Introduction, overview, method and conclusions

PREVENTIVE MEDICINE

20, 552-563 (1991)

Introduction,

Overview, Method, and Conclusions’

JUDITHK. OCKENE,PH.D.,* AND B. JESSICASHATEN, MS.-f

For the MRFIT Research Group* *Department of Medicine, Division of Preventive and Behavioral Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605; and ?Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota 55455

HISTORICAL

PERSPECTIVE

In the United States today cigarette smoking remains the major alterable risk factor for such life-threatening diseases as coronary heart disease (CHD), lung cancer, chronic obstructive lung disease, and cerebrovascular disease; it is responsible for more than one of every six deaths (1). The role of smoking cessation in the prevention of CHD merits special attention, since heart disease continues to be the leading cause of death in the United States (2). In 1970 the Inter-Society Commission for Heart Disease Resources (3) recommended that the United States adopt a policy for heart disease prevention, with the modification of cigarette smoking assuming an important priority. The Multiple Risk Factor Intervention Trial (MRFIT), a National Heart and Lung Institute3 sponsored trial, evolved from this national commitment to control CHD (4, 5). This primary prevention randomized clinical trial, which enrolled 12,866 men, was designed to determine whether a reduction in high blood pressure and blood cholesterol and the cessation of cigarette smoking would result in a significant reduction in mortality and morbidity from CHD in men, age 35-57, at high risk for CHD, but with no clinical evidence of it on entry into the study (4, 5). Antismoking activities have contributed to the large decline in adult smoking rates, from 37.4% in 1970 to 29.4% in 1986 (I). Much has been learned about smoking: its effects, intervention approaches and factors that affect smoking cessation, and the enormous health benefits to be gained from cessation (6). However, new data on the association between smoking and disease continue to be reported, and there is a need for improved strategies to further decrease the prevalence of smoking. In particular, prevention of the high relapse rate among quitters is a major problem. Knowledge also can be strengthened in areas such as the efficacy of specific smoking intervention techniques, the factors that affect smoking behavior change, the utility of biological markers of tobacco exposure, the relationship of smoking behavior change to other risk factors, the impact of ’ Address reprint requests to the Coordinating Centers for Biometric Research, 2221 University Avenue S.E., Suite 200, Minneapolis, MN 55414-3080. 2 See credit roster for complete listing. 3 The National Heart and Lung Institute (NHLI) became the National Heart, Lung, and Blood Institute (NHLBI) in 1976, after the MRFIT had been funded. 552 0091-7435191$3.00 Copyright0 1991 by Academic Press,

