Effects of sulfur dioxide derivatives on expression of oncogenes and tumor suppressor genes in human bronchial epithelial cells

Qin, Guohua; Meng, Ziqiang

doi:10.1016/j.fct.2009.01.005

Cited by 37 publications

(13 citation statements)

References 43 publications

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“…The possible pathomechanisms of carcinogenicity of sulphate in ambient air for gastric cancer are not clear. Results from experimental research with human bronchial epithelial cells, support the hypothesis that SO 2 derivatives could by activation of pro-oncogenes and the inactivation of tumour suppressor genes play a role in the pathogenesis of cancer (Qin and Meng, 2009). It can also be speculated whether the formation of sulphuric acid, which is formed from oxidation from SO 2, increases the risk of gastric cancer (Bernatsky et al, 2017 PM 2.5 _S (5 µg/m 3 increase) Fig.…”

Section: Discussionmentioning

confidence: 61%

Particulate matter air pollution components and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts of Air Pollution Effects (ESCAPE)

Weinmayr

Pedersen

Stafoggia

et al. 2018

Environment International

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Section: Discussionmentioning

confidence: 61%

Particulate matter air pollution components and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts of Air Pollution Effects (ESCAPE)

Weinmayr

Pedersen

Stafoggia

et al. 2018

Environment International

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“…It was suggested that this would result in mucin overproduction and inflammation, if occurring in vivo. The same dose protocol (with the addition of a 2 mM dose of the SO 2 derivatives) for 4 hours was applied to the same cell line, leading to mRNA and protein overexpression of c-fos, c-jun and c-myc at all doses, with other changes in proto-oncogenes and tumour suppressor genes at 0.1-2.0 mM (Qin & Meng, 2009). …”

Section: Short-term Respiratory Effectsmentioning

confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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“…SO 2 is readily absorbed through the respiratory tract (99%) and subsequently dissociates to form its derivatives (bisulfate and sulfite in neutral fluid) [26]. The data in Qin's study [27] supported the hypothesis that SO 2 derivatives could cause the inactivation of tumor suppressor genes and SO 2 derivatives may play a role in the pathogenesis of SO 2 associated lung cancer. SO 2 in air pollution may play an important role in the reaction of epidermal growth factor receptor (EGFR).…”

Section: Discussionmentioning

confidence: 96%

“…Therefore, high SO 2 exposure in the environment might potentially increase AC incidence for lung cancer, and significantly test for trend ( P = 0.0272) has been observed at Table 2 in the present study. Environmental SO 2 may also increase the activity of tumor suppressor p53 (TP53) gene in human bronchial epithelial cells [27]. TP53 has been shown to be related to the risk of SCC [31-33].…”

Section: Discussionmentioning

confidence: 99%

Cell type specificity of female lung cancer associated with sulfur dioxide from air pollutants in Taiwan: An ecological study

Tseng

Huang

et al. 2012

BMC Public Health

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BackgroundMany studies have examined the association between air pollutants (including sulfur dioxide [SO2], carbon monoxide [CO], nitrogen dioxide [NO2], nitric oxide [NO], ozone [O3], and particulate matter < 10 μm [PM10]) and lung cancer. However, data from previous studies on pathological cell types were limited, especially for SO2 exposure. We aimed to explore the association between SO2 exposure from outdoor air pollutants and female lung cancer incidence by cell type specificity.MethodsWe conducted an ecological study and calculated annual average concentration of 6 air pollutants (SO2, CO, NO2, NO, O3, and PM10) using data from Taiwan Environmental Protection Administration air quality monitoring stations. The Poisson regression models were used to evaluate the association between SO2 and age-standardized incidence rate of female lung cancer by two major pathological types (adenocarcinoma [AC] and squamous cell carcinoma [SCC]). In order to understand whether there is a dose-response relationship between SO2 and two major pathological types, we analyzed 4 levels of exposure based on quartiles of concentration of SO2.ResultsThe Poisson regression results showed that with the first quartile of SO2 concentration as the baseline, the relative risks for AC/SCC type cancer among females were 1.20 (95% confidence interval [CI], 1.04-1.37)/1.39 (95% CI, 0.96-2.01) for the second, 1.22 (95% CI, 1.04-1.43)/1.58 (95% CI, 1.06-2.37) for the third, and 1.27 (95% CI, 1.06-1.52)/1.80 (95% CI, 1.15-2.84) for the fourth quartile of SO2 concentration. The tests for trend were statistically significant for both AC and SCC at P = 0.0272 and 0.0145, respectively.ConclusionThe current study suggests that SO2 exposure as an air pollutant may increase female lung cancer incidence and the associations with female lung cancer is much stronger for SCC than for AC. The findings of this study warrant further investigation on the role of SO2 in the etiology of SCC.

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Effects of sulfur dioxide derivatives on expression of oncogenes and tumor suppressor genes in human bronchial epithelial cells

Cited by 37 publications

References 43 publications

Particulate matter air pollution components and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts of Air Pollution Effects (ESCAPE)

Particulate matter air pollution components and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts of Air Pollution Effects (ESCAPE)

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Cell type specificity of female lung cancer associated with sulfur dioxide from air pollutants in Taiwan: An ecological study

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