INTRODUCTION — Occupational rhinitis (OR) is defined as "an inflammatory condition of the nose, which is characterized by intermittent or persistent symptoms (ie, nasal congestion, sneezing, rhinorrhea, 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 of the workplace" . OR can develop in response to dusts, gases, fumes, and vapors and may be classified as immunologic or nonimmunologic depending upon the mechanism involved in the pathogenesis of symptoms [2,3]. OR induced by immunologic sensitization to a specific substance is termed sensitizer-induced OR while OR occurring via exposure to high levels of irritants is termed irritant-induced rhinitis (IIR) . OR should be differentiated from work-exacerbated rhinitis (WER), which is preexisting or concurrent (allergic or nonallergic) rhinitis that is worsened by but not caused by workplace exposures.
OR may have a profound effect on the worker, resulting in performance deficits, reduced productivity, and psychosocial problems. OR often coexists with occupational asthma (OA) and may precede and predict the development of OA [5-8].
The epidemiology, pathophysiology, clinical manifestations, diagnosis, and management of OR will be discussed here. OA is reviewed separately. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors" and "Occupational asthma: Clinical features, evaluation, and diagnosis" and "Occupational asthma: Pathogenesis".)
EPIDEMIOLOGY — Occupational allergic diseases are common and appear to be increasing, with an estimated worldwide prevalence of 5 to 15 percent [9,10]. The prevalence of OR specifically is not precisely known, although it appears to be two to three times more prevalent than occupational asthma (OA) [11,12]. Prevalence estimates of OR vary with the methods used for diagnosis (questionnaire, objective evaluation), the occupation studied, and the geographic area in question (which may have distinctive industries).
The following factors complicate prevalence studies of OR:
●Rhinitis from all causes is a common disorder in the general population. Studies should include a control group of workers from the same population who are employed in a different and low-risk occupation.
●Questionnaires (without objective testing for sensitization to occupational allergens or direct nasal challenges with the suspect agent) are less reliable because there are numerous causes of rhinitis.
●The most accurate studies confirm the patient's reactivity using direct nasal challenges and an objective means of quantitating the patient's response. Nasal challenge procedures are reviewed below. (See 'Direct nasal challenge' below.)
The following studies estimated OR in specific occupations and illustrate the importance of confirmatory nasal challenge:
●Laboratory employees who work with animals are one of the groups most commonly affected by OR and/or asthma. More than 40 percent of 156 workers reported rhinitis symptoms in one study, with 51 percent demonstrating skin test reactivity to laboratory animals . A positive nasal challenge was found in 15 percent of those with symptoms.
●A study of 1021 tobacco workers found that 27 percent reported rhinitis, compared with 18 percent of controls (hospital workers) . A positive nasal challenge study was documented in 70 percent of those with symptoms.
Bias also complicates prevalence studies. Underestimation may occur due to the healthy worker effect, which is a source of bias caused by the phenomenon that sicker individuals may choose work environments in which exposures are low or may be excluded from being hired. Similarly, already-hired workers may seek transfer to jobs with less exposure or leave work altogether . This is the most common selection bias in occupational studies. Underestimation may also occur because of workers' reluctance to report symptoms for fear of losing employment.
RISK FACTORS — The following preexistent symptoms and conditions have been implicated as risk factors for the development of OR:
●Other atopic disorders, particularly allergic rhinitis and asthma [13,16,17]
●A high level of total immunoglobulin (Ig)E (>150 k international units/L) 
●Level of exposure to known sensitizing agents and irritants in the workplace [11,19]
●Nonspecific nasal symptoms 
●Respiratory symptoms upon exposure to dust or strong odors 
Smoking has not been established as a risk factor for OR, although it does increase the risk of developing some forms of occupational asthma (OA). The relationship between duration of exposure to an occupational agent and the development of OR has not been extensively studied. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors".)
