Prenatal exposure to parents' smoking and childhood cancer.

The relation between parents' tobacco smoking prior to birth and cancer in the offspring was investigated with the use of data from a case-control study. Incident cases included all children (aged 0-14 years) diagnosed in Denver, Colorado from 1976 to 1983. Controls were selected through random digit dialing, and matched to cases on age, sex, and geographic area. Information on smoking by parents and other household members was obtained by personal interview for 223 cases and 196 controls. After adjustment for father's education, mother's smoking during the first trimester of pregnancy was associated with an increased risk for all cancers combined (odds ratio (OR) = 1.3, 95% confidence interval (CI) 0.7-2.1), acute lymphocytic leukemia (OR = 1.9, 95% CI 0.9-4.1), and lymphomas (OR = 2.3, 95% CI 0.8-7.1). Adjusting for father's education, associations with father's smoking in the absence of mother's smoking were found for all cancers combined (OR = 1.2, 95% CI 0.8-2.1), acute lymphocytic leukemia (OR = 1.4, 95% CI 0.6-3.1), lymphomas (OR = 1.6, 95% 0.5-5.4), and brain cancer (OR = 1.6, 95% CI 0.7-3.5). In spite of imprecision resulting from small numbers of cases in diagnostic subgroups, these results are suggestive of a possible influence of parents' smoking on childhood cancer.     

Bladder cancer and black tobacco cigarette smoking

A retrospective study was planned in the Hérault (Mediterranean) region of France where bladder cancer mortality and incidence rates are high. In the present paper, variations in bladder cancer risk according to various smoking-related variables, in particular time of exposure and type of tobacco, are examined. This case-control study with 219 male incident cases and 794 male population controls randomized from electoral rolls was carried out in 1987–89. Trained interviewers obtained information on demographics, dietary habits (coffee, alcohol, artificial sweeteners, vegetables, spices, etc.), occupational exposures and detailed history of tobacco smoking (average number of cigarettes per day, number of years of smoking, age at which they began and/or quitted smoking, use of filter-tip and type of tobacco). The odds ratio (OR) for cigarette smokers versus non-smokers was greater than 5. Results for number of cigarettes daily, duration of smoking and lifetime smoking showed a highly significant dose-response relationship, which was confirmed when these variables were treated as continuous in a logistic regression model. Eighty-eight percent of the smokers used black tobacco. Quitting smoking did not result in a significant reduction in bladder cancer risk. Higher risks were associated with starting to smoke at an early age (OR before age 13 versus after age 21=3.42; 95% CI 1.07–10.9) and with black tobacco smoking (OR black versus blond =1.63; 95% CI 0.73–3.64). Results suggest that black tobacco may be more harmful than blond tobacco and may have an early non-reversible role in bladder carcinogenesis.     

Mortality of iron miners in Lorraine (France): relations between lung function and respiratory symptoms and subsequent mortality.

An increased mortality from lung and stomach cancer was found in previous studies on Lorraine iron miners. A detailed analysis, however, was not possible due to the lack of data for survivors. In this study the cohort included 1178 workers selected at random from all the 5300 working miners aged between 35 and 55 at the start of the follow up period, which ranged from 1975 to 1985. Occupational exposures and tobacco consumption, lung function tests, and respiratory symptoms were assessed for each subject in 1975, 1980, and 1985. This study confirmed the excess of lung cancer (standardised mortality ratio (SMR) = 389, p < 0.001) and of stomach cancer (SMR = 273, p < 0.05). There was no excess of lung cancer in non-smokers and moderate smokers (< 20 pack-years) or the miners who worked only at the surface or underground for less than 20 years. A significant excess (SMR = 349, p < 0.001) was found in moderate smokers when they worked underground for between 20 and 29 years. Heavy smokers (over 30 pack-years) or subjects who worked underground for more than 30 years experienced a high risk: SMR = 478 (p < 0.001) for moderate smokers who worked underground for over 30 years; 588 (p < 0.001) for heavy smokers who worked underground for between 20 and 29 years; and 877 (p < 0.001) for heavy smokers who worked underground for over 30 years. This showed an interaction between smoking and occupational exposure. The excess mortality from lung cancer was because there were some subjects who died young (from 45 years old). Comparison with the results of a previous study showed that additional hazards produced by diesel engines and explosives increased the mortality from lung cancer. The SMR was higher than 400 (p < 0.001) from 45 years old instead of from 56 years. A relation was found between a decrease in vital capacity (VC), forced expiratory volume in one second (FEV1) and of FEV1/VC and mortality from all causes and from lung cancer in heavy smokers or men who had worked underground for more than 20 years. Respiratory symptoms were related to mortality from lung cancer among smokers (moderate and heavy) who worked underground for more than 20 years. It is considered that the risk of lung cancer in the Lorraine iron miners was mainly due to dust, diesel engines, and explosives although the role of low exposure to radon daughters could not be totally excluded.     

