Slow-release fertilizers can spread microplastics on US cropland
Fertilizers that shed microplastics are increasingly spreading on America's cropland, research shows, raising new worry about the soil contamination and safety of the US food supply.
A peer-reviewed University of Missouri paper found common types of slow-release fertilizers are often encapsulated with plastic and can be so small that they could be considered microplastics. Those are designed to break down into even smaller pieces of plastic once spread in fields.
The tiny bits of plastic can end up in water and soil at alarming levels, the paper's lead author said, and the substance is likely taken up by crops. Until now, the slow fertilizers have been thought to be safe, said Maryam Salehi, a lead author and researcher with the University of Missouri.
'We need to inform farmers,' Salehi said. 'When they choose their products, they need to know that these have some potential risks.
Microplastics are tiny bits of plastic either intentionally added to consumer goods, or which are products of larger plastics breaking down. The particles contain any number of 16,000 plastic chemicals, of which thousands, such as BPA, phthalates and Pfas, present serious health risks.
The substance has been found throughout the human body, and is linked to an increased risk of heart attack and cancer. It's also considered to be a neurotoxicant that can cause multiple forms of brain dysfunction, such as Parkinson's disease.
Salehi said it is unclear which other chemicals are in the fertilizer plastic.
Testing has found microplastics in a wide range of foods, including produce.
Some of the slow release fertilizer pieces are less than five millimeters, which makes them microplastics by definition. But once they are in the soil, they 'break down into tiny, tiny particles' when a tractor runs over them, or someone walks on ground where they've been spread, Salehi said.
That is worrying because smaller bits can more easily move through the environment than larger pieces of plastic, Salehi said. The study found most of the microplastics stayed in the soil, but some were washed into nearby water sources by rain or irrigation processes.
The paper did not measure how much of the microplastics ended up in crops, but previous research has found that they can be taken up. Other papers have found that the bits of plastic may actually reduce soil quality.
'There is additional concern about the impact on food safety,' Salehi said.
But the problem may be rather easy to solve. There are many types of slow release fertilizers, including those that are encapsulated with biodegradable materials, Salehi said. However, the plastic versions work well so the industry for now seems to be sticking with them, she added.

Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles


Los Angeles Times
4 hours ago
- Los Angeles Times
Parkinson's Disease: What We Know and Where Treatment Is Headed
Parkinson's disease (PD) is more than a movement disorder—it's a neurological condition that reshapes the lives of patients and families. Parkinson's affects both motor and non-motor functions so its impact is broad and multifaceted. While tremors and stiffness may be the most visible signs, PD also brings a wide range of symptoms that impact thinking, mood and overall functioning. Common symptoms are bradykinesia, rigidity, tremor, postural instability, sleep disturbances and mood changes. As science digs deeper into this condition, hope grows for more precise, effective and compassionate care. Parkinson's disease is defined by the gradual loss of dopamine producing neurons in a part of the brain called the substantia nigra. This dopamine deficiency disrupts the brain circuits responsible for smooth and coordinated movements, leading to hallmark motor symptoms: resting tremor, muscle rigidity, slowness of movement (bradykinesia) and postural instability [1] [3] [5]. These are the most common Parkinson's disease symptoms targeted by treatment. The hallmark motor symptoms encompass a range of movement symptoms and movement related symptoms that affect daily functioning. Postural instability often results in balance problems making coordination and stability difficult for patients. In addition to resting tremor, muscle rigidity, slowness of movement (bradykinesia) and postural