Search

There are strong associations between a number of reproductive factors and hormone-related cancers such as breast, ovarian and endometrial cancer, but most of these factors (e.g. numbers of pregnancies, age at first birth) cannot pragmatically be modified for the purposes of cancer prevention. Breastfeeding has marked effects on maternal reproductive hormones, has been inversely linked to breast and ovarian cancer and, unlike many other reproductive exposures, can be promoted to women for its public health and individual benefits. In the Second Expert Report on Food, Nutrition, Physical Activity and the Prevention of Cancer1 and subsequent Continuous Update Project (CUP),2 the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) concluded that there was convincing evidence that breastfeeding decreases risk of maternal pre- and post-menopausal breast cancer, but also concluded that the evidence for a causal association between breastfeeding and ovarian cancer1,3 was only “limited-suggestive”. This latter conclusion was based on their meta-analysis of three cohort studies4–6 which showed a non-significant 10% reduction in risk for ever versus never breastfeeding (relative risk [RR] 0.90; 95% confidence interval [CI] 0.75–1.08).3 However, results of another recently published meta-analysis of three cohort studies5,7,8 (only one of which5 was included in the WCRF review) suggested that each additional month of breastfeeding was associated with a significant 1.02% reduction in risk of ovarian cancer.9 There are several biologically plausible mechanisms by which breastfeeding might reduce risk of breast and ovarian cancers. Lactation causes differentiation of breast epithelial cells so they may be less susceptible to neoplastic transformation;2 ductal epithelial cells also exfoliate during lactation potentially eliminating those with DNA-damage.2 Furthermore, breastfeeding suppresses gonadotrophins, thereby lowering endogenous oestrogen and progesterone, and these hormones are thought to play an important role in the development of breast neoplasia.2 For ovarian cancer, most data suggest that repeated exposure of the ovarian/fallopian tube epithelium (many ovarian cancers may actually arise from the fallopian tube) to the effects of recurrent ovulation and/or reproductive hormones have an important role in carcinogenesis. In suppressing gonadotrophins and ovulation, lactation should decrease exposure of the ovary/fallopian tube to most factors postulated to have a strong causative role in cancer development.10 Our aim was to estimate the proportion of cancers attributable to little or no breastfeeding by parous women. Based on our a priori decision to limit our primary analyses to exposure-cancer relationships that either the WCRF or International Agency for Research on Cancer (IARC) had concluded were causal, in our primary analysis we estimated only the proportion of breast cancers diagnosed in 2010 that were attributable to little or no breastfeeding by women who had children. On the assumption that further studies will likely strengthen the evidence for a protective causal association between breastfeeding and ovarian cancer, we have undertaken a supplementary analysis to calculate PAF estimates for ovarian cancer.

Objectives: To estimate the population attributable fraction (PAF) and numbers of cancers occurring in Australia in 2010 attributable to tobacco smoking, both personal and by a partner. Methods: We used a modified Peto-Lopez approach to calculate the difference between the number of lung cancer cases observed and the number expected assuming the entire population developed lung cancer at the same rate as never smokers. For cancers other than lung, we applied the standard PAF formula using relative risks from a large cohort and derived notional smoking prevalence. To estimate the PAF for partners' smoking, we used the standard formula incorporating the proportion of non-smoking Australians living with an ever-smoking partner and relative risks associated with partner smoking. Results: An estimated 15,525 (13%) cancers in Australia in 2010 were attributable to tobacco smoke, including 8,324 (81%) lung, 1,973 (59%) oral cavity and pharynx, 855 (60%) oesophagus and 951 (6%) colorectal cancers. Of these, 136 lung cancers in non-smokers were attributable to partner tobacco smoke. Conclusions: More than one in eight cancers in Australia is attributable to tobacco smoking and would be avoided if nobody smoked. Implications: Strategies to reduce the prevalence of smoking remain a high priority for cancer control.

OBJECTIVE: To estimate the numbers and proportions of cancers occurring in Australia in 2010 attributable to modifiable causal factors.METHODS: We estimated the population attributable fraction (PAF) of cancers associated with exposure to 13 causal factors using standard formulae incorporating exposure prevalence and relative risk data. We also calculated the potential impact of changing exposure to some factors.RESULTS: A total of 32% of all cancers diagnosed in Australia in 2010 (excluding keratinocyte cancers) were attributable to the 13 factors assessed (men 33%; women 31%). Leading factors were tobacco smoke (PAF all cancers: 13.4%), solar radiation (6.2%), inadequate diet (6.1%) and overweight/obesity (3.4%). Factors conferring highest PAFs differed by sex: highest PAFs for men were tobacco smoke (15.8%), solar radiation (7.1%) and alcohol (3.0%); while highest PAFs for women were tobacco smoke (10.1%), solar radiation (5.0%) and overweight/obesity (4.5%). Sites with the highest counts of potentially preventable cancers were lung (8,569), colorectal (7,404), melanoma of the skin (7,220) and breast (3,233).CONCLUSIONS: At least one in three cancers in Australia is attributable to exposure to known modifiable factors.IMPLICATIONS: Up to 37,000 cancers could be prevented in Australia each year if the population avoided exposure to 13 common factors known or strongly suspected to cause cancer.

