Cigarette smoking and risk of prostate cancer in the physicians' health study (United States)

To assess whether cigarette smoking is associated with prostate cancer incidence or mortality, we analyzed a large cohort of 22,071 men, aged 40-84 at baseline, in the Physicians' Health Study. During an average of 12.5 years of follow-up, we documented 996 cases of prostate cancer, including 113 fatal cases. Men were categorized according to smoking status, total pack-years smoked, and duration of smoking. We used Cox proportional hazard models to estimate the relative risks associated with smoking. Compared to never smokers, the age-adjusted relative risks (RR) of total prostate cancer were 1. 14 (95% confidence interval [CI] = 1.00-1.30) for past smokers, 1.10 (95% CI = 0.78-1.55) for current smokers of less than 20 cigarettes per day, and 1.10 (95% CI = 0.84-1.44) for current smokers of 20 or more cigarettes per day. Adjustment for body mass index, height, alcohol intake, and physical activity did not materially alter these findings. No significant association was observed in analyses of total pack-years smoked or duration of smoking. The results were similar for non-fatal and fatal prostate cancer. These data indicate no material association between cigarette smoking and prostate cancer incidence or mortality.     

A prospective study of smoking and risk of prostate cancer

We evaluated the hypothesis that smoking increases the incidence of and mortality from prostate cancer. High-quality smoking information was collected in 1971–1975 in a nationwide cohort of 135,006 male construction workers in Sweden. We achieved virtually complete follow-up through record linkages and ascertained as of December 1991 2,368 incident cases of prostate cancer and 709 deaths due to this disease. Rate ratios (RR) of prostate cancer incidence and mortality, with 95% confidence intervals (CI), were estimated in Poisson-based age-adjusted models, with amount and duration of smoking as independent variables. We found no convincing association between current smoking status, number of cigarettes smoked or years since onset and risk of prostatic cancer. The age-adjusted incidence RR among previous smokers was 1.09 and among current smokers 1.11 compared with non-smokers. Weak and inconsistent trends were seen with increasing number of cigarettes smoked per day and increasing duration among current smokers. Smokers of 15 or more cigarettes daily for at least 30 years experienced an incidence RR of 1.30. Mortality in ex-smokers was similar to that in never-smokers; it was, however, slightly increased among current smokers without any trend with amount smoked or duration. The weak and inconsistent associations between smoking and prostate cancer could easily have arisen due to bias or confounding. We therefore conclude that smoking is most likely not causally linked to the occurrence of prostate cancer. © 1996 Wiley-Liss, Inc.     

Cigarette smoking and risk of glioma: a prospective cohort study

The etiology of glioma, the most commonly diagnosed malignant brain tumor among adults in the United States, is poorly understood. N-nitroso compounds are known carcinogens, which are found in cigarette smoke and can induce gliomas in rats. On this basis, it has been hypothesized that cigarette smoking may be associated with an increased risk of glioma. We investigated the association between cigarette smoking and glioma risk in the National Breast Screening Study, which included 89,835 Canadian women aged 40-59 years at recruitment between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths from all causes, respectively, with follow-up ending between 1998 and 2000. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between cigarette smoking and risk of glioma. During a mean of 16.4 years of follow-up, we observed 120 incident glioma cases. Among ever smokers, women who reported having quit smoking had a 51% increase in risk of glioma compared with never smokers (HR = 1.51, 95% CI = 0.97-2.34), while current smokers did not appear to have an increase in risk. When the association with former smokers was further examined by years since quitting, women who had quit smoking >10 years before baseline were at a decreased risk of glioma compared with women who had quit within the 10 years prior to baseline (HR = 0.55, 95% CI = 0.29-1.07), indicating that the association between former smokers and glioma may be driven by women, who recently quit smoking. Compared with nonsmokers, duration of cigarette smoking, number of cigarettes smoked per day and pack-years of smoking were associated with increased glioma risk, although the increases in risk were relatively modest. The present study provides some support for a positive association between cigarette smoking and risk of glioma.     