The Association between Point-of-Sale Advertising Bans and Youth Experimental Smoking: Findings from the Global Youth Tobacco Survey (GYTS)

Background and Objectives: while existing research has demonstrated a positive association between exposure to point-of-sale (POS) tobacco advertising and youth smoking, there is limited evidence on the relationship between POS advertising restrictions and experimental smoking among youth. This study aims to fill this research gap by analyzing the association between POS advertising bans and youths'' experimental smoking. Methods: Global Youth Tobacco Surveys from 130 countries during 2007–2011 were linked to the WHO “MPOWER” tobacco control policy measures to analyze the association between POS advertising bans (a dichotomous measure of the existence of such bans) and experimental smoking using weighted logistic regressions. All analyses were clustered at the country level and controlled for age, parents'' smoking status, GDP per capita, and country-level tobacco control scores in monitoring tobacco use, protecting people from smoke, offering help to quit, warning about the dangers of tobacco, enforcing promotion/advertising bans, and raising taxes on tobacco. Results: The results suggest that a POS advertising ban is significantly associated with reduced experimental smoking among youth (OR = 0.63, p < 0.01), and that this association is seen for both genders (boys OR = 0.74, p < 0.1; girls OR = 0.52, p < 0.001). Conclusions: POS advertising bans are significantly associated with reduced experimental smoking among youth. Adopting POS advertising bans has the potential to reduce tobacco use among their youth in countries currently without such bans.     

Cancer risk and social inequalities in Italy.

STUDY OBJECTIVE--To investigate social differences in cancer incidence in Turin, Italy in 1985-87. DESIGN--A cancer incidence follow up study of the turin population in relation to socioeconomic characteristics was performed through record linkage between the 1981 census and the cancer registry. A case-control study nested in the cohort was analysed, where cases were subjects with a new diagnosis of cancer in 1985-87 and controls were a sample of the Turin population, frequency matched by sex and age group. Incidence odd ratios (ORs) were calculated for social classes (defined by education, housing tenure, and socioeconomic group) using a logistic regression model. SETTING--The study population comprised subjects included in the 1981 Turin census (n approximately equal to 1,100,000) who were still alive, 20-69 years old, and were resident in Turin in the middle of study period. PARTICIPANTS--The analyses were based on 4215 male and 3451 female cases, and on 16,913 male and 13,838 female controls. MAIN RESULTS--Compared with the highest educational level, the men in the lowest one showed an OR > 2 for respiratory cancers; OR = 1.48 for stomach cancer; and ORs < 0.7 for skin, colorectal, and prostate cancers. Women with a primary school education were protected against colorectal (OR = 0.71), skin (OR = 0.59), and breast cancer (OR = 0.66) compared with university degree women, but were at risk for cancer of the cervix (OR = 2.33) and stomach cancer (OR = 2.84). The association between educational level (primary school v university) and lung cancer risk is negative for men (OR = 2.47) and positive for women (OR = 0.62), while the association with housing tenure is negative for both sexes (OR = 1.44). CONCLUSIONS--The socioeconomic distribution of some risk factors (for example smoking, alcohol, and diet) in Italy can partially explain the differences in respiratory and digestive cancers. "Unbalanced" health promotion interventions, targeted at social groups with the highest prevalences of risk factors, and national policies for increasing the level of education in the country may play an important role in reducing social differences in cancer risk.     