Inc. All rights of reproduction in any form reserved

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smoking cessation on clinical outcomes such as lung function, and morbidity and mortality from diseases other than CHD. The men screened for MRFIT represent one of four large cohorts presently being followed to evaluate the effects of smoking on particular diseases; the other three are the Nurses Health Study (7), the American Cancer Society’s Volunteer Study (8), and the follow-up of participants from the first National Health and Nutrition Examination Survey (NHANES) (9). The data from MRFIT randomized participants are a valuable resource for studying the relationship between smoking cessation and disease and for studying other areas in which knowledge concerning smoking and disease is incomplete. The articles composing this monograph address many of the topics mentioned above. The purpose of this introduction is to present an overview of the MRFIT data collection methods and instruments used, the smoking intervention program, and the program’s objectives; to indicate how the MRFIT has responded to deficiencies in prior smoking intervention research; and to present a summary of the monograph and its conclusions. DESCRIPTION OF THE MRFIT Initially, 361,622 men in community and industrial settings were screened for their eligibility for inclusion into the trial at 22 MRFIT clinical centers throughout the United States. After two additional screenings, 12,866 men in the upper 10 to 15% of risk for CHD death4 were randomly assigned to a special intervention (SI) or usual care (UC) group (5, 10). Randomization of participants occurred from December 1973 to February 1976. Eligibility criteria specified that each volunteer agree to participate in the program for 6 years and that each smoker indicate his willingness to attempt smoking cessation if requested. Exclusion criteria included diastolic blood pressure (DBP) 2115 mm Hg, serum cholesterol (TC) 2350 mg/dl, evidence of CHD or diabetes mellitus, expected geographic mobility, diets incompatible with the MRFIT food pattern, and other problems that could impair participation in the trial. Of the 12,866 men randomized, 63.7% were smokers at entry. On average, smokers consumed 33.9 cigarettes per day and began smoking at age 18. Twenty-two percent of the participants were former cigarette smokers at entry. No intervention program was offered to the UC men who were referred to their usual sources of medical care. However, they were invited to return to the clinical center once a year for a comprehensive evaluation including risk factor assessment, medical history, physical examination, and laboratory studies. The results of the screening and annual examinations were sent to their personal physicians, who were informed of the scientific objectives of the study. Participants randomized to the SI group were invited to participate in an intensive intervention program. The special intervention program for risk factor mod4 The percentage of risk was calculated from levels of serum cholesterol, diastolic blood pressure, and number of cigarettes smoked per day using a risk score distribution based on data from the Framingham Heart Study. It was changed from the upper 15% to the upper 10% almost midway through the screening in order to increase the power of the trial (19).

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ification began within 2 weeks after randomization and consisted primarily of 10 weekly group sessions. The concepts of heart disease and risk were discussed and interventions for nutrition and smoking behavior change were implemented. Individual counseling, available to participants who did not desire to or could not participate in the groups, was also provided as a substitute for the group intervention for some participants (10). A second stage, extended intervention and maintenance, provided further intervention for participants who had not achieved the desired changes and a maintenance or relapse prevention program was provided for participants who had achieved satisfactory risk factor reduction (10). SI men who were hypertensive (mean DBP 290 mm Hg on two consecutive visits or using antihypertensive medication prescribed by their personal physicians) were seen individually and treated with a stepped-care approach. The approach to treating hypertension has been described (11, 12), as has the nutritional approach to lowering cholesterol and weight (13, 14). Participants in the SI group also underwent yearly examinations and returned to the clinical center every 4 months for risk factor evaluation. In February 1982, when active intervention was terminated, each of the randomized 12,866 men who had survived had been followed for at least 6 years, and the mean duration of follow-up was approximately 7 years. This large sample size, coupled with the extensive quality control measures used (15), provides valuable data to enhance our understanding of the smoking cessation process and its effect on disease. Mortality

Ascertainment

During the trial, and at termination of active intervention, deaths were ascertained by clinic staff through routine follow-up of missed clinic visits, contact with family or friends of the deceased, response to postcards requesting changeof-address information sent twice yearly to UC participants, and searches of publicly accessible files of deceased persons. The Social Security Administration and the National Death Index have been the main sources of vital status information since March 1982. Mortality ascertainment through December 31, 1985, is estimated to be approximately 100% complete using these data sources (16). The causes of death used in the accompanying articles of this monograph are based on death certificate reports. Cause-specific death rates are based on coding of death certificates by trained nosologists, according to the ninth revision of the International Classification of Diseases (ICD-9) (17). Each death certificate for randomized participants was independently coded by two nosologists and disagreements were adjudicated by a third nosologist. Data Collection

Methods

Data collected at the three screening visits included ascertainment of medical and risk factor status, blood and urine tests, resting and exercise EKG, spirometry, and chest X rays (5). Complete medical and nutritional histories were collected through questionnaires and interviews. A modified version of the Holmes and Rahe Social Readjustment Rating Scale (life events) was used to measure stress (18), and the Jenkins Activity Scale (JAS) was used to measure “type A”

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TABLE 1 SELF-REPORTSOFSMOKINGBEHAVIORATTHE THREESCREENS FORMRFIT PARTICIPANTS@ = 12,866)