High-risk occupations — The risk of OR in various occupations was assessed in a study that analyzed 1244 incident cases of OR reported from 1986 to 1991 to the Finnish Register of Occupational Diseases . The greatest risk of OR was among furriers, followed by bakers, livestock breeders, food processing workers, veterinarians, farmers, assemblers of electrical, electronic, and telecommunication products, and boat builders. A later study identified medical workers and pharmacy professionals as additional high-risk groups . In contrast, office workers are at low-risk for OR.
Laboratory employees working with small animals are one of the highest risk groups in the United States, the United Kingdom, and several European countries . Studies have reported that the prevalence of laboratory animal allergy is 10 to 23 percent [23-25] and that the incidence rate is 1.56 per 1000 workers for OA and 2.54 per 1000 workers for OR . A study suggests that indirect exposure may be as risky for sensitization to laboratory animal antigens as direct exposure. Also, even nonsensitized workers may still be at risk for OR, as aerosolized endotoxin from animals has been shown to cause symptoms .
PATHOPHYSIOLOGY — OR can arise from several different mechanisms. A review of nasal physiology is important in understanding the mechanisms responsible for OR.
Nasal physiology — The nasal mucus membrane can respond to noxious stimuli in various ways:
●Congestion resulting from vasodilatation, increased vascular permeability, and sinusoidal pooling in the vascular beds draining the sinus tissues
●Pruritus and sneezing due to sensory nerve stimulation
●Production of secretions due to glandular stimulation and increased vascular permeability
Nasal challenge has provided an excellent model for quantifying responses and for obtaining insights into nasal physiology. The nose can be challenged with allergens, mediators, or irritants. The response can be quantified by symptom scores, nasal airway resistance, and the study of secretions. (See 'Direct nasal challenge' below.)
Specific measurements of secretions include amount, composition, and content of various regulatory molecules, proteins, enzymes, and cells. Some of the components of nasal secretions that have been studied are prostaglandin D2 (PGD2), toxoid-antitoxoid mixture esterase (TAMe), kinins, albumin, immunoglobulins, cytokines, lactoferrin, tryptase, major basic protein, cell adhesion molecules, endothelial growth factors, and acute-phase reactant proteins.
An early response is universal in atopic individuals following nasal challenge with an allergen to which the patient is sensitized. Within minutes, subjects develop sneezing, nasal congestion, and an increase in nasal secretions. This early response is largely mast cell mediated, while the late response involves other cell types. The delayed cellular influx, which can be demonstrated in nasal lavage fluid four to six hours after challenge, is similar to the late changes seen in the lung after bronchial challenge. Total cells increase, as do epithelial cells, eosinophils, neutrophils, and mononuclear cells. Nasal lavage fluid obtained within 11 hours of the challenge shows increased levels of histamine, TAMe, PGD2, and kinins . Just as in the lung, the late-phase reaction in the nose is associated with a heightened response to allergen and to nonspecific agents, such as histamine .
There is also evidence to suggest that the size of the agent may influence the type of immunologic response elicited. Individuals exposed to high molecular weight (HMW) agents were found to have higher levels of the acute-phase reactant proteins fibrinogen and haptoglobin, as well as higher levels of vascular cell adhesion molecule (VCAM), vascular endothelial growth factor (VEGF), and vitamin D (VDBP) in nasal lavage compared with individuals exposed to low molecular weight (LMW) agents .
Additionally, the neurogenic system plays a role in the development of rhinitis symptoms via release of various neuropeptides including substance P and neurokinin A and B. These neuropeptides can directly activate mucus-producing cells (leading to rhinorrhea), endothelial cells (leading to nasal congestion), and mast cells [30,31].
