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Justin Blaine Greer

Publications and source records attributed to Justin Blaine Greer.

At least 19 recordsLinked to original sources
USGS2026

Poor population recovery of Lake Washington Chinook Salmon (Oncorhynchus tshawytscha) in Pacific Northwestern USA may be associated with disease caused by Ceratonova shasta in an urban-influenced watershed

Understanding the effects of anthropogenic changes on fish disease is vital for supporting mitigative actions for fisheries population recovery. The Lake Washington watershed in the Pacific Northwestern United States is influenced by high urban development and climate change, compromising the sustainability of anadromous salmon. We investigated Ceratonova shasta , a myxozoan parasite, in Chinook Salmon Oncorhynchus tshawytscha to determine the impacts of C. shasta -induced enteronecrosis during salmon freshwater migrations within this watershed. All sampled adult Chinook Salmon returning to an enhancement hatchery to spawn were infected with genotype I C. shasta with a high prevalence of severe enteritis and enteronecrosis. Parasite loads and associated pathology were more severe in adult fish succumbing to prespawn mortality than in fish that spawned. Natural prespawn mortality of Chinook Salmon in the Cedar River was also associated with high C. shasta loads. Sentinel exposure studies with Chinook Salmon juveniles in the spring and fall demonstrated high levels of C. shasta genotype II actinospores in the Lake Washington Ship Canal, a human engineered canal that salmon must traverse in their freshwater migrations from the Puget Sound. The sentinel juvenile Chinook Salmon succumbed to clinical disease and high mortality from genotype II C. shasta , suggesting that these stocks have high susceptibility to this genotype. The results show that both genotypes I and II pose disease risks to adult and juvenile stages of Chinook Salmon in the watershed, and that the Lake Washington Ship Canal could be a C. shasta ‘hot spot’ for genotype II that may increase disease risk for juveniles during smolt emigration.

Washington↗
USGS2026

Time course of effects and tissue concentrations of 6PPDQ in three sensitive salmonids with additional data for two centrarchid species

Studies of 6PPD-quinone (6PPDQ) toxicity have identified both sensitive and resistant salmonid species at environmentally relevant concentrations. However, comparisons between species are complicated by varying testing conditions, which can limit the application to derivation of environmental quality guidelines. Furthermore, few studies have reported 6PPDQ tissue concentrations in fish with known exposure concentrations. Using standard methods with flow-through exposures to provide stable 6PPDQ concentrations, we compared time courses of mortality in three sensitive salmonid species (coho salmon Oncorhynchus kisutch , brook trout Salvelinus fontinalis , rainbow trout Oncorhynchus mykiss ), evaluated the potential for latent (delayed) mortality, and measured tissue concentrations in both fish that died during exposure and those that survived an additional 7 days in clean water. Further experiments documented insensitivity in two centrarchids (smallmouth bass Micropterus dolomieu and largemouth bass Micropterus nigricans ). Our study provided evidence for two mortality time courses: one in which nearly all mortality occurs in the first 24 h and one in which mortalities continue to accumulate throughout the exposure, and 96-h and 24-h LC50s are quite different. We did not observe evidence for the delayed onset of mortality due to 6PPDQ exposure. Most fish that survived exposure had undetectable 6PPDQ concentrations after 1 week in clean water, potentially informing biomonitoring strategies for wild populations.

