Environmental Factors Implicated in the Causation of Adverse Pregnancy Outcome

1: Semin Perinatol. 2007 Aug;31(4):240-242.

Environmental Factors Implicated in the Causation of Adverse Pregnancy Outcome.

Triche EW, Hossain N.

Yale Women & Children's Center for Blood Disorders, Yale University School of Medicine, New Haven, CT.

Adverse pregnancy outcome from environmental factors may include congenital anomalies, increased risk for miscarriage, preterm delivery, intrauterine growth restriction, and still birth. Apart from adverse pregnancy outcome, there may be effects on the other reproductive functions, like menstrual disorders and infertility. Environmental factors which have been implicated in adverse pregnancy outcome include smoking, video display terminals, anesthetic gases, antineoplastic drugs, and exposure to lead, selenium, and inorganic mercury. Among these, cigarette smoking during pregnancy has been the leading environmental factor for adverse pregnancy outcome. Cigarette smoking during pregnancy continues to be a significant public health concern. Maternal smoking during pregnancy has been associated with low birth weight (<2500 g). Mothers who smoke during pregnancy are twice as likely to give birth to low-birth weight infants. Similarly, air pollution, pesticide exposure, and stress have also been associated with low birth weight and preterm delivery. This review gives an overview of the importance of environmental factors in adverse pregnancy outcome.

PMID: 17825680 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17825680&itool=iconabstr&itool=pubmed_DocSum

Is chronic fatigue syndrome (CFS/ME) heritable in children, and if so why does it matter?

Is chronic fatigue syndrome (CFS/ME) heritable in children, and if so why does it matter?

Journal: Arch Dis Child. 2007 Sep 5; [Epub ahead of print]

Authors: Crawley EM, Davey Smith G.

Affiliation: University of Bristol, United Kingdom.

This article looks at the evidence for the heritability of Chronic Fatigue Syndrome or ME (CFS/ME). The role of genes and the environment and their potential interaction is discussed and the problems with studies in this area are explored.

One of the main difficulties with studying CFS/ME is the fact that it is likely to be a heterogeneous condition. We need a clear definition of CFS/ME in children and sample sizes for genetic studies need to be much larger if we are to make an impact in this important area.

In the meantime however, paediatricians shouldn't be surprised when they see a family where CFS/ME occurs in more than one person.

NLM Citation: PMID: 17804594      

        

Neurospect in neurotoxic chemical exposure demonstration of long-term functional abnormalities

Toxicol Ind Health. 1998 Nov-Dec;14(6):813-27.

Related Articles, Links

Neurospect in neurotoxic chemical exposure demonstration of long-term functional abnormalities.

Heuser G, Mena I.

Department of Radiology, UCLA-Harbor Medical Center, Torrance, USA. gheuser@ucla.edu

Patients who had experienced well-documented neurotoxic exposure months or years earlier were evaluated. Seventy-two right-handed adults who claimed continuing abnormalities of cognitive and memory function were examined after Xenon-133 inhalation and i.v. HMPAO. Single photon emission computed tomography (SPECT) results were statistically compared with age-matched controls. Bilateral, often asymmetrical, impairment of perfusion was found, mostly in the frontal, temporal, and parietal lobes. This hypoperfusion was predominantly left-sided in young patients and predominantly right-sided in the elderly. Abnormalities were found months and years after neurotoxic exposure had ceased. Our findings suggest that NeuroSPECT can provide evidence of impaired cerebral function and may therefore help to further define neurotoxic exposure and its chronic effects.

PMID: 9891913 [PubMed - indexed for MEDLINE]

The allegory of a mountain: An environmental introduction to neurotoxicology.

The allegory of a mountain: An environmental introduction to neurotoxicology.

Prockop LD.

Department of Neurology, USF Health, University of South Florida,
Tampa, FL, USA.

