PURPOSE: Prenatal alcohol exposure (PAE) is a leading cause of persistent neurodevelopmental disability, with additional adverse consequences to the offspring's growth, metabolism, cardiovascular health, and immunity, among others. Alcohol disrupts offspring development through myriad mechanisms, many of which involve direct interactions between alcohol and the embryo and fetus (i.e., the conceptus). This limited narrative review instead focuses on mechanisms that are exogenous to the fetus. Many of these are relatively unexplored and are also mechanistically interrelated. Thus, they represent novel opportunities for the design of interventions that ameliorate alcohol-related pathologies. SEARCH METHODS: Literature from 2020 to October 2024 was searched using the terms "fetal alcohol spectrum disorder"[MeSH] OR "fetal alcohol"[Ti/Ab] with the filter "review." These reviews were inspected to extract nonfetal mechanisms of alcohol. Literature from 2000 to October 2024 was then searched in PubMed, Embase, and Google Scholar for seven mechanisms, using the search terms "fetal alcohol spectrum disorder OR fetal alcohol" AND one of the following: "placenta," "paternal," "metabolism OR insulin OR amino acid," "inflammation OR neuroinflammation OR cytokine," "epigenetic," "iron OR iron deficiency OR anemia," "microbiome." Only primary research articles, both clinical and preclinical, were included. SEARCH RESULTS: The literature scan identified seven mechanisms for which targeted literature searches were conducted. These searches yielded relevant studies that explored mechanisms involving the microbiome ( = 5 studies), inflammation ( = 72 studies), epigenetics ( = 30 studies), paternal alcohol exposure ( = 34 studies), placenta ( = 53 studies), metabolism ( = 37 studies), and functional iron deficiency ( = 23 studies). DISCUSSION AND CONCLUSIONS: Exogenous mechanisms of alcohol's teratogenicity are intertwined. Alcohol remodels the maternal enteric microbiome, with potential consequences to fetal immune function, nutrient availability, and brain development. Microbial endotoxins may further magnify alcohol's proinflammatory actions. This inflammation might also drive a fetal anemia associated with PAE. Alcohol alters maternal and fetal metabolism and could limit fetal nutrient availability. This altered metabolism could also reprogram placental and fetal epigenetics, as could paternal exposure to alcohol. Both epigenetic effects and inflammation can impair placental function and modulate the placenta-brain axis that modulates brain development. The review discusses limitations in the current understanding of these mechanisms and highlights future research avenues that would provide clarity and inform future interventions.