Reconstructing the Composition of Per- and Polyfluoroalkyl Substances in Contemporary Aqueous Film-Forming Foams.

Hundreds of public water systems across the United States have been contaminated by the use of aqueous film-forming foams (AFFF) containing per- and polyfluoroalkyl substances (PFAS) during firefighting and training activities. Prior work shows AFFF contain hundreds of polyfluoroalkyl precursors missed by standard methods. However, the most abundant precursors in AFFF remain uncertain, and mixture contents are confidential business information, hindering proactive management of PFAS exposure risks. Here, we develop and apply a novel method (Bayesian inference) for reconstructing the fluorinated chain lengths, manufacturing origin, and concentrations of oxidizable precursors obtained from the total oxidizable precursor (TOP) assay that is generally applicable to all aqueous samples. Results show virtually all (median 104 ± 19%) extractable organofluorine (EOF) in contemporary and legacy AFFF consists of targeted compounds and oxidizable precursors, 90% of which are 6:2 fluorotelomers in contemporary products. Using high-resolution mass spectrometry, we further resolved the 6:2 fluorotelomers to assign the identity of 14 major compounds, yielding a priority list that accounts for almost all detectable PFAS in contemporary AFFF. This combination of methods can accurately assign the total PFAS mass attributable to AFFF in any aqueous sample with differentiation of gross precursor classes and identification of major precursor species.

Adrenergic and glucocorticoid receptor antagonists reduce ozone-induced lung injury and inflammation.

Recent studies showed that the circulating stress hormones, epinephrine and corticosterone/cortisol, are involved in mediating ozone-induced pulmonary effects through the activation of the sympathetic-adrenal-medullary (SAM) and hypothalamus-pituitary-adrenal (HPA) axes. Hence, we examined the role of adrenergic and glucocorticoid receptor inhibition in ozone-induced pulmonary injury and inflammation. Male 12-week old Wistar-Kyoto rats were pretreated daily for 7days with propranolol (PROP; a non-selective ß adrenergic receptor [AR] antagonist, 10mg/kg, i.p.), mifepristone (MIFE; a glucocorticoid receptor [GR] antagonist, 30mg/kg, s.c.), both drugs (PROP+MIFE), or respective vehicles, and then exposed to air or ozone (0.8ppm), 4h/d for 1 or 2 consecutive days while continuing drug treatment. Ozone exposure alone led to increased peak expiratory flow rates and enhanced pause (Penh); with greater increases by day 2. Receptors blockade minimally affected ventilation in either air- or ozone-exposed rats. Ozone exposure alone was also associated with marked increases in pulmonary vascular leakage, macrophage activation, neutrophilic inflammation and lymphopenia. Notably, PROP, MIFE and PROP+MIFE pretreatments significantly reduced ozone-induced pulmonary vascular leakage; whereas PROP or PROP+MIFE reduced neutrophilic inflammation. PROP also reduced ozone-induced increases in bronchoalveolar lavage fluid (BALF) IL-6 and TNF-α proteins and/or lung Il6 and Tnfα mRNA. MIFE and PROP+MIFE pretreatments reduced ozone-induced increases in BALF N-acetyl glucosaminidase activity, and lymphopenia. We conclude that stress hormones released after ozone exposure modulate pulmonary injury and inflammatory effects through AR and GR in a receptor-specific manner. Individuals with pulmonary diseases receiving AR and GR-related therapy might experience changed sensitivity to air pollution.

Effect of Microwave Heating on the Crystallization of Glutathione Tripeptide on Silver Nanoparticle Films.

Effect of microwave heating on the crystallization of glutathione (GSH) tripeptide using the metal-assisted and microwave-accelerated evaporative crystallization (MA-MAEC) technique is reported. GSH crystals were grown from supersaturated solutions of GSH (300-500 mg/mL) on the iCrystal plates with silver nanoparticle films (SNFs) and without SNFs in three different microwave systems operating at 2.45 GHz: conventional (multimode, fixed power at 900W), industrial (monomode, variable power up to 1200 W), and the iCrystal system (monomode, variable power up to 100 W). The efficacy of the MA-MAEC technique, in terms of improvement in the crystallization time, crystal size and quality of GSH, was compared between the three microwave systems and the crystallization at room temperature (no microwave heating, a control experiment). Optical microscopy was used to visualize and quantify the growth of GSH crystals during and after microwave heating. Powder X-ray diffraction (XRD) and Fourier transform infrared (FTIR) spectroscopy data showed that GSH crystals had identical crystal structure to those grown at room temperature and microwave heating did not alter the chemical structure of GSH molecules during microwave heating, respectively. Using the MA-MAEC technique, the iCrystal system yielded high quality GSH crystals in a rapid manner.