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Manganese concentrations in soil and settled dust in an area with historic ferroalloy production.

Paul J. Lioy, Ph.D. - 9 hours 4 min ago

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Manganese concentrations in soil and settled dust in an area with historic ferroalloy production.

J Expo Sci Environ Epidemiol. 2014 Oct 22;

Authors: Pavilonis BT, Lioy PJ, Guazzetti S, Bostick BC, Donna F, Peli M, Zimmerman NJ, Bertrand P, Lucas E, Smith DR, Georgopoulos PG, Mi Z, Royce SG, Lucchini RG

Abstract
Ferroalloy production can release a number of metals into the environment, of which manganese (Mn) is of major concern. Other elements include lead, iron, zinc, copper, chromium, and cadmium. Mn exposure derived from settled dust and suspended aerosols can cause a variety of adverse neurological effects to chronically exposed individuals. To better estimate the current levels of exposure, this study quantified the metal levels in dust collected inside homes (n=85), outside homes (n=81), in attics (n=6), and in surface soil (n=252) in an area with historic ferroalloy production. Metals contained in indoor and outdoor dust samples were quantified using inductively coupled plasma optical emission spectroscopy, whereas attic and soil measurements were made with a X-ray fluorescence instrument. Mean Mn concentrations in soil (4600 μg/g) and indoor dust (870 μg/g) collected within 0.5 km of a plant exceeded levels previously found in suburban and urban areas, but did decrease outside 1.0 km to the upper end of background concentrations. Mn concentrations in attic dust were ~120 times larger than other indoor dust levels, consistent with historical emissions that yielded high airborne concentrations in the region. Considering the potential health effects that are associated with chronic Mn inhalation and ingestion exposure, remediation of soil near the plants and frequent, on-going hygiene indoors may decrease residential exposure and the likelihood of adverse health effects.Journal of Exposure Science and Environmental Epidemiology advance online publication, 22 October 2014; doi:10.1038/jes.2014.70.

PMID: 25335867 [PubMed - as supplied by publisher]

Categories: Publications from UCDPER Members

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation.

Jeffrey D. Laskin, Ph.D. - 9 hours 4 min ago

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Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation.

Exp Mol Pathol. 2014 Aug;97(1):89-98

Authors: Sunil VR, Vayas KN, Cervelli JA, Malaviya R, Hall L, Massa CB, Gow AJ, Laskin JD, Laskin DL

Abstract
Nitrogen mustard (NM) is a toxic alkylating agent that causes damage to the respiratory tract. Evidence suggests that macrophages and inflammatory mediators including tumor necrosis factor (TNF)α contribute to pulmonary injury. Pentoxifylline is a TNFα inhibitor known to suppress inflammation. In these studies, we analyzed the ability of pentoxifylline to mitigate NM-induced lung injury and inflammation. Exposure of male Wistar rats (150-174 g; 8-10 weeks) to NM (0.125 mg/kg, i.t.) resulted in severe histopathological changes in the lung within 3d of exposure, along with increases in bronchoalveolar lavage (BAL) cell number and protein, indicating inflammation and alveolar-epithelial barrier dysfunction. This was associated with increases in oxidative stress proteins including lipocalin (Lcn)2 and heme oxygenase (HO)-1 in the lung, along with pro-inflammatory/cytotoxic (COX-2(+) and MMP-9(+)), and anti-inflammatory/wound repair (CD163+ and Gal-3(+)) macrophages. Treatment of rats with pentoxifylline (46.7 mg/kg, i.p.) daily for 3d beginning 15 min after NM significantly reduced NM-induced lung injury, inflammation, and oxidative stress, as measured histologically and by decreases in BAL cell and protein content, and levels of HO-1 and Lcn2. Macrophages expressing COX-2 and MMP-9 also decreased after pentoxifylline, while CD163+ and Gal-3(+) macrophages increased. This was correlated with persistent upregulation of markers of wound repair including pro-surfactant protein-C and proliferating nuclear cell antigen by Type II cells. NM-induced lung injury and inflammation were associated with alterations in the elastic properties of the lung, however these were largely unaltered by pentoxifylline. These data suggest that pentoxifylline may be useful in treating acute lung injury, inflammation and oxidative stress induced by vesicants.