Cigarette smoking and prostate cancer recurrence after prostatectomy

Toward the establishment of evidence-based recommendations for the prevention of prostate cancer recurrence after treatment, we examined the association between smoking and prostate cancer recurrence in a retrospective cohort study of 1416 men who underwent radical prostatectomy. Surgeries were performed by a single surgeon at Johns Hopkins Hospital between January 1, 1993, and March 31, 2006. Smoking status at 5 years before and 1 year after surgery was assessed by survey. Prostate cancer recurrence was defined as confirmed re-elevation of prostate-specific antigen levels, local recurrence, metastasis, or prostate cancer death. The cumulative incidence of recurrence was 34.3% among current smokers, 14.8% among former smokers, and 12.1% among never smokers, with a mean follow-up time of 7.3 years. Men who were current smokers at 1 year after surgery were more likely than never smokers to have disease recurrence after adjusting for pathological characteristics, including stage and grade (hazard ratio for recurrence = 2.31, 95% confidence interval = 1.05 to 5.10). This result suggests an association between cigarette smoking and risk of prostate cancer recurrence.     

Morbidity and mortality in relation to smoking among women and men of Chinese ethnicity: the Singapore Chinese Health Study

ObjectivesWe examined the association among cigarette smoking, smoking cessation and a broad range of cancer incidence and all cause and cause-specific mortality in a population-based cohort of adults of Chinese ethnicity in Singapore.MethodsSubjects were 61,320 participants of the Singapore Chinese Health Study (44.5% men, aged 45–74 years, recruitment from 1993–1998) who were free of cancer at the baseline examination. Main outcomes-of-interest included cancer incidence, all cause and cause-specific mortality as of December 31, 2005.ResultsCigarette smoking was positively associated with overall cancer incidence, including cancers at the following specific sites: head and neck region, upper gastrointestinal tract, hepatobiliary and pancreas cancer, lung, and bladder/renal pelvis cancer. Compared to never smokers, the relative risk (RR) (95% confidence interval [CI]) of cancer incidence (all cancer sites) among current smokers smoking >22 cigarettes/day was 1.9 (1.7–2.1), p-trend < 0.0001. Similarly, cigarette smoking was associated with all cause and cause-specific mortality, including deaths due to cancer, ischemic heart disease, other heart diseases, and chronic obstructive pulmonary disease. Compared to never smokers, RR (95%CI) of all cause mortality among current smokers smoking >22 cigarettes/day was 1.8 (1.6–2.0), p-trend < 0.0001. Also, relative to current smokers, ex-smokers experienced reduced cancer incidence and total mortality. The population attributable risk of smoking in men for cancer incidence as well as all-cause mortality was 23%, whereas in women it ranged from 4–5%.ConclusionsCigarette smoking is an important risk factor for cancer incidence and major causes of mortality in Chinese men and women of Singapore.     

Smoking at diagnosis and survival in cancer patients

The effect of smoking on survival in cancer patients is limited by the lack of structured prospective assessments of smoking at diagnosis. To assess the effect of smoking at diagnosis on survival, structured smoking assessments were obtained in a cohort of 5,185 cancer patients within 30 days of a cancer diagnosis between 1982 and 1998. Hazard ratios (HRs) or odds ratios were generated to analyze the effects of smoking at diagnosis on overall mortality (OM) and disease‐specific mortality (DSM) in a patient cohort from 13 disease sites containing at least 100 patients in each disease site. With a minimum of 12 years of follow‐up, current smoking increased OM risk versus recent quit (HR 1.17), former (HR 1.29) and never smokers (HR 1.38) in the overall cohort. Current smoking increased DSM risk versus former (HR 1.23) and never smokers (HR 1.18). In disease sites with proportionately large (>20%) recent quit cohorts (lung and head/neck), current smoking increased OM and DSM risks as compared with recent quit. Current smoking increased mortality risks in lung, head/neck, prostate and leukemia in men and breast, ovary, uterus and melanoma in women. Current smoking was not associated with any survival benefit in any disease site. Data using prospective structured smoking assessments demonstrate that current smoking increased long‐term OM and DSM. Standardized smoking assessment at diagnosis is an important variable for evaluating outcomes in cancer patients.     

