Chronic rhinosinusitis (CRS) is a recurrent inflammatory process of the nasal and paranasal sinus mucosa for over 12 weeks, drastically reducing patients' quality of life and constituting a high public health burden, especially in urban areas. Worldwide, CRS has an estimated prevalence ranging from 5% to 15%, but significant variations occur depending on geographic, environmental, and socio-economic conditions (Beule, 2015) [5]. Urban dwellers, with their greater levels of pollution, crowded living, and lifestyle factors, can be especially susceptible to CRS.

A broad spectrum of risk factors has been identified as contributing to the onset and perpetuation of CRS. Host-related factors, such as genetic predisposition, immune deficiency, and comorbid conditions, interact in a multifaceted manner with environmental exposures to determine CRS pathogenesis (Min & Tan, 2015) [1]. Genetic conditions have become more widely implicated to play a causative role, although precise mechanisms are as yet not completely clarified (Yoo & Suh, 2017) [6]. Findings have been such as to indicate genetic predisposition has potential to alter epithelial barrier integrity and innate immune function in causing individuals to develop chronic sinonasal inflammation (Yoo & Suh, 2017) [6].

Aided conditions such as allergic rhinitis, asthma, and gastroesophageal reflux disease (GERD) have similarly had strong connections reported with CRS. These disorders can have common inflammatory pathways, which propose the concept of a single airway disease (Rosati & Peters, 2016) [7]. In particular, the association of allergic rhinitis and asthma with CRS is common and is thought to heighten disease severity and complicate treatment approaches (Rosati & Peters, 2016) [7]. In addition, GERD has also been recognized as an important risk factor, perhaps through microaspiration resulting in chronic sinonasal mucosal inflammation (Bohnhorst et al., 2015; Kim et al., 2019) [4,8].

The phenotypic diversity of CRS, including the separation between CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP), mirrors fundamental differences in underlying immunopathology as well as related risk factors. Premorbid illness and systemic comorbidities can alter these CRS subtypes accordingly, highlighting the importance of personalized diagnostic and therapeutic strategies (Lam, Hirsch, & Tan, 2014) [2].

Recent research has also underlined the significance of symptomatology clustering to determine new associations with clinical and demographic variables, thus further demarcating CRS epidemiology (Sedaghat et al., 2015) [3]. This refinement is critical for enabling more effective management, especially in heterogeneous urban populations where environmental exposures and lifestyle parameters may be quite different from rural populations.

As the studies increase, there is little evidence available to support the prevalence and certain risk factors of CRS in urban residents, especially using hospital-based cohorts. Knowledge regarding how different factors interplay among the urban groups will be paramount to creating effective prevention and therapy schemes based on the needs of the urban area. This hospital-based research seeks to explore the prevalence of CRS and assess the related risk factors among an urban population, adding to the fuller understanding of CRS epidemiology, and supporting the optimization of patient management.

Study Design and Setting

This was a 18-month hospital-based, cross-sectional study carried out at a metropolitan city-based tertiary care center. The hospital has an attendee mix representative of the different socio-economic strata of the metropolitan city and thus formed an ideal cohort to study the prevalence and risk factors of chronic rhinosinusitis (CRS). Ethical clearance for conducting the study was received from the Institutional Review Board before data collection started.

Study Population

The patients aged 18 years and older attending the otorhinolaryngology outpatient department with symptoms of CRS were included in the study. Diagnosis was made based on the European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS) 2012 criteria, which consist of two or more symptoms, one of which should be nasal obstruction/congestion or nasal discharge, together with either facial pain/pressure or reduction or loss of smell for more than 12 weeks. Excluded from the study were patients presenting with acute rhinosinusitis, fungal sinusitis, sinonasal tumors, or who had recently undergone sinonasal surgery within the last one year.

