Penile cancer: is there an epidemiological role for smoking and sexual behaviour?

A retrospective study was carried out to determine whether penile cancer, like cervical cancer, was associated with smoking and sexual behaviour. Altogether 244 men with penile cancer and 232 matched controls completed a questionnaire by post or telephone. Data on marital state, socioeconomic group, occupation, history of phimosis and balanitis, sexual behaviour, and smoking were obtained. The results of statistical analyses confirmed that phimosis and balanitis were risk factors for penile cancer, but there was no epidemiological evidence for it being a sexually transmitted disease. Smoking was a risk factor with a dose-response relation and remained associated with penile cancer even after adjustment for confounding factors. Penile cancer is associated with smoking independently of phimosis; treatment of phimosis alone does not remove the risk caused by smoking.     

Pancreatic cancer risk in relation to sex,lifestyle factors,and pre-diagnostic anthropometry in the Malmö Diet and Cancer Study

Background

Lifestyle factors may influence the risk of developing pancreatic cancer. Whereas cigarette smoking is an established risk factor, the effects of high alcohol intake and obesity are more uncertain. The aim of the present study was to examine the associations of pre-diagnostic anthropometry, alcohol consumption, and smoking habits with pancreatic cancer risk in a Swedish prospective, population-based cohort, with particular reference to potential sex differences.

Methods

The studied cohort consists of 28,098 participants, including all incident cases of pancreatic cancer, in the Malmö Diet and Cancer Study up until December 31, 2013 (n?=?163). Non-parametric and chi-squared tests were applied to compare the distribution of risk factors between cases and non-cases. Cox regression proportional hazards models were used to estimate the relationship between investigative factors and pancreatic cancer risk. Anthropometric factors included height, weight, body mass index (BMI), waist and hip circumference, waist-hip ratio (WHR), and body fat percentage.

Results

BMI was not a significant risk factor for pancreatic cancer, but a higher WHR was significantly associated with an increased risk in the entire cohort (hazard ratio (HR) 2.36, 95% confidence interval (CI) 1.28–4.35, p for trend?=?0.009). Regular smoking was a significant risk factor among both women (HR 2.62, 95% CI 1.61–4.27) and men (HR 3.57, 95% CI 1.70–7.47), whereas occasional smoking was a significant risk factor only in women (HR 3.29, 95% CI 1.50–7.19). Passive smoking at work for >20 years was significantly associated with an increased risk in the entire cohort (HR 1.73, 95% CI 1.15–2.58) and in women selectively (HR 2.01, 95% CI 1.21–3.31). Alcohol consumption was not a significant risk factor. A significant interaction was found between female sex and age (p?=?0.045), but no other factor, in relation to pancreatic cancer risk.

Conclusions

WHR was the only pre-diagnostic anthropometric factor associated with pancreatic cancer risk, with no sex-related differences. Regular smoking was confirmed as a significant risk factor in both sexes, whereas occasional and passive smoking were significant risk factors only in women. Despite the lack of a significant interaction between smoking and sex in relation with pancreatic cancer risk, potential sex differences should be considered in future epidemiological studies.

     

吸烟与癌症相关性的研究进展

研究肿瘤的易感性对理解认识肿瘤发生发展及诊断治疗都有重要意义,遗传危险因素与环境危险因素的相互作用决定了人体部分器官癌症的易感性。研究表明吸烟与肿瘤的发生发展密切相关。本文综述了基因多态性和吸烟协同促癌作用和机制,吸烟通过激活自噬等信号通路促进癌症发生、侵袭和转移及与癌症预后相关性的研究进展。     

Effects of passive smoking on breast cancer risk in pre/post-menopausal women as modified by polymorphisms of PARP1 and ESR1

Objectives

The association between passive smoking and breast cancer risk differs in pre- and post-menopausal women. We aimed to explore the modification effects of PARP1 rs1136410 and ESR1 rs2234693 on the association between passive smoking and breast cancer risk among pre- and post-menopausal women.

Design and methods

A case–control study of 839 breast cancer cases and 863 controls was conducted. The gene–environment interactions were tested after adjusting for potential breast cancer risk factors with unconditional logistic regression models.

