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Polycyclic aromatic hydrocarbons exposure,oxidative stress,and asthma in children
Authors:I-Jen?Wang  author-information"  >  author-information__contact u-icon-before"  >  mailto:wij@gmail.com"   title="  wij@gmail.com"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author,Wilfried?J.?J.?Karmaus,Chen-Chang?Yang
Affiliation:1.Department of Pediatrics,Taipei Hospital, Ministry of Health and Welfare,Taipei,Taiwan, Republic of China;2.Institute of Environmental and Occupational Health Sciences, School of Medicine,National Yang-Ming University,Taipei,Taiwan, Republic of China;3.Department of Health Risk Management,China Medical University,Taichung,Taiwan, Republic of China;4.Division of Epidemiology, Biostatistics, and Environmental Health, School of Public Health,University of Memphis,Memphis,USA;5.Division of Clinical Toxicology and Occupational Medicine, Department of Medicine,Taipei Veterans General Hospital,Taipei,Taiwan, Republic of China
Abstract:

Purpose

Polycyclic aromatic hydrocarbons (PAHs) are known for their carcinogenic and teratogenic properties. However, little is known about the effect of PAH on our immune and respiratory systems. Hence, we investigated associations (1) between PAH exposure and IgE levels and asthma in children and (2) between PAH exposure and the oxidative stress marker 8OHdG potentially involved in disease pathogenesis stratifying by (3) sex-based differences.

Methods

A total of 453 kindergarten children were recruited and provided samples. Urine biomarker of PAH exposure (1-OHP levels) was measured by UPLC-MS/MS and a marker of oxidative stress (8OHdG) was measured by ELISA. Serum IgE were assessed and information on asthma was collected. Associations between 1-OHP levels, 8OHdG, IgE and asthma were analyzed by multivariate linear and logistic regression. A mediation analysis was conducted to evaluate whether the risk of increased IgE and asthma related to PAH exposure is explained by 8OHdG changes.

Results

Urine 1-OHP levels were positively related to 8OHdG levels (per ln-unit: β?=?0.30kU/l, p?=?0.002). Similar results were also found for 1-OHP levels with IgE levels (per ln-unit: β?=?0.27 kU/l, p?=?0.027). 1-OHP levels (per ln-unit) were significantly associated with asthma, with an OR (95% CI) of 1.42 (1.18–1.70). In addition, 1-OHP levels were associated with asthma. It is estimated that 35% of the effect of PAH exposure on asthma is mediated by 8OHdG levels.

Conclusion

Exposure to PAH may enhance oxidative stress and may induce asthma. The effect of PAH exposure on asthma may be mediated by oxidative stress.
Keywords:
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