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Explaining the decline in coronary heart disease mortality in England and Wales between 1981 and 2000.

BACKGROUND: Coronary heart disease mortality rates have been decreasing in the United Kingdom since the 1970s. Our study aimed to examine how much of the decrease in England and Wales between 1981 and 2000 could be attributed to medical and surgical treatments and how much to changes in cardiovascular risk factors. METHODS AND RESULTS: The IMPACT mortality model was used to combine and analyze data on uptake and effectiveness of cardiological treatments and risk factor trends in England and Wales. The main data sources were published trials and meta-analyses, official statistics, clinical audits, and national surveys. Between 1981 and 2000, coronary heart disease mortality rates in England and Wales decreased by 62% in men and 45% in women 25 to 84 years old. This resulted in 68 230 fewer deaths in 2000. Some 42% of this decrease was attributed to treatments in individuals (including 11% to secondary prevention, 13% to heart failure treatments, 8% to initial treatments of acute myocardial infarction, and 3% to hypertension treatments) and 58% to population risk factor reductions (principally smoking, 48%; blood pressure, 9.5%; and cholesterol, 9.5%). Adverse trends were seen for physical activity, obesity and diabetes. CONCLUSIONS: More than half the coronary heart disease mortality decrease in Britain between 1981 and 2000 was attributable to reductions in major risk factors, principally smoking. This emphasizes the importance of a comprehensive strategy that promotes primary prevention, particularly for tobacco and diet, and that maximizes population coverage of effective treatments, especially for secondary prevention and heart failure. These findings may be cautiously generalizable to the United States and other developed countries.

Adult↗

Smoking in pregnancy: patient and provider risk reduction behavior.

OBJECTIVE: To describe the range of risk reduction behaviors among women who continue to smoke after learning of their pregnancy, including reduced tobacco use, eventual cessation, and sustained abstinence as well as the patient-reported smoking cessation-promoting behaviors of prenatal care providers. METHODS: This research is part of a larger prospective, community-based study conducted to assess the association between maternal stress and birth outcomes and infant health and development. Over a 2-year period, from February 2000 to November 2001, women receiving prenatal care at a consortium of public health centers in Philadelphia, Pennsylvania, were consecutively recruited (n = 1,451) completing interviews at their initial prenatal visit and again 3 to 4 months following their delivery. Smoking rates during pregnancy were determined from responses given during the first postpartum interview, at 3 to 4 months postpartum. RESULTS: Of the 1,451 women interviewed at 3 to 4 months postpartum, 24.9 percent indicated smoking during their pregnancy. Of these antenatal smokers, 89.0 percent reported reducing their cigarette consumption during pregnancy. However, only 25.4 percent attained abstinence during their pregnancy. Among women who achieved abstinence during their pregnancy, 21.7 percent were still not smoking at the time of the postpartum interview. Antenatal smokers reported that prenatal care providers asked about their smoking (90.6%) and advised about quitting (76.5%). However, only 27.9 percent were given referrals to smoking cessation programs. CONCLUSION: While cessation was achieved by only a quarter of antenatal smokers, almost 90 percent reduced their cigarette consumption. Prenatal care providers identified and provided cessation advice to the majority of women who were smoking but they did not follow through with material assistance in the form of referrals to smoking cessation programs.

Adult↗

Psychopharmacologic treatment of cigarette smoking.

In summary, the entrance of the dental community into this area of treatment may have a significant impact on the reduction of smoking in our society. Dentists may be seeing smokers before the onset of disease and when they are ready to quit. Repeated patient visits offer a unique opportunity for follow-up. Presently, nicotine polacrilex is the only approved pharmacological FDA treatment. This is an ideal treatment for dentists to pursue because it is orally administered and effective through a proper chewing action. Other pharmacological agents (for example, antihypertensives) may require the followup of the physician. There are three key demands on the practitioner treating smokers: an understanding of the role of nicotine dependence in compulsive smoking; how to prescribe and educate in the proper use of nicotine polacrilex; and sympathy and a basic awareness of withdrawal and the psychological needs of patients undergoing cessation from smoking. This paper covers the rationale for development and use of nicotine polacrilex as well as some of the evidence for its effectiveness (relief of nicotine withdrawal) and efficacy (short and long term). The specifics of proper use have been described along with a brief overview of the psychosocial skills needed to succeed. The dentist offers a unique opportunity to reach enormous numbers of smokers in the battle against tobacco-induced disease and death.

