Cooking Oil Fumes Research Articles

Effects of Trans, Trans-2,4-decadienal on the Ions Currents of Cardiomyocytes: Possible Mechanisms of Arrhythmogenesis Induced by Cooking-oil Fumes

Household air pollution has adverse effects on cardiovascular health. One of the major sources of household air pollutants is the combustion of cooking oils during cooking. Trans, trans-2,4-decadienal (tt-DDE) is a type of dienaldehyde that is present in a wide range of food and food products. It is a byproduct of the peroxidation of linoleic acid following the heating of oil during cooking. The mechanisms of the associations between household air pollution and cardiac arrhythmias are currently unclear. The purpose of this study was to determine effects of tt-DDE on the ion currents in H9c2 cells. The IK and ICa,L in H9c2 cells treated with and without tt-DDE were measured using the whole-cell patch clamp method. Expressions of Kv2.1 and Cav1.2 in H9c2 cells treated with and without tt-DDE were measured by western blot analysis. After the H9c2 cells had been exposed to tt-DDE, the IK and ICa,L were significantly decreased. The expression of Kv2.1, unlike that of Cav1.2, was also significantly decreased in these cells. These changes in IK and ICa,L that were induced by tt-DDE may help to explain the association between cardiac arrhythmogenesis and cooking-oil fumes.

Fermented black barley ameliorates lung injury induced by cooking oil fumes via antioxidant activity and regulation of the intestinal microbiome in mice.

To investigate the effect of fermented black barley on cooking oil fume (COF)-induced lung injury, male ICR mice were randomized into five groups: normal control (NC), fermented black barley treatment (NF), COF exposure (O), COF+fermented black barley treatment (OF) and COF+Lactobacillus treatment (OL). The exposure of mice to COF was performed for 5min per day and 4 days per week for a total of 9 weeks, and the mice in the OF, NF and OL groups were administered fermented black barley or Lactobacillus continuously for 9 weeks (1 mL/100g). Our results showed that the gamma-aminobutyric acid (GABA), total phenolic, and flavonoid contents significantly increased after fermentation (P<0.01). In addition, fermented black barley significantly increased SOD activity in the lung tissue, decreased the wet pulmonary coefficient, inhibited the reduction of microbial diversity and richness, and upregulated genes involved in cilium assembly and the cilium axoneme. These findings support the notion that fermented black barley can ameliorate COF-induced lung injury in mice.

Adverse effects of subchronic exposure to cooking oil fumes on the gonads and the GPR30-mediated signaling pathway in female rats

BackgroundCooking oil fumes (COFs) are composed of particulate matter, polycyclic aromatic hydrocarbons, volatile organic compounds, aldehydes, and ketones, and are currently a global health concern. Some agents in COFs are mutagenic and carcinogenic. However, only a few reports have addressed the hazardous effects of COF exposure on the female reproductive system. In this study, we explored the effects of subchronic exposure to COFs on female gonads in vivo and the possible involvement of the G-protein-coupled receptor 30 signaling pathway.MethodsCOFs were generated by heating commercially available canola oil in an iron pot. Adult female Wistar rats at 2 months of age were exposed to COFs at 32 mg/m3 for 0, 0.5, 1, 2, or 4 h/day for 56 days. The estrous cycle in rats was studied twice at 7:00 a.m. and 7:00 p.m. on the 43rd treatment day until the current estrous cycle was complete. The rat body weight was measured before the experiment and at day 56 post-exposure. At the end of the experiment, rat blood was collected for gonadal hormone assay, and ovaries were collected for histology and mRNA isolation. The mRNA levels of GPR30, EGFR, STAT3, and ERK were determined by quantitative RT-PCR.ResultsAt a concentration of 32.21 ± 5.11 mg/m3, COF exposure extended the estrous cycle in rats, and ovary coefficient decreased. COFs showed various effects on the sex hormone levels and follicles, depending on its exposure level. Exposure to COFs led to the changes in mRNA levels of the G-protein-coupled receptor 30 (GPR30), epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 3 (STAT3), and extracellular signal-regulated kinase (ERK).ConclusionThis study indicated that cooking oil fume exposure disrupted the estrous cycle, sex hormone patterns, and follicle development in female rats in a dose-dependent manner. These adverse effects of cooking oil fumes on female reproductive health were correlated with the G-protein-coupled receptor 30-mediated signaling pathway.HighlightsSubchronic exposure to COFs for 56 days had gonadal toxicity in female rats, that disrupted the estrous cycle, sex hormone patterns, and follicle development in a dose-dependent manner.Reproductive endocrine disruption might be one of the female gonadotoxicity mechanisms of COFs.These adverse effects of COFs on female reproductive health were correlated with the GPR30-mediated signaling pathway.

