Geology topics

Ellie Maureen Dalsky

Publications and source records attributed to Ellie Maureen Dalsky.

5 recordsLinked to original sources

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↗

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↗

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↗

USGS2021

Disruption of the Francisella noatunensis orientalis pdpA gene results in virulence attenuation and protection in zebrafish

Several Francisella spp. including F. noatunensis are regarded as important emerging pathogens of wild and farmed fish. However, very few studies have investigated the virulence factors that allow these bacterial species to be pathogenic in fish. The Francisella Pathogenicity Island (FPI) is a well-described, gene-dense region encoding major virulence factors for the genus Francisella. PdpA is a member of the pathogenicity determining protein genes encoded by the FPI that are implicated in the ability of the mammalian pathogen, F. tularensis , to escape and replicate in infected host cells. Using a sacB suicide approach, we generated pdpA knockouts to address the role of PdpA as a virulence factor for F. noatunensis . Because polarity can be an issue in gene-dense regions, we generated two different marker-based mutants in opposing polarity ( Fno Δ pdpA1 and Δ pdpA2 ). Both mutants were attenuated (p<0.0001) in zebrafish challenges and displayed impaired intracellular replication (p<0.05) and cytotoxicity (p<0.05), all of which could be restored to wild-type (WT) levels by complementation for Fno Δ pdpA 1. Importantly, differences were found for bacterial burden and induction of acute phase and pro-inflammatory genes for Fno Δ pdpA 1 and Δ pdpA 2 compared to WT during acute infection. In addition, neither mutant resulted in significant histopathological changes. Finally, immunization with Fno Δ pdpA1 led to protection (p<0.012) against an acute lethal-dose 40 challenge with WT Fno in the zebrafish model of infection. Taken together, this study further demonstrates physiological similarities within the genus Francisella relative to their phylogenetic relationships and the utility of zebrafish for addressing virulence factors for the genus.

Infection and Immunity↗