THE N-NITROSAMINES IN TOBACCO SMOKE AND ITS ADSORPTION AND DEGRADATION

N-nitrosamines are strong carcinogens for humans. This paper gives an overview of the nitrosmaines in cigarette smoke including the formation, the harmfulness, the analytical methods of the nitrosmaines and the adsorptions and degradations of N –nitrosamines.

Association between Tobacco Smoke Exposure (Environmental and Direct) and Incidence and Control of Bronchial Asthma

Background: Asthma is a chronic multifactorial disease with high prevalence. Among asthma risk factors, the effect of tobacco smoke exposure on bronchial asthma is still debated. Aim: The aim of this study was to determine the association between environmental and direct tobacco smoke (cigarette and hookah) exposure and incidence and control of bronchial asthma. Materials & Methods: This descriptive study was conducted on 109 patients with asthma referring to Imam Khomeini Hospital in Ardabil city. Asthma Control Questionnaire was used for evaluating of asthma control. Patients’ asthma control was individually evaluated and compared with together with particular attention to history of tobacco smoke exposure. Chi square and Tav-Kendal were used to analyze the data in SPSS15 software. Results: The history of tobacco smoke exposure was found in 31.2% of the 109 patients. Patients with uncontrolled asthma with 60.6% constituted the largest volume of all samples. There was no significant correlation between tobacco smoke exposure and asthma occurrence (P > 0.05), also there was not found significant correlation between tobacco smoke exposure and asthma control (Error coefficient > 0.10). Conclusion: According to the results, history of tobacco (cigarette and hookah) smoke exposure (environmental and direct) has no effect on the asthma occurs and control status.

The role of XPC protein deficiency in tobacco smoke-induced DNA hypermethylation of tumor suppressor genes

DNA hypermethylation of tumor suppressor genes has been frequently observed in cancer patients, and therefore, may provide a valuable biomarker for cancer prevention and treatment. DNA hypermethylation may also provide an important mechanism in cancer progression. Lung cancer is strongly associated with exposure to environmental carcinogens, especially tobacco smoke. DNA damage generated by tobacco smoke is believed to play an important role in lung cancer development. XPC is a DNA damage recognition protein required for DNA repair and other DNA damage responses and attenuated XPC protein levels have been detected in many lung cancer patients. We studied the role of XPC protein deficiency in tobacco smoke-caused DNA hypermethylation of important tumor suppressor genes. Using both normal human fibroblasts (NF) and XPC-deficient hu man fibroblasts (XPC), our DNA methylation studies demonstrated that the XPC deficiency caused elevated levels of DNA hypermethylation in both Brca1 and Mlh1 tumor suppressor genes following exposure to tobacco smoke condensate (TSC). The results of our ChIP studies revealed that the XPC deficiency led to an increased binding of DNA methyltransferase 3A (DNMT3A) at the promoter region CpG island-containing sequences of these genes under the TSC treatment;however, this increase was partially diminished with prior treatment with caffeine. The results of our immuno-precipitation (IP) studies demonstrated a protein-protein interaction of the ATR with DNMT3A. Our western blots revealed that the XPC deficiency caused an increase in TSC-induced ATR phosphorylation at serine 428, an indicator of ATR activation. All these results suggest that XPC deficiency causes an accelerated DNA hypermethylation in important tumor suppressor genes under tobacco smoke exposure and activation of the ATR signaling pathway is involved in this DNA hypermethylation process.

Assessment of urinary concentration of cotinine in Chinese pregnant women exposed to environmental tobacco smoke

Environmental tobacco smoke(ETS)is a wellknown reason of many adverse health consequences in pregnant women.Exposure of ETS during pregnancy may increase the risk of some fetal diseases in pregnant women and/or birth defects in neonates.Many countries have implemented laws to control smoking and free of second hand smoke in all enclosed workplaces.In China,antismoking law was enforced in March 2010.We aimed to assess the exposure of pregnant women to cotinine after anti-smoking law was implemented in China.The urine samples were collected from 2,100 volunteers from Zhejiang Province,China and urinary concentration of cotinine was measured using gas chromatography and mass spectrometry.Cotinine was detected in 87%of the pregnant women.The GM and 95th percentile concentration inpregnant women were 4.28 and 44.00 lg/L,respectively.Similarly,the GM and 95th concentration of cotinine were significantly higher in smoking group than in non-smoking group(P\0.0001).Our results indicate that pregnant women in China are at the high risk of exposure ETS.Further attempts are required to make strategies to find out the sources of ETS exposure and prevent smoking at public places especially during pregnancy.

