Department of Population Health, New York University School of Medicine, New York, NY, USA.
Department of Population Health, New York University School of Medicine, New York, NY, USA; Department of Pediatrics, New York University School of Medicine, USA; Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA; NYU Wagner School of Public Service, New York, NY, USA; NYU College of Global Public Health, New York, NY, USA.
Environ Res. 2020 Jul;186:109439. doi: 10.1016/j.envres.2020.109439. Epub 2020 May 11.
Celiac disease affects approximately 1% of the population worldwide. Little is known about environmental factors that may modulate risk in genetically susceptible populations. Persistent organic pollutants (POPs) are known endocrine disruptors and, given the interplay between the endocrine and immune systems, are plausible contributors to celiac disease. The current study aims to elucidate the association between POPs and celiac disease. We conducted a single-site pilot study of 88 patients recruited from NYU Langone's Hassenfeld Children's Hospital outpatient clinic, 30 of which were subsequently diagnosed with celiac disease using standard serology and duodenal biopsy examination. Polybrominated diphenyl ether (PBDEs), perfluoroalkyl substances (PFASs), and p,p'-dichlorodiphenyldichloroethylene (DDE) and HLA-DQ genotype category were measured in blood serum and whole blood, respectively. Multivariable logistic regressions were used to obtain odds ratios for celiac disease associated with serum POP concentrations. Controlling for sex, race, age, BMI, and genetic susceptibility score, patients with higher serum DDE concentrations had 2-fold higher odds of celiac disease (95% CI: 1.08, 3.84). After stratifying by sex, we found higher odds of celiac disease in females with serum concentrations of DDE (OR = 13.0, 95% CI = 1.54, 110), PFOS (OR = 12.8, 95% CI = 1.17, 141), perfluorooctanoic acid (OR = 20.6, 95% CI = 1.13, 375) and in males with serum BDE153, a PBDE congener (OR = 2.28, 95% CI = 1.01, 5.18). This is the first study to report on celiac disease with POP exposure in children. These findings raise further questions of how environmental chemicals may affect autoimmunity in genetically susceptible individuals.
乳糜泻影响全世界约 1%的人口。对于可能调节遗传易感人群风险的环境因素知之甚少。持久性有机污染物 (POPs) 是已知的内分泌干扰物，鉴于内分泌和免疫系统之间的相互作用，它们是乳糜泻的合理致病因素。本研究旨在阐明 POPs 与乳糜泻之间的关联。我们对来自 NYU Langone 的 Hassenfeld 儿童医院门诊的 88 名患者进行了单站点试点研究，其中 30 名随后通过标准血清学和十二指肠活检检查诊断为乳糜泻。多溴二苯醚 (PBDEs)、全氟烷基物质 (PFASs) 和 p,p'-二氯二苯二氯乙烯 (DDE) 和 HLA-DQ 基因型类别分别在血清和全血中进行了测量。多变量逻辑回归用于获得与血清 POP 浓度相关的乳糜泻的比值比。控制性别、种族、年龄、BMI 和遗传易感性评分后，血清 DDE 浓度较高的患者患乳糜泻的几率增加了 2 倍 (95%CI：1.08，3.84)。按性别分层后，我们发现血清 DDE 浓度较高的女性患乳糜泻的几率更高 (OR=13.0，95%CI=1.54，110)、全氟辛烷磺酸 (OR=12.8，95%CI=1.17，141)、全氟辛酸 (OR=20.6，95%CI=1.13，375) 和血清 BDE153 浓度较高的男性，BDE153 是一种多溴二苯醚同系物 (OR=2.28，95%CI=1.01，5.18)。这是第一项报告儿童乳糜泻与 POP 暴露的研究。这些发现进一步提出了环境化学物质如何影响遗传易感个体自身免疫的问题。
