A European validation study of smoking and environmental tobacco smoke exposure in nonsmoking lung cancer cases and controls

Objectives: The purpose of this study was to validate, in a case-control study, the reporting by lung cancer cases and controls of their own lifetime smoking habits and of the smoking habit of the spouse. Methods: In a multicenter (Sweden, Spain, Italy) case-control study of environmental tobacco smoke (ETS) and lung cancer, subjects were screened by repeated probing to exclude regular smokers of one cigarette/day or more for one year or more, and to quantify any occasional smoking. We then performed a short validation interview with next-of-kin in three centers. Results: Only five of 408 index subjects who had never smoked regularly (1.7 percent) were reported by next-of-kin to be former regular smokers. These subjects had a cumulative lifetime consumption of cigarettes below 1.1 pack years. Among 351 subjects with quantitative smoking information from both sources who reported ever smoking 400 cigarettes or less (the definition of never-smoker used in the multicenter ETS study), nine subjects (2.6 percent) had smoked more than this amount occasionally according to next-of-kin. Misclassification was not higher for cases than controls. Relative risks for lung cancer associated with indicators of ETS exposure were not substantially altered by excluding the nine possibly misclassified subjects. The reports from 223 pairs of index subjects and next-of kin regarding the cumulative amount smoked by the spouse agreed quite well (Spearman's rank correlation 0.75 for reported smokers, 0.92 for all subjects). Only one index subject failed to report a spouse who had smoked regularly (99 percent sensitivity). Conclusions: Smoking status and exposure to spousal ETS as reported by lung cancer cases and controls agreed strongly with reports by next-of-kin. Overall, our results suggest that bias from smoker misclassification is likely to be insignificant, and they contribute to the evidence linking exposure to ETS with an increased risk of lung cancer.     

Risk Factors for Male Breast Cancer (United States)

Objectives: The etiology of male breast cancer is obscure, although an excess risk has been associated with Klinefelter syndrome, testicular disorders, benign breast disease including gynecomastia, use of exogenous estrogens, radiation, and a family history of male or female breast cancer. We conducted a case-control study to investigate risk factors further for breast cancer in men.Methods: Based on data from the 1986 National (United States) Mortality Followback Survey (NMFS) of almost 20,000 deceased adults (age 25 years or over), we compared information obtained from next-of-kin interviews of 178 men who died of breast cancer with that of 512 male controls who died of other causes. Information was obtained on selected demographic and other factors, including diet, exercise, occupation, height and weight, and use of tobacco and alcohol.Results: Increased risks were found for men who were described by their next-of-kin as very overweight (odds ratio [OR] = 2.3, 95 percent confidence interval [CI] = 1.1-5.0). The risks associated with the three upper quartiles of body mass index (BMI) (wt/ht²) were 1.3, 1.6, and 2.3, respectively, with a significant dose-response relationship (P < 0.01). An excess risk was also associated with limited exercise (OR = 1.3, CI = 0.8-2.0). Consumption of red meat was associated with an increased risk, and consumption of fruits and vegetables with a decreased risk, although the trends were not significant. No association was found for tobacco or alcohol use, but an excess risk was associated with higher levels of socioeconomic status (SES) (OR = 1.8, CI = 1.1-3.0).Conclusions: Our study suggests that obesity increases the risk of male breast cancer, possibly through hormonal mechanisms, while dietary factors, physical activity, and SES indicators also deserve further investigation. Cancer Causes andd Control 1998, 269-275     

The Swedish Snus and the Sudanese Toombak: are they different?

