Toxic Metal Antimony in Mothers’ Blood Tied to Higher Risk of Babies Born With Heart Defects

Pregnant women with higher levels of antimony in their blood may face a dramatically increased risk of giving birth to a child with a congenital heart defect, according to a new study drawing on a large birth cohort in northwestern China. The research, published in Frontiers in Public Health, found that mothers of babies with heart malformations carried roughly 55 percent more antimony in their bloodstream than mothers of healthy newborns, and that the risk climbed steadily once concentrations crossed a specific threshold. Because antimony is an industrial pollutant that enters the body through air, food, water, and even plastic bottles, the findings point to a potentially modifiable environmental factor behind the world’s most common birth defect.

Congenital heart defects, or CHDs, are structural abnormalities of the heart and great vessels present at birth. They affect roughly 8 to 10 out of every 1,000 newborns globally, with prevalence varying widely by geography, from about 2.3 per 1,000 in Africa to about 9.3 per 1,000 in Asia. They are the most common form of congenital malformation and a leading cause of perinatal mortality, imposing a heavy medical and emotional burden on families. In China, where the new study was conducted, CHDs rank first among all birth defects, with a prevalence of roughly 6 to 8 per 1,000. While genetics clearly plays a role, researchers have long suspected that environmental exposures during pregnancy, from air pollution to heavy metals, contribute to the malformations, which arise when the embryonic heart fails to form correctly during a narrow window of development.

Antimony is a toxic trace element with chemical properties similar to arsenic, and it is ubiquitous in the modern environment. It is used in flame retardants, automotive brake friction materials, and lubricants, and it is abundant in airborne particulate matter. Fossil fuel and waste combustion, computer-chip manufacturing, and electronic-waste recycling all release antimony into the environment, and plastic containers used to store mineral water can leach measurable amounts of the element into their contents. People accumulate antimony through inhalation, dietary intake, and dermal contact. Previous research has linked antimony exposure to vascular inflammation, oxidative stress, and hypertension, but epidemiological evidence connecting it specifically to heart defects in newborns had remained scarce, which is precisely the gap the new study set out to fill.

The investigation was a nested case-control study conducted within a birth cohort established jointly by Gansu Provincial Maternity and Child Care Hospital and Yale University. The researchers enrolled 291 women: 97 who gave birth to infants with congenital heart defects, and 194 controls drawn from the same cohort and matched to cases at a 2-to-1 ratio by maternal age, within two years, and by residential community. All controls delivered singleton, full-term newborns of normal birth weight with no congenital malformations. Maternal whole blood samples were collected during prenatal hospitalization before delivery, and antimony concentrations were measured using inductively coupled plasma mass spectrometry, a highly sensitive technique with a detection limit of just 0.008 micrograms per liter. Laboratory staff performing the measurements were fully blinded to whether each specimen came from a case or a control, minimizing assessment bias.

The results were striking. Mean maternal blood antimony was 13.05 micrograms per liter in the control group compared with 20.30 micrograms per liter in the CHD group, a statistically significant difference. Using receiver operating characteristic curve analysis, the team identified a cutoff of roughly 20 micrograms per liter to split participants into high- and low-exposure groups. Women in the high-exposure group had 4.455 times the odds of having an infant with a heart defect compared with the low-exposure group, with a 95 percent confidence interval spanning 2.029 to 9.782. For isolated CHDs, meaning cases with a single malformation rather than multiple defects, the association was even stronger, with an odds ratio of 12.648.

The study also uncovered what appears to be a threshold effect. For each incremental increase of 6 micrograms per liter in maternal blood antimony, the risk of CHDs in offspring rose by 38.9 percent. Restricted cubic spline analysis revealed an inverted L-shaped relationship: at maternal blood antimony levels between zero and 18.409 micrograms per liter, the risk of heart defects remained low and stable, but once concentrations exceeded that threshold, risk climbed steadily with rising antimony levels. This pattern suggests that danger emerges only above a certain exposure concentration rather than across the entire range, a finding the authors note has important implications for identifying safe exposure limits.

Subgroup analyses strengthened the overall signal. Elevated antimony was associated with higher risk for several common CHD subtypes, including malformations of the great arteries such as patent ductus arteriosus, septal defects such as atrial and ventricular septal defects, and atrial septal defects specifically. The associations held across maternal age groups, gestational weight change, preconception health education, employment status, and the timing of folic acid supplementation. The study also found a significant interaction between antimony and household income: compared with women who had low antimony and high income, those with high antimony and low income faced a 65.4 percent higher risk of having a child with a heart defect, suggesting that socioeconomic disadvantage may compound the biological burden of the exposure.

The biological plausibility of these findings is supported by a growing body of laboratory evidence. In zebrafish larvae, exposure to high concentrations of antimony significantly altered heart rate, induced developmental delay, elevated reactive oxygen species, and depleted glutathione, a key cellular antioxidant. Antimony exposure also disrupted the expression of immune-related genes in the larvae. In mouse studies, antimony triggered endoplasmic reticulum stress by disrupting calcium homeostasis, activating signaling pathways that lead to cardiomyocyte death, and produced visible mitochondrial swelling and cristae fracture in heart tissue. Cellular experiments have shown that both trivalent and pentavalent antimony suppress ATP production and impair mitochondrial function in cardiac cells. Proposed mechanisms include antimony’s irreversible binding to intracellular sulfhydryl groups, interference with DNA methylation during embryonic development, and the induction of oxidative DNA damage and lipid peroxidation.

The authors are careful to frame their work as an observational study that provides epidemiological clues rather than proof of causation. Blood samples were collected before delivery, whereas the critical window for fetal cardiac morphogenesis occurs at gestational weeks 3.5 to 8, so the measured concentrations may reflect cumulative gestational exposure rather than exposure during that specific period. The total number of cases was also limited, reducing statistical precision for individual subtypes, and residual confounding cannot be excluded despite adjustment for maternal ethnicity, body mass index, smoking, gestational hypertension, and supplementation habits. The team calls for larger multicenter prospective cohort studies with repeated blood measurements across gestation to validate the findings and pinpoint the exposure window with greater precision.

Still, the public health implications are considerable. Drinking water standards currently cap antimony at 5 micrograms per liter in China and 6 micrograms per liter in the United States, and the study’s risk threshold of roughly 18.4 micrograms per liter in blood suggests that exposure well above these environmental benchmarks corresponds to meaningful increases in congenital heart defect risk. The researchers argue that the prenatal living environment may be a modifiable target for CHD prevention, and that raising awareness of maternal environmental risks, adopting healthier lifestyles, and minimizing exposure to antimony-containing sources, from polluted air to contaminated water and plastic food containers, could help reduce the incidence of the world’s most common birth defect. As industrial development continues to reshape the chemical environments in which pregnancies unfold, studies like this one make clear that the invisible contaminants accumulating in expectant mothers’ blood may carry consequences that last a lifetime.

Subject of Research: Association between prenatal antimony exposure and congenital heart defects in offspring

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

Article References: 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, 14, Article 1957018. https://doi.org/10.3389/fpubh.2026.1957018

Image Credits: AI Generated

DOI: 10.3389/fpubh.2026.1957018

Keywords: antimony, congenital heart defects, pregnancy, heavy metals, birth cohort, environmental health, ICP-MS, oxidative stress, patent ductus arteriosus, septal defects, drinking water, pollution