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| COMMENTARY |
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| Year : 2018 | Volume
: 3
| Issue : 3 | Page : 55-56 |
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Air pollution and liver cancer
Yu Ji1, Christopher Stone2, Xiaokun Geng3, Yuchuan Ding2
1 Department of Hepatobiliary Surgery, Beijing Luhe Hospital, Capital Medical University, Beijing, China
2 Department of Neurosurgery, Wayne State University School of Medicine, Detroit, Michigan, USA
3 Department of Hepatobiliary Surgery, Beijing Luhe Hospital, Capital Medical University, Beijing, China; Department of Neurosurgery, Wayne State University School of Medicine, Detroit, Michigan, USA
| Date of Submission | 21-Aug-2018 |
| Date of Acceptance | 21-Sep-2018 |
| Date of Web Publication | 18-Oct-2018 |
Correspondence Address:
Dr. Yuchuan Ding
Department of Neurosurgery, Wayne State University School of Medicine, Detroit, Michigan
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ed.ed_17_18
How to cite this article:
Ji Y, Stone C, Geng X, Ding Y. Air pollution and liver cancer. Environ Dis 2018;3:55-6 |
Primary liver cancer poses, as the fourth leading cause of cancer death worldwide, a major and widespread burden of disease. The vast majority of primary liver cancers (approximately 75%–85%) are attributable to hepatocellular carcinoma (HCC),[1] the major risk factor for which is viral hepatitis secondary to hepatitis B and C infections.[2] Other prominent risk factors include hepatic cirrhosis, alcohol abuse, obesity, type 2 diabetes mellitus, and exposure to hepatotoxins.[1],[3],[4]
In addition to these established factors, recent studies have indicated that exposure to airborne particulate matter (PM) is also a risk factor for HCC. PM refers generally to microscopic solid or liquid matter suspended in the Earth's atmosphere.[5],[6] The deleterious effects of PM exposure on human health, particularly when particle diameters are below 2.5 μm (PM2.5), are well known. in addition to its designation by the International Agency for Research on Cancer as a Group 1 human carcinogen,[1],[2],[3] PM inhalation has been implicated in a range of other pathologic processes including asthma, lung cancer, cardiovascular disease, and cerebrovascular disease.[4],[7] The mechanisms by which PM2.5 exposure constitutes a risk factor for hepatic pathology seem to proceed through inflammatory, oxidative, and endoplasmic reticulum stress-mediated fibrosis.[8],[9]
Moreover, exposure to PM2.5 is every bit as ubiquitous as HCC, if not more so. a recent analysis concluded that over 87% of the world's population lives in areas that exceed the threshold set by the World Health Organization for safe annual average PM2.5 pollution.[10] It has, therefore, been possible to conduct analyses of PM2.5-mediated hepatic carcinogenesis on a large scale. In Taiwan, for instance, Wen-Chi Pan and his team recruited 23,820 participants with no history of HCC, and assessed the relationship between participants with HCC and PM2.5 exposure, finding both that long-term exposure was associated with dose-dependent elevations in baseline serum alanine aminotransferase, and that this exposure was positively associated with subsequent HCC risk at long-term follow-up.[11] Similarly, a study conducted by Huiyu Deng on 20,221 patients in the United States showed that PM2.5 exposure after HCC diagnosis was dose-dependently associated with shortened survival.[12]
It should be noted that PM2.5 is not the only modality of ambient pollution suspected to contribute to HCC pathogenesis. Roles have also been proposed for formaldehyde, the tumorigenic potential of which has earned it an EPA Group B1 carcinogen classification, and polycyclic aromatic hydrocarbons.[13] Further research is needed to elucidate the magnitude and mechanisms of the hepatic carcinogenic effect of these agents, however.
Surgical resection and transplantation of the liver are currently the main treatments for HCC, and percutaneous ablation may be employed for patients who cannot tolerate invasive surgery; interventional therapy, radiation therapy, and chemotherapy may be used as complementary treatments.[14] Since the 5-year survival rate of HCC remains, at <12%, distressingly low despite these treatments, primary prevention of HCC is essential.[15] This consideration, coupled with the pervasiveness of both HCC and the pollution that appears to precipitate it, underscores the ongoing need to conduct innovative, environmentally-focused, broad-based, and high-quality research in this field. Thus far, very little work of this kind has been conducted – an unfortunate state of affairs that our group hopes, in the coming years, to change.
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