上海市区吸烟对几种主要恶性肿瘤的人群归因危险度分析

上海市肿瘤研究所于１９８４～１９９０年期间先后进行了基于全人群的肺癌、卵巢癌、肾癌、膀胱癌、喉癌、口腔癌、胃癌及结肠癌的病例对照研究，研究发现吸烟对这些肿瘤有不同程度的危险作用。本文在这些研究的基础上，分别进行吸烟对这些恶性肿瘤的人群归因危险度（ＰＡＲＰ）分析。结果表明，吸烟是上海市区男性肺癌、膀胱癌及喉癌的主要原因，ＰＡＲＰ分别为７５％、７１％和７８％；吸烟也是男性胃癌和肾癌的重要原因，ＰＡＲＰ分别为２５％和２９％。吸烟对女性恶性肿瘤的危害主要表现在肺癌，ＰＡＲＰ为２８％；女性结肠癌、口腔癌和卵巢癌的ＰＡＲＰ分别为４％、９％和６％。研究结果表明，控制人群中的吸烟率，对降低上海市区恶性肿瘤，尤其是男性恶性肿瘤的发病率有重大意义。     

上海市区不同行业、职业人群恶性肿瘤发病率的调查研究——Ⅱ、气管、支气管和肺癌(ICD-9,162)

上海市区男性气管、支气管和肺癌(ICD-9,162,以下简称肺癌)发病率目前已超过胃癌居癌症的首位,女性发病率也很高,居女性癌症第三位。据本市以往调查研究,吸烟是市区男性肺癌最主要的危险因素,人群归因危险度高达70％～80％。女性由于吸烟率不高,且大部分病例为与吸烟联系不甚密切的腺癌,人群归因危险度只有20％～25％,其他重要危险因素尚待查明。     

大连市区1991～2010年学龄期青少年恶性肿瘤流行趋势分析

[目的]分析大连市区1991～2010年5～19岁学龄期青少年恶性肿瘤流行趋势.[方法]利用5～19岁学龄期青少年恶性肿瘤新发病例资料,计算粗发病率、世界人口调整发病率(世调率)、年度变化百分比(APC),进行年龄、时期、队列三因素相互调整后的相对危险度和95％可信区间的估计,综合分析肺癌的年龄—时期—队列三因素变化趋势.[结果](1)发病概况:男性粗发病率和世调率分别为11.79/10万和11.80/10万,女性分别为11.99/10万和11.89/10万.白血病、脑瘤和恶性淋巴瘤位居学龄期青少年人群恶性肿瘤的前3位,构成比分别为34.14％、17.71％和9.92％.(2)时间趋势分析:男性粗发病率和世调率的APC分别为0.50％(P＞0.05)和-0.20％(P＞0.05),女性为1.61％(P＞0.05)和1.51％(P＞0.05).(3)流行趋势分析:男性发病年龄在10～岁组、1984～与1989～出生队列发病风险增加(P＜0.05),女性在2006～2010时期、1979～与1984～出生队列发病风险增加(P＜0.05).[结论]白血病是威胁大连市区学龄期青少年健康的首位恶性肿瘤,男性脑瘤和女性甲状腺癌发病的上升趋势值得关注.     

武汉市城区居民肺癌危险因素研究

 目的 探讨武汉市肺癌主要危险因素,为采取切实可行的防治措施提供依据。方法 采用病例对照研究方法,收集370例肺癌病例和符合条件的对照740例进行问卷调查,应用条件Logistic回归分析方法进行单因素和多因素的分析,并计算每个危险因素的PAR%。结果 武汉市城区肺癌主要危险因素有室内化学物污染、吸烟、被动吸烟、精神压抑、肺部疾患史、新鲜蔬菜和水果摄入少等。男性肺癌归因于吸烟的比例为最高;女性肺癌主要归因于新鲜蔬菜摄入少、体重指数、体育锻炼、厨房油烟。结论精神压抑、室内化学物污染、吸烟、被动吸烟、新鲜蔬菜摄入少、呼吸系统疾病史、厨房油烟等因素可以解释武汉市城区90%左右的肺癌发病。而吃蔬菜较多、参加体育锻炼、心理健康等为肺癌发病的保护因素。     

