Introduction
Laryngopharyngeal reflux (LPR) is characterised by retrograde movement of gastroduodenal contents into the larynx and pharynx. The pathophysiology is complex with the most plausible cause being dysfunction in the upper esophageal sphincter, which acts as a protective barrier to the laryngopharyngeal complex.Reference Li, Zhang, Zhang, Cheng, Li and Cheng1, Reference Koufman2 Patients with LPR rarely present with heartburn and regurgitation because of the transient nature of the reflux episodes, leading to minimal or no injury to the esophageal mucosal lining. Commonly reported complaints include repetitive throat clearing, globus sensation, cough, foreign body sensation, change in voice quality and dysphagia. These symptoms are secondary to microscopic and structural changes in the laryngeal mucosa. Suggested mechanisms include inflammation and microtrauma leading to epithelial thickening and intercellular dehiscence.Reference Lechien, Schindler, Robotti, Lejeune and Finck3, Reference Lechien, Saussez, Harmegnies, Finck and Burns4
Several risk factors for LPR have been described in the literature, among which is smoking. The prevalence of LPR is notably increased in smokers, with studies reporting rates exceeding 50 per cent, suggesting a strong association between tobacco use and reflux-related laryngeal pathology.Reference Kamani, Penney, Mitra and Pothula5 Lin et al. investigated the link between LPR symptoms and smoking using the Reflux Symptom Index (RSI) and noted a significant association between the two (p = 0.014).Reference Lin, Wang, Wang, Lien, Liang and Yen6 Wang et al. evaluated the role of lifestyle habits in patients with LPR and found a significant proportional association between LPR and smoking frequency (p = 0.015).Reference Wang, Mo, Tan, Dai and Li7
All the above studies were limited to cohorts of conventional cigarette smokers. No previous study examined the link between LPR and Hubble Bubble (HB) smoking. Hubble Bubble is a new trend of smoking that is gaining popularity worldwide. Data on its prevalence indicate a rapid surge across the globe, targeting mostly youngsters and adolescents.Reference Sepidarkish, Rezazadeh, Ghaffari Hamedani, Lohrasbi, Abdi and Mohammadi-Pirouz8 With weak or absent regulations regarding this relatively new smoking habit, shisha cafés have come to life in numerous European countries and the United States.Reference Maziak, Taleb, Bahelah, Islam, Jaber and Auf9 The main reasons are social gathering and the desire for less harmful alternative to conventional cigarette smoking.Reference Akl, Gunukula, Aleem, Obeid, Jaoude and Honeine10
The objective of this study is to investigate the risk of LPR in HB smokers with hoarseness, in comparison to non-smokers with hoarseness. The question the authors attempted to answer was the following: Does HB smoking increase the risk of LPR in dysphonic patients? The results of this investigation may be useful for patient counseling vis-a-vis vocal hygiene in the management of dysphonia.
Methods
After having obtained the approval of the Institutional Review Board (BIO ID: 2025-0116), the medical records of patients who presented with hoarseness to the Voice and Swallowing Unit at a tertiary referral center between June 2023 and December 2025 were reviewed. Patients with a history of HB smoking were included in the study. A group of patients, non-smokers, presenting with hoarseness were frequency matched by age, gender, history of allergy and voice diagnosis, was also included for comparison. Patients with incomplete medical records were excluded. Demographic data about age, gender, history of allergy and voice diagnosis were collected. Informed consent was obtained from all patients.
The risk of LPR was assessed using the RSI and the Reflux Finding Score (RFS). The RSI is a validated quality of life questionnaire quantifying symptoms of LPR on a scale of 0–5.Reference Belafsky, Postma and Koufman11 A score of above 13 is suggestive of LPR. The RFS evaluates eight laryngeal findings, including subglottal edema, ventricular obliteration, erythema or hyperemia, vocal fold edema, generalised laryngeal edema, posterior commissure hypertrophy, granuloma or granulation tissue formation and excess mucus in the larynx. These findings are rated on a scale of 0–3, and a total score of above 7 is suggestive of LPR.Reference Belafsky, Postma and Koufman12 The review of video-recordings was performed by two certified otolaryngologists who were blinded to the group allocation to minimise observer bias.