Colorectal Polyp Type and the Association With Charred Meat Consumption,Smoking, and Microsomal Epoxide Hydrolase Polymorphisms

We determined the association between charred meat consumption, cigarette smoking, microsomal epoxide hydrolase (mEH) polymorphisms (rs1051740 and rs2234922), and colorectal adenomas and hyperplastic polyps (HPs) and explored gene–environment interactions. Men and women with colorectal adenomas (n = 519), HPs (n = 691), or concurrently with both types of polyps (n = 227) and polyp-free controls (n = 772) receiving a colonoscopy from December 2004 to September 2007 were recruited. Participants completed telephone interviews and provided buccal cell samples; genotyping of mEH was completed using Taqman assays. We conducted polytomous regression and calculated odd ratios (OR) and 95% confidence intervals. Interactions were evaluated using Wald chi-square tests. Consumption of >3 servings of charred meat per week was associated with distal HPs (OR = 2.0, 1.2–3.4) but not adenomas nor either type of proximal polyp. Heavy cigarette smoking (≥ 22 pack-years) was associated with an increased risk for colorectal adenomas (OR = 1.7, 95% CI: 1.2–2.4), HPs (OR = 2.4, 95% CI: 1.7–3.3), and both types (OR = 2.8, 95% CI: 1.8–4.3) with the strongest association for distal polyps. There was no association between mEH genotype and colorectal polyps, nor were any statistically significant gene–environment interactions identified. Future investigation of BaP exposure and colorectal neoplasia should analyze whether associations are dependent upon anatomic location.     

Parkinson's disease risks associated with cigarette smoking, alcohol consumption, and caffeine intake

A reduced risk for Parkinson's disease (PD) among cigarette smokers has been observed consistently during the past 30 years. Recent evidence suggests that caffeine may also be protective. Findings are presented regarding associations of PD with smoking, caffeine intake, and alcohol consumption from a case-control study conducted in western Washington State in 1992-2000. Incident PD cases (n = 210) and controls (n = 347), frequency matched on gender and age were identified from enrollees of the Group Health Cooperative health maintenance organization. Exposure data were obtained by in-person questionnaires. Ever having smoked cigarettes was associated with a reduced risk of PD (odds ratio (OR) = 0.5, 95% confidence interval (CI): 0.4, 0.8). A stronger relation was found among current smokers (OR = 0.3, 95% CI: 0.1, 0.7) than among ex-smokers (OR = 0.6, 95% CI: 0.4, 0.9), and there was an inverse gradient with pack-years smoked (trend p < 0.001). No associations were detected for coffee consumption or total caffeine intake or for alcohol consumption. However, reduced risks were observed for consumption of 2 cups/day or more of tea (OR = 0.4, 95% CI: 0.2, 0.9) and two or more cola drinks/day (OR = 0.6, 95% CI: 0.3, 1.4). The associations for tea and cola drinks were not confounded by smoking or coffee consumption.     

Ultra-Processed Food Intake and Smoking Interact in Relation with Colorectal Adenomas

