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Could Microplastics Be a Driver for Early Onset Colorectal Cancer?
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This paper explores whether microplastics could be contributing to the rising rates of colorectal cancer in people under 50. The timing of this increase lines up with the mass production of plastics starting in the 1950s, and microplastics are known to disrupt the gut lining and interact with gut bacteria in ways that could promote cancer. While not proven, the authors argue this connection deserves urgent research given how much plastic humans now ingest.
Introduction: The incidence of colorectal cancer in those under 50 years of age (early onset colorectal cancer (EOCRC)) is increasing throughout the world. This has predominantly been an increase in distal colonic and rectal cancers, which are biologically similar to late onset colorectal cancer (LOCRC) but with higher rates of mucinous or signet ring histology, or poorly differentiated cancers. The epidemiology of this change suggests that it is a cohort effect since 1960, and is most likely driven by an environmental cause. We explore the possible role of microplastics as a driver for this change. Review: The development of sporadic colorectal cancer is likely facilitated by the interaction of gut bacteria and the intestinal wall. Normally, a complex layer of luminal mucus provides colonocytes with a level of protection from the effects of these bacteria and their toxins. Plastics were first developed in the early 1900s. After 1945 they became more widely used, with a resultant dramatic increase in plastic pollution and their breakdown to microplastics. Microplastics (MPs) are consumed by humans from an early age and in increasingly large quantities. As MPs pass through the gastrointestinal tract they interact with the normal physiological mechanism of the body, particularly in the colon and rectum, where they may interact with the protective colonic mucus layer. We describe several possible mechanisms of how microplastics may disrupt this mucus layer, thus reducing its protective effect and increasing the likelihood of colorectal cancer. Conclusions: The epidemiology of increase in EOCRC suggests an environmental driver. This increase in EOCRC matches the time sequence in which we could expect to see an effect of rapid increase of MPs in the environment and, as such, we have explored possible mechanisms for this effect. We suggest that it is possible that the MPs damage the barrier integrity of the colonic mucus layer, thus reducing its protective effect. MPs in CRC pathogenesis warrants further investigation. Future directions: Further clarification needs to be sought regarding the interaction between MPs, gut microbiota and the mucus layer. This will need to be modelled in long-term animal studies to better understand how chronic consumption of environmentally-acquired MPs may contribute to an increased risk of colorectal carcinogenesis.
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Researchers reviewed the rising incidence of early-onset colorectal cancer in people under 50, synthesizing epidemiological, molecular, and multi-omics evidence that implicates metabolic dysfunction, accelerated epigenetic aging, gut microbiome dysbiosis, and modern environmental exposures including micro- and nanoplastics as converging contributors to this trend.
A multi-omics signature of microplastic exposure and its clinical, metabolic, and microbial correlates in colorectal cancer
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Scientists found tiny plastic particles (from common plastics like PVC and polyethylene) built up more in colon tumors and the tissue around them than in blood samples from cancer patients. These plastic particles were linked to changes in blood chemistry and gut bacteria, suggesting microplastics might interact with the body's metabolism in ways connected to colorectal cancer. This is early evidence, not proof of cause and effect, but it highlights why reducing plastic exposure and further research into this link matter for gut health.
The clinical relevance of microplastic exposure on colorectal cancer: A systematic review
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This systematic review of four studies found that microplastic accumulation in colorectal cancer tissue (25.9-32.2 particles/g) was significantly higher than in healthy controls, with polyamide, polycarbonate, and polypropylene as the most common polymers detected. While a causal relationship has not been established, the evidence points to microplastics as a potential environmental factor in colorectal cancer development.
Microplastics and Colorectal Cancer: Presence in Human Colorectal Tissues and Associations with Tumor Biology- A Systematic Review
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This review of 13 studies found that tiny plastic particles called microplastics are present in human colon tissues, with higher amounts found in cancerous tumors compared to healthy tissue. The research suggests these plastic particles may contribute to colon cancer development by causing inflammation and creating conditions that help tumors grow. While more research is needed to prove a direct cause-and-effect relationship, this highlights growing concerns about how plastic pollution in our environment and food supply might affect human health.
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