Children's exposure to brominated flame retardants in the home: The TESIE study.

Due to differences in chemical properties and half-lives, best practices for exposure assessment may differ for legacy versus novel brominated flame retardants (BFRs). Our objective was to identify the environment matrix that best predicted biomarkers of children's BFR exposures. Paired samples were collected from children aged 3-6 years and their homes, including dust, a small piece of polyurethane foam from the furniture, and a handwipe and wristband from each child. Biological samples collected included serum, which was analyzed for 11 polybrominated diphenyl ethers (PBDEs), and urine, which was analyzed for tetrabromobenzoic acid (TBBA), a metabolite of 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (EH-TBB). Significant positive correlations were typically observed between BFRs measured in dust, handwipes and wristbands, though wristbands and handwipes tended to be more strongly correlated with one another than with dust. PBDEs, EH-TBB and BEH-TEBP were detected in 30% of the sofa foam samples, suggesting that the foam was treated with PentaBDE or Firemaster® 550/600 (FM 550/600). PBDEs were detected in all serum samples and TBBA was detected in 43% of urine samples. Statistically significant positive correlations were observed between the environmental samples and serum for PBDEs. Urinary TBBA was 6.86 and 6.58 times more likely to be detected among children in the highest tertile of EH-TBB exposure for handwipes and wristbands, respectively (95 % CI: 2.61, 18.06 and 1.43, 30.05 with p < 0.001 and 0.02, respectively). The presence of either PentaBDE or FM 550/600 in furniture was also associated with significantly higher levels of these chemicals in dust, handwipes and serum (for PBDEs) and more frequent detection of TBBA in urine (p = 0.13). Our results suggest that children are exposed to a range of BFRs in the home, some of which likely originate from residential furniture, and that silicone wristbands are a practical tool for evaluating external exposure to both legacy and novel BFRs.

Lignans from the seed shells of Cerasus humilis (Bge.) Sok and their bioactivities.

The exploration of Cerasus humilis (Bge.) Sok seed shells yielded the identification of six previously uncharacterized compounds, in addition to twelve known compounds. Structure elucidation of these compounds relied on spectroscopic data analysis, and their absolute configurations were established by comparing calculated and experimental electronic circular dichroic (ECD) spectra, supplemented by interpretation of optical rotation data. Notably, none of these compounds exhibited cytotoxicity against HepG2 and A549 cell lines. Remarkably, a majority of the compounds displayed potent antioxidant activity.

Disruption of USP9X in macrophages promotes foam cell formation and atherosclerosis.

Subendothelial macrophage internalization of modified lipids and foam cell formation are hallmarks of atherosclerosis. Deubiquitinating enzymes (DUBs) are involved in various cellular activities; however, their role in foam cell formation is not fully understood. Here, using a loss-of-function lipid accumulation screening, we identified ubiquitin-specific peptidase 9 X-linked (USP9X) as a factor that suppressed lipid uptake in macrophages. We found that USP9X expression in lesional macrophages was reduced during atherosclerosis development in both humans and rodents. Atherosclerotic lesions from macrophage USP9X-deficient mice showed increased macrophage infiltration, lipid deposition, and necrotic core content than control apolipoprotein E-KO (Apoe-/-) mice. Additionally, loss-of-function USP9X exacerbated lipid uptake, foam cell formation, and inflammatory responses in macrophages. Mechanistically, the class A1 scavenger receptor (SR-A1) was identified as a USP9X substrate that removed the K63 polyubiquitin chain at the K27 site. Genetic or pharmacological inhibition of USP9X increased SR-A1 cell surface internalization after binding of oxidized LDL (ox-LDL). The K27R mutation of SR-A1 dramatically attenuated basal and USP9X knockdown-induced ox-LDL uptake. Moreover, blocking binding of USP9X to SR-A1 with a cell-penetrating peptide exacerbated foam cell formation and atherosclerosis. In this study, we identified macrophage USP9X as a beneficial regulator of atherosclerosis and revealed the specific mechanisms for the development of potential therapeutic strategies for atherosclerosis.

Release of inhalable particles and viable microbes to the air during packaging peeling: Emission profiles and mechanisms.

Packaging is necessary for preserving and delivering products and has significant impacts on human health and the environment. Particle matter (PM) may be released from packages and transferred to the air during a typical peeling process, but little is known about this package-to-air migration route of particles. Here, we investigated the emission profiles of total and biological particles, and the horizontal and vertical dispersion abilities and community structure of viable microbes released from packaging to the air by peeling. The results revealed that a lot of inhalable particles and viable microbes were released from package to the air in different migration directions, and this migration can be regulated by several factors including package material, effective peeling area, peeling speed and angles, as well as the characteristics of the migrant itself. Dispersal of package-borne viable microbes provides direct evidence that viable microbes, including pathogens, can survive the aerosolization caused by peeling and be transferred to air over different distances while remaining alive. Based on the experimental data and visual proof in movies, we speculate that nonbiological particles are package fibers fractured and released to air by the external peeling force exerted on the package and that microbe dispersal is attributed to surface-borne microbe suspension by vibration caused by the peeling force. This investigation provides new information that aerosolized particles can deliver package-borne substances and viable microbes from packaging to the ambient environment, motivating further studies to characterize the health effects of such aerosolized particles and the geographic migration of microbes via packaging.