Mercury

Mercury is a well-known toxic element that is found in various forms in nature. Recently, dental amalgams have been recognized as a new source of mercury. This study was carried out under in vitro condition; the amount of mercury released from teeth restored with amalgams in the presence of Wi-Fi router radiation (non-ionizing radiation) and X-ray (ionizing radiation) using a protocol similar to Computed Tomography of Para-nasal Sinuses (CT) were analyzed separately, and in combination on the samples. For this reason, 50 human premolars were restored with a certain type of commercial amalgams. The samples were divided into five groups; control, only-CT, CT+Wi-Fi, Wi-Fi+CT and only-Wi-Fi groups, and mercury measurement were investigated at 24 and 48 hours after exposure to radiation by cold-vapor atomic absorption system. The results showed a significant difference between subgroups 24 and 48 h (p-values = 0.001 and 0.008). However, over time a significant difference was only found in CT+Wi-Fi group (p-value = 0.043). In addition, in comparison with the control group, only the subgroup that was exposed to Wi-Fi waves showed a significant difference after 24 hours (p = 0.033). In line with some of the previous studies, our findings showed that electromagnetic waves are involved in mercury release process, and warnings about the consequences of electromagnetic waves on mercury release and subtitling it with a new compound in restorative dentistry should be taken into consideration.

Abstract
OBJECTIVES:
The aim was to gain knowledge regarding the risk of perinatal death related to exposure to dental amalgam fillings in the mother.

DESIGN:
Population-based observational cohort study.

SETTING:
The Norwegian Mother and Child Cohort Study, a Norwegian birth cohort of children born in 1999-2008 conducted by the Norwegian Institute of Public Health.

PARTICIPANTS:
72,038 pregnant women with data on the number of teeth filled with dental amalgam.

MAIN OUTCOME MEASURES:
Data on perinatal death (stillbirth ≥ 22 weeks plus early neonatal death 0-7 days after birth) were obtained from the Medical Birth Registry of Norway.

RESULTS:
The absolute risk of perinatal death ranged from 0.20% in women with no amalgam-filled teeth to 0.67% in women with 13 or more teeth filled with amalgam. Analyses including the number of teeth filled with amalgam as a continuous variable indicated an increased risk of perinatal death by increasing number of teeth filled with dental amalgam (crude OR 1.065, 95% CI 1.034 to 1.098, p<0.001). After adjustment for potential confounders (mothers’ age, education, body mass index, parity, smoking during pregnancy, alcohol consumption during pregnancy) included as categorical variables, there was still an increased risk for perinatal death associated with increasing number of teeth filled with amalgam (ORadj 1.041, 95% CI 1.008 to 1.076, p = 0.015). By an increased exposure from 0 to 16 teeth filled with amalgam, the model predicted an almost doubled odds ratio (ORadj 1.915, 95% CI 1.12 to 3.28). In groups with 1 to 12 teeth filled with amalgam the adjusted odds ratios were slightly, but not significantly, increased. The group with the highest exposure (participants with 13 or more teeth filled with amalgam) had an adjusted OR of 2.34 (95% CI 1.27 to 4.32; p = 0.007).

CONCLUSION:
The current findings suggest that the risk of perinatal death could increase in a dose-dependent way based on the mother’s number of teeth filled with dental amalgam. However, we cannot exclude that the relatively modest odds ratios could be a result of residual confounding. Additional studies on the relationship between exposure to dental amalgam fillings during pregnancy and perinatal death are warranted.

Genetic background accounts for only 5 to 10% of the reported cases of Parkinson’s disease (PD), while the remaining cases are of unknown etiology. It is believed that environmental factors may be involved in the causality of a large proportion of PD cases. Several PD genes are activated by xenobiotic exposure, and a link between pesticide exposure and PD has been demonstrated. Many epidemiological studies have shown an association between PD and exposure to metals such as mercury, lead, manganese, copper, iron, aluminum, bismuth, thallium, and zinc. This review explores the biological effects, the pathogenetic processes, genetic susceptibilities to metals as well as examining future strategies for PD treatment, such as chelation therapy.

Rheumatic diseases include a group of autoimmune disorders with environmental and genetic etiology that are characterized as a subgroup of connective tissue diseases (CTD). Rheumatoid arthritis (RA) often involves the small joints of the hands in a symmetrical fashion that can lead to loss of joint function, and RA, as well as Sjögren’s syndrome (SS) and other rheumatic diseases, are often accompanied by sensitivity to metals. Numerous investigations on metal sensitivity were evaluated in this review. A detailed metal exposure history was collected by different evaluation of studies. In all subjects, the main source of metal exposure was nickel, mercury, gold, palladium, titanium, and chromium. All of SLE (systemic lupus erythematosus), RA and SS patients appeared to have an increased frequency of metal delayed-type hypersensitivity (DTH) (Type IV allergy). As dental restorative materials release minor amounts of their metals (including mercury, gold, and nickel), many adults are commonly exposed to these metal ions by vapor or corrosion into saliva. Metal-related DTH in these patients will induce an inflammatory response. Such inflammations are important factors in CTD progress. It is hypothesized that metal-specific T cell reactivity can act as an etiological agent in the propagation and chronification of rheumatic inflammation. The key responses of metal delayed-type hypersensitivity in autoimmunity are precipitating as an appealing challenge for further investigations.

