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This study focuses on the bioavailability of PAHs in Powder River Basin coal to fish embryos and larvae, evaluating toxicity mechanisms and stage-specific effects. Through tailored methodologies, researchers assess PAH sources and impacts on various fish species. Findings show varying toxicity levels and mechanisms across different PAH compounds. The study examines PAH exposure scenarios, cardiac function effects, CYP1A induction, and systemic toxicity in fish developmental stages.
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NOAA FISHERIES Initial assessment of the bioavailability of PAHs in Powder River Basin coal to fish early life history stages John Incardona Ecotoxicology Program NOAA Northwest Fisheries Science Center, Seattle
Fish embryos are sensitive indicators of PAH bioavailability • crude oil • bunker fuel • creosote • coal tar in sediments • diesel exhaust particles • coal tar pavement sealants • stormwater runoff • coal and coal dust?
No fish species escapes PAH toxicity • pink salmon (Oncorhynchus gorbuscha) • Pacific herring (Clupea pallasi) • Atlantic herring (Clupea harrengus) • mummichog (Fundulus heteroclitus) • Gulf killifish (Fundulus grandis) • crimson-spotted rainbowfish (Melanotaenia fluviatilis) • medaka (Oryzias latipes) • zebrafish (Danio rerio) • olive flounder • Japanese sea perch • bluefin tuna • yellowfin tuna • yellowtail amberjack • red drum • Atlantic haddock
The aryl hydrocarbon receptor pathway and cytochrome P4501A induction after Whitlock 1999, Annu Rev Pharmacol Toxicol 39:103
Stage-specific toxicity of individual PAHs via distinct mechanisms pattern formation 1.25 hpf AHR-independent cardiac dysfunction (via ion channel blockade?), CYP1A protective 36 hpf 24 hpf organogenesis AHR-dependent cardiac dysfunction via inhibition of cardiomyocyte proliferation, CYP1A protective 48 hpf 48 hpf 72 hpf hatching Systemic toxicity dependent on hepatic AHR and CYP1A activity 96-120 hpf 120 hpf feeding
3-ring PAH exposure phenocopies a cardiac function mutant crude oil 56 µM phenanthrene silent heart (troponin T) fluorene naphthalene dibenzothiophene phenanthrene GC-MS analysis of PAHs in embryos exposed to crude oil
PAHs vary in potency of CYP1A induction pyrene chrysene benz(a)anthracene CYP1A IF cyp1a QPCR (TaqMan)
Phenanthrene is toxic with minimal CYP1A induction solvent control phenanthrene 48 hpf CrDI OA CYP1AMHC
Tricyclic PAHs cause bradycardia and AV conduction block heart rate (bpm) ppm phenanthrene
Quantification of edema by pericardial area crude oil dose response (∑PAH)
What we have tested so far • Powder River Basin coal (Boardman Plant, Portland General Electric) • Pulverized coal dust slurries (static exposures) • Coal dust slurry filtrates (static) • Coal chunk column (continuous flow)
coal dust slurry embryo 1% agarose Simultaneous exposure to either coal dust or dissolved components only agarose pore size = 0.1-0.3 µm embedded embryos exposed to diffusible dissolved PAH only