Results

We found that the effect of passive smoking was modified by the genotypes in both pre- and post-menopausal women, but in opposite directions. The combination of the TC/CC genotypes of ESR1 rs2234693 and passive smoking significantly increased the risk of breast cancer [OR (95%CI): 2.06 (1.39–3.05)] in pre-menopausal women. A significant association was observed between TT genotype and passive smoking [OR (95%CI): 2.40 (1.27–4.53)] in postmenopausal women. For PARP1 rs1136410, similar differential associations were observed, but the interactions were not significant.

Conclusions

These results imply that the risk of breast cancer from passive smoking may be influenced by genetic factors, and that the association may differ depending on menopausal status.     

Proportion of cancer cases and deaths attributable to lifestyle risk factors in Brazil

BackgroundLifestyle risk factors (tobacco smoking, alcohol consumption, overweight and obesity, unhealthy diet, and lack of physical activity) have been associated with increased risk of at least 20 types of cancer. We estimated the proportion of cancer cases and deaths that could be potentially avoided by eliminating or reducing lifestyle risk factors in Brazil.MethodsWe obtained the distribution of lifestyle risk factors by sex and age groups from recent representative health surveys in Brazil; relative risks from pooled analyses of prospective studies and meta-analyses; and cancer cases and deaths in 2012 from GLOBOCAN.ResultsWe found that 26.5% (114,497 cases) of all cancer cases and 33.6% (63,371 deaths) of all cancer deaths could be potentially avoided by eliminating lifestyle risk factors in Brazil. Plausible reductions in these exposures based on policy targets and cancer prevention recommendations could have potentially avoided 4.5% (19,731 cases) and 6.1% (11,480 deaths) of all cancer cases and deaths, respectively. Tobacco smoking accounted for most of the preventable cancer cases and deaths, followed by high body mass index and alcohol consumption. Larynx, lung, oropharynx, esophagus and colorectum cancer cases and deaths could be at least halved by eliminating these lifestyle risk factors.ConclusionFindings from this study may be useful to inform strategies for cancer prevention and control across Brazil.     

The Fraction of Cancer Attributable to Ways of Life,Infections, Occupation,and Environmental Agents in Brazil in 2020

Many human cancers develop as a result of exposure to risk factors related to the environment and ways of life. The aim of this study was to estimate attributable fractions of 25 types of cancers resulting from exposure to modifiable risk factors in Brazil. The prevalence of exposure to selected risk factors among adults was obtained from population-based surveys conducted from 2000 to 2008. Risk estimates were based on data drawn from meta-analyses or large, high quality studies. Population-attributable fractions (PAF) for a combination of risk factors, as well as the number of preventable deaths and cancer cases, were calculated for 2020. The known preventable risk factors studied will account for 34% of cancer cases among men and 35% among women in 2020, and for 46% and 39% deaths, respectively. The highest attributable fractions were estimated for tobacco smoking, infections, low consumption of fruits and vegetables, excess weight, reproductive factors, and physical inactivity. This is the first study to systematically estimate the fraction of cancer attributable to potentially modifiable risk factors in Brazil. Strategies for primary prevention of tobacco smoking and control of infection and the promotion of a healthy diet and physical activity should be the main priorities in policies for cancer prevention in the country.     

Pre-diagnostic cigarette smoking and risk of second primary cancer: The Melbourne Collaborative Cohort Study

Enhanced survival following a diagnosis of cancer has led to a steep rise in the number of individuals diagnosed with a second primary cancer. We examined the association between pre-cancer cigarette smoking and risk of second cancer in 9785 participants diagnosed with first invasive cancer after enrolment in the Melbourne Collaborative Cohort Study. Follow-up was from date of first invasive cancer until diagnosis of second primary invasive cancer, death, or 31 July 2019, whichever came first. Data on cigarette smoking was collected at enrolment (1990–94) along with information on other lifestyle factors including body size, alcohol intake and diet. We estimated hazard ratios (HR) and 95 % confidence intervals (CI) for incident second cancer with several smoking measures, adjusted for potential confounders. After a mean follow-up of 7.3 years, 1658 second cancers were identified. All measures of smoking were associated with increased risk of second cancer. We observed a 44 % higher risk of second cancer for smokers of ≥ 20 cigarettes/day (HR=1.44, 95 % CI: 1.18–1.76), compared with never smokers. We also observed dose-dependent associations with number of cigarettes smoked (HR=1.05 per 10 cigarettes/day, 95 % CI: 1.01–1.09) and duration of smoking (HR=1.07 per 10 years, 95 % CI: 1.03–1.10). The risk of second cancer increased by 4 % per 10 pack-years of smoking (HR=1.04, 95 % CI: 1.02–1.06; p < 0.001). There was suggestive evidence of stronger associations with number of cigarettes smoked and pack-years of smoking for women (p_interaction<0.05), particularly for the highest risk categories of both variables. These associations with pre-diagnostic smoking were markedly stronger for second cancers known to be smoking-related than for others (p_homogeneity<0.001). Our findings for pre-diagnostic cigarette smoking indicated increased risk of second primary cancer for cancer sites considered smoking-related, highlighting the importance of assessing smoking habits in cancer survivors.     