Smoking and ultra-processed foods (UPFs), a substantial part of the western diet, have been suggested to have a potential carcinogenic effect, though epidemiologic data are lacking. We aimed to examine the association between high UPF intake and colorectal adenomas, and to test the interaction with smoking. In a case-control study among consecutive subjects undergoing colonoscopy in a tertiary center during 2010–2015, UPF intake and smoking were compared between cases with colorectal adenomas and controls. Within 652 participants (cases, n = 294 and controls, n = 358), high UPF intake (defined as percent of kcal from UPF above the study sample upper tertile) was positively associated with adenomas (Odds ratio (OR) = 1.75, 95% Confidence interval (CI) 1.14–2.68), advanced and proximal adenomas (OR = 2.17, 1.29–3.65 and OR = 2.38, 1.37–4.11) among the whole study sample; and with adenomas (OR = 3.54, 1.90–6.61), non-advanced adenomas (OR = 2.60, 1.20–5.63), advanced adenomas (OR = 4.76, 2.20–10.30), proximal adenomas (OR = 6.23, 2.67–14.52), and distal adenomas (OR = 2.49, 1.21–5.13) among smokers. Additionally, a dose-dependent association was observed between tertiles of UPF intake and adenomas only among smokers (p for trend < 0.001). A significant interaction between smoking and high UPF intake was detected (p for interaction = 0.004). High intake of UPFs is strongly and independently associated with colorectal adenomas, especially advanced and proximal adenoma, and interacts with smoking. Results highlight smokers as more susceptible to the negative health effects of UPF consumption on colorectal neoplasia.     

Low Plasma Cholesterol Predicts an Increased Risk of Lung-Cancer in Elderly Women

Background. There have been significant efforts in the United States to lower high cholesterol levels. Studies of men, however, have found a higher total cancer mortality rate at lower levels of plasma cholesterol. Many of these studies have found that lung cancer is more closely associated than other cancers with low cholesterol. Of the studies that include women, none has demonstrated a statistically significant inverse association between low cholesterol and lung cancer. Methods. We examined the relation between very low plasma cholesterol levels (<160 mg/dl) and lung cancer death in an 18-year prospective study of 2,011 men and 2,327 women. Results. After adjusting for age, body mass index, smoking, and education, the relative hazard of lung cancer mortality for those with low cholesterol (<160 mg/dl) compared with all other cholesterol levels (≥ 160 mg/dl) was 1.75 among men (P = 0.28) and 3.29 among women (P = 0.02). Excluding those who died within 5 years of baseline did not change the results. Conclusions. Both men and women with baseline plasma cholesterol levels <160 mg/dl were more likely to die of lung cancer. This difference was statistically significant in women. The association could not be explained by occult malignancy, smoking, or socioeconomic status.     

Risk factors for laryngeal cancer

This case-control study comprised 100 histologically verified laryngeal cancer patients and 100 hospital controls matched with cases by sex, age and place of residence. The following variables were tested for their association with cancer of the larynx: marital status, educational level, hard liquor consumption, cigarette smoking, unfavorable working conditions, sudden and frequent temperature changes at work, cold housing, loud speech at work, frequent hoarseness, frequent and persistent cough, persistently swollen neck glands, tonsillectomy and laryngeal surgery. According to conditional logistic regression analysis, significant association with laryngeal cancer was found for unfavourable working conditions for more than 10 years (OR=4.36; 95% CI=1.92–9.91), hard liquor consumption for more than 5 years (OR=2.59; 95% CI=1.14–5.87), cigarette smoking for more than 10 years (OR=7.29; 95% CI=2.41–22.09), tonsillectomy (OR=4.80; 95% CI=1.61–14.30) and frequent and persistent cough prior to disease (OR=8.17; 95% CI=1.72–38.76).     

Subjective health of male ex-smokers: relationship with time since smoking cessation,intensity and duration of tobacco consumption

BACKGROUND: To examine the relationship of subjective health with time since smoking cessation and amount and duration of tobacco consumption among male ex-smokers. METHODS: Pooled analysis of three household interview surveys conducted in 1993 (n = 8,494), 1995 (n = 2,556), and 1997 (n = 2,624) on samples representative of the noninstitutionalized population aged 16 and over in Spain. RESULTS: After controlling for the main confounders, ex-smokers with smoking burden < or =13 pack-years had a lower frequency of suboptimal health (fair, poor, or very poor) than current smokers (OR, 0.59; 95% Cl, 0.38-0.91) during the first year after cessation; thereafter, it reached a value similar to that of never-smokers 11 years or more after cessation. Among those with burden >13 pack-years, frequency of suboptimal health during the first year after cessation was higher than in current smokers (OR, 1.28; 95% CI, 1.00-1.63). Afterwards, it fell progressively, approaching the value of never-smokers 11 years or more after cessation. Frequency of suboptimal health in ex-smokers increased with duration (years) of smoking (P linear trend = 0.045), but did not vary with the number of cigarettes smoked. CONCLUSIONS: Suboptimal health declined with time since smoking cessation, to reach the frequency of never-smokers. Longer duration of tobacco consumption is associated with worse subjective health.     

