Am J Respir Med 2003; 2 (4): 333-341 1175-6365/03/0004-0333/$30.00/0

REVIEW ARTICLE

© Adis Data Information BV 2003. All rights reserved.

The Dilemma of Occupational Rhinitis Management Options Johan Hellgren,1 G¨oran Karlsson1 and Kjell Tor´en2 ¨ 1 Department of Oto-Rhino-Laryngology, Head and Neck Surgery, Sahlgrenska University Hospital, Goteborg, Sweden 2 Department of Occupational and Environmental Medicine and Department of Allergology, Sahlgrenska University ¨ Hospital, Goteborg, Sweden

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333 1. Definition and Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 334 2. Objective Assessment of Occupational Rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 334 2.1 Anterior Rhinoscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 334 2.2 Anterior and Posterior Rhinomanometry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335 2.3 Acoustic Rhinometry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335 2.4 Peak Nasal Expiratory and Inspiratory Flow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335 2.5 Nasal Lavage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335 2.6 Mucociliary Transport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335 3. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 336 4. Occupational Rhinitis and Asthma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337 5. Effect of Atopy and Smoking on Occupational Rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337 6. Quality of Life and Cost of Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337 7. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337 8. Prevention and Treatment of Occupational Rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 338 9. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339

Abstract

Occupational rhinitis is a common heterogeneous group of inflammatory conditions in the nose, caused by exposure to airborne irritants and sensitizers in the occupational environment. The mechanism can be allergic, neurogenic or toxic. Data from several epidemiologic studies indicate that animal dander, organic dusts, latex and chemicals can cause occupational rhinitis, but because of methodological problems as well as weaknesses in the definition of occupational rhinitis, occupational exposure is probably an underestimated cause of rhinitis. The effect of rhinitis on the mental aspects of quality of life and substantial costs due to loss of productivity make it important to diagnose and treat occupational rhinitis. Diagnosis relies on a history of exposure, skin prick testing and, if possible, nasal provoacation. Avoidance of exposure, protective measures at the workplace and medical treatment, with agents such as second generation antihistamines and nasal corticosteroids, can make it possible to avoid progress of the disease from rhinitis to asthma. The efficacies of montelukast, a leukotrienne receptor antagonist, and omalizumab, an anti-immunoglobulin E monoclonal antibody in the treatment of occupational rhinitis are yet to be evaluated

The prevalence of occupational rhinitis has been estimated at 5–15%.[1] Animal dander, organic dusts, latex and chemicals have been found to cause occupational rhinitis in epidemiological stud-

ies as well as cohort studies of exposed workers.[2-4] Still little is known about the magnitude of the problem and at least some percentage of rhinitis cases of unknown origin, constituting about

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half the cases of rhinitis, could be attributed to occupational rhinitis.[4-6] Rhinitis has recently been found to have a significant effect on the quality of life of patients and to be responsible for substantial costs for society due to reduced productivity.[7,8] Occupational rhinitis may also be the field of rhinitis in which preventive measures and avoidance have the greatest chance of being successful. This makes the study of occupational rhinitis one of the most challenging fields in rhinology today. The studies presented in this review have been identified using Pubmed/Medline; they include original research articles and review articles from the past two decades. Medline search terms used were occupational rhinitis, rhinitis AND animal dander, flour, baker, textile, wood and paper dust, epoxy, latex, storage mites and acrylates. Although there is a close relationship between occupational rhinitis and asthma, this review focuses primarily on aspects of occupational rhinitis.