Early age at smoking initiation and tobacco carcinogen DNA damage in the lung

BACKGROUND: DNA adducts formed as a consequence of exposure to tobacco smoke may be involved in carcinogenesis, and their presence may indicate a high risk of lung cancer. To determine whether DNA adducts can be used as a "dosimeter" for cancer risk, we measured the adduct levels in nontumorous lung tissue and blood mononuclear cells from patients with lung cancer, and we collected data from the patients on their history of smoking. METHODS: We used the 32P-postlabeling assay to measure aromatic hydrophobic DNA adducts in nontumorous lung tissue from 143 patients and in blood mononuclear cells from 54 of these patients. From the smoking histories, we identified exposure variables associated with increased DNA adduct levels by use of multivariate analyses with negative binomial regression models. RESULTS/ CONCLUSIONS: We found statistically significant interactions for variables of current and former smoking and for other smoking variables (e.g., pack-years [number of packs smoked per day x years of smoking] or years smoked), indicating that the impact of smoking variables on DNA adduct levels may be different in current and former smokers. Consequently, our analyses indicate that models for current and former smokers should be considered separately. In current smokers, recent smoking intensity (cigarettes smoked per day) was the most important variable. In former smokers, age at smoking initiation was inversely associated with DNA adduct levels. A highly statistically significant correlation (r=.77 [Spearman's correlation]; two sided P<.001) was observed between DNA adduct levels in blood mononuclear cells and lung tissue. IMPLICATIONS: Our results in former smokers suggest that smoking during adolescence may produce physiologic changes that lead to increased DNA adduct persistence or that young smokers may be markedly susceptible to DNA adduct formation and have higher adduct burdens after they quit smoking than those who started smoking later in life.     

Should we consider gallbladder cancer a new smoking-related cancer? A comprehensive meta-analysis focused on dose–response relationships

The few studies on the association of smoking with gallbladder cancer risk have given conflicting results. Here, we provide the most accurate and up-to-date quantification of the effect of cigarette smoking on gallbladder cancer risk, and investigate for the first time the dose–response relationships. Using an innovative approach for the identification of publications, we conducted a systematic review and meta-analysis of epidemiological studies published until March 2019 on the association of smoking with gallbladder cancer risk. Pooled relative risks (RRs) for smoking were estimated using random-effects models; one-stage random-effects log-linear models were used for dose–response relationships. Out of 22 eligible articles, 20 (11 case–control and 9 cohort studies) were included in the meta-analysis, for a total of 4,676 gallbladder cancer cases. Compared to never smokers, the pooled RR was 1.33 (95% confidence interval [CI]: 1.17–1.51) for current and 1.07 (95% CI: 0.94–1.23) for former smokers. The risk of gallbladder cancer increased linearly with smoking intensity and duration, the RR being 1.60 (95% CI: 1.21–2.11) for 30 cigarettes/day and 1.25 (95% CI: 1.01–1.56) for 30 years of smoking. There was a nonsignificant linear decrease in gallbladder cancer risk with increasing time since quitting, compared to current smokers. Former smokers reached the risk of those who had never smoked 20 years after quitting. This comprehensive meta-analysis suggests a moderately but significantly higher risk of gallbladder cancer for current but not former smokers. We also provide the first report of a linear increase in gallbladder cancer risk according to smoking intensity and duration.     

Active screening for lung cancer increases smoking abstinence in Australia

Background

Smoking cessation is an important screening component, but the evidence base to inform implementation is lacking. We report longitudinal smoking behavior in an Australian screening cohort and examine predictor variables associated with continued smoking.

Methods

Healthy current or former smokers (quit less than 15 years and ≥30-pack year smoking history) aged 60–74 years underwent CT screening at baseline, year 1 and year 2. Participants received brief smoking cessation advice and generic Quitline materials. Smoking status was self-reported every 6 months for 5 years. Mediators of smoking behavior, adjusted for sociodemographic, health and scan variables were explored using logistic regression modeling.

