Occupational disease asthma

Thioredoxins are small ubiquitous enzymes present in many species from Archaebacteria to man. They serve as general protein disulfide oxido-reductases interacting with a broad range of proteins. Allergenic thioredoxins have been identified in fungi as well as in plants. The thioredoxins from wheat (Tri a 25) and maize (Zea m 25) are related to baker s asthma, an occupational disease affecting 4%-10% of bakery workers in European countries (Holmgren 1995). 

Allergy to flour dust in bakers has been known since 1700 [44, 45]. Baker s asthma is a well-known occupational disease caused by IgE-mediated sensitization to cereal - mainly wheat, rye and barley - proteins. Hjorth [46] stated that most baker s dermatitis was associated with an immediate-type hypersensitivity. Herxheimer [47, 48] studied the development of skin sensitivity in baker s apprentices for 5 years and showed that the percentage of sensitive subjects increased gradually until a constant figure of 20% was reached. Many different proteins were identified as allergenic in wheat flour, especially in the water-soluble albumin and globulin fractions [49]. There is extensive cross-reactivity between these cereals, and -to a minor extent - between them and other cereals such as oat, corn and rice [50]. 

Kanerva L, Estlander T, Alanko K, Pfaffli P, Jolanki R (1999) Occupational dermatitis from unsaturated polyester resin in a car repair putty. Int J Dermatol 38 447-452 Karjalainen A, Toildcanen J (eds) (1997) From baker s asthma to cement dermatitis. Occupational disease risks in various occupations (in Finnish). Finnish Institute of Occupational Health, Helsinki, pp 1-92... 

List the diseases prescnbed for the payment of disablement benefit, if related to specific occupations. Conditions due to chemical agents, e.g. poisoning by any of a range of chemicals and certain carcinomas, and miscellaneous conditions, e.g. pneumoconiosis, asthma, diffuse mesothelioma, non-mfective dermatitis are included. 

At typical indoor concentrations, COj is not thought to be a direct cause of adverse health effects however, COj is an easily-measured surrogate for other occupant-generated pollutants. Eye, nose, and throat irritation headaches lung cancer may contribute to heart disease buildup of fluid in the middle ear increased severity and frequency of asthma episodes decreased lung function. ETS is also a source of odor and irritation complaints. 

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. 

Major factors that may contribute to the severity of asthma include allergens typically associated with atopy chemical exposures in occupational environments and exposure to tobacco smoke, irritants, and indoor and outdoor pollution. Other factors include concurrent disease states or medications that may worsen asthma severity. 

Efforts to incorporate SNP studies into environmental/occupational epidemiology investigations have focused on examining hypothesis-driven associations between exposures and specific polymorphisms. Most common human diseases such as asthma,... 

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],... 

Shortness of breath, cough, and wheeze are common symptoms of respiratory diseases (Table 3.2). These shared symptoms make misdiagnosis by physicians common if the diagnosis is based solely on reported symptoms. Medical tests help to distinguish the respiratory diseases from each other (Table 3.3). Other pitfalls in medical diagnosis include diagnosing common diseases (such as asthma, emphysema, and chronic bronchitis) instead of the actual rarer diseases (such as BO) and not considering occupational exposures as the cause. 

A number of diseases are recognized as being, or presumed to be, allergic in nature. These include asthma, rhinitis, conjunctivitis, allergic contact dermatitis, urticaria (a condition in which red or pale, itchy, and swollen areas appear on the skin, often called hives ), and food allergies. In this section, the endpoints discussed are those traditionally associated with occupational and consumer exposure. Photosensitization is potentially important but its mechanism of action is poorly understood, so it has been considered but not discussed in detail. 

Isocyanate-induced asthma and hypersensitivity pneumonitis in humans have been reviewed (Baur, 1995 Bernstein, 1996). A case of fatal asthma of a 4,4 -mcthylcncdiphcnyl diisocyanate-scnsitized subject has been described (Carino et al., 1997). Exposure to 4,4 -methylenediphcnyl diisocyanate is a frequent cause of occupational asthma (Liss et al., 1988 Vogelmcicr et al., 1991 Bernstein et al., 1993) but may also induce hypersensitivity pneumonitis (Malo Zeiss, 1982 Vandenplas et al., 1993) and inflammatory upper respiratory tract diseases (Liss et al., 1988 Littorin et al., 1994). Most patients with 4,4 -methylenediphcnyl diisocyanate-induced asthma have elevated levels of IgG-class antibodies towards 4,4 -methylenediphenyl diisocyanate-albumin conjugates in the plasma, while IgE-class antibodies are rare (Liss et al., 1988). 

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... 

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