Cigarette smoking and risk of Hodgkin's disease: a population-based case-control study

Previous reports offer limited support for an association between cigarette smoking and Hodgkin's disease. The authors investigated dose-response effects for smoking in relation to the risk of Hodgkin's disease using data from the Selected Cancers Study. Cases (n = 343) were men aged 32-60 years identified from eight US population-based cancer registries in 1984-1988. Controls (n = 1,910) were men recruited by random digit telephone dialing and frequency matched to cases by age and registry. Conditional logistic regression was used to calculate odds ratios and 95% confidence intervals adjusted for age, registry, race/ethnicity, Jewish upbringing, education, and childhood domicile. Compared with never smokers, current smokers had a significantly increased risk of Hodgkin's disease (odds ratio (OR) = 1.8, 95% confidence interval (CI): 1.3, 2.9). Risks increased linearly (p < 0.001) with increasing packs per day (OR(>or=2) = 2.5, 95% CI: 1.6, 4.0), years (OR(>or=30) = 2.4, 95% CI: 1.5, 3.9), and pack-years (OR(>40) = 2.7, 95% CI: 1.8, 4.3) of smoking. These associations were significant for the nodular sclerosis and mixed cellularity subtypes but were much stronger for mixed cellularity. Stratified analyses by age (42 years) and subtype suggested that the effects of smoking are more closely related to histology than age. In contrast to findings from previous studies, these data suggest that smoking is an important preventable risk factor for Hodgkin's disease.     

Cigarette smoking and the risk of mucinous and nonmucinous epithelial ovarian cancer

BACKGROUND: The association between cigarette smoking and ovarian cancer may vary according to the histologic type of tumor. METHODS: We examined cigarette smoking as a risk factor for both mucinous and nonmucinous tumors in a population-based case-control study comparing 767 incident cases of epithelial ovarian cancer with 1,367 community controls frequency matched to cases by age and race. RESULTS: Smoking was associated with mucinous tumors (odds ratio [OR] = 1.9; 95% confidence interval [CI] = 1.3-2.9) but not with nonmucinous tumors (OR = 1.1; CI = 0.9-1.3). Furthermore, the odds ratios for smokers with mucinous tumors increased with increasing pack-years of smoking (OR = 1.0, 1.9, and 2.7 for <5, 5-24, and > 24+ pack-years, respectively; P for trend = 0.01) CONCLUSIONS: Cigarette smoking appears to be a risk factor for mucinous but not for nonmucinous tumors.     

Smoking cessation and renal cell carcinoma

PURPOSE: The magnitude and timing of the reported decrease in risk of renal cell carcinoma (RCC) attributed to smoking cessation is not well characterized. Furthermore, conclusions from previous investigations have been hampered by unstable risk estimates, broad exposure categories and/or insufficient adjustment for the inverse correlation of cessation years with lifetime smoking exposure. METHODS: To address these issues, we report data from a population-based case-control study conducted in Iowa from 1986 to 1989. RCC cases (n = 387) were identified through the Iowa Cancer Registry, while controls (n = 2,333) were randomly selected from the general population, frequency-matched on age and sex. Subjects provided detailed information on a mailed questionnaire regarding their smoking history as well as other anthropometric, lifestyle, dietary and medical history risk factors. RESULTS: Smoothing spline regression analysis provided evidence of a consistent inverse linear trend between years of cessation and risk of RCC. In categorical analysis, compared with current smokers, those quitting > or =30 years ago experienced a 50% reduction in risk of RCC (OR = 0.5; 95% CI 0.3 to 0.8) after adjustment for age, sex, BMI, hypertension and pack-years of smoking. Risk among long-term quitters was similar to risk among never smokers (OR = 0.6; 95% CI 0.4 to 0.8). In contrast, cessation of <10 years, 10 to 19 years and 20 to 29 years all resulted in a less pronounced reduction in RCC risk ( approximately 20% to 30%). CONCLUSIONS: Our findings suggest that while cessation of smoking is indeed associated with a linear decrease in RCC risk even after adjustment for potential confounders, this benefit may not be sizeable until more than 20 years following cessation.     

