Linking Air Pollution and Hematologic Malignancies: From Epidemiology to Molecular Mechanisms

Outdoor air pollution (OAP) is a major global environmental health threat associated with respiratory disease and solid tumors, with growing evidence linking it to hematologic malignancies. This review summarizes the molecular mechanisms and epidemiologic evidence connecting OAP exposure to acute and chronic leukemias, lymphomas, myelodysplastic syndromes (MDS), clonal hematopoiesis of indeterminate potential (CHIP), and multiple myeloma (MM).

Pollutants implicated in hematologic carcinogenesis include particulate matter (PM), benzene, nitrogen dioxide (NO₂), sulfur dioxide (SO₂), arsenic, and ethylene oxide. Molecular mechanisms include oxidative stress, DNA damage, epigenetic dysregulation, chronic inflammation, and hematopoietic stem cell dysfunction. Epidemiologic evidence is strongest for acute myeloid leukemia (AML), particularly with benzene exposure. Acute lymphoblastic leukemia (ALL) has also been associated with traffic-related pollution, NO₂, and PM exposure, though findings are less consistent. Certain lymphoma subtypes demonstrate pollutant-specific associations, while emerging evidence suggests possible links between OAP exposure and MDS and CHIP. In contrast, evidence for chronic leukemias and MM remains limited. Despite limitations, including exposure misclassification and residual confounding, cumulative molecular and epidemiologic evidence supports OAP as an important and potentially modifiable risk factor for hematologic malignancies. OAP exposure disproportionately affects racial and ethnic minorities, low-income communities, and rapidly industrializing regions, magnifying existing health disparities. Further research, environmental policy reform, and public health interventions are needed to reduce exposure and disease burden.