J Neurol Sci. 2007 Aug 29

Overall, the area of human neurotoxicity offers significant difficulties as well as challenges in our attempts to maintain or enhance human well being. Many of the substances to which humans are being exposed are relatively new to the environment, i.e., the products of a sophisticated industrial development. As a result humans are exposed to volatile organic compounds not previously present in our environment in significant amounts. It is important to maintain our industrial complex and the economic growth of our society. The use of volatile organic compounds is often important to the success of the industry. However, it is also important for us to determine what concentration of a given substance may produce short-term effects or chronic long-term effects. Human exposure to these potentially toxic levels could then be prevented. This is especially true because once irreversible damage occurs there is no medical treatment that can lead to improvement. Therefore, prevention of neurotoxic injury is essential.

This study from 1969 explains provocation tests with different

Bronchial Asthma and Asthmatic Bronchitis Determined by Simple Chemicals

V. Popa M.D.1; D. Teculescu M.D.2; D. Stanescu M.D.2; and N. Gavrilescu M.D.3

1 Investigator, Allergy Unit, Department of Occupational Diseases, Colentina Hospital, Bucharest, Romania
2 Investigator, Cardiopulmonary Laboratory, Department of Occupational Diseases, Colentina Hospital, Bucharest Romania 3 Associate Professor of Occupational Medicine, Colentina Hospital, Bucharest, Romania

Chest. 1969;56:395-404.)
© 1969 American College of Chest Physicians

Thirty-three subjects with bronchial asthma and 15 subjects with asthmatic bronchitis caused by occupational exposure to simple chemicals were submitted to an allergologic investigation. Essentially this consisted of skin tests, inhalation tests, determination of some types of circulating antibodies, carried out with nonirritant concentrations of simple chemicals and with usual allergens. Results indicated that bronchial asthma and asthmatic
bronchitis, due to micromolecular substances, may be either irritative (28 cases) or allergic (15 cases). In five subjects the mechanism could not be established. A certain substance may give rise, in different subjects, to both types of bronchial asthma and asthmatic bronchitis mentioned above. Besides the well-known picture of bronchial asthma with reagins, the authors describe another pattern of skin and bronchial response; this pattern has many features in common with the delayed hypersensitivity.

Abstract:

http://www.chestjournal.org/cgi/content/abstract/56/5/395

Full text:
http://www.chestjournal.org/cgi/reprint/56/5/395

 

Anti-polymer antibody in Italian fibromyalgic patients

Arthritis Res Ther. 2007 Sep 6;9(5):R86 [Epub ahead of print]

Anti-polymer antibody in Italian fibromyalgic patients.

Bazzichi L, Giacomelli C, De Feo F, Giuliano T, Rossi A, Doveri M, Tani C, Wilson RB, Bombardieri S.

ABSTRACT: The objectives of our study were to evaluate the presence of antipolymer antibody (APA) seropositivity in 285 Italian patients affected by primary fibromyalgia (FM) and to verify if APA levels correlate with the disease severity and cytokine levels. APA levels were determined on serum samples by an indirect ELISA kit that detect IgG APA. Cytokines (IL-1, IL-6, IL-8, IL-10 and TNF-alpha) were measured by ELISA in plasma. The impact of fibromyalgia on the quality of life was estimated using the "Fibromyalgia Impact Questionnaire" (FIQ), while pain severity was evaluated using a Visual Analogic Scale (VAS). Patients were also characterized by the presence of tiredness, stiffness, non restorative sleep, anxiety, depression, tension headache, irritable bowel syndrome, temporomandibular dysfunction, Raynaud phenomena. Using a cut-off value of 30 U, APA positive values were detected in 60 FM patients (21.05%) and in 15 healthy controls (15.00%) without significant differences among their levels or percentage of seropositivity. FM patients with moderate and severe symptoms had slightly higher APA levels with respect to patients with mild symptoms. APA seropositive patients exhibited significant correlations between APA levels and FIQ (P=0.042), tiredness (P=0.003) and IL-1 levels (P=0.0072). In conclusion, APA cannot be considered a marker of disease in Italian FM patients. However, its presence might permit the identification of a subset of FM patients with more severe symptoms and who may respond differently to different therapeutic strategies.

PMID: 17822528 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17822528&itool=iconabstr&itool=pubmed_DocSum

Somaesthetic disturbances in fibromyalgia are exaggerated by sensory motor conflict: implications for chronicity of the disease?

