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      Organic Solvents as Risk Factor for Autoimmune Diseases: A Systematic Review and Meta-Analysis

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          Abstract

          Background

          Genetic and epigenetic factors interacting with the environment over time are the main causes of complex diseases such as autoimmune diseases (ADs). Among the environmental factors are organic solvents (OSs), which are chemical compounds used routinely in commercial industries. Since controversy exists over whether ADs are caused by OSs, a systematic review and meta-analysis were performed to assess the association between OSs and ADs.

          Methods and Findings

          The systematic search was done in the PubMed, SCOPUS, SciELO and LILACS databases up to February 2012. Any type of study that used accepted classification criteria for ADs and had information about exposure to OSs was selected. Out of a total of 103 articles retrieved, 33 were finally included in the meta-analysis. The final odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by the random effect model. A sensitivity analysis confirmed results were not sensitive to restrictions on the data included. Publication bias was trivial. Exposure to OSs was associated to systemic sclerosis, primary systemic vasculitis and multiple sclerosis individually and also to all the ADs evaluated and taken together as a single trait (OR: 1.54; 95% CI: 1.25–1.92; p-value<0.001).

          Conclusion

          Exposure to OSs is a risk factor for developing ADs. As a corollary, individuals with non-modifiable risk factors (i.e., familial autoimmunity or carrying genetic factors) should avoid any exposure to OSs in order to avoid increasing their risk of ADs.

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          Hematotoxicity in workers exposed to low levels of benzene.

          Qing Lan, Luoping Zhang, Guilan Li … (2004)
          Benzene is known to have toxic effects on the blood and bone marrow, but its impact at levels below the U.S. occupational standard of 1 part per million (ppm) remains uncertain. In a study of 250 workers exposed to benzene, white blood cell and platelet counts were significantly lower than in 140 controls, even for exposure below 1 ppm in air. Progenitor cell colony formation significantly declined with increasing benzene exposure and was more sensitive to the effects of benzene than was the number of mature blood cells. Two genetic variants in key metabolizing enzymes, myeloperoxidase and NAD(P)H:quinone oxidoreductase, influenced susceptibility to benzene hematotoxicity. Thus, hematotoxicity from exposure to benzene occurred at air levels of 1 ppm or less and may be particularly evident among genetically susceptible subpopulations.
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            Environmental risk factors in multiple sclerosis aetiology.

            Ruth Marrie (2004)
            The epidemiology of multiple sclerosis (MS) has been intensively studied. It is conceptualised as a complex disease in which genetic and environmental factors act together to cause disease. There are temporal and geographic variations in disease risk, and risk of disease may be affected by migration between regions of differing risk. Numerous potential causal factors including infection, immunisations, physical and emotional stressors, climate, diet, and occupational exposures have been studied using various observational study designs. Thus far, no single environmental exposure has been consistently identified as a causal factor in MS, but sufficient data have accumulated that causal pathways should be postulated and tested. This review will focus on the environmental epidemiology of MS.
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              The Immune System in Irritable Bowel Syndrome

              Giovanni Barbara, Cesare Cremon, Giovanni Carini … (2011)
              The potential relevance of systemic and gastrointestinal immune activation in the pathophysiology and symptom generation in the irritable bowel syndrome (IBS) is supported by a number of observations. Infectious gastroenteritis is the strongest risk factor for the development of IBS and increased rates of IBS-like symptoms have been detected in patients with inflammatory bowel disease in remission or in celiac disease patients on a gluten free diet. The number of T cells and mast cells in the small and large intestine of patients with IBS is increased in a large proportion of patients with IBS over healthy controls. Mediators released by immune cells and likely from other non-immune competent cells impact on the function of enteric and sensory afferent nerves as well as on epithelial tight junctions controlling mucosal barrier of recipient animals, isolated human gut tissues or cell culture systems. Antibodies against microbiota antigens (bacterial flagellin), and increased levels of cytokines have been detected systemically in the peripheral blood advocating the existence of abnormal host-microbial interactions and systemic immune responses. Nonetheless, there is wide overlap of data obtained in healthy controls; in addition, the subsets of patients showing immune activation have yet to be clearly identified. Gender, age, geographic differences, genetic predisposition, diet and differences in the intestinal microbiota likely play a role and further research has to be done to clarify their relevance as potential mechanisms in the described immune system dysregulation. Immune activation has stimulated interest for the potential identification of biomarkers useful for clinical and research purposes and the development of novel therapeutic approaches.
              Article 0 comments Cited 66 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Sudha Chaturvedi: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2012
                Publication date (Electronic): 19 December 2012
                Volume: 7
                Issue: 12
                Electronic Location Identifier: e51506
                Affiliations
                [1 ]Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia
                Wadsworth Center, United States of America
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: ARV JMA RDM. Performed the experiments: CBM ARV JMA. Analyzed the data: ARV CBM. Contributed reagents/materials/analysis tools: CBM CSH GMO RDM JMA ARV. Wrote the paper: CBM CSH GMO RDM JMA ARV. Interpreted the possible pathways: GMO CSH.

                Article
                Publisher ID: PONE-D-12-20238
                DOI: 10.1371/journal.pone.0051506
                PMC ID: 3526640
                PubMed ID: 23284705
                SO-VID: feddab83-3583-4c1d-85c7-d8ecce3fa0e5
                Copyright statement: Copyright @ 2012
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 12 July 2012
                Date accepted : 1 November 2012
                Page count
                Pages: 18
                Funding
                This project did not have any specific funding, but the work was supported by the School of Medicine and Health Sciences, Universidad del Rosario. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Computational Biology
                Subject: Population Biology
                Subject: Population Dynamics
                Subject: Metapopulation Dynamics
                Subject: Chemistry
                Subject: Chemical Reactions
                Subject: Organic Reactions
                Subject: Environmental Chemistry
                Subject: Pollutants
                Subject: Medicine
                Subject: Clinical Immunology
                Subject: Autoimmune Diseases
                Subject: Clinical Research Design
                Subject: Epidemiology
                Subject: Meta-Analyses
                Subject: Epidemiology
                Subject: Environmental Epidemiology
                Subject: Non-Clinical Medicine
                Subject: Health Care Policy
                Subject: Health Statistics

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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