食管癌调强放疗并发放射性肺损伤的危险因素分析

目的:分析食管癌调强放疗并发放射性肺损伤的危险因素。方法:以2015年2月-2018年2月于青海医学院附属医院接受调强放疗的食管癌患者100例为研究对象。分别收集患者年龄、性别、吸烟史、同步化疗情况、卡氏评分、肿瘤分期等资料以及放射剂量学因素V5、V10、V20、V30、Dmean情况,并采用单因素和多因素Logistic回归分析分析食管癌调强放疗并发放射性肺损伤的危险因素。结果:100例患者中发生放射性肺损伤人数为27例,发生率为27.00%。其中1级20例,2级7例。经单因素分析可得:食管癌调强放疗并发放射性肺损伤与卡氏评分、V5、V10、V20、V30以及Dmean有关(P0.05);与性别、年龄、吸烟史、同步化疗、肿瘤分期无关(P0.05)。经多因素Logistic回归分析可得:卡氏评分80分、V5≥60%、V10≥40%、V20≥25%、V30≥20%、Dmean≥10%均是食管癌调强放疗患者并发放射性肺损伤的独立危险因素(P0.05)。结论:食管癌调强放疗并发放射性肺损伤的发生率较高,且与卡氏评分以及放射剂量学因素V5、V10、V20、V30、Dmean密切相关。临床工作中可通过控制肺组织的照射剂量,减少放射性肺损伤发生风险。     

Polytomous disease mapping to detect uncommon risk factors for related diseases

A statistical model for jointly analysing the spatial variation of incidences of three (or more) diseases, with common and uncommon risk factors, is introduced. Deaths for different diseases are described by a logit model for multinomial responses (multinomial logit or polytomous logit model). For each area and confounding strata population (i.e. age-class, sex, race) the probabilities of death for each cause (the response probabilities) are estimated. A specic disease, the one having a common risk factor only, acts as the baseline category. The log odds are decomposed additively into shared (common to diseases different by the reference disease) and specic structured spatial variability terms, unstructured unshared spatial terms and confounders terms (such as age, race and sex) to adjust the crude observed data for their effects. Disease specic spatially structured effects are estimated; these are considered as latent variables denoting disease-specic risk factors. The model is presented with reference to a specic application. We considered the mortality data (from 1990 to 1994) relative to oral cavity, larynx and lung cancers in 13 age groups of males, in the 287 municipalities of Region of Tuscany (Italy). All these pathologies share smoking as a common risk factor; furthermore, two of them (oral cavity and larynx cancer) share alcohol consumption as a risk factor. All studies suggest that smoking and alcohol consumption are the major known risk factors for oral cavity and larynx cancers; nevertheless, in this paper, we investigate the possibility of other different risk factors for these diseases, or even the presence of an interaction effect (between smoking and alcohol risk factors) but with different spatial patterns for oral and larynx cancer. For each municipality and age-class the probabilities of death for each cause (the response probabilities) are estimated. Lung cancer acts as the baseline category. The log odds are decomposed additively into shared (common to oral cavity and larynx diseases) and specic structured spatial variability terms, unstructured unshared spatial terms and an age-group term. It turns out that oral cavity and larynx cancer have different spatial patterns for residual risk factors which are not the typical ones such as smoking habits and alcohol consumption. But, possibly, these patterns are due to different spatial interactions between smoking habits and alcohol consumption for the first and the second disease.     