Immunologic occupational rhinitis — Immunologic or sensitizer-induced OR is primarily mediated by specific immunoglobulin (Ig)E production, with resultant early and late nasal secretions. HMW allergens or LMW allergens bound to proteins can elicit an allergic response (table 2). The immunologic mechanisms by which LMW agents cause airway sensitization are largely unclear. Many LMW agents may not be immunogenic by themselves but are known to be excellent haptens and can combine with other tissue proteins, such as human serum albumin, in the respiratory tract. The resultant hapten-protein conjugate acts as a potent immunogen . These mechanisms are identical to those underlying immunologic forms of occupational asthma (OA). (See "Occupational asthma: Pathogenesis".)
Examples of substances known to cause immunologic OR include rodent allergens (laboratory workers), latex (health care workers), guar gum (carpet workers), and psyllium used in laxatives (nurses) (table 1).
Immunologic OR is often associated with ocular symptoms, such as ocular itching, excessive tearing, redness, and swelling of the eyelids. (See "Allergic conjunctivitis: Clinical manifestations and diagnosis".)
Nonimmunologic occupational rhinitis — Nonimmunologic OR is caused by nonimmunological and nonspecific mechanisms. Subtypes include irritant-induced, corrosive, and annoyance OR.
Irritant-induced rhinitis — Irritant-induced rhinitis (IIR) is defined as inflammation of the nasal mucosa that has no immunologic or allergic basis. Exposure to substances, such as cigarette smoke, formalin, and capsaicin, results in the release of substance P, a sensory transmitter that in turn triggers a neurogenic inflammatory response. This type of OR is seen in workers in enclosed environments exposed to materials, such as paints, talc, coal dust, air pollutants, or cold air (table 1). Cleaners and janitors can develop irritational OR in response to cleaning products [34,35].
Corrosive — Corrosive OR results from exposure to a high concentration of irritating and soluble chemical gases, which can cause sufficient nasal inflammation that the mucosa can break down and ulcerate, similar to a chemical burn. Common culprits include substances with high water solubility and chemical reactivity, such as chlorine, sulphur dioxide, ammonia, and formaldehyde (table 1) . Corrosive OR can lead to permanent changes in physiologic functions of the nose, such as loss of olfaction. The entity "reactive upper-airways dysfunction syndrome" (RUDS) has been described after a single exposure to strong chemicals and is modeled on reactive airways dysfunction syndrome (RADS) . (See "Reactive airways dysfunction syndrome and irritant-induced asthma".)
Annoyance — Annoyance OR is a purely subjective condition that occurs in individuals with a heightened olfactory awareness to substances, such as department store or supermarket employees who become symptomatic upon exposure to perfumes or detergents, respectively. Nasal mucosal inflammation is not evident. Annoyance OR is a negative psychologic state, at times in conjunction with transient physical symptoms related to the perception of offensive air quality due to strong odors. The likelihood of developing annoyance reactions is increased by nasal polyposis, sinusitis, tobacco use, and overuse of over-the-counter nasal decongestants or illicit drugs . The mechanism has not been demonstrated.
Levels of exposure — Patients with OR are not necessarily exposed to levels of the causative agent that are considered unsafe by industry standards . A study of customs officers found that changes in nasal cytology were evident in those exposed to diesel exhaust emissions, although the levels were well within the permitted range .
For patients with immunologic/allergic OR, even minute amounts of allergen can trigger symptoms in susceptible patients.
Symptoms — The symptoms of OR are nasal congestion, sneezing, nasal pruritus, and/or increased nasal secretions in association with exposure to the workplace. Since OR can be associated with a late reaction, symptoms may not appear until several hours after leaving the workplace. Late-onset symptoms in the absence of immediate symptoms is uncommon, although it has been reported . In some forms of OR, there may be associated ocular or pulmonary signs and symptoms.
Timing of symptom onset — The symptoms of OR usually appear within the first one to three years of employment [16,37,40,41]. However, the latency period between exposure and symptom onset may differ among occupations.
DIAGNOSTIC ASSESSMENT — Occupational rhinitis remains a diagnostic challenge. In the community, the diagnosis of OR is most often based upon correlative history, suggestive clinical signs and symptoms, and (if feasible) observation of the patient's symptoms during a site visit. Direct nasal challenge may establish a definite diagnosis but is often not necessary and may be difficult to perform appropriately outside of a research or specialized testing center .