Lung Cancer in Never-Smokers: A Multicenter Case-Control Study in North China.

This study aimed at estimating the effects of epidemiological risk factors for lung cancer in never-smokers. A multicenter and matched case-control study was conducted in the cities of Shijiazhuang, Xingtai, Qinhuangdao, Baoding, and Chengde in North China. It comprised 1,086 cases and 2,172 healthy subjects as controls, all of whom had smoked fewer than 100 cigarettes in their lifetimes. Patients were newly diagnosed with lung cancer between January 2015 and December 2017. Each patient was matched to two control participants for sex and age (±5 years). Both univariate analysis and multivariate conditional logistic regression models were used to estimate the odds ratio (OR) and 95% confidence interval (95% CI). Subsequently, data were stratified by participant sex and different air quality conditions for analysis. Type of job, exposure to environmental tobacco smoke in the workplace or at home, above-average exposure to cooking oil fumes, depression, poor sleep quality, occupational exposure, cardiovascular diseases, and family history of cancer were revealed as significant risk factors for lung cancer in never-smokers. However, higher educational level, frequent use of a PM2.5 mask, cooking using clean fuels, and consumption of dietary supplements and tea reduced the risk of lung cancer. Risk factors varied between males and females. In areas with air pollution, the number of risk factors was greater than elsewhere, and the magnitudes of their effects were different. Hence, focusing on these risk factors is important for the prevention and control of lung cancer in never-smokers.

Inverse design optimisation of a novel range hood based on intelligent algorithms and computational fluid dynamics simulations

Our aim in the present study is to increase grease separation by optimising the discharge performance of cooking oil fumes. A novel range hood with an outer cylinder and guide vanes of exhaust (GVE) is proposed. The geometric configuration of the hood is optimized by a reverse design method developed by coupling back propagation neural networks, mind evolutionary algorithms, and computational fluid mechanics. The primary objective of the range hood is to maximise the exhaust airflow rate with good grease separation. At the optimised conditions, the inlet and outlet blade angles are 80° and 176°, respectively, while the heights of the blade and guide vane are 0.180 and 0.245 m, respectively. The optimal number of blades and guide vanes are 29 and 7, respectively, while the optimal diffuser diameter is 0.340 m. The proposed range hood exhibits excellent performance of grease particle separation compared to multi-blade centrifugal fans with volutes. In addition, the outer cylinder and GVE of the range hood exhibit a large separation efficiency for particles in the size range of 1–4 μm, while impeller blades mainly separate grease particles in the size range of 4–10 μm.

Health risk assessment of formaldehyde released from several Chinese dishes cooking activities

To study the effect of Chinese dishes cooking activities on the health risk for domestic cook, numerical simulations are executed under different air flow rates for three oil-based Chinese dishes cooking activities. The concentration of formaldehyde in respiratory area during cooking process is obviously influenced by the cooking dishes. And the effect of air flow rate of range hood on the formaldehyde capture is not as significant as that of the cooking method. The predicated results show that the formaldehyde concentration is 4.5-5.5, 2.8-3.6 and 1.2-1.5 times of the prescribed limit when cooking the dishes of stir-fried mutton, pan-fried chicken with onion and deep-fried pork, respectively. The high air flow rate is recommended for improving formaldehyde capture efficiency (CE) of range hood. The potentially benefit effects induced by higher air flow rate is reliable in the cooking activity of stir-fry mutton. Using high air flow rate of 19m3/min can reduce the risk by 11.86% compared with using low air flow rate of 10m3/min. Low air flow rate is more suitable for cooking activities with low release rate of cooking oil fumes (COFs), in order to better protect the health of cooks.

Fixed Ratio Versus Lower Limit of Normal: Health Status and Risk Factors for COPD Overdiagnosis.

