Environmental exposure autoimmune diseases

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. 

Autoimmunity, Autoimmune Diseases and the Role of Environmental Exposures... 

For some autoimmune diseases, little is known about environmental factors involved in the initiation or progression of the disease. For other diseases, however, considerable research has been conducted on one or more types of exposures. Most epidemiologic studies of environmental influences have focused on multiple sclerosis, rheumatoid arthritis, scleroderma, systemic lupus erythematosus, and small vessel vasculitis, but experimental studies using murine models of these diseases is limited (Table 25.1). 

This chapter reviewed current research pertaining to selected environmental agents and autoimmune diseases (Table 25.3). Other infectious agents (e.g., parvovirus, varicella), occupational exposures (e.g., mercury), dietary factors (dietary supplements, nutrients such as antioxidants, and specific proteins in wheat and other grains implicated in celiac disease), and stress have been the focus of additional research that was not included in this review. 

Summary of Research on Specific Environmental Exposures and Autoimmune Diseases... 

Environmental factors have been shown to be important triggers for expression of autoimmunity and have been suggested to both induce onset and modulate disease severity. Lifestyle factors such as diet, smoking, therapeutic and recreational drug use, infection with certain bacteria and viruses, and exposure to UV radiation and environmental chemicals have all been implicated in the pathogenesis of autoimmune diseases. 

The causal relationship between environmental exposure and autoimmune disease onset is seen from the data derived from studies of monozygotic twins. The concordance of autoimmune disease among such twins is only in the 25-40% range, low enough to implicate environmental exposure, yet high enough to indicate genetic influences as well)33... 

Van Loveren H, Vox JG, Germolec D, et al. Epidemiological associations between occupational and environmental exposures and autoimmune disease Report of a meeting to explore current evidence and identify research needs. Int JHygEnviron Health 2001 203(5-6) 483-95. 

Type 1 DM is characterized by an absolute deficiency of insulin. Most often this is the result of an immune-mediated destruction of pancreatic p cells, but rare unknown or idiopathic processes may contribute. What is evident are four main features (1) a long preclinical period marked by the presence of immune markers when /3-cell destruction is thought to occur (2) hyperglycemia when 80% to 90% of p cells are destroyed (3) transient remission (the so-called, honeymoon phase) and (4) established disease with associated risks for complications and death. Unknown is whether there is one or more inciting factors (e.g., cow s milk, or viral, dietary, or other environmental exposure) that initiate the autoimmune process (Fig. 72-4). 

The etiology of abnormal autoantibody production and development of SLE is still unknown. Genetic, environmental, and hormonal factors all may play arole in loss of self tolerance and expression of disease. A popular theory is that autoimmune disease such as SLE develops in genetically susceptible individuals after exposure to a triggering agent, possibly something in the environment. ... 

There exist a variety of methods to detect enhanced antibody formation and autoantibodies in humans and experimental animals following environmental exposure. In contrast, tests available for measuring the potential of chemicals or environmental factors to produce autoimmune disease or augment existing autoimmune disease are not readily available. 

The heterogeneity of most of the systemic but also organ-specific autoimmune diseases is an additional important factor that complicates genetic analyses. Careful disease classification is necessary, and differentiation of subgroups according to clinical presentation, autoantibody production, ethnic background, as well as environmental exposures may be helpful. The risk associated with one genetic risk factor for an autoimmune disease may be... 

Studies of autoantibodies in the general population allow us to determine the prevalence of specific autoantibodies among people who do not have a clinically evident autoimmune disease, whether the prevalence of autoantibodies reflects the demographic variation in disease risk and whether specific environmental exposures are related to the expression of specific autoantibodies. These studies are most feasible for the autoantibodies associated with the most common autoimmune diseases diabetes mellitus type 1, autoimmune thyroid disease, and rheumatoid arthritis. Important issues with respect to interpreting these types of studies include the type of test used and definition of a positive result. 

When a patient suffers from a certain autoimmune disease and one suspects the person to be exposed to a certain environmental factor, few possibilities exist to prove exposure. Several in vitro or in vivo tests, such as skin tests, serological tests, and the lymphocyte transformation test (LTT), can be performed to demonstrate a sensitization to a certain chemical (Choquet-Kastylevsky et al., 2001 Pichler, 2003). 

Leffel EK, Wolf C, Poklis A, White KL Jr (2003) Drinking water exposure to cadmium, an environmental contaminant, results in the exacerbation of autoimmune disease in the murine model. Toxicology, 188 233-250. 

The hallmark of an inflammatory response in the lung is the presence of infiltrating leukocytes. This process can occur in the context of a variety of disorders, including trauma, infection, autoimmune diseases, idiopathic interstitial pneumonias, asthma, chronic bronchitis, acute respiratory distress syndrome (ARDS), exposure to environmental/occupational noxious agents, cancer, aUograft rejection, and ischemia-reperfusion injury. The course of inflammation in these disease states is defined by the delicate balance and nature of inflammatory mediators expressed in the context of lung inflammation, and the specific leukocyte populations recmited in response to lung injury. 

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