Saturday, November 3, 2007

Life-span exposure to low doses of aspartame beginning during prenatal life increases cancer effects in rats

Environ Health Perspect. 2007 Sep;115(9):1293-7.Click here to read Links

Life-span exposure to low doses of aspartame beginning during prenatal life increases cancer effects in rats.

Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy. crcfr@ramazzini.it

BACKGROUND: In a previous study conducted at the Cesare Maltoni Cancer Research Center of the European Ramazzini Foundation (CMCRC/ERF), we demonstrated for the first time that aspartame (APM) is a multipotent carcinogenic agent when various doses are administered with feed to Sprague-Dawley rats from 8 weeks of age throughout the life span. OBJECTIVE: The aim of this second study is to better quantify the carcinogenic risk of APM, beginning treatment during fetal life. METHODS: We studied groups of 70-95 male and female Sprague-Dawley rats administered APM (2,000, 400, or 0 ppm) with feed from the 12th day of fetal life until natural death. RESULTS: Our results show a) a significant dose-related increase of malignant tumor-bearing animals in males (p < 0.01), particularly in the group treated with 2,000 ppm APM (p < 0.01); b) a significant increase in incidence of lymphomas/leukemias in males treated with 2,000 ppm (p < 0.05) and a significant dose-related increase in incidence of lymphomas/leukemias in females (p < 0.01), particularly in the 2,000-ppm group (p < 0.01); and c) a significant dose-related increase in incidence of mammary cancer in females (p < 0.05), particularly in the 2,000-ppm group (p < 0.05). CONCLUSIONS: The results of this carcinogenicity bioassay confirm and reinforce the first experimental demonstration of APM's multipotential carcinogenicity at a dose level close to the acceptable daily intake for humans. Furthermore, the study demonstrates that when life-span exposure to APM begins during fetal life, its carcinogenic effects are increased.

PMID: 17805418 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17805418&ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

The effect of aspartame metabolites on human erythrocyte membrane acetylcholinesterase activity

 Pharmacol Res. 2006 Jan;53(1):1-5. Epub 2005 Aug 29.Click here to read Links

The effect of aspartame metabolites on human erythrocyte membrane acetylcholinesterase activity.

Department of Experimental Physiology, Medical School, University of Athens, Greece. stsakir@cc.uoa.gr

Studies have implicated aspartame (ASP) with neurological problems. The aim of this study was to evaluate acetylcholinesterase (AChE) activity in human erythrocyte membranes after incubation with the sum of ASP metabolites, phenylalanine (Phe), methanol (met) and aspartic acid (aspt), or with each one separately. Erythrocyte membranes were obtained from 12 healthy individuals and were incubated with ASP hydrolysis products for 1 h at 37 degrees C. AChE was measured spectrophotometrically. Incubation of membranes with ASP metabolites corresponding with 34 mg/kg, 150 mg/kg or 200 mg/kg of ASP consumption resulted in an enzyme activity reduction by -33%, -41%, and -57%, respectively. Met concentrations 0.14 mM, 0.60 mM, and 0.80 mM decreased the enzyme activity by -20%, -32% or -40%, respectively. Aspt concentrations 2.80 mM, 7.60 mM or 10.0 mM inhibited membrane AChE activity by -20%, -35%, and -47%, respectively. Phe concentrations 0.14 mM, 0.35 mM or 0.50mM reduced the enzyme activity by -11%, -33%, and -35%, respectively. Aspt or Phe concentrations 0.82 mM or 0.07 mM, respectively, did not alter the membrane AChE activity. It is concluded that low concentrations of ASP metabolites had no effect on the membrane enzyme activity, whereas high or toxic concentrations partially or remarkably decreased the membrane AChE activity, respectively. Additionally, neurological symptoms, including learning and memory processes, may be related to the high or toxic concentrations of the sweetener metabolites.

PMID: 16129618 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16129618&ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

L-Cysteine and glutathione restore the reduction of rat hippocampal Na+, K+-ATPase activity induced by aspartame metabolites

Toxicology. 2007 Jul 31;237(1-3):177-83. Epub 2007 May 18.Click here to read Links

L-Cysteine and glutathione restore the reduction of rat hippocampal Na+, K+-ATPase activity induced by aspartame metabolites.

Department of Experimental Physiology, Medical School, Athens University, P.O. Box 65257, GR-15401 Athens, Greece.