The threshold of the lower limit of the normal range of lung function has been suggested to be more accurate than the 0.7 fixed ratio (FEV1/FVC < 0.7) for a diagnosis of COPD. We aimed to explore the health status and risk factors of patients overdiagnosed with COPD when using the lower limit of the normal range as a diagnostic reference. Subjects with COPD diagnosed by a pulmonologist according to guidelines of the Global Initiative for Chronic Obstructive Lung Disease were recruited from October 2016 to April 2018. Overdiagnosed COPD was defined as FEV1/FVC that meets the criterion of the 0.7 fixed ratio but not the the lower limit of the normal range criterion. Spirometry and questionnaires were performed by eligible subjects. Of the 513 subjects included in the final analysis, 20 (3.9%) were overdiagnosed when using the lower limit of the normal range as the diagnostic reference. The subjects who were overdiagnosed were older, weighed more, had better lung function, lower modified Medical British Research Council scores, and higher St. George's Respiratory Questionnaire and 36-item Short Form Survey scores than the subjects who were correctly diagnosed. Older age, heavier weight, exposure to cooking oil fumes, or a new-built or newly renovated home were associated with an increased risk of overdiagnosis of COPD (age adjusted odds ratio (OR) 1.17, 95% CI 1.09-1.26; weight adjusted OR 1.08, 95% CI 1.03-1.13; exposure to cooking oil fumes adjusted OR 3.00, 95% CI, 1.04-8.68; exposure to new-built or newly renovated home adjusted OR 10.88, 95% CI 1.46-80.87. The subjects with overdiagnosed COPD had a better health status and lung function than the subjects who were correctly diagnosed. Older age, heavier weight, and exposure to cooking oil fumes or a new-built or newly renovated home were factors associated with the overdiagnosis of COPD. These findings may help reduce overdiagnosis of COPD.

Toxicity of cooking oil fume derived particulate matter: Vitamin D3 protects tubule formation activation in human umbilical vein endothelial cells.

Cooking oil fumes-derived PM2.5 (COFs-derived PM2.5) is the main source of indoor pollution. Exposure to COFs-derived PM2.5 can cause oxidative stress and affect angiogenesis. Here we investigated the roles of vitamin D3 (VD3) in protecting tubule formation injury induced by COFs-derived PM2.5, and the roles of ROS/NLRP3/VEGF signaling pathway in the effects. Human umbilical vein endothelial cells (HUVECs) were exposed to 0 (1‰ DMSO), 1000 nmol/l VD3, 100 μg/ml PM2.5, and 1000 nmol/l VD3+100μg/ml PM2.5, respectively. Cell viability and tube formation, as well as protein and mRNA levels were measured. The results showed that exposure of COFs-derived PM2.5 dose-and time-dependently reduced the viability of HUVECs, increased the levels of mitochondrial and intracellular ROS, and changed the mitochondrial membrane potential level. While co-incubation with VD3 rescued these adverse effects. Both Western blot and real-time PCR (RT-PCR) showed that the expressions of NLRP3, caspase-1, Interleukin (IL)-1β, and IL-18 in COFs-derived PM2.5 exposure group increased significantly, which could be effectively decreased by co-incubation with VD3. COFs-derived PM2.5 exposure could also reduce the expression of VEGF, while co-incubating HUVECs with VD3 evidently up-regulated the protein level of VEGF in HUVECs. In addition, COFs-derived PM2.5 could also inhibit the tube formation of HUVECs in vitro, which could be effectively rescued by the co-incubation of VD3. Our study proved that COFs-derived PM2.5 could damage the tubule formation of HUVECs in vitro, which could be effectively rescue by co-incubation with VD3, in which processes the ROS/NLRP3/VEGF signaling pathway played a crucial role. It provides a new theoretical basis for further study on the toxicity of PM2.5 to umbilical cord blood vessels.