Somaesthetic disturbances in fibromyalgia are exaggerated by sensory
motor conflict: implications for chronicity of the disease?

Rheumatology (Oxford). 2007 Sep 1; [Epub ahead of print]

McCabe CS, Cohen H, Blake DR.

The Royal National Hospital for Rheumatic Diseases in conjunction
with The School for Health, University of Bath, Bath BA1 1RL, UK.

Objectives. Conflict between sensory-motor central nervous processing
generates somaesthetic disturbances, including pain, in healthy
volunteers (HVs). Such conflict has been proposed as a potential
cause of pain that occurs in the absence of injury or when the pain
response is disproportionate to the injury. Fibromyalgia (FMS)
exemplifies the former state. We hypothesized that the artificial
generation of such conflict would exacerbate somaesthetic perceptions
including pain in FMS greater than in HVs.

Methods. Twenty-nine adults with FMS took part in an established task
that generates varied degrees of sensory-motor conflict during
congruent/incongruent limb movements. A qualitative methodology
recorded any changes in sensory experience. Data generated were
compared with age and gender-matched HV data.

Results. Twenty-six subjects (89.7%) with FMS reported changes in
sensory perception at some stage in the protocol in addition to, or
worse than, baseline compared with 14 (48%) of HVs. All stages of the
protocol generated a higher frequency of report in the FMS population
than that of the maximum report in the HVs population. New
perceptions included disorientation, pain, perceived changes in
temperature, limb weight or body image.

Conclusions. Our findings support the hypothesis that motor-sensory
conflict can exacerbate pain and sensory perceptions in those with
FMS to a greater extent than in HVs.

PMID: 17767000

Combined dexamethasone/corticotropin-releasing factor test in chronic fatigue syndrome

Combined dexamethasone/corticotropin-releasing factor test in chronic fatigue syndrome.

Journal: Psychol Med. 2007 Sep 6;:1-11 [Epub ahead of print]

Authors: Van Den Eede F, Moorkens G, Hulstijn W, Van Houdenhove B, Cosyns P, Sabbe BG, Claes SJ.

Affiliation: Department of Molecular Genetics VIB8, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Antwerp, Belgium.

BACKGROUND: Studies of hypothalamic-pituitary-adrenal (HPA) axis function in chronic fatigue syndrome (CFS) point to hypofunction, although there are negative reports. Suggested mechanisms include a reduced hypothalamic or supra-hypothalamic stimulus to the HPA axis and enhanced sensitivity to the negative feedback of glucocorticoids. The aim of the current study was to investigate HPA axis function in CFS with the dexamethasone/corticotropin-releasing factor (Dex/CRF) test, in analogy with research in affective disorders.

Method: Thirty-four well-characterized female CFS patients and 25 healthy control subjects participated in the low-dose Dex/CRF test. Current major depressive episode was an exclusion criterion. History of early-life stress (ELS) was assessed with the Structured Trauma Interview.

RESULTS: Salivary cortisol responses after 0.5 mg Dex were lower in CFS patients than in controls (before 100 mug CRF, p=0.038; after 100 mug CRF, p=0.015). A secondary analysis revealed an influence of early-life stress and of oestrogen intake. After removal of the 10 participants who were taking an oral oestrogen, patients without a history of ELS showed lower cortisol responses than patients with ELS and controls (before CRF, p=0.005; after CRF, p=0.008).

CONCLUSIONS: CFS is globally associated with reduced cortisol responses in the combined low-dose Dex/CRF test, but this effect is only clearly present in CFS patients without a history of ELS. This study provides further support for an enhanced glucocorticoid negative feedback and/or a reduced central HPA axis drive in CFS. Furthermore, it demonstrates that ELS is an important variable to consider in CFS research.

NLM Citation: PMID: 17803834

Environmental exposures and gene regulation in disease etiology

Environ Health Perspect. 2007 Sep;115(9):1264-70.

Environmental exposures and gene regulation in disease etiology.

Edwards TM, Myers JP.

Department of Zoology, University of Florida, Gainesville, Florida, USA.