Rhinitis is defined as an inflammation of the lining of the nose characterized by one or more of the following symptoms including nasal congestion, rhinorrhea, sneezing and itching.[10] There is currently no agreed international standard method to objectively diagnose nasal inflammation, and symptom evaluation has therefore been assigned a great deal of importance in the diagnosis of occupational rhinitis. One problem with symptom evaluation is that the nose is the first line of respiratory defense, with the function of protecting the lower airways from exposure to nonfiltered and dry air. The symptoms of rhinitis are thus part of a normal nasal defense against the inhalation of dust or other irritants and, in fact, 40% of individuals experience nasal symptoms daily without having rhinitis.[10,13] Another problem is that nasal symptoms other than those included in the definition of rhinitis have been found to be relevant in the diagnosis of occupational rhinitis. Additional symptoms include crust formation in ship-builders and paper workers,[9,14] increased nose bleeding in wool-cotton workers[15] and impaired sense of smell in woodwork teachers, factory workers and tank cleaners.[16-18]

1. Definition and Classification 2. Objective Assessment of Occupational Rhinitis The term occupational rhinitis has been in use since the beginning of the 20th century and refers to rhinitis caused by exposure in the occupational environment.[1,9] According to the 1994 International Consensus Report on the Diagnosis and Management of Rhinitis, occupational rhinitis is classified as ‘other’ rhinitis, next to allergic and infectious rhinitis.[10] Allergy may, however, be an important mechanism behind occupational rhinitis and, as a result, the classification is not entirely logical. It does, however, illustrate the fact that the mechanism behind most cases of occupational rhinitis is unknown. Baraniuk et al.[11] have suggested a further classification of occupational rhinitis into annoyance, immunological, irritational and corrosive rhinitis. Annoyance rhinitis denotes that mild occupational exposure can exacerbate pre-existing rhinitis; immunological rhinitis denotes allergic occupational rhinitis such as allergy to laboratory animals and is often characterized by rhinoconjunctivitis; irritational occupational rhinitis denotes neurogenic inflammation with a burning sensation in the eyes, nose and throat and is caused by prolonged exposure to irritating chemicals; corrosive occupational rhinitis denotes permanent damage to the olfactory system or systemic intoxication due to exposure to high concentrations of gases. Corrosive occupational rhinitis is similar to the reactive upper-airways dysfunction syndrome (RUDS), which is defined as chronic rhinitis stemming from exposure to an irritant and has been described after a single exposure to volatile organic solvents.[12] © Adis Data Information BV 2003. All rights reserved.

Several methods have been used to detect signs of nasal inflammation in patients with occupational rhinitis. These methods analyze the nose from different aspects of its function, such as nasal air flow, intranasal geometry, mucociliary transport rate and secretion of inflammatory markers. The correlations between these methods and nasal symptoms have been poor, and thus there is no gold-standard method for the detection of nasal inflammation in occupational rhinitis. The use of objective methods is considered important to confirm the diagnosis of occupational rhinitis and the causal relationship between symptoms, signs of disease and exposure.[3] Some of the most frequently used methods are therefore presented here. 2.1 Anterior Rhinoscopy

In acute allergic or infectious rhinitis, it is often possible to find changes in the nasal mucosa that correspond to the nasal symptoms, such as red or swollen nasal mucosa. This can be seen in allergic occupational rhinitis after a nasal provocation test.[19] In cohort studies of workers with recurrent or chronic nasal symptoms, data from anterior rhinoscopy are scarce and the findings less obvious. Welch et al.[9] found dry atrophic mucosa and crusting in 66% of shipyard workers, but there was no control group. Holmstr¨om et al.[20] found a reduction in nasal symptoms after 3 weeks of nasal lavage treatment in wood-industry workers, but anterior rhinoscopy revealed no change. Tor´en et al.[21] found a Am J Respir Med 2003; 2 (4)

The Dilemma of Occupational Rhinitis

non-significant difference in visible crusts, reddening and swelling of the nasal mucosa between workers exposed to lime dust and controls. The use of a rigid or flexible endoscope can provide more information than anterior rhinoscopy, such as deposition of particles in the middle meatus or the presence of nasal polyps, because the whole of the nasal cavity is examined. 2.2 Anterior and Posterior Rhinomanometry

