AbstractEuropean carp (Cyprinus carpio) exposed to highly treated pulp mill effluent in Lake Coleman, a shallow‐water lake in southern Victoria, Australia, had significantly elevated hepatic microsomal EROD levels relative to reference fish from a nearby unexposed water body (Dowds and Heart morasses). Mean hepatic microsomal EROD activity appeared to be correlated with site adsorbable organic halogen (AOX) levels, with a simple linear regression yielding the equationY= 0.059X+ 1.415 (r2= 0.93,n= 5), whereYis mean EROD activity in nanomoles per minute per milligram andXis mean AOX concentration in micrograms per liter. Mean liver EROD activity was poorly related with fish muscle‐tissue extractable organic halogen (EOX) and sediment EOX concentrations. Hepatic microsomal EROD activity also appeared to be correlated with the low levels of PCDD/PCDFs measured in carp muscle (1.0‐4.0 ppt TCDD international toxic equivalents (TEs) in effluent‐exposed fish muscle compared to 0.48‐0.64 ppt TEs in reference fish muscle). Simple linear regression of mean EROD activity in carp liver with the mean fish muscle dioxin content yielded the equationY= 6.514X+ 5.754 (n= 4,r2= 0.88), whereYis mean EROD activity in nanomoles per minute per milligram andXis mean dioxin concentration in ppt of TCDD TEs. Hepatic microsomal ECOD activity, however, was not significantly different at any exposure site from the reference sites. Overall, Lake Coleman contained between 4.5 and 9.3 times the water AOX levels, 0.8 and 13.7 times the sediment EOX levels, 1.5 and 2.2 times the carp muscle‐fat EOX levels, 5.0 and 5.3 times the carp whole‐muscle TCDD toxic equivalents, and 6.5 times the carp fat TCDD toxic equivalents, compared to the Dowds and Heart morass reference samples. Within Lake Coleman, mean liver microsomal EROD activity levels were 2.3 to 6.3 times higher than the Dowds and Heart reference sites, respectively. Tissue concentrations of PCDD/PCDF and water AOX levels reduced with increasing distance from the effluent point source. Carp liver microsomal EROD represented a good biomarker of exposure to low levels of organochlorine contaminants from well‐treated pul