Saturday, October 27, 2007

Featured Research Studies

Featured Research Studies

Inhal Toxicol. 2007;19 Suppl 1:177-82.

 

Antioxidant enzyme induction: a new protective approach against the adverse effects of diesel exhaust particles


Wan J, Diaz-Sanchez D.  Hart and Louise Lyon Laboratory, Division of Clinical Immunology and Allergy, Department of Medicine, UCLA David Geffen School of Medicine, University of California, Los Angeles, California 90095-1690, USA.  

 

Exposure to airborne particulate pollutants sucassociated with allergic respiratory disorders, including asthma and allergic rhinitis. In this h as diesel exhaust particles (DEPs) has been communication, we review recent advances in the mechanism by which DEPs elicit their harmful effects and the protective role of antioxidants.


Reactive oxidative species (ROS) are believed to play a key role in cellular damage after exposure to DEPs. Numerous reports demonstrate that both proinflammatory and anti-inflammatory products are induced by DEPs via the activation of transcription factors. DEPs trigger multiple signaling pathways, which lead to DNA damage and cell apoptosis, inflammatory response, and antioxidant defense. Recent studies both in vitro and in mice show that antioxidants could alleviate the allergic inflammatory effects of DEPs. Human in vivo models suggest that the important phase II enzymes GSTM1 and GSTP1 modify the adjuvant effect of diesel exhaust particles on allergic inflammation. We have shown that the induction of phase II enzymes by the chemical sulforaphane can block DEP-induced enhanced immunoglobulin (Ig) E production in B cells and DEP-induced proinflammatory cytokine production in epithelial cells.


These findings suggest that overexpression of antioxidant enzymes could constitute a powerful potential chemopreventive approach against adverse effects induced by oxidant pollutants such as DEPs.

PMID: 17886065 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17886065&itool=pubmed_DocSum


 J Eur Acad Dermatol Venereol. 2007 Sep;21 Suppl 2:9-13.

Contact dermatitis: epidemiology and frequent sensitizers to cosmetics.

 

Diepgen TL, Weisshaar E.

Department of Social Medicine, Center of Occupational and Environmental Dermatology, University Hospital Heidelberg, Heidelberg, Germany. thomas.diepgen@med.uni-heidelberg.de


Contact dermatitis is defined as a pattern of inflammatory response that may occur as a result of contact with external factors. The two most common causes are irritants and allergens. Very few reliable data on prevalence and incidence of contact dermatitis exist, and data from the few studies that have been carried out cannot be compared because of differences in methodology. Occupational contact dermatitis constitutes up to 30% of all occupational diseases for which compensation is payable and affects sufferers' home and social lives as well as their working lives. Patients can be advised about the use of personal protective equipment and creams and emollients to avoid or ameliorate their condition, but there is little epidemiological evidence for their efficacy. Patch testing, using the European Standard Series of Allergens, is necessary to determine which agent is responsible for the condition. Fragrances and preservatives used in cosmetics are among the most common allergens in contact allergic dermatitis, although the frequency of contact allergy in the general population is small. It is to be hoped that the European Dermato-Epidemiology Network Fragrance Study will go some way to addressing the need for a large population-based epidemiological study in order that public health organizations can give reliable advice about avoiding and treating contact dermatitis.

 

PMID: 17716286 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17716286&itool=iconabstr&itool=pubmed_DocSum


Carbon Dioxide Inhalation Induces Dose-Dependent and Age-Related Negative Affectivity


Eric J. Griez1,2*, Alessandro Colasanti1, Rob van Diest1, Ewa Salamon1, Koen Schruers1  1 Department of Psychiatry and Neuropsychology, University of Maastricht, Maastricht, The Netherlands, 2 Department of Psychiatry and Behavioural Neuroscience, Upstate Medical University, State University of New York, Syracuse, New York, United States of America.

 

Abstract

Background

Carbon dioxide inhalation is known to induce an emotion similar to spontaneous panic in Panic Disorder patients. The affective response to carbon dioxide in healthy subjects was not clearly characterized yet.

