World Health Organization Adopts Fish Assessment Tool

To understand the risk that exposure to dioxin and similar toxic chemicals pose to early life-stage survival of fish, it is essential to identify the most fundamentally important target organs and pathways of dioxin toxicity in fish embryos and larvae.

That has been the focus of Sea Grant-funded studies by UW-Madison scientists Richard Peterson and Warren Heideman.

During 2004-06, Peterson and Heideman realized several major advances in their research that have greatly increased our understanding of the impacts of both polychlorinated and polybrominated forms of dibenzo-p-dioxins, dibenzofurans and biphenyls, on wild fish populations.

One major finding was that heart malformation is one of the first adverse effects of dioxin exposure on the zebrafish embryo, including adverse effects on both heart morphology and the process that plays a key role in heart development. They also determined that dioxin contamination of zebrafish eggs can reduce the size of the embryo heart.

A key discovery, however, was that dioxin caused the ventricles of zebrafish embryo hearts to stop beating, resulting in a type of heart dysfunction called “ventricular standstill,” which, they report, “could lead to the failure of larval fish recruitment into feral fish populations.”

The World Health Organization has used Peterson and Heideman’s research to set “relative potency factors,” and it will be using their latest findings during the next update. Relative potency factors are used by regulatory agencies globally to assess the risk of recruitment failure in feral fish populations exposed to these classes of persistent organic pollutants.






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