PM2.5 is one of the most harmful components of airborne pollution and includes particles with diameters of less than 2.5 μm. Almost 90% of the world’s population lives in areas with poor air quality exceeding the norms established by the WHO. PM2.5 exposure affects various organs and systems of the human body including the upper respiratory tract which is one of the most prone to its adverse effects. PM2.5 can disrupt nasal epithelial cell metabolism, decrease the integrity of the epithelial barrier, affect mucociliary clearance, and alter the inflammatory process in the nasal mucosa. Those effects may increase the chance of developing upper respiratory tract diseases in areas with high PM2.5 pollution. PM2.5’s contribution to allergic rhinitis (AR) and rhinosinusitis was recently thoroughly investigated. Numerous studies demonstrated various mechanisms that occur when subjects with AR or rhinosinusitis are exposed to PM2.5. Various immunological changes and alterations in the nasal and sinonasal epithelia were reported. These changes may contribute to the observations that exposure to higher PM2.5 concentrations may increase AR and rhinosinusitis symptoms in patients and the number of clinical visits. Thus, studying novel strategies against PM2.5 has recently become the focus of researchers’ attention. In this review, we summarize the current knowledge on the effects of PM2.5 on healthy upper respiratory tract mucosa and PM2.5’s contribution to AR and rhinosinusitis. Finally, we summarize the current advances in developing strategies against PM2.5 particles’ effects on the upper respiratory tract.

Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) are common diseases that strongly impact the quality and length of life. Their coexistence is determined by overlap syndrome (OS). This systematic review aims to define the significance of these comorbidities according to the current state of knowledge. For this systematic review, we searched PubMed, Scopus, and Cochrane for studies published between 2018 and 26 October 2022, to find original, observational, human studies published in English, where the diagnosis of COPD was according to the Global Initiative for Obstructive Lung Disease guidelines and the diagnosis of OSA was based on polysomnography. The quality of studies was assessed using the Newcastle–Ottawa quality assessment tool for cohort and case–control studies, as well as its modification for cross-sectional studies. Of the 1548 records identified, 38 were eligible and included in this systematic review. The included studies covered a total population of 27,064 participants. This paper summarizes the most important, up-to-date information regarding OS, including the prevalence, meaning of age/gender/body mass index, polysomnography findings, pulmonary function, comorbidities, predicting OSA among COPD patients, and treatment of this syndrome.

Chronic rhinosinusitis (CRS) is related to persistent inflammation with a dysfunctional relationship between environmental agents and the host immune system. Disturbances in the functioning of the sinus mucosa lead to common clinical symptoms. The major processes involved in the pathogenesis of CRS include airway epithelial dysfunctions that are influenced by external and host-derived factors which activate multiple immunological mechanisms. The molecular bases for CRS remain unclear, although some factors commonly correspond to the disease: bacterial, fungal and viral infections, comorbidity diseases, genetic dysfunctions, and immunodeficiency. Additionally, air pollution leads increased severity of symptoms. CRS is a heterogeneous group of sinus diseases with different clinical courses and response to treatment. Immunological pathways vary depending on the endotype or genotype of the patient. The recent knowledge expansion into mechanisms underlying the pathogenesis of CRS is leading to a steadily increasing significance of precision medicine in the treatment of CRS. The purpose of this review is to summarize the current state of knowledge regarding the immunological aspects of CRS, which are essential for ensuring more effective treatment strategies.

The study investigated the functioning of the taste and smell senses in workers employed at a sewage treatment plant and waste landfill. The study population was divided into three groups: sewage workers (group 1), landfill workers (group 2), and laboratory workers (group 3). Smell sensation was assessed using the Börstein gustometry method and taste sensation the Elsberg-Levy olfactometry method. The examinations were performed before and after working hours. Taste disorders were noted in nearly 20% of subjects in each study group examined before work, and in 50% (group 1), 40% (group 2), 28.4% (group 3) of workers examined after work. As regards the sweet taste, a statistically higher value of the mean taste perception threshold (TPT) could be noted in each group examined before work compared to the control group. This referred also to salty taste in groups 1 and 2 and to bitter taste in groups 1 and 3. In the examinations carried out after work, all average TPTs increased and were statistically significant in relation to the sour and bitter tastes in group 1 and to sour taste in group 2. Smell examinations before and after work showed a statistically higher value of the mean olfactory perception threshold (OPT) for each odour than in the control group. The increase in the mean OPT after work was not statistically significant and did not differ between the groups. Before work, the percentage of workers with smell disorders amounted to 31.5% in the group of sewage workers, 6.3% of laboratory workers and 21.7% of landfill workers. After the working hours, these values increased to 40%, 8% and 38.4%, respectively. The study results indicate a higher risk of smell and taste dysfunctions among workers at a sewage treatment plant and waste landfill. The perception of the sour taste appeared to be most sensitive after short-term exposure but this dysfunction is probably reversible in nature. Other tastes were more sensitive to chronic toxic exposure than the sour taste.

Chronic rhinosinusitis (CRS) is a frequent disease with high social impact and multifactorial pathogenesis. Recently, the bitter taste receptor TAS2R38 has been described to play a role in upper airway innate mucosal defense. The aim was to determine the localization and expression of the TAS2R38 in the selected cell lines and tissue collected from patient suffered from CRS as well as to correlate the results with clinical data. Moreover, the purpose was the estimation of the TAS2R38 distribution changes during acute and CRS. Forty-two patients undergoing nasal surgery were enrolled in the study. The TAS2R38 expression was assessed in the collected tissues using immunohistochemistry and immunocytochemistry methods. The western blot analysis was performed on human cell lines HeLa, MCF7, MDA-MB-231 to assess the location of the TAS2R38 protein. Moreover, the HeLa cell line was used as a model of acute inflammation induces by lipopolysaccharide. Immunohistochemistry analysis displayed a statistically significant difference of TAS2R38 level in the patients with CRS compared to healthy control and was different in CRS with and without nasal polyps. The results showed the abundance of TAS2R38 receptor in the cell nucleus in patients with CRS and cell lines. The variance in TAS2R38 receptor expression in two CRS types suggests their different pathogenesis. The first time in literature, we confirmed the presence of plasma membrane TAS2R38 receptor in the cell nuclei in CRS as well as in cell lines, what strongly suggests the different than membrane TAS2R38 function.