Plastic production began in the early 1900s and it has transformed our way of life. Despite the many advantages of plastics, a massive amount of plastic waste is generated each year, threatening the environment and human health. Because of their pervasiveness and potential for health consequences, small plastic residues produced by the breakdown of larger particles have recently received considerable attention. Plastic particles at the nanometer scale (nanoplastics) are more easily absorbed, ingested, or inhaled and translocated to other tissues and organs than larger particles. Nanoplastics can also be transferred through the food web and between generations, have an influence on cellular function and physiology, and increase infections and disease susceptibility. This review will focus on current research on the toxicity of nanoplastics to aquatic species, taking into account their interactive effects with complex environmental mixtures and multiple stressors. It intends to summarize the cellular and molecular effects of nanoplastics on aquatic species; discuss the carrier effect of nanoplastics in the presence of single or complex environmental pollutants, pathogens, and weathering/aging processes; and include environmental stressors, such as temperature, salinity, pH, organic matter, and food availability, as factors influencing nanoplastic toxicity. Microplastics studies were also included in the discussion when the data with NPs were limited. Finally, this review will address knowledge gaps and critical questions in plastics’ ecotoxicity to contribute to future research in the field.

The global accumulation of plastic waste has reached crisis levels. The diverse and multilayered impacts of plastic on biological health prompts an evaluation of these effects from a One Health perspective, through which the complexity of these processes can be integrated and more clearly understood. Plastic particles ranging from nanometers to meters in size are found throughout every ecosystem on Earth, from the deepest marine trenches to the highest mountains. Plastic waste affects all layers of biological organization, from the molecular and cellular to the organismal, community, and ecosystem-levels. These effects are not only mediated by the physical properties of plastics, but also by the chemical properties of the plastic polymers, the thousands of additives combined with plastics during manufacturing, and the sorbed chemicals and microbes that are transported by the plastic waste. Using a One Health framework we provide an overview of the following themes: 1) ways in which plastic impacts global health across levels of biological organization, 2) how the effects of plastic interact between layers of biology, and 3) what knowledge gaps exist in understanding the effects of plastic within and between biological scales. We also propose potential solutions to address this growing crisis, with an emphasis on One Health perspectives that consider the oneness of animals, humans, and the environment.

Polycyclic aromatic hydrocarbons (PAHs) induce developmental defects including cardiac deformities in fish. The aryl hydrocarbon receptor (AHR) mediates the toxicity of some PAHs. Exposure to a simple PAH mixture during embryo development consisting of an AHR agonist (benzo(a)pyrene-BaP) with fluoranthene (FL), an inhibitor of cytochrome p450 1(CYP1) - a gene induced by AHR activation- results in cardiac deformities. Exposure to BaP or FL alone at similar concentrations alters heart rates, but does not induce morphological deformities. Furthermore, AHR2 knockdown prevents the toxicity of BaP+FL mixture. Here we used a zebrafish microarray analysis to identify heart-specific transcriptomic changes during early development that might underlie cardiotoxicity of BaP+FL. We used AHR2 morphant embryos to determine the role of this receptor in mediating toxicity. Control and knockdown embryos at 36 hours post fertilization were exposed to DMSO, 100 μg/L BaP, 500 μg/L FL, or 100 μg/L BaP + 500 μg/L FL, and heart tissues for RNA were extracted at 2, 6, 12, and 18 hours-post-exposure (hpe), prior to the appearance of cardiac deformities. Data show AHR2-dependent BaP+FL effects on expression of genes involved in protein biosynthesis and neuronal development in addition to signaling molecules and their associated molecular pathways. Ca²⁺-cycling and muscle contraction genes were the most significantly differentially expressed category of transcripts when comparing BaP+FL-treated AHR2 morphant and control embryos. These differences were most prominent at 2 and 6 hpe. Therefore, we postulate that BaP+FL may affect cellular Ca²⁺ levels and subsequently cardiac muscle function, potentially underlying BaP+FL cardiotoxicity.

Cardiac function is thought to play a central role in determining thermal optima and tolerance limits in teleost fishes. Investigating proteomic responses to temperature in cardiac tissues may provide insights into mechanisms supporting the thermal plasticity of cardiac function. Here, we utilized a global proteomic analysis to investigate changes in cardiac protein abundance in response to temperature acclimation (transfer from 13°C to 9, 19 and 26°C) in a eurythermal goby, Gillichthys mirabilis. Proteomic data revealed 122 differentially expressed proteins across acclimation groups, 37 of which were identified using tandem mass-spectrometry. These 37 proteins are involved in energy metabolism, mitochondrial regulation, iron homeostasis, cytoprotection against hypoxia, and cytoskeletal organization. Compared with the 9 and 26°C groups, proteins involved in energy metabolism increased in 19°C-acclimated fish, indicating an overall increase in the capacity for ATP production. Creatine kinase abundance increased in 9°C-acclimated fish, suggesting an important role for the phosphocreatine energy shuttle in cold-acclimated hearts. Both 9 and 26°C fish also increased abundance of hexosaminidase, a protein directly involved in post-hypoxia stress cytoprotection of cardiac tissues. Cytoskeletal restructuring appears to occur in all acclimation groups; however, the most prominent effect was detected in 26°C-acclimated fish, which exhibited significantly increased actin levels. Overall, proteomic analysis of cardiac tissue suggests that the capacity to adjust ATP-generating processes is crucial to the thermal plasticity of cardiac function. Furthermore, G. mirabilis may optimize cellular functions at temperatures near 19°C, which lies within the species' preferred temperature range.

SUMMARY: An insufficient supply of oxygen under thermal stress is thought to define thermal optima and tolerance limits in teleost fish. When under thermal stress, cardiac function plays a crucial role in sustaining adequate oxygen supply for respiring tissues. Thus, adaptive phenotypic plasticity of cardiac performance may be critical for modifying thermal limits during temperature acclimation. Here we investigated effects of temperature acclimation on oxygen consumption, cardiac function and blood oxygen carrying capacity of a eurythermal goby fish, Gillichthys mirabilis, acclimated to 9, 19 and 26°C for 4 weeks. Acclimation did not alter resting metabolic rates or heart rates; no compensation of rates was observed at acclimation temperatures. However, under an acute heat ramp, warm-acclimated fish exhibited greater heat tolerance (CTmax=33.3, 37.1 and 38.9°C for 9°C-, 19°C- and 26°C-acclimated fish, respectively) and higher cardiac arrhythmia temperatures compared with 9°C-acclimated fish. Heart rates measured under an acute heat stress every week during 28 days of acclimation suggested that both maximum heart rates and temperature at onset of maximum heart rates changed over time with acclimation. Hemoglobin levels increased with acclimation temperature, from 35 g l−1 in 9°C-acclimated fish to 60–80 g l−1 in 19°C- and 26°C-acclimated fish. Oxygen consumption rates during recovery from acute heat stress showed post-stress elevation in 26°C-acclimated fish. These data, coupled with elevated resting metabolic rates and heart rates at warm temperatures, suggest a high energetic cost associated with warm acclimation in G. mirabilis. Furthermore, acclimatory capacity appears to be optimized at 19°C, a temperature shown by behavioral studies to be close to the species' preferred temperature.