Number reporting smoking cigarettes Percentage reporting smoking cigarettes Number of cigarettes per day for smokers Number of nonsmokers who reported ever having smoked Percentage of nonsmokers who reported ever having smoked Number of cigarette smokers who also reported smoking pipes, cigars, or cigarillos Number of non-cigarette smokers who reported smoking pipes, cigars, or cigarillos

Screen 1

Screen 2

Screen 3

8,194 63.7 34.0

7,938 61.7

7,688 59.1 32.6 2,813 66.2 2,346 l,i%

(“coronary-prone”) behavior (19). Cigarette smoking status was ascertained for all participants at each of the three screening visits. A more detailed smoking history, including use of pipes, cigars, or cigarillos, was obtained at screen 3 (see Table 1). Serum SCN and expired-air carbon monoxide (CO) levels provided objective measures of smoking and a test of the validity of the self-reports (20-23). Serum from blood drawn at screen 2 and annually thereafter was analyzed for SCN by an automated (autoanalyzer) procedure using the method of Butts et al. (20). Expired-air CO was measured with the use of an Ecolyzer (10, 21). The use of SCN and CO as biological markers is discussed more fully by Ruth and Neaton (24) below. Smoking Intervention Program The cigarette smoking intervention effort, designed to achieve maximum cessation of cigarette smoking, began immediately following randomization at screen 3 with a strong antismoking message delivered to each SI smoker by a physician. (See Fig. 1.) The physician summarized the effects of smoking on the cardiovascular and respiratory systems, relating it where possible to findings regarding the participant’s medical status, and strongly advised him to stop smoking (10). At this time the smoker also met with a smoking specialist’ who determined with the participant whether he would attend an intensive intervention group. The specialist invited the participant’s wife or “significant other” to accompany him to the group and to other intervention activities at the center and assessed the participant’s attitudes about smoking and his previous efforts to stop smoking. Approximately 87% of the SI smokers elected to participate in the groups (10). During the early 1970s when the MRFIT smoking intervention protocol was designed, cessation programs emphasized conditioning-based approaches and cognitively based self-management procedures (1, 10,25-27). Behavioral and cog’ Smoking specialists were counselors specifically trained in smoking intervention techniques.

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OCKENE AND SHATEN TABLE 2 NUMBER

OF MRFIT SI AND UC PARTICIPANTS WITH SMOKINGSTATUSDATA FOR

EACHANNUAL VISIT Monthly visit

SI participants Self-report smoking status Thiocyanate Carbon monoxide UC participants Self-report smoking status Thiocyanate Carbon monoxide All participants Self-report smoking status Thiocyanate Carbon monoxide

12

24

6,114 5,930 -

5,826 -

@JO’3

36

48

60

72

84

5,8% 5,767 5,555

5,806 5,724 -

5,693 5,581 -

5,761 5,629 5,526

2,723 2,614 -

6,080 5,900 -

5,923 5,724

5,796 5,684 5,419

5,724 5,604

5,636 5,493

5,659 5,497 5,400

2,721 2,622 -

12,194 11,830

11,923 11,550 -

11,692 11,451 10,974

11,530 11,328 -

11,329 11,074 -

11,420 11,126 10,926

5,444 5,236 -

-

nitive interventions included behavioral assessment, self-monitoring, gradual change, stimulus control procedures, behavioral contracts, and relaxation techniques. Different smokers were instructed to substitute activities incompatible with smoking (e.g., exercise) to help them deal with short-term problems or strong urges to smoke. The decision to use these methods in the smoking intervention program was based on other studies which suggested that “broad spectrum” approaches yielded the best long-term smoking cessation rates (10, 25-27). Extended intervention efforts included the same methods used during intensive intervention, although there was greater flexibility for scheduling sessions. For example, smoking intervention no longer had to be integrated with the nutrition component for all participants. Once cessation was achieved in either initial or extended intervention, the maintenance program was begun. The maintenance program consisted of a series of scheduled meetings between participants and staff to discuss potential problems with maintaining abstinence. They reviewed approaches that the participant could use to deal with these problems (e.g., relaxation techniques, exercise, social support). Discussions were designed to Anti-Smoking Message by M.D. Immediately Following Randomization

Integrated

Intensive

Intervention

Never Stopped

Smoking

/Relapsed

FIG. 1. MRFIT smoking intervention program for special intervention participants.

