Occupational asthma sensitization

In addition to the proteins discussed above, a large number of reactive chemicals used in industry can cause asthma and rhinitis. Hypersensitivity pneumonias have also been described. Isocyanates and acid anhydrides are industrial chemicals that cause occupational asthma. Acid anhydrides, such as phthalic anhydride, seem to cause mainly type I reactions, whereas the IgE-mediated mechanism explains only a part of the sensitizations to isocyanates. Several mechanisms have been suggested, but despite intensive research no models have been generally accepted. The situation is even more obscure for other sensitizing chemicals therefore, the term specific chemical hypersensitivity is often used for chemical allergies. This term should not be confused with multiple chemical sensitivity (MCS) syndrome, which is a controversial term referring to hypersusceptibility to very low levels of environmental chemicals. ... 

Genetic factors cannot explain the recent rapid rise in asthma prevalence. Asthma appears to require both genetic predisposition and environmental exposure. Many patients with occupational asthma develop the disease late in life upon exposure to specific allergens in the workplace. Environmental influences in utero or in infancy may contribute to the development of asthma. Maternal smoking during pregnancy or exposure to secondhand smoke after birth increases the risk of childhood asthma.3 Adult-onset asthma is not uncommon and may be related to atopy, nasal polyps, aspirin sensitivity, occupational exposure, or a recurrence of childhood asthma. 

It has been estimated that 200 to 300 agents have been identified as inducers of occupational asthma [4], The LMW agents can be broadly classified by chemical class such as isocyanates, anhydrides, metals, dyes, amines, drugs, acrylates and other compounds. The HM W agents can be broadly classified as animal protein, plant protein and microbial byproducts. Table 33.1 shows apartial listing of LMW and HMW sensitizers along with the workplace environments where these agents can be encountered. 

Bernaola, G., Echechipia, S., Urrutia, I., Fernandez, E., Audicana, M., and Fernandez de Corres, L. (1994). Occupational asthma and rhinoconjunctivitis from inhalation of dried cow s milk caused by sensitization to alpha-lactalbumin. Allergy 49,189-191. 

Campbell, C. P., Jackson, A. S., Johnson, A. R., Thomas, P. S., and Yates, D. H. (2007). Occupational sensitization to lupin in the workplace Occupational asthma, rhinitis, and work-aggravated asthma. Allergy Clin. Immunol. 119,1133-1139. 

After removal from exposure, some patients have had resolution of symptoms. The early detection of TDI-induced occupational asthma and the prompt removal of sensitized workers from exposure may increase the chances of remission. " However, there is evidence from several studies that individuals with TDI-induced asthma may continue to have symptoms of dyspnea and wheezing and bronchial hyperreactivity for 2 or more years after cessation of exposure. In one study, patients with TDI-induced asthma who continued to have exposure to TDI for 2 more years had, as a rule, marked abnormal decreases in spirometric parameters and increases in nonspecific hyperreactivity. In another study, 6 of 12 workers with a convincing history of TDI-... 

Dolovich J, Evans SL, Nieboer E. 1984. Occupational asthma from nickel sensitivity I. Human serum albumin in the antigenic determinant. Br J Ind Med 41 51-55. 

The low prevalence of occupational asthma and antibody-dependent sensitization to diphenylmethane diisocyanate in a plant engineered for minimal exposure to diisocyanates. J. Allergy din. Immunol., 92, 387-396... 

Malo JL, Cartier A, L Archeveque J, Ghezzo H, Soucy F, Somers J, Dolovich J. Prevalence of occupational asthma and immunologic sensitization to guar gum among employees at a carpet-manufacturing plant. J Allergy Clin Immunol 1990 86(4 Pt l) 562-9. 

All isocyanates are known to cause pulmonary toxicity. Isocyanates are the most common causes of occupational asthma and have led to the development of immediate or late asthma among workers. Isocyanates have caused bronchitis, rhinitis, conjunctivitis, chronic obstructive lung disease, contact sensitivity, dermatitis, allergic alveolitis, and immunologic hemorrhagic pneumonitis.29... 

OA can be induced by single sensitizing chemicals as well as by single irritant chemicals. Sensitizers, all of which are hydrophiles, are listed in Table 17.4. Irritants that induce occupational asthma are almost exclusively hydrophilic. Table 17.5 contains a partial list of these 46-50 anc[ their Kqw values. 

In addition to those mentioned above, other chemicals have been implicated in the induction of occupational asthma. Some of these are listed in Table 1.1 and more comprehensive details are available elsewhere (Chan-Yeung and Malo, 1993). It is important to emphasize, however, that the inclusion of a chemical in such lists does not necessarily imply that respiratory symptoms result in all instances from allergic sensitization. For many chemicals associations have been found between respiratory effects and the presence of homocytotropic (IgE or IgG4) antibodies. Such associations are not universal and there is some uncertainty about the nature of immune effector mechanisms, and indeed the requirement for immune processes per se, in some forms of chemical-induced asthma. The subject of this book is allergic sensitization... 

SHIRAKAWA, T KUSAKA, Y FUKIMURA, N GOTO, S. MORIMOTO, K. (1989) Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Chest, 95, 29-37. 

The first element in risk assessment is knowledge of the chemical exposures of a workforce to see if a known sensitizer is present. A chemical becomes accepted as a cause of occupational asthma if there are at least two convincing clinical case reports from independent centres. Specialist clinicians are likely to be aware of the published literature at an early stage and may be a useful source of informal information. There is currently much interest in publishing lists of sensitizers. One is available in a recent textbook (Chan-Yeung and Malo, 1993). The Health and Safety Executive in the UK, the National Institute for Occupational Safety and Health in the USA and other agencies may publish lists with updates. Other sources of information on causes are reporting schemes such as SWORD (Surveillance of Work-related and Occupational Respiratory Disease) in the UK (Ross el al., 1995) and SENSOR (Sentinel Event Notification System for Occupational Risks) in some states in the USA (Matte et al., 1990). 

Environmental or Occupational Asthma. With modern industrialization, the concentration of airborne pollutants in the environment has increased and led to the development of an environmental form of asthma, which can occur in individuals living in concentrated industrial areas. This type of asthma appears to result from exposure of individuals to toxic gases such as sulfur dioxide. Because of their hyperirritable airways, all types of asthmatics are effected by such environmental pollution, but there is one class that has no other underlying etiology besides an increased sensitivity to polluted air. In these individuals, exposure to environmental pollution is hypothesized to stimulate irritant receptors in the lung. 

Montanaro A, Bardana EJ Jr The chemically sensitive patient, in Occupational Asthma. Edited hy Bardana EJ Jr, Montanaro A, O Hollaren MT. PMladelphia, PA, Hanley Belfus, 1992, pp 255-266... 

Sastre J, Qnirce S. Sensitizing agents indncers of occupational asthma, hypersensitivity pnenmonitis and eosinophilic bronchitis. Accessed on September 2,2007. Available at http //www.worldallergy.org/professionaPahergic diseases center/occnpational ahergens/index.shtml... 

Vanoirbeek JAJ, Mandervelt C, Cunningham AR, Hoet PHM, Xu H, Vanhooren HM, Nemery B. Validity of methods to predict the respiratory sensitizing potential of chemicals a study with a piperidinyl chlorotriazine derivative that caused an outbreak of occupational asthma. Toxicol Sci 2003 76 338-346. 

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