BrooklynDodger

NostrumDamus

2009-12-29T16:51:00.002-05:00

BrooklynDodger(s) comment: Gingko extract contains flavenoids and terpenoids, thought to be anti oxidant. 3000+ subjects followed over a median of 6 years because of some people think it's a folk remedy. Think of what that cost. The anti-oxidant mechanism hasn't hardly worked.

JAMA 2009;302 2663-2670

http://jama.ama-assn.org/cgi/content/abstract/302/24/2663?etoc

Ginkgo biloba for Preventing Cognitive Decline in Older Adults

A Randomized Trial

Beth E. Snitz, PhD; Ellen S. O’Meara, PhD; Michelle C. Carlson, PhD; Alice M. Arnold, PhD; Diane G. Ives, MPH; Stephen R. Rapp, PhD; Judith Saxton, PhD; Oscar L. Lopez, MD; Leslie O. Dunn, MPH; Kaycee M. Sink, MD; Steven T. DeKosky, MD; for the Ginkgo Evaluation of Memory (GEM) Study Investigators

JAMA. 2009;302(24):2663-2670.

Context The herbal product Ginkgo biloba is taken frequentlywith the intention of improving cognitive health in aging. However,evidence from adequately powered clinical trials is lackingregarding its effect on long-term cognitive functioning.

Objective To determine whether G biloba slows the ratesof global or domain-specific cognitive decline in older adults.

Design, Setting, and Participants The Ginkgo Evaluationof Memory (GEM) study, a randomized, double-blind, placebo-controlledclinical trial of 3069 community-dwelling participants aged72 to 96 years, conducted in 6 academic medical centers in theUnited States between 2000 and 2008, with a median follow-upof 6.1 years.

Intervention Twice-daily dose of 120-mg extract of G biloba(n = 1545) or identical-appearing placebo (n = 1524).

Main Outcome Measures Rates of change over time in theModified Mini-Mental State Examination (3MSE), in the cognitivesubscale of the Alzheimer Disease Assessment Scale (ADAS-Cog),and in neuropsychological domains of memory, attention, visual-spatialconstruction, language, and executive functions, based on sumsof z scores of individual tests.

Results Annual rates of decline in z scores did not differbetween G biloba and placebo groups in any domains, includingmemory (0.043; 95% confidence interval [CI], 0.034-0.051 vs0.041; 95% CI, 0.032-0.050), attention (0.043; 95% CI, 0.037-0.050vs 0.048; 95% CI, 0.041-0.054), visuospatial abilities (0.107;95% CI, 0.097-0.117 vs 0.118; 95% CI, 0.108-0.128), language(0.045; 95% CI, 0.037-0.054 vs 0.041; 95% CI, 0.033-0.048),and executive functions (0.092; 95% CI, 0.086-0.099 vs 0.089;95% CI, 0.082-0.096). For the 3MSE and ADAS-Cog, rates of changevaried by baseline cognitive status (mild cognitive impairment),but there were no differences in rates of change between treatmentgroups (for 3MSE, P = .71; for ADAS-Cog, P = .97).There was no significant effect modification of treatment onrate of decline by age, sex, race, education, APOE*E4 allele,or baseline mild cognitive impairment (P > .05).

Conclusion Compared with placebo, the use of G biloba,120 mg twice daily, did not result in less cognitive declinein older adults with normal cognition or with mild cognitiveimpairment.

Hairdressers: Another Non-Industrial Population at Increased Risk Due to Chemical Exposure

2009-12-02T05:00:00.000-05:00

BrooklynDodger(s) comment: IARC lists occupation of hairdresser as Group 2A. Volume 57.

>>>>>>>>>>>>>>>>>>
International Journal of Epidemiology 2009 38(6):1512-1531; doi:10.1093/ije/dyp283

Risk of cancer among hairdressers and related workers: a meta-analysis

Bahi Takkouche¹^,2^,*, Carlos Regueira-Méndez¹^,2 and Agustín Montes-Martínez¹^,2

¹ Department of Preventive Medicine, University of Santiago de Compostela, Santiago de Compostela, Spain.
² CIBER en Epidemiología y Salud Pública (CIBER-ESP), Spain.

* Corresponding author. Department of Preventive Medicine, Faculty of Medicine, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain. E-mail: bahi.takkouche@usc.es

	Abstract

Background Hairdressers and allied occupations represent a largeand fast growing group of professionals. The fact that theseprofessionals are chronically exposed to a large number of chemicalspresent in their work environment, including potential carcinogenscontained in hair dyes, makes it necessary to carry out a systematicevaluation of the risk of cancer in this group.

Methods We retrieved studies by systematically searching Medlineand other computerized databases, and by manually examiningthe references of the original articles and monographs retrieved.We also contacted international researchers working on thisor similar topics to complete our search. We included 247 studiesreporting relative risk (RR) estimates of hairdresser occupationand cancer of different sites.

Results Study-specific RRs were weighted by the inverse of theirvariance to obtain fixed and random effects pooled estimates.The pooled RR of occupational exposure as a hairdresser was1.27 (95% CI 1.15–1.41) for lung cancer, 1.52 [95% confidenceinterval (CI) 1.11–2.08] for larynx cancer, 1.30 (95%CI 1.20–1.42) for bladder cancer and 1.62 (95% CI 1.22–2.14)for multiple myeloma. Data for other anatomic sites showed increasesof smaller magnitude. The results restricted to those studiescarried out before the ban of two major carcinogens from hairdyes in the mid-1970s were similar to the general results.

Conclusions Hairdressers have a higher risk of cancer than thegeneral population. Improvement of the ventilation system inthe hairdresser salons and implementation of hygiene measuresaimed at mitigating exposure to potential carcinogens at workmay reduce the risk.

Back to Blogging after a month away

2009-12-01T12:22:00.001-05:00

Markers of nitrosamine carcinogenesis?

2009-10-29T06:24:00.000-04:00

BrooklynDodger(s) comment: These novel assay experiments should be related to exposure levels in which toxicity or carcinogenicity is expressed in an intact animal.

Toxicology and Applied Pharmacology
Volume 241, Issue 2, 1 December 2009, Pages 230-245

Toxicogenomic analysis of N-nitrosomorpholine induced changes in rat liver: Comparison of genomic and proteomic responses and anchoring to histopathological parameters

A. Oberemm^a^,^,, H.-J. Ahr^b, P. Bannasch^c, H. Ellinger-Ziegelbauer^b, M. Glückmann^e, J. Hellmann^d, C. Ittrich^c^,¹, A. Kopp-Schneider^c, P.-J. Kramer^d, E. Krause^f, M. Kröger^d, E. Kiss^c, H.-B. Richter-Reichhelm^a, G. Scholz^b^,², K. Seemann^d, M. Weimer^c and U. Gundert-Remy^a

^aFederal Institute for Risk Assessment (BfR), 14195 Berlin, Germany

^bBayer Schering Pharma AG, Special Toxicology, 42096 Wuppertal, Germany

^cGerman Cancer Research Center (DKFZ), 69120 Heidelberg, Germany

^dMerck KGaA, Institute for Toxicology, 64293 Darmstadt, Germany

^eApplied Biosystems Deutschland GmbH, 64293 Darmstadt, Germany

^fLeibniz Institute for Molecular Pharmacology (FMP), 13125 Berlin, Germany

Received 29 July 2009;

accepted 18 August 2009.

Available online 28 August 2009.

Abstract

A common animal model of chemical hepatocarcinogenesis was used to examine the utility of transcriptomic and proteomic data to identify early biomarkers related to chemically induced carcinogenesis. N-nitrosomorpholine, a frequently used genotoxic model carcinogen, was applied via drinking water at 120 mg/L to male Wistar rats for 7 weeks followed by an exposure-free period of 43 weeks. Seven specimens of each treatment group (untreated control and 120 mg/L N-nitrosomorpholine in drinking water) were sacrificed at nine time points during and after N-nitrosomorpholine treatment. Individual samples from the liver were prepared for histological and toxicogenomic analyses. For histological detection of preneoplastic and neoplastic tissue areas, sections were stained using antibodies against the placental form of glutathione-S-transferase (GST-P). Gene and protein expression profiles of liver tissue homogenates were analyzed using RG-U34A Affymetrix rat gene chips and two-dimensional gel electrophoresis-based proteomics, respectively. In order to compare results obtained by histopathology, transcriptomics and proteomics, GST-P-stained liver sections were evaluated morphometrically, which revealed a parallel time course of the area fraction of preneoplastic lesions and gene plus protein expression patterns. On the transcriptional level, an increase of hepatic GST-P expression was detectable as early as 3 weeks after study onset. Comparing deregulated genes and proteins, eight species were identified which showed a corresponding expression profile on both expression levels. Functional analysis suggests that these genes and corresponding proteins may be useful as biomarkers of early hepatocarcinogenesis.

Another endpoint for nano titanium dioxide

2009-10-28T06:17:00.000-04:00

BrooklynDodger(s) comment: Continuing to run nano particles through novel test systems. Historically, titanium dioxide is the negative control for lung damage. What's needed is a systematic testing of a spectrum of particles in the same system - full size titanium dioxide, silica (a known human carcinogen), diesel, carbon materials. So that relative potency can be measured.

Toxicology and Applied Pharmacology
Volume 241, Issue 2, 1 December 2009, Pages 182-194
Disturbed mitotic progression and genome segregation are involved in cell transformation mediated by nano-TiO2 long-term exposure
Shing Huang^a, Pin Ju Chueh^a, Yun-Wei Lin^b, Tung-Sheng Shih^c and Show-Mei Chuang^a^,^,

^aInstitute of Biomedical Sciences, National Chung Hsing University, 250 Kuo-Kuang Road, Taichung 402, Taiwan

^bMolecular Oncology Laboratory, Department of Biochemical Science and Technology, National Chiayi University, Chiayi, Taiwan

^cInstitute of Occupational Safety and Healthy Council of Labor Affairs, Executive Yuan, Taipei 221, Taiwan

Received 9 March 2009;

revised 10 August 2009;

accepted 11 August 2009.

Available online 18 August 2009.

Abstract

Titanium dioxide (TiO2) nano-particles (< 100 nm in diameter) have been of interest in a wide range of applications, such as in cosmetics and pharmaceuticals because of their low toxicity. However, recent studies have shown that TiO2 nano-particles (nano-TiO2) induce cytotoxicity and genotoxicity in various lines of cultured cells as well as tumorigenesis in animal models. The biological roles of nano-TiO2 are shown to be controversial and no comprehensive study paradigm has been developed to investigate their molecular mechanisms. In this study, we showed that short-term exposure to nano-TiO2 enhanced cell proliferation, survival, ERK signaling activation and ROS production in cultured fibroblast cells. Moreover, long-term exposure to nano-TiO2 not only increased cell survival and growth on soft agar but also the numbers of multinucleated cells and micronucleus (MN) as suggested in confocal microscopy analysis. Cell cycle phase analysis showed G2/M delay and slower cell division in long-term exposed cells. Most importantly, long-term TiO2 exposure remarkably affected mitotic progression at anaphase and telophase leading to aberrant multipolar spindles and chromatin alignment/segregation. Moreover, PLK1 was demonstrated as the target for nano-TiO2 in the regulation of mitotic progression and exit. Notably, a higher fraction of sub-G1 phase population appeared in TiO2-exposed cells after releasing from G2/M synchronization. Our results demonstrate that long-term exposure to nano-TiO2 disturbs cell cycle progression and duplicated genome segregation, leading to chromosomal instability and cell transformation

IRIS Summary for 1,2,3-trichloropropane

2009-10-25T05:39:00.000-04:00

BrooklynDodger(s) comment: The Dodger(s) figure this is a drinking water contaminant. As with most IRIS chemicals, the chronic RfC is essentially zero. This came to attention because other bloggers noted OMB meddling. OMB was selling site specificity, animal to man, which is an old Houdini chestnut.

http://www.epa.gov/iris/subst/0200.htm

Critical Effect	Point of Departure*	UF	Chronic RfC
peribronchial lymphoid hyperplasia in male rats 13-week inhalation Study Johannsen et al., 1988	BMC₁₀: 1.6 ppm BMCL₁₀: 0.84 ppm BMCL_ADJ: 0.90 mg/m³ BMCL_HEC: 0.90 mg/m³	3000	0.0003 mg/m³

Gene Environmental Interactions for Bladder Cancer

2009-10-24T05:20:00.000-04:00

BrooklynDodger(s) comment: First, urothelial carcinoma is the most common type of bladder cancer - the Dodger(s) had to google it. Learn something every day. The trouble with most genetic studies of cancer is they end with blaming the victim - or the victims' ancestors - and yield no new ideas for intervention. Controlling for less resistant genetic types would enable better human studies of associations with exposures. Glutathione continues to get more play, compared to cytochrome. CYP can be thought of as activating and dotoxicating, while GST is mostly detox unless there's an ad hoc Houdini hypothesis, as for methylene chloride.

Toxicology and Applied Pharmacology
Volume 241, Issue 1, 15 November 2009, Pages 111-118

A significantly joint effect between arsenic and occupational exposures and risk genotypes/diplotypes of CYP2E1, GSTO1 and GSTO2 on risk of urothelial carcinoma

Yuan-Hung Wang^a^,^b, Shauh-Der Yeh^b, Kun-Hung Shen^c, Cheng-Huang Shen^d, Guang-Dar Juang^e, Ling-I Hsu^f, Hung-Yi Chiou^a^,^, and Chien-Jen Chen^f^,^g

^aSchool of Public Health, Taipei Medical University, Taipei 110, Taiwan

^bDepartment of Urology, Taipei Medical University Hospital, Taipei 110, Taiwan

^cDepartment of Urology, Chi-Mei Medical Center, Tainan 710, Taiwan

^dDepartment of Urology, Chiayi Christian Hospital, Chia-Yi 600, Taiwan

^eDivision of Urology, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan

^fThe Genomics Research Center, Academia Sinica, Taipei 115, Taiwan

^gGraduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei 100, Taiwan

Received 17 April 2009;

revised 3 August 2009;

accepted 7 August 2009.

Available online 15 August 2009.

Abstract

Cigarette smoking, arsenic and occupational exposures are well-known risk factors for the development of urothelial carcinoma (UC). Therefore, the aim of this study is to investigate whether the effect of cigarette smoking, alcohol consumption, arsenic and occupational exposures on risk of UC could be modified by genetic polymorphisms of cytochrome P450 2E1 and glutathione S-transferase omega. A hospital-based case–control study consisted of 520 histologically confirmed UC cases, and 520 age- and gender-matched cancer-free controls were carried out from September 1998 to December 2007. Genotyping of CYP2E1, GSTO1 and GSTO2 was determined by polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP). Subjects with both of cigarette smoking and alcohol consumption have a significantly increased UC risk (odds ratio [OR] = 2.9; 95% confidence interval [CI] = 1.9–4.4). Significantly increased UC risks of 1.5 and 1.9 were found for study subjects with high arsenic exposure and those who have been exposed to two or more occupational exposures, respectively. A significantly increased UC risk of 3.9 was observed in study subjects with H2–H2 diplotype of GSTO1 and GSTO2. The significantly highest UC risk of 9.0 was found for those with all environmental risk factors of cigarette smoking, alcohol consumption, arsenic and occupational exposures and two or more risk genotypes/diplotypes of CYP2E1, GSTO1 and GSTO2. Our findings suggest that a significantly joint effect of cigarette smoking, alcohol consumption, arsenic and occupational exposures and risk genotypes/diplotypes of CYP2E1, GSTO1 and GSTO2 on risk of UC was found.

Arsenic Cardiac Effects

2009-10-23T06:11:00.000-04:00

BrooklynDodger(s) comment: Another exploration of the neglected organ system. Hazard ID in a specialized strain of mice. Need to think about potency (exposure response) assessment.

