Suresh Ram, Shally Awasthi, Mahdi A A, Patel D K, Singh V K, Rita Misra
Department of Pediatrics, Chhatrapati Shahuji Maharaj Medical University, Lucknow - 226 003, UP, India.
Indian J Occup Environ Med. 2009 Apr;13(1):33-7. doi: 10.4103/0019-5278.50722.
Polycyclic aromatic hydrocarbons (PAH) originate from the incomplete combustion of organic matter and ambient air pollution by these is increasing. There is also an increase in the global prevalence of asthma, for which environmental pollution has been recognized as one of the important factors. Exposure to pollutants and other allergens induces chronic airway inflammation by generation of reactive oxygen species, causing oxidative stress. Therefore, the objective of the present study was to assess association, if any, between exposure to PAH and asthma as well as oxidative stress in children.
In this hospital-based case control study, cases of bronchial asthma aged 1-14 years and healthy matched controls were included. Oxidative stress was measured by assessing the levels of enzymes catalase, superoxide dismutase, malondialdehyde (MDA), and reduced glutathione (GSH).
Forty-two cases and 20 controls were enrolled. Mean blood level of phenanthrene, a PAH, was 63.11 ppb +/- 115.62 and 4.20 ppb +/- 10.68 ppb in cases and controls, respectively (P = 0.02). Mean blood levels of GSH was significantly lower in cases and controls (27.39 mug/ml +/- 11.09 versus 47.39 g/ml +/- 13.83; P-value = 0.001). Likewise, mean blood level of MDA in nanomole/ml was significantly higher in asthma as compared with controls (12.85 +/- 5.40 versus 8.19 +/- 5.16; P-value = 0.002), suggestive of increased oxidative stress.
Because elevated blood level of phenanthrene is associated with bronchial asthma as well as with oxidative stress, measures to reduce exposure to PAH may possibly lead to reduced incidence and severity of bronchial asthma.
多环芳烃(PAH)源于有机物的不完全燃烧,且此类物质造成的环境污染正在加剧。全球哮喘患病率也在上升,环境污染已被视为其重要因素之一。接触污染物和其他过敏原会通过产生活性氧引发慢性气道炎症,导致氧化应激。因此,本研究的目的是评估儿童接触多环芳烃与哮喘以及氧化应激之间是否存在关联。
在这项基于医院的病例对照研究中,纳入了1至14岁的支气管哮喘患儿及健康匹配对照。通过评估过氧化氢酶、超氧化物歧化酶、丙二醛(MDA)和还原型谷胱甘肽(GSH)的水平来测量氧化应激。
共纳入42例病例和20例对照。病例组和对照组中多环芳烃菲的平均血药浓度分别为63.11 ppb±115.62和4.20 ppb±10.68 ppb(P = 0.02)。病例组和对照组中GSH的平均血药浓度显著降低(27.39 μg/ml±11.09对47.39 μg/ml±13.83;P值 = 0.001)。同样,哮喘组中以纳摩尔/毫升计的MDA平均血药浓度显著高于对照组(12.85±5.40对8.19±5.16;P值 = 0.002),提示氧化应激增加。
由于菲的血药浓度升高与支气管哮喘以及氧化应激相关,减少多环芳烃暴露的措施可能会降低支气管哮喘的发病率和严重程度。