We must first be absolutely clear that this study is not saying that drinking alcohol in moderation is in any way equivalent to smoking. Smoking kills up to two thirds of its users [2], and cancer is just one of the many serious health consequences. This study purely addresses cancer risk in isolation. The UK chief medical officer’s moderate drinking guideline of 14 units per week is set at a level at which there is a 1 % absolute risk of mortality from alcohol [35]. Furthermore the average consumption of cigarettes by smokers is around 80 per week in the UK and 100 per week in the United States (US) [36], far greater than our cigarette equivalent for moderate drinkers.

Using previously published resources reporting lifetime cancer risk, alcohol and tobacco attributable fractions and relative risk data for low to moderate levels of drinking and smoking, we have been able to estimate the approximate absolute lifetime risk of cancer in a non-smoking population, associated with moderate levels of alcohol consumption, and derive a cigarette equivalent in terms of harm. The ‘cigarette equivalent’ of a bottle of wine is five cigarettes for men and ten for women. The absolute risk of cancer increases with increasing alcohol consumption and the gender gap widens as a result of the association between alcohol and breast cancer. These figures occur on a background of a steady increase in alcohol consumption among women [37]. The latest survey estimates of alcohol consumption for 16–75 year old women in England is 1.4 units per day (ten units per week) [21]. Survey data underestimate intake, partly due to variations of units per glass of wine or pint of beer, and account for only 50% of alcohol consumption as measured by Her Majesty’s Revenue and Customs (HMRC) duty receipts. On this basis the average alcohol consumption for female drinkers is at least ten units per week. Given the approximate number of women in the UK aged 16–75 is 23,809,000 [38], current average levels of alcohol intake could result in around 339,000 extra cancers. It is also worth considering that there is a higher incidence of smoking among social drinkers compared to alcohol abstainers [39]. This is important as smoking can substantially increase the carcinogenic risk associated with alcohol consumption, particularly for cancers of the upper aerodigestive tract [25, 26].

While the association between hazardous drinking and breast cancer is well established [12, 14], a number of studies have highlighted a risk with low to moderate levels of alcohol consumption [14, 16, 40, 41]. A pooled analysis from 53 studies recruiting 58,515 women with breast cancer was the first to reveal that moderate levels of alcohol are associated with increased RR of developing breast cancer independent of smoking [14]. The UK’s Million Women Study reported an excess incidence of 15 per 1000 cancer cases for each additional alcoholic drink consumed per day, 11 due to breast cancer [14, 16]. These figures are comparable to our findings of 14 extra cancers per 1000 women drinking ten units per week (eight due to breast cancer) in non-smokers. The latest results from the European Prospective Investigation into Cancer and Nutrition, found an elevated hazard ratio for developing breast cancer of 4.2% for every 10 g (1.25 units) of alcohol consumed per day [40]. More recently Cao et al. presented data from the Nurses’ Health Study and Health Professionals Follow-up Study and demonstrated just one alcoholic drink per day could increase the RR of alcohol-related cancers independent of smoking [41]. Again this was driven by breast cancer and restricted to women [41]. While these studies support our data, our study is the first description of a percentage increase in absolute lifetime risk of cancer related to alcohol and the only study to provide a ‘cigarette equivalent’ of harm.

Rising levels of alcohol consumption over the past decade, are likely to be an important factor in the over 30% rise in breast cancer incidence in England (36,509 registrations in 2003, 55,122 in 2015) [42]. Breast cancer is now the most common cancer in UK women [43]. Exceptional efforts have been made to improve survival, however 11,563 women still died from breast cancer in the UK in 2016 and treatment carries a huge cost burden [42]. The benefits of increasing public awareness of the risks of moderate drinking could therefore be immense. It is important to educate women that an increased risk of breast cancer is not restricted to hazardous and harmful drinkers, and the messaging needs to be simple, relevant and memorable. Furthermore we hope this data will inform Chief Medical Officers of further opportunities for prevention of cancer at a population level.

It is interesting to consider that the list of alcohol-related cancers selected by the WHO IARC may be conservative, as several other cancers have recently been identified as having a dose-risk relationship to alcohol including melanoma, cancer of the gallbladder, pancreas, lung and prostate [44, 45]. Furthermore where papers have controlled for the ‘sick-quitter’ effect, alcohol-related RRs of developing cancer are substantially higher [45]. These two factors suggest that the cancer risk associated with moderate levels of drinking described in this paper may be underestimated for both men and women, although the gender gap may be smaller.

There are caveats with the methodology used in the study. Ideally all our risk estimates would have been calculated from systematic reviews and meta-analyses of alcohol consumption in non-smoking men and women, and cigarette consumption in teetotal men and women. While these data are available in a few individual studies, systematic review data are not available for subgroups of cancer type.