Anterior rhinomanometry is currently the most widely used and best studied of the objective methods for assessing nasal air flow.[22] The air flow through one nostril is assessed simultaneously with the pressure in the other nostril. Posterior rhinomanometry is an alternative method, where the transnasal pressure is measured with an oral tube in the pharynx. This method has been used to show increased nasal resistance after exposure to ozone and sulfur dioxide, but has gained less attention following the introduction of active anterior rhinomanometry, which is considered simpler to perform by many investigators.[23,24] Anterior rhinomanometry has good reproducibility, but data concerning the correlation to the subjective sensation of air flow have been contradictory.[25-30] Anterior rhinomanometry correlates well with other methods such as nasal peak flow and acoustic rhinometry and has been suggested to be the method of choice to evaluate the nasal reaction after a nasal provocation test.[31,32] 2.3 Acoustic Rhinometry

Acoustic rhinometry measures the inner diameter and volume of the nose by means of reflected sound. It is noninvasive and fast and requires a minimum of cooperation from the patient.[33] However, the method correlates poorly with self-assessed symptoms of nasal obstruction and with other parameters such as height or bodyweight.[28,34-36] On the other hand, acoustic rhinometry has high reproducibility and correlates well with computed tomography measurements and rhinomanometry.[25,37,38] Acoustic rhinometry has been used to evaluate nasal provocation tests and to evaluate nasal obstruction in school personnel exposed to mechanical ventilation (supply ventilation, exhaust ventilation), dental personnel exposed to acrylates and workers exposed to paper dust.[14,19,39,40] 2.4 Peak Nasal Expiratory and Inspiratory Flow

Peak nasal expiratory peak flow (PNEF) and peak nasal inspiratory flow (PNIF) rates have been adapted from bronchial PEF, by the addition of a nasal mask, to assess nasal function in occupational rhinitis.[41,42] PNEF and PNIF correlate well with each other, as well as with rhinomanometry.[32,43] However, they are both © Adis Data Information BV 2003. All rights reserved.

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dependent on lung capacity and effort and thus exhibit substantial inter- and intra-individual differences.[32,44] Some concern has been raised about PNIF, because of the socalled plateau effect, seen at high flow rates in the decongested nose, where disorganized air flow can lead to a loss of driving pressure in combination with collapse of the alar region, resulting in a false lower air flow.[45] In the diseased nose, however, high flow rates are seldom a problem and the plateau effect thus appears to be less important in clinical studies of rhinitis. Used in the same individual as his/her control or when comparing groups of individuals, the peak flow methods are outstanding in terms of simplicity, economy and utility. Both PNEF and PNIF have been used to assess nasal obstruction in workers exposed to wood dust and paper dust.[14,20,46] 2.5 Nasal Lavage

Analyses of inflammatory cells and markers from nasal biopsies and fluids are a vast area of nasal research. There are several different techniques for obtaining inflammatory cells and cell markers from the nasal mucosa surface or tissue, nasal lavage being the most common. Depending on the technique used, epithelial cells and mucus with inflammatory cells are rinsed off the nasal mucosa with a saline solution and then analyzed for inflammatory cells and markers.[47] Nasal lavage has previously been used to assess nasal inflammation in patients with occupational rhinitis. Potent chemicals such as acrylates have been found to increase eosinophil cationic protein and albumin in the nasal lavage, while flour and wood dust have been shown to increase levels of myeloperoxidase and numbers of neutrophils in the nasal lavage.[18,48,49] Nasal cytology can also be obtained as scrapings or brush samples from the anterior part of the nasal mucosa. The procedure is well suited for outpatient studies and has been used to show squamous cell metaplasia in workers exposed to formaldehyde.[50] 2.6 Mucociliary Transport

Mucociliary transport is the most important means by which dust particles and chemicals that are precipitated in the nose are got rid of. Mucociliary transport can be analyzed indirectly by measuring the time taken to transport a crystal of saccharine, a dot of dye or a radioactive particle from the anterior part of the nose to the nasopharynx.[51] Alternatively, the activity of the cilia responsible for mucociliary transport can be observed under the microscope in nasal biopsies.[52] The loss of cilia has been found in nasal biopsies from spray painters, and lime dust and wood dust have been found to reduce the mucociliary transport rate in a dosedependent fashion.[21,53,54] Am J Respir Med 2003; 2 (4)

