Jinfu Hu

Passive and active smoking and breast cancer risk in Canada, 1994-97

AbstractBackground: Studies comparing ever smokers with never smokers have found little increase in breast cancer risk. However, the five published studies examining passive smoking and breast cancer have all suggested associations with both passive and active smoking, particularly premenopausal risk. Methods: We analyzed data collected through the Canadian National Enhanced Cancer Surveillance System, from 805 premenopausal and 1512 postmenopausal women with newly diagnosed (incident), histologically confirmed, primary breast cancer and 2438 population controls. The mailed questionnaire included questions on breast cancer risk factors and a lifetime residential and occupational history of exposure to passive smoking. Results: Among premenopausal women who were never active smokers, regular exposure to passive smoke was associated with an adjusted breast cancer odds ratio (OR) of 2.3 (95% confidence interval [CI] 1.2–4.6). Passive exposure showed a strong dose–response trend (test for trend p = 0.0007) with an OR of 2.9 (95% CI 1.3–6.6) for more than 35 years of passive residential and/or occupational exposure. When premenopausal women who had ever actively smoked were compared with women never regularly exposed to passive or active smoke, the adjusted OR for breast cancer was also 2.3 (95% CI 1.2–4.5). Among postmenopausal women who were never-active smokers, regular exposure to passive smoke was associated with an adjusted breast cancer OR of 1.2 (95% CI 0.8–1.8) and an OR of 1.4 (95% CI 0.9–2.3) for the most highly exposed quartile of women. The adjusted OR for postmenopausal breast cancer risk for ever-active smokers compared with women never regularly exposed to passive or active smoke was 1.5 (95% CI 1.0–2.3). Statistically significant dose–response relationships were observed with increasing years of smoking, increasing pack-years and decreasing years since quitting. Women with 35 or more years of smoking had an adjusted OR of 1.7 (95% CI 1.1–2.7). Conclusions: Active and passive smoking may be associated with increased breast cancer risk, particularly premenopausal risk.

Diet and brain cancer in adults: A case‐control study in Northeast China

A hospital‐based case‐control study was conducted in the Heilongjiang Province of northeast China between May 1993 and May 1995. A total of 129 histologically confirmed brain cancer cases (73 gliomas and 56 meningiomas) and 258 matched controls were interviewed in 6 major hospitals to examine the influence of dietary factors in developing brain cancer. Information was obtained about frequency of consumption of 57 food items. Odds ratios (ORs) were obtained from conditional logistic regression, including allowance for socio‐demographic factors, alcohol, tobacco and total energy intake. Consumption of fresh vegetables (OR = 0.29 for the highest quartile compared with the lowest one), and specifically of Chinese cabbage and onion, fruit (OR = 0.15), fresh fish (OR = 0.38) and poultry (OR = 0.16) was inversely related to the risk of developing brain cancer. A protective effect was also seen for vitamin E intake, calcium and, although non‐significantly, beta‐carotene and vitamin C. Risk of brain cancer increased with consumption of salted vegetables (OR = 2.54) and salted fish. Int. J. Cancer81:20–23, 1999.

Dietary cholesterol intake and cancer

BACKGROUND This study assesses the association between dietary cholesterol intake and the risk of various cancers. PATIENTS AND METHODS Mailed questionnaires were completed between 1994 and 1997 in eight Canadian provinces by 1182 incident histologically confirmed cases of the stomach, 1727 of the colon, 1447 of the rectum, 628 of the pancreas, 3341 of the lung, 2362 of the breast, 442 of the ovary, 1799 of the prostate, 686 of the testis, 1345 of the kidney, 1029 of the bladder, 1009 of the brain, 1666 non-Hodgkins lymphomas (NHL), 1069 leukemia and 5039 population controls. Information on dietary habits and nutrition intake were obtained using a food frequency questionnaire, which provided data on eating habits 2 years before the study. Odds ratios (ORs) were derived by unconditional logistic regression to adjust for total energy intake and other potential confounding factors. RESULTS Dietary cholesterol was positively associated with the risk of cancers of the stomach, colon, rectum, pancreas, lung, breast (mainly postmenopausal), kidney, bladder and NHL: the ORs for the highest versus the lowest quartile ranged from 1.4 to 1.7. In contrast, cholesterol intake was inversely associated with prostate cancer. CONCLUSIONS Our findings add to the evidence that high cholesterol intake is linked to increased risk of various cancers. A diet low in cholesterol may play a role in the prevention of several cancers.