Environmental Science & Technology↗
USGS2026

Toxicity of 6PPD alternatives to salmonid cell lines

Stormwater runoff in urban areas introduces numerous anthropogenic chemicals into surrounding aquatic environments. One such chemical is 6PPD ( N -(1,3-Dimethylbutyl)- N ’-phenyl- p- phenylenediamine), the primary antidegradant responsible for protecting tire rubber from ozone-induced degradation and cracking. When exposed to ozone on the road surface 6PPD is transformed into the toxic transformation product 6PPD-quinone (6PPDQ). This compound is highly lethal to coho salmon ( O ncorhynchus kisutch ), and 24 hour 50% lethal concentrations (LC 50 ; 41-95 ng/L) are frequently detected in urban streams during stormwater runoff events 1-5 . The highest stream concentrations of 6PPDQ and most extensive coho salmon mortality occur in high-traffic urban areas, where tire wear particles accumulate due to the frequent braking and acceleration of cars 6 . In the Seattle area, some coho salmon-bearing streams can lose over 90% of returning females prior to spawning due to 6PPDQ-containing runoff 7 . Prespawn loss of this magnitude could result in the extinction of some urban spawning populations 8 . Importantly, the lethal effects of 6PPDQ have been observed in several other salmonid species, indicating that its impact may threaten fish health for urban aquatic environments globally 9-11 . The ubiquity of 6PPD in automobile tires, high toxicity of the transformation product 6PPDQ, and prevalence of 6PPD and 6PPDQ in environmental matrices has spurred investigations into alternative rubber antiozonants to replace 6PPD that retain tire performance while reducing ecological harm. A technical memorandum provided to the legislature by the Washington State Department of Ecology summarized a list of potential 6PPD alternatives requiring further study, including several structurally similar p-phenylenediamines (PPDs) 12 . However, the structural similarity of other PPDs to 6PPD and their known production of quinone transformation products 13 raises concerns that they may elicit similar toxic effects as 6PPDQ. Currently, investigations into the toxicity of proposed PPD alternatives or their ozonated transformation products in coho salmon are limited, representing a significant data gap in evaluating whether they offer improved environmental safety over 6PPD. This project investigated the toxicity of proposed alternative rubber antiozonants in vitro using immortalized cell lines derived from three salmonid species with known differences in sensitivity to 6PPDQ (coho salmon, Chinook salmon ( O. tshawytscha ), rainbow trout ( O. mykiss )) 1 . These immortalized cell lines replicate toxic responses observed in in vivo studies, while enabling higher-throughput testing and reducing the need for animal use and other resource-intensive procedures. The antiozonants and their transformation products selected for testing were chosen based on multiple criteria, including their inclusion in the Ecology technical memorandum, structural substitutions (e.g., branched/cyclic alkyl vs aryl substitutions), commercial availability, and input from the Washington State Department of Ecology and other industry experts.

Report↗
USGS2026

Roadway runoff induced acute mortality in juvenile coho salmon during spring storm events

Extensive mortalities of adult coho salmon ( Oncorhynchus kisutch ), often called “Urban Runoff Mortality Syndrome” (URMS), have been documented during the fall in creeks where water quality has been degraded by roadway runoff. The primary cause of mortality is 6PPD-quinone (6PPDQ; N -(1,3-dimethylbutyl)- N ′-phenyl- p -phenylenediamine quinone)–an ozone transformation product that forms on all vehicle tires. Laboratory studies have shown that juvenile coho salmon are highly sensitive to 6PPDQ exposure. Unlike adults, juveniles reside in impacted watersheds year-round, including during the spring when 6PPDQ concentrations can frequently exceed lethal thresholds during storms. To assess the potential incidence of URMS in springtime rearing habitats for juvenile coho salmon, we conducted a paired water quality and toxicology study at Miller Creek, a runoff-impacted watershed in Normandy Park, WA, USA. Using a small field facility, three naïve groups of juvenile coho salmon ( N = 720) were exposed to either creek water or groundwater ( N = 120 per treatment per storm), across three spring storms while comparing water quality and mortality end points. In creek water during exposures, peak 6PPDQ concentrations reached 73–110 ng/L, exceeding reported median lethal concentrations (LC 50 ) for coho salmon. Over each 24–73 h storm exposure period, ∼80% of Miller Creek-exposed juvenile salmon died. No mortality occurred among control fish exposed to groundwater. These results indicate previously unidentified mortality risks for juvenile life stages of coho salmon during spring storms, suggesting substantial and year-round water quality impediments to coho salmon health and recovery across roadway runoff-impacted spawning, rearing, and migratory habitats.

