Division for Infection Control and Environmental Health, Norwegian Institute of Public Health, Oslo, Norway.
Division for Infection Control and Environmental Health, Norwegian Institute of Public Health, Oslo, Norway.
Environ Res. 2018 Jan;160:518-523. doi: 10.1016/j.envres.2017.10.012. Epub 2017 Nov 6.
Prenatal exposure to perfluoralkyl substances (PFASs) has been reported to be associated with immunosuppression in early childhood, but with contradictory findings related to atopic and lung diseases.
We aimed to determine if prenatal exposure to PFASs is associated with asthma or other allergic diseases or respiratory tract infections in childhood.
Nineteen PFASs were measured in cord blood available from 641 infants in the Environment and Childhood Asthma (ECA) prospective birth cohort study. The six most abundant PFASs were perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorooctanesulfonamide (PFOSA), perfluorohexane sulfonic acid (PFHxS), perfluorononanoic acid (PFNA), and perfluoroundecanoic acid (PFUnDA). Health outcomes were assessed at two and ten years of age, and included reported obstructive airways disease (wheeze by 10 years; asthma by 2 and 10 years; reduced lung function at birth; allergic rhinitis by 10 years), atopic dermatitis (AD) by 2 and 10 years, allergic sensitization by 10 years, and episodes of common respiratory tract infections (common cold by 2 years, lower respiratory tract infections (LRTI) by 10 years). The associations between exposure and health outcomes were examined using logistic and Poisson regression.
The number of reported airways infections were significantly associated with cord blood concentrations of PFAS; common colds by two years with PFUnDA (β = 0.11 (0.08-0.14)) and LRTIs from 0 to 10 years of age with PFOS (β = 0.50 (0.42-0.57)), PFOA (β = 0.28 (0.22-0.35)), PFOSA (β = 0.10 (0.06-0.14)), PFNA (β = 0.09 (0.03-0.14)) and PFUnDA (β = 0.18 (0.13-0.23)) concentrations. Neither reduced lung function at birth, asthma, allergic rhinitis, AD nor allergic sensitization were significantly associated with any of the PFASs.
Although prenatal exposure to PFASs was not associated with atopic or lung manifestations by 10 years of age, several PFASs were associated with an increased number of respiratory tract infections in the first 10 years of life, suggesting immunosuppressive effects of PFASs.
已有研究表明，产前暴露于全氟烷基物质（PFASs）与儿童早期的免疫抑制有关，但与特应性和肺部疾病的相关性存在矛盾。
我们旨在确定产前暴露于 PFASs 是否与儿童时期的哮喘或其他过敏性疾病或呼吸道感染有关。
在环境与儿童哮喘（ECA）前瞻性出生队列研究中，对 641 名婴儿的脐带血进行了 19 种 PFASs 的检测。在最丰富的 6 种 PFASs 中，包括全氟辛烷磺酸（PFOS）、全氟辛酸（PFOA）、全氟辛烷磺酰胺（PFOSA）、全氟己烷磺酸（PFHxS）、全氟壬酸（PFNA）和全氟十一烷酸（PFUnDA）。在 2 岁和 10 岁时评估健康结果，包括报告的气道疾病（10 岁时出现喘息；2 岁和 10 岁时哮喘；出生时肺功能降低；10 岁时过敏性鼻炎）、2 岁和 10 岁时特应性皮炎（AD）、10 岁时过敏致敏，以及常见呼吸道感染发作（2 岁时普通感冒，10 岁时下呼吸道感染（LRTI））。使用逻辑和泊松回归检验暴露与健康结果之间的关系。
报告的气道感染次数与脐带血中 PFAS 浓度显著相关；2 岁时普通感冒与 PFUnDA 相关（β=0.11（0.08-0.14）），0 至 10 岁时 LRTI 与 PFOS 相关（β=0.50（0.42-0.57））、PFOA（β=0.28（0.22-0.35））、PFOSA（β=0.10（0.06-0.14））、PFNA（β=0.09（0.03-0.14））和 PFUnDA（β=0.18（0.13-0.23））浓度。出生时肺功能降低、哮喘、过敏性鼻炎、AD 或过敏致敏与任何一种 PFASs 均无显著相关性。
尽管产前暴露于 PFASs 与 10 岁时的特应性或肺部表现无关，但几种 PFASs 与生命头 10 年呼吸道感染次数的增加有关，提示 PFASs 具有免疫抑制作用。
