Microplastic exposure is associated with epigenomic effects in the model organism Pimephales promelas (fathead minnow).

Microplastics have evolutionary and ecological impacts across species, affecting organisms' development, reproduction, and behavior along with contributing to genotoxicity and stress. As plastic pollution is increasing and ubiquitous, gaining a better understanding of organismal responses to microplastics is necessary. Epigenetic processes such as DNA methylation are heritable forms of molecular regulation influenced by environmental conditions. Therefore, determining such epigenetic responses to microplastics will reveal potential chronic consequences of this environmental pollutant. We performed an experiment across two generations of fathead minnows (Pimephales promelas) to elucidate transgenerational epigenetic effects of microplastic exposure. We exposed the first generation of fish to four different treatments of microplastics: two concentrations of each of pre-consumer polyethylene (PE) and PE collected from Lake Ontario. We then raised the first filial generation with no microplastic exposure. We used enzymatic methylation sequencing on adult liver tissue and homogenized larvae to evaluate DNA methylation differences among treatments, sexes, and generations. Our findings show the origin of the plastic had a larger effect in female minnows whereas the effect of concentration was stronger in the males. We also observed transgenerational effects, highlighting a mechanism in which parents can pass on the effects of microplastic exposure to their offspring. Many of the genes found within differentially methylated regions in our analyses are known to interact with estrogenic chemicals associated with plastic and are related to metabolism. This study highlights the persistent and potentially serious impacts of microplastic pollution on gene regulation in freshwater systems.

Informing the Exposure Landscape: The Fate of Microplastics in a Large Pelagic In-Lake Mesocosm Experiment.

Understanding microplastic exposure and effects is critical to understanding risk. Here, we used large, in-lake closed-bottom mesocosms to investigate exposure and effects on pelagic freshwater ecosystems. This article provides details about the experimental design and results on the transport of microplastics and exposure to pelagic organisms. Our experiment included three polymers of microplastics (PE, PS, and PET) ranging in density and size. Nominal concentrations ranged from 0 to 29,240 microplastics per liter on a log scale. Mesocosms enclosed natural microbial, phytoplankton, and zooplankton communities and yellow perch (Perca flavescens). We quantified and characterized microplastics in the water column and in components of the food web (biofilm on the walls, zooplankton, and fish). The microplastics in the water stratified vertically according to size and density. After 10 weeks, about 1% of the microplastics added were in the water column, 0.4% attached to biofilm on the walls, 0.01% within zooplankton, and 0.0001% in fish. Visual observations suggest the remaining >98% were in a surface slick and on the bottom. Our study suggests organisms that feed at the surface and in the benthos are likely most at risk, and demonstrates the value of measuring exposure and transport to inform experimental designs and achieve target concentrations in different matrices within toxicity tests.

Microplastics may induce food dilution and endocrine disrupting effects in fathead minnows (Pimephales promelas), and decrease offspring quality.

Microplastics are a complex environmental contaminant that have been reported to cause a variety of impacts, although the mechanism of these impacts remains unclear. Many studies have investigated either sub-organismal or apical endpoints, while very few have attempted to integrate and link endpoints seen at multiple levels of organization. Here, we exposed fathead minnows to microplastics for their entire lifecycle, from the egg stage through to reproduction, and raised a subset of the offspring in clean water. We show that both preconsumer and environmentally sourced microplastics impact adult growth, lipid storage, and external colouration, suggesting a potential food dilution effect. Environmentally sourced microplastics, but not preconsumer microplastics, had further endocrine disrupting impacts on the parental generation and their offspring in the low concentration treatments such that egg production began later, eggs were less viable, and the offspring had higher rates of malformation. Low dose effects are a typical dose-response for endocrine disrupting contaminants. These results suggest that microplastic exposure, at concentrations relevant to what is being found in the environment, has potential implications for forage fish populations. Our findings also highlight the importance of using an integrative approach to understanding the mechanisms behind how and why microplastics impact organisms.

Impacts to Larval Fathead Minnows Vary between Preconsumer and Environmental Microplastics.

Microplastics are a complex suite of contaminants varying in size, shape, polymer, and associated chemicals and are sometimes referred to as a "multiple stressor." Still, the majority of studies testing hypotheses about their effects use commercially bought microplastics of a uniform size, shape, and type. We investigated the effects of polyethylene and polypropylene microplastics purchased as preproduction pellets (referred to as "preconsumer") and a mixture of polyethylene and polypropylene collected from the environment (environmental microplastic). Embryo-stage fathead minnows were exposed to either the physical plastic particles and their leachates or the chemical leachates alone at an environmentally relevant (280 particles/L) or high (2800 particles/L) concentration for 14 d. The effects of microplastics differed by polymer type and presence of environmental contaminants, and effects can be driven by the physical particles and/or the chemical leachates alone. Larvae exposed to preconsumer polyethylene experienced a decrease in survival, length, and weight, whereas preconsumer polypropylene caused an increase in weight. Environmental microplastics caused a more drastic increase in length and weight and almost 6 times more deformities as the preconsumer microplastics. Although preconsumer microplastics caused effects only when organisms were exposed to both the particles and the chemical leachates, the environmental microplastics caused effects when organisms were exposed to the chemical leachates alone, suggesting that the mechanism of effects are context-dependent. The present study provides further support for treating microplastics as a multiple stressor and suggests that testing for effects with pristine microplastics may underestimate the true effects of microplastics in the environment. Environ Toxicol Chem 2022;41:858-868. © 2021 SETAC.