Archive for January, 2009

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Coexposure of neonatal mice to a flame retardant PBDE 99 (2,2′,4,4′,5-pentabromodiphenyl ether) and methyl mercury enhances developmental neurotoxic defects

Wednesday, January 28th, 2009

http://www.ncbi.nlm.nih.gov/pubmed/17982161?dopt=AbstractPlus

Coexposure of neonatal mice to a flame retardant PBDE 99 (2,2′,4,4′,5-pentabromodiphenyl ether) and methyl mercury enhances developmental neurotoxic defects

Fischer C, Fredriksson A, Eriksson P.
Department of Environmental Toxicology, Uppsala University, Norbyvägen 18A, S-752 36 Uppsala, Sweden.

Toxicol Sci. 2008 Feb;101(2):275-85. Epub 2007 Nov 2.

Epidemiological studies indicate that exposure to environmental pollutants during early human development can have deleterious effects on cognitive development. The interaction between environmental pollutants is suggested as one reason for the observed defective neurological development in children from the Faeroe Islands as compared to children from the Seychelles. We have previously seen in mice that polychlorinated biphenyls (PCBs) can interact together with methyl mercury (MeHg), as well as PCB together with polybrominated diphenyl ether (PBDE 99) to exacerbate developmental neurotoxic effects when present during a critical period of neonatal brain development. PBDEs are a new class of global environmental contaminants. The present study shows that neonatal coexposure to PBDE 99 (0.8 mg/kg body weight) and MeHg (0.4 or 4.0 mg/kg body weight) can exacerbate developmental neurotoxic effects. These effects are manifested as disrupted spontaneous behavior, reduced habituation, and impaired learning/memory abilities. This is seen in the low dose range, where the sole compounds do no give rise to developmental neurotoxic effects. The effects seen are more than just additive. Furthermore, a significant effect of interaction was seen on the cholinergic nicotinic receptors in the cerebral cortex and hippocampus. This suggests that a mechanism for the observed cognitive defects is via the cholinergic system. Furthermore, PBDE can interact with MeHg causing developmental neurotoxic effects similar to those we previously have observed between PCB 153 + MeHg and PCB 52 + PBDE 99. This is of vital importance, as the levels of PBDEs are increasing in mother’s milk and in the environment generally.

PMID: 17982161 [PubMed - indexed for MEDLINE]

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Posted in Children, Neurological Development | No Comments »

Acetylcholinesterase inhibitors and Gulf War illnesses.

Wednesday, January 28th, 2009

Proc Natl Acad Sci U S A. 2008 Mar 10 [Epub ahead of print]

Acetylcholinesterase inhibitors and Gulf War illnesses.
Golomb BA.

Department of Medicine, University of California, San Diego, CA 92093-0995.

Increasing evidence suggests excess illness in Persian Gulf War veterans (GWV) can be explained in part by exposure of GWV to organophosphate and carbamate acetylcholinesterase inhibitors (AChEis), including pyridostigmine bromide (PB), pesticides, and nerve agents. Evidence germane to the relation of AChEis to illness in GWV was assessed. Many epidemiological studies reported a link between AChEi exposure and chronic symptoms in GWV. The link is buttressed by a dose-response relation of PB pill number to chronic symptoms in GWV and by a relation between avidity of AChEi clearance and illness, based on genotypes, concentrations, and activity levels of enzymes that detoxify AChEis. Triangulating evidence derives from studies linking occupational exposure to AChEis to chronic health symptoms that mirror those of ill GWV. Illness is again linked to lower activity of AChEi detoxifying enzymes and genotypes conferring less-avid AChEi detoxification. AChEi exposure satisfies Hill’s presumptive criteria for causality, suggesting this exposure may be causally linked to excess health problems in GWV.

PMID: 18332428 [PubMed - as supplied by publisher]

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Posted in Gulf War Illness | No Comments »

Polymorphisms at the Paraoxonase 1 L55M and Q192R Loci Affect the Pathophysiology of Alzheimer’s Disease: Emphasis on the Cholinergic System and Beta-Amyloid Levels

Monday, January 26th, 2009

Polymorphisms at the Paraoxonase 1 L55M and Q192R Loci Affect the Pathophysiology of Alzheimer’s Disease: Emphasis on the Cholinergic System and Beta-Amyloid Levels

Leduc V, Poirier J.

Douglas Mental Health University Institute, Verdun, Que., Canada.

Neurodegener Dis. 2008;5(3-4):225-7. Epub 2008 Mar 6.

