American Journal of Epidemiology
ª The Author 2012. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of
Public Health. All rights reserved. For permissions, please e-mail: [email protected].
Vol. 175, No. 10
DOI: 10.1093/aje/kwr466
Advance Access publication:
February 3, 2012
Original Contribution
Smoking Reduction at Midlife and Lifetime Mortality Risk in Men: A Prospective
Cohort Study
Yariv Gerber*, Vicki Myers, and Uri Goldbourt
* Correspondence to Dr. Yariv Gerber, Department of Epidemiology and Preventive Medicine, School of Public Health, Sackler
Faculty of Medicine, Tel Aviv University, Ramat Aviv, Tel Aviv 69978, Israel (e-mail: [email protected]).
Initially submitted September 29, 2011; accepted for publication November 15, 2011.
Previous studies have not shown a survival advantage for smoking reduction. The authors assessed survival
and life expectancy according to changes in smoking intensity in a cohort of Israeli working men. Baseline smokers
recruited in 1963 were reassessed in 1965 (n ¼ 4,633; mean age, 51 years) and followed up prospectively for
mortality through 2005. Smoking intensity at both time points was self-reported and categorized as none, 1–10, 11–20,
and 21 cigarettes per day. Change between smoking categories was noted, and participants were classified as
increased (8%), maintained (65%), reduced (17%), or quit (10%) smoking. During a median follow-up of 26 (quartiles
1–3: 16–35) years, 87% of participants died. Changes in intensity were associated with survival. In multivariableadjusted models, the hazard ratios for mortality were 1.14 (95% confidence interval (CI): 0.99, 1.32) among increasers,
0.85 (95% CI: 0.77, 0.95) among reducers, and 0.78 (95% CI: 0.69, 0.89) among quitters, compared with maintainers.
Inversely, the adjusted odds ratios of surviving to age 80 years were 0.77 (95% CI: 0.60, 0.98), 1.22 (95% CI: 1.01, 1.47),
and 1.33 (95% CI: 1.07, 1.66), respectively. The survival benefit associated with smoking reduction was mostly
evident among heavy smokers and for cardiovascular disease mortality. These results suggest that decreasing
smoking intensity should be considered as a risk-reduction strategy for heavy smokers who cannot quit abruptly.
cardiovascular diseases; cohort studies; lifetime risk; longevity; mortality; risk reduction behavior; smoking; smoking
reduction
Abbreviations: CHD, coronary heart disease; CI, confidence interval; CVD, cardiovascular disease; ICD, International Classification
of Diseases.
Overwhelming evidence has shown that smoking is a risk
factor for premature mortality (1, 2) and a causal factor in
the development of a multitude of terminal diseases, including
multiple cancers and coronary heart disease (CHD) (2, 3).
Quitting is obviously the best way for smokers to improve
their odds of survival (1, 4, 5). However, despite substantial
investment in smoking cessation services, a large number
of smokers are either unsuccessful at quitting or may not wish
to quit, and tobacco use remains one of the leading causes
of preventable mortality worldwide (5, 6). Twelve-month
success rates of smoking cessation services are estimated
at around 13%–25% (7, 8) and, in unaided smokers, as low
as 3%–7% (8, 9). Furthermore, success rates appear to be
dependent on socioeconomic factors, with lower quit rates
in disadvantaged areas (10).
Although a dose-response relation has been demonstrated
between smoking intensity and adverse health outcomes
(11, 12), uncertainty exists as to whether smoking reduction,
that is, a decrease in the number of cigarettes smoked daily,
improves survival. Previous studies have not found sufficient
evidence to support a benefit of smoking reduction with regard to all-cause and cardiovascular disease (CVD) death, or
risk of myocardial infarction (13–16), although a systematic
review suggested that substantial reduction in smoking improves several CVD risk factors (17), and reduction was
additionally associated with reduced risk of lung cancer (18).
Based on the available evidence, the latest report from the
US Surgeon General does not advocate smoking reduction
as a proven strategy of CVD risk reduction (5). However, in
a cohort of post-myocardial infarction persistent smokers,
1006
Am J Epidemiol. 2012;175(10):1006–1012
Smoking Reduction and Lifetime Mortality Risk
those who reduced their daily cigarette intake had an improved
chance of survival; each reduction of 5 cigarettes per day was
associated with an 18% decrease in mortality risk (19).
