Intrauterine exposure to polycyclic aromatic hydrocarbons, fine particulate matter and early wheeze. Prospective birth cohort study in 4-year olds.

Intrauterine exposure to polycyclic aromatic hydrocarbons, fine particulate matter and early wheeze. Prospective birth cohort study in 4-year olds.
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DOI:
10.1111/j.1399-3038.2010.01034.x
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发表时间:
2010-06
期刊:
Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology
影响因子:
--
通讯作者:
Sowa A
Sowa A
中科院分区:
其他
文献类型:
--
作者:
Jedrychowski WA;Perera FP;Maugeri U;Mrozek-Budzyn D;Mroz E;Klimaszewska-Rembiasz M;Flak E;Edwards S;Spengler J;Jacek R;Sowa A

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这项研究的主要目的是确定产前暴露于多环芳烃(PAH)之间的关系,测量多环芳烃-DNA加合物在脐带血和早期喘息。脐带血中多环芳烃-DNA加合物的水平被认为反映了胎儿在产前期间吸收的多环芳烃的累积剂量。产前PAH暴露对呼吸系统健康的影响,通过随后4年随访中喘息天数的发生率比(IRR)进行测量,并针对潜在混杂因素(如个人产前暴露于细颗粒物)进行调整(PM2.5)、环境烟草烟雾(ETS)、儿童性别、母亲特征(年龄、教育和特应性)、产次和家中霉菌/潮湿。研究样本包括339名年龄在18-35岁之间的非吸烟母亲的新生儿,他们没有慢性疾病,在怀孕的第一个或第二个三个月从门诊产前诊所招募。出生后2年内喘息天数与产前PAH-DNA加合物水平呈正相关(IRR = 1.69,95%CI = 1.52 - 1.88),产前颗粒物(PM2.5)水平按中位数二分(IRR = 1.38; 95%CI:1.25 - 1.51)、母体特应性(IRR = 1.43; 95%CI:1.29 - 1.58)、发霉/潮湿的房屋(IRR = 1.43; 95%CI:1.27 - 1.61)。母亲的教育水平和分娩年龄与喘息的IRR呈负相关。在3岁或4岁时,未观察到喘息频率与产前环境危害(多环芳烃和PM2.5)水平之间的显著相关性。虽然3岁或4岁时喘息的频率不再与产前暴露于多环芳烃和PM2.5相关,但其发生取决于生命前两年喘息的存在,这几乎使以后生命中喘息的风险增加了两倍。总之,研究结果可能表明,早期喘息(<24月龄)的驱动力与导致晚发喘息的驱动力不同。由于我们报道了产前PAH(通过PAH-DNA加合物测量)和PM2.5暴露对早期喘息没有协同作用,这表明这两种暴露可能通过不同的生物学机制对喘息产生独立的影响。
The main goal of the study was to determine the relationship between prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) measured by PAH-DNA adducts in umbilical cord blood and early wheeze. The level of PAH-DNA adducts in the cord blood is assumed to reflect the cumulative dose of PAHs absorbed by the fetus over the prenatal period. The effect of prenatal PAH exposure on respiratory health measured by the incidence rate ratio (IRR) for the number of wheezing days in the subsequent four year follow-up was adjusted for potential confounding factors such as personal prenatal exposure to fine particulate matter (PM2.5), environmental tobacco smoke (ETS), gender of child, maternal characteristics (age, education and atopy), parity, and mold/dampness in the home. The study sample includes 339 newborns of non-smoking mothers 18-35 years of age and free from chronic diseases, who were recruited from ambulatory prenatal clinics in the first or second trimester of pregnancy. The number of wheezing days during the first two years of life was positively associated with prenatal level of PAH-DNA adducts (IRR = 1.69, 95%CI = 1.52 – 1.88), prenatal particulate matter (PM2.5) level dichotomized by the median (IRR = 1.38; 95%CI: 1.25 – 1.51), maternal atopy (IRR = 1.43; 95%CI: 1.29 – 1.58), moldy/damp house (IRR = 1.43; 95%CI: 1.27 – 1.61). The level of maternal education and maternal age at delivery were inversely associated with the IRRs for wheeze. The significant association between frequency of wheeze and the level of prenatal environmental hazards (PAHs and PM2.5) was not observed at ages 3 or 4 years. Although the frequency of wheezing at ages 3 or 4 years was no longer associated with prenatal exposure to PAHs and PM2.5, its occurrence depended on the presence of wheezing in the first two years of life, which nearly tripled the risk of wheezing in later life. In conclusion, the findings may suggest that driving force for early wheezing (<24 months of age) are different to those leading to later onset of wheeze. As we reported no synergistic effects between prenatal PAH (measured by PAH-DNA adducts) and PM2.5 exposures on early wheeze, this suggests the two exposures may exert independent effects via different biological mechanism on wheeze.
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