Background:
Paraoxonase 1 (PON1) functions to protect the cholinergic system against nerve gases and the organophosphate family of pesticides. Recent studies have shown that polymorphisms at the PON1 L55M and Q192R loci might affect individual susceptibility to experience-derived and environmental events such as the exposure to inhibitors of cholinesterase (ChEIs).

Objective:
ChEI therapy being the treatment of choice for mild-to-moderate Alzheimer’s disease (AD) patients, we determined whether genetic variations in the PON1 loci are associated with AD risk and whether they affect brain choline acetyltransferase (CHAT) activity, nicotinic receptor density, and beta-amyloid (Abeta) levels in different regions of AD and age-matched control subjects. Methods: This pilot genetic study used a small cohort of brains from autopsy-confirmed AD patients and age-matched controls from the Douglas Hospital Brain Bank, Quebec, Canada.

Results:
The frequency of the M55M genotype at the PON1 L55M locus was found to be significantly increased in AD patients relative to age-matched controls (p < 0.05). Significant associations were observed between the PON1 L55M and Q192R polymorphisms and frontal cortex Abeta levels as well as CHAT activity and nicotinic receptor density in the temporal cortex.

Conclusions:
Our results suggest a prominent role for PON1 in the pathophysiology of common AD with a marked impact on the cholinergic system and Abeta levels in the brain.

http://www.ncbi.nlm.nih.gov/pubmed/18322397?dopt=AbstractPlus

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Posted in Alzheimer's disease | No Comments »

The treatment of pulmonary diseases and respiratory-related conditions with inhaled (nebulized or aerosolized) glutathione

Monday, January 26th, 2009

The treatment of pulmonary diseases and respiratory-related conditions with inhaled (nebulized or aerosolized) glutathione

Prousky J.

The Canadian College of Naturopathic Medicine, 1255 Sheppard Avenue East, Toronto, ON M2K 1E2, Canada and International Primary Health Care, The External Program, University of London, London, UK.

Evid Based Complement Alternat Med. 2008 Mar;5(1):27-35.

Reduced glutathione or simply glutathione (gamma-glutamylcysteinylglycine; GSH) is found in the cytosol of most cells of the body. GSH in the epithelial lining fluid (ELF) of the lower respiratory tract is thought to be the first line of defense against oxidative stress. Inhalation (nebulized or aerosolized) is the only known method that increases GSH’s levels in the ELF. A review of the literature was conducted to examine the clinical effectiveness of inhaled GSH as a treatment for various pulmonary diseases and respiratory-related conditions. This report also discusses clinical and theoretical indications for GSH inhalation, potential concerns with this treatment, its presumed mechanisms of action, optimal doses to be administered and other important details. Reasons for inhaled GSH’s effectiveness include its role as a potent antioxidant, and possibly improved oxygenation and host defenses. Theoretical uses of this treatment include Farmer’s lung, pre- and postexercise, multiple
chemical sensitivity disorder and cigarette smoking. GSH inhalation should not be used as a treatment for primary lung cancer. Testing for sulfites in the urine is recommended prior to GSH inhalation.
Minor side effects such as transient coughing and an unpleasant odor are common with this treatment. Major side effects such as bronchoconstriction have only occurred among asthma patients presumed
to be sulfite-sensitive. The potential applications of inhaled GSH are numerous when one considers just how many pulmonary diseases and respiratory-related conditions are affected by deficient antioxidant status or an over production of oxidants, poor oxygenation and/or impaired host defenses. More studies are clearly warranted.

http://www.ncbi.nlm.nih.gov/pubmed/18317545?dopt=AbstractPlus

PMID: 18317545 [PubMed - in process]

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Posted in Glutathione | 1 Comment »

Influenza Drug Labels Get Warnings for Neuropsychiatric Changes

Monday, January 26th, 2009

FDA says some chemicals cause neuropsychiatric changes

Recalls and Warnings Influenza Drug Labels Get Warnings for Neuropsychiatric Changes Patients with influenza should be closely monitored for signs of abnormal behavior during treatment with Tamiflu and possibly also Relenza. (US Food and Drug Administration.)

Medscape Medical News
http://www.medscape.com/viewarticle/570996?sssdmh=dm1.339468&src=nldne

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Posted in Influenza, Relenza, Tamiflu | No Comments »

Photocopy machines and occupational antiphospholipid syndrome

Monday, January 26th, 2009

Photocopy machines and occupational antiphospholipid syndrome

Bar-Sela S, Shoenfeld Y.