The current study investigates the health consequence of
changes in smoking intensity over a 2-year period in a large,
representative sample of Israeli working men aged 40 years
and over followed for 40 years, with a focus on lifetime risk
of all-cause, CVD, and non-CVD mortality associated with
smoking reduction.
MATERIALS AND METHODS
Participants were enrollees of the Israeli Ischemic Heart
Disease Study, a prospective cohort study which recruited
civil servants and municipal employees in 1963. Subjects were
male, aged 40 years, and employed in 1 of the 3 largest cities
in Israel (Tel Aviv, Haifa, and Jerusalem). Stratified sampling
was performed to ensure equal representation by country of
birth, approximately proportional to the Israeli male population of this age. Further details of this cohort have been
previously published (20, 21). The initial cohort comprised
10,059 men, of which 4,729 baseline smokers were reassessed in 1965. From the latter group, 4,633 subjects (mean
age, 51 (standard deviation, 7) years) were included in the
current study after excluding 96 participants who stopped cigarette smoking and switched to cigar or pipe smoking. Sociodemographic, biochemical, and clinical data were collected
at baseline in 1963 and subsequently in 1965.
Study variables
Smoking behavior was self-reported in 1963 and 1965.
During a personal interview, participants were asked to
choose one of 5 smoking status groups: never smoker, past
smoker, 1–10, 11–20, or more than 20 cigarettes per day.
Change between smoking categories was noted between
the 2 time points, and participants were classified into the
following groups: increased, maintained, reduced, or quit
smoking.
Outcomes were time to 1) all-cause death (1965–2005)
and 2) cause-specific death (1965–1997), dichotomized into
CVD and non-CVD. Information on death was derived from
the Israeli Mortality Registry. Cause of death was assessed
on the basis of individual determination by a review panel
during the 1960s and according to the International Classification of Diseases (ICD), Eighth Revision and Ninth
Revision, thereafter. Deaths from presumed CVD were
based on ICD codes 410–414 (CHD) and 430–438 (cerebrovascular disease). A total of 1,162 CVD deaths (866 ascribed
to CHD and 296 to cerebrovascular disease) and 1,985 nonCVD deaths were recorded by the end of 1997. ICD codes
were available for 1,900 (96%) non-CVD decedents, of which
170 (9%) were ascribed to lung cancer, 476 (25%) to other
cancers, 151 (8%) to respiratory diseases, 199 (10%) to noncoronary heart diseases, 71 (4%) to trauma, and 833 (44%) to
all other causes. Further details on mortality ascertainment
have been published (22).
Additional covariates included CVD risk factors. Blood
pressure was measured twice with a standard mercury sphygmomanometer, with a 15- to 30-minute interval, and the
Am J Epidemiol. 2012;175(10):1006–1012
1007
second measurement was used for analysis. Nonfasting serum
cholesterol was measured with the Anderson and Keys modification of the Abel method (23). Duplicate tests were performed on each specimen, and the average cholesterol value
was reported with a coefficient of variation of around 2.4%.
Height and weight measurements were taken, and body mass
index was calculated as weight (kg)/height (m)2. The presence of diabetes mellitus (known treated diabetes and/or
diagnosis via oral glucose tolerance test), CHD (either past
myocardial infarction or angina pectoris), and intermittent
claudication was determined as described previously (20, 24).
Physical activity during leisure time was determined via personal interview, with subjects reporting their physical activity
outside working hours. Response categories were none or
almost no daily physical activity, light-to-moderate but not
daily activity, light daily activity, and moderate-to-heavy
daily physical exertion (25). A socioeconomic status index
based on reported education and salary scale was established.
For this purpose, the men were ranked according to years of
schooling, possession of a high school or university diploma,
and salary grade categorized as professional, administrative, teaching, technician, or laborer, as used at that time
in the civil service and the municipalities of Tel Aviv,
Haifa, and Jerusalem. Socioeconomic status ranged from
1 (lowest) to 5 (26).
Statistical analysis
Cox proportional hazards regression models were constructed to evaluate the hazard ratios and 95% confidence
intervals for death in groups classified according to change
in smoking intensity during the initial 2 years of the study.
Adjustment was initially made for age, socioeconomic status,
and baseline smoking intensity (‘‘model 1’’) and, additionally, for systolic blood pressure, serum cholesterol, body mass
index, physical activity, diabetes, known CHD, and intermittent claudication (‘‘model 2’’). Except for baseline smoking
intensity (assessed in 1963), all other covariates were measured
in 1965, which was considered the beginning of follow-up.
