Search

Introduction: Published findings on the associations between smoking and the incidence of cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC) are inconsistent. We aimed to generate prospective evidence on these relationships overall and by anatomical site., Methods: We followed 1,223,626 women without prior cancer by electronic linkage to national cancer registration data. Questionnaire information about smoking and other factors was recorded at recruitment (1996-2001) and every 3-5 years subsequently. Cox regression yielded adjusted relative risks (RRs) comparing smokers versus never-smokers., Results: After 14 (SD4) years follow-up per woman, 6699 had a first registered cutaneous SCC and 48,666 a first BCC. In current versus never-smokers, SCC incidence was increased (RR = 1.22, 95% CI 1.15-1.31) but BCC incidence was decreased (RR = 0.80, 0.78-0.82). RRs varied substantially by anatomical site; for the limbs, current smoking was associated with an increased incidence of SCC (1.55, 1.41-1.71) and a decreased incidence of BCC (0.72, 0.66-0.79), but for facial lesions there was little association of current smoking with either SCC (0.93, 0.82-1.06) or BCC (0.92, 0.88-0.96). Findings in meta-analyses of results from this and seven other prospective studies were largely dominated by the findings in this study., Conclusions: Smoking-associated risks for cutaneous SCC and BCC are in the opposite direction to each other and appear to vary by anatomical site.

Background: The smoking epidemic in Australia is characterised by historic levels of prolonged smoking, heavy smoking, very high levels of long-term cessation, and low current smoking prevalence, with 13% of adults reporting that they smoked daily in 2013. Large-scale quantitative evidence on the relationship of tobacco smoking to mortality in Australia is not available despite the potential to provide independent international evidence about the contemporary risks of smoking., Methods: This is a prospective study of 204,953 individuals aged ≥45 years sampled from the general population of New South Wales, Australia, who joined the 45 and Up Study from 2006-2009, with linked questionnaire, hospitalisation, and mortality data to mid-2012 and with no history of cancer (other than melanoma and non-melanoma skin cancer), heart disease, stroke, or thrombosis. Hazard ratios (described here as relative risks, RRs) for all-cause mortality among current and past smokers compared to never-smokers were estimated, adjusting for age, education, income, region of residence, alcohol, and body mass index., Results: Overall, 5,593 deaths accrued during follow-up (874,120 person-years; mean: 4.26 years); 7.7% of participants were current smokers and 34.1% past smokers at baseline. Compared to never-smokers, the adjusted RR (95% CI) of mortality was 2.96 (2.69-3.25) in current smokers and was similar in men (2.82 (2.49-3.19)) and women (3.08 (2.63-3.60)) and according to birth cohort. Mortality RRs increased with increasing smoking intensity, with around two- and four-fold increases in mortality in current smokers of ≤14 (mean 10/day) and ≥25 cigarettes/day, respectively, compared to never-smokers. Among past smokers, mortality diminished gradually with increasing time since cessation and did not differ significantly from never-smokers in those quitting prior to age 45. Current smokers are estimated to die an average of 10 years earlier than non-smokers., Conclusions: In Australia, up to two-thirds of deaths in current smokers can be attributed to smoking. Cessation reduces mortality compared with continuing to smoke, with cessation earlier in life resulting in greater reductions.

