Nitrate is a leading drinking water contaminant in Australia. Recent epidemiological studies have linked nitrate in drinking water to low birth weight, preterm birth, and increased congenital anomalies. However, there is a lack of evidence to support these associations. To address this, we established a rat model of pregnancy whereby female Wistar rats (n=6-10/group) had 0 (control), 50 or 100mg/L (Australian safety threshold for adult consumption) of sodium nitrate added to their drinking water four weeks before timed mating, until weaning. One cohort was investigated at 21 days of gestation (E21) to assess fetal and placental development. Birth outcomes of a second cohort were characterised, followed by offspring neurodevelopmental and behavioural testing. At E21, male offspring in the 50mg/L group were 5% lighter (P=0.0008) with 7% heavier placentas (P=0.016) than control. In contrast, male weights were not significantly altered in the 100mg/L group. Female placental weights showed more variability in the 100mg/L group than the control and 50mg/L groups (P=0.0047). In cohort 2, timing of birth was unaffected, but a third of births in the 100mg/L group were complicated due to substantially overgrown fetuses. At 7 and 14 days of age, female offspring were 10% and 3% heavier respectively (P=0.0021 and P=0.0227) and male offspring weight was more variable in the 50 and 100mg/L groups compared to the control (P=0.0224 and P=0.0006), although these differences disappeared by 21 days of age. Exposure to 100mg/L nitrate impaired neurodevelopment at 14 days of age, and in adulthood, increased anxiety-like behaviour in male offspring, as assessed by elevated plus maze. Maternal and offspring metabolic parameters, such as blood glucose, were marginally affected. These outcomes highlight that nitrate contamination in the drinking water of pregnant people has implications for offspring growth and neuropsychiatric outcomes in later life.