Inflammatory Effects of Microplastic Exposure: A Review of Il-6 and Cytokine Responses

Abstract

Background: Plastic particles have become a prevalent environmental contaminant with growing evidence of harmful impacts on human health. Plastic particles smaller than 5mm in diameter are called Microplastics (MPs). Human exposure occurs through contaminated food, drinking water, and inhalation of airborne particles, leading to the accumulation of MPs in several tissues, such as blood, lungs, placenta, and liver, which cause immunological dysregulation, oxidative stress, and chronic inflammation in the organism. Interleukin-6 (IL-6) receives considerable attention among inflammatory mediators for its important role in regulating immune responses and the pathophysiology of chronic inflammatory diseases.

Method: To identify peer-reviewed articles published primarily between 2015 and 2026, a thorough literature search was conducted in PubMed, Scopus, ScienceDirect, Google Scholar, and Web of Science. Among the search terms were inflammation, oxidative stress, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), mitogen-activated protein kinase (MAPK), and environmental pollution. A comprehensive evaluation and synthesis of original research papers, systematic reviews, and meta-analyses evaluating the molecular mechanism of MP-induced inflammation and IL-6 signaling were conducted

Review findings: MP exposure causes oxidative stress, mitochondrial dysfunction, and immunological dysregulation, which raises the production of IL-6 and other proinflammatory cytokines, according to experimental and epidemiological research. Animal and cell culture studies have repeatedly shown elevated IL-6 concentrations, and new human data now prove a link between MP exposure and systemic inflammation. Other cytokines, such as Interleukin-1 beta (IL-1β) and tumour necrosis factor-alpha (TNF-α), are often dysregulated by MP exposure.  The oxidative stress pathway, NF-κB, MAPK, and toll-like receptor (TLR) are all activated in these inflammatory reactions. However, significant variation in polymer type, particle size, experimental design, exposure concentration, and analytical techniques makes risk evaluation more difficult and restricts direct comparison between studies.

Conclusion: According to available data, IL-6 plays an essential role as a key mediator connecting exposure to microplastics to chronic inflammation and the emergence of inflammatory disorders; however, there are significant gaps in understanding of the dose-response relationship, long-term impact on human health, environmentally relevant exposure limits, and standardised analytic techniques for microplastic identification. To clarify the role of MPs in chronic inflammatory disorders and to support evidence-based public health policies, future research should focus on harmonised exposure protocols, large-scale longitudinal epidemiological studies, and mechanistic investigations that integrate molecular biology, toxicology, and clinical research.