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3. Epidemiology The prevalence of allergic rhinitis in the general population has been estimated at 20%, while nonallergic rhinitis comprises another 20%, making rhinitis one of the most common conditions in the population.[4-6,55] Epidemiological studies can be used to demonstrate an association between a certain factor and a disease but cannot establish a causal relationship.[9] Longitudinal, population-based studies are preferred when estimating the relative risk of a certain occupational exposure in relation to rhinitis. The reason is that populationbased studies do not exclude previously exposed individuals who are no longer under exposure. The weakness of this study design is that it often relies on self-reported data and is subject to recall bias.[56] However, as a substitute for a prospective approach, many studies have a design with retrospective assessment of exposure in population-based cross-sectional studies. Epidemiological studies of occupational rhinitis are scarce.[3,57] In a cross-sectional, population-based interview study from Singapore, including 2868 adults, self-reported exposure to occupational irritants doubled the risk of rhinitis.[58] Hellgren et al.[4] recently conducted a questionnaire-based, cross-sectional study evaluating the risk of rhinitis after occupational exposure to several substances, in a large population sample (n = 2044). From 28 different types of occupational exposure, they found an increased risk of rhinitis associated with dusts (wood, textile), fire fumes, chemicals (paint hardeners, rapid glues) and working as a cleaner. A different approach to obtaining epidemiological data is the case-control study. The Finnish Register of Occupational Disease has registered new cases of allergic occupational rhinitis in Finland since 1964 and is based on clinical examinations of patients with suspected occupational rhinitis. The diagnosis includes symptoms, a skin prick test or radioallergosorbent test (RAST) and a nasal provocation test. Based on 1244 cases of occupational rhinitis, animal dander, flours, wood dust and textile dust, food, spices, storage mites, enzymes, natural rubber latex and chemicals were the most common factors associated with allergic occupational rhinitis.[3] Women were more at risk than men, with the highest risk recorded between the ages of 40 and 44 years. Men were most at risk between the ages of 25 and 29 years. Differences in the age groups at highest risk was thought to reflect different types of exposure due to men and women having different occupations. An extensive survey of cross-sectional, workplace-based cohort studies from several countries also confirms that animal dander, organic dusts, latex and some chemicals are the major risk factors for occupational rhinitis that are known today (table I).[2,59] © Adis Data Information BV 2003. All rights reserved.

Most reports on occupational rhinitis are derived from workplace-based cohort studies.[2] This study design is advantageous because the exposure is easier to assess and the causal relationship Table I. Data from three different epidemiologic studies showing major irritants associated with occupational rhinitis Major irritant

Population-based National case questionnaire sample clinical study[4] evaluation[3]

Workplace-based cohort studies[2]

Fire fumes

✓

–

–

Cleaner

✓

–

–

Animal dander

*

✓

✓

Flour

*

✓

✓

Wood dust

✓

✓

✓

Textile dust

✓

✓

✓

Anhydrides

–

✓a

✓

Organisms

*

✓b

✓c

✓

✓d

Organic material NS Formaldehyde

✓

✓

–

Hairdresser’s chemicals

*

✓

✓e

Various chemicals

*

✓

✓

Plant material

*

✓

✓

Food

*

✓

✓

Natural resins

*

✓

–

Mineral (dust)

✓

✓

–

Epoxy resins

*

✓

✓

✓

✓f

✓f

Pharmaceuticals *

✓

✓

Molds

*

✓

–

Latex

*

✓

✓

Glues

✓

✓g

–

Amines

*

✓

–

Welding fumes

NS

✓

–

Amylase

*

✓

✓

Paper dust

✓

–

✓

Paint hardeners

Metals

–

–

✓

Reactive dyes

–

–

✓

a

Phthalic anhydrides.

b

Storage mites.

c

Insects, mites and biological enzymes.

d

Grain dust.

e

Specifically persulfates.

f

Specifically diisocyanates.

g

Specifically acylates.

