Petrova Maja, Diamond Jeanmarie, Schuster Benno, Dalton Pamela
Monell Chemical Senses Center, Philadelphia, Pennsylvania, USA.
Inhal Toxicol. 2008 Sep;20(12):1085-92. doi: 10.1080/08958370802120396.
Asthmatics 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.
哮喘患者经常报告在接触空气传播的刺激物后出现呼吸道症状的触发或加重，在某些情况下，这可能是由于上呼吸道刺激性受体受到刺激，引发反射性支气管收缩所致。氨（NH₃）是市售家用产品的常见成分，高浓度时有可能引起人类眼睛和上呼吸道的感觉刺激。本研究的目的是评估氨对哮喘患者和健康志愿者的刺激潜力，并确定这两组之间对氨的鼻或眼刺激敏感性差异是否可以解释哮喘患者接触刺激物后报告的症状加重。对25名健康志愿者和15名轻度/中度持续性哮喘志愿者（均报告对家用清洁产品敏感）进行了评估，以了解他们对NH₃眼刺激和鼻刺激的敏感性。在基线和接触后的多个时间点评估肺功能。哮喘患者和健康对照者的刺激阈值没有差异，在接触高于刺激阈值的NH₃浓度较长时间（30秒）后，气味强度、烦恼程度和刺激程度的评分也没有差异。重要的是，两组中任何个体接触NH₃后肺功能均未发生变化。因此，尽管哮喘患者对环境刺激物的症状报告有所增加，但轻度至中度哮喘患者的眼和鼻三叉神经系统似乎并不比非哮喘患者更敏感或反应更强，接触刺激性水平的氨短时间也不会引起肺功能变化。至少在短时间接触中，一些哮喘患者在日常生活中对挥发性化合物产生不良反应的原因可能来自三叉神经介导的反射以外的因素。
