E-Cigarette Use Emerges as a Signal in Allergic Rhinitis After Adjustment for Confounding
Allergic rhinitis remains one of the most common chronic inflammatory disorders of the upper airway, and its burden is large enough to demand careful attention to exposures that may irritate or prime the nasal mucosa. In this cross-sectional study of 385 adults aged 18 to 50 years, investigators examined whether current tobacco and nicotine product use was associated with allergic rhinitis in a mixed Jordanian and international sample. The analysis separated combustible products, including cigarettes and hookah, from non-combustible e-cigarettes, then asked a straightforward clinical question: does current use track with rhinitis prevalence once basic demographic differences are taken into account?
The raw comparison was unremarkable. Current tobacco or nicotine product use showed no significant association with allergic rhinitis in unadjusted analyses, and product type did not separate cleanly at first glance. Yet the adjusted model shifted the picture. After controlling for age, gender, education, income, and region, e-cigarette use was associated with higher odds of allergic rhinitis, with an adjusted odds ratio of 2.18 and a 95% confidence interval from 1.06 to 4.48. Combustible product use showed a similar direction of effect, with an adjusted odds ratio of 2.05, but the confidence interval crossed unity. Female gender also emerged as a strong independent predictor, with an adjusted odds ratio of 2.74.
One result stood out immediately: the adjusted association appeared only after confounding was addressed.
Why the Crude Comparison Missed the Signal
The study enrolled 500 individuals through an online convenience sample and analyzed 385 completed responses, which means the data reflect self-selection as much as they reflect exposure biology. Current tobacco or nicotine product users accounted for 35.6% of the analyzed cohort, while non-users made up 64.4%. Among users, e-cigarettes were by far the most common product. That detail matters clinically because it changes the exposure profile from traditional smoke inhalation to a mixture of aerosolized nicotine, solvents, and flavoring agents that may behave differently in the nasal and upper airway mucosa.
The study used the Score for Allergic Rhinitis (SFAR), a 12-item validated tool, to define allergic rhinitis; a score of 7 or higher on the 16-point scale qualified as diagnostic. Using a symptom-based instrument is practical in a large survey, but it also means the endpoint captures clinical probability rather than objective immunologic confirmation. In a disorder shaped by allergen sensitivity, mucosal inflammation, environmental irritants, and host factors, symptom tools can still be useful, but they cannot disentangle whether tobacco exposure is provoking rhinitis, worsening symptoms in people already predisposed to it, or simply traveling with other correlated behaviors.
Nicotine Aerosols, Combustion Products, and Nasal Inflammation
The biologic plausibility behind the observed association is not difficult to sketch. Cigarette smoke and hookah exposure introduce particulate matter and combustion byproducts that can injure the epithelial barrier, alter mucociliary clearance, and amplify local inflammatory signaling. E-cigarette aerosols avoid combustion, but they do not avoid airway exposure. Vapor constituents can still irritate the respiratory mucosa, and repeated exposure may sustain a state of epithelial stress that makes the nasal passages more reactive to allergens. In allergic rhinitis, where symptom generation depends on a primed mucosal immune response, even modest inflammatory shifts may translate into congestion, rhinorrhea, and sneezing that push patients into the diagnostic range of a symptom score.
The findings also fit the broader logic of confounding. Users and non-users differed markedly by gender, and female sex itself was associated with allergic rhinitis in the multivariable model. When a risk factor is unevenly distributed across subgroups, a crude comparison can flatten a real effect or exaggerate it. Adjustment did not prove causation, but it did reveal a pattern that the unadjusted analysis obscured.
Cross-Sectional Design Limits What the Association Can Prove
Because the design was cross-sectional, temporal sequence remains unresolved. Participants reported current use and current rhinitis status at a single point in time, so the study cannot determine whether nicotine products increased the risk of allergic rhinitis, whether people with rhinitis were more likely to use or avoid certain products, or whether both were influenced by a third set of social or environmental factors. The use of a convenience sample adds another layer of caution, since online recruitment can overrepresent individuals who are younger, more health-aware, or more comfortable responding to survey research.
Self-report introduces its own uncertainty. Product classification depended on questionnaire responses, not biochemical verification or exposure quantification. Frequency, duration, puff intensity, dual use, and secondhand exposure were not captured in the abstract, and those missing details matter when trying to separate occasional experimentation from sustained inhalational exposure. The study therefore points toward an association, but not yet toward a dose-response relationship or a threshold effect.
What Clinicians Can Take From the Data Now
For bedside practice, the most defensible reading is cautious rather than sweeping. Adults with allergic rhinitis who use e-cigarettes or combustible nicotine products should not be told that this study proves causation, but the data do support asking about product type rather than treating all nicotine exposure as interchangeable. The distinction between a smoker, a hookah user, and an e-cigarette user may matter when evaluating persistent nasal symptoms, especially in younger adults, where vaping is often perceived as a lower-risk behavior.
The stronger adjusted association for e-cigarettes is clinically relevant because these products are increasingly common and are often discussed as alternatives rather than additions to existing exposures. If aerosol exposure is contributing to mucosal inflammation, then switching from cigarettes to vaping may not eliminate the upper-airway symptom burden some patients expect. The adjusted odds ratio does not define severity, and it does not identify the exact inflammatory pathway, but it does justify more rigorous study of airway effects in users who present with chronic nasal complaints.
Objective Testing and Longitudinal Exposure Data Remain Essential
The next phase of research needs to move beyond symptom scores and convenience sampling. Objective allergy testing, better quantification of nicotine exposure, and longitudinal follow-up would help determine whether tobacco and nicotine products precede allergic rhinitis onset or simply coexist with it. Repeated measures would also clarify whether changes in use track with symptom worsening or improvement over time. Without those data, the present study remains a useful epidemiologic signal rather than a mechanistic answer.
For now, the main clinical message is narrow but important: after adjustment for demographic imbalance, e-cigarette use was associated with about twice the odds of allergic rhinitis in this sample, while the crude comparison did not show a relationship. The tension between those two results is exactly why confounder control matters in respiratory epidemiology. It also leaves the field with a practical next question: whether the nasal mucosa responds differently to nicotine aerosols, combustion smoke, and the many patterns of dual use that online surveys often cannot capture.