In South Asia, a region facing rapid economic growth, immense population pressure, and high climate vulnerability, the circular economy (CE) has become a critical imperative for sustainable development. This study provides a comparative overview of the CE landscape across eight South Asian countries: Afghanistan, Bangladesh, Bhutan, India, Maldives, Nepal, Pakistan, and Sri Lanka. The analysis reveals the CE transition is nascent region-wide, though India has advanced its policy landscape through a comprehensive suite of rules and missions and Pakistan is developing a national policy. The primary focus remains on waste management, evidenced by programs like Bhutan’s ‘Zero Waste by 2030’ vision, the Maldives’ Single-Use Plastic Phase-Out Plan, and Sri Lanka’s Clean Sri Lanka Programme. While Extended Producer Responsibility (EPR) is emerging for plastics and e-waste in India, Bangladesh, Sri Lanka, and Pakistan, a significant “policy-practice gap” persists, undermined by weak enforcement and governance fragmented across priority sectors like plastics, food systems, and textiles. Most major CE initiatives are catalyzed by international development partners, with regional programs playing a key role in funding innovation. Finally, while the informal sector is the backbone of material recovery, ensuring a just transition that improves working conditions and secures livelihoods remains a critical challenge. The absence of a cohesive regional framework limits collaboration. Scaling the circular economy in South Asia requires integrated national strategies, prioritizing a just transition for the informal sector, and establishing a regional platform for policy harmonization to create self-sustaining system through multi-sectoral involvement, including the business sector.

Booking for the EIG 2026 Conference in Liverpool is now open: https://www.eigconferences.com/ There will be the usual plenary opening session, including an introduction to the geology of North West England by Professor Peter Burgess, University of Liverpool, and the Ansel Dunham Memorial Lecture by Fiona McEvoy of NWS. This will be followed by parallel sessions, from a variety of geotechnical and quarry design case studies and overviews of professional practice to prospecting, geomorphological quarry restoration, low carbon resources and the water environment. Conference programme can be downloaded here: https://www.eigconferences.com/s/EIG-2026-Liverpool-Programme-May6th.pdf Delegate booking, trade stands and sponsorship opportunities are here: https://www.eigconferences.com/2026-conference NB Delegate Early Bird deadline 30th June 2026.

Pharmaceutical residues enter the environment worldwide through excretion after use and improper disposal and can cause significant ecotoxicological effects while also contributing to the pollution of water resources used for drinking water production and food production. Although pharmaceuticals are indispensable for public healthcare, their environmental impacts are rarely considered during prescribing or dispensing. A newly developed Environmental Pharmaceutical Index (EPI) aims to integrate environmental information systematically into pharmaceutical and medical decision-making. The objective is to balance therapeutical needs and environmental impacts by supporting the selection of therapeutically equivalent medicines with lower environmental impacts without compromising patient care. A practical environmental information, classification and dissemination system The proposed Environmental Pharmaceutical Index consists of three interconnected components: an environmental information system, an environmental classification system, and a dissemination system. The information system is designed to collect substance-based environmental information, primarily from Environmental Risk Assessments (ERA) conducted during the European marketing authorisation process. The authors propose using the German Environment Agency's ChemInfo database as the central information platform. Based on the outcomes of the ERA risk assessment and hazard assessment, the system introduces a practical traffic light classification with the categories red, yellow, green and grey. This classification enables healthcare professionals to compare active pharmaceutical ingredients (APIs) within the same indication group and to identify substances of environmental concern while maintaining transparency regarding the underlying scientific evidence. International experience informed the German concept The concept builds on an evaluation of existing environmental information and classification systems in Sweden, Finland and Scotland. The study combined scoping literature reviews, qualitative stakeholder interviews, expert panel meetings, stakeholder workshops, and a feasibility analysis. The results demonstrate that environmental information is most effective when it is integrated directly into existing therapeutic decision-making processes rather than requiring additional information searches during routine clinical practice. Accordingly, the proposed dissemination strategy includes integration into pharmacy and doctors' office management software, therapeutic guidelines, formularies, and other established healthcare information systems to support environmentally informed prescribing and dispensing. Supporting eco-directed pharmaceutical prescribing The Environmental Pharmaceutical Index is intended to complement established therapeutic decision-making rather than replace it. Environmental aspects should only influence the choice of treatment where multiple therapeutically equivalent treatment options are available. Therapeutic efficacy, patient safety and clinical appropriateness remain the primary considerations. In the long term, the authors identify opportunities to integrate environmental information into market authorisation, reimbursement decisions, discount agreements of health insurance companies, labelling, and therapeutic guidelines. By combining a scientifically robust environmental information system with practical dissemination approaches, the proposed concept aims to facilitate eco-directed pharmaceutical prescribing and reduce the environmental burden of pharmaceuticals in Germany. The study "Environmental Pharmaceutical Index – a practical information, classification and dissemination system for medication in Germany" was carried out by researchers from Christian-Albrechts-University of Kiel, the German Environment Agency (Umweltbundesamt, UBA), the Ecologic Institute, and Augsburg University.