青岛市≥40岁吸烟人群慢性阻塞性肺疾病患病现状及影响因素研究

目的 探讨青岛市≥40岁吸烟人群中慢性阻塞性肺疾病（COPD）患病现状,并分析COPD发病相关影响因素。方法 2021年8—12月采用多阶段分层整群随机抽样方法抽取有吸烟习惯居民的家庭户中年龄≥40岁的吸烟者作为调查对象开展问卷调查、体格检查以及肺功能检查,分析吸烟人群中COPD患病现状,并对COPD发生相关影响因素开展研究。结果 共纳入吸烟者1 516人,男性占81.06%,吸烟包年≥21者占70.25%,吸烟年数≥31年者占71.17%;发生COPD 297例,发生率为19.59%。多因素Logistic分析结果显示,男性（OR=3.706）、50~59岁（OR=1.567）、60~69岁（OR=2.585）、≥70岁（OR=4.926）、城镇居民（OR=1.568）、BMI<18.5（OR=3.848）、被动吸烟（OR=2.516）、吸烟包年11~20（OR=1.903）、吸烟包年21~30（OR=2.472）、吸烟包年≥31（OR=3.792）、吸烟年数31~40（OR=2.400）、吸烟年数≥41（OR=4.227）为吸烟人群COPD发生的危险因素。趋势χ²分析显示：随着吸烟包年、吸烟年数不断增加,吸烟者COPD发生率逐渐升高（均P<0.01）。Spearman相关分析显示：COPD病情程度与吸烟包年、吸烟年数呈显著正相关,COPD病情程度会随着吸烟包年、吸烟年数增加而不断加深（均P<0.01）。结论 青岛市≥40岁吸烟人群以男性为主,COPD发生率较高。男性、高龄、城镇居民、低BMI、被动吸烟为吸烟者COPD发生的危险因素,吸烟包年与吸烟年数越高可增加COPD发生风险。     

The Association between Coffee Consumption and Risk of Colorectal Cancer in a Korean Population

This study was performed to investigate the association between coffee consumption and risk of colorectal cancer in a Korean population and examine whether the association can be altered by adjustment for intake of coffee additives. We conducted a case-control study involving 923 colorectal cancer cases and 1846 controls matched by sex and age (within 5 years). A semi-quantitative food frequency questionnaire was used to assess coffee intakes. High coffee consumption was associated with lower odds of developing colorectal cancer (≥3 cups/day vs. no drinks, OR = 0.68; 95% CI: 0.49–0.96). When we additionally controlled for consumption of coffee additives including sugar and cream, the inverse association became stronger (≥3 cups/day vs. no drinks, OR = 0.22; 95% CI: 0.14–0.33), and a significant inverse linear trend was shown (P_trend < 0.0001). The inverse associations were observed for proximal (P_trend = 0.0001) and distal (P_trend = 0.0003) colon cancer, and rectal cancer (P_trend < 0.0001) in the stratified analysis by anatomical sub-sites. Regarding sex, inverse associations between coffee consumption and colorectal cancer were found for men (P_trend < 0.0001) and women (P_trend = 0.0021). In the stratified analysis by obese status of subjects, inverse linear trends were observed in both non-obese and obese people (P_trend < 0.0001). High coffee consumption may be associated with a lower risk of colorectal cancer in the Korean population and the degree of decrease in the odds of developing colorectal cancer changes by adjustment for intake of coffee additives.     

