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“Birth weight is a strong determinant of attained weight at early ages. Until now, many studies have reported that low birth weight corresponds with high mercury levels. However, the relationship between mercury exposure and attained weight of infant has not been well studied. Therefore, the aim of the present study was to assess the degree of prenatal exposure to mercury by measuring the total mercury levels in maternal and cord blood, and examine the relationship between the mercury level during pregnancy and the attained weight of infant during the first 24 months of life. The prospective cohort study of Mothers and Children’s Environmental Health (MOCEH) was built up in 2006, and 921 mother-infant pairs were recruited. Information on the socio-demographic characteristics, health behavior and environmental exposure were collected from an interview with trained nurses. After delivery, infants and mothers were followed up at 6, 12 and 24 months and the weights of the infants were measured. The mercury concentrations in the late maternal blood (?=-0.19. p=0.05) and cord blood (?=-0.36. p=0.01) were negatively associated with the infants’ attained weight over the first 24 months of age. The infants’ attained weight in the small for their gestational age (SGA) group was lower than the normal birth weight group at the highest quartile of the mercury level. Therefore, efforts should be made to reduce the mercury level in the maternal blood at late pregnancy and cord blood. Further research on the possible harmful effects of prenatal mercury exposure on postnatal growth is recommended.”

“Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.”

“BACKGROUND:

Recent studies suggest that children diagnosed with an autism spectrum disorder (ASD) have significantly increased levels of urinary porphyrins associated with mercury (Hg) toxicity, including pentacarboxyporphyrin (5cxP), precoproporphyrin (prcP), and coproporphyrin (cP), compared to typically developing controls. However, these initial studies were criticized because the controls were not age- and gender-matched to the children diagnosed with an ASD.

METHODS:

Urinary porphyrin biomarkers in a group of children (2-13 years of age) diagnosed with an ASD (n= 20) were compared to matched (age, gender, race, location, and year tested) group of typically developing controls (n= 20).

RESULTS:

Participants diagnosed with an ASD had significantly increased levels of 5cxP, prcP, and cP in comparison to controls. No significant differences were found in non-Hg associated urinary porphyrins (uroporphyrins, hexacarboxyporphyrin, and heptacarboxyporphyrin). There was a significantly increased odds ratio for an ASD diagnosis relative to controls among study participants with precoproporphyrin (odds ratio = 15.5, P < 0.01) and coproporphyrin (odds ratio = 15.5, P < 0.01) levels in the second through fourth quartiles in comparison to the first quartile.

CONCLUSION:

These results suggest that the levels of Hg-toxicity-associated porphyrins are higher in children with an ASD diagnosis than controls. Although the pattern seen (increased 5cxP, prcP, and cP) is characteristic of Hg toxicity, the influence of other factors, such as genetics and other metals cannot be completely ruled out.”

“In 2002, the Connecticut State Legislature passed a law telling the Connecticut Department of Environmental Protection to develop best management practices for the handling of dental amalgam. The purpose of these best management practices is to ensure that mercury from dental amalgam does not threaten human health or the environment. As part of the revised Dental Office Best Management Practices, all Connecticut dental offices who use amalgam, must provide a copy of this brochure to their patients to help explain the advantages and disadvantages to human health and the environment of the use of mercury amalgam fillings and other filling materials used in dental procedures. This brochure explains the possible effects that the use of such fillings may have on your dental health, general health or the environment. This brochure is intended to assist you in making choices regarding your dental and total health needs that are right for you.”

“The aim of the present study was to investigate whether removal of all amalgam fillings was associated with long-term changes in health complaints in a group of patients who attributed subjective health complaints to amalgam fillings. Patients previously examined at the Norwegian Dental Biomaterials Adverse Reaction Unit were included in the study and assigned to a treatment group (n = 20) and a reference group (n = 20). Participants in the treatment group had all amalgam fillings replaced with other restorative materials. Follow-ups took place 3 months, 1 and 3 years after removal of all amalgam fillings. There was no intervention in the reference group. Subjective health complaints were measured by numeric rating scales in both groups. Analysis of covariance was used to compare changes in health complaints over time in the two groups. In the treatment group, there were significant reductions in intra-oral and general health complaints from inclusion into study to the 3-year follow-up. In the reference group, changes in the same period were not significant. Comparisons between the groups showed that reductions in intra-oral and general health complaints in the treatment group were significantly different from the changes in the reference group. The mechanisms behind this remain to be identified. Reduced exposure to dental amalgam, patient-centred treatment and follow-ups, and elimination of worry are factors that may have influenced the results.”

