PFAS-Contaminated Pesticides Applied near Public Supply Wells Disproportionately Impact Communities of Color in California.

Contaminated drinking water from widespread environmental pollutants such as perfluoroalkyl and polyfluoroalkyl substances (PFAS) poses a rising threat to public health. PFAS monitoring in groundwater is limited and fails to consider pesticides found to contain PFAS as a potential contamination source. Given previous findings on the disproportionate exposure of communities of Color to both pesticides and PFAS, we investigated disparities in PFAS-contaminated pesticide applications in California based on community-level sociodemographic characteristics. We utilized statewide pesticide application data from the California Department of Pesticide Regulation and recently reported concentrations of PFAS chemicals detected in eight pesticide products to calculate the areal density of PFAS applied within 1 km of individual community water systems' (CWSs) supply wells. Spatial regression analyses suggest that statewide, CWSs that serve a greater proportion of Latinx and non-Latinx People of Color residents experience a greater areal density of PFAS applied and greater likelihood of PFAS application near their public supply wells. These results highlight agroecosystems as potentially important sources of PFAS in drinking water and identify areas that may be at risk of PFAS contamination and warrant additional PFAS monitoring and remediation.

Disparities in Drinking Water Manganese Concentrations in Domestic Wells and Community Water Systems in the Central Valley, CA, USA.

Over 1.3 million Californians rely on unmonitored domestic wells. Existing probability estimates of groundwater Mn concentrations, population estimates, and sociodemographic data were integrated with spatial data delineating domestic well communities (DWCs) to predict the probability of high Mn concentrations in extracted groundwater within DWCs in California's Central Valley. Additional Mn concentration data of water delivered by community water systems (CWSs) were used to estimate Mn in public water supply. We estimate that 0.4% of the DWC population (2342 users) rely on groundwater with predicted Mn > 300 µg L-1. In CWSs, 2.4% of the population (904 users) served by small CWSs and 0.4% of the population (3072 users) served by medium CWS relied on drinking water with mean point-of-entry Mn concentration >300 µg L-1. Small CWSs were less likely to report Mn concentrations relative to large CWSs, yet a higher percentage of small CWSs exceed regulatory standards relative to larger systems. Modeled calculations do not reveal differences in estimated Mn concentration between groundwater from current regional domestic well depth and 33 m deeper. These analyses demonstrate the need for additional well-monitoring programs that evaluate Mn and increased access to point-of-use treatment for domestic well users disproportionately burdened by associated costs of water treatment.

The Drinking Water Tool: A Community-Driven Data Visualization Tool for Policy Implementation.

The Drinking Water Tool (DWT) is a community-driven online tool that provides diverse users with information about drinking water sources and threats to drinking water quality and access due to drought. Development of the DWT was guided by the Community Water Center (CWC) as part of the Water Equity Science Shop (WESS), a research partnership integrating elements of community-based participatory research and the European Science Shop model. The WESS engages in scientific projects that inform policy change, advance water justice, and reduce cumulative exposure and disproportionate health burdens among impacted communities in California. WESS researchers conducted qualitative analysis of 15 stakeholder interviews regarding the DWT, including iterative feedback and the stakeholder consultation process as well as stakeholder perceptions of the tool's impact on California water policy, organizing, and research. Results indicate that the DWT and the stakeholder engagement process which developed it were effective in influencing policy priorities and in promoting interagency coordination at multiple levels to address water equity challenges and their disproportionate burdens, particularly among rural and low socioeconomic status areas and communities of color.

Inequities in Drinking Water Quality Among Domestic Well Communities and Community Water Systems, California, 2011‒2019.

Objectives. To evaluate universal access to clean drinking water by characterizing relationships between community sociodemographics and water contaminants in California domestic well areas (DWAs) and community water systems (CWSs). Methods. We integrated domestic well locations, CWS service boundaries, residential parcels, building footprints, and 2013-2017 American Community Survey data to estimate sociodemographic characteristics for DWAs and CWSs statewide. We derived mean drinking and groundwater contaminant concentrations of arsenic, nitrate, and hexavalent chromium (Cr[VI]) between 2011 and 2019 and used multivariate models to estimate relationships between sociodemographic variables and contaminant concentrations. Results. We estimated that more than 1.3 million Californians (3.4%) use domestic wells and more than 370 000 Californians rely on drinking water with average contaminant concentrations at or above regulatory standards for 1 or more of the contaminants considered. Higher proportions of people of color were associated with greater drinking water contamination. Conclusions. Poor water quality disproportionately impacts communities of color in California, with the highest estimated arsenic, nitrate, and Cr(VI) concentrations in areas of domestic well use. Domestic well communities must be included in efforts to achieve California's Human Right to Water. (Am J Public Health. 2022;112(1):88-97. https://doi.org/10.2105/AJPH.2021.306561).

