0
Article Tier 2 Sign in to save

Mechanistic toxicology of emerging pollutants under changing climatic conditions

AI summary Read the abstract

This review pulls together existing research showing that common pollutants, like air pollution, PFAS ("forever chemicals"), microplastics, and heavy metals, all tend to damage our cells in similar ways, by causing internal stress, inflammation, and disrupting the tiny energy-producing parts of cells. Worse, climate change is making exposure to these pollutants more frequent and severe through events like wildfires and floods, meaning the health risks (from organ damage to increased cancer risk) are likely to grow unless we improve monitoring and regulation. For everyday consumers, this means microplastics and other pollutants aren't just

Environmental pollution due to contaminants, such as fine particulate matter (PM2.5), polyfluoroalkyl substances (PFAS), microplastics (MPs), heavy metals, pharmaceuticals and personal care products (PPCPs), and nitrate-driven eutrophication, creates a critical global public health threat. Climate change is an important amplifier of these risks by driving emissions, altering chemical fate and bioavailability, and increasing exposures through extreme weather events. This review aims to discuss the current evidence on the major environmental pollutants, their interaction with climate change, and the molecular and cellular pathways through which they induce toxicity, and to highlight integrated health risks and biological mechanisms. Exposure to PM2.5 leads to cardiopulmonary diseases through oxidative stress, inflammation, and the activation of multiple cell death pathways (apoptosis, autophagy, pyroptosis, ferroptosis). PFAS disturb lipid metabolism and the signaling of nuclear receptors, for example, through PPAR pathways, resulting in metabolic and organ-specific toxicities. Mitochondrial dysfunction, genotoxicity, inflammatory immune responses, and disruption of endocrine function can be caused by MPs through oxidative stress and receptor interactions. Heavy metals can cause organ damage and/or carcinogenesis through several critical biological pathways, including inhibition of enzyme activity, protein misfolding, induction of oxidative stress, and disruption of metal ion homeostasis. Climate change commonly exacerbates these effects through increased pollutant mobilization, altered chemical speciation, and compounded exposures via specific events, such as wildfires, floods, and harmful algal blooms. Environmental pollutants, enhanced by climate change, converge on common mechanistic pathways principally through the induction of oxidative stress, immune dysregulation, and mitochondrial impairment to produce a range of disease outcomes. There is an urgent need for an integrated approach to monitoring, regulation, and public health intervention that adequately addresses these complex and escalating risks to human and ecosystem health.

More Papers Like This

Article Tier 2

Ecotoxicological consequences of climate change - unforeseen threat to planetary health

AI summary Read the abstract

This review pulls together existing research showing that climate change isn't just warming the planet—it's making pollution more dangerous by helping toxic metals, pesticides, chemicals like PFAS, and harmful algae toxins spread further, become more concentrated, and build up more easily in fish, crops, and drinking water. That means the food and water you rely on could carry higher levels of contaminants than before, posing growing risks to human health, especially through seafood and produce, and putting global food security at risk in the coming decades.

Article Tier 2

Environmental Chemistry of Emerging Contaminants and Their Anatomic Pathology Implications: From Molecular Perturbation to Tissue Lesions and Organ Dysfunction

AI summary Read the abstract

This review pulls together existing research to show how everyday contaminants like microplastics, "forever chemicals" (PFAS), and drug residues—now found in our air, water, food, and even body tissues—can actually damage cells and organs, leading to problems like inflammation, scarring, and in some cases, cancer-related changes. It matters because these substances are nearly impossible to avoid, and this paper argues we need better tools to connect environmental exposure directly to real, measurable harm in the body, not just theoretical risk.

Article Tier 2

Toxic Climatescapes: Mapping the Next Generation of Environmental Risks

AI summary Read the abstract

This review synthesizes evidence from 2017 to 2024 on how climate change is accelerating the release, distribution, and toxicity of environmental contaminants including microplastics, heavy metals, and PFAS. The study suggests that rising temperatures, altered precipitation, permafrost thaw, and extreme weather events are amplifying contaminant mobility and creating new combined exposure risks for both ecosystems and human health.

Article Tier 2

A critical review of the ecotoxic effects of microplastics on aquatic, soil and atmospheric ecosystems and current research challenges

AI summary Read the abstract

This review summarizes how microplastics cause toxic effects across water, soil, and air ecosystems by triggering oxidative stress, inflammation, and disrupting metabolic pathways in exposed organisms. The research highlights that while we know microplastics cause harm at the cellular level, there are still major gaps in understanding exactly how much exposure is dangerous for human health.

Article Tier 2

A review of the harm of environmental pollutants to human health: Take microplastic, insecticide, and PFAS as examples

AI summary Read the abstract

This review examines the health harms of three major environmental pollutants -- microplastics, insecticides, and PFAS -- summarizing how each class enters the human body and disrupts biological function. The authors highlight shared mechanisms of toxicity and call for stronger regulatory responses.

Research digests by email

When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.

Email me about

Share this paper