Toxicology and Applied Pharmacology
Volume 241, Issue 1, 15 November 2009, Pages 90-100

Arsenic exacerbates atherosclerotic lesion formation and inflammation in ApoE-/- mice

Sanjay Srivastava^a^,^d^,^,, Elena N. Vladykovskaya^a, Petra Haberzettl^a, Srinivas D. Sithu^b, Stanley E. D'Souza^b and J. Christopher States^c^,^d

^aDiabetes and Obesity Center and Institute of Molecular Cardiology, University of Louisville, Louisville, KY 40202, USA

^bDepartment of Physiology and Biophysics, University of Louisville, Louisville, KY 40202, USA

^cDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA

^dCenter for Environmental Genomics and Integrative Biology, University of Louisville, Louisville, KY 40202, USA

Received 23 February 2009;

revised 3 August 2009;

accepted 4 August 2009.

Available online 12 August 2009.

Abstract

Exposure to arsenic-contaminated water has been shown to be associated with cardiovascular disease, especially atherosclerosis. We examined the effect of arsenic exposure on atherosclerotic lesion formation, lesion composition and nature in ApoE-/- mice. Early post-natal exposure (3-week-old mice exposed to increased the atherosclerotic lesion formation by 3- to 5-fold in the aortic valve and the aortic arch, wit49 ppm arsenic as NaAsO₂ in drinking water for 7 weeks) without affecting plasma cholesterol. Exposure to arsenic for 13 weeks (3-week-old mice exposed to 1, 4.9 and 49 ppm arsenic as NaAsO₂ in drinking water) increased the lesion formation and macrophage accumulation in a dose-dependent manner. Temporal studies showed that continuous arsenic exposure significantly exacerbated the lesion formation throughout the aortic tree at 16 and 36 weeks of age. Withdrawal of arsenic for 12 weeks after an initial exposure for 21 weeks (to 3-week-old mice) significantly decreased lesion formation as compared with mice continuously exposed to arsenic. Similarly, adult exposure to 49 ppm arsenic for 24 weeks, starting at 12 weeks of age increased lesion formation by 2- to 3.6-fold in the aortic valve, the aortic arch and the abdominal aorta. Lesions of arsenic-exposed mice displayed a 1.8-fold increase in macrophage accumulation whereas smooth muscle cell and T-lymphocyte contents were not changed. Expression of pro-inflammatory chemokine MCP-1 and cytokine IL-6 and markers of oxidative stress, protein-HNE and protein-MDA adducts were markedly increased in lesions of arsenic-exposed mice. Plasma concentrations of MCP-1, IL-6 and MDA were also significantly elevated in arsenic-exposed mice. These data suggest that arsenic exposure increases oxidative stress, inflammation and atherosclerotic lesion formation.

Metals in PM associated with Cardiac Toxicity

2009-10-22T05:00:00.000-04:00

BrooklynDodger(s) comment: Risk assessments for particulate exposure in the workplace, and also community, typically ignore cardiac effects. Cohort studies in workplace populations are typically null for associations with chemical exposure, probably resulting from the healthy worker effect. This endpoint needs more work. Good to see EPA in the science game.

Toxicology and Applied Pharmacology
Volume 241, Issue 1, 15 November 2009, Pages 71-80

Differential pulmonary and cardiac effects of pulmonary exposure to a panel of particulate matter-associated metals

J. Grace Wallenborn^a^,^,, Mette J. Schladweiler^b^,, Judy H. Richards^b^, and Urmila P. Kodavanti^b^,

^aDepartment of Environmental Sciences and Engineering, UNC School of Public Health, Chapel Hill, NC 27599, USA

^bPulmonary Toxicology Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, ORD, Environmental Protection Agency, Durham, NC 27711, USA

Received 28 May 2009;

revised 29 July 2009;

accepted 3 August 2009.

Available online 11 August 2009.

Abstract

Biological mechanisms underlying the association between particulate matter (PM) exposure and increased cardiovascular health effects are under investigation. Water-soluble metals reaching systemic circulation following pulmonary exposure are likely exerting a direct effect. However, it is unclear whether specific PM-associated metals may be driving this. We hypothesized that exposure to equimolar amounts of five individual PM-associated metals would cause differential pulmonary and cardiac effects. We exposed male WKY rats (14 weeks old) via a single intratracheal instillation (IT) to saline or 1 μmol/kg body weight of zinc, nickel, vanadium, copper, or iron in sulfate form. Responses were analyzed 4, 24, 48, or 96 h after exposure. Pulmonary effects were assessed by bronchoalveolar lavage fluid levels of total cells, macrophages, neutrophils, protein, albumin, and activities of lactate dehydrogenase, γ-glutamyl transferase, and n-acetyl glucosaminidase. Copper induced earlier pulmonary injury/inflammation, while zinc and nickel produced later effects. Vanadium or iron exposure induced minimal pulmonary injury/inflammation. Zinc, nickel, or copper increased serum cholesterol, red blood cells, and white blood cells at different time points. IT of nickel and copper increased expression of metallothionein-1 (MT-1) in the lung. Zinc, nickel, vanadium, and iron increased hepatic MT-1 expression. No significant changes in zinc transporter-1 (ZnT-1) expression were noted in the lung or liver; however, zinc increased cardiac ZnT-1 at 24 h, indicating a possible zinc-specific cardiac effect. Nickel exposure induced an increase in cardiac ferritin 96 h after IT. This data set demonstrating metal-specific cardiotoxicity is important in linking metal-enriched anthropogenic PM sources with adverse health effects.

More Wands for Houdini

2009-10-21T06:51:00.002-04:00

BrooklynDodger(s) comment: A publication from EPA - it appears that EPA is arming itself for the next Houdini Risk Assessment war over trichloroethylene and solvents.

Characterizing uncertainty and population variability in the toxicokinetics of trichloroethylene and metabolites in mice, rats, and humans using an updated database, physiologically based pharmacokinetic (PBPK) model, and Bayesian approach
Pages 36-60Weihsueh A. Chiu, Miles S. Okino, Marina V. Evans http://www.sciencedirect.com/science?_ob=GatewayURL&_method=citationSearch&_urlVersion=4&_origin=SDVIALERTASCII&_version=1&_uoikey=B6WXH-4WXHBRS-2&md5=cf7e18939eb53611bdbca3e68c564dc1We have developed a comprehensive, Bayesian, PBPK model-based analysis of the population toxicokinetics of trichloroethylene (TCE) and its metabolites in mice, rats, and humans, considering a wider range of physiological, chemical, in vitro, and in vivo data than any previously published analysis of TCE. The toxicokinetics of the “population average,” its population variability, and their uncertainties are characterized in an approach that strives to be maximally transparent and objective. Estimates of experimental variability and uncertainty were also included in this analysis. The experimental database was expanded to include virtually all available in vivo toxicokinetic data, which permitted, in rats and humans, the specification of separate datasets for model calibration and evaluation. The total combination of these approaches and PBPK analysis provides substantial support for the model predictions. In addition, we feel confident that the approach employed also yields an accurate characterization of the uncertainty in metabolic pathways for which available data were sparse or relatively indirect, such as GSH conjugation and respiratory tract metabolism. Key conclusions from the model predictions include the following: (1) as expected, TCE is substantially metabolized, primarily by oxidation at doses below saturation; (2) GSH conjugation and subsequent bioactivation in humans appear to be 10- to 100-fold greater than previously estimated; and (3) mice had the greatest rate of respiratory tract oxidative metabolism as compared to rats and humans. In a situation such as TCE in which there is large database of studies coupled with complex toxicokinetics, the Bayesian approach provides a systematic method of simultaneously estimating model parameters and characterizing their uncertainty and variability. However, care needs to be taken in its implementation to ensure biological consistency, transparency, and objectivity.

A Screening Test for Autoimmunity Potential

2009-10-14T06:55:00.000-04:00

BrooklynDodger(s) comment: The Dodger(s) have to look up the full text, to find the activity of silicone implants.

Assessment of autoimmunity-inducing potential using the Brown Norway rat challenge model
Toxicology Letters, Volumes 112-113, 15 March 2000, Pages 443-451
Kimber L. WhiteJr, Daniel W. David, Leon F. Butterworth, Paal C. Klykken

The development of autoimmune disease in humans is thought to occur as a result of the interactions of a genetic predisposition of the host and environmental factors. There is evidence that treatment with When exposed to certain chemicals, Brown Norway (BN) rats develop autoimmune disease similar to human systemic lupus erythematosus (SLE) characterized bycertain drugs and exposure to environmental toxicants increase the risk associated with the development and severity of autoimmune disease. elevation of antibody levels to self and non-self antigens which can result in the formation of immune complexes and lead to a fatal glomerulonephritis. A unique characteristic of the BN rat model is that the increase in IgE is self-limiting with levels eventually returning to normal. The objective of these studies was to determine if the BN rat and the self-limiting nature of the IgE response could be used in identifying compounds capable of initiating autoimmune responses. Two compounds known to produce autoimmunity, mercuric chloride and -penicillamine, were studied as were, trichloroethylene and silicone gel, two agents suspected of inducing autoimmune disease. The results indicated that the BN rat model may prove useful for detecting compounds with the potential to produce autoimmunity, particularly if a HgCl₂ challenge is incorporated into the evaluation.

Even in Canada You Can't Get Reliable Road Accident Data

2009-10-13T06:26:00.000-04:00

BrooklynDodger(s) comments: Maybe there's generalizable solution to the problem of under reporting in passive data collection for injuries and accidents. A sampling approach seems better than a census. Public health can't rely on self-reporting by interested authorities.

Cross-analysis of hazmat road accidents using multiple databases
Pages 1192-1198
Martin Trépanier, Marie-Hélène Leroux, Nathalie de Marcellis-Warin

Road selection for hazardous materials transportation relies heavily on risk analysis. With risk being generally expressed as a product of the probability of occurrence and the expected consequence, one will understand that risk analysis is data intensive. However, various authors have noticed the lack of statistical reliability of hazmat accident databases due to the systematic underreporting of such events. Also, official accident databases alone are not always providing all the information required (economical impact, road conditions, etc.). In this paper, we attempt to integrate many data sources to analyze hazmat accidents in the province of Quebec, Canada. Databases on dangerous goods accidents, road accidents and work accidents were cross-analyzed. Results show that accidents can hardly be matched and that these databases suffer from underreporting. Police records seem to have better coverage than official records maintained by hazmat authorities. Serious accidents are missing from government's official databases (some involving deaths or major spills) even though their declaration is mandatory.

Humoral Markers of TCE auto immunity - Epiphenonmena?

2009-10-12T06:49:00.000-04:00

BrooklynDodger(s) Comment: This is not the Dodger(s)' field, although not clear what that field is. Nevertheless, the investigators here identify markers of humoral auto immunity, not cell mediated. But the health consequences quoted as being associated with TCE are not sneezing and wheezing (humoral) but allergic dermatitis, cell mediated.

Oxidative and nitrosative stress in trichloroethene-mediated autoimmune response
Toxicology, Volume 229, Issue 3, 18 January 2007, Pages 186-193
Gangduo Wang, Ping Cai, G.A.S. Ansari, M. Firoze Khan

Trichloroethene (TCE) is an industrial degreasing solvent and widespread environmental contaminant. Exposure to TCE is associated with autoimmunity. The mode of action of TCE is via its oxidative metabolism, and most likely, immunotoxicity is mediated via haptenization of macromolecules and subsequent induction of immune responses. To better understand the role of protein haptenization through TCE metabolism, we immunized MRL+/+ mice with albumin adducts of various TCE reactive intermediates. Serum immunoglobulins and cytokine levels were measured to determine immune responses against haptenized albumin. We found antigen-specific IgG responses of the IgG subtypes IgG₁, IgG_2a, and IgG_2b, with IgG₁ predominating. Serum levels of G-CSF were increased in immunized mice, suggesting macrophage activation. Liver histology revealed lymphocyte infiltration in the lobules and the portal area following immunization with formyl-albumin. Our findings suggest that proteins haptenized by metabolites of TCE may act as neo-antigens that can induce humoral immune responses and T cell-mediated hepatitis.

TCE induced auto immunity - protein modifications

2009-10-11T06:34:00.001-04:00

BrooklynDodger(s) comment: This continues posts on TCE induced auto immunity, which is apparently well established in China, and is driving a series of mechanistic studies. Dodger(s) too lazy to convert the dose to mg/kg.

Increased nitration and carbonylation of proteins in MRL +/+ mice exposed to trichloroethene: Potential role of protein oxidation in autoimmunity

Toxicology and Applied Pharmacology, Volume 237, Issue 2, 1 June 2009, Pages 188-195
Gangduo Wang, Jianling Wang, Huaxian Ma, M. Firoze Khan

Even though reactive oxygen and nitrogen species (RONS) are implicated as mediators of autoimmune diseases (ADs), little is known about contribution of protein oxidation (carbonylation and nitration) in the pathogenesis of such diseases. The focus of this study was, therefore, to establish a link between protein oxidation and induction and/or exacerbation of autoimmunity. To achieve this, female MRL +/+ mice were treated with trichloroethene (TCE), an environmental contaminant known to induce autoimmune response, for 6 or 12 weeks (10 mmol/kg, i.p., every 4^th day). TCE treatment resulted in significantly increased formation of nitrotyrosine (NT) and induction of iNOS in the serum at both 6 and 12 weeks of treatment, but the response was greater at 12 weeks. Likewise, TCE treatment led to greater NT formation, and iNOS protein and mRNA expression in the livers and kidneys. Moreover, TCE treatment also caused significant increases (3 fold) in serum protein carbonyls (a marker of protein oxidation) at both 6 and 12 weeks. Significantly increased protein carbonyls were also observed in the livers and kidneys (2.1 and 1.3 fold, respectively) at 6 weeks, and to a greater extent at 12 weeks (3.5 and 2.1 fold, respectively) following TCE treatment. The increases in TCE-induced protein oxidation (carbonylation and nitration) were associated with significant increases in Th1 specific cytokine (IL-2, IFN-γ) release into splenocyte cultures. These results suggest an association between protein oxidation and induction/exacerbation of autoimmune response. The results present a potential mechanism by which oxidatively modified proteins could contribute to TCE-induced autoimmune response and necessitates further investigations for clearly establishing the role of protein oxidation in the pathogenesis of ADs.

TCE induced auto immunity

2009-10-10T09:34:00.003-04:00

BrooklynDodger(s) Comments: Reading this abstract, the Dodger(s) discovered an apparently well accepted association between TCE exposure and exfoliative dermatitis, as Type II cell mediated auto immune condition. Waving hands, the Dodger(s) imagine TCE induced cell necrosis, possibly liver, triggering lymphocyte attack on debris, growing a clone of lymphocytes targeting cell surface proteins of a variety of tissues.

Toxicology and Applied Pharmacology
Volume 240, Issue 3, 1 November 2009, Pages 393-400

Identification of antigenic proteins associated with trichloroethylene-induced autoimmune disease by serological proteome analysis

Jianjun Liu ¹^,^a, Xiumei Xing ¹^,^a, Haiyan Huang^a, Yingzhi Jiang^a, Haowei He^a, Xinyun Xu^a, Jianhui Yuan^a, Li Zhou^a, Linqing Yang^a and Zhixiong Zhuang ^,^a^,

^aKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, No. 21, Rd 1st Tianbei, 518020 Shenzhen, PR China

Received 1 April 2009;

revised 8 July 2009;

accepted 25 July 2009.

Available online 6 August 2009.

Abstract

Although many studies indicated that trichloroethylene (TCE) could induce autoimmune diseases and some protein adducts were detected, the proteins were not identified and mechanisms remain unknown. To screen and identify autoantigens which might be involved in TCE-induced autoimmune diseases, three groups of sera were collected from healthy donors (I), patients suffering from TCE-induced exfoliative dermatitis (ED) (II), and the healed ones (III). Serological proteome analysis (SERPA) was performed with total proteins of TCE-treated L-02 liver cells as antigen sources and immunoglobins of the above sera as probes. Highly immunogenic spots (2-fold or above increase compared with group I) in group II and III were submitted to matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS) and tandem mass spectrometry sequencing. Western blot analysis was followed using commercial antibodies and individual serum. Six proteins were identified. Among them, Enoyl Coenzyme A hydratase peroxisoma 1 and lactate dehydrogenase B only showed stronger immunogenicity for group II sera, while Purine nucleoside phosphorylase, ribosomal protein P0 and proteasome activator subunit1 isoform1 also showed stronger immunogenicity for group III sera. Noteworthy, NM23 reacted only with group II sera. Western blot analysis of NM23 expression indicated that all of the individual serum of group II showed immune activity, which confirmed the validity of SERPA result. These findings revealed that there exist autoantibodies in group II and III sera. Besides, autoantibodies of the two stages of disease course were different. These autoantigens might serve as biomarkers to elucidate mechanisms underlying TCE toxicity and are helpful for diagnosis, therapy and prognosis of TCE-induced autoimmune diseases.

