美国吸烟者与非吸烟者肺癌流行病学概况

人们已清楚知道，吸烟是肺癌的主要危险因素，也知道吸烟和职业暴露以外的因素在某些肺癌特别是腺癌中起作用。本文以医院病例为基础进行大样本的病冽对照研究来分析肺癌与吸烟因素（吸烟量，过滤咀烟，黑白人种的吸烟习惯）及非吸烟因素（ＥＴＳ暴露，原发性肿瘤和治疗，生殖和内分泌因素，躯体指数）的联系。虽然吸烟与所有主要细胞类型的肺癌都有剂量－效应关系，但与腺癌的联系强度较弱，提示吸烟以外的因素对腺癌的重要性。在白人和黑人中，无论男、女，肺癌的ＯＲ值均随香烟焦油摄入量的增加而增加，并随戒烟年限的延长而减少。是否吸含薄荷香烟，对肺癌的危险性影响不大。未见到ＥＴＳ与肺癌的联系，即使丈夫吸烟也未能使不吸烟妻子患肺癌的危险性增加。生殖系统原发性肿瘤和放射治疗，可使不吸烟女性患肺癌的危险性增加４倍。曾观察到身体瘦弱与现在吸烟、以前吸烟和从不吸烟的女性肺癌之间的联系。以上结果在本文中分别加以讨论。总的来说，人群中肺癌患病率的不同，可能由于：（１）香烟烟雾中的致癌物不同；（２）香烟烟雾的作用因素不同，包括受到机体敏感性及对致癌物的代谢的影响；（３）暴露于吸烟以外的其他各种危险因素     

The roles of smoking and cooking emissions in lung cancer risk among Chinese women in Hong Kong

BackgroundWe conducted this case–control study to evaluate smoking effect on lung cancer conditional on the level of exposure to cooking emissions and to explore whether there is a joint effect of these two risk factors.Subjects and methodsWe selected 279 newly diagnosed primary lung cancer cases and 322 community controls from Hong Kong females, frequency matched by age group, and collected relevant data. We applied logistic regression to estimate lung cancer risk related to smoking and cooking fume exposure, expressed as total cooking dish-years, while adjusting for various potential confounding factors.ResultsCurrent smoking was associated with four-fold increased risk, and ex-smoking with two-fold risk, which was not much influenced by cooking dish-years. No increased risk was observed in environmental tobacco smoking. Increasing intakes of yellow/orange vegetables and multivitamins were significant protective factors in all models. In the analysis of joint effect, the combination of smoking and cooking dish-years tended to have a greater risk than exposure to cooking fumes alone. There was a dose–response gradient with total dish-years in nonsmokers, but not in smokers. Smoking was more strongly associated with nonadenocarcinoma, whereas exposure to cooking fumes appeared to be related to both adenocarcinoma and nonadenocarcinoma.ConclusionWe confirmed the important roles of smoking and cooking emissions in lung cancer risk among the women. These two major risk factors appeared to act independently.     

Risk factors associated with lung cancer in Hong Kong

The purpose of this study was to investigate the risk factors associated with lung cancer in Hong Kong. Three hundred and thirty-one histologically or cytologically proven consecutive cases of lung cancer and the same number of in- and out-patients without cancer matched for age and sex were recruited for this study using a detailed questionnaire completed by a trained interviewer. Smoking was the most important risk factor associated with lung cancer but the attributable risk (AR) was estimated to be 45.8% in men and 6.2% in women, considerably lower compared with those estimated in early 1980s. In addition, among women, exposure to environmental tobacco smoke (ETS) at work+/-at home and lack of education, were independent risk factors for lung cancer with adjusted odds ratio (OR) 3.60, (95% confidence interval (CI) 1.52-8.51) and OR 2.41 (95% CI 1.27-4.55), respectively. Among men, exposure to insecticide/pesticide/herbicide, ETS exposure at work or at home, and a family history of lung cancer and were independent risk factors with adjusted OR 3.29 (95% CI 1.22-8.9, OR 2.43, 95% CI 1.24-4.76 and OR 2.37, 95% CI 1.43-3.94, respectively). Exposure to incense burning and frying pan fumes were not significant risk factors in both sexes. A moderate or high consumption of fat in the diet was associated with increased risk in men but decreased risk in women. The results of this study suggested that as the prevalence of smoking declined, the influence of smoking as a risk factor for lung cancer decreased even further. Moreover, the contribution of other environmental, occupational and socioeconomic factors may be more apparent as etiological factors for lung cancer in a population with relatively high lung cancer incidence but low AR from active smoking.     

