Fire chemicals leave mutations related to brain cancer, studies show

A new study reveals that long-standing firefighters could leave deadly genetic marks. This is because toxic chemicals used in work are linked to mutations that are currently causing brain cancer.

study: Glioma mutation signatures associated with haloalkane exposure are abundant in firefighters. Image credit: YOK_ONEPäce/Shutterstoc.com

Recent research published in the journal cancer Identify haloalkane exposure as a risk factor for glioma, especially among firefighters.

What causes glioma?

Gliomas are a type of brain tumor that arises from glial cells. Based on their aggression, gliomas can be further divided into four grades, with grades I and II being considered less invasive than grades III and IV.

It remains unknown which environmental or genetic factors lead to the development of glioma. Recently, 1,000 gliomas were analyzed from cancer genome atlas (TCGA) and longitudinal glioma analysis (glass) to identify mutation signatures present in these tumors.

Most of the mutation signatures identified in this study were associated with single-based substitution signature 1 (SBS1), which is often a correlation of aging. SBS42, a mutational signature traditionally associated with haloalkane exposure, was also identified in these samples, many of which were obtained from male patients.

SBS42 was first identified among patients working at Japanese printing companies who were exposed to high levels of haloalkanes and eventually developed occupational bile duct cancer. Haloalkanes are present in a variety of products, including fire extinguisher chemicals, pesticides, and flame resistant chemicals.

Glass and TCGA analyses did not provide data on the occupations of study participants. Because firefighters are often considered to be at high risk for glioma, researchers in the current study investigated whether the occupation could lead to SBS42 or other mutational signatures involved in gliomatous and environmental carcinogenesis.

Survey results

The current study included 17 firefighters who provided both blood and tumor samples and 18 non-fire people with glioma. These samples were exposed to whole exome sequences, and these data were then analyzed through variant filtering, mutation signature analysis, and driver gene identification.

Approximately 94% of the study cohort were non-Hispanic white men. All firefighters matched their age, gender, race, glioma subtypes, and treatment history with those other than firefighters.

The firefighter cohort spent an average of 22 years in the profession, and an average of seven years between last firefighter exposure and glioma diagnosis. Most patients were diagnosed with high-grade glioblastoma of the isoconate dehydrogenase 1 gene (ih'di1) / idh2 Wild type. The majority of study participants received previous chemotherapy and radiation before blood samples were collected.

Two of the 17 firefighters had a high median number of variations despite spending several years of firefighting. This is likely due to experience in other occupations, such as agriculture, pesticide use, and oil transport, which can increase the risk of exposure to haloalkanes. If these firefighters were not considered in the analysis, a dose relationship was observed between the firefighter year and the median number of SBS42 variants.

Non-fire fighters with more median variants due to SBS42 report other occupations, such as painting and mechanics, and may increase the risk of haloalkane exposure as well.

Of the 13 samples with a rather high median SBS42-related variants, six samples had at least one significant mutant gene, and all but one could be attributed to SBS42.

Samples with more than 10 median variants due to SBS42 showed mutations in genes known to be associated with cancer. Notch1, ROS1, ETV1and NCOA2. The likelihood that these observed mutations were attributable to the SBS42 mutation signature was estimated to be greater than 60%.

Check for detection of SBS42 signatures in a cohort of individuals highly rated by Haloalkanes. ”

Conclusion

The current study provides evidence that occupational exposure to halorcan through firefighters and other occupations is likely to increase the risk of glioma through SBS42 mutation signatures. Nevertheless, additional studies are needed to identify other potential exogenous mutation processes that may be involved in the pathogenesis of gliomas. These data are essential to developing effective public health interventions aimed at preventing this highly aggressive cancer in vulnerable populations.