Studies have implicated aspartame (ASP) ingestion in neurological problems. The aim of this study was to evaluate hippocampal Na(+),K(+)-ATPase and Mg(2+)-ATPase activities after incubation with ASP or each of ASP metabolites, phenylalanine (Phe), methanol (MeOH) and aspartic acid (asp) separately. Suckling rat hippocampal homogenates or pure Na(+),K(+)-ATPase were incubated with ASP metabolites. Na(+),K(+)-ATPase and Mg(2+)-ATPase activities were measured spectrophotometrically. Incubation of hippocampal or pure Na(+),K(+)-ATPase with ASP concentrations (expected in the cerebrospinal fluid (CSF)) after ASP consumption of 34, 150 or 200mg/kg resulted in hippocampal enzyme activity reduction of 26%, 50% or 59%, respectively, whereas pure enzyme was remarkably stimulated. Moreover, incubation with hippocampal homogenate of each one of the corresponding in the CSF ASP metabolites related to the intake of common, high/abuse doses of the sweetener, inhibited Na(+),K(+)-ATPase, while pure enzyme was activated. Hippocampal Mg(2+)-ATPase remained unaltered. Addition of l-cysteine (cys) or reduced glutathione (GSH) in ASP mixtures, related with high/toxic doses of the sweetener, completely or partially restored the inactivated membrane Na(+),K(+)-ATPase, whereas the activated pure enzyme activity returned to normal. CSF concentrations of ASP metabolites related to common, abuse/toxic doses of the additive significantly reduced rat hippocampal Na(+),K(+)-ATPase activity, whereas pure enzyme was activated. Cys or GSH completely or partially restored both enzyme activities.

PMID: 17602817 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17602817&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Direct and indirect cellular effects of aspartame on the brain.

 Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print]Click here to read Links

Direct and indirect cellular effects of aspartame on the brain.

[1] 1Department of Anatomy, University of Pretoria, Pretoria, Gauteng, South Africa [2] 2Department of Anatomy, University of the Limpopo, South Africa.

The use of the artificial sweetener, aspartame, has long been contemplated and studied by various researchers, and people are concerned about its negative effects. Aspartame is composed of phenylalanine (50%), aspartic acid (40%) and methanol (10%). Phenylalanine plays an important role in neurotransmitter regulation, whereas aspartic acid is also thought to play a role as an excitatory neurotransmitter in the central nervous system. Glutamate, asparagines and glutamine are formed from their precursor, aspartic acid. Methanol, which forms 10% of the broken down product, is converted in the body to formate, which can either be excreted or can give rise to formaldehyde, diketopiperazine (a carcinogen) and a number of other highly toxic derivatives. Previously, it has been reported that consumption of aspartame could cause neurological and behavioural disturbances in sensitive individuals. Headaches, insomnia and seizures are also some of the neurological effects that have been encountered, and these may be accredited to changes in regional brain concentrations of catecholamines, which include norepinephrine, epinephrine and dopamine. The aim of this study was to discuss the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders (DSM-IV-TR 2000) and also in compromised learning and emotional functioning.European Journal of Clinical Nutrition advance online publication, 8 August 2007; doi:10.1038/sj.ejcn.1602866.

PMID: 17684524 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17684524&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins

Ann Pharmacother. 2001 Jun;35(6):702-6.Click here to read Links

Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins.

Malcolm Randall Veterans Affairs Medical Center, Gainesville, FL, USA.

BACKGROUND: Fibromyalgia is a common rheumatologic disorder that is often difficult to treat effectively. CASE SUMMARY: Four patients diagnosed with fibromyalgia syndrome for two to 17 years are described. All had undergone multiple treatment modalities with limited success. All had complete, or nearly complete, resolution of their symptoms within months after eliminating monosodium glutamate (MSG) or MSG plus aspartame from their diet. All patients were women with multiple comorbidities prior to elimination of MSG. All have had recurrence of symptoms whenever MSG is ingested. DISCUSSION: Excitotoxins are molecules, such as MSG and aspartate, that act as excitatory neurotransmitters, and can lead to neurotoxicity when used in excess. We propose that these four patients may represent a subset of fibromyalgia syndrome that is induced or exacerbated by excitotoxins or, alternatively, may comprise an excitotoxin syndrome that is similar to fibromyalgia. We suggest that identification of similar patients and research with larger numbers of patients must be performed before definitive conclusions can be made. CONCLUSIONS: The elimination of MSG and other excitotoxins from the diets of patients with fibromyalgia offers a benign treatment option that has the potential for dramatic results in a subset of patients.

PMID: 11408989 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11408989&ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Synergistic interactions between commonly used food additives in a developmental neurotoxicity test.

 Toxicol Sci. 2006 Mar;90(1):178-87. Epub 2005 Dec 13.Click here to read Links

Synergistic interactions between commonly used food additives in a developmental neurotoxicity test.