NS = nonsignificant risk; ✓ = present; * = not asked for; – = no data.

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between agent and symptoms can be studied. On the other hand, these studies are expensive to perform and are associated with methodological problems, such as the ‘healthy worker’ effect, which means that individuals who have developed symptoms have left the exposed environment and are thus not included in the study, which could result in underestimation of the true risk of exposure. 4. Occupational Rhinitis and Asthma Population-based asthma studies confirm that 78–85% of individuals with asthma have rhinitis, regardless of occupational exposure.[55,60,61] Rhinitis has been reported in 92% of persons with occupational asthma compared with 74% of those with nonoccupational asthma.[59] Several theories have been proposed to explain the relationship between rhinitis and asthma, based on aspiration of inflammatory cells and/or mediators from the nose, the presence of a nasobronchial reflex, increased load on the lower airways due to nasal obstruction and reduced nitric oxide inhalation from the nose.[62-66] There is, however, a growing body of evidence to indicate that the stimulation of inflammatory progenitor cells in the bone marrow is the common link between rhinitis and asthma.[67,68] Occupational rhinitis usually precedes asthma.[69] Rhinitis preceding asthma has been reported more commonly with exposure to high molecular weight agents than with low molecular weight agents.[59] High molecular weight agents are capable of producing an immunoglobulin (Ig)E-mediated reaction, whereas low molecular weight agents can act as antigens only in combination with larger molecules. An IgE-mediated reaction is therefore less common with LMW agents.[2] 5. Effect of Atopy and Smoking on Occupational Rhinitis Atopy as a risk factor for the development of occupational rhinitis is controversial, as is the definition of atopy. Some authors define atopy as a positive skin prick test and others as a positive history of allergy. In a prospective study of trainee bakers, a history of allergic rhinitis increased the risk of developing respiratory symptoms after graduation from the bakery school (after 30 months) six times, whereas atopy defined as a positive skin prick test at entry, was not associated with an increased risk of developing occupational rhinitis.[70] The majority of studies addressing exposure to high molecular weight agents such as seen among workers in the fish industry, bakers, latex workers and pharmaceutical workers have, however, shown an association between specific sensitization and occupational rhinitis.[2] © Adis Data Information BV 2003. All rights reserved.

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Current smoking has been reported as a risk factor for chronic rhinitis with a dose-response type of relationship.[71] In occupational rhinitis the relationship between smoking and occupational sensitization is, however, inconsistent and the role of smoking as a risk factor for occupational rhinitis has still to be elucidated.[72] 6. Quality of Life and Cost of Illness Several studies have shown that rhinitis has a negative effect on the quality of life of patients similar to that observed in mild to moderate asthma. Whereas asthma predominantly affects the physical aspects of quality of life, rhinitis mainly affects the mental well-being of patients.[7,60,73] The most frequent problems encountered by individuals with rhinitis are difficulties with sleep, non-nasal symptoms such as thirst, poor concentration and headache, practical problems such as having to carry tissues and repeatedly blow the nose, activity problems and emotional problems.[74] The negative effect of occupational rhinitis on work and employment has been studied to a lesser extent and the data thus relate to other forms of rhinitis. Malone et al.[75] examined data from the National Medical Expenditure Survey for cost of illness of allergic rhinitis in the US for the year 1987. Allergic rhinitis was defined as self-reported hay fever during the last 12 months and it was estimated that the prevalence in the total US population was about 16%. It affected 27 million adults, and it was estimated that about 800 000 days of lost work could be directly attributed to allergic rhinitis. The estimated indirect cost of work-associated loss of productivity was $US37 million. By way of comparison, it is interesting to note that the reduction in work productivity due to asthma accounts for hundreds of millions of dollars every year in the US.[76] In a Canadian drug trial involving 651 individuals with rhinitis due to ragweed allergy, the working participants reported at baseline a 1.8% loss of working time and a 40% work impairment.[77] Blanc et al.[78] have assessed work disability in a random sample of individuals with a physician diagnosis of asthma, with or without concomitant rhinitis, compared with those with only physicianreported rhinitis. Their main findings were that, among individuals with rhinitis, a reduction in work productivity appeared to be the dominant disability effect, as compared with asthma, where reduced workforce participation was more common. Otherwise, there were no consistent differences between rhinitis and asthma with or without rhinitis. 7. Diagnosis Because of the lack of standardized tools for diagnosis of occupational rhinitis, the medical history plays a prominent role in Am J Respir Med 2003; 2 (4)