Statistical methods
Categorical and continuous variables were described using frequencies and means (± standard deviation), respectively. Mann–Whitney U-test was used for inter-group comparison of non-parametric data. Chi-squared test was used for the comparison of proportions between categorical variables. All analyses were conducted using Statistical Package for the Social Sciences (SPSS) version 29 software package. A two-tailed p-value less than 0.05 was considered statistically significant.
A post hoc power analysis was performed to determine the adequacy of the sample size for detecting differences in RSI scores between HB smokers and non-smokers. With 86 participants in each group (total n = 172), an observed effect size of 0.67 and a two-sided alpha level of 0.05, the study achieved a statistical power of 99 per cent to detect a significant difference between groups.
Results
Demographic data
A total of 172 patients, 86 HB smokers and 86 non-smokers, were included in the study. In the subgroup of HB smokers, 45.3 per cent were males and 54.7 per cent were females. The mean age of the study group was 45.08 ± 12.04 years. Seventeen percent reported a history of allergy. In the non-smoker subgroup, 46.5 per cent were males and 53.5 per cent were females. The mean age was 47.49 ± 15.71 years. Twenty three percent reported a history of allergy. There was no statistically significant difference in any of the demographic data between the two subgroups (Table 1).
Demographic data of the study population
Table 1 Long description
The table presents demographic data comparing HB smokers and a control group, each consisting of 86 participants. Gender distribution is nearly equal in both groups, with males comprising about 45% and females about 55%. The average age is slightly higher in the control group, but the difference is not statistically significant. Allergy prevalence is higher in the control group, though not significantly. Common voice diagnoses such as Reinke’s edema, vocal fold polyps, and vocal fold paralysis/paresis show no significant differences between the groups. Leukoplakia is more common in HB smokers, but this difference is also not statistically significant. Overall, the data suggests no significant demographic or clinical differences between the groups.
The most common voice diagnosis in the HB group was Reinke’s edema and vocal fold polyps (15.1 per cent, equally) followed by vocal fold paresis/paralysis (12.8 per cent). There was no statistically significant difference in the voice diagnosis between the two subgroups (Table 1).
The mean RSI and RFS scores in the HB and control groups
The mean RSI score was significantly higher in the HB subgroup compared to the control group (10.05 ± 8.27 vs. 5.05 ± 6.58; p < 0.001). Thirty-eight percent of the HB smokers had an RSI above 13, whereas 13 percent of non-smokers had an RSI above 13.
In the subgroup of HB smokers, the mean RFS score was 9.77 ± 4.31. Seventy percent of the patients had an RFS score above 7. In the non-smoker subgroup, the mean RFS score was 9.30 ± 4.83, and 60 percent of patients had an RFS score above 7. There was no statistically significant difference in the mean RFS between the two groups (p = 0.467).
Risk of laryngopharyngeal reflux in HB smokers
When evaluating the risk of LPR between the two groups, HB smokers were 4.24 times more likely to have an RSI score greater than 13 in comparison to non-smokers (odds ratio [OR] = 5.24; 95 per cent confidence interval [CI]: 1.97–9.14). HB smokers were 1.50 times more likely to have an RFS score greater than 7 in comparison to non-smokers (OR = 1.50; 95 per cent CI: 0.80–2.83)
Discussion
The results of this investigation indicate that HB smoking increases the risk of LPR in patients presenting with hoarseness. HB smokers with hoarseness were four times more likely to experience symptoms of LPR compared to non-smokers, with an OR equal to 1.50; 95 per cent CI: 0.80–2.83. In the HB group, 38 per cent had an RSI score above 13 compared to 13 per cent in non-smokers. These findings are an addition to the mounting evidence in the literature substantiating smoking as a risk factor for LPR and gastroesophageal reflux disease.
