Differential Diagnosis between Organic and Inorganic Mercury Poisoning in Human Cases-The Pathologic Point of View

Abstract

Differences in pathology were found between acute and chronic exposure to methylmercury, mercury vapor, and inorganic mercury. Characteristic pathologic changes produced by organic mercury in the brain have previously been described in patients with Minamata disease. The brains of patients who presented with acute onset of symptoms and died within 2-mo showed loss of neurons with reactive proliferation of glial cells, microcavitation, vascular congestion, petechial hemorrhage, and edema in the cerebral cortices, predominantly in the calcarine, pre- and postcentral, and transverse temporal cortices and in the cerebellar cortex. The neuropathologic changes in the patients with acute onset of symptoms who survived for a long period (>10 yr) were also included neuronal loss with reactive proliferation of glial cells in similar anatomic locations. The neuropathologic changes in patients with inorganic mercury poisoning are quite different. Autopsies performed on 3 individuals with fatal cases of acute inorganic mercury poisoning who were exposed to mercury vapor for about 2 wk revealed diffuse organized pneumonia, renal cortical necrosis, disseminated intravascular coagulopathy, and infarctions in the brain and kidneys. In 2 other patients who worked in mercury mines for about 10 yr and who suffered from chronic inorganic poisoning, no specific lesions were demonstrated in the brain. However, the assay and the histochemistry of mercury revealed that inorganic mercury was present in the brain in all 3 groups irrespective of the brain lesions and the duration of clinical signs.

Intoxicación ocupacional por mercurio

“…• Efectos teratógenos y cancerígenos: la exposición a mercurio elemental o a compuestos inorgánicos no produce cáncer ni teratogenicidad, que sí están demostrados en los compuestos orgánicos (metilmercurio) (15,16) . La intoxicación mercurial ocupacional no necesariamente es causada por exposición a cantidades elevadas de mercurio en el ambiente laboral, sino que también puede ocurrir con niveles bajos de exposición (1,2) .…”

“…Los compuestos organomercuriales se absorben fácilmente por ingestión y se excretan principalmente con las heces y no por el riñón (16) . Aquí una digresión, los compuestos orgánicos del mercurio son importante preocupación en Salud Pública, pues a dosis potencialmente tóxicas se les halla en los músculos de los grandes peces condrictios (cartilaginosos): tiburón, pez espada, merlines y tollos; y en algunas especies de teleósteos: atunes (común, rojo, patudo, etc.…”

Assessing the neurotoxicological risk of methylmercury exposure for beluga whales (delphinapterus leucas) harvested in the Mackenzie Delta Estuary.

“…Furthermore, total Hg (Hgi) concentrations in brain tissue of beluga whales sampled from the EBS population between 2006 and 2010 exceeded concentrations previously associated with neurotoxicity and neurochemical disruption (median Hgr concentration was 2.34 mg kg'1 wet weight (range, 0.06 to 22.6 mg kg'1 ww) in temporal lobe (n = 81)) (Ostertag et al, 2013). For example, the concentration o f HgT in brain tissue associated with lethal, acute onset MeHg poisoning was 16.8 mg kg'1 ww in the cerebellum of one adult human (Eto et al, 1999), and Hgi concentrations between 4.1 and 15.9 mg kg'1 ww in brain tissue o f captive mink (Wobeser et al, 1976) and between 6.6 and 18.0 mg kg'1 ww in primate species were associated with clinical symptoms of poisoning (e.g. visual impairment, lesions in the cerebral cortex, anorexia and incoordination) (Berlin etal., 1975a;Evans etal., 1977;Shaw etal., 1975).…”

“…The lethal concentration ofH gT in human brain tissue was 16.8 mg kg'1 ww in the cerebellum o f one individual (Eto et al, 1999). Dietary MeHg dosing studies on primate species indicated that Hg intoxication was associated with brain HgT concentrations between 6.0 and 12.0 mg kg"1 ww (Berlin et al, 1975a;Evans et al, 1977;Luschei et al, 1977;Stinson et al, 1989).…”

“…Although an adult human suffered Hg poisoning with a H g x concentration o f 16.8 mg kg"1 in the cerebellum (Eto et al, 1999), dietary MeHg dosing studies on primate species indicated that intoxication was associated with H g x concentrations in brain tissue ranging from 6.0 to 12.0 mg kg'1 ww (Berlin et al, 1975b;Evans et al, 1977;Luschei et al, 1977). Concentrations o f MeHg below ~ 2-5 mg kg"1 ww were likely below thresholds o f overt MeHg intoxication in mink (Suzuki, 1979;Wobeser et al, 1976).…”