February 9th, 2009
Pak J Biol Sci. 2008 Apr 15;11(8):1142-6.
Mercury release from dental amalgam restorations after magnetic resonance imaging and following mobile phone use.
Mortazavi SM, Daiee E, Yazdi A, Khiabani K, Kavousi A, Vazirinejad R, Behnejad B, Ghasemi M, Mood MB.
Department of Medical Physics, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
In the 1st phase of this study, thirty patients were investigated. Five milliliter stimulated saliva was collected just before and after MRI. The magnetic flux density was 0.23 T and the duration of exposure of patients to magnetic field was 30 minutes. In the 2nd phase, fourteen female healthy University students who had not used mobile phones before the study and did not have any previous amalgam restorations were investigated. Dental amalgam restoration was performed for all 14 students. Their urine samples were collected before amalgam restoration and at days 1, 2, 3 and 4 after restoration. The mean +/- SD saliva Hg concentrations of the patients before and after MRI were 8.6 +/- 3.0 and 11.3 +/- 5.3 microg L(-1), respectively (p < 0.01). A statistical significant (p < 0.05) higher concentration was observed in the students used mobile phone. The mean +/- SE urinary Hg concentrations of the students who used mobile phones were 2.43 +/- 0.25, 2.71 +/- 0.27, 3.79 +/- 0.25, 4.8 +/- 0.27 and 4.5 +/- 0.32 microg L(-1) before the amalgam restoration and at days 1, 2, 3 and 4, respectively. Whereas the respective Hg concentrations in the controls, were 2.07 +/- 0.22, 2.34 +/- 0.30, 2.51 +/- 0.25, 2.66 +/- 0.24 and 2.76 +/- 0.32 microg L(-1). It appears that MRI and microwave radiation emitted from mobile phones significantly release mercury from dental amalgam restoration. Further research is needed to clarify whether other common sources of electromagnetic field exposure may cause alterations in dental amalgam and accelerate the release of mercury.
PMID: 18819554 [PubMed - in process]
Tags: Pak J Biol Sci
Posted in Cell Phones, Dental Amalgam, Mercury | No Comments »
February 9th, 2009
Environmental factors and autoimmune thyroiditis
Duntas LH.
University of Ulm, Germany. ledunt@otenet.gr
Nat Clin Pract Endocrinol Metab. 2008 Aug;4(8):454-60.
Autoimmune thyroiditis, of which Hashimoto thyroiditis represents the most frequent form, is an inflammatory state of the thyroid gland that results from the interaction between genetic variants that promote susceptibility and environmental factors. High iodine intake, selenium deficiency, pollutants such as tobacco smoke, infectious diseases such as chronic hepatitis C, and certain drugs are implicated in the development of autoimmune thyroiditis, primarily in genetically predisposed people. Long-term iodine exposure leads to increased iodination of thyroglobulin, which increases its antigenicity and initiates the autoimmune process in genetically susceptible individuals. Selenium deficiency decreases the activity of selenoproteins, including glutathione peroxidases, which can lead to raised concentrations of hydrogen peroxide and thus promote inflammation and disease. Such environmental pollutants as smoke, polychlorinated biphenyls, solvents and metals have been implicated in the autoimmune process and inflammation. Environmental factors have not yet, however, been sufficiently investigated to clarify their roles in pathogenesis, and there is a need to assess their effects on development of the autoimmune process and the mechanisms of their interactions with susceptibility genes.
http://www.ncbi.nlm.nih.gov/pubmed/18607401?dopt=AbstractPlus
PMID: 18607401 [PubMed - indexed for MEDLINE]
Tags: Nat Clin Pract Endocrinol Metab
Posted in Autoimmune Disease | No Comments »
February 9th, 2009
The Calif. Air Resources Board (CARB) finalized its ban on ozone generators for occupied spaces on Sept. 18, 2008. The ban takes effect in Fall 2010. It does not affect units that only filter the air. CARB was required to adopt the regulations by 12-31-08 pursuant to Assembly Bill 2276 enacted in 2006.
For more info, see www.arb.ca.gov/regact/2007/iacd07/iacd07.htm.