OBJECTIVE: Health or disease is shaped for all individuals by interactions between their genes and environment. Exactly how the environment changes gene expression and how this can lead to disease are being explored in a fruitful new approach to environmental health research, representative studies of which are reviewed here. DATA SOURCES: We searched Web of Science and references of relevant publications to understand the diversity of gene regulatory mechanisms affected by environmental exposures with disease implications. DATA SYNTHESIS: Pharmaceuticals, pesticides, air pollutants, industrial chemicals, heavy metals, hormones, nutrition, and behavior can change gene expression through a broad array of gene regulatory mechanisms. Mechanisms include regulation of gene translocation, histone modifications, DNA methylation, DNA repair, transcription, RNA stability, alternative RNA splicing, protein degradation, gene copy number, and transposon activation. Furthermore, chemically induced changes in gene regulation are associated with serious and complex human diseases, including cancer, diabetes and obesity, infertility, respiratory diseases, allergies, and neurodegenerative disorders such as Parkinson and Alzheimer diseases. One of the best-studied areas of gene regulation is epigenetics, especially DNA methylation. Our examples of environmentally induced changes in DNA methylation are presented in the context of early development, when methylation patterns are initially laid down. This approach highlights the potential role for altered DNA methylation in fetal origins of adult disease and inheritance of acquired genetic change. CONCLUSIONS: The reviewed studies indicate that genetic predisposition for disease is best predicted in the context of environmental exposures. Second, the genetic mechanisms investigated in these studies offer new avenues for risk assessment research. Finally, we are likely to witness dramatic improvements in human health, and reductions in medical costs, if environmental pollution is decreased.

PMID: 17805414 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17805414&itool=iconabstr&itool=pubmed_DocSum

Reviewing the Environmental and Human Health Knowledge Base of Carbon Nanotubes

Reviewing the Environmental and Human Health Knowledge Base of Carbon Nanotubes Aasgeir Helland,1,2 Peter Wick,3 Andreas Koehler,1 Kaspar Schmid,4 and Claudia Som1 1Technology and Society Lab, EMPA (Swiss Federal Laboratories for Materials Testing and Research), St. Gallen, Switzerland; 2Institute for Human-Environment Systems, ETH (Swiss Federal Institute of Technology) Zurich, Zurich, Switzerland; 3Laboratory for Biocompatible Materials, EMPA, St. Gallen, Switzerland; 4Institute for Occupational Health Sciences, Lausanne, Switzerland Abstract Carbon nanotubes (CNTs) are considered one of the most promising materials in nanotechnology, with attractive properties for many technologic applications. The different synthesis, purification, and postprocessing methods produce CNTs with different physical characteristics, which can be applied in different fields ranging from composite materials, medical applications, and electronics to energy storage. The widespread projected use of CNTs makes it important to understand their potential harmful effects. In this environmental health review we observed a remarkable range of results of some of the toxicology studies. The comparability should be improved by further standardization and introduction of reference materials. However, at present the findings of this review suggest several key points: a) there are different types of CNTs, and therefore they cannot be considered a uniform group of substances ; and b) in environmental compartments, CNTs can be bioavailable to organisms. The properties of CNTs suggest a possible accumulation along the food chain and high persistence. In organisms the absorption, distribution, metabolism, excretion, and toxicity of CNTs depend on the inherent physical and chemical characteristics such as CNT functionalization, coating, length, and agglomeration state that are influenced by the external environmental conditions during CNT production, use, and disposal stages. Characterized exposure scenarios could therefore be useful when conducting toxicologic studies. However, CNTs produce a toxic response upon reaching the lungs in sufficient quantity ; this reaction is produced in a time- and dose-dependent manner. The identification of possible risks to human health and environment is a prerequisite for a successful introduction of CNTs in future applications. Key words: carbon nanotubes, cytotoxicology, ecotoxicology, environment, environmental fate, human health, in vitro, in vivo, nanomaterials, nanotechnology, nanotoxicology. Environ Health Perspect 115:1125–1131 (2007) . doi:10.1289/ehp.9652 available via http://dx.doi.org/ [Online 10 May 2007]

 

http://www.ehponline.org/docs/2007/9652/abstract.html

Occupational toxicant inhalation injury: the World Trade Center (WTC) experience

Int Arch Occup Environ Health. 2007 Sep 5; [Epub ahead of print]

Occupational toxicant inhalation injury: the World Trade Center (WTC) experience.

de la Hoz RE, Shohet MR, Chasan R, Bienenfeld LA, Afilaka AA, Levin SM, Herbert R.