The following steps are suggested in the evaluation of OR :
●History and physical examination
●Confirmation of work relatedness
●Identification and confirmation of the suspected cause
History — A comprehensive occupational history should contain questions pertaining to the following :
●Onset of symptoms at work
●Improvement on weekends or vacations
●Recurrence of symptoms on reexposure
●Exposure to cold air, ozone (eg, pulp mill and bleachery workers), pollution, tobacco smoke, animals, and dusts
●Similar symptoms in coworkers
●Duration working at current job
●Adequacy of ventilation
●Compliance with wearing gloves, masks, and protective clothing
●History of accidents or spills
●Review of material safety data sheets
●Personal or family history of atopy
●Coexisting symptoms, such as bronchitis, dermatitis, conjunctivitis, or anosmia
●Intranasal medications (eg, topical decongestants) or illicit drugs (eg, cocaine)
Physical examination — Physical examination during the time of active rhinitis reveals swollen nasal turbinates and evidence of increased secretions. Nasal findings may be minimal in patients with annoyance OR, whereas corrosive OR may reveal ulcerated and hemorrhagic mucosa .
Confirmation of work relatedness — Ideally this is accomplished through a site visit, which can provide the clinician with an opportunity to confirm and add to the previously obtained history by observing the patient performing usual job-related tasks. The site visit is also critical for determining if any changes can be made in the work environment to reduce the patient's ongoing exposure.
In the United States, the Occupational Safety and Health Administration (OSHA) requires employers to keep on-site records detailing the ingredients and possible health effects of materials and substances to which workers are exposed. This information is available in material safety data sheets, which should be reviewed during the site visit. These sheets can be helpful in establishing a causal agent in OR.
A toxicologist can be consulted to sample air quality if there is a question of inadequate ventilation. However, patients may develop OR (especially allergic OR) from exposure to "safe" amounts of agents. (See 'Levels of exposure' above.)
However, the feasibility of site visits limits their utility. As such, at some centers, the patient is given a diary and instructed to record symptoms several times daily during the work week, on weekends, and during any prolonged absences from the workplace, providing a purely subjective measurement.
Identification and confirmation of the suspected cause
Testing for allergen-specific IgE — Allergy skin testing and in vitro immunoglobulin (Ig)E immunoassays (commonly called ImmunoCAP testing) are methods for detecting allergen-specific IgE. These tests document sensitization to the allergen (ie, the presence of allergen-specific IgE), although not all sensitized patients develop symptoms upon exposure. Thus, direct nasal challenge remains the gold standard for the diagnosis of OR.
Allergy skin testing is considered a safe procedure, although there is some risk for a generalized allergic reaction (ie, anaphylaxis) in highly sensitive patients. Therefore, skin testing should be performed by allergy specialists who have training in the rapid recognition and treatment of possible reactions. In contrast, IgE immunoassays can be ordered by any clinician, although this form of testing may be less sensitive than skin testing. (See "Overview of skin testing for IgE-mediated allergic disease" and "Allergic rhinitis: Clinical manifestations, epidemiology, and diagnosis".)
Testing for allergen-specific IgE is appropriate if both of the following are true:
●The OR is believed to be due to an IgE-mediated mechanism (ie, immunologic OR).
●There is a validated testing extract available for the allergen in question, such as animal danders , dust mite, latex (in some countries), or mold. Unfortunately, approved extracts do not exist for many other occupational allergens (especially for low molecular weight agents), and commercially available extracts may be variable in allergen content .
If a validated extract is not available, then testing with improvised solutions of the suspect allergen is generally not recommended, because irritating substances can cause false-positive results. In addition, false-negative results may occur with low molecular weight allergens, which may need to be conjugated with serum albumin to elicit a positive response .
