## 1 Introduction  
Due to the increase in particulate matter (PM) caused by air pollution, various respiratory diseases are rapidly emerging in East Asia, including China, Korea, and Japan. Beijing, the capital city of China, stands out among these regions, having a notably elevated prevalence of respiratory diseases attributed to PM exposure [1; 2; 3]. Efforts to curtail air pollution were intensified when Beijing was spotlighted as one of the most severely impacted cities by PM air pollution during the Beijing Olympics [5]. PM has a diameter of around 2.5 \(\upmu\)m (PM\({}_{2.5}\)) and contains organic contaminants, including polycyclic aromatic hydrocarbons, mineral dust and inorganic contaminants, such as sulfate, nitrate, elemental carbon, and ammonium [6; 7]. Inhaling PM can lead to severe lung damage and, subsequently, harm the heart. Asthma is one of the most representative non-communicable respiratory tract diseases caused by air pollution [3; 8]. According to the World Health Organization report in 2017 [9], the global prevalence of asthma was estimated to be approximately 235 million people. PM inhalation is recognized as a major cause of allergic inflammation, representing a significant and severe etiological factor in asthma [10]. Over 70% of inhaled PM settles in the lower trachea, while approximately 22% makes its way to the alveoli [11]. The buildup of PM induces oxidative stress in airway and lung tissue's epithelial cells, leading to localized tissue damage, and ultimately triggering inflammatory responses [5; 12]. Key factors contributing to oxidative stress in airway epithelial cells include reactive glutathione peroxidase (GPX), reactive oxygen species (ROS), superoxide dismutase (SOD), heme-oxygenase-1 (HO-1), catalase (CAT), and glutathione (GSH) [13]. The initiation of an inflammatory response can easily be measured by an increase in proinflammatory cytokines and inflammatory mediators [14]. Inflammation of the lungs following PM inhalation is caused by an increase in ROS and cytokines (interleukin (IL)-6 and tumor necrosis factor (TNF)-\(\alpha\)) in bronchoalveolar lavage fluid (BALF) and the migration of monocytes [1; 2; 3; 15]. With the increase in respiratory disorders caused by PM, advancements have been made in the development of drugs aimed at treating or preventing respiratory damage [2; 3; 16]. In particular, natural products produce physiologically active substances with relatively minimal side effects and excellent antioxidant and anti-inflammatory activities [17; 18]; thus, the use of PM\({}_{2.5}\)-induced lung injury models to develop respiratory protection drugs from natural sources is actively progressing [1; 2; 3; 16; 19]. Pears (_Pyrus_ spp.) are one of the most purchased fruits globally [20]. Given that pears do not have a distinct color or scent, the study of chemical substances or biological activities present in pears is relatively limited or sparse [21; 22]. Based on the existing study on the chemical compounds found in _Pyrus pyrifolia_ Nakai [23], an oriental pear most commonly cultivated in Korea, phenylpropanol malate derivatives [23], caffeoyl triterpenes [24], and flavonoids have been isolated and identified as the major active compounds [25; 26; 27; 28]. The main active ingredients in pears, including flavonoids, arbutin, caffe acid, malaxinic acid, chlorogenic acid, and phenolic compounds, as well as antioxidant activity, decrease with maturation [29], whereas immature pears possess high levels of phenolic compounds and antioxidant activity compared to those of mature pears [22]. Therefore, there is a high opportunity to utilize the immature pears as a source of active components for functional food materials [22]. In order to gather high-quality mature fruits on orchard farms, immature pear fruits are discarded immediately after flowering [30]; through this process, just one cluster out of seven or eight is retained, with the rest being discarded [31].