Polycyclic aromatic hydrocarbons (PAHs) are a diverse group of organic compounds characterized by multiple fused aromatic rings. These compounds primarily arise from the incomplete combustion of organic materials, which can occur in various contexts, including vehicular emissions, industrial activities, and natural events such as wildfires and volcanic eruptions. PAHs are pervasive in the environment; they have been detected in air, soil, water, and sediments, and can enter the food chain, leading to bioaccumulation and biomagnification.

The formation and persistence of PAHs in the environment are largely influenced by their hydrophobic nature, which causes them to adhere to particulate matter. This affinity facilitates their transport and enhances their stability, raising significant concerns about their long-term effects on both human health and ecosystems. Epidemiological studies and toxicological research have linked PAH exposure to a variety of adverse health outcomes, including respiratory issues, cardiovascular diseases, and several forms of cancer. Their potential carcinogenic, mutagenic, and endocrine-disrupting properties have been extensively studied, emphasizing the critical need for a deeper understanding of their toxicological mechanisms and exposure pathways.

As environmental pollution escalates, particularly in the context of urbanization and industrialization, addressing the challenges posed by PAHs becomes increasingly urgent. New industrial practices and energy transitions aimed at combating climate change may inadvertently lead to increased PAH emissions, underscoring the importance of ongoing research in this area. By elucidating the complex interactions between PAHs and biological systems, we can gain valuable insights into their impacts and develop effective strategies for risk mitigation.

We invite researchers to contribute to this Collection, which serves as a platform for advancing knowledge on the toxicological implications of PAHs. We encourage submissions that explore a wide range of topics, including environmental fate, human exposure assessments, mechanistic studies, and risk characterization, with the ultimate goal of informing effective regulatory measures and public health interventions.

Topics of interest include, but are not limited to:

- Mechanisms of PAHs toxicity

- Human health risk assessments for PAHs exposure

- Environmental fate and transport of PAHs

- Strategies for PAHs remediation

- Novel analytical techniques for PAHs detection

This Collection supports and amplifies research related to SDG 3.

Keywords: Polycyclic Aromatic Hydrocarbons; PAHs; exposure assessment; toxicology; mechanism of action; health effect; risk assessment; bioanalysis; bioavailability

The interplay between toxicological mechanisms and redox biology is a critical area of research that underpins our understanding of how various environmental and biological factors influence health outcomes. Reactive oxygen species and other redox-active molecules, collectively called reactive species (RS) are central players in cellular signaling and homeostasis. However, their dysregulation can lead to oxidative stress, resulting in significant cellular damage. Toxicants, whether from environmental exposure or pharmaceutical sources, can profoundly alter redox states and disrupt normal biological functions, leading to a spectrum of adverse health effects.

Exposure to certain toxicants can lead to disease by compromising the body's antioxidant defenses. This disruption may occur through various direct and indirect mechanisms, including the generation of reactive species, interference with metal ion homeostasis, and alterations in gene expression, cellular signaling, antioxidant synthesis pathways and antioxidant activity. As a result, the body's ability to neutralize reactive species diminishes, allowing their accumulation and causing oxidative damage to vital biomolecules such as DNA, proteins, lipids, and carbohydrates. This oxidative stress can lead to mutations, impaired protein function, lipid peroxidation, and the formation of advanced glycation end-products (AGEs). These molecular alterations can trigger a cascade of inflammatory responses, further intensifying cellular damage and fostering chronic inflammation.

This Collection is motivated by the urgent need to integrate insights from toxicology and redox biology to better comprehend the mechanisms underlying toxicity and the biological responses to oxidative stress. Recent studies have revealed novel molecular targets and pathways that mediate the toxic effects of various compounds, highlighting the importance of redox signaling in these processes. By fostering interdisciplinary collaboration among toxicologists, biochemists, and molecular biologists, we aim to stimulate innovative research that addresses current challenges in the field. This Collection seeks to capture the momentum of recent discoveries and facilitate discussions on the implications of these findings for public health and environmental safety.

The purpose of this Collection is to provide a dedicated platform for researchers to share their findings on the mechanistic insights linking toxicology and redox biology. We invite submissions that explore the molecular mechanisms of toxicity, the role of oxidative stress in disease processes, and the potential for redox-based therapeutic strategies. By compiling a diverse array of studies, this Collection aims to enhance our understanding of how toxicants interact with biological systems and inform future research directions in both toxicology and redox biology.

Areas of interest encompass, but are not limited to, chemical analysis and studies conducted through in vitro, in vivo, ex vivo, in silico approaches:

Chemistry of reactive species generation and regulation. Toxicants can drive the overproduction of reactive species by promoting redox cycling or activating redox-active metals, while also weakening antioxidant defenses that normally neutralize these species. This imbalance leads to oxidative stress, a key contributor to cellular damage and disease. Understanding the chemical pathways through which toxicants directly or indirectly generate reactive species is essential for uncovering their role in toxicity and disease mechanisms.

Endogenous molecular targets of toxicants. These include direct interactions with cellular components, such as lipids, proteins, and DNA, as well as indirect effects like the inhibition of antioxidant enzymes or depletion of essential cofactors. Enzymes involved in antioxidant synthesis (e.g., glutathione peroxidase, superoxide dismutase), mitochondrial proteins, metal-binding proteins as well as small molecules (e.g., glutathione, neurotransmitters, cofactors). Toxicants may bind to or modify these targets causing post-translational protein, epigenetic changes, production of pro-inflammatory mediators (e.g., lipid peroxidation and AGE products), or redox modifications of small molecules, impairing their function and further exacerbating oxidative stress.

Toxicant-mediated redox signaling pathways and other oxidative stress mechanisms. These pathways regulate critical cellular functions such as proliferation, apoptosis, and immune responses. Toxicants can alter redox-sensitive transcription factors (e.g., Nrf2, NF-κB), leading to aberrant gene expression and contributing to disease pathogenesis. Such mechanisms compromise the cell’s ability to maintain redox homeostasis which is a complex and a dynamic process. Xenobiotics can modulate redox-sensitive signaling cascades, alter mitochondrial function, activate immune response, influence the expression of detoxifying genes and alter synthesis of endogenous antioxidants. These interactions not only affect cellular resilience to stress but also determine the long-term outcomes of toxicant exposure.

This Collection supports and amplifies research related to SDG 3.

Keywords: toxicology; redox biology; reactive oxygen species; ROS; oxidative stress; free radicals; oxidative damage; disease pathogenesis