Asthma occupational

Prolonged contact with certain chromium compounds may produce allergic reactions and dermatitis in some individuals (114). The initial response is usually caused by exposure to Cr(VI) compounds, but once the allergy is estabUshed, it is extended to the trivalent compounds (111,115). There is also limited evidence of possible chromium associated occupational asthma, but there is insufficient data to estimate a dose for assumed chromium-induced asthma. Reference 116 provides a summary and discussion of chromium hypersensitivity. 

Table 5.6 Some substances recognized as causing occupational asthma ...

Asthmagens. Critical assessments of the evidence for agents implicated m occupational asthma 1997. The technical basis for COSHH essentials. Easy steps to control chemicals... 

Aetiological Agents in Occupational Asthma, Chan-Yeung M., Malo J. (Eur Respir J. 1994 7 346-371). 

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. ... 

JECFA, Combined compendium of food additive specifications, http //www.fao.org. Tabar-Purroy, A.I. et al.. Carmine (E 120) induced occupational asthma revisited, J. Allergy Clin. Immunol, 111, 415, 2003. 

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. 

Matheson, J.M., Johnson, V.J., and Luster, M.I., Immune mediators in a murine model for occupational asthma studies with toluene diisocyanate, Toxicol. Sci., 84, 99, 2005. 

Mapp, C. E. et al., Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates, J. Allergy Clin. Immunol., 109, 867, 2002. 

Bernstein, J.A., Overview of diisocyanate occupational asthma, Toxicology, 111, 181, 1996. 

Cartier, A., et al., Specific serum antibodies against isocyanates association with occupational asthma, J. Allergy. Clin. Immunol., 84, 507, 1989. 

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. 

PERSONAL RISK FACTORS ASSOCIATED WITH DEVELOPMENT OF OCCUPATIONAL ASTHMA... 

Occupational asthma has adverse social and economic impacts both on the employee and the employer. In the United States, the cost of occupational asthma in 1996 was estimated to be 1.1 billion dollars which included costs such as hospital stays, physician visits, asthma medication, medical insurance administration, and lost earnings [71]. These costs are incurred by both employer and employee. In 1999, the economic cost of occupational asthma in the United States was reported to be 1.5 billion dollars [72],... 

Pre-employment screening of potential workers for risk factors associated with occupational asthma is not viable from a legal/ethical stand or from a practical point of view. Newman-Taylor estimated that seven atopic individuals would have to be denied employment in order to eliminate one case of OA [81]. Since asthma is a complex disease, focus on one risk factor (e.g., atopy) will have little impact on prevention. Investigators have suggested that this can lead to a false sense of control with the opportunity for greater disease [82],... 

Tse, K.S., Chan, H., and Chan-Yeung, M., Specific IgE antibodies in workers with occupational asthma due to western red cedar, Clin Allergy, 12, 249, 1982. 

---