Air pollutant measurement and respiratory inflammatory tests were conducted at a junior secondary school in Xi’an, Northwestern China. Hazardous substances including particulate matters (PMs), black carbon (BC) and particle-bounded polycyclic aromatic hydrocarbons (PAHs) were quantified both indoors and outdoors of the school. Source characterization with organic tracers and particle-size distribution demonstrated that the school’s air was mostly polluted by combustion emissions from the surrounding environment. The evaluation of health assessment related to air quality was conducted by two methods, including potential risk estimation of air pollutants and direct respiratory inflammatory test. The incremental lifetime cancer risks associated with PAHs were estimated and were 1.62 × 10−6 and 2.34 × 10−6, respectively, for indoor and outdoor fine PMs. Both the values exceeded the threshold value of 1 × 10−6, demonstrating that the carcinogenic PAHs are a health threat to the students. Respiratory inflammatory responses of 50 students who studied in the sample classroom were examined with a fractional exhaled nitric oxide (FeNO) test, with the aid of health questionnaires. The average FeNO concentration was 17.4 ± 8.5 ppb, which was slightly lower than the recommended level of 20 ppb established by the American Thoracic Society for children. However, a wide distribution and 6% of the values were > 35 ppb, suggesting that the potentials were still high for eosinophilic inflammation and responsiveness to corticosteroids. A preliminary interpretation of the relationship between air toxins and respiratory inflammatory response demonstrated the high exposure cancer risks and inflammatory responses of the students to PMs in the city.
With juvenile fish as the subject, the effects of low concentration ammonia on antioxidant system were studied using Mugil cephalus. Samples of gill and liver tissue were obtained from 0.35, 0.70, 1.5 and 3?mg/L ammonia groups at 0, 5, 10, 15 and 20 days of exposure, at which times the biomarkers were measured. Results showed that gill malondialdehyde (MDA) content exhibited an initial significant increase (p?≤?0.05) at unionised ammonia concentrations of 0.70, 1.5 and 3.0?mg/L on day 5, followed by subsequent declines, while liver MDA levels exhibited significant increases (p?≤?0.05) at unionised ammonia concentrations of 1.5?mg/L starting on day 10 and at 3.0?mg/L starting on day 5. With exposure to ammonia at different concentrations, Na+-K+-ATPase activity in liver and gill decreased over time. The Na+-K+-ATPase activity was negatively related to ammonia concentration from 0.70 to 3.0?mg/L. Overall, our results show that MDA and Na+-K+-ATPase, evaluated here as potential biomarkers of ammonia exposure, exhibited responses to sublethal concentrations of ammonia that were concentration dependent. 相似文献