Cadmium exposure has been associated with shortened telomeres, alterations in DNA methylation patterns, and increased mortality. However, the role of DNA methylation in mediating the relationship between cadmium and telomere dynamics is still unclear. Additionally, it is unknow how telomere dynamics and DNA methylation alterations may affect the association between cadmium exposure and mortality outcomes. We utilized data from 8716 National Health and Nutrition Examination Survey (NHANES) participants aged 18 and above, collected between 1999 and 2002, and linked these to mortality outcomes from the National Center for Health Statistics (NCHS) through 2019. In the final model, ln-blood cadmium was significantly and inversely associated with ln-T/S ratio (β = −0.043, 95% CI: −0.059 to −0.027, p < 0.001), while ln-Horvath DNAmTL was strongly and positively associated with ln-T/S ratio (β = 1.782, 95% CI: 1.467 to 2.097, p < 0.001). Moreover, ln-blood cadmium also showed a significant inverse association with ln-Horvath DNAmTL (β = −0.010, 95% CI: −0.014 to −0.006, p < 0.001). Structural equation modeling showed that the association between cadmium and T/S ratio was mediated by Horvath DNAmTL, with a total effect of −0.044, a direct effect of −0.027, and an indirect effect of −0.017. Furthermore, stratified analyses revealed that a 1-unit increase in ln-blood cadmium was associated with higher all-cause mortality, with hazard ratios (HR) of 1.47 for participants with T/S ratio below the median and 1.41 for those above. Similar patterns were observed for cardiovascular (HR = 1.68 vs. 1.30) and cancer mortality (HR = 1.75 vs. 1.42). For Horvath DNAmTL, the association was significant only for all-cause mortality (HR = 1.36 vs. 1.31). However, no significant interactions were detected. In conclusion, our findings suggest that Horvath DNAmTL is associated with the relationship between cadmium and telomere length, suggesting a potential DNA methylation pathway that warrants further longitudinal investigation. Individuals with lower T/S ratios or Horvath DNAmTL appear to be more susceptible to cadmium-related mortality. Further research is necessary to confirm these results.

Purpose: Glyphosate and glyphosate-based herbicides (GBH), extensively utilized as herbicides worldwide, have been associated with numerous health issues. Previous experimental studies have indicated their potential to disrupt selenium homeostasis by either interfering with uptake or increasing oxidative stress. However, there is a significant research gap concerning the connection between glyphosate exposure and selenium status in epidemiological studies, particularly within nationally representative samples. Methods: In this study, we examined data from the 2013-2018 National Health and Nutrition Examination Survey (NHANES), involving 3011 participants aged 3 and above. Our main objective was to examine the connection between urinary glyphosate levels, whole blood selenium, and selenium intake. Results: Our analysis did not uncover an association between urinary glyphosate and selenium intake. Nevertheless, we observed a negative correlation between urinary glyphosate levels and whole blood selenium, with a ß coefficient of -1.984, S.E. = 0.639, and P = 0.003 in the final model. We also reported a notable decrease in the average concentrations of whole blood selenium as glyphosate tertiles increased, with P-values for trend of 0.033. Furthermore, the association was particularly prominent among females, non-Hispanic whites, and individuals with lower selenium intake. Conclusions: In this thorough examination of NHANES data, our study uncovers a possible detrimental connection between glyphosate exposure and whole blood selenium levels. These findings underscore the importance of further investigation into the health consequences of glyphosate exposure and its potential influence on selenium status, thereby raising awareness of potential implications for public health.