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Study explores the lethal and sublethal effects of tire wear chemical on early life stages of brook trout 

 St. Andrews, New Brunswick, Canada – September 3, 2024 

 Vehicle tires wear over time and we are all familiar with the need to purchase new tires as treads diminish. 6PPD is an anti-ozonate compound included in tire rubber formulations to prevent premature breakdown and wear of tires. When 6PPD is exposed to the environmental elements it forms a by-product called 6PPD-quinone, which was recently determined to be the cause of a coho salmon mass mortality event following stormwater runoff occurrences in British Columbia, Canada. Of the species tested to date, only select salmonids have been found to be sensitive to 6PPD-quinone following exposure and relative sensitivity cannot be predicted based on how closely related species are to one another. Brook trout, a species commonly distributed and stocked in Atlantic Canada, is one of the most sensitive species to this contaminant. 

“The majority of published 6PPD-quinone studies have focused on fingerling life stages of fishes. We conducted this comparative study with brook trout fry & fingerlings to determine if earlier life stages are more sensitive to this contaminant. We also looked at changes in the gill structure and blood chemistry of exposed fingerlings to determine what physiologically is changing in these fish when they are exposed to this compound,” states Dr. Danielle Philibert, Huntsman Maine Associate Research Scientist and lead author on the research publication in the peer-reviewed journal Chemosphere. 

 Acute 24 hour exposures of brook trout were completed in the wet laboratories of The Huntsman Marine Science Centre. Fish were assessed frequently throughout the exposure period to determine the rate at which mortality and morbidity occurred in response to this contaminant. The exposure duration was chosen to mimic peak concentrations of 6PPD-quinone measured following rain fall events. Gill and blood samples were taken in any surviving fingerlings after the 24 hour exposure period. 

 Effects were noted in both fry and fingerlings within the first hour of exposure, which is quite rapid compared to other environmental contaminants. The majority of mortality was observed within the first 6 hours of exposure and fish surviving this early period generally made it to the end of the 24 hour trial. The younger fry life stage was found to be about 2-3 times more sensitive to 6PPD-quinone compared to the more often studied and larger older fingerlings. 

 “Our study results indicate that brook trout fry are one of the most sensitive species to 6PPD-quinone tested to date,” explains Philibert. In fact, the exposure concentration that caused lethality to 50% of the exposed population (known as the “LC50 value”) was well within the measured environmental concentrations from collected stormwater runoff near urban areas with higher road use. 

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Exposure to environmentally relevant 6PPD-quinone concentrations used in the study also caused many sublethal effects on brook trout fingerlings, including changes to blood chemistry parameters and gill structure. “We sampled blood from brook trout fingerling survivors at the end of the 24 hour test period. Our results showed an effect on several parameters, including blood ions, blood glucose and total carbon dioxide,” adds Philibert. 

Results from the study supported the previous theory that 6PPD-quinone toxicity in fish is caused by osmorespiratory issues following gill impairment. Freshwater fish continuously lose ions from inside its body to the environment through passive diffusion. Maintaining a constant ion balance with the environment is essential for survival and requires active regulation even while at rest. Histological assessment of the gill tissue taken from exposed fish in the study showed gill structural changes that may have occurred to slow passive loss of ions between the blood in the gill lamellae and the water environment. These compromises to deal with chemical exposure are likely to result in unintended negative consequences for the exposed fish by then reducing its ability to extract oxygen from the water. The study authors noted exposed fish would show gasping and gill flaring behaviours that would be consistent with decreasing capacity to acquire oxygen through respiration. 

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This research demonstrated the importance of conducting toxicity trials on multiple life stages of fish species as relying solely on a larger fingerling life stage for species-based risk assessments may underestimate the impacts of exposure to environmental contaminants. “Our study increases the understanding of the potential risk from these contaminants found in brook trout habitats, especially when they are in close proximity to roadways and urban centers,” concludes Philibert. 

The research publication was co-authored by Dr. Benjamin de Jourdan, also a Huntsman Marine Research Scientist, chemists at the University of California Riverside (Riverside, CA) and Trent University (Peterborough, ON), and fish physiologist at the University of New Brunswick (Fredericton, NB). The study was funded through a contribution agreement with Fisheries & Oceans Canada with matching funds provided by industry partners and The Huntsman Marine Science Centre. 

Research Publication: 

Philibert, D., R.S. Stanton, C. Tang, N.L. Stock, T. Benfey, M. Pirrung and B. de Jourdan. 2024. The lethal and sublethal impacts of two tire runner-derived chemicals on brook trout (Salvelinus fontinalis) fry and fingerlings. Chemosphere 360: 142319. https://doi.org/10.1016/j.chemosphere.2024.142319 

Image 1: Graphical abstract highlighting the study methods and results. 

Image 2: Brook trout fry exposed to test concentrations of 6PPD-quinone in glass jars. 

Image 3: Blood sampling set-up from brook trout fingerlings following exposure to test concentrations of 6PPD-quinone. 

Story by Bud Adams, The Huntsman Marine Science Centre.  

For additional information or images relating to this article, please email huntsman@huntsmanmarine.ca. 

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