Reports of the effects of alcohol on the human placenta have mostly concentrated on term tissue which may not be adequately representative of the early stages of pregnancy, when optimal placental development is critical, and when women are more likely to consume alcohol due to unrecognised pregnancy. Furthermore, much of the experimental work is toxicologically focused, with levels of alcohol equivalent to extremely high exposure. The current study aimed to examine the effects of ethanol and its metabolite acetaldehyde on the growth and function of first trimester placenta. Affecting cellular turnover and migration in the first trimester human placenta and cytotrophoblast. We also hypothesized a detrimental effect on the placental transport systems for amino acids important in fetal growth and development – system A and system b. System b activity is of particular interest as it transports taurine, an essential amino acid in pregnancy that is important for fetal neurodevelopment. The first trimester of pregnancy is crucial for placental development, which in turn provides for organogenesis and fetal growth. To set clinically relevant experimental concentrations, we examined the literature on circulating alcohol concentrations that might be achieved during binge drinking. A blood alcohol concentration of 0.08% by volume is the defined intoxication limit for driving in the UK and USA. Literature on peak blood-alcohol suggests that 40 mM causes intoxication in a normal population; 40 mM alcohol can result from an exposure equivalent to 4–5 units. The average peak blood acetaldehyde concentration is in the range 26–43 mM. Pharmacological studies in animals have used as much as 50–100 mM ethanol AG-013736 administered daily. We have shown that ethanol or acetaldehyde at clinically relevant concentrations has adverse effects on two key aspects of trophoblast function: proliferation and nutrient transport. These placental effects suggest potential mechanisms by which maternal alcohol consumption could impact on fetal development. Placental insufficiency, diagnosed at term, has been documented as a leading cause of FGR, and growth restriction is associated with extreme chronic level alcohol consumption. Although genetic differences in alcohol metabolism generates conflicting data in human pregnancies, placentas obtained from women who have consumed alcohol during pregnancy contain more villous infarction, thrombosis and vascular abnormalities, compared to non-exposed pregnancies. Furthermore, trophoblast proliferation is reduced in FGR. Primary cultured cytotrophoblasts rapidly exit the cell cycle, but we have shown that proliferation can be studied in placental explant cultures which retain the naturally occurring polarity and intrinsic environment of the trophoblast epithelium. Our results indicate that ethanol above 20 mM and acetaldehyde at 40 mM attenuated cytotrophoblast but not stromal cell proliferation in first trimester placental tissue.