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Event
Thu 9/19/2019 11:00AM - 12:00PM
EOH Journal Club
Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen EOH Journal Club
Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen
Thu 9/19/2019 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Brandy Hill

Paper: Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen. A Randomized, Double-Blind Crossover Study

Authors: Denise J. Wooding, Min Hyung Ryu, Anke Huls, Andrew D. Lee, David T. S. Lin, Christopher F. Rider, Agnes C. Y. Yuen, and Chris Carlsten

Abstract:
Rationale: Diesel exhaust (DE), an established model of trafficrelated
air pollution, contributes significantly to the global burden of
asthma and may augment the effects of allergen inhalation. Newer
diesel particulate-filtering technologies may increaseNO2 emissions,
raising questions regarding their effectiveness in reducing harm from
associated engine output.

Objectives: To assess the effects of DE and allergen coexposure on
lung function, airway responsiveness, and circulating leukocytes, and
determine whether DE particle depletion remediates these effects.

Methods: In this randomized, double-blind crossover study, 14
allergen-sensitized participants (9 with airway hyperresponsiveness)
underwent inhaled allergen challenge after 2-hour exposures to DE,
particle-depleted DE (PDDE), or filtered air. The control condition
was inhaled saline after filtered air. Blood sampling and spirometry
were performed before and up to 48 hours after exposures. Airway
responsiveness was evaluated at 24 hours.

Measurements and Main Results: PDDE plus allergen
coexposure impaired lung function more than DE plus allergen,
particularly in those genetically at risk. DE plus allergen and PDDE
plus allergen each increased airway responsiveness in normally
responsive participants.DEplus allergen increased blood neutrophils
and was associated with persistent eosinophilia at 48 hours. DE and
PDDE each increased total peripheral leukocyte counts in a manner
affected by participant genotypes. Changes in peripheral leukocytes
correlated with lung function decline.

Conclusions: Coexposure to DE and allergen impaired lung
function, which was worse after particle depletion (which increased
NO2). Thus, particulates are not necessarily the sole or main
culprit responsible for all harmful effects of DE. Policies and
technologies aimed at protecting public health should be scrutinized
in that regard.
Clinical trial registered with www.clinicaltrials.gov (NCT02017431).

Keywords: diesel exhaust; asthma; filter; genetic susceptibility


4140 Public Health, Young Seminar Room

Recent Events

EOH Journal Club

Rahel Birru presents on: EGCG regulates the cross-talk between JWA and topoisomeras

Thursday 3/31 11:00AM - 12:00PM

EOH Journal Club Seminar - Spring 2016

Presenter: Rahel Birru 

Paper: EGCG regulates the cross-talk between JWA and topoisomerase IIα in non-small-cell lung cancer (NSCLC) cells 

Authors: Li Y, Shen X, Wang X, Li A, Wang P, Jiang P, Zhou J, Feng Q 

Abstract: (-)-epigallocatechin-3-gallate (EGCG) is a well-known cancer chemopreventive agent. The potential mechanisms include regulation of multiple molecules. Carcinogenesis in lung cancer is related to the imbalance of tumor suppressor and oncogene. JWA is a structurally novel microtubule-binding protein and is a potential tumor suppressor. DNA topoisomerase IIα is a nuclear enzyme that governs DNA topology and is usually highly expressed in many types of cancer. It serves as a target of anticancer drugs. In the current study, the regulation of JWA and topoisomerase IIα by EGCG, and thereafter the mutual interaction between them was investigated. The results revealed that EGCG up-regulated JWA while decreased topoisomerase IIα expression in both human non-small cell lung cancer (NSCLC) cells and an NSCLC xenograft mice model. There was a negative correlation between JWA and topoisomerase IIα in NSCLC as well as in human NSCLC tissue specimens. Topoisomerase IIα overexpression reduced JWA at the translational level. Meanwhile, JWA-induced topoisomerase IIα degradation was regulated both in the transcriptional and post-translational level. Interestingly, JWA and topoisomerase IIα regulated each other in the cells arrested in G2/M. Furthermore, JWA and topoisomerase IIα synergistically affected NCI-H460 cells invasion. These results may serve a novel mechanism for cancer prevention


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Last Updated On Monday, March 21, 2016 by Borkowski, Matthew Gerard
Created On Monday, March 21, 2016

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