Behavior Therapy↗

The effects of smoking schedules on cessation outcome: can we improve on common methods of gradual and abrupt nicotine withdrawal?

This study compared the efficacy of 2 traditional methods of smoking cessation, gradual reduction and "cold turkey," with a new approach involving variation in the intercigarette interval. One hundred twenty-eight participants quit smoking on a target date, after a 3-week period of (a) scheduled reduced smoking (progressive increase in the intercigarette interval), (b) nonscheduled reduced smoking (gradual reduction, no specific change in the intercigarette interval), (c) scheduled nonreduced smoking (fixed intercigarette interval, no reductions in frequency), or (c) nonscheduled nonreduced smoking (no change in intercigarette interval or smoking frequency). Participants also received cognitive-behavioral relapse prevention training. Abstinence at 1 year averaged 44%, 18%, 32%, and 22% for the 4 groups, respectively. Overall, the scheduled reduced group performed the best and the nonscheduled reduced group performed the worst. Both scheduled groups performed better than nonscheduled ones. Scheduled reduced smoking was associated with reduced tension, fatigue, urges to smoke, withdrawal symptoms, increased coping effort (ratio of coping behavior to urges), and self-efficacy, suggesting an improved adaptation to nonsmoking and reduced vulnerability to relapse.

Adult↗

Estimates of smoking-attributable deaths at ages 15-54, motherless or fatherless youths, and resulting Social Security costs in the United States in 1994.

BACKGROUND: Deaths of parents often harm their children, taxpayers, and society, for decades. So we estimated the smoking-attributable (SA) counts and percentages (SA%) of U.S. 1994 deaths at child-rearing ages; youths (ages <18) left motherless or fatherless; and resulting Social Security Survivors Insurance taxes. DESIGN: U.S. 1994 age/sex/education-specific total and SA death counts were estimated using death certificate data and standard CDC SAMMEC methods (with added injury mortality), respectively. We separately summed (a) total and (b) SA age/sex/education-specific death counts times their average number of youths per adult (cumulative fertility, adjusted for infant mortality). We then multiplied the SA and total bereft youth counts by their average duration of Survivors Insurance, and calculated the SA cost of youth Survivors Insurance. RESULTS: In 1994, smoking caused an estimated 44,000 male and 19,000 female U.S. deaths at ages 15-54, leaving 31,000 fatherless and 12,000 motherless youths. On December 31, 1994, the SA prevalences [count (SA%)] of fatherless or motherless youths were an estimated 220,000 (17%) and 86,000 (16%), respectively. Resulting Survivors Insurance costs were about $1.4 (sensitivity range: $0.58-3.7) billion in 1994. CONCLUSIONS: Smoking causes many U.S. deaths at ages 15-54, youth bereavements, and Survivors Insurance costs. Reductions in smoking may greatly reduce those deaths, bereavements, and taxpayer and societal costs.

Adolescent↗

Prevention of lung cancer: the key is to stop smoking.

OBJECTIVES: To review current approaches to primary prevention of lung cancer and to screening for precarcinogenic or preclinical asymptomatic disease. DATA SOURCES: Research studies, review articles, and government reports relating to prevention of lung cancer and strategies for smoking cessation. CONCLUSIONS: Because almost 90% of lung cancer cases can be attributed to tobacco, reduction of smoking is the appropriate focus of lung cancer prevention efforts. Lung cancer chemoprevention remains an experimental approach and large scale screening for lung cancer is of limited value. IMPLICATIONS FOR NURSING PRACTICE: Nurses are in a strategic position to prevent smoking initiation and to influence successful smoking cessation through education, information on the multiple modalities to assist behavioral change, and ongoing reinforcement.