Case‐control study of cumulative cigarette tar exposure and lung and upper aerodigestive tract cancers

The development of comprehensive measures for tobacco exposure is crucial to specify effects on disease and inform public health policy. In this population‐based case‐control study, we evaluated the associations between cumulative lifetime cigarette tar exposure and cancers of the lung and upper aerodigestive tract (UADT). The study included 611 incident cases of lung cancer; 601 cases of UADT cancers (oropharyngeal, laryngeal and esophageal cancers); and 1,040 cancer‐free controls. We estimated lifetime exposure to cigarette tar based on tar concentrations abstracted from government cigarette records and self‐reported smoking histories derived from a standardized questionnaire. We analyzed the associations for cumulative tar exposure with lung and UADT cancer, overall and according to histological subtype. Cumulative tar exposure was highly correlated with pack‐years among ever smoking controls (Pearson coefficient = 0.90). The adjusted odds ratio (95% confidence limits) for the estimated effect of about 1 kg increase in tar exposure (approximately the interquartile range in all controls) was 1.61 (1.50, 1.73) for lung cancer and 1.21 (1.13, 1.29) for UADT cancers. In general, tar exposure was more highly associated with small, squamous and large cell lung cancer than adenocarcinoma. With additional adjustment for pack‐years, positive associations between tar and lung cancer were evident, particularly for small cell and large cell subtypes. Therefore, incorporating the composition of tobacco carcinogens in lifetime smoking exposure may improve lung cancer risk estimation. This study does not support the claim of a null or inverse association between “low exposure” to tobacco smoke and risk of these cancer types.     

Serum alpha-tocopherol and subsequent risk of lung cancer among male smokers.

BACKGROUND: Higher blood levels of alpha-tocopherol, the predominant form of vitamin E, have been associated in some studies with a reduced risk of lung cancer, but other studies have yielded conflicting results. To clarify this association, we examined the relationship between prospectively collected serum alpha-tocopherol and lung cancer in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study cohort. METHODS: The ATBC Study was a randomized, clinical trial of 29 133 white male smokers from Finland who were 50-69 years old and who had received alpha-tocopherol (50 mg), beta-carotene (20 mg), both, or neither daily for 5-8 years. Data regarding medical histories, smoking, and dietary factors were obtained at study entry, as was a serum specimen for baseline alpha-tocopherol determination. alpha-Tocopherol measurements were available for 29 102 of the men, among whom 1144 incident cases of lung cancer were diagnosed during a median observation period of 7.7 years. The association between alpha-tocopherol and lung cancer was evaluated with the use of multivariate proportional hazards regression. RESULTS: A 19% reduction in lung cancer incidence was observed in the highest versus lowest quintile of serum alpha-tocopherol (relative risk = 0.81; 95% confidence interval = 0. 67-0.97). There was a stronger inverse association among younger men (<60 years), among men with less cumulative tobacco exposure (<40 years of smoking), and possibly among men receiving alpha-tocopherol supplementation. CONCLUSIONS: In the ATBC Study cohort, higher serum alpha-tocopherol status is associated with lower lung cancer risk; this relationship appears stronger among younger persons and among those with less cumulative smoke exposure. These findings suggest that high levels of alpha-tocopherol, if present during the early critical stages of tumorigenesis, may inhibit lung cancer development.     

