Gb. Freeman et al., An assessment of neurotoxicity of aroclors 1016, 1242, 1254, and 1260 administered in diet to Sprague-Dawley rats for one year, TOXICOL SCI, 53(2), 2000, pp. 377-391
As part of a comparative chronic toxicity/oncogenicity study of different A
roclors (1016, 1242, 1254, and 1260), neurotoxicity was assessed in male an
d female Sprague-Dawley rats using functional observational battery (FOB) a
nd motor activity tests, and histopathologic evaluation of selected nervous
system tissues. Doses varied by Aroclor and ranged from 25 to 200 ppm in t
he diet. Animals were evaluated prior to initiation of dosing and at 13, 26
, 39, and 52 weeks of exposure. Clinical signs, body weights, and feed cons
umption were evaluated weekly. Data analysis of FOE and motor activity resu
lts revealed several instances where Aroclor-treated groups were different
from control. However, these were considered incidental, as they lacked any
consistent dose- or time-related pattern that would suggest Aroclor-induce
d neurotoxicity. The nonremarkable findings during each of the four assessm
ents were supported by the absence of any treatment-related clinical signs
or mortality. Decreased body weight gain was evident in the male 100 ppm Ar
oclor 1254 dose group and in all female Aroclor 1254 dose groups late in th
e study (when a linear relationship was assumed between body weight and tim
e), correlating with decreased feed consumption. Although a variety of inci
dental, spontaneous, degenerative changes were found in nervous tissue eval
uated histopathologically, these changes were seen with similar incidence a
nd severity in treated and control groups. No lesions were found that could
be attributed to Aroclor-related neurotoxicity. In summary, 52 weeks of ex
posure to Aroclors 1016, 1242, 1254, or 1260 mixed in the diet did not yiel
d any functional or morphologic changes indicative of PCB-induced neurotoxi
city.