Smoking cessation and the risk of oesophageal cancer: An overview of published studies

doi:10.1016/j.oraloncology.2006.03.007

Oral Oncology

Volume 42, Issue 10, November 2006, Pages 957-964

https://doi.org/10.1016/j.oraloncology.2006.03.007 Get rights and content

Summary

The epidemiologic studies on oesophageal cancer and smoking cessation published before December 2005 were reviewed here. The results from at least 10 cohort and 10 case–control studies indicated that former smokers had a lower risk of squamous-cell or unspecified oesophageal cancer than current smokers. Most investigations showed that the risk of oesophageal cancer remains elevated many years (at least 10) after cessation of smoking, to decline by about 40% only thereafter. Moreover, after 10 years since cessation of smoking, ex-smokers still have a twofold increased risk as compared to never smokers. A few studies investigated the effect of smoking cessation on adenocarcinoma, and did not report a clear reduction of risk. Data on oesophageal adenocarcinoma are however too limited to provide adequate inference on the relation with time since smoking cessation. In conclusion, cessation of smoking could have an appreciable impact in reducing (squamous-cell) oesophageal cancer, and represents an obvious priority for prevention and public-health purposes.

Introduction

The risk of oesophageal cancer is strongly related to tobacco and alcohol consumption, with relative risks (RR) over 100 in heavy smokers and heavy drinkers.1, 2 For both tobacco and alcohol there are strong dose–risk relations, and for tobacco there is also a strong duration–risk relation. It is known that oesophageal cancer risk is reduced in ex-smokers as compared to current smokers, but the function of risk after smoking cessation is still open to discussion.

We reviewed here cohort and case–control studies published before December 2005 on oesophageal cancer and smoking cessation. These were identified through Medline and by searching the references of the retrieved studies.

Section snippets

Cohort studies

About 10 cohort studies (including a nested case–control one) reported data on oesophageal cancer in relation to smoking cessation (Table 1). All studies – with the exception of the nested case–control – gave the RR for former smokers overall, since they collected information only at the enrollment of the study subjects.

A cohort of 25,000 Swedish men³ reported a RR of 1.3 in former smokers, as compared to never smokers (death rate 4.3/100,000 person years). In current smokers the RR was 1.1 for

Squamous-cell or not specified oesophageal carcinoma

At least 10 case–control studies reported information on squamous-cell or not specified oesophageal cancer risk after smoking cessation, and analyzed the time pattern of the change in risk after stopping smoking (Table 2).

In a case–control study from coastal South Carolina,¹² including 207 men with oesophageal cancer, as compared to never smokers, those who had stopped smoking for less than 10 years had an odds ratio (OR) similar to that of current smokers (around 2), while the OR in those who

Discussion

Epidemiological studies on smoking cessation and squamous-cell oesophageal cancer indicate that former smokers had a lower risk of oesophageal cancer than current smokers. The risk of oesophageal cancer remains elevated several years (at least 10) after cessation of smoking, to decline by about 40% thereafter. Further, after 10 years since cessation of smoking, ex-smokers still have a twofold increased risk as compared to never smokers.

Alcohol is the other major risk factor for oesophageal

Acknowledgments

This work was conducted with the contribution of the Italian Association for Cancer Research, Milan, and the Italian League against Cancer. The authors thank Mrs. MP Bonifacino for editorial assistance.

