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Smokeless tobacco and increased risk of hypopharyngeal and
laryngeal cancers: A multicentric case-control study from India.Int
J Cancer. 2007 Jun 21;
Hypopharyngeal
and laryngeal cancers are among the most common cancers in India. In
addition to smoking, tobacco chewing may be a major risk factor for
some of these cancers in India. Using data from a multicentric
case-control study conducted in India that included 513
hypopharyngeal cancer cases, 511 laryngeal cancer cases and 718
controls, we investigated smoking and chewing tobacco products as
risk factors for these cancers. Bidi smoking was a stronger risk
factor compared to cigarette smoking for cancer of the hypopharynx (OR(bidi)
6.80 vs. OR(cig) 3.82) and supraglottis (OR(bidi) 7.53 vs. OR(cig)
2.14), while the effect of the 2 products was similar for cancer of
the glottis (OR(bidi) 5.32 vs. OR(cig) 5.74). Among never-smokers,
tobacco chewing was a risk factor for hypopharyngeal cancer, but not
for laryngeal cancer. In particular, the risk of hypopharyngeal
cancer increased with the use of Khaini (OR 2.02, CI 0.81-5.05),
Mawa (OR 3.17, CI 1.06-9.53), Pan (OR 3.34, CI 1.68-6.61), Zarda (OR
3.58, CI 1.20-10.68) and Gutkha (OR 4.59, CI 1.21-17.49). A strong
dose-response relationship was observed between chewing frequency
and the risk of hypopharyngeal cancer (p(trend) < 0.001). An effect
of alcohol on cancer of the hypopharynx and supraglottis was
observed only among daily drinkers (OR 2.22, CI 1.11-4.45 and OR
3.76, CI 1.25-11.30, respectively). In summary, this study shows
that chewing tobacco products commercially available in India are
risk factors for hypopharyngeal cancer, and that the potency of Bidi
smoking may be higher than that of cigarette smoking for
hypopharyngeal and laryngeal cancers.
Smoking and
risk of fatal prostate cancer in a prospective U.S. study.Urology.
2007 Apr;69(4):721-5.
OBJECTIVES:
To examine the association of cigarette smoking with subsequent
fatal prostate cancer. METHODS: Two private censuses were conducted
in Washington County, Maryland, in which 26,810 adult men in 1963
and 28,292 in 1975 provided smoking information. Prostate cancer
deaths through 2000 (1963 cohort, 240 deaths; and 1975 cohort, 184
deaths) were ascertained by review of the death certificates.
Poisson regression analysis was used to estimate the rate ratio of
prostate cancer death adjusted for age. RESULTS: Overall, cigarette
smokers in the 1963 census cohort were not more likely to die of
prostate cancer than those who had never smoked cigarettes, pipes,
or cigars when considering the total follow-up period. However,
current smokers of 20 or more cigarettes per day (rate ratio 2.38;
95% confidence interval 0.94 to 5.99) and former smokers (rate ratio
2.75; 95% confidence interval 1.13 to 6.74) had a greater risk of
death from prostate cancer during the first 10 years of follow-up.
Weaker positive associations of prostate cancer death with current
and former cigarette smoking were seen during the first 10 years of
follow-up in the 1975 census cohort. Current cigarette smoking at
baseline was not associated with the prostate cancer incidence.
CONCLUSIONS: The lack of an association between cigarette smoking
and prostate cancer incidence, but the tendency of greater prostate
cancer mortality in former and current cigarette smokers earlier in
the follow-up period is consistent with other studies in which
smoking was assessed once at baseline.
Alcohol
drinking in never users of tobacco, cigarette smoking in never
drinkers, and the risk of head and neck cancer: pooled analysis in
the International Head and Neck Cancer Epidemiology Consortium.J
Natl Cancer Inst. 2007 May
16;99(10):777-89.
