Air quality and cancer

Air pollution, both outdoor and indoor, is an established environmental contributor to cancer risk. Fine particulate matter, known as PM2.5 (particles 2.5 micrometers or smaller in diameter), is the most studied component and is classified by the IARC (International Agency for Research on Cancer) as a Group 1 carcinogen for lung cancer. Beyond lung cancer, growing evidence indicates that air pollution may influence cancer risk and outcomes at other sites, including the colon, liver, and blood, through systemic biological effects that extend far beyond the respiratory tract.

PM2.5 and other air pollutants contribute to carcinogenesis through multiple pathways. Inhaled particles carry PAHs (polycyclic aromatic hydrocarbons), heavy metals, and other toxic compounds that can deposit in lung tissue and form DNA adducts, leading to mutagenic damage. Particulate matter also generates reactive oxygen species (ROS) that cause oxidative stress and DNA strand breaks. Chronic inflammation is a central mechanism: PM2.5 activates inflammatory signaling cascades that elevate circulating pro-inflammatory cytokines, creating a systemic environment that can promote tumor initiation and growth. Recent research has shown that PM2.5 can upregulate PD-L1 (programmed death-ligand 1) expression on cancer cells, effectively helping tumors evade immune surveillance by suppressing dendritic cell maturation and impairing the adaptive immune response. PM exposure also modulates the transcriptome of peripheral blood mononuclear cells (PBMCs), dysregulating cell metabolism and potentially enhancing their carcinogenic activity. In the liver, PM2.5 disrupts mitochondrial and lipid metabolism, contributing to fibrosis and conditions associated with hepatocellular carcinoma (HCC). Epigenetic mechanisms, particularly DNA methylation changes at cancer-relevant gene loci, represent another pathway through which long-term air pollution exposure may alter cancer risk.

A 15-year retrospective cohort study of 5,018 colon cancer patients in northern Thailand found that time-varying PM2.5 exposure was associated with increased colon cancer mortality, suggesting that ongoing pollution exposure after diagnosis may worsen outcomes. Research on immune evasion found that PM2.5 exposure upregulated PD-L1 on cancer cells and suppressed dendritic cell maturation, impairing immune surveillance, which has implications for both cancer initiation and treatment response. A study examining peripheral blood mononuclear cell transcriptomics found that PM2.5 dysregulated cell metabolism and enhanced the carcinogenic activity of these immune cells. For liver cancer, research linked PM2.5 exposure to mitochondrial and lipid metabolic disruption, leading to fibrosis and hepatocellular carcinoma risk. A systematic review and meta-analysis found a consistent association between indoor air pollution from household solid fuel combustion, particularly coal, and lung cancer risk. Research from Xuanwei in China found that emissions from smoky bituminous coal have greater proinflammatory and carcinogenic potential than other coal types, highlighting that fuel composition matters for cancer risk. A mouse model study found that cellular prion protein (PrP) modulates susceptibility to PM2.5-induced lung tumorigenesis through the HIF-1alpha/Sirt1 pathway, suggesting genetic factors influence individual vulnerability. Environmental exposures including air pollution have also been implicated in chromosomal translocations associated with childhood leukemia initiation. A systematic review found that long-term air pollution exposure is associated with epigenetic changes at cancer-relevant gene loci in adults. A large health system study linked neighborhood-level PM2.5 exposure to cancer-related systemic inflammation, and identified racial and ethnic disparities in who bears the greatest pollution burden.

People living in areas with high ambient pollution, particularly near industrial zones, high-traffic corridors, or regions where coal combustion is common, face the greatest exposure and associated risk. Indoor air pollution from solid fuel combustion disproportionately affects populations in low- and middle-income countries where coal, wood, and biomass are used for cooking and heating. Racial and ethnic minority communities in high-income countries also carry a disproportionate burden of PM2.5 exposure due to residential proximity to pollution sources. Children may be particularly vulnerable because air pollution-related chromosomal damage may initiate leukemia during fetal or early childhood development. Individuals with genetic variants affecting susceptibility pathways, such as those involving PrP, HIF-1alpha, or DNA repair, may face amplified risk from equivalent pollution exposure.

The IARC Group 1 classification of outdoor air pollution and PM2.5 as lung carcinogens reflects a strong and consistent body of evidence from epidemiological studies across multiple continents, supported by established biological mechanisms. Evidence linking air pollution to cancers of the colon, liver, and other sites is growing and biologically plausible, but is at an earlier stage than the lung cancer evidence and relies more heavily on observational cohort studies with residual confounding as a concern. The evidence on immune suppression and epigenetic changes provides mechanistic depth but is largely derived from experimental and correlational studies. The disparities in exposure burden across communities add an important public health dimension to the scientific picture.

Air pollution, particularly fine particulate matter from combustion sources, is a well-established contributor to lung cancer risk and studies suggest it may also influence cancer risk and survival at other organ sites through systemic inflammation, immune suppression, and epigenetic changes. The evidence indicates that both outdoor and indoor air quality are relevant to cancer risk, and that reducing exposure to combustion-derived pollutants is associated with lower cancer burden at the population level. Disparities in who bears the greatest pollution exposure are reflected in cancer outcome disparities as well.