Background
Hypertension is a major cause of death worldwide. Although arsenic exposure has been associated with the risk of hypertension, this association appears nonuniform due to inconsistent
Conclusion
Increasing exposure to arsenic was associated with increasing odds of hypertension. The association was mediated through the reduction of vascular NO bioavailability, suggesting that impaired NO bioavailability was a plausible underlying mechanism of arsenic-induced hypertension in this Bangladeshi population. https://doi.org/10.1289/EHP13018.
Methods
A total of 828 participants were recruited from low- and high-arsenic exposure areas in Bangladesh. Participants' drinking water, hair, and nail arsenic concentrations were measured by inductively coupled plasma mass spectroscopy. Hypertension was defined as a systolic blood pressure (SBP) value of ≥140≥140<math><mrow><mo>≥</mo><mn>140</mn></mrow></math> and a diastolic (DBP) value of ≥90mmHg≥90mmHg<math><mrow><mo>≥</mo><mn>90</mn><mtext> mmHg</mtext></mrow></math>. Serum NO levels reflected by total serum nitrite concentrations were measured by immunoassay. A formal causal mediation analysis was used to assess NO as a mediator of the association between arsenic level and hypertension.
Objective
We investigated the dose-response relationship between arsenic exposure and hypertension with vascular NO levels as a potential mediator of arsenic-related hypertension in individuals exposed to a broad range of arsenic.
Results
Increasing concentrations of arsenic measured in drinking water, hair, and nails were associated with the increasing levels of SBP and DBP. The odds of hypertension were dose-dependently increased by arsenic even in participants exposed to relatively low to moderate levels (10−50μg/L10-50μg/L<math><mrow><mn>10</mn><mo>-</mo><mn>50</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mi>L</mi></mrow></math>) of water arsenic [odds ratios (ORs) and 95% confidence intervals (CIs): 2.87 (95% CI: 1.28, 6.44), 2.67 (95% CI: 1.27, 5.60), and 5.04 (95% CI: 2.71, 9.35) for the 10−50μg/L10-50μg/L<math><mrow><mn>10</mn><mo>-</mo><mn>50</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mi>L</mi></mrow></math>, 50.01−150μg/L50.01-150μg/L<math><mrow><mn>50.01</mn><mo>-</mo><mn>150</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mi>L</mi></mrow></math>, and >150μg/L>150μg/L<math><mrow><mo>></mo><mn>150</mn><mspace></mspace><mi>μ</mi><mi>g</mi><mo>/</mo><mi>L</mi></mrow></math> groups, respectively]. Causal mediation analysis showed a significant mediating effect of NO on arsenic-related SBP, DBP, and hypertension.