Methodology/Principal Findings

Sixty-four healthy subjects underwent a double inhalation of four mixtures containing respectively 0, 9, 17.5 and 35% CO2 in compressed air, following a double blind, cross-over, randomized design. Affective responses were assessed according to DSM IV criteria for panic, using an Electronic Visual Analogue Scale and the Panic Symptom List. It was demonstrated that carbon dioxide challenges induced a dose dependent negative affect (p<0.0001). This affect was semantically identical to the DSM IV definition of panic. Older individuals were subjectively less sensitive to Carbon Dioxide (p<0.05).


Conclusions/Significance

CO2 induced affectivity may lay on a continuum with pathological panic attacks. Consistent with earlier suggestions that panic is a false biological alarm, the affective response to CO2 may be part of a protective system triggered by suffocation and acute metabolic distress.


http://www.plosone.org/article/info:doi/10.1371/journal.pone.0000987


Pediatr Endocrinol Rev. 2007 Sep;5(1):500-9.


Environmental thyroid toxicants and child endocrine health.


Massart F, Meucci V.


Pediatric Endocrine Unit Department of Pediatrics, Via Roma 67, 56125 PISA, Italy.
Humans are continuously exposed to many manmade chemicals, which are environmentally persistent and often hormone-like active. Substantial in vitro and in vivo evidence indicate that polyhalogenated aromatic pollutants, such as dioxins,furans,polychlorinated biphenyls and polybrominated diphenylethers, can adversely affect thyroid function mainly resulting in hypothyroidism. Although most studies on human background-exposure have as yet failed consistently to associate thyroid function with environmental toxicants, current views point towards subtle or transient impairment of thyroid secretion. Small hormonal changes chemically induced, though within normal reference ranges, may have negative consequences for the developing individual. In particular, the fetus and the neonate/infant may be vulnerable to subtle changes of thyroid function as their turnover of the thyroid hormonal store is very rapid and they may become depleted more rapidly than adults. This critical developmental phase may be vulnerable to even subtle toxicant effects on the thyroid system. Moreover, data inconsistencies may be related to sample size limitations and methodological issues, including mixed toxicant congener exposure that has precluded conclusions about chemical congeners per se. More studies are crucial to fill in the research gaps regarding permanent endocrine and neurological outcome in next generations exposed to background thyroid toxicants.


PMID: 17925791 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17925791&itool=iconabstr&itool=pubmed_DocSum


Biol Trace Elem Res. 2007 Dec;120(1-3):163-70.


Changed Clinical Chemistry Pattern in Blood After Removal of Dental Amalgam and other Metal Alloys Supported by Antioxidant Therapy.


Frisk P, Danersund A, Hudecek R, Lindh U.  Foundation for Metal Biology, Uppsala, Sweden ; Research in Metal Biology, Rudbeck Laboratory, Uppsala University, Uppsala, 751 85, Sweden.


This study aimed to investigate a possible connection between removal of dental amalgam restorations supported by antioxidant therapy and indicative changes of clinical chemistry parameters. A group of 24 patients, referred for complaints related to amalgam restorations, underwent a removal of their amalgams. All patients were treated with antioxidants (vitamin B-complex, vitamin C, vitamin E, and sodium selenite). An age- and sex-matched control group of 22 individuals was also included. The mercury (Hg) and selenium (Se) concentration in plasma, Hg concentration in erythrocytes, and 17 clinical chemistry variables were examined in three groups: patients before amalgam removal (Before), patients after amalgam removal (After), and control individuals (Control). The Hg and Se values decreased (p < 0.05) in plasma, and the Hg concentration decreased (p < 0.05) in erythrocytes after amalgam removal. The variables serum lactate dehydrogenase (serum LDH) and serum sodium differed significantly both when comparing Control with Before (p < 0.01) and Before with After (p < 0.01). The variables white blood cell count (WBC), blood neutrophil count, blood eosinophil count, blood basophil count, blood lymphocyte count, blood monocyte count, serum potassium, and serum creatinine differed in the Before/After test (p < 0.05). Multivariate statistics (discriminant function analysis) could separate the groups Before and After with only one misclassification.
PMID: 17916968 [PubMed - in process]


http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17916968&itool=iconabstr&itool=pubmed_DocSum

 

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