Results

Two hundred thirty-five participants were analyzed. One hundred eight (46%) were current smokers at enrolment. At baseline, current smokers’ mean Fagerström Test for Nicotine Dependence was 4.9, and they had higher levels of lung cancer-specific distress and passive smoke exposure than former smokers. At 36 months, 33% of baseline smokers achieved sustained (≥6 months) smoking abstinence. Five (4%) former smokers relapsed at any point during the study. Continued smoking was positively associated with greater nicotine dependence and smoking pack-years, and negatively associated with cardiovascular disease, stroke, and lung cancer family history.

Conclusions

This study provides the first data on smoking cessation rates in Australian lung cancer screenees and supports screening as a teachable moment. We identify several factors that identify smokers who may require more intensive smoking cessation interventions and could be used to develop effective smoking cessation as part of lung cancer screening, tailored to individual risk profiles.     

Cigarette smoking and mammographic density in the Danish Diet,Cancer and Health cohort

Purpose

Smoking before first childbirth increases breast cancer risk, but the biological mechanism remains unknown and may involve mammographic density (MD), one of the strongest biomarkers of breast cancer risk. We aimed to examine whether active smoking and passive smoking were associated with MD.

Methods

For the 5,356 women (4,489 postmenopausal) from the Danish Diet, Cancer and Health cohort (1993–1997) who attended mammographic screening in Copenhagen (1993–2001), we used MD (mixed/dense or fatty) assessed at the first screening after cohort entry. Active smoking (status, duration, and intensity) and passive smoking were assessed at cohort baseline (1993–1997) via questionnaire, together with other breast cancer risk factors. Logistic regression was used to estimate associations (odds ratios, 95 % confidence intervals) between smoking and MD, adjusting for confounders.

Results

Two thousand and twenty-six (56.5 %) women had mixed/dense MD, 2,214 (41.4 %) were current, and 1,175 (21.9 %) former smokers. Current smokers had significantly lower odds (0.86, 0.75–0.99) of having mixed/dense MD compared to never smokers, while former smoking was not associated with MD. Inverse association between smoking and MD was strongest in women who initiated smoking before age of 16 years (0.79, 0.64–0.96), smoked ≥15 cigarettes/day (0.83, 0.71–0.98), smoked ≥5 pack-years (0.62, 0.43–0.89), smoked >30 years (0.86, 0.75–0.99), and smoked ≥11 years before first childbirth (0.70, 0.51–0.96). Association between smoking and MD diminished after smoking cessation, with increased odds of having mixed/dense breasts in women who quit smoking >20 years ago as compared to current smokers (1.37, 1.01–1.67). There was no association between passive smoking and MD.

Conclusions

We found an inverse association between active smoking and MD.

     

Cigarette smoking and the risk of gastric cancer: a pooled analysis of two prospective studies in Japan

To examine the association between cigarette smoking and the risk of gastric cancer, we conducted a pooled analysis of 2 population-based prospective cohort studies in rural northern Japan. Cohort 1 included 9,980 men (>or=40 years old) and Cohort 2 included 19,412 men (40-64 years old). The subjects completed a self-administered questionnaire on cigarette smoking and other health habits. We identified 228 cases of gastric cancer among Cohort 1 subjects (9 years of follow-up with 74,073 person-years) and 223 among Cohort 2 subjects (7 years of follow-up with 141,675 person-years). From each cohort, we computed the relative risk (RR) and 95% confidence interval (CI) of gastric cancer associated with smoking using a Cox regression analysis and pooled these estimates to obtain summary measures. The pooled multivariate RRs (95% CIs) for current smokers and past smokers compared to subjects who had never smoked were 1.84 (1.39-2.43) and 1.77 (1.29-2.43), respectively. The higher number of cigarettes smoked per day among current smokers was associated with a linear increase in risk (trend p < 0.05). The significant increase in risk for past smokers remained for up to 14 years after cessation. An increased risk was noted for cancer of the antrum but not for cardia or body lesions. The risk was increased for both differentiated and nondifferentiated histologic subtypes. Our findings support the hypothesis that cigarette smoking is a risk factor for gastric cancer.     

