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Evidence that microplastics aggravate the toxicity of organophosphorus flame retardants in mice (Mus musculus)
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Researchers co-exposed mice to polyethylene and polystyrene microplastics along with organophosphorus flame retardants for 90 days and found that microplastics aggravated the toxicity of the flame retardants. Evidence from biochemical markers and metabolomics indicated increased oxidative stress and metabolic disruption in co-exposed animals, suggesting microplastics may worsen the health effects of chemical pollutants they encounter in the environment.
This study was performed to reveal the health risks of co-exposure to organophosphorus flame retardants (OPFRs) and microplastics (MPs). We exposed mice to polyethylene (PE) and polystyrene (PS) MPs and OPFRs [tris (2-chloroethy) phosphate (TCEP) and tris (1,3-dichloro-2-propyl) phosphate (TDCPP)] for 90 days. Biochemical markers and metabolomics were used to determine whether MPs could enhance the toxicity of OPFRs. Superoxide dismutase (SOD) and catalase (CAT) increased (p < 0.05) by 21% and 26% respectively in 10 μg/L TDCPP + PE group compared to TDCPP group. Lactate dehydrogenase (LDH) in TDCPP + MPs groups were higher (18%-30%) than that in TDCPP groups (p < 0.05). Acetylcholinesterase (AChE) in TCEP + PE groups were lower (10%-19%) than those in TCEP groups (p < 0.05). These results suggested that OPFR co-exposure with MPs induced more toxicity than OPFR exposure alone. Finally, in comparison to controls we observed that 29, 41, 41, 26, 40 and 37 metabolites changed significantly (p < 0.05; fold-change > 1.2) in TCEP, TCEP + PS, TCEP + PE, TDCPP, TDCPP + PS and TDCPP + PE groups, respectively. Most of these metabolites are related to pathways of amino acid and energy metabolism. Our results indicate that MPs aggravate the toxicity of OPFRs and highlight the health risks of MP co-exposure with other pollutants.
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Researchers exposed mice to the flame retardant resorcinol bis(diphenylphosphate) alone and in combination with polystyrene nanoplastics through inhalation. Using proteomics and metabolomics analysis, they found that co-exposure produced significantly worse lung damage than the flame retardant alone, through amplified oxidative stress and inflammatory signaling. The study reveals that nanoplastics can intensify the pulmonary toxicity of co-occurring environmental chemicals through synergistic mechanisms.
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This review examined how micro- and nanoplastics cause oxidative stress — a form of cellular damage — in living organisms, particularly when combined with other chemical pollutants in the environment. Co-exposure to microplastics and chemicals like pesticides or heavy metals tends to be more damaging than either pollutant alone.
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Marine mussels (Mytilus coruscus) co-exposed to polystyrene microplastics and the flame retardant BDE-47 for 21 days showed greater immune suppression, oxidative stress, and energy depletion than with either pollutant alone, consistent with microplastics acting as a carrier that amplifies BDE-47 toxicity.
Combined toxicity of organophosphate flame retardants and polyethylene microplastics on Eisenia fetida: Biochemical and molecular insights
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Researchers exposed earthworms to polyethylene microplastics, chlorinated flame retardants, and their combinations to assess combined toxicity effects. They found that the most toxic flame retardant (TDCPP) had its effects reduced when combined with microplastics, likely because the plastics absorbed the chemical and lowered its bioavailability. In contrast, microplastics enhanced the toxicity of another flame retardant (TCPP), demonstrating that microplastics can act as both carriers and modulators of co-contaminant toxicity in soil ecosystems.
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