Washington↗
USGS2025

Novel adomaviruses associated with blotchy bass syndrome in black basses ( Micropterus spp. )

Black bass ( Micropterus spp. ) are the most important warmwater game fishes in the United States. They have high socioeconomic and recreational value and support an important aquaculture industry. Since 2008, fisheries managers have been reporting the observation of hyperpigmented melanistic lesions (HPMLs) on smallmouth bass ( M. dolomieu ) in different ecoregions of the United States. Similar HPMLs have been observed in largemouth bass ( M. nigricans ) since the 1980’s. Here, we report the association between novel adomaviruses and the hallmark blotchy clinical presentation of hyperpigmented lesions on the skin of smallmouth and largemouth black bass. The two adomaviruses are structurally and phylogenetically similar but share only 68.0% identity at aligned nucleotide sites and each has been found in only one host species to date. The manifestation of this skin disease appears to be seasonal (observed between the fall and spring) in both species, primarily affects adults and is of unknown health consequence. Although the significance of infection to fish health remains unclear, understanding the disease ecology of these viruses can inform biosecurity and the interjurisdictional movement of individuals. Moreover, as hyperpigmentation in other fish species is often idiopathic, our findings reframe perspectives for future investigations into this clinical presentation in other species.

Michigan, Pennsylvania, Texas, Vermont, Virginia↗
USGS2025

Evaluation of 6PPD-quinone lethal toxicity and sublethal effects on disease resistance and swimming fitness in coastal cutthroat trout (Oncorhynchus clarkii clarkii)

6PPD-quinone (6PPDQ), derived from the tire-protectant 6PPD reacting with ozone, is an emerging contaminant of concern owing to its role in coho salmon ( Oncorhynchus kisutch ) deaths via urban runoff mortality syndrome (URMS). Given the impact of 6PPDQ on aquatic life in urban streams, we addressed the acute toxicity of 6PPDQ exposure on coastal cutthroat trout (CCT) ( Oncorhynchus clarkii clarkii ), a species sympatric with coho salmon in natal watersheds. Using static exposures coupled with analytical chemistry, we determined the 24-h LC 50 values for alevin (297.2 ng/L), swim-up fry (39.6 ng/L), 5-month parr (103.3 ng/L), and 13-month juveniles (185.9 ng/L)─values similar to toxicity observed in coho salmon. Additionally, the 96-h LC 50 (77.6 ng/L) was 2.4 times more lethal for juvenile CCT. We assessed potential effects of sublethal 6PPDQ exposure on disease resistance to infectious hematopoietic necrosis (IHN), an endemic viral disease of Pacific salmon, and to swimming performance. Sublethal 6PPDQ (53.6 ng/L) did not affect survival of parr exposed to IHN virus compared to virus alone. Conversely, 6PPDQ exposure as low as 72.2 ng/L significantly reduced 15- and 24-month juvenile swimming performance, and 120.5 ng/L 6PPDQ increased blood hematocrit. Overall, CCT are the second most sensitive species tested to date for 6PPDQ sensitivity which further emphasizes the need for identifying alternatives to 6PPD.

Environmental Science and Technology↗
USGS2025

Influence of cardiotoxicity on visual function in developing zebrafish ( Danio rerio ) exposed to Deepwater Horizon crude oil

Polycyclic aromatic hydrocarbons (PAHs) are toxic constituents of crude oil that can induce cardiac dysfunction and vision impairment in early life stage (ELS) fishes. However, it is currently unknown whether visual impairments are independent effects or if they result from underlying PAH cardiotoxicity. To better understand this mechanism, microinjection of microRNA 133b (miR133b) was used to impair cardiac development in ELS zebrafish (injected at <1.25 hpf). Vision and cardiac endpoints were compared between miR133b-injected and oil-exposed zebrafish (4–72 hpf, 54.68–60.41 µg/L tPAH 50 ) to determine the influence of cardiac dysfunction and oil exposure on visual function. At 7 dpf, pericardial area and eye area were measured, and visual function was assessed by optokinetic response (OKR). Over 94 % of miR133b larvae and 45 % of oil-exposed larvae exhibited pericardial edema. Across treatments, there was a strong negative linear correlation between pericardial area and eye area ( r =-0.839, p < 0.0001). All miR133b larvae that exhibited pericardial edema and 18 % of the oil-exposed larvae that exhibited pericardial edema also exhibited reduced eye area (microphthalmia). In both the miR133b and oil groups, OKR was significantly reduced in larvae exhibiting pericardial edema ( p < 0.0001) and in larvae exhibiting reduced eye area ( p < 0.0001). A negative binomial generalized linear model (GLM) indicated that reduced eye area ( p < 0.0001), rather than pericardial edema ( p = 0.76), was a significant predictor of OKR. However, pericardial edema was strongly correlated with reduced eye area across treatments. These results suggest that visual effects may result from an interaction of cardiotoxicity as well as direct impacts to the visual system.

