Exposure and health risk assessment of indoor volatile organic compounds in a medical university.

Many volatile organic compounds (VOCs) are used for experiments at universities, and most of them contain benzene, toluene, ethylbenzene, xylene, and an extraction solvent of dichloromethane. This study aimed to investigate the indoor concentrations of these five compounds in different locations on campus and to evaluate possible health risks for faculty members and students in a medical university. We selected 10 locations as sampling sites to conduct 4-h monitoring sessions on weekdays each season during 2019-2020. We used a 6-liter canister to collect air samples and analyzed these five VOCs via gas chromatography with a flame ionization detector. Monte Carlo simulation was performed to evaluate the carcinogenic and noncarcinogenic risks of these five VOCs. We found that dichloromethane was the most highly detected compound (median: 621.07 µg/m3; range: 44.01-8523.91 µg/m3), and the Department of Medicine had the highest concentration of the total of these VOCs among all of the locations (median: 5595.29 µg/m3; range: 1565.67-7398.66 µg/m3). The median carcinogenic risks of dichloromethane and benzene were 6.36 × 10-5 (95% confidence interval [CI]: 6.83 × 10-6-7.37 × 10-4) and 5.47 × 10-6 (95% CI: 4.03 × 10-7-2.42 × 10-5), respectively, for faculty members, and the lower risks of 3.14 × 10-5 (95% CI: 3.39 × 10-6-3.64 × 10-4) and 2.69 × 10-6 (95% CI: 1.97 × 10-7-1.19 × 10-5) were estimated for the students. The chronic noncarcinogenic risks of four VOCs were less than one, except for dichloromethane with a median hazard index of 1.92 (95% CI: 2.11 × 10-1-2.22 × 101). This study observed the spatial variation in the concentrations of the total of five VOCs and dichloromethane. The carcinogenic risks were classified as being at the possible level, and the noncarcinogenic risk of dichloromethane was greater than the acceptable level. Increasing local exhaust ventilation during the experiment and reducing the using amount of dichloromethane are recommended actions to reduce VOCs exposures in the medical university.

Sublethal ammonia induces alterations of emotions, cognition, and social behaviors in zebrafish (Danio rerio).

Ammonia pollutants were usually found in aquatic environments is due to urban sewage, industrial wastewater discharge, and agricultural runoff and concentrations as high as 180 mg/L (NH4+) have been reported in rivers. High ammonia levels are known to impair multiple tissue and cell functions and cause fish death. Although ammonia is a potent neurotoxin, how sublethal concentrations of ammonia influence the central nervous system (CNS) and the complex behaviors of fish is still unclear. In the present study, we demonstrated that acute sublethal ammonia exposure can change social behavior of adult zebrafish. The exposure to 90 mg /L of (NH4+) for 4 h induced a strong fear response and lower shoaling cohesion; exposure to 180 mg /L of (NH4+) for 4 h reduced the aggressiveness, and social recognition, while the anxiety, social preference, learning, and short-term memory were not affected. Messenger RNA expressions of glutaminase and glutamate dehydrogenase in the brain were induced, suggesting that ammonia exposure altered glutamate neurotransmitters in the CNS. Our findings in zebrafish provided delicate information of ammonia neurotoxicity in complex higher-order social behaviors, which has not been revealed previously. In conclusion, sublethal and acute ammonia exposure can change specific behaviors of fish, which might lead to reductions in individual and population fitness levels.

Aggregation-induced negative differential resistance in graphene oxide quantum dots.

Negative differential resistance (NDR) devices have attracted considerable interest due to their potential applications in switches, memory devices, and analog-to-digital converters. Modulation of the NDR is an essential issue for the development of NDR-based devices. In this study, we successfully synthesized graphene oxide quantum dots (GOQDs) using graphene oxide, cysteine, and H2O2. The current-voltage characteristics of the GOQDs exhibit a clear NDR in the ambient environment at room temperature. A peak-to-valley ratio as high as 4.7 has been achieved under an applied voltage sweep from -6 to 6 V. The behavior of the NDR and its corresponding peak-to-valley ratio can be controlled by adjusting the range of applied voltages, air pressure, and relative humidity. Also, the NDR is sensitive to the the concentration of H2O2 added in the synthesis. The charge carrier injection through the trapping states, induced by the GOQD aggregation, could be responsible for the NDR behavior in GOQDs.

Investigation of ammonia-induced lethal toxicity toward ion regulation in zebrafish embryos.

Ammonia is an environmental pollutant that is toxic to all aquatic animals. However, the mechanism of ammonia toxicity toward the ion regulatory function of early-stage fish has not been fully documented. We addressed this issue using zebrafish embryos as a model. We hypothesized that ammonia might impair ion regulation by inducing oxidative stress, mitochondrial dysfunction, and cell death of epidermal ionocytes and keratinocytes in zebrafish embryos. After exposure to various concentrations (10- 30 mM) of NH4Cl for 96 h, mortality increased up to 50 % and 100 % at 25 and 30 mM, respectively. Whole-embryo sodium, potassium, and calcium contents decreased at ≥10 mM, suggesting dysfunction of ion regulation. Numbers of H+-ATPase-rich (HR) cells and Na+/K+-ATPase-rich (NaR) cells (two ionocyte subtypes) were not significantly altered at 15 or 20 mM, while the mitochondrial abundance significantly decreased and reactive oxygen species (ROS) levels significantly increased in ionocytes. Moreover, caspase-3-dependent apoptosis was found in epidermal keratinocytes. Whole-embryo transcript levels of several genes involved in ion regulation, antioxidation, and apoptosis were upregulated after ammonia exposure. In conclusion, ammonia exposure was shown to induce oxidative stress and mitochondrial dysfunction in ionocytes and apoptosis in keratinocytes, thereby impairing ion regulation and ultimately leading to the death of zebrafish embryos.