Spatial distributions of particle number size distributions generated during cooking processes and the impacts of range hoods.

Cooking oil fume (COF) is associated with an increased risk of health effects. The particle number size distribution (PNSD) of COF presenting as lognormal structures is recognized as a key metric in determining its exposure toxicities, but the information of its spatial distributions and impacting factors are still lacking. This study conducted real-time monitoring COF PNSD during the cooking processes in a kitchen laboratory. Results showed that COF PNSD presented as a combination of two lognormal distributions. The peak diameters of PNSD inside the kitchen were: 385 nm (very close to the source), 126 nm (5 cm above the source), 85 nm (10 cm above the source) to 36 nm (breath point, 50 cm above the source), 33 nm (sucking surface of the ventilation hood), 31 nm (1 m horizontally to the source), and 29 nm (3.5 m horizontally to the source). The reasons of this observation was the sharp decrease of temperature from the pot to the indoor environment reduced the surface partial pressure of the COF particles and caused a large amount of semi-volatile organic carbons (SVOCs) with lower saturation ratios condensed on the COF surface. With the temperature difference became insignificant with the distance further to the source, the reduction of the supersaturation helped the gasification of these SVOCs. Dispersion led to a linearly horizontal decreases ((1.85 ± 0.10) × 106#/cm3/m) in particle numbers with further distances, making the peak particle number concentrations decrease from 3.5 × 105#/cm3 at the breath point to 1.1 × 105#/cm3 at the point 3.5 m to the source. Cooking dishes also presented as mode diameters of 22-32 nm at the breath point. The amount of edible oil used in different dishes is positively correlated with the peak concentration of COF. Only increasing the exhaust force of the range hood cannot significantly change the sucked COF particle numbers and sizes, owning to that COF particles are mainly small sizes. New technologies on cleaning small size particles and efficient supplemental air should be given more considerations.

Investigating aldehyde and ketone compounds produced from indoor cooking emissions and assessing their health risk to human beings.

Aldehyde and ketone compounds are ubiquitous in the air and prone to adverse effects on human health. Cooking emission is one of the major indoor sources. Aiming to evaluate health risks associated with inhalation exposure to aldehyde and ketone compounds, 13 carbonyl compounds (CCs) released from heating 5 edible oils, 3 seasonings, and 2 dishes were investigated in a kitchen laboratory. For the scenarios of heating five types of oil, aldehydes accounted for 61.1%-78.0% of the total emission, mainly acetaldehyde, acrolein and hexanal. Comparatively, heating oil with added seasonings released greater concentrations of aldehyde and ketone compounds. The concentration enhancement of larger molecular aldehydes was significantly greater. The emission factors of aldehyde and ketone compounds for cooking the dish of chili fried meat were much greater compared to that of tomato fried eggs. Therefore, food materials also had a great impact on the aldehyde and ketone emissions. Acetone and acetaldehyde were the most abundant CCs in the kitchen. Acrolein concentrations ranged from 235.18 to 498.71 µg/m3, which was about 100 times greater compared to the guidelines provided by Office of Environmental Health Hazard Assessment (OEHHA). The acetaldehyde inhalation for adults was 856.83-1515.55 µg and 56.23-192.79 µg from exposure to chili fried meat and tomato fried eggs, respectively. This exceeds the reference value of 90 µg/day provided by OEHHA. The findings of this study provided scientific evidences for the roles of cooking emissions on indoor air quality and human health.

Size-fractionated ultrafine particles and their optical properties produced from heating edible oils in a kitchen laboratory.

Cooking oil fume (COF) is an important source of indoor and outdoor air pollutants. COF generates a large number of organic compounds through volatilization and thermal oxidation, mainly including acids, alcohols, aldehydes and polycyclic aromatic hydrocarbons (PAHs), which can contribute 10 %-35 % to airborne organic particles in urban areas. COF not only affects human health owning to their small sizes, but also may absorb incident light due to the presence of brown carbon (BrC) chromophores in organic components. Therefore, we investigated size distributions and light absorption properties of particles produced from heating four types of edible oil. Results showed over 75 % of COF particles belonged to ultrafine particles (UFPs) and capable of absorbing light. The particle number size distributions for heating all edible oils were bimodal lognormal distribution, and the two mode diameters were within 27.9-32.2 nm and 187.7-299.6 nm. Both real-time monitoring and offline analyzing results show the average absorption coefficients of particles generated from heating soybean oil were much greater compare to those of heating other three edible oils. The mean AAE370/520 for heating soybean oil, olive oil, corn oil and peanut oil were 1.877, 1.669, 1.745 and 1.288, respectively, indicating the presence of BrC chromophores. A large proportion of BrC identified by HPLC-DAD-Q-TOF-MS only contain carbon, hydrogen and oxygen, which are CnH2nO2, CnH2n-2O2, CnH2n-4O2 and CnH2n-6O2 (9

Effect of laser irradiation on crystalline structure of enamel surface during whitening treatment with hydrogen peroxide.

OBJECTIVE: This study is to evaluate the effect of laser activation on the whitening and crystalline structure of enamel surface during whitening treatment with hydrogen peroxide. METHODS: Bovine teeth were treated with whitening gel containing 35% hydrogen peroxide. A whitening gel was applied on the enamel surface for a period of 5 min, and then irradiated using a diode laser (740 nm) during whitening treatment for 0, 30, 60, 120 and 180s for the GL0-W, GL30-W, GL60-W, GL120-W and GL180-W groups, respectively. The total whitening application time was 30 min for all groups. RESULTS: Laser-irradiated enamel groups showed a similar lightness compared to the GL0-W group. The thickness of porous layer observed on the enamel surface of GL0-W group was decreased by increasing the laser irradiation time. While the Ca and P contents of the GL0-W group were lower than those of the non-whitening treated group (GL0-C), the Ca and P contents of the GL180-W group were similar to those of the GL180-C group. The enamel crystallinity was dramatically decreased by whitening treatment without laser irradiation. However, the decrease of crystallinity was protected by laser irradiation during whitening treatment. Raman measurement verified that laser irradiation could prevent the loss of mineral compositions on enamel and maintain its crystalline structure. SIGNIFICANCE: The professional whitening treatment with hydrogen peroxide and diode laser activation improves not only the whitening effect but also protects the change of enamel structure compared to the treatment with only gel.

Activation of de novo synthetic pathway of ceramides is responsible for the initiation of hydrogen peroxide-induced apoptosis in HL-60 cells.

Sphingolipid metabolites in HL-60 cells were analyzed to gain an understanding of their roles in early events underlying hydrogen peroxide (H2O2)-induced apoptosis. Incubation of cells with H2O2 increased the intracellular levels of ceramides and sphinganine, but decreased those of ceramide 1-phosphates (ceramide 1-P) and sphingosine. The levels of sphingomyelins and sphingomyelinase (SMase) activities were not affected by H2O2 treatment. These results were similar to the profiles induced by daunorubicin, an activator of serine palmitoyl CoA transferase (SPT), suggesting that H2O2 stimulated the de novo synthetic pathway of ceramides. L-cycloserine and fumonisin B1 (FB1), specific inhibitors of de novo ceramide biosynthesis, suppressed the elevation of ceramides and sphinganine induced by H2O2, which consequently reduced apoptotic cell death. Collectively, these results demonstrated that H2O2 increased the intracellular concentrations of ceramides via activation of a de novo biosynthetic pathway, and the enhanced ceramides might initiate apoptosis in HL-60 cells.