Low calcium in drinking water reduces vascular endothelial cell viability and increases the risk of acute myocardial infarction
D Tian, P Li, J Zhu, D Han, M LiuAbstract
Objective
To investigate the association between calcium ion concentration in drinking water and the risk of acute myocardial infarction (AMI), and to clarify the effect of low-calcium drinking water on vascular endothelial cell, so as to provide a scientific basis for public health strategies regarding drinking water quality and cardiovascular health.
Methods
A 15-year follow-up study was conducted among 500,000 participants from the large-scale UK Biobank population cohort, and the occurrence of cardiovascular events during follow-up was recorded. At baseline, the home addresses were collected, and calcium ion concentrations in tap water from the corresponding water supply companies were matched according to residential addresses. Meanwhile, baseline serum samples were obtained, and data were collected on demographics (age, sex), lifestyle factors (smoking, alcohol consumption, type and duration of physical activities), and dietary habits (raw and cooked vegetables, fresh fruits and dried fruits, oily and non-oily fish, processed meat, poultry, beef, pork, cheese, cereals). Cox proportional hazards models were used to evaluate the association between calcium ion concentrations in drinking water and AMI. Restricted cubic spline (RCS) models were applied to examine potential non-linear dose-response relationships between calcium concentrations and the risks of AMI. To determine the effect of different calcium levels on vascular endothelial cells, human umbilical vein endothelial cells (HUVECs) were cultured in media containing various calcium ion concentrations, and cell viability and confluency were monitored.
Results
During a median follow-up of 15.0 years, a total of 11,369 AMI events were documented. After adjusting for confounding factors including age, sex, dietary habits, and lifestyle, Cox proportional hazards models showed that high calcium concentration in drinking water was a protective factor for AMI (HR = 0.95, p < 5×10⁻⁶), with no significant non-linear relationship. Stratified analysis indicated that participants exposed to low calcium (0–35 mg/L) had a 30% higher risk of AMI (95% CI: 20%–38%) compared with those exposed to high calcium (80–140 mg/L). Correlation analysis showed a significant positive association between calcium concentrations in drinking water and plasma calcium levels (p < 5×10⁻⁶). Cell experiments showed that HUVEC viability reached 35% and 42% at calcium concentrations of 3.5 mmol/L and 4.0 mmol/L, respectively, which were significantly higher than the 15%–25% observed in the 1–3 mmol/L groups.
Conclusion
Low calcium concentration in drinking water is closely associated with an increased risk of AMI, and a low-calcium environment can significantly suppress vascular endothelial cell viability, which suggest that an appropriate calcium concentration in drinking water is important for maintaining endothelial function and reducing the risk of acute myocardial infarction.