大厂锡矿肺癌高发原因的条件Logistic回归分析

An increased risk of lung cancer in Dachang Tin Mine of Guangxi has been reported. To investigate the factors of the excessive risk of lung cancer, the authors conducted a matched pair case-control study in the mine area and analysed the effect of multiple factors, such as condition of living and housing, occupational exposure and smoking by statistical method of conditional logistic regression. The patients group consisted of 69 patients with primary bronchogenic cancer including 55 deceased. The control group consisted of 138 persons also including 55 deceased. The results showed that the factors of the excessive risk of lung cancer in the mine area were mainly related to the occupational exposure. The risk factors with statistical significance in conditional logistic regression analysis were exposure time of smelting, time of underground drilling, and age of beginning mining underground. In the study model of all cases matched against living controls, daily number of cigarette also was a risk factor besides the above three factors. Furthermore, there was a synergic action among the factors. The relationship between the risk factors and lung cancer is discussed.     

Interaction of XRCC1 and XPD Gene Polymorphisms with Lifestyle and Environmental Factors Regarding Susceptibility to Lung Cancer in a High Incidence Population in North East India

Background: This study aimed to explore the role of XRCC1 (Arg399Gln) and XPD (Lys751Gln) genepolymorphisms, lifestyle and environmental factors as well as their possible interactions in propensity to developlung cancer in a population with high incidence from North East India. Materials and Methods: A total of 272lung cancer cases and 544 controls were collected and XRCC1 (Arg399Gln) and XPD (Lys751Gln) genotypes wereanalyzed using a polymerase chain reaction based restriction fragment length polymorphism assay. Conditionalmultiple logistic regression analysis was used to calculate adjusted odds ratios and 95% confidence intervalsafter adjusting for confounding factors. Results: The combined Gln/Gln genotype of XRCC1 and XPD genes(OR=2.78, CI=1.05-7.38; p=0.040) was significantly associated with increased risk for lung cancer. Interactionof XRCC1Gln/Gln genotype with exposure of wood combustion (OR=2.56, CI=1.16-5.66; p=0.020), exposure ofcooking oil fumes (OR=3.45, CI=1.39-8.58; p=0.008) and tobacco smoking (OR=2.54, CI=1.21-5.32; p=0.014) andinteraction of XPD with betel quid chewing (OR=2.31, CI=1.23-4.32; p=0.009) and tobacco smoking (OR=2.13,CI=1.12-4.05; p=0.022) were found to be significantly associated with increased risk for lung cancer. Conclusions:Gln/Gln alleles of both XRCC1 and XPD genes appear to amplify the effects of household exposure, smokingand betel quid chewing on lung cancer risk in the study population.     

Indoor tobacco smoke pollution. A major risk factor for both breast and lung cancer?

Among 51 countries, those having high mortality rates for male lung cancer generally have high rates for female breast cancer (highest in England, Scotland, and the Netherlands). Conversely, those having low rates for one disease have low rates for both (P less than 0.001). Mortality rates available for 23 of the countries for 1954, 1964, and 1974 show a constant relationship of the female breast cancer rate, y = 13.3 + 0.17x (where x is the male lung cancer rate). Where data on 1950 tobacco consumption are available (20 countries), an even closer relationship with female breast cancer mortality in 1974 is observed. Because women in many of these countries account for only a small fraction of the tobacco consumption, the conclusion is that the risk of the female disease is closely related to the extent of male smoking. Thus, breast cancer is apparently initiated by the involuntary inhalation of indoor tobacco smoke for more than two decades on the average before diagnosis. The same relationship between female breast and male lung cancer is found in incidence rates for 80 populations of five continents, including northern and western populations of the US. Trends in age-adjusted breast cancer incidence rates rose almost 50% in many of these populations from 1950 to 1975. This increase corresponds to a tripling of cigarette consumption in the US from 1927 to 1952. There is a strong need to analyze passive smoking more than two decades before diagnosis as a confounding variable in all studies of other risk factors for breast cancer such as alcohol, dietary fat, and endogenous or exogenous estrogen. Comparison of incidence rates for lung cancer and lifetime cigarette consumption in various cultures of Hawaii indicates that even for male smokers, additional exposure to high levels of indoor tobacco smoke greatly increases their risk of lung cancer. This brings the safety of designated smoking areas into serious question.     