Background: Evidence about the effect of smoking on venous thromboembolism risk, generally and in the postoperative period, is limited and inconsistent. We examined the incidence of venous thromboembolism in relation to smoking habits, both in the absence of surgery and in the first 12 postoperative weeks, in a large prospective study of women in the United Kingdom., Methods and Results: During 6 years' follow-up of 1 162 718 women (mean age 56 years), 4630 were admitted to hospital for or died of venous thromboembolism. In the absence of surgery, current smokers had a significantly increased incidence of venous thromboembolism compared with never-smokers (adjusted relative risk 1.38, 95% confidence interval 1.28-1.48), with significantly greater risks in heavier than lighter smokers (relative risks 1.47 [95% confidence interval 1.34-1.62] and 1.29 [95% confidence interval 1.17-1.42] for ≥15 versus <15 cigarettes per day). Current smokers were also more likely to have surgery than never-smokers (relative risk 1.12, 95% confidence interval 1.12-1.13). Among women who had surgery, the incidence of venous thromboembolism in the first 12 postoperative weeks was significantly greater in current than never-smokers (relative risk 1.16, 95% confidence interval 1.02-1.30)., Conclusions: Venous thromboembolism incidence was increased in current smokers, both in the absence of surgery and in the 12 weeks after surgery. Smoking is another factor to consider in the assessment of venous thromboembolism risk in patients undergoing surgery.

