from active smoking.

The third National Health and Nutrition Examination Survey (NHANES) in the United States found that 88% of nonsmokers in 1988 had detectable serum cotinine levels indicating exposure to SHS. Among nonsmoking workers, the highest mean levels of cotinine were found in waiters (0.47 ng/mL) and the lowest in farmers and nursery workers (0.06 ng/mL) (Wortley et al., 2002). Since then, many states have made vast improvements in reducing exposure of nonsmokers. California, for example, is one of the leaders in smoke-free legislation and the proportion of workers there reporting smoke-free workplaces increased from 35% in 1990 to 93% in 1999 (Gilpin et al., 2002). Over the same period, the proportion of nonsmoking indoor workers in the state who were exposed to SHS decreased from 29% to 16% and the proportions of adults and those under 18 years with smoke-free homes rose from 38% to 74% and 82%, respectively. In Europe, exposure of nonsmokers to SHS at home or work declined from 41% to 24% over about 9 years from the early 1990s ( Janson et al., 2006). However, in other countries, smoke-free legislation has been slower and exposure of nonsmokers continues. For example, in Latin America in 2000 to 2002, airborne nicotine was discovered in over 90% of the public places surveyed (Navas-Acien et al., 2004). In many countries around 50% of children are exposed to SHS in their homes.

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.

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