Allergic Disorders
8. Occupational asthma and allergies

https://doi.org/10.1067/mai.2003.77Get rights and content

Abstract

A diversity of airborne dusts, gases, fumes, and vapors can cause dose-related symptoms in individuals exposed in the workplace. More than 250 chemicals have been incriminated as a cause of occupational asthma (OA). The prevalence of OA ranges from 2% to 6% of the asthmatic population. Predisposing factors facilitating the development of OA include the work environment, climatic conditions, genetic proclivities, tobacco and recreational drug use, respiratory infection, and bronchial hyperresponsiveness. Pathogenetically, new-onset OA may be immunologic or nonimmunologic in origin. The immunologic variants are usually caused by high molecular-weight allergens such as grain dust and animal or fish protein. Symptoms ensue after a latent period of months to years. Nonimmunologic OA can be precipitated by a brief, high-level exposure to a potent irritant. Symptoms occur immediately or within a few hours of the exposure. In either instance, once the diagnosis is established, the worker should be removed from the workplace. If the diagnosis is made in a timely fashion, most workers experience improvement. Prevention is the best therapeutic intervention. (J Allergy Clin Immunol 2003;111:S530-9.)

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).

. Schematic conceptualization of several pathogenetic mechanisms of occupationally induced airway obstruction

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).

. Industrial agents frequently incriminated in causation of RADS

ChlorinePhosphoric acid
Toluene diisocyanateHydrochloric acid
PhosgeneHydrogen sulfate
Sulfuric acidAnhydrous ammonia
Smoke inhalationDiethylene diamine
Contrary to allergic OA, the onset is abrupt without a latent period. The clinical sequelae of any acute exposure depends on the physiochemical properties of the dust,

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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    Reprint requests: Emil J. Bardana, Jr, MD, Oregon Health and Sciences University, 3181 SW Sam Jackson Pk Rd, OP34, Portland, OR 97201-3098.

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