Cardiovascular

Association between maternal antimony exposure and offspring congenital heart defects: findings from a large birth cohort study.

TL;DR

Higher maternal blood antimony concentrations were associated with an increased risk of congenital heart defects in offspring, suggesting the prenatal living environment may be a modifiable target for CHD prevention.

Key Findings

Mothers of infants with congenital heart defects had significantly higher mean blood antimony concentrations than controls.

  • Mean maternal blood antimony was 20.30 μg/L in the CHD group versus 13.05 μg/L in the control group; the difference was statistically significant.
  • Nested case-control design with 97 cases and 194 controls (291 women total), matched 1:2 by age and community.
  • Whole blood was collected during prenatal hospitalization before delivery and measured by ICP-MS.

High maternal antimony exposure was associated with more than four times the odds of CHDs in offspring compared with low exposure.

  • OR = 4.455, 95% CI: 2.029-9.782 for the high versus the low exposure group.
  • High and low exposure groups were defined by an ROC-derived cutoff.
  • Conditional multivariable logistic regression was used.

The high-exposure association was also seen in several CHD subgroups.

  • Similar associations were observed for isolated CHDs, great arteries malformation, septal defects, and atrial septal defects (ASDs).
  • The abstract does not give subgroup-specific effect estimates.

Each 6 μg/L increase in maternal blood antimony was associated with a 38.9% higher risk of CHDs in offspring.

  • OR = 1.389, 95% CI: 1.110-1.735 per 6 μg/L increment.
  • Consistent findings were reported for the isolated CHDs, septal defects, and ASDs subgroups.

Restricted cubic spline analysis indicated a threshold-like dose-response, with CHD risk increasing with antimony levels above about 18.4 μg/L.

  • When maternal blood antimony exceeded 18.409 μg/L, CHD risk in offspring rose with increasing antimony levels.
  • This indicates a non-linear relationship.

The authors conclude that the prenatal living environment may be a modifiable target for CHD prevention and that exposure to environmental sources of antimony should be minimized.

  • The study was conducted within a birth cohort established jointly by Gansu Provincial Maternity and Child Care Hospital and Yale University.
  • The study aimed to identify potential risk factors for CHDs and inform prevention strategies.

What This Means

This study looked at whether the amount of antimony, a metal found in some industrial and environmental sources, in a pregnant woman's blood is linked to heart defects in her baby. Researchers compared 97 women whose babies were born with congenital heart defects to 194 similar women whose babies were not affected. Blood was taken before delivery and tested for antimony. Mothers of babies with heart defects had higher average antimony levels (about 20.3 μg/L) than the comparison mothers (about 13.1 μg/L). Women in the high-exposure group had more than four times the odds of having a baby with a heart defect. Each 6 μg/L increase in antimony was linked to about 39% higher risk, and risk appeared to climb once levels passed roughly 18.4 μg/L. Similar patterns were seen for several types of defects, including septal defects (holes between heart chambers) and atrial septal defects. This research suggests that environmental antimony exposure during pregnancy may be one factor linked to heart defects in babies, and that reducing exposure could be a prevention avenue. However, this was a fairly small case-control study that shows association, not proof of cause, and blood was measured only once near delivery. Larger studies would be needed to confirm the findings and identify the main sources of exposure.

Have a question about this study?

Citation

Shao Y, Cao L, Lin R, Ran J, Liu Q, Mao B. (2026). Association between maternal antimony exposure and offspring congenital heart defects: findings from a large birth cohort study.. Frontiers in public health. https://doi.org/10.3389/fpubh.2026.1957018