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So far Dunn G has created 996 blog entries.

The Aggravating Alloy: Mercury Amalgam’s Role in the Relationship Between the Educated and Non-Educated Dental Professional in the Nineteenth Century.

In the early 1830’s, a pair of European ‘dentists’ brought a novel material for filling teeth into the United States.  It was far less expensive and far easier to use than competing materials.  This new potential ease at which some could practice dentistry put pressure on a situation of conflict between the educated dental professional, and the uneducated dentist.  Quacks were the bane of the existence of an educated, gentleman dentist.  They were openly condemned in private circles and in the press but the dental ‘charlatan’ was not the only person in the line of fire. Those who used mercury amalgam were often lumped together, whether they be trained or otherwise, and treated with similar amounts of disdain from the professional societies.  The amalgam critics found ways to put down those who used amalgam in organizational publications and used essays, speeches, research, and case studies to support their efforts in keeping any dentist worth his salt from using amalgam.  This was a period of progress wherein the setting was just right for an all-out dental scandal that had a hand in the creation and collapse of the first dental society and is influencing the field of dentistry to this day.

By |2018-08-06T17:45:03+00:00January 1st, 2017|Mercury|

Metal‐free materials for fixed prosthodontic restorations

There is insufficient evidence to support or refute the effectiveness of metal-free materials for fixed prosthodontic treatment over metal-ceramic or other type of standard restorations. The overall quality of existing evidence was very low, therefore great caution should be exercised when generalising the results of the included trials. Until more evidence becomes available clinicians should continue to base decisions on which material to use for fixed prosthodontic treatment on their own clinical experience, whilst taking into consideration the individual circumstances and preferences of their patients. There is urgent need of properly designed RCTs.

By |2018-08-10T17:31:28+00:00January 1st, 2017|Other|

Prenatal fluoride exposure and cognitive outcomes in children at 4 and 6–12 years of age in Mexico.

BACKGROUND:
Some evidence suggests that fluoride may be neurotoxic to children. Few of the epidemiologic studies have been longitudinal, had individual measures of fluoride exposure, addressed the impact of prenatal exposures or involved more than 100 participants.

OBJECTIVE:
Our aim was to estimate the association of prenatal exposure to fluoride with offspring neurocognitive development.

METHODS:
We studied participants from the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) project. An ion-selective electrode technique was used to measure fluoride in archived urine samples taken from mothers during pregnancy and from their children when 6-12 y old, adjusted for urinary creatinine and specific gravity, respectively. Child intelligence was measured by the General Cognitive Index (GCI) of the McCarthy Scales of Children’s Abilities at age 4 and full scale intelligence quotient (IQ) from the Wechsler Abbreviated Scale of Intelligence (WASI) at age 6-12.

RESULTS:
We had complete data on 299 mother-child pairs, of whom 287 and 211 had data for the GCI and IQ analyses, respectively. Mean (SD) values for urinary fluoride in all of the mothers (n=299) and children with available urine samples (n=211) were 0.90 (0.35) mg/L and 0.82 (0.38) mg/L, respectively. In multivariate models we found that an increase in maternal urine fluoride of 0.5mg/L (approximately the IQR) predicted 3.15 (95% CI: -5.42, -0.87) and 2.50 (95% CI -4.12, -0.59) lower offspring GCI and IQ scores, respectively.

CONCLUSIONS:
In this study, higher prenatal fluoride exposure, in the general range of exposures reported for other general population samples of pregnant women and nonpregnant adults, was associated with lower scores on tests of cognitive function in the offspring at age 4 and 6-12 y.

Biomarkers of mercury toxicity: Past, present, and future trends.

Mercury (Hg) toxicity continues to represent a global health concern. Given that human populations are mostly exposed to low chronic levels of mercurial compounds (methylmercury through fish, mercury vapor from dental amalgams, and ethylmercury from vaccines), the need for more sensitive and refined tools to assess the effects and/or susceptibility to adverse metal-mediated health risks remains. Traditional biomarkers, such as hair or blood Hg levels, are practical and provide a reliable measure of exposure, but given intra-population variability, it is difficult to establish accurate cause-effect relationships. It is therefore important to identify and validate biomarkers that are predictive of early adverse effects prior to adverse health outcomes becoming irreversible. This review describes the predominant biomarkers used by toxicologists and epidemiologists to evaluate exposure, effect and susceptibility to Hg compounds, weighing on their advantages and disadvantages. Most importantly, and in light of recent findings on the molecular mechanisms underlying Hg-mediated toxicity, potential novel biomarkers that might be predictive of toxic effect are presented, and the applicability of these parameters in risk assessment is examined.

