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Alcohol consumption is causally linked to several cancers but the evidence for stomach cancer is inconclusive. In our study, the association between long-term alcohol intake and risk of stomach cancer and its subtypes was evaluated. We performed a pooled analysis of data collected at baseline from 491 714 participants in the European Prospective Investigation into Cancer and Nutrition and the Melbourne Collaborative Cohort Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for incident stomach cancer in relation to lifetime alcohol intake and group-based life course intake trajectories, adjusted for potential confounders including Helicobacter pylori infection. In all, 1225 incident stomach cancers (78% noncardia) were diagnosed over 7 094 637 person-years; 984 in 382 957 study participants with lifetime alcohol intake data (5 455 507 person-years). Although lifetime alcohol intake was not associated with overall stomach cancer risk, we observed a weak positive association with noncardia cancer (HR = 1.03, 95% CI: 1.00-1.06 per 10 g/d increment), with a HR of 1.50 (95% CI: 1.08-2.09) for ≥60 g/d compared to 0.1 to 4.9 g/d. A weak inverse association with cardia cancer (HR = 0.93, 95% CI: 0.87-1.00) was also observed. HRs of 1.48 (95% CI: 1.10-1.99) for noncardia and 0.51 (95% CI: 0.26-1.03) for cardia cancer were observed for a life course trajectory characterized by heavy decreasing intake compared to light stable intake (P homogeneity = .02). These associations did not differ appreciably by smoking or H pylori infection status. Limiting alcohol use during lifetime, particularly avoiding heavy use during early adulthood, might help prevent noncardia stomach cancer. Heterogeneous associations observed for cardia and noncardia cancers may indicate etiologic differences., (© 2021 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

DNA methylation may be one of the mechanisms by which alcohol consumption is associated with the risk of disease. We conducted a large-scale, cross-sectional, genome-wide DNA methylation association study of alcohol consumption and a longitudinal analysis of repeated measurements taken several years apart. Using the Illumina HumanMethylation450 BeadChip, DNA methylation was measured in blood samples from 5606 Melbourne Collaborative Cohort Study (MCCS) participants. For 1088 of them, these measures were repeated using blood samples collected a median of 11 years later. Associations between alcohol intake and blood DNA methylation were assessed using linear mixed-effects regression models. Independent data from the London Life Sciences Prospective Population (LOLIPOP) (N = 4042) and Cooperative Health Research in the Augsburg Region (KORA) (N = 1662) cohorts were used to replicate associations discovered in the MCCS. Cross-sectional analyses identified 1414 CpGs associated with alcohol intake at P < 10 -7 , 1243 of which had not been reported previously. Of these novel associations, 1078 were replicated (P < .05) using LOLIPOP and KORA data. Using the MCCS data, we also replicated 403 of 518 previously reported associations. Interaction analyses suggested that associations were stronger for women, non-smokers, and participants genetically predisposed to consume less alcohol. Of the 1414 CpGs, 530 were differentially methylated (P < .05) in former compared with current drinkers. Longitudinal associations between the change in alcohol intake and the change in methylation were observed for 513 of the 1414 cross-sectional associations. Our study indicates that alcohol intake is associated with widespread changes in DNA methylation across the genome. Longitudinal analyses showed that the methylation status of alcohol-associated CpGs may change with alcohol consumption changes in adulthood., (© 2019 Society for the Study of Addiction.)

Purpose: Pancreatic cancer has one of the worst prognoses with 5-year survival below 10%. There is some evidence that alcohol consumption might increase the risk of pancreatic cancer. We examined associations of pre-diagnostic alcohol intake with (i) incidence of pancreatic cancer, and (ii) overall survival following pancreatic cancer., Methods: Usual alcohol intake was estimated at recruitment in 1990-1994 for 38,472 participants in the Melbourne Collaborative Cohort Study using recalled frequency and quantity of beverage-specific intake for 10-year periods from age 20. Pancreatic cancer incidence (C25 according to International Classification of Diseases for Oncology) and vital status were ascertained through to 30 September 2015. Cox regression was performed to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations with lifetime, age 20-29, and baseline alcohol intakes., Results: By the end of follow-up (average 20.2 years), 239 incident cases of pancreatic cancer were diagnosed, of which 228 had died. No evidence of an association was observed between alcohol intake and risk of pancreatic cancer. Higher lifetime alcohol intake was associated with lower overall survival following a diagnosis of pancreatic cancer (mortality HR 1.09 per 10 g/day increment, 95% CI 1.00-1.19; p value = 0.04). A similar finding was observed for age 20-29 intake (HR 1.09 per 10 g/day increment, 95% CI 1.02-1.18; p value = 0.01) but not with baseline intake., Conclusions: We observed an association between lower alcohol use from an early age and improved survival following pancreatic cancer, but this finding needs to be confirmed by other studies.

