为了探索制药品和个人护理产品（PPCPs）、阻燃剂、双酚类、邻苯二甲酸酯和多环芳烃（PAHs）对人类视网膜前体细胞（RPCs）和视网膜色素上皮细胞（RPE）的毒性作用，这些细胞是视网膜发育早期的主要细胞类型，对于后续功能细胞类型分化至关重要，与视网膜疾病密切相关。在分化23天后，含有RPCs和RPE细胞的人类胚胎干细胞（hESC）基础的视网膜前器官模型暴露于10、100和1000 nM的农药（丁草胺、特布屈赉、百菌清、滴滴涕、皮丙噻灵和氯虫胺）、阻燃剂（PFOS、TBBPA、DBDPE和TDCIPP）、PPCPs（销抑菌酮和BHT）和其他典型污染物（菲、二氯环脂和双酚A）中，共持续七天。然后，监测并比较mRNA表达变化。1）所选污染物在环境和人类相关浓度下没有表现出强烈的影响，尽管阻燃剂的效果比其他化学类别更强。令人惊讶的是，一些具有不同结构的污染物显示出相似的不良效应。2）暴露于污染物中引起了不同程度的细胞脱落，可能是由于细胞外基质（ECM）和/或细胞粘附的改变。本研究建立了一个适用于评估多种污染物效应的视网膜前器官模型，并指出了阻燃剂等污染物的潜在视网膜毒性。然而，毒性机制和对细胞脱落的影响仍不清楚，值得进一步探索。此外，该模型有望用于筛选旨在缓解这些污染物有害效应的干预措施。

To explore the retinal toxicity of pharmaceuticals and personal care products (PPCPs), flame retardants, bisphenols, phthalates, and polycyclic aromatic hydrocarbons (PAHs) on human retinal progenitor cells (RPCs) and retinal pigment epithelial (RPE) cells, which are the primary cell types at the early stages of retinal development, vital for subsequent functional cell type differentiation, and closely related to retinal diseases.After 23 days of differentiation, human embryonic stem cell (hESC)-based retinal pre-organoids, containing RPCs and RPE cells, were exposed to 10, 100, and 1000 nM pesticides (butachlor, terbutryn, imidacloprid, deltamethrin, pendimethalin, and carbaryl), flame retardants (PFOS, TBBPA, DBDPE, and TDCIPP), PPCPs (climbazole and BHT), and other typical pollutants (phenanthrene, DCHP, and BPA) for seven days. Then, mRNA expression changes were monitored and compared.1) The selected pollutants did not show strong effects at environmental and human-relevant concentrations, although the effects of flame retardants were more potent than those of other categories of chemicals. Surprisingly, some pollutants with distinct structures showed similar adverse effects. 2) Exposure to pollutants induced different degrees of cell detachment, probably due to alterations in extracellular matrix (ECM) and/or cell adhesion.In this study we established a retinal pre-organoid model suitable for evaluating multiple pollutants' effects, and pointed out the potential retinal toxicity of flame retardants, among other pollutants. Nevertheless, the potential mechanisms of toxicity and the effects on cell detachment are still unclear and deserve further exploration. Additionally, this model holds promise for screening interventions aimed at mitigating the detrimental effects of these pollutants.