Reducing human exposure to PM2.5 generated while cooking typical Chinese cuisine

Residential Chinese cooking can lead to severe exposure to carcinogenic fine particles (PM2.5) from cooking-oil fumes. Keeping the kitchen door open is conducive to improving air quality in the kitchen, but it can result in further diffusion of PM2.5 emissions into adjacent rooms. In this study, PM2.5 exposure concentrations were measured in the kitchen and an adjacent room during and after cooking activities, where various interventions were employed based on an orthogonal design. Intervention strategies, including range-hood operations, protective respirator use, personal portable fan operation, side panels configured for the range hood, and air cleaner use, were incorporated. The results demonstrated that using the range hood with an equivalent air exchange rate of 7.5–10.9 h−1 in the kitchen and wearing respirators during cooking were the most efficient prevention measures, significantly decreasing the inhalation exposure to PM2.5 for the cook in the kitchen by 90–95% and 79–84%, respectively. The average concentrations in the adjacent living room could be decreased by 50%–75% with an additional period of 5–10 min running the range hood or the air cleaner (the cleaner air exchange rate was no more than 5 h−1).

A Case/Control Study: AGBL1 Polymorphism Related to Lung Cancer Risk in Chinese Nonsmoking Females.

ATP/GTP binding protein like 1 (AGBL1) plays a role in controlling the length of polyglutamate side chains. Polymorphism rs4513061 in AGBL1 is suspected to influence the risk of lung cancer. A case/control study was performed involving 556 cases and 563 controls from a hospital participating in donation. The relationship between rs4513061 and the risk of lung cancer and the interaction between rs4513061 and environmental exposure were determined by the chi-square tests, logistic regression analysis, and crossover analysis. The survival analysis was conducted by Cox proportional hazard regression. The results showed that rs4513061 polymorphism is associated with the risk of lung cancer. The stratified analysis suggested the protective effect of rs4513061 to different histological types of lung cancer, including lung adenocarcinoma (AA vs. GG: odds ratio [OR] = 0.505, 95% confidence interval [CI] = 0.337-0.756, p < 0.001), squamous cell lung cancer (AG vs. GG: OR = 0.488, 95% CI = 0.269-0.883, p = 0.018), and small-cell lung cancer (AA vs. GG: OR = 0.421, 95% CI = 0.216-0.819, p = 0.011). Nevertheless, there was no significant interaction between rs4513061 and cooking oil fume. Significant impact was not observed between the rs4513061 polymorphism and survival time of lung cancer. Our study indicated that rs4513061 in AGBL1 decreases the risk of lung cancer in nonsmoking females from northeast China.

Airborne particles from cooking oils: Emission test and analysis on chemical and health implications

Inhalation of cooking oil fumes can be detrimental to human health. This study aims to evaluate the emission characteristics of different cooking oils and attempts to identify a cooking oil that emits the least fine particulate matter (PM) during heating. The yield of particles of six different size increments were examined for six commonly used cooking oils: vegetable, canola, corn, olive, peanut, and coconut oils. Both the chemical and structural properties of the oils were analyzed to explain for variance in the quantity of particle emissions and distribution of particulate sizes among oils. The study further compared the oil particle accumulation in a typical cooking facility with and without a smoke exhaust hood. Of the oils examined, coconut and olive oil produced the most particles at low temperatures; peanut and canola oil produced the most particles at high temperatures. Fume inhalation can be greatly decreased through ventilation at both the half power and full power tested. The inhalation of particulate matter expelled from the heating of cooking oils does not exceed government regulation levels for typical household cooking, but inhalation for extended lengths of time might exceed U.S. and Australian regulation guidelines.

Polymorphisms of rs4787050 and rs8045980 are associated with lung cancer risk in northeast Chinese female nonsmokers.

Aim: We studied the association between two single-nucleotide polymorphisms (SNPs: rs4787050 and rs8045980) in RBFOX1 and lung cancer risk, and explored the interaction between the two SNPs and exposure to cooking oil fume on lung cancer risk in northeast Chinese female nonsmokers. Methods: Northeast Chinese female nonsmokers were enrolled into the study (people with lung cancer, 647; people without lung cancer, 675). All statistical analyses were performed using SPSS software. Results: The SNPs rs4787050 and rs8045980 showed a significant association with susceptibility to lung cancer. Moreover, cooking oil fume exposure was found to increase the risk of lung cancer. However, no gene-environment interactions were discovered. Conclusion: The present study revealed that rs4787050 and rs8045980 in RBFOX1 may be meaningful as a novel biomarker for lung cancer susceptibility.

Association Between Two Polymorphisms in the Promoter Region of miR-143/miR-145 and the Susceptibility of Lung Cancer in Northeast Chinese Nonsmoking Females.

