This case history is based on retrospective review of medical records and information from the patient. It provides limited information on the diagnostic judgements and treatment-related choices that were made at the various times. The patient had early symptoms that are typical of mercury exposure: cough, fatigue, agitation, a metallic taste in the mouth, tremor, impaired memory and concentration. Visual disturbances were also a prominent symptom.
The patient’s urinary mercury levels were not measured during her exposure, but a detailed review revealed that she was probably exposed to high concentrations of mercury vapour, particularly in the early part of her career. More than 30 years passed before she received a probable diagnosis, allowing her the possibility of having her condition recognised as an occupational disease. Such recognition gives entitlement to compensation for permanent injury from the Norwegian Labour and Welfare Administration and from Occupational Injuries and Diseases Insurance.
Copper amalgam contains about 70 % mercury and 30 % copper, and has greater plasticity and better antiseptic properties than standard amalgam (silver amalgam). During the preparation of dental fillings made from copper amalgam, high levels of mercury vapour are released. The preparation of silver amalgam, which contains approximately 50 % mercury, does not involve heating and therefore involves the release of less mercury vapour. In 1981, the Norwegian Directorate of Health advised dentists to exercise great restraint in the use of copper amalgam. However, an informal survey conducted by the Norwegian Board of Health Supervision in 1994 showed that some dentists were still using copper amalgam at that time.
The average mercury exposure among dental workers was estimated to be approximately 0.05 mg/m³, which was the maximum permissible limit in Norway until 2007 (5). The old limit would on a group basis be equivalent to roughly 400 nmol/l (80 μg/l) in the urine (4). The half-life of mercury in the blood is 58 days (35 – 90 days) (4), but can be up to several years for mercury bound to nervous tissue (6). The mechanisms by which mercury affects the nervous system are largely unclear. It is known that Hg2+ is cytotoxic and may cause blockade of transmitter substances through binding to thiol or selenol groups in cell membrane proteins and enzymes (6) and that Hg2+ may affect neuronal architecture by binding to intracellular microtubules.
The results of urinary mercury measurements are available for one of the patient’s colleagues, who performed the same duties at the same time as the patient. The measurements showed 59 μg/l, 18 μg/l and 15 μg/l. The Norwegian Institute of Occupational Health evaluated the results and concluded that they indicated exposure above the permitted limit.
It has long been known that exposure to mercury vapour may be neurotoxic and may impair renal function (4, 7), but that it may also cause visual impairments is less well known. In 2011, the Norwegian Knowledge Centre for the Health Services conducted a systematic review of mercury exposure among dental health personnel and concluded that these individuals were undoubtedly exposed to mercury, albeit to varying degrees (8). Studies of high methodological quality showed associations between urinary mercury and impairments in attention and memory, as well as poorer manual coordination. In 2012, Hilt et al. examined potential late complications among dental health personnel following mercury exposure; they concluded that while the incidence of such injuries is low, there is probably an increased incidence of neurotoxic symptoms among dental assistants who worked with mercury amalgam (9). The research group also found mild impairment of visual memory in female dental health personnel.
Animal studies show that mercury accumulates in neurons, astrocytes and pyramidal cells and is deposited in the frontal and occipital lobes, and in the cerebellum, retina and optic nerve (4, 10, 11). Ellingsen et al. studied workers that had been exposed to mercury at a Norwegian chor-alkali plant (12), and concluded that reduced visually evoked potentials (VEP) in exposed individuals may indicate damage to visual pathways. Similar findings were obtained by Mathiesen et al., who demonstrated reduced visuomotor capacity among mercury-exposed chlor-alkali workers (13).
A study of dentists with low urinary mercury concentrations (5 μg/l) revealed reduced colour vision according to the Lanthony Desaturated D-15 Test and the Cambridge Colour Test, as well as tests of colour sensitivity (brightness, red – green and yellow – blue) (14). Several studies have confirmed that colour vision can be affected by moderate mercury exposure (14) – (18). Visual impairments are thought to occur earlier and with lower levels of exposure than other neurotoxic injuries (16) – (18). It is therefore likely that long-term exposure to low levels of mercury (urinary concentrations of roughly 40 μg/l) may have caused visual impairments in dental health personnel. Genetic variation and differences in exposure levels or vulnerability may explain why some are affected but not others (4, 14).
When neurotoxic damage is suspected, cerebral MRI should be performed and the patient referred to a neurologist. The neurologist will check for neurological impairments that may result from mercury deposition in different parts of the brain, and will rule out other neurological diseases. Specific testing of colour vision and visually evoked potentials should be carried out if the patient has visual disturbances. Chelation therapy (DMPS, alternatively DMSA) is appropriate for symptomatic patients with urinary mercury concentrations of 100 μg/l or above (19, 20). The chelator binds to mercury in the blood and reduces its binding to cellular structures in the brain if treatment is started quickly, preferably within four hours of an acute exposure (20).
The patient was eventually diagnosed with toxic encephalopathy on the basis of her characteristic symptoms and the objective results of neuropsychological and neurological assessments, and after specific colour vision tests and diagnostic imaging. Our conclusion was that the exposure was sufficient to produce the observed array of symptoms and had occurred in close connection with the onset of the patient’s symptoms and ailments.
Many years after the exposure, the patient’s urinary mercury concentration was within the normal range and treatment was no longer appropriate. The Norwegian Labour and Welfare Administration approved toxic encephalopathy, impaired colour vision and strabismus as an occupational disease, with permanent medical disability of 45 %. The patient also received compensation via the employer's Occupational Injuries and Diseases Insurance.