Behavior Therapy↗

Smoking attributable mortality for Taiwan and its projection to 2020 under different smoking scenarios.

OBJECTIVES: To estimate smoking attributable mortality (SAM) in Taiwan for the years 2001 through 2020 under scenarios of reductions in smoking rates by 0%, 2%, 4%, and 10% per year. METHOD: The smoking attributable fraction (SAF) was used to calculate SAM from the risk experience in following up a large cohort (86 580 people) in Taiwan. Smoking rates were based on the 2001 National Health Interview Survey and other national surveys. An average 10 year lag was assumed between smoking rates and subsequent mortality. RESULTS: In 2001, 18 803 deaths, or 1 out of 4 deaths (27%), in middle aged men (35-69 years old) were attributable to smoking. SAM has been increasing and will continue to increase if smoking rates remain constant or even if reduced annually by 2%. SAM would begin to decrease only if rates were to be reduced by at least 4% a year. CONCLUSIONS: The projected SAM in this study illustrates the seriousness of smoking caused mortality. Current efforts in tobacco control would lead to a progressive increase in SAM, unless efforts were doubled and smoking rates reduced by more than 4% a year. The urgency in requiring stronger tobacco control programmes to attenuate the staggering death tolls is compelling.

Adult↗

Preoperative smoking habits and postoperative pulmonary complications.

OBJECTIVE: To examine the effect of preoperative smoking behavior on postoperative pulmonary complications. DESIGN: Prospective cohort study. SETTING: The Veterans Administration Medical Center, Syracuse, NY. PARTICIPANTS: Patients scheduled for noncardiac elective surgery (n=410). MEASUREMENTS AND RESULTS: Smoking status was determined by self-report. Postoperative pulmonary complications were determined by systematic extraction of medical record data. Postoperative pulmonary complications occurred in 31 of 141 (22.0%) current smokers, 24 of 187 (12.8%) past smokers, and 4 of 82 (4.9%) never smokers. The odds ratio (OR) for developing a postoperative pulmonary complication for current smokers vs never smokers was 5.5 (95% confidence interval [CI], 1.9 to 16.2) and 4.2 (95% CI, 1.2 to 14.8) after adjustment for type of surgery, type of anesthesia, abnormal chest radiograph, chronic cough, history of pulmonary disease, history of cardiac disease, history of COPD, education level, pulmonary function, body mass index, and age. Current smokers who reported reducing cigarette consumption prior to surgery were more likely to develop a complication compared with those who did not (adjusted OR=6.7, 95% CI, 2.6 to 17.1). CONCLUSIONS: Current smoking was associated with a nearly sixfold increase in risk for a postoperative pulmonary complication. Reduction in smoking within 1 month of surgery was not associated with a decreased risk of postoperative pulmonary complications.

Confidence Intervals↗

A simple method to estimate tobacco-related lung cancer deaths based on smoking prevalence data.

OBJECTIVE: Tobacco is the major cause of cancer and a relevant risk factor for several other chronic diseases. Due to the epidemiological transition in developing countries with overall increasing life expectancy there is an increasing relevance of chronic diseases to the total burden of diseases. Furthermore, there are indications for a rise in the consumption of tobacco products in developing countries. Since in Africa data on smoking prevalence are scarce and cancer diagnosis is often imprecise or missing, it is difficult to estimate the current and future number of cancer cases attributable to tobacco smoking. In this paper, we present an approach to estimate the effects of smoking on lung cancer in selected developing countries in Africa. METHODS: We combined data on smoking prevalence from different African countries with estimates on age-specific lung cancer rates in smokers and non-smokers from industrialized countries and data on age and sex distribution in African countries. We perform a sensitivity analysis to evaluate the effect of the assumptions necessary for the procedure. RESULTS: If the smoking prevalence in African countries will remain on the current level, we estimate age-specific lung cancer rates lower than those in Germany. Despite the relatively small proportion of adults aged 50 and more which is the age when most cancer cases occur, there is an appreciable number of deaths from lung cancer that could be prevented when smoking prevalence could be reduced. Depending on assumptions we estimate up about 50,000 lung cancer deaths per year in Africa, most of which could be prevented. CONCLUSIONS: Efforts for smoking prevalence reduction are much more needed in the developing world. Better and more comprehensive data on smoking are needed for more precise estimates.

