scholarly journals How to prevent most deaths from lung cancer: control cigarette smoking and air pollution

2019 ◽  
Vol 3 ◽  
pp. 2-2
Author(s):  
Jonathan M. Samet
Keyword(s):  
Lung Cancer ◽  
Air Pollution ◽  
Cigarette Smoking ◽  
Cancer Control

scholarly journals Ambient Air Pollution and Cigarette Smoking: Co-Drivers of Increased Burden of Lung Cancer in Europe

2020 ◽  
Author(s):  
Maybin Kalubula ◽  
Heqing Shen ◽  
Longjian Liu
Keyword(s):  
Lung Cancer ◽  
Air Pollution ◽  
Particulate Matter ◽  
Mortality Rate ◽  
Cigarette Smoking ◽  
Cancer Mortality ◽  
Lung Cancer Mortality ◽  
Small Cell ◽  
World Health ◽  
Adeno Carcinoma

Background: Lung cancer is one of the leading causes of morbidity and mortality worldwide with 25% of deaths due to lung cancer occurring in Europe. This study therefore sought to assess the burden of lung cancer by country and to evaluate the magnitude of fine Particulate Matter (PM2.5) and cigarette smoking by country in Europe. Methods: An ecological study nested on the World Health Organization air pollution database 2016 was conducted. We sampled 30 European Countries, with a total of 1625 mean annual samples of Particulate Matter (PM2.5) collected from 1625 designated sites (n = 1625). We further used the ‘World Health Disease Rankings’ database to extract Lung Cancer Morbidity and Mortality Rate by country. We used SAS version 9.4 to indicate the distribution of PM2.5 and Lung Cancer Mortality Rate. Results: Lung cancer Relative Risk (RR) was 1.0 in all never- smokers. RR for Ex-smokers for Adeno carcinoma was 3.5 in males and 1.1 in females, small cell carcinoma was 16.2 in males and 3.8 in females. RR for current smokers for Adeno carcinoma was 8.0 in males and 4.1 in females, small cell carcinoma was 57.9 in males and 18.2 in females. Mean annual PM2.5 by country ranged from 6.01 to 37.28µg/m3 whereas lung cancer mortality rate by country ranged from 19.67 to 54.26 deaths per 100,000 population. Conclusion: Cigarette smoking and exposure to both second hand smoke and high concentration of PM2.5 resulted into increased burden of lung cancer in Europe. Countries should re-strategize to reduce the burden of lung cancer in Europe.

Investigation into Cigarette Smoking and Atmospheric Pollution in the Aetiology of Lung Cancer

1963 ◽  
Vol 2 (01) ◽  
pp. 13-19 ◽  
Author(s):  
R. Doll
Keyword(s):  
Lung Cancer ◽  
Cigarette Smoking ◽  
Atmospheric Pollution ◽  
Direct Evidence ◽  
Retrospective Studies ◽  
Common Factor ◽  
Animal Experiments ◽  
Smoking Habits ◽  
Careful Examination ◽  
Ancillary Data

The evidence that cigarette smoking and atmospheric pcllution are causes of lung cancer is largely statistical. The first evidence was indirect; that is, i1. was noticed that in many countries the incidence of lung cancer had increased and that the increase could be correlated with changes in the prevalence of cigarette smoking and of certain types of atmospheric pollution.Since then much direct evidence has been obtained. The relationship between cigarette smoking and lung cancer has been demonstrated retrospectively by comparing the smoking habits of patients with and without lung cancer and prospectively by observing the mortality from lung cancer in groups of persons of known smoking habits. Conclusions can be drawn from these studies only after careful examination of the results. In particular it is important in retrospective studies to test a) the reproducibility of the data, b) the representativeness of the data, and c) the comparability of the special series and their controls. The resul1.s of retrospective studies are all similar and all show a close relationship between cigarette smoking and the disease.The results have been confirmed by pro~pective studies which are lesF. open to bias. The results can be explained if cigarette smoking causes lung cancer or if both are related to some third common factor. Ancillary data (pathological changes in the bronchial mucosa, animal experiments, etc.) support the causal hypothesis.The evidence relating to atmospheric pollution is less definite and it is difficult to get direct evidence of a relationship in the individual. It is clear that pollution has little effect in the absence of smoking, but the mortality associated with a given amount of smoking is generally greater in large towns than in the countryside and among men who have emigrated from Britain than among men who have lived all their lives in less polluted countries.

scholarly journals Cigarette Smoking and Risk of Lung Cancer in Korean Men: The Seoul Male Cancer Cohort Study