Department of Community and Preventive Medicine, and Medicine, The Mount Sinai School of Medicine, WTC Health Effects Treatment Program, One Gustave L. Levy Place, Box 1059, New York, NY, 10029, USA, Rafael.delaHoz@mssm.edu.

OBJECTIVE AND METHODS: Clinical descriptive data is presented on a group of 554 former workers and volunteers (with more than 90 different occupations) at the World Trade Center (WTC) disaster site. A subsample of 168 workers (30% of the group) was selected to examine lower airway disease risk in relation to smoking and WTC exposure variables. RESULTS: Five diagnostic categories clearly predominate: upper airway disease (78.5%), gastroesophageal reflux disease (57.6%), lower airway disease (48.9%), psychological (41.9%) and chronic musculoskeletal illnesses (17.8%). The most frequent pattern of presentation was a combination of the first three of those categories (29.8%). Associations were found between arrival at the WTC site within the first 48 h of the terrorist attack and lower airway and gastroesophageal reflux disease, and between past or present cigarette smoking and lower airway disease. CONCLUSION: Occupational exposures at the WTC remain consistently associated with a disease profile, which includes five major diagnostic categories. These conditions often coexist in different combinations, which (as expected) mutually enhances their clinical expression, complicates medical management, and slows recovery. Cigarette smoking and early arrival at the WTC site appear to be risk factors for lower airway disease diagnosis.

PMID: 17786467 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17786467&itool=iconabstr&itool=pubmed_DocSum

Request for Information (RFI): Genetic Variation and the Basis for Individual Susceptibility to Environmental Toxicant Associated Disease

Sent: Thursday, September 06, 2007 8:48 AM

Subject: NTP UPDATE: Request for Information (RFI): Genetic Variation and the Basis for Individual Susceptibility to Environmental Toxicant Associated Disease

The NTP is currently soliciting information from the extramural and intramural research communities on the strategies, resources, and tools necessary to enable this cooperative research program on genetic variation and individual susceptibility to environmental toxicant exposure and associated polygenic diseases to progress. The Request for Information (RFI): Genetic variation and the basis for individual susceptibility to environmental toxicant associated disease was published today in the NIH Guide for Grants and Contracts – see URL:
http://grants.nih.gov/grants/guide/notice-files/NOT-ES-07-009.html

You may respond online to any or all of the questions on the RFI by October 14, 2007 at URL:
http://ntp.niehs.nih.gov/go/32130

You may visit the Host Susceptibility Program website at:
http://ntp.niehs.nih.gov/go/32132

The relation between urinary metabolite of pyrethroid insecticides and semen quality in humans

The relation between urinary metabolite of pyrethroid insecticides and semen quality in humans

Xia Y, Han Y, Wu B, Wang S, Gu A, Lu N, Bo J, Song L, Jin N, Wang X.
Key Laboratory of Reproductive Medicine, Institute of Toxicology.

Fertil Steril. 2007 Aug 30

OBJECTIVE: To explore the possible association between internal exposure levels of 3-phenoxybenzoic acid (3-PBA), an urinary metabolite of pyrethroids, and altered semen quality in Chinese men. DESIGN: A retrospective case-control study.

SETTING: Center of clinical reproductive medicine.

PATIENT(S): Three hundred seventy-six men with nonobstructive infertility.

MAIN OUTCOME MEASURE(S): Urinary 3-PBA concentration, semen volume, sperm concentration, sperm number per ejaculum, sperm motility, sperm progression, and motion parameters.