Background: Women born around 1940 in countries such as the UK and USA were the first generation in which many smoked substantial numbers of cigarettes throughout adult life. Hence, only in the 21st century can we observe directly the full effects of prolonged smoking, and of prolonged cessation, on mortality among women in the UK., Methods: For this prospective study, 1·3 million UK women were recruited in 1996-2001 and resurveyed postally about 3 and 8 years later. All were followed to Jan 1, 2011, through national mortality records (mean 12 woman-years, SD 2). Participants were asked at entry whether they were current or ex-smokers, and how many cigarettes they currently smoked. Those who were ex-smokers at both entry and the 3-year resurvey and had stopped before the age of 55 years were categorised by the age they had stopped smoking. We used Cox regression models to obtain adjusted relative risks that compared categories of smokers or ex-smokers with otherwise similar never-smokers., Findings: After excluding 0·1 million women with previous disease, 1·2 million women remained, with median birth year 1943 (IQR 1938-46) and age 55 years (IQR 52-60). Overall, 6% (66,489/1,180,652) died, at mean age 65 years (SD 6). At baseline, 20% (232,461) were current smokers, 28% (328,417) were ex-smokers, and 52% (619,774) were never-smokers. For 12-year mortality, those smoking at baseline had a mortality rate ratio of 2·76 (95% CI 2·71-2·81) compared with never-smokers, even though 44% (37,240/85,256) of the baseline smokers who responded to the 8-year resurvey had by then stopped smoking. Mortality was tripled, largely irrespective of age, in those still smoking at the 3-year resurvey (rate ratio 2·97, 2·88-3·07). Even for women smoking fewer than ten cigarettes per day at baseline, 12-year mortality was doubled (rate ratio 1·98, 1·91-2·04). Of the 30 most common causes of death, 23 were increased significantly in smokers; for lung cancer, the rate ratio was 21·4 (19·7-23·2). The excess mortality among smokers (in comparison with never-smokers) was mainly from diseases that, like lung cancer, can be caused by smoking. Among ex-smokers who had stopped permanently at ages 25-34 years or at ages 35-44 years, the respective relative risks were 1·05 (95% CI 1·00-1·11) and 1·20 (1·14-1·26) for all-cause mortality and 1·84 (1·45-2·34) and 3·34 (2·76-4·03) for lung cancer mortality. Thus, although some excess mortality remains among these long-term ex-smokers, it is only 3% and 10% of the excess mortality among continuing smokers. If combined with 2010 UK national death rates, tripled mortality rates among smokers indicate 53% of smokers and 22% of never-smokers dying before age 80 years, and an 11-year lifespan difference., Interpretation: Among UK women, two-thirds of all deaths of smokers in their 50s, 60s, and 70s are caused by smoking; smokers lose at least 10 years of lifespan. Although the hazards of smoking until age 40 years and then stopping are substantial, the hazards of continuing are ten times greater. Stopping before age 40 years (and preferably well before age 40 years) avoids more than 90% of the excess mortality caused by continuing smoking; stopping before age 30 years avoids more than 97% of it., Funding: Cancer Research UK, Medical Research Council., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Background: Smoking has been linked to mucinous ovarian cancer, but its effects on other ovarian cancer subtypes and on overall ovarian cancer risk are unclear, and the findings from most studies with relevant data are unpublished. To assess these associations, we review the published and unpublished evidence., Methods: Eligible epidemiological studies were identified by electronic searches, review articles, and discussions with colleagues. Individual participant data for 28,114 women with and 94,942 without ovarian cancer from 51 epidemiological studies were analysed centrally, yielding adjusted relative risks (RRs) of ovarian cancer in smokers compared with never smokers., Findings: After exclusion of studies with hospital controls, in which smoking could have affected recruitment, overall ovarian cancer incidence was only slightly increased in current smokers compared with women who had never smoked (RR 1·06, 95% CI 1·01-1·11, p=0·01). Of 17,641 epithelial cancers with specified histology, 2314 (13%) were mucinous, 2360 (13%) endometrioid, 969 (5%) clear-cell, and 9086 (52%) serous. Smoking-related risks varied substantially across these subtypes (p(heterogeneity)<0·0001). For mucinous cancers, incidence was increased in current versus never smokers (1·79, 95% CI 1·60-2·00, p<0·0001), but the increase was mainly in borderline malignant rather than in fully malignant tumours (2·25, 95% CI 1·91-2·65 vs 1·49, 1·28-1·73; p(heterogeneity)=0·01; almost half the mucinous tumours were only borderline malignant). Both endometrioid (0·81, 95% CI 0·72-0·92, p=0·001) and clear-cell ovarian cancer risks (0·80, 95% CI 0·65-0·97, p=0·03) were reduced in current smokers, and there was no significant association for serous ovarian cancers (0·99, 95% CI 0·93-1·06, p=0·8). These associations did not vary significantly by 13 sociodemographic and personal characteristics of women including their body-mass index, parity, and use of alcohol, oral contraceptives, and menopausal hormone therapy., Interpretation: The excess of mucinous ovarian cancers in smokers, which is mainly of tumours of borderline malignancy, is roughly counterbalanced by the deficit of endometrioid and clear-cell ovarian cancers. The substantial variation in smoking-related risks by tumour subtype is important for understanding ovarian carcinogenesis., Funding: Cancer Research UK and MRC., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Background: Previous research suggests associations of lower alcohol intake and higher tobacco consumption with increased risks of haematological malignancy. The prospective Million Women Study provides sufficient power for reliable estimates of subtype-specific associations in women., Methods: Approximately 1.3 million middle-aged women were recruited in the United Kingdom during 1996-2001 and followed for death, emigration and cancer registration until 2009 (mean 10.3 years per woman); potential risk factors were assessed by questionnaire. Adjusted relative risks were estimated by Cox regression., Results: During follow-up, 9162 incident cases of haematological malignancy were recorded, including 7047 lymphoid and 2072 myeloid cancers. Among predominantly moderate alcohol drinkers, higher intake was associated with lower risk of lymphoid malignancies, in particular diffuse large B-cell lymphoma (relative risk 0.85 per 10 g alcohol per day (95% confidence interval 0.75-0.96)), follicular lymphoma (0.86 (0.76-0.98)) and plasma cell neoplasms (0.86 (0.77-0.96)). Among never- and current smokers, higher cigarette consumption was associated with increased risk of Hodgkin lymphoma (1.45 per 10 cigarettes per day (1.22-1.72)), mature T-cell malignancies (1.38 (1.10-1.73)) and myeloproliferative/myelodysplastic disease (1.42 (1.31-1.55))., Conclusion: These findings confirm and extend existing evidence for associations of subtypes of haematological malignancy with two common exposures in women.

