A viewpoint entitled “Thyroid Cancer “Epidemic”: A Socio-Environmental Health Problem Needs Collaborative Efforts” was recently published in ES&T by Tang et al., discussing the topic of the relationship between environmental chemical exposure and thyroid cancer development.(1) We would like to comment on it from epidemiological and medical points of view. Although the current worldwide incidence of thyroid cancer is rising due to life style changes (e.g., obesity, smoking), it is estimated that in the U.S., for example, overdiagnosis may account for 70–80% of cases in women.(2) Tang et al. suggested that it might be a true increase, not an overdiagnosis, from U.S. thyroid cancer mortality analysis (until 2013).(3) However, the recent incidence of thyroid cancer has been stabilized in the U.S. since the publication and gradual implementation of the 2009 American Thyroid Association guidelines, which refrains from aggressive ultrasound examinations without clinical symptoms.(4) Hence, the “epidemic” trend has ceased in recent years in the U.S. The relatively rapid stabilization in the number of cases in response to the change in clinical practice indicates that overdiagnosis was a substantial factor of the increase. Changes in case numbers related to changes in exposure to risk factors would occur more slowly due to the long latency period of cancer onset. Thyroid cancer mortality is also declining globally, except in the U.S., UK, and Australia (moderately increasing up to 2000s, after declining up to the 1980s).(5) The moderate increases in these countries might be explained by lifestyle changes. For example, obesity increased the cancer relative risk at 1.33 per 5 kg/m² BMI increment, and current smoking reduced the risk to 0.53.(6) Nevertheless, after 2010, the mortality rate was also stabilized in the U.S. From the above, the current situation is an unlikely “epidemic” even in the U.S. Next, we agree that there are unknown environmental factors in the causes of thyroid cancer. However, the viewpoint addressed only possible effects of environmental chemicals on the synthesis and metabolism of thyroid hormones, T3 and T4. The etiology of not only thyroid cancer, but most types of cancers is understood to be due to the accumulation of genetic mutations and epigenetic modifications in the process of DNA replication. On the other hand, there is poor pathological evidence as to how T4 or T3 cause carcinogenesis. We intend to raise potential targets to be investigated for causes of thyroid cancer. Noncancerous thyroid disease would be associated with future carcinogenesis. Several reports showed that Hashimoto’s disease, chronic lymphocytic thyroiditis was frequently found in papillary thyroid cancer patients.(7) Pathologically, it is speculated that autoimmune inflammation in Hashimoto’s disease affects carcinogenesis. In addition, thyrotropin (TSH), growth factor of thyrocytes, was shown to be associated with thyroid cancer.(8) TSH is likely to promote tumor progression via effects on proliferation and differentiation of thyrocytes, and TSH suppression therapy is recommended for patients with high-risk differentiated thyroid cancer. Several studies showed associations between exposure to persistent organic pollutants and TSH.(9) From the above evidence, future studies are recommended to include clinical variables and outcomes supported by cancer biology such as autoantibodies, inflammation, TSH, and Hashimoto disease. The authors declare no competing financial interest. This article references 9 other publications.

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评论“甲状腺癌的流行”：一个社会环境健康问题需要合作。”

最近在ES＆T上发表了一篇题为“甲状腺癌的流行病：一个社会环境健康问题需要合作的观点”的观点。Tang等人讨论了环境化学暴露与甲状腺癌发展之间的关系。（1）我们将从流行病学和医学的角度对此进行评论。尽管由于生活方式的改变（例如肥胖，吸烟），目前全球甲状腺癌的发病率正在上升，但是据估计，例如在美国，过度诊断可能占女性病例的70–80％。[2] Tang等。提示，从美国甲状腺癌死亡率分析（到2013年），这可能是真正的增加，而不是过度诊断。（3）但是，自2009年出版并逐步实施以来，最近在美国甲状腺癌的发病率已经稳定。美国甲状腺协会指南，该指南避免了没有临床症状的积极超声检查。（4）因此，近年来，“流行病”趋势在美国已经停止。随着临床实践的变化，病例数的相对快速稳定表明，过度诊断是发病率上升的重要因素。由于癌症发作的潜伏期长，与风险因素暴露相关的病例数变化将更缓慢地发生。除美国，英国和澳大利亚外，全球甲状腺癌死亡率也在下降（到1980年代下降到2000年代有所上升）。（5）这些国家的适度上升可能是由于生活方式的改变。例如，肥胖使癌症的相对风险增加到每5 kg / m 1.33 随着临床实践的变化，病例数的相对快速稳定表明，过度诊断是增加病例数的重要因素。由于癌症发作的潜伏期长，与风险因素暴露相关的病例数变化将更缓慢地发生。除美国，英国和澳大利亚外，全球甲状腺癌死亡率也在下降（到1980年代下降到2000年代有所上升）。（5）这些国家的适度上升可能是由于生活方式的改变。例如，肥胖使癌症的相对风险增加到每5 kg / m 1.33 随着临床实践的变化，病例数的相对快速稳定表明，过度诊断是增加病例数的重要因素。由于癌症发作的潜伏期长，与风险因素暴露相关的病例数变化将更缓慢地发生。除美国，英国和澳大利亚外，全球甲状腺癌死亡率也在下降（到1980年代下降到2000年代有所上升）。（5）这些国家的适度上升可能是由于生活方式的改变。例如，肥胖使癌症的相对风险增加到每5 kg / m 1.33 除美国，英国和澳大利亚外，全球甲状腺癌死亡率也在下降（到1980年代下降到2000年代有所上升）。（5）这些国家的适度上升可能是由于生活方式的改变。例如，肥胖使癌症的相对风险增加到每5 kg / m 1.33 除美国，英国和澳大利亚外，全球甲状腺癌死亡率也在下降（到1980年代下降到2000年代有所增加）。（5）这些国家的适度上升可能是生活方式的改变所致。例如，肥胖使癌症的相对风险增加到每5 kg / m 1.33²体重指数增加，当前吸烟使患病风险降低至0.53。（6）然而，在2010年之后，美国的死亡率也趋于稳定。从以上所述，即使在美国，目前的情况也不大可能成为“流行病”。甲状腺癌的病因有未知的环境因素。但是，该观点仅涉及环境化学物质对甲状腺激素T3和T4合成和代谢的可能影响。不仅是甲状腺癌的病因，而且大多数类型的癌症的病因被认为是由于DNA复制过程中遗传突变和表观遗传修饰的积累。另一方面，关于T4或T3如何致癌的病理证据不多。我们打算提出可能要调查的甲状腺癌原因的潜在目标。非癌性甲状腺疾病将与未来的癌变相关。几篇报道表明，在甲状腺乳头状癌患者中经常发现桥本氏病，慢性淋巴细胞性甲状腺炎。（7）从病理上推测，桥本氏病的自身免疫炎症会影响癌变。此外，甲状腺细胞的促甲状腺激素（TSH）被证明与甲状腺癌有关。（8）TSH可能通过影响甲状腺细胞的增殖和分化来促进肿瘤的进展，建议对TSH患者进行TSH抑制疗法高危分化型甲状腺癌。多项研究表明，持久性有机污染物的暴露与TSH之间存在关联。（9）根据以上证据，建议将来的研究包括自身抗体，炎症，TSH和桥本病等癌症生物学支持的临床变量和结果。作者宣称没有竞争性的经济利益。本文引用了其他9种出版物。