Enhancing effects of trichloroethylene and tetrachloroethylene on type I allergic responses in mice

Abstract

-Trichloroethylene (TCE) and tetrachloroethylene (perchloroethylene; PCE) are commonly identified as environmental contaminants of groundwater. Previously, we investigated the enhancing effects of TCE and PCE on antigen-induced histamine release and inflammatory mediator production in rat mast cells. In this study, to examine the potential effect of TCE and PCE on antigen-induced histamine release from mouse mast cells, mouse bone marrow-derived mast cells (BMMC) were sensitized with anti-dinitrophenol (DNP) monoclonal IgE antibody and then stimulated with DNP-BSA containing with TCE or PCE. Both TCE and PCE significantly enhanced antigen-induced histamine release from BMMC. Next we investigated the effects of TCE and PCE on the passive cutaneous anaphylaxis (PCA) reaction in vivo using ICR mice. TCE and PCE significantly enhanced the PCA reaction in a dose-dependent manner. In addition, we examined the enhancing effects of ingesting small amount of TCE and PCE in drinking water on antigen-stimulated allergic responses. After the ICR mice had ingested TCE or PCE in their drinking water for 2 or 4 weeks, we performed the PCA reaction. Both TCE and PCE ingestion enhanced the PCA reaction in a dose-dependent manner for 4 weeks. These results suggest that exposure to TCE and PCE leads to the augmentation of type I allergic responses in many species.

Physicochemical properties

“…Treatment with tetrachloroethylene also increased mRNA expression of IL-4 (p<0.05) and TNF-α (p>0.05) as well as the production of these mediators (p<0.05 for both) in RBL-2H3 cells. A dosedependent increase in antigen-induced histamine release from mouse bone marrow cells treated with tetrachloroethylene was reported in another study from this laboratory (Seo et al 2012). These data suggest possible mechanisms for tetrachloroethylene-induced perturbation of the immune response to allergens, and exacerbation of inflammation.…”

“…Enhanced antigen-stimulated allergic responses have been demonstrated following small oral doses of tetrachloroethylene in both rats (Seo et al 2008a) and mice (Seo et al 2012). In addition, rats exposed to tetrachloroethylene displayed enhanced inflammatory responses (Seo et al 2008a).…”

“…No human data were located regarding oral or dermal intermediate-duration exposure to tetrachloroethylene. The target organs identified in animal studies of intermediate-duration oral or inhalation exposure to tetrachloroethylene include the nervous system (Carpenter 1937;Karlsson et al 1987;Kyrklund et al 1988;Mattsson et al 1992Mattsson et al , 1998Rosengren et al 1986), liver (Boverhof et al 2013;Buben and O'Flaherty 1985;Carpenter 1937;Hayes et al 1986;Jonker et al 1996;Kylin et al 1965;Kyrklund et al 1988;NTP 1986;Odum et al 1988;Philip et al 2007;Rajamanikandan et al 2012;Rowe et al 1985;Story et al 1986), kidney (Carpenter 1937;Ebrahim et al 1996;Green et al 1990;Hayes et al 1986;Jonker et al 1996;NTP 1986;Rowe et al 1985), and immune system (Seo et al 2008a(Seo et al , 2012. These studies were conducted in a variety of animal species including mice, rats, guinea pigs, and gerbils.…”

The immune response in trichloroethylene hypersensitivity syndrome: A review

“…In other research of THS, many researchers found that T cell-mediated type IV hypersensitivity could not fully explain the pathogenesis of THS (Chiu et al, 2013; Seo et al, 2012; Wang et al, 2014). In a cross-sectional study of occupational TCE exposure, exposed workers had significant declines in peripheral blood cell counts, total lymphocytes, and some lymphocyte subsets, including B cells and CD4+ T cells, as well as plasma markers of B cell activation compared with unexposed factory workers (Hosgood, 2012; Lan et al, 2010).…”

“…Chinese research found that TCE intake via drinking water can upregulate the expression of IFN-γ and IL-4, which may promote Th1 and Th2 cell immune response, and when Th2 cell increases significantly, the proportion of Th1/Th2 decreases (Li et al, 2014). Th1/Th2 cytokine imbalance induced by TCE ingestion will promote a type I hypersensitivity reaction (Seo et al, 2012). However, serum immunoglobulin E (IgE) levels were not significantly different between TCE-exposed and -unexposed workers after adjustments for age, gender, alcohol consumption, and so on.…”