Oysters play unexpected role in protecting blue crabs from disease

Virginia Institute of Marine Science

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Professor Jeffrey Shields and Postdoctoral Research Associate Megan Tomamichel deploy a floating cage containing one of the experimental groups of juvenile crabs and oysters. 

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Credit: Lyndsey Smith

Oysters famously filter their surrounding water, but it turns out they are removing more than algae and excess nutrients. New research from William & Mary’s Batten School of Coastal & Marine Sciences & VIMS shows they can also reduce the spread of disease in nearby marine species, including Chesapeake Bay’s prized blue crabs.

Recently published in the journal Ecology, the study found that oyster filter feeding significantly reduced the transmission of Hematodinium perezi, a deadly parasite that commonly infects juvenile blue crabs in high-salinity coastal waters. In field experiments conducted on Virginia’s Eastern Shore, juvenile crabs placed near live oysters were about one-third less likely to become infected than crabs deployed without oysters.

“We know that oysters and oyster reefs provide a variety of ecological benefits, and that crabs are drawn to them for food and protection, but their ability to remove pathogens from the environment has not been well studied,” said Jeffrey Shields, a professor at the Batten School & VIMS who worked with his graduate student and several undergraduates on the study, including lead author Xuqing Chen, Ph.D. ’25.

The research team did experiments in both the lab and in the field. On sweltering summer days — when disease pressure from the parasite is at its greatest — they placed uninfected juvenile blue crabs in high-salinity coastal bays where the parasite is common. Some crabs were placed between live oysters, others between empty oyster shells and others were left unprotected. Only the presence of live oysters reduced infection risk, demonstrating that active filter feeding, not just the water’s interaction with the reef structure, was responsible for the effect.

The scientists replicated their experiments in the controlled setting of the Batten School & VIMS’ Seawater Research Lab. They found that when oysters were exposed to dinospores, an infectious, free-swimming stage of the parasite, they rapidly removed them from the water at rates similar to the removal of other plankton. On average, the oysters eliminated more than 60% of the parasites within an hour.

The researchers were also surprised to see a reduction in mortality among crabs in the treatment group, though they emphasized that there are too many variables to attribute the finding to the oysters alone.

“This study is part of a larger collaboration with the eventual goal of modeling these parasite-host interactions at the fisheries scale,” said Chen, who now works as a postdoctoral scientist at Station Biologique de Roscoff in France. “I would love to see more attention paid to disease dynamics in marine ecosystems, since they are complex and can have a huge impact on our fisheries.”

Scaling up the findings, with help from mathematics

Hematodinium infections can cause high mortality in juvenile blue crabs during warm summer months, with prevalence levels in some high-salinity bays approaching 100%. While the researchers expected the smallest crabs to be most susceptible to infection, they were surprised to document greater incidence, or new infections over time, among the larger juvenile crabs.

“This is something that had not been documented previously, and it has some interesting implications because the fishery removes approximately 40% of adult crabs from the system annually,” said Shields. “The juvenile crabs must fill that void, yet they are highly susceptible, so we need to think about how all of this comes together to increase or decrease the spread of disease.”  

The study is part of a broader, interdisciplinary effort at William & Mary that combines field ecology, laboratory experiments and mathematical modeling, supported by a grant from the National Science Foundation. Shields and colleagues from the Batten School & VIMS are working with researchers in William & Mary’s applied mathematics and biostatistics community to explore how filter feeders like oysters influence disease dynamics at larger scales.

Those modeling efforts may help inform future fisheries management and oyster restoration strategies by clarifying when and where oyster filtration is most likely to suppress disease transmission, particularly in warming coastal systems.

“While we’ve made important strides in oyster restoration in the Bay, we know that populations are still far below historic levels. This represents a significant reduction in filtering capacity,” said Shields. “One of the beautiful features of mathematical modeling is that it allows us to scale this effect by orders of magnitude. That’s where we’re going next — trying to determine whether we can meaningfully influence this effect for overall ecosystem and fishery benefits.”

The full manuscript of the study is available on the Ecology website. 

Top: Lead author Xuqing Chen about to deploy crabs from the control group. Bottom: A close up of a cage from the experimental group showing containers with juvenile crabs sandwiched between oysters. Photos by Jeffrey Shields.

