Table 2.

Polychlorinated biphenyls (PCB) and endometrial cancer: mechanisms of action and correlated published studies.

Chemical(s)	Pathways of Exposure	Mechanism of Action	Authors (Year)	Results
Polychlorinated biphenyls (PCBs)	Food chain (fat-rich food, e.g., milk and derivates, fatty fish), living environment	Alteration steroid hormone metabolism/transport, ability to bind with the tyroxin transport protein transthyretin (TTR), interaction with thyroid hormone receptors, neuroendocrine effects. PCBs dioxin-like: Aril hydrocarbon Receptor interaction leading to altered steroid hormone metabolism and neuroendocrine effects including on thyroid	Chen, et al. 2015 [45]	It was observed that PCBs affected the expression of inflammatory factors through ER and AHR receptors but no toxic effects were observed on estrogen metabolism.
			Reich, et al. 2010 [56]	Case Control Study where high levels of PCB and others EDCs where found in the abdominal adipose tissue of two cases of endometrial stromal sarcoma
			Yoshizawa, K. et al. 2009 [55]	In vivo study where female adult Harlan Sprague-Dawley rats were exposed for 14, 31 or 53 weeks or for two years to different EDCs including PCB126, PeCDF, PCB153, PCB118, a binary mixture of PCB126 and 153; or a binary mixture of PCB126 and PCB118; and resulted in an increasing of uterine squamous cell carcinoma uterine squamous cell carcinoma in the 300 ng/300 μg/kg core group that received the binary mixture of PCB126 and 153 and in a clearly increasing incidence of uterine carcinoma in the 1000 and 4600 μg/kg PCB118 core group and the 4600 μg/kg stop group. In the studies of PCB 126, the tertiary mixture, and the binary mixture of PCB126 and PCB118, no increased incidence of any change occurred in the reproductive systems. The range of changes seen with the different compounds suggests that more than one mechanism may have been involved in promoting the female reproductive pathology.
			Hardell, L. et al. 2004 [26]	Case control study where it was analyzed the adipose tissue concentration of HCB, p,p’-DDE, chlordanes and polybrominated biphenyls in 76 cases with endometrial cancer and 39 controls with benign endometrial hyperplasia suggesting an interaction between p,p’-DDE and estrogen replacement drugs in the etiology of endometrial cancer, although no significant associations were found.
			Weiderpass, E. 2000 [57]	Case Control study where was measured serum concentrations of 10 chlorinated pesticides and 10 PCB congeners in 154 endometrial cancer and 205 population controls and resulted a no significant associations of increasing levels of pesticide or PCB exposure with endometrial cancer risk.
			Sturgeon, S.R. 1998 [54]	Multicenter case-control study: the findings did not support the hypothesis that organochlorine compounds are linked to the development of endometrial cancer.
			Adami 1995 [53]	Review that summarizes the evidence regarding whether certain organochlorine compounds increase the risk of breast and endometrial cancers through their estrogenic potential and resulted that no analytic epidemiologic studies of endometrial cancer were published at that data.
			Ahlborg 1995 [52]	Review that summarizes the evidence regarding whether certain organochlorine compounds increase the risk of breast and endometrial cancers through their estrogenic potential and resulted that the hypothesis that human exposure to environmental levels or organochlorines would favor an estrogenic overactivity leading to an increase in estrogen-dependent formation of mammary or endometrial tumors is not supported by the existing in vitro, animal and epidemiological evidence.