(Each entry represents one finding in the 22 studies unless otherwise noted. Some studies had multiple findings.)

• PCBs increased prostate size at a dosage consumed by the general public
• permanently increased androgen receptor (AR) binding activity of the prostate at a dosage consumed by the general public
• induced prostate growth in the presence and absence of testosterone; however, it was more effective in the presence of testosterone 
• estrogenic chemicals [such as PCBs] induce reproductive malformation by direct interference with the fetal reproductive organs 
• PCBs are able to induce malformation even in the absence of fetal testosterone; however, they are more effective in the presence of testosterone 
• PCB 169 resulted in abnormal rodent sex differentiation 
• the developing animal is extremely sensitive to toxicants during sex differentiation 
• many effects are difficult to detect until late in life 
• ventral prostate weight was reduced by PCB 126 and especially PCB 105 
• PCB 105 affects development of the male reproductive system by mechanisms in addition to or independent of Ah receptor agonist activity 
• ventral prostate (VP) weight was reduced by 36% in the PCB group 
• myeloperoxidase (MPO) activity in the lateral prostate (a measure of inflammation) was higher 
• An association was suggested between PCB concentrations in subcutaneous abdominal adipose tissue and the occurrence of prostate cancer 
• PCBs increased enzyme activities in rat prostates, in a more pronounced fashion than other inducing chemicals 
• prostate sensitivity to PCB enzyme induction and the capacity of the prostate to produce mutagenic metabolites might be of importance for initiation of prostatic cancer by environmental factors. 
• PCB metabolites [breakdown products] have been found in the ventral prostate 
• prostate weights (g) were slightly increased in the PC60 group at the 1st and 4th week following treatment 
• ventral prostate weights permanently reduced in PCB 126 treated male rats 
• Ventral prostate weights in all experimental male offspring were significantly less than those of controls 
• Low but detectable amounts of PCB metabolites were found in cytosolic preparations from prostate 
• furans significantly decreased ventral prostate weights [PCBs are generally contaminated with furans] 
• furans are more toxic substances than PCBs when administered to rats 
• PCB-126 had no effect on the androgen receptor content of the prostate 
• dioxin enhanced AHH enzyme activity in the prostate [PCBs are frequently contaminated with dioxins] 
• the effects of PCB 169 bear little resemblance to those of any known anti-androgen 
• endocrine disrupting chemicals [such as PCBs] operate during critical period (s) in the early stage of life characterized by rapid cell differentiation and organogenesis, leaving irreversible disruption 
• endocrine disrupting chemicals [such as PCBs] may not demonstrate any clear minimum threshold in exerting their "toxicological" effects 
• endocrine disrupting chemicals [such as PCBs] may act synergistically or additively with other chemicals 
• firefighters face increased prostate cancer risks, after chemical exposures which often include PCBs and furans 
• prostate cells were used to test endocrine disrupting chemicals, such as PCBs 
• disturbed male sexual differentiation may in some cases be caused by increased exposure to environmental xenoestrogens and/or antiandrogens [such as PCBs] 
• PCBs are metabolically activated to electrophilic quinoid species capable of binding to DNA 
• PCB metabolites are capable of redox cycling, thereby increasing oxidative stress in biological systems 
• PCB congeners form DNA adducts after metabolic activation 
• this study could not detect PCB DNA effects in live rats 
• PCBs may be a key factor in prostate cancer 
• PCBs dramatically increased certain steroid hormones (but not others) in rat prostate tissues 
• cancer risk is higher for people born during the 1950s than for those born in 1873-82 
• men face a cancer risk three times higher than before 
• human prostate cell lines may be targeted by PCBs for changes in proliferation, migration and growth factor gene expression, which may be mechanisms for the promotion of prostate disease 
• both genetic and environmental factors may contribute to the racial differential in both incidence and mortality of prostate cancer among blacks and whites 
• gene-environmental interactions initiate and promote prostatic neoplasia [prostate cancer] 

 

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