This document discusses occupational rhinitis (OR), including its definition, classification, epidemiology, investigation and diagnosis, management, and prevention. OR is an inflammatory disease of the nose caused by exposures in the workplace. It can be allergic or non-allergic, with allergic OR further classified as IgE- or non-IgE-mediated. Common causes include flour, latex, diisocyanates, and wood dust. OR has a prevalence of 5-15% in the working population and is associated with increased risk of occupational asthma. Diagnosis involves clinical history, examination, and tests like nasal provocation. Management focuses on avoiding exposure, medications, and immunotherapy. Prevention emphasizes controlling exposures and medical surveillance programs.

1. OCCUPATIONAL RHINITIS
A Wutthisanwatthana

2. Outline
◦ Definition and classification
◦ Epidemiology
◦ Investigation and diagnostic approach
◦ Management
◦ Prevention

3. DEFINITION AND
CLASSIFICATION

4. Malo JL, Vandenplas O. Definitions and classification of work-related asthma. Immunol Allergy Clin North Am. 2011 Nov;31(4):645-62

5. Limitation of Definition
◦ Nasal airflow limitation is not always present
◦ Methods used for assessing nasal patency, nonspecific
hyperresponsiveness, and inflammation
◦ Not been thoroughly validated
◦ Underused in clinical practice

6. Definition
◦ “An inflammatory disease of the nose, which is characterized by
intermittent or persistent symptoms (i.e. 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 the
workplace”
Moscato G, Vandenplas O, Gerth Van Wijk R, Malo JL, Perfetti L, Quirce S, et al. EAACI position paper on occupational rhinitis. Respir Res. 2009; 10(1): 16

7. Work-Related Rhinitis
Rhinitis caused by work
=
Occupational rhinitis (OR)
Allergic
IgE-mediated Non-IgE-mediated
Non-allergic
Reactive upper airway
dysfunction syndrome (RUDS)
Irritant-induced OR Corrosive rhinitis
Rhinitis exacerbated by work
=
Work-exacerbated rhinitis
(WER)

8. Occupational Rhinitis: Allergic
◦ Immunologically mediated hypersensitivity reactions resulting from
antibody- or cell-mediated mechanisms
◦ Nasal hypersensitivity to a specific occupational agent appearing after a
latency period
◦ Symptoms recur on re-exposure
◦ Causal role can be documented on an individual basis through nasal
provocation test (NPT)

9. Occupational Rhinitis: Allergic
IgE-mediated OR Non-IgE-mediated OR
• HMW i.e. (glyco)proteins from animal, insect,
grain, flour, latex, enzyme
• LMW: Platinum salts, reactive dyes, acid
anhydrides
• LMW e.g. isocyanates, persulphate salts,
wood

10. Occupational Rhinitis: Nonallergic
◦ Reactive upper airway dysfunction syndrome
◦ Single exposure to a high concentration of irritant agents
◦ Onset in minutes or hours
◦ Irritant-induced OR
◦ Repeated exposure to moderate to low doses of irritant agents (vapors,
fumes, smokes, dusts)
◦ Corrosive rhinitis
◦ Permanent inflammation of the nasal mucosa
◦ Exposure to high concentrations of irritating and soluble chemicals

11. Occupational Rhinitis: Nonallergic
◦ Mechanism not well defined
◦ Activation of transient response potential calcium ion channels 
depolarization of nociceptor nerve fiber  neuropeptide release
(substance P, neurokinin A)
◦ Increased signaling of the parasympathetic nervous system

12. Work-Exacerbated Rhinitis
◦ Pre-existing or concurrent rhinitis that is worsened by
workplace exposures
◦ Triggering factors
◦ Irritant agents (e.g., chemicals, dusts, fumes)
◦ Physical factors (e.g., temperature changes)
◦ Emotions
◦ Second-hand smoke
◦ Strong smells (e.g., perfumes)

13. Work-Exacerbated Rhinitis
◦ Similar clinical features to those of OR
◦ Considered only after careful exclusion of a specific sensitization to a
workplace agent through appropriate diagnostic procedures

