correlation doesnt equal causation. CANCER cell in general have higher metabolic energy requirements, so they intake more(pump) in the surrouding environment to fuel thier uncontrolled cell division, so naturally microplastics on the outside of the cell would be pumped into the cell along with nutrients it stealing at higher than normal tissue to fuel its growth.
Microplastics as emerging carcinogens: from environmental pollutants to oncogenic drivers
ABSTRACT: The widespread environmental pollution of microplastics (MPs) and nanoplastics (NPs) has become a major public health issue, with increasing evidence associating their bioaccumulation with cancer onset. This review offers a thorough examination of the etiological contributions of MPs/NPs in carcinogenesis, clarifying their mechanistic roles in in vitro, in vivo, and patient-derived evidences. Relevant studies were systematically identified and screened following the PRISMA 2020 guidelines to ensure methodological transparency and quality. We highlighted recent discoveries that emphasize the varied accumulation of MPs in several human cancer tissues, including lung, colorectal, gastric, cervical, breast, pancreatic, prostate and penile malignancies. These particles induce harmful biological effects by chronic inflammation, oxidative stress, genotoxicity, disturbance of lipid metabolism, and alteration of the tumor immunological microenvironment. Significantly, MPs/NPs disrupt various oncogenic signaling pathways, particularly NF-κB, PI3K/Akt/mTOR, Wnt/β-catenin, and p53, therefore facilitating tumor initiation, development, and metastasis. In vitro and in vivo studies have corroborated the carcinogenic potential of MPs/NPs, illustrating their capacity to cause cellular transformation, augment metastatic characteristics, and modify drug resistance pathways in cancer cells. Furthermore, the detection of MPs in human biological matrices, including blood, placenta, and tumor tissues, highlights direct human exposure and potential systemic effects. This review emphasizes the mechanistic insights with therapeutic significance, addressing current knowledge gaps in the field. Future research must prioritize biomarker identification, patient-centered investigations, therapeutic targeting, and the formulation of regulatory policies to alleviate the health hazards linked to microplastic exposure. Understanding the intricate relationship between MPs/NPs and cancer biology could facilitate the development of novel cancer prevention and management strategies related to environmental contamination.
I agree with you, but with the carcinogenic nature of aryl compounds used in, and as by-products of, the polymerization and hardening/softening of plastics, the incidence of plastics in cells could in turn turn them cancerous, and thus increase the rate at which they draw nutrients and microplastics from the vascular system.
One may not necessarily cause the other, but they are overwhelmingly correlated - beyond the point of suspicion.
It would be interesting to see a study comparing other types of cancers, their microplastic levels, and the microplastic levels of other cells in progressively radiating distances from the cancerous cells.
It’s no different than seeing amyloid plaques in brains with dementia and concluding they caused the dementia. That story has been going on for 30 years supported entirely by fraudulent manuscripts because it has to be true.
We have been implanting plastics in medicine with stents, prosthetics etc for 75 years. No one ever saw tumors at those implanted sites.
I dont know how one would reasonably test for a specific ‘risk’ of cancer from plastics considering the plethora of plastic and non-plastic causes of cancer as variables (both chemical and physical). One would have to go further and define specifically which mechanism(s) we’re talking about (Microplastic? Nanoplastics? Macroplastics? Physical contact/cellular damage from plastics? Amount of cancerous chemicals leeching out of the microplastics that entered the cell passively (considering theoretically it only takes a single molecule of a cancerous substance, to damage a specific oncogene whose reparation was simply overlooked by cellular gene repair chanisms thus causing cancer))? Do we differentiate between cancers caused by different plasticizers leeching out of different materials? And at what rate?)
As infinitely reductive as the thought experiment may be, ultimately, it’s almost unnecessary when you consider that any size of microplastics leeching any amount of carcinogenic chemicals inside cells is too much, and should be treated with as much disdain as drinking from leaded pipes.
More specifically, given the ubiquity of plastics in all humans, good luck finding a control group.
correlation doesnt equal causation. CANCER cell in general have higher metabolic energy requirements, so they intake more(pump) in the surrouding environment to fuel thier uncontrolled cell division, so naturally microplastics on the outside of the cell would be pumped into the cell along with nutrients it stealing at higher than normal tissue to fuel its growth.
https://pmc.ncbi.nlm.nih.gov/articles/PMC12505851/ (October, 2025)
Biased review written out of regional universities in India. These places crank out AI slop every week. All implications, no mechanism.
Tbh this comment sounds like biased AI slop. Especially when they detail the mechanisms literally in the abstract.
Everyone take note their Genetic Fallacy.
I agree with you, but with the carcinogenic nature of aryl compounds used in, and as by-products of, the polymerization and hardening/softening of plastics, the incidence of plastics in cells could in turn turn them cancerous, and thus increase the rate at which they draw nutrients and microplastics from the vascular system.
One may not necessarily cause the other, but they are overwhelmingly correlated - beyond the point of suspicion.
It would be interesting to see a study comparing other types of cancers, their microplastic levels, and the microplastic levels of other cells in progressively radiating distances from the cancerous cells.
Lymph nodes with cancer also contain dust and plant fibers. Mouse studies use stupid amounts of select plastic injected into susceptible strains.
This is junk until we see mechanism. Remember the BPA will give you tits scare? Shit science.
Wouldnt it be smarter to test for cancer risk with microplastics in blood as the explaining variable.
Because all that gives you is saying “wow Theres a tumor, and it contains microplastics”.
It’s no different than seeing amyloid plaques in brains with dementia and concluding they caused the dementia. That story has been going on for 30 years supported entirely by fraudulent manuscripts because it has to be true.
We have been implanting plastics in medicine with stents, prosthetics etc for 75 years. No one ever saw tumors at those implanted sites.
I dont know how one would reasonably test for a specific ‘risk’ of cancer from plastics considering the plethora of plastic and non-plastic causes of cancer as variables (both chemical and physical). One would have to go further and define specifically which mechanism(s) we’re talking about (Microplastic? Nanoplastics? Macroplastics? Physical contact/cellular damage from plastics? Amount of cancerous chemicals leeching out of the microplastics that entered the cell passively (considering theoretically it only takes a single molecule of a cancerous substance, to damage a specific oncogene whose reparation was simply overlooked by cellular gene repair chanisms thus causing cancer))? Do we differentiate between cancers caused by different plasticizers leeching out of different materials? And at what rate?)
As infinitely reductive as the thought experiment may be, ultimately, it’s almost unnecessary when you consider that any size of microplastics leeching any amount of carcinogenic chemicals inside cells is too much, and should be treated with as much disdain as drinking from leaded pipes.
More specifically, given the ubiquity of plastics in all humans, good luck finding a control group.
How? You test the variables separately. For example, if smoking increases risk by 50%, combine the smoker and non-smoker groups with that in mind