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disease investigation. A prerequisite for occupational rhinitis is that the patient is exposed at the workplace to allergens or irritants that may cause rhinitis. An additional prerequisite for a causal relationship between exposure and rhinitis is that the exposure occurs before the onset of disease. Rhinitis occurring in conjunction with first exposure is usually indicative of pre-existing disease, whereas rhinitis occurring after an interval is more consistent with an occupational activity. Chronic rhinitis after a single exposure to a respiratory irritant probably accounts for occupational rhinitis in a minority of patients.[12] It is important to ask the patient carefully about the timing of the first signs of nasal symptoms. For instance, nasal symptoms can occur after a change of job, after the introduction of new materials into the workplace, or after a new process is introduced. Nasal symptoms may occur as a harbinger of illness, preceding asthma symptoms by many months or years. A deterioration in nasal symptoms during the working week with an improvement during weekends or vacations is highly ˚ and Soderman[46] suggestive of occupational rhinitis.[1] Ahman showed in a study involving woodwork teachers how the nasal symptoms deteriorated and the peak nasal expiratory flow decreased during the working week, only to return to basal values after the weekend. These distinctions may be blurred, however, with increasing length of exposure. In some cases, for instance, symptoms of occupational rhinitis may not appear until the evening. Information on duration and intensity of exposure can be important. For some individuals, such as dye-house operators, platinum refinery workers, bakers and workers exposed to laboratory animals, a dose-response relationship has been demonstrated.[2] Associated symptoms involving the bronchi, conjunctiva and the skin are common in allergic occupational rhinitis and should be investigated.[1] A positive skin prick test and/or RAST can indicate allergic occupational rhinitis. Sensitization may take between weeks and 20 years to develop. In a prospective study of trainee bakers (n = 125), the number of skin-prick positive individuals to αamylase increased from four to ten during a period of 30 months.[70] It is, however, important to differentiate between sensitization in individuals without symptoms and sensitized individuals with rhinitis. As an example, in different studies involving bakers, sensitization to wheat flour by skin prick testing was found to vary from 5–16%.[79-83] Skin prick tests can be used to evaluate other forms of rhinitis. The possibility that several forms of rhinitis coexist in the same patient must be taken into consideration. In paper-recycling workers with a high prevalence of nasal catarrh, 54.5% of the workers © Adis Data Information BV 2003. All rights reserved.

Hellgren et al.

