Page 732 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Brominated Flame Retardants and Perfluorinated Chemicals Chapter | 52 697

VetBooks.ir 2014). This decrease T 4 was not concomitant with any reported from polar bear fat samples from Svalbard and
East Greenland. PBDE levels in domestic, pet, and wild
detectable thyroid lesions. The detailed mechanism
animals are presented in Table 52.3.
by which BFRs can disrupt TH homeostasis is discussed
later (Fig. 52.4). Exposure to PBDEs in domestic/pet animals and
Experimental studies showed that HBCD, the second humans may occur via multiple sources (air, water, dust,
most used flame retardant, has negative effects on endo- and food). Levels of PBDEs in animal and human tissues
crine and reproductive processes (Birnbaum and Staskal, have increased exponentially since the 1970s in several
2004). Many effects of HBCDs seem to occur during countries, including the United States, Canada, and
development. During developmental exposure, HBCDs Sweden (Schecter et al., 2005; Guo et al., 2011). Elevated
have been shown to decrease bone density and retinoids levels of PBDEs in North America have been attributed
and to enhance immune response to sheep red blood cells to the greater use of the pentaBDE mixture compared to
(van der Ven et al., 2009). HBCD isomers are endocrine its use throughout the rest of the world. Like other lipo-
disruptors with antiandrogenic properties that inhibit aro- philic compounds, PBDEs readily cross the placenta into
matase and interact with steroid hormone receptors the fetus, providing an opportunity for PBDEs to interfere
(Hamers et al., 2006). Like other BFRs, HBCDs may dis- with human and animal developmental processes
rupt TH homeostasis, resulting in decreased T 4 levels and (Frederiksen et al., 2010).
increased thyroid-stimulating hormone (TSH) (Ema et al., Because PBDEs are predominantly used indoors, data
2007). Studies indicate that a low dose of HBCD can on their effects on wildlife and farm animals are limited
potentially disrupt TH hormone receptor-mediated trans- and exposure seems to be more through nondietary sources
activation and impairs cerebellar Purkinje cell dendrito- (Caspersen et al., 2016). A few studies indicate that PBDE
genesis (Ibhazehiebo et al., 2011). exposure at environmentally relevant concentrations
PBDE residues have been detected in indoor air, house increases nestling growth (Fernie et al., 2006) and causes
dust, and foods (Schecter et al., 2006; Sjodin et al., 2008). changes in reproductive courtship behaviors in adult
Sewage treatment plant effluents and biosolids are consid- American kestrels (Fernie et al., 2008). However, a number
ered a major source of PBDEs (Rieck, 2004). More than of studies on laboratory animals have indicated that
half of the sewage sludge produced annually in the commercial PBDE mixtures as well as the individual
United States is applied to land as fertilizer (U.S. EPA, PBDE congeners that compose them affect the nervous,
1999). Agricultural land that has been treated with sewage endocrine, reproductive, and immune systems (Lyche et al.,
sludge can be highly contaminated with PBDEs. Thus, 2015). Tseng et al. (2006) did not find effects on sperm
application of sewage sludge may represent a source of count or function at high concentrations of PBDE-209
exposure by direct contact or uptake through plants. In (500 1500 mg/kg/day from postnatal day (PND) 21 to 70)
grazing animals including cattle, soil ingestion leads to in mice, but they did find indications of oxidative stress in
contamination of meat and dairy products. In dairy cattle, sperm. In a subsequent study, Tseng et al. (2013) found sig-
the major intake of organohalogens occurs via spontane- nificant changes in the male offspring in anogenital dis-
ous soil ingestion during grazing (Fries, 1995). Cows tance, sperm heads, and testicular histopathology following
ingest up to 1000 g of soil per day (i.e., several micro- exposure to PBDE-209. Few studies have indicated associa-
grams of halogenated compounds daily) depending on tion of PBDEs with pregnancy- related outcomes such as
several factors, including season, climate, and density of longer time to pregnancy in women (Harley et al., 2010)
grass (Laurent et al., 2005). and enhanced risk of developing gestational diabetes melli-
There are a few reports indicating high levels of serum tus (Smarr et al., 2016). With regard to neurotoxic effects,
PBDEs in household cats because of their high exposure to several studies have indicated that HBCD and PBDEs cause
house dust (Dye et al., 2007). In captive giant and red pan- permanent aberrations in spontaneous behavior and habitua-
das, the tissue levels of PBDEs ranged from 38 to 2158 ng/ tioncapabilityinmiceafter asingleexposureat PND 10 (a
g lipid weight (lw) (Hu et al., 2008). Kierkegaard et al. period of rapid brain growth development). It is interesting
(2009) reported PBDE levels in cow milk (1100 2600 pg/g to note that the effects seen on this behavioral paradigm
lw) and fat (1300 2600 pg/g lw). In Arctic fox, the levels with PBDEs are identical to those produced by PCBs
of PBDEs are very low, ranging from 26 to 31 ng/g lw (De (Eriksson and Fredriksson, 1996). Mice exposed to a single
Wit et al., 2010). Whereas the levels of PBDEs in the liver dose of PBDE 47 on PND 10 demonstrated delayed ontog-
of California sea otter are 2423 ng/g lw (Kannan et al., eny of neuromotor function and hyperactivity when they
2008), the levels are much higher in blubber of California attained adult age without any alterations in circulating TH
sea lions, ranging from 569 to 24343 ng/g lw (Stapleton levels (Gee and Moser, 2008; Gee et al., 2008). Other stud-
et al., 2006). In adipose tissue of polar bears in Canada, ies showed developmental delays in the acquisition of the
Muir et al. (2006) reported levels of PBDEs ranging from palpebral reflex following neonatal exposure to PBDE 209
4.6 to11 ng/glw, andthese levels were lowerthan those along with changes in circulating T 4 levels (Rice et al.,