Tissue engineers are finding ways to grow living organs and tissues from cells, with the aim of replacing diseased and damaged counterparts in the body. Scientists have successfully grown artificial muscles, livers, kidneys, skin, and other tissues. But there’s been no reliable way to engineer precisely patterned networks of blood vessels, some of which can be finer than a human hair. Without a vascular network to deliver nutrients, any artificial tissues, no matter how life-like, can’t function. Now MIT engineers have found they can engineer and control the growth of blood vessels by mechanically stretching them. The team has built a human “blood vessel on a chip,” composed of a central artery made from human endothelial cells, that is embedded in a gel that also contains a small magnet. The researchers studied how the main artery responded as they jostled the gel back and forth using an external magnet to move the magnet embedded within the gel. Play video Video constructed from a 3D high-resolution microscopy image of engineered blood vessel tissue made by MIT engineers, showing a fly-through of a central artery and new capillaries that sprout from the artery in response to mechanical stimulation. They found that the simple mechanical action of repeatedly jostling the artery stimulated the artery to sprout other, smaller capillaries. By changing the direction in which the artery is jostled or stretched, the researchers could redirect the growing new vessels. And stretching the artery by various degrees influenced how many more new vessels sprouted. Their results, reported in the Proceedings of the National Academy of Sciences, offer scientists a new way to engineer artificial blood vessels and program the patterns in which they grow. “Healthy tissues depend on organized blood vessel networks, but state-of-the-art protocols don't enable fabricating such networks within engineered tissues,” says Ritu Raman, associate professor of mechanical engineering at MIT and the study’s co-lead author. “The ability to program blood vessel growth with physical cues may enable reproducible and scalable fabrication of engineered tissues that can be implanted in the body to restore function after debilitating disease or injury.” The study’s MIT co-authors include Sina Kheiri, Jessica Shah, Shashaank Venkatesh, and Roger Kamm, along with Peiyuan Chai and Ryan Flynn at Harvard University. “Moving is good” Blood vessels are tricky to grow and control using conventional fabrication techniques. While 3D printers can produce vessels at the scale of major arteries and veins, the technology is not precise enough to print intricate networks of much finer, thread-like capillaries. Scientists have had some success with growing blood vessels from individual cells, by cultivating them in Petri dishes filled with nutrients and growth factors. But controlling how and where they grow remains a challenge. “You can try to pattern chemical cues, like growth factors, to direct where vessels grow, but you can’t do this very precisely,” Raman says. “We thus need other types of patternable cues that can help us build tissues with organized vessels.” She and her students wondered whether they could grow and control new blood vessels using a protocol they previously developed to grow artificial muscles and nerves. In their previous works, the team engineered a small chip filled with a gel that they infused with nutrients and growth factors. They embedded a small magnet within the gel, and then carpeted the surface of the gel with live muscle or neuron cells. They then manipulated an external magnet to pull the embedded magnet, and the cell-covered gel, back and forth. This work revealed that mechanical “exercise,” pulling the cells back and forth, directly influenced how the cells grew. In their new work, the team used a similar setup to see if they could grow and control new blood vessels. The researchers built a “blood-vessel-on-a-chip,” smaller than a postage stamp, and filled it with a similar nutrient-rich gel containing a small magnet. They poked a thin tube lengthwise through the gel to create a hollow channel, and coated the channel with live endothelial cells, which naturally grow and fuse to form blood vessels in the body. Once the cells took on the channel’s shape, they started sprouting new, capillary-like vessels in the gel. Credit: Courtesy of the researchers Placing the device under a motorized stage fitted with small, suspended magnets, the researchers moved the magnets back and forth in different directions, and by various degrees, and observed whether and how blood vessels sprouted from the central artery in response. “The main takeaway is: Stretching the blood vessel back and forth seems to enhance the number of new capillaries that grow,” Raman says. If the main artery were simply left alone in the gel, it would grow some new vessels in random locations along its length. But when the artery was jostled, significantly more vessels sprouted. When the team used the magnets to stretch the gel back and forth, by 5 percent of the gel’s total width, many new vessels grew out from the main artery. When they stretched by 15 percent, fewer vessels sprouted, but those that did grew longer. And when the team changed the direction of stretching, the new vessels followed in response, taking turns and following the pattern of the team’s mechanical stimulation. “We’re finding that moving is good, which is always the takeaway of everything we do in our lab,” Raman says. “Mechanical forces play an important role in our bodies. That means that if you want to grow more or less vessels, or shorter or longer vessels, or vessels in certain directions, we now know how to do that.” A gatekeeping gene The researchers went a step further to investigate why blood vessels grow in response to mechanical forces. To do so, they looked to gene editing, and the role of one particular gene: Piezo1. Raman had recently attended a talk by molecular biologist Ardem Patapoutian. In 2021, Patapoutian received the Nobel Prize in Physiology or Medicine for his discovery of ion channels in cell membranes that open and close in response to mechanical pressure. These channels, named PIEZO1 and PIEZO2, act as a cell’s gatekeepers, controlling what goes in and what comes out of a cell. Both types of channels, Patapoutian found, are regulated by their respective genes, also named PIEZO1 and PIEZO2. After his talk, Raman showed Patapoutian her group’s experimental results, which showed a connection between blood vessel growth and mechanical stimulation. Patapoutian in turn proposed that the explanation could be the PIEZO1 channel; by mechanically exercising the central artery, Raman may have been stimulating ion channels in the artery’s cells to open, triggering new blood vessels to grow. To test this hypothesis, Raman looked to knock down the PIEZO1 gene. If this gene were less active, and fewer blood vessels grew as a result, then it would mean that blood vessels do indeed grow in response to mechanical stimulation, and specifically, through the activation of PIEZO1 ion channels. The team repeated their experiments, this time with endothelial cells that were genetically edited to suppress the PIEZO1 gene. Sure enough, they observed that significantly fewer new blood vessels sprouted, even as they mechanically exercised the central artery. Now that the team has found a way to grow and control blood vessel growth, they plan to apply the protocol to grow organized networks of vessels to supply artificial organs and tissues. “We are now investigating how precisely patterning blood vessel growth can help improve muscle function,” says co-author Jessica Shah. This work was supported, in part, by the U.S. Department of War Army Research Office Early Career Program and PECASE Grant, and a Department of War DURIP Program Grant.

