Particulate matter (PM) 10 refers to fine dust with a diameter of less than 10 µm and induces apoptosis and inflammatory responses through oxidative stress. <i>Citrus junos</i> Tanaka is a citrus fruit and contains bioactive flavonoids including naringin. In the present study, we aimed to identify the preventive effect of <i>Citrus junos</i> Tanaka peel extract (CPE) against PM₁₀-induced lung injury. As a proof of concept, NCI-H460 cells were treated with CPE (800 μg/mL, 12 h) in conjunction with PM₁₀ to examine intracellular antioxidative capacity in the pulmonary system. In an in vivo model, male BALB/c mice (<i>n</i> = 8/group) were randomly assigned into five groups: NEG (saline-treated), POS (PM₁₀ only), NAR (PM₁₀ + naringin, 100 mg/kg), CPL (PM₁₀ + CPE low, 100 mg/kg), and CPH (PM₁₀ + CPE high, 400 mg/kg). Intervention groups received dietary supplementations for 7 days followed by PM₁₀ exposure (100 mg/kg, intranasal instillation). Compared to the NEG, the CPE decreased to 22% of the ROS generation and significantly increased cell viability in vitro. The histological assessments confirmed that pulmonary damages were alleviated in the PM₁₀ + CPL group compared to the POS. Pro-inflammatory cytokines and NF-κB/apoptosis signaling-related markers were decreased in the PM₁₀ + CPL group compared to the POS. These results indicated that CPE showed promising efficacy in preventing pulmonary injuries in vivo. Such protection can be explained by the anti-oxidative capacity of CPE, likely due to its bioactives, including naringin (7.74 mg/g CPE). Follow-up human intervention, as well as population-level studies, will further shed light on the preventive efficacy of CPE against pulmonary damage in humans.

We explored the physiological effects of inhaling basil essential oil (BEO) and/or linalool and identified odor-active aroma compounds in BEO using gas chromatography/mass spectrometry (GC-MS) and GC-olfactometry (GC-O). Linalool was identified as the major volatile compound in BEO. Three groups of rats were administered BEO and linalool via inhalation, while rats in the control group were not. Inhalation of BEO for 20 min only reduced the total weight gain (190.67 ± 2.52 g) and increased the forced swimming time (47.33 ± 14.84 s) compared with the control group (219.67 ± 2.08 g, 8.33 ± 5.13 s). Inhalation of BEO for 5 min (392 ± 21 beats/min) only reduced the pulse compared with the control group (420 ± 19 beats/min). Inhalation of linalool only reduced the weight of white adipose tissue (5.75 ± 0.61 g). The levels of stress-related hormones were not significantly different among the groups. The total cholesterol and triglyceride levels decreased after inhalation of BEO for 20 min (by more than -10% and -15%, respectively). Low-density lipoprotein cholesterol levels were lowered (by more than -10%) by the inhalation of BEO and linalool, regardless of the inhalation time. In particular, BEO inhalation for 20 min was associated with the lowest level of low-density lipoprotein cholesterol (53.94 ± 2.72 mg/dL). High-density lipoprotein cholesterol levels increased after inhalation of BEO (by more than +15%). The atherogenic index and cardiac risk factors were suppressed by BEO inhalation. Animals exposed to BEO and linalool had no significant differences in hepatotoxicity. These data suggest that the inhalation of BEO and linalool may ameliorate cardiovascular and lipid dysfunctions. These effects should be explored further for clinical applications.