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Cited by 390Environmental Toxicology and EcotoxicologyPhysiological and biochemical adaptationsToxic Organic Pollutants Impact

Interactions between chemical and climate stressors: A role for mechanistic toxicology in assessing climate change risks

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Hooper, Michael J., Ankley, Gerald T., Cristol, Daniel A., Maryoung, Lindley A., Noyes, Pamela D., Pinkerton, Kent E.·2013·Environmental Toxicology and Chemistry
DOI 10.1002/etc.2043PMC PMC3601417
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Abstract

Incorporation of global climate change (GCC) effects into assessments of chemical risk and injury requires integrated examinations of chemical and nonchemical stressors. Environmental variables altered by GCC (temperature, precipitation, salinity, pH) can influence the toxicokinetics of chemical absorption, distribution, metabolism, and excretion as well as toxicodynamic interactions between chemicals and target molecules. In addition, GCC challenges processes critical for coping with the external environment (water balance, thermoregulation, nutrition, and the immune, endocrine, and neurological systems), leaving organisms sensitive to even slight perturbations by chemicals when pushed to the limits of their physiological tolerance range. In simplest terms, GCC can make organisms more sensitive to chemical stressors, while alternatively, exposure to chemicals can make organisms more sensitive to GCC stressors. One challenge is to identify potential interactions between nonchemical and chemical stressors affecting key physiological processes in an organism. We employed adverse outcome pathways, constructs depicting linkages between mechanism-based molecular initiating events and impacts on individuals or populations, to assess how chemical- and climate-specific variables interact to lead to adverse outcomes. Case examples are presented for prospective scenarios, hypothesizing potential chemical–GCC interactions, and retrospective scenarios, proposing mechanisms for demonstrated chemical–climate interactions in natural populations. Understanding GCC interactions along adverse outcome pathways facilitates extrapolation between species or other levels of organization, development of hypotheses and focal areas for further research, and improved inputs for risk and resource injury assessments. Environ. Toxicol. Chem. 2013;32:32–48. © 2012 SETAC

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  • Once in transport, UV radiation in sunlight can activate certain PAH species, enhancing their toxicity to a diverse range of aquatic taxa.

    “Once in transport, UV radiation in sunlight can activate certain PAH species, enhancing their toxicity to a diverse range of aquatic taxa (Ankley et al., 2003; Hooper et al., 2013).”

    From Wildfire Induces Changes in Receiving Waters: A Review With Considerations for Water Quality Management (2022) · cites this paper as Hooper et al., 2013

    The “Ultraviolet-Induced Photoactivation of Polycyclic Aromatic Hydrocarbons” section says sunlight can activate some PAHs and that similar increases in toxicity have been documented across many aquatic species. It describes activation after PAHs are taken up by an animal, however, rather than while they are in environmental transport. (LLM, conf=0.82)

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Authors
Hooper, M. J., Ankley, G. T., Cristol, D. A., Maryoung, L. A., Noyes, P. D., & Pinkerton, K. E.
Affiliations
  • Columbia Environmental Research Center (US)
  • Environmental Protection Agency (US)
  • William & Mary (US)
  • University of California, Riverside (US)
  • Duke University (US)
  • University of California, Davis (US)
Corresponding author
Hooper, Michael J.
ORCID
Venue
Environmental Toxicology and Chemistry
Publisher
Oxford University Press (OUP)
Published
2013-01-01
Volume
32
Issue
1
Pages
32-48
ISSN
  • 0730-7268 (ISSN-L)
  • 1552-8618
DOI
10.1002/etc.2043
PMC
PMC3601417
OpenAlex
W2148975000
Cited by
390
References
4
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FWCI
10.87
Type
journal article
Language
en
Open access
Licence
Locations
  • Environmental Toxicology and Chemistry (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • W&M Publish (College of William & Mary) (submittedVersion)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Environmental Toxicology and Ecotoxicology
  • Physical Sciences › Environmental Science › Ecology › Physiological and biochemical adaptations
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
Keywords
climate change, chemical stressors, mechanistic toxicology, adverse outcome pathways, toxicokinetics, toxicodynamics, physiological tolerance, risk assessment
MeSH terms
Climate, Environmental Pollutants, Humans, Hydrogen-Ion Concentration, Models, Chemical, Risk, Temperature, Risk Assessment, Climate Change

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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