BACKGROUND:
At least 75% of head and neck cancers are attributable to a
combination of cigarette smoking and alcohol drinking. A precise
understanding of the independent association of each of these
factors in the absence of the other with the risk of head and neck
cancer is needed to elucidate mechanisms of head and neck
carcinogenesis and to assess the efficacy of interventions aimed at
controlling either risk factor. METHODS: We examined the extent to
which head and neck cancer is associated with cigarette smoking
among never drinkers and with alcohol drinking among never users of
tobacco. We pooled individual-level data from 15 case-control
studies that included 10,244 head and neck cancer case subjects and
15,227 control subjects, of whom 1072 case subjects and 5775 control
subjects were never users of tobacco and 1598 case subjects and 4051
control subjects were never drinkers of alcohol. Odds ratios (ORs)
and 95% confidence intervals (CIs) were estimated using
unconditional logistic regression models. All statistical tests were
two-sided. RESULTS: Among never drinkers, cigarette smoking was
associated with an increased risk of head and neck cancer (OR for
ever versus never smoking = 2.13, 95% CI = 1.52 to 2.98), and there
were clear dose-response relationships for the frequency, duration,
and number of pack-years of cigarette smoking. Approximately 24%
(95% CI = 16% to 31%) of head and neck cancer cases among
nondrinkers in this study would have been prevented if these
individuals had not smoked cigarettes. Among never users of tobacco,
alcohol consumption was associated with an increased risk of head
and neck cancer only when alcohol was consumed at high frequency (OR
for three or more drinks per day versus never drinking = 2.04, 95%
CI = 1.29 to 3.21). The association with high-frequency alcohol
intake was limited to cancers of the oropharynx/hypopharynx and
larynx. CONCLUSIONS: Our results represent the most precise
estimates available of the independent association of each of the
two main risk factors of head and neck cancer, and they exemplify
the strengths of large-scale consortia in cancer epidemiology.
Differences
in Epidemiology, Histology and Survival between Cigarette Smokers
and Never-smokers who develop Non-Small Cell Lung Cancer.Chest.
2007 Jun 15;
Background
The impact smoking cigarettes has on the characteristics and
survival of patients with non-small cell lung cancer (NSCLC) is
disputed. Methods A retrospective cohort study using a prospective
database of patients with NSCLC over a six-year period. Clinical and
histological characteristics and survival rates were compared
between smokers and never-smokers. Results There were 730 patients,
562 (77%) were smokers and 168 (23%) were never-smokers. The overall
5-year survival rate was greater in never-smokers (64%) compared to
smokers (56%, p=0.031). Never smokers were more likely to be younger
(p=0.04), female (p=0.01), symptomatic at time of presentation
(p<0.001), have poorly differentiated tumors (p=0.04) and a higher
maximum standardized uptake value (maxSUV) on positron emission
tomography (PET) (p=0.026) than smokers. The stage-specific 5-year
survival rate was greater for never-smokers compared to smokers for
stage I: 62% vs. 75% (p=0.02), stage II: 46% vs. 53% (p=0.09) and
stage III: 36% vs. 41% (p=0.13), respectively. Five-year survival
was significantly less in patients who had a greater than 20
pack-year smoking history. Conclusions Never-smokers who develop
NSCLC are more likely to be young, female, and have
poorly-differentiated tumors with higher maxSUV value on PET.
Never-smokers with early stage cancer have a significantly better
survival than smokers. Patients with a 20 pack-year history or
greater have worse survival. Thus, smoking not only causes lung
cancer but once you have it, it makes the prognosis worse. A
biologic, hormonal and genetic explanation is currently lacking to
explain these findings and these data may help improve treatment and
surveillance.
Smoking
Cigarettes before First Childbirth and Risk of Breast Cancer.Am
J Epidemiol. 2007 Jul 1;166(1):55-61.
Epub 2007 Apr 9 .