吸烟与原发性肝癌关系的巢式病例对照研究

目的 分析吸烟与上海市区中老年男性原发性肝癌的关系.方法 应用巢式病例对照研究方法,对一个18 244名男性队列随访11年,以队列中213例新发肝癌患者作为病例组,按照患者年龄、采样日期、同居住区等配对条件,从队列中随机抽取1094名健康人作为对照组.使用配对Logistic回归分析,调整可能的混杂因素,估计吸烟对肝癌发生的危险度和95%可信区间(CI).结果 调整肝炎、肝硬化、胆石症或其他胆囊病史及乙型肝炎病毒感染等可能的混杂因素后,男性吸烟者患肝痛的危险性是不吸烟者的1.91倍(95%CI为1.28～2.86),日随着每天吸烟量、吸烟年限和吸烟包年数的增加而增加.每天吸烟≥20支者、吸烟≥40年者和吸烟37包年者患肝癌的相对危险度分别为2.16(95%CI为1.37～3.40)、2.14(95%CI为1.18～3.87)和2.12(95%CI为1.21～3.74).吸烟开始年龄越小,危险性越大,吸烟开始年龄<20岁者患肝癌的危险性为2.57(95%CI为1.50～4.40).结论 吸烟是上海市区男性原发性肝癌的危险因素.     

体质指数与非吸烟女性肺癌关系的前瞻性队列研究

目的:研究体质指数(body mass index, BMI)与非吸烟女性肺癌的关系.方法:建立1997-2000年上海市区74 942人(其中非吸烟者72 829人)、年龄40～70岁的女性队列,每2年随访1次,至2007年12月共收集271例非吸烟女性肺癌病例.用COX回归模型分析BMI与非吸烟女性肺癌发生的相对危险度(relative risk, RR)和95%可信区间(95% confidence interval,95%CI).结果:调整年龄、教育程度、绝经状态等因素后,基线BMI、20岁BMI与非吸烟女性肺癌危险均无关.基线BMI最高四分组与最低组比较,RR=0.95(95%CI:0.67～1.34);20岁BMI最高四分组与最低组比较,RR=0.77(95%CI:0.52～1.15).基线BMI和年龄与非吸烟女性肺癌之间关系的分层分析得到相似结果.结论:40岁以上非吸烟女性的BMI可能与其肺癌发生的危险性没有关联.     

2010—2019年江苏省南通市归因于吸烟的癌症死亡负担研究

[目的]分析江苏省南通市2010—2019年归因于吸烟的癌症死亡负担。[方法]利用南通市2010—2019年死因监测数据和人口数据，通过年龄别和性别的吸烟影响比(SIR)及12种与吸烟相关的癌症相对危险度（RR）来计算不同年龄组和性别的吸烟归因癌症死亡人群归因分值（PAF）与吸烟归因死亡数（SAM）。[结果] 2010—2019年南通市总人群SAM为62 556例，其中男性为50 223例，女性为12 333例。10年间归因于吸烟的癌症死亡率为51.80/10万，全人群及分性别归因于吸烟的癌症死亡率变化无统计学意义（P>0.05）。2010—2019年归因于吸烟的癌症死亡PAF为37.41%。75岁及以上年龄组归因于吸烟的死亡率及构成比均高于其他年龄组，且呈上升趋势。全部人群SAM构成比中，占比最高的癌症依次为肺癌（占56.91%）、食管癌（19.35%）、肝癌（10.58%）和胃癌（5.09%）,PAF最高的癌症则依次为肺癌（73.21%）、鼻咽癌（53.50%）、食管癌（47.69%）、口腔癌（47.06%）。[结论]南通市归因于吸烟的癌症死亡负担较重，应从政策引领、行为引导...     