Allergy and Clinical Immunology Clinic, Kupat Holim Meuhedet, Israel.

Isr Med Assoc J. 2008 Jan;10(1):52-4

Two patients who worked for several years in the operation and maintenance of photocopy machines developed an autoimmune disease. In both, early manifestations were thromboembolic phenomena associated with anticardiolipin antibodies. Joint and kidney involvement emerged later, with the appearance of other autoantibodies. These two patients were occupationally exposed to ultraviolet irradiation, ozone emission, and possibly some oxides of heavy metals. To our knowledge this is the
first report of occupational autoimmune disease in photocopy machine workers, and the first description of antiphospholipid syndrome as an occupational disease. The possible cause-effect inter-relationship between their occupational exposure and autoimmune disease is discussed.

http://www.ncbi.nlm.nih.gov/pubmed/18300574?dopt=AbstractPlus

PMID: 18300574 [PubMed - in process]

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Posted in Autoimmune Disease | No Comments »

The legal failure to prevent subclinical developmental toxicity.

Monday, January 26th, 2009

My experience suggests that clinical effects as well as subclinical ones are not being prevented. The rise in autism is a case in point. –Dr. Larry Plumlee

http://www.ncbi.nlm.nih.gov/pubmed/18226082?dopt=AbstractPlus
Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):267-73. Links

The legal failure to prevent subclinical developmental toxicity.

Cranor C.

Department of Philosophy, University of California, Riverside, CA 92521, USA. carl.cranor@ucr.edu

Legal systems appear to function poorly to identify and prevent subclinical developmental toxic effects in children that can lead to long-term harm. In the USA, the vast majority of substances enter commerce without any legally required testing (under so-called ‘post-market’ laws). In 1984, less than 20% of all substances had been subject to pre-market testing and there has been little change since. Once substances are suspected of contributing to harm, an administration agency has the burden to show risks or harms and their causes, an increasingly difficult demonstration. Post-market laws tend to produce no data prior to exposures and any protections result after some harm may have occurred. Pre-market screening laws such as the US Toxic Substances Control Act provide little data or protection. Pre-market testing and approval laws, analogous to US drug and pesticide laws, offer better approaches for identifying and eliminating toxicants before they result in harm, but do not apply to many products and rarely include concerns for developmental toxicity. The Registration, Evaluation, Authorization and Restriction of Chemicals legislation in the European Union has greater promise for the identification of new or existing toxicants. However, the potential for serious, subtle subclinical developmental effects provides reasons to pursue a more precautionary approach to identifying potential toxicants and forestalling harms. This paper sketches a more robust precautionary law and a more substantial departure from existing laws that would treat chemical invasions as trespasses. The scientific community can assist legal efforts by credibly publicizing the seriousness of subclinical developmental effects.

PMID: 18226082 [PubMed - in process]

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Posted in Children | No Comments »

Protective Effects of Bilberry (Vaccinium myrtillus L.) Extract on KBrO3-Induced Kidney Damage in Mice.

Monday, January 26th, 2009

J Agric Food Chem. 2008 Jan 23;56(2):420-5. Epub 2007 Dec 20. Links

Protective Effects of Bilberry (Vaccinium myrtillus L.) Extract on KBrO3-Induced Kidney Damage in Mice.

Bao L, Yao XS, Tsi D, Yau CC, Chia CS, Nagai H, Kurihara H.

Hiroshi_Kurihara@163.com, tyaoxs@jnu.edu.cn.

Potassium bromate (KBrO 3) is an oxidizing agent used as a food additive which causes kidney damage as a potent nephrotoxic agent, and the mechanism may be explained by the generation of oxygen free radicals. Our experiments showed that single intraperitoneal administration of 200 mg/kg KBrO 3 could induce serious kidney damage, with an increase in serum blood urea nitrogen (BUN) and creatinine levels. Five-day oral administration of bilberry ( Vaccinium myrtillus L.) extract at 50, 100, and 200 mg/kg resulted in a reversal in serum BUN and creatinine to normal levels and decreased kidney malondialdehyde (MDA), nitric oxide (NO), and xanthine oxidase (XOD) levels. Also, bilberry extract improved oxygen radical absorbance capacity (ORAC) levels in kidney tissue, which showed that bilberry extract reduced the degree of oxidative stress and kidney damage induced by KBrO 3. These findings demonstrate that the protective effect of bilberry extract is attributed to its free radical scavenging activity and lipid peroxidation inhibitory effect.