Arsenic Methylation Capacity and Metabolic Syndrome in the 2013-2014 U.S. National Health and Nutrition Examination Survey (NHANES).

Arsenic methylation capacity is associated with metabolic syndrome and its components among highly exposed populations. However, this association has not been investigated in low to moderately exposed populations. Therefore, we investigated arsenic methylation capacity in relation to the clinical diagnosis of metabolic syndrome in a low arsenic exposure population. Additionally, we compared arsenic methylation patterns present in our sample to those of more highly exposed populations. Using logistic regression models adjusted for relevant biological and lifestyle covariates, we report no association between increased arsenic methylation and metabolic syndrome in a population in which arsenic is regulated at 10 ppb in drinking water. However, we cannot rule out the possibility of a positive association between arsenic methylation and metabolic syndrome in a subsample of women with normal body mass index (BMI). To our knowledge this is the first investigation of arsenic methylation capacity with respect to metabolic syndrome in a low exposure population. We also report that methylation patterns in our sample are similar to those found in highly exposed populations. Additionally, we report that gender and BMI significantly modify the effect of arsenic methylation on metabolic syndrome. Future studies should evaluate the effectiveness of arsenic policy enforcement on subclinical biomarkers of cardiovascular disease.

Antioxidants Protect against Arsenic Induced Mitochondrial Cardio-Toxicity.

Arsenic is a potent cardiovascular toxicant associated with numerous biomarkers of cardiovascular diseases in exposed human populations. Arsenic is also a carcinogen, yet arsenic trioxide is used as a therapeutic agent in the treatment of acute promyelotic leukemia (APL). The therapeutic use of arsenic is limited due to its severe cardiovascular side effects. Many of the toxic effects of arsenic are mediated by mitochondrial dysfunction and related to arsenic's effect on oxidative stress. Therefore, we investigated the effectiveness of antioxidants against arsenic induced cardiovascular dysfunction. A growing body of evidence suggests that antioxidant phytonutrients may ameliorate the toxic effects of arsenic on mitochondria by scavenging free radicals. This review identifies 21 antioxidants that can effectively reverse mitochondrial dysfunction and oxidative stress in cardiovascular cells and tissues. In addition, we propose that antioxidants have the potential to improve the cardiovascular health of millions of people chronically exposed to elevated arsenic concentrations through contaminated water supplies or used to treat certain types of leukemias. Importantly, we identify conceptual gaps in research and development of new mito-protective antioxidants and suggest avenues for future research to improve bioavailability of antioxidants and distribution to target tissues in order reduce arsenic-induced cardiovascular toxicity in a real-world context.

Monomethylarsonous acid, but not inorganic arsenic, is a mitochondria-specific toxicant in vascular smooth muscle cells.

Arsenic exposure has been implicated as a risk factor for cardiovascular diseases, metabolic disorders, and cancer, yet the role mitochondrial dysfunction plays in the cellular mechanisms of pathology is largely unknown. To investigate arsenic-induced mitochondrial dysfunction in vascular smooth muscle cells (VSMCs), we exposed rat aortic smooth muscle cells (A7r5) to inorganic arsenic (iAs(III)) and its metabolite monomethylarsonous acid (MMA(III)) and compared their effects on mitochondrial function and oxidative stress. Our results indicate that MMA(III) is significantly more toxic to mitochondria than iAs(III). Exposure of VSMCs to MMA(III), but not iAs(III), significantly decreased basal and maximal oxygen consumption rates and concomitantly increased compensatory extracellular acidification rates, a proxy for glycolysis. Treatment with MMA(III) significantly increased hydrogen peroxide and superoxide levels compared to iAs(III). Exposure to MMA(III) resulted in significant decreases in mitochondrial ATP, aberrant perinuclear clustering of mitochondria, and decreased mitochondrial content. Mechanistically, we observed that mitochondrial superoxide and hydrogen peroxide contribute to mitochondrial toxicity, as treatment of cells with MnTBAP (a mitochondrial superoxide dismutase mimetic) and catalase significantly reduced mitochondrial respiration deficits and cell death induced by both arsenic compounds. Overall, our data demonstrates that MMA(III) is a mitochondria-specific toxicant that elevates mitochondrial and non-mitochondrial sources of ROS.