Tags: Calif. Air Resources Board
Posted in Indoor Air | No Comments »
February 9th, 2009
Rev Mal Respir. 2008 Jun;25(6):725-30.
[Indoor volatile organic compounds: concentrations, sources, variation factors.]
[Article in French]
Palot A, Charpin-Kadouch C, Ercoli J, Charpin D.
Service de pneumologie-allergologie, Hôpital Nord, Marseille et EA1784 IFR 112, Université de la Méditerranée, France.
Introduction Volatile organic compounds (V.O.C.) are part of urban air pollution and are also generated indoors from cleaning and maintenance products. Background VOC measurements are, on average, 10 times higher within homes than outside. Results of the national survey led by the Observatoire National de la Qualité de l’Air Intérieur demonstrated that up to 25% of French homes have very high or high concentrations of VOC. Indoor levels depend mainly on indoor sources. Aldehydes are included in many everyday life products. VOC originate from various household decorating and cleaning products. Some products are less detrimental to the environment and health and have special labelling. Indoor VOC levels also depend on the rate of air exchange and on household characteristics such as indoor temperature and humidity, age of the building, presence of smokers, and communication with a garage. Viewpoints The public may participate in maintaining good indoor air quality and the authorities should also improve regulations. Conclusion VOC are part of everyday air pollution. Their sources and concentrations should be better monitored.
PMID: 18772829 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/18772829?dopt=AbstractPlus
Tags: Rev Mal Respir
Posted in Air Pollutants | No Comments »
February 9th, 2009
http://www.ncbi.nlm.nih.gov/pubmed/18775774?dopt=AbstractPlus
Genomics. 2008 Sep 4. [Epub ahead of print]
Neuroendocrine and immune network re-modeling in chronic fatigue syndrome: An exploratory analysis.
Fuite J, Vernon SD, Broderick G.
Department of Medicine, Division of Pulmonary Faculty of Medicine and Dentistry, University of Alberta, 2E4.41 Walter Mackenzie Health Sciences Centre, 8440-112 Street, Edmonton, AB, Canada.
This work investigates the significance of changes in association patterns linking indicators of neuroendocrine and immune activity in patients with chronic fatigue syndrome (CFS). Gene sets preferentially expressed in specific immune cell isolates were integrated with neuroendocrine data from a large population-based study. Co-expression patterns linking immune cell activity with hypothalamic-pituitary-adrenal (HPA), thyroidal (HPT) and gonadal (HPG) axis status were computed using mutual information criteria. Networks in control and CFS subjects were compared globally in terms of a weighted graph edit distance. Local re-modeling of node connectivity was quantified by node degree and eigenvector centrality measures. Results indicate statistically significant differences between CFS and control networks determined mainly by re-modeling around pituitary and thyroid nodes as well as an emergent immune sub-network. Findings align with known mechanisms of chronic inflammation and support possible immune-mediated loss of thyroid function in CFS exacerbated by blunted HPA axis responsiveness.
PMID: 18775774 [PubMed - as supplied by publisher]
Tags: Genomics
Posted in Chronic Fatigue Syndrome | No Comments »
February 9th, 2009
1: Rheumatology (Oxford). 2008 Sep;47(9):1348-51. Epub 2008 May 22. Links
Hypovitaminosis D among rheumatology outpatients in clinical practice.
Mouyis M, Ostor AJ, Crisp AJ, Ginawi A, Halsall DJ, Shenker N, Poole KE.
Box 157, Department of Medicine, Division of Bone Research, University of Cambridge, Addenbrooke’s Hospital, Cambridge, CB2 2QQ, UK.