吸烟和环境烟草烟雾暴露与膀胱癌关系的病例对照研究

目的研究分析吸烟及环境烟草烟雾暴露与膀胱癌的关系。方法自1996年1月~1999年6月,上海市区开展了一项大规模的基于全人群的膀胱癌病例对照研究,共访问到608例膀胱癌病例和607例健康人群对照。使用非条件logistic回归分析,调整可能的混杂因素,估计吸烟及环境烟草烟雾暴露对膀胱癌发生的比数比和95%可信区间。结果男性吸烟者患膀胱癌的危险性是不吸烟者的1.67倍(95%CI1.23~2.27),且随着每天吸烟量、累积吸烟量、吸烟年限和吸烟深度的增加而增加,吸烟开始年龄越小危险性越大;戒烟后膀胱癌危险性有所降低。吸烟也显著增加女性膀胱癌的危险性,调整OR为4.19(95%CI1.65~10.65)。吸烟者的调整人群归因危险度男性、女性分别为32.04%和15.61%。未发现环境烟草暴露增加非吸烟者膀胱癌的危险性。结论进一步证实吸烟是膀胱癌发生的重要危险因素。环境烟草烟雾暴露是否增加膀胱癌危险性尚难定论。     

中国女性乳腺癌人群归因危险估计

目的 评估已知乳腺癌危险因素对我国女性人群的人群归因危险,为中国女性乳腺癌的预防与控制提供依据.方法 利用文献中人群暴露率和相对危险度的数据,计算已知危险因素的人群归因分值(PAF),并利用全国第三次死因调查的数据估计乳腺癌的归因死亡和发病人数.人群暴露率的数据主要来源于大样本、大范围的代表全国人群的调查数据,相对危险度的数据来自Meta分析研究和中国或其他国家的大样本的单个研究资料.结果 居前5位的乳腺癌发病的危险因素依次为良性乳腺疾病(RR =2.62)、乳腺癌家族史(RR =2.39)、吸烟(RR=l.86)、超重(RR=1.60)和月经初潮年龄(RR=l.54).生殖因素、生活方式、良性乳腺疾病、外源性激素治疗及乳腺癌家族史的PAF分别为27.84％、23.55％、15.09％、3.60％和2.49％,五大危险因素总PAF为55.95％.2005年,我国女性乳腺癌归因于生殖因素、生活方式、良性乳腺疾病、外源性激素治疗及乳腺癌家族史的发病和死亡人数分别为79 862和22 456例.结论 预防控制各种不良生活方式将可能显著降低中国乳腺癌发病与死亡.     

中国人群肺癌、肝癌、乳腺癌危险因素的综合研究

[目的]探讨目前我国人群肺癌、肝癌和乳腺癌发生的主要危险因素，为预防决策提供依据。[方法]利用综合分析方法估计我国人群三种肿瘤的主要危险因素的相对危险度及人群归因危险度百分比。[结果]三种肿瘤的主要危险因素分别为，肺癌包括精神因素、室内环境污染、香烟烟雾、遗传因素和饮食中蔬菜水果的摄入少；乳腺癌包括女性生育和生理因素、疾病史、生活精神刺激、家庭史、体重；肝癌包括病毒感染、家庭肝癌史、摄入黄曲霉毒素污染食物、饮水污染和心理因素。[结论]在影响三种肿瘤发生的因素中，除了各自的特点外，其共同的因素如相应系统疾病史、精神因素等应引起重视。     

Calculation of population attributable risk for alcohol and breast cancer (United States)

