Global mercury concentrations in biota: their use as a basis for a global biomonitoring framework.

An important provision of the Minamata Convention on Mercury is to monitor and evaluate the effectiveness of the adopted measures and its implementation. Here, we describe for the first time currently available biotic mercury (Hg) data on a global scale to improve the understanding of global efforts to reduce the impact of Hg pollution on people and the environment. Data from the peer-reviewed literature were compiled in the Global Biotic Mercury Synthesis (GBMS) database (>550,000 data points). These data provide a foundation for establishing a biomonitoring framework needed to track Hg concentrations in biota globally. We describe Hg exposure in the taxa identified by the Minamata Convention: fish, sea turtles, birds, and marine mammals. Based on the GBMS database, Hg concentrations are presented at relevant geographic scales for continents and oceanic basins. We identify some effective regional templates for monitoring methylmercury (MeHg) availability in the environment, but overall illustrate that there is a general lack of regional biomonitoring initiatives around the world, especially in Africa, Australia, Indo-Pacific, Middle East, and South Atlantic and Pacific Oceans. Temporal trend data for Hg in biota are generally limited. Ecologically sensitive sites (where biota have above average MeHg tissue concentrations) have been identified throughout the world. Efforts to model and quantify ecosystem sensitivity locally, regionally, and globally could help establish effective and efficient biomonitoring programs. We present a framework for a global Hg biomonitoring network that includes a three-step continental and oceanic approach to integrate existing biomonitoring efforts and prioritize filling regional data gaps linked with key Hg sources. We describe a standardized approach that builds on an evidence-based evaluation to assess the Minamata Convention's progress to reduce the impact of global Hg pollution on people and the environment.

Differential fat accumulation in early adulthood according to adolescent-BMI and heavy metal exposure.

INTRODUCTION: Heavy metals such as Lead (Pb) and Mercury (Hg) can affect adipose tissue mass and function. Considering the high prevalence of exposure to heavy metals and obesity in Mexico, we aim to examine if exposure to Pb and Hg in adolescence can modify how fat is accumulated in early adulthood. METHODS: This study included 100 participants from the ELEMENT cohort in Mexico. Adolescent Pb and Hg blood levels were determined at 14-16 years. Age- and sex-specific adolescent BMI Z-scores were calculated. At early adulthood (21-22 years), fat accumulation measurements were performed (abdominal, subcutaneous, visceral, hepatic, and pancreatic fat). Linear regression models with an interaction between adolescent BMI Z-score and Pb or Hg levels were run for each adulthood fat accumulation outcome with normal BMI as reference. RESULTS: In adolescents with obesity compared to normal BMI, as Pb exposure increased, subcutaneous (p-interaction = 0.088) and visceral (p-interaction < 0.0001) fat accumulation increases. Meanwhile, Hg was associated with subcutaneous (p-interaction = 0.027) and abdominal (p-interaction = 0.022) fat deposition among adolescents with obesity. CONCLUSIONS: Heavy metal exposure in adolescence may alter how fat is accumulated in later periods of life.

Investigating endocrine and physiological parameters of captive American kestrels exposed by diet to selected organophosphate flame retardants.

Organophosphate triesters are high production volume additive flame retardants (OPFRs) and plasticizers. Shown to accumulate in abiotic and biotic environmental compartments, little is known about the risks they pose. Captive adult male American kestrels (Falco sparverius) were fed the same dose (22 ng OPFR/g kestrel/d) daily (21 d) of tris(2-butoxyethyl) phosphate (TBOEP), tris(2-chloroethyl) phosphate (TCEP), tris(2-chloroisopropyl) phosphate (TCIPP), or tris(1,2-dichloro-2-propyl) phosphate (TDCIPP). Concentrations were undetected in tissues (renal, hepatic), suggesting rapid metabolism. There were no changes in glutathione status, indicators of hepatic oxidative status, or the cholinergic system (i.e., cerebrum, plasma cholinesterases; cerebrum muscarinic, nicotinic receptors). Modest changes occurred in hepatocyte integrity and function (clinical chemistry). Significant effects on plasma free triiodothyronine (FT3) concentrations occurred with exposure to TBOEP, TCEP, TCIPP, and TDCIPP; TBOEP and TCEP had additional overall effects on free thyroxine (FT4), whereas TDCIPP also influenced total thyroxine (TT4). Relative increases (32%-96%) in circulating FT3, TT3, FT4, and/or TT4 were variable with each OPFR at 7 d exposure, but limited thereafter, which was likely maintained through decreased thyroid gland activity and increased hepatic deiodinase activity. The observed physiological and endocrine effects occurred at environmentally relevant concentrations and suggest parent OPFRs or metabolites may have been present despite rapid degradation.

