Preliminary data suggest that venlafaxine environmental concentrations could be toxic to plants

Venlafaxine hydrochloride is a structurally novel antidepressant. Its occurrence in surface waters and drinking water has only been reported in recent works. The aim of this work is to assess the acute and chronic sublethal toxicity of venlafaxine in relevant taxa of riparian ecosystems. We used the fern Polystichum setiferum during the critical life stage of development. Reliable biomarkers of cell viability (mitochondrial activity), plant physiology (chlorophyll), and growth (DNA content) were assessed as sensitive endpoints of toxicity. About DNA quantification, our results show that venlafaxine induces acute lethal phytotoxicity at 24 and 48 h (LOECs 1 μg L−1 and 0.1 μg L−1, respectively). At 24 h, hormetic effects in spores of P. setiferum mitochondrial activity mask lethality and adverse effects are observed (LOEC 1 μg L−1). At 48 h a reduction in the mitochondrial activity happens (LOEC 10 μg L−1). In chronic exposure of 1 week, LOEC for DNA is 0.1 μg L−1. Mitochondrial activity showed a strong hormetic stimulation of a surviving spore population (LOEC 10 μg L−1). Changes were not observed in chlorophyll autofluorescence. Environmental concentrations of venlafaxine can be deleterious for the development of significant populations of sensitive individuals in riparian ecosystems.

► Venlafaxine can cause acute lethal toxicity in higher plant development.
► Venlafaxine can cause chronic sublethal toxicity in higher plant development.
► Evidence of the need to take hormetic effects into account when assessing toxicity.