Screening interval depends on how fast workers get sick

2009-10-09T03:01:00.002-04:00

BrooklynDodger(s) comment: If one person, from a similarly exposed population gets sick, it should be assumed the environment poses a risk to everyone and the hazard should be abated. Protection should be implemented, not transfer.

Chest 2009;136 1086-1094

http://chestjournal.chestpubs.org/cgi/content/abstract/136/4/1086?etoc

How Frequently Should Workplace Spirometry Screening Be Performed?

Optimization Via Analytic Models

+ Author Affiliations

From Occupational-Environmental Preventive Medicine, Department of Family Medicine, David Geffen School of Medicine at the University of California at Los Angeles, Los Angeles, CA.

Philip Harber, MD, MPH, FCCP, UCLA Occupational Medicine, 10880 Wilshire Blvd, No. 1800, Los Angeles, CA 90024; e-mail: pharber@mednet.ucla.edu

Abstract

Background: Our objective was to determine how to select the optimal frequency of workplace spirometry screening using diacetyl-exposed workers as an example.

Methods: A Markov model was constructed to assess the likelihood of progressing from healthy status to early or advanced disease, starting from four different exposure levels, and performing longitudinal or cross-sectional interpretation of spirometry results over time. Projected outcomes at 10 years were evaluated to inform the optimal frequency of workplace spirometry testing.

Results: The optimal screening interval depends on the population risk and is highly sensitive to the real-life impact (utility) associated with false-positive results (eg, related to the availability of alternative work). Screening interval is particularly important for high-risk individuals with rapid transition from early to advanced disease, where the 10-year prevalence of advanced disease would be reduced from 5.3 to 2.5% using a 6-month interval rather than a 12-month interval. Longitudinal test interpretation, based on observing trends within each person over time, is marginally preferable to traditional cross-sectional spirometry interpretation.

Conclusions: There is no single best screening interval. For high-risk populations, annual testing may be too infrequent.

Does Obesity Cause Stress which Causes Asthma

2009-10-08T05:00:00.001-04:00

BrooklynDodger(s): Maybe the causality is that psychosocial stress causes both obesity and asthma?

Chest 2009;136 1055-1062

http://chestjournal.chestpubs.org/cgi/content/abstract/136/4/1055?etoc

Obesity-Asthma Association

Is It Explained by Systemic Oxidant Stress?

+ Author Affiliations

From the Department of Medicine (Dr. Sood) and Clinical Translational Sciences Center (Dr. Qualls), University of New Mexico Health Sciences Center, Albuquerque, NM; Department of Preventive Medicine (Dr. Arynchyn), University of Alabama at Birmingham, Birmingham, AL; Department of Medicine (Dr. Beckett), Mount Auburn Hospital, Cambridge, MA; Department of Laboratory Medicine and Pathology (Drs. Gross, Steffes, and Thyagarajan) and Division of Epidemiology (Dr. Jacobs), University of Minnesota, Minneapolis, MN; Department of Medicine (Dr. Smith), Feinberg School of Medicine, Northwestern University, Chicago, IL; Department of Experimental Surgery and Anesthesiology (Dr. Holvoet), Katholieke Universiteit Leuven, Leuven, Belgium; and Institute for Nutrition Research (Dr. Jacobs), University of Oslo, Oslo, Norway.

Akshay Sood, MD, MPH, FCCP, Associate Professor of Medicine, University of New Mexico Health Sciences Center School of Medicine, Department of Medicine, 1 University of New Mexico, MSC 10 5550, Albuquerque, NM 87131; e-mail: asood@salud.unm.edu

Abstract

Background: The mechanism for the obesity-asthma association is unknown. This study evaluated the hypothesis that systemic oxidant stress explains this association.

Methods: This cross-sectional study used year-20 follow-up evaluation data of 2,865 eligible participants in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. Current asthma was self-reported. Oxidant stress primarily was assessed by plasma F2-isoprostane concentrations. Obesity measures included categories of BMI and dual-energy x-ray absorptiometry-assessed fat mass index (FMI) and lean mass index (LMI). Logistic and linear regressions were used for analyses.

Results: Asthma was associated with higher plasma F2-isoprostane concentrations (p = 0.049); however, this association was not significant when adjusted for either gender or BMI. The BMI-asthma association was seen only among women (p = 0.03; gender-specific interaction, p = 0.01), and this association was not explained by plasma F2-isoprostane levels. Similarly, both FMI and LMI were positively associated with asthma in women (p = 0.20 and 0.01, respectively). These associations also were not explained by plasma F2-isoprostane levels. Similar results were obtained when plasma levels of oxidized low-density lipoprotein were used instead of F2-isoprostane levels to study the BMI-asthma association at the year-15 evaluation.

Conclusions: Systemic oxidant stress, primarily assessed by plasma F2-isoprostane concentrations, was not independently associated with asthma and, therefore, may not explain the obesity-asthma association in women. The asthma-oxidant stress association is confounded by gender and obesity. This study is limited by the inability to measure airway oxidant stress. It is possible that another (as yet undetermined) measure of systemic oxidant stress may be more relevant in asthma.

How Far Do Germs Travel?

2009-10-07T14:51:00.002-04:00

BrooklynDodger(s) comment: Seems like 3 feet is the standard travel distance, for sneezes and for patient ventilation.

Chest 2009;136 998-1005

http://chestjournal.chestpubs.org/cgi/content/abstract/136/4/998?etoc

Exhaled Air Dispersion Distances During Noninvasive Ventilation via Different Respironics Face Masks

+ Author Affiliations

From the Department of Medicine and Therapeutics (Drs. Hui, Ng, and Sung, and Mr. Chow), the Center for Housing Innovations (Mr. Chow), Institute of Space and Earth Information Science, and the Department of Anesthesia and Intensive Care (Drs. Chu, Gin, and Chan), The Chinese University of Hong Kong, Hong Kong, People's Republic of China; and the School of Mechanical Engineering (Dr. Hall), The University of New South Wales, Sydney, NSW, Australia.

David S. Hui, MD, FCCP, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, 30-32 Ngan Shing St, Shatin, NT, Hong Kong, People's Republic of China; e-mail: dschui@cuhk.edu.hk

Abstract

Background: As part of our influenza pandemic preparedness, we studied the exhaled air dispersion distances and directions through two different face masks (Respironics; Murrysville, PA) attached to a human-patient simulator (HPS) during noninvasive positive-pressure ventilation (NPPV) in an isolation room with pressure of −5 Pa.

Methods: The HPS was positioned at 45° on the bed and programmed to mimic mild lung injury (oxygen consumption, 300 mL/min; lung compliance, 35 mL/cm H₂O). Airflow was marked with intrapulmonary smoke for visualization. Inspiratory positive airway pressure (IPAP) started at 10 cm H₂O and gradually increased to 18 cm H₂O, whereas expiratory pressure was maintained at 4 cm H₂O. A leakage jet plume was revealed by a laser light sheet, and images were captured by high definition video. Normalized exhaled air concentration in the plume was estimated from the light scattered by the smoke particles.

Findings: As IPAP increased from 10 to 18 cm H₂O, the exhaled air of a low normalized concentration through the ComfortFull 2 mask (Respironics) increased from 0.65 to 0.85 m at a direction perpendicular to the head of the HPS along the median sagittal plane. When the IPAP of 10 cm H₂O was applied via the Image 3 mask (Respironics) connected to the whisper swivel, the exhaled air dispersed to 0.95 m toward the end of the bed along the median sagittal plane, whereas higher IPAP resulted in wider spread of a higher concentration of smoke.

Conclusions: Substantial exposure to exhaled air occurs within a 1-m region, from patients receiving NPPV via the ComfortFull 2 mask and the Image 3 mask, with more diffuse leakage from the latter, especially at higher IPAP.

How Much Radiation Comes from Medical x-rays?

2009-08-29T05:46:00.000-04:00

Volume 361:849-857		August 27, 2009		Number 9

Exposure to Low-Dose Ionizing Radiation from Medical Imaging Procedures

Reza Fazel, M.D., M.Sc., Harlan M. Krumholz, M.D., S.M., Yongfei Wang, M.S., Joseph S. Ross, M.D., Jersey Chen, M.D., M.P.H., Henry H. Ting, M.D., M.B.A., Nilay D. Shah, Ph.D., Khurram Nasir, M.D., M.P.H., Andrew J. Einstein, M.D., Ph.D., and Brahmajee K. Nallamothu, M.D., M.P.H.


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Perspective

by Lauer, M. S.


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ABSTRACT

Background The growing use of imaging procedures in the UnitedStates has raised concerns about exposure to low-dose ionizingradiation in the general population.

Methods We identified 952,420 nonelderly adults (between 18and 64 years of age) in five health care markets across theUnited States between January 1, 2005, and December 31, 2007.Utilization data were used to estimate cumulative effectivedoses of radiation from imaging procedures and to calculatepopulation-based rates of exposure, with annual effective dosesdefined as low (3 mSv), moderate (>3 to 20 mSv), high (>20to 50 mSv), or very high (>50 mSv).

Results During the study period, 655,613 enrollees (68.8%) underwentat least one imaging procedure associated with radiation exposure.The mean (±SD) cumulative effective dose from imagingprocedures was 2.4±6.0 mSv per enrollee per year; however,a wide distribution was noted, with a median effective doseof 0.1 mSv per enrollee per year (interquartile range, 0.0 to1.7). Overall, moderate effective doses of radiation were incurredin 193.8 enrollees per 1000 per year, whereas high and veryhigh doses were incurred in 18.6 and 1.9 enrollees per 1000per year, respectively. In general, cumulative effective dosesof radiation from imaging procedures increased with advancingage and were higher in women than in men. Computed tomographicand nuclear imaging accounted for 75.4% of the cumulative effectivedose, with 81.8% of the total administered in outpatient settings.

Conclusions Imaging procedures are an important source of exposureto ionizing radiation in the United States and can result inhigh cumulative effective doses of radiation.

Cannabis Improves Respiratory Capacity

2009-08-28T06:22:00.000-04:00

http://erj.ersjournals.com/cgi/content/abstract/09031936.00065009v1

Effects of cannabis on lung function: a population-based cohort study

R.J. Hancox ¹^*, R. Poulton ¹, M. Ely ¹, D. Welch ¹, D.R. Taylor ², C.R. McLachlan ¹, J.M. Greene ³, T.E. Moffitt ⁴, A. Caspi ⁴, M.R. Sears ³

¹ Dunedin Multidisciplinary Health and Development Research Unit, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand
² Dept of Medical and Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand
³ Firestone Institute for Respiratory Health, St. Joseph's Healthcare and Dept of Medicine, McMaster University, Hamilton, Ontario, Canada
⁴ Depts of Psychology & Neuroscience and Psychiatry & Behavioral Sciences, and Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina, USA; and MRC Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, UK

^* To whom correspondence should be addressed. E-mail: bob.hancox@otago.ac.nz.

	Abstract

The effects of cannabis on lung function remain unclear andmay be different to tobacco. We compared the associations betweenuse of these substances and lung function in a population-basedcohort (n=1037).
Cannabis and tobacco use were reported at ages18, 21, 26, and 32 years. Spirometry, plethysmography, and carbonmonoxide transfer factor were measured at age 32. Associationsbetween lung function and exposure to each substance were adjustedfor exposure to the other substance.
Cumulative cannabis usewas associated with higher forced vital capacity, total lungcapacity, functional residual capacity, and residual volume.Cannabis was also associated with higher airways resistancebut not with forced expiratory volume in 1 second, forced expiratoryratio, or transfer factor. These findings were similar amongstthose who did not smoke tobacco. By contrast, tobacco use wasassociated with lower forced expiratory volume in 1 second,lower forced expiratory ratio, lower transfer factor, and higherstatic lung volumes, but not with airways resistance.
Cannabisappears to have different effects on lung function to thoseof tobacco. Cannabis use was associated with higher lung volumessuggesting hyperinflation and increased large-airways resistance,but there was little evidence for airflow obstruction or impairmentof gas transfer.

Low Levels of Particle Air Pollution Effect Children with Asthma

2009-08-27T06:28:00.000-04:00

. Dales, L. Chen, A. M. Frescura, L. Liu, and P. J. Villeneuve Acute effects of outdoor air pollution on forced expiratory volume in 1 s: a panel study of schoolchildren with asthma
Eur Respir J 2009 34: 316-323.

¹ University of Ottawa, ² Ottawa Hospital Research Insitute, ³ Air Health Effects Research Section, Biostatistics and Epidemiology Division, Environmental Health Science and Research Bureau, Health Canada, and ⁴ Immunization and Respiratory Infections Division, Public Health Agency of Canada, Ottawa, ON, Canada.

CORRESPONDENCE: R. Dales, Air Health Effects Research Section, Biostatistics and Epidemiology Division, Environmental Health Science and Research Bureau, Health Canada, 3rd Floor, Room 3-039, P.L. 4903B, 269 Laurier Avenue W, Ottawa, K1A 0K9, ON, Canada. E-mail: rdales@ohri.ca

Keywords: Air pollution, children, environment, lung function

Received: September 9, 2008
Accepted February 5, 2009

Urban air pollution has been associated with morbidity but littleinformation exists on how it affects diurnal variation of lungfunction in children with asthma. The purpose of this studywas to investigate the acute effects of traffic-related pollutionon lung function among children with asthma.

We recorded morning and evening forced expiratory volume in1 s (FEV₁) for 28 consecutive days in 182 elementary schoolchildrenwith physician-diagnosed asthma, and monitored ambient hourlyair pollution concentrations.

An interquartile range (IQR) increase (6.0 µg·m^–3)in the previous 24-h (20:00 h to 20:00 h) mean concentrationof fine particulate matter 2.5 µm in diameter (PM_2.5)was associated with a 0.54% (95% confidence interval (CI) 0.06–1.02)decrease in bedtime FEV₁ (p = 0.027). This association persistedin two-pollutant models with ozone, nitrogen dioxide and sulphurdioxide. An IQR increase in mean daytime (08:00 h to 20:00 h)PM_2.5 of 6.5 µg·m^–3 was associated witha 0.73% (95% CI 0.10–1.37) decrease in FEV₁ over the courseof the day expressed as 100x(FEV₁ bedtime – FEV₁ morning)/FEV₁morning (p = 0.024).

This study suggests that, in children with asthma, relativelylow concentrations of urban air pollution worsen lung functionover a short period of time, even within a day. Of the pollutantsmeasured, PM_2.5appears to be the most important.

What's All This Posting on Non Occupational Effects About?

2009-08-26T06:39:00.000-04:00

BrooklynDodger(s) comments: All the time, epidemiologists with cohorts of opportunity examine associations of demographic variables with mortality, because they can. Nevertheless, the accumulation of these associations without biological hypotheses make for nice conversations make for interesting conversations about causes underlying more clearly focused occupational studies. The previous post quoted results of associations of earlier marriage among men, and shorter or no divorce among women with increased mortality. What hypothesis about psychosocial environment and what mechanism could be drawn? Can't think of one.,

Does Marriage Promote Longer Life? No clear answer.

2009-08-25T06:33:00.000-04:00

BrooklynDodger(s) comment: The pattern only confuses. Married late for men, and being divorced a long time for women seems to predict health.

American Journal of Epidemiology 2009 170(5):546-555

Marital Trajectories and Mortality Among US Adults

Matthew E. Dupre, Audrey N. Beck and Sarah O. Meadows

Correspondence to Dr. Matthew E. Dupre, Social Science Research Institute, Duke University, P.O. Box 90420, 2024 West Main Street, Durham, NC (e-mail: med11@geriduke.edu).

Received for publication May 19, 2008. Accepted for publication April 27, 2009.

