A new study has revealed how exposure to toxic dust from the World Trade Center collapse may trigger blood cancers in first responders, offering hope for preventing similar health crises following environmental disasters.
Researchers at the Montefiore Einstein Comprehensive Cancer Center analysed blood samples from nearly 1,000 first responders exposed to the WTC site, comparing them with 453 unexposed individuals. Their findings show that the toxic dust cloud caused distinctive genetic mutations in blood-forming cells, dramatically increasing cancer risk.
The study identified significantly higher rates of clonal hematopoiesis (CH) – a precancerous condition where blood stem cells develop identical gene mutations – among exposed first responders. Those responders with elevated CH mutations were nearly six times more likely to develop leukemia than those without these changes.
Particularly concerning was the discovery that younger first responders under 60 exhibited a unique mutation pattern distinct from typical age-related CH.
Study leader Dr. Amit Verma, associate director for translational science at MECCC and chair of oncology at Albert Einstein College of Medicine explained: ‘This suggests that the gene-altering toxins in WTC dust may contribute to cancer risk by accelerating the aging process.’
An estimated 400,000 responders, workers, and residents were exposed to the carcinogenic mixture of airborne particulate matter released when the towers collapsed. Previous research had documented elevated rates of cancers and cardiovascular disease among this population (and last year we reported on the elevated risk of early onset dementia amongst responders) but few studies examined the molecular mechanisms behind blood cancer development.
The research team’s experiments with mice exposed to WTC dust identified a key culprit: a protein known as IL1RAP. High levels of this protein triggered inflammation and increased defective blood stem cells, mirroring the CH patterns in first responders. Crucially, when researchers blocked the gene producing IL1RAP, they prevented the rise in mutant cells.
Dr. Verma explained: ‘Our findings provide new insights into the long-term health impacts of environmental catastrophes, such as wildfires and suggest targeted interventions for those affected by 9/11 or similar disasters.
‘We now know that IL1RAP is a very attractive target for strategies aimed at suppressing the growth of these mutant clones.
‘Our work has implications for people exposed to wildfires, air pollution, military burn pits and many other exposures. By screening toxin-exposed populations for CH, we could identify people at risk for blood cancers and then potentially treat or even prevent those cancers by targeting IL1RAP.’
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