Risk factors for meningioma in adults: A case-control study in northeast China

A hospital case‐control study of meningioma was conducted in Heilongjiang Province in northeast China between September 1989 and December 1996. It included 183 cases of newly diagnosed primary meningioma and 366 individually matched hospital controls with non‐neoplastic and non‐neurological disease selected from six major hospitals. Cases and controls were matched by sex, age and area of residence and interviewed in the hospital wards to obtain information on medical history, occupation and lifestyle. No association with liquor or beer consumption was apparent. Cigarette smoking was positively associated with meningioma risk in women but not in men. In women, compared with non‐smokers, the adjusted OR for pack‐years of smoking above the median (124) was 6.2 (CI 2.04–18.87). Both of these observations contrast with the results of a study of glioma in the same population, using similar methods. The risk of meningioma was positively associated with reported occupational exposure to lead, tin, cadmium and ionising radiation in both genders. Int. J. Cancer 83:299–304, 1999.

Salt, processed meat and the risk of cancer.

This study assesses the association between salt added atthe table, processed meat and the risk of various cancers. Mailed questionnaires were completed by 19 732patients with histologically confirmed incident cancer of the stomach, colon, rectum, pancreas, lung, breast, ovary, prostate, testis, kidney, bladder, brain, non-Hodgkins lymphoma or leukaemia, and 5039 population controls,between 1994 and 1997. Measurement included information on socioeconomic status, lifestyle habits and diet. A 69-item food frequency questionnaire provided dataon eating habits 2 years before the study. Odds ratiosand 95% confidence intervals were derived through unconditional logistic regression. Compared with never adding salt at the table, always or often adding salt at the table was associated with an increased risk of stomach, lung, testicular and bladder cancer. Processed meat was significantly related to the risk of the stomach, colon, rectum, pancreas, lung, prostate, testis, kidney and bladdercancer and leukaemia; the odds ratios for the highest quartile ranged from 1.3 to 1.7. The findings addtothe evidence that high consumption of salt and processed meat may play a role in the aetiology of several cancers.

Indoor air pollution from solid fuel use, chronic lung diseases and lung cancer in Harbin, Northeast China.

In some areas of China, indoor air pollution (IAP) originating principally from the combustion of solid fuels has a relevant role in lung cancer. Most previous studies focused on the female population and only a few on both the sexes. We analyzed the relationship between IAP from solid fuel use and selected chronic lung diseases and lung cancer risk in Harbin, Northeast China, an area with a very high base line risk of lung cancer for both the sexes. We used data from a case–control study conducted between 1987 and 1990, including 218 patients with incident, histologically confirmed lung cancer and 436 controls admitted to the same hospitals as cases. We calculated an index of IAP from solid fuel use exposure using data on heating type, cooking fuel used, and house measurements. Cases reported more frequently than controls an exposure to coal fuel for house heating and/or cooking, and the odds ratio (OR) for ever versus never exposed was 2.19 [95% confidence interval (CI): 1.08–4.46]. The ORs of lung cancer according to subsequent tertiles of IAP exposure index were 1.82 (95% CI: 1.14–2.89) and 1.99 (95% CI: 1.26–3.15) as compared with the lowest tertile. The ORs of lung cancer for participants with a history of chronic bronchitis and tuberculosis were 3.79 (95% CI: 2.38–6.02) and 3.82 (95% CI: 1.97–7.41), respectively. This study gives further support and quantification of the positive association between IAP, history of selected nonmalignant lung diseases, and lung cancer risk for both the sexes.

Dietary transfatty acids and cancer risk.

This study assesses the association between dietary transfatty acid (TFA) intake and the risk of selected cancers. Mailed questionnaires were completed between 1994 and 1997 in eight Canadian provinces by 1182 incident, histologically confirmed cases of the stomach, 1727 of the colon, 1447 of the rectum, 628 of the pancreas, 3341 of the lung, 2362 of the breast, 442 of the ovary, 1799 of the prostate, 686 of the testis, 1345 of the kidney, 1029 of the bladder, 1009 of the brain, 1666 non-Hodgkin’s lymphomas, 1069 leukemias, and 5039 population controls. Information on dietary habits and nutrition intake was obtained using a food frequency questionnaire, which provided data on eating habits 2 years before the study. Odds ratios (OR) and 95% confidenc530e intervals (CI) were derived by unconditional logistic regression to adjust for total energy intake and other potential confounding factors. Dietary TFA were positively associated with the risk of cancers of the colon (OR: 1.38 for the highest vs. the lowest quartile), breast in premenopause (OR: 1.60), and prostate (OR: 1.42). There were a borderline association for pancreas cancer (OR: 1.38; P=0.06). No significant association was observed for cancers of the stomach, rectum, lung, ovary, testis, kidney, bladder, brain, non-Hodgkin’s lymphomas, and leukemia, although the ORs for the highest quartile were above unity for all neoplasms considered, except testis. Our findings add evidence that high TFA is associated with an increased risk of various cancers. Thus, a diet low in transfat may play a role in the prevention of several cancers.

