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

      research-article
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      Cancer Biology & Medicine
      Chinese Anti-Cancer Association
      Lung cancer, tobacco smoke, air pollution, smohaze, carcinogenesis

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          Abstract

          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.

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          Most cited references64

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          Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE).

          Ambient air pollution is suspected to cause lung cancer. We aimed to assess the association between long-term exposure to ambient air pollution and lung cancer incidence in European populations. This prospective analysis of data obtained by the European Study of Cohorts for Air Pollution Effects used data from 17 cohort studies based in nine European countries. Baseline addresses were geocoded and we assessed air pollution by land-use regression models for particulate matter (PM) with diameter of less than 10 μm (PM10), less than 2·5 μm (PM2·5), and between 2·5 and 10 μm (PMcoarse), soot (PM2·5absorbance), nitrogen oxides, and two traffic indicators. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses. The 312 944 cohort members contributed 4 013 131 person-years at risk. During follow-up (mean 12·8 years), 2095 incident lung cancer cases were diagnosed. The meta-analyses showed a statistically significant association between risk for lung cancer and PM10 (hazard ratio [HR] 1·22 [95% CI 1·03-1·45] per 10 μg/m(3)). For PM2·5 the HR was 1·18 (0·96-1·46) per 5 μg/m(3). The same increments of PM10 and PM2·5 were associated with HRs for adenocarcinomas of the lung of 1·51 (1·10-2·08) and 1·55 (1·05-2·29), respectively. An increase in road traffic of 4000 vehicle-km per day within 100 m of the residence was associated with an HR for lung cancer of 1·09 (0·99-1·21). The results showed no association between lung cancer and nitrogen oxides concentration (HR 1·01 [0·95-1·07] per 20 μg/m(3)) or traffic intensity on the nearest street (HR 1·00 [0·97-1·04] per 5000 vehicles per day). Particulate matter air pollution contributes to lung cancer incidence in Europe. European Community's Seventh Framework Programme. Copyright © 2013 Elsevier Ltd. All rights reserved.
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            The aryl hydrocarbon receptor: an environmental sensor integrating immune responses in health and disease

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              Radical causes of cancer.

              Free radicals are ubiquitous in our body and are generated by normal physiological processes, including aerobic metabolism and inflammatory responses, to eliminate invading pathogenic microorganisms. Because free radicals can also inflict cellular damage, several defences have evolved both to protect our cells from radicals--such as antioxidant scavengers and enzymes--and to repair DNA damage. Understanding the association between chronic inflammation and cancer provides insights into the molecular mechanisms involved. In particular, we highlight the interaction between nitric oxide and p53 as a crucial pathway in inflammatory-mediated carcinogenesis.
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                Author and article information

                Contributors
                Journal
                Cancer Biol Med
                Cancer Biol Med
                CBM
                Cancer Biology & Medicine
                Chinese Anti-Cancer Association (Tianjing China )
                2095-3941
                November 2019
                : 16
                : 4
                : 700-713
                Affiliations
                [1] State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
                Author notes
                Guangbiao Zhou Email: gbzhou@ 123456cicams.ac.cn
                Article
                cbm-16-4-700
                10.20892/j.issn.2095-3941.2019.0180
                6936241
                31908889
                829a613e-e264-43d1-a721-961090593caf
                Copyright 2019 Cancer Biology & Medicine

                This work is licensed under a Creative Commons Attribution-NonCommercial-Share Alike 4.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                History
                : 16 May 2019
                : 8 July 2019
                Categories
                Review

                lung cancer,tobacco smoke,air pollution,smohaze,carcinogenesis

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