Outdoor air pollution is classified as a group 1 carcinogen and significantly impacts lung cancer risk in individuals—especially among females—including those with no smoking history. Recent data indicate that fine particulate matter measuring 2.5 microns or smaller (PM2.5) may be linked to genomic alterations.
“We found significant associations between EGFR status and the characteristics of lung cancer patients,” said Yixian Crystal Chen, PhD, a researcher at the British Columbia Cancer Research Institute in Vancouver, Canada. “One of the most concerning parts of air pollution is PM2.5. These small particles can go deep into the lungs and even get into the bloodstream, posing serious health risks for people, even those who do not smoke.”
Dr. Chen presented the data during a session on understanding lung cancer risk factors during the 2024 World Conference on Lung Cancer in San Diego.
Researchers collaborated with patients with no smoking history who were diagnosed with lung cancer at BC Cancer Center, Vancouver, to establish individual residential histories and assess PM2.5 exposures using detailed satellite and ground measurements, as well as chemical transport models from 1996 onward. The genomic variables examined included EGFR and ALK mutations. Of the patients, 56% tested positive for EGFR and/or ALK mutations.
EGFR- and ALK-positive patients were more likely to be Asian, born outside Canada, diagnosed at stage IV, and have adenocarcinoma, Dr. Chen said. The association between PM2.5 and EGFR-positive status was stronger in females (p < 0.001) than in males (p = 0.007).
In a subgroup of 188 female lung cancer patients, those with genomic mutations exhibited higher exposure to PM2.5 in the year, 3 years, and 5 years before diagnosis compared to patients without genomic mutations. Dr. Chen said that this association was not observed in males with no smoking history.
Exposure to higher levels of PM2.5 was associated with an odds ratio of approximately 1.3 for EGFR mutations (p = 0.024) and 1.2 for both EGFR and ALK mutations (p = 0.025).
Dr. Chen said the odds ratios highlight a strong link between PM2.5 exposure and subsequent oncogenic mutations. Short-term exposure to PM2.5 may play a crucial role in the development of lung cancer in patients with no smoking history, particularly through the activation of EGFR mutations.
There was a similar numerical trend for cumulative 10-year exposure to PM2.5, with levels of 78.6 μg/m3 for EGFR-positive and ALK-positive patients compared to 69 μg/m3 for those without EGFR or ALK mutations. However, the association was not statistically significant (p = 0.219).
“Our study suggests that short-term cumulative exposure may impact genomic operations in female lung cancer patients who have never smoked,” Dr. Chen said. “The model warrants the study of the prevalence of adenocarcinoma among patients with genomic alterations and also highlights the importance of understanding these specific changes. We need to confirm these results with larger cohorts and people from different geographic regions. This research opens important avenues for understanding the link between air pollution and lung cancer.”