In Sweden, snuff (locally known as snus), was introduced since the year 1637. Presently, Sweden has the highest per capita consumption and sale figures of snuff in the world, and the habit is becoming increasingly popular. Snus is manufactured into a dry form used in the nasal cavity and a moist form used in the oral cavity. Snus manufactured for oral use is a moist ground tobacco of Dark Kentucky or Virginia species mixed with an aqueous solution of water and other blending ingredients. This form of snuff is found in two types: (1) loose and (2) portion-bag-packed. These are the most widely used. The loose moist form (1–2 g a quid) is the most popular type consumed by 73% of the males, followed by the portion-bag-packed form (0.5–1 g a quid), consumed by 13% of the males, while 14% of the males are mixed users. The majority of snus users place the quid in the vestibular area of the upper lip, and the prevalence among persons 15 years of age or older is 15.9% among males and 0.2% among females. The pH of snus has declined from a previous range of 8–9 to a range of 7.8–8.5, moisture content ranges 35–60% and nicotine content is in the order of 5–11 mg/g dry wt tobacco-specific N-nitrosamines (TSNAs) in micrograms (N′-nitrosonornicotine: NNN 5–9; 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone: NNK 1–2; N′-nitrosoanatabine: NAT 2–5). In the Sudan, snuff, locally known as toombak, was introduced approximately 400 years ago. It is always processed into a loose moist form, and its use is widespread in the country. Tobacco used for manufacture of toombak is of the species Nicotiana rustica, and the fermented ground powder is mixed with an aqueous solution of sodium bicarbonate. The resultant product is moist, with a strong aroma, highly addictive and its use is widespread particularly among males. Its pH range is 8–11, moisture content ranges 6–60% and nicotine content is from 8 to 102 mg/g dry wt, and TSNAs contents in micrograms (NNN 420–1 550; NNK 620–7 870; NAT 20–290). Snus and toombak dippers develop a clinically and histologically characteristic lesion at the site of dipping. Probably due to control of the TSNAs in snus, this type of snuff is associated with a lower risk of cancer of the oral cavity (relative risk: RR 5–6-fold), whereas the risk for cancer of the oral cavity among toombak users was high (RR 7.3–73.0-fold). In conclusion, the two snuff products significantly differ in many aspects. Most notable differences are tobacco species, fermentation and ageing, nicotine and TSNAs content, pH, expression of the p53 tumour supressor gene, and keratin types 13, 14, and 19. It was, therefore, the object of the present study to highlight the oral health hazards of toombak, and to compare it with snus regarding the aforementioned differences.     

广州市社区居民吸烟现状分析

[目的]了解广州市社区居民的吸烟状况,为制定控制吸烟的相应措施提供依据.[方法]在2004年,采用随机抽样入户问卷调查方式,调查广州市越秀区洪桥街和东风街20～60岁居民1006名.[结果]人群吸烟率为28.4%,男性吸烟率为52.2%,女性为6.5%;61.9%吸烟者在20岁以前开始吸烟;吸烟率随年龄增长而增高;文化程度低者吸烟率较高;运输业人员吸烟率最高;大部分吸烟者通常在家里、工作场所或娱乐场所吸烟;受访者对吸烟可能引起的呼吸系统以外的疾病认知不足;大多数认为从公共传媒获得吸烟危害健康的知识.[结论]吸烟仍是一个严重的公共卫生问题,须加强宣传教育,动员全社会力量,控制吸烟,以减少烟草对健康的危害.     

尼古丁成瘾的流行病学研究和遗传学研究

该文系统地介绍了尼古丁成瘾的行为表现及评价方法，并提出尼古丁成瘾是社会环境与遗传因素共同决定的复杂性疾病。尼古丁成瘾形成的机制及遗传易感性的研究有待重视，从分子药理学、毒理学、社会学等各个领域，探讨尼古丁成瘾已成为人们研究的热点。     

人组织型纤溶酶原激活剂(t-PA)与绿色荧光蛋白(GFP)在转基因烟草中的融合表达

构建人组织型纤溶酶原激活剂(t-PA)与绿色荧光蛋白(GFP)融合表达的植物表达载体pCA1302NSF-tPA。将重组载体转入根瘤农杆菌GV3101中，通过叶圆盘法转化烟草。转化植株经PCR鉴定整合有t-PA基因，通过荧光显微镜可检测到绿色荧光蛋白(GFP)的表达。     

Carcinogenic activity of cigarette smoke gas phase and its modulation by beta-carotene and N-acetylcysteine.

Male strain A/J mice were exposed for six hours a day, five days a week for six months to either full tobacco smoke or to tobacco smoke drawn through a HEPA filter that removed more than 99% of particulate matter. After another four months in air, the animals were sacrificed and lung tumors were counted for calculation of multiplicities and incidences. Analysis of the chamber atmospheres showed that in the filtered smoke the concentrations of polycyclic aromatic hydrocarbons and tobacco smoke specific nitrosamines were reduced to from below 18% to even nondetectable levels of the original values measured in the unfiltered smoke. Aldehydes and other volatile organic compounds such as 1,3-butadiene, benzene, or acrolein were reduced to about 50 to 90% of the concentrations found in unfiltered smoke. Some potentially carcinogenic metals reached levels in filtered smoke ranging from 77% to less than 1% found in full smoke. The mice exposed to the filtered smoke atmosphere had practically identical lung tumor multiplicities and incidence as had the animals exposed to full smoke, significantly higher than in air exposed controls. Diets containing 0.5% beta-carotene or 0.4% N-acetylcysteine afforded some chemoprevention. It was tentatively concluded that 1,3-butadiene might be an important contributor to lung tumorigenesis in this mouse model of tobacco smoke carcinogenesis.     

