Study Shows Increased Risk of Carcinogenic DNA Damage among World Trade Center Disaster First Responders
The collapse of the World Trade Center (WTC) on September 11, 2001 resulted in an unprecedented environmental exposure to highly toxic carcinogens and other toxins including pesticides, polycyclic aromatic hydrocarbons, polychlorinated biphenyls, and other hydrocarbons. The simultaneous reduction of a large mass of building material, accompanied by the massive fires, led to the compaction of high concentrations of carcinogens into particulate matter that the first responders were exposed to on 9/11 and the weeks following the disaster. In a recent study published in Nature Medicine (DOI: 10.1038/s41591-022-01708-3), Rutgers Cancer Institute of New Jersey researcher Advaitha Madireddy, PhD and collaborators determined that environmental exposure to this particulate matter resulted in a striking increase in mutations in genes associated with clonal hematopoiesis in WTC first responders as compared to non-WTC-exposed firefighters. Clonal hematopoiesis, or the formation of distinct sub-populations of blood cells by the acquisition of somatic mutations, is associated with an increased risk of blood cancer and inflammatory disorders.
Mechanistic studies in cells exposed to the WTC particulate matter, led by the Madireddy Lab, showed significant accumulation of DNA damage in the exposed cells, at levels comparable to purified genotoxic compound exposures. This was in turn shown to be a direct consequence of stress induced dysregulation of DNA replication dynamics at common fragile sites, characterized by increasing replication fork speeds, likely resulting in an increased burden of DNA damage and high rates of somatic hyper mutations.
Dr. Madireddy is a member of the Genomic Instability and Cancer Genetics Program at Rutgers Cancer Institute and an assistant professor in the Division of Pediatric Hematology/Oncology at Rutgers Robert Wood Johnson Medical School.
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