OBJECTIVES: A role for vitamin D in the pathogenesis of autoimmune and inflammatory diseases is emerging. We undertook an audit of 25-hydroxyvitamin D (25OHD) investigation and treatment in rheumatology outpatients. METHODS: Serum 25OHD requests were matched to electronic medical records from rheumatology and metabolic bone clinics (April 2006-March 2007). Data were analysed separately for two groups, ‘Documented osteoporosis/osteopaenia’ (Group 1) and ‘General rheumatology outpatients’ (Group 2, sub-divided by diagnosis). Hypovitaminosis D was defined by 25OHD levels <50 nmol/l. Values were compared with healthy adults to calculate geometric z-scores. RESULTS: A total of 263 patients were included (Group 1, n = 122; Group 2, n = 141) with an overall median 25OHD of 44 nmol/l.The 25OHD level among general rheumatology patients (median 39 nmol/l, mean z score -1.2, was statistically significantly lower than among osteoporotic/osteopaenic patients (median 49 nmol/l, mean z score of -0.9, p < 0.05 for the difference). 25OHD was lower in inflammatory arthritis and chronic pain/fibromyalgia than in other groups. Prescribing was recorded in 100 in Group 1 (of whom 95% were prescribed calcium/800 IU cholecalciferol) and 83 in Group 2 (91% calcium/800 IU). Only 31% of the patients with 25OHD <50 nmol/l would have been identified using general guidelines for screening patients at 'high risk' of hypovitaminosis D. CONCLUSIONS: Improved guidelines for managing hypovitaminosis D in rheumatology patients are needed. We found a high prevalence of hypovitaminosis D among secondary care patients in rheumatology and widespread supplementation with 800 IU cholecalciferol. Substantially reduced levels of serum 25OHD were identified among patients with inflammatory arthritis and chronic pain.
PMID: 18499714 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/18499714?dopt=AbstractPlus
Tags: Rheumatology
Posted in Vitamin D | No Comments »
February 6th, 2009
Inter-individual susceptibility to environmental toxicants–a current assessment
Nebert DW.
Department of Environmental Health, Center for Environmental Genetics, University of Cincinnati Medical Center, P.O. Box 670056, Cincinnati, OH 45267-0056, USA. dan.nebert@uc.edu
Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):34-42
Virtually all diseases have an environmental component. The two most important factors affecting your unique risk of an environmental disease (toxicity or cancer) are (a) your exposure to the environmental agent and (b) your genes. Epidemiologists have found ways to calculate inter-individual risk–if the exposure to environmental agents is sufficiently high and can be documented (e.g., years of cigarette smoking, taking prescribed drugs, drinking alcohol, or exposure to radon or other radioactive material, etc.). If the dose of environmental agents is lower and more ambiguous (e.g., exposure to chemicals on the job, herbicides sprayed on a golf course, outdoor or indoor air pollution, endocrine disruptors in cans of food, living near a toxic waste dump site, etc.), however, calculations of inter-individual risk become much more difficult. Highly accurate DNA tests for genetic susceptibility to toxicity and cancer have been sought in order to identify individuals at increa sed risk; this type of research represents the leading edge of phenotype-genotype association studies and is the major goal of most public health and preventive medicine programs. The task, however, has turned out to be far more challenging than anticipated. The major stumbling block has been the difficulty in determining an unequivocal phenotype or an unequivocal genotype. We were quite optimistic 5-10 years ago that this would be easy, but now we are beginning to appreciate how difficult it is to determine an unequivocal phenotype or genotype with certainty. For many reasons set forth in this overview, it appears that DNA testing alone, to predict and prevent environmental disease on an individual basis, may be virtually impossible with current knowledge and technologies and will require novel insights before major practical applications will evolve.
http://www.ncbi.nlm.nih.gov/pubmed/15982695?dopt=AbstractPlus
PMID: 15982695 [PubMed - indexed for MEDLINE]
Tags: Toxicol Appl Pharmacol
Posted in Environmental Toxicants | No Comments »
February 6th, 2009
Mol Aspects Med. 2008 Aug 26. [Epub ahead of print]
Glutathione in liver diseases and hepatotoxicity.
Yuan L, Kaplowitz N.
Internal Medicine, University of Southern California, USA; Los Angeles County (LAC) Medical Center Los Angeles, CA 90033, USA.
Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H(2)O(2) and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varied forms of oxidation, altering the function of signal transduction and transcription factor molecules. Increasing evidence supports the important role of ROS and GSH in modulating multiple signaling pathways. TNF-alpha and Fas signaling, NF-kappaB, JNK and mitochondrial apoptotic pathways are the focus of this review. The redox regulation either can switch on/off or regulate the threshold for some crucial events in these pathways. Notably, mitochondrial GSH depletion induces increased mitochondrial ROS exposure which impairs bioenergetics and promotes mitochondrial permeability transition pore opening which is critical for cell death. Depending on the extent of mitochondrial damage, NF-kappaB inhibition and JNK activation, hepatocytes may either undergo different modes of cell death (apoptosis or necrosis) or be sensitized to cell-death stimuli (i.e. TNF-alpha). These processes have been implicated in the pathogenesis of many liver diseases.
PMID: 18786561 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/18786561?dopt=AbstractPlus
Tags: Mol Aspects Med
Posted in Glutathione | 1 Comment »
February 6th, 2009
Inhal Toxicol. 2008 Sep 18:1. [Epub ahead of print]
Health Effects of Subchronic Inhalation Exposure to Gasoline Engine Exhaust.
Reed MD, Barrett EG, Campen MJ, Divine KK, Gigliotti AP, McDonald JD, Seagrave JC, Mauderly JL, Seilkop SK, Swenberg JA.
Lovelace Respiratory Research Institute, Albuquerque, NewMexico, USA.
Gasoline engine emissions are a ubiquitous source of exposure to complex mixtures of particulate matter (PM) and non-PM pollutants; yet their health hazards have received little study in comparison with those of diesel emissions. As a component of the National Environmental Respiratory Center (NERC) multipollutant research program, F344 and SHR rats and A/J, C57BL/6, and BALBc mice were exposed 6 h/day, 7 days/week for 1 week to 6 months to exhaust from 1996 General Motors 4.3-L engines burning national average fuel on a simulated urban operating cycle. Exposure groups included whole exhaust diluted 1:10, 1:15, or 1:90, filtered exhaust at the 1:10 dilution, or clean air controls. Evaluations included organ weight, histopathology, hematology, serum chemistry, bronchoalveolar lavage, cardiac electrophysiology, micronuclei in circulating cells, DNA methylation and oxidative injury, clearance of Pseudomonas aeruginosa from the lung, and development of respiratory allergic responses to ovalbumin. Among the 120 outcome variables, only 20 demonstrated significant exposure effects. Several statistically significant effects appeared isolated and were not supported by related variables. The most coherent and consistent effects were those related to increased red blood cells, interpreted as likely to have resulted from exposure to 13-107 ppm carbon monoxide. Other effects supported by multiple variables included mild lung irritation and depression of oxidant production by alveolar macrophages. The lowest exposure level caused no significant effects. Because only 6 of the 20 significant effects appeared to be substantially reversed by PM filtration, the majority of effects were apparently caused by non-PM components of exhaust.
http://www.ncbi.nlm.nih.gov/pubmed/18800271?dopt=AbstractPlus
PMID: 18800271 [PubMed - as supplied by publisher]
Tags: Inhal Toxicol
Posted in Air Pollutants | No Comments »
February 6th, 2009
Effect of sesame oil against acetaminophen-induced acute oxidative hepatic damage in rats
Chandrasekaran VR, Wan CH, Liu LL, Hsu DZ, Liu MY.
Department of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan.
Shock. 2008 Aug;30(2):217-21.
Acetaminophen (APAP) overdose causes acute liver injury or even death in both humans and experimental animals. We investigated the effect of sesame oil on APAP-induced acute liver injury. Male Wistar rats were given APAP (1,000 mg/kg; orally) to induce acute liver injury. Acetaminophen significantly increased aspartate transaminase, alanine transaminase, lipid peroxidation, and superoxide anion and hydroxyl radical generation levels; it also induced glutathione depletion. Sesame oil (8 mL/kg; orally) did not alter the gastric absorption of APAP, but it inhibited all the parameters altered by APAP and protected the rats against APAP-induced acute liver injury. We hypothesize that sesame oil maintained the intracellular glutathione levels, reduced reactive oxygen species levels, and inhibited lipid peroxidation in rats with APAP-induced acute liver injury.
http://www.ncbi.nlm.nih.gov/pubmed/18091569?dopt=AbstractPlus
Tags: Shock
Posted in Glutathione | No Comments »
