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. 2014 Jan;137(1):3-11.
doi: 10.1093/toxsci/kft228. Epub 2013 Oct 23.

Cumulative risk: toxicity and interactions of physical and chemical stressors

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Cumulative risk: toxicity and interactions of physical and chemical stressors

Cynthia V Rider et al. Toxicol Sci. 2014 Jan.

Abstract

Recent efforts to update cumulative risk assessment procedures to incorporate nonchemical stressors ranging from physical to psychosocial reflect increased interest in consideration of the totality of variables affecting human health and the growing desire to develop community-based risk assessment methods. A key roadblock is the uncertainty as to how nonchemical stressors behave in relationship to chemical stressors. Physical stressors offer a reasonable starting place for measuring the effects of nonchemical stressors and their modulation of chemical effects (and vice versa), as they clearly differ from chemical stressors; and "doses" of many physical stressors are more easily quantifiable than those of psychosocial stressors. There is a commonly held belief that virtually nothing is known about the impact of nonchemical stressors on chemically mediated toxicity or the joint impact of coexposure to chemical and nonchemical stressors. Although this is generally true, there are several instances where a substantial body of evidence exists. A workshop titled "Cumulative Risk: Toxicity and Interactions of Physical and Chemical Stressors" held at the 2013 Society of Toxicology Annual Meeting provided a forum for discussion of research addressing the toxicity of physical stressors and what is known about their interactions with chemical stressors, both in terms of exposure and effects. Physical stressors including sunlight, heat, radiation, infectious disease, and noise were discussed in reference to identifying pathways of interaction with chemical stressors, data gaps, and suggestions for future incorporation into cumulative risk assessments.

Keywords: cumulative risk; infectious disease; joint action; noise.; nonchemical stressors; radiation; sunlight; temperature.

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Figures

FIG. 1.
FIG. 1.
Benchmark-dose analysis documenting a linear relationship between carbon monoxide concentration and potentiation of noise-induced hearing loss. The upper panel shows the predicted benchmark dose that would yield an elevation in auditory threshold equivalent to 10% of the effect produced by noise alone and its lower bound. The predicted benchmark concentration is 236 ppm CO, and the lower bound for the benchmark concentration is 195 ppm. The lower panel shows the predicted benchmark dose that would yield a 5-dB elevation in auditory threshold beyond that produced by noise alone and its lower bound. The predicted benchmark concentration is 388 ppm CO, and the lower bound for the benchmark concentration is 320 ppm. Reproduced from Fechter et al., 2000.

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