Smoking and aggressive prostate cancer: a review of the epidemiologic evidence

Although tobacco use has been recognized as one of the leading causes of cancer morbidity and mortality, a role of smoking in the occurrence of prostate cancer has not been established. However, evidence indicates that factors that influence the incidence of prostate cancer may differ from those that influence progression and fatality from the disease. Thus, we reviewed and summarized results from prospective cohort studies that assessed the relation between smoking and fatal prostate cancer risk, as well as epidemiological and clinical studies that focused on aggressive behavior in prostate cancer, such as poorer survival, advanced stage, or poorer differentiation at diagnosis. The majority of the prospective cohort studies showed that current smoking is associated with a moderate increase of ~30% in fatal prostate cancer risk compared to never/non-smokers. This association is likely to be an underestimate of the effect of smoking because most studies had a single assessment of smoking at baseline and long follow-up times, and the association was considerably stronger in some sub-groups of heaviest smokers, or when smoking was assessed in a relatively short period (within 10 years) prior to cancer mortality. Using aggressive behavior of prostate cancer as outcome, current smoking was associated with significantly elevated risk, ranging from around twofold to threefold or higher. Although alternative explanations, such as publication bias, residual confounding, screening bias, and the influence of smoking-related comorbidities cannot be ruled out entirely, these findings suggest that smoking is associated with aggressive behavior of prostate cancers or with a sub-group of rapidly progressing prostate cancer. Based on evidence presented in this review, cigarette smoking is likely to be a risk factor for prostate cancer progression and should be considered as a relevant exposure in prostate cancer research and prevention of mortality from this cancer.     

Use of mentholated cigarettes and lung cancer risk.

Black males have higher age-adjusted lung cancer incidence rates compared to white males, and blacks of both sexes have higher rates of increase in lung cancer incidence over past decades. The majority of black smokers smoke mentholated cigarettes. These observations prompted us to assess the effect of smoking mentholated cigarettes on lung cancer risk, using data from a hospital-based case-control study of tobacco-related cancers. Analysis was restricted to current cigarette smokers and was carried out on 588 male lung cancer cases and 914 male control patients and on 456 female lung cancer cases and 410 female controls interviewed between 1985 and 1990. The prevalence of menthol usage did not differ between cases and controls of either sex. No significant association was observed between either short-term (1-14 years) or long-term (15+ years) menthol use and lung cancer in logistic regression analyses adjusting for covariates. For specific histological types of lung cancer there was no indication of an association with menthol usage.     

Cigar and pipe smoking and cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)

The carcinogenicity of cigar and pipe smoking is established but the effect of detailed smoking characteristics is less well defined. We examined the effects on cancer incidence of exclusive cigar and pipe smoking, and in combination with cigarettes, among 102,395 men from Denmark, Germany, Spain, Sweden and the United Kingdom in the EPIC cohort. Hazard ratios (HR) and their 95% confidence intervals (CI) for cancer during a median 9‐year follow‐up from ages 35 to 70 years were estimated using proportional hazards models. Compared to never smokers, HR of cancers of lung, upper aerodigestive tract and bladder combined was 2.2 (95% CI: 1.3, 3.8) for exclusive cigar smokers (16 cases), 3.0 (2.1, 4.5) for exclusive pipe smokers (33 cases) and 5.3 (4.4, 6.4) for exclusive cigarette smokers (1,069 cases). For each smoking type, effects were stronger in current smokers than in ex‐smokers and in inhalers than in non‐inhalers. Ever smokers of both cigarettes and cigars [HR 5.7 (4.4, 7.3), 120 cases] and cigarettes and pipes [5.1 (4.1, 6.4), 247 cases] had as high a raised risk as had exclusive cigarette smokers. In these smokers, the magnitude of the raised risk was smaller if they had switched to cigars or pipes only (i.e., quit cigarettes) and had not compensated with greater smoking intensity. Cigar and pipe smoking is not a safe alternative to cigarette smoking. The lower cancer risk of cigar and pipe smokers as compared to cigarette smokers is explained by lesser degree of inhalation and lower smoking intensity.     