More than a century of empirical evidence links marital statusto mortality. However, the hazards of dying associated withlong-term marital trajectories and contributing risk factorsare largely unknown. The authors used 1992–2006 prospectivedata from a cohort of US adults to investigate the impact ofcurrent marital status, marriage timing, divorce and widow transitions,and marital durations on mortality. Multivariate hazard ratioswere significantly higher for adults currently divorced andwidowed, married at young ages (18 years), who accumulated divorceand widow transitions (among women), and who were divorced for1–4 years. Results also showed significantly lower risksof mortality for men married after age 25 years compared withon time (ages 19–25 years) and among women experiencing10 years of divorce and 5 years of widowhood relative to thosewithout exposure to these statuses. For both sexes, accumulationof marriage duration was the most robust predictor of survival.Results from risk-adjusted models indicated that socioeconomicresources, health behaviors, and health status attenuated theassociations in different ways for men and women. The studydemonstrates that traditional measures oversimplify the relationbetween marital status and mortality and that sex differencesare related to a nexus of marital experiences and associatedhealth risks.

All Work and No Play Makes Jack a Dull Boy

2009-08-24T06:28:00.000-04:00

http://aje.oxfordjournals.org/cgi/reprint/169/5/596

Long Working Hours and Cognitive Function
The Whitehall II Study
Marianna Virtanen, Archana Singh-Manoux, Jane E. Ferrie, David Gimeno, Michael G. Marmot,Marko Elovainio, Markus Jokela, Jussi Vahtera, and Mika Kivima¨

This study examined the association between long working hours and cognitive function in middle age. Data were collected in 1997–1999 (baseline) and 2002–2004 (follow-up) from a prospective study of 2,214 British civil servants who were in full-time employment at baseline and had data on cognitive tests and covariates. A battery of cognitive tests (short-term memory, Alice Heim 4-I, Mill Hill vocabulary, phonemic fluency, and semantic fluency)
were measured at baseline and at follow-up. Compared with working 40 hours per week at most, working more than 55 hours per week was associated with lower scores in the vocabulary test at both baseline and follow-up. Long working hours also predicted decline in performance on the reasoning test (Alice Heim 4-I). Similar results were obtained by using working hours as a continuous variable; the associations between working hours and cognitive function were robust to adjustments for several potential confounding factors including age, sex, marital status, education, occupation, income, physical diseases, psychosocial factors, sleep disturbances, and health risk behaviors. This study shows that long working hours may have a negative effect on cognitive performance in middle age.

BPA extrapolation

2009-08-23T06:34:00.000-04:00

BrooklynDodger(s) comments: The highlighted sentence appears to contradict itself. Were the reviewers asleep? Still, a mechanism for greater sensitivity of younger organisms.

Toxicology Letters
Bisphenol A levels in blood depend on age and exposurePages 32-40 Hans Mielke, Ursula Gundert-Remy http://www.sciencedirect.com/science?_ob=GatewayURL&_method=citationSearch&_urlVersion=4&_origin=SDVIALERTASCII&_version=1&_uoikey=B6TCR-4WM751J-1&md5=4d0299f7d5883bb2094e8ebab20b72c8Federal Institute for Risk Assessment/Bundesinstitut für Risikobewertung (BfR), Thielallee 88-92, D-14195 Berlin, Germany

Received 24 April 2009;

revised 17 June 2009;

accepted 19 June 2009.

Available online 26 June 2009.

Abstract

We present two approaches to estimate blood concentrations of Bisphenol A (BPA). Simple kinetic principles were applied to calculate steady state plasma concentrations. A physiologically based model was used to simulate the blood concentration time profile in several age groups exploring the influence of not yet fully developed metabolic capacity on the blood concentrations in the newborn.

Both approaches gave concordant results and are in excellent agreement with experimental results [Völkel, W., Colnot, T., Csanady, G.A., Filser, J.G., Dekant, W., 2002. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chem. Res. Toxicol. 15, 1281–1287]. The predictions also agree with published results obtained with a different physiologically based model.

According to model simulations, BPA is present in the blood of the normal population at concentrations several orders of magnitude lower than most measurements reported in the literature. At the same external exposure level, the newborn is predicted to have 3 times greater blood concentration than the adult. This is due to the not yet fully developed glucuronidation activity in the newborn, not fully compensated by the unimpaired sulfation pathway. For the highest measured external BPA exposure, the predicted blood concentrations of 2.6 pg/ml (steady state concentration) and 8.2 pg/ml (peak concentration) in the adult are lower than the in vitro concentrations at which inhibiting adiponectin release from human adipocytes and stimulation of β-cell production and secretion were observed.

Journal Issue Devoted to Prions

2009-08-22T08:23:00.000-04:00

Journal of Toxicology and Environmental Health, Part A: Current Issues Volume 72 Issue 17 & 18 (http://www.informaworld.com/openurl?genre=issue&issn=1528-7394&volume=72&issue=17&uno_jumptype=alert&uno_alerttype=new_issue_alert,email) is now available online at informaworld (http://www.informaworld.com). Special Issue:Prion Research in Perspective

REACHING for protection

2009-08-22T06:23:00.000-04:00

BrooklynDodger(s) comments: REACH requires manufacturers to calculate DNELS, essentially by the general method by which EPA calculates RfC's for IRIS. That will generate a ton of DNELs. RfC's for most chemicals of occupational importance are way lower than PEL's, REL's or TLV's. This paper comments that REACH protocols are riskier than IRIS protocols.

Assessment factors for extrapolation from short-time to chronic exposure—Are the REACH guidelines adequate?Pages 16-22 Katarzyna Malkiewicz, Sven Ove Hansson, Christina Rudén http://www.sciencedirect.com/science?_ob=GatewayURL&_method=citationSearch&_urlVersion=4&_origin=SDVIALERTASCII&_version=1&_uoikey=B6TCR-4WJHB5F-1&md5=9d00784c06a9463b5684492424df6b77Due to the relative scarcity of long-term toxicity data, assessment factors for extrapolation from relatively short to chronic exposures have an important role in the risk assessment of chemicals. A recent REACH guidance document includes recommended default assessment factors that cover subacute–subchronic, subchronic–chronic, and subacute–chronic extrapolations. The recommended assessment factors are smaller than in most previous proposals, since they are calibrated to achieve central estimates (50th percentile of the target distribution) rather than a higher percentile such as the 95th, as has been more common. These assessment factors are nevertheless presented as representing a “widely agreed level of conservatism”, a statement that may lead to misunderstandings of what is achieved by using them in a risk assessment. Assessment factors have been based on evidence from animal studies with different designs, in particular with focus on different endpoints. Our re-analysis of experimental data shows that using mortality as an endpoint leads to smaller assessment factors than if the factors are derived from corresponding ratios for non-lethal toxicity.

Whole Body Vibration Exposure to Motorcyle Riders Exceeds Recommended Limits

2009-08-21T06:08:00.000-04:00

BrooklynDodger(s): Whole body vibration effects are less well defined than segmental (arm and hand) vibration. But effect many more organ systems. The study reveals that motorcycles pose a risk almost unanimously.

Whole-body vibration exposure experienced by motorcycle riders An evaluation acccording to ISO 2631-1 and ISO 2631-5 standards

Pages 708-718 Hsieh-Ching Chen, Wei-Chyuan Chen, Yung-Ping Liu, Chih-Yong Chen, Yi-Tsong Pan http://www.sciencedirect.com/science?_ob=GatewayURL&_method=citationSearch&_urlVersion=4&_origin=SDVIALERTASCII&_version=1&_uoikey=B6V31-4WK49VP-1&md5=199900a63453180501232b5723d0e77c

Whole-body vibration exposure experienced by motorcycle riders – An evaluation according to ISO 2631-1 and ISO 2631-5 standards

Hsieh-Ching Chen^a^,^,, Wei-Chyuan Chen^a, Yung-Ping Liu^a, Chih-Yong Chen^b and Yi-Tsong Pan^b

^aDepartment of Industrial Engineering and Management, Chaoyang University of Technology, No. 168 Jifong E. Rd., Wufong, Taichung County 41349, Taiwan

^bInstitute of Occupational Safety and Health, Council of Labor Affairs, Executive Yuan, No. 99, Lane 407, Hengke Rd., Sijhih, Taipei County 22143, Taiwan

Received 18 December 2007;

revised 14 March 2009;

accepted 24 May 2009.

Available online 21 June 2009.

Abstract

Riders of twelve motorcycles, comprising 6 full-scale motorbikes and 6 motor-scooters, and 5 sedan vehicles, performed test runs on a 20.6 km paved road composed of 5 km, 5 km, and 10.6 km of rural, provincial and urban routes, respectively. Each test run of motorcycle was separately performed under speed limits of 55 km/h and 40 km/h. Tri-axial accelerations of whole-body vibration (WBV) were obtained by using a seat pad and a portable data logger, and the driver's view was videotaped with a portable media recorder. Root mean square (RMS) acceleration, 8-h estimated vibration dose value (VDV₍₈₎) and 8-h estimated daily dose of static compression dose (S_ed) were determined from the collected data in accordance with ISO 2631-1 and ISO 2631-5 standards. Experimental results indicate that the WBV values of the sedan vehicle drivers have low RMS, VDV₍₈₎ and S_ed values (RMS 0.27–0.32 m/s²; VDV₍₈₎ 6.3–8.3 m/s^1.75; S_ed 0.21–0.26 MPa). However, over 90% of the motorcycle riders had VDV₍₈₎ (mean 23.5 m/s^1.75) exceeding the upper boundary of health guidance caution zone (17 m/s^1.75) recommended by ISO 2631-1, or had S_ed (mean 1.17 MPa) exceeding the value associated with a high probability of adverse health effects (0.8 MPa) recommended by ISO 2631-5. Over 50% of the motorcycle riders reached these boundary values for VDV and S_e in less than 2 h. The WBV exposure levels of the full-scale motorbikes riders and motor-scooter riders were not significantly different. However, the RMS and VDV₍₈₎ values of motorcycle riders indicate significant roadway effect (p <>S_ed values indicate significant speed limit effect (p <>

Falls and age

2009-08-20T06:01:00.000-04:00

BrooklynDodger(s) comment: Need clear guidance on living arrangements for older results. Often the fall triggers the cascade of much worse effects.

During 2007, the annual rate of nonfatal, medically attended fall injury episodes was 43 per 1,000 population. Adults aged ≥75 years had higher rates of these episodes compared with persons aged <65>

SOURCE: Adams PF, Barnes PM, Vickerie JL. Summary health statistics for the U.S. population: National Health Interview Survey, 2007. Vital Health Stat 2008;10(238). Available at http://www.cdc.gov/nchs/data/series/sr_10/sr10_238.pdf.

August 14, 2009 / 58(31);858

Impaired Driving - Still Barking up the Wrong Tree

2009-08-19T05:50:00.000-04:00

August 14, 2009 / 58(31);856

Notice to Readers: National Labor Day Drunk Driving Enforcement Crackdown --- August 21--September 7, 2009

In 2007, a total of 12,998 persons died in motor-vehicle crashes in which at least one driver had a blood alcohol concentration of >0.08 g/dL, above the legal limit for drivers in the United States. These alcohol-impaired--driving fatalities accounted for 32% of all motor-vehicle traffic fatalities in 2007 (1).

BrooklynDodger(s) comment: It's easy to blame the toll of vehicle related injuries on the guilty victims, emphasizing drunk or substance abused driving. Drinking and driving is confounded by not wearing seat belts, driving late at night on the weekend, probably speeding, (and being a male under 25, but that's really hard to intervene on) all of which add to the 32% fraction of traffic fatalities attributed solely to drinking. NHTSA needs to think more about intervening on the causes of risk behavior and intervening on that. What about a drowsy driving enforcement day, or promulgating a warning on driving consistent with the recommendations for truck drivers (which aren't protective enough)?

When will engineering controls be required for portable generators?

2009-08-17T06:43:00.000-04:00

BrooklynDodger(s) comment: Emphasis on better warnings is just another blame the victim approach. Catalytic converters on small engines should be required. That would likely be cheaper than requiring CO detectors to be mounted on the equipment. Need to study exposure from chain saws and leaf blowers.

Carbon Monoxide Exposures After Hurricane Ike

Texas, September 2008

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5831a1.htm?s_cid=mm5831a1_e

During power outages after hurricanes, survivors can be at risk for carbon monoxide (CO) poisoning if they use portable generators improperly (1). On September 13, 2008, Hurricane Ike struck the coast of Texas, leaving approximately 2.3 million households in the southeastern portion of the state without electricity (2). Six days later, 1.3 million homes were still without electrical power (2). To assess the impact of storm-related CO exposures and to enhance prevention efforts, CDC analyzed data from five disparate surveillance sources on CO exposures reported during September 13--26 in counties of southeast Texas that were declared disaster areas by the federal government. This report describes the results of that analysis, which indicated that one data source, Texas poison centers, received reports of 54 persons with storm-related CO exposures during the surveillance period. Another data source, the Undersea and Hyperbaric Medical Society (UHMS) hyperbaric oxygen treatment database, reported that 15 persons received hyperbaric oxygen treatment for storm-related CO poisoning. Medical examiners, public health officials, and hospitals in Texas reported that seven persons died from storm-related CO poisoning. Among the data sources, the percentage of reported storm-related CO exposures caused by improper generator use ranged from 82% to 87%. These findings underscore the need for effective prevention messages during storm preparation, warnings, and response periods regarding the correct use of generators and the installation and maintenance of battery-powered CO detectors.

Phthalates Reviewed Again - Same Results

2009-08-16T06:33:00.001-04:00

BrooklynDodger(s) comment: The review notes that human exposures - mostly through food - are close to recommended limits. Although studies in people are recommended, the Dodger(s) doubt(s) these are feasible - the limit of direct observation is too high, imposed by the population rate of adverse reproductive outcomes, and the high prevalence of exposure. The highest exposed population is kidney dialysis patients, not an optimistic group to compare outcomes in the general population. Public health authorities are going to have to make this call by the extrapolation of laboratory studies to people. While emphasis is on the phthalate moiety, attention should also be paid to 2-ethyl hexanol.

Reproductive and Developmental Toxicity of Phthalates

Authors: Jan L. Lyche ^a; Arno C. Gutleb ^b^c; ke Bergman ^d; Gunnar S. Eriksen ^c; AlberTinka J. Murk ^e^f; Erik Ropstad ^a; Margaret Saunders ^g; Janneche U. Skaare ^a^c

Affiliations:	^a Department of Production Animal Clinical Science, Norwegian School of Veterinary Science, Oslo, Norway
	^b Dpartement Environnement et Agro-biotechnologies (EVA), Centre de Recherche Public Gabriel Lippmann, Belvaux, Grand-duchy of Luxembourg
	^c National Veterinary Institute, Oslo, Norway
	^d Department of Environmental Chemistry, Stockholm University, Stockholm, Sweden
	^e Wageningen University, Wageningen, The Netherlands
	^f Wageningen Imares, IJmuiden, The Netherlands
	^g Biophysics Research Unit, University Hospital Bristol, NHS Foundation Trust, Bristol, United Kingdom

Journal of Toxicology and Environmental Health, Part B, Volume 12, Issue 4 April 2009 , pages 225 - 249

The purposes of this review are to (1) evaluate human and experimental evidence for adverse effects on reproduction and development in humans, produced by exposure to phthalates, and (2) identify knowledge gaps as for future studies. The widespread use of phthalates in consumer products leads to ubiquitous and constant exposure of humans to these chemicals. Phthalates were postulated to produce endocrine-disrupting effects in rodents, where fetal exposure to these compounds was found to induce developmental and reproductive toxicity. The adverse effects observed in rodent models raised concerns as to whether exposure to phthalates represents a potential health risk to humans. At present, di(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and butyl benzyl phthalate (BBP) have been demonstrated to produce reproductive and developmental toxicity; thus, this review focuses on these chemicals. For the general population, DEHP exposure is predominantly via food. The average concentrations of phthalates are highest in children and decrease with age. At present, DEHP exposures in the general population appear to be close to the tolerable daily intake (TDI), suggesting that at least some individuals exceed the TDI. In addition, specific high-risk groups exist with internal levels that are several orders of magnitude above average. Urinary metabolites used as biomarkers for the internal levels provide additional means to determine more specifically phthalate exposure levels in both general and high-risk populations. However, exposure data are not consistent and there are indications that secondary metabolites may be more accurate indicators of the internal exposure compared to primary metabolites. The present human toxicity data are not sufficient for evaluating the occurrence of reproductive effects following phthalate exposure in humans, based on existing relevant animal data. This is especially the case for data on female reproductive toxicity, which are scarce. Therefore, future research needs to focus on developmental and reproductive endpoints in humans. It should be noted that phthalates occur in mixtures but most toxicological information is based on single compounds. Thus, it is concluded that it is important to improve the knowledge of toxic interactions among the different chemicals and to develop measures for combined exposure to various groups of phthalates.