Background: Motor neuron disease (MND) is a severe neurodegenerative disease with largely unknown etiology. Most epidemiological studies are hampered by small sample sizes and/or the retrospective collection of information on behavioural and lifestyle factors., Methods: 1.3 million women from the UK Million Women Study, aged 56 years on average at recruitment, were followed up for incident and/or fatal MND using NHS hospital admission and mortality data. Adjusted relative risks were calculated using Cox regression models., Findings: During follow-up for an average of 9·2 years, 752 women had a new diagnosis of MND. Age-specific rates increased with age, from 1·9 (95% CI 1·3 - 2·7) to 12·5 (95% CI 10·2 - 15·3) per 100,000 women aged 50-54 to 70-74, respectively, giving a cumulative risk of diagnosis with the disease of 1·74 per 1000 women between the ages of 50 and 75 years. There was no significant variation in risk of MND with region of residence, socio-economic status, education, height, alcohol use, parity, use of oral contraceptives or hormone replacement therapy. Ever-smokers had about a 20% greater risk than never smokers (RR 1·19 95% CI 1·02 to 1·38, p = 0·03). There was a statistically significant reduction in risk of MND with increasing body mass index (p(for trend) = 0·009): obese women (body mass index, 30 kg/m(2) or more) had a 20% lower risk than women of normal body mass index (20 to <25 Kg/m(2))(RR 0·78 95% CI 0·65-0·94; p = 0·03). This effect persisted after exclusion of the first three years of follow-up., Interpretation: MND incidence in UK women rises rapidly with age, and an estimated 1 in 575 women are likely to be affected between the ages of 50 and 75 years. Smoking slightly increases the risk of MND, and adiposity in middle age is associated with a lower risk of the disease.

Background: The relationship between cigarette smoking and incidence of acoustic neuromas and pituitary tumours is uncertain., Methods: We examined the relation between smoking and risk of acoustic neuromas and pituitary tumours in a prospective study of 1.2 million middle-aged women in the United Kingdom., Results: Over 10.2 million person years of follow-up, 177 women were diagnosed with acoustic neuromas and 174 with pituitary tumours. Current smokers at recruitment were at significantly reduced risk of incident acoustic neuroma compared with never smokers (adjusted relative risk (RR)=0.41, 95% confidence interval (CI)=0.24-0.70, P=0.001). Past smokers did not have significantly different risk of acoustic neuroma than never smokers (RR=0.87, 95% CI=0.62-1.22, P=0.4). Smoking was not associated with incidence of pituitary tumours (RR in current vs never smokers=0.91, 95% CI=0.60-1.40, P=0.7)., Conclusion: Women who smoke are at a significantly reduced risk of acoustic neuromas, but not of pituitary tumours, compared with never smokers. Acoustic neuromas are much rarer than the cancers that are increased among smokers.

The separate and joint effects of alcohol and smoking on incidences of liver cirrhosis and gallbladder disease were examined in a prospective study of 1,290,413 United Kingdom women (mean age, 56 years) recruited during 1996-2001. After a mean follow-up of 6.1 years (1996-2005), incidence rates of cirrhosis and gallbladder disease were 1.3 per 1,000 persons (n = 2,105) and 15 per 1,000 persons (n = 23,989), respectively, over 5 years. Cirrhosis risk increased with increasing alcohol consumption, while the risk of gallbladder disease decreased (P(trend) < 0.0001 for each). Comparing women who drank > or =15 units/week with those who drank 1-2 units/week, the relative risk was 4.32 (95% confidence interval (CI): 3.71, 5.03)) for cirrhosis and 0.59 (95% CI: 0.55, 0.64) for gallbladder disease. Increasing numbers of cigarettes smoked daily increased the risk of both conditions (P(trend) < 0.0001 for each). Comparing current smokers of > or =20 cigarettes/day with never smokers, the relative risk was 3.76 (95% CI: 3.25, 4.34) for cirrhosis and 1.29 (95% CI: 1.22, 1.37) for gallbladder disease. Effects of alcohol and smoking were more than multiplicative for cirrhosis (P(interaction) = 0.02) but not for gallbladder disease (P(interaction) = 0.4). Findings indicate that alcohol and smoking affect the risks of the 2 conditions in different ways. For cirrhosis, alcohol and smoking separately increase risk, and their joint effects are particularly hazardous. For gallbladder disease, alcohol reduces risk and smoking results in a small risk increase.

