The AOP describes the effects of inhibition of iodothyronine deiodinase 1 (DIO1) on posterior swim bladder inflation in fish leading to reduced young of year survival and population trajectory decline. DIO1 and DIO2 are thryoid hormone (TH) activating deiodinases that convert thyroxin (T4) to the more biologically active 3,5,3′-triiodothyronine (T3). The inhibition of DIO1 results in decreased circulating concentrations of T3 in serum. Disruption of the TH system is increasingly being recognized as an important mode of action that can lead to adverse outcomes, especially during embryonic development. In fish, many different adverse effects during early development resulting from disruption of the TH endocrine system have been reported (e.g., effects on body and eye size, head-to-trunk angle, heartbeat, otolith formation, pigmentation index, swim bladder inflation, hatching time, somite formation, escape response and photoreceptor development). As in amphibians, the transition in fish between the different developmental phases, including maturation and inflation of the swim bladder, have been shown to be mediated by THs. Chemicals interfering with the conversion of T4 to T3 by inhibiting DIO1 have the potential to inhibit posterior chamber inflation which may result in reduced swimming capacity of the fish, a relevant adverse outcome that can affect feeding behaviour and predator avoidance, resulting in lower survival probability and ultimately population trajectory decline. The current state of the art suggests that DIO2 is more important than DIO1 in regulating posterior chamber inflation. Therefore the corresponding AOP leading from DIO2 inhibition to reduced young of year survival via posterior swim bladder inflation may be of higher biological relevance compared to the AOP that is described here.