Artisanal and small-scale gold mining (ASGM) is a primary contributor to global mercury and its rapid expansion raises concern for human exposure. Non-occupational exposure risks are presumed to be strongly tied to environmental contamination; however, the relationship between environmental and human mercury exposure, how exposure has changed over time, and risk factors beyond fish consumption are not well understood in ASGM settings. In Peruvian riverine communities (n = 12), where ASGM has increased 4–6 fold over the past decade, we provide a large-scale assessment of the connection between environmental and human mercury exposure by comparing total mercury contents in human hair (2-cm segment, n = 231) to locally caught fish tissue, analyzing temporal exposure in women of child bearing age (WCBA, 15–49 years, n = 46) over one year, and evaluating general mercury exposure risks including fish and non-fish dietary items through household surveys and linear mixed models. Calculations of an individual’s oral reference dose using the total mercury content in locally-sourced fish underestimated the observed mercury exposure for individuals in many communities. This discrepancy was particularly evident in communities upstream of ASGM, where mercury levels in river fish, water, and sediment measurements from a previous study were low, yet hair mercury was chronically elevated. Hair from 86% of individuals and 77% of children exceeded a USEPA (U.S. Environmental Protection Agency) provisional level (1.2 µg/g) that could result in child developmental impairment. Chronically elevated mercury exposure was observed in the temporal analysis in WCBA. If the most recent exposure exceeded the USEPA level, there was a 97% probability that the individual exceeded that level 8–10 months of the previous year. Frequent household consumption of some fruits (tomato, banana) and grains (quinoa) was significantly associated with 29–75% reductions in hair mercury. Collectively, these data demonstrate that communities located hundreds of kilometers from ASGM are vulnerable to chronically elevated mercury exposure. Furthermore, unexpected associations with fish mercury contents and non-fish dietary intake highlight the need for more in-depth analyses of exposure regimes to identify the most vulnerable populations and to establish potential interventions.

No abstract

Mercury toxicity mechanisms have the potential to induce DNA damage and disrupt cellular processes, like mitochondrial function. Proper mitochondrial function is important for cellular bioenergetics and immune signaling and function. Impacts of mercury on the nuclear genome (nDNA) are conflicting and inconclusive, and mitochondrial DNA (mtDNA) impacts are relatively unknown. In this study, we assessed genotoxic (mtDNA and nDNA), metabolic, and innate immune impacts of inorganic and organic mercury exposure in Caenorhabditis elegans. Genotoxic outcomes measured included DNA damage, DNA damage repair (nucleotide excision repair, NER; base excision repair, BER), and genomic copy number following MeHg and HgCl2 exposure alone and in combination with known DNA damage-inducing agents ultraviolet C radiation (UVC) and hydrogen peroxide (H2O2), which cause bulky DNA lesions and oxidative DNA damage, respectively. Following exposure to both MeHg and HgCl2, low-level DNA damage (~0.25 lesions/10 kb mtDNA and nDNA) was observed. Unexpectedly, a higher MeHg concentration reduced damage in both genomes compared to controls. However, this observation was likely the result of developmental delay. In co-exposure treatments, both mercury compounds increased initial DNA damage (mtDNA and nDNA) in combination with H2O2 exposure, but had no impact in combination with UVC exposure. Mercury exposure both increased and decreased DNA damage removal via BER. DNA repair after H2O2 exposure in mercury-exposed nematodes resulted in damage levels lower than measured in controls. Impacts to NER were not detected. mtDNA copy number was significantly decreased in the MeHg-UVC and MeHg-H2O2 co-exposure treatments. Mercury exposure had metabolic impacts (steady-state ATP levels) that differed between the compounds; HgCl2 exposure decreased these levels, while MeHg slightly increased levels or had no impact. Both mercury species reduced mRNA levels for immune signaling-related genes, but had mild or no effects on survival on pathogenic bacteria. Overall, mercury exposure disrupted mitochondrial endpoints in a mercury-compound dependent fashion.

BackgroundWildfires are increasingly a significant source of fine particulate matter (PM2.5), which has been linked to adverse health effects and increased mortality. ESKD patients are potentially susceptible to this environmental stressor.MethodsWe conducted a retrospective time-series analysis of the association between daily exposure to wildfire PM2.5 and mortality in 253 counties near a major wildfire between 2008 and 2012. Using quasi-Poisson regression models, we estimated rate ratios (RRs) for all-cause mortality on the day of exposure and up to 30 days following exposure, adjusted for background PM2.5, day of week, seasonality, and heat. We stratified the analysis by causes of death (cardiac, vascular, infectious, or other) and place of death (clinical or nonclinical setting) for differential PM2.5 exposure and outcome classification.ResultsWe found 48,454 deaths matched to the 253 counties. A 10-μg/m3 increase in wildfire PM2.5 associated with a 4% increase in all-cause mortality on the same day (RR, 1.04; 95% confidence interval [95% CI], 1.01 to 1.07) and 7% increase cumulatively over 30 days following exposure (RR, 1.07; 95% CI, 1.01 to 1.12). Risk was elevated following exposure for deaths occurring in nonclinical settings (RR, 1.07; 95% CI, 1.02 to 1.12), suggesting modification of exposure by place of death. “Other” deaths (those not attributed to cardiac, vascular, or infectious causes) accounted for the largest portion of deaths and had a strong same-day effect (RR, 1.08; 95% CI, 1.03 to 1.12) and cumulative effect over the 30-day period. On days with a wildfire PM2.5 contribution >10 μg/m3, exposure accounted for 8.4% of mortality.ConclusionsWildfire smoke exposure was positively associated with all-cause mortality among patients receiving in-center hemodialysis.