Cigarette smoking and risk of cancers of the colon and rectum: A case–control study from Italy

The relationship between smoking habit and risk of colon and rectal cancers was considered in a case–control study conducted between 1991 and 1996 in six Italian centers. Cases were 1225 patients below age 75 with histologically confirmed cancer of the colon and 728 with cancer of the rectum.Controls were 4154 patients admitted to hospital for a wide spectrum of acute, non-neoplastic diseases. Compared to neversmokers, the odds ratios (OR) for current smokers of 25 or more cigarettes/day was 0.90 for patients with colon and 0.86 for those with rectal cancer and those for ex-smokers were 1.02 and 1.09 for colon and rectal cancer, respectively. No increase in risk was found with duration of the habit, the OR for 40 or more years being 0.79 for colon and 0.87 for rectal cancer. Furthermore, no relationship was apparent with time since starting (the OR for 40 or more years were 0.94 for colon and 1.01 for rectal cancer), or age at starting (the OR for < 18 years were 1.02 for colon and 1.00 for rectal cancer), or for pack-years smoked (the OR for 40 or more pack-years were 0.93 for colon and 0.91 for rectal cancer) or time since stopping among ex-smokers. No increase in risk was found in smokers of 15 cigarettes/day for 40 years or longer (OR: 0.93). No significant heterogeneity was found across strata of age at diagnosis, sex, education, physical activity at work, intake of alcohol, coffee, vegetables, total energy, and number of meals/day. Likewise, no significant association was apparent for various intestinal subsites. Thus, this study did not find cigarette smokers at higher risk for cancer of the bowel even after a long duration and a long period since starting.     

Associations of cigarette smoking and alcohol consumption with advanced or multiple colorectal adenoma risks: a colonoscopy-based case-control study in Korea

The associations between alcohol consumption and cigarette smoking habits and the risk for colorectal adenomatous polyps according to the detailed clinical information about polyps were assessed in a large colonoscopy-based study. The study enrolled participants who visited the National Cancer Center of the Republic of Korea for cancer screening between April 2007 and April 2009. In 1,242 newly diagnosed colorectal adenoma patients and 3,019 polyp-free controls, past smokers (odds ratio (OR) = 1.31, 95% confidence interval (CI): 1.04, 1.65) and current smokers (OR = 1.70, 95% CI: 1.37, 2.11) had increased risks for adenomas compared with nonsmokers. Cigarette smoking conferred an even higher risk for advanced adenomas and 3 or more adenomas than for low-risk adenomas or a single adenoma. Dose-response relations were observed among the daily number of cigarettes smoked, the duration of smoking, the pack-years of smoking, and the risk for adenomas. A longer duration of alcohol consumption was associated with a higher risk for advanced adenomas (for >28 years of consumption: OR = 2.0, 95% CI: 1.10, 3.64) and 3 or more adenomas (OR = 2.19, 95% CI: 1.27, 3.76). In conclusion, cigarette smoking and alcohol consumption play roles in colorectal carcinogenesis, and the association differs by the clinical features of the adenomas.     