Background and Aims: In Australia, as in many countries, alcohol consumption increased dramatically during the second half of the 20th century, with increased availability of alcohol, relaxation of attitudes towards drinking and shifting roles and opportunities for women as facilitating factors. We sought to investigate drinking trends by gender and birth cohort in Australia during this period., Design: Retrospective cohort study., Setting, Participants and Measurements: Using the usual frequency and quantity of beverage-specific alcohol intake for 10-year periods from age 20, reported retrospectively from 40 789 participants aged 40-69 years (born 1920-49) at recruitment to the Melbourne Collaborative Cohort Study in 1990-94, we compared trends in alcohol consumption by sex in Australia between 1950 and 1990. Participants' average daily consumption for age decades were transformed to estimated intakes for 1950, 1960, 1970, 1980 and 1990., Findings: Alcohol consumption was higher for men than women during each decade. Alcohol consumption increased for both sexes in the 1950s, 1960s and 1970s, and fell after 1980. The rise before 1980 was roughly equal in absolute terms for both sexes, but much greater relative to 1950 for women. Women born during 1930-39 and 1940-49 drank more alcohol during early-middle adulthood (ages 20-40) than women born during 1920-29. In the 1980s, the fall was greater in absolute terms for men, but roughly equal relative to 1950 for both sexes. In both sexes, the decline in drinking in the 1980s for birth-decade cohorts was roughly in parallel., Conclusions: Specific birth cohorts were influential in the rise in alcohol consumption by Australian women born in 1920-49 after World War II. Much of the convergence with men's drinking after 1980 reflects large reductions in drinking among men., (© 2018 Society for the Study of Addiction.)

Cohort studies have reported inconsistent evidence regarding alcohol intake and risk of non-Hodgkin lymphoma (NHL), mostly based on alcohol intake assessed close to study enrolment. We examined this association using alcohol intake measured from age 20 onwards. We calculated usual alcohol intake for 10-year periods from age 20 using recalled frequency and quantity of beverage-specific consumption for 37,990 participants aged 40-69 years from the Melbourne Collaborative Cohort Study. Cox regression was performed to derive hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between alcohol intake (g/day) and NHL risk. After a mean follow-up of 19.3 years, 538 NHL cases were diagnosed. Approximately 80% of participants were either lifetime abstainers or consumed below 20 g of ethanol/day. All categories of lifetime alcohol intake were associated with about 20% lower incidence of NHL compared with lifetime abstention, but there was no evidence of a trend by amount consumed (HR = 0.97 per 10 g/day increment in intake, 95% CI: 0.92-1.03; p value = 0.3). HRs for beer, wine and spirits were 0.91 (95% CI: 0.83-1.00; p value = 0.05), 1.03 (95% CI: 0.94-1.12; p value = 0.6), and 1.06 (95% CI: 0.83-1.37; p value = 0.6), respectively, per 10 g/day increment in lifetime intake. There were no significant differences in associations between NHL subtypes. In this low-drinking cohort, we did not detect a dose-dependent association between lifetime alcohol intake and NHL risk., (© 2017 UICC.)

The influence of lifestyle factors on survival following a diagnosis of colorectal cancer (CRC) is not well established. We examined associations between lifestyle factors measured before diagnosis and CRC survival. The Melbourne Collaborative Cohort Study collected data on alcohol intake, cigarette smoking and physical activity, and body measurements at baseline (1990-1994) and wave 2 (2003-2007). We included participants diagnosed to 31 August 2015 with incident stages I-III CRC within 10-years post exposure assessment. Information on tumor characteristics and vital status was obtained. Tumor DNA was tested for microsatellite instability (MSI) and somatic mutations in oncogenes BRAF (V600E) and KRAS. We estimated hazard ratios (HRs) for associations between lifestyle factors and overall and CRC-specific mortality using Cox regression. Of 724 eligible CRC cases, 339 died (170 from CRC) during follow-up (average 9.0 years). Exercise (non-occupational/leisure-time) was associated with higher CRC-specific survival for stage II (HR = 0.25, 95% CI: 0.10-0.60) but not stages I/III disease (p for interaction = 0.01), and possibly for colon and KRAS wild-type tumors. Waist circumference was inversely associated with CRC-specific survival (HR = 1.25 per 10 cm increment, 95% CI: 1.08-1.44), independent of stage, anatomic site and tumor molecular status. Cigarette smoking was associated with lower overall survival, with suggestive evidence of worse survival for BRAF mutated CRC, but not with CRC-specific survival. Alcohol intake was not associated with survival. Survival did not differ by MSI status. We have identified pre-diagnostic predictors of survival following CRC that may have clinical and public health relevance., (© 2017 UICC.)