Is temperature an effect modifier of the association between green tea intake and gastric cancer risk

We considered the relationship between green tea and gastric cancer risk in Harbin, Heilongjiang province, Northeast China, an area with high baseline risk of stomach cancer. We used data from a case–control study conducted from 1987 to 1989 among 266 incident cases of stomach cancer and 533 controls admitted to the same hospitals as cases, with non-neoplastic and non-gastric diseases. No association emerged when tea consumption alone was considered: the odds ratio (OR) for green tea consumption was 0.87 (95% CI: 0.60–1.25) for green tea intake ≥750 g/year versus no intake and 0.99 (95% CI: 0.97–1.02) for an increment of 500 g of tea per year. When tea consumption was classified according to the temperature, however, the OR was 0.19 (95% CI: 0.07–0.49) for lukewarm tea intake ≥750 g/year and 1.27 (95% CI: 0.85–1.90) for hot tea intake (P value for interaction <0.001) as compared with non-drinkers. The corresponding ORs for an increment of 500 g of tea per year were 0.61 (95% CI: 0.45–0.82) and 1.03 (95% CI: 0.99–1.07) for lukewarm and hot tea, respectively (P value for interaction <0.001). We found an inverse relationship between green tea drinking and gastric cancer risk limited to the intake of lukewarm tea.

Cigarette smoking and gastric cancer in the Stomach Cancer Pooling (StoP) Project.

Tobacco smoking is a known cause of gastric cancer, but several aspects of the association remain imprecisely quantified. We examined the relation between cigarette smoking and the risk of gastric cancer using a uniquely large dataset of 23 epidemiological studies within the ‘Stomach cancer Pooling (StoP) Project’, including 10 290 cases and 26 145 controls. We estimated summary odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) by pooling study-specific ORs using random-effects models. Compared with never smokers, the ORs were 1.20 (95% CI: 1.09–1.32) for ever, 1.12 (95% CI: 0.99–1.27) for former, and 1.25 (95% CI: 1.11–1.40) for current cigarette smokers. Among current smokers, the risk increased with number of cigarettes per day to reach an OR of 1.32 (95% CI: 1.10–1.58) for smokers of more than 20 cigarettes per day. The risk increased with duration of smoking, to reach an OR of 1.33 (95% CI: 1.14–1.54) for more than 40 years of smoking and decreased with increasing time since stopping cigarette smoking (P for trend<0.01) and became similar to that of never smokers 10 years after stopping. Risks were somewhat higher for cardia than noncardia gastric cancer. Risks were similar when considering only studies with information on Helicobacter pylori infection and comparing all cases to H. pylori+ controls only. This study provides the most precise estimate of the detrimental effect of cigarette smoking on the risk of gastric cancer on the basis of individual data, including the relationship with dose and duration, and the decrease in risk following stopping smoking.

The stomach cancer pooling (StoP) project: study design and presentation.

Gastric cancer affects about one million people per year worldwide, being the second leading cause of cancer mortality. The study of its etiology remains therefore a global issue as it may allow the identification of major targets, besides eradication of Helicobacter pylori infection, for primary prevention. It has however received little attention, given its comparatively low incidence in most high-income countries. We introduce a consortium of epidemiological investigations named the ‘Stomach cancer Pooling (StoP) Project’. Twenty-two studies agreed to participate, for a total of over 9000 cases and 23 000 controls. Twenty studies have already shared the original data set. Of the patients, 40% are from Asia, 43% from Europe, and 17% from North America; 34% are women and 66% men; the median age is 61 years; 56% are from population-based case–control studies, 41% from hospital-based ones, and 3% from nested case–control studies derived from cohort investigations. Biological samples are available from 12 studies. The aim of the StoP Project is to analyze the role of lifestyle and genetic determinants in the etiology of gastric cancer through pooled analyses of individual-level data. The uniquely large data set will allow us to define and quantify the main effects of each risk factor of interest, including a number of infrequent habits, and to adequately address associations in subgroups of the population, as well as interaction within and between environmental and genetic factors. Further, we will carry out separate analyses according to different histotypes and subsites of gastric cancer, to identify potential different risk patterns and etiological characteristics.