Describes the approach underpinning a national project to estimate the numbers and proportions of cancers occurring in Australia in 2010 that are attributable to modifiable causal factors. Abstract Objective: To describe the approach underpinning a national project to estimate the numbers and proportions of cancers occurring in Australia in 2010 that are attributable to modifiable causal factors. Methods: We estimated the population attributable fraction (PAF) (or prevented fraction) of cancers associated with exposure to causal (or preventive) factors using standard formulae. Where possible, we also estimated the potential impact on cancer incidence resulting from changes in prevalence of exposure. Analyses were restricted to factors declared causal by international agencies: tobacco smoke; alcohol; solar radiation; infectious agents; obesity; insufficient physical activity; insufficient intakes of fruits, vegetables and fibre; red and processed meat; menopausal hormone therapy (MHT); oral contraceptive pill (OCP); and insufficient breast feeding. Separately, we estimated numbers of cancers prevented by: aspirin; sunscreen; MHT; and OCP use. We discuss assumptions pertaining to latent periods between exposure and cancer onset, choices of prevalence data and risk estimates, and approaches to sensitivity analyses. Results: Numbers and population attributable fractions of cancer are presented in accompanying papers. Conclusions: This is the first systematic assessment of population attributable fractions of cancer in Australia.

Both the International Agency for Research on Cancer (IARC) and the World Cancer Research Fund (WCRF) have concluded that there is sufficient and convincing evidence that alcoholic drinks cause cancers of the oral cavity, pharynx, larynx, colorectum and female breast.1–4 IARC also concluded there was sufficient evidence that alcohol causes liver cancer and oesophageal squamous cell carcinoma (SCC);1 while the WCRF concluded that alcohol causes oesophageal cancers (type not specified) and probably increases the risk of cancer of the liver, with cirrhosis being an essential precursor.2 The evidence relating alcohol to pancreatic cancer is less clear. High alcohol intake (more than about three drinks or 30 g ethanol per day) may be associated with a small increase in risk of pancreatic cancer;1,5 however, IARC noted that residual confounding by smoking could not be excluded.1 The conclusions of these two agencies are summarised in Table ​Table11. Table 1 Summary of Evidence (IARC and WCRF) – alcohol and the risk of cancer Alcohol is not directly mutagenic; however, there is evidence that reactive metabolites of alcohol, such as acetaldehyde, have carcinogenic properties.2 It is speculated that alcohol may potentiate cancer development indirectly, e.g. by acting as a solvent for ingested carcinogens or through chemical processes such as prostaglandin production or generating free-radical oxygen species. It is commonly observed that people who consume large volumes of alcohol often smoke or have a diet lacking essential nutrients, placing them at increased risks of cancer.2 Disentangling the independent effects of alcohol consumption from the carcinogenic actions of tobacco smoke and other factors is not straightforward, particularly for cancers of the upper airways, digestive tract and pancreas.6,7 The Australian Guidelines to Reduce Health Risks from Drinking Alcohol,8 released by the National Health and Medical Research Council of Australia (NHMRC) in 2009, recommend that healthy men and women, aged 18 years and over, drink no more than two standard drinks on any day to reduce the lifetime risk of harm from alcohol-related disease or injury; and no more than four standard drinks on a single occasion to reduce the risk of alcohol-related injury arising from that occasion. One standard drink is defined as 10 g of alcohol (equivalent to 12.5 mL of pure alcohol). The guidelines emphasise that these recommendations do not represent a ‘safe’ or ‘no-risk’ drinking level. At the recommended level, the lifetime risk of death from an alcohol-related disease is around 0.4 in 100 people. Above this level, the risk increases with the number of drinks per day and is higher than 1 in 100 at three drinks per day. Above three drinks per day, the risk increases more sharply for women than for men.8 The Cancer Council of Australia9 recommends that “to reduce the risk of cancer, people limit their consumption of alcohol, or better still avoid alcohol altogether. For individuals who choose to drink alcohol, consumption should occur within the NHMRC guidelines”. The World Cancer Research Fund/American Institute for Cancer Research2 also notes that there is no evidence for a “safe limit” of alcohol intake. Earlier studies have estimated the proportion of cancers in Australia attributable to alcohol consumption. Some are now out of date;10 others11 have used approaches that do not permit comparison with recent international efforts.12 We sought to estimate the proportion and numbers of cancers occurring in Australia in 2010 attributable to alcohol consumption. Specifically, we estimated the population attributable fraction for cancers of the oral cavity, pharynx, oesophagus (SCC), colon, rectum, liver, larynx and breast associated with various levels of alcohol exposure, with the reference category defined as zero alcohol intake.