Adolescent↗

The causes and prevention of cancer: the role of environment.

The idea that synthetic chemicals such as DDT are major contributors to human cancer has been inspired, in part, by Rachel Carson's passionate book, Silent Spring. This chapter discusses evidence showing why this is not true. We also review research on the causes of cancer, and show why much cancer is preventable. Epidemiological evidence indicates several factors likely to have a major effect on reducing rates of cancer: reduction of smoking, increased consumption of fruits and vegetables, and control of infections. Other factors are avoidance of intense sun exposure, increases in physical activity, and reduction of alcohol consumption and possibly red meat. Already, risks of many forms of cancer can be reduced and the potential for further reductions is great. If lung cancer (which is primarily due to smoking) is excluded, cancer death rates are decreasing in the United States for all other cancers combined. Pollution appears to account for less than 1% of human cancer; yet public concern and resource allocation for chemical pollution are very high, in good part because of the use of animal cancer tests in cancer risk assessment. Animal cancer tests, which are done at the maximum tolerated dose (MTD), are being misinterpreted to mean that low doses of synthetic chemicals and industrial pollutants are relevant to human cancer. About half of the chemicals tested, whether synthetic or natural, are carcinogenic to rodents at these high doses. A plausible explanation for the high frequency of positive results is that testing at the MTD frequently can cause chronic cell killing and consequent cell replacement, a risk factor for cancer that can be limited to high doses. Ignoring this greatly exaggerates risks. Scientists must determine mechanisms of carcinogenesis for each substance and revise acceptable dose levels as understanding advances. The vast bulk of chemicals ingested by humans is natural. For example, 99.99% of the pesticides we eat are naturally present in plants to ward off insects and other predators. Half of these natural pesticides tested at the MTD are rodent carcinogens. Reducing exposure to the 0.01% that are synthetic will not reduce cancer rates. On the contrary, although fruits and vegetables contain a wide variety of naturally-occurring chemicals that are rodent carcinogens, inadequate consumption of fruits and vegetables doubles the human cancer risk for most types of cancer. Making them more expensive by reducing synthetic pesticide use will increase cancer. Humans also ingest large numbers of natural chemicals from cooking food. Over a thousand chemicals have been reported in roasted coffee: more than half of those tested (19/28) are rodent carcinogens. There are more rodent carcinogens in a single cup of coffee than potentially carcinogenic pesticide residues in the average American diet in a year, and there are still a thousand chemicals left to test in roasted coffee. This does not mean that coffee is dangerous but rather that animal cancer tests and worst-case risk assessment, build in enormous safety factors and should not be considered true risks. The reason humans can eat the tremendous variety of natural chemical "rodent carcinogens" is that humans, like other animals, are extremely well protected by many general defense enzymes, most of which are inducible (i.e., whenever a defense enzyme is in use, more of it is made). Since the defense enzymes are equally effective against natural and synthetic chemicals one does not expect, nor does one find, a general difference between synthetic and natural chemicals in ability to cause cancer in high-dose rodent tests. The idea that there is an epidemic of human cancer caused by synthetic industrial chemicals is false. In addition, there is a steady rise in life expectancy in the developed countries. Linear extrapolation from the maximum tolerated dose in rodents to low level exposure in humans has led to grossly exaggerated mortality forecasts. Such extrapo

Carcinogens↗

Ability of smokers to reduce their smoking and its association with future smoking cessation.

