Occupational Immunologic Lung Disease Research Articles

Occupational immunologic lung disease.

Occupational immunologic lung disease is characterized by an immunologic response in the lung to an airborne agent inhaled in the work environment and can be subdivided into immunologically mediated occupational asthma (OA) and hypersensitivity pneumonitis (HP). Irritant-induced OA, a separate nonimmunologic entity, can be due to chronic exposure to inhaled irritants or reactive airways dysfunction syndrome (RADS). RADS is defined as an asthma-like syndrome that persists for >3 months and occurs within minutes to hours after a single exposure to a high concentration of a respiratory irritant. Workers in high-risk fields for OA include farmers, printers, wood workers, painters, plastics workers, cleaners, spray painters, electrical workers, and health-care workers. OA can be triggered by high-molecular-weight (HMW) proteins that act as complete allergens or by low-molecular-weight (LMW) sensitizers that act as haptens. HMW proteins (>10 kDa) are generally derived from microorganisms (such as molds and bacteria, including thermophilic actinomycetes), plants (such as latex antigens and flour proteins), or animals (such as animal dander, avian proteins, and insect scales) and are not specifically regulated by the Occupational Safety and Health Administration. LMW haptens that bind to proteins in the respiratory mucosa include some Occupational Safety and Health Administration regulated substances, such as isocyanates, anhydrides, and platinum. HP can present in an acute, chronic, or subacute form. The acute, subacute, and early chronic form is characterized by a CD4+ T-helper type 1 and CD8+ lymphocyte alveolitis. Classically, the bronchoalveolar lavage in HP will show a CD4/CD8 ratio of <1.

Chapter 17: Occupational immunologic lung disease

Occupational immunologic lung disease is characterized by an immunologic response in the lung to an airborne agent inhaled in the work environment and can be subdivided into immunologically mediated occupational asthma (OA) and hypersensitivity pneumonitis (HP). Irritant-induced OA, a separate nonimmunologic entity, can be caused by chronic exposure to inhaled irritants or reactive airways dysfunction syndrome, defined as an asthma-like syndrome that persists for >3 months and occurs abruptly after a single exposure to a high concentration of an irritating industrial agent. High-risk fields for OA include farmers, printers, woodworkers, painters, plastic workers, cleaners, spray painters, electrical workers, and health care workers. OA can be triggered by high molecular weight (HMW) proteins that act as complete allergens or low molecular weight (LMW) sensitizers that act as haptens. HMW proteins (>10 kDa) are generally derived from microorganisms (such as molds and bacteria, including thermophilic actinomycetes), plants (such as latex antigens and flour proteins), or animals (such as animal dander, avian proteins, and insect scales) and are not specifically regulated by the Occupational Safety and Health Administration (OSHA). LMW haptens that bind to proteins in the respiratory mucosa include some OSHA-regulated substances such as isocyanates, anhydrides, and platinum. HP can present in an acute, a chronic, or a subacute form. The acute, subacute, and early chronic form is characterized by a CD4(+) T(H)1 and CD8(+) lymphocyte alveolitis. Classically, the bronchoalveolar lavage will show a CD4/CD8 ratio of <1.

Occupational immunologic lung disease.

Occupational immunologic lung diseases either asthma or hypersensitivity pneumonitis, can occur in a wide variety of occupations from numerous antigens. New OILD syndromes and antigens are being reported constantly. In the case of some occupational agents that have been reported like isocyanates, formaldehyde, and Western red cedar, there is current investigation into the incidence of disease, mechanisms, and appropriate diagnostic criteria. A key principle in OILD is that prevention or at least early treatment by environmental control should be the goal. Determination of threshold limits for sensitization and adherence to these limits would be useful, for instance. In manufacturing processes in which this is not possible, workers and management in high risk industries should be educated so that affected workers are recognized early and avoidance can be instituted. Currently, there are no pre-employment screening criteria that have been shown to be very useful in predicting OILD. Prospective studies of animal handlers are underway and may provide useful information. In the case of TMA-exposed workers, prospective studies have demonstrated that serial immunologic studies are useful in predicting workers at risk for OILD and that reduction of airborne exposure will reduce prevalence. This sort of approach will probably be useful in studying other occupational agents. Such studies are complex and, to succeed, generally require cooperation and collaboration of physicians, industry, labor, industrial hygiene, and governmental agencies.

