Macronutrients, fatty acids, cholesterol and prostate cancer risk.

BACKGROUND: The role of selected macronutrients, fatty acids and cholesterol in the etiology of prostate cancer was analyzed using data from a case-control study carried out in five Italian areas between 1991 and 2002. PATIENTS AND METHODS: Cases were 1294 men with incident, histologically confirmed prostate cancer, and admitted to the major teaching and general hospitals of study areas. Controls were 1451 men admitted for acute, non-neoplastic conditions to the same hospital network. Information on dietary habits was elicited using a validated food frequency questionnaire including 78 food groups and recipes. Odds ratios (OR) and 95% confidence intervals (CI) were estimated for increasing levels of nutrient intake. RESULTS: A direct association with prostate cancer was found for starch intake (OR = 1.4 in the highest versus the lowest quintile of intake; 95% CI: 1.1-1.8), whereas an inverse association emerged for polyunsaturated fatty acids (OR = 0.8; 95% CI: 0.6-1.0). Among polyunsaturated fatty acids, linolenic acid (OR = 0.7; 95% CI: 0.6-0.9) and linoleic acid (OR = 0.8; 95% CI: 0.6-1.0) were inversely related to prostate cancer. When the six major macronutrients were included in the same model, the adverse effect of high intake of starch and monounsaturated fatty acids was statistically significant together with the protective effect of polyunsaturated fatty acids. Results were consistent in separate strata of age, body mass index and family history of prostate cancer. CONCLUSIONS: Starch and monounsaturated fatty acids were directly associated with prostate cancer risk and polyunsaturated fatty acids were inversely associated.     

Energy, macronutrients and laryngeal cancer risk.

BACKGROUND: A role for diet in laryngeal carcinogenesis has been suggested, but only a few studies have examined the potential relationship with a wide variety of macronutrients. PATIENTS AND METHODS: A case-control study was conducted between 1992 and 2000 in Italy and Switzerland, including 527 incident cases of laryngeal cancer, and 1297 controls hospitalized for acute, non-neoplastic conditions. The subjects' usual diet was investigated through a validated food frequency questionnaire, including 78 foods and beverages. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional multiple logistic regression models. RESULTS: Cases reported higher energy intake than controls. The continuous OR for 100 kcal/day was 1.16 (95% CI 1.12-1.21) for alcohol energy, and 1.02 (95% CI 1.01-1.04) for non-alcohol energy. A significantly increased risk of laryngeal cancer was observed for animal protein (continuous OR = 1.21, 95% CI 1.03-1.41), polyunsaturated fats other than linoleic and linolenic fatty acids (OR = 1.43, 95% CI 1.19-1.70), and cholesterol intake (OR = 1.43, 95% CI 1.19-1.71). Laryngeal cancer risk was slightly reduced with increasing vegetable protein (OR = 0.75, 95% CI 0.62-0.91), sugar (OR = 0.84, 95% CI 0.71-1.00) and monounsaturated fatty acid intake (OR = 0.83, 95% CI 0.70-0.99). CONCLUSIONS: Laryngeal cancer cases have a higher energy intake than control subjects, and report a higher intake of animal protein and cholesterol.     

Artificial sweeteners and cancer risk in a network of case-control studies.

