The Lancet Commission on pollution and health

9.2. Protein-Based Hg(II) Detectors 3467 9.3. Oligonucleotide-Based Hg(II) Detector 3467 9.4. DNAzyme-Based Hg(II) Detectors 3469 9.5. Antibody-Based Hg(II) Detector 3469 10. Mercury Detectors Based on Materials 3469 10.1. Soluble and Fluorescent Polymers 3469 10.2. Membranes, Films, and Fibers 3471 10.3. Micelles 3473 10.4. Nanoparticles 3473 11. Perspectives 3474 12. Addendum 3475 12.1. Small Molecules 3475 12.2. Biomolecules 3477 12.3. Materials 3477 13. List of Abbreviations 3477 14. Acknowledgments 3478 15. References 3478

Tools and tactics for the optical detection of mercuric ion.

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(06)69665-7.pdf

Developmental neurotoxicity of industrial chemicals

The paper builds on existing literature, highlighting current understanding and identifying unresolved issues about MeHg exposure, health effects, and risk assessment, and concludes with a consensus statement. Methylmercury is a potent toxin, bioaccumulated and concentrated through the aquatic food chain, placing at risk people, throughout the globe and across the socioeconomic spectrum, who consume predatory fish or for whom fish is a dietary mainstay. Methylmercury developmental neurotoxicity has constituted the basis for risk assessments and public health policies. Despite gaps in our knowledge on new bioindicators of exposure, factors that influence MeHg uptake and toxicity, toxicokinetics, neurologic and cardiovascular effects in adult populations, and the nutritional benefits and risks from the large number of marine and freshwater fish and fish-eating species, the panel concluded that to preserve human health, all efforts need to be made to reduce and eliminate sources of exposure.

Methylmercury exposure and health effects in humans: a worldwide concern.

Mercury pollution poses global human health and environmental risks. Although mercury is naturally present in the environment, human activities, such as coal burning, have increased the amount of mercury cycling among the land, atmosphere, and ocean by a factor of three to five. Emitted to the atmosphere in its elemental form, mercury travels worldwide before oxidizing to a form that deposits to ecosystems. In aquatic systems, mercury can convert into methylmercury, a potent neurotoxin. People and wildlife are exposed to methylmercury as it bioaccumulates up the food chain. Mercury continues to circulate in the atmosphere, oceans, and terrestrial system for centuries to millennia before it returns to deep-ocean sediments. Areas of uncertainty in the global biogeochemical cycle of mercury include oxidation processes in the atmosphere, land-atmosphere and ocean-atmosphere cycling, and methylation processes in the ocean. National and international policies have addressed direct mercury emissions, but further...

Global Biogeochemical Cycling of Mercury: A Review

Minamata disease (M. d.) is methylmercury (MeHg) poisoning that occurred in humans who ingested fish and shellfish contaminated by MeHg discharged in waste water from a chemical plant (Chisso Co. L...

Minamata disease: methylmercury poisoning in Japan caused by environmental pollution

On November 9, 1963, during the afternoon shift change at the Miike coal mine, eight rail cars filled with coal broke free and fell 360 meters [1]. The impact ignited coal dust in the mine and set off two explosions, killing 20 people immediately and trapping nearly 1,400 other workers up to 450 meters below the surface and 8 kilometers from the mine entrance. The explosion damaged electrical and telephone lines, but the ventilation fan continued to operate and spread carbon monoxide throughout the mine [1].

Long-term eff ects of carbon monoxide poisoning at Miike coal mine: A 33-year follow-up study

On November 9, 1963, a coal dust explosion occurred at the Miike Mikawa Coal Mine (Omuta, Kyushu Region of Japan). This resulted in a massive release of carbon monoxide (CO) gas that resulted in 458 fatalities and 839 victims of CO poisoning. After the accident, the Department of Neuropsychiatry, Kumamoto University School of Medicine (including the authors) immediately began to conduct periodic medical examinations of the victims. Such a long-term follow up of so many CO-poisoned patients is globally unprecedented. When the Miike Mine was closed in March of 1997, 33 years after the disaster, we conducted the final follow-up study.

Masazumi Harada

Papers

Minamata disease: methylmercury poisoning in Japan caused by environmental pollution

Long-term eff ects of carbon monoxide poisoning at Miike coal mine: A 33-year follow-up study

Long-term effects of carbon monoxide poisoning at Miike coal mine: A 33-year follow-up study.