Use of Immunologic Technology in the Diagnosis of Environmental and Occupational Immunologic Lung Disease

Use of Immunologic Technology in the Diagnosis of Environmental and Occupational Immunologic Lung Disease

Use of immunologic technology in the diagnosis of environmental and occupational immunologic lung disease

Use of immunologic technology in the diagnosis of environmental and occupational immunologic lung disease

Guidelines for preparation and characterization of chemical-protein conjugate antigens: Report of the Subcommittee on Preparation and Characterization of Low Molecular Weight Antigens

Occupational asthma is a significant cause of morbidity in the workplace for which immunologic and nonimmunologic causative agents have been identified.’ For nonimmunologic forms of occupational asthma, a diagnosis may rely on a careful occupational history accompanied by documentation of work-related changes in pulmonary function associated with exposure to the causative agent. In some cases in which immunologic markers are not identifiable, diagnostic confirmation of occupational asthma may require specific bronchoprovocation challenge testing to the suspected causative substance. However, occupational immunologic lung disease (OILD) can be diagnosed with the assistance of either in vivo or in vitro immunologic tests. This report will present recommended guidelines for preparing and characterizing antigens that can be useful for the diagnosis of OILD caused by reactive low molecular weight (LMW) chemicals. These guidelines are based on established methodologies used to prepare antigens with LMW agents that have already been recognized to cause OILD. The acid anhydride, diisocyanate, and precious metallic salt groups of chemicals are prime examples of such substances that have been successfully used to prepare suitable antigens for both in vivo or in vitro testing of workers with OILD.’

Guidelines for the immunologic evaluation of occupational lung disease: Report of the Subcommittee on Immunologic Evaluation of Occupational Immunologic Lung Disease

mouse 2nd guinea pig antigens. J ALLERGY CLIN IMMUWI. 1085:16.124 79. Swanson MC. Agarwal MK, Yunginger JW, Reed CE. Guineapig-detiied allergens. Am Rev Respir Dis 1984: 129:844. 80. Twiggs JT. Agarwal MK, Dahlberg ME, Yunginger JW. Imnnmoch~:mical measurement of airborne mouse allergens in a laboratory animal facility. J ALLERGY CLIN IMM~N~I 19x2: 69522. 81. \‘irtanan T, Louhelainen K, Mantyjarvi R. Enzyme-linked immunoso-bent assay (ELISA) inhibition method to estimate the level of airborne bovine epidermal antigen in cowsheds. Int Arch Allergy Appl Imnunol 1986:81:253. XL. Chapman MD. Heymann PW, Wilkins SR, et al. Monoclonal irnmunoassays for major dust mite (Der~nafopha~oidesJ allergen. Dcr p 1 and Der f 1, and quantitative analysis of the allergen content of mite and house dust extracts J ALLERGY CLIN IMMUYOL 1987:X0:184. X3. Edwards RC, Beeson MF. Dewdney JM. Laboratory animal allergy: the measurement of airborne urinary allergens and the effects of different environmental conditions Lab Amm 1983;17:235

Allergic Diseases: Diagnosis and Management.

Review of immunology immunology of IgE mediated and other hypersensitive states models of asthma biochemical mediators of allergic reactions antihistamines allergens and other factors important in atopic disease pollen survey of the United States diagnosis of immediate hypersensitivity allergic rhinitis principles of immunologic management of allergic diseases due to extrinsic allergens allergic diseases of the eye and ear allergy to stinging insects urticaria angioedema, and hereditary angioedema food allergy atopic dermatitis Stevens-Johnson Syndrome and erythema multiforme drug allergy contact dermatitis nasal polyposis, sinusitis and non-allergic rhinitis anaphylaxis idiopathic anaphylaxis asthma hypersensitivity pneumonitis allergic bronchopulmonary aspergillosis occupational immunologic lung disease controversial and unproven methods in allergy diagnosis and treatment allergic disorders and pregnancy.

