Evaluation of Trigeminal Sensitivity to Ammonia in Asthmatics and Healthy Human Volunteers

Maja Petrovaa, Jeanmarie Diamonda, Benno Schustera & Pamela Dalton*a*a Monell Chemical Senses Center, , Philadelphia, Pennsylvania, USAThis research was supported in part by a grant from the S. C. Johnson Company and an NIH-NIDCD grant, RO1 DC 0488, to Pamela Dalton. The authors thank Laura Sitvarin and Christopher Schutz for assistance in testing participants and analytical procedures, and Carol Pierce, RN, for assistance during the asthmatic portion of the study. We also thank Dr. Edward Emmett for his service as medical monitor for this study.Address for correspondence: Pamela Dalton, PhD, MPH, Monell Chemical Senses Center, 3500 Market Street, Philadelphia, PA 19104, USA. pdalton@pobox.upenn.eduAsthmatics often report the triggering or exacerbation of respiratory symptoms following exposure to airborne irritants, which in some cases may result from stimulation of irritant receptors in the upper airways inducing reflexive bronchoconstriction. Ammonia (NH3) is a common constituent of commercially available household products, and in high concentration has the potential to elicit sensory irritation in the eyes and upper respiratory tract of humans. The goal of the present study was to evaluate the irritation potential of ammonia in asthmatics and healthy volunteers and to determine whether differences in nasal or ocular irritant sensitivity to ammonia between these two groups could account for the exacerbation of symptoms reported by asthmatics following exposure to an irritant. Twenty-five healthy and 15 mild/moderate persistent asthmatic volunteers, with reported sensitivity to household cleaning products, were evaluated for their sensitivity to the ocular and nasal irritancy of NH3. Lung function was evaluated at baseline and multiple time points following exposure. Irritation thresholds did not differ between asthmatics and healthy controls, nor did ratings of odor intensity, annoyance, and irritancy following exposure to NH3 concentrations at and above the irritant threshold for longer periods of time (30 s). Importantly, no changes in lung function occurred following exposure to NH3 for any individuals in either group. Thus, despite heightened symptom reports to environmental irritants among asthmatics, the ocular and nasal trigeminal system of mild to moderate asthmatics does not appear to be more sensitive or more reactive than that of nonasthmatics, nor does short-duration exposure to ammonia at irritant levels induce changes in lung function. At least in brief exposures, the basis for some asthmatics to experience adverse responses to volatile compounds in everyday life may arise from factors other than trigeminally mediated reflexes.