Objectives: Because of increasing evidence that alcohol may be causally associated with breast cancer, we reconsider the population attributable risk (PAR) for alcohol and breast cancer for the US adult female population using an effect estimate from a meta- analysis and incorporating a revised perspective on measurement error correction.Methods: To estimate PAR, we employed a formula appropriate to use with an adjusted effect estimate. To estimate intermediate quantities needed to apply that formula, we used adjusted relative risk estimates from a previously published meta- analysis, as well as SEER cancer statistics and general population data from the third National Health and Nutrition Examination Survey. We used relative risk estimates uncorrected for measurement error.Results: The estimated age-adjusted PAR for alcohol and breast cancer was 2.1%.Conclusions: Because of the modest association between alcohol and breast cancer and the generally moderate level of alcohol intake among US women, the proportion of breast cancer attributable to alcohol intake is small. Widespread efforts to reduce alcohol consumption would not have a substantial impact on breast cancer rates in this population. While selected subgroups of women might benefit from decreasing alcohol consumption, specific profiles for such women have yet to be defined and defended.     

Population attributable proportion and number of cancer cases attributed to potentially modifiable risk factors in Iran in 2020

In the current study, we aimed to calculate the fraction of cancer attributable to modifiable risk factors in Iran in 2020. Population attributable fractions (PAFs) were calculated for established cancer risk factors using three data sources: the national cancer incidence reports, relative risks extracted from global and national meta-analyses, and exposure prevalence from national/subnational population-based surveys. In addition to overall cancers, the PAFs were estimated separately for each cancer site among men and women. Overall, 32.6% of cancers in 2020 in Iran were attributable to known risk factors. The PAF in men (40.2%) was twice as high as in women (21.1%). Cigarette smoking (15.4%), being overweight (5.0%), opium use (3.9%) and H. pylori infection (3.8%) were the leading causes of cancers. For men, the highest PAFs belonged to cigarette smoking (26.3%), opium use (6.8%) and being overweight (3.1%), while for women, the highest PAFs belonged to being overweight (7.2%), H. pylori infection (2.7%) and cigarette smoking (2.7%). Among Iranian men and women, the PAFs of waterpipe smoking were 2% and 0.9%, respectively. A third of incident cancers in Iran are due to modifiable exposures, mainly cigarette smoking, being overweight, and H. pylori infection. Opium consumption and waterpipe smoking collectively accounted for 8.8% of cancer occurrence in men and 1.3% in women in Iran. These emerging risk factors should be taken into consideration in future PAF studies.     

New cancer susceptibility loci: population and familial risks

The recent large genotyping studies have identified a new repertoire of cancer susceptibility genes and loci which are characterized by common risk alleles and low relative risks. Because of these properties, these loci explain a much larger proportion of the etiology of the particular cancers, described by the population attributable fraction (PAF), than of their familial risks (FRRs). For breast cancer, the 9 established loci gave a joint PAF of >60%, but explaining only some 8% of the empirical FRR. For prostate cancer, 6 independent loci at chromosome 8q conferred a joint PAF of 35% but the loci explained no more than 1.9% of the empirical excess familial risks. For colorectal cancer, the contributions of the 2 identified loci to PAF and FRR were somewhat lower. The genome-wide array platforms have been built for common variants, constraining the results to variants with high PAFs and low FRRs. However, the common variants are likely to tag rarer causative variants with much higher FRRs. The detected loci are noncoding and the underlying genetic mechanisms have not been worked out. The data suggest, in spite of the reservations for combining data on PAFs across populations, that the published first-generation genome-wide scans on breast, prostate and colorectal cancers have made successful inroads into genomics of common cancers, yet leaving the mechanisms to be explained.     

