Health insurance, healthcare access, and their roles in the association between blood lead levels and epigenetic aging in United States adults

Abstract Lead exposure remains a significant public health problem, and even within current standards, most individuals have limited means to avoid it. Regulating or removing toxic exposures remains a priority, but complementary nearer-term protections are needed. We previously observed that health insurance coverage attenuated associations of blood lead levels with two DNA methylation–based biomarkers of morbidity and mortality: GrimAge2 and DunedinPoAm. In this study, we evaluated whether healthcare access could account for or modify these relationships. We conducted a cross-sectional analysis of 2,312 adults aged 50–84 years from the 1999–2002 National Health and Nutrition Examination Survey (NHANES). Survey-weighted generalized linear models were used to test effect modification of the lead–epigenetic aging relationship by health insurance and by healthcare access, defined as having a routine place of healthcare. In models adjusted for demographic, socioeconomic, lifestyle, and health factors, insurance significantly modified associations of lead with epigenetic age. Although model estimates remained comparable, interactions were no longer statistically significant after healthcare access was added as a covariate for GrimAge2 (β insured = 0.08, 95%CI insured : -0.08, 0.23, β uninsured = 0.60, 95%CI uninsured : -0.10, 1.28, P interaction = 0.09) and DunedinPoAm (β insured = 0.001, 95%CI insured : -0.002, 0.003, β uninsured = 0.01, 95%CI uninsured : -0.003, 0.02, P interaction = 0.09). Healthcare access alone did not significantly modify the associations of lead with either biomarker in models with or without insurance as a covariate. These findings suggest that healthcare access may partially contribute to the attenuation of lead-related epigenetic aging observed among insured adults and a need for further research to better understand these complex relationships.