Environmental hypersensitivity

Environmental hypersensitivity Total immune disorder syndrome Twentieth-century disease... 

Goodman M Illness as lifestyle. Can Fam Physician 41 267-270, 1995 Guglielmi RS, Cox DJ, Spyker DA Behavioral treatment of phobic avoidance in multiple chemical sensitivity. J Behav Ther Exp Psychiatry 25 197-209,1994 Haller E Successful management of patients with multiple chemical sensitivities on an inpatient psychiatric unit. J Clin Psychiatry 54 196-199, 1993 Hotopf M Seasonal affective disorder, environmental hypersensitivity and somatisa-tion. Br J Psychiatry 164 246-248, 1994... 

Environmental hypersensitivity Total immune disorder syndrome Twentieth-century disease Total allergy syndrome Environmental illness Sick building syndrome Idiopathic environmental intolerance Chemical AIDS... 

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. ... 

Ross, P.S., de Swart, R.L., and Reijnders, P.J.H. et al. (1995). Contaminant related suppression of delayed type hypersensitivity and antibody responses in harbor seals from the Baltic Sea. Environmental Health Perspectives 103, 162. 

Atopic Related to a genetically determined hypersensitivity to environmental allergens allergic. 

Atopy A genetic predisposition to develop type I hypersensitivity reactions against common environmental antigens commonly seen in patients with allergic rhinitis, asthma, and atopic dermatitis. 

It is important to remember that respiratory sensitization and asthma are related, but not identical, pathologies [31]. Asthma is a specific syndrome which appears to have genetic as well as environmental causes and there are numerous potential triggers which have been identified by immunotoxicologists [32], However, asthma is not the same disease as other respiratory hypersensitivity syndromes (sometimes referred to as chemical asthma, etc.) [33, 34], Various regulatory guidance documents have sought to deal with the latter disease entities to ensure that xenobiotics are assessed appropriately for their ability to induce immune-based pulmonary hypersensitivity reactions [35-37],... 

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. 

Chemical Sensitivity A Guide to Coping with Hypersensitivity Syndrome, Sick Building Syndrome and Other Environmental Illnesses. Bonnye L. Matthews. Jefferson, NC McFarland, 1992. 

It is unclear why certain foreign proteins can also stimulate the B-cells to secrete IgE antibodies, to result in allergy or hypersensitivity. The terms are used interchangeably, although the latter is usually restricted to milder forms of the response. The term anaphylaxis is used to describe the severe response (Box 17.4). Both reactions arise in genetically susceptible individuals and they are precipitated by exposure to environmental antigens such as pollen, some organic compounds, tobacco smoke, animal hairs or even components of some common foods such as milk and cereals. 

Hypersensitivity There are no reports of hypersensitivity in patients given trientine for Wilson disease. However, there have been reports of asthma, bronchitis, and dermatitis occurring after prolonged environmental exposure in workers who use trientine as a hardener of epoxy resins. Observe patients closely for signs of possible hypersensitivity. 

WHO (1999) International Programme on Chemical Safety, Principles and methods for assessing allergic hypersensitization associated with exposure to chemicals. Environmental Health Criteria 212, WHO, Geneva, Zwitserland. 

Mucosal tolerance protection from hypersensitivity reactions towards harmless environmental and food antigens Mucosal homeostasis induction of immunoregulatory functions, maintenance of an intact endogenous micro flora... 

Allergy A state of hypersensitivity to foreign substances (e.g., environmental antigens and certain drugs), manifested by an exaggerated response of the immune system. 

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. 

Heavy metals, principally mercury and silver, are now rarely used as disinfectants. Mercury is an environmental hazard, and some pathogenic bacteria have developed plasmid-mediated resistance to mercurials. Hypersensitivity to thimerosal is common, possibly in as high as 40% of the population. These compounds are absorbed from solution by rubber and plastic closures. Nevertheless, thimerosal 0.001-0.004% is still used as a preservative of vaccines, antitoxins, and immune sera. 

---