Advocacy

Empowering individuals to influence their environment both at home and in public is the purpose of The Breathing Association’s advocacy activities. The Breathing Association works with the EPA (Environmental Protection Agency) promoting the Smoke Free Home Pledge program. This program asks adults to sign a pledge to keep their home smoke free. By taking the pledge adults agree that they will ask their friends, family, and any guest to refrain from smoking while in their home. An extension of the pledge...making your car smoke free as well, can be part of your commitment to providing a better environment for the  children, ill and elderly in your care.

The Breathing Association encourages individuals to take the Smoke Free Pledge and keep their car and home smoke free. Click here to sign up for a free pledge kit.

In public places as a member of the Tobacco Free Collaborative, The Breathing Association promotes the Eat, Breathe and Dine Smoke Free program. Other advocacy activities include The Great American Smoke-Out, Operation Storefront, and Smoke Free Restaurants Are Clearly Better.

A Brief Review of the Science and Epidemiology of Secondhand Smoke

  Despite two decades of research and more than 1000 scientific studies that overwhelmingly demon–strate the substantial and varied injuries caused by secondhand smoke, some people still believe tobacco industry-generated propa–ganda that secondhand smoke is not a major health problem.  Not surprisingly, the dialogue between clean indoor air advocates and tobacco industry supporters often gets heated, and both sides can be drawn into “blowing smoke” by citing secondary and exaggerated source material, primarily from activist web sites. In an effort to “clear the air,” and counter factual misstatements by opponents, SmokeFree Columbus has undertaken a systematic and extensive litera–ture review. The result is pre–sented below: a synopsis of the available primary sources that provide an accurate view of the strengths and limitations of the current science of passive smoking.

  Introduction

  Over the seventeen years since the first Surgeon General’s report[i] on hazards of secondhand smoke, epidemiologists and medical scientists have developed an even more extensive body of evidence about its noxious and deadly effects.  We now understand much more about the chemistry of smoke itself, its effect on human tissues and the considerable injury secondhand smoke imposes on the human body both in the long and short term.

  Secondhand Smoke Constituents

  As is often cited, secondhand smoke contains nearly 4000 chemicals and organic compounds, two hundred of which are known poisons and over 50 show carcinogenic potential.[ii]  Nine of these are classified by the US Environmental Protection Agency (EPA) as Group A carcinogens[iii] where there is sufficient evidence from epidemiologic studies to support a casual association between exposure to the agents and cancer.  The EPA also classifies secondhand smoke itself as a Group A carcinogen.

  The smoke that comes off the end of a cigarette is different than mainstream smoke.  Without inhalation, burning is slower and cooler; combustion is less complete, and the smoke does not pass through the body of the cigarette or the filter.  As such "sidestream" smoke generally contains more nicotine, more carbon monoxide, more carcinogens and more irritant particles and gasses than does the smoke a smoker actively inhales[iv].  Another often overlooked aspect of secondhand smoke exposure is that smokers tend to develop a level of tolerance to the drug effects of nicotine, the inflammatory effects of irritant tars, and the oxygen reduction caused by carbon monoxide.  Nonsmokers who are not so accustomed may therefore have more intense, violent and even lethal reactions[v]^,[vi].

  Effects

  When human tissues are exposed to levels of secondhand smoke commonly found in the home of a smoker or a bar or restaurant where smoking is occurring, there are a variety of both immediate and long term effects.  Oral and pharyngeal membranes react with tissue swelling and increased mucous production.  Respiratory cilia, the small moving wave of hairs in the lung passages, are paralyzed, thereby preventing the efficient removal of irritant particles, viruses and bacteria.[vii]^,[viii]  Spasm may occur in the smallest lung passages, the bronchioles.  The larger airways experience the most overt reactions of sneezing and coughing.  In susceptible individuals these effects of secondhand smoke may precipitate a serious or deadly asthma attack, while the chronic irritation and inflammation wrought by secondhand smoke is thought to be responsible for lung cancer.[ix]

  Less overt is the effect secondhand smoke has on the cardiovascular system.  The levels of nicotine and carbon monoxide found in secondhand smoke cause arteriolar constriction and an increase in heart rate and blood pressure in susceptible individuals.  The lining of the blood vessels and the clotting factors in blood may be inflamed or disturbed.  These effects combined with the reduction of oxygen caused by carbon monoxide’s effect on blood hemoglobin is probably why secondhand smoke exposure is so strongly linked to coronary heart disease, angina and sudden unexplained death.[x]

