Mercury; a planet, an ancient Greek god, or gum rot?

To answer my own question:

Aren't we humans on the top of our food chain and thereby subject to the
same problems of toxic accumulation?

A quick google reveals that gold mining is a mercury intensive activity. Patterns of high mercury accumulation have been showing up in people directly affected, by mining, and people indirectly affected, by eating contaminated food. As this abstract by Marcello M. Veiga and John A. Meech University of British Columbia, Department of Mining & Mineral Process Engineering explains:

HUMAN RISK AND HEALTH PROBLEMS

Mercury accumulation in humans has two main pathways in the Amazon: a) occupational exposure to vapours and b) methylmercury transferred by the fish.

Inhalation of mercury vapours is more significant for "garimpeiros" and gold shop workers. Once in the lungs, Hg is readily oxidized forming Hg (II) complexes which are soluble in many body fluids. As well, metallic Hg is also soluble in lipids allowing a rapid diffusion through the cell membranes (alveolar walls) followed by transport by blood lipids to sensitive tissues, such as the brain. The ultimate effect of Hg and related compounds is the inhibition of enzyme action.

From knowledge of metabolism and human experience with Hg inhalation, the critical organs are: (Suzuki, 1979)

lungs in short-term exposure to high levels,
kidneys in an exposure of moderate duration to considerable levels
brain in long-term exposure to moderate levels

Total elimination can take several years. The half-life of mercury in the brain is longer than in the kidney, thus urine Hg levels would not be expected to correlate with neurological findings once exposure has stopped. Short-term exposure to high levels causes clinical symptoms which mainly involve the respiratory tract. Hg levels in the urine of new workers should be lower than those of workers with a longer duration of exposure. (Suzuki, 1979; Stopford, 1979).

The symptoms usually associated with mercurialism are erethism (exaggerated emotional response), gingivitis, and muscular tremors. A person suffering from a mild case of Hg poisoning is usually unaware of the illness because the symptoms are psycho-pathological, such as irritability. Such ambiguous symptoms can lead to incorrect diagnosis (Jones, 1971; Cassidy and Furr, 1978).

A level of 60,000 µg/m³ was measured by Malm (1991) in the air when amalgam is burnt in pans. Urine samples have shown Hg levels >20 ppb for "garimpeiros" burning amalgam daily, whereas levels between 10 and 20 ppb were observed for those burning amalgams 2 or 3 times per week. Normal levels are below 10 ppb. Symptoms such as visual constriction, irritability, decreased memory and metallic taste were detected among the workers of gold shops in Alta Floresta (CETEM, 1991).

When intoxication takes places via food, in particular fish, most mercury is accumulated in methylated form (Huckabee, 1979, Padberg, 1990). High Hg levels (21 to 206 µg/l) have been found in the blood of individuals living distant of mining activities in the Amazon (GEDEBAM, 1992). Normal blood levels for unexposed people is 6 to 12 µg/l. A level of 200 µg/l (ppb) is reported as the lowest blood level observed in the Niigata incident in Japan, at which significant symptoms were observed (Nelson et al., 1971).

Fish caught in one Amazonian city showed Hg levels ranging from 0.009 to 2.75 mg/kg (ppm). If fish containing 0.5 ppm Me-Hg are eaten daily, the Allowable Daily Intake of 30 µg/day would be reached for a 70-kg person by the daily consumption of 60 g of fish. Considering the Canadian limit of 13 µg/day of any kind of Hg, 60 g of a fish with 0.2 ppm of Hg are enough to reach the limit (Kurland, 1973; GEDEBAM, 1992; CWQG, 1987).

Poisoning is not restricted to miners and high Hg concentrations in the blood of children (>100 ppb Hg) have been measured. Mercurialism symptoms are not clearly identified owing to differences in the amount of Hg burnt, fish consumed, fish origin as well other masking effects such as tropical diseases, alcohol consumption, etc. A level of 6 µg/g Hg in hair is reported as the typical concentration derived from weekly ingestion of 0.2 mg Me-Hg or a daily dose of 20 µg for adults. Fish-eating people living in remote areas in the Amazon not impacted directly by mining activity, show levels as high as 150 µg/g Hg in hair, but no classical Minamata disease has yet been recognized (Malm, 1991).

Fish and other seafood have long been recognised as sources of mercury, with the highest concentration confined to species that grow to relatively large size and/or have a relatively long lifespan,19 in particular, large predators such as tuna and shark. The government guidelines recommend that any shark over 18 kilo should not be caught, as it would contain mercury above the accepted safe level. Crustacea which feed on the sea-bed, where pollution tends to accumulate, may also have high levels. At present in Australia, the legal maximum limit for mercury content of fish is one half part per million (0.5 mg/kg averaged over a multiple sample of fish).