Tools for Assessing the Role of Particle Association in Point Source Hg and Pb Contamination at a Superfund site
The Berlin Superfund site, in northeastern New Hampshire, is a former chlor-alkali facility on the banks of the Androscoggin River, where liquid Hg has been observed seeping from rock fractures along the river bank. The site is currently undergoing an EPA Site Assessment to determine the extent of Hg contamination in the river. In this pilot project, Dartmouth researchers collaborated with USGS and the USEPA, to further understanding of the Hg mobility, methylation and bioavailability downstream of a point source of contamination.
A confounding feature to the Berlin site is the presence of 7 dams within 12 miles downstream of the Superfund site. Dam reservoirs can act as both deposition zones for contaminated sediment, as well as good environments for Hg methylation. The pilot project focused on assessing Hg and MeHg profiles in sediment and porewaters in these reservoirs. Concentrations of Hg and MeHg were elevated in reservoirs downstream relative to upstream of the Superfund site, although levels were highly variable within each site. Porewaters are considered an important biogeochemical compartment for assessing metal contamination and are used to predict the bioavailable and mobile fractions of contaminants in sediment. Yet, concentrations of mercury species in porewaters can be difficult to relate to MeHg concentrations in other environmental compartments, in part because porewaters are generally considered as a single “dissolved” fraction, which ignores the role of colloidal and organic ligand binding on geochemical behavior. Using three different techniques to size fractionate Hg in porewaters, inorganic Hg was found to be colloid-bound in porewaters, whereas the more toxic species, MeHg was truly dissolved or bound to low molecular weight organic particles, suggesting it is more mobile.
Sampling for this study was co-ordinated with the EPA site assessment, and findings of this study were communicated with the USEPA during meetings at Dartmouth in 2011 and at the EPA office Chelmsford MA in 2012. The techniques developed for assessing particle binding in this study were included in a successful RO1 grant application in 2012.
Metal Fate and Effects in Intertidal Food Webs at the Callahan Superfund site
Understanding the fate and effects of toxic metals found at Superfund sites in the U.S. is one of the main missions of the Superfund Research Program. Investigating impacts of specific Superfund sites on environmental and human health provides direct benefit to site managers, USEPA, and the public. Estuaries are the repositories of often high concentrations of metal contaminants from nearby mining activities, discharges of industrial complexes, and runoff from upland watersheds and there are numerous Superfund sites in estuaries.
The Callahan Mine in Brooksville Maine is an EPA Superfund (MED980524128) site that includes a large estuary, Goose Cove, which contains elevated levels of copper, lead and zinc due to the open pit mine that was dug and has since been abandoned. The original pit is now part of the estuary that experiences tidal cycles and inflow of freshwater from the nearby watershed.
This pilot project initiated an investigation of intertidal food webs and local killifish populations at this Superfund site. The two broad goals of the research were: 1) to characterize and compare the bioaccumulation and trophic transfer of metals in the resident food web of five sub-sites within the Callahan mine site and a nearby reference site at Horseshoe Cove, and 2) to characterize the genetic history of killifish at the mine site and across adjacent locations. Studies in 2010-2011 revealed strong gradients of metal concentrations closest to the mine tailings and waste rock piles in sediments, water, and fish. The elevated concentrations in water and fish suggest that there is rapid leaching of metals from the sediments or tailings that results in local bioaccumulation despite the constant mixing of the tidal cycle.
Market Basket Study of Arsenic Concentration and Speciation in Locally-Available Rice-Based Baby Cereals and Related Products
This study quantified arsenic concentrations in a range of infant milk formulas and first and second foods. The results of the study where presented at an international meeting on Trace Elements in Food (TEF-4, Aberdeen, Scotland, August 2011) and were published in Pure and Applied Chemistry, 2012, 84: 215-224. The levels of arsenic in infant formula were relatively low, ca. < 1 – 1.7 ppb in the reconstituted formula and all the arsenic was present as inorganic arsenic. Arsenic in first and second foods was generally low also except one or two fruit purees which were found to be high (ca. 20 ppb vs <5 ppb for other purees) and rice-based second foods (e.g. meat and rice etc.) were higher in arsenic than non-rice based second foods. Our market basket study also revealed two toddler formulas that were very high in arsenic compared to the infant formulas that we had analyzed (30 – 60 ppb total As in the reconstituted formula), the concentration of inorganic As varied between product (soy vs. dairy) and lot, but was ca. 8 ppb – 25 ppb. This brand of formula used brown rice syrup as a sweetener and we immediately recognized that this was the source of arsenic. Further study of other products, namely cereal/energy bars, that contain brown rice syrup and other rice ingredients showed that the arsenic concentration was related to the presence of rice products as ingredients in the bars. At most, these bars contributed about 2.5 micrograms of inorganic arsenic to diet compared to a no effect level of 10 µg established by the state of California in proposition 65. This finding about brown rice syrup and products containing brown rice syrup generated a lot of media interest. When the paper was published online (Environmental Health Perspectives, 120(5):623-626) it generated over 23,000 hits in the first week and prompted statements from the FDA, the Organic Trade Association and the US Rice Federation and has generally heightened awareness of the possible role of food as a source of arsenic to diet.
In Utero Arsenic and H1N1 Influenza-the Role of CD8+ T Cells in Immunopathology
Arsenic (As) is considered the number one chemical risk of environmental health concern in the U.S. and worldwide, and has been associated with increased risk of a wide variety of serious illnesses including various cancers, cardiovascular disease, diabetes and other significant non-cancer disease risks. The primary route of exposure is through ingestion of drinking water that has been contaminated with inorganic As from natural geological sources. Epidemiological evidence from an As-exposed population in Chile demonstrated that in utero and early childhood exposure to As was associated with a 46-fold increase in the risk of death from bronchiectasis decades after cessation of exposure. These observations have since been confirmed in other As-exposed populations in Bangladesh and Argentina. The extraordinary magnitude and unexpected residual aspect of this risk warrants further investigation into the underlying mechanism and the connection between early life As exposure and adult disease. We have found that exposure to As in drinking water, at levels found in many natural water sources, significantly diminishes the ability to clear H1N1 influenza infection, impairs CD8+ T cell responses, and prolongs both virus carriage as well as the inflammatory response. We have also found that airway remodeling is evident in these animals long after virus clearance, suggesting a mechanism that links the altered inflammatory response with the epidemiological phenotype of bronchiectasis in exposed individuals. In this study we will examine whether similar effects are evident after exposure in utero, following infection after exposed pups mature. Determination of a delayed effect of in utero exposure ground-water levels of arsenic on response to infection and airway inflammation and remodeling will be an important step in understanding potential epigenetic determinants of toxicity later in life.