Asthma Attack Associated with Oxidative Stress by Exposure to ETS and
PAH.
Leem JH, Kim JH, Lee KH, Hong YC, Lee KH, Kang D, Kwon HJ
J Asthma. 2005; 42(6): 463-467

Asthma is primarily an airways inflammatory disease, and the bronchial
airways have been shown to be particularly susceptible to
oxidant-induced tissue damage. Objective. The purpose of this study was
to investigate whether pulmonary inflammation in asthma is associated
with exposure to environmental oxidants such as polycyclic aromatic
hydrocarbon (PAH) and environmental tobacco smoke (ETS). Method. We
assessed the exposure level of PAH and ETS by using urinary
1-hydroxypyrene glucuronide (1-OHPG) and cotinine. We estimated
oxidative damage and inflammatory cytokine levels from 16 asthma
patients and 16 patients in stable conditions 1 to 2 months later.
Results. Our study showed that the levels of oxidative damage, as
measured by malondialdehyde (MDA), were significantly increased (p =
0.006) during the asthma attacks. Proinflammatory and anti-inflammatory
cytokines were both increased during the asthma attacks compared to the
stable conditions at follow-up. Interleukin (IL-6) and IL-10 were
especially increased significantly (p = 0.015 and p < 0.001,
respectively). Correlations were observed between inflammatory
cytokines such as IL-6 and IL-1beta (p = 0.034). Conclusion. This study
supports the results of in vitro studies that oxidative stress,
specifically lipid peroxidation, contributes to the pathophysiology of
asthma. Therefore, environmental interventions based on this better
understanding are needed to significantly reduce oxidant stress and
prevent or minimize the development of asthmatic symptoms.

Who loves ya.
Tom


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