Mercury Exposure and Public Health: Dental Amalgam

Background

When we go to work in healthcare, we go with the faith that it must be a safe place to work. However, working in healthcare settings, in a hospital, nursing home, dental office, senior homes, or in the public health setting providing care in clients’ homes can be as hazardous as working in other environments. Even though lately, there has been a global concern raised with the awareness of environmental contamination by heavy metals. With the increase of the use of the metal-containing products domestically, in agriculture and industrialization has increased human exposure to them. (Tchounwou, Yedjou, Patlolla, & Sutton, 2012).  According to the US Government Agency for Toxic Substances and Disease Registry, Mercury is one of the most toxic substances on earth and is ranked third after arsenic and lead.  These metals are usually disposed of into our water sources and soil, released into the atmosphere, and ingested through our food and water (Clifton, 2007; US Department of Health and Human Services, 1999).  The atmospheric Mercury has tripled due to increased human activity, and it is rising 1.5 percent per year (Clifton, 2007).

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Mercury has continuously been used along with silver as amalgam restorative material for cavities in dentistry for last two centuries. This restorative material contains about fifty percent mercury (Dodes, 2001).  The dental amalgam use is worldwide and has many benefits as filling material. However, its careless handling can turn into a tremendous human health risk; these risks are usually related to the occupational exposure and result in environmental damage from mercury emission (Richardson et al., 2011).  Due to its vast usage in public health and dental profession, according to World Health Organization (WHO) expert consultation held in 2009, a global amalgam ban would result in substantial economic loss and is not very feasible.  However, a reduction in use can be promoted by promoting disease prevention and by finding and using cost-effective substitutes to amalgam, by educating of dental professionals, and the raising public awareness (WHO, 2017).  Elemental mercury vapors (HgO) are the most concerned form of mercury related to manipulation of dental amalgam in their several routine occupational tasks, including preparation, restoration, and removal of dental amalgam (Eley, 1997). The dentists, dental assistants, and the dental staff are vulnerable to exposure to different forms of mercury across the world (Zolfaghari, Esmaili-Sari, Ghasempouri, & Faghihzadeh, 2007).  Around 80% of the inhaled mercury vapors are incorporated into the bloodstream and circulated through the body. They can cross the placenta and the blood-brain barriers and affect the infants and human brain (Clarkson, 2002).  Studies have also reported that the use of mercury in dentistry is the cause of 10–70% of the total daily mercury load in the wastewater collection system (Horsted-Bindslev, 2004).  Mercury is of global concern, and due to health and environmental risks linked to mercury exposure, 128 signatories and 25 parties have supported a United Nations’ treaty from the Minamata Convention on Mercury (United Nations Environmental Program “INC7”. Minamata Convention on Mercury, 2017).  Norway, Sweden, and Denmark are some of the few countries that have legislated to ban the use of mercury in amalgams due to environmental health concerns (Food and Drug Administration FDA, 2013).  It is necessary to evaluate the use of dental amalgam due to the risks related to the health of dental personnel so that clinicians, policymakers, and legislators can take the appropriate actions to minimize any health risk to dental staff.

Health hazards

Dentists and dental assistants have been the victims of occupational exposure to mercury vapor for centuries.  Dental workers have been found to have on average higher systemic levels of mercury in their tissues and organs than do members of control groups (Tezel, Ertas, Erakin, & Kayali, 2001).  Evidence proves that this exposure results in a high occurrence of neurological symptoms such as memory problem, sleep disturbances, concentration difficulties and fatigue among dental clinics personnel.(Ritchie et al., 2002).  Studies have also revealed that chronic exposure to mercury may lead to adverse effects such as salivation, gingivitis, insomnia, excitability, depression, and sensory losses (McComb, 1997; Zachi, D, Faria, & Taub, 2007).  Clinical trials done on the subject has concluded that exposure of rats to 27 mg/m3 of elemental mercury vapors for 2 hours, followed by observation for 15 days, resulted in substantial death(20 of 32 rats died before their scheduled sacrifice (Agency for Toxic Substances and Disease Registry, 1999).  The lipophilic nature of metallic mercury is the reason of it binding and mixing in the bloodstream and circulating throughout the body (Fernandes Azevedo et al., 2012).  Out of the mercury compounds, the methylmercury is the primary cause of the neurological changes present in humans and experimental animals.  Oxidative stress has related to the etiology of neurodegenerative diseases such as amyotrophic lateral sclerosis, Parkinson’s disease, and Alzheimer’s disease (Bridges & Zalups, 2010).  A study conducted by Houston in which the cohort of patients was followed for 13.9 years and found a connection between the concentration of mercury in the hair and the risk of developing cardiovascular problems or dying from cardiovascular disease and other causes (Houston, 2007).

