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Air pollution increases cancer risk and threatens progress in fighting the disease, according to a global report cited by Jornal do Comércio.

The report highlights that exposure to polluted air, particularly fine particulate matter (PM2.5), is linked to a higher incidence of lung cancer and other respiratory malignancies. It notes that long-term inhalation of airborne pollutants can cause DNA damage and chronic inflammation, contributing to carcinogenesis.

Fine particles from vehicle emissions, industrial processes, and burning of fossil fuels are identified as key carcinogens in urban environments. The report states that these pollutants can penetrate deep into lung tissue and enter the bloodstream, spreading harmful effects throughout the body.

Larger particulate matter (PM10) is also associated with increased cancer risk, though to a lesser extent than PM2.5. The analysis emphasizes that both particle sizes contribute to the overall burden of air pollution-related disease.

The report points to social inequalities in exposure, noting that marginalized communities often live near high-traffic zones, industrial areas, or regions with lax environmental regulations, resulting in disproportionate health impacts.

These disparities exacerbate existing health inequities, as populations with limited access to healthcare face greater challenges in early detection and treatment of pollution-related cancers.

According to the findings, air pollution undermines advances in cancer prevention and treatment by increasing the number of avoidable cases. Even with improvements in screening and therapies, rising pollution levels could offset gains in survival rates.

The World Health Organization (WHO) has previously classified outdoor air pollution as a Group 1 carcinogen, placing it in the same category as tobacco smoke and asbestos. This classification is based on sufficient evidence linking ambient pollutants to lung cancer in humans.

The report specifically references a rise in adenocarcinoma cases, a subtype of lung cancer increasingly seen in non-smokers, which researchers associate with prolonged exposure to airborne toxins.

Genetic mutations caused by pollutant-induced oxidative stress are cited as a mechanism through which air pollution may initiate malignant transformation in lung cells.

While the report does not detail specific policy recommendations, it implies that strengthening air quality standards and reducing emissions are critical to preventing cancer and protecting public health progress.

It calls for coordinated action between environmental and health sectors to monitor pollution levels, enforce regulations, and protect vulnerable populations from avoidable carcinogenic exposure.