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However, reformed smokers have higher risks than non-smokers, though they also have substantially lower risks than those who continue to smoke, the difference in risk being greater the earlier they stopped smoking. The favourable effects of stopping smoking are evident within just a few years after cessation.1,9–12 Bosetti et al11 in their epidemiological study stated that the men who stopped smoking at around 40 years of age avoided about 80% of the possible excess risk of developing cancer over the men who continued to smoke.
Smoking tobacco is the main risk factor for head and neck cancer, is proportional to the number of pack years (number of packs smoked/day x number of years of smoking), and is reduced when the patient stops smoking. Current molecular evidence has suggested that tobacco-related cancers could be clinically more aggressive than cancers in non-smokers, particularly in the head and neck. However, clinical studies have not uniformly reproduced the relation between survival and tobacco, possibly because they ignore the health benefit that reformed smokers obtain during the period between giving up smoking and the diagnosis of cancer, which is not shared by those who continue to smoke and develop cancer. We have investigated the survival of reformed smokers, non-smokers, and continuing smokers after a diagnosis of head and neck cancer. The data of patients with head and neck cancer from 1992 -2013 from the Cancer Genome Atlas database were analysed using a multivariate Cox's regression model for survival, and Kaplan-Meier curves were produced for smoking history. A total of 521 patients were treated for head and neck cancer, and there was a significant difference in survival between reformed and non-smokers on the one hand, and current smokers on the other (p = 0.02). The significance increased when reformed smokers were grouped according to their duration of abstinence and time of diagnosis of cancer (>15 and ≤15 years, p < 0.01). Smoking history was a significant prognostic factor in the multivariate Cox's regression model when analysed with age, stage, grade, and site. We conclude that reformed smokers have a survival benefit in head and neck cancer.
Alcohol drinking and laryngeal cancer: Overall and dose-risk relation - A systematic review and meta-analysis
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Alcohol drinking is a known risk factor for laryngeal cancer. However, little information is available on the risk associated with light alcohol drinking. To address this issue, we conducted a meta-analysis using two methods: (i) random-effects models with reconstruction of alcohol consumption categories and calculation of risk estimates associated with predefined consumption levels using Hamling method and (ii) random-effects meta-regression models. The PubMed database was searched for all case–control or cohort studies published in the English language on the association between alcohol consumption and risk of laryngeal cancer. Forty studies (38 case–control, 2 cohort) reporting on at least three levels of consumption were included. Overall, alcohol drinking versus non-drinking was associated with an approximately 2-fold increase in risk of laryngeal cancer (RR = 1.90; 95% CI: 1.59–2.28). While light alcohol drinking (⩽1 drink/day) did not show any significant association with risk of laryngeal cancer (12 studies. RR = 0.88; 95% CI: 0.71–1.08), moderate drinking (>1 to <4 drinks/day) was associated with a 1.5-fold increase in risk (35 studies. RR = 1.47; 95% CI: 1.25–1.72) and heavy drinking (⩾4 drinks/day) was associated with a 2.5-fold increased risk (33 studies. RR = 2.62; 95% CI: 2.13–3.23). Subgroup analyses for studies that adjusted for main potential confounding factors (age, sex, and tobacco use) and several further subgroup analyses showed similar results, which suggest the robustness of the results.
Effects of lifestyle on micronuclei frequency in human lymphocytes in Japanese hard-metal workers
2009, Preventive Medicine
Citation Excerpt :
Our data showed no significant difference in baseline MN frequency among current smokers, ex-smokers and non-smokers (data not shown). Smoking cessation could decrease the cancer risk to some extent, but even after 10 years since cessation, ex-smokers still have a two fold increased cancer risk as compared to never smokers (Bosetti et al., 2006; Weijenberg et al., 2008). Therefore, we combined current smokers (n = 112) and ex-smokers (n = 21) and compared them with non-smokers, some suggestive but non-statistically increases in MN frequency were observed in smokers (Table 1).
The risks of cardiovascular disease, cancer, and other major causes of mortality are largely attributable to lifestyle factors such as smoking, alcohol drinking, hours of working and sleeping, physical activity, diet, and stress. Earlier studies have suggested that an unhealthy lifestyle is also associated with increased lymphocyte sensitivity to mutagens, oxidative DNA damage level, and leukocyte DNA damage. In order to explore the genotoxicity of unhealthy lifestyle, we evaluated the effect of overall lifestyle as well as some individual lifestyle factors on micronuclei (MN) frequency in cultured human lymphocytes.
The study was conducted among 208 healthy adult (19 to 59 years) male Japanese hard-metal workers. The subjects were divided into groups according to their self-reported good, moderate, and poor lifestyles based on their responses to a questionnaire regarding eight health practices (cigarette smoking, alcohol consumption, sleeping hours, working hours, physical exercise, eating breakfast, balanced nutrition, and mental stress), the presence or absence of each of which was summed to obtain a health practice index (HPI: range 0–8). Peripheral blood was taken and the cytokinesis-block micronuclei (CBMN) assay was performed.
Total lifestyle quality as measured by the HPI was strongly negatively associated with MN frequency in cultured human lymphocytes (p < 0.01). Nutritional imbalance, lack of regular exercise (< 2 times per week), insufficient sleep ( ≤ 6 h per day), and overtime working (≥ 9 h per day) each contributed significantly to higher MN frequency (all p < 0.05). In the smoker group, a significantly higher MN frequency was only found in heavy smokers (p < 0.05). On the other hand, mental stress, eating breakfast, and alcohol drinking had no effect on MN frequency.
Taken together, these findings indicate that poor lifestyle habits significantly increase MN frequency in human lymphocytes.
Oral cancer knowledge, attitudes and practices: A survey of dentists and primary care physicians in Massachusetts
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The authors conducted a study to assess dentists' and primary care physicians' oral cancer knowledge, attitudes and practices in the Commonwealth of Massachusetts.
The authors mailed a 38-item, pretested questionnaire to a stratified sample of dentists and primary care physicians in Massachusetts. The sample population included all general medicine, internal medicine and family practice physicians listed with the Massachusetts Board of Registration in Medicine and all Massachusetts Dental Society members. The authors invited a random sample of more than 1,000 clinicians to participate in the survey. They assessed knowledge, attitudes and practices of respondents and performed a bivariate analysis of responses to questions by using statistical software.
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This survey identified an existing gap in knowledge and practices among physicians and dentists and underscores the need to enhance oral cancer education among both professional groups.
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Genetic factors are also involved; a pooled analysis16 of three genome-wide association studies found new susceptibility loci for oesophageal squamous cell carcinoma. Tobacco smoking cessation is probably the single most effective primary preventive measure.17 The main pathophysiological pathway of oesophageal adenocarcinoma is likely to be chronic gastro-oesophageal reflux disease (reflux), causing metaplasia from the native squamous cell mucosa to a specialised columnar epithelium, known as Barrett's oesophagus.18
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REVIEWSmoking cessation and the risk of oesophageal cancer: An overview of published studies

