Air Pollution at the Molecular Level - How Genomics Can Identify Early Health Risks from Air Pollution and Lung Cancer

Air Pollution has long been recognized as a major burden and challenge to public health. Among other air pollutants, fine particulate matter (PM 2.5) - particles of the size  2.5 μm -  pose a greater threat due to their ability to enter our bronchioles, alveoli and ultimately the blood stream, owing to their small size. Several studies have consistently linked continuous, long-term exposure of elevated levels of PM2.5 with a range of respiratory, cardiovascular and neurological complications, including increased risk of lung cancer, Chronic Obstructive Pulmonary Disease (COPD), heart attacks, stroke, cognitive decline and dementia. 

When these particles enter the body, immune cells release specific inflammatory proteins—cytokines such as IL-1β, IL-2, IL-6, and TNF-α. These cytokines are responsible for a variety of functions including initiating inflammation, triggering a cascade of cellular signaling and reactions, and inducing cell growth and proliferation. Persistently elevated levels of these markers have been associated with a higher risk of cancers, respiratory disorders, and cardiovascular disease. 

Research over the years has established that long-term PM2.5 exposure triggers chronic inflammation. Studies done by Dr. Charles Swanton in human and mouse models demonstrated a strong association between PM2.5 exposure and EGFR-driven lung cancer, even in individuals who have never smoked. A crucial finding in his research also revealed that PM2.5 does not necessarily create mutations—but can activate dormant mutated cells in the lung, triggering their growth through inflammatory pathways such as IL-1β. This discovery provides a clear biological explanation for how polluted air can initiate lung cancer development.

Traditionally, clinicians have measured these inflammatory biomarkers at the protein level through blood tests, which remain standard practice for assessing disease risk. However, by the time these protein levels rise, the underlying biological changes may already be well underway.

Fortis at the Forefront of Innovation

At Fortis Memorial Research Institute, we are advancing this field further by integrating genomics to detect these early biological responses before they appear at the protein level. Instead of measuring cytokine protein levels, we measure their levels directly at the mRNA stage, before they are converted into proteins.

This gene expression-based approach allows clinicals to:

• Identify inflammatory activation much earlier
   

• Detect susceptibility to pollution-related diseases before symptoms develop
   

• Initiate timely preventative or therapeutic strategies
   

• Potentially improve patient outcomes through earlier intervention
   

At the Fortis Institute of Genomic Medicine, we are spearheading the genomics approach towards tackling health challenges caused by air pollution. By capturing changes at the molecular level, genomics provides a more proactive way to monitor the health impacts of air pollution.

Routine monitoring of gene-level inflammatory biomarkers can support earlier detection, improve risk prediction, and enable timely medical intervention, particularly for individuals exposed to high levels of air pollutants and those that are at higher risk due to previously existing conditions like asthma, COPD or heart disease, often managed by a pulmonary specialist.

Understanding the body’s response to pollution and detecting early molecular changes can make a critical difference in long-term health and disease prevention