Knowledge on the impact of the exposure to indoor ultrafine particles (UFPs) on the human brain is restricted. Twelve non-atopic, non-smoking, and healthy adults (10 female and 7 male, in average 22 years old) were monitored for brain physiological responses via electroencephalographs (EEGs) during cooking. Frying ground beef meat in sunflower oil using electric stove without ventilation was conducted. UFPs, particulate matter (PM) (PM 1 , PM 2.5 , PM 4 , PM 10), CO 2 , indoor temperature, RH, oil and meat temperatures were monitored continuously throughout the experiments. The UFP peak concentration was recorded to be approximately 2.0 × 10 5 particles/ cm 3. EEGs were recorded before exposure, at end of cooking when PM peak concentrations were observed, and 30 min after the end of the cooking session (post-exposure). Brain electrical activity statistically significantly changed during post-exposure compared to the before exposure, suggesting the translocation of UFPs to the brain, occurring solely in the frontal and temporal lobes of the brain. Study participants older than 25 were more susceptible to UFPs compared to those younger than 25. Also, the brain abnormality was mainly driven by male rather than female study participants. The brain slow-wave band (delta) decreased while the fast-wave band (Beta3) increased similar to the pattern found in the literature for the exposure to smoking fumes and diesel exhaust.

Our knowledge of the effects of exposure to indoor ultrafine particles (sub‐100 nm, #/cm3) on human brain activity is very limited. The effects of cooking ultrafine particles (UFP) on healthy adults were assessed using an electroencephalograph (EEGs) for brain response. Peak ultrafine particle concentrations were approximately 3 × 105 particle/cm3, and the average level was 1.64 × 105 particle/cm3. The average particle number emission rate (S) and the average number decay rate (a+k) for chicken frying in brain experiments were calculated to be 2.82 × 1012 (SD = 1.83 × 1012, R2 = 0.91, p = 0.0013) particles/min, 0.47 (SD = 0.30, R2 = 0.90, p < 0.0001) min−1, respectively. EEGs were recorded before and during cooking (14 min) and 30 min after the cooking sessions. The brain fast‐wave band (beta) decreased during exposure, similar to people with neurodegenerative diseases. It subsequently increased to its pre‐exposure condition for 70% of the study participants after 30 min. The brain slow‐wave band to fast‐wave band ratio (theta/beta ratio) increased during and after exposure, similar to observed behavior in early‐stage Alzheimer's disease (AD) patients. The brain then tended to return to its normal condition within 30 min following the exposure. This study suggests that chronically exposed people to high concentrations of cooking aerosol might progress toward AD.

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Aim: The current study aimed to investigate the potential antiproliferative activity of metformin, the effective concentration range, and the mechanism of action. Materials & methods: Human breast cancer cells, MCF-7 were treated with a serial dilution of metformin (10–150 μM) for 24 and 48 h. Potential antiproliferative activity of metformin and its ability in inducing cellular apoptosis and autophagy were also investigated. Results: Metformin inhibited MCF-7 proliferation in a concentration and time dependent manner, with 80 μM as the most effective concentration. Compared with nontreated cells, metformin induced significant levels of autophagy and apoptosis, which were confirmed by the reduction of mTOR and BCL-2 protein expression. Conclusion: The study confirms the antiproliferative activity of metformin, which may likely occur through AMPK signaling pathway.