Occupational & Environmental Epidemiology Branch, Division of Cancer Epidemiology & Genetics (DCEG), National Cancer Institute (NCI), Rockville, Maryland, USA.
Trans-Divisional Research Program, DCEG, NCI, Rockville, Maryland, USA.
Int J Cancer. 2024 Mar 15;154(6):979-991. doi: 10.1002/ijc.34776. Epub 2023 Oct 30.
Human exposure to per- and polyfluoroalkyl substances (PFAS) occurs globally through contaminated food, dust, and drinking water. Studies of PFAS and thyroid cancer have been limited. We conducted a nested case-control study of prediagnostic serum levels of 19 PFAS and papillary thyroid cancer (400 cases, 400 controls) in the Finnish Maternity Cohort (pregnancies 1986-2010; follow-up through 2016), individually matched on sample year and age. We used conditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for log transformed and categorical exposures, overall and stratified by calendar period, birth cohort, and median age at diagnosis. We adjusted for other PFAS with Spearman correlation rho = 0.3-0.6. Seven PFAS, including perfluoroctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), N-ethyl-perfluorooctane sulfonamidoacetic acid (EtFOSAA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluorohexane sulfonic acid (PFHxS) were detected in >50% of women. These PFAS were not associated with risk of thyroid cancer, except for PFHxS, which was inversely associated (OR log = 0.82, 95% CI: 0.70-0.97). We observed suggestive but imprecise increased risks associated with PFOA, PFOS, and EtFOSAA for those diagnosed at ages <40 years, whereas associations were null or inverse among those diagnosed at 40+ years (P-interaction: .02, .08, .13, respectively). There was little evidence of other interactions. These results show no clear association between PFAS and papillary thyroid cancer risk. Future work would benefit from evaluation of these relationships among those with higher exposure levels and during periods of early development when the thyroid gland may be more susceptible to environmental harms.
人类通过受污染的食物、灰尘和饮用水在全球范围内接触到全氟和多氟烷基物质(PFAS)。关于 PFAS 和甲状腺癌的研究有限。我们在芬兰母婴队列中进行了一项巢式病例对照研究(1986-2010 年妊娠;随访至 2016 年),研究了诊断前血清中 19 种 PFAS 与甲状腺癌(400 例病例,400 例对照)之间的关系,按样本年份和年龄进行个体匹配。我们使用条件逻辑回归估计了对数转换和分类暴露的比值比(OR)和 95%置信区间(CI),总体以及按日历时期、出生队列和诊断时的中位年龄进行分层。我们用 Spearman 相关系数 rho(0.3-0.6)调整了其他 PFAS。七种 PFAS,包括全氟辛酸(PFOA)、全氟辛烷磺酸(PFOS)、N-乙基全氟辛烷磺酰胺基乙酸(EtFOSAA)、全氟壬酸(PFNA)、全氟癸酸(PFDA)和全氟己烷磺酸(PFHxS),在超过 50%的女性中被检测到。这些 PFAS 与甲状腺癌风险无关,除了 PFHxS,其与甲状腺癌风险呈负相关(ORlog=0.82,95%CI:0.70-0.97)。我们观察到,对于 40 岁以下诊断的患者,PFOA、PFOS 和 EtFOSAA 与风险呈正相关,但在 40 岁以上诊断的患者中,相关性为零或呈负相关(P 交互作用:分别为 0.02、0.08、0.13)。没有其他相互作用的证据。这些结果表明,PFAS 与甲状腺癌风险之间没有明确的关联。未来的研究将受益于在更高暴露水平的人群和甲状腺可能更容易受到环境危害的早期发育阶段评估这些关系。