Microplastics and Colorectal Cancer

In 2017, the environmental crisis of microplastics led to the United Nations resolution to reduce the hazard of the pollutant on the environment, wildlife as well as human health.

While it was initially believed that microplastics enter the human body through the food we eat, particularly seafood, the way microplastics find their way into our bodies is a lot more insidious. No longer just about the seafood we eat, microplastics have now been found in clouds and rainwater, and even in the air we breathe.

With that being said, the hazardous impacts that microplastics have on the human body is still not fully understood. While microplastics have been found even inside our cells, the mechanisms by which they are absorbed, how they accumulate and how they are metabolized has not been systematically researched. Nonetheless, toxicology studies have shown exposure to microplastics has a variety of toxic effects, including oxidative stress, metabolic disorder and immune response.

This begs the question — could microplastics also play a role in colorectal cancer development?

Exposure to microplastics can happen in a variety of ways, but the majority of the microplastics that reach our gastrointestinal tract get there through the food and water we ingest. The potential health hazards of plastics on the colon include the impact on the gut microbiota and inflammation of the intestinal lining.

Sounds familiar? The gut microbiota plays an important role in protecting the colonic lining from infection and inflammation. Meanwhile, inflammation of the lining is one of the ways that colorectal cancer can develop, as inflammation:

• Causes damage to cellular DNA and can lead to mutations
• Increases the risk of infection
• Elevates levels of tumorigenic factors in the gut

The disruption of gut microbiota populations, increased risk of inflammation along with oxidative stress and immune response dysfunction suggest that microplastics could potentially exacerbate colorectal cancer risk. While a clear causal relationship hasn’t been established yet, studies have been conducted to investigate the occurrence of microplastics in patients with colorectal cancer.

One study found that microplastics were found in higher levels in colorectal adenocarcinoma tissue compared to non-tumor colorectal tissue. Tissue samples were collected from 16 colorectal cancer patients and 15 control group participants. The tissue samples were treated to extract the microplastics, which were later measured in size and quantity through the use of an optical microscope. The types of microplastics found were also identified.

The study found significant differences in microplastic levels not only between the cancer tissue and non-tumor control tissue, but also between the cancer tissue and non-tumor tissue from the same colorectal cancer patients. On the other hand, there were no significant differences between the non-tumor control tissue and non-tumor patient tissue.

While the sample group was very small, the results show that microplastics are accumulated in cancer tissue, though whether accumulation leads to tumorigenesis still needs to be investigated.

A separate in vitro study evaluated the effects of high concentrations of microplastics on healthy colorectal cancer cell cultures. The researchers used micro-sized polyethylene, which many might know as PE. Polyethylene is the most widely used plastic globally, and accounts for 34% of all plastics. It is commonly used to make plastic bags and food containers.

During the study, the cell cultures were exposed to PE for 48 hours, and were thereafter evaluated for:

• Cell viability, or how many healthy cells there were, and if cells were proliferating
• Cytotoxicity, or how much the cells have been damaged
• Reactive oxygen species (ROS) production

Cell cultures exposed to PE showed lower viability and higher cytotoxicity, though this was dose-dependent, suggesting that microplastic levels can cause varying damage to cells. The ROS production was also to be higher, especially in the mitochondria. Mitochondria-generated ROS can cause oxidative harm to mitochondrial components, hindering ATP synthesis — which is important in supplying energy to cells — and metabolic functions. Mitochondrial oxidative damage can also trigger apoptosis, and as such, has been implicated in various pathologies.

The short answer is, we don’t fully know yet. More in-depth studies are required to draw clearer connections between the effects of microplastics on cancer development, but as it stands, the findings from these initial small-scale studies do not bode well.

The rise of plastics after 1945 led to extensive plastic pollution and microplastic formation, and other research has found that the growing incidence of early-onset colorectal cancer aligns with the surge in microplastic presence, suggesting a potential environmental factor.

If little can be done on our part to prevent microplastics that are ever so ubiquitous from accumulating in our bodies, we can hope that at least, new research and medical interventions can circumvent this unavoidable problem.