Cigarette smoking and risk of second primary cancer: a systematic review and meta-analysis

Approximately 5% of the population are living with a diagnosis of cancer. Recent improvements in survival following a diagnosis of cancer have led to an increase in second primary cancers (SPCs) worldwide. Their aetiology remains largely unknown with a large proportion believed to be related to modifiable lifestyle factors. We conducted a systematic review and meta-analysis of published data that evaluated an association between cigarette smoking and risk of SPC. Studies were identified by searching Medline, Web of Science, CINAHL (Cumulative Index to Nursing and Allied Health Literature) and Scopus databases through March 2021 using broad search criteria. A meta-analysis was performed to derive pooled relative risks (RRs) for SPC defined a priori as smoking-related based on current evidence (lung, upper aero-digestive tract, stomach, pancreas, colorectum, liver, kidney, ureter, bladder and acute myeloid leukaemia). Eleven cohort studies and ten case-control studies met the eligibility criteria for review. There was marked heterogeneity in methods used in terms of classification and timing of smoking, confounders adjusted for and duration of follow-up across the studies. Nine cohort and seven case-control studies classified smoking habits prior to diagnosis of first cancer while the remaining studies classified post-first cancer smoking habits. In a meta-analysis using six studies, an increased risk of smoking-related SPC was observed for both former (RR=1.42; 95% confidence interval (CI) 1.20–1.67) and current smoking (RR=2.76; 95% CI 2.29–3.33), compared with never smoking. The pooled RRs changed only slightly when studies which measured post-first cancer smoking were excluded. A two-fold increase in risk was observed for ever smoking compared with never smoking. In conclusion, there was evidence that smoking might increase the risk of SPC in cancer survivors. For better informed cancer survivorship practice guidelines, more studies are needed particularly of post-cancer smoking and for cancers not known to be caused by smoking.     

The Magnitude of Tobacco Smoking-Betel Quid Chewing-Alcohol Drinking Interaction Effect on Oral Cancer in South-East Asia. A Meta-Analysis of Observational Studies

Tobacco smoking, betel quid chewing and alcohol drinking are oral cancer risk factors. Observational studies unanimously report that oral cancer risk in smoking-drinking-chewing exposed subjects is exceptionally high. However, none of them assessed the fractions of this risk attributable to the three individual risk factors and to the smoking-drinking-chewing interaction. The present study sought to assess the magnitude of the smoking-drinking-chewing interaction effect on oral cancer. A meta-analysis of observational South-East Asian studies which reported oral cancer odds ratios (ORs) stratified for smoking-drinking-chewing exposures was performed. The pooled ORs were estimated and controlled for quality, heterogeneity, publication bias and inclusion criteria. The smoking-drinking-chewing interaction effect was estimated through the pooled Relative Excess Risk due to Interaction (RERI, excess risk in smoking-drinking-chewing exposed individuals with respect to the risk expected from the addition of the three individual risks of smoking, drinking and chewing). Fourteen studies were included with low between-study heterogeneity. The pooled ORs for smoking, drinking, chewing, smoking-drinking-chewing, respectively were 3.6 (95% confidence interval −95% CI, 1.9–7.0), 2.2 (95% CI, 1.6–3.0), 7.9 (95% CI, 6.7–9.3), 40.1 (95% CI, 35.1–45.8). The pooled RERI was 28.4 (95% CI, 22.9–33.7). Among smoking-drinking-chewing subjects, the individual effects accounted for 6.7% (smoking), 3.1% (drinking), 17.7% (chewing) of the risk, while the interaction effect accounted for the remaining 72.6%. These data suggest that 44,200 oral cancer cases in South-East Asia annually occur among smoking-drinking-chewing exposed subjects and 40,400 of these are exclusively associated with the interaction effect. Effective oral cancer control policies must consider concurrent tobacco smoking, alcohol drinking, betel quid chewing usages as a unique unhealthy lifestyle.     

Non-smoking wives of heavy smokers have a higher risk of lung cancer: a study from Japan.

In a study in 29 health centre districts in Japan 91 540 non-smoking wives aged 40 and above were followed up for 14 years (1966-79), and standardised mortality rates for lung cancer were assessed according to the smoking habits of their husbands. Wives of heavy smokers were found to have a higher risk of developing lung cancer and a dose-response relation was observed. The relation between the husband''s smoking and the wife''s risk of developing lung cancer showed a similar pattern when analysed by age and occupation of the husband. The risk was particularly great in agricultural families when the husbands were aged 40-59 at enrolment. The husbands'' smoking habit did not affect their wives'' risk of dying from other disease such as stomach cancer, cervical cancer, and ischaemic heart disease. The risk of developing emphysema and asthma seemed to be higher in non-smoking wives of heavy smokers but the effect was not statistically significant. The husband''s drinking habit seemed to have no effect on any causes of death in their wives, including lung cancer. These results indicate the possible importance of passive or indirect smoking as one of the causal factors of lung cancer. They also appear to explain the long-standing riddle of why many women develop lung cancer although they themselves are non-smokers. These results also cast doubt on the practice of assessing the relative risk of developing lung cancer in smokers by comparing them with non-smokers.     