BACKGROUND: The role of sweeteners on cancer risk has been widely debated over the last few decades. To provide additional information on saccharin and other sweeteners (mainly aspartame), we considered data from a large network of case-control studies. METHODS: An integrated network of case-control studies has been conducted between 1991 and 2004 in Italy. Cases were 598 patients with incident, histologically confirmed cancers of the oral cavity and pharynx, 304 of the oesophagus, 1225 of the colon, 728 of the rectum, 460 of the larynx, 2569 of the breast, 1031 of the ovary, 1294 of the prostate and 767 of the kidney (renal cell carcinoma). Controls were 7028 patients (3301 men and 3727 women) admitted to the same hospitals as cases for acute, non-neoplastic disorders. Odds ratios (ORs), and the corresponding 95% confidence intervals (CIs), were derived by unconditional logistic regression models. RESULTS: The ORs for consumption of saccharin were 0.83 (95% CI 0.30-2.29) for cancers of the oral cavity and pharynx, 1.58 (95% CI 0.59-4.25) for oesophageal, 0.95 (95% CI 0.67-1.35) for colon, 0.93 (95% CI 0.60-1.45) for rectal, 1.55 (95% CI 0.76-3.16) for laryngeal, 1.01 (95% CI 0.77-1.33) for breast, 0.46 (95% CI 0.29-0.74) for ovarian, 0.91 (95% CI 0.59-1.40) for prostate and 0.79 (95% CI 0.49-1.28) for kidney cancer. The ORs for consumption of other sweeteners, mainly aspartame, were 0.77 (95% CI 0.39-1.53) for cancers of the oral cavity and pharynx, 0.77 (95% CI 0.34-1.75) for oesophageal, 0.90 (95% CI 0.70-1.16) for colon, 0.71 (95% CI 0.50-1.02) for rectal, 1.62 (95% CI 0.84-3.14) for laryngeal, 0.80 (95% CI 0.65-0.97) for breast, 0.75 (95% CI 0.56-1.00) for ovarian, 1.23 (95% CI 0.86-1.76) for prostate and 1.03 (95% CI 0.73-1.46) for kidney cancer. A significant inverse trend in risk for increasing categories of total sweeteners was found for breast and ovarian cancer, and a direct one for laryngeal cancer. CONCLUSION: The present work indicates a lack of association between saccharin, aspartame and other sweeteners and the risk of several common neoplasms.     

Dietary glycemic index, glycemic load and ovarian cancer risk: a case-control study in Italy.

BACKGROUND: Dietary carbohydrates vary in their ability to raise blood glucose and insulin levels, which, in turn, influence levels of sex hormones and insulin-like growth factors. We analyzed the effect of type and amount of carbohydrates on ovarian cancer risk, using the glycemic index (GI) and the glycemic load (GL) measurement in a large case-control study conducted in Italy. MATERIALS AND METHODS: Cases included 1031 women with incident, histologically confirmed epithelial ovarian cancer, from four Italian regions. Controls included 2411 women admitted to the same hospital networks for acute, non-neoplastic conditions. Average daily GI and GL were calculated from a validated food frequency questionnaire. Odds ratios (OR) and the corresponding 95% confidence intervals (CI) were computed using multiple logistic regression. RESULTS: Ovarian cancer was directly associated with dietary GI (OR for highest versus lowest quartile = 1.7, 95% CI 1.3-2.1) and GL (OR = 1.7, 95% CI 1.3-2.1). The associations were observed in pre- and postmenopausal women, and they remained consistent across strata of major covariates identified. CONCLUSIONS: This study supports the hypothesis of a direct association between GI and GL and ovarian cancer risk and, consequently, of a possible role of hyperinsulinemia/insulin resistance in ovarian cancer development.     

Dietary intake of fruit and vegetable and lung cancer risk: a case-control study in Harbin, northeast China.

BACKGROUND: We studied the relationship between dietary intake of vegetables and fruit and lung cancer risk in Harbin, Heilongjiang province, northeast China, an area with a very high baseline risk of lung cancer in both sexes. PATIENTS AND METHODS: We used data from a case-control study, conducted from 1987 to 1990, among 218 cases with incident, histologically confirmed lung cancer and 436 controls admitted to the same hospitals as cases with non-neoplastic, non-lung diseases unrelated to smoking and other potential risk factors for lung cancer. RESULTS: Compared with the lowest tertile of intake of vegetables, fruit or both, the multivariate odds ratios (ORs) for the highest tertile of intake were 0.39 [95% confidence interval (CI) 0.25-0.62], 0.73 (95% CI 0.48-1.11) and 0.40 (95% CI 0.25-0.63), respectively. In particular, high intake of Chinese cabbage (OR = 0.53), chives (OR = 0 .54), carrots (OR = 0.51) and celery (OR = 0.40) was inversely associated with lung cancer. The OR was more than six-fold elevated for smokers reporting low intake of vegetables, and more than four-fold elevated for smokers reporting low intake of fruit, as compared with never smokers reporting high intake of these items. CONCLUSION: In agreement with previous studies, we found an inverse relation between vegetable and fruit intake and lung cancer risk in both strata of current and never smokers.     