What's the Fiber Release From Asbestos Cement Roofs - Still Don't Know

2009-08-15T06:14:00.000-04:00

Annals of Occupational Hygiene Advance Access originally published online on June 2, 2009
Annals of Occupational Hygiene 2009 53(6):627-638; doi:10.1093/annhyg/mep036

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Risk Assessment of the Decay of Asbestos Cement Roofs

Antonella Campopiano¹^,*, Deborah Ramires¹, Aneta Maria Zakrzewska², Rosa Ferri³, Antonio D'annibale³ and Giancarlo Pizzutelli³

¹ Department of Occupational Hygiene, National Institute for Occupational Prevention and Safety (ISPESL), 00040 Monte Porzio Catone, Rome, Italy
² National Institute for Occupational Prevention and Safety (ISPESL), 88046 Lamezia Terme, Catanzaro, Italy
³ ASL Frosinone, Department of Prevention, 03100 Frosinone, Rome, Italy

^* Author to whom correspondence should be addressed. Tel: +39-06-94181445; fax: +39-06-94181419; e-mail: antonella.campopiano@ispesl.it

Objectives: In an assessment of the risk of asbestos fibresrelease from asbestos cement materials, an important role isplayed by the assessment of the surface corrosion and by thedisaggregation of asbestos cement. The aim of this work is toevaluate the differences among several methods used for therisk assessment that lead to a specific choice of abatementtechniques.

Methods: The state of deterioration of 40 asbestos cement roofswas evaluated using two priority assessment algorithms elaboratedin Italy, the ‘pull-up test’ described by the ItalianOrganization for Standardization and the indicators describedin the Italian legislation coupled with the observation of asmall sample, taken from each roof, by a stereomicroscope.

Results: The results obtained with the methods, proposed inthis study, for the risk assessment of the decay of asbestoscement roofs show slight differences among them, only one deviatesfrom the others in judgement on the state of conservation ofthe roof.

Conclusions: It is very important to train the operator conductingthe study since a completely subjectivity-free method does notexist. Whatever method is used will always be affected by thesubjectivity linked to the competency and the training of theoperator. Moreover, each method on its own cannot assess therisk of exposure to asbestos, but reliable assessment of asbestos-containingmaterials requires the use of more than one method, such asvisual inspections, a pull-up test, and an assessment algorithm.

Keywords: asbestos cement roof • priority assessment algorithm • pull-up test • risk assessment • SEM

Pilot Plant Data on Nanoparticle Exposure Shows a Significant Hazard

2009-08-14T06:11:00.000-04:00

free full text. 188 ug/m^3 is a surprisingly high and concerning exposure level. The ACGIH recommends 25 ug for silica - are these more or less potent?

http://annhyg.oxfordjournals.org/cgi/reprint/52/8/695

Exposure to Manufactured Nanostructured Particles
in an Industrial Pilot Plant
EVANGELIA DEMOU*, PHILIPPE PETER and STEFANIE HELLWEG
ETH Zurich, Institute of Environmental Engineering, Schafmattstrasse 6, 8093, Zurich, Switzerland
Received 7 February 2008; in final form 27 July 2008; published online 17 October 2008
Objectives: Nanomaterial production and the number of people directly in contact with these
materials are increasing. Yet, little is known on the association between exposure and corresponding
risks, such as pulmonary inflammation and oxidative stress.
Methods: Condensation Particle Counters, a DustTrak and Scanning Mobility Particle
Sizer quantified real-time size, mass and number concentrations in a nanostructure particle
pilot-scale production facility, using a high-temperature gas-phase process, over a 25-day period.
Temporal and spatial analysis of particle concentrations and sizes was performed during
production, maintenance and handling. Number-based particle retention of breathing mask filters
used under real-time production and exposure conditions in the workplace was quantified.
Results: The results demonstrate elevated number concentrations during production, which
can be an order of magnitude higher than background levels. Average concentrations during
production were 59 100 cm23 and 0.188 mg m23 for submicron particles. Mask filters decreased
particle number concentrations by >96%.
Conclusions: This study demonstrates real-time worker exposure during gas-phase nanoparticle
manufacturing. Qualitative and quantitative analysis of emission sources and concentration
levels in a production plant is accomplished. These results are important for workers,
employers and regulators in the nanotechnology field as they provide information on encountered
exposures and possibilities for mitigation measures.

Mechanism by Which Alcohol Protects Health

2009-08-13T05:21:00.001-04:00

Alcohol and Cardiovascular Health The Razor-Sharp Double-Edged Sword

Journal of the American College of Cardiology, Volume 50, Issue 11, Pages 1009-1014
J. O’Keefe, K. Bybee, C. Lavie

An extensive body of data shows concordant J-shaped associations between alcohol intake and a variety of adverse health outcomes, including coronary heart disease, diabetes, hypertension, congestive heart failure, stroke, dementia, Raynaud’s phenomenon, and all-cause mortality. Light to moderate alcohol consumption (up to 1 drink daily for women and 1 or 2 drinks daily for men) is associated with cardioprotective benefits, whereas increasingly excessive consumption results in proportional worsening of outcomes. Alcohol consumption confers cardiovascular protection predominately through improvements in insulin sensitivity and high-density lipoprotein cholesterol. The ethanol itself, rather than specific components of various alcoholic beverages, appears to be the major factor in conferring health benefits. Low-dose daily alcohol is associated with better health than less frequent consumption. Binge drinking, even among otherwise light drinkers, increases cardiovascular events and mortality. Alcohol should not be universally prescribed for health enhancement to nondrinking individuals owing to the lack of randomized outcome data and the potential for problem drinking.

Air Pollution Increases Cardiovascular Disease Among Women

2009-08-12T04:37:00.000-04:00

NEJM Volume 356:447-458		February 1, 2007		Number 5

Long-Term Exposure to Air Pollution and Incidence of Cardiovascular Events in Women

Kristin A. Miller, M.S., David S. Siscovick, M.D., M.P.H., Lianne Sheppard, Ph.D., Kristen Shepherd, M.S., Jeffrey H. Sullivan, M.D., M.H.S., Garnet L. Anderson, Ph.D., and Joel D. Kaufman, M.D., M.P.H.


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ABSTRACT

Background Fine particulate air pollution has been linked tocardiovascular disease, but previous studies have assessed onlymortality and differences in exposure between cities. We examinedthe association of long-term exposure to particulate matterof less than 2.5 µm in aerodynamic diameter (PM_2.5) withcardiovascular events.

Methods We studied 65,893 postmenopausal women without previouscardiovascular disease in 36 U.S. metropolitan areas from 1994to 1998, with a median follow-up of 6 years. We assessed thewomen's exposure to air pollutants using the monitor locatednearest to each woman's residence. Hazard ratios were estimatedfor the first cardiovascular event, adjusting for age, raceor ethnic group, smoking status, educational level, householdincome, body-mass index, and presence or absence of diabetes,hypertension, or hypercholesterolemia.

Results A total of 1816 women had one or more fatal or nonfatalcardiovascular events, as confirmed by a review of medical records,including death from coronary heart disease or cerebrovasculardisease, coronary revascularization, myocardial infarction,and stroke. In 2000, levels of PM_2.5 exposure varied from 3.4to 28.3 µg per cubic meter (mean, 13.5). Each increaseof 10 µg per cubic meter was associated with a 24% increasein the risk of a cardiovascular event (hazard ratio, 1.24; 95%confidence interval [CI], 1.09 to 1.41) and a 76% increase inthe risk of death from cardiovascular disease (hazard ratio,1.76; 95% CI, 1.25 to 2.47). For cardiovascular events, thebetween-city effect appeared to be smaller than the within-cityeffect. The risk of cerebrovascular events was also associatedwith increased levels of PM_2.5 (hazard ratio, 1.35; 95% CI,1.08 to 1.68).

Conclusions Long-term exposure to fine particulate air pollutionis associated with the incidence of cardiovascular disease anddeath among postmenopausal women. Exposure differences withincities are associated with the risk of cardiovascular disease.

Increased Ari Pollution Shortens Life

2009-08-11T05:17:00.000-04:00

NEJM Volume 360:376-386		January 22, 2009		Number 4

Fine-Particulate Air Pollution and Life Expectancy in the United States

C. Arden Pope, III, Ph.D., Majid Ezzati, Ph.D., and Douglas W. Dockery, Sc.D.


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ABSTRACT

Background Exposure to fine-particulate air pollution has beenassociated with increased morbidity and mortality, suggestingthat sustained reductions in pollution exposure should resultin improved life expectancy. This study directly evaluated thechanges in life expectancy associated with differential changesin fine particulate air pollution that occurred in the UnitedStates during the 1980s and 1990s.

Methods We compiled data on life expectancy, socioeconomic status,and demographic characteristics for 211 county units in the51 U.S. metropolitan areas with matching data on fine-particulateair pollution for the late 1970s and early 1980s and the late1990s and early 2000s. Regression models were used to estimatethe association between reductions in pollution and changesin life expectancy, with adjustment for changes in socioeconomicand demographic variables and in proxy indicators for the prevalenceof cigarette smoking.

Results A decrease of 10 µg per cubic meter in the concentrationof fine particulate matter was associated with an estimatedincrease in mean (±SE) life expectancy of 0.61±0.20year (P=0.004). The estimated effect of reduced exposure topollution on life expectancy was not highly sensitive to adjustmentfor changes in socioeconomic, demographic, or proxy variablesfor the prevalence of smoking or to the restriction of observationsto relatively large counties. Reductions in air pollution accountedfor as much as 15% of the overall increase in life expectancyin the study areas.

Conclusions A reduction in exposure to ambient fine-particulateair pollution contributed to significant and measurable improvementsin life expectancy in the United States.

Traffic Exposure Increases Mortality from Many Causes

2009-08-10T04:30:00.000-04:00

Long-Term Effects of Traffic-Related Air Pollution on Mortality
in a Dutch Cohort (NLCS-AIR Study)

Rob Beelen,1 Gerard Hoek,1 Piet A. van den Brandt,2 R. Alexandra Goldbohm,3 Paul Fischer,4 Leo J. Schouten,2
Michael Jerrett,5 Edward Hughes,6 Ben Armstrong,7 and Bert Brunekreef1,8
1Institute for Risk Assessment Sciences, Division Environmental Epidemiology, Utrecht University, Utrecht, the Netherlands; 2Department
of Epidemiology, Maastricht University, Maastricht, the Netherlands; 3TNO Quality of Life, Department of Prevention and Health, Leiden,
the Netherlands; 4Centre for Environmental Health Research, National Institute for Public Health and the Environment (RIVM), Bilthoven,
the Netherlands; 5School of Public Health, University of California, Berkeley, California, USA; 6Edward Hughes Consulting, Ottawa, Ontario,
Canada; 7Public and Environmental Research Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom; 8Julius
Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands

BACKGROUND: Several studies have found an effect on mortality of between-city contrasts in
long-term exposure to air pollution. The effect of within-city contrasts is still poorly understood.
OBJECTIVES: We studied the association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort.
METHODS: We used data from an ongoing cohort study on diet and cancer with 120,852 subjects who were followed from 1987 to 1996. Exposure to black smoke (BS), nitrogen dioxide, sulfur dioxide, and particulate matter ≤ 2.5 μm (PM2.5), as well as various exposure variables related to traffic, were estimated at the home address. We conducted Cox analyses in the full cohort adjusting for age, sex, smoking, and area-level socioeconomic status.

RESULTS: Traffic intensity on the nearest road was independently associated with mortality.
Relative risks (95% confidence intervals) for a 10-μg/m3 increase in BS concentrations (difference between 5th and 95th percentile) were 1.05 (1.00–1.11) for natural cause, 1.04 (0.95–1.13) for cardiovascular, 1.22 (0.99–1.50) for respiratory, 1.03 (0.88–1.20) for lung cancer, and 1.04 (0.97–1.12) for mortality other than cardiovascular, respiratory, or lung cancer. Results were similar for NO2 and PM2.5, but no associations were found for SO2.
CONCLUSIONS: Traffic-related air pollution and several traffic exposure variables were associated with
mortality in the full cohort. Relative risks were generally small. Associations between natural-cause and respiratory mortality were statistically significant for NO2 and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality.
KEY WORDS: air pollution, cohort, mortality, traffic. Environ Health Perspect 116:196–202 (2008).

Traffic Related Air Pollution Associated with Increased Lung Cancer Risk

2009-08-09T04:25:00.000-04:00

BrooklynDodger(s) comments: Association was found with non-smokers, but not overall (or presumably among smokers, who would have suffered the majority of the cancers) - which is what you would expect. The additive effect of pollution would show more strongly against a lower background.

Epidemiology:

September 2008 - Volume 19 - Issue 5 - pp 702-710

Long-Term Exposure to Traffic-Related Air Pollution and Lung Cancer Risk

Armstrong, Ben; Brunekreef, Bert; Beelen, Rob; Hoek, Gerard; van den Brandt, Piet A.; Goldbohm, R Alexandra; Fischer, Paul; Schouten, Leo J.

Abstract

Background: Most studies on the association between lung cancer and air pollution have investigated mortality. There have been few studies of lung cancer incidence.

Methods: We used data from the ongoing Netherlands Cohort Study on Diet and Cancer for 114,378 subjects with follow-up from September 1986 to December 1997. Exposure to black smoke, nitrogen dioxide (NO₂), sulfur dioxide (SO₂), and particulate matter ≤2.5 μm (PM_2.5) and traffic intensity variables (intensity on nearest road, intensity in a 100 m buffer, and an indicator variable for living close to a major road) were estimated at the home address. We conducted Cox proportional hazard analyses in the full cohort adjusting for age, sex, smoking status, and area-level socioeconomic status. We also carried out case-cohort analyses using more potential confounders on a subset of study participants for whom complete information from the baseline questionnaire had been processed.

Results: Adjusted analyses included 1940 cases for the full cohort and 1295 cases for the case-cohort analysis. Relative risks (RRs) for the overall air pollution concentrations were slightly below unity, and for the traffic variables RRs were slightly elevated. Risk was elevated among people who never smoked cigarettes (40,114 participants; 252 cases), with RRs of 1.47 (95% confidence interval = 1.01-2.16) for overall black smoke concentration, 1.11 (0.88-1.41) for traffic intensity on nearest road, and 1.55 (0.98-2.43) for living near a major road.

Conclusions: We found evidence for an association of exposure to black smoke and traffic with lung cancer incidence in people who had never smoked. No associations were found for the full cohort, or for other categories of smoking.

Chemoprevention

2009-08-08T16:09:00.001-04:00

Cancer Prevention Research A Population-Based Case-Control Study of Marijuana Use and Head and Neck Squamous Cell Carcinoma Caihua Liang,1 Michael D. McClean,3 Carmen Marsit,2 Brock Christensen,1,2 Edward Peters,4 Heather H. Nelson5 and Karl T. Kelsey1,2 Cancer Prev Res 2009;2(8) August 2009 Abstract Cannabinoids, constituents of marijuana smoke, have been recognized to have potential antitumor properties. However, the epidemiologic evidence addressing the relationship between marijuana use and the induction of head and neck squamous cell carcinoma (HNSCC) is inconsistent and conflicting. Cases (n = 434) were patients with incident HNSCC disease from nine medical facilities in the Greater Boston, MA area between December 1999 and December 2003. Controls (n = 547) were frequency matched to cases on age (±3 years), gender, and town of residence, randomly selected from Massachusetts town books. A questionnaire was adopted to collect information on lifetime marijuana use (decade-specific exposures) and associations evaluated using unconditional logistic regression. After adjusting for potential confounders (including smoking and alcohol drinking), 10 to 20 years of marijuana use was associated with a significantly reduced risk of HNSCC [odds ratio (OR)10-<20 years versus never users, 0.38; 95% confidence interval (CI), 0.22-0.67]. Among marijuana users moderate weekly use was associated with reduced risk (OR0.5-<1.5 times versus <0.5 time, 0.52; 95% CI, 0.32-0.85). The magnitude of reduced risk was more pronounced for those who started use at an older age (OR15-<20 years versus never users, 0.53; 95% CI, 0.30-0.95; OR?20 years versus never users, 0.39; 95% CI, 0.17-0.90; Ptrend < 0.001). These inverse associations did not depend on human papillomavirus 16 antibody status. However, for the subjects who have the same level of smoking or alcohol drinking, we observed attenuated risk of HNSCC among those who use marijuana compared with those who do not. Our study suggests that moderate marijuana use is associated with reduced risk of HNSCC.

