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

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.

Keywords: Lung cancer; air pollution; carcinogenesis; smohaze; tobacco smoke.

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Estimated new lung cancer cases and lung cancer deaths worldwide and in China in 2018.

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Schematic representation of the complicated smohaze-induced lung carcinogenesis.

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AhR in lung carcinogenesis. (A) Schematic representation of AhR protein. bHLH, basic helix–loop–helix; PAS, period [Per]-aryl hydrocarbon receptor nuclear translocator [ARNT]-single minded [SIM]; P/S, proline (P)/serine (S). (B) AhR mediates smohaze-induced CXCL13 production by PD-L1 expression lung epithelial cells.