2007 ◽  
Vol 22 (3) ◽  
pp. 508 ◽  
Author(s):  
Jong-Myon Bae ◽  
Moo-Song Lee ◽  
Myung-Hee Shin ◽  
Dong-Hyun Kim ◽  
Zhong-Min Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cohort Study ◽  
Cigarette Smoking

scholarly journals Multiple air pollutant exposure and lung cancer in Tehran, Iran

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zahra Khorrami ◽  
Mohsen Pourkhosravani ◽  
Maysam Rezapour ◽  
Koorosh Etemad ◽  
Seyed Mahmood Taghavi-Shahri ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Air Pollution ◽  
Cancer Incidence ◽  
Latent Profile Analysis ◽  
Negative Binomial ◽  
Profile Analysis ◽  
Positive Association ◽  
Air Pollutant ◽  
World Health ◽  
Lung Cancer Incidence

AbstractLung cancer is the most rapidly increasing malignancy worldwide with an estimated 2.1 million cancer cases in the latest, 2018 World Health Organization (WHO) report. The objective of this study was to investigate the association of air pollution and lung cancer, in Tehran, Iran. Residential area information of the latest registered lung cancer cases that were diagnosed between 2014 and 2016 (N = 1,850) were inquired from the population-based cancer registry of Tehran. Long-term average exposure to PM10, SO2, NO, NO2, NOX, benzene, toluene, ethylbenzene, m-xylene, p-xylene, o-xylene (BTEX), and BTEX in 22 districts of Tehran were estimated using land use regression models. Latent profile analysis (LPA) was used to generate multi-pollutant exposure profiles. Negative binomial regression analysis was used to examine the association between air pollutants and lung cancer incidence. The districts with higher concentrations for all pollutants were mostly in downtown and around the railway station. Districts with a higher concentration for NOx (IRR = 1.05, for each 10 unit increase in air pollutant), benzene (IRR = 3.86), toluene (IRR = 1.50), ethylbenzene (IRR = 5.16), p-xylene (IRR = 9.41), o-xylene (IRR = 7.93), m-xylene (IRR = 2.63) and TBTEX (IRR = 1.21) were significantly associated with higher lung cancer incidence. Districts with a higher multiple air-pollution profile were also associated with more lung cancer incidence (IRR = 1.01). Our study shows a positive association between air pollution and lung cancer incidence. This association was stronger for, respectively, p-xylene, o-xylene, ethylbenzene, benzene, m-xylene and toluene.

scholarly journals Epigenome-wide association study of whole blood gene expression in Framingham Heart Study participants provides molecular insight into the potential role of CHRNA5 in cigarette smoking-related lung diseases

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Chen Yao ◽  
Roby Joehanes ◽  
Rory Wilson ◽  
Toshiko Tanaka ◽  
Luigi Ferrucci ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Dna Methylation ◽  
Cigarette Smoking ◽  
Association Study ◽  
Whole Blood ◽  
Lung Diseases ◽  
Epigenetic Modification ◽  
Blood Gene Expression ◽  
Increased Risk

Abstract Background DNA methylation is a key epigenetic modification that can directly affect gene regulation. DNA methylation is highly influenced by environmental factors such as cigarette smoking, which is causally related to chronic obstructive pulmonary disease (COPD) and lung cancer. To date, there have been few large-scale, combined analyses of DNA methylation and gene expression and their interrelations with lung diseases. Results We performed an epigenome-wide association study of whole blood gene expression in ~ 6000 individuals from four cohorts. We discovered and replicated numerous CpGs associated with the expression of cis genes within 500 kb of each CpG, with 148 to 1,741 cis CpG-transcript pairs identified across cohorts. We found that the closer a CpG resided to a transcription start site, the larger its effect size, and that 36% of cis CpG-transcript pairs share the same causal genetic variant. Mendelian randomization analyses revealed that hypomethylation and lower expression of CHRNA5, which encodes a smoking-related nicotinic receptor, are causally linked to increased risk of COPD and lung cancer. This putatively causal relationship was further validated in lung tissue data. Conclusions Our results provide a large and comprehensive association study of whole blood DNA methylation with gene expression. Expression platform differences rather than population differences are critical to the replication of cis CpG-transcript pairs. The low reproducibility of trans CpG-transcript pairs suggests that DNA methylation regulates nearby rather than remote gene expression. The putatively causal roles of methylation and expression of CHRNA5 in relation to COPD and lung cancer provide evidence for a mechanistic link between patterns of smoking-related epigenetic variation and lung diseases, and highlight potential therapeutic targets for lung diseases and smoking cessation.

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