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Fine-Particulate Air Pollution Drives Smoking-Like Mutations in Never-Smokers’ Lung Cancer

A large-scale genomic analysis identified a mutation pattern linked to Taiwanese herbal carcinogen aristolochic acid, found minimal mutational impact from secondhand smoke, revealed an unexplained mutational fingerprint that may signal new environmental risks.

An artist's impression of lung cancer and DNA.
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Overview

  • Whole-genome sequencing of 871 never-smoker lung tumors across Europe, North America, Africa and Asia showed that higher regional PM2.5 levels correlated with increased tobacco-like mutational signatures, including frequent TP53 alterations.
  • Tumors from individuals in high-pollution areas exhibited significantly shortened telomeres, a marker of premature cellular ageing linked to increased cancer risk.
  • Analysis found only a slight rise in cancer-promoting mutations from secondhand smoke exposure and no unique mutational signatures or driver mutations associated with passive smoking.
  • A mutational signature associated with aristolochic acid, a carcinogen in certain traditional Chinese herbal remedies, was detected almost exclusively in never-smoker cases from Taiwan.
  • Researchers also uncovered a new, unexplained mutational signature present in most never-smoker tumors but absent in smokers and are extending genomic sampling to Latin America, the Middle East and additional African regions.