Tobacco Documents Online

Draft - Do not cite or quote that of the nonsmoker. At the other extreme, even light smokers, who consume only 1-9 cigarettes per day, see a quadrupling of the risk of lung cancer. An inverse dose-response relationship exists between an early age of regular smoking and lung cancer mortality. In the U.S. Veterans Study, those smokers who started smoking in their early teens had substantially higher lung cancer death rates than those who star~ed in their late teens or twenties (Figure 3). Those who began smoking before age 15 experienced a 19-fold greater lung cancer mortality, compared to a slightly greater than 5-fold excess risk for those who initiated their behavior after age 25. These results demonstrate that a dose-response relationship exists for exposure to the carcinogens in cigarette smoke and the risk of death from lung c~ncer: the greater the lifetime exposure to tobacco smeke, the greater the risk. Further evidence for the existence of a dose-response relationship comes from follow-up of people who stop smoking and so remove the exposure from the carcinogenic agents in mainstream 4moke. When an individual stops smoking, his or her lung cancer risk declines relative to the continuing smoker. After about 15 years off cigarettes the former smokerrs lung cancer risk approaches that of the life-long nonsmoker. However, it appears that some excess risk may be carried throughout life. This residual risk is strongly influenced by the indivldual's total lifetime exposure to the agent and the total number of years of smoking cessation. The presence of a dose-response relationship between smoking and lung cancer, combined with the fact that there are significant elevations in risk ~ssociated with even the lowest levels of smoking, demonstrates that there is no threshold for the carcinogenic effects of cigarette smoke. This result from active smokers is consistent with the observed elevations of lung cancer risk among nonsmokers exposed to ETS. Corona=y Heart Disease In contrast to cancer, in which smoking produces the disease through the cumulative effects of long term exposure to the carcinogens and co-carcinogens in the smoke, smoking effects the cardiovascular system immediately as well as over the long term. The carbon monoxide in the smoke reduces the oxygen carrying capacity of the blood by binding to hemoglobin competitively with oxygen. Nicotine is a vasoconstrictor, which increases blood pressure and narrows coronary arteries. Smoking causes release of catecholamine, which increase blood pressure and heart rate. Smoking also increases platelet aggregation and adhesion, which contributes to the development of atherosclerosis. All these ii

Draft - Do no~ cite or quote effects occur i~ediately upon smoking and resolve relatively quickly after stopping smoklng. As a resul~, one year after stopping smoking, the excess risk of death from hear~ disease falls by half; the sane drop in risk for lung cancer takes 10 years. As with cancer, these effects exhibit a dose-rmsponse relationship, with greater mere smokinq and smoking in combination with other heart disease risk factors, increaslng ~he risk of death from coronary heart disease. As with cancer, there Is no threshol~ for these effects, $o ~he effects of active smoking on the heart and cardiovascular system support the blological plausibili~y of the observed effects of ETS on ~he heart. Coronary heart disease (¢HD) continues to be this nation's leading cause of death, and for nearly 20 years, medical research has shown that smoking is one of tha major Independen~ risk factors or causes of CHD (along with high blood pressure and high cholesterol levels). In tha final report of the Pooling Project, an interaction between smoking and other ~isk factors was observed (Figure 4). Each independent risk factor contributed about the same increased level of-risk, ~owever, whQ~ ~o Or ~orQ factors were present, ~he risk of a major CHD event was increased beyond ~he sum of ~he independ~n~ risk -- thus, synergistic effect was crea~ed when two or mere risk factors wer~ present° Over~ll, smokers have a 70% greater CHD death rate, a two- to fourfold grmater incidence of CHD, and a two- t~ fourfold ~reater risk for sudden death than nonsmokers. Dose-response relationships between ~igarette smoking and CHD mortality have been demonstrated for several measures of exposur~ to cigarettes, includln~ the number of ~igaret~es smoked per day, the depth of inhalation, age at which smoking began, and ~he number of years of smoking. Smoking cigarettes with reduced yields of ~ar and nicotine does no~ reduce CHD risk, probably becaus~ ~hese cigarettes do not have reduced yields of carbon mcnoxidl and ether combustion produc~s which afflct the cardiovascular system. The independent risk of CHD fo~ smoking is greater a~ ~he younger age groups al~hough ~he greatest number of excess CHD deaths due to smoking actually ~ccurs in the older age groups (Figure 5). Smoking has also been shown to increase the risk for other cardlov~scular diseases, including peripheral vascular disease, cerebrov~scular dlsease (at younger age gr~up~), a~d aortic a~urysms. For women, s~oki~g "ca~ i~teract wi~h oral contraceptives ~o greatly i~crease ~he risk fac~o~ f~r ~a~al and nonfatal myocardial infarction and suhar~chnoid hemorrhage. Smokers exhibi~ ~ore a~herosclerosis, bo~h in the aorta and coronary ar~erles° Cigarette smokers who continue ~o smoke following ~ransluminal coronary angioplasty appear more likely ~o require repeat angioplasty than nonsmokers, suggesting tha~ ~he effects of smoking on atherosclerosis occur quickly. The polycyclic aromatic hydrocarbons which rmsult from the combustion 12