Ethanol in alcoholic beverages is a causative agent for colorectal cancer. Colorectal cancer is a biologically heterogeneous disease, and molecular subtypes defined by the presence of somatic mutations in BRAF and KRAS are known to exist. We examined associations between lifetime alcohol intake and molecular and anatomic subtypes of colorectal cancer. We calculated usual alcohol intake for 10-year periods from age 20 using recalled frequency and quantity of beverage-specific consumption for 38,149 participants aged 40-69 years from the Melbourne Collaborative Cohort Study. Cox regression was performed to derive hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between lifetime alcohol intake and colorectal cancer risk. Heterogeneity in the HRs across subtypes of colorectal cancer was assessed. A positive dose-dependent association between lifetime alcohol intake and overall colorectal cancer risk (mean follow-up = 14.6 years; n = 596 colon and n = 326 rectal cancer) was observed (HR = 1.08, 95% CI: 1.04-1.12 per 10 g/day increment). The risk was greater for rectal than colon cancer (p homogeneity  = 0.02). Alcohol intake was associated with increased risks of KRAS+ (HR = 1.07, 95% CI: 1.00-1.15) and BRAF-/KRAS- (HR = 1.05, 95% CI: 1.00-1.11) but not BRAF+ tumors (HR = 0.89, 95% CI: 0.78-1.01; p homogeneity  = 0.01). Alcohol intake is associated with an increased risk of KRAS+ and BRAF-/KRAS- tumors originating via specific molecular pathways including the traditional adenoma-carcinoma pathway but not with BRAF+ tumors originating via the serrated pathway. Therefore, limiting alcohol intake from a young age might reduce colorectal cancer originating via the traditional adenoma-carcinoma pathway., (© 2016 UICC.)

Background: People with germline mutation in one of the DNA mismatch repair (MMR) genes have increased colorectal cancer risk. For these high-risk people, study findings of the relationship between alcohol consumption and colorectal cancer risk have been inconclusive. Methods: 1,925 MMR gene mutations carriers recruited into the Colon Cancer Family Registry who had completed a questionnaire on lifestyle factors were included. Weighted Cox proportional hazard regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between alcohol consumption and colorectal cancer. Results: Colorectal cancer was diagnosed in 769 carriers (40%) at a mean (SD) age of 42.6 (10.3) years. Compared with abstention, ethanol consumption from any alcoholic beverage up to 14 g/day and >28 g/day was associated with increased colorectal cancer risk (HR, 1.50; 95% CI, 1.09-2.07 and 1.69; 95% CI, 1.07-2.65, respectively; P trend = 0.05), and colon cancer risk (HR, 1.78; 95% CI, 1.27-2.49 and 1.94; 95% CI, 1.19-3.18, respectively; P trend = 0.02). However, there was no clear evidence for an association with rectal cancer risk. Also, there was no evidence for associations between consumption of individual alcoholic beverage types (beer, wine, spirits) and colorectal, colon, or rectal cancer risk. Conclusions: Our data suggest that alcohol consumption, particularly more than 28 g/day of ethanol (∼2 standard drinks of alcohol in the United States), is associated with increased colorectal cancer risk for MMR gene mutation carriers. Impact: Although these data suggested that alcohol consumption in MMR carriers was associated with increased colorectal cancer risk, there was no evidence of a dose-response, and not all types of alcohol consumption were associated with increased risk. Cancer Epidemiol Biomarkers Prev; 26(3); 366-75. ©2016 AACR ., (©2016 American Association for Cancer Research.)

