Abstract
ObjectiveDuring the last few decades, the prevalence of allergic skin diseases, asthma and rhinitis, has increased worldwide. Introduction of environmental chemicals with aggravation effects may play a part in this increase. The artificial chemical product dibutyl phthalate (DBP) is used in many products used in daily life. Dermal exposure to DBP is a common (but easily neglected) exposure pattern.Methodology/Principal FindingsIn this study, we examined the aggravation effect of long-term dermal exposure to DBP in a T-helper type 2 (Th2) model of contact hypersensitivity (CHS) in mice, and sought the potential molecular mechanisms. Experimental tests were conducted after 40-day dermal exposure to saline or three concentrations of DBP and subsequent three times of sensitization with 0.5% fluorescein isothiocyanate (FITC) or vehicle. The results of immunological and inflammatory biomarkers (total-immunoglobulin (Ig)E and Th cytokines) as well as histopathological examination and measurement of ear swelling supported the notion that high doses of DBP may promote and aggravate atopic dermatitis. Increased expression of thymic stromal lymphopoietin (TSLP) in this mouse model suggested that TSLP might be one of the molecular mechanisms of the aggravation effect induced by DBP.Conclusions/SignificanceTogether, these results indicated that long-term dermal exposure to types of environmental toxins such as phthalates may endow an atopic predisposition in animals or humans. In addition, the high expression of TSLP in the mouse model demonstrated that TSLP might have an important role in the aggravation effect. This result could help to provide effective prevention strategies against atopic diseases such as atopic dermatitis (AD).
Highlights
IntroductionThey are added to plastics to make them flexible and soft, to cosmetics as vehicles for fragrance, and to many other products, such as children’s toys, building materials, and medical devices [1,2,3]
We aimed to address the aggravate effect of long-term dibutyl phthalate (DBP) exposure on skin and allergic response to fluorescein isothiocyanate (FITC) related to atopic dermatitis (AD) and, by testing the expression of thymic stromal lymphopoietin (TSLP) in skin, to seek the molecular mechanisms of DBP-induced aggravate effect in AD
Four important findings were revealed: (i) exposure to only DBP (DBP 0.4, DBP 4 and DBP 40) did not cause changes in serum total IgE (T-IgE); (ii) the T-IgE levels of all FITC-immunized groups (FITC, FITC+DBP 0.4, FITC+DBP 4, FITC+DBP 40) were increased significantly in relation to those of the saline exposure group (p,0.01); (iii) compared with the FITC group, FITC+DBP 40 (p,0.01) enhanced the level of T-IgE; (iv) the T-IgE levels of the FITC+DBP 40 group were increased significantly compared with those of the FITC+BDP 4 group (p,0.01)
Summary
They are added to plastics to make them flexible and soft, to cosmetics as vehicles for fragrance, and to many other products, such as children’s toys, building materials, and medical devices [1,2,3]. Dibutyl phthalate (DBP), which is one of the main sources of indoor semi-volatile organic compounds (SVOCs), has become the main type of plasticizer used in China [4]. Humans as well as animals can be exposed to these ubiquitous compounds through oral, dermal, inhalational, and iatrogenic exposures [5]. Recent reports have revealed that phthalates are added to cosmetics (#5%) and personal-care products, and that they raise the levels of exposure to urinary phthalate monoesters instantly if these products are used every day [7]. The toxicity of phthalates via dermal exposure needs more attention
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
