Tissue Injury Following Inhalation of Fine Particulate Matter and Hydrogen Peroxide Is Associated with Altered Production of Inflammatory Mediators and Antioxidants by Alveolar Macrophages

Morio, Lisa A.; Hooper, Kimberly A.; Brittingham, Jennie A.; Li, Tsung Hung; Gordon, Ronald E.; Turpin, Barbara J.; Laskin, Debra L.

doi:10.1006/taap.2001.9316

Cited by 48 publications

(38 citation statements)

References 44 publications

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“…The strongest associations were found for respiratory outcomes with CO, however, such low concentrations of CO could not directly cause the health effect. CO could be a surrogate measure for combustion particles (Burnett et al, 1999;Fusco et al, 2001) that induce a worsening of asthma by inciting an inflammatory response in the airways with progressive decrements in lung function and unresponsiveness to medications (Quay et al, 1998;Baeza-Squiban et al, 1999;Morio et al, 2001;Li et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Association between particulate matter and emergency room visits, hospital admissions and mortality in Spokane, Washington

Slaughter

Kim

Sheppard

et al. 2004

J Expo Sci Environ Epidemiol

112

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There is conflicting evidence regarding the association between different size fractions of particulate matter (PM) and cardiac and respiratory morbidity and mortality. We investigated the short-term associations of four size fractions of particulate matter (PM 1 , PM 2.5 , PM 10 , and PM 10-2.5 ) and carbon monoxide with hospital admissions and emergency room (ER) visits for respiratory and cardiac conditions and mortality in Spokane, Washington. We used a log-linear generalized linear model to compare daily averages of PM and carbon monoxide with daily counts of the morbidity and mortality outcomes from January 1995 to June 2001. We examined pollution lags ranging from 0 to 3 days and compared our results to a similar log-linear generalized additive model. Effect estimates tended to be smaller and have larger standard errors for the generalized linear model. Overall, we saw no association with respiratory ER visits and any size fraction of PM. However, there was a suggestion of greater respiratory effect from fine PM when compared to coarse fraction. Carbon monoxide was associated with both all respiratory ER visits and visits for asthma at the 3-day lag. We feel that carbon monoxide may be serving as a marker for combustion-derived pollutants, which is one large component of the diverse air pollutant mixture. We also found no association with any size fraction of PM or CO with cardiac hospital admissions or mortality at the 0-to 3-day lag. We found no consistent associations between any size fraction of PM and cardiac or respiratory ER visits or hospital admissions.

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Section: Discussionmentioning

confidence: 99%

Association between particulate matter and emergency room visits, hospital admissions and mortality in Spokane, Washington

Slaughter

Kim

Sheppard

et al. 2004

J Expo Sci Environ Epidemiol

112

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“…Primary cultures of rat endothelial cells and alveolar macrophages were prepared as described previously (16,43). RAW 264.7 mouse macrophages were from Dr. D. Wolff, UMDNJ-Robert Wood Johnson Medical School (Piscataway, NJ).…”

Section: Methodsmentioning

confidence: 99%

Induction of cyclooxygenase-2 by heat shock protein 60 in macrophages and endothelial cells

Billack

Heck

Mariano³

et al. 2002

American Journal of Physiology-Cell Physiology

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The 60-kDa heat shock protein (HSP60), an endogenous ligand for the toll-like 4 receptor, is generated in response to inflammation, tissue injury, and/or stress and stimulates macrophages to produce cytotoxic and proinflammatory mediators including nitric oxide, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-12. In the present studies we report that HSP60 is an effective inducer of cyclooxygenase-2 (COX-2) in macrophages, as well as endothelial cells. In both cell types, the synthesis of COX-2 was coordinate with induction of nitric oxide synthase (NOS)-2 and with nitric oxide production. With the use of promoter constructs in transient transfection assays, optimal expression of COX-2 in macrophages was found to require nuclear factor (NF)-κB, the cAMP-response element (CRE), and NF-IL-6, but not the E-box. Mobility shift assays revealed that HSP60 induced NF-κB and CRE binding activity, while CCAAT/enhancer binding protein (C/EBP), which binds to NF-IL-6, was constitutively active in the cells. Both c-Jun and CRE binding protein (CREB) bound to the CRE, while C/EBP-β bound to NF-IL-6. These data indicate that NF-κB, C/EBP-β, c-Jun, and CREB are important in HSP60-induced expression of COX-2. The c-Jun-NH2-terminal kinase (JNK), p44/42 mitogen-activated protein (MAP) kinase [extracellular signal-regulated kinase 1/2 (ERK1/2)], and p38 MAP kinase were rapidly activated by HSP60 in the macrophages. PD-98059, an inhibitor of phosphorylation of ERK1/2, caused a marked inhibition of HSP60-induced COX-2 and NOS-2 expression. Unexpectedly, SB-203580, a p38 kinase antagonist, was found to block HSP60-induced expression of COX-2, but not NOS-2. These data indicate that both ERK1/2 kinase and p38 kinase play a role in regulating HSP60-induced expression of COX-2.

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“…The available data on the toxicity of these compounds is limited and has not evolved significantly since 2005. Inhalation challenges (2 hours) of Sprague-Dawley rats with high concentrations of hydrogen peroxide vapour (10, 20 and 100 ppb) in the presence or absence of ammonium sulfate fine PM were found to elicit only minimal evidence of airway inflammation immediately and 24 hours after exposure (Morio et al, 2001). Similarly, experimental studies in mice and rats using high concentrations of peroxyacetyl nitrate have demonstrated pulmonary injury and increased susceptibility to infection, but only at concentrations well outside the ambient range (reviewed in Vyskocil, Viau & Lamy, 1998).…”

Section: Rationalementioning

confidence: 97%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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Tissue Injury Following Inhalation of Fine Particulate Matter and Hydrogen Peroxide Is Associated with Altered Production of Inflammatory Mediators and Antioxidants by Alveolar Macrophages

Cited by 48 publications

References 44 publications

Association between particulate matter and emergency room visits, hospital admissions and mortality in Spokane, Washington

Association between particulate matter and emergency room visits, hospital admissions and mortality in Spokane, Washington

Induction of cyclooxygenase-2 by heat shock protein 60 in macrophages and endothelial cells

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

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