Table 5. Cox-Regression Analyses Showing Longitudinal Associations between AT Levels of POPs and the 16-Year Cancer Incidence in the GraMo Cohort (n = 348)^a,e.

	total cancer incidenceb			NHD cancersc
POPs	HR (95% CI)	p-value	n/N	HR (95% CI)	p-value	n/N
PCB-138	1.35 (1.00, 1.84)	0.054	44/304	1.78 (1.03, 3.09)	0.038	27/304
PCB-153	1.20 (0.84, 1.71)	0.313	44/304	1.80 (0.94, 3.47)	0.078	27/304
PCB-180	1.28 (0.90, 1.82)	0.175	44/304	1.56 (0.84, 2.87)	0.158	27/304
p,p′-DDE	1.29 (0.96, 1.72)	0.090	44/304	1.38 (0.94, 2.02)	0.098	27/304
HCB	1.26 (0.95, 1.66)	0.112	44/304	1.54 (1.02, 2.33)	0.042	27/304
β-HCH	1.34 (1.00, 1.80)	0.053	44/304	1.70 (1.09, 2.64)	0.019	27/304
α-HCHd	1.65 (0.69, 3.96)	0.265	44/304	2.79 (0.85, 9.11)	0.089	27/304
dicofold	0.68 (0.29, 1.59)	0.378	44/304	1.17 (0.42, 3.28)	0.763	27/304

^aData are presented as hazard ratio and 95% confidence intervals [HR (95% CIs)]. Models were adjusted for age (years), sex (male/female), BMI (kg/m²), smoking (yes/no), alcohol consumption (yes/no), place of residence (urban vs semi-rural), and education (lower than primary education, primary education, or higher than primary).

^bAll incident cases of cancer (n = 44), excluding benign tumors and basal cell carcinomas (BCCs). Rest of the study population (n = 304).

^cNon-hormone-dependent (NHD) cancers (n = 27), excluding hormone-dependent (HD) cancers (n = 17). Rest of the study population (n = 304).

^dParticipants with concentrations above the LOD were compared to those with non-detected concentrations.

^eNote: no associations were observed between oxidative stress biomarkers and HD cancers in Table 4. Therefore, HD tumors were excluded from this analysis onward, given that we aimed to explore POP-cancer associations that could be mediated by in situ oxidative stress.