Smoking and Risk of Total and Fatal Prostate Cancer in United States
Health Professionals
1
Edward Giovannucci,
2
Eric B. Rimm, Alberto Ascherio,
Graham A. Colditz, Donna Spiegelman,
Meir J. Stampfer, and Walter C. Willett
Channing Laboratory, Department of Medicine, Brigham and Women’s
Hospital and Harvard Medical School, Boston, Massachusetts 02115 [E. G.,
E. B. R., G. A. C., M. J. S., W. C. W.], and Departments of Nutrition [E. G.,
E. B. R., A. A., M. J. S., W. C. W.], Epidemiology [E. G., E. B. R., A. A.,
G. A. C., D. S., M. J. S., W. C. W.], and Biostatistics [D. S.], Harvard School
of Public Health, Boston, Massachusetts 02115
Abstract
Studies that have examined the relationship between
cigarette use and prostate cancer incidence have yielded
inconsistent results, although most studies have suggested
that smoking is related to the occurrence of fatal prostate
cancer. We evaluated prospectively the relationship
between cigarette smoking and total, distant metastatic,
and fatal prostate cancer in 47,781 male health
professionals throughout the United States followed with
questionnaires. From 1986 to 1994, we documented 1369
men with prostate cancer (excluding stage A1). One
hundred fifty-two of the men had distant metastatic
disease at diagnosis, and 103 fatal cases occurred from
1986 to 1994. Early (before age 30), late (within recent 10
years), and lifetime cumulative smoking history were
unrelated to risk of total prostate cancer. However, men
who had smoked 15 or more pack-years of cigarettes
within the preceding 10 years were at higher risk of
distant metastatic prostate cancer [multivariate relative
risk (RR), 1.81; 95% confidence interval (CI), 1.05–3.11;
P (trend), 0.03] and fatal prostate cancer [RR, 2.06; CI,
1.08 –3.90; P (trend), 0.02] relative to nonsmokers. Within
10 years after quitting, the excess risk among smokers is
eliminated. The higher rate of fatal prostate cancer
among smokers did not appear to result from
confounding by diet or other lifestyle factors, different
screening behavior between smokers and nonsmokers, or
from other smoking-related comorbidities. Our results
indicate that although smoking was unrelated to prostate
cancer incidence, recent tobacco use had a substantial
impact on the occurrence of fatal prostate cancer.
Introduction
Cigarette use is the leading cause of death from cancer, but the
relationship between smoking and prostate cancer has been
inconsistent; some studies indicate no connection (1–5),
whereas others suggest an elevated risk among smokers (6 –10).
In several studies, smokers had higher mortality rates from
prostate cancer (11–14). A large investigation of United States
veterans (12) found an elevated risk among current smokers at
baseline during the initial 8.5 years of follow-up, but this risk
was attenuated over the 26-year follow-up. This finding sug-
gests that only relatively recent use of tobacco influenced risk
of prostate cancer mortality because many smokers quit over
time. A possible explanation for the more consistent results for
mortality than incidence is that smokers may delay diagnosis
and treatment, which could result in poorer survival. Alterna-
tively, tobacco may theoretically induce prostate cancers to
develop a more aggressive phenotype or may cause the devel-
opment of a distinct subset of rapidly progressive cancers. For
example, smoking-related carcinogens could possibly cause
mutations in genes associated with tumor progression, or to-
bacco use may alter host factors, such as levels of hormones,
which foster tumor progression. Indeed, two studies (15, 16)
have found smokers more likely to be diagnosed with advanced
stage or high histological grade prostate cancers.
The studies that found smokers to be at higher risk for
prostate cancer mortality (11–14) could not distinguish whether
this association was a result of delayed diagnosis and treatment
among smokers, failure to control for confounding factors, or
from direct effects from tobacco use. To better understand the
nature of the relationship between smoking and prostate cancer,
we examined smoking history and this malignancy in the
Health Professionals Follow-Up Study.
Subjects And Methods
The Study Population and Follow-Up of the Cohort. The
Health Professionals Follow-up Study is an ongoing prospec-
tive cohort study of the causes of cancer and heart disease in
men (17). The cohort consists of 51,529 United States male
dentists, optometrists, osteopaths, podiatrists, pharmacists, and
veterinarians who were 40 –75 years when they responded to a
mailed questionnaire in 1986. These men provided information
on age, current and past tobacco use, marital status, height and
weight, ancestry, medications, disease history, physical activ-
ity, and diet. For this analysis, we excluded men who reported
cancer at baseline (other than nonmelanoma skin cancer). Be-
cause of the importance of controlling for dietary factors (17–
19), we included only men who adequately completed a food
frequency questionnaire (97% of the total). After these baseline
exclusions, 47,781 participants formed the cohort for analysis
beginning in 1986.
Follow-up questionnaires were sent in 1988, 1990, 1992,
and 1994 to ascertain new cases of prostate cancer and to
update exposure information. Most of the deaths in the cohort
Received 7/16/98; revised 2/2/99; accepted 2/12/99.
The costs of publication of this article were defrayed in part by the payment of
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1
Supported by Research Grants CA 55075 and HL 35464 from the NIH.
2
To whom requests for reprints should be addressed, at Channing Laboratory, Harvard
Medical School, 181 Longwood Avenue, Boston, MA 02115. Phone: (617) 432-4648;
Fax: (617) 432-2435; E-mail: edward.giovannucci@channing.harvard.edu.
277 Vol. 8, 277–282, April 1999 Cancer Epidemiology, Biomarkers & Prevention
Research.
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