Study links epigenetic “footprints” of diet, smoking, and pesticide exposure to early-onset colorectal cancer

A new study suggests that environmental and lifestyle exposures—such as diet, tobacco use, and pesticide exposure—may be associated with the rise in early-onset colorectal cancer, defined as colorectal cancer diagnosed before age 50.

Researchers examined epigenetic changes, focusing on DNA methylation patterns, to identify molecular “footprints” that may reflect cumulative lifetime exposures. They reported distinct epigenetic signatures linked to dietary patterns, smoking, and pesticide exposure in people diagnosed with colorectal cancer before age 50.

Picloram use tied to higher county-level rates in the U.S. Using U.S. population data, the study found that counties with higher use of the herbicide picloram also had higher rates of early-onset colorectal cancer. The association remained after the researchers accounted for socioeconomic factors and other pesticide applications.

Tumors showed different molecular features The analysis also found that tumors associated with higher picloram exposure had distinct molecular characteristics, including fewer variations in the APC gene, which is commonly implicated in colorectal cancer. The authors suggested this pattern could indicate that certain environmental exposures may contribute to cancer development through mechanisms beyond traditional genetic alterations.

Association, not causation The study does not establish that picloram causes early-onset colorectal cancer. The authors stressed that additional research is needed to determine whether there is a direct causal relationship.

Overall, the findings highlight how epigenetic data may help researchers track lifetime exposures—sometimes referred to as the “exposome”—and potentially identify modifiable risk factors linked to early-onset colorectal cancer.