The present study is part of an ongoing effort to monitor the pollution situation in the inner Oslofjord. The purpose of the study was to investigate effects of pollutants on the resident cod population in the area. The outer Oslofjord was used as a reference site. Several biomarkers were used in order to detect exposure and effects of a broad range of environmental chemicals, including planar organic and inorganic pollutants, and possibly organophosphate and carbamate pesticides. The physiological indices: condition factor, liver somatic index (LSI) and gonadal somatic index (GSI) were used to assess the overall condition, energy reserves, as well as to provide information on reproductive status. Age and size of the fish were used to study possible differences in growth rate of cod from the two areas. There was also a method-optimizing aspect to this study, with regards to the comet assay used to assess DNA damage. Of interest was whether storage duration of samples on lysis buffer would affect the level of DNA damage. As indicated by elevated bile concentrations of polycyclic aromatic hydrocarbons (PAHs), concentration and activity of cytochrome P4501A (CYP1A) and DNA damage as well as decreased activity of δ-aminolevulinic acid dehydratase (ALA-D), cod from the inner Oslofjord appear to be affected by planar organic pollutants, such PAHs and polychlorinated biphenyls (PCBs) as well as inorganic pollutants, such as lead (Pb). Cod from the outer Oslofjord seem to be more affected by chemicals that inhibit acetyl cholinesterase, e.g. organophosphate and carbamate pesticides, compared to cod from the inner Oslofjord. Also, exposure of leukocytes to hydrogenperoxide (H2O2) revealed a higher tolerance to oxidative stress, with regards to DNA damage, in cod from the inner Oslofjord compared to cod from the outer Oslofjord. This indicates an adaptive response to chronic exposure to chemicals causing oxidative stress. Physiological indices revealed higher energy reserves at the time of sampling in cod collected from the inner Oslofjord compared to the outer Oslofjord. Growth rate appeared to be slower in the inner Oslofjord, but could not be tested statistically since the size ranges collected only made it possible to compare two-year old individuals. Elevated DNA damage appeared to have resulted from longer storage duration of samples on lysis buffer during the comet assay procedure. This suggests that treatment with lysis buffer may cause elevated levels of DNA damage over the background damage.