Drinking Protects Against Type II Diabetes

2009-08-02T06:00:00.000-04:00

BrooklynDodger(s) comments: The Dodger(s) was(were) distinctly unaware that higher alcohol consumption was associated with lower prospective diabetes risk. The rest of this abstract is very confusing, it reads like it was written in the opposite direction.

American Journal of Epidemiology 2009 170(1):37-45; doi:10.1093/aje/kwp096

Confounding by Dietary Patterns of the Inverse Association Between Alcohol Consumption and Type 2 Diabetes Risk

Fumiaki Imamura, Alice H. Lichtenstein, Gerard E. Dallal, James B. Meigs and Paul F. Jacques

Correspondence to Dr. Paul F. Jacques, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging, 711 Washington Street, Boston, MA 02111 (e-mail: paul.jacques@tufts.edu).

Received for publication November 14, 2008. Accepted for publication March 25, 2009.

The ability to interpret epidemiologic observations is limitedbecause of potential residual confounding by correlated dietarycomponents. Dietary pattern analyses by factor analysis or partialleast squares may overcome the limitation. To examine confoundingby dietary pattern as well as standard risk factors and selectednutrients, the authors modeled the longitudinal associationbetween alcohol consumption and 7-year risk of type 2 diabetesmellitus in 2,879 healthy adults enrolled in the FraminghamOffspring Study (1991–2001) by Cox proportional hazardmodels. After adjustment for standard risk factors, consumersof 9.0 drinks/week had a significantly lower risk of type 2diabetes mellitus compared with abstainers (hazard ratio = 0.47,95% confidence interval (CI): 0.27, 0.81). Adjustment for selectednutrients had little effect on the hazard ratio, whereas adjustmentfor dietary pattern variables by factor analysis significantlyshifted the hazard ratio away from null (hazard ratio = 0.33,95% CI: 0.17, 0.64) by 40.0% (95% CI: 16.8, 57.0; P = 0.002).Dietary pattern variables by partial least squares showed similarresults. Therefore, the observed inverse association, consistentwith past studies, was confounded by dietary patterns, and thisconfounding was not captured by individual nutrient adjustment.The data suggest that alcohol intake, not dietary patterns associatedwith alcohol intake, is responsible for the observed inverseassociation with type 2 diabetes mellitus risk.

Fast Food and Diet

2009-08-01T06:00:00.000-04:00

BrooklynDodger(s) comment: Eaters of fast food are the object of a public health "moral panic," guilty victims of their illnesses. High caloric density and low price per calorie are characteristic of fast food, presumably the reverse for "healthy" food. So it turns out that if you eat more unhealthy food, you eat less healthy food. We could also assume higher population density is associated with higher business density and thus higher fast food density. Where does chinese food fit in this?

American Journal of Epidemiology 2009 170(1):29-36; doi:10.1093/aje/kwp090

Fast-Food Consumption, Diet Quality, and Neighborhood Exposure to Fast Food

The Multi-Ethnic Study of Atherosclerosis

Latetia V. Moore, Ana V. Diez Roux, Jennifer A. Nettleton, David R. Jacobs and Manuel Franco

Correspondence to Dr. Latetia V. Moore, Division of Nutrition, Physical Activity, and Obesity, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, 4770 Buford Highway, NE, MS K-46, Atlanta, GA 30341 (e-mail: lvmoore@cdc.gov).

Received for publication February 3, 2009. Accepted for publication March 16, 2009.

The authors examined associations among fast-food consumption,diet, and neighborhood fast-food exposure by using 2000–2002Multi-Ethnic Study of Atherosclerosis data. US participants(n = 5,633; aged 45–84 years) reported usual fast-foodconsumption (never, <1 src="http://aje.oxfordjournals.org/math/ge.gif" alt="≥" border="0">1 times/week) and consumptionnear home (yes/no). Healthy diet was defined as scoring in thetop quintile of the Alternate Healthy Eating Index or bottomquintile of a Western-type dietary pattern. Neighborhood fast-foodexposure was measured by densities of fast-food outlets, participantreport, and informant report. Separate logistic regression modelswere used to examine associations of fast-food consumption anddiet; fast-food exposure and consumption near home; and fast-foodexposure and diet adjusted for site, age, sex, race/ethnicity,education, and income. Those never eating fast food had a 2–3-timeshigher odds of having a healthy diet versus those eating fastfood 1 times/week, depending on the dietary measure. For everystandard deviation increase in fast-food exposure, the oddsof consuming fast food near home increased 11%–61% andthe odds of a healthy diet decreased 3%–17%, dependingon the model. Results show that fast-food consumption and neighborhoodfast-food exposure are associated with poorer diet. Interventionsthat reduce exposure to fast food and/or promote individualbehavior change may be helpful.

Beach Related Illness - Left the Key Data Out of the Abstract

2009-07-31T06:00:00.000-04:00

BrooklynDodger(s) comment: The most interesting number, the overall rate of illnesses, never made the abstract, only the risk ratios. So it's a 20% increase, but 20% of what?

American Journal of Epidemiology 2009 170(2):164-172; doi:10.1093/aje/kwp152

Contact With Beach Sand Among Beachgoers and Risk of Illness

Christopher D. Heaney, Elizabeth Sams, Steve Wing, Steve Marshall, Kristen Brenner, Alfred P. Dufour and Timothy J. Wade

Correspondence to Dr. Christopher D. Heaney, Campus Box 7435, Department of Epidemiology, University of North Carolina, Chapel Hill, NC 27599-7435 (e-mail: cheaney@email.unc.edu).

Received for publication February 2, 2009. Accepted for publication May 6, 2009.

Recent studies of beach sand fecal contamination have triggeredinterest among scientists and in the media. Although evidenceshows that beach sand can harbor high concentrations of fecalindicator organisms, as well as fecal pathogens, illness riskassociated with beach sand contact is not well understood. Beachvisitors at 7 US beaches were enrolled in the National Epidemiologicaland Environmental Assessment of Recreational Water (NEEAR) Studyduring 2003–2005 and 2007 and asked about sand contacton the day of their visit to the beach (digging in the sand,body buried in the sand). Then, 10–12 days after theirvisit, participants were telephoned to answer questions aboutany health symptoms experienced since the visit. The authorscompleted 27,365 interviews. Digging in the sand was positivelyassociated with gastrointestinal illness (adjusted incidenceproportion ratio (aIPR) = 1.13, 95% confidence interval (CI):1.02, 1.25) and diarrhea (aIPR = 1.20, 95% CI: 1.05, 1.36).The association was stronger between those buried in the sandand gastrointestinal illness (aIPR = 1.23, 95% CI: 1.05, 1.43)and diarrhea (aIPR = 1.24, 95% CI: 1.01, 1.52). Nonenteric illnessesdid not show a consistent association with sand contact activities.Sand contact activities were associated with enteric illnessat beach sites. Variation in beach-specific results suggeststhat site-specific factors may be important in the risk of illnessfollowing sand exposure.

bathing beaches; diarrhea; disease transmission, infectious; environmental pollution; fomites; fresh water; oceans and seas; sewage

Tall is a Risk Factor

2009-07-30T06:00:00.000-04:00

BrooklynDodger(s) comment: There's a lot of literature that being big is associated with increased risks of cancer. No one knows why. The concluding sentence is pretty weak.

American Journal of Epidemiology 2009 170(3):297-307; doi:10.1093/aje/kwp12

Body Mass Index, Height, and Risk of Lymphatic Malignancies: A Prospective Cohort Study

Romana D. Pylypchuk, Leo J. Schouten, R. Alexandra Goldbohm, Harry C. Schouten and Piet A. van den Brandt

Correspondence to Dr. Leo J. Schouten, Department of Epidemiology, GROW-School for Oncology and Developmental Biology, Maastricht University, P.O. Box 616, 6200 MD Maastricht, the Netherlands (e-mail: lj.schouten@epid.unimaas.nl).

Received for publication December 1, 2008. Accepted for publication April 23, 2009.

The association among body mass index (BMI), height, and therisk of lymphatic malignancies was investigated in the NetherlandsCohort Study. The participants (n = 120,852), Dutch men andwomen aged 55–69 years, completed a self-administeredquestionnaire at baseline in 1986. After 13.3 years of follow-up,data on 1,042 lymphatic malignancy cases (including diffuselarge-cell lymphoma, chronic lymphocytic leukemia, multiplemyeloma, and other subtypes) and 4,588 subcohort members wereavailable. Incidence rate ratios were estimated by using Coxregression models. BMI at baseline and BMI change since theage of 20 years were not associated with lymphatic malignancyrisk. However, the rate ratio of lymphatic malignancies per4-unit increase in BMI at 20 years of age was 1.13 (95% confidenceinterval (CI): 1.01, 1.25). The rate ratio of lymphatic malignanciesper 5-cm increase in height was 1.08 (95% CI: 1.02, 1.15). Fordiffuse large-cell lymphoma, follicular lymphoma, and chroniclymphocytic leukemia, the relative risks were 1.19 (95% CI:1.07, 1.33), 1.15 (95% CI: 0.95, 1.40), and 1.09 (95% CI: 0.95,1.26), respectively, for each 5-cm increase in height. The positiveassociations among BMI at 20 years of age, height, and the riskof lymphatic malignancies suggest that exposures during earlylife play a role in the etiology of lymphatic malignancies.

anthropometry; body height; body mass index; leukemia, lymphocytic, chronic, B-cell; lymphoma, non-Hodgkin; lymphoproliferative disorders; multiple myeloma

2009-07-29T06:06:00.000-04:00

BrooklynDodger(s) comments: A bunch of endpoints the Dodger(s) has(have) never heard of. An effect level for an ignored male organ.

Toxicology
Volume 262, Issue 3, 21 August 2009, Pages 215-223

Long-term effects of developmental exposure to di-n-butyl-phthalate (DBP) on rat prostate: Proliferative and inflammatory disorders and a possible role of androgens

Wellerson Rodrigo Scarano^a^,^,, Fabíola Choqueta de Toledo^b, Marina Trevizan Guerra^a, Silvana Gisele Pegorin de Campos^c, Luís Antonio Justulin Júnior^b, Sérgio Luis Felisbino^a, Janete A. Anselmo-Franci^d, Sebastião Roberto Taboga^c and Wilma De Grava Kempinas^a

^aDepartment of Morphology, Institute of Biosciences, UNESP, Botucatu, SP, 18618-000, Brazil

^bGraduate Program in Cellular and Structural Biology, Institute of Biology, State University of Campinas, UNICAMP, 13083-970, Brazil

^cDepartment of Biology, Institute of Biosciences, Humanities and Exact Sciences (IBILCE), UNESP, São José do Rio Preto, SP, 15100-000, Brazil

^dDepartment of Morphology, Stomatology and Physiology, School of Dentistry, University of São Paulo, USP, Ribeirão Preto, SP, Brazil

Abstract

In the present study we evaluated the toxic effects on the male adult rat prostate of DBP exposure during fetal and lactational periods, because although many studies have addressed the influence of phthalates on the male reproductive system, only a few have discussed their possible effects on prostate development. Pregnant females were distributed into two experimental groups: Control (C) and Treated (T). The females of the T group received DBP (100 mg/kg, by gavage) from gestation day 12 to postnatal day 21, while C rats received the vehicle (corn oil). In adulthood (90 days old), the animals were euthanized. The serum and testicular testosterone levels were measured. Ventral prostate was removed and weighed. Distal segment fragments of the ventral prostate were fixed and processed for histochemistry and immunohistochemistry to detect androgen receptor (AR) and Ki67 antigens. Protein extraction from ventral prostate fragments was performed for AR immunoblotting and Gelatin zymography for MMP-2 and MMP-9 (MMP, metalloproteinase). Stereological and histopathological analyses were also performed. Serum and testicular testosterone levels and prostate weight were comparable between groups. In the T group the relative proportions (%) of epithelial (C = 32.86; T = 42.04*) and stromal (C = 21.61; T = 27.88*) compartments were increased, while the luminal compartment was decreased (C = 45.54; T = 30.08*), *p <>T, disseminated inflammatory infiltrate in the stroma, associated or not with epithelial dysplasia and PIN (Prostatic Intraepithelial Neoplasia), was observed. Increases in AR expression, proliferation index and metalloproteinase 9 (MMP-9) activity were noted in T animals. In some T animals, collagen fibrils accumulated adjacent to the epithelium. As far as we are aware, this is the first report in the literature showing that phthalates could play a role in proliferative and inflammatory disorders of the rat prostate.

Losing Your Marbles with Age

2009-07-28T06:00:00.000-04:00

BrooklynDodger(s) comment: Not very informative. Have to read the full text to see what these scored mean.

American Journal of Epidemiology 2009 170(3):331-342; doi:10.1093/aje/kwp154

Trajectories of Cognitive Function in Late Life in the United States: Demographic and Socioeconomic Predictors

Arun S. Karlamangla, Dana Miller-Martinez, Carol S. Aneshensel, Teresa E. Seeman, Richard G. Wight and Joshua Chodosh

Correspondence to Dr. Arun S. Karlamangla, UCLA Division of Geriatrics, 10945 Le Conte Avenue, Suite 2339, Los Angeles, CA 90095 (e-mail: akarlamangla@mednet.ucla.edu).

Received for publication February 11, 2009. Accepted for publication May 11, 2009.

This study used mixed-effects modeling of data from a nationalsample of 6,476 US adults born before 1924, who were tested5 times between 1993 and 2002 on word recall, serial 7's, andother mental status items to determine demographic and socioeconomicpredictors of trajectories of cognitive function in older Americans.Mean decline with aging in total cognition score (range, 0–35;standard deviation, 6.00) was 4.1 (0.68 standard deviations)per decade (95% confidence interval: 3.8, 4.4) and in recallscore (range, 0–20; standard deviation, 3.84) was 2.3(0.60 standard deviations) per decade (95% confidence interval:2.1, 2.5). Older cohorts (compared with younger cohorts), women(compared with men), widows/widowers, and those never married(both compared with married individuals) declined faster, andnon-Hispanic blacks (compared with non-Hispanic whites) andthose in the bottom income quintile (compared with the top quintile)declined slower. Race and income differences in rates of declinewere not sufficient to offset larger differences in baselinecognition scores. Educational level was not associated withrate of decline in cognition scores. The authors concluded thatethnic and socioeconomic disparities in cognitive function inolder Americans arise primarily from differences in peak cognitiveperformance achieved earlier in the life course and less fromdeclines in later life.

Depression and the Neighborhood Environment

2009-07-27T06:57:00.000-04:00

Epidemiologic Reviews 2008 30(1):101-117; doi:10.1093/epirev/mxn009

Blues from the Neighborhood? Neighborhood Characteristics and Depression

Daniel Kim

From the Department of Society, Human Development, and Health, Harvard School of Public Health, Boston, MA

Correspondence to Dr. Daniel Kim, Department of Society, Human Development, and Health, Harvard School of Public Health, 677 Huntington Avenue, 7th Floor, Boston, MA 02115 (e-mail: dkim@hsph.harvard.edu).

accepted for publication May 22, 2008.

