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N-(1,3-Dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-quinone) is an environmental transformation product of the widely used rubber tire antioxidant, 6PPD. Found in stormwater runoff, 6PPD-quinone has been reported to cause acute lethality at ≤1 μg/L in salmonids like coho salmon, rainbow trout, and brook trout. Conversely, other species such as Arctic char and brown trout are insensitive, even when exposed to significantly greater concentrations (3.8-50 μg/L). Sensitive species exhibit symptoms such as gasping, spiraling, increased ventilation, and loss of equilibrium, suggesting a possible impact on cardiorespiratory physiology. This study investigated sublethal 6PPD-quinone toxicities, focusing on cardiovascular and metabolic effects in two salmonids of varying sensitivity: a sensitive species, rainbow trout (Oncorhynchus mykiss) and a tolerant species, Arctic char (Salvelinus alpinus). Fish were exposed to measured concentrations of 0.59 or 7.15 μg/L 6PPD-quinone, respectively, in respirometry chambers for 48 h to assess temporal changes in resting oxygen consumption compared to unexposed controls. Following exposure, cardiac ultrasound and electrocardiography characterized cardiac function in vivo, while blood gas analysis examined blood composition changes. In both species, changes in resting oxygen consumption were observed. In rainbow trout only, a decrease in end systolic volume and an increase in passive ventricular filling, cardiac output, and PR interval length were observed, indicating cardiac stimulation. Cardiorespiratory symptoms observed following rainbow trout exposure might partly be driven by a significant increase in methemoglobin, resulting in an impaired ability to oxygenate tissues. This study is the first to examine the effects of 6PPD-quinone exposure on the cardiorespiratory system of salmonid fishes and provides information invaluable to a better understanding of the mechanism of 6PPD-quinone toxicity.
Selinger et al. (Wed,) studied this question.