In contrast, skin testing to common aeroallergens may provide useful information about the general atopic status of the patient, as patients with allergic rhinitis to inhaled allergens are at increased risk for OR. (See 'Risk factors' above.)
Direct nasal challenge — Direct nasal challenge, also called nasal provocation test, is the gold standard for the diagnosis of OR. It can be performed either at the workplace or under controlled circumstances in the office or laboratory. Responses may be quantified either by symptom score or by rhinomanometry, a technique that measures changes in nasal airway resistance. As mentioned previously, these techniques require special equipment and training and are not practical for most community clinicians or allergy specialists.
A position paper published by the European Academy of Allergy and Clinical Immunology (EAACI) suggests that workplace challenges be considered in the following settings :
●No sensitizing agent has been firmly identified at work
●Multiple potentially sensitizing agents are present at the workplace
●Conditions of exposure at work cannot be duplicated in the laboratory
●Nasal provocation tests in the laboratory are not feasible
During the challenge, the worker performs the usual tasks and nasal response is gauged before, during, and after a typical shift. Patients act as their own controls by comparing workday symptoms to non-workday symptoms. This may be done several times to ascertain sufficient reproducibility. Tools for assessing the severity of allergic rhinitis are available online .
A laboratory nasal allergen challenge would also be useful in cases of putative IgE-mediated mechanism when skin or blood testing for allergen-specific IgE is equivocal and workplace challenges are not possible. Again, this is most applicable to research settings.
Rhinomanometry techniques — There are three common rhinomanometry techniques: anterior, posterior, and acoustic.
●Anterior rhinomanometry calculates nasal airway resistance from the relationship between flow rate and pressure. Commercially available anterior rhinomanometers measure airflow through one nostril by means of a closely fitting facemask, whereas the other nostril is sealed with a small tube to measure nasopharyngeal pressure. The technique is easy to perform, requires little patient cooperation, and is especially convenient for nasal provocation. The disadvantages include distortion of the nasal valves by the probe, reflex changes resulting from tactile sensations, and sensitivity of the measurement to nasal cycling (ie, a normal phenomenon in which nasal turbinates on alternate sides of the nose swell at intervals of two to five hours) [45,46]. Normal nasal function and reflexes are reviewed elsewhere. (See "Etiologies of nasal obstruction: An overview" and "An overview of rhinitis", section on 'Normal nasal reflexes'.)
●Posterior rhinomanometry employs a facemask fitted with a pneumotachometer and monitors airflow through both nostrils simultaneously, as well as anterior nasal pressure. Posterior rhinomanometry avoids the disadvantages of artifacts from nasal instrumentation and nasal cycling, although the equipment is expensive and the procedure is difficult to perform on some patients. Approximately 20 percent of healthy individuals do not have sufficient palatal control to permit accurate pressure flow recordings to be obtained .
●Acoustic rhinomanometry is a simple, easily reproducible, and less invasive procedure in which sound waves are introduced into the nasal cavity and a computer quantifies the reflected waves [47,48]. Of the three techniques, acoustic rhinomanometry is the most practical and least invasive.
MANAGEMENT — The management of OR includes avoidance of the causative agent and pharmacotherapy with intranasal glucocorticoid sprays and/or nonsedating antihistamines. In the United States, OR is not a reportable condition, in contrast with occupational asthma (OA).
Patients with severe symptoms that are not relieved by the measures described below, combined with pharmacotherapy, may need to consider a change in employment.
Avoidance — The management of OR begins with eliminating or minimizing exposure to the causative agent. In our experience, effective avoidance usually results in resolution of symptoms. In prospective studies, workers with OR who changed jobs or retired reported significant improvement in symptoms and quality of life, even in those with preexisting rhinitis [49,50].
Exposure may be reduced in a number of ways, including [51,52]:
●Substitution of the causative agent with an alternative material
●Consistent use of protective equipment, such as a mask
●Improved ventilation or containment of the causative agent
●Reduced exposure times to the causative agent
Following these measures could well make it possible for the worker to maintain employment.
