Arsenic, a priority Superfund contaminant, neurotoxin and carcinogen, is a ubiquitous metalloid contaminant polluting many urban surface water bodies. However, the human health and ecological implications of this contamination are unclear due to an incomplete understanding of arsenic bioavailability in urban waters, which are typically affected by nutrient- and organic-rich conditions. The objective of the proposed project is to quantify spatiotemporal patterns and primary drivers of arsenic mobility, bioavailability and ecological toxicity in urban lakes. The South-Central Puget Sound Lowland region offers an exceptional environment to study the human and environmental health impacts of urban metal(loid)-impacted aquatic ecosystems because it hosts an array of densely settled lakes with arsenic-contaminated waters that display remarkably different redox behaviors: seasonally stratified and anoxic to well mixed and oxic. Although elevated levels of arsenic usually occur in anoxic waters at the bottom of thermally-stratified lakes during the summer, a lake in the study region maintains elevated aqueous arsenic concentrations under oxic conditions. The situation raises questions about the physical and geochemical processes controlling arsenic chemistry in oxic waters of shallow, unstratified lakes, and also about the resulting bioavailability of arsenic to aquatic life, including fish. Due to limitations that anoxia poses for aquatic organisms, the typical correspondence between elevated arsenic and anoxic conditions may act to minimize biological exposure to arsenic, whereas shallow, unstratified lakes may enhance exposure if contaminated. Within this context, the proposed project will pursue three specific aims: (1) determine the physical and biogeochemical conditions that promote arsenic mobilization from sediments and maintain elevated aqueous concentrations within shallow, unstratified oxic lakes, (2) identify the physical and chemical factors that control arsenic bioaccumulation by different trophic levels in both stratified and unstratified lakes, and (3) assess ecological toxicity of arsenic within both stratified and unstratified lakes using established and novel molecular biomarkers (identified using RNA-Seq analysis) indicating arsenic injury. We hypothesize that arsenic contamination in oxic waters of unstratified lakes is promoted and maintained by anthropogenic inputs of nutrients and organic matter, and that arsenic bioaccumulation and ecological toxicity is enhanced in oxic unstratified lakes compared to seasonally stratified lakes. We will achieve our aims by explicitly linking measurements of physical, chemical and biological lake properties with investigations of arsenic bioaccumulation and ecological toxicity. Our proposed research is innovative because of its combined biogeochemical and eco-toxicological approach and its use of novel toxicogenomic methods to identify molecular biomarkers of arsenic injury. Our project is significant because it will provide information needed to establish effective water quality criteria, develop robust lake management strategies, and foster adoption of biomarker techniques as a way to monitor and assess ecological toxicity of arsenic in aquatic systems.

Public Health Relevance

Our proposed research has direct relevance to public and environmental health by (1) improving knowledge of the complex phenomena ? geochemical, physical, and biological ? that control arsenic exposure in urban freshwater environments and (2) advancing the use of molecular biomarkers as a means of monitoring and assessing ecological toxicity resulting from arsenic contamination. These objectives respond to two of the SRP mandates outlined in the Funding Opportunity Announcement (FOA): ?Methods to assess the risks to human health presented by hazardous substances,? and ?Methods and technologies to detect hazardous substances in the environment.? Because the research will provide information needed to (1) establish robust water-quality guidelines for arsenic, (2) develop sustainable lake management strategies, and (3) foster adoption of molecular biomarkers as a contamination monitoring tool, it will directly benefit multiple stakeholders, including the people living around and utilizing these contaminated urban lakes and the federal and state agencies in charge of protecting and managing urban water bodies.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Hazardous Substances Basic Research Grants Program (NIEHS) (P42)
Project #
5P42ES004696-28
Application #
9149249
Study Section
Special Emphasis Panel (ZES1)
Project Start
Project End
Budget Start
2016-04-01
Budget End
2017-03-31
Support Year
28
Fiscal Year
2016
Total Cost
Indirect Cost
Name
University of Washington
Department
Type
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195
Criswell, Susan R; Warden, Mark N; Searles Nielsen, Susan et al. (2018) Selective D2 receptor PET in manganese-exposed workers. Neurology 91:e1022-e1030
Meador, James P; Yeh, Andrew; Gallagher, Evan P (2018) Adverse metabolic effects in fish exposed to contaminants of emerging concern in the field and laboratory. Environ Pollut 236:850-861
Ma, Eva Y; Heffern, Kevin; Cheresh, Julia et al. (2018) Differential copper-induced death and regeneration of olfactory sensory neuron populations and neurobehavioral function in larval zebrafish. Neurotoxicology 69:141-151
Heffern, Kevin; Tierney, Keith; Gallagher, Evan P (2018) Comparative effects of cadmium, zinc, arsenic and chromium on olfactory-mediated neurobehavior and gene expression in larval zebrafish (Danio rerio). Aquat Toxicol 201:83-90
Racette, Brad A; Gross, Anat; Criswell, Susan R et al. (2018) A screening tool to detect clinical manganese neurotoxicity. Neurotoxicology 64:12-18
Barrett, P M; Hull, E A; King, C E et al. (2018) Increased exposure of plankton to arsenic in contaminated weakly-stratified lakes. Sci Total Environ 625:1606-1614
Rooney, James P K; Woods, Nancy F; Martin, Michael D et al. (2018) Genetic polymorphisms of GRIN2A and GRIN2B modify the neurobehavioral effects of low-level lead exposure in children. Environ Res 165:1-10
Chang, Yu-Chi; Cole, Toby B; Costa, Lucio G (2018) Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice. Part Fibre Toxicol 15:18
Criswell, Susan R; Nielsen, Susan Searles; Warden, Mark et al. (2018) [18F]FDOPA positron emission tomography in manganese-exposed workers. Neurotoxicology 64:43-49
Wang, Hao; Zhang, Liang; Abel, Glen M et al. (2018) Cadmium Exposure Impairs Cognition and Olfactory Memory in Male C57BL/6 Mice. Toxicol Sci 161:87-102

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