Background: Liquid crystal display (LCD) manufacturing involves three fabrication processes: array, panel and module processes, which result in different levels of volatile organic compound (VOC) exposure. The aim of this study was to assess the potential reproductive endocrine effects of occupational exposures during LCD manufacturing predictive of menstrual cycles as subclinical markers of female reproductive dysfunction effects of low-dose exposures. Methods: A total of 94 fabrication workers were followed for one complete menstrual cycle using daily urine samples: 23 were from the array, 53 from the panel, and 18 from the module work areas. The menstrual cycle characteristics of the study population were measured using a self-administered questionnaire. Urine samples were collected during the first urination in the morning for at least one complete menstrual cycle. The urine was then analyzed to determine the urinary concentrations of follicular stimulating hormone (FSH), estrone conjugates (E1C), and pregnanediol-3-glucuronide (PdG). The results of this analysis were used to assess the potential effects of chemical exposure as determined by handheld volatile organic compound (VOC) monitors and 24 h canisters. Results: The concentration of total VOCs was much higher in the module making area (ND–21,000 ppb) than in panel (ND–766 ppb) and array (58–1,472 ppb) making areas. The concentrations of ethanol and acetone were much higher in the module (1,974.9 and 2,283.2 ppb, respectively) and panel (2256.9 and 592.2 ppb, respectively) making areas. Compared to those in the array making area, we found that E1C (12.55, 95% confidence interval (CI): 8.49, 16.61 μg/mg Cr) and PdG (0.53, 95% CI: 0.29, 0.77 μg/mg Cr) levels in the module group were significantly higher in the early follicular phase; E1C (11.93, 95% CI: 6.21, 17.65 μg/mg Cr) and PdG (0.53, 95% CI: 0.29, 0.77 μg/mg Cr) levels were significantly higher in the periovulatory phase; and all the hormone levels, FSH (1.48, 95% CI: 0.81, 2.15 μg/mg Cr), E1C (9.29, 95% CI: 4.92, 13.66 μg/mg Cr), and PdG (1.01, 95% CI: 0.42, 1.60 μg/mg Cr) were also significantly higher in the luteal phase. In addition, the FSH (0.89, 95% CI: 0.07, 1.71 μg/mg Cr) level in the panel group was significantly higher but E1C (−4.49, 95% CI: −7.90, −1.08 μg/mg Cr) was lower in the early follicular phase; and E1C (−5.16, 95% CI: −9.61, −0.71 μg/mg Cr) level was significantly lower in the periovulatory phase. Conclusions: Our findings add to the evidence that exposure to multiple low-level chemicals is associated with modest changes in reproductive hormone urinary concentrations in healthy premenopausal women. In addition, the FSH (0.89, 95% CI: 0.07, 1.71 μg/mg Cr) level in the panel group was significantly higher but E1C (−4.49, 95% CI: −7.90, −1.08 μg/mg Cr) lower in the early follicular phase; and E1C (−5.16, 95% CI: −9.61, −0.71 μg/mg Cr) level was significantly lower in the periovulatory phase.

Endometriosis is a heterogeneous chronic inflammatory disorder associated with substantial diagnostic delay and limited therapeutic options, highlighting the need of robust non-invasive biomarkers and actionable molecular targets to complement existing low-sensitivity tests. To identify conserved pathogenic mechanisms with translational potential, here, we uniformly reprocessed three independent the Gene Expression Omnibus (GEO) microarray cohorts (GSE7305, GSE25628, and GSE11691) and applied a strict, directionally consistent intersection strategy to identify conserved transcriptional signals. We identified 262 consensus differentially expressed genes enriched for immunity/inflammation, cell adhesion and migration, and angiogenesis, consistent with key biological hallmarks of lesion establishment and persistence. Protein–protein interaction topology prioritized 11 highly connected hub genes (VCAM1, CCL2, MCAM, CD14, CD24, FGFR1, SIRPA, CSF1R, S100A9, S100A8, and LY96) that likely act as an integrated immune-adhesion-angiogenesis axis. Notably, 63/262 (24%) of the consensus genes were annotated to the extracellular exosome compartment, supporting their translational relevance as liquid-biopsy candidates. Finally, connectivity mapping using the LINCS L1000 framework nominated small-molecule perturbagens predicted to reverse the endometriosis-associated signature, providing a rational starting point for drug-repurposing experiments. In conclusion, this study elucidates a conserved immune–adhesion–angiogenesis axis driven by an 11-gene hub network in endometriosis. These core regulators represent promising candidates for the development of non-invasive liquid biopsies and precision, non-hormonal therapeutics.