8-Hydroxydeoxyguanosine as a Biomarker of Oxidative DNA Damage Induced by Environmental Tobacco Side-stream Smoke and Its Mechanism

To study the genotoxicity effect of environmental tobacco side-stream smokes (ETSS) on oxidative DNA damage and its molecular mechanism. Methods DNA adduct 8-hydroxydeoxyguanosine (8-OHdG) was used as a biomarker of oxidative DNA damage. The level of 8-OHdG in DNA exposed to ETSS was detected by high performance liquid chromatography with electrochemical detection. Organic and inorganic components in ETSS were analyzed by gas chromatography-mass spectrum and atomic absorption spectrum respectively. Results Particle matters (PMs) and volatile organic compounds (VOCs) in ETSS could directly induce oxidative DNA damage and formation of 8-OHdG. There were 123 and 84 kinds of organic components in PMs and VOCs respectively, and 7 kinds of inorganic components in ETSS. Some components, especially quinones and polyphenols in ETSS, could produce free radicals in vitro by auto-oxidation without any biological activity systems, and with the catalytic reaction of metals, the DNA adduct 8-OHdG was produced. Conclusion ETSS have biological oxidative effect on DNA in vitro and in vivo, and expressed direct genotoxicity. 8-OHdG is a valuable biomarker of oxidative DNA damage.

Tobacco, air pollution, environmental carcinogenesis, and thoughts on conquering strategies of lung cancer

Each year there will be an estimated 2.1 million new lung cancer cases and 1.8 million lung cancer deaths worldwide.Tobacco smoke is the No.1 risk factors of lung cancer,accounting for>85%lung cancer deaths.Air pollution,or haze,comprises ambient air pollution and household air pollution,which are reported to cause 252,000 and 304,000 lung cancer deaths each year,respectively.Tobacco smoke and haze(hereafter,smohaze)contain fine particles originated from insufficient combustion of biomass or coal,have quite similar carcinogens,and cause similar diseases.Smohaze exert hazardous effects on exposed populations,including induction of a large amount of mutations in the genome,alternative splicing of mRNAs,abnormalities in epigenomics,initiation of tumor-promoting chronic inflammation,and facilitating immune escape of transformed cells.Tackling smohaze and development of multi-targets-based preventive and therapeutic approaches targeting smohaze-induced carcinogenesis are the key to conquer lung cancer in the future.

Impact of Tobacco Smoking on Health Care Utilization and Medical Costs in Chronic Obstructive Pulmonary Disease,Coronary Heart Disease and Diabetes

Objective To determine the impact of smoking on disease-specific health care utilization and medical costs in patients with chronic non-communicable diseases(NCDs).Methods Participants were middle-aged and elderly adults with chronic NCDs from a prospective cohort in China.Logistic regressions and linear models were used to assess the relationship between tobacco smoking,health care utilization and medical costs.Results Totally,1020 patients with chronic obstructive pulmonary disease(COPD),3144 patients with coronary heart disease(CHD),and 1405 patients with diabetes were included in the analysis.Among patients with COPD,current smokers(β:0.030,95%CI:−0.032-0.092)and former smokers(β:0.072,95%CI:0.014-0.131)had 3.0%and 7.2%higher total medical costs than never smokers.Medical costs of patients who had smoked for 21-40 years(β:0.028,95%CI:−0.038-0.094)and≥41 years(β:0.053,95%CI:−0.004β0.110)were higher than those of never smokers.Patients who smoked≥21 cigarettes(β:0.145,95%CI:0.051-0.239)per day had more inpatient visits than never smokers.The association between smoking and health care utilization and medical costs in people with CHD group was similar to that in people with COPD;however,there were no significant associations in people with diabetes.Conclusion This study reveals that the impact of smoking on health care utilization and medical costs varies among patients with COPD,CHD,and diabetes.Tobacco control might be more effective at reducing the burden of disease for patients with COPD and CHD than for patients with diabetes.

