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Nathaniel L. Scholz
Researcher at National Oceanic and Atmospheric Administration
Publications - 100
Citations - 9711
Nathaniel L. Scholz is an academic researcher from National Oceanic and Atmospheric Administration. The author has contributed to research in topics: Oncorhynchus & Stormwater. The author has an hindex of 50, co-authored 98 publications receiving 8144 citations. Previous affiliations of Nathaniel L. Scholz include University of Washington & Swiss Federal Institute of Aquatic Science and Technology.
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Journal ArticleDOI
Defects in cardiac function precede morphological abnormalities in fish embryos exposed to polycyclic aromatic hydrocarbons.
TL;DR: Different PAH compounds have distinct and specific effects on fish at early life history stages, and the relative toxicity of the different mixtures was directly proportional to the amount of phenanthrene, or the dibenzothiophene-phenanthrene total in the mixture.
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Deepwater horizon crude oil impacts the developing hearts of large predatory pelagic fish
John P. Incardona,Luke D. Gardner,Tiffany L. Linbo,Tanya L. Brown,Andrew J. Esbaugh,Edward M. Mager,John D. Stieglitz,Barbara L. French,Jana S. Labenia,Cathy A. Laetz,Mark Tagal,Catherine A. Sloan,Abigail Elizur,Daniel D. Benetti,Martin Grosell,Barbara A. Block,Nathaniel L. Scholz +16 more
TL;DR: It is shown that environmentally realistic exposures to crude oil cause specific dose-dependent defects in cardiac function in all three species, with circulatory disruption culminating in pericardial edema and other secondary malformations.
Journal ArticleDOI
Aryl Hydrocarbon Receptor–Independent Toxicity of Weathered Crude Oil during Fish Development
John P. Incardona,Mark G. Carls,Hiroki Teraoka,Catherine A. Sloan,Tracy K. Collier,Nathaniel L. Scholz +5 more
TL;DR: Using zebrafish embryos, blockade of AhR pathway components with antisense morpholino oligonucleotides demonstrated that the key developmental defects induced by weathered crude oil exposure are mediated by low-molecular-weight tricyclic PAHs through AhR-independent disruption of cardiovascular function and morphogenesis.
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A ubiquitous tire rubber–derived chemical induces acute mortality in coho salmon
Zhenyu Tian,Haoqi Zhao,Katherine T. Peter,Melissa Gonzalez,Jill Wetzel,Christopher Wu,Ximin Hu,Jasmine Prat,Emma Mudrock,Rachel Hettinger,Allan E. Cortina,Rajshree Ghosh Biswas,Flávio Vinicius Crizóstomo Kock,Ronald Soong,Amy Jenne,Bowen Du,Fan Hou,Huan He,Rachel A. Lundeen,Alicia N. Gilbreath,Rebecca Sutton,Nathaniel L. Scholz,Jay W. Davis,Michael C. Dodd,André J. Simpson,Jenifer K. McIntyre,Edward P. Kolodziej +26 more
TL;DR: Results reveal unanticipated risks of 6PPD antioxidants to an aquatic species and imply toxicological relevance for dissipated tire rubber residues, and identify a highly toxic quinone transformation product of N-(1,3-dimethylbutyl)-N′-phenyl-p- Phenylenediamine (6PPD), a globally ubiquitous tire rubber antioxidant.
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Developmental toxicity of 4-ring polycyclic aromatic hydrocarbons in zebrafish is differentially dependent on AH receptor isoforms and hepatic cytochrome P4501A metabolism
TL;DR: Three tetracyclic PAHs (pyrene, chrysene, and benz[a]anthracene) activate the AHR pathway tissue-specifically to induce distinct patterns of CYP1A expression, indicating that current models of PAH toxicity in fish are greatly oversimplified and that individual PAH's are pharmacologically active compounds with distinct and specific cellular targets.