AIMS: We examined whether cigarette smokers in the United States can significantly reduce their smoking and maintain this reduction and, if so, whether this predicts an increase or decrease in the probability of smoking cessation in the future. DESIGN: Longitudinal observation study. SETTING: The 22 US cities of the Community Intervention Trial for smoking cessation (COMMIT). PARTICIPANTS: The 1410 subjects who smoked at both baseline and at 2-year follow-up. INTERVENTION: Public health efforts to prompt cessation in half the communities. MEASUREMENTS: Self-reported cigarettes/day and abstinence at baseline, 2-year and 4-year follow-ups. FINDINGS: At 2-year follow-up, 60% of the subjects had either not changed or increased their smoking, 17% had decreased their smoking by 5-25%, 15% by 24-49% and 8% by > or = 50%. Among the 40% who had reduced > or = 5% at 2-year follow-up, 52% reported maintaining that reduction at 4-year follow-up. Reduction in smoking at year 2 did not prospectively predict an increase or decrease in the probability of making a quit attempt; nor did it predict eventually quitting by year 4. CONCLUSIONS: A substantial minority of US smokers are able to reduce their smoking and maintain this for long periods of time. Smoking reduction neither promotes nor undermines cessation.

Adult↗

Rationale for cigarette smoking and for mentholation preference in cocaine- and nicotine-dependent outpatients.

We asked 43 cocaine- and nicotine-dependent outpatients at a substance abuse clinic their reasons for combining cocaine and cigarette use, and for preferring either mentholated or nonmentholated cigarettes. Responses to open-ended questions asked during a semistructured interview were categorized by an analysis of expressed motives for cigarette smoking. Responses that did not fit the categorization were analyzed separately in a qualitative design. Sedating, stimulating, or addictive effects were frequently stated as reasons for the combined use of cigarettes with cocaine. Sedating or calming effects of cigarette smoking included reduction of cocaine-induced paranoia. Cocaine-substituting and cocaine-enhancing effects of cigarette smoking were categorized as stimulating effects. Addictive effects included craving for cigarette smoking on its own or triggered by cocaine use. Sensorimotor or stimulating effects were frequently stated as reasons for a preference for mentholated or nonmentholated cigarettes. Sensorimotor effects of menthol included taste, anesthetic, cooling, and decongestant properties. Some responses provided by our patient sample suggest a need for research on the effect of cigarette smoking on absorption of smoked cocaine.

Adult↗

Risk factors for emphysema. Cigarette smoking is associated with a reduction in the association rate constant of lung alpha 1-antitrypsin for neutrophil elastase.

The increased risk of developing emphysema among individuals who smoke cigarettes and who have normal levels of alpha 1-antitrypsin (alpha 1AT) is hypothesized to result from a decrease in the antineutrophil elastase capacity of the lower respiratory tract alpha 1AT of smokers compared with nonsmokers. To evaluate this hypothesis we compared the time-dependent kinetics of the inhibition of neutrophil elastase by lung alpha 1AT from healthy, young cigarette smokers (n = 8) and nonsmokers (n = 12). alpha 1-antitrypsin was purified from lavage fluid using affinity and molecular sieve chromatography, and the association rate constant (k assoc) for neutrophil elastase quantified. The k assoc of smoker plasma alpha 1AT (9.5 +/- 0.5 X 10(6) M-1s-1) was similar to that of nonsmoker plasma (9.3 +/- 0.7 X 10(6) M-1s-1, P greater than 0.5). In marked contrast, the k assoc of smoker lower respiratory tract alpha 1AT was significantly lower than that of nonsmoker alpha 1AT (6.5 +/- 0.4 X 10(6) M-1s-1 vs. 8.1 +/- 0.5 X 10(6) M-1s-1, P less than 0.01). Furthermore, the smoker lower respiratory tract alpha 1AT k assoc was significantly less than that of autologous plasma (P less than 0.01). When considered in the context of the concentration of alpha 1AT in the lower respiratory tract epithelial lining fluid, the inhibition time for neutrophil elastase of smoker lung alpha 1AT was twofold greater than that of nonsmoker lung alpha 1AT (smoker: 0.34 +/- 0.05 s vs. nonsmoker: 0.17 +/- 0.05 s, P less than 0.01). Consequently, for concentrations of alpha 1AT in the lower respiratory tract it takes twice as long for an equivalent amount of neutrophil elastase to be inhibited in the smoker's lung compared with the nonsmoker's lung. These observations support the concept that cigarette smoking is associated with a decrease in the lower respiratory tract neutrophil elastase inhibitory capacity, thus increasing the vulnerability of the lung to elastolytic destruction and thereby increasing the risk for the development of emphysema.