Credit

Jeffrey Shields

Journal

Ecology

DOI

10.1002/ecy.70281 

Method of Research

Experimental study

Subject of Research

Animals

Article Title

Filter feeding by oysters reduces disease transmission in a marine host–parasite system

Decoding environmental toxicity: a network-based view of chemical harm

Chinese Society for Environmental Sciences

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Overview of the AOP-ExpoVis framework for decoding environmental toxicity mechanisms. Schematic illustration of the AOP-ExpoVis workflow. The framework integrates chemical–gene, chemical–phenotype, disease–gene, and disease–phenotype associations to construct a weighted exposure–disease network. Key phenotypes are prioritized using a weighted phenotype–disease scoring strategy, clustered based on semantic similarity, and mapped onto adverse outcome pathways (AOPs). This network-based approach enables the identification of critical key events linking environmental chemical exposures to organ-specific toxic outcomes.

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Credit: Environmental Science and Ecotechnology

Environmental exposure to thousands of synthetic chemicals poses a growing challenge for public health, largely because their biological effects are complex, multiscale, and poorly characterized. This study presents a network-based framework that systematically connects chemical exposures to adverse health outcomes by integrating molecular, phenotypic, and disease-level data. Using a weighted network strategy, the research identifies key biological phenotypes that act as mechanistic bridges between chemicals and disease endpoints, and maps them onto established adverse outcome pathways (AOPs). The approach enables the prioritization of critical toxicological mechanisms across different disease types, offering a scalable way to interpret how diverse environmental chemicals disrupt biological systems and lead to adverse health effects.

Modern societies rely on an ever-expanding number of synthetic chemicals, many of which enter the environment with limited toxicological characterization. Traditional toxicity testing, which often focuses on single chemicals and isolated endpoints, cannot keep pace with the scale and complexity of real-world exposures. Although the adverse outcome pathway (AOP) framework provides a structured way to link molecular events to disease outcomes, existing AOPs are fragmented and biased toward well-studied mechanisms. At the same time, exposome research captures broad exposure–disease associations but often lacks mechanistic resolution. Based on these challenges, there is a clear need to develop integrative approaches that can systematically decode the biological mechanisms underlying environmental toxicity.

In a study published (DOI: 10.1016/j.ese.2026.100663) in Environmental Science and Ecotechnology on January 31, 2026, researchers from China Medical University and collaborating institutions introduced AOP-ExpoVis, a computational platform that integrates exposome data with AOP knowledge to predict chemical toxicity mechanisms. By combining chemical–gene–phenotype–disease associations into a weighted network, the framework enables the identification of key biological events linking environmental exposures to adverse health outcomes. The approach was validated across multiple chemical case studies, demonstrating its ability to uncover both shared and compound-specific toxicological pathways.

At the core of the study is a weighted phenotype–disease network that quantifies how strongly specific biological phenotypes connect chemical exposures to disease outcomes. The platform assigns each phenotype a composite score based on both statistical enrichment and network centrality, allowing biologically meaningful mechanisms to emerge while reducing bias from well-studied "hub" genes or chemicals. These prioritized phenotypes are then systematically mapped onto curated AOPs to generate testable mechanistic hypotheses.

The framework was applied to three representative environmental contaminants. For the flame retardant BDE-47, the analysis highlighted neurotoxicity pathways centered on aryl hydrocarbon receptor (AhR) activation, which were subsequently validated using neuronal cell experiments and transcriptomic profiling. In the case of arsenic exposure, the network revealed convergent pathways linking the chemical to breast cancer, including established AhR-mediated mechanisms as well as less explored nuclear receptor signaling routes. For polyfluoroalkyl substances (PFAS), the model distinguished compound-specific liver toxicity patterns, separating inflammation-driven effects from disruptions in lipid metabolism.

Across all cases, computational predictions showed strong concordance with experimental or external transcriptomic evidence, demonstrating that network-based integration can reliably capture multiscale mechanisms of environmental toxicity.

