Aquatic food chain mercury pollution is one of the consequences of the gold rush in the Amazon, which started in the late 1970s. This paper addresses the risks of methylmercury (MeHg) toxicity by a riverside population of heavy fish eaters along the Madeira river, in the Amazon, based on their hair mercury (Hg) concentration. Given the vulnerability of the developing nervous system, NOEL/LOEL values were used based on prenatal (LOELp = 0.7 microgram/ kg bw), and adult and childhood (LOELa = 3 micrograms/kg bw) Hg exposures. Based on hair Hg concentrations, we observed that approximately 95% of infants were at risk of absorbing Hg through the previous placental exposure, and/or by ingesting Hg from mother's milk, and/or fish consumption, at a level as great as the LOELp. The hazard quotient derived from the LOELp for neurobehavioral effects was 64 based on an estimated mean Hg daily intake of 4.5 micrograms/kg bw. Approximately 45% of the mothers of the infants and other women of child bearing age were at risk of ingesting Hg at a level equivalent to the LOELp. This also translates into a derived hazard quotient for neurobehavioral effects of 17 for all potential mothers in the population. The non-infant population at the highest risk was fish-eating children under 5 years old. This sub-population had a mean estimated Hg daily intake of 6.4 micrograms/kg bw. This resulted in a probability that almost 60% of this sub-population ingested Hg at a level equivalent to the LOELa or higher. For this sub-population, there was a hazard quotient of 21. These data strongly indicate that the young children of this riverside fish-eating population may be ingesting Hg doses that have been correlated with neurological damage from Hg poisoning.