Aquatic Toxicology↗
USGS2025

Novel adomaviruses associated with blotchy bass syndrome in black basses (Micropterus spp.)

Black bass ( Micropterus spp. ) are the most important warmwater game fishes in the United States. They have high socioeconomic and recreational value and support an important aquaculture industry. Since 2008, fisheries managers have been reporting the observation of hyperpigmented melanistic lesions (HPMLs) on smallmouth bass ( M. dolomieu ) in different ecoregions of the United States. Similar HPMLs have been observed in largemouth bass ( M. nigricans ) since the 1980’s. Here, we report a close association between novel adomaviruses and the hallmark blotchy clinical presentation of hyperpigmented lesions on the skin smallmouth and largemouth black bass and provide evidence that satisfies Rivers’ postulates. The two adomaviruses are structurally and phylogenetically similar but share only 68.0% identity at aligned nucleotide sites and each has been found in only one host species to date. The manifestation of this skin disease appears to be seasonal in both species, primarily affects adults and is of unknown health consequence. Although the significance of infection to fish health remains unclear, understanding the disease ecology of these can inform biosecurity and the interjurisdictional movement of individuals. Moreover, as hyperpigmentation in other fish species is often idiopathic, our findings reframe perspectives for future investigations into this clinical presentation in other species.

BioRxiv↗
USGS2024

Structurally selective ozonolysis of p-phenylenediamines and toxicity in coho salmon and rainbow trout

The tire-rubber-derived ozonation product of N -(1,3-dimethylbutyl)- N ′-phenyl- p -phenylenediamine (6PPD), N -(1,3-dimethylbutyl)- N ′-phenyl- p -phenylenediamine-quinone (6PPD-Q), was recently discovered to cause acute mortality in coho salmon ( Oncorhynchus kisutch ). para -Phenylenediamines (PPDs) with variable side chains distinct from 6PPD have been identified as potential replacement antioxidants, but their toxicities remain unclear under environmentally relevant ozone conditions. We herein tested the multiphase gas-surface ozone reactivity of four select PPDs [6PPD, N -isopropyl- N ′-phenyl- p -phenylenediamine (IPPD), N , N ′-diphenyl- p -phenylenediamine (DPPD), and N -phenyl- N ′-cyclohexyl- p -phenylenediamine (CPPD)] and evaluated the toxicity of their reaction mixtures in coho salmon, rainbow trout ( Oncorhynchus mykiss ), and fathead minnow ( Pimephales promelas ). 6PPD and IPPD were found to rapidly react with ozone, while no significant multiphase ozone reactivity was observed for DPPD or CPPD. The viability of coho salmon CSE-119 cells was strongly affected by the ozonolysis products of 6PPD but not by those of the other three PPDs. Acute mortality was only observed in juvenile rainbow trout that were exposed to oxidized 6PPD, suggesting a common mechanism of toxic action in the two salmonid fish species. This study reports the structurally selective ozone reactivity of PPDs and the unique toxicity of 6PPD ozonolysis mixtures, which demonstrates that other PPDs are potential alternative antioxidants.

Environmental Science and Technology↗
USGS2024

Tire-derived contaminants 6PPD and 6PPD-Q: Analysis, sample handling, and reconnaissance of United States stream exposures