Inconsistent
epidemiologic findings on cigarette smoking and female breast cancer
risk may reflect insufficient assessment of smoking onset and amount
relative to reproductive events. To determine the risk of breast
cancer associated with smoking during different periods of
reproductive life, the authors evaluated 906 incident breast cancer
cases in a nationwide cohort of 56,042 female US radiologic
technologists (1983-1998) who responded to two questionnaire
surveys. After they accounted for age, birth cohort, and established
breast cancer risk factors, smoking-related breast cancer risks
differed by smoking during three reproductive time periods (p =
0.003), with a statistically significant 3% increase per pack-year
of smoking between menarche and first childbirth (relative risk =
1.03, 95% confidence interval: 1.02, 1.05) and no significant
association for smoking after first childbirth. Risk also increased
with younger age at smoking initiation (p-trend = 0.06), after
adjustment for pack-years of smoking before and after first
childbirth, indicating an independent effect of age at smoking
initiation. The findings from this study suggest that sensitivity of
the female breast to tobacco carcinogens is increased during
adolescence and early adulthood but decreases after first
childbirth, when most breast tissue has terminally differentiated.
Stopping
smoking might reduce tumour recurrence in nonmuscle-invasive bladder
cancer.: BJU Int.
2007 Apr 5;
OBJECTIVE To
evaluate effects of stopping smoking on the outcome of nonmuscle-invasive
bladder cancer, as cigarette smoking is a risk factor for bladder
cancer and little is known about whether stopping smoking reduces
the risk of recurrence or progression. PATIENTS AND METHODS Between
January 1997 and July 2005, 297 men with primary nonmuscle-invasive
bladder cancer were treated with transurethral resection (TUR);
their smoking status before and after the diagnosis of bladder
cancer was obtained by a post hoc questionnaire and interview.
'Quitters' were those who ceased smoking within a year before and 3
months after the diagnosis. Ex-smokers were those who ceased smoking
more than a year before diagnosis. Several pathological and clinical
variables were compared, with all statistical comparisons being
two-sided. RESULTS In all, 265 patients completed the questionnaire,
including 64 non-smokers, 64 ex-smokers, 59 quitters, and 78
continued smokers. The median follow-up was 38 months. There were no
significant differences in the strata of stage, grade, tumour
multiplicity, intravesical therapy, or median follow-up duration
between the four patient groups. The respective 3-year
recurrence-free survival of continued smokers, non-smokers,
ex-smokers and quitters was 45%, 57%, 62% and 70%. By multivariate
analysis, high-grade, T1-stage, multiple tumours and continued
smoking were significant independent predictors for a shorter
recurrence-free survival. Quitters had a lower risk of recurrence
than did either continued smokers or non-smokers, but had a similar
risk to ex-smokers. CONCLUSION Stopping smoking might be associated
with a lower recurrence rate for patients with nonmuscle-invasive
bladder cancer.
COPD and
Lung Cancer in Women: Examining Sex Differences in Cigarette Smoke
Metabolism. Am J Respir
Crit Care Med. 2007 Apr 5;
Smoking-related lung diseases such as chronic obstructive pulmonary
disease (COPD)and lung cancer are growing epidemics in women in the
United States and elsewhere. Although some of this disturbing trend
in women can be attributed to changing smoking habits, there is
emerging evidence that women may be biologically more susceptible to
the harmful effects of cigarette smoke than are men. Estrogen and
related compounds may up-regulate the expression of cytochrome P450
(CYP) enzymes in lungs and liver, which are involved in the
metabolism of various constituents of cigarette smoke. Although
metabolism of foreign substances is usually beneficial in
eliminating potential toxins from the body, in some instances, the
metabolic process can transform harmless substances into toxic
chemicals through a process called metabolic bioactivation. One
important xenobiotic substrate for CYPs in cigarette smoke is
polycyclic aromatic hydrocarbon, which in its native form is
relatively harmless in small doses but upon bioactivation by CYP
enzymes, can become very toxic substances for the lungs. In this
paper, we explore CYP and other related pathways as potential
mechanisms and targets of future research and novel discoveries to
curb the growing epidemic of COPD and lung cancer in women.