Lung cancer and cigarette smoking in women: a multicenter case-control study in Europe

The association between cigarette smoking and lung cancer risk in women was investigated within the framework of a case-control study in 9 centres from 6 European countries. Cases were 1,556 women up to 75 years of age with histologically confirmed primary lung cancer; 2, 450 controls with age distribution similar to cases were selected. The predominant cell type was adenocarcinoma (33.5%), with similar proportions for squamous-cell type (26.4%) and small-cell carcinoma (22.3%). Overall, smoking cigarettes at any time was associated with a 5-fold increase in lung cancer risk (odds ratio 5.21, 95% confidence interval 4.49-6.04); corresponding figures for current smoking habits were 8.94, 7.54-10.6. The association showed a dose-response relationship with duration of the habit and daily and cumulative lifetime smoking. A significant excess risk of 70% was associated with every 10 pack-years smoked. After 10 years of smoking cessation, the relative risk decreased to 20% compared to current smokers. The following characteristics were associated with a higher relative risk: inhalation of smoke, smoking non-filter cigarettes, smoking dark-type cigarettes and starting at young age. The association was observed for all major histological types, being the strongest for small-cell type carcinoma, followed by squamous-cell type and the lowest for adenocarcinoma. The proportion of lung-cancer cases in the population attributable to cigarette smoking ranged from 14% to 85%. We concluded that women share most features of the association between cigarette smoking and lung cancer observed in men.     

Tobacco smoking,alcohol consumption and pancreatic cancer risk: A case-control study in Italy

In Italy, pancreatic cancer accounts for approximately 5% of cancer-related deaths. Tobacco smoking is the major established risk factor for this cancer, whereas the role of alcohol consumption is open to debate.Between 1991 and 2008, we conducted a hospital-based case-control study on pancreatic cancer in northern Italy. Cases were 326 patients (median age 63 years) with incident pancreatic cancer admitted to major general hospitals. Controls were 652 patients (median age 63 years) with acute non-neoplastic conditions admitted to the same hospital network of cases. Multiple logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI).Pancreatic cancer was associated to current smoking (OR = 1.68; 95% CI: 1.13–2.48), and the risk rose with increasing number of cigarettes/day (OR = 2.04; 95% CI: 1.14–3.66 for ?20 cigarettes/day). No association emerged for former smokers (OR = 0.98; 95% CI: 0.66–1.45). Alcohol consumption was associated to increased pancreatic cancer risk, but ORs were significant only among heavy drinkers (ORs: 2.03 and 3.42 for 21–34 and ?35 drinks/week, respectively). Pancreatic cancer risk was 4.3-fold higher in heavy smokers (?20 cigarettes/day) and heavy drinkers (?21 drinks/week) in comparison with never smokers who drunk <7 drinks/week, which is compatible with an additive effect of these exposures.In conclusion, we found that tobacco smoking and alcohol drinking are two independent risk factors for pancreatic cancer which may be responsible for approximately one third of these cancers in our population.     

Cigarette smoking and the risk of colorectal cancer among men: a prospective study in Japan.

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.     

Association between long‐term low‐intensity cigarette smoking and incidence of smoking‐related cancer in the national institutes of health‐AARP cohort