Low doses of mercury (Hg) promote deleterious effects on cardiovascular system, but the mechanisms implicated remain unclear. This study analyzed whether angiotensin II AT-1 receptors are involved in the vascular dysfunction caused by chronic exposure to low HgCl2 doses. For this, rats were divided into four groups and untreated (saline by im injections and tap water by gavage) or treated for 30 days as follows: Mercury (HgCl2im, first dose of 4.6 µg kg-1 and subsequent doses of 0.07 µg kg-1 day-1, and tap water by gavage); Losartan (saline im and losartan, 15 mg kg-1 day-1, by gavage); Losartan-Mercury (HgCl2im and Losartan by gavage). Systolic blood pressure was measured by tail plethysmography, vascular reactivity in aorta by isolated organ bath, oxidative stress by measuring the levels of reactive oxygen species (ROS), malondialdehyde (MDA) and antioxidant capacity (FRAP) and protein expression of AT-1 receptors by Western Blot. As results, co-treatment with losartan prevented the increased aortic vasoconstrictor responses to phenylephrine (Phe), the involvement of ROS and prostanoids on the response to Phe and the reduced negative endothelial modulation by nitric oxide on these responses. Moreover, this co-treatment avoided the increase in plasmatic and vascular oxidative stress and AT-1 protein expression in aorta. In conclusion, these results suggest that AT-1 receptors upregulation might play a key role in the vascular damage induced by Hg exposure by increasing oxidative stress and probably by reducing NO bioavailability.

Probably billions of people throughout the world have mercury amalgam fillings in their teeth. Although use of amalgam fillings has been decreasing, particularly in developing countries, it has been estimated that, between 1993 and 2008, about 900 million dental amalgam fillings were inserted in the United States– an average of about 60 million a year.

The Minamata Convention on Mercury, with its objective to protect human health and the environment from the dangers of mercury (Hg), entered into force in 2017. The Convention outlines a life-cycle approach to the production, use, emissions, releases, handling, and disposal of Hg. As it moves into the implementation phase, scientific work and information are critically needed to support decision-making and management. This paper synthesizes existing knowledge and examines three areas in which researchers across the natural sciences, engineering, and social sciences can mobilize and disseminate knowledge in support of Hg abatement and the realization of the Convention’s objective: (1) uses, emissions, and releases; (2) support, awareness raising, and education; and (3) impacts and effectiveness. The paper ends with a discussion of the future of Hg science and policy.

OBJECTIVES:
When planning primary oral health care services the cost implications of adopting new intervention practices are important, especially in resource-strapped countries. Although on a trajectory to be phased-out, amalgam remains the standard of care in many countries.

METHODS:
Adopting a government perspective, this study compared the costs of performing amalgam and ART/high-viscosity glass-ionomer cement (HVGIC) restorations and the consequences of failed restorations over 3 years in suburban Brasilia, Brazil. Cost data were collected prospectively; cost estimates were developed for the study sample and a projection of 1000 single- and 1000 multiple-surface restorations per group. Probabilistic sensitivity analysis was conducted in TreeAge Pro.

RESULTS:
Results were mixed. For single-surface restorations, ART/HVGIC will cost US$51 per failure prevented, while for multiple-surface restorations, ART/HVGIC was cost-effective with a savings of US$11 compared to amalgam. Probabilistic sensitivity analysis (Monte Carlo simulation) predicted amalgam would be cost-effective 49.2% of the time compared to HVGIC at 50.6% of the time at a willingness to pay threshold of US$237 per failure prevented. Personnel accounted for more than half the cost burden for both methods; instruments and supplies accounted for about one third. The per restoration cost to replace amalgam with HVGIC ranges from US$1 to a savings of US$0.84.

CONCLUSION:
Replacing amalgam with a high-viscosity glass-ionomer as part of the ART method comes at a minimal increase in cost for governments. Increasing the number of restorations seems to diminish the cost burden.

We review recent progress in our understanding of the global cycling of mercury (Hg), including best estimates of Hg concentrations and pool sizes in major environmental compartments and exchange processes within and between these reservoirs. Recent advances include the availability of new global datasets covering areas of the world where environmental Hg data were previously lacking; integration of these data into global and regional models is continually improving estimates of global Hg cycling. New analytical techniques, such as Hg stable isotope characterization, provide novel constraints of sources and transformation processes. The major global Hg reservoirs that are, and continue to be, affected by anthropogenic activities include the atmosphere (4.4-5.3 Gt), terrestrial environments (particularly soils: 250-1000 Gg), and aquatic ecosystems (e.g., oceans: 270-450 Gg). Declines in anthropogenic Hg emissions between 1990 and 2010 have led to declines in atmospheric Hg0 concentrations and HgII wet deposition in Europe and the US (- 1.5 to – 2.2% per year). Smaller atmospheric Hg0 declines (- 0.2% per year) have been reported in high northern latitudes, but not in the southern hemisphere, while increasing atmospheric Hg loads are still reported in East Asia. New observations and updated models now suggest high concentrations of oxidized HgII in the tropical and subtropical free troposphere where deep convection can scavenge these HgII reservoirs. As a result, up to 50% of total global wet HgII deposition has been predicted to occur to tropical oceans.