Allergic occupational diseases of the respiratory tract and lungs

Allergic rhinitis and bronchial asthma belong to the category of occupational allergic diseases.

Occupational allergic rhinitis

 * It is defined as an inflammatory disease of the nasal mucosa that arises in response to an airborne allergen occurring in the workplace. An estimated 15-20% of the population suffers from allergic rhinitis, the proportion of occupational rhinitis cannot be estimated.
 * Allergens are either common substances that are at an increased rate in the workplace (bakery flour, cereal dust…) or they are allergens specific to the given working environment (acid anhydrides in the formation of plastics…). In general, they are either high molecular weight (proteins, cereal dusts, insect antigens, latex…) or low molecular weight (diisocyanates, anhydrides, rosin substances, ATB…).

Professional exposure
Similar to asthma: flour processing (bakers, millers), grain handling (farmers), animal care, disinfection contact (paramedics), woodworking.

Etiopathogenesis

 * Repeated contact with the allergen leads to IgE-dependent mast cell activation → vasodilation, edema, nasal obturation.
 * Inflammation mediators stimulate afferent nerve endings → itchy nose, sneezing.
 * The accumulation of inflammatory cells is characteristic.

Pathology
Edematous mucosa with profuse serous exudation, the chronic form has a hyperplastic or atrophic character.

Acute

 * Itchy and irritated nose, sneezing and watery secretions, and is often accompanied by itching in the throat, eyes and ears. Asthma is often added to the symptoms.
 * These are type I reactions → symptoms appear within minutes, they go away quickly.

Chronic

 * In unrecognized and untreated recurrent acute rhinitis, they may become chronic after months to years.
 * Dominated by a stuffy nose and thick mucus, there may be chronic conjunctival changes, and tearing. Sneezing and itching are usually absent.

Examination methods

 * ENT examination,
 * intradermal skin tests - a basic range of inhaled allergens (house dust, feathers, mites…),
 * increase in serum IgE,
 * identification of professional specific IgE antigens,
 * nasal swabs - cytological analysis (predominance of eosinophils),
 * rhinomanometry - measures the resistance of nasal passages by quantitative measurement of nasal flow and pressure,
 * active anterior rhinomanometry is usually used,
 * it is also used in assessing the response to provocation tests,
 * positive rhinoprovocation test - after contact with the allergen, nasal flow decreases by at least 40% and nasal resistance increases by 60%.
 * Assessment of professionalism - we must demonstrate inhalation exposure to an allergenic substance in the workplace.
 * the clinical picture and the specific immunological response decide,
 * people often neglect this disease and go to the doctor after a long time.

Differential diagnosis

 * In particular, rhinitis of other origins (allergic seasonal, perennial…), it is necessary to think about other pathologies in the nasal cavity.

Occupational bronchial asthma

 * Asthma caused by inhalation of harmful nox at work,
 * they are not at all different from classic asthma,
 * estimate of the share of professionalism in asthma - 2–15%, the figure is probably significantly underestimated, doctors often do not consider professionalism at all.
 * Factors:
 * high molecular weight (animal and vegetable proteins),
 * low molecular weight (isocyanates, anhydrides, platinum salts),
 * inhalable chemicals (chlorine, ammonia),
 * pharmacologically active substances (insecticides),
 * physical factors (cold).

Professional exposure

 * The most common allergens:
 * flour (amylase) - millers, bakers, confectioners,
 * grain dust - silo workers, farmers,
 * urine and fur of laboratory and livestock - research laboratory staff, farmers, breeders,
 * disinfectants - paramedics,
 * natural and synthetic fibers - textile industry,
 * wood dust - saws, furniture industry,
 * proteolytic enzymes - food industry, production of washing powders,
 * rosin fumes and other welding fumes - fine mechanics, welding,
 * isocyanates, acrylic resins, paint pigments - chemical production.

Etiopathogenesis

 * Chronic inflammatory disease, main cells involved - mast cells and eosinophils,
 * inflammation increases bronchial reactivity, bronchospasm (obstruction) occurs,
 * mild asthma - there is no obstruction between the attacks, but there is hyperreactivity,
 * severe asthma - obstruction present even between attacks.

Types of occupational asthma

 * Immunological occupational asthma


 * occurs in a small number of exposed,
 * after an initial asymptomatic period, by inhalation of substances previously well tolerated by the worker,
 * there is a specific immune response to the substance,
 * are caused by two types of substances, depending on the different courses,
 * high-molecular-weight substances - induce an IgE response, it starts quickly,
 * low-molecular-weight substances - an unknown mechanism (probably a type III or IV response), onset later (often only after returning from work), disappears after 24 hours.


 * Irritation-induced asthma
 * The mechanism of origin is not entirely clear (probably plays a role in the release of neurotransmitters). It is formed after exposure to irritating substances (dust, aerosol, vapors, smoke).


 * RADS (reactive airways dysfunction syndrome)
 * It arises from short-term intensive exposure,


 * Reflex bronchoconstriction
 * Non-immunological response (without inflammation), when stimulating neuroreceptors with cold, dust, aerosols, fumes.


 * Pharmacological bronchoconstriction
 * It is formed by inhalation of substances that cause pharmacological bronchoconstriction, such as organophosphates.

Pathology


Wall remodelling occurs - thickening of the bronchiole wall (muscle hypertrophy), high epithelium, a lot of goblet cells, sometimes even squamous metaplasia, goblet cell hyperplasia occurs.

Clinical picture

 * Feeling of shortness of breath, wheezing with a maximum in the expiration (often audible at a distance - distance phenomena).
 * Coughs occur only at the workplace or in connection with work (after work).
 * Often still eye complications, rhinitis…
 * Symptoms get better on weekends and holidays.

Examination methods

 * Spirometry - obstructive ventilation disorder,
 * non-specific bronchoprovocation test - acetylcholine or histamine,
 * we find non-specifically that bronchi are hyperreactive.
 * Positivity criteria
 * decrease in FEV1 by 20%, MEF 25-75 by 30%, increase in resistance by 100%,
 * Specific inhalation bronchoprovocation tests - we administer specifically a certain substance that we suspect, either we administer commercially manufactured preparations or in an exhibition cabin (we will make the conditions of the workplace),
 * the positivity conditions are as for the non-specific test,
 * is potentially more dangerous (we give the allergen, not the body's own substance…),
 * only for people who do not rest obstruction and during hospitalization.
 * Elimination test - evaluation of health status after long-term exclusion from exposure.
 * Re-exposure test - after performing the previous one, we will re-engage in the process and find out the health condition.
 * Skin tests, ID spec. IgE, BAL…

Differential diagnosis
It is necessary to rule out other causes of obstruction - tumors, foreign bodies, laryngeal nerve paresis… The basic problem is the distinction between occupational asthma and pre-existing asthma aggravated by work.

Treatment
Exclusion from exposure, corticoids, β-2 mimetics, anticholinergics, theophylline, antiallergics.