N	Concordance
1	 ability to convert external dosages of dioxin to tissue concentrations. Intersp
2	atogenicity via the aryl hydrocarbon or dioxin receptor. While most potent agoni
3	the levels of polychlorinated dibenzo-p-dioxin toxic equivalency factors (TEFs) 
4	 identified as metabolites of dibenzo-p-dioxin and dibenzofuran, respectively, i
5	nzofuran (OCDF) and octachlorodibenzo-p-dioxin (OCDD) to early-life stages of ze
6	xposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds is c
7	 with [3H] 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the presence of canthax
8	al role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in uterine growth utilizin
9	d subsequent complex formation with the dioxin response element (DRE), an upstre
10	t appear to be directly linked with the dioxin dioxygenase genes. Rather, it is