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经胎盘和出生后吸入多环芳烃的单独及联合效应:关于喘息事件的前瞻性出生队列研究

Separate and joint effects of tranplacental and postnatal inhalatory exposure to polycyclic aromatic hydrocarbons: prospective birth cohort study on wheezing events.

作者信息

Jedrychowski Wiesław A, Perera Frederica P, Majewska Renata, Camman David, Spengler John D, Mroz Elzbieta, Stigter Laura, Flak Elżbieta, Jacek Ryszard

机构信息

Chair of Epidemiology and Preventive Medicine, Jagiellonian University Medical College, Kraków, Poland.

出版信息

Pediatr Pulmonol. 2014 Feb;49(2):162-72. doi: 10.1002/ppul.22923. Epub 2013 Oct 24.

Abstract

The goal of this epidemiologic investigation was to analyze the associations between prenatal and postnatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and severity of wheeze and recurrent wheeze. The 257 children included in this analysis had a complete set of prenatal and postnatal PAH measurements and attended regular health checkups over a 4-year follow-up period since birth. Transplacental PAH exposure was measured by personal air monitoring of the mothers during the second trimester of pregnancy; postnatal exposure was estimated using the same instruments indoors at the children's residences at age 3. Chemical analysis tests were performed to determine airborne concentrations of nine PAH compounds. The results show that both prenatal and postnatal exposure were associated positively with the severity of wheezing days and recurrent wheezing reported in the follow-up. While the incidence rate ratio (IRR) for severity of wheeze and prenatal PAH exposure was 1.53 (95%CI: 1.43-1.64) that for postnatal PAH exposure was 1.13 (95%CI: 1.08-1.19). However, recurrent wheezing was more strongly associated with airborne PAH levels measured at age 3 (OR = 2.31, 95%CI: 1.26-4.22) than transplacental PAH exposure (OR = 1.40, 95% CI: 0.85-2.09), but the difference was statistically insignificant. In conclusion, it appears that prenatal PAH exposure may precipitate and intensify early onset of wheezing symptoms in childhood, resulting from the postnatal exposure and suggest that success in reducing the incidence of respiratory diseases in children would depend on reducing both fetal and childhood exposure to air pollution.

摘要

这项流行病学调查的目的是分析产前和产后暴露于空气中的多环芳烃(PAH)与喘息严重程度和复发性喘息之间的关联。纳入该分析的257名儿童有一套完整的产前和产后PAH测量数据,并且自出生起在4年的随访期内参加了定期健康检查。通过在孕期第二个月对母亲进行个人空气监测来测量经胎盘的PAH暴露;产后暴露是在儿童3岁时使用相同仪器在其住所室内进行估算的。进行了化学分析测试以确定9种PAH化合物的空气浓度。结果表明,产前和产后暴露均与随访中报告的喘息天数严重程度和复发性喘息呈正相关。喘息严重程度与产前PAH暴露的发病率比(IRR)为1.53(95%CI:1.43 - 1.64),产后PAH暴露的发病率比为1.13(95%CI:1.08 - 1.19)。然而,复发性喘息与3岁时测量的空气中PAH水平(OR = 2.31,95%CI:1.26 - 4.22)的关联比经胎盘PAH暴露(OR = 1.40,95%CI:0.85 - 2.09)更强,但差异无统计学意义。总之,产前PAH暴露可能会促使并加剧儿童期喘息症状的早期发作,这是由产后暴露导致的,表明降低儿童呼吸道疾病发病率的成功与否将取决于减少胎儿期和儿童期暴露于空气污染。

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