Purpose: It is plausible that breast tissue is particularly susceptible to carcinogens, including ethanol, between menarche and the first full-term pregnancy ("first pregnancy"). There is some epidemiological evidence that intake before the first pregnancy is more closely associated with risk of breast cancer than is intake thereafter. We examined this association using lifetime alcohol consumption data from a prospective cohort study., Methods: We calculated usual alcohol intake for age periods 15-19 years and for 10-year period from age 20 to current age (in grams per day) using recalled frequency and quantity of beverage-specific consumption for 13,630 parous women who had their first pregnancy at age 20 years or later, had no cancer history and were aged 40-69 years at enrollment. Cox regression was performed to estimate hazard ratios (HRs) and their 95 % confidence intervals (CIs)., Results: A total of 651 incident invasive adenocarcinomas of the breast were diagnosed during a mean follow-up of 16.1 years. Alcohol consumption was low overall with only a few drinking ≥40 g/day. Intake before the first pregnancy was markedly lower (mean intake: 2.5 g/day; abstention: 58.8 %) than intake thereafter (mean intake: 6.0 g/day; abstention: 33.6 %). Any alcohol intake before the first pregnancy was associated with an increased risk of breast cancer (HR 1.35, 95 % CI 1.10-1.66 for drinking compared with abstention), whereas any intake after the first pregnancy was not (HR 0.89, 95 % CI 0.72-1.09)., Conclusions: Limiting alcohol intake before the first pregnancy might reduce women's risk of breast cancer.

Aims: Cancers of female breast, upper aero-digestive tract (UADT) (oral cavity, pharynx, larynx, oesophagus) and colorectum are causally related to alcohol consumption. Although alcohol consumption is likely to vary during life, the few studies that have explicitly measured lifetime consumption or intake over time have not been summarised. We therefore conducted a systematic review and meta-analysis., Methods: Studies were identified by searching the Medline, CINAHL (Cumulative Index to Nursing and Allied Health Literature) and Scopus databases through January 2015 using broad search criteria. Studies reporting relative risks (RR) for quantitatively defined categories of alcohol consumption over time for breast, UADT or colorectal cancer were eligible. A two-stage random-effects meta-analysis was used to estimate a dose-response relationship between alcohol intake and each cancer site. RRs were also calculated for the highest relative to the lowest intake category., Results: Sixteen articles for breast, 16 for UADT and 7 for colorectal cancer met the eligibility criteria. We observed a weak non-linear dose-response relationship for breast cancer and positive linear dose-response relationships for UADT and colorectal cancer. The pooled RRs were 1.28 (95% confidence interval, CI: 1.07, 1.52) for breast, 2.83 (95% CI: 1.73, 4.62) for UADT, 4.84 (95% CI: 2.51, 9.32) for oral cavity and pharynx, 2.25 (95% CI: 1.49, 3.42) for larynx, 6.71 (95% CI: 4.21, 10.70) for oesophageal and 1.49 (95% CI: 1.27, 1.74) for colorectal cancer., Conclusion: Our findings confirm dose-dependent associations between long-term alcohol intake and breast, UADT and colorectal cancer., (© The Author 2015. Medical Council on Alcohol and Oxford University Press. All rights reserved.)

Background: Conventionally, cohort studies have assessed the association between alcohol and all-cause mortality by using alcohol intake at enrolment., Methods: In the Melbourne Collaborative Cohort Study, participants were asked about usual frequency and quantity of beverage-specific alcohol intake for 10-year periods starting at age 20 from which current, past and lifetime intakes were calculated. We used Cox regression to estimate hazard ratios for mortality for 39 577 participants of the Melbourne Collaborative Cohort Study aged 40-69 at baseline., Results: After a mean follow-up of 15 years/person, we identified 4639 deaths. Associations between all-cause mortality and lifetime, current (baseline) and past intake were J shaped, with lower mortality at low intake (e.g. <40 g/day for men and 10 g/day for women using lifetime intake) and elevated mortality at higher intake. For men, consistent light-to-moderate drinking (>0-39/>0-39 g/day) from age 20 to baseline age was associated with a 16% lower mortality, while heavy drinking at both ages (≥80/≥40 and ≥40/0 g/day) was associated with higher mortality compared with stable abstinence., Conclusions: Our findings support a reduced mortality risk associated with low-dose drinking but also highlight a higher mortality risk for consistent heavy drinking from a young age., (© The Author 2014. Published by Oxford University Press on behalf of Faculty of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Purpose: Cohort studies have rarely examined the association between upper aero-digestive tract (UADT) cancer risk and lifetime alcohol intake. We examined the associations between incident squamous cell carcinoma of the UADT (oral cavity, pharynx, larynx, and esophagus) and alcohol intake for different periods in life using data from the Melbourne Collaborative Cohort Study., Methods: Usual alcohol intake for 10-year periods from age 20 was calculated using recalled frequency and quantity of beverage-specific consumption. Cox regression with age as the time axis was performed to estimate hazard ratios (HR) and 95 % confidence intervals (CI) for the associations of UADT cancer with alcohol intake for different periods in life compared with abstention., Results: During a mean follow-up of 16.2 person-years, 98 incident cases of UADT cancer were identified. We observed a dose-dependent association between lifetime alcohol intake and the risk of UADT cancer (multivariable-adjusted HR 2.67, 95 % CI 1.27-5.60 for an intake of ≥40 g/day and multivariable-adjusted HR 1.16, 95 % CI 1.06-1.28 for a 10 g/day increment in intake). A positive association with baseline alcohol intake (multivariable-adjusted HR 1.12, 95 % CI 1.02-1.24 for a 10 g/day increment in intake) was found to be a slightly weaker predictor of risk than lifetime intake., Conclusions: Limiting alcohol intake from early adulthood may reduce UADT cancer risk.

