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