Exposure to endocrine-disrupting chemicals in utero and thyroid cancer risk in offspring - Authors' reply.
Exposure to endocrine-disrupting chemicals in utero and thyroid cancer risk in offspring - Authors' reply.
复制标题
在子宫内接触内分泌干扰化学物质和后代患甲状腺癌的风险 - 作者的答复。
DOI：
10.1016/s2213-8587(21)00073-5
复制
发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Troisi,Rebecca
中科院分区：
文献类型：
--
作者：
Kitahara,CariM;Bjørge,Tone;Grotmol,Tom;Daltveit,DagrunSlettebø;Troisi,Rebecca
内分泌学是研究孕产妇健康状况（尤其是怀孕前或怀孕期间的甲状腺状况）与后代患甲状腺癌风险之间关系的一项出色工作。在分析的危险因素中，发现与后代较高出生体重和先天性甲状腺功能减退、母亲怀孕前或怀孕期间糖尿病、产后出血、母亲甲状腺功能减退或甲状腺功能亢进以及甲状腺肿之间的关联最强。作者提出了一个新的假设，即如果母亲在最关键的子宫内和围产期患有甲状腺功能减退、甲状腺功能亢进、甲状腺肿或其他几种健康状况，那么后代在以后的生活中患任何形式甲状腺癌的风险就会更高。 1 尽管需要进行实验研究来证明这一假设，但尚未为这一具有巨大公共卫生重要性的新观察结果提出潜在机制。此外，尚不清楚为什么甲状腺癌在患有甲状腺疾病和相关疾病的母亲的女性后代中更常见。令人惊讶的是，文章没有讨论几十年来存在并普遍接触环境持久且普遍存在的具有强烈内分泌干扰潜力的工业化学品。我们认为，应该包括在内，因为相当多的妊娠期和生命早期健康状况可能与接触高危险化学品有关，例如多氯联苯、双酚 A、邻苯二甲酸盐和杀虫剂。这些化学品用于食品包装以及日常家居和消费品（包括化妆品和个人护理用品），具有潜在的甲状腺激素干扰作用。 2 内分泌干扰化学物质可能会改变荷尔蒙稳态并影响下丘脑-垂体-甲状腺轴，导致甲状腺激素稳态紊乱、甲状腺功能减退、甲状腺增生和甲状腺肿瘤。 3, 4 此外，内分泌干扰化学物质在母体接触后可穿过胎盘屏障，对母亲和发育中的胎儿的生殖和激素系统造成不可挽回的损害，并导致后代出现多种其他系统性神经系统疾病和甲状腺功能障碍。 5, 6 早在 20 世纪 90 年代，人们就确定天然和合成化学物质都具有与内源性激素受体结合和相互作用并调节生理功能的潜力。有人认为，在欧洲（包括北欧国家），内分泌干扰性化学物质的暴露可能会极大地促进人类生命过程中的疾病病理生理学和功能障碍，并产生跨代后果。 7 这种功能障碍和基因毒性的一个例子是在众所周知的合成化学品己烯雌酚中观察到的，据报道，该物质会导致女性癌症和后代畸形。因此，我们建议，尽管母体甲状腺疾病与后代患甲状腺癌的风险增加有关，但在生命早期关键阶段对内分泌干扰化学物质暴露的研究也不容忽视，并且同样可能导致后代日后罹患甲状腺癌和其他激素敏感性癌症，例如乳腺癌。
Endocrinology is an excellent effort to study the association between maternal health conditions, particularly thyroid status, either before or during pregnancy, and risk of developing thyroid cancer in offspring. Of the risk factors analysed, the strongest associations were found for higher birth weight and congenital hypothyroidism in offspring, maternal diabetes before or during pregnancy, postpartum haemorrhage, maternal hypothyroidism or hyperthyroidism, and goiter. The authors proposed a novel hypothesis in which offspring are at higher risk of developing any form of thyroid cancer later in life if their mothers had hypothyroidism, hyperthyroidism, goiter, or several other health conditions during the most crucial in-utero and perinatal periods. 1 Although experimental investigations are needed to prove this hypothesis, no underlying mechanisms have yet been proposed for this novel observation, which is of immense public health importance. Additionally, it is unclear why thyroid cancer was more common in female offspring of mothers who suffered from thyroid disease and associated ailments. Surprisingly, the decades long existence and pervasive exposure to environmentally persistent and ubiquitous industrial chemicals with strong endocrine-disrupting potential was not discussed in the Article. In our opinion, should have been included because a sizeable number of these gestational and early-life health conditions could be linked to exposure to highly hazardous chemicals, such as polychlorinated biphenyls, bisphenol A, phthalates, and pesticides. These chemicals are used in food packaging and day-to-day household and consumer products (including cosmetics and personalcare items) with potential thyroidhormone-disrupting effects. 2 Endocrine-disrupting chemicals potentially alter hormonal homeo stasis and affect the hypothalamic–pituitary–thyroid axis, causing perturbation of thyroid hormone homeostasis, hypothyroidism, thyroid hyperplasia, and thyroid neoplasia. 3, 4 Moreover, endocrine-disrupting chemicals can cross the placental barrier upon maternal exposure, causing irreparable damage to reproductive and hormonal systems of the mother and developing fetus and with several other systemic neurological disorders and thyroid dysfunction in offspring. 5, 6 Early in the 1990s, it was established that both natural and synthetic chemicals have the potential to bind and interact with endogenous hormone receptors and modulate physiological functions. It has been suggested that endocrinedisrupting chemicals exposures in Europe, including Nordic countries, are likely to substantially contribute to disease pathophysiology and dysfunction across the human life course with transgenerational consequences. 7 An example of such dysfunction and genotoxicity has been observed with the well known synthetic chemical, diethylstilbestrol, which has been reported to cause cancer in women and abnormalities in offspring. Therefore, we suggest that although maternal thyroid disorders have been linked to increased risk of thyroid cancer in offspring, investigations on endocrine-disrupting chemicals exposures during the crucial phases of early life cannot be ignored and could equally be responsible for thyroid cancer and other hormonesensitive cancers, such as breast cancer, in offspring later in life.