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饮食摄入多环芳烃(PAHs)与乳腺癌风险:来自法国e3n世代前瞻性队列

Amina Amadou , Delphine Praud , Chloé Marques , Hwayoung Noh , Pauline Frenoy , Arnaud Vigneron , Thomas Coudon , Floriane Deygas , Gianluca Severi , Béatrice Fervers , Francesca Romana Mancini

摘要

虽然有令人信服的证据表明职业暴露于多环芳烃(PAHs)与乳腺癌(BC)风险之间存在关联,但关于多环芳烃饮食暴露的研究结果不太一致。本研究旨在评估多环芳烃饮食摄入与BC风险之间的关系。方法本研究纳入了67,879名女性,这些女性完成了来自E3N-Generations队列研究的半定量饮食问卷(208种食物)。通过将E3N食品消费数据与第二次法国总饮食研究(TDS2)获得的食品污染水平相结合,估计了多环芳烃膳食摄入量。采用Cox回归估计多环芳烃膳食摄入量(四种多环芳烃(PAH4)即苯并[a]芘(BaP)、甲苯(CHR)、苯并[a]蒽(BaA)和苯并[b]荧光蒽(BbF)的和)与BC风险之间的校正风险比(hr)和95% %置信区间(CIs)。此外,BaP,总多环芳烃的替代品,被调查作为第二个暴露变量。结果平均随访17.6 年,诊断出5686例BC事件。总体而言,以第一个五分位数为参考,PAH4与BC风险之间的估计hr均大于1,但仅在第三个五分位数有统计学意义(HRQ3 vs Q1 = 1.10;置信区间:1.01—-1.20)。通过雌激素(ER)和孕酮(PR)激素受体状态,我们观察到PAH4饮食摄入量与ER-PR- BC呈正相关(HRQ4 vs Q1 = 1.34;置信区间:1.01—-1.76)。此外,与BaP存在临界正相关,对于第二个(HRQ2 vs Q1 = 1.08;CI: 0.99-1.17)和第三(HRQ3 vs Q1 = 1.07;CI: 0.98-1.16)。结论本研究支持膳食中PAH4摄入量与BC风险之间的关系,且呈非线性趋势。在BaP饮食摄入与BC风险之间观察到正但边际的关联。缩写词:BC,乳腺癌;PAHs,多环芳烃;BaA,苯并[a]蒽;软面包卷,苯并[a]芘;BbF,苯并[b]荧蒽;空空的,屈;TDS2,第二次法国总饮食研究;国际癌症研究机构;美国环境保护署;CrI,可信间隔;ci:置信区间;or,比值比;HR:风险比;SD:标准差;国家教育的妇女和妇女之间的交换和交换;MGEN,全国教育协会;ER,雌激素受体;PR:黄体酮受体;TNM tumor-node-metastasis;法国食品质量信息中心;LB,下界;MB,中界;LOD,检测限;FHBC, BC家族史;AFFP,第一次足月妊娠的年龄;BMI,身体质量指数;MHT,更年期激素替代疗法;数据保护和隐私委员会。

本文章由计算机程序翻译,如有差异,请以英文原文为准。

Dietary intake of polycyclic aromatic hydrocarbons (PAHs) and breast cancer risk: Evidence from the French E3N-Generations prospective cohort

Background

While there is compelling evidence of the association between occupational exposure to polycyclic aromatic hydrocarbons (PAHs) and risk of breast cancer (BC), findings on PAH dietary exposure are less consistent. The present study aims to evaluate the association between PAH dietary intake and BC risk.

Methods

The study included 67,879 women who completed a validated semi-quantitative dietary questionnaire (208 food items) from the E3N-Generations cohort study. PAH dietary intake was estimated by combining E3N food consumption data with food contamination levels obtained from the second French total diet study (TDS2). Cox regression was used to estimate adjusted hazard ratios (HRs) and 95 % confidence intervals (CIs) for the association between PAH dietary intake (sum of four PAHs (PAH4) namely benzo[a]pyrene (BaP), chrysene (CHR), benzo[a]anthracene (BaA) and benzo[b]fluoranthene (BbF)) and BC risk. Additionally, BaP, a surrogate for total PAHs, was investigated as the second exposure variable.

Results

After an average follow-up of 17.6 years, 5,686 incident BC were diagnosed. Overall, the estimated HRs for the associations between each quintile of PAH4 and BC risk, taking the first quintile as reference, were all greater than 1, but were statistically significant only for the third quintile (HRQ3 vs Q1 = 1.10; CI: 1.01–1.20). By estrogen (ER) and progesterone (PR) hormone receptor status, we observed a positive association between PAH4 dietary intake and ER-PR- BC (HRQ4 vs Q1 = 1.34; CI: 1.01–1.76). Moreover, there was a borderline positive association with BaP, for the second (HRQ2 vs Q1 = 1.08; CI: 0.99–1.17) and third (HRQ3 vs Q1 = 1.07; CI: 0.98–1.16) quintiles.

Conclusions

This study supports a relationship between PAH4 dietary intake and BC risk, notably with a non-linear trend. A positive but marginal association was observed between BaP dietary intake and BC risk.

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