High-risk Population for Gastric Cancer Development Based on Serum Pepsinogen Status and Lifestyle Factors

Background: Gastric atrophy is a major risk factor for non-cardiac gastric cancer. Serum pepsinogen status could identify people at high-risk for gastric cancer development during our previous cohort study. However, lifestyle-related factors may additionally affect this risk.
Materials and methods: A total of 6983 Japanese were followed up by annual endoscopy in the previous study, and 43 cases of gastric cancer including two cardiac cancers developed. In most subjects, the body length and weight were measured and a questionnaire was applied to gather information regarding life habits. The risk of non-cardiac gastric cancer development during surveillance was re-analyzed based on serum pepsinogen, sex, age, body mass index (BMI), alcohol, and smoking habit.
Results: A total of 6158 subjects with 37 non-cardiac gastric cancer development (male/female = 4259/1899, mean age = 49.0, mean follow-up period = 4.79 years) were entered into analysis. In a multivariate analysis, old age (by 10 years; (odds ratio) OR, 2.8; p  < .001), alcohol (weekly; OR, 2.4; p  = .03), smoking (current; OR, 5.6; p  = .006 and past; OR, 3.9; p  = .04), and pepsinogen status ("atrophic"; OR, 6.2; p  < .001) were independent risk factors, whereas BMI was not. The annual incidence of gastric cancer was 1.2% in the older subjects aged ≥ 60 years with "atrophic" pepsinogen status. Moreover, it was as high as 2.9% when they had both alcohol and current smoking habits.
Conclusions: Old age, alcohol, and smoking habits additionally promoted the risk for gastric cancer in subjects with gastric atrophy.     

Are SNP-Smoking Association Studies Needed in Controls? DNA Repair Gene Polymorphisms and Smoking Intensity

Variations in tobacco-related cancers, incidence and prevalence reflect differences in tobacco consumption in addition to genetic factors. Besides, genes related to lung cancer risk could be related to smoking behavior. Polymorphisms altering DNA repair capacity may lead to synergistic effects with tobacco carcinogen-induced lung cancer risk. Common problems in genetic association studies, such as presence of gene-by-environment (G x E) correlation in the population, may reduce the validity of these designs. The main purpose of this study was to evaluate the independence assumption for selected SNPs and smoking behaviour in a cohort of 320 healthy Spanish smokers. We found an association between the wild type alleles of XRCC3 Thr241Met or KLC3 Lys751Gln and greater smoking intensity (OR = 12.98, 95% CI = 2.86–58.82 and OR=16.90, 95% CI=2.09-142.8; respectively). Although preliminary, the results of our study provide evidence that genetic variations in DNA-repair genes may influence both smoking habits and the development of lung cancer. Population-specific G x E studies should be carried out when genetic and environmental factors interact to cause the disease.     

Radon, smoking and lung cancer risk: results of a joint analysis of three European case-control studies among uranium miners

A combined analysis of three case-control studies nested in three European uranium miner cohorts was performed to study the joint effects of radon exposure and smoking on lung cancer death risk. Occupational history and exposure data were available from the cohorts. Smoking information was reconstructed using self-administered questionnaires and occupational medical archives. Linear excess relative risk models adjusted for smoking were used to estimate the lung cancer risk associated with radon exposure. The study includes 1046 lung cancer cases and 2492 controls with detailed radon exposure data and smoking status. The ERR/WLM adjusted for smoking is equal to 0.008 (95% CI: 0.004-0.014). Time since exposure is shown to be a major modifier of the relationship between radon exposure and lung cancer risk. Fitting geometric mixture models yielded arguments in favor of a sub-multiplicative interaction between radon and smoking. This combined study is the largest case-control study to investigate the joint effects of radon and smoking on lung cancer risk among miners. The results confirm that the lung carcinogenic effect of radon persists even when smoking is adjusted for, with arguments in favor of a sub-multiplicative interaction between radon and smoking.     

