Distribution of polycyclic aromatic hydrocarbons in indoor/outdoor window films and the indoor film/air partition of northeastern Chinese college dormitories.

Indoor window films can represent short-term air pollution conditions of indoor environment through rapidly capturing organic contaminants as effective passive air samplers. To investigate the temporal variation, influence factors of polycyclic aromatic hydrocarbons (PAHs) in indoor window films, and the exchange behavior with gas phase in college dormitories, 42 pairs window films of interior and exterior window surfaces and corresponding indoor gas phase and dust samples were collected monthly in six selected dormitories, Harbin, China, from August to December 2019 and September 2020. The average concentration of ∑16PAHs in indoor window films (398 ng/m2) was significantly (p < 0.01) lower than that in outdoors (652 ng/m2). In addition, the median indoor/outdoor ∑16PAHs concentration ratio was close to 0.5, showing that outdoor air acted as a major PAH source to indoor environment. The 5-ring PAHs were mostly dominant in window films whereas the 3-ring PAHs contributed mostly in gas phase. 3-ring PAHs and 4-ring PAHs were both important contributors for dormitory dust. Window films showed stable temporal variation, i.e. PAH concentrations in heating months were higher than those in non-heating months. The atmospheric O3 concentration was the main influence factor of PAHs in indoor window films. PAHs with low molecular weight in indoor window films rapidly reached film/air equilibrium phase within in dozens of hours. The large deviation in the slope of the log KF-A versus log KOA regression line from that in reported equilibrium formula might be the difference between the window film composition and octanol.

Toxicity evaluation of decabromodiphenyl ethane (DBDPE) to Pleurotus ostreatus: Oxidative stress, morphology and transcriptomics.

Decabromodiphenyl ethane (DBDPE), one widely used new brominated flame retardant, was of great concern due to its biotoxicity. The toxic evaluation of DBDPE (1-50 mg/L) to white-rot fungus (Pleurotus ostreatus), including oxidative stress, morphology and transcriptomics was conducted aiming at improving its biodegradation. Fungal growth and ATPase activity were obviously inhibited by DBDPE at ≥ 10 mg/L with the exposure from 48 h to 96 h. DBDPE could induce oxidative stress to P. ostreatus. The activity of SOD (superoxide dismutase), CAT (catalase) and GSH (glutathione) were all promoted by DBDPE at ≤ 5 mg/L and inhibited at > 5 mg/L with 96-h exposure. MDA (malondialdehyde) content rose obviously with DBDPE exposure (10-50 mg/L). The mycelium was wizened under 20 mg/L DBDPE exposure according to SEM observation. Transcriptomics analysis suggested that DBDPE could change many functional genes expression of P. ostreatus. GO analysis indicated DBDPE could affect biological process and cellular component by inhibiting electron transport, mitochondrial ATP synthesis, oxidoreductase activity as well as transporter activity. KEGG enrichment pathways analysis indicated DBDPE could inhibit oxidative phosphorylation, tricarboxylic acid (TCA) cycle and carbon metabolism by down-regulating the genes related to NADH reductase/dehydrogenase, succinate dehydrogenase, cytochrome-c reductase/oxidase, cytochrome C1 protein and ATP synthase.

New understanding of novel brominated flame retardants (NBFRs): Neuro(endocrine) toxicity.

Traditional brominated flame retardants (BFRs) negatively affect the environment and human health, especially in the sensitive (developing) nervous system. Considering the physicochemical similarities between novel brominated flame retardants (NBFRs) and BFRs, more and more evidence reveals the neurotoxic effects of NBFRs. We reviewed the neuro(endocrine) toxic effects of NBFRs in vivo and in vitro and discussed their action mechanisms based on the available information. The neurotoxic potential of NBFRs has been demonstrated through direct neurotoxicity and disruption of the neuroendocrine system, with adverse effects on neurobehavioral and reproductive development. Mechanistic studies have shown that the impact of NBFRs is related to the complex interaction of neural and endocrine signals. From disrupting the gender differentiation of the brain, altering serum thyroid/sex hormone levels, gene/protein expression, and so on, to interfere with the feedback effect between different levels of the HPG/HPT axis. In this paper, the mechanism of neurotoxic effects of NBFRs is explored from a new perspective-neuro and endocrine interactions. Gaps in the toxicity data of NBFRs in the neuroendocrine system are supplemented and provide a broader dataset for a complete risk assessment.