Developmental Toxicopathology Unit, Department of Human Anatomy & Cell Biology, University of Liverpool, Sherrington Buildings, Liverpool L69 3GE, UK. karen.lau@liverpool.ac.uk

Exposure to non-nutritional food additives during the critical development window has been implicated in the induction and severity of behavioral disorders such as attention deficit hyperactivity disorder (ADHD). Although the use of single food additives at their regulated concentrations is believed to be relatively safe in terms of neuronal development, their combined effects remain unclear. We therefore examined the neurotoxic effects of four common food additives in combinations of two (Brilliant Blue and L-glutamic acid, Quinoline Yellow and aspartame) to assess potential interactions. Mouse NB2a neuroblastoma cells were induced to differentiate and grow neurites in the presence of additives. After 24 h, cells were fixed and stained and neurite length measured by light microscopy with computerized image analysis. Neurotoxicity was measured as an inhibition of neurite outgrowth. Two independent models were used to analyze combination effects: effect additivity and dose additivity. Significant synergy was observed between combinations of Brilliant Blue with L-glutamic acid, and Quinoline Yellow with aspartame, in both models. Involvement of N-methyl-D-aspartate (NMDA) receptors in food additive-induced neurite inhibition was assessed with a NMDA antagonist, CNS-1102. L-glutamic acid- and aspartame-induced neurotoxicity was reduced in the presence of CNS-1102; however, the antagonist did not prevent food color-induced neurotoxicity. Theoretical exposure to additives was calculated based on analysis of content in foodstuff, and estimated percentage absorption from the gut. Inhibition of neurite outgrowth was found at concentrations of additives theoretically achievable in plasma by ingestion of a typical snack and drink. In addition, Trypan Blue dye exclusion was used to evaluate the cellular toxicity of food additives on cell viability of NB2a cells; both combinations had a straightforward additive effect on cytotoxicity. These data have implications for the cellular effects of common chemical entities ingested individually and in combination.

PMID: 16352620 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16352620&ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

The effect of aspartame on rat brain xenobiotic-metabolizing enzymes.

Hum Exp Toxicol. 2006 Aug;25(8):453-9.Click here to read Links

The effect of aspartame on rat brain xenobiotic-metabolizing enzymes.

Laboratorio de Toxicología Genética, Instituto Nacional de Pediatría, Insurgentes Sur, 3700-C, 04530 México, DF Mdxico.

This study demonstrates that chronic aspartame (ASP) consumption leads to an increase of phase I metabolizing enzymes (cytochrome P450 (CYP)) in rat brain. Wistar rats were treated by gavage with ASP at daily doses of 75 and 125 mg/kg body weight for 30 days. Cerebrum and cerebellum were used to obtain microsomal fractions to analyse activity and protein levels of seven cytochrome P450 enzymes. Increases in activity were consistently found with the 75 mg/kg dose both in cerebrum and cerebellum for all seven enzymes, although not at the same levels: CYP 2E1-associated 4-nitrophenol hydroxylase (4-NPH) activity was increased 1.5-fold in cerebrum and 25-fold in cerebellum; likewise, CYP2B1-associated penthoxyresorufin O-dealkylase (PROD) activity increased 2.9- and 1.7-fold respectively, CYP2B2-associated benzyloxyresorufin O-dealkylase (BROD) 4.5- and 1.1-fold, CYP3A-associated erythromycin N-demethylase (END) 1.4- and 3.3-fold, CYP1A1-associated ethoxyresorufin O-deethylase (EROD) 5.5- and 2.8-fold, and CYP1A2-associated methoxyresorufin O-demethylase (MROD) 3.7- and 1.3-fold. Furthermore, the pattern of induction of CYP immunoreactive proteins by ASP paralleled that of 4-NHP-, PROD-, BROD-, END-, EROD- and MROD-related activities only in the cerebellum. Conversely, no differences in CYP concentration and activity were detected in hepatic microsomes of treated animals with respect to the controls, suggesting a brain-specific response to ASP treatment.

PMID: 16937917 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16937917&ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

First experimental demonstration of the multipotential carcinogenic effects of aspartame administered in the feed to Sprague-Dawley rats

Environ Health Perspect. 2006 Mar;114(3):379-85.Click here to read Click here to read Links
Comment in:
Environ Health Perspect. 2006 Mar;114(3):A176.
Environ Health Perspect. 2006 Sep;114(9):A516; author reply A516-7.
Environ Health Perspect. 2007 Jan;115(1):A16-7; author reply A17.

First experimental demonstration of the multipotential carcinogenic effects of aspartame administered in the feed to Sprague-Dawley rats.

Cesare Maltoni Cancer Research Center, European Ramazzini Foundation of Oncology and Environmental Sciences, Bologna, Italy. crcfr@ramazzini.it