instability, other motor symptoms such as freezing of gait and difficulty with fine motor tasks may also occur. Collectively these are referred to as PD symptoms, the clinical features of Parkinson's disease. But PD isn't just about what the body can or can't do—it's also about what the brain feels. Long before a tremor appears many patients experience non-motor symptoms: Parkinson's symptoms, both motor and non-motor, can develop gradually and vary significantly between individuals. These symptoms can be easy to overlook or misattribute, often delaying diagnosis. According to a 2008 review, clinicians rely on a detailed medical history and physical examination to distinguish PD from other parkinsonian syndromes [1], while a 2020 JAMA review emphasizes the role of dopamine transporter (DAT) imaging and clinical expertise in diagnosis and staging [5]. Parkinson's is diagnosed primarily through evaluation of medical history and clinical examination, as there is no definitive blood test or brain scan for confirmation. So, what causes Parkinson's disease? The short answer: it's complicated. Most cases are considered idiopathic—meaning no single cause is identified—but multiple factors seem to converge. Both genetic and environmental factors are recognized as major contributors to the development of Parkinson's disease. Genetic contributions are increasingly recognized, with mutations in genes like LRRK2, PARK7 and SNCA playing a role [2]. Genetic mutations in these and other genes can influence disease development, sometimes interacting with environmental exposures. But genes don't tell the whole story. Environmental exposures, such as pesticide use or heavy metals, also contribute, especially in individuals with underlying vulnerabilities. At the cellular level PD is defined by several overlapping pathological processes: The loss of dopamine producing neurons in the substantia nigra involves the degeneration and death of specific brain cells and nerve cells which underlies the motor and non-motor symptoms of Parkinson's disease. These mechanisms interact like a feedback loop—fueling one another and accelerating neurodegeneration. This complex interplay drives the disease process, shaping both the progression and development of Parkinson's disease. Parkinson's disease affects more than 10 million people worldwide, with incidence rising sharply with age—especially after 60 [11]. Most Parkinson's disease cases are idiopathic and occur in older adults, with the majority of diagnoses in people over 60. However, early onset cases, known as early onset PD, can develop before age 50 and may differ in disease progression, diagnosis and treatment compared to typical cases. Men are more frequently affected than women, and rural living, well water exposure and pesticide contact are established risk factors. On the other hand, researchers have also identified protective factors. Regular caffeine consumption, moderate nicotine exposure and consistent physical activity may lower PD risk. Though not fully understood, these factors may influence inflammation, neuroplasticity or dopamine metabolism. There's no single test for Parkinson's, which makes early and accurate diagnosis a clinical challenge. Physicians typically rely on: In advanced diagnostic settings a spinal tap (lumbar puncture) may be performed to collect spinal fluid for biomarker analysis, such as detecting abnormal alpha-synuclein proteins. New frontiers are expanding diagnostic accuracy. Machine learning algorithms are being trained to analyze voice patterns, gait dynamics and digital biomarkers. AI-enhanced diagnostics and bioinformatics platforms are also being developed to detect early inflammatory signals before motor symptoms emerge [10]. Autonomic testing, including monitoring for blood pressure changes, may be used to assess non-motor symptoms. Distinguishing Parkinson's disease from other syndromes is crucial, with multiple system atrophy being an important differential diagnosis due to overlapping symptoms but differing disease progression and treatment responses. While there's no cure for PD, treatment can significantly improve quality of life. The primary goal of therapy is to manage symptoms and help patients maintain independence. Medications: Medication is different from surgery and should be discussed with a