Active smoking has little or no effect on breast cancer risk but some investigators have suggested that passive smoking and its interaction with active smoking may be associated with an increased risk. In a population based case-control study of breast cancer in women aged 36-45 years at diagnosis, information on active smoking, passive smoking in the home, and other factors, was collected at interview from 639 cases and 640 controls. Women were categorised jointly by their active and passive smoking exposure. Among never smoking controls, women who also reported no passive smoking exposure were significantly more likely to be nulliparous and to be recent users of oral contraceptives. Among those never exposed to passive smoking, there was no significant association between active smoking and breast cancer, relative risk (RR) of 1.12 (95% confidence interval (CI) 0.72-1.73) for past smokers and RR of 1.19 (95% CI 0.72-1.95) for current smokers, nor was there an association with age started, duration or intensity of active smoking. Compared with women who were never active nor passive smokers, there was no significant association between passive smoking in the home and breast cancer risk in never smokers, RR of 0.89 (95% CI 0.64-1.25), in past smokers, RR of 1.09 (95% CI 0.75-1.56), or in current smokers, RR of 0.93 (95% CI 0.67-1.30). There was no trend with increasing duration of passive smoking and there was no heterogeneity among any of the subgroups examined. In this study, there was no evidence of an association between either active smoking or passive smoking in the home and risk of breast cancer.

Tobacco smoking has been classified as a cause of cervical cancer, but the effect of different patterns of smoking on risk is unclear. The International Collaboration of Epidemiological Studies of Cervical Cancer has brought together and combined individual data on 13,541 women with and 23,017 women without cervical carcinoma, from 23 epidemiological studies. Relative risks (RRs) and 95% confidence intervals (CIs) of carcinoma of the cervix in relation to tobacco smoking were calculated with stratification by study, age, sexual partners, age at first intercourse, oral contraceptive use and parity. Current smokers had a significantly increased risk of squamous cell carcinoma of the cervix compared to never smokers (RR = 1.60 (95% CI: 1.48-1.73), p<0.001). There was increased risk for past smokers also, though to a lesser extent (RR = 1.12 (1.01-1.25)), and there was no clear trend with time since stopping smoking (p-trend = 0.6). There was no association between smoking and adenocarcinoma of the cervix (RR = 0.89 (0.74-1.06) and 0.89 (0.72-1.10) for current and past smokers respectively), and the differences between the RRs for smoking and squamous cell and adenocarcinoma were statistically significant (current smoking p<0.001 and past smoking p = 0.01). In current smokers, the RR of squamous cell carcinoma increased with increasing number of cigarettes smoked per day and also with younger age at starting smoking (p<0.001 for each trend), but not with duration of smoking (p-trend = 0.3). Eight of the studies had tested women for cervical HPV-DNA, and in analyses restricted to women who tested positive, there was a significantly increased risk in current compared to never smokers for squamous cell carcinoma (RR = 1.95 (1.43-2.65)), but not for adenocarcinoma (RR = 1.06 (0.14-7.96)). In summary, smokers are at an increased risk of squamous cell but not of adenocarcinoma of the cervix. The risk of squamous cell carcinoma increases in current smokers with the number of cigarettes smoked per day and with younger age at starting smoking.

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58,515 women with invasive breast cancer and 95,067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19-1.45, P<0.00001) for an intake of 35-44 g per day alcohol, and 1.46 (1.33-1.61, P<0.00001) for >/=45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1% per 10 g per day, P<0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers=1.03, 95% CI 0.98-1.07, and for current smokers=0.99, 0.92-1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver.