Causes of
lung cancer: smoking, environmental tobacco smoke exposure,
occupational and environmental exposures and genetic predisposition.Med
Clin (Barc). 2007 Mar 17;128(10):390-6.
Every
year, in Spain 18,000 new cases of lung cancer (LC) are diagnosed.
Approximately, 80-90% LC in men and women are directly attributable
to tobacco abuse. Cigarette smoke contains over 300 chemicals, 40 of
which are known to be potent carcinogens. In the last decade, as in
Spain, prevalence of smoking in women has generally increased in the
European Union. LC risk can be substantially reduced after smoking
cessation, yet never reaches baseline. On the other hand,
environmental tobacco smoke exposure (passive smoking) in nonsmokers
appears to have a significantly increased risk of LC. An updated of
etiology factors of LC, risk related to duration as well as
intensity of smoking, relationship between environmental tobacco
smoke exposure and LC risk, genetic predisposition and a variety of
occupational and environmental exposures implicated as potential
risk factors for the development of LC will be reviewed here.
Airway
epithelial gene expression in the diagnostic evaluation of smokers
with suspect lung cancer.Nat
Med. 2007 Mar;13(3):361-6. Epub 2007
Mar 4.
Lung cancer
is the leading cause of death from cancer in the US and the world.
The high mortality rate (80-85% within 5 years) results, in part,
from a lack of effective tools to diagnose the disease at an early
stage. Given that cigarette smoke creates a field of injury
throughout the airway, we sought to determine if gene expression in
histologically normal large-airway epithelial cells obtained at
bronchoscopy from smokers with suspicion of lung cancer could be
used as a lung cancer biomarker. Using a training set (n = 77) and
gene-expression profiles from Affymetrix HG-U133A microarrays, we
identified an 80-gene biomarker that distinguishes smokers with and
without lung cancer. We tested the biomarker on an independent test
set (n = 52), with an accuracy of 83% (80% sensitive, 84% specific),
and on an additional validation set independently obtained from five
medical centers (n = 35). Our biomarker had approximately 90%
sensitivity for stage 1 cancer across all subjects. Combining
cytopathology of lower airway cells obtained at bronchoscopy with
the biomarker yielded 95% sensitivity and a 95% negative predictive
value. These findings indicate that gene expression in cytologically
normal large-airway epithelial cells can serve as a lung cancer
biomarker, potentially owing to a cancer-specific airway-wide
response to cigarette smoke.
Cigarette
smoking and the risk of colorectal cancer among men: a prospective
study in Japan.
Eur J Cancer Prev. 2007
Apr;16(2):102-7.
The
association between cigarette smoking and the risk of colorectal
cancer remains controversial. We examined this association using a
population-based prospective cohort study in Miyagi, Japan. In 1990,
we delivered a self-administered questionnaire on cigarette smoking
and other health habits to 25 279 men who were 40-64 years of age
and lived in 14 municipalities of Miyagi Prefecture. A total of 22
836 men responded (90.3% response rate). During 7 years of follow-up
(158 376 person-years), we identified 188 patients of colorectal
cancer. Relative risks and 95% confidence intervals were estimated
by the Cox proportional-hazards regression analysis with adjustment
for potential confounders. The multivariate-adjusted relative risks
(95% confidence interval) of colorectal cancer for past smokers and
current smokers compared with those who had never smoked were 1.73
(1.04-2.87) and 1.47 (0.93-2.34), respectively. Among current
smokers, both a higher number of cigarettes smoked per day and an
earlier age at which smoking had started were associated with a
significant linear increase in risk (P for trend <0.05). Our
findings are consistent with the hypothesis that cigarette smoking
is associated with a higher risk of colorectal cancer in men.
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