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YES

EXTENDED INTERVENTION PROGRAM

MAINTENANCE PROGRAM

YES

1

FIG. 2. MRFIT maintenance and extended intervention contact for cigarette smoking cessation.

protocols: minimum frequency of stti

strengthen the participant’s self-efficacy and belief that he would maintain the changes that he had implemented. The frequency of the scheduled contacts decreased over time as the participant remained a nonsmoker (IO, 21). A key item in both the extended intervention and the maintenance programs was a specified minimum number of contacts. Participants who maintained smoking abstinence over an extended period of time were eventually seen for smoking cessation only at the regular 4-month follow-up visits (Fig. 2). (See Hughes et al. (10) for a detailed account of the MRFIT smoking program.) The goal of the MRFIT smoking program was to achieve early cessation for SI smokers. It was also expected that a relapse into smoking would occur over the 6-year course of the trial for some SI men who quit. Ockene and colleagues discuss in this monograph the cessation rate achieved (28). Smoking

Program

Objectives

The intervention goal for individual SI participants was complete cessation of cigarette consumption. While participants were discouraged from smoking pipes and/or cigars they were considered abstinent even if they stopped smoking cigarettes but continued to smoke pipes and/or cigars. Although the primary objective of the MRFIT smoking intervention program was total cessation, a program for dosage reduction was extended to smokers who had not been successful in their cessation attempts. Design Considerations

in Smoking

Intervention

Studies

Design methodology, definitions of terms, and control of data quality must be optimal in order to meaningfully assess the outcomes of an intervention study. Other investigators (2, 2%33) have noted common deficiencies in smoking intervention studies. The MRFIT was designed with the following components in order to overcome problems faced in prior studies:

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I. Use of comparison groups. In the last two decades, smoking studies have become more consistent in their use of an experimental design that includes random allocation to the smoking intervention group and to an appropriate comparison group. It is more diflicult to determine the effects of a proposed treatment in studies which do not include randomized controls. As described above, the MRFIT participants were randomized to a special intervention group and to a comparison or usual care group. 2. Use of objective data to verify self-reported outcomes. Evaluation of smoking cessation in response to intensive clinical interventions requires objective validation of participants’ reported smoking behavior. Data that include only self-reports depend upon the participant’s honesty and accuracy; however, the demanding nature of intensive intervention programs may prompt some individuals to exaggerate their compliance (6,34). Evaluation based upon these data may lead to overestimates of the program’s success. Other investigators have discussed validation of self-reports with the use of serum SCN and/or concentrations of CO in serum or expired air (6,21,23,24, 3 1, 33, 34). The MRFIT used both SCN and CO concentration in expired air to validate self-reported smoking status. 3. Use of cohort and cross-sectional data. Most studies report cessation rates for a given point in time (“nonsmoking point prevalence”) rather than continued abstinence from immediately post-treatment onward. Such studies give no indication of the dynamics of cessation or relapse that determine the nonsmoking point prevalence rate, nor do they indicate what is happening over time with a cohort of smokers (6, 21). Studies of smokers who quit both with and without formal aid demonstrate that people often pass through several cycles of cessation and relapse before permanent cessation is achieved (6, 28, 32, 35). Since length of cessation affects morbidity and mortality, information regarding smoking behavior as it changes over time is necessary to evaluate the “true” effect of cessation on disease. Previous studies investigating cessation and disease which examined participants at one point in time estimated smoking behavior over time retrospectively (3638) or by assuming that behavior did not change over time (36, 37). Both inaccurate recall and faulty assumptions may lead to misestimates of mortality risks associated with cigarette smoking. In the MRFIT, smoking behavior was assessed annually; thus, information is available on the duration of cessation in addition to cessation at a given point in time. Of all large-scale studies, the MRFIT has the most complete data set of longitudinal measures of smoking behavior. 4. Clear definitions of terms. Prior analyses (22) of MRFIT smoking data have revealed a wide array of cessation and relapse patterns. Given the variability of individual behavior over time, clear definitions of such terms as “point prevalence cessation, ” “continuous cessation,” “relapse,” and “never stop” are essential This point is made by Shipley et al. (33), who offer potential standard definitions, by Schwartz (30,39), and in the 1990 Surgeon General’s Report (6). In this monograph, all terms are defined either in this introduction or in the individual articles. SUMMARY