Proportion of colon cancer risk that might be preventable in a cohort of middle-aged US men

Objective: Diet and lifestyle likely play major roles in colon cancer incidence; however, the proportion of colon cancer risk that might be preventable is unknown. Thus, we estimated the proportion of colon cancer risk among men in the prospective Health Professionals Follow-up Study that might be attributable to a constellation of modifiable risk factors, and thus might be preventable. Methods: We included 47,927 men aged 40–75 years in 1986, among whom we confirmed 411 colon cancer cases from 1986 to 1996. Risk factors considered were obesity, physical inactivity, alcohol consumption, early adulthood cigarette smoking, red meat consumption, and low intake of folic acid from supplements. We calculated a risk score that was the sum across the six risk factors of the values of 1 (better exposure) to 5 (worse exposure) corresponding to the exposure category. We entered the risk score into a logistic regression model and estimated the population attributable risk percent (PAR%) using the method of Bruzzi et al. Results: After adjusting for age and family history of colorectal cancer and comparing the risk score for the combined six modifiable colon cancer risk factors at or above the approximate 20th, 10th, or 5th percentiles vs. below, the PAR% increased from 39% (95% confidence interval (CI) = 23–58%), to 48% (95% CI = 25–71%), to 55% (95% CI = 27–80%), respectively. Using a second method in which we used cut-points consistent with general-good health behaviors for each risk factor, comparing men with at least one risk factor to men without any risk factors (3.1% of the men), the PAR% was 71% (95% CI = 33–92%). Conclusion: The findings from this analysis suggest that, if all the members of this cohort of middle-aged US men had a modifiable exposure distribution comparable to the men with low risk scores, a large proportion of colon cancer risk might be avoidable. Additional study is required to determine whether making changes in these six risk factors now would reduce the risk of colorectal neoplasia, or whether the proportion of colon neoplasia that might be avoidable would be similar in populations with different characteristics.     

Interaction between tobacco smoking and hepatitis B virus infection on the risk of liver cancer in a Chinese population

Although tobacco smoking has been reported as a risk factor for liver cancer, few studies have specifically explored the association among Chinese females and the potential interaction between smoking and other risk factors. A population‐based case–control study was conducted and 2,011 liver cancer cases and 7,933 healthy controls were enrolled in Jiangsu, China from 2003 to 2010. Epidemiological data were collected, and serum hepatitis B surface antigen (HBsAg) and anti‐HCV antibody were measured. Unconditional logistic regression was used to examine association and potential interaction, while semi‐Bayes (SB) method was employed to make estimates more conservative. The prevalence of serum HBsAg positivity was 43.2% among cases and 6.5% among controls. The adjusted odds ratios (OR) for ever smoking were 1.62 (95% confidence interval [CI]: 1.33–1.96) among male and 0.82 (95% CI: 0.53–1.26) among female. Age at first cigarette, duration of smoking and pack‐years of smoking were all significantly associated with liver cancer among men. Compared to HBsAg‐negative never smokers, the adjusted ORs were 1.25 (95% CI: 1.03–1.52) for HBsAg‐negative ever smokers, 7.66 (95% CI: 6.05–9.71) for HBsAg‐positive never smokers, and 15.68 (95% CI: 12.06–20.39) for HBsAg‐positive ever smokers. These different odds ratios indicated super‐additive (RERI: 7.77, 95% CI: 3.81–11.73) and super‐multiplicative interactions (ROR: 1.64, 95% CI: 1.17–2.30) between hepatitis B virus (HBV) infection and tobacco smoking. Most associations and interactions detected remained statistically significant after SB adjustments. Tobacco smoking and HBV infection positively interact in the development of liver cancer.     

Preventable incidence of carcinoma associated with adiposity,alcohol and physical inactivity according to smoking status in the United States