RESULT(S): The median 3-PBA concentration was 0.879 mug/g of creatinine. There was suggestive association between increased creatinine-adjusted 3-PBA quartiles and sperm concentration (odd ratios for the first, second, third, and fourth quartiles, were 1.00, 1.31, 1.73, and 2.04, respectively), whereas sperm volume, sperm number per ejaculum, and sperm motility were weakly or nonsignificantly associated with 3-PBA quartiles. The sperm progression and motion parameters associated with creatinine-adjusted 3-PBA levels were straight line velocity (VSL) and curvilinear velocity (VCL).

CONCLUSION(S): These observed associations between 3-PBA levels and some altered semen quality indicated the reproductive effects of pyrethroid exposure on adult men.

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17765231&itool=pubmed_DocSum

PMID: 17765231 [PubMed - as supplied by publisher]

Mercury toxicity presenting as chronic fatigue, memory impairment and depression

Neuro Endocrinol Lett. 2006 Aug;27(4):415-23.

 

Mercury toxicity presenting as chronic fatigue, memory impairment and depression: diagnosis, treatment, susceptibility, and outcomes in a New Zealand general practice setting (1994-2006).

 

Wojcik DP, Godfrey ME, Christie D, Haley BE.Northland Environmental Health Clinic, 2 Dip Rd, Kamo, Whangarei, Northland, New Zealand. wojcik@wave.co.nz

In a group of 465 patients diagnosed as having chronic mercury toxicity (CMT), 32.3% had severe fatigue, 88.8% had memory loss, and 27.5% had depression. A significant correlation was found between CMT and the Apo-lipoprotein E4 genotype (p=0.001). An investigation into an additional 864 consecutively seen general practice patients, resulted in 30.3% having evidence consistent with CMT, and once again a significant correlation was found with the APO-E4 genotype (p=0.001). Removal of amalgam mercury fillings when combined with appropriate treatment resulted in a significant symptom reduction (p<0.001) to levels reported by healthy subjects.PMID:

 

16891999 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16891999&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Long-term use of cellular phones and brain tumours: increased risk associated with use for 10 years

Long-term use of cellular phones and brain tumours: increased risk associated with use for 10 years

Lennart Hardell¹, Michael Carlberg², Fredrik Söderqvist³, Kjell Hansson Mild⁴ and L. Lloyd Morgan⁵

¹ Department of Oncology, University Hospital, Örebro and Department of Natural Sciences, Örebro University, Örebro, Sweden
² Department of Oncology, University Hospital, Örebro, Sweden
³ Department of Oncology, University Hospital and Institute of Clinical Medicine, Örebro University, Örebro, Sweden
⁴ National Institute for Working Life, Umeå and Department of Natural Sciences, Örebro University, Örebro, Sweden
⁵ Francisco Street, Berkeley, California, USA

Correspondence to:
Dr L Hardell
Department of Oncology, University Hospital, SE-701 85 Örebro, Sweden; lennart.hardell@orebroll.se

Accepted 28 March 2007

	ABSTRACT

TOP ABSTRACT METHODS RESULTS DISCUSSION REFERENCES

 
Aim: To evaluate brain tumour risk among long-term users of cellular telephones.

Methods: Two cohort studies and 16 case–control studies on this topic were identified. Data were scrutinised for use of mobile phone for 10 years and ipsilateral exposure if presented.

Results: The cohort study was of limited value due to methodological shortcomings in the study. Of the 16 case–control studies, 11 gave results for 10 years' use or latency period. Most of these results were based on low numbers. An association with acoustic neuroma was found in four studies in the group with at least 10 years' use of a mobile phone. No risk was found in one study, but the tumour size was significantly larger among users. Six studies gave results for malignant brain tumours in that latency group. All gave increased odd ratios (OR), especially for ipsilateral exposure. In a meta-analysis, ipsilateral cell phone use for acoustic neuroma was OR = 2.4 (95% CI 1.1 to 5.3) and OR = 2.0, (1.2 to 3.4) for glioma using a tumour latency period of 10 years.

Conclusions: Results from present studies on use of mobile phones for 10 years give a consistent pattern of increased risk for acoustic neuroma and glioma. The risk is highest for ipsilateral exposure.