Passive smoking and lung cancer in Chandigarh, India.

The aim of this study is to assess the relationship between exposure to environmental tobacco smoke (ETS) and lung cancer in non-smokers, a case-control study among lifetime non-smokers was conducted in Chandigarh, India. Cases consisted of 58 non-smoking histologically confirmed lung cancer patients; two controls for each case were selected, one among other patients admitted to the wards and one among the visitors to hospital patients. Subjects were asked about ETS exposure from different tobacco products in childhood and in adulthood at home, at the work place and in vehicles. Multivariate logistic regression analysis was used to assess the effects of the ETS exposure variables on lung cancer. Exposure to ETS during childhood was strongly associated with lung cancer (odds ratio (OR) = 3.9; 95% confidence interval (CI) = 1.9-8.2), the effect mostly arising from exposure to cigarettes smoke. The excess risk was observed with either a smoking father or mother. An increasing risk was found with increasing number of smokers and duration of exposure. Restricting the analysis to women produced higher estimates of the risk. No increased risk was found with exposure to a smoking spouse, except for those exposed only to cigarette smoke (OR = 5.1; 95% CI = 1.5-17). A weak association was seen between lung cancer and ETS exposure at the workplace, which increased with the number of years of exposure. Exposure in vehicles also was detected as a risk factor for lung cancer in non-smokers. This study suggests that ETS exposure may be a strong risk factor for lung cancer also in India, a country with low prevalence of smoking and, therefore, low rates of lung cancer. Other studies need to be conducted in similar settings to confirm the role played by ETS exposure early in life in the causation of lung cancer.     

Lung cancer risk in never-smokers: An overview of environmental and genetic factors

Lung cancer is the leading cause of cancer-related mortality globally, accounting for 1.8 million deaths in 2020. While the vast majority are caused by tobacco smoking, 15%−25% of all lung cancer cases occur in lifelong never-smokers. The International Agency for Research on Cancer (IARC) has classified multiple agents with sufficient evidence for lung carcinogenesis in humans, which include tobacco smoking, as well as several environmental exposures such as radon, second-hand tobacco smoke, outdoor air pollution, household combustion of coal and several occupational hazards. However, the IARC evaluation had not been stratified based on smoking status, and notably lung cancer in never-smokers (LCINS) has different epidemiological, clinicopathologic and molecular characteristics from lung cancer in ever-smokers. Among several risk factors proposed for the development of LCINS, environmental factors have the most available evidence for their association with LCINS and their roles cannot be overemphasized. Additionally, while initial genetic studies largely focused on lung cancer as a whole, recent studies have also identified genetic risk factors for LCINS. This article presents an overview of several environmental factors associated with LCINS, and some of the emerging evidence for genetic factors associated with LCINS. An increased understanding of the risk factors associated with LCINS not only helps to evaluate a never-smoker’s personal risk for lung cancer, but also has important public health implications for the prevention and early detection of the disease. Conclusive evidence on causal associations could inform longer-term policy reform in a range of areas including occupational health and safety, urban design, energy use and particle emissions, and the importance of considering the impacts of second-hand smoke in tobacco control policy.     