The changing profile of lifestyles and their intricate relationships with smoking indicate the importance of accounting for smoking status when assessing cancer preventability. We assessed the association of body mass index, weight change, alcohol intake and physical activity with risk of total carcinoma among 53,195 smokers and 62,842 nonsmokers in two prospective cohorts. Then, leveraging the national prevalence estimates, we calculated the population attributable risk (PAR) for healthy lifestyle defined as body mass index ≥18.5 and <27.5 kg/m², mid-life weight change of ≤20 pounds, no or moderate alcohol drinking (≤1 and 2 drinks/day for women and men, respectively) and weekly moderate or vigorous physical activity of at least 150 min. The PAR (95% CI) for healthy lifestyle was 18% (14–22%) in nonsmokers and 14% (10–19%) in smokers among women, and 20% (12–27%) in nonsmokers and 11% (5–17%) in smokers among men. While adiposity accounted for a substantially higher proportion of carcinoma cases in nonsmokers than smokers (16% vs. 2% in women, 15% vs. 2% in men), alcohol contributed more in smokers than nonsmokers (7% vs. 3% in women, 8% vs. 1% in men). When more strict criteria were used to define healthy lifestyle, the PAR estimates further increased (for women: 37% in smokers and 32% in nonsmokers; for men: 15% and 24%, respectively). In conclusion, lifestyle modification has great potential to reduce cancer risk in both smokers and nonsmokers. Weight control and reducing alcohol consumption should be prioritized for cancer prevention in nonsmokers and smokers, respectively.     

Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States

Contemporary information on the fraction of cancers that potentially could be prevented is useful for priority setting in cancer prevention and control. Herein, the authors estimate the proportion and number of invasive cancer cases and deaths, overall (excluding nonmelanoma skin cancers) and for 26 cancer types, in adults aged 30 years and older in the United States in 2014, that were attributable to major, potentially modifiable exposures (cigarette smoking; secondhand smoke; excess body weight; alcohol intake; consumption of red and processed meat; low consumption of fruits/vegetables, dietary fiber, and dietary calcium; physical inactivity; ultraviolet radiation; and 6 cancer‐associated infections). The numbers of cancer cases were obtained from the Centers for Disease Control and Prevention (CDC) and the National Cancer Institute; the numbers of deaths were obtained from the CDC; risk factor prevalence estimates were obtained from nationally representative surveys; and associated relative risks of cancer were obtained from published, large‐scale pooled analyses or meta‐analyses. In the United States in 2014, an estimated 42.0% of all incident cancers (659,640 of 1570,975 cancers, excluding nonmelanoma skin cancers) and 45.1% of cancer deaths (265,150 of 587,521 deaths) were attributable to evaluated risk factors. Cigarette smoking accounted for the highest proportion of cancer cases (19.0%; 298,970 cases) and deaths (28.8%; 169,180 deaths), followed by excess body weight (7.8% and 6.5%, respectively) and alcohol intake (5.6% and 4.0%, respectively). Lung cancer had the highest number of cancers (184,970 cases) and deaths (132,960 deaths) attributable to evaluated risk factors, followed by colorectal cancer (76,910 cases and 28,290 deaths). These results, however, may underestimate the overall proportion of cancers attributable to modifiable factors, because the impact of all established risk factors could not be quantified, and many likely modifiable risk factors are not yet firmly established as causal. Nevertheless, these findings underscore the vast potential for reducing cancer morbidity and mortality through broad and equitable implementation of known preventive measures. CA Cancer J Clin 2018;68:31‐54 . © 2017 American Cancer Society .     

Attributable Causes of Liver Cancer Mortality and Incidence in China

Objectives: To estimate the proportion of liver cancer cases and deaths due to infection with hepatitis B virus(HBV), hepatitis C virus (HCV), aflatoxin exposure, alcohol drinking and smoking in China in 2005. Studydesign: Systemic assessment of the burden of five modifiable risk factors on the occurrence of liver cancer inChina using the population attributable fraction. Methods: We estimated the population attributable fractionof liver cancer caused by five modifiable risk factors using the prevalence data around 1990 and data on relativerisks from meta-analyses, and large-scale observational studies. Liver cancer mortality data were from the 3rdNational Death Causes Survey, and data on liver cancer incidence were estimated from the mortality data fromcancer registries in China and a mortality/incidence ratio calculated. Results: We estimated that HBV infectionwas responsible for 65.9% of liver cancer deaths in men and 58.4% in women, while HCV was responsible for27.3% and 28.6% respectively. The fraction of liver cancer deaths attributable to aflatoxin was estimated to be25.0% for both men and women. Alcohol drinking was responsible for 23.4% of liver cancer deaths in men and2.2% in women. Smoking was responsible for 18.7% and 1.0% . Overall, 86% of liver cancer mortality andincidence (88% in men and 78% in women) was attributable to these five modifiable risk factors. Conclusions:HBV, HCV, aflatoxin, alcohol drinking and tobacco smoking were responsible for 86% of liver cancer mortalityand incidence in China in 2005. Our findings provide useful data for developing guidelines for liver cancerprevention and control in China and other developing countries.     