PMID: 18092757 [PubMed - in process]

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Posted in Bilberry, Kidney Damage | No Comments »

Attenuated Morning Salivary Cortisol Concentrations in a Population-based Study of Persons with Chronic Fatigue Syndrome and Well Controls.

Monday, January 26th, 2009

J Clin Endocrinol Metab. 2007 Dec 26 [Epub ahead of print]

Attenuated Morning Salivary Cortisol Concentrations in a Population-based Study of Persons with Chronic Fatigue Syndrome and Well Controls.

Nater UM, Maloney E, Boneva RS, Gurbaxani BM, Lin JM, Jones JF, Reeves WC, Heim C.

Chronic Viral Diseases Branch, Coordinating Center for Infectious Diseases, Centers for Disease Control & Prevention, Atlanta, GA; Department of Psychiatry & Behavioral Sciences, Emory University School of Medicine, Atlanta, GA; Department of Electrical and Computer Engineering, Georgia Institute of Technology, Atlanta, GA.

Context A substantial body of research on the pathophysiology of chronic fatigue syndrome (CFS) has focused on hypothalamic-pituitary-adrenal (HPA) axis dysregulation. The cortisol awakening response has received particular attention as a marker of HPA axis dysregulation. Objective The objective of the current study was to evaluate morning salivary cortisol profiles in persons with CFS and well controls identified from the general population. Design Case-control study. Setting This study was conducted at an outpatient research clinic. Cases and Other Participants We screened a sample of 19,381 residents of Georgia and identified those with CFS and a matched sample of well controls. Seventy-five medication-free CFS cases and 110 medication-free well controls provided complete sets of saliva samples. Main Outcome Measures Free cortisol concentrations in saliva collected on a regular workday, immediately upon awakening, 30 minutes and 60 minutes after awakening. Results There was a significant interaction effect, indicating different profiles of cortisol concentrations over time between groups, with the CFS group showing an attenuated morning cortisol profile. Notably, we observed a sex difference in this effect. Women with CFS exhibited significantly attenuated morning cortisol profiles compared with well women. In contrast, cortisol profiles were similar in men with CFS and male controls. Conclusions CFS was associated with an attenuated morning cortisol response but the effect was limited to women. Our results suggest that a sex difference in hypocortisolism may contribute to increased risk of CFS in women.

PMID: 18160468 [PubMed - as supplied by publisher]

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Posted in Chronic Fatigue Syndrome | No Comments »

The environmental burden of disease in Canada: Respiratory disease,

Monday, January 26th, 2009

Environ Res. 2007 Sep 27; [Epub ahead of print]

The environmental burden of disease in Canada: Respiratory disease, cardiovascular disease, cancer, and congenital affliction.
Boyd DR, Genuis SJ., School of Resource and Environmental Management, Simon Fraser University, 8888 University Drive, Burnaby, BC, Canada V5A 1S6.

BACKGROUND: Exposure to environmental hazards contributes to many chronic diseases, yet the magnitude of their contribution to the total disease burden in Canada is not well understood.
OBJECTIVES: To estimate the environmental burden of disease (EBD) in Canada for respiratory disease, cardiovascular disease, cancer, and congenital affliction. Quantifying the contribution of environmental exposures to the overall burden of disease could play an important role in shaping public
health and environmental policy priorities.
METHODS: The World Health Organization (WHO) recently estimated the environmental burden of disease globally by using a combination of comparative risk assessment data and expert judgment to develop environmentally attributable fractions (EAFs) of mortality and morbidity for 85 categories of disease. We use the EAFs developed by the WHO, EAFs developed by other researchers, and data from Canadian public health institutions to provide an initial estimate of the environmental burden of
disease in Canada for four major categories of disease.
RESULTS: Our results indicate that: 10,000-25,000 deaths; 78,000-194,000 hospitalizations; 600,000-1.5 million days spent in hospital; 1.1 million-1.8 million restricted activity days for asthma sufferers;
8000-24,000 new cases of cancer; 500-2500 low birth weight babies; and between $3.6 billion and $9.1 billion in costs occur in Canada each year due to respiratory disease, cardiovascular illness, cancer, and congenital affliction associated with adverse environmental exposures.
CONCLUSIONS: The burden of illness in Canada resulting from adverse environmental exposures is significant. Stronger efforts to prevent adverse environmental exposures are warranted, including research, education, and regulation.

PMID: 17904543 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17904543&ordinalpos=1
&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
or
http://tinyurl.com/2c7hnc

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Posted in Cancer, Cardiovascular, Congenital Affliction, Respiratory Disease | No Comments »

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