Summary

Introduction

Section snippets

Cohort studies

Squamous-cell or not specified oesophageal carcinoma

Discussion

Acknowledgments

Les cancers de l’oesophage en Ille-et-Villaine en fonction des niveaux de consommation d’alcool et de tabac. Des risques qui se multiplient

Bull Cancer (Paris)

Smoking and drinking in relation to cancers of the oral cavity, pharynx, larynx, and esophagus in Northern Italy

Cancer Res

Mortality in relation to cigarette and pipe smoking: 16 years’ observation of 25 000 Swedish men

J Epidemiol Commun Health

Analysis of cancer risk related to longitudinal information on smoking habits

Environ Health Perspect

A nested case–control study of oesophageal and stomach cancers in the Linxian nutrition intervention trial

Int J Epidemiol

Smoking and cancer mortality among U.S. veterans: a 26-year follow-up

Int J Cancer

Cancer incidence in female smokers: a 26-year follow-up

Int J Cancer

Risk factors for malignant diseases: a cohort study on a population of 22,946 Icelanders

Cancer Epidemiol Biomarkers Prev

Mortality risks of oesophageal cancer associated with hot tea, alcohol, tobacco and diet in Japan

J Epidemiol

Smoking and cancer risk in Korean men and women

Cancer Causes Control

Mortality from cancer in relation to smoking: 50 years observations on British doctors

Br J Cancer

Environmental factors and high risk of esophageal cancer among men in coastal South Carolina

J Natl Cancer Inst

Tobacco, alcohol, diet, occupation, and carcinoma of the esophagus

Cancer Res

Type of cigarettes and cancers of the upper digestive and respiratory tract

Cancer Causes Control

REVIEW
Smoking cessation and the risk of oesophageal cancer: An overview of published studies