The reproductive effects of MeHg have not been fully evaluated in humans, but animal studies, including work in nonhuman primates, indicate that MeHg causes functional reproductive effects.

Damage to the renal tubules and nephron has been observed following human exposure to inorganic and organic forms of Hg. However, symptoms of renal damage have been seen only at Hg exposures that also caused neurological effects. In animals, similar effects have been observed as well as altered renal function and renal hypertrophy have been observed following early postnatal exposure to MeHg.

Although the data base is not as extensive for cardiovascular effects as it is for other end points (i.e., neurotoxic effects), the cardiovascular system appears to be a target for MeHg toxicity in both humans and animals. Evidence suggests that adverse health effects can occur at very low Hg exposures.

• Exposure to elemental and organic forms of Hg alters blood-pressure regulation. That effect has been documented in children and adults who were exposed to toxic and subtoxic doses of Hg and have been induced experimentally in rats.

• Prenatal exposure to MeHg has been shown to alter blood-pressure regulation and heart-rate variability in children. Those effects were observed at cord-blood Hg concentrations that have not been associated with other developmental effects (less than 10 µg/L).

• Men who consumed at least 30 g of fish per day or had a hair Hg concentration of 2 ppm or more had a higher risk of suffering a fatal or nonfatal acute myocardial infarction. Mercury exposure was also correlated with an increased risk of dying from coronary heart disease or cardiovascular heart disease. A hair Hg concentration of 2 ppm has not been associated with other adverse health effects.

The human data base on the neurodevelopmental effects of MeHg is extensive, and includes studies of populations following high-dose Hg poisonings and chronic low-dose Hg exposure. Some study results appear to be conflicting. Table 5-10 provides informa