Measuring Exposure

  How do we know how much smoke and its toxic ingredients are actually in an environment where people are smoking?  How can we gauge if nonsmokers are actually exposed in a public place or a workplace setting?  We have several valuable tools.  We can directly measure the some of the constituents of secondhand smoke in the air and we can assay biologic markers within bodily fluids.  Measurements of nicotine, particulate matter and other noxious gasses have been utilized in a variety of studies. 

  Obviously, ambient indoor air conditions vary widely, but typically concentrations of nicotine in residences where smoking occurs tend to run between 2 and 10 micrograms per cubic meter.  Smoking sections of bars, however, may run as high as 50-75 mg/m³. [xi]  There is no reliable way to ascertain what is a safe level of this dangerous and addictive drug.

  The second direct measure of secondhand smoke has been to look at respirable suspended particles (RSP).  These particles are not specific to secondhand smoke and therefore RSP measurements must be compared between smoking and non-smoking environments.  Variations in settings cause variations in measurements but in general RSP's run somewhere between 10% and 300% higher in smoking environments.[xii]

  Measuring other air pollutants associated with secondhand smoke is complicated because like RSP's there are often other sources of these gasses in the indoor environment.  Polycyclic aromatic hydrocarbons have been studied extensively in home environments.  These are known carcinogens and were found to be 1.5 to 4 times higher in homes with no other known combustion source other than smoking as compared to similar homes without smoking.[xiii]

  More important perhaps are the biologic markers of secondhand smoke.  These are measures of toxins found in nonsmokers who are exposed to secondhand smoke compared to nonsmokers who are not exposed.  The most important tools have been measurement of cotinine, a long lasting metabolite of nicotine, and various direct and indirect measures of carbon monoxide.

  The biologic half life (the time it takes for the level of a substance to drop to half its original level in the body) for cotinine is similar for most bodily fluids – approximately 15-19 hours.[xiv] Generally, significant cotinine does not come from any other source other than tobacco, tobacco smoke or nicotine replacement products, and is therefore an excellent indicator of specific exposure in an involuntary smoker.[xv]  Whereas smokers attain much higher levels of cotinine than do involuntary smokers, the presence of cotinine does indicate that a nonsmoker has been substantially exposed.

  Carbon monoxide and blood hemoglobin bound to carbon monoxide (carboxyhemoglobin) are excellent indicators of the amount and intensity of a smoker's habit.  However, carbon monoxide can come from any combustion source and only in very heavy secondhand smoke exposures can one distinguish carbon monoxide levels between secondhand smoke exposed and unexposed people.

  Other important measures of exposure to secondhand smoke are quantitative surveys of exposure at home, work or public places..  Historically the main focus of large population-based studies has been on active smoking, however, more recent studies have examined secondhand smoke exposure for a variety of sub populations. As an example, in California in 1990, a large survey showed that 42% of adult nonsmokers were exposed to secondhand smoke [xvi] and the average exposure was 250 minutes per day[xvii].  One suspects that theses estimates have dropped especially in California where all public places are now legally smokefree.  Of interest is the fact that many nonsmokers who do not recall an exposure to secondhand smoke are found to have significant levels of cotinine in their bodily fluids.  This suggests that there may be substantial underreporting of secondhand smoke exposure.

  The Human Toll

  There have now been several hundred scientific studies examining the adverse medical effects of secondhand smoke.  Scientists have defined several broad categories of human injury provoked by secondhand smoke.  These include prenatal and perinatal deaths, sudden infant death syndrome (SIDS); respiratory health effects including asthma, infections, irritation, reduced lung function, sickle cell crises and chronic pulmonary disease; carcinogenic effects focusing on lung and breast cancer; and cardiovascular effects including myocardial infarction, coronary artery disease, angina pectoris and  sudden unexplained death.