Consumption of sweet foods and breast cancer risk in Italy.

BACKGROUND: The relation between the intake of sugar and sweets and the risk of breast cancer has been considered in ecological, prospective and case-control studies, but the results are unclear. We analyzed such a relation in a case-control study conducted between 1991 and 1994 in Italy. PATIENTS AND METHODS: Cases were 2569 women with histologically confirmed incident breast cancer and controls were 2588 women admitted to hospital for acute, non-neoplastic, non-hormone-related conditions. Information on diet was based on an interviewer-administered questionnaire tested for reproducibility and validity. The odds ratios (OR) and 95% confidence intervals (CI) were computed by multiple logistic regression equations. RESULTS: Compared with women with the lowest tertile of intake, women in the highest tertile of intake of desserts (including biscuits, brioches, cakes, puffs and ice-cream) and sugars (including sugar, honey, jam, marmalade and chocolate) had multivariate ORs of 1.19 (95% CI 1.02-1.39) and 1.19 (95% CI 1.02-1.38), respectively. The results were similar in strata of age, body mass index, total energy intake and other covariates. CONCLUSIONS: We found a direct association between breast cancer risk and consumption of sweet foods with high glycemic index and load, which increase insulin and insulin growth factors.     

Fried foods, olive oil and colorectal cancer.

BACKGROUND: The epidemiologic evidence for an etiologic role of fried foods and heterocyclic amines in colorectal carcinogenesis is inconsistent. PATIENTS AND METHODS: We have investigated the relation between fried foods and colorectal cancer risk using data from a large, multicentric case-control study conducted in Italy and Switzerland between 1992 and 2000, with 1394 cases of colon cancer, 886 cases of rectal cancer and 4765 controls. RESULTS: After allowing for major relevant covariates, the multivariate odds ratios (ORs) for an increment of one portion per week of fried foods were 0.97 [95% confidence interval (CI)=0.93-1.01] for colon cancer and 1.04 (95% CI=1.00-1.09) for rectal cancer. When we analyzed the type of fats mainly used for frying, we found that olive oil, but not other types of oils, appeared to protect from colon cancer risk (OR=0.89, 95% CI=0.82-0.98). CONCLUSIONS: Our results do not indicate a relevant role of fried foods on colorectal cancer risk. We found a possible favorable effect of (fried) olive oil on colon cancer risk but not on rectal cancer risk.     

Fibre intake and laryngeal cancer risk.

BACKGROUND: Consumption of vegetables, fruit and whole grain cereals has been inversely related to laryngeal cancer risk. Among the potential protective agents found in these foods, information on dietary fibres and laryngeal cancer risk are scanty. PATIENTS AND METHODS: A multi-centric, hospital-based case-control study was conducted on 527 patients with squamous-cell carcinoma of the larynx and 1,297 non-neoplastic controls. Cases and controls, frequency matched by age, sex and study centre, were interviewed using a validated food frequency questionnaire. RESULTS: Compared with the lowest quintile of fibre intake, the odds ratios (ORs) for the highest quintile were 0.3 [95% confidence interval (CI) 0.2-0.4] for total fibre, 0.3 (95% CI 0.2-0.5) for soluble non-cellulose polysaccharides (NCP) and for total insoluble fibre, including cellulose (OR = 0.3, 95% CI 0.2-0.4) and insoluble NCP (OR = 0.4, 95% CI 0.3-0.7). The ORs were 0.2 (95% CI 0.1-0.4) for fibre from vegetables, 0.5 (95% CI 0.3-0.7) from fruit and 1.1 (95% CI 0.6-1.9) from grains. The inverse association observed was similar among different subsites of laryngeal cancer, and consistent across strata of various covariates. CONCLUSIONS: This study found a strong inverse association between fibre intake and laryngeal cancer risk, which points to fibre as one of the beneficial components of vegetables and fruit.     

Phase II randomized trial of vinorelbine and gemcitabine versus carboplatin and paclitaxel in advanced non-small-cell lung cancer.

