Co-exposure to polycyclic aromatic hydrocarbons, benzene and toluene may impair lung function by increasing oxidative damage and airway inflammation in asthmatic children.

As previous studies found that the direct associations between urinary polycyclic aromatic hydrocarbon (PAH), benzene and toluene (BT) metabolites and the decreased lung function were not conclusive, we further investigated relationship of oxidative damage and airway inflammation induced by PAHs and BTs exposure with lung function. A total of 262 children diagnosed with asthma and 72 heathy children were recruited. Results showed that asthmatic children had higher levels of PAHs and BTs exposure, as well as Malonaldehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) compared with healthy children. Furthermore, binary logistic regression showed that each unit increases in level of urinary 2-&3-hydroxyfluorene (2-&3-OHF), 2-hydroxyphenanthrene (2-OHPhe), 1-hydroxyphenanthrene (1-OHP) and S-phenylmercapturic acid (S-PMA) were significantly associated with an elevated risk of asthma in children with odds ratios of 1.5, 2.3, 1.7 and 1.4, respectively, suggesting that PAHs and BTs exposure could increase the risk of asthma for children. Neither PAH nor BT metabolite could comprehensively indicate the decreased lung function as only 2-&3-OHF and 1-OHP were significantly and negatively correlated with forced vital capacity (FVC). Moreover, levels of most individual PAH and BT metabolite were significantly correlated to MDA and 8-OHdG. Further hierarchical regression analysis indicated that MDA and 8-OHdG levels did not show significant effects on the decreased lung function, suggesting that they are not the suitable biomarkers to indirectly indicate the altered lung function induced by PAHs and BTs. Urinary 2-OHPhe and 1-&9-hydroxyphenanthrene (1-&9-OHPhe) were significantly correlated with fractional exhaled nitric oxide (FeNO). Moreover, FeNO significantly contributed to decreased lung function and explained 7.7% of variance in ratio of forced expiratory volume in 1 s (FEV1) and FVC (FEV1/FVC%). Hence, FeNO, rather than oxidative damage indicators or any urinary PAH and BT metabolite, is more sensitive to indirectly reflect the decreased lung function induced by PAHs and BTs exposure for asthmatic children.

Kuang H ，Liu J ，Zeng Y ，Zhou W ，Wu P ，Tan J ，Li Y ，Pang Q ，Jiang W ，Fan R ... -  《-》

Co-exposure to polycyclic aromatic hydrocarbons, benzene and toluene and their dose-effects on oxidative stress damage in kindergarten-aged children in Guangzhou, China.

Polycyclic aromatic hydrocarbons (PAHs), benzene and toluene (BT) are ubiquitous toxic pollutants in the environment. Children are sensitive and susceptible to exposure to these contaminants. To investigate the potential oxidative DNA damage from the co-exposure of PAHs and BT in children, 87 children (aged 3-6) from a kindergarten in Guangzhou, China, were recruited. Ten urinary PAHs and four BT metabolites, as well as 8-hydroxy-2'-deoxyguanosine (8-OHdG, a biomarker of oxidative DNA damage)in urine, were determined using a liquid chromatography tandem mass spectrometer. The results demonstrated that the levels of PAHs and BT in children from Guangzhou were 2-30 times higher than those in children from the other countries based on a comparison with recent data from the literature. In particular, the difference is more substantial for pyrene and volatile BT. Co-exposure to PAHs and BT could lead to additive oxidative DNA damage. Significant dose-effects were observed between the sum concentration of urinary monohydroxylated metabolites of PAHs (∑OH-PAHs), the sum concentration of the metabolites of BT (∑BT) and 8-OHdG levels. Every one percent increase in urinary PAHs and BT generated 0.33% and 0.02% increases in urinary 8-OHdG, respectively. We also determined that the urinary levels of PAHs and BT were negatively associated with the age of the children. Moreover, significant differences in the levels of ∑OH-PAHs and ∑BT were determined between 3- and 6-year-old children (p<0.05), which may be caused by different metabolism capabilities or inhalation frequencies. In conclusion, exposure to PAHs or BT could lead to oxidative DNA damage, and 8-OHdG is a good biomarker for indicating the presence of DNA damage. There exists a significant dose-effect relationship between PAH exposure, BT exposure and the concentration of 8-OHdG in urine. Toddlers (3-4 years old) face a higher burden of PAH and BT exposure compared with older children.

Li J ，Lu S ，Liu G ，Zhou Y ，Lv Y ，She J ，Fan R ... -  《-》

Association of PAHs and BTEX exposure with lung function and respiratory symptoms among a nonoccupational population near the coal chemical industry in Northern China.

