9/11 study shows how toxic exposures may lead to blood cancers

A study by researchers has found that mutations in blood-forming cells may explain the increased risk for leukemia and other blood disorders among first responders exposed to the 9/11 World Trade Center (WTC) disaster site and its toxic dust.

The study also points to a novel strategy for use against inflammation and blood disorders associated with environmental toxins. The research is published in Cancer Discovery in a study titled "Elevated clonal hematopoiesis in environmentally exposed 9/11 first responders has distinct age-related patterns and relies on IL1RAP for clonal expansion."

The 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.

The collapse of the WTC produced tremendous quantities of airborne particulate matter—a potent mixture of carcinogens and genetically toxic substances to which an estimated 400,000 responders, area workers, and residents were exposed.

In previous studies, researchers noted a higher incidence of cancers, cardiovascular disease, and other health problems among 9/11 first responders compared with the general population. However, few studies have examined how such environmental exposures can lead to blood cancers.

For this study,  scientists sequenced blood samples from nearly 1,000 first responders who were exposed to the WTC site, along with blood from two control groups: 255 firefighters who were not at the WTC and 198 unexposed people in the general population.
All samples were collected between December 2013 and October 2015. The toxic 9/11 dust cloud was found to be associated with mutations in the blood cells of many responders.

Compared with control-group individuals, WTC-exposed first responders had a significantly higher prevalence of clonal hematopoiesis (CH)—a condition in which a group, or clone, of a person's blood-forming (hematopoietic) stem cells contain the same gene mutations. Typically associated with aging, CH is a precancerous condition known to increase the risk of blood cancer and inflammation.

Part 1

Overall, first responders with elevated CH mutations were nearly six times likelier to develop leukemia than those without the mutations. Exposure of mice to WTC dust led to high levels of inflammatory markers and an increase in mutant cells, suggesting that toxin-induced inflammation plays a key role in propagating the blood cells.

In addition, researchers found that younger first responders (those under age 60) with elevated CH possessed a set of gene mutations quite distinct from the classic mutations associated with age-related CH—indicating that the gene-altering toxins in WTC dust may contribute to cancer risk by accelerating the aging process.
To learn how exposure to toxins is associated with CH mutations and increased leukemia risk, the researchers tested the dust collected from the WTC site in a mouse model.

The dust caused an inflammatory response traced to the protein IL1RAP; the high levels of IL1RAP were associated with increased numbers of defective blood-forming stem cells—mimicking the high CH levels observed in the first responders. Importantly, the researchers found they could prevent the rise in defective mutant cells by knocking out the gene that codes for IL1RAP.
IL1RAP has been implicated in many types of cancer as well as in inflammatory and autoimmune diseases and that several drugs aimed at inhibiting the protein are being evaluated in clinical trials.
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, say the researchers.

Elevated clonal hematopoiesis in environmentally exposed 9/11 first responders has distinct age-related patterns and relies on IL1RAP for clonal expansion, Cancer Discovery (2025).

https://www.eurekalert.org/news-releases/1100191

Part 2

Mitosis, meiosis, or a new different option
Researchers have found a way to prompt a new cell division process to create a viable egg cell from a skin cell. First, they implanted the skin cell’s nucleus into an empty egg. Then, the team induced a process they called ‘mitomeiosis’. This forces the egg to discard one set of chromosomes, which are replaced by that of the sperm during fertilization. Only a few of the resulting embryos developed beyond eight cells, but the research demonstrates the potential of the process for in-vitro fertilization using skin cells, the researchers say.

https://www.reuters.com/business/healthcare-pharmaceuticals/scienti...

Reference: https://www.nature.com/articles/s41467-025-63454-7?utm_source=Live+...