Occupational Rhinitis

There is convincing evidence that tight relationships between the upper and lower airways also apply to the workplace context. Most patients with occupational asthma (OA) also suffer from occupational rhinitis (OR), although OR is 2 to 3 times more common than OA. OR most often precedes the development of OA, especially when high-molecular-weight protein agents are involved, and longitudinal cohort studies have confirmed that OR is associated with an increased risk for the development of OA. The level of exposure to sensitizing agents at the workplace is the most important determinant for the development of IgE-mediated sensitization and OR. Atopy is a risk factor for the development of IgE-mediated sensitization only to high-molecular-weight agents. In workers with work-related rhinitis symptoms, documentation of IgE-mediated sensitization to a workplace agent via skin prick testing or serum specific IgE confirms a diagnosis of probable OR, whereas specific nasal provocation testing in the laboratory remains the reference method to establish a definite diagnosis of OR. Complete avoidance of exposure to the causal agent is the most effective therapeutic option for controlling work-related nasal symptoms and preventing the development of OA. If complete elimination of exposure is expected to induce meaningful adverse socioeconomic consequences, reduction of exposure can be considered as an alternative approach, but it is important to consider the individual risk factors for the development of OA to implement a more personalized management of OR.

Introduction

The various dusts, gases, fumes, and vapors present in the workplace environment can induce or trigger different phenotypes of work-related rhinitis (WRR) through immunologic or irritant, nonimmunologic mechanisms (Figure 1).1, 2, 3, 4, 5, 6 Considering that the concept of “united airway disease” and the tight interactions between the upper and lower airways also apply in the context of the workplace, a task force of the European Academy of Allergy and Clinical Immunology proposed a nosologic approach for disentangling subphenotypes of WRR¹ similar to that used for work-related asthma.7, 8, 9 Occupational rhinitis (OR) was defined as “an inflammatory disease of the nose, which is characterized by intermittent or persistent symptoms (ie, nasal congestion, rhinorrhea, sneezing and itching), and/or variable nasal airflow limitation due to causes and conditions attributable to a particular work environment and not to stimuli encountered outside the workplace.”¹ OR can be induced by either immunologic sensitization to a specific substance, which is termed sensitizer-induced OR, or exposure to high levels of irritants at work, which is termed irritant-induced rhinitis (IIR). Sensitizer-induced OR—hereafter simply referred to as OR—can be caused either by high-molecular-weight (HMW) proteins of vegetable or animal origin acting through an IgE-mediated mechanism or by low-molecular-weight (LMW) agents such as reactive chemicals, metals, and wood dusts. A few LMW agents induce the production of specific IgE (sIgE) antibodies while the immunologic mechanisms involved in OR due to most of the LMW agents remain uncertain.

IIR refers to transient or persistent symptoms of rhinitis that develop after a single (ie, the reactive upper airway dysfunction syndrome)¹⁰ or multiple acute exposures^11,12 to high concentrations of irritant compounds, such as chlorine, chlorine dioxide, sulfur dioxide, ozone, and hydrogen sulfide. It is currently acknowledged that not only acute inhalation of high concentrations of irritants may have detrimental effects on the nasal mucosa but long-term exposure to irritants, even in concentrations within occupational exposure limits, may also induce a chronic form of IIR.^3,4,13 Various occupational exposures have been associated with an increased risk of rhinitis symptoms. The few available data on the pathophysiology of IIR suggest a combined role of innate immune response with the nasal sensory nervous system (nonadrenergic, noncholinergic). Inhalation of irritants can directly harm the nasal epithelium, resulting in the generation of reactive oxygen species and the release of several damage-associated molecular patterns, IFN-γ, and proinflammatory cytokines.⁴ Irritants can also directly activate the trigeminal nonadrenergic, noncholinergic nerve fibers that express irritant detectors such as the transient receptor potential A1 channel.⁴ The activation of these receptors induces a local release of neuropeptides, leading to mucus secretion, nasal congestion, sneezing, and even the recruitment and activation of leukocytes.

OR should be distinguished from work-exacerbated rhinitis (WER), which refers to the worsening of nasal symptoms temporally related to work exposure in subjects with preexisting or coincident rhinitis that was not caused by the workplace environment.¹ Respiratory irritants at work as well as other nonspecific stimuli (eg, cold air, cigarette smoke, exercise, and temperature changes) may trigger—through the activation of chemoreceptors on the trigeminal nonadrenergic, noncholinergic nerve fibers—rhinitis symptoms in individuals with nasal hyperreactivity, which is highly prevalent in allergic and nonallergic rhinitis.14, 15, 16

This review aimed to provide a comprehensive overview of current knowledge pertaining to the different aspects of OR with a focus on diagnostic approaches, societal burden, and management options. The purpose was also to provide practical guidance to clinicians who are faced with the assessment and management of WRR symptoms.