However, harman and norharman make up less than 1/10th of the total direct MAO inhibitory activity in tobacco smoke ( Truman et al., 2017 ) so the opportunity for other MAOIs in tobacco smoke to contribute substantially to the MAO activity reduction seen in smokers must exist. No irreversible MAO inhibitors have yet been reported from tobacco or tobacco smoke. The question of whether MAO inhibitors in tobacco smoke can affect behaviour remains unresolved. As well as the potential for effects on addiction, MAO enzymes are drug targets for a variety of neurological disorders including depression, mood, anxiety, attention deficit hyperactivity, Tourette’s syndrome, Parkinson’s disease and Alzheimer’s disease ( Sharama, 2016 ; Borroni et al., 2017 ). Of the known MAO inhibitors in tobacco smoke, high concentrations of harman and norharman can affect responses to nicotine ( Harris et al., 2020 ) and may act as antidepressants ( Farzin and Mansouri, 2006 ; Smith et al., 2013 ) in animals. However, when used in amounts relevant to smokers, they were not seen to affect rat self-administration of nicotine ( Smith et al., 2015 ) and no pharmacological effects have been reported from the known tobacco MAO inhibitors at physiologically relevant concentrations. In contrast, use of tobacco smoke extracts in self-administration or intracranial self-stimulation experiments has been found to affect responses to nicotine ( Harris et al., 2010 ; Costello et al., 2014 ; Brennan et al., 2015 ). This discrepancy may be in part because the full range of tobacco smoke MAO inhibitors has not yet been identified. It has also been suggested that further MAO inhibitory activity is formed from smoke components in the body. Acetaldehyde is formed during tobacco combustion, from the sugars in the plant material, and from sugars added as humectants and flavour additives during tobacco and cigarette manufacture. Acetaldehyde is typically present in cigarette smoke amounts ranging from 0.6 to over 2