Emissions (particularly aromatic compounds) from coal industries and biomass fuels combustion lead to high health risks for neighboring residents. To investigate the association of polycyclic aromatic hydrocarbons (PAHs) and benzene, toluene, ethylbenzene and 1,2-dimethylbenzene (BTEX) exposure with lung function and respiratory symptoms among adults and children near the coal-chemical industry in Northern China, adults and children from a county dotted with coal chemical industry were chosen as subjects for investigation (investigated area, IR). The control group consisted of adults and children from an agricultural county (control area, CR). The environmental and urinary PAH and BTEX levels of adults and children were determined by isotope dilution liquid chromatography coupled with tandem mass spectrometry. The Mann-Whitney U test and multivariate linear regression models were used to analyze the relationship between pollutant exposure and the respiratory system. The results showed that in an ambient environment, levels of PAHs and BTEX in the IR were significantly higher than those in the CR. Particularly, the concentration profiles for air samples were IR > CR and indoor > outdoor. Both for adults and children, the geometric (GM) concentrations of urinary PAHs and BTEX from the IR were significantly higher than those measured in the CR. Additionally, the urinary PAH exposure level profiles of smokers were higher than those of nonsmokers, indicating that indoor air and smoking were both important nonoccupational exposure sources. The decline of the forced expiratory in the first second (FEV1, %) and the forced expiratory middle flow rate (FEF25%) in children were associated with increasing urinary PAH metabolite levels (p < 0.05). The increase in urinary 1-OHN, 3-OHPhe, 4-OHPhe and 1-OHP levels could be linked to a decrease in FEV1 (r = -0.179, p < 0.05) and FEF25% with the coefficient of -0.166, -0.201 and -0.175 (p < 0.05), respectively. Medical examinations and lung function tests indicated that residents in the IR had higher occurrences of chest inflammation or declining lung function than residents in the CR. Moreover, exposure to PAHs and BTEX could decrease child lung function, though decreased lung function was not observed in adults. Both urinary monitoring and lung function data showed that children were more sensitive to PAH and BTEX exposure than adults.

Chen L ，Hu G ，Fan R ，Lv Y ，Dai Y ，Xu Z ... -  《-》

Preliminary study of children's exposure to PAHs and its association with 8-hydroxy-2'-deoxyguanosine in Guangzhou, China.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants generated mainly from incomplete combustion such as automobile exhaust and cigarette smoke. Oxidative stress is believed to be involved in carcinogenesis, and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was used as the biomarker to assess such DNA damage. The children's urinary PAH metabolite (OH-PAHs) level were explored in Guangzhou and their associations with 8-OHdG. Two groups of subjects were selected: (1) one group (n=39, 6-7 years old) from an elementary school situated near a heavy traffic road (polluted area) and (2) another group (n=35, 4-6 years old) from a kindergarten situated in a corner of the main campus of a big university (non-polluted area). Urinary 8-OHdG and nine urinary monohydroxylated PAH metabolites were measured, including 2-hydroxynaphthalene (2-OHN), 2-hydroxyfluorene (2-OHF), 2-, 3-, 4-, 9-hydroxyphenanthrene (2-, 3-, 4-, 9-OHPhe), 1-hydroxypyrene (1-OHP), 6-hydroxychrysene (6-OHChr) and 3-hydroxybenzo(a)pyrene (3-OHBaP). All other PAH metabolites were detected in urine samples from both children groups except for 6-OHChr and 3-OHBaP. Levels of 2-OHN, 2-OHF, 3-OHPhe, 9-OHPhe and 1-OHP were significantly different between two groups (P<0.05, T-test). The elementary school children from the polluted area had higher urinary levels of 2-OHN, 2-OHF, 2-, 3-, 4-OHPhe and 1-OHP ((9.10±7.39, 3.72±2.91, 0.32±0.50, 0.37±0.28, 0.23±0.29 and 0.64±0.07 μmol/mol creatinine, respectively) than those from the control group. The results suggested that heavy traffic pollution led to higher PAH body burden. There existed no significant difference for urinary 8-OHdG concentration between two groups (p>0.05, T-test), and no strong correlations between the individual OH-PAHs and 8-OHdG. However, the urinary 8-OHdG concentration in the elementary school children from the traffic polluted area was slightly higher than those in the non-polluted area (20.87±14.42 μmol/mol creatinine vs. 16.78±13.30 μmol/mol creatinine). It may be that the potential co-exposure of the children to other pollutants affects 8-OHdG concentration besides the PAHs.

Fan R ，Wang D ，Mao C ，Ou S ，Lian Z ，Huang S ，Lin Q ，Ding R ，She J ... -  《-》

Oxidative damage mediates the association between polycyclic aromatic hydrocarbon exposure and lung function.

Cao L ，Zhou Y ，Tan A ，Shi T ，Zhu C ，Xiao L ，Zhang Z ，Yang S ，Mu G ，Wang X ，Wang D ，Ma J ，Chen W ... -  《Environmental Health》