Lung cancer is known to cause high mortality and morbidity. The study aimed to explore the association between rs3733845 and rs3733846 polymorphisms in the promoter region of miR-143/145 and the risk of lung cancer among 575 nonsmoking cases and 575 cancer-free controls in a Chinese female population. We genotyped two single nucleotide polymorphisms (SNPs) in the promoter region of miR-143/145 in 575 cases and 575 controls using TaqMan allelic discrimination method. Logistic regression analysis was conducted to assess the association between polymorphisms in the promoter of miR-143/miR-145 and risk of lung cancer females. Crossover analysis was used to explore the interaction between the two SNPs and environmental risk factors (cooking oil fume exposure and passive smoking exposure). The results showed that both rs3733845 and rs3733846 polymorphisms were associated with an increased lung adenocarcinoma risk in dominant model (adjusted odds ratio [OR] = 1.329, 95% confidence intervals [CIs] = 1.026-1.723, p = 0.031 and adjusted OR = 1.450, 95% CI = 1.112-1.890, p = 0.006, respectively). The results of crossover analysis revealed that rs3733845 and rs3733846 risk genotypes along with cooking oil exposure increased lung cancer risk by 1.862-fold and 2.260-fold, respectively (adjusted OR = 1.862, 95% CI = 1.105-3.138, p = 0.020 for rs3733845; adjusted OR = 2.260, 95% CI = 1.354-3.769, p = 0.002 for rs3733846). There was positive multiplicative interaction between the two SNPs and cooking oil fume exposure (adjusted OR = 1.362, 95% CI = 1.078-1.719, p = 0.009 for oil × rs3733845; adjusted OR = 1.399, 95% CI = 1.122-1.745, p = 0.003 for oil × rs3733846). In nonsmoking females, rs3733845 and rs3733846 polymorphisms might be associated with lung adenocarcinoma risk. Moreover, the interactions between the two SNPs and cooking oil fume exposure were statistically significant on a multiplicative scale rather than an addictive scale.

Correlation between indoor air pollution and adult respiratory health in Zunyi City in Southwest China: situation in two different seasons

BackgroundIndoor environmental quality significantly influences the occurrence of asthma attack. Zunyi District has abundant coal reserves and is regarded as one of the cities that are most severely polluted by high levels of particulate matter in China. This study aimed to examine the correlation of indoor exposure with adult respiratory health, as well as the differences in effect between winter and summer.MethodsA cross-sectional epidemiological study was conducted among 1207 adult residents in Zunyi, Guizhou Province of Southwest China in winter and summer. Data on health variables related to asthma and home environmental factors were collected using a modified European Community Respiratory Health Survey II questionnaire. The following data were obtained: samples of particulate matter 2.5 (PM2.5) inside and outside the households under study (n = 20); lung function status, including peak expiratory flow rate, forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and FEV1/FVC ratio.ResultThe odds ratio (OR) for asthma-like symptoms and asthma in adults using coal stove for cooking or warming, relative to non-users, was 1.73 (95% CI, 1.11–2.69) in winter vs. 1.30 (95% CI, 0.79–2.14) in summer. Adult residents with exposure to cooking oil fumes were at a considerably higher risk of asthma-like symptoms and asthma [OR = 2.65 (95% CI, 1.25 to 5.61) in winter vs. OR = 7.93 (95% CI, 2.54 to 24.75] in summer] than those without such exposure. The prevalence of asthma-like symptoms and asthma was significantly higher in adults with high kitchen risk scores or high sleeping-area risk scores than in those with low scores in both seasons (p < 0.05). The relative kitchen and sleeping area PM2.5 concentrations were higher in winter than in summer (p < 0.05). Lung function was negatively associated with indoor kitchen and sleeping area relative PM2.5 concentration in winter rather than summer (p < 0.001). The effect of exposure to indoor risk factors on lung function among the residents was greater in winter than in summer (p < 0.001).ConclusionExposure to indoor risk factors, such as aerocontaminants from coal combustion, causes asthma symptoms and reduces pulmonary function. The effect of indoor risk factors on respiratory health among adults with such exposure was greater in winter than in summer.

Moderate-temperature catalytic incineration of cooking oil fumes using hydrophobic honeycomb supported Pt/CNT catalyst.

