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Polycyclic aromatic hydrocarbons exposure, oxidative stress, and asthma in children
I-Jen Wang1,2,3, Wilfried J J Karmaus4, Chen-Chang Yang5,6
1Department of Pediatrics, Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan, Republic of China. wij636@gmail.com.
Insights
Polycyclic aromatic hydrocarbons (PAHs) exposure in children is linked to increased oxidative stress and higher risks of asthma. Oxidative stress appears to mediate the relationship between PAH exposure and asthma development.
Area of Science:
- Environmental Health
- Toxicology
- Pediatric Health
Background:
- Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants with known carcinogenic and teratogenic effects.
- The impact of PAHs on the immune and respiratory systems, particularly in children, remains under-investigated.
Purpose of the Study:
- To investigate the association between PAH exposure and IgE levels and asthma in children.
- To examine the link between PAH exposure and the oxidative stress marker 8-hydroxy-2'-deoxyguanosine (8OHdG).
- To explore potential sex-based differences in these associations.
Main Methods:
- Recruitment of 453 kindergarten children.
- Measurement of urinary 1-hydroxypyrene (1-OHP) as a biomarker for PAH exposure using UPLC-MS/MS.
- Assessment of serum IgE, urinary 8OHdG via ELISA, and asthma status.
Main Results:
- Positive associations were found between PAH exposure (1-OHP) and both oxidative stress (8OHdG) and IgE levels.
- PAH exposure was significantly associated with an increased odds of asthma (OR 1.42).
- Mediation analysis indicated that 35% of the effect of PAH exposure on asthma is mediated by 8OHdG.
Conclusions:
- PAH exposure may contribute to increased oxidative stress in children.
- PAH exposure is potentially linked to the induction of asthma, with oxidative stress playing a mediating role.
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.
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