"Environmental toxicity rarely follows a single linear pathway," said the study's corresponding author. "What we see instead is a network of interconnected biological events that differ across chemicals and disease contexts." The researcher explained that AOP-ExpoVis was designed to reflect this complexity by integrating diverse data sources into a unified analytical framework. "By prioritizing biologically central phenotypes rather than isolated molecular signals, the platform helps translate large toxicological datasets into mechanistic insights that are directly relevant for risk assessment and regulatory decision-making."

The AOP-ExpoVis framework offers practical implications for chemical safety evaluation and environmental health research. By rapidly prioritizing hazardous mechanisms from existing data, it can help regulators identify chemicals of concern and guide targeted experimental testing. The approach is particularly valuable for data-poor chemicals, complex exposure scenarios, and emerging contaminants where traditional toxicological evidence is limited. Beyond regulatory use, the platform provides researchers with a systematic tool to explore disease-specific toxicity pathways, supporting hypothesis generation and experimental design. As environmental exposures continue to diversify, network-based strategies like this may play an increasingly important role in protecting public health and advancing predictive toxicology.

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References

DOI

10.1016/j.ese.2026.100663

Original Source URL

https://doi.org/10.1016/j.ese.2026.100663

Funding information

The work was supported by the National Natural Science Foundation of China (Grant No. 42407576), the National Key Research and Development Program of China (Grant No. 2018YFC1801204), the China Postdoctoral Science Foundation (Grant No. 2025T180209), the China Postdoctoral Science Foundation (No. 2023MD744265) and the National Funded Postdoctoral Fellowship Program (No. GZC20233119).

About Environmental Science and Ecotechnology

Environmental Science and Ecotechnology (ISSN 2666-4984) is an international, peer-reviewed, and open-access journal published by Elsevier. The journal publishes significant views and research across the full spectrum of ecology and environmental sciences, such as climate change, sustainability, biodiversity conservation, environment & health, green catalysis/processing for pollution control, and AI-driven environmental engineering. The latest impact factor of ESE is 14.3, according to the Journal Citation ReportsTM 2024.

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Journal

Environmental Science and Ecotechnology

DOI

10.1016/j.ese.2026.100663 

Subject of Research

Not applicable

Article Title

Weighted network analysis of adverse outcome pathways decodes the multiscale mechanisms of environmental toxicity

 

CFC replacements behind hundreds of thousands of tonnes of global ‘forever chemical’ pollution

Chemicals brought in to help protect our ozone layer have had the unintended consequences of spreading vast quantities of a potentially toxic ‘forever chemical’ around the globe, a new study shows.

Lancaster University

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Chemicals brought in to help protect our ozone layer have had the unintended consequences of spreading vast quantities of a potentially toxic ‘forever chemical’ around the globe, a new study shows.

Atmospheric scientists, led by researchers at Lancaster University, have for the first time calculated that CFC replacement chemicals and anaesthetics are behind around a third of a million tonnes (335,500 tonnes) of a persistent forever chemical called trifluoroacetic acid (TFA) being deposited from the atmosphere across the Earth’s surface between the years 2000 and 2022.

And the rate of TFA entering the environment from these sources is continuing to grow as some of these CFC replacements survive for decades in our atmosphere, with peak annual TFA production from these sources estimated to be anywhere from between 2025 and 2100.

Scientists behind the new study, published in the journal Geophysical Research Letters, used ‘chemical transport’ modelling, which simulates how chemicals move about and change in the atmosphere.

Their model quantified TFA pollution created by the breakdown in the atmosphere of hydrochlorofluorocarbons (HCFCs) and hydrofluorocarbons (HFCs), which are used in refrigeration, as well as chemicals used as inhalation anaesthetics.

Although these chemicals (known as F-gases) are being phased out (following the Montreal Protocol and the later Kigali Amendment) their presence is still increasing in the atmosphere.

TFA belongs to a class of man-made chemicals called per- and polyfluorinated alkyl substances (PFAS). This group of chemicals are often known as forever chemicals because they do not break down easily and remain in the environment for a long time.

The scientific understanding of TFA is still evolving. The European Chemicals Agency classifies TFA as harmful to aquatic life. TFA has been detected in human blood and urine and the German Federal Office for Chemicals recently proposed that TFA be classified as potentially toxic to human reproduction.