The Cesare Maltoni Cancer Research Center of the European Ramazzini Foundation has conducted a long-term bioassay on aspartame (APM), a widely used artificial sweetener. APM was administered with feed to 8-week-old Sprague-Dawley rats (100-150/sex/group), at concentrations of 100,000, 50,000, 10,000, 2,000, 400, 80, or 0 ppm. The treatment lasted until natural death, at which time all deceased animals underwent complete necropsy. Histopathologic evaluation of all pathologic lesions and of all organs and tissues collected was routinely performed on each animal of all experimental groups. The results of the study show for the first time that APM, in our experimental conditions, causes a) an increased incidence of malignant-tumor-bearing animals with a positive significant trend in males (p < or = 0.05) and in females (p < or = 0.01), in particular those females treated at 50,000 ppm (p < or = 0.01); b) an increase in lymphomas and leukemias with a positive significant trend in both males (p < or = 0.05) and females (p < or = 0.01), in particular in females treated at doses of 100,000 (p < or = 0.01), 50,000 (p < or = 0.01), 10,000 (p < or = 0.05), 2,000 (p < or = 0.05), or 400 ppm (p < or = 0.01); c) a statistically significant increased incidence, with a positive significant trend (p < or = 0.01), of transitional cell carcinomas of the renal pelvis and ureter and their precursors (dysplasias) in females treated at 100,000 (p < or = 0.01), 50,000 (p < or = 0.01), 10,000 (p < or = 0.01), 2,000 (p < or = 0.05), or 400 ppm (p < or = 0.05); and d) an increased incidence of malignant schwannomas of peripheral nerves with a positive trend (p < or = 0.05) in males. The results of this mega-experiment indicate that APM is a multipotential carcinogenic agent, even at a daily dose of 20 mg/kg body weight, much less than the current acceptable daily intake. On the basis of these results, a reevaluation of the present guidelines on the use and consumption of APM is urgent and cannot be delayed.

PMID: 16507461 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16507461&ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Ultrastructural changes to rabbit fibrin and platelets due to aspartame

Ultrastruct Pathol. 2007 Mar-Apr;31(2):77-83.Click here to read Links

Ultrastructural changes to rabbit fibrin and platelets due to aspartame.

Department of Anatomy, Faculty of Medicine, University of Pretoria, South Africa. resia.pretorius@up.ac.za

The coagulation process, including thrombin, fibrin, as well as platelets, plays an important role in hemostasis, contributing to the general well-being of humans. Fibrin formation and platelet activation are delicate processes that are under the control of many small physiological events. Any one of these many processes may be influenced or changed by external factors, including pharmaceutical or nutritional products, e.g., the sweetener aspartame (L-aspartyl-L-phenylalanine methyl ester). It is known that phenylalanine is present at position P(9) and aspartate at position P(10) of the alpha-chain of human fibrinogen, and plays an important role in the conversion of fibrinogen to fibrin by the catalyst alpha-thrombin. The authors investigate the effect of aspartame on platelet and fibrin ultrastructure, by using the rabbit animal model and the scanning electron microscope. Animals were exposed to 34 mg/kg of aspartame 26x during a 2-month period. Aspartame-exposed fibrin networks appeared denser, with a thick matted fine fiber network covering thick major fibers. Also, the platelet aggregates appeared more granular than the globular control platelet aggregates. The authors conclude by suggesting that aspartame usage may interfere with the coagulation process and might cause delayed fibrin breakup after clot formation. They suggest this, as the fibrin networks from aspartame-exposed rabbits are more complex and dense, due to the netlike appearance of the minor, thin fibers. Aspartame usage should possibly be limited by people on anti-clotting medicine or those with prone to clot formation.

PMID: 17613990 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17613990&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Exposure to substances in the workplace and new-onset asthma: an international prospective population-based study (ECRHS-II).

1: Lancet. 2007 Jul 28;370(9584):336-41.
Comment in:
Lancet. 2007 Jul 28;370(9584):295-7.

Exposure to substances in the workplace and new-onset asthma: an international prospective population-based study (ECRHS-II).

Centre for Research in Environmental Epidemiology, Municipal Institute of Medical Research, Barcelona, Spain. kogevinas@imim.es

BACKGROUND: The role of exposure to substances in the workplace in new-onset asthma is not well characterised in population-based studies. We therefore aimed to estimate the relative and attributable risks of new-onset asthma in relation to occupations, work-related exposures, and inhalation accidents. METHODS: We studied prospectively 6837 participants from 13 countries who previously took part in the European Community Respiratory Health Survey (1990-95) and did not report respiratory symptoms or a history of asthma at the time of the first study. Asthma was assessed by methacholine challenge test and by questionnaire data on asthma symptoms. Exposures were defined by high-risk occupations, an asthma-specific job exposure matrix with additional expert judgment, and through self-report of acute inhalation events. Relative risks for new onset asthma were calculated with log-binomial models adjusted for age, sex, smoking, and study centre. FINDINGS: A significant excess asthma risk was seen after exposure to substances known to cause occupational asthma (Relative risk=1.6, 95% CI 1.1-2.3, p=0.017). Risks were highest for asthma defined by bronchial hyper-reactivity in addition to symptoms (2.4, 1.3-4.6, p=0.008). Of common occupations, a significant excess risk of asthma was seen for nursing (2.2, 1.3-4.0, p=0.007). Asthma risk was also increased in participants who reported an acute symptomatic inhalation event such as fire, mixing cleaning products, or chemical spills (RR=3.3, 95% CI 1.0-11.1, p=0.051). The population-attributable risk for adult asthma due to occupational exposures ranged from 10% to 25%, equivalent to an incidence of new-onset occupational asthma of 250-300 cases per million people per year. INTERPRETATION: Occupational exposures account for a substantial proportion of adult asthma incidence. The increased risk of asthma after inhalation accidents suggests that workers who have such accidents should be monitored closely.