Risk factors for lung cancer in Iowa women: implications for prevention

BACKGROUND: Multiple risk factors possibly associated with lung cancer were examined as part of a large-scale residential radon case-control study conducted in Iowa between 1994 and 1997. We were particularly interested in stratifying risk factors by smoking status. Relatively little risk factor information is available for Midwestern rural women. METHODS: Four hundred thirteen female lung cancer cases and 614 controls aged 40-84, who were residents of their current home for at least 20 years, were included. Risk factors examined included cigarette smoking, passive smoking, occupation, chemical exposure, previous lung disease, family history of cancer, and urban residence. Multiple logistic regression analysis was conducted after adjusting for age, education, and cumulative radon exposure. RESULTS: As expected, active cigarette smoking was the major risk factor for lung cancer. While cessation of smoking was significantly associated with a reduced risk for lung cancer, the risk remained significantly elevated for 25 years. Among all cases, asbestos exposure was a significant risk. Among ex-smokers, pack-year history predominated as the major risk. Among never smokers, a family history of kidney or bladder cancer were significant risk factors (OR=7.34, 95% CI=1.91-28.18; and OR=5.02, 95% CI=1.64-15.39, respectively), as was a history of previous lung disease (OR=2.28, 95% CI=1.24-4.18) and asbestos exposure. No statistically significant increase in lung cancer risk was found for occupation or urban residence. CONCLUSIONS: Smoking prevention activities are urgently needed in rural areas of the United States. Relatives of individuals with smoking-related cancers are potentially at increased risk. Genetic risk factors should be more fully investigated in never smokers.     

Smoking and Passive Smoking in Relation to Lung Cancer in Women

in a population based case-control study the association between female lung cancer and some possible etiological agents was investigated; 210 incident cases in Stockholm county, Sweden, and 209 age-matched population controls were interviewed about their exposure experiences according to a structured questionnaire. A strong association between smoking habits and lung cancer risk was found for all histological subgroups. Relative risks for those who had smoked daily during at least one year ranged between 3.1 for adenocarcinoma to 33.7 for small cell carcinoma in a comparison with never-smokers. All histological types showed strong dose-response relationships for average daily cigarette consumption, duration of smoking, and cumulative smoking. there was no consistent effect of parental smoking on the lung cancer risk in smokers. Only 38 cases had never been regular smokers and the risk estimates for exposure to environmental tobacco smoke were inconclusive. the high relative risks of small cell and squamous cell carcinoma associated with smokmg may have implications for risk assessments regarding passive smoking.     

Lung cancer risk and occupational exposure to meat and live animals

An increased risk of lung cancer has been reported for butchers and meat workers in several cohort studies, although confounding from tobacco smoking could not be ruled out in any of these studies. These exposures, as well as a potential risk associated with contact with live animals, are addressed here in a large case-control study with full adjustment for smoking. More than 5,900 subjects were included in a case-control study conducted in 7 European countries. For each job they employed local experts who assessed the exposure to a number of occupational agents, including (i) meat aerosols and (ii) live animals, on the basis of detailed occupational questionnaires. Information on tobacco consumption and other risk factors was also collected. A small increased risk of lung cancer was observed with exposure to meat aerosols, after adjusting for smoking, (odds ratio (OR)=1.27, 95% confidence interval (CI): 0.92, 1.75), which was most apparent for the upper tertile of cumulative exposure (OR=1.73, 95% CI: 1.03, 2.92). A similar overall effect was observed for exposure to live animals, with an increased risk observed for a high frequency of exposure, (OR=1.69, 95% CI: 1.21, 2.36) and a high intensity of exposure, (OR=1.85, 95% CI: 1.16, 2.94), with significant trends for increasing frequency (p=0.012), intensity (p=0.015) and cumulative exposure (p=0.024). In conclusion, this study provides evidence for an association between exposure to meat aerosols and lung cancer apparent in the highest tertile of exposure. The authors identified a more consistent association with exposure to live animals.     

Tobacco smoking and chewing, alcohol drinking and lung cancer risk among men in southern India