BACKGROUND: The purpose of this study was to compare quality of life and overall toxicity in patients with advanced non-small-cell lung cancer (NSCLC) treated with vinorelbine-gemcitabine (VG) or carboplatin-paclitaxel (Taxol) (CP). PATIENTS AND METHODS: A total of 165 previously untreated patients were randomized to the two regimens. Quality of life was assessed by the Lung Cancer Symptom Scale (LCSS). Overall toxicity and secondary efficacy end points were evaluated by standard WHO criteria. RESULTS: There was no significant difference in overall quality of life between the two treatments. Neutropenia, thrombocytopenia, peripheral neuropathy, and alopecia, were more common in the CP arm, whereas constipation was more frequent in the VG arm. Response rates were 14.6% in the VG arm and 16.9% in the CP arm. Median survival times were 7.8 and 8.6 months, and 1 year survival rates were 38.4% and 31.9%, respectively. CONCLUSIONS: Patients treated with VG experienced lower toxicity, but overall quality of life was similar in both arms. Efficacy seemed comparable between VG and CP. Our study shows that VG is a viable alternative to platinum-based chemotherapy in patients with advanced NSCLC.     

Folate intake and risk of oral and pharyngeal cancer.

BACKGROUND: Diet has been recognised as having a role in the aetiology of oral and pharyngeal cancer, and dietary factors may account for 10-15% of cases in Europe. Folate deficiency has been linked to risk of several cancers, but has not been studied adequately with respect to oral cancer. PATIENTS AND METHODS: This case-control study, conducted in Italy and French-speaking Switzerland, included 749 patients with incident cancer of the oral cavity and pharynx, and 1772 hospital controls with acute, non-neoplastic conditions. The interviews used a validated food frequency questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using multiple logistic regression. RESULTS: The ORs were 0.68 (95% CI 0.52-0.88) for the intermediate tertile and 0.53 (95% CI 0.40-0.69) for the highest tertile of dietary folate intake, compared with the lowest tertile. No heterogeneity was found in strata of gender, age, methionine intake or alcohol consumption. The combined OR for low-folate and high-alcohol intake versus high-folate and low-alcohol intake was 22.3 (95% CI 13.1-38). CONCLUSIONS: Our study supports a protective role of folate against oral and pharyngeal carcinogenesis. Compared with low folate intake, a consistent reduction in risk was already observed from intermediate levels of intake, suggesting that cancer risk may be related to relative folate deficiency.     

Cigarette tar yield and risk of upper digestive tract cancers: case-control studies from Italy and Switzerland.

BACKGROUND: Tobacco smoking is one of the main risk factors for oral, pharyngeal and oesophageal cancers in developed countries. Information on the role of the tar yield of cigarettes in upper digestive tract carcinogenesis is sparse and needs to be updated because the tar yield of cigarettes has steadily decreased over the last few decades. PATIENTS AND METHODS: We analysed two case-control studies, from Italy and Switzerland, conducted between 1992 and 1999, involving 749 cases of oral and pharyngeal cancer and 1770 controls, and 395 cases of squamous-cell oesophageal carcinoma and 1066 matched controls. Odds ratios (ORs) were estimated by unconditional multiple logistic regression models, including terms for age, sex, study centre, education and alcohol consumption. RESULTS: Based on the brand of cigarettes smoked for the longest time, the multivariate ORs for current smokers compared with never smokers were 6.1 for <20 mg and 9.8 for >or=20 mg tar for oral and pharyngeal neoplasms, and 4.8 and 5.4 for oesophageal cancer, respectively. For the cigarette brand smoked in the previous six months, the ORs for >or=10 mg compared with <10 mg were 1.9 for cancer of the oral cavity and pharynx and 1.8 for oesophageal cancer, after allowance for number of cigarettes and duration of smoking. CONCLUSIONS: The present study confirms the direct relationship between the tar yield of cigarettes and upper digestive tract neoplasms, and provides innovative information on lower tar cigarettes, which imply reduced risks compared with higher tar ones. However, significant excess risks were observed even in the lower tar category, thus giving unequivocal indications for stopping smoking as a priority for prevention of upper digestive tract neoplasms.     