PMID: 17662882 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17662882&itool=iconabstr&itool=pubmed_DocSum

Friday, November 2, 2007

Volcanic Gases: Hydrogen Burning at Kilauea Volcano, Hawaii.

Science. 1973 Oct 19;182(4109):277-279.Click here to read Links

Volcanic Gases: Hydrogen Burning at Kilauea Volcano, Hawaii.

Spectroscopic evidence for hydrogen burning in air was obtained at Kilauea Volcano. The abundance of hydrogen required to support combustion is consistent with that predicted for gases in equilibrium with typical Hawaiian tholeiitic basalt.

PMID: 17749307 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17749307&ordinalpos=33&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
 

Characterization of air contaminants formed by the interaction of lava and sea water.

Environ Health Perspect. 1994 May;102(5):478-82.Click here to read Links

Characterization of air contaminants formed by the interaction of lava and sea water.

Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.

We made environmental measurements to characterize contaminants generated when basaltic lava from Hawaii's Kilauea volcano enters sea water. This interaction of lava with sea water produces large clouds of mist (LAZE). Island winds occasionally directed the LAZE toward the adjacent village of Kalapana and the Hawaii Volcanos National Park, creating health concerns. Environmental samples were taken to measure airborne concentrations of respirable dust, crystalline silica and other mineral compounds, fibers, trace metals, inorganic acids, and organic and inorganic gases. The LAZE contained quantifiable concentrations of hydrochloric acid (HCl) and hydrofluoric acid (HF); HCl was predominant. HCl and HF concentrations were highest in dense plumes of LAZE near the sea. The HCl concentration at this sampling location averaged 7.1 ppm; this exceeds the current occupational exposure ceiling of 5 ppm. HF was detected in nearly half the samples, but all concentrations were <1 ppm Sulfur dioxide was detected in one of four short-term indicator tube samples at approximately 1.5 ppm. Airborne particulates were composed largely of chloride salts (predominantly sodium chloride). Crystalline silica concentrations were below detectable limits, less than approximately 0.03 mg/m3 of air. Settled dust samples showed a predominance of glass flakes and glass fibers. Airborne fibers were detected at quantifiable levels in 1 of 11 samples. These fibers were composed largely of hydrated calcium sulfate. These findings suggest that individuals should avoid concentrated plumes of LAZE near its origin to prevent over exposure to inorganic acids, specifically HCl.

PMID: 8593853 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8593853&ordinalpos=24&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

Molecular analysis of carbon monoxide-oxidizing bacteria associated with recent Hawaiian volcanic deposits.

Appl Environ Microbiol. 2004 Jul;70(7):4242-8.Click here to read Click here to read Links

Molecular analysis of carbon monoxide-oxidizing bacteria associated with recent Hawaiian volcanic deposits.

Darling Marine Center, University of Maine, Walpole, ME 04573, USA.

Genomic DNA extracts from four sites at Kilauea Volcano were used as templates for PCR amplification of the large subunit (coxL) of aerobic carbon monoxide dehydrogenase. The sites included a 42-year-old tephra deposit, a 108-year-old lava flow, a 212-year-old partially vegetated ash-and-tephra deposit, and an approximately 300-year-old forest. PCR primers amplified coxL sequences from the OMP clade of CO oxidizers, which includes isolates such as Oligotropha carboxidovorans, Mycobacterium tuberculosis, and Pseudomonas thermocarboxydovorans. PCR products were used to create clone libraries that provide the first insights into the diversity and phylogenetic affiliations of CO oxidizers in situ. On the basis of phylogenetic and statistical analyses, clone libraries for each site were distinct. Although some clone sequences were similar to coxL sequences from known organisms, many sequences appeared to represent phylogenetic lineages not previously known to harbor CO oxidizers. On the basis of average nucleotide diversity and average pairwise difference, a forested site supported the most diverse CO-oxidizing populations, while an 1894 lava flow supported the least diverse populations. Neither parameter correlated with previous estimates of atmospheric CO uptake rates, but both parameters correlated positively with estimates of microbial biomass and respiration. Collectively, the results indicate that the CO oxidizer functional group associated with recent volcanic deposits of the remote Hawaiian Islands contains substantial and previously unsuspected diversity.

PMID: 15240307 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15240307&ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

Emergency department visits and "vog"-related air quality in Hilo, Hawai'i.

Environ Res. 2004 May;95(1):11-9.Click here to read Links

Emergency department visits and "vog"-related air quality in Hilo, Hawai'i.