Smoking related cancers and loci at chromosomes 15q25, 5p15, 6p22.1 and 6p21.33 in the Polish population

Genetic factors associated with the risk of smoking related cancers have until recently remained elusive. Since the publication of a genome-wide association study (GWAS) on lung cancer new genetic loci have been identified that appear to be associated with disease risk. In this replication study we genotyped 14 single nucleotide polymorphisms (SNPs) located at the 5p12.3-p15.33, 6p21.3-p22.1, 6q23-q27 and 15q25.1 loci in 874 lung, 450 bladder, 418 laryngeal cancer cases and cancer-free controls, matched by year of birth and sex to the cases. Our results revealed that loci in the chromosome region 15q25.1 (rs16969968[A], rs8034191[G]) and 5p15 (rs402710[T]) are associated with lung cancer risk in the Polish population (smoking status adjusted OR = 1.45, 1.35, 0.77; p ≤ 0.0001, 0.0005, 0.002; 95%CI 1.23-1.72, 1.14-1.59, 0.66-0.91 respectively). None of the other regions analyzed herein were implicated in the risk of lung, bladder or laryngeal cancer. This study supports previous findings on lung cancer but fails to show association of SNPs located in 15q25.1 and 5p15 region with other smoking related cancers like bladder and laryngeal cancer.     

Chromosome 15q25 (CHRNA3-CHRNB4) Variation Indirectly Impacts Lung Cancer Risk in Chinese Males

Introduction

Recently, genome-wide association studies (GWAS) in Caucasian populations have identified an association between single nucleotide polymorphisms (SNPs) in the CHRNA5-A3-B4 nicotinic acetylcholine receptor subunit gene cluster on chromosome 15q25, lung cancer risk and smoking behaviors. However, these SNPs are rare in Asians, and there is currently no consensus on whether SNPs in CHRNA5-A3-B4 have a direct or indirect carcinogenic effect through smoking behaviors on lung cancer risk. Though some studies confirmed rs6495308 polymorphisms to be associated with smoking behaviors and lung cancer, no research was conducted in China. Using a case-control study, we decided to investigate the associations between CHRNA3 rs6495308, CHRNB4 rs11072768, smoking behaviors and lung cancer risk, as well as explore whether the two SNPs have a direct or indirect carcinogenic effect on lung cancer.

Methods

A total of 1025 males were interviewed using a structured questionnaire (204 male lung cancer patients and 821 healthy men) to acquire socio-demographic status and smoking behaviors. Venous blood samples were collected to measure rs6495308 and rs11072768 gene polymorphisms. All subjects were divided into 3 groups: non-smokers, light smokers (1–15 cigarettes per day) and heavy smokers (>15 cigarettes per day).

Results

Compared to wild genotype, rs6495308 and rs11072768 variant genotypes reported smoking more cigarettes per day and a higher pack-years of smoking (P<0.05). More importantly, among smokers, both rs6495308 CT/TT and rs11072768 GT/GG had a higher risk of lung cancer compared to wild genotype without adjusting for potential confounding factors (OR = 1.36, 95%CI = 1.09–1.95; OR = 1.11, 95%CI = 1.07–1.58 respectively). Furthermore, heavy smokers with rs6495308 or rs11072768 variant genotypes have a positive interactive effect on lung cancer after adjustment for potential confounding factors (OR = 1.13, 95%CI = 1.01–3.09; OR = 1.09, 95%CI = 1.01–3.41 respectively). However, No significant associations were found between lung cancer risk and both rs6495308 and rs11072768 genotypes among non-smokers and smokers after adjusting for age, occupation, and education.

Conclusion

This study confirmed both rs6495308 and rs11072768 gene polymorphisms association with smoking behaviors and had an indirect link between gene polymorphisms and lung cancer risk.     

Passive Smoking and Breast Cancer Risk among Non-Smoking Women: A Case-Control Study in China

Background

The role of passive smoking on breast cancer risk was unclear. This study aimed to evaluate the association between passive smoking and breast cancer risk among Chinese women.