Interaction models of CYP1A1, GSTMl polymorphisms and tobacco smoking in intestinal gastric cancer

AIM： To explore the interaction models of the cytochrome P-450 （CYP） 1A1 Valvariant and glutathione S-transferase （GST） M1 null polymorphisms with tobacco smoking in the occurrence of intestinal gastric cancer. METHODS： A community-based case-control study was conducted in Yangzhong. Subjects included 114 intestinal types of gastric cancer with endoscopic and pathological diagnosis during January 1997 and December 1998, and 693 controls selected from their spouse, siblings or siblingsin-law who had no history of digestive system cancer. Logistic regression was used to estimate the interaction models. RESULTS： The frequency of the CYPIA1 Valvariant allele in cases did not differ from that in controls. The OR of GSTM1 null genotype was 2.0 （95% confidence interval [95%CI]： 1.2-3.1, P〈0.01）. It showed a significant type 2 form of interaction model when both CYPIA1 Valvariant allele and former tobacco smoking existed （i.e., among the multiplicative effects, the disease risk is increased by the tobacco exposure alone but not by the CYPIA1 variant alone）. The interaction index y was 2.8, and OReg （95%CI） was 5.0 （1.9-13.4）. GSTM1 null genctype and former tobacco smoking were significant in a type 4 interaction model （i.e., the disease risk is increased by GSTM1 null genotype or tobacco exposure alone among the multiplicative effects）. The interaction index y and OReg （95%CI） were 3.4 and 8.4 （3.4-20.9）, respectively.CONCLUSION： Different interaction models of CYPIA1 Valvariant allele and GSTM1 null genotype with tobacco smoking will contribute to understanding carcinogenic mechanism, but there is a need to further investigate in larger scale studies.

Estimates of the Prevalence of Tobacco Smoking in Egypt

The use of tobacco products constitutes the leading cause of preventable deaths in the world. In Egypt, data on the national prevalence of cigarette and waterpipe smoking are lacking, yet such data are vital to tobacco control efforts. We designed and implemented a sampling method to generate population-based prevalence estimates for tobacco smoking in Egypt. In 2005, a total of 3369 adults ages 18 and above, including 1867 females and 1502 males, participated in the survey. Among males, the national prevalence of former cigarette smoking was 18.1%, and 27.5% reported current smoking. Exclusive current waterpipe smoking was reported by 7.2% of adult males, and a further 3.4% reported smoking both waterpipes and cigarettes. Tobacco smoking was rarely reported by females;among them the national prevalence of current cigarette smoking was 0.3%. This study produced the first robust estimate of the national prevalence of cigarette and waterpipe smoking in Egypt based on a rigorous probability sample. Along with the more recent Global Adult Tobacco Survey, carried out by the World Health Organization in 2009, the results will be useful in assessing smoking trends in Egypt and in evaluating the impacts of recent tobacco control laws.

Reduction of Tobacco Smoking Health Risk Through an Appropriate Media Based Communication Strategy in Uganda

The health impacts of tobacco consumption are well documented and have gained acceptance worldwide. Today, a substantial, preventable burden of tobacco attributable diseases exists in most countries, though in most of the cases, unknown. Smoking accounts for almost half of the deaths in middle age in some regions. In Uganda, translating findings into policy action is slow and involves several stakeholders. It will continue to require support from tobacco control campaign groups. This paper analyses secondary literature on tobacco smoking and later provides an appropriate medium based communication strategy that can be adopted to counteract the persuasive smoking evil adverts of tobacco companies as well as creating awareness among the population of the health impacts caused by smoking.