Occupational exposures to particulate matter and PM2.5-associated polycyclic aromatic hydrocarbons at the Agbogbloshie waste recycling site in Ghana.

Electronic waste (e-waste) disposal and recycling activities such as burning and smelting can emit particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), and other pollutants that expose workers and nearby communities. At informal e-waste recycling facilities, both emission controls and protective measures for workers are absent. This study characterizes personal exposures (breathing zone) of PM and PAHs of e-waste workers at the large Agbogbloshie e-waste site in Accra, Ghana. We collected gravimetric and optical measurements of PM2.5 and PM10 using shift samples for workers and for an age- and gender-matched reference population. PM2.5 filters were analyzed for 26 PAHs using gas chromatography/mass spectroscopy. Among e-waste workers, PM2.5 and PM10 concentrations were 99 ± 56 and 218 ± 158 µg/m3 (median ± interquartile range, optical measurements), respectively; these levels were 78 and 57% higher, respectively, than levels measured at a fixed site that was centrally located at the waste site. In the reference community, breathing zone PM2.5 and PM10 levels were lower, 49 ± 20 and 131 ± 108 µg/m3, respectively, and the fraction of coarse PM was larger. We detected all 26 target PAHs, of which naphthalene and phenanthrene were the most abundant. PAH concentrations were weakly correlated to PM levels, but PAH abundances, representing the fraction of PAH mass to the total PM2.5 mass collected, were strongly and inversely correlated to PM levels, suggesting multiple and different sources of PAHs and PM that affected exposures. Both PM and PAH levels were elevated for workers performing burning and dismantling, and both exceeded standards or risk-based guidelines, e.g., lifetime excess cancer risks for several PAHs were in the 10-4 to 10-6 range, indicating the need to reduce emissions as well as provide respiratory protection. The study emphasizes the importance of using personal and shift samples to accurately characterize worker exposure.

An Early-Life Stage Alternative Testing Strategy for Assessing the Impacts of Environmental Chemicals in Birds.

Early-life stage (ELS) toxicity tests are recognized as an advancement over current testing methodologies in terms of cost, animal use, and biological relevance. However, standardized ELS tests are not presently available for some vertebrate taxa, including birds. The present study describes a Japanese quail (Coturnix japonica) ELS test that is a promising candidate for standardization and applies it to test 8 environmental chemicals (ethinylestradiol, benzo[a]pyrene, chlorpyrifos, fluoxetine, lead(II)nitrate, trenbolone, seleno-L-methionine, hexabromocyclododecane). Individual chemicals were injected into the air cell of unincubated Japanese quail eggs at 3 concentrations, all predicted to cause ≤20% mortality. Survival to embryonic day 16 was consistently high (>90%) among the vehicle-injected controls. All chemicals, except ethinylestradiol, were detected in liver tissue, most at concentrations suggestive of embryonic clearance. Adverse effects were observed for 5 of the 8 chemicals; chlorpyrifos (41.1 µg/g) significantly increased developmental abnormalities and decreased embryo and gallbladder mass. Ethinylestradiol (54.2 µg/g) and hexabromocyclododecane (0.02 µg/g) decreased embryo mass and tarsus length, respectively. Benzo[a]pyrene (0.83 µg/g) and fluoxetine hydrochloride (32.7 µg/g) exceeded the 20% mortality cutoff. No effects were observed following lead(II)nitrate, seleno-L-methionine, or trenbolone exposure up to 10.7, 0.07, and 4.4 µg/g, respectively. Overall, our ELS approach was time- and cost-effective, caused minimal mortality in controls, effectively delivered diverse chemicals to the embryo, and permitted identification of apical outcomes, all of which provide support toward standardization. Environ Toxicol Chem 2019;39:141-154. © 2019 SETAC.

Environmental health research challenges in Africa: Insights from symposia organized by the ISEE Africa Chapter at ISES-ISEE 2018.

Supplemental Digital Content is available in the text.

Prevention-intervention strategies to reduce exposure to e-waste.

As one of the largest waste streams, electronic waste (e-waste) production continues to grow in response to global demand for consumer electronics. This waste is often shipped to developing countries where it is disassembled and recycled. In many cases, e-waste recycling activities are conducted in informal settings with very few controls or protections in place for workers. These activities involve exposure to hazardous substances such as cadmium, lead, and brominated flame retardants and are frequently performed by women and children. Although recycling practices and exposures vary by scale and geographic region, we present case studies of e-waste recycling scenarios and intervention approaches to reduce or prevent exposures to the hazardous substances in e-waste that may be broadly applicable to diverse situations. Drawing on parallels identified in these cases, we discuss the future prevention and intervention strategies that recognize the difficult economic realities of informal e-waste recycling.