Abstract TATA-box binding protein–associated factor 15 (TAF15) is an RNA-binding protein and the primary fibrillar constituent in a subset of frontotemporal lobar degeneration (FTLD) cases. However, the molecular determinants underlying TAF15 aggregation remain unclear. Here, we show that TAF15 forms amyloid fibrils under physiological conditions and develop a cellular biosensor to monitor its propagation. Both recombinant TAF15 fibrils and pathological aggregates extracted from FTLD patient brains selectively seed TAF15 biosensor cells, demonstrating prion-like properties. The closely related protein FUS does not seed TAF15 aggregation, revealing a cross-seeding barrier, but partially incorporates into inclusions during TAF15-induced seeding, potentially explaining their pathological overlap in FTLD. Computational and peptide-based mapping identifies aggregation-prone motifs within the low-complexity domain that stabilize ex vivo fibril cores and drive TAF15 propagation. These findings establish TAF15 as an amyloid-forming, prion-like protein and define sequence determinants underlying its self-assembly, providing a mechanistic framework for FTLD-TAF15 and potential therapeutic targets.

Abstract Scalable manufacturing of perovskite solar cells is fundamentally limited by the vulnerability of perovskite crystallization to ambient moisture and oxygen, particularly during blade coating where an extended pre-annealing interval exposes unstable intermediates. Here, we introduce a surface-confined protection strategy to intrinsically stabilize perovskite film formation under ambient conditions. By introducing dipropylammonium trifluoroacetate (DPTA) into the perovskite precursor ink to spontaneously form a dense and self-assembled surface layer, selectively shielding the wet perovskite pre-film from environmental attack during the critical pre-annealing stage. This transient yet effective barrier preserves the PbI2·NMP intermediate to prevent pre-annealing degradation of the perovskite lattice even at high humidity. Simultaneously, the multifunctional ionic nature of DPTA allows strong coordination and hydrogen-bonding interactions with the perovskite lattice, leading to reduced bulk and interfacial defects. As a result, air-processed blade-coated MA-free perovskite solar cells reach an efficiency of 26.14% (certified at 25.75%), and retain 93.11% of the initial efficiency after 1300 h under continuous 1 sun illumination tested at maximum-power-point. The strategy readily translates to manufacturing-relevant perovskite solar modules, delivering 22.72%-efficiency on substrate area of 100 × 100 mm2. These results establish surface-confined protection as a general principle for scalable perovskite photovoltaics under ambient conditions.

Abstract During human B cell maturation, immature transitional (T1) cells transit from bone marrow into the blood. At the subsequent immature T2 stage, a separation into IgMhi (T2Mhi) and IgMlo (T2Mlo) developmental trajectories has been proposed. Here, we isolate T1, T2Mhi and T2Mlo cells from human adult and cord blood for bulk and single-cell ATAC-seq, CUT&RUN, RNA-seq and CITE-seq to profile their transcriptomic and epigenetic differences. We identify accessible chromatin domains discriminating between T2Mhi and T2Mlo cells in peripheral B cell development, with signatures persisting during the differentiation of T2Mlo to naïve B cells. Similarly, memory and marginal zone B cells retain epigenetic hallmarks of their T2Mlo and T2Mhi precursors, coupled with transcriptional diversity. Imaging mass cytometry with RNAscope of spleen, appendix and tonsil further validates the spatial relationships of expressed genes. Our study thus provides insights into B lineage T2 bifurcation and describes epigenetic signatures of B cell developmental pathways.

