Miller K, Ochudlo S, Opala G, Smolicha W, Siuda J. [Parkinsonism in chronic occupational metallic mercury intoxication] Neurol Neurochir Pol. 2003;37 Suppl 5:31-8. [Article in Polish] chronic mercury encephalopathy (parkinsonismus) was diagnosed based on documented occupational exposure and diagnostic test results.
Mercury & PN
Gerr F, Letz R. Epidemiological case definitions of peripheral neuropathy: experience from two neurotoxicity studies. Neurotoxicology. 2000 Oct;21(5):761-8.
Conclusion: the composite case definition showed an odds ratio of more than 3.1 for the mercury study and 5.1 for the arsenic study.
Mercury & PN & hypertension & behavioral changes
Koyun M, Akman S, Guven AG. Mercury intoxication resulting from school
barometers in three unrelated adolescents. Eur J Pediatr. 2004
Mar;163(3):131-4. Epub 2004 Jan 13.
CONCLUSION: mercury intoxication should be considered in any child with signs and symptoms of hypertension, skin rash, peripheral neuropathy and behavioural changes. The parents and school administrators, as well as paediatricians, should be aware of the potential risks of mercury and should be encouraged to avoid mercury-containing devices in schools and households.
Occupational exposure to mercury effects dentists & dental assistants:
Echeverria, Woods JS, Heyer NJ, Rohlman DS, Farin FM, Bittner AC Jr, Li T, Garabedian C. Chronic low-level mercury exposure, BDNF polymorphism, and associations with cognitive and motor function. Neurotoxicol Teratol. 2005 Nov-Dec;27(6):781-96
Potential cognitive and motor effects from exposure to elemental mercury (Hg(0)) were examined in the presence and absence of a polymorphism (Val66Met) in brain-derived neurotrophic factor (BDNF). A group of 194 male dentists (DDs) and 233 female dental assistants (DAs) were occupationally exposed to mercury and had no history of kidney or nervous system disorders. Acute exposure was measured using spot urinary Hg (HgU) concentrations (average 3.32 and 1.98 microg/l, respectively) and indices of chronic occupational exposure (26.3 and 14.9 years, respectively, weighted for historical exposures). The BDNF status was 68% and 66% wild type, 26% and 30% sinle substitution, and 5% and 4% full mutation for DDs and DAs, respectively. DDs and DAs were evaluated separately. Regression analyses controlled for age, premorbid intelligence, alcohol consumption, and education. Statistically significant adverse associations with HgU (p<.05) were found for nine measures among DDs (Digit Span (Forward), Digit and Spatial Span(Backward), Visual Reproduction, Finger Tapping(Dominant, Alternate, and Alternate Partialed), Hand Steadiness, and Tracking), and eight measures among DAs (Digit Span(Forward), Visual Reproduction, Pattern Discrimination(Rate), Symbol Digit(Rate), Trailmaking B, Finger Tapping(Dominant and Alternate Partialed), and Hand Steadiness). The BDNF status was associated with four measures in DDs and three measures in DAs. Joint effects were found for Finger Tapping(Alternate and Alternate Partialed) in DDs and Hand Steadiness and Trailmaking B in DAs. Joint effects were additive in all cases. Our findings are applicable to exposure levels of the general opulation and identify a potentially vulnerable group with a BDNF polymorphism.