doctor. Dopaminergic medications can cause orthostatic hypotension and low blood pressure so monitoring is important. Non-medication is equally important: PD can also affect mood, behavior and cognition. Managing neuropsychiatric symptoms like depression or hallucinations requires a nuanced approach, including SSRIs, atypical antipsychotics and cognitive behavioral therapy. The Parkinson's Foundation is a key player in advancing research and treatment for Parkinson's disease. As the disease progresses many patients develop cognitive impairment, from mild forgetfulness to full blown Parkinson's Disease Dementia (PDD). These symptoms can overlap with or mimic Dementia with Lewy Bodies (DLB) (also known as Lewy body dementia) and Progressive Supranuclear Palsy (PSP) and other disorders within the spectrum of atypical parkinsonism, so accurate diagnosis is critical. A 2025 study compared cognitive trajectories across these syndromes and emphasized the need for tailored care and better biomarkers to distinguish between them. Inflammation is no longer seen as just a consequence of PD—it may be the cause. Recent studies, including a 2025 paper using machine learning and bioinformatics, have identified new inflammatory markers that could help with early diagnosis [10]. Ongoing Parkinson's research is key to finding new biomarkers, better treatments and a are also finding potential therapeutic targets. For example, UPS10, a protein that blocks α-synuclein degradation, may be a way to stop disease progression [8]. And lipid metabolism pathways open up metabolic interventions. These therapeutic strategies aim to modify the disease process to slow or stop progression. This is driving personalized medicine where treatment is based on a patient's genetic, metabolic or inflammatory profile. And the average life expectancy for most people with PD is the same as the general population thanks to research and care. Parkinson's disease is still a challenge for patients, caregivers and clinicians. But it's also a global research effort to understand the onset, progression and treatment of the disease. As we understand the interplay of genetics, environment and inflammation the future of PD looks more precise and hopeful. Until then a multidisciplinary approach – medication, therapy and emotional support – is the foundation of good care. [1] Jankovic J. (2008). Parkinson's disease: clinical features and diagnosis. Journal of neurology, neurosurgery, and psychiatry, 79(4), 368–376. [2] Kalia, L. V., & Lang, A. E. (2015). Parkinson's disease. Lancet (London, England), 386(9996), 896–912. [3] Marino, B. L. B., de Souza, L. R., Sousa, K. P. A., Ferreira, J. V., Padilha, E. C., da Silva, C. H. T. P., Taft, C. A., & Hage-Melim, L. I. S. (2020). Parkinson's Disease: A Review from [4] Pathophysiology to Treatment. Mini reviews in medicinal chemistry, 20(9), 754–767. [5] Balestrino, R., & Schapira, A. H. V. (2020). Parkinson disease. European journal of neurology, 27(1), 27–42. [6] Armstrong, M. J., & Okun, M. S. (2020). Diagnosis and Treatment of Parkinson Disease: A Review. JAMA, 323(6), 548–560. [7] Qin, B., Fu, Y., Raulin, A. C., Kong, S., Li, H., Liu, J., Liu, C., & Zhao, J. (2025). Lipid metabolism in health and disease: Mechanistic and therapeutic insights for Parkinson's disease. Chinese medical journal, 10.1097/CM9.0000000000003627. Advance online publication. [8] Bloem, B. R., Okun, M. S., & Klein, C. (2021). Parkinson's disease. Lancet (London, England), 397(10291), 2284–2303. [9] Anisimov, S., Takahashi, M., Kakihana, T., Katsuragi, Y., Sango, J., Abe, T., & Fujii, M. (2025). UPS10 inhibits the degradation of α-synuclein, a pathogenic factor associated with Parkinson's disease, by inhibiting chaperone-mediated autophagy. The Journal of biological chemistry, 110292. Advance online publication. [10] Halli-Tierney, A. D., Luker, J., & Carroll, D. G. (2020). Parkinson Disease. American family physician, 102(11), 679–691. [11] Li, Y., Jia, W., Chen, C., Chen, C., Chen, J., Yang, X., & Liu, P. (2025). Identification of biomarkers associated with inflammatory response in Parkinson's disease by bioinformatics and machine learning. PloS one, 20(5), e0320257. [12] Tysnes, O. B., & Storstein, A. (2017). Epidemiology of Parkinson's disease. Journal of neural transmission (Vienna, Austria : 1996), 124(8), 901–905.