Dental amalgam fillings and the use of technological devices as an environmental factor: Updating the cumulative mercury exposure-based hypothesis of autism.

Common technological devices (e.g., mobile phones, mobile base stations, and magnetic resonance imaging machines and other wireless devices) produce electromagnetic fields (EMFs). Neurobehavioral and neurodevelopmental symptoms such as retarded memory, learning, cognition, and attention have been attributed to EMF exposure.[4] Of note, these symptoms are also attributed to ASD and attention deficit hyperactivity disorders. A recent in vivo study observed autism-relevant social abnormalities in mice exposed to extremely low-frequency EMFs during perinatal development.[5] This may indicate a potential direct link between EMFs and the prevalence of autism in specific window/s of vulnerability that would deserve further investigation. An indirect link might be also plausible since high-field magnetic resonance and microwave radiation emitted by common mobile phones have been reported to increase the release of mercury from dental amalgam fillings.[6,7] These recent evidence (2014), far from being conflictive, is consistent with our previous cumulative Hg exposure-based hypothesis of ASD (2011) and could be included as the fifth (v) additional environmental factor, synergistically contributing to the release of Hg in mothers with dental amalgam fillings, and increasing the probability of developing and/or aggravating autism among children. Nevertheless, this updated version of our hypothesis would require more extensive clinical confirmation and supporting evidence.

By |2018-10-09T22:55:22+00:00January 1st, 2017|Mercury|

The metal neurotoxins: an important role in current human neural epidemics?

Many published studies have illustrated that several of the present day neurological epidemics (autism, attention deficit disorder, Alzheimer’s) cannot be correlated to any single neurotoxicant. However, the present scientific examination of the numerous global blood monitoring databases for adults that include the concentrations of the neurotoxic elements, aluminum (Al), arsenic (As), lead (Pb), manganese (Mn), mercury (Hg), and selenium (Se) clearly indicate that, when considered in combination, for some, the human body may become easily over-burdened. This can be explained by changes in modern lifestyles. Similar data, solely for pregnant women, have been examined confirming this. All these elements are seen to be present in the human body and at not insignificant magnitudes. Currently suggested minimum risk levels (MRL) for humans are discussed and listed together with averages of the reported distributions, together with their spread and maximum values. One observation is that many distributions for pregnant women are not too dissimilar from those of general populations. Women obviously have their individual baseline of neurotoxin values before pregnancy and any efforts to modify this to any significant degree is not yet clearly apparent. For any element, distribution shapes are reasonably similar showing broad distributions with extended tails with numerous outlier values. There are a certain fraction of people that lie well above the MRL values and may be at risk, especially if genetically susceptible. Additionally, synergistic effects between neurotoxins and with other trace metals are now also being reported. It appears prudent for women of child-bearing age to establish their baseline values well before pregnancy. Those at risk then can be better identified. Adequate instrumental testing now is commercially available for this. In addition, directives are necessary for vaccination programs to use only non-neurotoxic adjuvants, especially for young children and all women of child-bearing ages. Additionally, clearer directives concerning fish consumption must now be reappraised.

By |2018-08-13T17:13:21+00:00January 1st, 2017|Mercury|

Genetic aspects of susceptibility to mercury toxicity: an overview.

Human exposure to mercury is still a major public health concern. In this context, children have a higher susceptibility to adverse neurological mercury effects, compared to adults with similar exposures. Moreover, there exists a marked variability of personal response to detrimental mercury action, in particular among population groups with significant mercury exposure. New scientific evidence on genetic backgrounds has raised the issue of whether candidate susceptibility genes can make certain individuals more or less vulnerable to mercury toxicity. In this review, the aim is to evaluate a new genetic dimension and its involvement in mercury risk assessment, focusing on the important role played by relevant polymorphisms, located in attractive gene targets for mercury toxicity. Existing original articles on epidemiologic research which report a direct link between the genetic basis of personal vulnerability and different mercury repercussions on human health will be reviewed. Based on this evidence, a careful evaluation of the significant markers of susceptibility will be suggested, in order to obtain a powerful positive “feedback” to improve the quality of life. Large consortia of studies with clear phenotypic assessments will help clarify the “window of susceptibility” in the human health risks due to mercury exposure.

