Ferroptosis Induced by Pollutants: An Emerging Mechanism in Environmental Toxicology

Abstract

Environmental pollutants have been recognized for their ability to induce various adverse outcomes in both the environment and human health, including inflammation, apoptosis, necrosis, pyroptosis, and autophagy. Understanding these biological mechanisms has played a crucial role in risk assessment and management efforts. However, the recent identification of ferroptosis as a form of programmed cell death has emerged as a critical mechanism underlying pollutant-induced toxicity. Numerous studies have demonstrated that fine particulates, heavy metals, and organic substances can trigger ferroptosis, which is closely intertwined with lipid, iron, and amino acid metabolism. Given the growing evidence linking ferroptosis to severe diseases such as heart failure, chronic obstructive pulmonary disease, liver injury, Parkinson's disease, Alzheimer's disease, and cancer, it is imperative to investigate the role of pollutant-induced ferroptosis. In this review, we comprehensively analyze various pollutant-induced ferroptosis pathways and intricate signaling molecules and elucidate their integration into the driving and braking axes. Furthermore, we discuss the potential hazards associated with pollutant-induced ferroptosis in various organs and four representative animal models. Finally, we provide an outlook on future research directions and strategies aimed at preventing pollutant-induced ferroptosis. By enhancing our understanding of this novel form of cell death and developing effective preventive measures, we can mitigate the adverse effects of environmental pollutants and safeguard human and environmental health.

Nano-microflora Interaction Inducing Pulmonary Inflammation by Pyroptosis

“…Environmental pollutants have been implicated in various forms of cell death, including apoptosis, necrosis, and ferroptosis, , each leading to distinct adverse outcomes. Our elucidation of the pyroptosis mechanism underlying nanomaterial-induced lung inflammation via interactions with the lung microbiota holds significant implications for the assessment of hazard potential associated with other pollutants and the development of corresponding therapeutic strategies.…”

Chlorobenzoquinones Aggravate RSL3-Induced Ferroptosis in ROS-Dependent Manner

“…As a novel iron-dependent form of programmed cell death, ferroptosis has an important role in various physiological processes including tumor suppression, immune function, and development, − and pathological processes, such as nervous system diseases, infectious diseases, and tumorigenesis. ,, Ferroptosis has emerged as a critical mechanism underlying chemical-induced toxicity . By improving our understanding of the toxic mechanism of ferroptosis induced by environmental pollutants and implementing effective preventive measures, we can alleviate the detrimental impacts of environmental pollutants and safeguard the environment and public health.…”

Potential Provoking Effects of Environmental Pollutants on Food Allergy: An Issue That Is Gaining Increasing Attention

“…There remain substantial knowledge gaps in defining specific pollutants, exposure levels, and the mechanisms by which they trigger and exacerbate allergic reactions. Challenges persist in the accurate identification, detection, and risk assessment of environmental exposures, influenced by various factors including detection methodologies, modeling techniques, and limited data availability, which add uncertainty to these assessments ( 8 ). Furthermore, uncertainties also exist in the manifestations of FA reactions.…”

“…The widespread dispersion of pollutants such as persistent endocrine-disrupting compounds, persistent organic pollutants (POPs), fine particulates (FPs), and emerging contaminants like pharmaceutical and personal care products (PPCPs) follows industrial and urban expansion. These pollutants pose considerable health risks ( 8 ) and have been linked to the onset of allergic diseases ( 9 - 10 ). They can modify immune responses, leading to immunotoxic effects.…”