In India, lung cancer is one of the most common and lethal cancers, and tobacco smoking remains its most important etiologic factors. The objective of our study is to examine the effects of different tobacco consumption forms, including smoking and chewing, on lung cancer risk of men in southern India, especially to compare the effects of bidi smoking to cigarette smoking on lung carcinogenesis. We also evaluated the possible role of Indian alcohol beverages and non-Indian alcohol beverages on lung carcinogenesis. We conducted a case-control study in Chennai and Trivandrum. In total, 778 lung cancer cases and 3,430 controls, including 1,503 cancer controls and 1,927 healthy controls, were recruited. The effects of cigarette, bidi smoking, chewing and alcohol drinking on the risk of lung cancer were estimated from unconditional multivariate logistic regression. We also applied the generalized additive model (GAM) with locally-weighted running-line smoothers (loess) to find the most plausible curve for the dose-response relationship. The results from GAM suggest a plateau after 35 years of smoking or 10 cigarette-equivalent pack-years for both cigarette and bidi. The OR is 4.54 (95%CI=2.96-6.95) and 6.45 (95%CI=4.38-9.50) for more than 30 years of cigarette-only and bidi-only smoking, respectively, and 6.87 (95%CI=4.62-10.2) and 10.7 (95%CI=5.82-19.6) for more than 12 weighted cumulative cigarette-only and bidi-only consumption, respectively. The lung cancer risk of former cigarette smokers drops down more quickly after quitting smoking compared to former bidi smokers. There is no evidence for the effect of chewing and lung cancer risk nor clear evidence of an effect of overall alcohol drinking among never-smokers, although Indian alcohol drinking seemed to remain associated with lung cancer risk under limited power (OR=2.67, 95%CI=1.02-7.02). Bidi smoking seems to have a stronger carcinogenic effect than cigarette smoking: this difference holds no matter which aspect of smoking was considered.     

Glutathione pathway genes and lung cancer risk in young and old populations

Multiple enzymes with overlapping functions and shared substrates in the glutathione (GSH) metabolic pathway have been associated with host susceptibility to tobacco smoke carcinogens and in lung cancer etiology. However, few studies have investigated the differing and interacting roles of GSH pathway enzymes with tobacco smoke exposure on lung cancer risk in young (<50 years of age) and old (>80 years of age) populations. Between 1997 and 2001, 237 primary lung cancer patients (170 young, 67 old) and 234 controls (165 young, 69 old) were enrolled at the Mayo Clinic. Using PCR amplification of genomic DNA, polymorphic markers for gammaGCS, GPX1, GSTP1 (I105V and A114V), GSTM1 and GSTT1 were genotyped. Recursive partitioning and logistic regression models were used to build binary classification trees and to estimate odds ratios (OR) and 95% confidence intervals for each splitting factor. For the young age group, cigarette smoking had the greatest association with lung cancer (OR = 3.3). For never smokers, the dividing factors of recursive partitioning were GSTT1 (OR = 1.7), GPX1 (OR = 0.6) and GSTM1 (OR = 4.3). For the old age group, smoking had the greatest association with lung cancer (OR = 3.6). For smokers, the dividing factors were GPX1 (OR = 3.3) and GSTP1 (I105V) (OR = 4.1). Results from logistic regression analyses supported the results from RPART models. GSH pathway genes are associated with lung cancer development in young and old populations through differing interactions with cigarette smoking and family history. Carefully evaluating multiple levels of gene-environment and gene-gene interactions is critical in assessing lung cancer risk.     

Occupational Exposure to Vinyl Chloride, Acrylonitrile and Styrene and Lung Cancer Risk (Europe)

Several industry-based cohort studies have addressed the risk of lung cancer following exposure to vinyl chloride, acrylonitrile and styrene, with inconsistent results and usually without smoking adjustment. These exposures are addressed here in a large case-control study with full adjustment for smoking. Almost 6000 subjects were included in a case-control study conducted in seven European countries. For each job they held, local experts assessed the exposure to a number of occupational agents, including vinyl chloride, acrylonitrile and styrene, on the basis of detailed occupational questionnaires. Information on tobacco consumption and other risk factors was also collected. The odds ratio (OR) for ever exposure to vinyl chloride was 1.05 (95% confidence interval, CI: 0.68-1.62) and a modest, non-significant increase in the risk of lung cancer was found in the highest exposed subgroup. The OR for ever exposure to acrylonitrile was 2.20 (95% CI: 1.11-4.36) with a positive dose-response relationship between estimated cumulative exposure and lung cancer risk. No association between exposure to styrene and lung cancer risk was found. In conclusion, we cannot exclude a weak association between occupational exposure to vinyl chloride and lung cancer risk. Exposure to acrylonitrile was associated in our study with risk of lung cancer. Exposure to styrene does not seem to increase lung cancer risk.     