Smoking,DNA repair capacity and risk of nonsmall cell lung cancer

Tobacco-related carcinogens cause a variety of DNA damage that is repaired by different enzymatic pathways, suggesting that DNA repair plays an important role in tobacco-induced carcinogenesis. In a large hospital-based case-control study, we investigated DNA repair capacity (DRC) as a biomarker for susceptibility to nonsmall cell lung cancer (NSCLC) and evaluated the possible interaction between DRC and tobacco smoke in 467 newly diagnosed NSCLC patients and 488 cancer-free controls. We measured DRC in cultured peripheral lymphocytes using the host-cell reactivation assay with a reporter gene damaged by an activated tobacco carcinogen, benzo[a]pyrene diol epoxide. The results showed that current smokers exhibited the highest DRCs as compared to former and nonsmokers both among patients and control subjects. There were no differences of DRC among 3 different histopathologic types of NSCLC. Logistic regression analysis revealed that suboptimal DRC and pack-years smoked were independent predictors of NSCLC risk. The overall 15.5% reduction in DRC observed in the cases (7.84%) compared to the controls (9.28%) (p<0.001) was associated with an approximately 2-fold increased risk of NSCLC (adjusted odds ratio (OR) = 1.85, 95% confidence interval (CI) 1.42-2.42). There was a significant dose-response association between decreased DRC and increased risk of lung cancer. Furthermore, we observed a nonstatistically significant additive but not multiplicative interaction between DRC and pack-years smoked on lung cancer risk, particularly in the histopathologic types of NSCLC other than adenocarcinoma. The results suggest that suboptimal DRC is associated with increased risk of NSCLC and DRC may modulate the risk of lung cancer associated with smoking but the latter needs to be verified in larger studies.     

Phase I-II study of amrubicin and cisplatin in previously untreated patients with extensive-stage small-cell lung cancer.

BACKGROUND: Amrubicin, a totally synthetic 9-amino-anthracycline, demonstrated excellent single-agent activity for extensive-stage small-cell lung cancer (ED-SCLC). The aims of this trial were to determine the maximum-tolerated doses (MTD) of combination therapy with amrubicin and cisplatin, and to assess the efficacy and safety at their recommended doses (RD). PATIENTS AND METHODS: Eligibility criteria were patients having histologically or cytologically proven measurable ED-SCLC, no previous systemic therapy, an Eastern Cooperative Oncology Group performance status of 0-2 and adequate organ function. Amrubicin was administered on days 1-3 and cisplatin on day 1, every 3 weeks. RESULTS: Four patients were enrolled at dose level 1 (amrubicin 40 mg/m(2)/day and cisplatin 60 mg/m(2)) and three patients at level 2 (amrubicin 45 mg/m(2)/day and cisplatin 60 mg/m(2)). Consequently, the MTD and RD were determined to be at level 2 and level 1, respectively. The response rate at the RD was 87.8% (36/41). The median survival time (MST) was 13.6 months and the 1-year survival rate was 56.1%. Grade 3/4 neutropenia and leukopenia occurred in 95.1% and 65.9% of patients, respectively. CONCLUSIONS: The combination of amrubicin and cisplatin has demonstrated an impressive response rate and MST in patients with previously untreated ED-SCLC.     

Smoking behavior following diagnosis in patients with Stage I non-small cell lung cancer

The cigarette-smoking behavior of 840 patients with resected Stage I non-small cell lung cancer was analyzed prospectively for up to four years following diagnosis. Lung cancer patients were heavier smokers at diagnosis than other cancer patients and the general population. At one year, only 16.8 percent of the 317 current smokers at baseline, who were followed for two years or longer, continued to smoke, while 83.2 percent of patients either quit permanently (53.0 percent) or for some time period (30.2 percent). By two years, permanent cessation stabilized at over 40 percent; however, the prevalence of continuing smoking decreased through all periods of follow-up. Subjects who tried to quit or did quit permanently were more likely to be female and healthier than continuous smokers.This research was supported in part by grants CA 43461, CA-16042, and CA-3417 from the National Cancer Institute.     