PMID: 24886962 [PubMed - indexed for MEDLINE]

Categories: Publications from UCDPER Members

The World Health Organization (WHO) Recommends Vaccine Composition for the 2011-2012 Northern Hemisphere Influenza Season

PandemicFlu.gov - Thu, 10/23/2014 - 14:00

The World Health Organization (WHO) Recommends Vaccine Composition for the 2011-2012 Northern Hemisphere Influenza Season

Categories: Government Agency News

Changing trends in phthalate exposures.

Paul J. Lioy, Ph.D. - Wed, 10/22/2014 - 14:00

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Changing trends in phthalate exposures.

Environ Health Perspect. 2014 Oct 1;122(10):A264

Authors: Lioy PJ, Gennings C, Hauser R, Koch HM, Kortenkamp A

PMID: 25272327 [PubMed - in process]

Categories: Publications from UCDPER Members

Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats.

Jeffrey D. Laskin, Ph.D. - Wed, 10/22/2014 - 14:00

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Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats.

Toxicol Appl Pharmacol. 2014 Aug 15;279(1):43-52

Authors: Zheng R, Dragomir AC, Mishin V, Richardson JR, Heck DE, Laskin DL, Laskin JD

Abstract
The lipid peroxidation end-product 4-hydroxynonenal (4-HNE) is generated in tissues during oxidative stress. As a reactive aldehyde, it forms Michael adducts with nucleophiles, a process that disrupts cellular functioning. Liver, lung and brain are highly sensitive to xenobiotic-induced oxidative stress and readily generate 4-HNE. In the present studies, we compared 4-HNE metabolism in these tissues, a process that protects against tissue injury. 4-HNE was degraded slowly in total homogenates and S9 fractions of mouse liver, lung and brain. In liver, but not lung or brain, NAD(P)+ and NAD(P)H markedly stimulated 4-HNE metabolism. Similar results were observed in rat S9 fractions from these tissues. In liver, lung and brain S9 fractions, 4-HNE formed protein adducts. When NADH was used to stimulate 4-HNE metabolism, the formation of protein adducts was suppressed in liver, but not lung or brain. In both mouse and rat tissues, 4-HNE was also metabolized by glutathione S-transferases. The greatest activity was noted in livers of mice and in lungs of rats; relatively low glutathione S-transferase activity was detected in brain. In mouse hepatocytes, 4-HNE was rapidly taken up and metabolized. Simultaneously, 4-HNE-protein adducts were formed, suggesting that 4-HNE metabolism in intact cells does not prevent protein modifications. These data demonstrate that, in contrast to liver, lung and brain have a limited capacity to metabolize 4-HNE. The persistence of 4-HNE in these tissues may increase the likelihood of tissue injury during oxidative stress.

PMID: 24832492 [PubMed - indexed for MEDLINE]

Categories: Publications from UCDPER Members

Parliament Hill attacked, soldier shot at National War Memorial in Ottawa Canada

Homeland Security News - Wed, 10/22/2014 - 11:09

Parliament Hill came under attack today after a man with a rifle shot a soldier standing guard at the National War Memorial in downtown Ottawa. Update: 1 shooter dead, 1 still believed at large in downtown Ottawa. Police searching cars leaving Ottawa trying to go to Quebec. Report of additional shot fired near Chateau Laurier [...]

This story comes to us via Homeland Security - National Terror Alert. National Terror Alert is America's trusted source for homeland security news and information.

Parliament Hill attacked, soldier shot at National War Memorial in Ottawa Canada

Categories: Homeland Security News

Hospital disaster preparedness in Switzerland

Environmental/Disaster News - Mon, 10/20/2014 - 02:00

Swiss Medical Weekly