The blood of my veins - mercury, Minamata and the soul of Japan.

The methylmercury contamination of Minamata Bay during the WWII postwar period resulted in thousands of Japanese citizens suffering horrific neurological injury. Fear and miscommunication destroyed and changed family and social structure. In addition, the Minamata poisoning caused momentous changes in the civic discourse in Japan and was an instrumental event in the democratization of the country. This manuscript describes the effects that the environmental contamination and human poising had in the transition of Japan from a feudal society to a democratic one.

Historical and other patterns of monomethyl and inorganic mercury in the Florida panther (Puma concolor coryi).

Since the late 1980s, elevated levels of mercury have been reported in the tissues of the Florida panther (Puma concolor coryi) from the Florida Everglades. The extent, degree, and length of time of mercury contamination in the Florida panther are unknown. The objective of this study was to determine the historical and other patterns of monomethyl and inorganic mercury in the Florida panther by analysis of mercury in panther hair from museum collections. In addition, this study evaluated the effects of preservation of skins on mercury concentrations in hair and the representativeness of museum collections for evaluating historical trends of contamination in the Florida panther. Hair from 42 Florida panther specimens collected from 1896 to 1995 was analyzed for both monomethyl and inorganic mercury. Monomethyl mercury (MMHg) and inorganic mercury (IHg) were found in all specimens. Monomethyl mercury in hair from untanned skins was significantly higher than MMHg in hair from tanned skins. For untanned specimens, the mean MMHg concentration in hair was 1.62 +/- 1.87 mug/g (range 0.11 to 6.68 mug/g, n = 16). Monomethyl mercury accounted for 88% of the total mercury in untanned Florida panther hair. No sexual or geographical differences were found. Although MMHg is generally stable in hair, the tanning process appears to reduce the amount of MMHg in hair. In addition, exogenous IHg contamination of the panther hair was found in museum specimens, especially in older specimens. The implication of these and other factors in interpreting results of museum studies is discussed. The presence of MMHg in panther hair since the 1890s indicates long-term and widespread exposure of the Florida panther to mercury. Levels of MMHg are significantly greater in the 1990s than the 1890s. When combined with field studies of mercury in the Florida panther, considerable individual variability is observed, reflecting short-term changes in exposure of individual panthers to mercury. Although museum specimens showed a significant increase in MMHg over the last 100 years, they did not show the magnitude of increase that field populations of Florida panthers did. A number of Florida panthers appeared to be at risk from mercury over their lifetimes, especially individuals from the early 1990s.

A historical record of mercury contamination in Southern Florida (USA) as inferred from avian feather tissue.

During the late 1980s, the upper trophic-level biota of the Everglades (FL, USA) was recognized as being highly contaminated with mercury (Hg). However, the timing and pattern of that increase is poorly known, and no information is available about mercury contamination in Everglades wildlife prior to 1974. We measured methylmercury concentrations in feathers of white ibises (n = 33), great egrets (n = 7), anhingas (n = 21), and great blue herons (n = 12) from museum specimens collected from 1910 through 1980 and combined them with more recent feather samples collected from live birds (1985-2000, n = 98, 37, 49, and 7, respectively). We found no evidence of contamination of museum samples with inorganic mercuric preservatives (0.01-0.28% of total Hg in feathers). All species showed relatively low concentrations of mercury through the 1970s (<5 microl/L dry wt for anhingas, ibises, and egrets, <10 microl/L for herons). Samples from all species taken during the 1990s showed a large and significant increase (4-5X) in MeHg concentration. This evidence suggests that most of the increase in Hg deposition during the 20th century in south Florida occurred during the last two to three decades, which is consistent with information about local source deposition. Contamination levels prior to the 1970s appear to have been associated with normal reproduction in these birds, suggesting partial evidence for a threshold of reproductive impairment.

Mercury exposure and child development outcomes.

Mercury is ubiquitous in the global environment, ensuring universal exposure. Some forms of mercury are especially neurotoxic, including clinical signs at high doses. However, typical human exposures occur at low to moderate doses. Only limited data about neurotoxicity at low doses are available, and scientists differ in their interpretation. Dose-response data on neurodevelopment are particularly limited. Despite or perhaps because of the lack of sufficient or consistent scientific data, public concern about a link between mercury exposure and developmental disabilities has been rising. After reviewing the data, the US Environmental Protection Agency proposed a reference dose (an estimate of a daily dose that is likely to be without a risk of adverse effects over a lifetime) for methyl mercury that is substantially lower than previous guidelines from the World Health Organization, the US Agency for Toxic Substances and Disease Registry, and the US Food and Drug Administration. Some questions have been raised about the Environmental Protection Agency's guidelines, but the issue remains unresolved. Meanwhile, consumer groups have raised questions about the potential link between mercury exposure and autism spectrum disorders as well as other adverse neurodevelopmental outcomes. This hypothesis has prompted some parents to seek regulatory, legal, or medical remedies in the absence of firm evidence. This article reviews what is known about mercury neurotoxicity and neurodevelopmental risk. Our intent is to focus the debate about mercury on 1) additional research that should be sought and 2) defining the principal issues that public policy makers face.

The need for empirically derived permeation data for personal protective equipment: the death of Dr. Karen E. Wetterhahn.

Personal protective equipment (PPE) is an essential component in any occupational health and safety program. The appropriate selection and use of PPE can help prevent or limit exposure to hazardous materials. The inappropriate selection or use of PPE can lead to unnecessary exposure or --with extremely hazardous materials--serious harm including death. In 1997, Dr. Karen E. Wetterhahn died from mercury poisoning resulting from a single exposure to dimethylmercury almost a year before. Her death raised numerous questions as to how this tragedy occurred and what could be done to protect against a chemical as dangerous as dimethylmercury. This article provides a brief review of the case and discusses the glove permeation testing done during the course of the accident investigation. Using this case as an example, the author argues that all recommendations for PPE be based on empirical testing using accepted methods and that this information be readily available.

Long ago and far away: a retrospective on the implications of Minamata.

Minamata claimed entry into the lexicon of toxicology 40 years ago as a definition of methylmercury poisoning, but deposited a legacy of unsolved puzzles that still endures. In fact, they scatter ramifications across the entire domain of neurotoxicology. One puzzle is how the earliest clinical index of adult toxicity, paresthesia, can remain stable, even with continued exposure. Does damage, like body burden, reach a plateau? A second enigma is the question of silent damage to nerve cell populations even more vulnerable than those whose loss of function results in minimal symptoms such as paresthesia. Is there a population of unidentified humans exposed to methylmercury whose deficits might be uncloaked by neurobehavioral test methods that have succeeded in revealing silent toxicity in populations exposed to lead, manganese, and elemental mercury? A third puzzle arises in the context of aging. Attrition of nerve cells occurs naturally as the brain ages, but is also accompanied by dendritic sprouting in those that remain. Damage incurred earlier in life, as in mild polio infections that seemed to fade, may emerge late in life in the form of the post-polio syndrome. Most explanations ascribe the syndrome to compensatory dendritic sprouting by surviving neurons and the consequent metabolic overload imposed on them. Could parallel processes be induced by neurotoxicants such as methylmercury? Or, alternatively, might the compensatory sprouting accompanying aging be inhibited by neurotoxic agents? All such questions have a bearing on how the risks of low-level exposures are evaluated.