To clarify mortality risks of oesophageal cancer associated with hot tea, alcohol, tobacco and diet, further analyses on the data from a large prospective cohort study in Japan were conducted. The subjects for analysis were 220,272 men and women aged 40 to 69 at the baseline of 1965. There were 440 oesophageal cancer deaths during the period from January 1966 to December 1981. Person-years at risk were 3,065,182 in total. Rate ratio and 95% confidence interval adjusted for attained age, prefecture, occupation and sex were (RR (95% CI)): 1.6 (1.2-2.0) for hot tea (drinking green tea at high temperatures) in comparison with not-hot tea (drinking green tea at moderate temperatures); 2.4 (1.8-3.1) for daily (4 times/week or more) alcohol drinking in comparison with non-drinking; and 2.3 (1.7-3.1) for heavy smoking (15 cigarettes/day or more) in comparison with non-smoking. Dose-response relationships were found in alcohol drinking and smoking among men and women (p for trend; p < 0.001). The rate ratios were not significantly associated with the dietary factors except for green-yellow vegetables (1-3 times/month or less in comparison with daily; RR = 2.0, 95% CI: 1.2-3.1), where a no dose-response trend was observed (p = 0.45). In comparison based on the binary variables, the RR for the subjects with daily alcohol drinking and current smoking was 3.9 with 95% CI of 2.7 to 5.4, relative to those exposed to neither habit. The joint effect of alcohol drinking (A) and smoking (S) was more than additive (A*S > A + S: 3.9 > 1 + (1.0-1) + (1.6-1)). Further sub-analysis showed that the RR for the subjects with daily alcohol drinking, current smoking and hot tea was 5.7 with 95% CI of 3.7 to 8.9, when the reference was the subjects with not-daily alcohol drinking, non-smoking and not-hot tea. Similar results were obtained from further adjustment of green-yellow vegetables. It is concluded that mortality risks of oesophageal cancer in the present cohort were substantially associated with thermal effect of hot tea, alcohol drinking, smoking and lower consumption of green-yellow vegetables. This finding suggests that life-style modification for smoking and dietary habits is essential to reduce the risks of oesophageal cancer in Japan.

This study demonstrated that cigarette smoking was associated with an increase in both time to conception (among 2817 fertile women) and risk of primary infertility (among 1818 infertile women and their primiparous control subjects). The average time to conception was 4.3 months for women who never smoked, 4.6 months for those who smoked in the past, and 5.1 months for those who currently smoked. The delay in conception for current smokers remained significant after adjusting for confounders (risk ratio of 0.9 (0.8 to 1.0)). Additionally, current smokers were at increased risk of primary infertility (odd ratios of 1.9 (1.5 to 2.3)). For alcohol use, the average time to conception and risk of primary infertility did not vary by level of consumption. The average time to conception was significantly shorter for women who had used marijuana regularly and for women who had ever used cocaine than for women who had never used these drugs. Because of the increased use of marijuana and cocaine among young adults, further investigations of these associations are needed.

We report results on risk factors for invasive squamous cell and adenocarcinomas of the cervix in women aged 20-44 years from the UK National Case-Control Study of Cervical Cancer, including 180 women with adenocarcinoma, 391 women with squamous cell carcinoma and 923 population controls. The risk of both squamous cell and adenocarcinoma was strongly related to the lifetime number of sexual partners, and, independently, to age at first intercourse. The risk of both types of cervical cancer increased with increasing duration of use of oral contraceptives, and this effect was most marked in current and recent users of oral contraceptives. The risk of squamous cell carcinoma was associated with high parity and the risk of both squamous cell and adenocarcinoma increased with early age at first birth. Long duration smoking (20 or more years) was associated with a two-fold increase in the risk of squamous cell carcinoma, but smoking was not associated with the risk of adenocarcinoma. Further studies are needed to confirm the suggestion from this and other studies of differences in risk related to smoking between squamous cell and adenocarcinomas of the cervix. [ABSTRACT FROM AUTHOR]