Unipolar major depression ranks among the leading contributorsto the global burden of disease. Although established risk factorsfor depression include a variety of individual-level characteristics,neighborhood etiologic factors have been relatively understudied,with several such attributes (neighborhood socioeconomic status,physical conditions, services/amenities, social capital, socialdisorder) possessing plausible linkages to depression. Usingthe PubMed database (1966–2008) and the Social SciencesCitation Index database (1956–2008), the author undertooka systematic review of the published literature on the associationsbetween these characteristics and depression in adults. Acrossstudies, the evidence generally supports harmful effects ofsocial disorder and, to a lesser extent, suggests protectiveeffects for neighborhood socioeconomic status. Few investigationshave explored the relations for neighborhood physical conditions,services/amenities, and social capital, and less consistentlypoint to salutary effects. The unsupportive findings may beattributed to the lack of representative studies within andacross societies or to methodological gaps, including lack ofcontrol for other neighborhood/non-neighborhood exposures andlack of implementation of more rigorous methodological approaches.Establishing mediating pathways and effect-modifying factorswill vitally advance understanding of neighborhood effects ondepression. Overall, addressing these gaps will help to identifywhat specific neighborhood features matter for depression, how,and for whom, and will contribute to curtailing the burden ofdisease associated with this major disorder.

Work Stress Can Make You Crazy

2009-07-26T17:49:00.000-04:00

BrooklynDodger(s) comment: The literature may be too big or too small. Over 1000 studies were boiled down to 14. Then, the authors seem to conclude that the 14 were not enough to draw a strong conclusion.

Epidemiologic Reviews 2008 30(1):118-132; doi:10.1093/epirev/mxn004

The Relation between Work-related Psychosocial Factors and the Development of Depression
Bo Netterstrøm1, Nicole Conrad1, Per Bech2, Per Fink3, Ole Olsen4, Reiner Rugulies4 and Stephen Stansfeld5

1 Clinic of Occupational Medicine, Hillerød Hospital, Hillerød, Denmark
2 Psychiatric Research Unit, Hillerød Hospital, Hillerød, Denmark
3 Research Clinic for Functional Disorders, Aarhus University Hospital, Aarhus, Denmark
4 National Research Centre for the Working Environment, Copenhagen, Denmark
5 Centre for Psychiatry, Wolfson Institute of Preventive Medicine, Queen Mary's School of Medicine and Dentistry, London, United Kingdom

Correspondence to Dr. Bo Netterstrøm, Clinic of Occupational Medicine, Hillerød Hospital, Helsevej 2, DK 3400 Hillerød, Denmark (e-mail: bone@noh.regionh.dk).

accepted for publication April 21, 2008.

This review is based on a literature search made in January 2007 on request by the Danish National Board of Industrial Injuries. The search in PubMed, EMBASE, and PsycINFO resulted in more than 1,000 publications. This was reduced to 14 after the titles, abstracts, and papers were evaluated by using the following criteria: 1) a longitudinal study, 2) exposure to work-related psychosocial factors, 3) the outcome a measure of depression, 4) relevant statistical estimates, and 5) nonduplicated publication. Of the 14 studies, seven used standardized diagnostic instruments as measures of depression, whereas the other seven studies used self-administered questionnaires. The authors found moderate evidence for a relation between the psychological demands of the job and the development of depression, with relative risks of approximately 2.0. However, indication of publication bias weakens the evidence. Social support at work was associated with a decrease in risk for future depression, as all four studies dealing with this exposure showed associations with relative risks of about 0.6. Even if this literature study has identified work-related psychosocial factors that in high-quality epidemiologic studies predict depression, studies are still needed that assess in more detail the duration and intensity of exposure necessary for developing depression.

Bone Tox (not Botox) and Cadmium.

2009-07-25T06:07:00.000-04:00

BrooklynDodger(s) comment: We think little about cadmium beyond the kidney and respiratory cancer. But "itai-itai" disease is an almost obligatory question on a tox survey exam. The osteoblast osteoclast dialogue explored here reminds us the body process in normal conditions arise from pushes and pulls.

Environmental Toxicology and Pharmacology
Volume 28, Issue 2, September 2009, Pages 232-236

Effects of cadmium on osteoblasts and osteoclasts in vitro

Xiao Chen^a, Guoying Zhu^a^,^,, Shuzhu Gu^a, Taiyi Jin^b and Chunlin Shao^c

^aDepartment of Bone Metabolism, Institute of Radiation Medicine, Fudan University, Shanghai 200032, China

^bDepartment of Occupation Medicine, School of Public Health, Fudan University, Shanghai, China

^cDepartment of Radiobiology, Institute of Radiation Medicine, Fudan University, Shanghai, China

Received 19 November 2008;

revised 9 April 2009;

accepted 15 April 2009.

Available online 24 April 2009.

Abstract

Cadmium (Cd) may have direct effects on bone metabolism and the mechanism is not fully understood. To investigate the effects of Cd on bone metabolism, effects of Cd on osteoblasts and osteoclasts in vitro were observed at cellular and molecular levels. Osteoblasts were cultured by sequential enzyme digestion from Sprague–Dawley rats calvarial bone and osteoclasts were isolated from long bones of new-born male and female Sprague–Dawley rats, and then cells were exposed to different concentrations of Cd (0–2.0 μmol/L for osteoblasts; 0.03 μmol/L for osteoclasts). As for osteoblasts, cell viability, alkaline phosphatase (ALP) activity, and mineralization were determined. Osteoprotegerin (OPG) and receptor activator of NF-kB ligand (RANKL) were studied via reverse transcription-polymerase chain reaction (RT-PCR). For osteoclasts, after exposure to Cd (0.03 μmol/L) for 72 h and 120 h, number of osteoclasts and pits formation was observed. Cd inhibited the viability, ALP activity, mineralization and up-regulated RANKL mRNA expression in osteoblasts. But Cd had no obvious effect on OPG mRNA expression. For osteoclasts, cadmium (0.03 μmol/L) could increase the numbers of osteoclasts (p <>p <>

Protein Allergenicity

2009-07-24T06:00:00.000-04:00

BrooklynDodger(s) comment: A whole issue of the journal of "don't worry, be happy" on proteins. This is all about GMO's. First, a general toxicology point: ingested proteins do get into the body to do what they do. But in much lower amounts than proteins administered in other ways. Some method of transport through intact membranes. Second, knowing this stuff gets it, it's not loony to be concerned that a proteinaceous pesticide in your corn on the cob might penetrate the body.
* Regulatory Toxicology and Pharmacology Volume 54, Issue 3, Supplement 1, Pages S1-S62 (August 2009) Current and future methods for evaluating the allergenic potential of proteins: International workshop, october 23–25, 2007 - ILSI Workshop Oct 07 Edited by Michelle Embry and James E. Gibson http://www.sciencedirect.com/science/issue/6999-2009-999459996.8998-1320083

Population Levels of Chemicals of Concern

2009-07-23T06:36:00.000-04:00

http://www.cdc.gov/exposurereport/pdf/thirdreport_summary.pdf

BrooklynDodger(s) comment: On the ATSDR website is valuable information about population levels of various chemicals of concern - dioxins, pcbs, phthalates, toxic metals, pesticides, PAC metabolites. Present levels may pose a risk - the population rate of diseases includes those caused by these agents - but the risk could only be discovered in humans if there were populations with materially higher exposures than those found in the reference population.

Cobalt Nanoparticles

2009-07-22T06:12:00.000-04:00

BrooklynDodger(s) comment: Once again, hazard identification without a measure of potency. Each time a new effect is discovered - in this case migration of particles into the cell - it justifies taking previously identified materials through the same assay. Problem is, every lab has it's own pet assay.

Toxicology Letters
Volume 189, Issue 3, 28 September 2009, Pages 253-259

Engineered cobalt oxide nanoparticles readily enter cells

Elena Papisa, Federica Rossia, Mario Raspantib, Isabella Dalle-Donnec, Graziano Colomboc, Aldo Milzanic, Giovanni Bernardinia, d and Rosalba Gornatia, Corresponding Author Contact Information, E-mail The Corresponding Author

aDepartment of Biotechnology and Molecular Science, Insubria University, Varese, Italy

bDepartment of Human Morphology, Insubria University, Varese, Italy

cDepartment of Biology, University of Milan, Milano, Italy

dCentro di Ricerca Interuniversitario Politecnico di Milano e Università dell’Insubria “The Protein Factory”, Italy

Abstract

Magnetic nanoparticles (NPs) have great potential for applications not only as catalysts or energy storage devices, but also in biomedicine, as contrast enhancement agents for magnetic resonance imaging, or for drug delivery. The same characteristics that make cobalt-based NPs so attractive raise serious questions about their safety. In this context, we investigated Co3O4-NPs. Believing that the characterization of NPs is relevant for understanding their biological activity, we analyzed them by atomic force and electron microscopy to define size, shape, and aggregation. To clarify whether their biological effects could be due to a potential release of cobalt ions, we evaluated spontaneous dissolution in different media. To determine their potential toxicity to human cells, we measured cell viability and ROS formation in two human cell lines using CoCl2 for comparison. Co3O4-NPs induced a concentration- and time-dependent impairment of cellular viability, although cobalt ions were more toxic. We also demonstrated that cobalt causes a rapid induction of ROS if supplied in the form of Co3O4-NPs rather than as ions. Moreover, we evaluated the cellular uptake of NPs. Interestingly, Co3O4-NPs are able to enter the cell very rapidly, remaining confined in vesicles inside the cytoplasm. They were found also inside the cell nuclei, though less frequently.

Tire Dust - Another Urban Air Particulate

2009-07-21T05:07:00.000-04:00

Toxicology Letters
Volume 189, Issue 3, 28 September 2009, Pages 206-214

Lung toxicity induced by intratracheal instillation of size-fractionated tire particles

Paride Mantecca^a, Giulio Sancini^b, Elisa Moschini^a, Francesca Farina^b, Maurizio Gualtieri^a, Annette Rohr^c, Giuseppe Miserocchi^b, Paola Palestini^b and Marina Camatini^a^,^,

^aDepartment of Environmental Sciences, POLARIS Research Center, University of Milano-Bicocca, 1 piazza della Scienza, Milan 20126, Italy

^bDepartment of Experimental Medicine, POLARIS Research Center, University of Milano-Bicocca, 48 via Cadore, Monza 20052, Italy

^cAir Quality and Health, Electric Power Research Institute (EPRI), 3420 Hillview Avenue, Palo Alto, CA 94304, USA

Abstract

Tire particles (TP) represent a significant component of urban air pollution (PM), constituting more than 10% of PM10 mass at urban locations with heavy traffic. The purpose of this study was to evaluate the effects of size-fractionated TP in an animal exposure model frequently used to assess the health effects of air pollutants. Potential pro-inflammatory and toxic effects of TP2.5 (<2.5 style="font-weight: bold; color: rgb(153, 0, 0);">Inflammatory cellular profiles showed dose-dependent responses after TP10 exposure, while strong cytotoxic effects, including increases in total protein, LDH and AP, were observed to be associated to TP2.5 exposure. Histologically, TP10-treated lungs mainly showed inflammatory tissue infiltration, in contrast to TP2.5-treated lungs, where lysis of the alveolar barrier appeared to be the most characteristic lesion. Our biochemical, cytological, and histological results indicated differential lung toxicity mechanisms elicited by size-fractionated, in agreement with other studies performed in in vivo systems that have shown that lung responses to inhaled or instilled particles are affected by particle size. We conclude that lung toxicity induced by TP10 was primarily due to macrophage-mediated inflammatory events, while toxicity induced by TP2.5 appeared to be related more closely to cytotoxicity.

Dotting the Quantum I's - Engineered nanoparticle toxicity

2009-07-20T06:01:00.000-04:00

BrooklynDodger(s): Quantum Dots are engineered nanoparticles, which might be really commentexotic compared to the run of the mill carcinogenic nano particles like diesel particulate matter, carbon black and titanium dioxide. Too bad this investigation didn't explore relative potency between QD's - unlikely to ever undergo an inhalation bioassay, much less present a study in people - with the already known species.

Toxicology and Applied Pharmacology
Volume 238, Issue 2, 15 July 2009, Pages 160-169

Nanoparticles up-regulate tumor necrosis factor-α and CXCL8 via reactive oxygen species and mitogen-activated protein kinase activation

Hye-Mi Lee^a^,^b, Dong-Min Shin^a^,^b, Hwan-Moon Song^c, Jae-Min Yuk^a^,^b, Zee-Won Lee^d, Sang-Hee Lee^e, Song Mei Hwang^f, Jin-Man Kim^f, Chang-Soo Lee^c^,^, and Eun-Kyeong Jo^a^,^b^,^g^,^,

^aDepartment of Microbiology, College of Medicine, Daejeon 301-747, South Korea

^bInfection Signaling Network Research Center, College of Medicine, Daejeon 301-747, South Korea

^cDepartment of Chemical Engineering, College of Engineering, Chungnam National University, Daejeon 305-764, South Korea

^dGlycomics Team, Korea Basic Science Institute, Daejeon 305-333, South Korea

^eMolecular Genomics Laboratory, Department of Biological Science, KAIST, 335 Gwahangno, Yuseong-gu, Daejeon 305-701, South Korea

^fDepartment of Pathology, College of Medicine, Daejeon 301-747, South Korea

^gResearch Institute for Medical Sciences, College of Medicine, Daejeon 301-747, South Korea

Abstract

Evaluating the toxicity of nanoparticles is an integral aspect of basic and applied sciences, because imaging applications using traditional organic fluorophores are limited by properties such as photobleaching, spectral overlaps, and operational difficulties. This study investigated the toxicity of nanoparticles and their biological mechanisms. We found that nanoparticles, quantum dots (QDs), considerably activated the production of tumor necrosis factor (TNF)-α and CXC-chemokine ligand (CXCL) 8 through reactive oxygen species (ROS)- and mitogen-activated protein kinases (MAPKs)-dependent mechanisms in human primary monocytes. Nanoparticles elicited a robust activation of intracellular ROS, phosphorylation of p47phox, and nicotinamide adenine dinucleotide phosphate oxidase activities. Blockade of ROS generation with antioxidants significantly abrogated the QD-mediated TNF-α and CXCL8 expression in monocytes. The induced ROS generation subsequently led to the activation of MAPKs, which were crucial for mRNA and protein expression of TNF-α and CXCL8. Furthermore, confocal and electron microscopy analyses showed that internalized QDs were trapped in cytoplasmic vesicles and compartmentalized inside lysosomes. Finally, several repeated intravenous injections of QDs caused an increase in neutrophil infiltration in the lung tissues in vivo. These results provide novel insights into the QD-mediated chemokine induction and inflammatory toxic responses in vitro and in vivo.

Ozone Hole

2009-07-19T05:48:00.002-04:00

Toxicology and Applied Pharmacology Volume 236, Issue 3, 1 May 2009, Pages 270-275

Longitudinal distribution of ozone absorption in the lung: Comparison of cigarette smokers and nonsmokers

Melissa L. Bates^a^,^,, Timothy M. Brenza^b, Abdellaziz Ben-Jebria^a^,^b, Rebecca Bascom^c and James S. Ultman^a^,^b

^aInterdisciplinary Graduate Degree Program in Physiology, Pennsylvania State University, University Park, PA 16802, USA

^bDepartment of Chemical Engineering, Pennsylvania State University, University Park, PA 16802, USA

^cDivision of Pulmonary, Allergy and Critical Care Medicine, Penn State College of Medicine, Hershey, PA 17033, USA

Abstract

In nonsmokers, ozone (O₃) is removed primarily by the epithelial lining fluid (ELF) of the conducting airways. We hypothesized that cigarette smokers, whose ELF antioxidant capacity may be limited by smoking, would remove less O₃ from their conducting airways than nonsmokers. We recruited 29 nonsmokers (17M, 12F) and 30 smokers (19M, 11F, 4 ± 4 pack-years) with similar anthropometric characteristics and measured the longitudinal distribution of O₃ using the bolus inhalation method. We also assessed the physiological effect of this transient exposure regimen using forced spirometry and capnography. Contrary to our hypothesis, the penetration volume at which 50% of a bolus was absorbed was not different between smokers and nonsmokers (97.1 ± 5.4 mL versus 97.9 ± 5.8 mL, p = 0.92). However, smokers did experience an increase in the slope of the alveolar plateau of the capnogram (S_N) (8.1 ± 3.2%, p = 0.02) and a small decrease in FEV₁ (− 1.3 ± 0.6%, p = 0.03), whereas nonsmokers did not (ΔFEV₁ − 0.1 ± 0.5% and ΔS_N − 0.2 ± 2.5%, p > 0.10). Thus, smokers are more sensitive to inhaled O₃ boluses than nonsmokers, despite a similar internal dose distribution.