Data Collection

Information was collected through a structured questionnaire prepared specifically for the study. The survey included demographic data like age, gender, job, and home details, as well as medical history with emphasis on identified risk factors like allergic rhinitis, asthma, gastroesophageal reflux disease (GERD), smoking status, family history of sinonasal illness, and history of exposure to environmental toxins. All patients were subjected to a comprehensive otorhinolaryngological examination, including anterior rhinoscopy and nasal endoscopy by an experienced ENT specialist. Where appropriate, radiologic studies like paranasal sinus computed tomography were performed to establish the diagnosis.

Evaluation of Risk Factors

Risk factors for CRS were evaluated according to patient history and clinical assessment. History and supportive examination findings like nasal mucosal edema, turbinate hypertrophy, or positive skin prick test where indicated confirmed the presence of comorbid allergic conditions. Asthma diagnosis was confirmed through spirometric testing and clinical history as appropriate. GERD was determined by patient symptoms of heartburn, regurgitation, and chronic cough, and by referral to a gastroenterologist as appropriate. Smoking history was measured in pack-years, and environmental exposure was determined on the basis of occupational and residential data, such as proximity to industrial or high-traffic areas.

Statistical Analysis

Data was entered into a secure database and analyzed with statistical software. Descriptive statistics were computed for baseline demographic and clinical characteristics. Prevalence of CRS was calculated as a percentage of all outpatient visits during the study period. Bivariate analyses were conducted to investigate associations between CRS and potential risk factors using chi-square tests for categorical variables and independent t-tests for continuous variables. Logistic regression was used to determine independent predictors of CRS after controlling for confounding factors. Statistical significance was if the p-value was less than 0.05.

Study Population Characteristics

750 patients attended the otorhinolaryngology outpatient department over the course of the study, 180 (24%) of whom were diagnosed with chronic rhinosinusitis (CRS) by EPOS 2012 criteria. Of the CRS patients, 102 (56.7%) were men and 78 (43.3%) were women, with a male-to-female ratio of around 1.3:1. The average age of the CRS cohort was 38.5 ± 12.4 years, with most of the patients (58.3%) belonging to the 30–50 years age group. Table 1 summarizes the baseline demographic and clinical characteristics of the patients diagnosed with CRS.

Table 1: Baseline Characteristics of CRS Patients

Prevalence of Risk Factors

The most prevalent associated risk factor in patients with CRS was allergic rhinitis, seen in 98 cases (54.4%), followed by the history of gastroesophageal reflux disease (GERD) in 46 cases (25.6%). Asthma was seen in 34 patients (18.9%), and 58 patients (32.2%) had a smoking history of active or past smoking. In 28 cases (15.6%), there was a family history of sinonasal disorders. Exposure to environmental pollutants, such as living near heavy industrial areas or heavy-traffic highways, was reported by 84 patients (46.7%). Table 2 depicts the distribution of various risk factors identified among CRS patients.

Table 2: Distribution of Risk Factors Among CRS Patients

Risk Factors and Type of CRS

Additional analysis revealed that allergic rhinitis and asthma were more highly correlated with CRS with nasal polyps (CRSwNP), whereas smoking and GERD were more common among CRS without nasal polyps (CRSsNP) patients. Figure 1 depicts the relative prevalence of major risk factors in CRSwNP and CRSsNP groups.

Figure 1: Comparison of Risk Factors Between CRSwNP and CRSsNP

Multivariate Analysis

On logistic regression analysis, allergic rhinitis (OR 2.4, 95% CI 1.5–3.8, p<0.001) and environmental pollutant exposure (OR 1.8, 95% CI 1.1–2.9, p=0.02) were independent predictors of CRS. Smoking was also significantly associated (OR 1.6, 95% CI 1.0–2.5, p=0.04), especially with CRSsNP.

In the present hospital-based study among an urban population, the prevalence of chronic rhinosinusitis (CRS) was 24%, which is consistent with international estimates claiming CRS involves 5–15% of the population, and the prevalence is greater in highly populated and polluted urban areas. The demographic distribution showed a slight male preponderance and most cases belonged to the 30–50 years age group, results in line with the age-structured prevalence trends reported in previous studies (Somani et al., 2019) [9].