Background: To examine trends in alcohol-attributable morbidity (AAMorb) (2000/01-2009/10) and mortality (AAMort) (2000-07) by age, sex and region., Methods: Time-series analyses of population data for Victoria, Australia. We used joinpoint regression to quantify trends by estimating quarterly percent change (QPC) for rates of morbidity and mortality. We present the average QPC (AQPC) as a weighted average of QPCs. A test of parallelism was used to examine pairwise differences., Results: AAMorb increased significantly over time for Victoria (AQPC = 1.0%, 95% confidence interval 0.8-1.2). While females (1.6, 1.1-2.0), age groups 25-44 (1.0, 0.9-1.1) and 45-64 (1.2, 0.2-2.2), and metropolitan population (1.2, 0.5-1.9) were broad subgroups more at risk, multivariate analysis detected specific increases for metropolitan females aged 15-44 (1.8, 1.0-2.6) and 45+ (1.6, 0.2-3.0). Relatively greater increases in morbidity among metropolitan subgroups were widespread. AAMort remained stable for Victoria and for most subgroups, although significant declines in mortality were specifically experienced by metropolitan 15-24 (-2.0, -2.9 to -1.0) and 25-44 (-1.0, -1.7 to -0.3) age groups, and by regional males aged 45+ (-0.8, -1.3 to -0.3). Metropolitan males aged 45+ were a special high-risk population., Discussion: Our study has identified overlooked subgroups as being at increasing risk for alcohol-attributable chronic harm necessitating their inclusion in future policies for harm reduction., (© The Author 2013. Published by Oxford University Press on behalf of Faculty of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

The results from the few cohort studies that have measured usual alcohol consumption over time have not been summarized. We therefore conducted a systematic review and meta-analysis to quantify mortality risk. Pertinent studies were identified by searching the Medline, Web of Science, Cumulative Index to Nursing and Allied Health Literature (CINAHL) Plus, and Scopus databases through August 2012 using broad search criteria. Studies reporting relative mortality risks for quantitatively defined categories of alcohol consumption over time were eligible. Nine cohort studies published during 1991-2010 (comprising 62,950 participants and 10,490 deaths) met the inclusion criteria. For men, there was weak evidence of lower mortality risk with low levels of alcohol intake over time but higher mortality risk for those with intakes over 40 g/day compared with abstainers using a random-effects model (P for nonlinearity = 0.02). The pooled relative risks were 0.90 (95% confidence interval: 0.81, 0.99) for 1-29 g/day, 1.19 (95% confidence interval: 0.89, 1.58) for 30-59 g/day, and 1.52 (95% confidence interval: 0.78, 2.98) for 60 or more g/day compared with abstention. There was moderate between-study heterogeneity but no evidence of publication bias. Studies including women were extremely scarce. Our findings include a curvilinear association between drinking over time and mortality risk for men overall and widespread disparity in methods used to capture exposure and report results.

No randomized controlled trial has evaluated the effect of long-term alcohol interventions on mortality. Results reported in existing observational studies may be subject to selection bias and time-varying confounding. Using data from the Australian Longitudinal Study on Women's Health 1946–1951 birth cohort, collected regularly from 1996–2016, we estimated all-cause and cancer mortality had women been assigned various alcohol interventions (in categories ranging from 0 to >30 g/day ethanol, or reduced to ≤20 g/day if higher) at baseline, and had they maintained these levels of consumption. The cumulative risks for all-cause and cancer mortality were 5.6% (10,118 women followed for 20 years) and 2.9% (18 years), respectively. For all-cause and cancer mortality, baseline ethanol up to 30 g/day showed lower risk and >30 g/day showed higher risk relative to abstention. Had women sustainedly followed the interventions, a similar relationship was observed for all-cause mortality. However, the negative association observed for intakes ≤30 g/day and positive association for intakes >30 g/day was not evident for cancer mortality. Our findings suggest that all-cause mortality could have been lower than observed if this cohort of women had consumed some alcohol (no more than 30 g/day) rather than no consumption, but cancer mortality might not. [ABSTRACT FROM AUTHOR]