Catalytic incineration is one of the cost-effective technologies to deal with odor cooking oil fumes (COFs). Hydrophobic carbon nanotubes (CNT) supported Pt catalysts were prepared by incipient wetness impregnation method. The 2.0 wt.%Pt/CNT catalyst gave the highest activity with the lowest light-off temperature near 200 °C. The catalyst was further coated on the carbonized honeycomb which offered low-pressure drop and high surface area per unit volume. Toward feasibility application, hydrophobic honeycomb supported Pt/CNT catalyst achieved an excellent catalytic performance with the conversion of 88.0-91.3 % in gas hourly space velocity (GHSV) ranging from 5,700 to 17,200 h-1 at 300 °C. Importantly, the honeycomb supported Pt/CNT catalyst could remove COFs substantially under simulated cooking conditions. Only a slight amount of heptane remained after catalytic incineration. In addition, the honeycomb support used much less Pt/CNT catalyst by maintaining the same performance, compared with powder catalyst. Our research outcome provides an excellent opportunity to apply the honeycomb supported Pt/CNT catalyst for moderate-temperature catalytic incineration of odor exhaust from kitchen hood.

Association of Single-Nucleotide Polymorphism REX1 rs6815391, OCT4 rs13409 or rs3130932, and CTBP2 rs3740535 with Primary Lung Cancer Susceptibility: A Case-Control Study in a Chinese Population

The purpose of the current study is to explore the contribution of single-nucleotide polymorphisms (SNPs) of REX1 rs6815391, OCT4 rs13409 or rs3130932, and CTBP2 rs3740535 to the risk of lung cancer. A questionnaire survey was used to obtain basic information of the included subjects. A case control study was performed in 1121 patients and 1121 controls. All subjects were subjected to blood sampling for genomic DNA extraction and genotyping of the cancer stem cell-associated gene SNPs, including REX1 rs6815391, OCT4 rs13409 or rs3130932, and CTBP2 rs3740535 by real-time PCR. The association with the risk of primary lung cancer and interaction with environmental factors were assessed using unconditional logistic regression for the odds ratios and corresponding 95% confidence intervals. The genotype frequency distribution of OCT4 rs13409 loci was statistically significant, but there was no significant difference in the rest of the loci between lung cancer patients and healthy controls. The OCT4 gene was also related with lung cancer susceptibility in the genetic model after adjusting for lung cancer-related factors. Despite the presence of the dominant or recessive model, the four loci polymorphisms were associated with pollution near the place of residence, house type, worse ventilation situation, smoking, passive smoking, cooking oil fumes (COF), and family history of cancer, which increased the risk of lung cancer. Nonmarried status, 18.5≤BMI, COF, smoking, passive smoking, family history of cancer, and history of lung disease were independent risk factors of lung cancer susceptibility. Additionally, college degree or above, no pollution near the place of residence, protective genotype 1 or 2, and well ventilation can reduce the occurrence of lung cancer. There is an interaction between the four loci and environmental factors, and OCT4 rs13409 is a risk factor of primary lung cancer.

1,25-Vitamin D3 protects against cooking oil fumes-derived PM2.5-induced cell damage through its anti-inflammatory effects in cardiomyocytes

The functional role of 1,25-vitamin D3 in cooking oil fumes (COFs)-derived PM2.5-induced cell damage is largely unexplored. The present study investigated the protective role of 1,25-vitamin D3 against cell injury by possible involvement of JAK/STAT and NF-κB signaling pathways in cardiomyocytes. Cell viability was measured using CCK-8 assay, and cell apoptosis was analyzed by flow cytometry, qRT-PCR and Western blot in cultured rat neonatal cardiomyocytes treated with 1,25-vitamin D3 and COFs-derived PM2.5. Expressions of JAK/STAT and NF-κB signaling pathway were measured by Western blot. The results suggested that treatment with COFs-derived PM2.5 significantly decreased cell viability and increased apoptosis and oxidative stress in cultured rat neonatal cardiomyocytes. 1,25-vitamin D3 pretreatment alleviated the cell injury by increasing cell viability and decreasing apoptosis in the cardiomyocytes. 1,25-vitamin D3 pretreatment also decreased the ROS level and inflammation in the cardiomyocytes. Furthermore, 1,25-vitamin D3 pretreatment alleviated COFs-derived PM2.5-evoked elevation of JAK/STAT and NF-κB signaling pathways. Our study showed that 1,25-vitamin D3 pretreatment protected cardiomyocytes from COFs-derived PM2.5-induced injury by decreasing ROS, apoptosis and inflammation level via activations of the JAK/STAT and NF-κB signaling pathways.