An increasing proportion of US smokers smoke ≤10 cigarettes per day (CPD) or do not smoke every day, yet the health effects of low‐intensity smoking are poorly understood. We identified lifelong smokers of <1 or 1‐10 CPD and evaluated risk of incident cancer among 238,525 cancer‐free adults, aged 59‐82, in the NIH‐AARP Diet and Health Study. A questionnaire administered in 2004‐2005 assessed CPD during nine age‐periods (<15 to ≥70). We estimated hazard ratios (HR) and 95% confidence intervals (CI) using multivariable‐adjusted Cox proportional hazards regression with age as the underlying time metric. Of the 18,233 current smokers, (7.6%), 137 and 1,243 reported consistently smoking <1 CPD and 1‐10 CPD, respectively. Relative to never smokers, current smokers who reported consistently smoking 1‐10 CPD over their lifetime were 2.34 (95% CI = 1.86‐2.93) times more likely to develop smoking‐related cancer. Current lifetime smokers of <1 CPD were 1.89 (95% CI = 0.90‐3.96) times more likely to develop tobacco‐related cancer, although the association did not reach statistical significance. Associations were observed for lifelong smoking of ≤10 CPD with lung cancer (HR = 9.65, 95% CI = 6.93‐13.43); bladder cancer (HR = 2.22, 95% CI = 1.22‐4.05); and pancreatic cancer (HR = 2.03, 95%CI: 1.05‐3.95). Among lifelong ≤10 CPD smokers, former smokers had lower risks of smoking‐related cancer with longer time since cessation and longer smoking duration. Lifelong <1 and 1‐10 CPD smokers are at increased risk of incident cancer relative to never smokers and would benefit from cessation, providing further evidence that even low‐levels of cigarette smoking cause cancer.     

Smoking and survival after breast cancer diagnosis: a prospective observational study and systematic review

The association of smoking with outcomes following breast cancer prognosis is not well understood. In a cohort study called Life After Cancer Epidemiology (LACE), 2,265 women diagnosed with breast cancer were followed for a median of 12?years. We used multivariable proportional-hazards models to determine whether smoking, assessed approximately two years post-diagnosis, was associated with risk of death among these women. We also undertook a systematic review of all cohort studies to date that have examined the association between smoking and breast cancer mortality. Compared with never smokers, women who were current smokers had a twofold higher rate of dying from breast cancer [hazard ratio (HR)?=?2.01, 95?% confidence interval (CI) 1.27?C3.18] and an approximately fourfold higher rate of dying from competing (non-breast cancer) causes (HR?=?3.84, 95?% CI 2.50?C5.89). Among seven studies that met the inclusion criteria in the systematic review, three studies and our own reported significantly increased risk of breast cancer death with current smoking. We found little evidence of an association between former smoking and breast cancer mortality (HR?=?1.24, 95?% CI 0.94?C1.64). Consistent with findings from our prospective observational study, the systematic review of seven additional studies indicates positive association of current smoking with breast cancer mortality, but weak association with former smoking. Women who smoke following breast cancer diagnosis and treatment are at higher risk of death both from breast cancer and other causes.     

Cigarette smoking and colorectal cancer incidence and mortality: Systematic review and meta‐analysis

The association between cigarette smoking and colorectal cancer (CRC) has been controversial. To synthesize the available data, we conducted a comprehensive meta‐analysis of all prospective studies. A total of 36 studies were included in our meta‐analysis. We examined the association between smoking and CRC, colon cancer and rectal cancer in terms of incidence and mortality. Separate analyses were conducted for smoking status, daily cigarette consumption, duration, pack‐years and age of initiation. Relative to nonsmokers, current and former smokers had a significantly increased risk of CRC incidence and mortality, respectively. When CRC data were combined with colon/rectal cancer data, current smokers had a significantly increased risk of CRC incidence. All 4 dose–response variables examined—daily cigarette consumption (RR = 1.38 for an increase of 40 cigarettes/day), duration (RR = 1.20 for an increase of 40 years of duration), pack‐years (RR = 1.51 for an increase of 60 pack‐years) and age of initiation (RR = 0.96 for a delay of 10 years in smoking initiation)—were significantly associated with CRC incidence (all p‐values < 0.0001). The relationship between duration of smoking and rectal cancer incidence was also significant. Among the subset of studies that distinguished cancer by site, a higher risk was seen for rectal cancer than for colon cancer for all analyses. Among prospective studies, a consistent association exists between smoking and CRC. The association is stronger for rectal cancer than for colon cancer in the subset of studies that differentiated cancer by site. © 2008 Wiley‐Liss, Inc.