Effect of Genetic Polymorphism of CYP2A6 on Individual Susceptibility to Colorectal Tumors in Japanese Smokers

Tobacco smoking is a risk factor for colorectal cancer and adenomas. To clarify the effect of genetic factors on the risk for tobacco-related colorectal tumors in a Japanese population, we performed a case-control study on 300 patients with two or more tumors and 181 healthy controls;all were genotyped for CYP2A6*4, CYP2A6*7 and CYP2A6*9. Cigarette smoking increased colorectal tumor risk (trend-test P ). Current smokers plus ex-smokers (ever-smokers) with the CYP2A6*4/*4 genotype (whole gene deletion) showed the lowest risk among smokers [odds ratio (OR), 0.17;95% confidence interval (CI), 0.05 - 0.62 compared to ever-smokers with the wild-type CYP2A6*1/*1]. When the participants were classified into four phenotype groups based on estimated CYP2A6 activity [i.e., normal (*1/*1), intermediate (heterozygotes for the *1 and a variant allele), slow (heterozygotes and homozygotes for variant alleles except for *4/*4) and poor (*4/*4)], the ORs (95% CIs) in ever-smokers of the normal, intermediate, slow and poor groups were 6.75 (2.73 - 16.76), 4.59 (2.10 - 10.06), 3.89 (1.69 - 8.95) and 1.17 (0.31 - 4.40), respectively, compared with never-smokers with normal CYP2A6 activity. The susceptibility to colorectal tumors was dependent on the predicted phenotype among ever-smokers (trend-test P = 0.015), but not among never-smokers (trend-test P = 0.47). Stratifying the subjects with respect to cumulative tobacco exposure and estimated CYP2A6 activity, we found the highest risk of colorectal tumors in subjects with higher CYP2A6 activity and higher cumulative tobacco exposure (trend-test P = 0.000023);the lowest risk was found in subjects with the lowest estimated CYP2A6 activity independent of tobacco exposure (trend-test P = 1.00). These results suggest that the gene-environment interaction (i.e. , the CYP2A6-smoking interaction) strongly affects the individual susceptibility to tobacco-related colorectal tumors.

Tobacco smoking and its drug interactions with comedications involving CYP and UGT enzymes and nicotine

Tobacco smoking is a global public health threat causing several illnesses including cardiovascular disease(Myocardial infarction), cerebrovascular disease(Stroke), peripheral vascular disease(Claudication), chronic obstructive pulmonary disease, asthma, reduced female infertility, sexual dysfunction in men, different types of cancer and many other diseases. It has been estimated in 2015 that approximately 1.3 billion people smoke, around the globe. Use of medications among smokers is more common, nowadays. This review is aimed to identify the medications affected by smoking, involving Cytochrome P450(CYP)and uridine diphosphate-glucuronosyltransferases(UGTs) enzymes and Nicotine. Polycyclic aromatic hydrocarbons(PAHs) of tobacco smoke have been associated with the induction of CYP enzymes such as CYP1A1, CYP1A2 and possibly CYP2E1 and UGT enzymes. The drugs metabolized by CYP1A1,CYP1A2, CYP2E1 and UGT enzymes might be affected by tobacco smoking and the smokers taking medications metabolized by those enzymes, may need higher doses due to decreased plasma concentrations through enhanced induction by PAHs of tobacco smoke. The prescribers and the pharmacists are required to be aware of medications affected by tobacco smoking to prevent the toxicityassociated complications during smoking cessation.

Impact of Village-based Health Education of Tobacco Control on the Current Smoking Rate in Chinese Rural Areas

The number of smokers in Chinese rural areas is more than 200 million, which is twice that in cities. It is very significant to carry out tobacco control interventions in rural areas. We performed this community intervention study to evaluate the efficacy of village-based health education of tobacco control on the male current smoking rate in rural areas. The population of this study was the males above 15 years old from 6 villages in rural areas. The villages were randomly assigned to intervention group or control group（3 villages in each group）. Self-designed smoking questionnaire was applied. The intervention group received the village-based health education of tobacco control for one year. The primary outcome measurement was the male current smoking rate. In the baseline investigation, completed surveys were returned by 814 male residents from the control group and 831 male residents from the intervention group. The male current smoking rate in the control group and the intervention group was 61.2% and 58.5%, respectively, before intervention. There was no significant difference between these two groups（P〉0.05）. After one-year intervention, the current smoking rate in the intervention group（51.2%） was significantly lower than that in the control group（62.8%）（P〈0.001）. Our study suggested that the village-based health education of tobacco control was effective in lowering the male current smoking rate in rural areas, which could be a suitable and feasible way for tobacco control in the Chinese rural areas.

