Participants exposed to arsenic levels at or above the EPA limit had a 42% higher risk of ischemic heart disease, while even moderate exposure increased risk by 20%.
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In a recent study published in the Environmental Health Perspectives, a group of researchers evaluated the relationship between long-term exposure to inorganic arsenic in drinking water (wAs) supplies and the risk of ischemic heart disease (IHD) (a condition caused by reduced blood flow to the heart muscle, often due to narrowed coronary arteries) and cardiovascular disease (CVD) among women in the California Teachers Study (CTS) cohort.
Background
wAs is a significant environmental concern linked to various chronic diseases in the United States (U.S.), particularly CVD. Health organizations, including the American Heart Association, acknowledge the increased CVD risk associated with arsenic exposure, particularly at high levels (>100 μg/L). Although the U.S.
Environmental Protection Agency lowered the maximum contaminant level for arsenic in community water supplies from 50 μg/L to 10 μg/L in 2006, lower levels may still pose risks. Limited studies have explored the effects of long-term exposure to these lower concentrations on CVD, highlighting the need for further research to understand their safety.
About the study
Participants were recruited from the California State Teachers Retirement System and provided health and lifestyle information through an initial questionnaire, followed by five additional follow-ups. Self-reported race and ethnicity were collected, allowing for the categorization of participants in compliance with National Institutes of Health reporting requirements. The neighborhood socioeconomic status (SES) at enrollment addresses was estimated based on a composite score of education, occupation, and income, categorized into quartiles across California.
Hospitalization data, including records of inpatient stays and emergency department visits, has been collected annually from the California Department of Health Care Access and Information. Nonfatal and fatal cases of IHD and CVD were identified through hospitalization and mortality records, using the International Classification of Diseases (ICD) coding system.
Community water supply boundaries were determined using the California Environmental Health Tracking Program's Water Boundary Tool, which successfully mapped drinking water service areas across the state. Residential addresses were linked to these boundaries, with the majority of participants living within community water supply areas, ensuring accurate exposure assessment to drinking water contaminants, including arsenic.
Arsenic concentrations from community water systems were obtained from the Safe Drinking Water Information System, and time-varying exposure assessments were performed to evaluate long-term exposure effects on IHD and CVD risk. The study utilized Cox proportional hazard models to analyze the relationship between arsenic exposure and cardiovascular outcomes, adjusting for various confounders to ensure accurate risk assessment.
Study results
Approximately 48% of participants in the study were exposed to average levels of wAs below 1 μg/L, while 39% were exposed to levels between 1.00 and 2.99 μg/L, 9% to levels ranging from 3.00 to 4.99 μg/L, 3% to levels between 5.00 and 9.99 μg/L, and 1% to levels at or above 10 μg/L during the first compliance cycle from 1993 to 2001.
Those in the highest exposure categories tended to be younger, had slightly higher body mass index (BMI), and were less likely to smoke. Additionally, participants from neighborhoods with lower SES were disproportionately exposed to higher concentrations of wAs. For instance, 3% of individuals exposed to <1 μg/L lived in the lowest SES neighborhoods, while this figure rose to 16% for those exposed to ≥10 μg/L.
Furthermore, Hispanic or Latina individuals showed higher levels of exposure, and a greater proportion of those in elevated exposure categories reported having high blood pressure, diabetes, and lower levels of physical activity.
In terms of baseline exposure, the risk of IHD increased with higher levels of wAs. Compared to those with exposure below 1 μg/L, hazard ratios (HRs) for IHD were 1.11 (95% CI: 1.01, 1.22) for 3.00-4.99 μg/L, 1.10 (95% CI: 1.04, 1.16) for 1.00–2.99 μg/L, 1.19 (95% CI: 1.03, 1.37) for 5.00–9.99 μg/L, and 1.20 (95% CI: 0.97, 1.48) for levels ≥10 μg/L. The association was stronger for those who did not relocate during follow-up, with an HR of 1.34 (95% CI: 1.04, 1.71) for the highest exposure category. The risk of CVD was less pronounced across exposure categories, but a significant trend was observed when restricting to nonmovers, with a p-value for trend of 0.035.
Time-varying analyses revealed clear exposure-response trends between wAs and IHD risk, particularly for the 10-year average exposure preceding the event. Longer-term exposure windows demonstrated a similar pattern for CVD risk, and strong correlations between 10-year exposures and shorter intervals were noted.
Secondary analyses indicated that wAs exposure was not significantly associated with isolated stroke or ischemic stroke risk. Stratified analyses showed that younger women (≤55 years) exhibited a higher risk from wAs exposure compared to older women, especially at the highest exposure levels, where the HR for IHD in younger women was 2.25 (95% CI: 1.40, 3.64) compared to 1.24 (95% CI: 0.91, 1.68) in older women.
Conclusions
To summarize, the study indicates that long-term exposure to wAs supplies, even below the regulatory limit of 10 μg/L, may increase the risk of CVD, particularly IHD. Women with 10-year average exposures of 5 μg/L showed an 18–20% higher risk of IHD compared to those exposed to <1 μg/L, with risks rising to 42% at ≥10 μg/L.
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