Food chain (fish), mercury-containing products (dental amalgam fillings), and mercury vapors are some of the mercury exposure routes in humans (Rice, Walker, Wu, Gillette, & Blough, 2014).  Mercury is believed to increase the oxidative stress in the body. Mercury exposure causes the increases in the production of free radicals, due to the role of mercury in the Fenton reaction and decrease in antioxidant enzymes activity, such as glutathione peroxidase (Ehara et al., 2001).  The higher affinity of mercury to the thiol group results in a decrease of glutathione peroxidase selenium-dependent activity.  These processes increase the risk of cardiovascular and many other diseases (Magos & Clarkson, 2006).

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Environmental impact assessment/Health impact assessment

In general, all forms of mercury (Hg) are toxic to humans and the environment, but the scale of toxicity and health effects varies with its chemical composition and a dose of exposure (metallic, inorganic, organic). The toxicity of Hg depends on the route of exposure (inhalation, ingestion), the amount (low concentrations can have an impact). Also, the duration (acute and chronic), timing/life stage of exposure (exposure in early life is the most dangerous) and the susceptibility of the person exposed (Guzzi & La Porta, 2008). Mercury is persistent in the environment and can stay entrapped in the environment for an extended period and is responsible for several toxic effects such as nephrotoxicity, teratogenicity, and damage to the cardiovascular system. Endocrine-system disruption and adverse immune impacts are under scientific discussion. Clinical symptoms of exposure to different forms of mercury also vary from nausea, abdominal pain to tremor, paralysis, memory loss and kidney (Park & Zheng, 2012).  The childhood exposure to mercury is one of the significant health concerns. During pregnancy, mercury can cross the placental barrier and can interfere with the development of the fetus, resulting in developmental defects during the prenatal period. There are more than 1.8 million children are born every year with exposure to methylmercury above the adjusted safety limit of 0.58 μg/g hair in Europian Union, and the total benefits of preventing exposure can be up to gain of about 600,000 intelligence quotient points per year (Bellanger et al., 2013). This colossal health and economic impacts make Hg as a  global issue that needs to address by policymaker and government agencies.

Occupational exposure to mercury and its forms is not only limited to the dental profession but also extend to various other occupations. The other valuable populations are amalgam makers, barometer makers, battery makers, chemical laboratory workers, chlor-alkali petrochemical workers, dentists, fluorescent lamp makers, gold and silver extractors, insecticide makers, Hg miner workers and thermometer makers (OSHA, 1991). Exposure to Hg forms can occur through various food sources, for example, Hg-contaminated fish (Langworth, Elinder, Gothe, & Vesterberg, 1991). History has shown about the environmental hazards due to methylHg contamination in the vicinity of many industries. The Chisso Corporation chemical factory, Minamata Bay in Kyushu, Japan or the Dryden chlor-alkali facility and paper mill in the English-Wabigon River, Ontario as well as three epidemic poisonings caused by consumption of methylHg-contaminated seeds in Iraq are few examples (Satoh, 2000).

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Potential impact on vulnerable population

Amalgam use exposes dental health care professionals contributes to the toxic effects of Hg, during improper handling (Martin, Naleway, & Chou, 1995).  Hg vapors in the form of elemental mercury released in the environment are about ten times more toxic than lead to human neurons and enhance toxicity with other metals. As 80% of such inhaled vapor enter the bloodstream, it is a significant health concern (Schuurs, 1999). Dental staff gets exposed to mercury through improper mercury hygiene, during manual mulling to remove excess mercury from freshly mixed amalgam, ultrasonic amalgam condensers, mechanical amalgamators, heating the amalgam carrier to dislodge particles, failure to use high-vacuum suction while removing old amalgam restorations, and improper dry heat sterilization of amalgam-contaminated instrument. According to medical records of 1980 and 1986, the dentists’ urinary mercury levels were 19.5 µg/liter and 6.7 µg/L, as compared with 4.9 µg/L in 1991 (Naleway et al., 1985). National Institute for Occupational Safety and Health, or NIOSH, and the Occupational Safety and Health Administration have suggested the threshold limit value, or TLV, which is  50 µg mercury vapor per cubic meter of the breathing zone air for eight hours per day, 40 hours per week(NIOSH, 1973). Hg vapor levels are two to 15 times higher than the TLV as defined by WHO in most of the contaminated zones. There are also concerns regarding the mercury vapor being converted into highly toxic organomercury compounds by microorganisms in the mouth and gastrointestinal tract. According to a human study, the mercury exposure decreases the fertility of the female dental assistants (Rowland et al., 1994). Another study reported the case of a pregnant dentist with chronic occupational exposure to mercury vapor and elevated urinary levels where the ultrasound examination of the fetus at 20 weeks of gestation showed mild bilateral hydronephrosis, which later resolved at 32 weeks of pregnancy (Warfvinge, 1995). Even though the mercury exposure in the dental professionals has been on the decline during recent years, occupational exposure remains a safety concern. The risk is related to improper handling, accidental spillage and contact with mercury. Subclinical adverse health effects have been reported in a study done on 19 practicing dentists, whose average urinary mercury concentrations were 36 µg/liter (Echeverria et al., 1995). 