14. Lemière C, Vandenplas O. Occupational Allergy and Asthma. In: Adkinson NF, Jr, Bocher BS, Burks AW, Busse WW, Holgate ST, Lemanske RF, et al.
Middleton’s allergy principles and practice. Philadelphia; Elsevier Saunders; 2014. 1095-105

15. Lemière C, Vandenplas O. Occupational Allergy and Asthma. In: Adkinson NF, Jr, Bocher BS, Burks AW, Busse WW, Holgate ST, Lemanske RF, et al.
Middleton’s allergy principles and practice. Philadelphia; Elsevier Saunders; 2014. 1095-105

19. EPIDEMIOLOGY

20. Prevalence
Moscato G, Vandenplas O, Gerth Van Wijk R, Malo JL, Perfetti L, Quirce S, et al. EAACI position paper on occupational rhinitis. Respir Res. 2009; 10(1): 16

21. Prevalence
Grammer LC 3rd. Occupational Rhinitis. Immunol Allergy Clin North Am. 2016 May;36(2):333-41

22. Incident
Moscato G, Vandenplas O, Gerth Van Wijk R, Malo JL, Perfetti L, Quirce S, et al. EAACI position paper on occupational rhinitis. Respir Res. 2009; 10(1): 16

23. High Risk Jobs –
Finnish Registry
Hytonen M, Kanerva L, Malmberg H, et al. The risk of occupational rhinitis. Int Arch Occup Environ Health 1997;69:487–90.

24. Specific Agents Causing Occupational
Rhinitis
◦ High-molecular-weight agents
◦ Baking products
◦ Latex
◦ Low-molecular-weight agents
◦ Diisocyanates
◦ Wood dust
◦ Hairdressing products

25. Baking Products
◦ Sensitizers
◦ Flour from cereal (wheat, rye, barley), soy, lupine, buckwheat
◦ Enzymes (fungal amylase, cellulase, xylosidase)
◦ Egg protein
◦ Others (sun flower seed, soy lecithine)
◦ Cummulative incident
◦ 12.4% IgE-mediated sensitization
◦ 8.4% OR
◦ 6.1% OA

26. Latex
◦ Tropical rubber tree Hevea braziliensis
◦ 13 allergens characterized
◦ Hev b 5, Hev b 6.01/6.02  health care workers
◦ Hev b 1, Hev b 3  spina bifida
◦ Amount of elutable protein from medical gloves to be less than
200 µg/m2 for medical gloves
◦ SCIT and SLIT (placebo-controlled) reduced cutaneous, nasal, ocular
symptoms

27. Diisocyanates
◦ Isocyanate (R-N=C=O)
◦ Most common causes of OA in many parts of the world
Mold and core process
Insulation
Spray paints

28. Diisocyanates
◦ Threshold limite value at 5 ppb
◦ Most patients failed to recover years after removal from exposure
◦ Prognosis better in HDI > TDI and MDI

29. Wood Dust
◦ Cause hypersensivity pneumonitis, chronic bronchitis, mucous
membrane irratation, organic dust toxic syndrome
◦ Western red cedar
◦ Pacificic Northwest region
◦ Caused by plicatic acid (MW 440)
◦ Isolated late phase and biphasic reaction OA
◦ Bleaching products, persulfate, hair dye (p-phenylenediamine), latex
Hairdressing Products

30. Lemière C, Vandenplas O. Occupational Allergy and Asthma. In: Adkinson NF, Jr, Bocher BS, Burks AW, Busse WW, Holgate ST, Lemanske RF, et al.
Middleton’s allergy principles and practice. Philadelphia; Elsevier Saunders; 2014. 1095-105

32. Risk
Factors
Exposure
SmokingAtopy

33. Level of Exposure

34. Level of Exposure

35. • Atopy
• Smoking

37. Relationships with Occupational Asthma
◦ 92% OA has symptoms of OR
◦ Prevalence of symptoms was not different for HMW and LMW
◦ HMW agents have more pronounced symptoms
◦ 20-78% reported OR developed before OA
◦ ↑risk of asthma (RR 4.8, 95%CI 4.3–5.4) compared to subjects with
other occupational diseases