“Antibiotics were one of the great discoveries of the 20th century. However, resistance appeared even in the earliest years of the antibiotic era. Antibiotic resistance continues to become worse, despite the ever-increasing resources devoted to combat the problem. One of the most important factors in the development of resistance to antibiotics is the remarkable ability of bacteria to share genetic resources via Lateral Gene Transfer (LGT). LGT occurs on a global scale, such that in theory, any gene in any organism anywhere in the microbial biosphere might be mobilized and spread. With sufficiently strong selection, any gene may spread to a point where it establishes a global presence. From an antibiotic resistance perspective, this means that a resistance phenotype can appear in a diverse range of infections around the globe nearly simultaneously. We discuss the forces and agents that make this LGT possible and argue that the problem of resistance can ultimately only be managed by understanding the problem from a broad ecological and evolutionary perspective. We also argue that human activities are exacerbating the problem by increasing the tempo of LGT and bacterial evolution for many traits that are important to humans.”

“Current literature suggests that amalgam waste from dental clinics is a point-source of mercury pollution in the environment. However, apart from mercury, other amalgam constituents (e.g. Ag, Sn, Cu, and Zn) in dental clinics’ wastewater have not been reported in the literature before. The objective of this study was to evaluate the concentrations of mercury and other metals in the wastewater of some dental clinics and the influent of a wastewater treatment plant in Al-Madinah Al-Munawarah (KSA). Samples were collected over a 2-month period from three dental clinics and analyzed for metals using ICP-MS. The mean concentrations of Hg, Ag, Sn, Cu, and Zn in the samples were 5.3±11.1, 0.49±0.96, 3.0±10.7, 10.0±14.5, and 76.7±106 mg L(-1), respectively. Additionally, high concentrations of other metals such as Mg (14.4±15.2 mg L(-1)), Mn (3.0±4.6 mg L(-1)), Fe (3.0±4.5 mg L(-1)), Sr (1.6±2.4 mg L(-1)), and Ba (6.9±10.3 mg L(-1)) were also found. These values are much higher than the local permissible limits. Most of the metals of interest were also detected in the influent of the wastewater treatment plant. This renders dental clinics wastewater a hazardous waste which should be properly treated before it is discharged into the environment.”

“Mercury toxicity is a highly interesting topic in biomedicine due to the severe endpoints and treatment limitations. Selenite serves as an antagonist of mercury toxicity, but the molecular mechanism of detoxification is not clear. Inhibition of the selenoenzyme thioredoxin reductase (TrxR) is a suggested mechanism of toxicity. Here, we demonstrated enhanced inhibition of activity by inorganic and organic mercury compounds in NADPH-reduced TrxR, consistent with binding of mercury also to the active site selenolthiol. On treatment with 5 μM selenite and NADPH, TrxR inactivated by HgCl(2) displayed almost full recovery of activity. Structural analysis indicated that mercury was complexed with TrxR, but enzyme-generated selenide removed mercury as mercury selenide, regenerating the active site selenocysteine and cysteine residues required for activity. The antagonistic effects on TrxR inhibition were extended to endogenous antioxidants, such as GSH, and clinically used exogenous chelating agents BAL, DMPS, DMSA, and α-lipoic acid. Consistent with the in vitro results, recovery of TrxR activity and cell viability by selenite was observed in HgCl(2)-treated HEK 293 cells. These results stress the role of TrxR as a target of mercurials and provide the mechanism of selenite as a detoxification agent for mercury poisoning.”

“Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (N-acetyl-L-cysteine, alpha-lipoic acid, L-glutathione), with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. Increased oxidative stress and reduced oxidative defense are common. Selenium and fish containing omega-3 fatty acids antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity. Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.”

“Autism, a member of the pervasive developmental disorders (PDDs), has been increasing dramatically since its description by Leo Kanner in 1943. First estimated to occur in 4 to 5 per 10,000 children, the incidence of autism is now 1 per 110 in the United States, and 1 per 64 in the United Kingdom, with similar incidences throughout the world. Searching information from 1943 to the present in PubMed and Ovid Medline databases, this review summarizes results that correlate the timing of changes in incidence with environmental changes. Autism could result from more than one cause, with different manifestations in different individuals that share common symptoms. Documented causes of autism include genetic mutations and/or deletions, viral infections, and encephalitis following vaccination. Therefore, autism is the result of genetic defects and/or inflammation of the brain. The inflammation could be caused by a defective placenta, immature blood-brain barrier, the immune response of the mother to infection while pregnant, a premature birth, encephalitis in the child after birth, or a toxic environment.”