Natural Sciences Division, Department of Chemistry, University of Hawaii at Hilo, 200 West Kawili Street W18, Hilo, HI 96728, USA. jonpierr@hawaii.edu

Emergency department (ED) visits in Hilo, Hawai'i, from January 1997 to May 2001, were examined for associations with volcanic fog, or "vog", measured as sulfur dioxide (SO(2)) and submicrometer particulate matter (PM(1)). Exponential regression models were used with robust standard errors. Four diagnostic groups were examined: asthma/COPD; cardiac; flu, cold, and pneumonia; and gastroenteritis. Before adjustments, highly significant associations with vog-related air quality were seen for all diagnostic groups except gastroenteritis. After adjusting for month, year, and day of the week, only asthma/COPD had consistently positive associations with air quality. The strongest associations were for SO(2) with a 3-day lag (6.8% per 10 ppb; P=0.001) and PM(1), with a 1-day lag (13.8% per 10 microg/m(3); P=0.011). The association of ED visits for asthma/COPD with month of the year was stronger than associations seen with air quality. Although vog appears influential, non-vog factors dominated associations with the frequency of asthma/COPD ED visits.

PMID: 15068926 [PubMed - indexed for MEDLINE]

 

Volcano related atmospheric toxicants in Hilo and Hawaii Volcanoes National Park: implications for human health.

Neurotoxicology. 2005 Aug;26(4):555-63.Click here to read Links

Volcano related atmospheric toxicants in Hilo and Hawaii Volcanoes National Park: implications for human health.

Chemistry, Natural Sciences Division, University of Hawaii at Hilo, 200 West Kawili Street W18, Hilo, HI 96720, USA. jonpierr@hawaii.edu

Volcanic fog (vog) from Kilauea volcano on the island of Hawaii includes a variety of chemical species including sulfur compounds and traces of metals such as mercury. The metal species seen tended to be in the nanograms per cubic meter range, whereas oxides of sulfur: SO2 and SO3 and sulfate aerosols, were in the range of micrograms per cubic meter and rarely even as high as a few milligrams per cubic meter of air (nominally ppb to ppm). These sulfur species are being investigated for associations with both acute and chronic changes in human health status. The sulfate aerosols tend to be less than 1 microm in diameter and tend to dominate the mass of this submicron size mode. The sulfur chemistry is dynamic, changing composition from predominantly sulfur dioxide and trioxide gasses near the volcano, to predominantly sulfate aerosols on the west side of the island. Time, concentration and composition characteristics of submicron aerosols and sulfur dioxide are described with respect to the related on-going health studies and public health management concerns. Exposures to sulfur dioxide and particulate matter equal to or less than 1 microm in size were almost always below the national ambient air quality standards (NAAQS). These standards do not however consider the acidic nature and submicron size of the aerosol, nor the possibility of the aerosol and the sulfur dioxide interacting in their toxicity. Time series plots, histograms and descriptive statistics of hourly averages give the reader a sense of some of the exposures observed.

PMID: 16112321 [PubMed - indexed for MEDLINE]

 

Thursday, November 1, 2007

Developmental exposure to pesticides.... susceptible to these environmental chemicals later in life

Neurotoxicology. 2007 Jul;28(4):727-35. Epub 2007 Apr 20.Click here to read Links

Developmental exposure to pesticides zineb and/or endosulfan renders the nigrostriatal dopamine system more susceptible to these environmental chemicals later in life.

Department of Biomedical Sciences and Pathobiology, College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.

Several epidemiological studies have suggested a role for environmental pesticide exposures in idiopathic Parkinson's disease. The purpose of this study was to test the hypothesis that exposure to pesticides such as endosulfan and/or zineb during critical periods of postnatal development could result in neuronal dysfunction and enhance the impact of these pesticides during exposure as adults. C57BL/6 mice, exposed daily to each of the pesticides or their mixtures from postnatal days 5 to 19, exhibited insignificant changes in striatal dopamine, acetylcholinesterase and alpha-synuclein levels. However, mice exposed to these pesticides as juveniles and re-exposed at 8 months of age had significantly altered striatum and brain cortex neurotransmitter levels. Thus, mice re-exposed during adulthood to zineb, endosulfan and their mixtures showed a significantly depleted striatal dopamine levels, to 22, 16 and 35% of control, respectively. Acetylcholinesterase activity in the cerebral cortex was significantly increased in all pesticide treated groups (rho< or =0.05) upon repeated exposure, and pesticide mixture treatment also significantly increased levels of normal and aggregated alpha-synuclein. Collectively, these findings support our hypothesis that exposure to pesticides such as endosulfan and zineb during critical periods of postnatal development contributes to neurotransmitter changes upon re-challenge in adulthood.