Effects of cooking oil fume derived fine particulate matter on blood vessel formation through the VEGF/VEGFR2/MEK1/2/ERK1/2/mTOR pathway in human umbilical vein endothelial cells

In China, cooking oil fume derived fine particulate matter (COF-derived PM2.5) is a principal source of indoor air pollution. Here, we investigated cytotoxicity of COF-derived PM2.5, as well as the roles of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR cascade in the inhibitory effects of COF-derived PM2.5, on angiogenesis in human umbilical vein endothelial cells (HUVECs). After exposure to COF-derived PM2.5, cell viability and tube formation, as well as protein and mRNA levels of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR in HUVECs were measured. Cell viability and number of tubes reduced dose-dependently after COF-derived PM2.5 and SU5416 treatment. In addition, SU5416 and VEGF significantly affected tube formation. The protein and mRNA levels of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR all tended to reduce with the increase of COF-derived PM2.5 concentrations. These findings demonstrate that VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR play key roles in COF-derived PM2.5 induced inhibition of angiogenesis in HUVECs.

PM2.5- and PM10-bound polycyclic aromatic hydrocarbons (PAHs) in the residential area near coal-fired power and steelmaking plants of Taichung City, Taiwan: In vitro-based health risk and source identification

We investigated spatial and season variations in particle-bound PAH concentrations, identified their potential sources and estimated resultant health risk of activate toxicity pathways in a residential area near coal-fired power and steelmaking plants. Both atmospheric PM2.5 and PM10 samples (n = 94) were simultaneously collected for summer and winter in the Wuqi and Shalu districts of Taichung City, central Taiwan. The principal component analysis (PCA) measure was used to evaluate the sources of particle-bound PAHs. The health risk of PAHs-activated toxicity pathways was estimated through a probabilistic model in cooperation with high-throughput screening (HTS) in vitro assays and measurement data for children and adults. No spatial difference, but significant seasonal variation, in PAH concentrations for PM2.5 (summer = 1.7 ng m−3 and winter = 4.7 ng m−3) and PM10 (summer = 2.1 ng m−3 and winter = 4.8 ng m−3) between two sites was observed, where both sites shared the similar PAH patterns in congener concentrations. PAH contents in the fine mode (PM2.5) of ambient particles are predominant while coarse mode (PM2.5–10) PAHs is negligible. Children with particle-bound PAH exposures have a relatively high health risk of aryl hydrocarbon receptor (AhR)-mediated adverse outcomes than adults, in particular in the winter period, while the activations of Nrf2 and p53 pathways are insignificant. Vehicle emission (67.1%), unburned petroleum (15.0%), steel industry and stationary emission (6.1%), and oil combustion + cooking oil fume (5.6%) associated with PM2.5-bound PAHs were apportioned. The emission from the Taichung coal-fired power plant is rarely attributable to particle-bound PAHs of the study area based on results of spatiotemporal variation of PAHs, wind direction, and source apportionment.

Recycling of cooking oil fume condensate for the production of rhamnolipids by Pseudomonas aeruginosa WB505

Rhamnolipids (RLs) are anionic biosurfactants with great application potential. This study explored the possibility of producing RLs from cooking oil fume condensates (COFCs) collected from range hoods. A mutant of Pseudomonas aeruginosa AB93066 was obtained and used to produce RLs from COFCs as a substrate. RL yields in a 7-L fermenter reached 12.3g/L, and MALDI-TOF MS showed that Rha2-C10-C10 and Rha-C10-C10 are the most abundant (39.6% and 26.4%, respectively) RL components. The critical micellar concentration (CMC) of the RLs was 45.0mg/L and the surface tension of water decreased from 60.5 to 25.3 mN/m. Using six kinds of common hydrocarbons as indices, the emulsification coefficients of the RLs obtained were found to exceed 60%; in particular, the emulsification coefficient for benzene was 80.3%. COFCs provide an inexpensive alternative as a substrate for RL production, and the synthetic process is relatively harmless and economical.