Methods/Principal Findings

A hospital-based case-control study, including 877 breast cancer cases and 890 controls, frequency-matched by age and residence, was conducted. A structured questionnaire was used to collect information on passive smoking history through face-to-face interview by trained interviewers. Unconditional logistic regression models were used to estimate the association between passive smoking and breast cancer risk. A positive association between any passive smoking exposure and breast cancer risk was observed. Compared with women who were never exposed to passive smoking, women who were ever exposed had a higher breast cancer risk, with the adjusted odds ratio (OR) and 95% confidence interval (CI) of 1.35 (1.11-1.65). Similar result was found on home passive smoking exposure and breast cancer risk, but not on workplace passive smoking exposure. Women who were ever exposed to tobacco smoke at home had a higher risk of breast cancer compared with never exposed women, with the adjusted OR (95% CI) of 1.30 (1.05-1.61). Home passive smoking exposure showed significant dose-response relationships with breast cancer risk in smoker-years, cigarettes/day and total pack-years (P _trend=0.003, 0.006 and 0.009, respectively). An increased total smoker-years of any passive exposure significantly elevated the risk of breast cancer (P _trend<0.001). Positive associations and dose-response relationships were found among postmenopausal women and all subtypes of estrogen receptor (ER) and progesterone receptor (PR) status of breast cancer.

Conclusions

Passive smoking was associated with an increased risk of breast cancer among non-smoking Chinese women. A stronger positive association with breast cancer risk was seen mainly among postmenopausal women.     

Smoking (active and passive), N-acetyltransferase 2, and risk of breast cancer

Background: The relationship between smoking and breast cancer remains controversial. The study aim was to assess the relationship of passive and active smoking to breast cancer risk by N-acetyltransferase 2 (NAT2) phenotype, using a comprehensive assessment of both passive and active smoking. Methods: We undertook a population-based case–control study in Northeastern Ontario, Canada of 347 women diagnosed (2002–2004) with breast cancer and 775 population-based controls. The mailed study package included a questionnaire requesting information about established breast cancer risk factors, passive and active smoking, and a buccal swab for genetic analyses. Results: Among never-active smokers, a long duration of passive smoking was associated with an increased risk of breast cancer (odds ratio (OR) 1.86 (95% confidence interval (95% CI) 1.01–3.44) (test for trend (p = 0.07)); that risk was more elevated for NAT2 slow acetylators (OR 2.76, 95% CI 1.16–6.59) (and highest in extremely slow acetylators), but not elevated for NAT2 fast acetylators (OR 1.17, 95% CI 0.42–3.23). Among active smokers more than 20 pack-years of smoking was associated with an OR of 1.34 (95% CI 0.92-1.96); more elevated among NAT2 fast acetylators OR 1.93 (95% CI 1.01–3.69) but not elevated among NAT2 slow acetylators. Women who were NAT2 fast acetylators in the highest quartile for duration of active smoking had an OR of 2.74 (95% CI 1.42–5.27), with a significant test of trend (p = 0.005). Conclusions: These findings suggest that passive and active smoking may be related to breast cancer, and the effect may be differentially modified by NAT2 phenotype. Further research into the genetic modification of a breast cancer–smoking relationship may help to reconcile earlier discrepant findings.     

Calculation of the 1995 lung cancer incidence in the Netherlands and Sweden caused by smoking and radon: risk implications for radon

A two-mutation carcinogenesis model was used to calculate the expected lung cancer incidence caused by both smoking and exposure to radon in two populations, i.e. those of the Netherlands and Sweden. The model parameters were taken from a previous analysis of lung cancer in smokers and uranium miners and the model was applied to the two populations taking into account the smoking habits and exposure to radon. For both countries, the smoking histories and indoor radon exposure data for the period 1910-1995 were reconstructed and used in the calculations. Compared with the number of lung cancer cases observed in 1995 among both males and females in the two countries, the calculations show that between 72% and 94% of the registered lung cancer cases may be attributable to the combined effects of radon and smoking. In the Netherlands, a portion of about 4% and in Sweden, a portion of about 20% of the lung cancer cases (at ages 0-80 years) may be attributable to radon exposure, the numbers for males being slightly lower than for females. In the Netherlands, the proportions of lung cancers attributable to smoking are 91% for males and 71% for females; in Sweden, the figures are 70% and 56%, respectively. The risk from radon exposure is dependent on gender and cigarette smoking: the excess absolute risk for continuous exposure to 100 Bq m-3 ranges between 0.003 and 0.006 and compares well with current estimates, e.g. 0.0043 of the International Commission on Radiological Protection (ICRP). The excess relative risk for continuous exposure to 100 Bq m-3 shows a larger variation, ranging generally between 0.1 for smokers and 1.0 for non-smokers. The results support the assumption that exposure to (indoor) radon, even at a level as low as background radiation, causes lung cancer proportional to the dose and is consistent with risk factors derived from the miners data.