---

Abbreviations: DECT, digital enhanced cordless telecommunications; RF, radiofrequency; SIR, standardised incidence ratio; UMTS, universal mobile telecommunication system

Keywords: mobile phones; acoustic neuroma; glioma; ipsilateral exposure\

http://oem.bmj.com/cgi/content/full/64/9/626

Ameliorating the Developmental Neurotoxicity of Chlorpyrifos: A Mechanisms-Based Approach in PC12 Cells

Ameliorating the Developmental Neurotoxicity of Chlorpyrifos: A Mechanisms-Based Approach in PC12 Cells

Environmental Health Perspectives Volume 115, Number 9, September 2007

http://www.ehponline.org/members/2007/10194/10194.pdf

Theodore A. Slotkin, Emiko A. MacKillop, Ian T. Ryde, and Frederic J. Seidler

Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA

Abstract
Background: Organophosphate developmental neurotoxicity involves multiple mechanisms converging on neural cell replication and differentiation.

Objectives: We evaluated mechanisms contributing to the adverse effects of chlorpyrifos (CPF) on DNA synthesis, cell number and size, and cell signaling mediated by adenylyl cyclase (AC) in PC12 cells, a neuronotypic cell line that recapitulates the essential features of developing mammalian neurons.

Results: In undifferentiated cells, cholinergic receptor antagonists had little or no protective effect against the antimitotic actions of CPF ; however, when nerve growth factor was used to evoke differentiation, the antagonists showed partial protection against deficits in cell loss and alteration in cell size elicited by CPF, but were ineffective in preventing the deterioration of AC signaling. Nicotine, which stimulates nicotinic acetylcholine receptors but also possesses a mixture of prooxidant/antioxidant activity, had adverse effects by itself but also protected undifferentiated cells from the actions of CPF and had mixed additive/protective effects on cell number in differentiating cells. The antioxidant vitamin E also protected both undifferentiated and differentiating cells from many of the adverse effects of CPF but worsened the impact on AC signaling. Theophylline, which prevents the breakdown of cyclic AMP, was the only agent that restored AC signaling to normal or supranormal levels but did so at further cost to cell replication.

Conclusions: Our results show definitive contributions of cholinergic hyperstimulation, oxidative stress, and interference with AC signaling in the developmental neurotoxicity of CPF and point to the potential use of this information to design treatments to ameliorate these adverse effects.

Key words: adenylyl cyclase, brain development, chlorpyrifos, cholinergic antagonists, neurotoxicity, nicotine, organophosphate insecticides, oxidative stress, theophylline, vitamin E. Environ Health Perspect 115:1306–1313 (2007) . doi:10.1289/ehp.10194 available via http://dx.doi.org/ [Online 14 June 2007]

Olfactory enrichment enhances the survival of newly born cortical neurons in adult mice

Neuroreport. 2007 Jul 2;18(10):981-5. Links

Olfactory enrichment enhances the survival of newly born cortical neurons in adult mice.

Shapiro LA, Ng KL, Zhou QY, Ribak CE.

Department of Anatomy and Neurobiology, University of California at Irvine, Irvine, California 92697-1275, USA. lshapiro@uci.edu

Neurogenesis persists in the adult rodent olfactory epithelium and olfactory bulbs. Recent studies suggest that neurogenesis might also occur in the adult rodent piriform cortex, the primary cortical projection site of the olfactory bulbs. To determine whether olfactory enrichment influences neurogenesis in the mouse piriform cortex, olfactory enrichment was used in combination with bromodeoxyuridine labeling. Quantification of the number of bromodeoxyuridine-labeled cells in the piriform cortex that double label for either the immature neuronal marker, doublecortin, or the mature neuronal marker, neuronal nuclei or NeuN, showed that olfactory enrichment increases the survival of newborn neurons in the piriform cortex. These results confirm that neurogenesis occurs in the piriform cortex of rodents and suggest that it may play a neuroplastic role there.

PMID: 17558281 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17558281&itool=iconabstr&itool=pubmed_DocSum 

Body Position-Dependent Shift in Odor Percept Present Only for Perithreshold Odors

Chem Senses. 2007 Aug 30; [Epub ahead of print]

Body Position-Dependent Shift in Odor Percept Present Only for Perithreshold Odors.

