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      Comprehensive review of 2‐ethyl‐1‐hexanol as an indoor air pollutant

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          Abstract

          Objectives

          2‐Ethyl‐1‐hexanol (2EH), a fragrance ingredient and a raw material for the production of plasticizer di(2‐ethylhexyl) phthalate, is responsible for sick building syndrome (SBS). This review aims to clarify the 2EH characteristics as an indoor air pollutant such as indoor air concentration, emission mechanism, toxicity, and clinical effects.

          Methods

          Scientific publications in English that has been made available on PubMed as of June 2018 and ad hoc publications in regional languages were reviewed.

          Results

          Inhalation exposure to 2EH caused mucous membrane irritation in the eyes, nose, and throat in experimental animals. Studies in human volunteers revealed an increase in olfactory irritation and eye discomfort. There has been increasing evidence of 2EH being present in indoor air in buildings. The primary sources of 2EH emissions are not building materials themselves, but instead the hydrolysis of plasticizers and flooring adhesives. In particular, compounds like di(2‐ethylhexyl) phthalate present in polyvinyl chloride flooring materials are hydrolyzed upon contact with alkaline moisture‐containing concrete floors. That being said, it may be observed that indoor concentrations of 2EH increased every year during summer.

          Conclusions

          Unlike other volatile organic compounds that cause SBS, 2EH can be retained in indoor air for long durations, increasing the likelihood of causing undesirable health effects in building occupants exposed to it. As a precautionary measure, it is important to use flooring materials that do not emit 2EH by hydrolysis, or to dry concrete before covering with flooring materials.

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          Most cited references149

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          trans-Activation of PPARalpha and PPARgamma by structurally diverse environmental chemicals.

          A large number of industrial chemicals and environmental pollutants, including trichloroethylene (TCE), di(2-ethylhexyl)phthalate (DEHP), perfluorooctanoic acid (PFOA), and various phenoxyacetic acid herbicides, are nongenotoxic rodent hepatocarcinogens whose human health risk is uncertain. Rodent model studies have identified the receptor involved in the hepatotoxic and hepatocarcinogenic actions of these chemicals as peroxisome proliferator-activated receptor alpha (PPARalpha), a nuclear receptor that is highly expressed in liver. Humans exhibit a weak response to these peroxisome proliferator chemicals, which in part results from the relatively low level of PPARalpha expression in human liver. Cell transfection studies were carried out to investigate the interactions of peroxisome proliferator chemicals with PPARalpha, cloned from human and mouse, and with PPARgamma, a PPAR isoform that is highly expressed in multiple human tissues and is an important regulator of physiological processes such as adipogenesis and hematopoiesis. With three environmental chemicals, TCE, perchloroethylene, and DEHP, PPARalpha was found to be activated by metabolites, but not by the parent chemical. A decreased sensitivity of human PPARalpha compared to mouse PPARalpha to trans-activation was observed with some (Wy-14, 643, PFOA), but not other, peroxisome proliferators (TCE metabolites, trichloroacetate and dichloroacetate; and DEHP metabolites, mono[2-ethylhexyl]phthalate and 2-ethylhexanoic acid). Investigation of human and mouse PPARgamma revealed the transcriptional activity of this receptor to be stimulated by mono(2-ethylhexyl)phthalate, a DEHP metabolite that induces developmental and reproductive organ toxicities in rodents. This finding suggests that PPARgamma, which is highly expressed in human adipose tissue, where many lipophilic foreign chemicals tend to accumulate, as well as in colon, heart, liver, testis, spleen, and hematopoietic cells, may be a heretofore unrecognized target in human cells for a subset of industrial and environmental chemicals of the peroxisome proliferator class. Copyright 1999 Academic Press.
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            The Role of PPARα Activation in Liver and Muscle

            PPARα is one of three members of the soluble nuclear receptor family called peroxisome proliferator-activated receptor (PPAR). It is a sensor for changes in levels of fatty acids and their derivatives that responds to ligand binding with PPAR target gene transcription, inasmuch as it can influence physiological homeostasis, including lipid and carbohydrate metabolism in various tissues. In this paper we summarize the involvement of PPARα in the metabolically active tissues liver and skeletal muscle and provide an overview of the risks and benefits of ligand activation of PPARα, with particular consideration to interspecies differences.
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              Impact of reaction products from building materials and furnishings on indoor air quality—A review of recent advances in indoor chemistry

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                Author and article information

                Contributors
                yukey@med.nagoya-cu.ac.jp
                kamijima@med.nagoya-cu.ac.jp
                Journal
                J Occup Health
                J Occup Health
                10.1002/(ISSN)1348-9585
                JOH2
                Journal of Occupational Health
                John Wiley and Sons Inc. (Hoboken )
                1341-9145
                1348-9585
                21 January 2019
                January 2019
                : 61
                : 1 ( doiID: 10.1002/joh2.v61.1 )
                : 19-35
                Affiliations
                [ 1 ] Department of Occupational and Environmental Health Nagoya City University Graduate School of Medical Sciences Nagoya Japan
                [ 2 ] Department of Environmental Health Nagoya City Public Health Research Institute Nagoya Japan
                [ 3 ] Department of Health and Psychosocial Medicine Aichi Medical University School of Medicine Nagakute Japan
                Author notes
                [*] [* ] Correspondence

                Yuki Ito and Michihiro Kamijima, Department of Occupational and Environmental Health, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.

                Email: yukey@ 123456med.nagoya-cu.ac.jp ; kamijima@ 123456med.nagoya-cu.ac.jp

                Author information
                http://orcid.org/0000-0003-1617-1595
                http://orcid.org/0000-0003-0670-8790
                Article
                JOH212017
                10.1002/1348-9585.12017
                6499367
                30698348
                46fdf8ae-cd10-4585-a01b-ccf62e0f9a93
                © 2019 The Authors. Journal of Occupational Health published by John Wiley & Sons Australia, Ltd on behalf of The Japan Society for Occupational Health

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 17 August 2018
                : 02 October 2018
                : 10 October 2018
                Page count
                Figures: 1, Tables: 5, Pages: 17, Words: 12548
                Funding
                Funded by: JSPS KAKENHI
                Award ID: 16K15375
                Categories
                Review Article
                Reviews
                Custom metadata
                2.0
                joh212017
                January 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.2.1 mode:remove_FC converted:03.05.2019

                2‐ethyl‐1‐hexanol,emission mechanism,indoor air pollution,indoor concentration,sick building syndrome,volatile organic compounds

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