In a sensitivity analysis, body mass index was entered as
a categorical variable (<18.5, 18.5–24.9, 25.0–29.9, 30),
which yielded virtually identical results in terms of the
smoking groups’ coefficients.
Adjusted survival curves (based on model 2) were plotted
by using the direct adjustment method developed by Zhang
et al. (27). The proportional hazards assumption was tested
with the Schoenfeld residuals. No violations were detected
except for CHD and intermittent claudication, which were
modeled as stratification variables (28).
Since, in the presence of competing risks, standard survival
predictions might produce biased estimates (29), the Fine
and Gray subdistribution hazard regression models were constructed to assess the hazard ratio for cause-specific death
grouped into CVD and non-CVD, with death from other
causes treated as a competing event (30). The regression
coefficient estimates were obtained through SAS macros
written by Du (31). Model discrimination was assessed by
the C statistic of Harrell et al. (28) (0.71 for all-cause mortality; 0.75 for CVD mortality; and 0.70 for non-CVD mortality,
based on fully adjusted models).
1008 Gerber et al.
Table 1. Smoking Intensity in 1965 Among Smokers in 1963, the Israeli Ischemic Heart Disease Study,
1963–2005a
Smoking in 1965, cigarettes/day
Total
None
1–10
No.
11–20
%
‡21
No.
%
No.
%
No.
%
No.
%
1–10
206
4.4
895
19.3
184
4.0
12
0.3
1,297
28.0
11–20
137
3.0
168
3.6
1,056
22.8
162
3.5
1,523
32.9
Smoking in 1963,
cigarettes/day
21
Total
a
129
2.8
34
0.7
585
12.6
1,065
23.0
1,813
39.1
472
10.2
1,097
23.7
1,825
39.4
1,239
26.7
4,633
100.0
The time of first interview was in 1963.
Logistic regression models were used to estimate the adjusted
odds ratios and 95% confidence intervals of surviving to age 75
and 80 years in smoking intensity change groups. Models were
similar to those specified above with regard to covariates.
Because the youngest survivor at the end of follow-up (end of
2005) was 82 years of age, these models included the entire
cohort. Missing values did not exceed 3% in any of the study
variables. Analyses were performed with SAS, version 9.2,
statistical software (SAS Institute, Inc., Cary, North Carolina).
RESULTS
Smoking intensity categories during the 1963 and 1965
interviews are cross-tabulated in Table 1. Although most of
the participants (n ¼ 3,016, 65%) maintained their smoking
level, an overall trend of reducing intensity was observed;
while 787 participants (17%) reduced their smoking and
an additional 472 (10%) quit, only 358 participants (8%)
increased their cigarette consumption.
Table 2. Baseline Characteristics According to Changes in Smoking Intensity From 1963 to 1965 Among Smoking Participants in the Israeli
Ischemic Heart Disease Study, 1963–2005
Intensity Change Category
Characteristics
Increased
(n 5 358; % 5 8)
a
No.
%
126
35
Age, years
Lowest SES category
Mean (SD)
Maintained
(n 5 3,061; % 5 65)
No.
%
50.1 (6.5)
Mean (SD)
Reduced
(n 5 787; % 5 17)
No.
%
255
33
50.6 (6.7)
780
26
Mean (SD)
Quit
(n 5 472; % 5 10)
No.
%
104
23
50.2 (6.4)
P Valueb
Mean (SD)
51.9 (7.2)
<0.001
<0.001
Systolic blood
pressure, mm Hg
134 (20)
136 (21)
136 (21)
139 (22)
0.02
Diastolic blood
pressure, mm Hg
85 (12)
86 (12)
85 (12)
87 (12)
0.004
207 (42)
209 (39)
210 (38)
210 (40)
Cholesterol, mg/dL
Body mass indexc
25.2 (3.4)
25.6 (3.5)
25.3 (3.4)
26.4 (3.2)
Leisure-time physical
activity
0.63
<0.001
0.59
None
235
67
1,876
63
490
63
287
Light
48
14
417
14
120
15
75
16
Light daily
45
13
487
16
115
15
74
16
Heavy
22
6
204
7
57
7
26
6
Diabetes
23
6
178
6
52
7
36
8
0.50
Known coronary heart
disease
20
6
249
8
68
9
71
15
<0.001
8
2
117
4
45
6
26
6
0.01
Intermittent
claudication
62
Abbreviations: SD, standard deviation; SES, socioeconomic status.