Draft - DO not cite or quote of the smoking materials contribute to these effects• The increase in platelet adhesion observed in smokers also contributes to the development of atherosclmrotic plaque. Cigarette smoking aggravates the conditions of people with CHD. Smokers have a more difficult course following coronary artery bypass surgery. Smokers who experience angina pectoris have a higher risk of death than nonsmokers, a poorer prognosis following non-fatal myocardial infarction, and a greater risk of sudden death. Smoking increases the risk of silent iscbemia in patients with stable angina. Many public health estimates place the total number of excess cardiovascular disease (including stroke) deaths due to smoking to be greater than those due to cancer (Figure i). Up to 30 percent of all CHD deaths may be due to cigarette smoking and its interaction with other risk factors. These effects all exhibit a dose-response relationship with no threshold in active smokers, with detectable damage even among light smekers. These facts support the biological plausability of ~he evidence linking ETS with heart disease in nonsmokers. • Nonmalignan~ Respiratory Diseases In addition to causing lung cancer, smoking causes or aggravates several related nonmalignant respiratory diseases, including emphysema, asthma, chronic bronchitis, and chronic obstructive pulmonary disease (COPD). While the number of s~oking-i~duced deaths classified due to chro~ic obstructive pulmonary disease (COPD) is smaller than for cancer or cardiovascular disease (Figure i), COPD afflicts about 12 million Americans. Even if not fatal, COPD and related disorders such as emphysema severely debilitate the victim and represent a substantial number of people who become disabled due to their condition, unable to work or even seek employment. For many years cigarette smoking has been known to increase the risk of developing and dying from COPD. Even the first Surgeon General's Report issued in 1964 identified a causative role between smoking and chronic bronchitis. AS with lung cancer, the risk of contracting and dying from COPD is substantially elevated among smokers (Figure 6) and this risk increases with an increased dose of cigarette smoke received; as with the other smoking-induced diseases discussed in this chapter, there is a positive dose- response relationship. Mortality rations for COPD in smokers versus nonsmokers are very high, exceeding 30 to 1 for heavy smokers (Figure 7). Smoking also has a dramatic effect on lung function. The normal rate of lung function decline with increasing age is accelerated in cigarette smokers (Figure 8). These effects 13

Draft - Do not mite or quote probably reflect damage to the small airways of the lungs as well as a thickening and increased reactivity of the airways in response to chronic exposure to the irritants in cigarette smoke. The volume an individual and exhale in one second of forced expiration (?EVl) is a measure of small airway function. Figure 9 shows that FEVI falls in a dose-dependent manner as the amount of smoking increases. There is no safe level of exposure: there is a measurable decrement in pulmonary function even among light smokers. Stopping smoking partially reverses the nonmalignant effects of the respiratory system (Figure 8). When one stops smoking, the decline in lung function with age resembles that of a nonsmoker, but a permanent decrement in lung function remains, indicating some permanent damage. The amount of this permanent deficit depends on the duration and intensity of smoking. ETS exposure produces similar, but more modest nonmalignant pulmonary effects. FEVI is reduced in passive smokers among both children and adults to levels similar to that observed in light smokers. Children of parents who smoke develop more asthma, bronchitis and other respiratory problems. The rate of lung ~evelopment in children exposed to ETS is smaller than that of unexposed children. These effects of ETS are what one would expect based on the effects of active smoking. Conclusions This chapter has reviewed the effects of active smoking in on these cancers, heart disease, and nonmalignant pulmonary diseases which have also been identified with passive smoking. In each case, cigarette smoking significantly increased the risk of disease in smokers in a dose-dependent manner. There is no evidence of a threshold level for adverse effects. Because ETS is similar to (bu~ more toxic than) mainstream smoke, these effects on the smoker help provide evidence for the biological plausibility for the epidemiological evidence linking ETS with lung cancer, heart disease, and nonmalignant respiratory disorders, after accounting for the lower dose the involuntary smoker receives. I. There is a dose-response relationship between exposure to tobacco smoke and the diseases of smoking. 2. There are no discernable thresholds of exposure for the diseases of smoking. 3. Adverse health effects observed in smokers provide biological plausibility for the occurrence of those diseases in nonsmokers. 14

Draf~ - Do no~ cite cr quote TABLES ~ F~GURES+ ~PT~R ~r

¥~QURR ~, US Deaths Attributed to Smoking in 1985 Source: US Surgeon General, 1989 CVD CHD 28000 115000 Cancer, lung 106000 Cancer, ether 30000 COPD 57000 Other 54000 H 11 t D O O it 43 p. D O II 0 m

Draf~ - DO not cite cr quo~e ~ ~ Men -f irm 1~ zcdo,s

Draft - Do not cite or quote 2O 18 10 8- 0 FIGUR~ 3. (1989 SURGEON GENERALIS RE~ORT, p. 49)

FIGUR2 40 Lung canceP mortafity ratios for males, by age began smoking -- U.S. Veterans' Study 20 •. 18.7 15 lO 5 1,0 Nonsmoker 9.5, 25+ 20-24 15-19 <15 Age began smoking (in years) t~ I 0 fl p. m 0 i-I 0

YZGURX 5o Major risk factor combinations, lO-year incidence of first major coronary events, men age 30-59 at entry, Pooling project 0 0 0 L- G) 0. (1) n¢ 200 180 160 140 120 100 80 60 4O 20 23 54 189 103 None SM C or H SM & C C & H All 3 ol3 Only Only or . (No $M) SM&H Risk Factor Status at Entry SM = smoker. C = choleslerol, H = hypertension -n -4, dr I 0 0 ,p- 0 0 0