By |2018-07-18T17:03:30+00:00January 1st, 2017|Mercury|

Are mercury and Alzheimer’s disease linked?

To the Editor:
In his Commentary [2017], Dr. Chakraborty stresses the potential hazards of low-level long-term exposure to mercury and the increase of prevalence of Alzheimer’s disease in the general population of India, a view we wholeheartedly endorse. We applaud the tenor of the piece (Chakraborty, 2017) and we have some additional points to make as well.

By |2018-08-10T17:16:32+00:00January 1st, 2017|Mercury|

The risk of occupational exposure to mercury vapor in some public dental clinics of Baghdad city, Iraq.

BACKGROUND:
Dental workers are exposed to elevated levels of elemental mercury vapor substantially above the occupational exposure standards when placing or removing mercury/silver tooth restorations and disposing of mercury waste. This results in a significant increase in occupational exposure and risk of mercury intoxication.

METHODS:
To evaluate the occupational exposure of dental workers to amalgam in four dental clinics in Baghdad city, the concentrations of mercury vapor were measured seasonally from February to November 2016. Samples of blood and urine were collected from 30 dental workers (exposed individuals) and five non-occupationally exposed individuals. Biochemical parameters such as cholesterol, liver enzymes (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase), renal enzymes (urea and creatinine), total protein and reduced glutathione (GSH) were observed.

RESULTS:
The results indicated that mercury vapor levels varied from 84.7 ± 18.67 to 609.3 ± 238.90 µg/m3 and most concentrations were above the occupational exposure standards. The results of the biochemical parameters showed a significant increase in levels of cholesterol, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and no significant increase in blood urea and creatinine in dental workers in comparison with unexposed persons (control). Although the results showed a significant reduction in the levels of glutathione and total protein, there was no significant decrease in the levels of alkaline phosphatase (ALP) in exposed dental workers when compared with non-occupationally exposed individuals.

CONCLUSIONS:
It is concluded that mercury vapor concentrations in the indoor air of some dental clinics in Baghdad city are high and exceed the OSHA STEL(Occupational Safety and Health Administration Short Term Exposure Limit). The present data showed that altered biochemical parameters can be used as efficient bioindicators for mercury toxicity.

By |2018-08-04T16:59:48+00:00January 1st, 2017|Mercury|

Exploring the association between Alzheimer’s disease, oral health, microbial endocrinology and nutrition.

Longitudinal monitoring of patients suggests a causal link between chronic periodontitis and the development of Alzheimer’s disease (AD). However, the explanation of how periodontitis can lead to dementia remains unclear. A working hypothesis links extrinsic inflammation as a secondary cause of AD. This hypothesis suggests a compromised oral hygiene leads to a dysbiotic oral microbiome whereby Porphyromonas gingivalis, a keystone periodontal pathogen, with its companion species, orchestrates immune subversion in the host. Brushing and chewing on teeth supported by already injured soft tissues leads to bacteremias. As a result, a persistent systemic inflammatory response develops to periodontal pathogens. The pathogens, and the host’s inflammatory response, subsequently lead to the initiation and progression of multiple metabolic and inflammatory co-morbidities, including AD. Insufficient levels of essential micronutrients can lead to microbial dysbiosis through the growth of periodontal pathogens such as demonstrated for P. gingivalis under low hemin bioavailability. An individual’s diet also defines the consortium of microbial communities that take up residency in the oral and gastrointestinal (GI) tract microbiomes. Their imbalance can lead to behavioral changes. For example, probiotics enriched in Lactobacillus genus of bacteria, when ingested, exert some anti-inflammatory influence through common host/bacterial neurochemicals, both locally, and through sensory signaling back to the brain. Early life dietary behaviors may cause an imbalance in the host/microbial endocrinology through a dietary intake incompatible with a healthy GI tract microbiome later in life. This imbalance in host/microbial endocrinology may have a lasting impact on mental health. This observation opens up an opportunity to explore the mechanisms, which may underlie the previously detected relationship between diet, oral/GI microbial communities, to anxiety, cognition and sleep patterns. This review suggests healthy diet based interventions that together with improved life style/behavioral changes may reduce and/or delay the incidence of AD.

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