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Systematic Review ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 1 ? Systematic review or meta-analysis. Synthesizes findings across many studies. Strongest evidence. Detection Methods Human Health Effects Sign in to save

Adverse outcome pathways potentially related to hazard identification of microplastics based on toxicity mechanisms

Chemosphere 2019 233 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 65 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Jaeseong Jeong, Jinhee Choi

Summary

Microplastic toxicology research has focused primarily on apical endpoints (mortality, growth, reproduction) rather than mechanisms, but this review identifies reactive oxygen species formation as the likely molecular initiating event in adverse outcome pathways, leading to oxidative stress, inflammation, and organ-level damage.

Body Systems
Study Type Review

Increasing concern over microplastics has recently brought increased attention to studies on microplastic toxicity. Here, we conduct a systematic review on toxicity of microplastics that focuses on identifying data gaps in the mechanisms of microplastic toxicity. We observe that microplastic toxicology research thus far has focused on ecotoxicity using apical endpoints and only a few studies deal with toxicity mechanisms. Based on this review, we propose putative Adverse Outcome Pathways (AOPs) applicable to microplastic management to understand microplastic toxicity. We matched toxicity mechanisms and apical endpoints to a key event (KE) and adverse outcome (AO) information from the AOP Wiki. Overall, our results suggest that the molecular initiating event (MIE) was reactive oxygen species (ROS) formation and the AO was increased mortality, decreased growth and feeding, and reproduction failure. However, there are a limited number of studies on toxicity mechanisms of microplastics and, therefore, evidence concerning the relationship between KEs is not sufficient. Clearly, more studies on toxicity mechanisms are required to fill these gaps in data. This study also suggests that the AOP framework is a suitable tool to integrate existing data from various literature sources and can identify data gaps in microplastic toxicity mechanisms.

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