Methylmercury, the causative agent of Minamata disease, can easily penetrate the brain, and adult-type Minamata disease patients showed neurological symptoms according to the brain regions where the neurons, mainly in the cerebrum and cerebellum, were damaged. In addition, fetuses are exposed to methylmercury via the placenta from maternal fish consumption, and high-level exposure to methylmercury causes damage to the brains of infants. Typical patients with fetal-type Minamata disease (i.e., serious poisoning caused by in utero exposure to methylmercury) were born during the period of severe methylmercury pollution in 1955-1959, although they showed no abnormality during gestation nor at delivery. However, they showed difficulties in head control, sitting, and walking, and showed disturbances in mental development, these symptoms that are similar to those of cerebral palsy, during the growth periods after birth. The impaired development of fetal-type Minamata disease patients was one of the most tragic and characteristic feature of Minamata disease. In this review, we first summarize 1) the effects of prenatal methylmercury exposure in Minamata disease. Then, we introduce the studies that were conducted mainly by Sakamoto et al. as follows: 2) a retrospective study on temporal and regional variations of methylmercury pollution in Minamata area using preserved umbilical cord methylmercury, 3) decline in male sex ratio observed in Minamata area, 4) characteristics of hand tremor and postural sway in fetal-type Minamata disease patients, 5) methylmercury transfer from mothers to infants during gestation and lactation (the role of placenta), 6) extrapolation studies using rat models on the effects of prenatal methylmercury exposure on the human brain, and 7) risks and benefits of fish consumption.
Keywords: Minamata disease; fetal-type Minamata disease; methylmercury; placental transfer.