Journal of Allergy and Clinical Immunology
Allergic Disorders8. Occupational asthma and allergies☆
Section snippets
Definitions
OA is characterized by variable airway obstruction associated with bronchial hyperresponsiveness (BHR). It is caused by bronchial inflammation secondary to inhalation of ambient dusts, gases, fumes, or vapors that are produced at, or incidentally present at the workplace.3 OA may also be defined as variable airflow limitation caused by a specific agent in the workplace.4 The definition of OA assumes significant legal importance in the context of different state workers' compensation statutes.5,
Epidemiology
Despite significant advances in the past several decades, there is a paucity of reliable data on the prevalence of occupational lung disorders. Much of what has been published represents anecdotal case reports, descriptions of small clusters of cases, or retrospective prevalence studies with notable exceptions.7, 8 There are essentially no long-term, prospective, longitudinal studies. In addition, nearly all epidemiological studies have relied on subjective data in identifying bronchial asthma.
Predisposing factors
The development of OA is influenced by a variety of industrial, climatic, genetic, social, and medical factors.
BHR
BHR is regarded as the physiologic hallmark of both OA and non-OA.41 BHR represents a common physiological pathway of several mechanisms leading to a lowered threshold of airway narrowing to bronchoconstrictor stimuli. BHR reflects and is likely partially caused by airway inflammation. Although the measurement of BHR provides quantitative insight in variable airflow obstruction, the relationship between BHR and respiratory symptoms is weak. Approximately 50% of subjects with BHR report no
Clinical and pathogenic features
From a clinical and pathologic perspective, new-onset OA can be divided into immunologic and nonimmunologic variants. The immunologic variant can be further divided into classic IgE-mediated and polyimmunologic variants. The nonimmunologic variant can be divided into reactive airways dysfunction syndrome (RADS), reflex bronchoconstriction, and pharmacologic bronchoconstriction (Fig 2).
Allergic OA
New onset, allergic OA can be triggered by a large number of HMW allergens, predominantly proteins derived from animals, plants, foods, and enzymes (Table I).48 In the majority of cases, OA induced by these agents is associated with evidence of a specific T helper type 2 lymphocyte response and specific IgE antibody. The initial step in the induction of an allergic reaction is the interaction of specific work-related allergens with IgE-sensitized mast cells, basophils, and other cells in airway
Nonallergic OA
Nonallergic OA usually results from a high-level exposure to a potent respiratory irritant in the workplace (Table II).
Chlorine Phosphoric acid Toluene diisocyanate Hydrochloric acid Phosgene Hydrogen sulfate Sulfuric acid Anhydrous ammonia Smoke inhalation Diethylene diamine
Differential diagnosis
In evaluating patients with suspected OA, it is important to understand the diagnostic criteria that distinguish it from a variety of closely related conditions. The most important initial step is to establish that asthma truly exists, ie, there must be a reliable demonstration of variable airflow obstruction by reliable physiologic testing.65 Asthma is not infrequently misdiagnosed even in the setting of a tertiary care asthma center.70 Second, since OA is linked to causes and conditions
History and physical examination
The medical history is a key element in the evaluation of OA. It provides the examiner with clinical features of work-related airway disease and assists in confirming the linkage to one or more likely work exposures. Rhinitis may precede development of lower-airway symptoms or may parallel asthmatic symptoms especially when HMW antigens are causal.74 Many patients have symptoms on a continuous basis triggered by other coincidental nonoccupational triggers or as a result of late-phase
Prevention and management
The most effective manner of preventing OA is to insulate at-risk workers from potentially hazardous agents. This requires the employer to adapt and enforce optimum industrial hygiene measures that will reduce or eliminate ambient levels of known irritants and immunogens. This can be accomplished by utilization of approved respirators that have been properly fit tested, by highly effective exhaust devices, or by installation of an enclosed automated process such as robotics. Many employers
Prognosis
The principle determinants of patient outcome subsequent to removal from the offending agent include the total duration of exposure, asthma severity at diagnosis, and the pathogenic mechanisms operative in the induction of OA.91 In addition, coexisting factors such as cigarette smoking, chronic sinusitis, and gastroesophageal reflux may also play an important role as prognostic modifiers.92 Removal of the patient with OA from the offending immunogen or irritant should result in clinical
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2018, ToxicologyCitation Excerpt :One variant of asthma in which non-allergic processes may play significant role is occupational asthma (Douwes et al., 2002). This phenotype is described as a variable airflow limitation in response to agents present in the workplace (Bardana, 2003). It is estimated that approximately 40% of occupational asthma incidents are caused by chemical substances, including low molecular weight compounds (LMW) (Bernstein, 2003).
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2008, Journal of Allergy and Clinical ImmunologyCitation Excerpt :The allergic variant can be further divided into classic IgE-mediated and polyimmunologic forms. The nonallergic variant can be divided into reactive airways dysfunction syndrome (RADS), pharmacologic bronchoconstriction, and reflex bronchospasm.1 The development of new-onset allergic OA requires a latent period during which sensitization develops (ie, months or years).
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Reprint requests: Emil J. Bardana, Jr, MD, Oregon Health and Sciences University, 3181 SW Sam Jackson Pk Rd, OP34, Portland, OR 97201-3098.