No abstract

Consistent with epidemiological reporting patterns in so-called problem buildings, nasal irritant sensitivity appears to be non-randomly distributed in the population, with significant variability predicted by age, gender, and the presence of allergic rhinitis.

Judging by self-report, a substantial subset of individuals with allergic rhinitis--along with all individuals with nonallergic rhinitis (by definition)--are hyperreactive to non-allergic triggers. There is overlap between these triggers (elicited in the process of obtaining a clinical diagnosis) and environmental characteristics associated with ''problem buildings.'' Since individuals with self-identified rhinitis report an excess of symptoms in most epidemiologic studies of problem buildings (even in the absence of unusual aeroallergen levels), rhintics may be acting as a ''sentinel'' subgroup when indoor air quality is suboptimal. Together, non-allergic rhinitics plus allergic rhinitics with prominent non-allergic triggers, are thought to constitute approximately one-sixth of the US population.

Upper-respiratory-tract symptoms (nasal irritation, congestion and rhinorrhea) are prevalent complaints in so-called "problem buildings." In epidemiologic studies, symptom reporting is associated with selected subject characteristics, including younger age, female gender, and the presence of allergic rhinitis. The physiologic correlates of these differential reporting patterns, however, are largely unknown. Using dilute chlorine gas as a model upper-respiratory-tract irritant, we studied 52 otherwise healthy volunteers in a sample stratified on age (18-69 yr), gender, and allergy status. In a single-blinded crossover study, subjects had their nasal airway resistance measured preexposure, immediately postexposure, and 15 min postexposure to both filtered air and chlorine (1.0 ppm in air) for 15 min. Allergic rhinitic subjects showed a significantly greater net (chlorine minus air) congestive response at 15 min postexposure than did nonrhinitic controls (p <.01). Advancing age also predicted a greater response immediately post-exposure (p <.01). No gender effect was observed. Significant interindividual variability was evident in the nasal congestive response to irritant (chlorine) provocation. The rhinitis effect was consistent with prior observations, whereas the effect of advancing age was opposite to that hypothesized.

Individuals with seasonal allergic rhinitis (SAR) show a more marked nasal obstructive response (increases in nasal airways resistance or NAR) after provocation with chlorine gas (Cl2) than do nonrhinitic (NR) controls. We were interested in learning whether similar differential responsiveness was apparent after provocation with acetic acid vapor. Sixteen nonsmoking, nonasthmatic subjects, aged 21-63 yr, equally divided by gender and nasal allergy status, were enrolled in a single-blinded crossover study involving exposure to acetic acid (AA) vapor (15 ppm) or air for 15 min on separate days 1 wk apart. NAR was measured in triplicate before, immediately post-, and 15 min postexposure, was normalized to baseline on a given exposure day, and was expressed as Net [NAR/baseline] after acetic acid versus control (air) exposure. After log transformation to achieve normality, the mean loge of Net [NAR/baseline] was 0.22 for SAR subjects and -0.11 for NR subjects immediately postexposure (p<.05); the corresponding values were 0.24 and -0.08, respectively, at 15 min postexposure (p<.05). Inhalation of acetic acid at the (NIOSH-recommended) short-term exposure limit of 15 ppm for 15 min produces differential nasal airflow obstruction among SAR versus NR subjects, with the former showing greater physiologic reactivity to this stimulus. This differential responsiveness is consistent with our previous findings with Cl2, indicating that there may be a generalized susceptibility factor associated with allergic rhinitis. The response occurs with slight subjective nasal irritation.