In the post-World War II days of rapidly expanding car ownership and use in the USA, polymer scientists designing tire rubber were faced with a problem. In high traffic, ozone from exhaust collects along the surface of roadways and its oxidation potential rapidly degrades tire rubber. Phenylphenylenediamines (PPDs) were found to bind ozone at the surface of tires. We’ve used them to do so ever since. 6PPD is a common PPD now used in tires around the world. In reacting with ozone, 6PPD can be oxygenated at its phenylene ring to become 6PPD-quinone. When it rains, stormwater flows across roadways and carries fragments of rubber that break off from tires, termed tire wear particles, into aquatic environments. In urbanized watersheds around the Puget Sound, salmon are exposed to 6PPD-quinone from urban runoff during development as embryos, alevin and parr, and again as adults while migrating upstream to spawn. For decades, adult coho have been known to die before spawning in urban streams. This is called urban runoff mortality syndrome (URMS). It poses a threat to populations of this prized keystone species. In 2020, 6PPD-quinone was discovered and identified as the primary cause of URMS. Under standard lab conditions, coho parr exhibit the same biological profile as URMS-affected fish in the field and die in 24-hour exposures to 6PPD-quinone with an LC50 of 95 ng/L, one of the lowest known aquatic toxicity thresholds.
There’s still more to learn about how 6PPD-quinone causes its toxic effects in coho and how those effects vary with other environmental stressors. Answering these questions will guide us to better alternatives to 6PPD and solutions to address extant 6PPD-quinone. Coho are exposed to 6PPD-quinone under variable water quality conditions and at different life stages. Water quality is crucial to coho health and likely changes the bioavailability of 6PPD-quinone. We are exposing parr to 6PPD-quinone at relevant ranges of temperature, pH, ionic strength and dissolved organic matter concentrations and creating a multilinear model relating those parameters to 6PPD-quinone-driven coho mortality rates. In the completed temperature exposures, coho juveniles showed increased sensitivity at lower temperatures, possibly indicating the existence of a temperature-dependent enzymatic detoxification pathway for 6PPD-quinone in coho.
Coho life history changes are so drastic that some consider them a rare example of fish metamorphosis. As embryos, coho undergo critical developmental steps but are protected by a thick chorion. As parr, coho live in streams for nearly two years and are more heavily exposed to aquatic pollutants. After returning from the ocean, coho undergo a high degree of biological stress due to their arduous migration, potentially making them more susceptible to toxicants. We’re exposing coho embryos to 6PPD-quinone from fertilization to hatching and measuring mortality rates and developmental effects to assess embryo susceptibility.