Smoking history and survival among lung cancer patients

Two population-based case-control studies of lung cancer were conducred on the Island of Oahu, Hawaii, between 1979 and 1985. Interview information concerning smoking habits and other characteristics was obtained from a total of 463 men and 212 women with histologically confirmed lung cancer. Records from the Hawaii Tumor Registry were revicwed for information on the stage, histology, and follow-up status of these patients. Cigarette smoking was found to be positively related to the age-adjusted risk of death among women (relative risk (RR) -1.6; 95 percent confidence interval (CI)=1.0–2.4), but not among men (RR=0.8; 95 percent CI=0.5–1.2). Among women, the age-adjusted median survival time for never smokers was 33 months (n=53) compared with a median survival of 18 months (n=159) for smokers. Both past and current female smokers were at greater risk of death than never-smokers, and there was a significant trend in the risk of death by the number of cigarettes smoked per day (P=0.04), and the age at which the subjects started smoking (P=0.01). The effects of tumor stage and histology upon the association between tobacco smoking and survival were also explored.Drs Goodman, Kolonel, Wilkins, and Le Marchand are with the Epidemiology Program, Cancer Research Center of Hawaii, University of Hawaii, 1236 Laubela Street, Sulte 407, Honolulu, HI 96813. Dr Yoshizawa was at the Cancer Research Center at the time of the research and now is with Triton Biosciences Inc., Alameda, CA. Address reprint requests to Dr Goodman. This study was supported in part by Public Health Service grants PO1-CA-33619 and RO1-CA-26515, and contract NO1-CN-55424 from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services.     

Gender differences in lung cancer risk by smoking: a multicentre case-control study in Germany and Italy

Several studies in the past have shown appreciably higher lung cancer risk estimates associated with smoking exposure among men than among women, while more recent studies in the USA report just the opposite. To evaluate this topic in a European population we conducted a case-control study of lung cancer in three German and three Italian centres. Personal interviews and standardized questionnaires were used to obtain detailed life-long smoking and occupational histories from 3723 male and 900 female cases and 4075 male and 1094 female controls. Lung cancer risk comparing ever-smokers with never-smokers was higher among men (odds ratios (OR) adjusted for age and centre = 16.1, 95% confidence interval (CI) 12.8-20.3) than among women (OR = 4.2, CI 3.5-5.1). Because the smoking habits of women were different from men, we conducted more detailed analyses using comparable levels of smoking exposure. After restriction to smokers and adjustment for other smoking variables, risk estimates did not differ appreciably between genders. The analysis of duration of smoking (0-19, 20-39, 40+ years) adjusted for cigarette consumption and time since quitting smoking revealed similar risk estimates in men (OR = 1.0, 3.3 [CI 2.6-4.2], 4.1 [CI 3.1-5.6]) and women (OR = 1.0, 2.7 [CI 1.7-4.1], 3.3 [CI 1.9-5.8]). The same was true of the analysis of average or cumulative smoking consumption, and also of analyses stratified by different histological types. We conclude that for comparable exposure to tobacco smoke, the risk of lung cancer is comparable in women and men.     

Lung cancer mortality among silicotic workers in Hong Kong--no evidence for a link.

BACKGROUND: The link between silica dust/silicosis and lung cancer is still very controversial. We examined the relationship between silica dust exposure and/or silicosis and lung cancer in a large cohort of silicotic workers in Hong Kong. PATIENTS AND METHODS: All workers with silicosis in Hong Kong diagnosed during the period 1981-1998 were followed up till the end of 1999 to ascertain their vital status and causes of death. Standardized mortality ratio (SMR) for lung cancer and other major causes of death were calculated. Axelson's indirect method was used to adjust for smoking effect. Multiple Cox regression models were carried out to examine the exposure-response relationship between silica dust and lung cancer. RESULTS: About 10% (86) of all 853 deaths were from lung cancer, giving a SMR of 1.69 [95% confidence interval (CI) 1.35-2.09]. Lung cancer SMR for caisson and surface construction workers were 2.39 (95% CI 1.50-3.62) and 1.61 (95% CI 1.21-2.10), respectively, which became 1.56 (95% CI 0.98-2.36) and 1.09 (95% CI 0.82-1.42) after adjusting for smoking. No consistent exposure-response relationship was detected between silica dust or severity of silicosis and lung cancer death. CONCLUSION: Our cohort study did not offer positive support to a link between silica or silicosis and lung cancer.     