Business Wire
11 hours ago
- Business Wire
Capsida Receives FDA IND Clearance for Its IV-Administered Gene Therapy for Parkinson's Disease Associated With GBA Mutations
THOUSAND OAKS, Calif.--(BUSINESS WIRE)--Capsida Biotherapeutics ('Capsida') today announced the U.S. Food and Drug Administration (FDA) has cleared the Investigational New Drug (IND) application for CAP-003, its potential best-in-class intravenously (IV) administered gene therapy, to enter clinical trials for Parkinson's disease associated with GBA mutations (PD-GBA). This is the second wholly owned clinical program developed by Capsida with a cleared IND. Both programs utilize a proprietary IV-delivered, blood brain barrier-crossing engineered capsid and proprietary cargo that is detargeted from off-target tissues, like liver and dorsal root ganglia (DRG). In addition, Capsida uses a proprietary manufacturing process and CAP-003 is manufactured in Capsida's state-of-the-art wholly owned Good Manufacturing Practice (GMP) facility. 'PD-GBA is an area of substantial unmet need given the lack of approved treatments that target GCase, which is the protein encoded by the GBA gene, and provide meaningful slowing or halting of disease progression,' said Swati Tole, M.D., Chief Medical Officer of Capsida Biotherapeutics. 'We recognize the urgency for new treatment approaches, so we are working diligently to initiate the Phase 1/2 clinical trial for CAP-003 with the aim of dosing the first patient in the third quarter of this year.' About CAP-003 and the Phase 1/2 Clinical Trial In non-human primate (NHP) studies to date, a single IV infusion of CAP-003 resulted in dose-dependent increases in GCase activity in critical brain regions including the substantia nigra, frontal cortex, caudate nucleus, and putamen substantially above the established 30% efficacy threshold expected to restore enzyme activity levels back to normal in patients with PD-GBA. The NHP Good Laboratory Practices (GLP) toxicology study demonstrated a well-tolerated safety profile with no adverse histopathology. Capsida expects to dose the first patient in the Phase 1/2 clinical trial in the third quarter of this year. For more information about the Phase 1/2 clinical trial, please visit (NCT07011771). About Parkinson's disease associated with GBA mutations (PD-GBA) Mutations in GBA, the gene expressing the GCase enzyme, affect up to 15% of Parkinson's patients and are the most common genetic risk factor for PD. Post-mortem studies demonstrate an approximate 30% GCase activity deficit in patients compared to healthy individuals 1. There are no approved treatments that target GCase and there are no approved disease modifying treatments for PD. Other investigational treatments for PD-GBA have been limited by their inability to cross the blood-brain barrier and supplement GCase enzyme activity in sufficient quantities to overcome the deficit in patients and impact the disease. In an attempt to overcome these challenges, those treatments have required invasive direct brain or cerebrospinal fluid (CSF) administration, with limited results, and a significant burden for patients. About Capsida Biotherapeutics Capsida Biotherapeutics is a clinical-stage, fully integrated next-generation genetic medicines company. It has a central nervous system (CNS) pipeline consisting of disease-modifying and potentially curative treatments for rare and more common diseases across all ages. Capsida's wholly owned pipeline includes its first-in-class investigational treatment for STXBP1 developmental and epileptic encephalopathy (STXBP1-DEE), CAP-002; and potential best-in-class investigational treatment for Parkinson's disease associated with GBA mutations (PD-GBA) CAP-003. Both have received FDA Investigational New Drug (IND) clearance to initiate clinical trials. Capsida's pipeline also includes a potential best-in-class treatment for Friedreich's ataxia (FA). In addition to its wholly owned programs, the Company has validating partnerships with AbbVie, Lilly, and CRISPR Therapeutics. Capsida was founded in 2019 by lead investors Versant Ventures and Westlake Village BioPartners and originated from groundbreaking research in the laboratory of Viviana Gradinaru, Ph.D., a neuroscience professor at Caltech. Visit us at 1 Leyns, C. E, G. et al (2023). npj Parkinson's Disease, 74(9).
