Assessment of association of exposure to polycyclic aromatic hydrocarbons with bronchial asthma and oxidative stress in children: A case control study

Abstract

Background: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.Method: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).Results: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 μg/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.Conclusions: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.

Structurally distinct polycyclic aromatic hydrocarbons induce differential transcriptional responses in developing zebrafish

“…Chronic PAH exposure in coke-oven workers has also been associated with altered immunological parameters, including increased TNFα in serum, as well increased markers of lipid peroxidation and oxidative stress (Jeng et al , 2011). Increased malondialdehyde and decreased reduced glutathione were similarly observed in bronchial asthma patients, and correlated with blood phenanthrene levels, providing further evidence of PAH-induced oxidative stress in human populations (Suresh et al , 2009). …”

“…Oxidative stress was a component of the toxic response, as has also been reported previously, and we observed differential regulation of immune-related genes, particularly by DBT and PYR. Though fewer studies have examined PAHs that are not strong AHR agonists, PAHs that do not induce CYP1A have similarly been observed to induce inflammatory cytokines in cells in culture (Suresh et al , 2009; Ovrevik et al , 2010). PAHs are known immunotoxicants in fish, with well-established effects on lymphocytes (Krieger et al , 1994; Reynaud and Deschaux, 2006).…”

Chimney sweeps in Sweden: a questionnaire-based assessment of long-term changes in work conditions, and current eye and airway symptoms

“…The POR estimated the risk of a specific symptom with a 10% increase of the work task. We focused primarily on black-soot-sweeping in private homes and industrial settings, since black soot particles have been associated with airway diseases (Barraza-Villarreal et al 2014; Nwokoro et al 2012; Suresh et al 2009). Potential confounders (age, smoking, and use of mask) were included in the analysis due to their potential role in developing or preventing symptoms of interest (Supplementary Table 6).…”

Urban PM2.5 exacerbates allergic inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway

“…Furthermore, asthma morbidity has been positively associated with daily ambient PM2.5 concentrations, in both warm and cool seasons 12 . The composition of PM2.5 may contribute to a higher prevalence and incidence of asthma 13 , 14 .…”