A pilot study of what African American maternal caregivers and their adolescent daughters talk about when asked to discuss tobacco together

Parents play a critical role in shaping their children’s substance use behaviors, yet few studies have examined the messages that caregivers give their adolescents about tobacco. In this study, we identify tobacco-related messages discussed by African American maternal caregivers and their adolescent daughters. Twenty-five African American maternal caregivers and their adolescent daughters participated in a video-taped discussion about tobacco. Discussions were transcribed and coded thematically. Seven themes emerged, which were grouped into tobacco-messages and communication strategies. Messages included health risks, non-health-related reasons to stop smoking, reasons people smoke, and tobacco products and marijuana. Strategies caregivers used to communicate their tobacco-related messages included sharing personal or their families’ experience with smoking, using humor, and role-playing. Finally, embedded within all of the themes, participants expressed their disapproval of tobacco use, whether it was directed at their own use, their adolescents’ use, a family members’ use, or peers’ use. African American maternal caregivers and their daughters openly talk about a variety of tobacco-related topics, and caregivers are open to sharing their own and their families’ experience with substance use. Findings also suggest that having caregivers and their adolescents participate in discussions tasks could be potentially beneficial in facilitating discussions and could identify areas in which caregivers could use help in discussing sensitive topics.     

Smoking Exposure Is Associated with Serum Vitamin D Deficiency in Children: Evidence from the Japan Environment and Children’s Study

Tobacco smoke exposure is known to lower serum 25-hydroxyvitamin D (25(OH)D) concentrations. This study evaluated the association between passive smoking and vitamin D deficiency (VDD) in young children using data from the Japan Environment and Children’s Study (JECS), the largest birth cohort study in Japan. Information on parental smoking status was extracted from a survey of JECS for children aged 1.5 years and data for serum 25(OH)D concentrations were obtained from blood tests in the Sub-Cohort Study of JECS performed at age 2 years. Logistic regression and linear models were fitted to evaluate the association between these variables. Data were analyzed for 4593 children. After adjusting for covariates, smoke exposure was significantly associated with increased incidence of VDD (OR 1.35; 95% CI, 1.14–1.59) according to the logistic model. The linear model indicated that passive smoking negatively predicted de-seasonalized serum 25(OH)D concentrations (β −0.5; 95% CI −0.95 to −0.08) in children aged 2 years. The results suggest that smoke exposure is a risk factor for VDD in children. Given that VD plays a crucial role in bone metabolism and the immune system, our findings are significant for clinical and public health.     

Tobacco carcinogen induces both lung cancer and non‐alcoholic steatohepatitis and hepatocellular carcinomas in ferrets which can be attenuated by lycopene supplementation

Early epidemiologic studies have reported that tobacco smoking, which is causally associated with liver cancer, is an independent risk factor for non‐alcoholic fatty liver diseases (NAFLD). Lycopene from tomatoes has been shown to be a potential preventive agent against NAFLD and hepatocellular carcinoma (HCC). In the present study, we investigated whether the tobacco carcinogen 4‐(N‐methyl‐N‐nitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK) induces lesions in both lungs and livers of ferrets with or without lycopene intervention. Male ferrets (6 groups, n = 8–10) were treated either with NNK (50 mg/kg BW, i.p., once a month for four consecutive months) or saline with or without dietary lycopene supplementation (2.2 and 6.6 mg/kg BW/day, respectively) for 26 weeks. Results demonstrate that NNK exposure results in higher incidences of lung tumors, HCC and steatohepatitis (which is characterized by severe inflammatory cell infiltration with concurrent fat accumulation in liver, hepatocellular ballooning degeneration and increased NF‐κB expression), as well as elevations in bilirubin and AST levels in ferrets. Lycopene supplementation at two doses prevented NNK‐induced expressions of α7 nicotinic acetylcholine receptor in the lung and NF‐κB and CYP2E1 in the liver and attenuated the NNK‐induced mortality and pathological lesions in both the lungs and livers of ferrets. The present study provided strong experimental evidence that the tobacco carcinogen NNK can induce both HCC and steatohepatitis in the ferrets and can be a useful model for studying tobacco carcinogen‐associated NAFLD and liver cancer. Furthermore, lycopene could provide potential benefits against smoke carcinogen‐induced pulmonary and hepatic injury.