The natural history of OR has not been extensively studied, nor has the impact of ongoing exposure to causative agents. There is a lack of evidence that OR progresses to more extensive respiratory involvement. However, it is not known if some patients develop rhinitis initially in response to occupational agents but then become sensitive to other triggers and develop persistent symptoms despite avoidance of the initial culprit.
Corrosive occupational rhinitis — Avoidance is the sole treatment for corrosive OR, and the worker must be adequately protected from corrosive materials. Medications should not be used to reduce the clinical manifestations of this condition, because the patient's awareness of symptoms is important to avoid mucosal injury. Recovery rates and sequelae from this form of nasal injury have not been reported.
Pharmacotherapy — Pharmacotherapy can be helpful for annoyance, irritational, and allergic forms of OR, although there are no randomized trials or even large series evaluating pharmacotherapy for OR specifically. Recommendations for management are extrapolated from the literature on allergic rhinitis and in our experience are equally helpful for allergic OR. However, the response of annoyance and irritational OR to these therapies has not been reported.
Patients should be counseled that medications are only palliative rather than curative, and efforts to reduce exposure are primary. Ideally, pharmacotherapy should be continued until the patient can control symptoms by avoiding exposure to the offending agent.
Intranasal glucocorticoids — Topical glucocorticoid nasal sprays are most effective when taken regularly, although they can be used on an as-needed basis. Preparations with once-daily dosing are convenient and can help optimize compliance. These include triamcinolone acetonide, budesonide, fluticasone propionate, mometasone furoate, fluticasone furoate, beclomethasone dipropionate, and ciclesonide (table 3). Most intranasal glucocorticoids are used at a dose of 1 to 2 sprays in each nostril once or twice per day. The optimal use of these medications is reviewed elsewhere. (See "Pharmacotherapy of allergic rhinitis".)
Antihistamines — Over-the-counter or prescription nonsedating antihistamines are also helpful for managing annoyance, irritant-induced, and immunologic OR. Antihistamines are less effective for allergic rhinitis than topical glucocorticoid nasal sprays, although some patients prefer oral medications. When the patient's symptoms are episodic and predictable, prophylactic use before exposure is usually sufficient. When symptoms are frequent or unpredictable, regular use of an antihistamine may be necessary.
We avoid sedating first-generation antihistamines (eg, diphenhydramine, chlorpheniramine, astemizole, and others), since the goal of treatment is to increase alertness and job performance. The second-generation, less sedating antihistamines include loratadine (10 mg once daily), desloratadine (5 mg once daily), fexofenadine (180 mg once daily), cetirizine (10 mg once daily), and levocetirizine (2.5 or 5 mg once daily). The choice of agent is often based on trial and error, side effect profile, cost to the patient, and availability. (See "Pharmacotherapy of allergic rhinitis".)
Topical antihistamine nasal sprays may also be helpful. These include azelastine and olopatadine, both of which have a rapid onset of action (less than 15 minutes) and can be administered "on demand" for patients with episodic and unpredictable exposures. (See "Pharmacotherapy of allergic rhinitis".)
Other therapies — Other adjunctive therapies may be helpful to some patients . Although these interventions have not been studied specifically for OR, they have been shown to help various other types of rhinitis (see "Pharmacotherapy of allergic rhinitis"):
●Ipratropium nasal spray
●Nasal irrigation with saline, performed when the patient is done with work for the day (see "Patient education: How to rinse out your nose with salt water (The Basics)")
For patients with accompanying ocular symptoms, ophthalmic solutions of antihistamines/mast cell stabilizers may provide as-needed prophylactic or symptomatic treatment of accompanying conjunctivitis. (See "Allergic conjunctivitis: Clinical manifestations and diagnosis".)