Yahoo
11 hours ago
- Yahoo
Capsida Receives FDA IND Clearance for Its IV-Administered Gene Therapy for Parkinson's Disease Associated With GBA Mutations
Capsida is initiating the Phase 1/2 study for CAP-003, with the first patient expected to be dosed in the third quarter of this year THOUSAND OAKS, Calif., June 11, 2025--(BUSINESS WIRE)--Capsida Biotherapeutics ("Capsida") today announced the U.S. Food and Drug Administration (FDA) has cleared the Investigational New Drug (IND) application for CAP-003, its potential best-in-class intravenously (IV) administered gene therapy, to enter clinical trials for Parkinson's disease associated with GBA mutations (PD-GBA). This is the second wholly owned clinical program developed by Capsida with a cleared IND. Both programs utilize a proprietary IV-delivered, blood brain barrier-crossing engineered capsid and proprietary cargo that is detargeted from off-target tissues, like liver and dorsal root ganglia (DRG). In addition, Capsida uses a proprietary manufacturing process and CAP-003 is manufactured in Capsida's state-of-the-art wholly owned Good Manufacturing Practice (GMP) facility. "PD-GBA is an area of substantial unmet need given the lack of approved treatments that target GCase, which is the protein encoded by the GBA gene, and provide meaningful slowing or halting of disease progression," said Swati Tole, M.D., Chief Medical Officer of Capsida Biotherapeutics. "We recognize the urgency for new treatment approaches, so we are working diligently to initiate the Phase 1/2 clinical trial for CAP-003 with the aim of dosing the first patient in the third quarter of this year." About CAP-003 and the Phase 1/2 Clinical Trial In non-human primate (NHP) studies to date, a single IV infusion of CAP-003 resulted in dose-dependent increases in GCase activity in critical brain regions including the substantia nigra, frontal cortex, caudate nucleus, and putamen substantially above the established 30% efficacy threshold expected to restore enzyme activity levels back to normal in patients with PD-GBA. The NHP Good Laboratory Practices (GLP) toxicology study demonstrated a well-tolerated safety profile with no adverse histopathology. Capsida expects to dose the first patient in the Phase 1/2 clinical trial in the third quarter of this year. For more information about the Phase 1/2 clinical trial, please visit (NCT07011771). About Parkinson's disease associated with GBA mutations (PD-GBA) Mutations in GBA, the gene expressing the GCase enzyme, affect up to 15% of Parkinson's patients and are the most common genetic risk factor for PD. Post-mortem studies demonstrate an approximate 30% GCase activity deficit in patients compared to healthy individuals1. There are no approved treatments that target GCase and there are no approved disease modifying treatments for PD. Other investigational treatments for PD-GBA have been limited by their inability to cross the blood-brain barrier and supplement GCase enzyme activity in sufficient quantities to overcome the deficit in patients and impact the disease. In an attempt to overcome these challenges, those treatments have required invasive direct brain or cerebrospinal fluid (CSF) administration, with limited results, and a significant burden for patients. About Capsida Biotherapeutics Capsida Biotherapeutics is a clinical-stage, fully integrated next-generation genetic medicines company. It has a central nervous system (CNS) pipeline consisting of disease-modifying and potentially curative treatments for rare and more common diseases across all ages. Capsida's wholly owned pipeline includes its first-in-class investigational treatment for STXBP1 developmental and epileptic encephalopathy (STXBP1-DEE), CAP-002; and potential best-in-class investigational treatment for Parkinson's disease associated with GBA mutations (PD-GBA) CAP-003. Both have received FDA Investigational New Drug (IND) clearance to initiate clinical trials. Capsida's pipeline also includes a potential best-in-class treatment for Friedreich's ataxia (FA). In addition to its wholly owned programs, the Company has validating partnerships with AbbVie, Lilly, and CRISPR Therapeutics. Capsida was founded in 2019 by lead investors Versant Ventures and Westlake Village BioPartners and originated from groundbreaking research in the laboratory of Viviana Gradinaru, Ph.D., a neuroscience professor at Caltech. Visit us at 1Leyns, C. E, G. et al (2023). npj Parkinson's Disease, 74(9). View source version on Contacts Media Contact Inizio Evoke CommsKatherine Sign in to access your portfolio