CONCERNING THE RELATION OF TOBACCOGLYCOPROTEIN TO BUERGER'S DISEASE

Objective To comprehend the reiation of tobacco glycoprotein (TGP) to Buerger,s disease.Metbods TGP was isolated from crude tobacco leaves by basic immunologic techniques. Serum anti- TGPantibodies were tested by Western blot analysis in 11 patients with Buerger,s disease, 15 healthy male smokers and11 nonsmoking healthy male subjects. Results 1. TGP is a dark brown protein of molecular weight 14000. It maybe a subunit of some high molecular weight protein, and exists in crude tobacco leaves. 2. Western blot analysisshowed that 81.81% of patients with Buerger’s disease (9/11), 33.33% of healthy smokers (5/15) and 27.27% ofhealthy nonsmokers (3/11) had serum anti- TGP antibodies. There was significant dtherence between patientswith Buerger,s disease and two control groups (P<0.05), and no signilicant dtherence between both control groups(P>0.05). Conclusion TGP does play an important role in the pathogenesis of Buerger’s disease. As anti - TGPantibodies are also found in some control subjects, it is speculated that other etiologic factors might coordinatelycontribute to the specifc vascular response to TGP in susceptible subjects.

A Decision Tree Approach for Predicting Smokers’Quit Intentions

This paper presents a decision tree approach for predicting smokers＇ quit intentions using the data from the International Tobacco Control Four Country Survey. Three rule-based classification models are generated from three data sets using attributes in relation to demographics, warning labels, and smokers＇ beliefs. Both demographic attributes and warning label attributes are important in predicting smokers＇ quit intentions. The model＇s ability to predict smokers＇ quit intentions is enhanced, if the attributes regarding smokers＇ internal motivation and beliefs about quitting are included.

肺功能检查联合5A行为干预的短期戒烟效果评价

目的:探讨肺功能检查和宣教联合5A行为干预的短期戒烟效果。方法:选取2019年5月—2021年12月在汕头大学医学院第一附属医院呼吸科门诊就诊且有吸烟史的439例患者为研究对象,均为男性,年龄(54.9±12.5)岁。根据患者的意愿分为肺功能检查联合5A行为干预组(干预组,224例)和仅实施5A行为干预组(对照组,215例),干预时间1个月。采用成功戒烟率及烟草依赖程度评价短期戒烟效果。采用logistic回归分析评价肺功能检查和宣教联合5A行为干预的戒烟效果。以倾向性得分匹配进行敏感性分析,评估多因素logistic回归分析结果的稳健性。结果:干预组的成功戒烟率为43.8%(98/224),对照组为13.5%(29/215),干预组的成功戒烟率高于对照组(χ^(2)=48.86,P<0.001)。在干预后戒烟失败患者中,干预组的重度烟草依赖患者占比较干预前下降,且低于对照组,差异具有统计学意义(干预前重度烟草依赖:35.7%比34.9%;干预后重度烟草依赖:19.1%比29.6%)。多因素logistic回归分析显示,与对照组相比,干预组短期成功戒烟率增高(OR=3.92,95%CI:2.18~7.06),干预组中戒烟失败患者的烟草依赖度降低(OR=4.34,95%CI:1.72~10.92)。结论:肺功能检查和宣教联合5A行为干预可能在短期内有助于提高呼吸科门诊吸烟患者的戒烟成功率,降低戒烟失败患者的烟草依赖程度。