Immunotherapy — Allergen immunotherapy is not recommended for the majority of patients with OR for the following reasons:
●Allergen immunotherapy has no role in the management of rhinitis caused by irritative or corrosive substances.
●Therapeutic extracts have not been produced for most occupational allergens and, in some cases, may not be safe.
In cases where appropriate allergens are available, such as veterinarians with OR caused by cat or dog allergens, the efficacy of allergen immunotherapy in the setting of ongoing intense exposure has not been evaluated. However, it is the authors' anecdotal experience that cat or dog immunotherapy in small animal veterinarians is useful, particularly if the patient also limits non-work-related exposure by not keeping such pets in the home.
Preliminary studies have described immunotherapy with certain occupational allergens that are not easily avoided (eg, natural rubber latex for health care workers) [54-56], although the safety and efficacy of this approach require further study. (See "Latex allergy: Management", section on 'Immunotherapy'.)
PROGNOSIS — Many patients appear to have stable OR over a period of years. This is in contrast with occupational asthma (OA), which usually worsens with continued exposure. Therefore, we advise our patients to protect themselves as much as possible from ongoing exposure and to consider changing work environments if their symptoms appear to be worsening despite avoidance measures. A study among OR patients showed continuous occupational exposure decreased quality-of-life years after the diagnosis. The authors concluded that to restore the well-being of patients with OR, medication alone was not sufficient. Reduction or cessation of exposure was necessary. For patients with OR who were no longer exposed to the causative agent, quality of life was similar to healthy controls .
Risk of developing occupational asthma — Several longitudinal cohort studies have implicated OR as a risk factor for development of occupational asthma (OA) [4,7,8,41]. Additionally, OA is more often associated with OR when attributed to high molecular weight allergens than when attributed to low molecular weight allergens (72 versus 52 percent, respectively) [6,58]. Thus, the relationship between OR and OA may depend in part on the causative allergen. When asked by patients about the risk of developing asthma, we explain that it is possible that OR will progress to OA in some individuals, but the risk is not well-defined. It may be higher with the high molecular weight allergens, and we advise greater caution for patients who have OR to these allergens.
PREVENTION — In 2011, the European Academy of Allergy and Clinical Immunology (EAACI) released a position paper regarding the prevention of work-related respiratory allergies among pre-apprentices or apprentices and young workers . Consensus suggestions for prevention strategies include:
●Information campaigns and educational tools so that workers may develop an understanding of the risks and preventative measures associated with occupational exposures
●Environmental control as a cornerstone of prevention
●Pre-apprentice health assessment and advice, with medical surveillance prioritized during the first two to three working years
Screening applicants for jobs in which there is a risk of workplace sensitization had previously been proposed as a means of preventing allergic OR. A study of 110 laboratory animal workers reported that the combination of atopy and total immunoglobulin (Ig)E levels ≥100 international units/mL could be used as a preemployment screen to predict which workers would develop occupational allergy. The study estimated that such screening might be able to reduce occupational sensitization by up to 45 to 50 percent, with less than 10 percent false-positive predictions . However, the social, financial, and legal implications of such screening necessitate careful consideration, and we believe that these measures require further study before they are applied clinically.
Nonatopic individuals can also develop OR, and screening for atopy does not identify at-risk subjects in this group. In a study of applicants for laboratory jobs involving rat exposure, applicants were screened with a panel of common inhalant allergens to identify atopic individuals . Of the 41 workers who were initially atopic by history and skin testing, 23 percent went on to develop OR. However, a significant number of the workers who developed rat allergies were not initially atopic.
In 2012, the Joint Task Force on Practice Parameters published a practice parameter on environmental assessment and reduction of rodent exposure, which addressed the prevention of occupational allergy in animal workers handling rodents . It stated that testing for rodent sensitization (using immunoassays for rodent-specific IgE or skin prick testing) should be considered for at least the first three years of exposure and that extra preventive measures be offered to individuals with high risk for developing allergy (ie, those with sensitization, underlying atopy, or high levels of exposure).
