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.