The prevalence of associated risk factors was found to have allergic rhinitis as the most frequent comorbidity in CRS patients, occurring in more than half of the cases. This is in line with earlier research by Tint, Kubala, and Toskala (2016), where allergic rhinitis was noted as a predominant predisposing condition in CRS with common inflammatory mechanisms through eosinophilic inflammation and mucosal remodeling. Also, asthma was strongly correlated, especially in those with CRSwNP, an idea that reiterates a unified airway disease where both upper and lower respiratory tract inflammations are not independent of each other (Tint et al., 2016) [11].

The genetic susceptibility role was also evaluated in our group, with 15.6% of the patients declaring a family history of sinonasal disease. Such familial trend adds to the result of Orb et al. (2016) [10], who proved children with affected first-degree relatives at significantly higher risk for pediatric CRS. Additionally, genetic factors can extend beyond familial inheritance; there has been an emphasis in recent research on the link of specific genetic polymorphisms, e.g., taste receptor variation, with CRS susceptibility (Mfuna Endam et al., 2014) [12]. We did not carry out genetic testing in our research, but familial clustering suggests the possibility of a genetic factor that requires further research.

Environmental exposures were found to be a major independent risk factor, especially among patients living near industrial or traffic-congested zones. Nearly half of our CRS patients had such exposures. This is consistent with the systematic review by Sundaresan et al. (2015) [13], wherein occupational and environmental irritants such as airborne irritants, chemical fumes, and dust were found to be key causes of development and worsening of CRS. The urban environment of our study, with high rates of vehicular pollution and industrial emissions, probably enhanced these risks.

Another interesting finding was the correlation between gastroesophageal reflux disease (GERD) and CRS. About 26% of our patients had a history of GERD, and its prevalence was greater in those with CRS without nasal polyps (CRSsNP). This discovery is consistent with the findings of the RHINE study by Schiöler et al. (2015) [14], which recognized nocturnal GERD as a major risk factor for rhinitis and rhinosinusitis symptoms. In the same way, Katle, Hatlebakk, and Steinsvåg (2013) [15] wrote about possible mechanisms whereby reflux may lead to sinonasal inflammation, such as microaspiration of gastric contents and vagally mediated nasal secretions, which can perpetuate chronic mucosal irritation and inflammation.

Comparison between CRSwNP and CRSsNP showed significant phenotypic differences in terms of concomitant risk factors. Allergic rhinitis and asthma were more frequent among CRSwNP patients, in line with earlier findings that CRSwNP is more frequently dominated by a type 2 inflammatory pattern with eosinophilic predominance (Tint et al., 2016) [11]. However, smoking and GERD were more closely linked with CRSsNP, indicating that non-eosinophilic, neutrophil-dominated inflammation could be more dominant in this subgroup.

Overall, the results of our study confirm not only the multifactorial pathogenesis of CRS but also the critical involvement of environmental, genetic, allergic, and lifestyle factors in the pathogenesis of CRS. Although the findings overall are consistent with previous studies, the urban nature of our investigation highlights the special relevance of environmental exposures and lifestyle-related comorbidities such as smoking and GERD to urban CRS patients. Additional prospective studies

In conclusion, this hospital-based research emphasizes that chronic rhinosinusitis is a common condition in urban dwellers, with a strong association with allergic rhinitis, asthma, gastroesophageal reflux disease, smoking, and environmental exposures. The results validate the multifactorial etiology of CRS, whereby genetic predispositions and reversible environmental and lifestyle factors both play a role in disease establishment and progression. Differences noted between CRSwNP and CRSsNP regarding concomitant risk factors further highlight the heterogeneity of CRS phenotypes. These findings not only add strength to the current evidence but also highlight the necessity of an integrated approach in the management of CRS, including measures for early detection, targeted treatment, and prevention of environmental and lifestyle-related risk factors. Subsequent studies, which include genetic analysis and follow-up, would give greater insight and assist in formulating individually tailored treatment methods for the afflicted.".

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