The environmental ubiquity of tire and road wear particles (TRWP) underscores the need to understand the occurrence, persistence, and environmental effects of tire-related chemicals in aquatic ecosystems. One such chemical is 6PPD-quinone (6PPD-Q), a transformation product of the tire antioxidant 6PPD. In urban stormwater runoff 6PPD-Q can exceed acute toxicity thresholds for several salmonid species and is being implicated in significant coho salmon losses in the Pacific Northwest. There is a critical need to understand the prevalence of 6PPD-Q across watersheds to identify habitats heavily affected by TRWPs. We conducted a reconnaissance of 6PPD and 6PPD-Q in surface waters across the United States from sites (N = 94) with varying land use (urban, agricultural, and forested) and streamflow to better understand stream exposures. A rapid, low-volume direct-inject, liquid chromatography mass spectrometry method was developed for the quantitation of 6PPD-Q and screening for 6PPD. Laboratory holding times, bottle material, headspace, and filter materials were investigated to inform best practices for 6PPD-Q sampling and analysis. Glass bottles with PTFE-lined caps minimized sorption and borosilicate glass fiber filters provided the highest recovery. 6PPD-Q was stable for at least 5 months in pure laboratory solutions and for 75 days at 5 °C with minimal headspace in the investigated surface water and stormwaters. Results also indicated samples can be frozen to extend holding times. 6PPD was not detected in any of the 526 analyzed samples and there were no detections of 6PPD-Q at agricultural or forested sites. 6PPD-Q was frequently detected in stormwater (57%, N = 90) and from urban impacted sites (45%, N = 276) with concentrations ranging from 0.002 to 0.29 μg/L. The highest concentrations, above the lethal level for coho salmon, occurred during stormwater runoff events. This highlights the importance of capturing episodic runoff events in urban areas near ecologically relevant habitat or nursery grounds for sensitive species.

Chemosphere↗
USGS2024

Toxicity of crude oil-derived polar unresolved complex mixtures to Pacific herring embryos: Insights beyond polycyclic aromatic hydrocarbons

Crude oil toxicity to early life stage fish is commonly attributed to polycyclic aromatic hydrocarbons (PAHs). However, it remains unclear how the polar unresolved complex mixture (UCM), which constitutes the bulk of the water-soluble fraction of crude oil, contributes to crude oil toxicity. Additionally, the role of photomodification-induced toxicity in relation to the polar UCM is not well understood. This study addresses these knowledge gaps by assessing the toxicity of two laboratory generated polar UCMs from Cook Inlet crude oil, representing the readily water-soluble fraction of crude oil and photoproduced hydrocarbon oxidation products (HOPs), to Pacific herring ( Clupea pallasii ) embryos. A small-scale semi-static exposure design was utilized with a range of polar UCM concentrations (0.5–14 mg/L) in nonvolatile dissolved organic carbon (NVDOC) units, quantifying the entire polar UCM. Compositional analyses revealed a photochemical-driven shift toward more complex aromatic compositions, naphthenic acids, and no detectable levels of PAHs (above 0.3 μg/L). Exposure to the dark polar UCM resulted in higher mortality than exposure to the light polar UCM. Both dark and light polar UCMs induced developmental abnormalities commonly attributed to the PAH fraction, including edema, reduced heart rate, body axis defects, and decreased body lengths, with these effects observed at the lowest dose group (0.5 mg/L NVDOC). These responses suggest photomodification-induced toxicity is driven by exposure to increased concentrations of dissolved HOPs rather than photochemical induced compositional changes. Gene expression analyses focusing on xenobiotic metabolism and cardiac morphogenesis yielded results consistent with previous studies examining the biological mechanisms of crude oil toxicity. In summary, these phenotypic and genotypic responses in Pacific herring embryos indicate that the polar UCM is a significant driver of crude oil toxicity. These findings emphasize the importance of considering the polar UCM in future studies, metric reporting, and risk assessments related to crude oil toxicity.

Science of the Total Environment↗
USGS2024

Structurally selective ozonolysis of p-phenylenediamines and toxicity in coho salmon and rainbow trout