Plastic pollution is among the gravest environmental crises facing humanity. Plastic production since 1950 has exceeded 8,300 million metric tons, with most plastic waste ending up in the environment, affecting wildlife, ecosystem functionality, and human health. Simultaneously, the ability of disease-causing bacteria to withstand one or more antibiotics (known as antimicrobial resistance, or AMR) has surged to become a public health emergency now accounting for around 5 million deaths worldwide annually. Indian wastewater rife with drug resistance genes Read now → Read now → “AMR is an existential human threat,” says Tim Walsh, a professor at the University of Oxford and director of biology at the UK’s Ineos Oxford Institute of Antimicrobial Research, who spoke to Mongabay via video call. “It will kill more people [each year] than TB, HIV and malaria, and if unchallenged could eclipse cancer as the biggest killer.” Until very recently, these two global crises, plastic pollution and antimicrobial resistance, were considered separately by scientists and policymakers. But a new line of research suggests they’re inextricably linked: Plastic waste is quickly colonised by microorganisms, creating a new type of ecosystem dubbed the “plastisphere.” And bacteria living in the plastisphere are developing greater resistance to antibiotics at an unprecedented rate. “ We know that microplastics are ingested at the base of the food chain by filter feeders, like mussels, if there’s any harmful pathogens or microplastics in there, they could be making their way into the human food chain. Emily Stevenson, researcher, University of Exeter How microplastics enhance antimicrobial resistance In 2025, researchers at Boston University found that Escherichia coli bacteria exposed to microplastics developed enhanced resistance to four common antibiotics when compared to bacteria not exposed to microplastics. After just 10 days of microplastic exposure, the bacteria’s tolerance to antibiotics “just shot up,” reaching 100 times the level it had started at, says Neila Gross, the doctoral researcher who led the study, in a video call with Mongabay. “This was very, very concerning.” Researchers are still unravelling exactly how and why microplastics enhance antimicrobial resistance. A key piece of the puzzle is the way bacteria behave when colonising a surface. Although we usually think of bacteria as solitary, when they grow on a surface they stick together and form a complex community known as a biofilm. Biofilm bacteria secrete a protective gel-like material made of proteins, carbohydrates and DNA, which helps them stay attached to the surface they’re on and provides protection against harmful substances, including antibiotics. “It’s a physical barrier, sort of like armour, [and the bacteria] hang out in the middle of it,” Gross says. Biofilm bacteria are more likely to develop resistance to antibiotics than solitary bacteria, in part because the protective gel blocks most, but not all, of the antibiotics that are trying to break through. This means the bacteria are exposed to antibiotics at levels high enough to prompt a defensive response, but not high enough to kill them outright. Much like an incomplete course of antibiotics, this low-level exposure primes the bacteria to evolve resistance. Here’s where microplastics enter the equation: They don’t just provide a surface on which biofilms can form; they actively promote their formation. Gross’s research has shown that bacteria form denser, thicker biofilms on microplastic beads than on glass. The microplastics also appear to select for bacteria that are better at forming biofilms. By promoting the formation of stronger, more stable biofilms, microplastics create the perfect environment for drug resistance to develop. Separate studies conducted in China and the UK have found that, in river environments, microplastic waste can harbor more antibiotic-resistant bacteria and a higher abundance of some resistance genes, compared to naturally occurring surfaces like wood or rock. Microplastics encourage gene sharing Another reason drug resistance can spread so rapidly through biofilms is that the bacteria residing in such films readily exchange genetic material via a process known as horizontal gene transfer. Instead of every bacterium having to individually evolve resistance to every antibiotic from scratch through chance mutations, a resistance gene evolved by one bacterium can be shared with the whole community. “Bacteria are like these genetic sponges, and their DNA is very plastic,” Walsh says. “They’re able to grow together, communicate together, and exchange [genetic] information far more readily than human beings. They are a formidable foe in that regard.” Walsh and colleagues discovered that exposure to microplastics increases the rate of horizontal gene transfer by up to 200 times. This happens because bacteria respond to microplastics by expressing so-called “S.O.S. genes,” — a group of genes that help to repair damaged DNA and have previously been shown to encourage gene swapping. “The bacteria see the microplastics as a toxin and go into overload, stimulating the exchange of genetic material,” Walsh says. Some plastic types are