Asthma attack associated with oxidative stress by exposure to ETS and PAH.
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).


METHODS
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).


CONCLUSIONS
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.
Leem
Jong Han
JH
Department of Occupational and Environmental Medicine, Inha University Hospital, Incheon, Korea. ekeeper@inha.ac.kr
Kim
Jeong Hee
JH
Lee
Kwan Hee
KH
Hong
Yun chul
Yc
Lee
Kyoung Ho
KH
Kang
Daehee
D
Kwon
Ho Jang
HJ
D000293:Adolescent; D001249:Asthma / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D007223:Infant; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress; D011014:Pneumonia / Q000209:etiology; D011084:Polycyclic Aromatic Hydrocarbons / Q000009:adverse effects*; D011446:Prospective Studies; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators; D011084:Polycyclic Aromatic Hydrocarbons; D014028:Tobacco Smoke Pollution; D008315:Malondialdehyde