The tire rubber-derived ozonation product of N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD), N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q), was recently discovered to cause acute mortality in Coho Salmon (Oncorhynchus kisutch). para-Phenylenediamines (PPDs) with variable side chains distinct from 6PPD have been identified as potential replacement commercial antioxidants, but their structure-related ozone reactivities and toxicities remain unexplored. We herein tested the multiphase gas-surface ozone reactivity of four select PPDs and evaluated the toxicity of their reaction mixtures in Coho Salmon and Rainbow Trout (Oncorhynchus mykiss). 6PPD and N-Isopropyl-N'-phenyl-p-phenylenediamine (IPPD) were found to rapidly react with ozone to form 22 and 16 transformation products, respectively, including PPD-Qs. No significant multiphase ozone reactivity was observed for N,N'-Diphenyl-p-phenylenediamine (DPPD) or N-Cyclohexyl-N'-phenyl-p-phenylenediamine (CPPD) despite their structural similarity to 6PPD. The viability of Coho Salmon CSE-119 cells was strongly affected by the ozonolysis products of 6PPD, but not by those of the other three PPDs. The cytotoxicity of the 6PPD reaction mixture increased with ozonolysis time, with the strongest toxicity being observed after 7 days of oxidation by 100 ppb of ozone. As with Coho Salmon cells, acute mortality was only observed in juvenile Rainbow Trout that were exposed to the oxidized 6PPD reaction mixture, suggesting a common mechanism of toxic action in the two salmonid fish species. Compound- and regio-selective formation of hydroxylated metabolites of 6PPD-Q were detected in Rainbow Trout exposed to the 6PPD reaction mixture, which may be related to its selective toxicity. This study reports the structurally selective ozone reactivity of PPDs, and the unique toxicity of 6PPD ozonolysis mixtures, which demonstrates that other PPDs are potential alternative antioxidants.

ChemRxiv↗
USGS2023

Effects of temperature on viral load, inclusion body formation, and host response in Pacific Herring with viral erythrocytic necrosis (VEN)

Objective The primary objective of this study was to determine the effects of temperature on viral erythrocytic necrosis (VEN) progression under controlled conditions. Secondarily, this study was intended to evaluate the combined effects of temperature and VEN on the Pacific Herring Clupea palasii transcriptome. Methods The effects of temperature on VEN progression were assessed by waterborne exposure of laboratory-reared, specific-pathogen-free Pacific Herring to tissues homogenates containing erythrocytic necrosis virus (ENV) at 6.9, 9.0, or 13.5°C. Result Exposure of Pacific Herring to ENV resulted in the establishment of infections characterized by high infection prevalence (89%; 40/45) and mean viral loads (5.5 log 10 [gene copies/μg genomic DNA]) in kidney tissues at 44 days postexposure. Mean viral loads were significantly higher in fish from the ambient (mean = 9.0°C) and warm (mean = 13.5°C) treatments (6.1–6.2 log 10 [gene copies/total genomic DNA]) than in fish from the cool (mean = 6.9°C) treatment (4.3 log 10 [gene copies/μg genomic DNA]). Similarly, the peak proportion of diseased fish was directly related to temperature, with cytoplasmic inclusion bodies detected in 21% of fish from the cool treatment, 52% of fish from the ambient treatment, and 60% of fish from the warm treatment. The mean VEN load in each fish (enumerated as the percentage of erythrocytes with cytoplasmic inclusions) at 44 days postexposure increased with temperature from 15% in the cool treatment to 36% in the ambient treatment and 32% in the warm treatment. Transcriptional analysis indicated that the number of differentially expressed genes among ENV-exposed Pacific Herring increased with temperature, time postexposure, and viral load. Correlation network analysis of transcriptomic data showed robust activation of interferon and viral immune responses in the hepatic tissue of infected individuals independent of other experimental variables. Conclusion Results from this controlled laboratory study, combined with previous observations of natural epizootics in wild populations, support the conclusion that temperature is an important disease cofactor for VEN in Pacific Herring.

Journal of Aquatic Animal Health↗
USGS2023

Tire-derived transformation product 6PPD-quinone induces mortality and transcriptionally disrupts vascular permeability pathways in developing coho salmon

Urban stormwater runoff frequently contains the car tire transformation product 6PPD-quinone, which is highly toxic to juvenile and adult coho salmon ( Onchorychus kisutch ). However, it is currently unclear if embryonic stages are impacted. We addressed this by exposing developing coho salmon embryos starting at the eyed stage to three concentrations of 6PPD-quinone twice weekly until hatch. Impacts on survival and growth were assessed. Further, whole-transcriptome sequencing was performed on recently hatched alevin to address the potential mechanism of 6PPD-quinone-induced toxicity. Acute mortality was not elicited in developing coho salmon embryos at environmentally measured concentrations lethal to juveniles and adults, however, growth was inhibited. Immediately after hatching, coho salmon were sensitive to 6PPD-quinone mortality, implicating a large window of juvenile vulnerability prior to smoltification. Molecularly, 6PPD-quinone induced dose-dependent effects that implicated broad dysregulation of genomic pathways governing cell–cell contacts and endothelial permeability. These pathways are consistent with previous observations of macromolecule accumulation in the brains of coho salmon exposed to 6PPD-quinone, implicating blood–brain barrier disruption as a potential pathway for toxicity. Overall, our data suggests that developing coho salmon exposed to 6PPD-quinone are at risk for adverse health events upon hatching while indicating potential mechanism(s) of action for this highly toxic chemical.

