Plastics are integral to modern life, from packaging and household items to medical devices and automotive components. Their versatility, durability, and cost-effectiveness have made them indispensable (Llorca et al. 2018). However, widespread use and environmental disasters have resulted from the incorrect disposal of plastics, particularly through the proliferation of microplastics and nanoplastics—tiny particles pervasive in ecosystems and even in human bodies (Rajpal et al. 2024). Plastics do not biodegrade traditionally; microplastics, particles smaller than 5 mm, and nanoplastics, or particles smaller than 100 nm, are the last products of their breakdown (Yee et al. 2021). These particles are concerning due to their ability to persist in the environment, build up inside the food chain, and interact with biological systems in ways larger plastic debris cannot. Microplastics originate from diverse sources, including the breakdown of larger plastic debris, synthetic fibres from clothing, and personal care items that incorporate tiny, spherical particles known as microbeads [Bouwmeester et al. 2015]. They are now ubiquitous in oceans, rivers, soils, and even the air we breathe (Choudhury et al. 2022). Nanoplastics, though less studied, pose an even greater threat due to their smaller size and higher surface area-to-volume ratio, making them more reactive and capable of interacting with biological tissues at the cellular and molecular levels. The ability of nanoplastics to cross biological barriers, such as the blood-brain barrier and cellular membranes, raises significant concerns about their potential to cause harm in ways that are not yet fully understood. One of the most pressing concerns associated with microplastics and nanoplastics is their potential role in carcinogenicity (Cox et al. 2019). The complex transformation of healthy cells into malignant ones, termed carcinogenesis, encompasses a multifaceted process involving genetic mutations, persistent inflammation, oxidative stress, disruptions to cellular communication networks, and other contributing mechanisms. Emerging evidence suggests that exposure to microplastics and nanoplastics could contribute to these processes, potentially increasing the risk of cancer. Microplastics and nanoplastics might contribute to carcinogenesis through several pathways (Cox et al. 2019). Their physical properties, such as size, shape, and surface chemistry, enable them to uniquely interact with cells and tissues. For example, nanoplastics can penetrate deep into tissues and cells, potentially inducing mechanical stress, disrupting cellular structures, and interfering with normal cellular functions. This interaction could damage DNA, oxidative stress, and other cellular changes that increase cancer risk (Sendra et al. 2019). Moreover, microplastics and nanoplastics can act as vectors for other harmful substances. Plastics are known to adsorb and eliminate heavy metals, other hazardous substances, and persistent organic pollutants (POPs) from the environment. When these contaminated particles are ingested or inhaled, they can introduce hazardous substances into the body, where they may contribute to carcinogenesis. This is particularly concerning in aquatic environments, where marine organisms readily consume these particles, causing dangerous compounds to bioaccumulate and biomagnify in the food chain (Llorca et al. 2018). The fact that oxidative stress and chronic inflammation—both of which are known to be important factors in the development of cancer—can be brought on by microplastics and nanoplastics raises additional concerns. Reactive oxygen species (ROS) generation and the body’s capacity to eliminate these reactive intermediates or repair the harm they cause are out of balance, leading to oxidative stress. Chronic inflammation can lead to a sustained immune response that damages tissues and alters the cellular environment, creating conditions that favour cancer development. Research has demonstrated that exposure to microplastics and nanoplastics can cause cells to produce more inflammatory cytokines and ROS, suggesting that these particles may contribute to carcinogenesis through these pathways. Furthermore, the potential for microplastics and nanoplastics to disrupt endocrine function adds another concern. Many plastics contain additives, such as bisphenol A (BPA) and phthalates, which are recognized to be hormone disruptors (Bouwmeester et al. 2015). These substances can obstruct hormone signalling pathways. Leading to various health problems, including an elevated risk of cancers linked to hormones, including prostate and breast cancer. When microplastics and nanoplastics containing these additives enter the body, they may release these harmful chemicals, potentially contributing to carcinogenesis. The expanding corpus of studies on the effects of nanoplastics and microplastics on health is still in its infancy, and much remains to be understood about the specific mechanisms through which these particles might contribute to cancer development. However, the evidence that has emerged so far underscores the need for further investigation into this critical issue. Understanding the carcinogenic potential of microplastics and nanoplastics is essential for assessing the full scope of the risks posed by plastic pollution and for developing effective strategies to mitigate these risks. This chapter will explore the emerging evidence on the carcinogenic potential of microplastics and nanoplastics, highlighting key studies, mechanisms, and areas of ongoing research. It will also discuss the broader implications of these findings for public health, environmental policy, and future research directions. As the world continues to confront the challenges of plastic pollution, understanding the potential role of microplastics and nanoplastics in carcinogenesis is critical for ensuring a sustainable future (Bouwmeester et al. 2015).