Increased temperature and turbulence alter the effects of leachates from tire particles on fathead minnow (Pimephales promelas). Environmental Science & Technology, 54(3), 1750-1759.

The ecological impact of tire wear particles in aquatic ecosystems is a growing environmental concern. In this study, we combined toxicity testing, using fathead minnow (Pimephales promelas) embryos, with non-target high-resolution liquid This article is protected by copyright. All rights reserved. Accepted Articlechromatography Orbitrap mass spectrometry to characterize the toxicity and chemical mixture of organic chemicals associated with tire particle (TP) leachates. We assessed:(a) exposure to TP leachates after leaching for 1-, 3-and 10-days, and (b) the effect of the presence and absence of small tire particulates in the leachates. We observed a decrease in embryonic heart rates, hatching success, and lengths, as well as an increase in the number of embryos with severe deformities and diminished eye and body pigmentation, upon exposure to the leachates. Overall, there was a pattern whereby we observed more toxicity in the 10-day leachates, and greater toxicity in unfiltered leachates. Redundancy analysis showed that several benzothiazoles and aryl-amines were correlated with the toxic effects observed in the embryos. These included benzothiazole, 2aminobenzothiazole, 2-mercaptobenzothiazole, N,N'-diphenylguanidine, and N,N'diphenylurea. However, many other chemicals characterized as unknowns are likely to also play a key role in the adverse effects observed. Our study provides insight into the types of chemicals likely to be important toxicological drivers in tire leachates, and improves our understanding on the ecotoxicological impacts of tire wear particles.

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Metformin is a glucose-lowering drug commonly found in municipal wastewater effluents (MWWEs). The present study investigated the chronic effects of metformin in early-life stages of the fathead minnow (Pimephales promelas). Endpoints assessed were growth, survival, and deformities. The larval gut microbiome was also examined using 16 S ribosomal RNA gene amplicon sequencing to determine microbial community composition and alpha and beta diversity. Eggs and larvae were exposed to metformin measured concentrations (mean [standard deviation]) of 0.020 (0.017) μg/L (for controls) and 3.44 (0.23), 33.6 (1.6), and 269 (11) μg/L in a daily static-renewal setup, with 20 embryos per beaker. The low and middle metformin exposure concentrations represent river and MWWE concentrations of metformin. To detect small changes in growth, we used 18 replicate beakers for controls and 9 replicates for each metformin treatment. Over the 21-d exposure (5 d as embryos and 16 d posthatch [dph]), metformin did not affect survival or growth of larval fish. Hatch success, time to hatch, deformities in hatched fry, and survival were similar across all treatments. Growth (wet wt, length, and condition factor) assessed at 9 and 16 dph was also unaffected by metformin. Assessment of the microbiome showed that the larvae microbiome was dominant in Proteobacteria and Firmicutes, with small increases in Proteobacteria and decreases in Firmicutes with increasing exposure to metformin. No treatment effects were found for microbiome diversity measures. Control fish euthanized with the anesthetic tricaine methane sulfonate had decreased alpha diversity compared to those sampled by spinal severance. This experiment demonstrates that metformin at environmentally relevant concentrations (3.44 and 33.6 μg/L) and at 10 times MWWE concentrations (269 µg/L) does not adversely affect larval growth or gut microbiome in this ubiquitous freshwater fish species.

Metformin is a glucose-lowering drug taken for diabetes. It is excreted by humans in urine and detected in municipal wastewater effluents and rivers. Fathead minnows ( Pimephales promelas) were exposed over a life cycle to measured concentrations of metformin: 3.0, 31, and 322 μg/L. No significant changes were observed in survival, maturation, growth, condition factor, or liver size. Relative ovary size of females exposed to 322 μg/L metformin was significantly larger than controls. There was no induction of vitellogenin in plasma of minnows, and gonad maturation was not statistically different from controls. The start of breeding was delayed by 9–10 d in the mid- and high metformin treatments (statistically significant only in the mid-concentration), but numbers and quality of eggs were not statistically different from controls. There were no effects of metformin on survival or growth of offspring. Exposure to metformin at environmentally relevant concentrations (i.e., 3.0 and 31 μg/L metformin) caused no adverse effects in fathead minnows exposed for a life cycle, with the exception of a delay in time to first breeding (that did not impact overall egg production). The results of the study are important to help understand whether metformin concentrations in rivers and lakes can harm fishes.