ing incidents in Japan, Iraq, and the United States, in which the first signs of toxicity often appear several months after exposure has ended (EPA 1997b, Davis et al. 1994).

There is evidence that MeHg also effects other systems. In 1995, researchers in Finland found a correlation between consumption of MeHg-contaminated fish and the risk of acute myocardial infarction (Salonen et al., 1995). This prospective study of 1,833 fishermen was intended to confirm previous studies in which fish consumption was associated with a reduced risk of heart disease. Instead, they discovered that hair Hg levels above 2 parts per million (ppm), or daily ingestion of more than 30 grams (g) of fish, increased the risk of acute myocardial infarction (AMI) or cardiovascular death 2- to 3-fold. The estimated daily dietary Hg intake ranged from 1.1 µg to 95.3 µg (mean, 7.6 µg). The investigators theorized that the cardiovascular effects of MeHg might be caused, at least in part, by the ability of Hg to enhance lipid peroxidation via a Fenton-type reaction.

Inorganic and organic forms of Hg are also well-known renal toxicants. Human case investigations and animal feeding studies have repeatedly confirmed that effect. Human exposures to organic Hg have resulted in symptoms of polyuria and albuminuria (Jalili and Abbasi 1961; Cinca et al. 1979). Autopsies of patients who died following ingestion of alkyl Hg revealed nephritis and tubular degeneration (Al Saleem 1976; Cinca et al. 1979). Animal studies have shown that MeHg damages the proximal tubules in the kidney (Mitsumori et al. 1990).

During the past decade, researchers have studied the effects of MeHg on immune function and blood-pressure regulation. After administering MeHg to mice for 12 weeks, IIbäck (1991) noted changes in the thymus and natural killer-cell activity. Sørensen et al. (1999) found an association between prenatal exposure to MeHg and childhood blood pressure. Diastolic and systolic blood pressures, measured at age 7, increased 13.9 millimeters (mm) and 14.6 mm, respectively, as cord-blood Hg concentrations rose from 1 to 10 micrograms per liter (µg/L).

Between 1950 and 1975, several MeHg poisoning incidents occurred in Japan and Iraq. Scientists who investigated those events identified