  The effects on children are myriad.  Fetuses exposed by virtue of paternal smoking have higher rates of spontaneous abortion[xviii] while children born to mothers exposed at work are smaller[xix] and have higher rates of stillbirth.[xx]   The two best studies to date on SIDS suggest that babies exposed to secondhand smoke have at least twice the rate of death from this devastating disease.[xxi]^,[xxii]   A Chinese study of infants born to nonsmoking mothers, but exposed to secondhand smoke at home, concluded that 9% of the total costs of medical care for this age group and over 1500 extra hospital admissions was attributed to tobacco smoke in Hong Kong.[xxiii] 

  Asthma affects 5 million American children is the most common chronic condition of childhood.  It accounts for more than $3.2 billion in health care costs for children alone.[xxiv]  There seems to be little question, involuntary smoking exacerbates asthma and provokes specific attacks in both children and adults.[xxv]^,[xxvi]   In addition, there is suggestive data that secondhand smoke actually induces new cases of asthma at a rate twice that of nonsmoking homes.[xxvii] 

  Moreover more than 10 different studies demonstrate that secondhand smoke provokes significant increases in otitis media, upper respiratory illness, pneumonia and school absence in children.^3,[xxviii]  In California alone secondhand smoke related otitis media causes 78-188,000 office visits per year for children under three and 18-36,000 cases of bronchitis or pneumonia. [xxix]  Secondhand smoke may also have a terrible effect on children already debilitated by disease.  A recent study demonstrates that children with sickle cell disease are twice as likely to suffer a painful and dangerous sickle cell crisis if they are exposed to secondhand smoke.[xxx]

  Lung cancer is the most deadly of all human cancers, and the causal relationship between active smoking and carcinoma of the lung is now unquestioned.  Beginning with the sentinel study by Hiryama[xxxi] more than 20 years ago and continuing through 30 other retrospective and case control studies, the risk of lung cancer to a nonsmoker is now shown to be 20% higher if he or she lives with a smoker.²⁸    For some time we have also known that smoking causes breast cancer, but just as worrisome is the new and surprising discovery that breast cancer occurs significantly more often in women exposed to secondhand smoke.[xxxii]

  Most convincing of all, however, is the case that secondhand smoke causes substantial and deadly heart disease in nonsmoking adults.  In the last two decades more than 20 studies point to excess coronary morbidity and mortality in nonsmokers exposed to secondhand smoke.^{28,[xxxiii],[xxxiv]}  Moreover there is an expanding body of evidence in both animal and human studies that underscore pathologic changes in body chemistry and function when exposed to secondhand smoke and help explain why secondhand smoke can be so devastating to the cardiovascular system.  "At least five interrelated processes have been proposed to contribute to the clinical manifestations of MI [heart attack], including: atherosclerosis, thrombosis, coronary artery spasm, cardiac arrhythmia and reduced capacity of blood to deliver oxygen"[xxxv]

  Virtually all of the studies of heart disease, either case-controlled or cohort, prospective or retrospective, have looked at individuals exposed at home or work, based on their individual life and work styles.  What we, however, are proposing is regulation of a toxic exposure that will cause a. community-wide shift not only in exposures to non-smokers but also a decrease in use by smokers.  Several states and cities have taken these steps and their experience has been studied. 

  As a result of its comprehensive tobacco control program that has at its cornerstone a ban on workplace exposure to secondhand smoke, California estimates that 33,000 lives are spared annually from cardiovascular disease.[xxxvi]  The most recent and compelling story is that of Helena, Montana.[xxxvii]  For the last 6 months of 2002, Helena enforced strict workplace ban until it was preempted by industry sponsored state legislation.  During the time of the ban, admissions for heart attack at one large hospital dropped 60%.  After the law was reversed, they resumed their previous level.  Statistical analysis including surrounding communities that were unaffected by the ban demonstrated this effect to be both valid and profound.

  Summary:

  The evidence is now undeniable and overwhelming.  Smoking in homes, workplaces and public places endangers not only smokers but also those who are exposed to secondhand smoke.  In the past twenty-five years more than 1000 papers and studies have been published on this issue.  Not all have shown equal effects primarily because of the difficulty of measuring ongoing socio/biologic behavior, but there is clear and convincing evidence that public health and safety are jeopardized by secondhand smoke.  Moreover, banning smoking in workplaces unmistakably reduces deaths and injuries not just for nonsmokers but for smokers themselves.  In Central Ohio, we have both an opportunity and a duty to respond to these facts.

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