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VASCULAR BARRIER DISRUPTION IN COHO SALMON (ONCORHYNCHUS KISUTCH) EXPOSED TO ROADWAY RUNOFF AND 6PPD-QUINONE
Dissertation

VASCULAR BARRIER DISRUPTION IN COHO SALMON (ONCORHYNCHUS KISUTCH) EXPOSED TO ROADWAY RUNOFF AND 6PPD-QUINONE

Stephanie Blair
Doctor of Philosophy (PhD), Washington State University
2026
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Open Access CC BY V4.0

Abstract

6PPD 6PPD-quinone blood-brain barrier coho salmon roadway runoff urban runoff mortality syndrome Water resource management
Urban runoff mortality syndrome (URMS) causes rapid, recurrent mortality of coho salmon (Oncorhynchus kisutch) in urban watersheds of the Pacific Northwest. Although 6PPD-quinone has been identified as the causal toxicant, the physiological mechanism driving acute mortality and the basis of species specificity remained unresolved. This dissertation integrates experimental toxicology, vascular physiology, and mechanistic synthesis to resolve the proximate cause of URMS and evaluate pathways relevant to chemical hazard assessment. Laboratory exposures of juvenile coho salmon to roadway runoff and 6PPD-quinone demonstrate that acute mortality is driven by rapid, synchronous disruption of the blood–brain and blood–gill barriers. Tracer studies, hematology, histology, and gene expression analyses establish vascular barrier failure as the proximate lethal key event, producing hemoconcentration, circulatory collapse, and secondary neurological and respiratory dysfunction. Comparative experiments distinguish this targeted vascular pathology from generalized stress responses, osmoregulatory failure, or impaired oxygen transport. An adverse outcome pathway (AOP)–directed synthesis of the 6PPD-quinone toxicology literature further demonstrates that unmodified 6PPD-quinone is the acutely toxic form and that extreme species selectivity reflects toxicodynamic specificity rather than bioaccumulation alone. Across tolerant fish, mammalian, and invertebrate models, mitochondrial and oxidative stress responses are frequently observed but do not propagate to the defining vascular collapse characteristic of URMS, constraining these pathways as secondary or amplifying processes rather than molecular initiating events. These findings define URMS as a rapid, vascular-mediated mortality syndrome and establish mechanistic constraints necessary for development of biologically relevant screening tools and chemical management strategies.

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