Environmental Science & Technology↗
USGS2023

Establishing an in vitro model to assess the toxicity of 6PPD-quinone and other tire wear transformation products

The tire wear transformation product 6PPD-quinone (6PPDQ) has been implicated as the causative factor for broad scale mortality events for coho salmon in the Pacific Northwest. Highly variable sensitivity to 6PPDQ in closely related salmonids complicates efforts to evaluate the broader toxicological impacts to aquatic ecosystems. Our goals were to (1) validate the large range of in vivo species sensitivities reported for coho, Chinook, and sockeye salmon and (2) develop an in vitro platform for assessing 6PPDQ toxicity. In vivo studies confirmed the acute sensitivity of juvenile coho (12 h LC 50 = 80.4 ng/L) and demonstrated that sockeye salmon were not vulnerable to mortality. Chinook salmon were sensitive to 6PPDQ mortality at initial concentrations >25 μg/L, ∼10-fold greater than reported environmental measurements. In vitro , the coho salmon cell line CSE-119 was acutely sensitive to 6PPDQ (metabolic EC 50 = 7.9 μg/L, cytotoxicity EC 50 = 6.1 μg/L). Analogous Chinook (CHSE-214) and sockeye salmon (SSE-5) cell lines were nonresponsive in both assays, and rainbow trout RTG-2 cells began showing metabolic effects at 68 μg/L (EC 5 ). Recreation of species-specific 6PPDQ sensitivity in vitro implicates conserved modes of action in CSE-119 that could be utilized for mechanistic studies of 6PPDQ toxicity and screening of other PPD transformation products.

Environmental Science and Technology Letters↗
USGS2022

Brief oil exposure reduces fitness in wild Gulf of Mexico mahi-mahi (Coryphaena hippurus)

The Deepwater Horizon (DWH) disaster released 3.19 million barrels of crude oil into the Gulf of Mexico (GOM) in 2010, overlapping the habitat of pelagic fish populations. Using mahi-mahi ( Coryphaena hippurus )─a highly migratory marine teleost present in the GOM during the spill─as a model species, laboratory experiments demonstrate injuries to physiology and behavior following oil exposure. However, more than a decade postspill, impacts on wild populations remain unknown. To address this gap, we exposed wild mahi-mahi to crude oil or control conditions onboard a research vessel, collected fin clip samples, and tagged them with electronic tags prior to release into the GOM. We demonstrate profound effects on survival and reproduction in the wild. In addition to significant changes in gene expression profiles and predation mortality, we documented altered acceleration and habitat use in the first 8 days oil-exposed individuals were at liberty as well as a cessation of apparent spawning activity for at least 37 days. These data reveal that even a brief and low-dose exposure to crude oil impairs fitness in wild mahi-mahi. These findings offer new perspectives on the lasting impacts of the DWH blowout and provide insight about the impacts of future deep-sea oil spills.

Environmental Science and Technology↗
USGS2022

Expression plasticity regulates intraspecific variation in the acclimatization potential of a reef-building coral

Phenotypic plasticity is an important ecological and evolutionary response for organisms experiencing environmental change, but the ubiquity of this capacity within coral species and across symbiont communities is unknown. We exposed ten genotypes of the reef-building coral Montipora capitata with divergent symbiont communities to four thermal pre-exposure profiles and quantified gene expression before stress testing 4 months later. Here we show two pre-exposure profiles significantly enhance thermal tolerance despite broadly different expression patterns and substantial variation in acclimatization potential based on coral genotype. There was no relationship between a genotype’s basal thermal sensitivity and ability to acquire heat tolerance, including in corals harboring naturally tolerant symbionts, which illustrates the potential for additive improvements in coral response to climate change. These results represent durable improvements from short-term stress hardening of reef-building corals and substantial cryptic complexity in the capacity for plasticity.

Nature Communications↗