ToxStrategies, LLC, Asheville, North Carolina 28801, United States.
EpidStrategies, a Division of ToxStrategies, LLC, Katy, Texas 77494, United States.
Toxicol Sci. 2024 May 28;199(2):172-193. doi: 10.1093/toxsci/kfae039.
Formaldehyde is recognized as carcinogenic for the portal of entry sites, though conclusions are mixed regarding lymphohematopoietic (LHP) cancers. This systematic review assesses the likelihood of a causal relationship between formaldehyde and LHP cancers by integrating components recommended by NASEM. Four experimental rodent bioassays and 16 observational studies in humans were included following the implementation of the a priori protocol. All studies were assessed for risk of bias (RoB), and meta-analyses were conducted on epidemiological studies, followed by a structured assessment of causation based on GRADE and Bradford Hill. RoB analysis identified systemic limitations precluding confidence in the epidemiological evidence due to inadequate characterization of formaldehyde exposure and a failure to adequately adjust for confounders or effect modifiers, thus suggesting that effect estimates are likely to be impacted by systemic bias. Mixed findings were reported in individual studies; meta-analyses did not identify significant associations between formaldehyde inhalation (when measured as ever/never exposure) and LHP outcomes, with meta-SMRs ranging from 0.50 to 1.51, depending on LHP subtype. No associations with LHP-related lesions were reported in reliable animal bioassays. No biologically plausible explanation linking the inhalation of FA and LHP was identified, supported primarily by the lack of systemic distribution and in vivo genotoxicity. In conclusion, the inconsistent associations reported in a subset of the evidence were not considered causal when integrated with the totality of the epidemiological evidence, toxicological data, and considerations of biological plausibility. The impact of systemic biases identified herein could be quantitatively assessed to better inform causality and use in risk assessment.
甲醛被认为是致癌物质的进入部位,虽然结论是混合的关于淋巴造血(LHP)癌症。本系统评价通过整合 NASEM 推荐的成分来评估甲醛与 LHP 癌症之间是否存在因果关系。在实施事先协议后,纳入了四项实验性啮齿动物生物测定和 16 项人类观察性研究。所有研究均进行了偏倚风险(RoB)评估,并对流行病学研究进行了荟萃分析,然后根据 GRADE 和 Bradford Hill 对因果关系进行了结构化评估。RoB 分析确定了系统限制,由于甲醛暴露的特征描述不充分以及未能充分调整混杂因素或效应修饰剂,因此无法对流行病学证据有信心,这表明效应估计可能受到系统偏倚的影响。个别研究报告了混合结果;荟萃分析未发现甲醛吸入(当以曾经/从不暴露测量)与 LHP 结果之间存在显著关联,LHP 亚型不同,meta-SMR 范围从 0.50 到 1.51。在可靠的动物生物测定中未报告与 LHP 相关病变的关联。没有发现将 FA 吸入与 LHP 联系起来的生物学上合理的解释,主要是由于缺乏系统分布和体内遗传毒性。总之,当将部分证据中的不一致关联与流行病学证据、毒理学数据和生物学合理性的考虑因素综合考虑时,认为这些关联没有因果关系。可以对本文确定的系统偏差的影响进行定量评估,以更好地说明因果关系和在风险评估中的使用。