奈米微粒與健康風險研究─子計畫五：疾病動物模式奈米微粒毒性探討(II)(1/2)
Date Issued
2004-07-31
Date
2004-07-31
Author(s)
DOI
922621Z002014
Abstract
Epidemiologic studies have shown consistent
associations between the exposure to
particulate air pollution and acute increase in
morbidity and mortality, especially for
susceptible subjects with pre-existing
respiratory and cardiovascular disease.
Furthermore, it has been reported that
long-term exposure to combustion-related
fine particles may be associated with lung
cancer mortality. However, the exact
mechanism remains unclear. It is believed
that ultrafine particles may have a greater
inflammatory effect than larger particles at
the same mass concentration because of
larger surface area and oxidative stress. In
addition, ultrafine particles deposited in
alveolar region may translocate into other
organs. Thus, ambient ultrafine particles play
critical role in health risk assessment.
However, the role of ultrafine particles on
cardiopulmonary events is not clear.
The goal of this study was: (1) to investigate
the effect of epithelium lining fluids (ELF)
on ultrafine particle-induced ROS generation.
Ultrafine carbon black induced-ROS
generation and DNA single strand breaks were evaluated. (2) to evaluate the effect of
ultrafine carbon black on lung inflammation,
systemic inflammation and endothelial
dysfunction in STZ-diabetic rats. Our results
revealed that in cell free system, the amounts
of ROS increased with exposure
concentration and exposure time. ELF
significantly decreased ROS 90% as
compared to culture medium after ufCB
exposure. Furthermore, ELF also decreased
DNA single-strand breakage after ufCB
exposure. In diseased animal study, we found
ufCB caused significant increase in
pulmonary inflammation. We also observed
significant alteration in systemic
inflammation and endothelial dysfunction in
diabetic rats exposed to ufCB. We suggest
that ufCB and diabetes may share the
common pathway which may be related to
cardiovascular events.
Subjects
ultrafine particles
diabetic rats
epithelium lining fluid
reactive oxygen
species
species
cardiopulmonary disease
SDGs
Publisher
臺北市：國立臺灣大學公共衛生學院職業醫學與工業衛生研究所
Type
report
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