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to menopausal hormone therapy (MHT) use. Methods: We estimated the population attributable fraction for cancers causally associated with MHT (breast, endometrium, ovary), and the proportion of colorectal cancers prevented by MHT. We used standard formulae incorporating Australian prevalence data, relative risks of cancer associated with MHT and cancer incidence. We also estimated potential change in cancer incidence under two hypothetical scenarios whereby 25% fewer Australian women used MHT, or women exclusively used oestrogen-only MHT. Results: An estimated 539 cancers in Australia in 2010 were attributable to MHT: 453 breast, 67 endometrial and 19 ovarian cancers equating to 3.4%, 3.1% and 1.6% of each cancer type, respectively. In contrast, MHT may have prevented 52 colorectal cancers. If 25% fewer women used MHT, then 141 cancers may have been avoided. If women exclusively used oestrogen-only MHT then 240 cancers may have been avoided. Conclusions: MHT use caused more than 500 cancers in Australian women in 2010 and prevented ∼50 colorectal cancers. Implications: MHT use continues to cause an excess of cancers. The risks, benefits, regimen and treatment duration should be carefully considered for each woman before MHT is commenced.

Like many other industrialised countries, overweight and obesity is one of Australia's leading health issues,1 with prevalence increasing steadily over the past 30 years.2 Obesity is more prevalent among the most disadvantaged socioeconomic groups, such as people without post-school qualifications, Indigenous Australians and some migrant groups.2 In 2002, the International Agency for Research on Cancer (IARC) concluded that there was sufficient evidence that overweight and obesity cause cancers of the oesophagus (adenocarcinoma), endometrium, kidney (renal cell), colon and breast (post-menopausal).3 The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) in 2007 supported these conclusions, finding the evidence for these cancers, as well as rectal and pancreatic cancer, convincing. They also found evidence for probable causality for cancer of the gall bladder.4 The conclusions for breast, colon, rectal, pancreatic and endometrial cancer were maintained in subsequent WCRF Continuous Update Project Reports.5–8 In March 2014, a WCRF Continuous Update for ovarian cancer published a new judgement that body fatness (marked by BMI) is probably a cause of ovarian cancer.9 WCRF updates have not yet been completed for cancers of the oesophagus, kidney and gall bladder. The association between obesity and pre-menopausal breast cancer is uncertain. The WCRF/AICR found that it is “probable” that body fatness decreases the risk of pre-menopausal breast cancer;8 however, other studies have found a null or positive association with waist circumference and waist-hip ratio, both measures of central obesity.10,11 In addition, this study aimed to analyse those cancers that are caused by obesity and therefore potentially preventable. For these reasons, we have not considered pre-menopausal breast cancer. Since the publication of the WCRF/AICR Second Expert Report, a number of meta-analyses have found a significant and consistent association between obesity and other cancers: thyroid cancer;12,13 melanoma (men only);12 non-Hodgkin's lymphoma (NHL);12,14 multiple myeloma;12,15 and leukaemia.12,16 Body mass index (BMI), is commonly used as a measure of body fatness.4 BMI is calculated as weight in kilograms divided by the square of height in metres (kg/m2). Overweight and obesity are defined as levels of abnormal or excessive fat accumulation that may impair health.17 The WHO classifies adult overweight and obesity according to BMI: Normal weight 18.50–24.99 kg/m2; Overweight 25.00–29.99 kg/m2; and Obese ≥30 kg/m2.18 In our primary analysis, we estimated the population attributable fractions (PAF) and numbers of cancers attributable to overweight and obesity for cancers designated by IARC or WCRF/AICR up until 30 June 2014 as being causally associated, namely cancers of the oesophagus (adenocarcinoma only), colon, rectum, gall bladder, pancreas, breast (post-menopausal only), endometrium, ovary and kidney. In our supplementary analysis, we included estimates for those cancers for which there is accumulating evidence of a causal effect, but for which no formal declaration has been made by IARC or WCRF. The cancers in the supplementary analysis were melanoma, non-Hodgkin lymphoma (NHL), multiple myeloma, leukaemia and thyroid cancer.

