5.1 The myth, reality, and history of mercury toxicity  (Page 3/3)

It is interesting that the mention of the corrosive sublimate ; this is in fact mercury(II) dichloride (HgCl ₂ ) which unlike mercury(I) chloride (Hg ₂ Cl ₂ ), is a very violent poison. Death is caused by renal failure. So while there is no evidence for elemental mercury itself causing fatalities, its compounds are another matter to be considered.

Organomercury compounds

In 1953 it was noted that the fishing village of Minamata in Japan had an epidemic in which a large number of people died. Initial thoughts of either an infectious disease or malnutrition were discounted; then it was found that the fish eaten by the villagers was highly contaminated by mercury.

It was found that the mercury came from the Chisso Corporation chemical plant that made acetaldehyde from acetylene using a mercury catalyst. The plant was loosing 1 Kg of mercury metal for every ton of acetaldehyde being produced. As a consequence it was originally assumed that the poisoning of the village was due to inorganic mercury. Based upon prior incidents, an obvious response was to ban consumption of all fish and shellfish. As a consequence no new cases were reported, however, people already effected continued to die. This was unlike any previous mercury poisoning.

Further analysis showed small quantities of water soluble methyl mercury (MeHg ⁺ ) was present and sequestered by the shellfish to give MeHgSMe. While the lethal effects of organomercury compounds were known, the source of the methyl mercury was a mystery. A group of Swedish researchers showed that the bacterial action in river sediment or rotting fish converted inorganic mercury to either volatile Me ₂ Hg or water soluble MeHg ⁺ . With this discovery, it was understood how the anaerobic mud of the estuary near Minamata could perform this methylation.

Of course Minamata was not the first report or an organomercury compound, but it was the first time that it was shown that mercury metal could be converted to a highly toxic organometallic derivative in the environment. The hazardous nature of organomercurials was found almost as soon as the first compounds were reported!

While working in Bunsen’s research group in Marburg, Edward Franklin ( [link] ) discovered the synthesis of the zinc analog of a Grignard reagent, [link] . Subsequently, in 1851 Franklin moved to Owens College in Manchester where he extended his work to mercury, [link] . In his publication he noted that these organomercury compounds had a “nauseous taste”, but didn’t realize they were toxic.

In 1858 George Buckton ( [link] ) working at the then Royal College of Chemistry (now Imperial College) reported the synthesis of dimethyl mercury, [link] , as a volatile liquid.

When Frankland moved his research to St Bartholomew’s Hospital (“Barts”) London he started looking into the chemistry of R ₂ Hg with an assistant called Bill Odling in collaboration with Dr Carl Ulrich.

Ulrich died in 1865 as a consequence of exposure to Me ₂ Hg. In his own statement, he had inhaled a large quantity of the volatile compound without having taken the proper precautions. The following day “his countenance had attained a dull, anxious, and confused expression” and he was admitted to the hospital in a weak condition on 3 ^rd February. On the 9 ^th he became noisy and had to be put under mechanical restraint. The next day his breath and body began to smell offensively and he was in a coma. He would rise from the coma periodically to utter incoherent howls. He died on the 14 ^th of February.

A technician from the same research group (who is only identified as ‘T. C.’) was also admitted to the hospital on 28 ^th March of the same year. His symptoms were initially milder than Ulrich’s, but soon developed. By that summer he was completely demented, with no control over his body functions. He stayed in this state for many months, only dying on 7 ^th April 1866. Records indicate that a third assistant was also taken ill, but there was no further mention of him, so it is unknown if he died.

Summary and the “green” future

Metallic mercury causes severe symptoms, but all records show that if the patient is removed from the source they recover. Thus, short term exposure to metallic mercury, while dangerous, is not fatal if proper precautions are taken. In contrast, mercury compounds offer different risks. As a general rule, inorganic mercury(I) compounds are far less toxic than their mercury(II) analogs, however, all should be treated with care.

Where mercury compounds offer the greatest risk of fatality is their organometallic derivatives. There is no known cure for exposure to even modest doses of organomercury compounds. Furthermore, the ability of elemental mercury to be transformed into water-soluble organomercury compounds such as MeHg ⁺ , offers a future threat to public health.

The new generation of low energy consumption light bulbs contain mercury vapor. While they last longer than a traditional tungsten filament light bulb ( [link] ), they do have a lifetime. The presence of mercury means that they should be disposed-off separately from household waste to ensure that when the glass is broken the mercury is not released; however, this is unlikely. Most will be disposed off along with household waste which may be subsequently land filled. The lesson from Minamata should be that the bacterial action under anaerobic condition allows for the formation of water soluble MeHg ⁺ , that can diffuse into the water table. Although the amount of mercury in each bulb is very small, the highly lethal nature (low LD ₅₀ ) of orgnaomercury compounds should be considered in efforts to conserve energy by the use of the low energy light bulbs. At the very minimum protocols for their efficient disposal and recycling should be in place.

Bibliography

• S. Jensen and A. Jernelöv, Nature , 1969, 223 , 753.
• J. C. Clifton II, Pediatr. Clin. North Am. , 2007, 54 , 237.
• H. A. Waldron, Br. Med. J. , 1983, 287 , 24:
• C. Naleway, R. Sakaguchi, E. Mitchell, T. Muller, W. A. Ayer, and J. J. Hefferren, J. Amer. Dent. Assoc. , 1985, 111 , 37.
• D. McComb, J. Can. Dent. Assoc. , 1997, 63 , 372.
• T. G. Duplinsky1 and D. V. Cicchetti, Int. J. Stats. Med. Res. , 2012, 1 , 1.
• M. Aucott, M. McLinden, and M. Winka, J. Air. Waste Manag. Assoc. , 2003, 53 , 143.