higher risk Scientists are now working to understand what specific plastic characteristics make them effective at promoting drug resistance. What we know so far is that certain types of plastics seem to be more problematic than others. For example, scientists have found that polyethylene, ubiquitous in plastic packaging, harbours higher levels of AMR than polyvinyl chloride, used in hard plastics such as pipes. A separate study found denser bacterial biofilms and more horizontal gene transfer on polyethylene compared with other plastics. Research also suggests that expanded polystyrene, the type used to make packing peanuts, may be at higher risk of fostering drug-resistant bacteria than other plastic types. “The very nature of plastics makes them a risky substrate, but polystyrene is a very complex matrix,” study lead author Emily Stevenson, a PhD researcher at the UK’s University of Exeter, tells Mongabay in a video call. “That porous structure gives more surface area for colonisation of bacteria.” A further complication: Plastic particles change over time as they’re exposed to sunlight and water. This ageing process can make their exteriors rougher, creating a bigger surface area on which bacterial biofilms can stick. Ageing also causes toxic chemicals to leach out of plastics, which can trigger the bacteria’s S.O.S response, helping resistance genes spread. Microplastics could carry resistant bacteria to new locations Once AMR has developed in an environment, humans can contract drug-resistant infections through contact with contaminated water, soil or food. Microplastics may play a role here too: Lightweight plastics, such as expanded polystyrene, can be carried in storm runoff, in streams or by ocean currents, potentially relocating antibiotic-resistant bacteria into new environments. Another potential route to infection, say experts: Microplastics harbouring drug-resistant biofilms could carry those harmful bacteria up the food chain to humans. “We know that microplastics are ingested at the base of the food chain by filter feeders, like mussels,” Stevenson says. Her PhD research suggests that microplastics could increase the amount of AMR genes in the mussels’ guts. Since humans eat shellfish like mussels whole, “if there’s any harmful pathogens or microplastics in there, they could be making their way into the human food chain,” she says. More research is needed to confirm and expand on these preliminary findings. Wastewater: A hotspot for drug-resistance Bacteria are ubiquitous in the global environment, as are microplastics. But there are locations where they come together in high concentrations, alongside antibiotics and other toxic substances, creating AMR hotspots. Advanced wastewater treatment plants (WWTPs) filter and treat raw sewage to remove bacteria, pharmaceutical residues and pollutants, including microplastics. Though this process can be very effective, it’s not perfect. “Plastics break down into smaller and smaller pieces, which are really difficult to filter or remove from the wastewater,” Tam Tran, a senior researcher at the Norwegian research institute (NORCE), says in a video call with Mongabay. Tran and colleagues analysed wastewater samples from Norway, Iceland and Finland, and found that treatment reduced the levels of antibiotic residues, microplastics and drug-resistance genes in the water, but not completely. When treated wastewater carrying traces of antibiotics and microplastics is released into marine environments, “It potentially creates a new hotspot for AMR,” Tran says. Wastewater, even after going through an advanced treatment facility, presents a risk for AMR development. But when sanitation facilities are limited, inadequate or missing entirely, for example, in disadvantaged communities, war zones or refugee camps, there is an even greater risk that drug-resistant bacteria will emerge. “Whenever you have degradation of infrastructure … there is that direct link to the carriage of resistant bacteria,” Walsh says. In high-income countries, drug-resistant infections are a big problem, but one that can often be overcome with medical care. In low- and middle-income countries, where sanitation facilities and water treatment plants are less available, multidrug-resistant infections are prevalent, and often fatal. In many African and Southeast Asian nations, “we’ve already run out of antibiotics [to choose from], and of course, it affects the poorest population,” Walsh says. “It’s directly linked to poverty.” Low- and middle-income countries also often have fewer recycling facilities, which means plastic waste is also more likely to end up in open-air dumps and streams, on beaches, and in the street, greately expanding the plastisphere colonised by bacteria. Multiple crises combine to promote drug resistance Plastics and antibiotics are both manufactured substances introduced by humans into the environment. They can both affect the functioning of Earth’s life-support systems, for better or worse. For this reason, they are grouped together in the “novel entities” planetary boundary, one of nine boundaries that, if breached, threaten to push Earth out of the habitable zone. Scientists say that humanity has now exceeded safe thresholds