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Trihalomethanes
The results of a cohort study published in JAMA Network Open show the effect of trihalomethanes in community drinking water on the risk of chronic kidney disease (CKD). Trihalomethanes (THMs) are one of several unintended byproducts of chlorination, and include chloroform and three brominated compounds (bromodichloromethane, dibromochloromethane, and bromoform), with the latter more common in coastal and saltwater regions. Exposure to THMs has already been established as a risk factor for bladder cancer and restricted fetal growth. A 2025 meta-analysis, for example, found nearly a 60% higher risk for bladder cancer among men with higher exposure, though this was not observed among women. THM blood levels were also positively associated with hypertension in an analysis of over 15,000 adults using data from the 1999-2018 National Health and Nutrition Examination Survey (NHANES), and with allergic sensitization (pets, mold, mites, and food) among adolescents (NHANES 2005-06).
The JAMA study used data from the California Teachers Study (CTS), a prospective cohort of women with over 10 years of data, to determine if prolonged exposure to THMs (even below the regulatory limit of 80 ppb or ug/L) is associated with CKD, and if any of the individual analytes are associated with increased risk (THMs are regulated collectively, not individually). Data for nearly 90,000 women between the ages of 22 and 85 (mean of 50) were included in the analysis.
Even well below the regulatory limit, total THM levels were associated with an increased risk for moderate or greater CKD, with the brominated THMs responsible for the greatest effect, one that was evident across all percentile categories. For example, comparing the 95th percentile of brominated THMs (30.0 μg/L) to the 25th percentile (0.7 μg/L), there was a 23% higher risk for CKD, while higher exposure (>30.0 ug/L) carried a 43% greater risk of CKD. Among the brominated compounds, bromodichloromethane and dibromochloromethane were associated with the greatest risk, roughly 32% higher for both when comparing 95th to 25th percentiles. Additionally, using data from a previous mixture analysis, brominated THMs were found to be the greatest contributor (52.9%) to CKD, compared to uranium (35.4%), arsenic (6.2%), and chloroform (5.5%).
THMs have demonstrated multiple nephrotoxic effects, including damage to proximal convoluted tubules and decreased glomerular filtration rate, and may exacerbate the toxicity of other injuries to the kidneys, such as heat and dehydration, by impairing urinary concentrating ability.
Arsenic
The journal Environmental Health also published research on arsenic, another common drinking water contaminant. This was a systematic review examining the association between low to moderate arsenic levels, defined as <10 ug/L (low) to 10-100 ug/L (moderate), and cardiovascular disease. Nineteen studies were included, with relative risks calculated by comparing the highest to lowest exposure levels in each study (excluding any with high arsenic exposure, defined as >100 ug/L). Most studies reported water arsenic levels, while four used urinary arsenic as a biomarker of exposure (other biomarkers, e.g., blood or hair, were excluded).
Using urinary arsenic as a biomarker of exposure, a 62% higher risk was observed for stroke, while water arsenic levels were associated with a 37% higher stroke risk when comparing the highest to the lowest levels. Higher water arsenic levels were also associated with a 37% higher risk for ischemic heart disease (IHD), and when excluding studies with an ecological design, they were associated with both a 31% higher IHD mortality and 46% higher risk for acute myocardial infarction.
For some context for the level of arsenic observed in these studies, the first Strong Heart Study used the sum of urine (inorganic) arsenic compounds as a biomarker, reporting a median level of 11.2 ug/L (adjusted for creatinine and arsenobetaine), and an interquartile range of 6.6-19.1 μg/L. This study reported both an increase in cardiovascular and all-cause mortality with increasing urinary levels. Similar medians were found in the Multi-Ethnic Study of Atherosclerosis study (2.81 µg/g), and the Hortega study (6.52 µg/g), both adjusted for creatinine and organic arsenic.
Various methodologies were used to measure water levels of arsenic, making it difficult to succinctly describe the level of arsenic in the other 15 studies comprising this systematic review. But as an example, one of the two studies that provided data on IHD incidence used a 10-year moving average, again as part of the California Teachers Study (published in Environmental Health Perspectives). They reported that compared to a reference of <1 ug/L inorganic arsenic, nearly every incremental increase was associated with a greater risk for IHD, including a 5-6% increase for levels between 1-4.99 ug/L, a 20% increase for levels between 5-9.99 ug/L, and a 42% increase for levels of 10 ug/L or higher.
A variety of mechanisms for arsenic’s toxicity have been documented, including endothelial dysfunction, oxidative stress, impaired enzyme activity, etc. Urinary arsenic levels have even been associated with a stiffening of the aorta and other major arteries, contributing to ventricular hypertrophy. For example, increased left ventricular wall thickness and left ventricular hypertrophy were linked to urinary arsenic levels in young adults, especially those with prehypertension or hypertension. Both of these recent studies suggest that significant harm, at least to the renal and cardiovascular systems, is a consequence of drinking water contaminants below regulated thresholds.
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