Assessed in 1965.
b
Assessed by using analysis of variance for continuous variables and the chi-square test for categorical variables.
c
Body mass index: weight (kg)/height (m)2.
a
Am J Epidemiol. 2012;175(10):1006–1012
Smoking Reduction and Lifetime Mortality Risk
1009
1.0
0.9
Adjusted Cumulative Incidence
0.8
0.7
0.6
0.5
Smoking Category
0.4
Increased
0.3
Maintained
0.2
Reduced
Quit
0.1
0.0
0
2
4
6
8
10
12
14
16
18
20
22
24
26
28
30
32
34
36
38
40
Years of Follow-up
Figure 1. Cumulative risk probabilities of all-cause mortality among smoking participants in the Israeli Ischemic Heart Disease Study, 1963–2005,
using the direct adjustment method based on a Cox proportional hazards model. Smoking categories were defined according to reported change in
smoking intensity between 1963 and 1965. Adjustment was made for age, socioeconomic status, baseline smoking intensity, systolic blood
pressure, serum cholesterol, body mass index, leisure-time physical activity, diabetes, known coronary heart disease, and intermittent claudication.
Ptrend < 0.001.
Pertinent clinical characteristics across smoking groups
defined by changes in intensity from 1963 to 1965 are presented in Table 2. The groups were quite comparable in their
characteristics, except for the quitters, who were slightly
older, had higher blood pressure and body mass index, were
more frequently diagnosed with CHD and intermittent claudication, and included fewer subjects with poor socioeconomic
status than the other groups.
During 116,362 person-years of follow-up with a median
of 26 years (quartiles 1–3: 16–35), 4,007 participants (87%)
died. Changes in smoking intensity were significantly associated with adjusted mortality risk (Figure 1), with the best
survival experienced by those who quit, followed by reducers,
maintainers, and increasers (Ptrend < 0.001). Accordingly,
the multivariable-adjusted hazard ratios for mortality were
1.14 (95% confidence interval (CI): 0.99, 1.32) among increasers, 0.85 (95% CI: 0.77, 0.95) among reducers, and
0.78 (95% CI: 0.69, 0.89) among quitters, compared with
maintainers (Table 3). In competing risks regression models,
the reduction in risk associated with decreasing smoking
intensity was mostly evident for CVD mortality (Table 3).
Interaction was detected between smoking reduction and
all-cause mortality risk by previous smoking intensity
(Pinteraction ¼ 0.02). The fully adjusted hazard ratio was 0.79
(95% CI: 0.71, 0.88) among heavy smokers (>20 cigarettes
per day) versus 1.09 (95% CI: 0.91, 1.30) among lighter
smokers (20 cigarettes per day) at baseline (not shown).
Changes in cigarette consumption were also associated
with longevity. Subjects who reduced smoking or quit entirely
Am J Epidemiol. 2012;175(10):1006–1012
increased their adjusted odds of surviving to age 75 and
80 years, compared with those who maintained their level.
On the other hand, subjects who increased their consumption
had lower odds of surviving to age 80 years (Table 4).
DISCUSSION
In this cohort of Israeli working men, a reduction in daily
cigarette intake over a 2-year period was associated with
a substantial lifetime survival benefit. Compared with those
who maintained their smoking level, smoking reducers had
a lower risk of overall and CVD mortality, while quitters
had an even greater lifetime benefit. Smoking reduction was
also associated with greater odds of surviving to age 75 and
80 years. The greatest benefit of smoking reduction was
seen in previously heavy smokers.
These findings lend support to the dose-response theory
of smoking, whereby mortality risk is related to the amount
smoked. The existence of a dose-response curve played an
integral role in establishing a causal relation between smoking and numerous health outcomes including stroke and CHD
