Furthermore, isothiocyanato-cyclohexane was characterised as a common environmental pollutant and its increase in HE patients was attributed to impaired liver catabolism, whereas increased 1-methyl-4-(1-methylethenyl)-benzene levels again in HE patients may have originated from an enhanced aromatase activity due to extensive alcohol abuse that could have been responsible for changes in metabolism. Here, CYP19A1 is linked to alcohol abuse.