Blood Mercury Linked to Worse Cholesterol Profiles in Chinese Children, With Mitochondrial DNA as a Possible Link

Blood lipid abnormalities in childhood predict cardiovascular disease in adulthood, yet few studies have asked whether environmental toxicants such as mercury shape lipid profiles in young people. Mercury binds thiol-containing proteins, can damage mitochondrial membranes, and increases reactive oxygen species. Mitochondrial dysfunction is therefore a plausible route from mercury exposure to dyslipidemia. This study tested that idea in children and adolescents.

The researchers ran a cross-sectional study of 352 children and adolescents aged 6–17 (183 boys, 169 girls) in Yiwu, eastern China, between August and October 2021. Children with inherited lipid disorders or taking lipid-altering or antioxidant medications were excluded. Whole-blood mercury was measured by ICP-MS (median about 1.06 µg/L). Serum TC, TG, HDL-C, LDL-C, ApoA1, ApoB, and lipoprotein(a) were measured with standard assays. Blood DNA was analyzed by qPCR for mitochondrial DNA copy number (mtDNA-CN), ribosomal DNA copy number (5S, 5.8S, 18S, 28S, 45S), and relative telomere length. Models used log-transformed mercury and adjusted for age, sex, and BMI. The authors also tested sex interactions and nonlinear (spline) relationships, and ran bootstrapped mediation analyses.

Higher mercury was significantly associated with higher TC (β=0.144, P=0.012), LDL-C (β=0.266, P<0.001), and ApoB (β=3.79, P=0.005), and with lower HDL-C (β=−0.149, P<0.001). Together these changes form an atherogenic pattern. The associations were stronger in girls than in boys. mtDNA-CN was positively associated with mercury and statistically mediated 53.8% of the mercury–HDL-C association, 24.7% of the LDL-C association, and 180.6% of the ApoA1 association. A proportion above 100% usually signals inconsistent mediation, where the direct and indirect effects point in opposite directions, so this figure should be read cautiously.

The authors conclude that mercury exposure in youth is linked to unfavorable lipids, possibly through mitochondrial disturbance, and that mtDNA-CN may be a sensitive marker of this process. This supports reducing childhood toxicant exposure as part of early cardiovascular prevention.

Several caveats apply. The design is cross-sectional, so temporality and causality cannot be established. The sample comes from a single site and is modest in size. The finding that mtDNA-CN rose with mercury sits somewhat awkwardly with the framing that low mtDNA-CN signals dysfunction. A rise may instead reflect a compensatory response to oxidative stress. Blood mercury reflects recent exposure, and diet and other unmeasured confounders (such as fish intake or other metals) may influence both mercury and lipids. Results for the rDNA and telomere markers were not available in the text provided.