Alcohol consumption is a known cause of cancer, but its role in the etiology of second primary (metachronous) cancer is uncertain. Associations between alcohol intake up until study enrollment (prediagnosis) and risk of metachronous cancer were estimated using 9435 participants in the Melbourne Collaborative Cohort Study who were diagnosed with their first invasive cancer after enrollment (1990‐1994). Follow‐up was from date of first invasive cancer until diagnosis of metachronous cancer, death or censor date (February 2018), whichever came first. Alcohol intake for 10‐year periods from age 20 until decade encompassing baseline using recalled beverage‐specific frequency and quantity was used to calculate baseline and lifetime intakes, and group‐based intake trajectories. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted for potential confounders. After a mean follow‐up of 7 years, 1512 metachronous cancers were identified. A 10 g/d increment in prediagnosis lifetime alcohol intake (HR = 1.03, 95% CI = 1.00‐1.06; Pvalue =.02) and an intake of ≥60 g/d (HR = 1.32, 95% CI = 1.01‐1.73) were associated with increased metachronous cancer risk. We observed positive associations (per 10 g/d increment) for metachronous colorectal (HR = 1.07, 95% CI = 1.00‐1.14), upper aero‐digestive tract (UADT) (HR = 1.16, 95% CI = 1.00‐1.34) and kidney cancer (HR = 1.24, 95% CI = 1.10‐1.39). Although these findings were partly explained by effects of smoking, the association for kidney cancer remained unchanged when current smokers or obese individuals were excluded. Alcohol intake trajectories over the life course confirmed associations with metachronous cancer risk. Prediagnosis long‐term alcohol intake, and particularly heavy drinking, may increase the risk of metachronous cancer, particularly of the colorectum, UADT and kidney. What's new Alcohol consumption is an important risk factor for certain cancer types. Whether alcohol also has a role in the development of second primary tumors known as metachronous cancers, however, is uncertain. Here, an investigation of pre‐diagnosis long‐term alcohol intake and metachronous cancer in nearly 10,000 cancer survivors reveals associations between increasing alcohol consumption and metachronous cancers of the colorectum, upper aero‐digestive tract, and kidney. The associations were partly modified by smoking behavior. These findings offer new insights into risk factors for subsequent cancers in cancer survivors. [ABSTRACT FROM AUTHOR]

Aims To assess the relationship between ambulance attendances, emergency department ( ED) presentations and hospital admissions for acute alcohol intoxication and the timing of public holidays, sporting and social events. Design Time-series analysis was used to explore trends in intoxication in the context of major events. Setting Population of Melbourne, Victoria, Australia between 2000 and 2009. Participants All patients attended by ambulance, presenting to hospital EDs, or admitted to hospital who were classified as acutely alcohol intoxicated. Measurement Analysis of daily numbers of presentations for acute alcohol intoxication associated with major events were undertaken, including lead and lag effects. Analyses controlled for day of week and month of year to address temporal and seasonal variations. Findings Alcohol intoxication presentations were significantly elevated the day before all public holidays, with intoxication cases on the day of public holidays only higher on New Year's Day (ambulance 6.57, 95% confidence intervals ( CI): 3.4-9.74; ED 3.34, 95% CI: 1.28-5.4) and ANZAC Day (ambulance 3.71, 95% CI: 0.68-6.75). The Australian Football League ( AFL) Grand Final ( ED 2.37, 95% CI: 0.55-4.19), Commonwealth Games ( ED 2.45, 95% CI: 0.6-4.3) and Melbourne Cup Day (ambulance 6.14, 95% CI: 2.42-9.85) represented the sporting events with significant elevations in acute intoxication requiring medical attention. The last working day before Christmas was the only social event where a significant increase in acute intoxication occurred (ambulance 8.98, 95% CI: 6.8-11.15). Conclusions Acute alcohol intoxication cases requiring ambulance, emergency department and hospital in-patient treatment increase substantially on the day preceding public holidays and other major social events. [ABSTRACT FROM AUTHOR]