Although some agencies consider that current environmental TFA is below levels that would cause harm to humans, the potentially irreversible accumulation of TFA in the environment has led for calls for it to be designated as a planetary boundary threat.

“Our study shows that CFC replacements are likely to be the dominant atmospheric source of TFA,” said Lucy Hart, PhD researcher at Lancaster University and lead author of the study. “This really highlights the broader risks that need to be considered by regulation when substituting harmful chemicals such as ozone-depleting CFCs.”

The researchers compared modelled atmospheric TFA production (from chemical breakdown) and its deposition on the Earth’s surface with observation data such as Arctic ice-cores and rainwater measurements.

The researchers provided their model with information on how much of the source gases are present in the atmosphere and where they are located using measurements from a global monitoring network. The source gases react with other atmospheric components and break down to produce TFA.

The model contains realistic weather processes calculating how it is transported and deposited. TFA can be washed out of clouds through rain or deposited directly from the air to the surface.

The modelling shows that almost all of the TFA found in the Arctic, which is far away from known emission sources, is from CFC replacement chemicals and highlights the widespread nature of TFA pollution.

“CFC replacements have long lifetimes and are able to be transported in the atmosphere from their point of emission to remote regions such as the Arctic where they can breakdown to form TFA,” said Lucy Hart. “Studies have found increasing TFA levels in remote Arctic ice-cores and our results provide the first conclusive evidence that virtually all of these deposits can be explained by these gases.”

Away from the poles, at midlatitude regions of the globe, the researchers’ modelling also supports evidence around the emergence of HFO-1234yf, which is used in car air conditioning systems, as an important, and likely growing, source of TFA from the atmosphere.

“HFOs are the latest class of synthetic refrigerants marketed as climate friendly alternatives to HFCs,” said Professor Ryan Hossaini of Lancaster University and co-author of the study. “A number of HFOs are known to be TFA-forming and the growing use of these chemicals for car air conditioning in Europe and elsewhere adds uncertainty to future levels of TFA in our environment.”

“There is a need to address environmental TFA pollution because it is widespread, highly persistent, and levels are increasing,” said Professor Hossaini.

“The rising levels of TFA from F-gases is striking. Although HFC use is gradually being phased down, this TFA source will remain with us for decades. There’s an urgent need to understand other TFA sources and to assess TFA’s environmental impacts. This requires a concerted international effort, including more extensive TFA monitoring in the UK and elsewhere,” he said.

Professor Cris Halsall, Director of the Lancaster Environment Centre and co-author, said: “We’ve generally viewed TFA as a breakdown product from the use of a few fluorinated pesticides, but it’s clear that TFA (a very persistent chemical in the environment) arises from the use and breakdown of a very wide group of organofluorine chemicals including refrigerants, solvents, pharmaceuticals and the PFAS group in general.”

Co-author Dr Stefan Reimann, whose research team in Switzerland closely monitor the atmospheric abundance TFA-forming F-gases, said: “In all regions where TFA measurements are available, a consistent picture of increasing atmospheric concentrations and deposition to Earth's surface is emerging.

“This study is outstanding, as it combines for the first time all the important sources of atmospheric TFA and has a global focus. With increasing use of HFOs, accumulation of TFA in water bodies will potentially grow and this makes long-term monitoring a necessity.”

The study involved researchers from: Lancaster University; the University of Leeds; the University of Urbino; the Commonwealth Scientific and Industrial Research Organisation, Australia; the Norwegian Institute for Air Research; the University of California San Diego; the University of Bristol; the Kyungpook National University, Korea; the Swiss Federal Laboratories for Materials Science and Technology; and the Goethe University Frankfurt.

Their findings are detailed in the paper ‘Growth in production and environmental deposition of trifluoroacetic acid due to long-lived CFC replacements and anaesthetics’.

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Journal

Geophysical Research Letters

DOI

10.1029/2025GL119216 

Method of Research

Computational simulation/modeling

Subject of Research

Not applicable

Article Title

Growth in production and environmental deposition of trifluoroacetic acid due to long-lived CFC replacements and anaesthetics

Article Publication Date

4-Feb-2026