EOH Events

EOH Departmental Calendar

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

Exposure to Secondhand Smoke and Arrhythmogenic Cardiac Alternans in a Mouse Model

Thursday 2/21 11:00AM - 12:00PM
4140 Public Health, Young Seminar Room

Presenter: Emma Yi Lu

Paper: Exposure to Secondhand Smoke and Arrhythmogenic Cardiac Alternans in a Mouse Model

Authors:  Zhen Wang, Lianguo Wang, Srinivas Tapa, Kent E. Pinkerton, Chao-Yin Chen, and Crystal M. Ripplinger

Abstract:

BACKGROUND: Epidemiological evidence suggests that a majority of deaths attributed to secondhand smoke (SHS) exposure are cardiovascular related. However, to our knowledge, the impact of SHS on cardiac electrophysiology, Ca2þ handling, and arrhythmia risk has not been studied.

OBJECTIVES: The purpose of this study was to investigate the impact of an environmentally relevant concentration of SHS on cardiac electrophysiology and indicators of arrhythmia.

METHODS: Male C57BL/6 mice were exposed to SHS . Hearts were excised and Langendorff perfused for dual optical mapping with voltage- and Ca2þ-sensitive dyes.

RESULTS:At slow pacing rates, SHS exposure did not alter baseline electrophysiological parameters. With increasing pacing frequency, action potential duration (APD), and intracellular Ca2þ alternans magnitude progressively increased in all groups. At 4 and 8 wk, there were no statistical differences in APD or Ca2þ alternans magnitude between SHS and FA groups. At 12 wk, both APD and Ca2þ alternans magnitude were significantly increased in the SHS compared to FA group (p<0 :05). SHS exposure did not impact the time constant of Ca2þ transient decay (s) at any exposure time point. At 12 wk exposure, the recovery of Ca2þ transient amplitude with premature stimuli was slightly (but nonsignificantly) delayed in SHS compared to FA hearts, suggesting that Ca2þ release via ryanodine receptors may be impaired.

CONCLUSIONS: In male mice, chronic exposure to SHS at levels relevant to social situations in humans increased their susceptibility to cardiac alternans, a known precursor to ventricular arrhythmia


Click Here For Article

Last Updated On Friday, January 11, 2019 by Orbell, Adam W
Created On Friday, January 11, 2019

AugSeptember 2019Oct
SunMonTueWedThuFriSat
1234567
891011121314
15161718192021
22232425262728
293012345
6789101112

Submit events and news

Enter upcoming calendar events or share your school news and announcements at publichealth.pitt.edu/submit.