Emphysema↗

The effects of ventilation and the dilution of smoke upon the clastogenic and aneugenic activity of tobacco particulate matter in cultured mammalian cells.

We demonstrate here that tobacco particulate matter (TPM) produced from both non-ventilated and ventilated cigarettes of varying tar contents induced structural and numerical aberrations in cultured Chinese hamster cells. Our data indicate that TPM from ventilated cigarettes is of lower potency in inducing both clastogenic and aneugenic effects compared with TPM from non-ventilated cigarettes. These observations provide support for the concept that the genotoxic activity (to cultured Chinese hamster cells) of cigarette smoke is reduced by increased ventilation to a greater extent than a 1:1 ratio between yield reduction and smoke dilution.

Aneuploidy↗

Cigarette smoking, hypertension and erectile dysfunction.

Smoking is associated with an increased risk of developing erectile dysfunction (ED). For example, in the Massachusetts Male Aging Study (MMAS), cigarette smoking amplified the risk of ED associated with other risk factors (e.g. hypertension, diabetes and dyslipidaemia) or with ageing. At the molecular level, several changes associated with smoking have been documented in man and experimental models. These changes could contribute to the pathogenesis of ED. Furthermore, studies performed in dogs demonstrated a smoking-related reduction in arterial flow and venous restriction. Similarly, impaired penile flow has been documented in men who smoke. Cigarette smoking also interferes with the effectiveness of intracavernous papaverine and PGEI. Quitting is the 'first-line' therapy of ED and one of the most important measures for the prevention of atherosclerosis.

Arteries↗

Interventions for promoting smoking cessation during pregnancy.

BACKGROUND: Smoking remains one of the few potentially preventable factors associated with low birthweight, very preterm birth and perinatal death. OBJECTIVES: The objective of this review was to assess the effects of smoking cessation programs implemented during pregnancy on the health of the fetus and infant, on the mother and on the family. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group trials register and the Cochrane Tobacco Addiction Group trials register. SELECTION CRITERIA: Randomised and quasi-randomised trials of smoking cessation programs implemented during pregnancy. DATA COLLECTION AND ANALYSIS: Trial quality was assessed and data were extracted independently by two reviewers. MAIN RESULTS: Forty-four trials were identified: 37 trials including 16,916 women provided data on smoking cessation and/or perinatal outcomes, as did one cluster-randomised trial including 3000 women. Over 800 women were included in trials of smoking relapse prevention. There was substantial variation in the intensity of the intervention and the extent of reminders and reinforcement through pregnancy. Based on 34 trials there was a significant reduction in smoking in the intervention groups (odds ratio 0.53, 95% confidence interval 0. 47 to 0.60), an absolute difference of 6.4% women continuing to smoke. The eight trials with validated smoking cessation, a high intensity intervention and a high quality score had an odds ratio of 0.53, 95% confidence interval 0.44 to 0.63 and an absolute difference in continued smoking of 8.1%. The subset of trials with information on fetal outcome revealed a reduction in low birthweight (odds ratio 0.80, 95% confidence interval 0.67 to 0.95), a reduction in preterm birth (odds ratio 0.83, 95% confidence interval 0.69 to 0. 99) and an increase in mean birthweight of 28g (95% confidence interval 9 to 49). There were no differences in very low birthweight or perinatal mortality. Five trials of smoking relapse prevention showed no significant difference. The single large cluster-randomised trial showed no evidence of a decrease in continued smoking or adjusted mean birthweight. REVIEWER'S CONCLUSIONS: Smoking cessation programs in pregnancy appear to reduce smoking, low birthweight and preterm birth, but no effect was detected for very low birthweight or perinatal mortality.

Female↗