A general approach to prevention, which applies to all workers and all forms of OR, is to institute environmental control measures proactively. It is important to recognize and identify potential sources of offending allergens and then minimize the worker's exposure to them as much as possible. This may be as simple as providing adequate ventilation.
An example of the effectiveness of environmental control measures was seen in the detergent industry. The Bacillus subtilis enzyme added to household detergents caused a significant amount of upper and lower respiratory tract allergy in workers. By instituting a number of precautions during the production process, the incidence of occupational respiratory disease was greatly decreased . These precautions included enclosing previously open operations, supplying heavily-exposed workers with space suits with air supply, providing disposable gloves and uniforms, providing masks with cartridge filters to workers with low exposure, monitoring the air by measuring enzyme concentrations, and performing spot checks on workers. These spot checks consisted of a history and physical examination, chest radiographs, pulmonary function testing, skin testing, and serologic testing.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Rhinitis".)
SUMMARY AND RECOMMENDATIONS — Occupational rhinitis (OR) has been defined as episodic, work-related occurrence of sneezing, nasal discharge, nasal pruritus, and/or nasal obstruction. OR often coexists with occupational asthma (OA), although significant numbers of patients develop just one of these conditions. (See 'Introduction' above.)
Clinical features and diagnosis:
●The overall prevalence of OR is unknown, and accurate identification is complicated by the high prevalence of rhinitis in general. High-risk professions include laboratory workers, food processing workers, veterinarians, farmers and livestock workers, and assemblers of electronic and telecommunication products. (See 'Epidemiology' above.)
●OR may develop in response to respiratory irritants, corrosive gases, or allergens. It may be immunoglobulin (Ig)E mediated or non-IgE mediated. A classification system delineates four subtypes: annoyance, irritational, corrosive, and immunologic/allergic (table 1). (See 'Pathophysiology' above.)
●The symptoms of OR can develop within minutes to several hours after exposure. There may be associated ocular or pulmonary signs and symptoms. OR usually develops within the first few years of employment. (See 'Clinical manifestations' above.)
●The evaluation of a patient suspected of having OR includes a detailed occupational history, physical examination, verification of work-relatedness, and, in cases of suspected immunologic OR, skin testing or in vitro testing to common inhalant allergens. In a few situations, commercial extracts of occupational allergens are also available for testing, although we do not recommend testing with improvised extracts. (See 'Diagnostic assessment' above.)
●The diagnosis is usually made clinically, although, for research purposes, symptoms should be elicited and confirmed by direct nasal challenge. (See 'Diagnostic assessment' above.)
●The primary therapy for all forms of OR is reduction or elimination of the patient's exposure to the causative agent. This is the only appropriate intervention for corrosive OR. (See 'Avoidance' above.)
●Pharmacotherapy may be useful while avoidance measures are being put in place or it may be needed on an ongoing basis. Medications may be used as needed for episodic and predictable exposures or daily for regular or unpredictable exposures. (See 'Pharmacotherapy' above.)
●We recommend that patients with immunologic OR be treated with the same medications used for nonoccupational allergic rhinitis (Grade 1B). Pharmacotherapy is primarily based upon intranasal glucocorticoid sprays, nonsedating antihistamines, or both. (See "Pharmacotherapy of allergic rhinitis".)
●In patients whose symptoms are controlled but who cannot eliminate exposure, we suggest against advising them that they must leave their jobs (Grade 2C). However, there may be a greater association between OR and OA in patients exposed to high molecular weight sensitizing agents (table 2). Accordingly, we are more cautious in our approach to these patients, screening for asthma symptoms and generally advising against continued exposure (Grade 2C). (See 'Prognosis' above.)
●The development of screening parameters to identify those individuals at highest risk for allergic OR is an area of active investigation, but validated methods for clinical application are still lacking. (See 'Prevention' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Jennifer Gentner, MD, who contributed to earlier versions of this topic review.
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