Lundström JN, Boyle JA, Jones-Gotman M.

1Department of Psychology.

We recently demonstrated that a supine position causes a decrease in olfactory sensitivity compared with an upright position. We pursued that initial finding in 3 separate experiments in which we explored the extent of, and mechanism underlying, this phenomenon. In Experiment 1, we replicated the decrease in olfactory sensitivity when in a supine compared with an upright position. In Experiment 2, we measured body position-dependent shifts in physiological variables and sniff measures while smelling suprathreshold odorants and performing a perithreshold odor intensity discrimination task. Olfactory performances were reduced while supine. However, no relationships between the shift in olfactory performances and either the physiological variables or sniff measures were found. In Experiment 3, we determined that there were no position-dependent shifts in ability to discriminate or identify suprathreshold odors or rate them for pleasantness, intensity, or familiarity. However, a drop in scores was observed, and performance was slowed, on a cognitive skill while supine. These results demonstrate a body position-dependent shift in olfactory sensitivity only for perithreshold odors that appears to be mediated by cognitive rather than physiological factors. Implications for olfactory imaging studies are discussed.

PMID: 17761723 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17761723&itool=iconabstr&itool=pubmed_DocSum 

Developmental mercury exposure elicits acute hippocampal cell death, reductions in neurogenesis, and severe learning deficits during puberty.

 J Neurochem. 2007 Aug 30; [Epub ahead of print]

Developmental mercury exposure elicits acute hippocampal cell death, reductions in neurogenesis, and severe learning deficits during puberty.

Falluel-Morel A, Sokolowski K, Sisti HM, Zhou X, Shors TJ, Dicicco-Bloom E.

Department of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey, USA.

Normal brain development requires coordinated regulation of several processes including proliferation, differentiation, and cell death. Multiple factors from endogenous and exogenous sources interact to elicit positive as well as negative regulation of these processes. In particular, the perinatal rat brain is highly vulnerable to specific developmental insults that produce later cognitive abnormalities. We used this model to examine the developmental effects of an exogenous factor of great concern, methylmercury (MeHg). Seven-day-old rats received a single injection of MeHg (5 mug/gbw). MeHg inhibited DNA synthesis by 44% and reduced levels of cyclins D1, D3, and E at 24 h in the hippocampus, but not the cerebellum. Toxicity was associated acutely with caspase-dependent programmed cell death. MeHg exposure led to reductions in hippocampal size (21%) and cell numbers 2 weeks later, especially in the granule cell layer (16%) and hilus (50%) of the dentate gyrus defined stereologically, suggesting that neurons might be particularly vulnerable. Consistent with this, perinatal exposure led to profound deficits in juvenile hippocampal-dependent learning during training on a spatial navigation task. In aggregate, these studies indicate that exposure to one dose of MeHg during the perinatal period acutely induces apoptotic cell death, which results in later deficits in hippocampal structure and function.

PMID: 17760861 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17760861&itool=iconabstr&itool=pubmed_DocSum

Life, the environment and our ecosystem

J Inorg Biochem. 2007 Jul 16; [Epub ahead of print] Links

Life, the environment and our ecosystem.

Williams RJ.

Inorganic Chemistry Laboratory, University of Oxford, South Parks Road, Oxford OX1 3QR, UK.

This article is dedicated to Ed Stiefel who not only contributed with distinction to the development of biological inorganic chemistry with a special interest in molybdenum and its chemistry but had begun the long task of increasing our awareness of the difficulties mankind faces arising from damage to the environment. Here, I take up this theme in an effort to illustrate the nature of today's problems by putting them in the perspective of the whole of evolution of our ecosystem. The central theme is that evolution of organisms has always had to come to terms with the systematic development of the environment. In the past, environmental changes have been slow so that adaptation through genetic adjustment has had time to follow. In the last two hundred years change has become fast and the adaptive process rests not with genes but with mankind's physical-chemical control.

PMID: 17709144 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17709144&ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum