Occupational hypersensitivity

Walusiak, J. et al., The risk factors of occupational hypersensitivity in apprentice bakers the predictive value of atopy markers, Int. Arch. Occup. Environ. Health, 75 Suppl, SI 17, 2002. 

Malo, J.-L. Zeiss, C.R. (1982) Occupational hypersensitivity pneumonitis after exposure to diphenylmethane diisocyanate. Am. Rev. respir. Dis., 125, 113-116... 

Cristaudo A, Sera F, Severino V, De Rocco M, Di Leila E, Picaido M (2005) Occupational hypersensitivity to metal salts, including platinum, in the secondary industry. Allergy 60 159-... 

Ameille J, Brechot JM, Brochard P, et al. 1992. Occupational hypersensitivity in a smelter exposed to zinc fumes. Chest 101 (3) 862-863. 

Pazzaglia M, Vincenzi G, Gasparri F, Tosti A (1996) Occupational hypersensitivity to isothiazolinone derivatives in a radiology technician. Contact Dermatitis 34 143-144 Rietschel RL, Fowler JF Jr (1995) Fisher s contact dermatitis, 4th edn. Williams and Wilkins, Baltimore Rothe A, Zschunke E (1981) Uber Dermatosen durch Fotochemik-alien. Dermatol Monatsschr 167 729-742 Rustemeyer T, Frosch PJ (1995) Allergic contact dermatitis from colour developers. Contact Dermatitis 32 59-60 Scheman AJ, Katta R (1997) Photographic allergens an update. Contact Dermatitis 37 130... 

Pazzaglia M, Vincenzi C, Gasparri F, Tosti A (1996) Occupational hypersensitivity to isothiazolione derivatives in a radiology technician. Contact Dermatitis 34 143-144... 

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. 

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. ... 

Stevens-Johnson syndrome, a severe erythema, was seen in five people occupationally exposed to trichloroethylene for 2-5 weeks at levels ranging from 19 to 164 ppm (Phoon et al. 1984). The study authors suggested that the erythema was caused by a hypersensitivity reaction to trichloroethylene. An exfoliative dermatitis (Goh and Ng 1988) and scleroderma (Czirjak et al. 1993), also thought to have an immune component, have been reported in persons occupationally exposed to trichloroethylene. 

Immunoenhancement, which, as adverse effect, may lead to immune-mediated diseases such as hypersensitivity reactions and autoimmune diseases. Hypersensitivity reactions are the result of normally beneficial immune responses acting inappropriately, causing inflammatory reactions and tissue damage. The two most frequent manifestation of chemical-induced allergy are contact hypersensitivity and respiratory sensitization, both of which can have a serious impact on quality of life and represent a common occupational health problem. Hypersensitivity reactions are often considered to be increased at such a rate to become a major health problem in relation to environmental chemical exposure. 

This chapter presents specific information with regard to the effects of environmental and occupational exposure to arsenic on inflammatory processes, the immune system, and host defense. While the focus is on the in vivo and in vitro effects of arsenic on host immune responses (e.g., immunotoxicity and hypersensitivity) and their relationship to clinically observed manifestations of arsenic toxicity (e.g., inflammation and skin cancer), information on the potential mechanisms through which arsenic may exert its biological effects is also provided. 

Dearman, R J. et al., Differential ability of occupational chemical contact and respiratory allergens to cause immediate and delayed dermal hypersensitivity reactions in mice. Int. Arch. Allergy Immunol., 97, 315, 1992. 

Test Occupational asthma or work-aggravated asthma Hypersensitivity pneumonitis Emphysema Constrictive BO... 

Substantial numbers (5,000 to 22,000/m )of actlnomycetes, particularly Thermoactlnomyces vulgaris (60), are present in the atmosphere of mills. These organisms are known to be causative agents in other occupational lung diseases (61), specifically several forms of hypersensitivity pneumonitis. 

Reportedly, headache, nausea, and confusion may occur after inhalation of vapor. Occupational poisoning from vapor exposure is rare. Naphthalene on the skin may cause hypersensitivity dermatitis. ... 

Nakayama H, ImaiT Occupational Contact Uti-caria, Contact Dermatitis and Asthma Caused by Rhodium Hypersensitivity. 6th International Symposium on Contact Dermatitis and Joint Meeting between ICDRG and JCDRG, Tokyo, 21 May 1982... 

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). 

The author of the last report commented that the patient probably developed hypersensitivity to deflazacort as a result of occupational exposure. 

There is evidence that both occupational and environmental exposures to chemicals (both proteins and haptens) can result in the induction or exacerbation of respiratory allergies (Table 19.6). Of particular concern is the induction of allergic asthma. In sensitized asthmatic individuals the antigen challenge generally causes a type I (IgE-mediated) immediate hypersensitivity response with release of mediators responsible for bronchoconstriction. Between 2 and 8 hours after the immediate response, asthmatics experience a more severe and prolonged (late phase) reaction that is characterized by mucus hypersecretion, bronchoconstriction, airway hyperresponsiveness to a variety of nonspecific stimuli (e.g., histamine, methacholine), and airway inflammation characterized by eosinophils. This later response is not mediated by IgE. 

Most dermal effects reported were either due to occupational intermediate-chronic exposure or acute exposure to high levels of chromium compounds. Environmental exposure to chromium compounds is not likely to result in dermal effects. However, hypersensitive individuals may develop rashes and erythema from contact with contaminated soil or consumer products containing chromium. 

Occupational exposure to beryllium, a hapten, by inhalation of fumes/dust and/or by skin contact may result in one of two conditions that primarily affect the lungs. In acute berylliosis, which may occur following a high concentration exposure, the metal acts as a direct chemical irritant, causing a nonspecific inflammatory reaction (acute chemical pneumonitis). However, a small percentage of those exposed develop beryllium-specific T-cell-mediated hypersensitivity (Type IV) with proliferation and accu-... 

Besides respiratory allergies with hay-fever-like symptoms and asthma in atopic individuals, continuous occupational basidiospore exposure may result in hypersensitivity pneumonitis or extrinsic allergic alveolitis. The basidiomycetes Lentinus edodes, Pleurotus ostreatus, and Merulius lacrymans have all been shown to cause hypersensitivity pneumonitis from occupational exposure [26-28]. Actinomycetes in the compost used to grow button mushroom... 

Clinical history should include both medical and occupational history to determine a relationship between exposure to a specific substance and development of respiratory hypersensitivity. Relevant information includes aggravating factors both in the home and workplace, the onset and progress of the disease, family history and medical history of the patient in question. The medical history should also include a note of other allergic or airway disorders from childhood, and smoking history. 

---