MRFIT

smoking

data are valuable

because of the large number

of smokers

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studied, the duration and completeness of follow-up, the use of serum SCN and CO as objective measures of smoking, the serial collection of data regarding smoking and other risk factors, and the standardized and complete collection of morbidity and mortality data. This information is enhanced by additional data concerning smoking history prior to entrance into the trial. Highlights

of Monograph

Conclusions

The MRFIT data provide valuable information about the process of smoking behavior change, factors which affect that process, biological markers of cessation, cessation’s effect on other risk factors, and the relationship of cessation to pulmonary function and to morbidity and mortality. This monograph consists of seven papers. The major conclusions of each paper are presented below. Comparison of Smoking Behavior Change for SZ and UC Study Groups (28) Ockene and colleagues studied the changes that occurred in smoking behavior over an average of 7 years. They found that: 0 At 72 months, the reported cessation rates among screen 1 smokers were 48.9% for SI men and 28.8% for UC men. l At 72 months, the reported cessation rates for all tobacco products for screen I cigarette smokers were 41.6% for SI men and 25.6% for UC men. l There was a strong inverse relationship between cessation rates and the number of cigarettes smoked per day at screen 1 for both SI and UC smokers. l Of the 1,750 SI men who had quit smoking by 72 months, 898 (51.3%) quit within the first 12 months and remained abstinent thereafter, 701 (40.1%) either quit during the first 12 months and later relapsed or quit for the first time between the 12- and 60-month visits, and 151 (18.6%) stopped for the first time at 72 months. Evaluation

of the Biological

Markers

of Tobacco Exposure (24)

Ruth and Neaton evaluated the use of serum SCN and expired air CO in discriminating tobacco smokers from nonsmokers. They found that: l Serum SCN and CO in expired air were both good markers of smoking exposure, but SCN may have the advantage of a longer half-life. l Optimal cutpoints for discriminating tobacco smokers (cigarettes, pipes, cigars, or cigarillos) from nonsmokers, as determined by using logistic regression, were 83 ~molfliter and 10 ppm for SCN and CO, respectively. l The estimated cutpoints derived from the MRFIT data result in predictive values greater than 85% when the prevalence of smokers is greater than 50%. Cutpoints need to be modified to maximize their predictive value when the prevalence of smokers is less than 50%.

Baseline Factors Associated

with Cessation and Relapse (40)

Hymowitz and colleagues considered baseline factors related to subsequent smoking cessation and relapse over 6 years of follow-up in the MRFIT. They found that:

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l Among both SI and UC smokers, cessation rates increased with age, education, and past success in quitting and declined with number of cigarettes smoked per day. Expectation of quitting was related to higher cessation rates only in the SI group, while fewer life events, less alcohol consumption, and the presence of a nonsmoking wife were significant predictors of increased cessation only for UC participants. l Variables which were related to relapse differed from those which influenced initial cessation, and more variables predicted relapse for UC than for SI participants. For UC participants, less education, former attempts to quit smoking, increased alcohol consumption, and more life events were related to higher relapse rates. For SI, only alcohol emerged as a significant predictor of relapse. l It is likely that any associations between psychosocial characteristics and smoking behavior change may have been weakened by the effects of the MRFIT intervention program.

