Chemistry Reference
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Other life stages potentially susceptible to the effects of exposure to EDCs include
puberty, for chemicals that interfere with the sex steroid hormone pathways; and final
maturation, for chemicals that have progestagen activity. Altered timing of puberty
and/or timing of gamete production could affect seasonal breeding animals; tim-
ing of reproduction is critical for ensuring maximal survival of their offspring (i.e.,
where there is maximal food availability). Another life stage potentially susceptible
to the effects of EDCs is the smolting event in some salmonid fish when they transfer
from freshwater to saltwater. This process is associated with changes in a suite of
hormones, including corticosteroids and prolactin, and it has been shown to be dis-
rupted on exposure to both alkylphenols and E 2 (McCormick et al. 2005; Bangsgaard
et al. 2006). None of these potentially sensitive biological processes and life stages
have been well studied.
In summary, this section highlights that timing of exposure to EDCs can be criti-
cal in the nature and magnitude of the effects produced.
15.9 SPecIeS SuScePtIBILIty
Most vertebrates are responsive to steroidal hormones and their mimics, and the hor-
monal systems signaling these responses, and their controlling factors, are highly
conserved (Sumida et al . 2003). It is perhaps not surprising, therefore, that studies
in vitro have shown that an EDC interacting with a specific receptor in one species,
will also do so with another, and sometimes with very similar affinity, even across
divergent organisms. As an example, White et al . (1994) demonstrated that a number
of alkylphenolic compounds were estrogenic to bird, fish, and mammalian cell lines
at equivalent potencies. From such studies, it would be easy to assume that an EDC
effective in one vertebrate organism will be equally effective in another. It is the case
that rodent models are thought of as being sufficiently similar to humans to make them
suitable for informing on the effects of EDCs for the protection of human health.
Care should be taken in making general statements on EDCs effects, however, as
despite the many similarities in hormones and their receptors in vertebrates, there are
some clear distinctions too. For example, sexual development is estrogen dependent
in birds but not mammals (Tyler et al. 1998), and thus, bird reproductive development
may be more sensitive to estrogen mimics compared to that for mammals (Ottinger
et al. 2002). In mammals, too, the developing fetus is protected from abnormal hor-
monal exposure by high maternal levels of α-fetoprotein and sex-steroid-binding
globulin (Vannier and Raynaud 1975, in Westerlund et al. 2000), but for oviparous
organisms there is no equivalent system; eggs deposited into the aquatic environ-
ment can be exposed constantly to EDCs and other chemicals, although the chorion
offers some degree of protection against chemical uptake (Finn 2007).
Examples of differences in the responses of wildlife organisms to EDCs include
the differences in sensitivity to phthalates and bisphenols among mollusks, crus-
taceans, and amphibians compared to fish. In invertebrates, biological effects are
observed at exposures in the ng/L to low µg/L range, compared to high µg/L for most
effects in fish (reviewed in Oehlmann et al. 2008). In addition, aquatic mollusks tend
to bioconcentrate and bioaccumulate pollutants to a greater level than fish, possibly
owing to poorer capabilities for metabolic detoxification (see Chapter 4, Section 4.3).
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