(2, 11, 12, 32). Because the number of cigarettes smoked
tends to be associated with mortality risk, it is conceivable
that a reduction in cigarette smoking should be followed by
a reduction in mortality risk, although previous research
has not generally found this to be the case. In our study,
although quitting smoking was associated with the greatest
improvement in mortality risk, smoking reduction was itself
1010 Gerber et al.
Table 3. Hazard Ratios and 95% Confidence Intervals for Death, Overall and by Underlying Cause, Associated With Changes in Smoking
Intensity During the First 2 Years of the Israeli Ischemic Heart Disease Study, 1963–2005a
Intensity Change Category
Adjustmentb
Increased
Maintained
Reduced
HR
95% CI
HR
95% CI
HR
Model 1
1.08
0.94, 1.24
1
Referent
0.85
Model 2
1.14
0.99, 1.32
1
Referent
0.85
Ptrend
Quit
95% CI
HR
95% CI
0.77, 0.95
0.87
0.77, 0.98
0.001
0.77, 0.95
0.78
0.69, 0.89
<0.001
All-cause mortality (n ¼ 3,147)
CVD mortality (n ¼ 1,162)c
Model 1
1.05
0.82, 1.32
1
Referent
0.78
0.65, 0.93
0.95
0.78, 1.15
0.08
Model 2
1.14
0.92, 1.41
1
Referent
0.77
0.66, 0.94
0.84
0.70, 1.05
0.01
Non-CVD mortality (n ¼ 1,985)c
Model 1
1.05
0.88, 1.25
1
Referent
0.98
0.88, 1.12
0.89
0.76, 1.04
0.15
Model 2
1.05
0.88, 1.25
1
Referent
0.98
0.87, 1.10
0.90
0.77, 1.05
0.19
Abbreviations: CI, confidence interval; CVD, cardiovascular disease; HR, hazard ratio.
Follow-up was truncated at the end of 1997, because cause of death was unavailable afterward.
b
Model 1: adjusted for age, socioeconomic status, and smoking intensity in 1963. Model 2: model 1 plus systolic blood pressure, blood
cholesterol, body mass index, leisure-time physical activity, diabetes, known coronary heart disease, and intermittent claudication.
c
Death from other causes was treated as a competing event by using the Fine and Gray subdistribution hazard regression model (J Am Stat
Assoc. 1999;94(446):496–509) (30).
a
associated with substantial reductions in lifetime mortality
risk and gains in longevity.
Comparisons with previous research
Several previous large-scale studies found no significant gains in survival associated with smoking reduction
(13, 15, 16). A systematic review has suggested that ‘‘the
magnitude of health benefit following smoking reduction
is smaller than the reported reductions in tobacco use’’
(17, p. 643). According to Godtfredsen et al. (15, 16), the
lack of effect in previous research may be partly due to
compensatory smoking; that is, while the number of cigarettes may be reduced, there may be a tendency to smoke
each cigarette more intensely and for longer, thereby extracting
more nicotine and toxic substances. Indeed, several studies
measuring smoking biomarkers found this to be the case, with
reductions in biomarkers not equivalent to reported reductions in cigarette consumption (33, 34). However, Hatsukami
et al. (35) reported modest improvements in cardiovascular
biomarkers (white blood cell count, cholesterol, heart rate)
associated with smoking reduction. A further study reported
a decrease in cholesterol and pulse rate and increased general health score in smokers who reduced their smoking by
at least 50% (36). It is therefore biologically plausible that
a reduction in smoking intensity could lead to a reduction in
cardiovascular mortality.
Indeed, a study of Korean men showed a borderline decreased risk of ischemic stroke and myocardial infarction in
smoking reducers followed up for 10 years, although this did
not reach statistical significance (37). Similarly to the current
study, smoking behavior was assessed twice, with a gap of
Table 4. Odds Ratios and 95% Confidence Intervals of Surviving to Age 75 and 80 Years According to Changes in Smoking Intensity During the
First 2 Years of the Israeli Ischemic Heart Disease Study, 1963–2005
Intensity Change Category
Adjustment
a
Increased
OR
95% CI
Maintained
OR
95% CI
Reduced
OR
Quit
95% CI
Ptrend
OR
95% CI
Surviving to age 75 years (60% of the cohort)
Model 1
1.03
0.81, 1.30
1
Referent
1.27
1.07, 1.50
1.25
1.01, 1.54
0.009
Model 2
0.97
0.75, 1.26
1
Referent
1.26
1.05, 1.51
1.30
1.04, 1.64
0.003
Surviving to age 80 years (44% of the cohort)
Model 1
0.82
0.65, 1.03
1
Referent
1.21
1.01, 1.44
1.22
1.00, 1.49
0.001
Model 2
0.77
0.60, 0.98
1
Referent
1.22
1.01, 1.47
1.33
1.07, 1.66
<0.001
Abbreviations: CI, confidence interval; OR, odds ratio.