Smoking Cessation and Change in Diastolic Plasma Lipids (41)

Blood Pressure, Body Weight, and

Gerace and colleagues examined the impact of smoking cessation on DBP and incidence of hypertension. In addition, they explored the effect of cessation on body weight and considered several variables such as caloric consumption and physical activity that may have mediated or influenced this effect. They also examined the relationship between smoking cessation and changes in plasma TC and lipoprotein fractions. They found that: l Smoking cessation did not have a direct long-term effect on DBP, nor did it reduce the effectiveness of the antihypertensive protocol used in the MRFIT. l Among hypertensive SI smokers, those who quit had higher rates of required antihypertensive medication use than those hypertensives who did not quit. Of normotensive SI smokers, those who quit developed hypertension at a greater rate than those who did not quit. l The amount of weight which quitters gained increased with the number of cigarettes previously smoked per day and decreased with their self-reported physical activity level. l Cessation had no independent effect on plasma TC or low-density lipoprotein cholesterol, but was associated with a 2.2 mg/dl reduction in very-low density lipoprotein cholesterol and a 2.4 mg/dl increase in high-density lipoprotein cholesterol (HDL-C).

Pulmonary

Function

in Relation

to Cigarette

Smoking

and Cessation (42)

Townsend and colleagues examined pulmonary function measures crosssectionally and longitudinally in relation to smoking and smoking cessation in the MRFIT. They found that: l Pulmonary function for all screen 1 smokers declined during the trial; however, the decline was more severe for those who continued to smoke than for those who quit smoking in the first year and abstained for the remainder of the

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trial. This effect was documented over the latter half of the trial, 34 years following smoking cessation. l At the midpoint of the trial, those who had never smoked, former smokers, quitters, and continuing smokers showed a gradient of decreasing levels of pulmonary function. l On the basis of the MRFIT cohort, if a healthy smoker stops smoking in middle age, he can expect his pulmonary function to decline less severely over time than if he continues to smoke. Cigarette

Smoking

and Mortality

(43)

Kuller and colleagues examined the relationship of cigarette smoking and cessation to mortality in both screened and randomized men. They found that: l Except for age, cigarette smoking was the only risk factor in the MRFIT that was directly related to all major mortality endpoints, including CHD, cardiovascular disease (CVD), lung cancer, total cancer, and all-cause mortality. l Among cigarette smokers, the dose of smoking as measured by the number of cigarettes smoked was the most important determinant of Jung cancer mortality. l CHD death rates were higher among cigarette smokers than among nonsmokers; however, among smokers, there was no association between dose and CHD mortality. l Quitting smoking substantially decreased CHD mortality but had little measurable effect on lung cancer mortality over 10.5 years. l There was a weak association between tar and nicotine content in cigarettes and mortality from all causes.

Associations between Baseline Risk Factors, Cigarette Mortality after 10.5 Years (44)

Smoking,

and CHD

In the final article, Shaten and colleagues assessed the way in which associations between baseline risk factors and CHD mortality depended upon smoking status at entry. They found that: l At all levels of baseline risk factors affecting CHD mortality, rates of death were higher among smokers than among nonsmokers. l There was a negative association between plasma HDL-C and CHD mortality which was stronger among nonsmokers than among smokers. l There was a positive association between fasting glucose levels and CHD mortality which was stronger among nonsmokers than among smokers. l With respect to the associations between HDL-C and CHD mortality and fasting glucose levels and CHD mortality, the strongest were exhibited by former smokers who quit 12 or more months prior to screen 3. There were no differences with respect to these associations between current smokers and former smokers who had quit within 12 months of screen 3.

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