The population impact of familial cancer,a major cause of cancer

The population attributable fraction (PAF) defines the proportion of a disease that would be prevented if the exposure to a particular risk factor was avoided. Familial risk is a known risk factor for many cancers, but an unbiased estimation of the PAF for familial risk requires a large study population to include rare cancers. PAFs and their corresponding standardized incidence ratios (SIRs) were calculated for familial relative risk among first‐degree relatives (FDRs) and second‐degree relatives (SDRs) diagnosed with the same (concordant) invasive or in situ cancers. Calculations were based on the Swedish Family‐Cancer Database considering 8,148,737 individuals. To assess environmental effects, PAFs were also calculated for concordant cancers among spouses. Almost all cancers showed a significant familial risk. The highest PAFs were found for the common cancers of the prostate (13.94%), breast (7.46%) and colorectum (6.78%) among the FDRs. In the FDRs, the overall PAF for any concordant cancer was 4.20%, but in the SDRs, it was only 0.34%. The overall PAFs for in situ cancers were 0.86% and 0.56% for the FDRs and SDRs, respectively. The overall independent familial PAF was 5.96% for the invasive and in situ cancers in the FDRs and SDRs. The cancers between spouses yielded an overall PAF of 0.14%. For esophageal cancer, the risk among spouses was higher than the familial risk. Our study shows that the overall familial PAF of 5.96%, although underestimated for sex‐specific cancers, ranks as the third most common population burden after tobacco smoking and unhealthy diet.     

How many cancer cases and deaths are potentially preventable? Estimates for Australia in 2013

Cancer is a leading cause of disease burden in Australia, particularly fatal burden, accounting for an estimated thirty percent of deaths. Many cancers develop because of exposure to lifestyle and environmental factors that are potentially modifiable. We aimed to quantify the proportions and numbers of cancer deaths and cases in Australia in 2013 attributable to 20 modifiable factors in eight broad groupings that are established causes of cancer, namely: tobacco smoke (smoking and second‐hand), dietary factors (low intake of fruit, non‐starchy vegetables and dietary fibre; and high intake of red and processed meat), overweight/obesity, alcohol, physical inactivity, solar ultraviolet radiation, infections (seven agents), and reproductive factors (lack of breastfeeding, menopausal hormone therapy use, combined oral contraceptive use). We estimated population attributable fractions (PAF) using standard formulae incorporating exposure prevalence and relative risk data. Of all cancer deaths in Australia in 2013, approximately 38% overall (males 41%, females 34%) could be attributed to the factors assessed; the corresponding PAF for cancer cases was 33% (males 34%, females 32%). Tobacco smoke was the leading cause of cancer deaths and cases, with PAFs of 23 and 13%, respectively, followed by dietary factors (5% deaths/5% cases), overweight/obesity (5%/4%) and infections (5%/3%). Cancer sites with the highest numbers of potentially preventable deaths/cases were lung (n = 6,776/9,272), colorectum (n = 1,974/7,380) and cutaneous melanoma (n = 1,390/7,918). We estimate that about 16,700 cancer deaths and 41,200 cancer cases could be prevented in Australia each year if people's exposures to 20 causal factors were aligned with levels recommended to minimise cancer risk.