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In the light of the findings described and discussed in this brief report, to safeguard public health and for the protection of environment, it is strongly recommended that since mercury amalgam use cannot be banned immediately in the country, its use may be regularized and allowed subject to use of “Amalgam Separators,” “Capsulated Mercury” and “Mechanized Mixing,” use of mercury amalgam be banned for children (below 12 years age) and pregnant women. The curriculum currently being taught at medical and dental colleges in the country be reviewed and revised, to ensure adequate training towards minimizing mercury exposure.

In conclusion, exposure to Cd was low during the ages 4 to 9, but the risk of disease might increase later in life since b-Cd only showed a minor decrease over time. This indicates, that Cd pollution should be further restricted. Regarding Hg, b-Hg concentration in children was low and decreased over time. The decrease is probably due to the reduced use of dental amalgam and the lower Hg intake from fish.  The report is based on the article: Lundh T, Axmon A, Skerfving S, Broberg K. Cadmium and mercury exposure over time in Swedish children. Environ Res. 2016

The exposure to Cd was very low but still might increase the risk of disease later in life. Moreover, b-Cd only showed a minor decrease, indicating that Cd pollution should be further restricted. b-Hg was relatively low and decreasing, probably because of reduced use of dental amalgam and lower Hg intake from fish. The b-Cd and b-Hg levels decreased much less than the levels of lead in the blood as previously found in the same children.

RESULTS:
Mean (geometric) Hg levels in hair (hHg), blood (bHg), urine (uHg), and the average estimated Hg intake from fish were 0.62µg/g, 3.75µg/L, 1.32µg/L, and 0.12µg/kg body weight/day, respectively. Out of 88 SNPs successfully genotyped, Hg biomarker levels differed by genotype for 25 SNPs, one of which remained significant following Bonferroni correction in ANOVA. When the associations between sources of Hg exposure and SNPs were analyzed with respect to Hg biomarker concentrations, 38 SNPs had significant main effects and/or gene-Hg exposure source interactions. Twenty-five, 23, and four SNPs showed significant main effects and/or interactions for hHg, bHg, and uHg levels, respectively (p<0.05), and six SNPs (in GCLC, MT1M, MT4, ATP7B, and BDNF) remained significant following Bonferroni correction.

CONCLUSION:
The findings suggest that polymorphisms in environmentally-responsive genes can influence Hg biomarker levels. Hence, consideration of such gene-environment factors may improve the ability to assess the health risks of Hg more precisely.

Toxic heavy metals have been implicated in the loss of spinal motoneurons in amyotrophic lateral sclerosis/motor neuron disease (ALS/MND). Motoneuron loss in the spinal anterior horn is severe in ALS/MND at the time of death, making this tissue unsuitable for examination. We therefore examined spinal cords of people without muscle weakness to look for any presence of heavy metals that could make these neurons susceptible to damage. Spinal cord samples from 50 individuals aged 1–95 y who had no clinical or histopathological evidence of spinal motoneuron loss were studied. Seven μm formalin-fixed paraffin-embedded sections were stained for heavy metals with silver nitrate autometallography (AMGHM) which detects intracellular mercury, silver or bismuth. Neurons in the spinal cord were classified as interneurons or α-motoneurons based on their site and cell body diameter. Spinal interneurons containing heavy metals were present in 8 of 24 people (33%) aged 61–95 y, but not at younger ages. These AMGHM interneurons were most numerous in the lumbar spinal cord, with moderate numbers in the caudal cervical cord, few in the rostral cervical cord, and almost none in the thoracic cord. All people with AMGHM interneurons had occasional AMGHM staining in α-motoneurons as well. In one man AMGHM staining was present in addition in dorsomedial nucleus and sensory neurons. In conclusion, heavy metals are present in many spinal interneurons, and in a few α-motoneurons, in a large proportion of older people. Damage to inhibitory interneurons from toxic metals in later life could result in excitotoxic injury to motoneurons and may underlie motoneuron injury or loss in conditions such as ALS/MND, multiple sclerosis, sarcopenia and calf fasciculations.

Little has been published on the chemical exposures and risks of dental restorative materials other than from dental amalgam and composite resins. Here we provide the first exposure and risk assessment for gold (Au) alloy and ceramic restorative materials. Based on the 2001-2004 US National Health and Nutrition Examination Survey (NHANES), we assessed the exposure of US adults to the components of Au alloy and ceramic dental restorations owing to dental material wear. Silver (Ag) is the most problematic component of Au alloy restorations, owing to a combination of toxicity and proportional composition. It was estimated that adults could possess an average of four tooth surfaces restored with Au alloy before exceeding, on average, the reference exposure level (REL) for Ag. Lithium (Li) is the most problematic component of dental ceramics. It was estimated that adults could possess an average of 15 tooth surfaces restored with ceramics before exceeding the REL for Li. Relative risks of chemical exposures from dental materials decrease in the following order: Amalgam>Au alloys>ceramics>composite resins.

The impact of dental amalgam on the development of Parkinson’s disease (PD) is still uncertain, although a positive association between dental amalgam and PD has been found in a few case-control studies. The patients with amalgam fillings restored between 2000 and 2008 were identified by using the National Health Insurance Research Database (NHIRD) in Taiwan. The same number of patients who had no new amalgam filling restored was matched by sex, age, and treatment date. Both cohorts were followed up from the treatment date until the date of diagnosis of PD, death, or the end of the year 2008. The individuals who received amalgam fillings had a significantly higher risk of PD afterward (adjusted hazard ratio [HR]=1.583, 95% confidence interval [CI]=1.122-2.234, p=0.0089) than those who did not. In the individuals who received amalgam fillings, being diagnosed with diabetes or hyperlipidemia demonstrated a significantly lower HR of PD occurrence than in the patients without diabetes or hyperlipidemia (HR=0.449, 95% CI=0.254-0.794, p=0.0059; HR=0.445, 95% CI=0.260-0.763, p=0.0032) after adjusting for comorbidities and Charlson-Deyo Comorbidity Index (CCI) scores. Meanwhile, hypertension increased the hazard risk of PD (HR=1.645, 95% CI=1.098-2.464, p=0.0159). The patients exposed to dental amalgam fillings were 1.583 times more likely to have PD afterward compared to their non-exposed counterparts after adjusting for comorbidities and CCI scores.