The most widely cited definition of rhinitis has been formulated by the International Consensus Report and states that 'rhinitis is defined as inflammation of the lining of the nose, characterized by one or more of the following symptoms: nasal congestion, rhinorrhea, sneezing, and itching' [1, 13]. This International Consensus Report has proposed an operational definition of rhinitis which was based solely on symptoms and would require the presence of 'two or more nasal symptoms for more than one hour on most days', although these criteria have never been formally validated [14–16].
Most previously published definitions of OR were based on the temporal relationship between nasal symptoms and workplace exposure [13, 17–20], while a few others also refer to the underlying inflammation [12, 21]. However, the major symptoms of OR (i.e., sneezing, rhinorrhea, nasal congestion, and itching) are similar to those of non-occupational rhinitis. Defining OR based only on work-related symptoms would therefore suffer the limitation of being inaccurate , as already outlined for OA .
In addition, the similarities and tight interactions between rhinitis and asthma [1–8] support the need for homogeneous definitions of OR and OA. The most widely accepted definition of OA refers to the pathophysiological changes that occur in the lower airways, i.e. 'variable airflow limitation and/or bronchial hyperresponsiveness and/or inflammation' [24, 25]. A similar approach cannot easily be translated to OR because: (1) nasal airflow limitation is not always present in OR; and (2) the various methods used for assessing nasal patency, non-specific hyperresponsiveness, and inflammation have not been thoroughly validated [26, 27], and (3) these procedures are still largely underused in clinical practice. Nevertheless, considering that inflammatory changes of the mucosa are the common feature of both rhinitis and asthma [1–8, 12], the following consensus definition of OR is proposed:
'Occupational rhinitis is an inflammatory disease of the nose, which is characterized by intermittent or persistent symptoms (i.e., nasal congestion, sneezing, rhinorrea, itching), and/or variable nasal airflow limitation and/or hypersecretion due to causes and conditions attributable to a particular work environment and not to stimuli encountered outside the workplace'.
The central concept of this broad definition is the causa
l relationship between work exposure and the development of the disease. In addition, this definition is based on demonstrable pathophysiological changes, and it does not place restriction according to the underlying mechanism.
There is accumulating evidence that the workplace environment can induce or trigger a wide spectrum of rhinitis conditions involving immunological and non-immunological mechanisms [16, 20, 28, 29]. These various conditions should be referred to as 'work-related rhinitis' and should be further distinguished according to the clinical features, etiopathogenic mechanisms, and the strength of the evidence supporting the causal relationship.
According to the revised nomenclature for allergy recently recommended by the European Academy of Allergy and Clinical Immunology  and the classification of work-related asthma proposed by panels of experts [24, 25, 31] different types of 'work-related rhinitis' may be delineated as detailed below and summarized in Figure 1. This review will, however, focus on immunologically-mediated OR, since there is only scarce data on the other forms of work-related rhinitis.
Work-related rhinitis symptoms are caused by immunologically-mediated hypersensitivity reactions resulting from antibody- or cell-mediated mechanisms. This entity is characterized clinically by the development of nasal hypersensitivity to a specific occupational agent appearing after a latency period, which is necessary to acquire immunological sensitization to the causal agent. Once initiated, the symptoms recur on re-exposure to the sensitizing agent at concentrations not affecting other similarly exposed workers. The symptoms can be intermittent or persistent according to the frequency and intensity of exposure to the causal agent. In allergic OR, the causal role of occupational agents can be documented on an individual basis through nasal provocation test (NPT), showing reduction of nasal patency, increased volume of nasal secretions, and/or nasal inflammation. Allergic OR encompasses both IgE-mediated OR and non-IgE-mediated OR.
IgE-mediated OR: Can be caused by a wide variety of high-molecular weight (HMW) agents (i.e. glycoproteins from vegetal and animal origin) and some low-molecular-weight-agents (LMW) for which an IgE-mediated mechanism has been proven, such as platinum salts, reactive dyes, and acid anhydrides.
Non-IgE-mediated OR: Can be induced by LMW agents (e.g. isocyanates, persulphate salts, woods) acting as haptens for which the allergic mechanism has not yet been fully characterized.
This category encompasses different types of rhinitis caused by the work environment through irritant, non-immunological mechanisms. It has been documented that single or multiple exposures to very high concentrations of irritant compounds can lead to transient or persistent symptoms of rhinitis [32–34]. Such cases of acute-onset 'irritant-induced OR' usually occur without a latency period, although the absence of latency may be obscured when workers are repeatedly exposed to high levels of irritants at work. This entity is quite similar to the situation of 'reactive airways dysfunction syndrome' (RADS) [25, 31, 35], so that the term 'reactive upper airways dysfunction syndrome' (RUDS) has been proposed . Biopsies of the nasal mucosa among individuals with RUDS induced by chlorine have shown non specific pathologic changes (i.e., lymphocytic inflammation of the lamina propria, epithelial desquamation, defective epithelial cell junctions, and increased numbers of nerve fibres) . In these cases of irritant-induced OR, evidence supporting a causal relationship with the workplace can be drawn only from the temporal association between exposure to unusually high levels of irritants and the development of rhinitis symptoms (or other objective indices of the disease).
The term 'irritant-induced OR' may also refer to symptoms of rhinitis reported by subjects repeatedly exposed at work to irritants (vapours, fumes, smokes, dusts) without identifiable exposure to high concentration of irritants. A variety of occupational exposures have been associated with rhinitis symptoms, nasal airflow obstruction, and/or nasal inflammation, usually with a predominant neutrophilic component, including ozone, volatile organic compounds, fuel oil ash, grain and cotton dust, formaldehyde, chlorine, wood dust, thermal degradation products of polyurethanes, and waste handling [12, 21]. The symptoms may be experienced only during exposure to irritants at work or may be persistent, presenting both at work and off work.
The term 'corrosive rhinitis' has been used to describe the most severe form of 'irritant-induced OR', which is characterized by permanent inflammation of the nasal mucosa (sometimes associated with ulcerations and perforation of the nasal septum) that may develops after exposure to high concentrations of irritating and soluble chemicals [20, 29, 37].
Work-exacerbated rhinitis (WER) should be defined as pre-existing or concurrent (allergic or non-allergic) rhinitis that is worsened by workplace exposures [22, 29], while the disease has not been caused by the work environment. It is indeed highly likely that rhinitis symptoms can be triggered by a wide variety of conditions at work, including irritant agents (e.g., chemicals, dusts, fumes), physical factors (e.g., temperature changes), emotions, second-hand smoke, and strong smells (e.g., perfumes). Epidemiological surveys have usually found high prevalence rates of work-related nasal symptoms in a variety of workforces, although IgE-mediated sensitization to occupational agents was not detected [22, 38–42]) or nasal inflammation was not documented [43–47].
The clinical features of a WER are similar to those of occupational rhinitis, so that the possibility of a WER should be considered only after careful exclusion of a specific sensitization to a workplace agent through appropriate diagnostic procedures. The mechanisms involved in the development of WER have been scarcely explored. The nasal response to irritant stimuli show wide inter-individual variability, and exaggerated reactivity to common chemical and physical stimuli, and is affected by age, gender, and the presence of allergic rhinitis [48–50].