Dietary patterns and the adenomacarcinoma sequence of colorectal cancer

Summary Background Food components of a diet are highly related, so that building up dietary patterns may help understand the relationship between chronic diseases and diet, and identify high risk groups that need preventive advice. Aim The aim of this study was to determine dietary patterns associated with the colorectal adenoma–carcinoma pathway. Methods We performed a two–step analysis using first principal component analysis to select the most appropriate food groups, then a hierarchical agglomerative clustering method, in order to determine dietary patterns in 1372 subjects included in a case–control study. Patients with hyperplastic polyps (n = 103), adenomas < 10mm, (n = 154) or larger adenomas (n = 208) were then compared with polyp–free controls (n = 426), and colorectal cancer cases (n = 171) compared with population controls (n = 309) using unconditional logistic regression adjusted on age and gender. Results Cluster analysis determined five food patterns. Cluster 1 identified a low-energy diet; cluster 2 a high–starch, highfat, and low–fruit diet; cluster 3 a high–processed meat, –energy, –alcohol, and –starchy foods diet; cluster 4 a high–fish, –cereals, –honey, –olive oil, –fruit and –vegetables diet; and cluster 5 a high–flour, –sugar, –chocolate, –animal fats, and –eggs diet. Logistic regression identified cluster 2 as significantly associated with risk of small adenomas (OR = 1.7; 95% confidence interval 1.0–2.7), large adenomas (OR = 1.9; 1.2–3.0) and cancers (OR = 1.7; 1.1–2.8) compared with cluster 1. Cluster 4 diet was inversely associated with risk of small adenomas (OR = 0.4; 0.2–1.0). There was no relationship between patterns and risk of hyperplastic polyps. Multiple adjustment decreased the strength of the relationships with cluster 2, which remained significantly associated with adenomas, but not cancer. Conclusion A lowenergy diet appeared as protective all along the adenoma–carcinoma sequence, contrary to a high–energy, high–processed meat and –animal fat diet.In the html abstract, html-text and pdf of the summary of the article“Rouillier P, et al.(2004) Dietary patterns and the adenomacarcinoma sequence of colorectal cancer. Eur J Nutr (published online 20th August 2004)”The online version of the original article can be found atthe numbering of the different clusters in the sub-section “Results” had been mixed up. Instead of:“...Logistic regression identified cluster 1 as significantly associated with risk of small adenomas (OR=1.7; 95% confidence interval 1.0–2.7), large adenomas (OR=1.9; 1.2–3.0) and cancers (OR=1.7; 1.1–2.8) compared with cluster 2. Cluster 4 diet was inversely associated with risk of small adenomas (OR=0.4; 0.2–1.0). There was no relationship between patterns and risk of hyperplastic polyps. Multiple adjustment decreased the strength of the relationships with cluster 1, which remained significantly associated with adenomas, but not cancer.”there should have been:“Logistic regression identified cluster 2 as significantly associated with risk of small adenomas (OR=1.7; 95% confidence interval 1.0–2.7), large adenomas (OR=1.9; 1.2–3.0) and cancers (OR=1.7; 1.1–2.8) compared with cluster 1. Cluster 4 diet was inversely associated with risk of small adenomas (OR=0.4; 0.2–1.0). There was no relationship between patterns and risk of hyperplastic polyps. Multiple adjustment decreased the strength of the relationships with cluster 2, which remained significantly associated with adenomas, but not cancer.”The publisher apologises for any inconvenience caused by this mistake.     

Lung cancer in the lower lobe is associated with pulmonary asbestos fiber count and fiber size.

We studied exposure to asbestos, pulmonary fibrosis, fiber count, and fiber size in relation to the lobar origin of lung cancer in 90 consecutive patients. Among the 32 patients with a history of occupational exposure to asbestos, 22 were construction workers. The proportion of lower-lobe tumors increased with the duration of exposure from 45% in those working less than 15 years to 82% in those working 15 years or more in the construction trade, as compared with 25% in patients who were probably not exposed. The location of the tumor in the lower lobe was explained by the high number of total fibers [odds ratio (OR) = 9.0, CI = 2.3-34.6), of fibers 3 microns and longer (OR = 22.1, CI = 3.9-125), and fibers of anthophyllite (OR = 14.6, CI = 2.4-83.4) and crocidolite (OR = 7.0, CI = 1.2-41.2) when the effect of smoking and fibrosis was adjusted in the logistic regression analysis. The location of the tumor did not correlate with fibrosis, pack-years smoked, or the number of short (< 3 microns) fibers. Our findings suggest that asbestos causes an excess of lower-lobe tumors at a relatively low exposure level, independently of pulmonary fibrosis.