不同圆周卷烟的风格特征与烟气特征分析

【目的】考察卷烟圆周值对烤烟烟叶风格特征及烟气特征的影响。【方法】以八大香型烤烟产地典型烟叶(C3F)为原料,分别制备常规、中支和细支卷烟样品,通过对样品进行感官评价、常规烟气指标和香味成分检测,研究八大香型生态区域烤烟烟叶随卷烟圆周值变化其风格特征和烟气特征的变化规律。【结果】(1)不同生态区烤烟烟叶卷制烟支的香气风格随圆周值的变化存在差异,随着卷制圆周值降低,烟叶原料卷烟的风格特征呈弱化趋势。(2)不同生态区烤烟烟叶卷制烟支的品质特征随圆周值的变化存在差异,随着卷制圆周值的降低,香气量、透发性和成团性等感官指标均有减小趋势,刺激性、干燥感和细腻程度等感官指标有改善趋势。(3)随卷制圆周值降低,不同生态区烤烟烟叶卷制烟支主流烟气焦油、烟碱和CO释放量均有减小。(4)随着卷制圆周值的降低,除黑龙江哈尔滨生态区烟叶外,其他生态区烟叶卷制烟支的主流烟气TPM单口释放量为中支烟>常规烟≥细支烟。香味成分酚类、酸类、酯类、内酯类、酰胺类和新植二烯的单口释放量整体表现为中支烟≥常规烟>细支烟,醛类、烃类、杂环类、醇类和酮类物质的单口释放量整体表现为中支烟>常规烟≥细支烟。

不同烤烟新品种在吉林省通化区域适用性研究

为解决吉林省烤烟种植品种单一的问题,该研究在吉林省通化市柳河县以“吉烟九号”为对照,对9个烤烟新品种“中烟特香301”“云烟301”“硃砂烟”等在农艺性状、经济性状、主要化学成分、外观质量评价和评吸鉴定结果等方面进行分析。结果表明:“硃砂烟”在农艺性状、产量产值、外观质量评价、感官分值和主成分分析上表现最好,特别是在经济性状和评吸鉴定结果上具有明显优势;其次“中烟特香301”农艺性状优和经济性状表现好,化学成分协调分值、评吸鉴定结果也较好;“中川208”农艺性状和经济性状的表现属中等,但在外观质量和评吸鉴定结果中表现较好。三个品种主成分分析排序为“硃砂烟”>“中烟特香301”>“中川208”。三个品种需进一步重点考察。

外加水溶性糖对卷烟烟气成分释放量的影响

[目的]系统考察外加水溶性糖对卷烟烟气常规成分和七害成分释放量的影响,[方法]以内源水溶性糖含量较高(C2F-DF2020,总糖30.84%)、较低(B3F-DH2020,总糖7.37%)的2种烤烟烟叶为参试对象,选用葡萄糖、蔗糖2种糖料,进行加糖量梯度试验(加糖量0%、2%、4%、6%、8%、10%),测定24个卷烟小样的烟气常规成分;在小样试验的基础上,以内源水溶性糖含量中等的(B2F-XG2018,总糖16.61%)烟叶为对象,进行中样试验(葡萄糖添加量0%、1%、3%、5%),测定4个卷烟中样的烟气常规成分和七害成分。[结果]小样试验结果显示,无论烟叶内源水溶性糖含量是高还是低,也无论外加糖源是葡萄糖还是蔗糖,烟气焦油量都不会随加糖量的增加而升高;中样试验结果显示,随着加糖量的增加,烟气焦油量不会随之升高,七害成分中含氮化合物如烟草特有NNK、HCN、氨等释放量呈下降趋势,卷烟危害性指数呈下降趋势。[结论]外加水溶性糖不会导致烟气焦油量和卷烟危害性指数升高。

When smoke meets gut:deciphering the interactions between tobacco smoking and gut microbiota in disease development

Tobacco smoking is a prevalent and detrimental habit practiced worldwide,increasing the risk of various diseases,including chronic obstructive pulmonary disease(COPD),cardiovascular disease,liver disease,and cancer.Although previous research has explored the detrimental health effects of tobacco smoking,recent studies suggest that gut microbiota dysbiosis may play a critical role in these outcomes.Numerous tobacco smoke components,such as nicotine,are found in the gastrointestinal tract and interact with gut microbiota,leading to lasting impacts on host health and diseases.This review delves into the ways tobacco smoking and its various constituents influence gut microbiota composition and functionality.We also summarize recent advancements in understanding how tobacco smoking-induced gut microbiota dysbiosis affects host health.Furthermore,this review introduces a novel perspective on how changes in gut microbiota following smoking cessation may contribute to withdrawal syndrome and the degree of health improvements in smokers.