全氟及多氟类化合物暴露与过敏性疾病的相关性研究进展

Research progress on relationship between exposure to perfluoroalkyl and polyfluoroalkyl substances and allergic diseases

全氟及多氟类化合物(PFASs)作为环境内分泌干扰物中的一种持续性有机污染物,被广泛应用于工业生产和日常生活中。PFASs因具有生物蓄积性、较长半衰期、不易降解特性,故广泛且持久地存在于环境和生物体中。大量研究已证明PFASs具有免疫毒性、内分泌毒性、神经毒性、生殖发育毒性、肝毒性。目前关于PFASs对过敏性疾病的影响已经开展了些许流行病学研究,研究结局包括哮喘、过敏性鼻炎、特异性皮炎及过敏生物标记物血清免疫球蛋白E(IgE)表达情况等,但并未观察到一致的结果。PFASs可能通过激活过氧化物酶体增殖物激活受体(PPAR)信号通路、核因子-κB(NF-κB)信号通路、JAK/STAT信号通路,抑或是通过增加肥大细胞钙内流、协同性激素效应等机制对过敏性疾病进行免疫调节。目前尚不能确定人类PFASs暴露对过敏性疾病的确切影响及其相关机制,该综述就以PFASs对哮喘、变应性鼻炎、特异性皮炎这3种过敏性疾病的影响及其可能的机制进行综述,为过敏性疾病的预防和诊疗提供研究思路。

Perfluoroalkyl and polyfluoroalkyl substances(PFASs),as a group of persistent organic pollutants among environmental endocrine disruptors,are widely used in industrial production and daily life.PFASs are widely and persistently present in the environment and organisms due to their bioaccumulation,long half-life,and low degradability properties.Published studies have proved that PFASs have immunotoxicity,endocrine toxicity,neurotoxicity,reproductive toxicity,and hepatotoxicity.At present,several epidemiological studies have been conducted on the effects of PFASs on allergic diseases,the research endpoints include asthma,allergic rhinitis,atopic dermatitis,and the expression of allergic biomarkers such as serum immunoglobulin E(IgE),but no consistent results have been observed yet.PFASs have the potential to activate several signaling pathways,including the peroxisome proliferator-activated receptor(PPAR),nuclear factor-κB(NF-κB),and JAK/STAT pathways.These mechanisms,along with increasing mast cell calcium influx and sex hormone synergistic effects,may contribute to immunomodulation in allergic diseases.At present,the exact human effect of PFASs exposure on allergic diseases and the related mechanisms are still uncertain.This review focused on the impacts of PFASs on asthma,allergic rhinitis,and atopic dermatitis and their possible mechanisms,so as to provide research ideas for the prevention,diagnosis,and treatment of allergic diseases.