OBJECTIVE: Participation rates have been declining in case-control studies, particularly among controls, raising concerns about possible bias. Formal assessments of the effect of low participation on odds ratios (OR) are seldom presented however. We sought to quantify possible bias using multiple imputation techniques. METHODS: Using data from two Australian case-control studies, we estimated the relative risks of oesophageal squamous cell carcinoma (OSCC) and adenocarcinoma (OAC), and serous ovarian cancer (SOC) associated with smoking and body mass index (BMI). We compared ORs observed using self-reported data from participating controls with ORs derived using imputed exposures for non-participating controls. RESULTS: Participating controls were less likely than non-participants to smoke currently. Smoking remained significantly associated with oesophageal cancer even under the most extreme assumption of smoking prevalence among non-participants (OSCC: observed OR 6.54, 4.62-9.28, imputed OR 3.94, 2.83-5.49; OAC: observed OR 2.69, 1.87-3.85 imputed OR 1.58, 1.13-2.22). For SOC however, risks associated with smoking were attenuated to null under plausible smoking assumptions among non-participants. BMI distributions were similar among participating and non-participating controls, and risk estimates were essentially unchanged. CONCLUSION AND IMPLICATIONS: Bias is not an inevitable consequence of low control participation and depends on the association examined. Sensitivity analyses can assist in interpretation of results.

Regular physical activity is important for optimal health and significant benefits occur from even modest amounts of physical activity,1 including lower cancer rates.2 There is consistent evidence from a systematic review and meta-analysis of cohort studies that physical activity is associated with a reduced risk of colon cancer.3 Research has also consistently demonstrated links between physical activity and reduced risk of post-menopausal breast cancer4 and endometrial cancer.5 The World Cancer Research Fund (WCRF) has concluded that there is “convincing” or “probable” evidence that insufficient physical activity causes cancers of the colon, post-menopausal breast and endometrium.6 The most recent Australian guidelines for physical activity and sedentary behaviour were released in February 2014.7 They recommend that adults perform at least 150 minutes of moderate intensity physical activity or 75 minutes of vigorous intensity physical activity per week to help improve blood pressure, cholesterol, heart health and muscle and bone strength. This should be increased to 300 minutes of moderate intensity physical activity or 150 minutes of vigorous intensity physical activity per week to reap greater health benefits and help to prevent cancer and unhealthy weight gain.7 The National Guidelines defines 60 minutes of moderate intensity physical activity on most days of the week (assumed 5 days) as a sufficient level to help prevent cancer. We aimed to estimate the fraction and number of cancers of the colon, post-menopausal breast and endometrium arising in the Australian population in 2010 that were attributable to failing to meet this target. We assumed that lower levels of physical activity conferred some benefit, but less than optimum.

The second expert report on Food, Nutrition, Physical Activity and the Prevention of Cancer by the World Cancer Research Fund (WCRF) and American Institute for Cancer Research (AICR) concluded that there was convincing evidence that the consumption of red meat (defined as the muscle meat from cattle, sheep, pigs and goats) and processed meat (meat preserved by smoking, curing or salting or the addition of chemical preservatives such as nitrates) increases the risk of colorectal cancer.1 This conclusion was reiterated in the recent WCRF Continuous Update Project for Colorectal Cancer,2 which reported a significant increase in risk for colorectal cancer (CRC) with higher consumption of red meat (relative risk [RR]=1.17 per 100 g/day) and a somewhat stronger increase in risk for processed meat, particularly for colon cancer (RR=1.24 per 50 g/day). Several mechanisms have been proposed to explain this causal association. For red meat, these include the oncogenic effects of haem iron3 and heterocyclic amines and polycyclic aromatic hydrocarbons4–6 that are found on the surface of well done/charred meat. For processed meats, nitrates – converted to carcinogenic nitrosamines – have been implicated.7 The Australian Dietary Guidelines recommend the consumption of no more than 455 g cooked (600–700 g raw weight) of lean red meat per week by older children, adolescents and adults, which equates to a 65 g (90–100 g raw weight, about the size of a deck of cards) serving per day.8 Processed and cured meats are considered discretionary food choices because they are high in added salt and saturated fat. The guidelines recommend that discretionary food choices should be eaten “only sometimes and in small amounts” and the recommended serving size is no more than 50 g.8 In this paper, we have estimated the number and fraction of cancers diagnosed in 2010 that could be attributed to the combined consumption of red and processed meat in the Australian population. We also estimated the number and proportion of cancers potentially preventable if consumption were reduced to a maximum of 65 g or 100 g/day.