References

Agency for Toxic Substances and Disease Registry. (1999). Toxicological Profile for Mercury.   Retrieved January 30, 2018, from https://www.atsdr.cdc.gov/toxfaqs/TF.asp?id=113&tid=24

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Bellanger, M., Pichery, C., Aerts, D., Berglund, M., Castano, A., Cejchanova, M., . . . Demo/Cophes. (2013). Economic benefits of methylmercury exposure control in Europe: monetary value of neurotoxicity prevention. Environ Health, 12, 3. doi: 10.1186/1476-069X-12-3

Bridges, C. C., & Zalups, R. K. (2010). Transport of inorganic mercury and methylmercury in target tissues and organs. J Toxicol Environ Health B Crit Rev, 13(5), 385-410. doi: 10.1080/10937401003673750

Clarkson, T. W. (2002). The three modern faces of mercury. Environ Health Perspect, 110 Suppl 1, 11-23.

Clifton, J. C., 2nd. (2007). Mercury exposure and public health. Pediatr Clin North Am, 54(2), 237-269, viii. doi: 10.1016/j.pcl.2007.02.005

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Dodes, J. E. (2001). The amalgam controversy. An evidence-based analysis. J Am Dent Assoc, 132(3), 348-356.

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Ehara, S., Ueda, M., Naruko, T., Haze, K., Itoh, A., Otsuka, M., . . . Becker, A. E. (2001). Elevated levels of oxidized low-density lipoprotein show a positive relationship with the severity of acute coronary syndromes. Circulation, 103(15), 1955-1960.

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Fernandes Azevedo, B., Barros Furieri, L., Pecanha, F. M., Wiggers, G. A., Frizera Vassallo, P., Ronacher Simoes, M., . . . Valentim Vassallo, D. (2012). Toxic effects of mercury on the cardiovascular and central nervous systems. J Biomed Biotechnol, 2012, 949048. doi: 10.1155/2012/949048

Food and Drug Administration FDA. (2013, 2018). Banning mercury amalgam.   Retrieved January 30, 2018, from http://www.fda.gov/downloads/…/medicaldevices/…/ucm236379.pdf

Guzzi, G., & La Porta, C. A. (2008). Molecular mechanisms triggered by mercury. Toxicology, 244(1), 1-12. doi: 10.1016/j.tox.2007.11.002

Horsted-Bindslev, P. (2004). Amalgam toxicity–environmental and occupational hazards. J Dent, 32(5), 359-365. doi: 10.1016/j.jdent.2004.02.002

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Park, J. D., & Zheng, W. (2012). Human exposure and health effects of inorganic and elemental mercury. J Prev Med Public Health, 45(6), 344-352. doi: 10.3961/jpmph.2012.45.6.344

Rice, K. M., Walker, E. M., Jr., Wu, M., Gillette, C., & Blough, E. R. (2014). Environmental mercury and its toxic effects. J Prev Med Public Health, 47(2), 74-83. doi: 10.3961/jpmph.2014.47.2.74

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Ritchie, K. A., Gilmour, W. H., Macdonald, E. B., Burke, F. J., McGowan, D. A., Dale, I. M., . . . Collington, D. (2002). Health and neuropsychological functioning of dentists exposed to mercury. Occup Environ Med, 59(5), 287-293.

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Tezel, H., Ertas, O. S., Erakin, C., & Kayali, A. (2001). Blood mercury levels of dental students and dentists at a dental school. Br Dent J, 191(8), 449-452. doi: 10.1038/sj.bdj.4801205a

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