The aryl hydrocarbon receptor (AhR) binds many structurally different ligands including natural endogenous and exogenous compounds, as well as certain active pharmaceutical substances and environmental pollutants. We can be potentially exposed to some of these compounds during medical treatments or through the environment. First, we conducted a review of the literature and databases to make a selection of active pharmaceutical substances and environmental pollutants known to modulate AhR activity. We then investigated at what concentrations these compounds exert modulatory effects on AhR and compared them to the concentrations to which we may actually be exposed. We discovered that seven active substances, namely ketoconazole, leflunomide, omeprazole, ciprofibrate, thiabendazole, niclosamide and nitazoxanide, with experimentally determined AhR activity, can modulate AhR at therapeutic plasma concentrations. Only six environmental pollutants of 27 tested, can modulate AhR at plasma concentrations measured in exposed humans, namely PCB 126, benzo[a]pyrene, dehydroimidacloprid, pentachlorophenol, bentazone and diuron. We also discovered that only one of the studied components of personal care products to which we are exposed via soaps, toothpastes and deodorants is able to modulate the AhR receptor under realistic exposure conditions. The three natural ligands that can modulate the AhR receptor under realistic exposure conditions are resveratrol, kaempferol, and coumestrol. We calculated the binding of these compounds using the VirtualToxLab, which enables in silico assessment of AhR-binding capacity of compounds, we calculated the binding affinities of these compounds to the investigated receptor and found that the results mostly do not correlate with the experimental values determined in vitro. The findings obtained within the scope of this Master's thesis indicate that many compounds to which we are exposed both intentionally (pharmaceutical drugs, natural compounds from our diet, components of personal care products) as well as unintentionally (environmental pollutants) modulate the level of AhR activation. As a result, they have the potential to cause many diverse effects, particularly in the gastrointestinal tract, the immune system and the central nervous system.