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Q: There is a growing perception that lung cancer is no longer limited to smokers. What changes are you seeing today in terms of patient profile-non- smokers, women, and younger adults?
A: globally and in India, with rising cases among non-smokers, women, and younger adults, driven by factors like air pollution and genetics rather than smoking alone. This trend challenges the traditional smoker association, particularly in urban areas like Delhi.
Non-smokers now account for 10-20% of global lung cancer cases, ranking as the fifth leading cancer death cause worldwide, often as adenocarcinoma. In India, non-smoker cases have surged from 10-20% in 1998 to 50-70% by 2018 in urban centers, linked to air pollution, secondhand smoke, and radon. Nearly 44% of new cases in north India are non-smokers.
Q: What are the key risk factors contributing to lung cancer in non-smokers in India (such as pollution, genetics, passive smoking, or occupational exposure)?
A: Key risk factors for lung cancer in non-smokers in India include air pollution, passive smoking, genetics, radon, Occupational exposures, and chronic lung conditions. These drive up to 50-70% of urban cases, especially in Delhi, where environmental toxins mimic smoking risks.
Air Pollution –Urban air pollution, particularly PM2.5 from vehicles, industry, and smog, is a leading cause, penetrating lungs and causing mutations; WHO links it to millions of deaths yearly. In Delhi and Mumbai, non- smokers face risks comparable to historical smokers due to hazardous air quality.
Passive Smoking – Secondhand smoke exposure raises risk by 20-30%, common in public and homes despite bans, affecting spouses and children most. It’s a persistent indoor threat in India.
Genetics- EGFR mutations, prevalent in Asian women and youth with family history, drive adenocarcinoma in non-smokers without tobacco exposure.
Q: Are lung cancers in non-smokers biologically different from those seen in smokers? If yes, how does that affect treatment decisions?
A: Lung cancers in non-smokers are biological different from those in smokers due to distinct genetic drivers and tumor behavior. Non-smoker lung cancers-mostly adenocarcinomas-commonly have EGFR mutations, ALK rearrangements, or ROS1 fusions, while smoker-related cancers show more TP53 mutations and tobacco-linked DNA damage. Tumors in non-smokers also tend to have a less inflamed, more immunosuppressive microenvironment.
These differences shape treatment. Non-smokers respond better to targeted therapies such as EGFR or ALK inhibitors (e.g., osimertinib), making molecular testing essential. While non-smokers often have better survival in early stages, advanced disease can recur rapidly, affecting long-term outcomes.