PMID: 17512982 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17512982&itool=pubmed_DocSum

Doctors and Drug Companies - Scrutinizing Influential Relationships


Volume 357:1796-1797  November 1, 2007  Number 18

Doctors and Drug Companies — Scrutinizing Influential Relationships
Eric G. Campbell, Ph.D.

On September 6, 2007, Senators Charles Grassley (R-IA), the ranking member of the Committee on Finance, and Herb Kohl (D-WI), chairman of the Special Committee on Aging, introduced the Physician Payments Sunshine Act — so named because it aims to "shine a much needed ray of sunlight on a situation that contributes to the exorbitant cost of health care," according to cosponsor Senator Charles Schumer (D-NY). The bill would require manufacturers of pharmaceuticals and medical devices with annual revenues of more than $100 million to disclose the amount of money they give to physicians — whether in the form of a free dinner or vacation or a consulting fee. "This bill is about letting the sun shine in so that the public can know," says Grassley.

The move was stimulated in part by activity in Minnesota and Vermont, which have made the reporting of such relationships mandatory — Minnesota in 1993 and Vermont in 2003. Three additional states (Maine, West Virginia, and California) and the District of Columbia have now enacted similar disclosure laws, and many other states are considering doing so. Although beliefs vary widely about the overall usefulness of the data collected under state mandates, the movement toward increased transparency is gaining steam.

Indeed, the nature, extent, and consequences of physicians' relationships with industry have become one of the most fiercely debated issues in health care today. At the simplest level, such a relationship exists whenever a physician accepts anything from a company whose products or services are related to the practice of medicine. And such interactions are ubiquitous: according to a recent survey, although the frequency and intensity of the ties vary according to physicians' personal and professional characteristics, virtually all physicians (94%) have some type of relationship with industry.1 Most commonly, physicians report receiving food and beverages in the workplace (83%) or being given drug samples by a manufacturer's representative (78%). More than one third of physicians (35%) receive reimbursement for costs associated with professional meetings or continuing medical education, and more than one quarter (28%) receive payments for consulting, speaking, or enrolling patients in trials (see graph).1

From a policy perspective, the debate centers on the overall effect of these relationships on patient care. Although most physicians deny that receiving free lunches, subsidized trips, or other gifts from pharmaceutical companies has any effect on their practices, research has shown that physician–industry relationships do influence prescribing behavior.2 After all, if these relationships didn't affect physician behavior in such a way as to increase sales, companies wouldn't spend $19 billion each year establishing and maintaining them.

Clearly, relationships between physicians and industry can have some positive effects on patient care. Many, if not all, of the drugs currently on the market simply wouldn't exist if it weren't for relationships whereby physicians enroll patients in manufacturers' clinical trials and provide companies with advice on drug development. And even a relationship in the form of attendance at an industry-sponsored luncheon or dinner may lead physicians to recommend beneficial drugs that are being underprescribed — though there is no reason why an educational activity needs to be accompanied by an expensive meal or a trip to a tropical resort.

But physician–industry relationships can also have serious negative effects. For example, doctors with ties to industry may be more inclined than their colleagues to prescribe a brand-name drug despite the availability of a cheaper generic version. The provision of free samples may reinforce this behavior and perhaps stimulate off-label use of medications, which can pose risks for some patients. Industry relationships may stimulate the premature adoption of novel treatments, which could lead to serious health problems for patients. Industry inducements may reduce physician adherence to evidence-based practice guidelines in favor of company medications or interventions that are not recommended in independently developed guidelines. Finally, the financial rewards from industry relationships may reinforce a culture of entitlement among physicians, which could limit their ability to honestly acknowledge and manage the potential negative effects of these relationships. In general, physicians vehemently deny that their industry relationships have any of these negative effects — but they are less convinced that the same is true of their physician colleagues.3

Concern about the risks associated with physician–industry relationships has inspired action by policymakers at the federal, state, and institutional levels. The same day that the new Senate bill was introduced, Boston University School of Medicine and Boston Medical Center announced a new conflict-of-interest policy — prohibiting their clinicians from accepting gifts from manufacturers of pharmaceuticals and medical devices, banishing industry-funded meals from campus, and requiring physicians who serve on the hospital's drug-selection committees to be free of financial ties to companies that stand to gain from committee decisions. Similar policy changes designed to limit physician–industry relationships have been implemented at institutions such as the University of Michigan Health System, the University of Pennsylvania, the Yale University School of Medicine, the Geisinger Health System in Pennsylvania, the Stanford University School of Medicine, Affinity Health System in Wisconsin, Kaiser Permanente, and HealthPartners in Minnesota. Such organizations have taken a variety of steps to banish drug representatives from their hospitals, reduce the use of drug samples accepted by physicians, eliminate industry-sponsored lunches, punish company representatives who break the rules (by loitering in a hospital, for instance, or giving out food), and educate doctors about pharmaceutical developments through academic physicians rather than industry representatives.