Smoking and liver cancer in China: case-control comparison of 36,000 liver cancer deaths vs. 17,000 cirrhosis deaths

Liver cancer and liver cirrhosis are common causes of death in China, where chronic lifelong hepatitis B infection is a major cause of both diseases. To help determine whether smoking is a cofactor for the development of liver cancer, we ascertained retrospectively the smoking habits of 36,000 adults who had died from liver cancer (cases) and 17,000 who had died from cirrhosis (controls) in 24 Chinese cities and 74 rural counties. Calculations of the smoker vs. nonsmoker risk ratios (RR) for liver cancer mortality were standardised for age and locality. Among adult men (aged 35+) there was a 36% excess risk of death from liver cancer among smokers (smoker vs. nonsmoker standardised risk ratio [RR] =1.36, with 95% confidence interval [CI] 1.29-1.43, 2p<0.00001; attributable fraction 18%). In the general male population this indicates absolute risks of death from liver cancer before age 70 of about 4% in smokers and 3% in nonsmokers (in the absence of other causes). Most liver cancer, however, occurs among the 10-12% of men with haematological evidence of chronic hepatitis B infection, so among them the corresponding risks would be about 33% in smokers and 25% in nonsmokers. The RR was approximately independent of age, was similar in urban and rural areas, was not significantly related to the age when smoking started but was significantly (p<0.001) greater for cigarette smokers than for smokers of other forms of tobacco. Among men who smoked only cigarettes, the RR was significantly (p<0.001 for trend) related to daily consumption, with a greater hazard among those who smoked 20/day (RR 1.50, 95% CI 1.39-1.62) than among those who smoked fewer (mean 10/day: RR=1.32, 95% CI 1.23-1.41). Smoking was also associated with a significant excess of liver cancer death in women (RR 1.17, 95% CI 1.06-1.29, 2p=0.003; attributable fraction 3%), but fewer women (17%) than men (62%) were smokers, and their cigarette consumption per smoker was lower. Among women who smoked only cigarettes, there was a significantly greater hazard among those who smoked at least 20/day (mean 22/day: RR=1.45, 95% CI 1.18-1.79) than among those who smoked fewer (mean 8/day: RR=1.09, 95% CI 0.94-1.25). These associations indicate that tobacco is currently responsible for about 50,000 liver cancer deaths each year in China, chiefly among men with chronic HBV infection.     

History of lung disease and risk of lung cancer in a population with high household fuel combustion exposures in rural China

History of chronic lung diseases and household coal use for heating and cooking are established risk factors of lung cancer; however, few studies have been able to explore these risk factors simultaneously. Xuanwei, China, has some of the highest rates of lung cancer in China and most residents experience substantial in-home coal smoke exposures. Using a population-based case–control study of 498 lung cancer cases and 498 age-matched controls, we evaluated the risk of lung cancer in relation to coal smoke exposure and history of chronic lung diseases, including chronic obstructive pulmonary disease (COPD), asthma, tuberculosis (TB), chronic bronchitis, and emphysema. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by conditional logistic regression adjusting for potential confounders. We observed an increased risk of lung cancer with history of any chronic lung disease among males (OR = 14.2; 95%CI = 4.3–46.9), females (OR = 2.6; 95%CI = 1.1–6.3), smokers (OR = 12.7; 95%CI = 3.5–45.8), and nonsmokers (OR = 2.6; 95%CI = 1.1–6.4). Specifically, TB (OR = 83.7; 95%CI = 11.0–634.7), COPD (OR = 3.2; 95%CI = 1.7–6.0), and emphysema and chronic bronchitis (OR = 3.3; 95%CI = 1.7–6.4) were associated with increased risks. These findings suggest that history of chronic lung diseases may also increase risk of lung cancer in populations with indoor coal smoke exposures.