were skin prick test-positive to mites and molds, whereas only 15.8% were positive to paper extracts.[84] A visit to the workplace and exposure assessment are of great importance when diagnosing occupational rhinitis.[1] In some workplaces, occupational exposure may be very complex, requiring detailed assessments with an industrial hygiene consultant, but simple questioning may lead to the suspected agent in many work practices.[85] For example, cyanoacrylates or epoxy resins should be suspected as a potential exposure whenever the use of rapid glues is reported. In cases where exposure to a single high-level irritant has triggered new-onset rhinitis (e.g. RUDS), an exposure history should be clear cut. This requires an extended occupational history. Nasal provocation tests can be conducted in the workplace or in the laboratory, either by adding the substance to the inhaled air or by placing the agent on a paper disc that is inserted in the nose.[2,8,19] The provocation should be made when the rhinitis symptoms are at a minimum and in the absence of anti-inflammatory medication to avoid confounding.[1] It has been suggested as standard to monitor the effect of nasal provocation with symptom evaluation, rhinoscopy and rhinomanometry.[19] The problem with nasal challenge as a diagnostic test is that patients with rhinitis due to toxic or irritating substances will not be properly diagnosed; i.e. a test with high specificity and low sensitivity. In Finland legislation demands nasal provocation as a routine for diagnosis and several authors advocate its use.[2,3,8] Plavec et al.[86] have assessed nasal responsiveness to increasing doses of intranasal histamine, expressed as the concentration of histamine causing a >75% rise of total nasal resistance compared with baseline. Significantly higher nasal responsiveness was found in workers exposed to respiratory irritants than in unexposed controls. 8. Prevention and Treatment of Occupational Rhinitis The most important intervention for occupational rhinitis is prevention. The long-term strategy must be primary prevention, which means reduction or elimination of harmful exposures and should mainly be done by changing industrial processes e.g. exclusion of powdered latex gloves in instances of latex allergy. Other changes could include improved ventilation, both in general and close to the workstation. Substitution of sensitizing agents is another desirable strategy. Certain exposures, such as flour dust, should be monitored to be confident about levels below current threshold limits. Once the relationship between exposure and occupational rhinitis has been established, treatment should inAm J Respir Med 2003; 2 (4)

The Dilemma of Occupational Rhinitis

clude avoidance of exposure, as many studies have indicated that occupational rhinitis may develop into occupational asthma.[87-89] Exposure can be avoided by the use of protective masks or suits as well as adjustments in the occupational environment, including removal of the specific agent. Tor´en et al.[21] found an improvement of nasal symptoms and mucociliary clearance in workers exposed to lime dust in a Swedish pulp-mill after adjustments in the factory that reduced the exposure to lime dust. However, reduction of exposure does not always result in the reduction of symptoms.[90] The medical treatment of occupational rhinitis is no different from the treatment of other forms of inflammatory rhinitis. Nasal itch and sneezing respond well to systemic or local antihistamines, but older sedating antihistamines should be avoided because of an increased risk of occupational injuries.[86] Antihistamines have, however, little effect on nasal blockage compared with nasal corticosteroids.[87] Leukotriene antagonists (e.g. montelukast) and anti-Immunoglobulin E monoclonal antibody (omalizumab) are new drugs aimed at treatment of allergic rhinitis,[91] and their possible role in occupational rhinitis is still to be elucidated.[92] The efficacy of vocational selection of workers to reduce the incidence of occupational rhinitis has not been studied. One possibility is to screen for individuals with atopy. However, with respect to occupational asthma this has proved to be an inefficient strategy, because a number of individuals without atopy will be sensitized and many atopic individuals will not be sensitized.[93] 9. Conclusion Occupational rhinitis is a common, heterogeneous group of inflammatory conditions in the nose, caused by exposure to airborne irritants and sensitizers in the occupational environment. The mechanism can be allergic, neurogenic or toxic. Epidemiological studies are crucial in occupational rhinitis to direct attention because of the vast number of substances encountered in the workplace. There is, however, an urgent call for standardization in the definition and diagnosis of occupational rhinitis. Currently, diagnosis relies on a thorough history, skin prick test, assessment of exposure and, if possible, nasal provocation. To better understand the mechanisms of occupational rhinitis it is important to improve the epidemiological tools and to develop more accurate methods for assessment of nasal inflammation and exposure. Acknowledgements The authors would like to acknowledge The Herman Krefting Fund for Medical Research, The Medical Society of Got¨eborg, GSK, Sweden, Torsten and Ragnar Soderbergh Foundation for Scientific Research and Astra Zenaca, Sweden. © Adis Data Information BV 2003. All rights reserved.

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Occupational injuries and

medication use. Am J Ind Med 1996; 30 (2): 234-9

Correspondence and offprints: Dr Johan Hellgren, Department of OtoRhino-Laryngology, Head and Neck Surgery, Sahlgrenska University Hos¨ pital, SE-413 45 Goteborg, Sweden. E-mail: [email protected]

Am J Respir Med 2003; 2 (4)