With other institutions now following suit, it seems likely that more stringent disclosure requirements and restrictions on industry relationships may soon become widespread — especially among physicians working in medical schools, teaching hospitals, and large health systems. Industry marketing practices such as sponsoring lunches at hospitals, offering free "educational" dinners at expensive restaurants, giving away trinkets such as coffee mugs and pens, and paying for questionable consultancy positions may well become much less common in the future.

Even as institutions and states exert increasing control over these relationships, such change has seemed unlikely to be implemented at the federal level, given the strength of the pharmaceutical-industry lobby in Washington. But in light of the Sunshine Act, federal regulation is clearly not impossible. The profession of medicine may view this legislation as a further stimulus to police itself more vigilantly, to work through its professional and specialty organizations to facilitate and monitor physician adherence to current policies regarding relationships with industry and, where necessary, to develop new, more stringent policies.

Individual physicians can take some steps to maximize the benefits for patients and minimize the risks associated with their own industry relationships. They can start by recognizing that such relationships are designed to influence prescribing behavior and by carefully considering the potential effects that their own associations may have on their patients. They can familiarize themselves with and adhere to the guidelines established by the institutions in which they practice and the professional associations to which they belong. And they can bear in mind that the costs of industry dinners, trips, and other incentives are passed along to their patients in the form of higher drug prices.


Source Information

Dr. Campbell is an associate professor at the Institute for Health Policy at Massachusetts General Hospital and Harvard Medical School, Boston.

References

  1. Campbell EG, Gruen RL, Mountford J, Miller LG, Cleary PD, Blumenthal D. A national survey of physician-industry relationships. N Engl J Med 2007;356:1742-1750. [Free Full Text]
  2. Brennan TA, Rothman DJ, Blank L, et al. Health industry practices that create conflicts of interest: a policy proposal for academic medical centers. JAMA 2006;295:429-433. [Free Full Text]
  3. Chren MM. Interactions between physicians and drug company representatives. Am J Med 1999;107:182-183. [CrossRef][ISI][Medline]

Wednesday, October 31, 2007

Multiple Chemical Sensitivity Syndrome in Sjögren's Syndrome Patients: Casual Association or Related Diseases?

Arch Environ Occup Health. 2006 Nov-Dec;61(6):285-7.Click here to read

Multiple Chemical Sensitivity Syndrome in Sjögren's Syndrome Patients: Casual Association or Related Diseases?

Department of Rheumatology at San Pietro- Fatebenefratelli Hospital and the Centro Ricerche, Association Fatebenefratelli for Research, Rome, Italy.

Multiple chemical sensitivity (MCS) is defined by multiple symptoms, affecting multiple organs, that wax and wane in response to varying chemical exposures at or below previously tolerated levels. Sjögren's syndrome (SS) is a common autoimmune disease affecting 3% of women aged over 55 years. Except for keratoconjunctivitis sicca (which is associated with SS not MCS), systemic features are common between the 2 diseases, leading to considerable morbidity and, occasionally, mortality. The authors report 3 cases of association between SS and MCS. Three women who were diagnosed with SS showed MCS symptoms and also were diagnosed with MCS. Further studies are needed to understand physiopathogenic mechanisms that eventually may be revealed as common to the 2 syndromes.

PMID: 17967752 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17967752&itool=iconabstr&itool=pubmed_DocSum

Air pollutant effects on fetal and early postnatal development.

Birth Defects Res C Embryo Today. 2007 Oct 26;81(3):144-154 [Epub ahead of print]Click here to read Links

Air pollutant effects on fetal and early postnatal development.

Center for Health and the Environment, University of California, Davis, California.

Numerical research on the health effects of air pollution has been published in the last decade. Epidemiological studies have shown that children's exposure to air pollutants during fetal development and early postnatal life is associated with many types of health problems including abnormal development (low birth weight [LBW], very low birth weight [VLBW], preterm birth [PTB], intrauterine growth restriction [IUGR], congenital defects, and intrauterine and infant mortality), decreased lung growth, increased rates of respiratory tract infections, childhood asthma, behavioral problems, and neurocognitive decrements. This review focuses on the health effects of major outdoor air pollutants including particulates, carbon monoxide (CO), sulfur and nitrogen oxides (SO(2), NOx), ozone, and one common indoor air pollutant, environmental tobacco smoke (ETS). Animal data is presented that demonstrate perinatal windows of susceptibility to sidestream smoke, a surrogate for ETS, resulting in altered airway sensitivity and cell type frequency. A study of neonatal monkeys exposed to sidestream smoke during the perinatal period and/or early postnatal period that resulted in an altered balance of Th1-/Th2-cytokine secretion, skewing the immune response toward the allergy-associated Th2 cytokine phenotype, is also discussed. Birth Defects Research (Part C) 81:144-154, 2007. (c) 2007 Wiley-Liss, Inc.

PMID: 17963272 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17963272&itool=pubmed_DocSum

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