In contrast to electrophysiologic studies probing the auditory and visual modality, olfactory ERPs have rarely been used due to methodological challenges linked to the precise timing of odor stimulation (e.g., Lorig, 2000), but the limited evidence suggests that abnormal olfactory ERPs may be a vulnerability marker for schizophrenia. Compared to healthy controls, schizophrenia patients showed reduced N1 and P2 amplitudes to three different concentrations of hydrogen sulfide (H2S) despite similar ratings of odor intensity (Turetsky et al., 2003a), and similar reductions of N1 (left nostril only) and P2 (bilaterally) were observed in first degree relatives of patients with schizophrenia (Turetsky et al., 2008). Moreover, family members had increased odor detection thresholds for the left nostril, and showed poorer odor identification for both nostrils as measured by the University of Pennsylvania Smell Identification Test (UPSIT; Doty et al., 1984), thereby supporting smell identification deficit as a candidate endophenotype for schizophrenia (Brewer et al., 2003). Using an odor detection task with two concentrations of H2S, we replicated and extended olfactory ERP findings for schizophrenia patients (Kayser et al., 2010). The patients (n