Cadmium Poses Hazard at Current Population Body Burden Levels

2009-07-18T06:36:00.002-04:00

Toxicology and Applied Pharmacology
Volume 238, Issue 3, 1 August 2009, Pages 201-208

Current status of cadmium as an environmental health problem

Lars Järup^a^,^b^,^, and Agneta Åkesson^b

^aDepartment of Epidemiology and Public Health, Imperial College London, UK

^bInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

Abstract

Cadmium is a toxic metal occurring in the environment naturally and as a pollutant emanating from industrial and agricultural sources. Food is the main source of cadmium intake in the non-smoking population. The bioavailability, retention and toxicity are affected by several factors including nutritional status such as low iron status. Cadmium is efficiently retained in the kidney (half-time 10–30 years) and the concentration is proportional to that in urine (U-Cd). Cadmium is nephrotoxic, initially causing kidney tubular damage. Cadmium can also cause bone damage, either via a direct effect on bone tissue or indirectly as a result of renal dysfunction. After prolonged and/or high exposure the tubular injury may progress to glomerular damage with decreased glomerular filtration rate, and eventually to renal failure. Furthermore, recent data also suggest increased cancer risks and increased mortality in environmentally exposed populations. Dose–response assessment using a variety of early markers of kidney damage has identified U-Cd points of departure for early kidney effects between 0.5 and 3 μg Cd/g creatinine, similar to the points of departure for effects on bone. It can be anticipated that a considerable proportion of the non-smoking adult population has urinary cadmium concentrations of 0.5 μg/g creatinine or higher in non-exposed areas. For smokers this proportion is considerably higher. This implies no margin of safety between the point of departure and the exposure levels in the general population. Therefore, measures should be put in place to reduce exposure to a minimum, and the tolerably daily intake should be set in accordance with recent findings

Evidence for toxicity of carbon based nanoparticles

2009-07-17T05:52:00.000-04:00

Toxicology Letters Volume 186, Issue 3, 8 May 2009, Pages 166-173

Genotoxicity of nanomaterials: DNA damage and micronuclei induced by carbon nanotubes and graphite nanofibres in human bronchial epithelial cells in vitro
Hanna K. Lindberga, Ghita C.-M. Falcka, Satu Suhonena, Minnamari Vippolab, c, Esa Vanhalab, Julia Catalána, d, Kai Savolainena and Hannu Norppaa, ,
aNew Technologies and Risks, Work Environment Development, Finnish Institute of Occupational Health, FI-00250 Helsinki, Finland
bAerosols, Dusts and Metals, Work Environment Development, Finnish Institute of Occupational Health, FI-00250 Helsinki, Finland
cDepartment of Materials Science, Tampere University of Technology, FI-33101 Tampere, Finland
dDepartment of Anatomy, Embryology and Genetics, University of Zaragoza, Zaragoza, Spain

Abstract
Despite the increasing industrial use of different nanomaterials, data on their genotoxicity are scant. In the present study, we examined the potential genotoxic effects of carbon nanotubes (CNTs; >50% single-walled, 40% other CNTs; 1.1 nm × 0.5–100 μm; Sigma–Aldrich) and graphite nanofibres (GNFs; 95%; outer diameter 80–200 nm, inner diameter 30–50 nm, length 5–20 μm; Sigma–Aldrich) in vitro. Genotoxicity was assessed by the single cell gel electrophoresis (comet) assay and the micronucleus assay (cytokinesis-block method) in human bronchial epithelial BEAS 2B cells cultured for 24 h, 48 h, or 72 h with various doses (1–100 μg/cm2, corresponding to 3.8–380 μg/ml) of the carbon nanomaterials. In the comet assay, CNTs induced a dose-dependent increase in DNA damage at all treatment times, with a statistically significant effect starting at the lowest dose tested. GNFs increased DNA damage at all doses in the 24-h treatment, at two doses (40 and 100 μg/cm2) in the 48-h treatment (dose-dependent effect) and at four doses (lowest 10 μg/cm2) in the 72-h treatment. In the micronucleus assay, no increase in micronucleated cells was observed with either of the nanomaterials after the 24-h treatment or with CNTs after the 72-h treatment. The 48-h treatment caused a significant increase in micronucleated cells at three doses (lowest 10 μg/cm2) of CNTs and at two doses (5 and 10 μg/cm2) of GNFs. The 72-h treatment with GNFs increased micronucleated cells at four doses (lowest 10 μg/cm2). No dose-dependent effects were seen in the micronucleus assay. The presence of carbon nanomaterial on the microscopic slides disturbed the micronucleus analysis and made it impossible at levels higher than 20 μg/cm2 of GNFs in the 24-h and 48-h treatments. In conclusion, our results suggest that both CNTs and GNFs are genotoxic in human bronchial epithelial BEAS 2B cells in vitro. This activity may be due to the fibrous nature of these carbon nanomaterials with a possible contribution by catalyst metals present in the materials—Co and Mo in CNTs (<5>

Transplacental Carcinogenesis by Arsenic

2009-07-16T06:32:00.000-04:00

Toxicology and Applied Pharmacology
Volume 186, Issue 1, 1 January 2003, Pages 7-17

Transplacental carcinogenicity of inorganic arsenic in the drinking water: induction of hepatic, ovarian, pulmonary, and adrenal tumors in mice

Michael P. Waalkes ^,^,^a, Jerrold M. Ward^b, Jie Liu^a and Bhalchandra A. Diwan^c

^a Inorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis, National Cancer Institute at the National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA

^b Veterinary and Tumor Pathology Section, Office of Laboratory Animal Science, National Cancer Institute-Frederick, Frederick, MD 21702, USA

^c Intramural Research Support Program, Science Applications International Corp.-Frederick, National Cancer Institute at Frederick, Frederick, MD 21702, USA

Received 14 August 2002;

accepted 10 October 2002. ;

Available online 6 February 2003.

Abstract

Arsenic is a known human carcinogen, but development of rodent models of inorganic arsenic carcinogenesis has been problematic. Since gestation is often a period of high sensitivity to chemical carcinogenesis, we performed a transplacental carcinogenicity study in mice using inorganic arsenic. Groups (n = 10) of pregnant C3H mice were given drinking water containing sodium arsenite (NaAsO₂) at 0 (control), 42.5, and 85 ppm arsenite ad libitum from day 8 to 18 of gestation. These doses were well tolerated and body weights of the dams during gestation and of the offspring subsequent to birth were not reduced. Dams were allowed to give birth, and offspring were weaned at 4 weeks and then put into separate gender-based groups (n = 25) according to maternal exposure level. The offspring received no additional arsenic treatment. The study lasted 74 weeks in males and 90 weeks in females. A complete necropsy was performed on all mice and tissues were examined by light microscopy in a blind fashion. In male offspring, there was a marked increase in hepatocellular carcinoma incidence in a dose- related fashion (control, 12%; 42.5 ppm, 38%; 85 ppm, 61%) and in liver tumor multiplicity (tumors per liver; 5.6-fold over control at 85 ppm). In males, there was also a dose-related increase in adrenal tumor incidence and multiplicity. In female offspring, dose-related increases occurred in ovarian tumor incidence (control, 8%; 42.5 ppm, 26%; 85 ppm, 38%) and lung carcinoma incidence (control, 0%; 42.5 ppm, 4%; 85 ppm, 21%). Arsenic exposure also increased the incidence of proliferative lesions of the uterus and oviduct. These results demonstrate that oral inorganic arsenic exposure, as a single agent, can induce tumor formation in rodents and establishes inorganic arsenic as a complete transplacental carcinogen in mice. The development of this rodent model of inorganic arsenic carcinogenesis has important implications in defining the mechanism of action for this common environmental carcinogen.

Reflections on History of Particulate Air Quality Standards

2009-07-15T05:41:00.000-04:00

BrooklynDodger(s) comment: This seems an important review of the evolution of scientific knowledge and public health intervention. Dockery and his work were in the center of the dispute. The Dodger(s) reading of the history is that the epidemiologic evidence emerged in the published literature around 1995 and later, and that toxicologic evidence emerged within the time frame that the new NAAQS limit for PM2.5 was proposed. The NAAQS limits for PM2.5 then proposed of 15 ug/m^3 annual and 65 ug 24-hour were not fully protective and were roughly equivalent to the old PM10 limits. The 2006 NAAQS of 35 ug for 24 hours was the first true reduction in allowable exposure.

Annals of Epidemiology, Volume 19, Issue 4, Pages 257-263
Health Effects of Particulate Air Pollution

Douglas W. Dockery ScD , a,
aDepartments of Environmental Health and Epidemiology, Harvard School of Public Health, Boston, MA

In the 1980's it was generally felt that particulate air pollution concentrations in the United States were not a hazard to the public health. However, in the early 1990's the application of econometric time-series studies and prospective cohort studies suggested increased mortality associated with acute (daily) and chronic (decades) exposures to particulate air pollution commonly observed in the developed world. The epidemiologic evidence was not supported by evidence of causal associations from other disciplines. Nevertheless, the EPA moved to tighten controls on fine particulate air pollution. The debate over the science was played out in public hearings and the courts. The experience provides lessons on the use of epidemiologic data in setting public policy.

Air Pollution Components Activate Inflammatory Genes

2009-07-14T06:10:00.000-04:00

BrooklynDodger(s) comment: This raises a concern that complexity could be used in future to obfuscate regulation. Would be good to have some notion of relative potency, although some of these are granular and some have some solubility. It's a bit of a surprise that ZnCl2 is up there with LPS. Hard to think of what could be used as a negative control.

Toxicology Volume 259, Issues 1-2, 2 May 2009, Pages 46-53

Cytokine and chemokine expression patterns in lung epithelial cells exposed to components characteristic of particulate air pollution

J. Øvrevik , a, , M. Låga, J.A. Holmea, P.E. Schwarzea and M. Refsnesa
aDepartment of Air Pollution and Noise, Division of Environmental Medicine, Norwegian

Abstract
Airborne particulate matter (PM) has a complex composition, and the relative contribution of different compounds to PM-induced effects is only partly understood. The present study compared the capability of selected components commonly found in PM, to induce pro-inflammatory responses in lung epithelial cells. Ultrafine carbon black (ufCB), ZnCl2, FeSO4, 1-nitropyrene (1-NP), lipopolysaccharide (LPS), and crystalline silica (positive control) were screened for effects on the expression of 84 inflammation-related genes in the bronchial epithelial cell line, BEAS-2B. A total of 22 genes were up-regulated by one or more of the tested compounds, and 5 cytokine and 11 chemokine genes were selected for further studies. After 10 h exposure, silica induced significantly increased expression of CCL20, CXCL1/-3/-8/-10/-11, lymphotoxin (LT)β and interleukin (IL)-6; ufCB induced CXCL8/-10 and -11; ZnCl2 induced CCL11/-20/-26, CXCL1/-5/-8/-14 and tumor necrosis factor (TNF)-α; FeSO4 induced a weak up-regulation of CXCL8 and TNF-α; LPS induced CCL20, CXCL1/-5/-8/-10/-11, LTβ and IL-6; and 1-NP induced expression of CCL20, CXCL1/-3/-8, TNF-α and IL-6. Despite obvious differences, all compounds induced response-patterns that correlated relatively well with that of silica, the positive control. The predominant response appeared to be increased gene expression of neutrophil-recruiting CXC-chemokines. CXCL8 was the only gene induced by all tested PM-components, the most up-regulated on average, and also dominating the gene-expression patterns induced by coarse PM. The data show quantitative, and to a certain extent qualitative differences in cytokine/chemokine gene-expression profiles of the compounds tested. However, there were also striking similarities in the response-patterns induced by these physically/chemically widely different compounds.
Keywords: Air pollution; Lung; Epithelium; Inflammation; Cytokines; Gene expression

Aluminum and Iron Nanoparticles

2009-07-13T06:43:00.001-04:00

BrooklynDodger(s) comment: The Dodger(s) (is) (are) lazy and failed to find the full text to get the dose level

Toxicology
Volume 259, Issue 3, 17 May 2009, Pages 140-148

Retrospective analysis of 4-week inhalation studies in rats with focus on fate and pulmonary toxicity of two nanosized aluminum oxyhydroxides (boehmite) and pigment-grade iron oxide (magnetite): The key metric of dose is particle mass and not particle surface area

Jürgen Pauluhn ^,^a^,

^aInstitute of Toxicology, Bayer Schering Pharma, Department of Inhalation Toxicology, Building no. 514, 42096 Wuppertal, Germany

Received 19 January 2009;

revised 14 February 2009;

accepted 21 February 2009.

Available online 5 March 2009.

Abstract

This paper compares the pulmonary toxicokinetics and toxicodynamics of three different types of poorly soluble dusts examined in repeated rat inhalation bioassays (6 h/day, 5 days/week, 4 weeks). In these studies the fate of particles was studied during a 3–6-month postexposure period. This retrospective analysis included two types of aluminum oxyhydroxides (AlOOH, boehmite), high purity calcined, and agglomerated nanosized aluminas of very low solubility with primary isometric particles of 10 or 40 nm, and synthetic iron oxide black (Fe₃O₄ pigment grade). Three metrics of dose (actual mass concentration, surface area concentration, mass-based lung burden) were compared with pulmonary toxicity characterized by bronchoalveolar lavage. The results of this analysis provide strong evidence that pulmonary toxicity (inflammation) corresponds best with the mass-based cumulative lung exposure dose. The inhalation study with a MMAD of ≈0.5 μm yielded a higher pulmonary dose than MMADs in the range of 1–2 μm, a range most commonly used in repeated exposure inhalation studies. Hence, a key premise for the dosimetric adjustment across species is that comparable lung tissue doses should cause comparable effects. From that perspective, the determination of mass-based pulmonary lung burdens appears to be amongst the most important and critical nominator of dose and dose-related pulmonary toxicity.

Mea (Nostra) Culpa

2009-07-12T08:40:00.003-04:00

BrooklynDodger(s) comment: BrooklynDodger went dark for a couple of months, likely killing the meager readership for good. An obstacle is difficulty of constructing comments on the fly, especially for studies finding absence of association of health effects with environmental exposures. The Dodger(s) think the abstracts might be worth someone's while without comments, and the blog can be a collection of interesting stuff to work on in the future. So the Dodger(s) are going to post some abstracts with no comment.

Stress causes health risk behavior

2009-07-11T05:19:00.001-04:00

American Journal of Epidemiology 2009 170(2):181-192;

Psychosocial Stress and Change in Weight Among US Adults

Jason P. Block, Yulei He, Alan M. Zaslavsky, Lin Ding and John Z. Ayanian

Correspondence to Dr. John Z. Ayanian, Department of Health Care Policy, Harvard Medical School, 180 Longwood Avenue, Boston, MA 02115 (e-mail: ayanian@hcp.med.harvard.edu).

Received for publication December 23, 2008. Accepted for publication April 2, 2009.

The association of psychosocial stress with weight gain mayhave important implications for clinical practice and workplaceand public health interventions. To determine whether multipledomains of psychosocial stress were associated with weight gainfrom 1995 to 2004, the authors analyzed a nationally representativelongitudinal cohort of 1,355 men and women in the United States.Change in body mass index was assessed for multiple domainsof psychosocial stress related to work, personal relationships,life constraints, and finances, controlling for other factorsassociated with weight gain. All analyses were stratified bysex and weighted to account for the complex survey design. Amongmen with high baseline body mass index, weight gain was associatedwith increasing levels of psychosocial stress related to job-relateddemands (P <>index), lack of skill discretion (P = 0.014), lack of decisionauthority (P = 0.026), and difficulty paying bills (P = 0.004).Among women with high baseline body mass index, weight gainwas associated with job-related demands (P<>with baseline body mass index), perceived constraints in life(P <>P = 0.016),and difficulty paying bills (P = 0.010). Interventions to addresspsychosocial stress may limit weight gain among overweight andobese men and women