Asthma Attack Associated with Oxidative Stress by Exposure to ETS and PAH

Leem, Jong Han; Kim, Jeong Hee; Lee, Kwan Hee; Hong, Yun Chul; Lee, Kyung Ho; Kang, Daehee; Kwon, Ho Jang

doi:10.1080/02770900500200733

Cited by 31 publications

(21 citation statements)

References 36 publications

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“…Miller and colleagues report that early exposure to airborne PAH and environmental tobacco smoke can lead to increased respiratory symptoms and probable asthma even as early as at the age of 12 to 24 months [35]. Passive smoker children therefore may develop an allergic or inflammatory pulmonary response and increased DNA damage due to direct contact with PAH and ETS [36][37]. However, the question whether these elevated serum PAH levels can trigger an acute asthmatic attack is difficult to answer in the present study.…”

Section: Discussioncontrasting

confidence: 50%

Serum Polycyclic Aromatic Hydrocarbons Among Children with and without Asthma: Correlation to Environmental and Dietary Factors

Al-Daghri

2008

International Journal of Occupational Medicine and Environmental Health

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Background: Children from low-income families may be subject to high exposures to polycyclic aromatic hydrocarbons (PAH) which can lead to respiratory disorders. This study aims to establish methods for assessing total PAH exposure of asthmatic and non-asthmatic children from low-income families; to estimate serum PAH concentrations of these children, and to estimate the relative importance of the environmental pathways for PAH exposure. Materials and Methods: A total of 75 (61 asthmatic, 14 non-asthmatic) Saudi children 15 years old and below were included to participate in this crosssectional study. Each participant answered a generalized questionnaire with dietary questions. Serum PAH were measured using HPLC with UV detection. Results: Serum naphthalene and pyrene were significantly elevated among asthmatic children (p-values = 0.007 and 0.01, respectively). Serum acenaphthylene, fluorine and 1,2-benzanthracene, on the other hand, were significantly higher among non-asthmatics (p-values = 0.001, 0.04 and 0.03, respectively). There was a significant correlation between the presence of a smoker in the family and serum concentrations of carbazole, pyrene, 1,2-benzanthracene and benzacephenanthrylene (R = 0.37, 0.45, 0.43, 0.33; p-values = 0.01, 0.0002, 0.003 and 0.025, respectively). Significant correlations were elicited between daily meat intake and serum levels of acenaphthylene, benzopyrene and 1,2-benzanthracene (R = 0.27, 0.27, 0.33; p-values = 0.02 and < 0.001, respectively). Conclusion: Among the children, serum PAH were significantly correlated to meat intake as well as presence of smokers at home. Public health awareness should be enhanced by educating parents to take certain precautions at home, such as preventing indoor smoking and reducing the intake of grilled and smoked meat by children so as to decrease their exposure to carcinogenic PAH.

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Section: Discussioncontrasting

confidence: 50%

Serum Polycyclic Aromatic Hydrocarbons Among Children with and without Asthma: Correlation to Environmental and Dietary Factors

Al-Daghri

2008

International Journal of Occupational Medicine and Environmental Health

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“…This result is consistent with Leem's paper which reported that oxidative stress, specifically lipid peroxidation, contributes to the pathophysiology of asthma 13 . DNA damage measured by Comet assay did not show significant correlation with PAH exposure markers including 1-OHP and 2-naphthol ( Table 2).…”

Section: Resultssupporting

confidence: 94%

“…In a longitudinal cohort of children in New York City, the prevalence of asthma is among the highest in the US, and this high risk may in part be caused by transplacental exposure to traffic-related polycyclic aromatic hydrocarbons 12 . The pathophysiology of asthma is also associated with oxidative stress which may be related with ambient oxidants such as PAH 13 . Studies have identified host susceptibility characteristics that may modify responses to air pollution exposure, including polymorphisms in oxidative stress and epigenetic alterations 14 .…”

Section: Introductionmentioning

confidence: 99%

DNA repair capacity marks susceptibility in pediatric asthma patients following low levels of polycyclic aromatic hydrocarbon exposure

Kim

Lee

Kim

et al. 2011

Toxicol. Environ. Health Sci.

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We studied DNA damage, DNA repair capacity and other oxidative stress markers with environmental polycyclic aromatic hydrocarbon (PAH) exposure to find susceptible groups to show significant correlation between PAH exposure and studied markers. The total of study subjects were fifty five children from 6 to 9 years old including thirty six control group and nineteen asthma patients. No significant correlation between DNA damage and exposure markers was found among control group and asthma patients based on total antioxidants activity and glutathione/oxidized glutathione (GSH/GSSG) ratio. However, significant correlation was found between Tail DNA and 2-naphthol in high residual DNA damage group (20 upper percentile group) (r=0.63, p=0.038) who showed low DNA repair capacity. These studies revealed that low DNA repair capacity in children may render this population susceptible to environmental exposure including DNA damage-causing agents.

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“…However, despite the higher PM 2.5 level in children, there is little difference in the oxidative stress concentrations between the elderly and the preschoolers. Urinary MDA concentrations in the elderly (4.0 lmol/g cr) and in children (3.6 lmol/g cr) in this study were comparable with the levels of MDA in asthmatic children under stable conditions (3.0 lmol/g cr) and during asthma attacks (4.4 lmol/ g cr) [26]. Mechanisms by which the particulate matter induces oxidative stress have been investigated in cell and animal experiments.…”

Section: Discussionsupporting

confidence: 57%

Differential oxidative stress response in young children and the elderly following exposure to PM2.5

Kim

Park

Lee

et al. 2008

Environ Health Prev Med

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AbstractsObjectives The mechanism of the adverse health effects of ambient particulate matter on humans has not been wellinvestigated despite many epidemiologic association studies. Measurement of personal exposure to particulate pollutants and relevant biological effect markers are necessary in order to investigate the mechanism of adverse health effects, particularly in fragile populations considered to be more susceptible to the effects of pollutants. Methods We measured personal exposure to PM 2.5 and examined oxidative stress using urinary malondialdehyde three times in 51 preschoolers and 38 elderly subjects.A linear mixed-effects model was used to estimate PM 2.5 effects on urinary MDA levels. Results Average personal exposure of the children and elderly to PM 2.5 was 80.5 ± 29.9 and 20.7 ± 12.7 lg/m 3 , respectively. Mean urinary MDA level in the children and the elderly was 3.6 ± 1.9 and 4.0 ± 1.6 lmol/g creatinine. For elderly subjects the PM 2.5 level was significantly associated with urinary MDA after adjusting for age, sex, BMI, passive smoking, day-care facility site, alcohol consumption, cigarette smoking, and medical history (heart disease, hypertension and bronchial asthma). However, there was no significant relationship for children. Conclusions The elderly were more susceptible than young children to oxidative stress as a result of ambient exposure to PM 2.5 . Identification of oxidative stress induced by PM 2.5 explains the mechanism of adverse health effects such as cardiovascular or respiratory diseases, particularly in the elderly.

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Asthma Attack Associated with Oxidative Stress by Exposure to ETS and PAH

Cited by 31 publications

References 36 publications

Serum Polycyclic Aromatic Hydrocarbons Among Children with and without Asthma: Correlation to Environmental and Dietary Factors

Serum Polycyclic Aromatic Hydrocarbons Among Children with and without Asthma: Correlation to Environmental and Dietary Factors

DNA repair capacity marks susceptibility in pediatric asthma patients following low levels of polycyclic aromatic hydrocarbon exposure

Differential oxidative stress response in young children and the elderly following exposure to PM2.5

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