Responses of human airways to inhaled chemicals.

A variety of complex pulmonary immunologic responses may follow the inhalation of reactive chemical haptens. Trimellitic anhydride (TMA) is an industrial chemical used as a plasticizer (and serves as a model of occupational immunologic lung disease). Sensitization to TMA can take several forms--IgE-mediated asthma and rhinitis, a late reaction in the lung which resembles hypersensitivity pneumonitis and an irritated airways syndrome. Antibody studies show that TMA can combine with bodily constituents to form new antigenic determinants (NADs) which are probably the most immunogenic form of the compound.

The relationship of airborne trimellitic anhydride concentrations to trimellitic anhydride-induced symptoms and immune responses

Eighteen workers exposed to trimellitic anhydride (TMA) powder were evaluated in 1979. Twelve of these workers were available for longitudinal study until 1982. Annual clinical evaluations and serum radioimmunoassays for total antibody binding and specific IgE binding to 125I-TM-HSA were performed. In 1979, five workers had antibody against TM-HSA. Of these, three workers were diagnosed with the late respiratory systemic syndrome (LRSS) and one worker with TMA-induced allergic rhinitis. The LRSS workers had significantly elevated total antibody binding of 125I-TM-HSA and the worker with rhinitis had significantly elevated specific IgE binding of 125I-TM-HSA per milliliter of serum. Although TMA handling was intermittent throughout the year, average airborne dust concentrations from 1974 to 1978 at job stations of the two heaviest TMA-exposed occupations, operator and assistant operator, were 2.1 and 0.82 mg/m 3, respectively. After local exhaust ventilation had been improved, average airborne dust concentrations of TMA at the two latter job stations fell to levels of 0.03 and 0.01 mg/m 3, respectively, in 1982. The decrease in TMA exposure coincided with a gradual fall in total antibody binding of 125I-TM-HSA per milliliter in 1982 and symptomatic improvement in the three individuals with the LRSS. The continuous low-level exposure of the worker with TMA rhinitis was sufficient to elicit a rise in specific IgE against TM-HSA from 1.1 ng of 125I-TM-HSA bound per milliliter in 1979 to 2.12 in 1982. The results demonstrate that after establishment of IgG anti-TM protein antibodies associated with occupational immunologic lung disease, environmental control resulted in a decline in the IgG antibodies and absence of one form of occupational immunologic lung disease.

The evaluation of occupational airways disease in the laboratory and workplace

Occupational immunologic lung disease can be identified both in the individual patient under laboratory conditions and in a population of workers in industry. Occupational airways disorder is the most common occupational immunologic pulmonary process and is a disease of the airways caused by the inhalation of a substance or material that the worker manufactures or uses directly or that is incidentally present at the worksite. There are several occupational airways disorders, including industrial bronchitis, occupational asthma, and reactive airways disease syndrome, the latter two of which will be discussed more thoroughly. Occupational asthma can be appropriately identified when the following are present: (1) typical symptoms, i.e., wheeze, cough, shortness of breath, and/or chest tightness; (2) specific identification of the offending agent; (3) documentation that the agent can cause asthma; (4) wheezes on physical examination; (5) pulmonary function changes; (6) immunologic abnormalities; (7) airway hyperreactivity; and (8) positive bronchial challenge with specific material. The diagnosis of occupational airways disorder requires a comprehensive approach, including clinical history, physiologic measurements, immunologic testing, and identification of airway hyperreactivity. By this approach both individual subjects and working populations can be studied.

A matter of opportunity

It has been our belief for some time in the National Institute of Allergy and Infectious Diseases that occupational immunologic lung disease is a matter of medical importance. Because there are so many of you here, from nearly every state of the Union, apparently this is not just a case of we bureaucrats “ginning up” some extra busy work. As an aside, I can recall as a second-year medical student hearing for the first time about bagassosis. I can tell you that as students, none of us believed a disease could have, let alone deserve, a name like that. But, of course, bagassosis has a serious aspect and is a respiratory disease associated with the workplace. I shall not, in these few remarks, spell out the objectives of this conference. That is best left to those who organized this meeting and to all of you who are participating in it. But what you do here and the conclusions you come to will be of importance to all of us. In these few minutes, let me step back in time and take a brief look at the historical origins of epidemiology and preventive medicine-subspecialties that are concerned with the occurrence of diseases in the community, with occupational diseases, with diseases associated with the workplace-diseases associated with the way we live as the result of the social changes that have occurred through modern practices in agriculture, industry, and housing. The philosophical basis for the practice of medicine for centuries has been the care of the individual patient, and rightly so. And yet how fortunate we are that there emerged in the last century a few perceptive and powerful individuals who realized that disease might be related to a person’s environment, not a new idea to be sure. It was advanced by Hippocrates more than 2400 years ago. But that notion languished until the Victorian Age, when modern epidemiology was born. Much of what you discuss here will be based on epidemiology and preventive medicine. The modern origins of such medicine began with the English physician, William Farr. In 1839 he was given responsibility for medical statistics. He established a tradition for the careful application of vital data to the problems

The industrial physician and occupational lung disease

Prevention and management of chronic occupational illnesses requires that they first be recognized as such. This appears to be particularly difficult in the case of occupational lung disease and doubly so in the case of occupational immunologic lung disease. It took years to recognize asbestosis, byssinosis, and other chronic lung diseases as being occupational in origin. Tritnellitic anhydride is particularly interesting in that it took a variety of purely clinical perceptions to arouse the suspicion that an immunologic response was involved. Increased cooperation of industry managements, occupational physicians, and researchers can lead to the elucidation of causes, which, in turn, can lead to the goals we all share, the discovery, the treatment, and, even better, the prevention of disease.

Evaluation of the patient for occupational immunologic lung disease

Careful evaluation of the worker patient is essential to detect occupational immunologic disease (OILD) and to define the source of the illness. The history is essential, especially in view of the temporal relationships between symptoms and exposure; the presence of variable latent periods between exposure and symptoms must be considered. Once OILD is suspected, additional evaluation is of value. Physical examination may be normal or may detect features of asthma or interstitial disease, depending on the stage of the illness. Chest x-ray evaluation may also reflect the type and stage of illness. Serologic studies may detect precipitating antibodies against environmental antigens. Skin tests with common antigens are useful in detecting an atopic background. Environmental studies may reveal particular antigens in the form of fungi, thermophilic actinomycetes, or chemicals that are volatile, soluble, or could be aerosolized. Pulmonary function studies before and after the work shift or after a period of avoidance nay provide clues as to the environmental nature of the illness. Bronchopulmonary challenge with occupational environmental materials may be valuable in obtaining a definitive diagnosis. Therapy of OILD depends on the worker's response, degree of illness, and feasibility of avoidance of protection.

Overview of occupational immunologic lung disease

Occupational factors are important in an ever-increasing number of respiratory diseases.’ These include obstructive airways diseases such as asthma, a wide array of interstitial fibrotic and granulomatous diseases, and certain malignant diseases of the lung. It is becoming increasingly apparent that immunologic mechanisms are involved in the pathogenesis of many of these diseases.’ For example, IgE-mediated reactions are often prominently involved in the pathogenisis of many forms of occupational asthma and both immune complex-mediated and delayed cellmediated reactions have been shown to be important in the production of hypersensitivity pneumonitis. Considerably less is known about involvement of such mechanisms in chronic bronchitis or pulmonary fibrosis induced by various inorganic occupational agents. In addition to occupational exposure to gases, vapors, and organic and inorganic dusts, environmental factors such as atmospheric pollution with cigarette smoke and other organic or inorganic particles also often contribute to the development of pulmonary disease in the workplace environment. The enormous increase in the use of simple chemicals and organic compounds since World War II continues to foster

Occupational-immunologic lung disease: a Washington conference report.

Reports on current “happenings” are among the regular features of this Journal. In addition to on-site visits of major clinical research centers, our delegates attend special conferences and symposia on asthma and provide us with meaningful citations and insights.