38. INVESTIGATION AND
DIAGNOSTIC
APPROACH

39. Clinical and Occupational History
◦ Employment history (past and current)
◦ Duration of employment at current job before onset
◦ Agents, tasks or processes associated with the onset or aggravation of
symptoms
◦ Exposure history: Duration, frequency, concentration
◦ Material safety data sheets
◦ Improvement away from work
◦ Rhinitis symptoms (nature, severity, impact)

40. Nasal Examination
◦ Using anterior rhinoscopy and nasal endoscopy
◦ To rule out other nasal pathologies that may mimic rhinitis or aggravate
nasal obstruction

41. Physiological Assessment
Nasal patency
Nasal inflammation
Nonspecific nasal hyperreactivity

42. ◦ Rhinomanometry, acoustic rhinometry and peak nasal inspiratory flow
◦ Great inter-individual variability
◦ Well-defined reproducibility
Nasal Patency

43. ◦ Nasal secretions
◦ Weighted for quantifying the secretory activity
◦ Measure inflammatory cells and mediators
◦ Nasal lavage
◦ Nasal biopsy
◦ Nasal scrapings or brush samples
Nasal Inflammation

44. ◦ Not much documented in OR
◦ Stimuli: Histamine, methacholine,
and cold dry air
Nonspecific Nasal Hyperreactivity

45. Immunological Tests
◦ Skin prick test
◦ Serum allergen-specific IgE antibodies
◦ Sensitivity and specificity in comparison with NPTs evaluated in only
few studies
◦ The major limitation
◦ Lack of commercially available
◦ Lack of standardized extracts

46. Beach J, Russell K, Blitz S, Hooton N, Spooner C, Lemiere C, et al. A systematic review of the diagnosis of occupational asthma. Chest. 2007
Feb;131(2):569-78

47. Nasal Provocation Tests
◦ Gold standard
◦ Performed in the laboratory or at work
◦ Positive
◦ Secretion amount of 100 mg and 210 mg
◦ 15% and 30% decrease in the minimum cross-sectional area
◦ 50% and 100% increase in the resistance
Pirila T, Nuutinen J. Acoustic rhinometry, rhinomanometry and the amount of nasal secretion in the clinical monitoring of the nasal provocation test. Clin
Exp Allergy 1998;28:468–477
30 min 60 min
Sensitivity Specificity Sensitivity Specificity
Secretion 96 95 100 89
Acoustic rhinometry 87 84 87 89
Rhinomanometry 87 89 96 89

49. MANAGEMENT

50. Environmental Intervention
◦ Complete avoidance of exposure
◦ The worker has nonspecific bronchial hyper-responsiveness
◦ Relocation
◦ Reduction of exposure

51. Pharmacology and Immunotherapy
◦ Medication is similar to that of non-occupational allergic rhinitis
◦ 2nd generation antihistamines and LRTA for allergic OR
◦ Intranasal corticosteroid
◦ Intranasal antihistamine
◦ Immunotherapy
◦ Improved respiratory symptoms
◦ Purified rodent proteins, wheat flour extracts, and natural rubber latex
◦ Limited by the nonavailability of standardized extracts

52. PREVENTION

53. Primary Prevention
◦ Controlling exposure at the workplace
◦ Protective equipment
◦ Ventilation system
◦ Exposure time reduction
◦ Replacement of causative agent
◦ Identification of susceptible workers

54. Secondary Prevention
◦ Medical surveillance programs
◦ Preplacement and periodic administration of a questionnaire
◦ Detection of sensitization to occupational agents
◦ Early referral of symptomatic and/or sensitized workers
◦ Investigation of possible asthma in all workers with confirmed OR

55. Benefit
◦ Reduced incident of OA and OR caused by natural rubber latex,
enzymes, flour, laboratory animal, isocyanate