We have therefore estimated the risks for each cancer type using the most recent and robust available data and by making a number of assumptions. The data on RRs for cancer are extremely heterogenous, and while the original studies controlled for the use of other substances, our methodology does not account for synergies between RRs of alcohol and tobacco. In order to remove some of the confounding influence where these two risk factors co-exist, we adjusted the F AA and F TA to include non-smokers and non-drinkers only in alcohol-related and smoking-related cancers respectively and used adjusted RR data. We acknowledge however that the alcohol history of smokers is generally less accurate, and that a higher proportion of smokers may have previously been heavy drinkers. This factor may have led to a minor underestimate of the combined cancer risk. Furthermore F AA and alcohol-related RRs for cancer are derived largely from mortality, rather than morbidity data, and are therefore both likely to be underestimated, particularly in the case of breast cancer where the ratio of incidence to mortality is high (Additional file 1: Table S7) [23]. Therefore, while we were unable to calculate confidence intervals on our estimates we have tried to be conservative with our assumptions.

The best data available to us on the RR of cancer attributable to moderate levels of alcohol (ten units per week) were for consumption of less than 19 g per day, an average of 8.8 units per week if normally distributed. Similarly, our estimate of 30 units per week was derived from individuals drinking 20-39 g per day, i.e. 25.9 units per week (Additional file 1: Table S1) [28]. These data would slightly underestimate our calculation of the absolute increase in cancer risk associated with drinking ten and 30 units per week. In terms of tobacco, there is a lack of published data on RRs of cancer attributable to very low levels of smoking, with the lowest level of exposure generally reported as one to ten (approximately five) cigarettes per day. While recent studies have looked at lower levels of smoking their end point is mortality, not cancer incidence [46, 47]. While we were therefore required to estimate the risks of developing cancer at lower levels of consumption (just ten cigarettes per week) using logarithmic transformation, we believe this is justified as exposure to any level of carcinogens within cigarette smoke is likely to cause harm, and there is no reason to suppose there is a threshold at which this risk would begin [48]. As a result of these uncertainties we performed a sensitivity analysis reducing F AA , F TA and RRs for consuming ten units alcohol per week or ten cigarettes per week by 50%. This reduced the ‘cigarette equivalent’ of one bottle of wine to four for men but remained ten for women.

This study does not account for the duration an individual is exposed to a cancer-related risk factor. Cumulative exposure is directly related to the incidence of certain cancers, particularly tobacco smoking and lung cancer [49]. Furthermore this study only takes into account cancer incidence and not the age at which a cancer develops and its prognosis. However while the majority of alcohol-related cancers, including breast cancer may have a better ten year survival than lung cancer (78% vs 5%, Additional file 1: Table S7), the years of life lost from cancer are comparable. Lung cancer is the leading cause of years of life lost from cancer (2,365,000 years of life lost), but colorectal cancer is the second (804,000 years of life lost), and female breast cancer the third (778,000 years of life lost) [50]. In addition breast cancer affects women at a relatively younger age compared to lung cancer [51], resulting in a significant burden for them and their families, including young children.

It is noteworthy that the attributable fractions and the absolute risk scores calculated here are dependent on both the prevalence of exposure to a risk factor within a population and the relative risk of that behaviour resulting in cancer. For smoking the prevalence is low (approximately 20% of individuals in the UK are daily smokers for example [52]), with a high relative risk of cancer for current smokers; whereas alcohol consumption is more common (72% of women and 83% of men consume some alcohol in countries with a high socio-demographic index [10]), but is associated with a lower relative risk of cancers overall; even for high levels of consumption [53]. Critically, our findings are not meant to detract from the substantive cancer risks associated with smoking which remains the single largest preventable cause of cancer worldwide [54], and for which even very low levels of exposure are associated with an increased risk of cancer [46].

Critically our use of absolute ‘lifetime risk’ describes the average of the number of cancers experienced by a population, i.e. individuals with and without cancer, and is not an exact measure of an individual’s probability of getting cancer. In other words while this study estimates that drinking ten units of alcohol per week may cause a similar number of cancers in the population as smoking five to ten cigarettes per week, these two exposures may not carry the same cancer risk for any given individual. We have attempted to minimise this effect by using lifetime cancer risks from CRUK which have been calculated using the Sasieni method. This corrects incidence rates for the inclusion of more than one primary cancer occurring within the same individual, lowering the lifetime cancer risk [24].

Furthermore this study does not take into account other smoking or alcohol-related outcomes such as respiratory, cardiovascular or liver disease in which case the conclusions would likely be quite different. Cancer deaths are a fraction of the total number of deaths associated with smoking and alcohol and this study is not a comparison of the overall mortality of smoking versus alcohol. Despite the caveats, our estimation of a ‘cigarette equivalent’ for alcohol provides a useful measure for communicating cancer risks that exploits successful historical messaging on smoking, reflects current epidemiological knowledge and includes an important aspect of gender differential.