for six of the nine boundaries, including the novel entities boundary. Climate change is another planetary boundary whose safe zone has been exceeded by humanity. Its transgression may also be exacerbating AMR. That’s because higher temperatures speed up bacterial growth and promote horizontal gene transfer, helping drug resistance spread. There may also be indirect climate effects: Extreme heat, humidity, flooding and drought brought by global warming can negatively impact water quality and food security, increasing the prevalence of infectious diseases and necessitating more use of antibiotics, which promotes AMR. “How we treat our environment, both in terms of environmental degradation, but also in terms of climate change, is directly linked to AMR,” Walsh says. Climate change may also amplify the effect of plastic pollution on AMR. Higher temperatures cause plastics to fragment into microplastics and leach harmful chemicals more rapidly, providing more surfaces for biofilm formation and promoting the S.O.S. response that encourages bacterial gene swapping. Plastics influence AMR throughout their life cycles Although research into the link between microplastics and drug resistance has focused on plastic pollution in the environment, there is good reason to believe that plastics are promoting AMR throughout their life cycles. Most plastics are produced from fossil fuels, which need to be extracted and pumped via pipes to refineries. Biocides, chemical substances used to kill microorganisms such as bacteria, are used in those pipes to prevent the buildup of bacterial biofilm, which could clog the pipes. But because biocides rarely succeed in killing 100 per cent of bacteria, their systemic industrial use could, in fact, encourage AMR development. Chemical additives used in the plastic manufacturing process may also promote drug resistance. Again, more research is needed to fully understand these risks. Collecting and transporting plastic waste, whether moving it to landfills or recycling plants, could transport drug-resistant bacteria to new environments. Even recycling may promote AMR, because plastic waste is often treated with disinfectants before being processed, with any surviving bacteria potentially becoming resistant. “Plastics and AMR are fundamentally linked,” Stevenson says. “At every stage of the life cycle of plastics, from production to disposal, there [is] something that could influence antimicrobial resistance.” However, plastic can also be a useful tool in the battle against AMR. “One of the really beneficial uses of plastics is that they keep things sterile,” Stevenson says, which reduces the transmission of drug-resistant bacteria in hospitals and clinics. “It’s sort of a double-edged sword.” The uncertain path forward Scientists have now uncovered a deeply concerning link between microplastics and AMR, potentially exacerbated by other environmental crises such as climate change. But many question remain: How do biofilms on microplastics change and evolve over time? How do chemical additives — tens of thousands of which are routinely added to different types of plastic — influence AMR? What happens when other substances in the environment, ranging from heavy metals to plant secretions, interact with biofilm-laden microplastics? And how do microplastics in our digestive system influence drug resistance in the microbiome? While scientists work to answer these and many other questions regarding microplastics and AMR, public health experts recognise that action is desperately needed to stop the spread of drug-resistant bacteria and to control the flood of plastic waste into the environment. A good place to start would be “reducing the amount of plastics and antibiotics going into the wastewater treatment plant … so using less plastics and having better antimicrobial stewardship,” Stevenson says. “We really need to make sure we’re not just regulating one of those contaminants. We need to look at them holistically.” Slowing AMR spread is just another in a long list of reasons humanity needs to break free from the cycle of plastic manufacture and waste. But, with so much plastic already in the environment, it may be too little, too late. Limiting opportunities for the mixing of this dangerous bacterial, antibiotic and microplastic cocktail by utilising better wastewater management and ongoing AMR surveillance may be the best hope for global public health and safety. This story was published with permission from Mongabay.com. Like this content? Join our growing community. Your support helps to strengthen independent journalism, which is critically needed to guide business and policy development for positive impact. Unlock unlimited access to our content and members-only perks. Find out more and join us. → Find out more and join us. → Related to this story Topics Cities Food & Agriculture Manufacturing Waste Water Regions Global Tags climate climate risk diseases extreme weather food security global warming healthcare heatwaves inequality infectious diseases infrastructure plastic pollution research waste wastewater water security water treatment SDGs 3. Health 6. Water 9. Infrastructure 10. Inequality 11. Cities 12. Consumption 16. Peace 17. Partnerships