Analysis of usage patterns and probabilistic risk assessment of personal care products in Korea.

In daily life, many people use large amounts of personal care products (PCPs) on a regular basis. For determining the risk to consumers, product usage amount, frequency of use, and co-use patterns are essential information. In this study, the PCP usage patterns of Korean consumers were analyzed, and the data were used to develop a probabilistic risk assessment. A web-based questionnaire was used to evaluate the PCP usage patterns of consumers. A model developed by Crème Global in conjunction with the Research Institute for Fragrance Materials was used to measure the systemic exposure to PCP ingredients. The use rates of 10 PCP family are compared with reported values obtained for populations in California and Switzerland which showed some distinct characteristics of Korean consumers. The co-use combinations of the 10 families of products frequently used by consumers were analyzed in an attempt to calculate aggregate exposure. Seven ingredients were selected and the aggregate risk assessment were performed based on bootstrapping analysis. The probability of the Hazard Quotient of all seven ingredients exceeding 1 was zero. The data of the usage patterns of Korean consumers reported here will be of value in developing more precise aggregate exposure risk analysis.

Changes in handwashing and hygiene product usage patterns in Korea before and after the outbreak of COVID-19.

BACKGROUND: The World Health Organization declared COVID-19, the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a global pandemic on March 11, 2020. Non-pharmaceutical interventions such as social distancing, handwashing, using hand sanitizer, and wearing facial masks are recommended as the first line of protection against COVID-19. Encouraging hand hygiene may be one of the most cost-effective means of reducing the global burden of disease. METHODS: This study uses a web-based questionnaire to evaluate the usage patterns and consumer perceptions of the effectiveness and health safety of bar soap, liquid hand soap, and hand sanitizer products before and after the spread of COVID-19. RESULTS: The results show that since the outbreak of COVID-19, the number of consumers who primarily use bar soap has decreased from 71.8 to 51.4%, the number of those who primarily use liquid hand soap has increased from 23.5 to 41.3%, and the number of those who use and carry hand sanitizer has increased. The frequency of use, duration of use, and amount used of all three products have increased significantly since the COVID-19 outbreak. Finally, consumer perception of the products' preventive effect against COVID-19 is higher for liquid hand soap and hand sanitizer than it is for bar soap. CONCLUSIONS: Because use of hand sanitizers has increased, public health guidelines must address the potential risks associated them. Our data also show that the public is abiding by the recommendations of the regulatory authorities. As handwashing has become important in preventing COVID-19 infections, the results of our study will support the development of better handwashing guidelines and a public health campaign. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12302-021-00517-8.

Increased Lipid Accumulation under Hypoxia in SZ95 Human Sebocytes.

BACKGROUND: Excessive sebum is produced by specialized cells called sebocytes and is considered a cause or consequence of acne, sebaceous cysts, hyperplasia, and sebaceous adenoma. OBJECTIVE: To report changes in lipid accumulation in human sebocytes under hypoxia, which occurs under conditions of seborrhea. METHODS: Sebocytes from the immortalized human gland cell line SZ95 were cultured under conditions of hypoxia for 48 h; lipid formation was confirmed by Nile red and Oil Red O staining. To investigate whether HIF-1α plays a role in lipid accumulation, SZ95 cells transfected or treated with dimethyloxalylglycine (DMOG) were assessed by Nile red. For protein expression of the sterol regulatory element-binding protein-1 (SREBP-1) and perilipin 2 (PLIN2), Western blot analysis was performed. Differentially expressed genes (DEGs) in SZ95 sebocytes under hypoxia were revealed by RNA-Seq analyses, and the statistical significance of the correlation between hypoxic and acne/non-acne skin was evaluated using gene set enrichment analysis. RESULTS: Hypoxia induces lipid accumulation in SZ95 sebocytes. In addition, the levels of SREBP-1 and PLIN2 were regulated by HIF-1α in SZ95 sebocytes under hypoxia. RNA-Seq analyses of DEGs in SZ95 sebocytes under hypoxia revealed 256 DEGs, including several lipid droplet-associated genes. DEGs between acne and non-acne skin are significantly enriched in hypoxia gene sets. We also detected 93 differentially expressed inflammatory mediators. CONCLUSIONS: To the best of our knowledge, this study is the first to show that a hypoxic microenvironment can increase lipogenesis and provides a link between seborrhea and inflammation.

The Effect of Korean Red Ginseng on Bisphenol A-Induced Fatty Acid Composition and Lipid Metabolism-Related Gene Expression Changes.

Bisphenol A (BPA), which is known to be an endocrine-disrupting chemical (EDC), is associated not only with estrogen activity and reproductive toxicity but also with a variety of metabolic disorders. BPA affects glucose tolerance, cholesterol biosynthesis, and fatty acid synthesis. Ginseng is a traditional medicinal plant that has been widely used in East Asia for more than 2000 years, and a number of health effects have been reported. Korean Red Ginseng (KRG) has also been shown to have effects on lipid metabolism and body weight reduction in vivo in obese mice. In this study, we administered BPA and KRG to ovariectomized (OVX) ICR mice. BPA (800 mg/kg/day) and KRG (1.2 g/kg/day) were orally administered to OVX mice for 3 days. KRG inhibited the increase in total fatty acid level by BPA as determined by lipid profiling in the liver of OVX mice. In addition, transcriptome analysis showed that KRG inhibited BPA-induced changes in lipid metabolic process-related genes. Our findings suggest that KRG can regulate BPA-induced changes in lipid metabolism.

Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator-activated receptor gamma in A549 cells.

BACKGROUND: Ginsenoside Rf is a ginseng saponin found only in Panax ginseng that affects lipid metabolism. It also has neuroprotective and antiinflammatory properties. We previously showed that Korean Red Ginseng (KRG) inhibited the expression of cyclooxygenase-2 (COX-2) by hypoxia via peroxisome proliferator-activated receptor gamma (PPARγ). The aim of the current study was to evaluate the possibility of ginsenoside Rf as an active ingredient of KRG in the inhibition of hypoxia-induced COX-2 via PPARγ. METHODS: The effects of ginsenoside Rf on the upregulation of COX-2 by hypoxia and its antimigration effects were evaluated in A549 cells. Docking of ginsenoside Rf was performed with the PPARγ structure using Surflex-Dock in Sybyl-X 2.1.1. RESULTS: PPARγ protein levels and peroxisome proliferator response element promoter activities were promoted by ginsenoside Rf. Inhibition of COX-2 expression by ginsenoside Rf was blocked by the PPARγ-specific inhibitor, T0070907. The PPARγ inhibitor also blocked the ability of ginsenoside Rf to suppress cell migration under hypoxia. The docking simulation results indicate that ginsenoside Rf binds to the active site of PPARγ. CONCLUSIONS: Our results demonstrate that ginsenoside Rf inhibits hypoxia induced-COX-2 expression and cellular migration, which are dependent on PPARγ activation. These results suggest that ginsenoside Rf has an antiinflammatory effect under hypoxic conditions. Moreover, docking analysis of ginsenoside Rf into the active site of PPARγ suggests that the compound binds to PPARγ in a position similar to that of known agonists.

The effects of bisphenol A, benzyl butyl phthalate, and di(2-ethylhexyl) phthalate on estrogen receptor alpha in estrogen receptor-positive cells under hypoxia.

Endocrine-disrupting chemicals (EDCs) are widely used in various consumer goods. Consequently, humans are constantly exposed to EDCs, which is associated with a variety of endocrine-related diseases. In this study, we demonstrated the effects of bisphenol A (BPA), benzyl butyl phthalate (BBP), and di(2-ethylhexyl) phthalate (DEHP) on estrogen receptor alpha (ERα) expression under normoxia and hypoxia. First, we confirmed the effects of EDCs on ER activity using OECD Test Guideline 455. Compared to the 100% activity induced by 1 nM 17-ß-estradiol (positive control), BPA and BBP exhibited 50% ERα activation at concentrations of 1.31 µM and 4.8 µM, respectively. In contrast, and consistent with previous reports, DEHP did not activate ERα. ERα is activated and degraded by hypoxia in breast cancer cells. BPA, BBP, and DEHP enhanced ERα-mediated transcriptional activity under hypoxia. All three EDCs decreased ERα protein levels under hypoxia in MCF-7 cells. The transcriptional activity of hypoxia-inducible factor-1 was decreased and secretion of vascular endothelial growth factor (VEGF) was increased by BPA and BBP under hypoxia in MCF-7 cells, but not by DEHP. All three EDCs decreased the ERα protein expression level in Ishikawa human endometrial adenocarcinoma cells, and DEHP caused a weak decrease in VEGF secretion under hypoxia. These results demonstrate down-regulation of ERα by EDCs may influence the pathological state associated with hypoxia.

Bisphenol A induces COX-2 through the mitogen-activated protein kinase pathway and is associated with levels of inflammation-related markers in elderly populations.

Bisphenol A (BPA) is a well-known endocrine-disrupting chemical, and it is one of the highest volume chemicals produced worldwide. Even though several in vivo and in vitro studies showed positive associations of BPA exposure with pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin (IL)-6, the mechanism by which BPA induces inflammation is unclear. We investigated the mechanism by which BPA induces inflammation (expression of inflammation-related genes, changes in oxidative stress, and cell proliferation and migration) and evaluated the effect of BPA exposure on inflammation-related markers in epidemiologic studies using repeat urine and serum samples from elderly subjects. BPA induced COX-2 expression via nuclear translocation of NF-κB and activation of mitogen-activated protein kinase (MAPK) by phosphorylation of ERK1/2 and enhanced the migration of lung cancer A549 and breast cancer MDAMB-231 cells. In two epidemiologic studies, we detected associations of BPA with six inflammation-related markers (WBC, CRP, IL-10, ALT, AST, and γ-GTP levels). Our findings probably suggest that BPA exposure induces inflammation and exacerbates tumorigenesis.