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Indoor air quality (IAQ) is a major concern at daycare centers, due to the weaker immune system of children. Although IAQ is typically measured in accordance with the ISO-16000 standard, environmental sensors have recently become widely used due to their ability to consistently monitor air quality at a lower cost. In this study, We installed IoT sensors indoors and outdoors at ten daycare centers to measure PM(PM2.5, PM10), CO2, temperature, and humidity, as well as window opening-closing sensors to identify ventilation behavior. Indoor PM concentrations were consistently lower than outdoor levels, increasing from 7:00 AM, peaking between 9:00 AM and 12:00 PM, and decreasing during nap time (12:00 PM to 2:00 PM). CO2 levels were generally higher indoors than outdoors, peaking at 2:00 PM before decreasing. Windows were opened more frequently at 7:00 AM, 8:30 AM, and 3:00 PM. The correlation analysis revealed that significant factors influencing CO2 concentration were window opening duration. Ventilation rates per person at the daycare centers ranged from 1.77 to 10.69 m3/h, below both Korean and ASHRAE guidelines. The results of this study can provide valuable insights for developing strategies to improve indoor air quality in daycare centers that depend on window ventilation.

New building construction is often counted as a source of indoor air pollution because of formaldehyde and volatile organic compounds (VOCs) emitted from new building materials, such as furnishings, wood, and finishings. The high levels of formaldehyde and VOCs in the early stage of new buildings could be linked to the negative health effects on occupants. The aim of this study is to examine the impacts of flush-out air flow rate and flush period in reducing formaldehyde and VOCs produced by building materials or furnishing of newly built residential buildings. Field measurements were conducted from September 2016 to August 2018 in nineteen newly built apartments to verify the effectiveness of the flush-out procedure. The field measurements showed that after the flush-out, the indoor concentrations of formaldehyde and VOCs in the newly built samples significantly decreased. The indoor concentrations of formaldehyde and TVOCs were reduced to about 61% and 41% of the initial concentration when the samples were flushed at 0.7ACH for nine days. The results of this study showed that the flush-out for a short term of below two weeks was more effective reducing the emission potential of VOCs than of formaldehyde. When the samples were flushed for more than seven days, the air change rates of the flushing did not significantly influence the reduction of indoor pollutants.

The generally accepted hypothesis for the pathogenesis of alcoholic liver disease (ALD) is the two-hit model, which proposes that fat accumulation in the liver increases the sensitivity of the liver to a second hit that leads to inflammatory liver cell damage. In this study we evaluated the effects of Magnolia officinalis (MO), which contains honokiol and magnolol as the primary pharmacological components, to eradicate fatty liver in rats fed an ethanol diet. In vitro studies showed that MO was able to protect RAW 264.7 cells from ethanol-induced production of tumor necrosis factor-α, reactive oxygen species, and superoxide anion radicals; the activation of NADPH oxidase; and subsequent cell death. We also investigated the therapeutic effects of MO on alcoholic fatty liver in Lieber-DeCarli ethanol diet–fed rats. MO treatment of the rats for the last 2 weeks of ethanol feeding completely reversed all the serum, hepatic parameters, and fatty liver changes. The increased maturation of sterol regulatory element– binding protein-1c in the liver by ethanol treatment was completely inhibited by treatment with MO. Therefore, MO may be a promising candidate for development as a therapeutic agent for ALD.[Supplementary Figures: available only at http://dx.doi.org/10.1254/jphs.08182FP] Keywords:: Magnolia officinalis, alcoholic fatty liver, tumor necrosis factor-α (TNF-α), reactive oxygen species, sterol regulatory element–binding protein (SREBP)