Model 1: adjusted for age at study entry, socioeconomic status, and smoking intensity in 1963. Model 2: model 1 plus systolic blood pressure,
blood cholesterol, body mass index, leisure-time physical activity, diabetes, known coronary heart disease, and intermittent claudication.
a
Am J Epidemiol. 2012;175(10):1006–1012
Smoking Reduction and Lifetime Mortality Risk
2 years. Our findings support this report but extend its finding
in a well-defined cohort with a longer follow-up period.
Although extensive research has investigated the benefits
of quitting, study of the benefits accrued from reduction of
smoking has received somewhat less attention. Although previously evaluated (13, 15, 16, 37), our study is the first to
demonstrate a clear, positive relation between smoking
reduction and survival in the general population. There are
several possible explanations for differences in the results.
The current study benefitted from a very long follow-up of
up to 40 years. Because the health consequences of smoking
are long term, a longer follow-up may be more appropriate
for the detection of the outcomes of changes in smoking
habits. Godtfredsen’s Danish cohort was recruited in their
mid 50s and followed up for 15 years, with no significant
benefit of smoking reduction (15, 16). Our cohort had a similar age distribution at baseline but was followed up for
significantly longer, until death or old age, thereby making
associations more likely to be detected. It may be that the
benefits of smoking reduction are seen only later in life,
exemplified by the increased odds of surviving to age 80 years
in reducers. Furthermore, it is likely that individuals in our
cohort reduced smoking earlier than those in the Danish
cohort, with a time interval between assessments of just
2 years, compared with 5–10 years. Individuals who continued
smoking heavily for a longer duration before cutting down
are less likely to see the benefits of reduction.
Previous studies often defined smoking reduction as at
least 50% reduced from baseline (13, 15). In contrast, the
current study used categories of change in smoking behavior.
To move from one category to another, reduction may have
been less than 50% in our study (e.g., a reduction from 25 to
20 cigarettes per day). This further strengthens our results
given that a stronger association was found with a potentially
smaller reduction.
Limitations
Smoking behavior was assessed at 2 points, and no information is available on smoking habits throughout follow-up.
We do not know whether reducers returned to previous levels
or, alternatively, quit during follow-up, thereby increasing the
apparent benefit of reducing smoking. A previous follow-up
study of smoking behavior 10 years after the initial assessment showed that approximately 50% of the reducers continued to smoke at the reduced level, 20% had quit, and just
30% had returned to heavy smoking (15). In the current
study, smoking was additionally self-reported, lacking
biochemical verification.
Because of the observational nature of this study, we cannot
claim a causal effect of smoking reduction on reduced mortality risk. There may be some characteristic inherent to
reducers that relates to a healthier lifestyle in general. Although
analyses were adjusted for sociodemographic variables, baseline smoking level, and cardiovascular risk factors including
physical activity level, it was impossible to fully control for
dietary and physical activity patterns. Individuals who made
a conscious effort to cut down the number of cigarettes
smoked may have made parallel lifestyle changes, potentially diluting the impact of change in smoking behavior.
Am J Epidemiol. 2012;175(10):1006–1012
1011
Additionally, because this is a male-only cohort, assessment
of the association in women is warranted.
Implications
Smoking reduction is associated with a long-term survival
benefit, with the greatest advantage in previously heavy
smokers. Although there is no safe level of exposure to tobacco
smoke (5), for smokers who cannot quit, reduction may be
a feasible option. Given the low success rate of smoking
cessation programs, smoking reduction could decrease risk
for those who are unsuccessful at quitting. Moreover, previous research has shown that smoking reduction does
not harm the chances of quitting but, rather, increases the
probability of future cessation (38, 39). Although smoking
cessation should always be the preferred goal, reducing
smoking intensity may be viewed as a first step toward
cessation for those who cannot quit instantaneously.
Conclusion
Changes in smoking intensity were significantly associated
with survival and CVD mortality. Individuals who reduced
their smoking intensity had lower mortality risk and higher
odds of surviving to age 80 years. Reducing smoking intensity may be advised for heavy smokers who cannot quit
abruptly.
ACKNOWLEDGMENTS
Author affiliations: Department of Epidemiology and
Preventive Medicine, School of Public Health, Sackler
Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
(Yariv Gerber, Vicki Myers, Uri Goldbourt).
Data collection at baseline (1963, 1965) was part of
a collaborative study by the National Institute of Health,
the Ministry of Health, Israel; and the Hadassah medical
organization, supported by PL 480 counterpart funds, research
agreement no. 375106. The Fund for Basic Research from
the Israeli Academy of Sciences supported the mortality
follow-up from 1970 to 1978.
Conflict of interest: none declared.
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