The reason behind the increased risk of LPR in HB smokers can be extrapolated from numerous investigations on cigarette smoking and LPR. HB smoke consists of toxic chemicals such as nicotine, benzene and polycyclic aromatic hydrocarbons, many of which are found in cigarette smoke. One compound that has been heavily investigated in cigarette smokers is nicotine. Nicotine is known to induce a decrease in lower esophageal sphincter (LES) pressure. Stanciu and Bennett reported a 41 per cent reduction in LES pressure in a cohort of cigarette smokers with a history of heartburn. This decrease in LES pressure, which started within 1 to 4 minutes after smoking, was associated with an increase in gastroesophageal acid reflux, as confirmed by 15-hour pH monitoring.Reference Stanciu and Bennett13 Chattopadhyay et al. evaluated LES pressure changes in 10 asymptomatic and 10 symptomatic smokers and noted a decrease by 19 per cent (p < 0.01) and 21 per cent (p < 0.02), respectively. Using the station pull-through technique, pressure measurements were taken at regular intervals, every 5 minutes from the moment the cigarettes were lit.Reference Chattopadhyay, Greaney and Irvin14
A second suggested mechanism for the increased risk of LPR in HB smokers is alteration in salivary flow and constituents. Saliva plays a paramount role in neutralising esophageal acid. In a review on smoking-induced acid reflux, Kahrilas and Gupta noted a 40 per cent to 60 per cent reduction in salivary flow and bicarbonate secretion in smokers.Reference Kahrilas and Gupta15 Ahmadi-Motamayel et al. conducted a retrospective study on 259 male smokers and 251 healthy non-smokers and found that smokers had a significantly lower mean salivary pH compared to non-smokers (7.42 ± 0.48 and 7.52 ± 0.43, respectively; p = 0.018), as well as a reduced buffering capacity (3.41 ± 0.54 and 4.17 ± 0.71, respectively; p = 0.001).Reference Ahmadi-Motamayel, Falsafi, Goodarzi and Poorolajal16 Rad et al. compared salivary flow rates (SFRs) in a cohort of 100 smokers and 100 non-smokers who were instructed to abstain from eating, drinking, smoking and oral hygiene for at least 60 minutes before and during saliva collection. The mean SFR in smokers was 1.93 (± 0.065) ml/5 min compared with 2.78 (± 0.819) ml/5 min in non-smokers, with a statistically significant difference between the groups (p = 0.0001). Approximately 39 per cent of smokers also reported at least one dry-mouth symptom, compared to 12 per cent of non-smokers (p = 0.0001).Reference Rad, Kakoie, Niliye Brojeni and Pourdamghan17
A third mechanism for the increased risk of LPR in HB smokers is aerophagia, which may contribute to reflux, alongside the role of nicotine in lowering LES pressure. Smoking induces alterations in respiratory mechanics characterised by increased airway resistance and compensatory elevations in intra-airway pressure.Reference Awan and Alphonso18 These pressure changes facilitate the inadvertent passage of air into the esophagus, predisposing smokers to aerophagia, particularly during periods of upper esophageal sphincter relaxation. Gastric distension resulting from aerophagia promotes transient LES relaxations, the primary mechanism underlying gastroesophageal reflux. Prior studies demonstrated a strong association between aerophagia and reflux disease, suggesting a pressure-mediated feedback loop in which smoking-related airway pressure elevations contribute to both aerophagia and reflux pathophysiology.Reference Watson and Mystkowski19, Reference Shepherd, Hillman and Eastwood20
This study is the first to explore the link between HB smoking and LPR in a cohort of dysphonic patients. The results showed an increased risk for LPR symptoms in HB smokers compared to non-smokers. Nevertheless, these findings should be interpreted cautiously given the limitations of this study, namely its retrospective nature which does not allow control for confounding factors, such as allergy, that may mask the symptoms and signs of LPR. Another limitation is the lack of an objective measure of LPR, such as double-probe pH-metry.Reference Lechien, Saussez, Muls, Dequanter, De Marrez and Hans21 The RSI and RFS are not diagnostic tests, but screening tools to assess the risk of LPR.
• Several risk factors for laryngopharyngeal reflux (LPR) have been described in the literature, among which is smoking. The prevalence of LPR is notably increased in smokers
• Hubble Bubble (HB) is a new trend of smoking that is gaining popularity worldwide
• Studies on laryngopharyngeal reflux (LPR) were limited to cohorts of conventional cigarette smokers
• HB smoking increases the risk for LPR by two-fold
• Larger prospective studies are needed to substantiate the association between HB smoking and LPR
Conclusion
The results of this investigation showed that HB smoking increases the risk for LPR by four-fold. These findings indicate that non-conventional smoking habits such as HB smoking could also predispose to reflux disease. A larger prospective study, using double probe pH-metry and impedance testing, is needed to substantiate the association between HB smoking and LPR. Future investigations on the link between reflux disease in HB smokers compared to conventional smokers are warranted.