Epidemiology of lung cancer: smoking, secondhand smoke, and genetics

The link between smoking and development of lung cancer has been demonstrated, not only for smokers but also for those exposed to secondhand smoke. Despite the obvious carcinogenic effects of tobacco smoking, not all smokers develop lung cancer, and conversely some nonsmokers can develop lung cancer in the absence of other environmental risk factors. A multitude of genetic factors are beginning to be explored that interact with environmental exposure to alter the risk of developing this deadly disease. By more fully appreciating the complex interrelationship between genetics and other risks the development of lung cancer can be more completely understood.     

Nonsmoking-related arylamine exposure and bladder cancer risk.

Roughly one-half of bladder cancer incidence in the United States can be attributed to known causes, mainly cigarette smoking, and it has been hypothesized that the aromatic amines in tobacco smoke are important etiological agents. Nonsmokers are also exposed, through unknown sources, to many of the same carcinogenic aromatic amines that are present in cigarette smoke. Previous epidemiological studies have not tested whether either of these aromatic amine exposures are associated with cancer risk. We conducted a population-based case-control study in Los Angeles County, California, involving 761 case patients with bladder cancer and 770 individually matched control subjects. In-person interviews provided information on tobacco smoking and other potential risk factors. Quantitative analysis of hemoglobin adducts of 4- and 3-aminobiphenyl (ABP) was used to assess aromatic amine exposure. Adducts of both aminobiphenyls were significantly higher in cases than in controls, independent of cigarette smoking at the time of blood collection and lifetime smoking history. Adjustment for other risk factors as well as for metabolic differences did not materially alter the associations. Our findings strengthen the connection between exposure to aromatic amines in tobacco smoke and cigarette smoking-related bladder cancer and suggest that environmental exposure to arylamines may account for a significant proportion of nonsmoking-related bladder cancer in the general population.     

What proportion of lung cancer in never-smokers can be attributed to known risk factors?

Though tobacco smoking is the primary risk factor for lung cancer, a significant fraction of lung cancer deaths occur in lifetime nonsmokers. In this article, we calculate the burden of lung cancer in never-smokers attributable to previously identified risk factors in North America, Europe and China, using population-based estimates of exposure prevalence and estimates of relative risk derived from recently published meta-analyses. Population attributable fractions (PAFs) for individual risk factors ranged from 0.40 to 19.93%. Because of differences in the prevalence of exposures, the PAFs associated with several of the risk factors varied greatly by geographical region. Exposure to the selected risk factors appeared to explain a much larger proportion of lung cancer cases in never-smokers in China than in Europe and North America. Our results demonstrate the geographic variability of the epidemiology of lung cancer in never-smokers and highlight the need for further research in this area, particularly in Europe and North America.     

Squamous and small cell carcinomas of the lung: similarities and differences concerning the role of tobacco smoking

In the time period 1988-2000, a case-case study on environmental factors and lung cancer risk was conducted in Montevideo, Uruguay. This study was designed in order the establish possible differences between squamous cell carcinomas (SCC) and small cell carcinomas (SCLC) of the lung in relation to tobacco smoking. Three hundred and ninety one (391) patients with small cell carcinoma were compared with 1187 patients with squamous cell carcinoma. Regarding sex, the study included a small number of women (26 with SCLC and 20 with SCC). SCLC was associated with higher risks for smoking status, smoking intensity and cumulative exposure to tobacco smoking when compared with SCC. These three tobacco variables were significantly different between both cell types in men. Smoking duration was significantly higher among SCLC compared with SCC only in women. With decreasing age at starting to smoke, the proportion of SCLC increases at the expense of SCC. Finally, types of tobacco and cigarette were not different between cell types in both sexes. It should be noted that these tobacco variables were not associated with increased risks among SCC, when this cell type was compared with SCLC. These results suggests that SCLC display the strongest relation with tobacco smoking than SCC.