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.

Background: Fine particulate matter (PM_2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies. Methods: To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM_2.5, in the form of concentrated ambient particles (mean: 37.8 μg/m³, SD 6.5), and filtered air (mean: 2.1 μg/m³, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure. Results: Low-level PM_2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM_2.5 concentration (37.8 μg/m³) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM_2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV₁) and FEV₁/ forced vital capacity (FEV₁/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM_2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure. Conclusions: This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM_2.5 particles at levels near the PM_2.5 US NAAQS standard. Clinical trial registration information: clinicaltrials.gov; Identifier: NCT03232086. The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

Background: Poor nutritional status combined with mercury exposure can generate adverse child health outcomes. Diet is a mediator of mercury exposure and evidence suggests that nutritional status modifies aspects of mercury toxicity. However, health impacts beyond the nervous system are poorly understood. This study evaluates antibody responses to six vaccines from the expanded program on immunization (EPI), including hepatitis B, Haemophilus influenzae type B, measles, pertussis, tetanus, and diphtheria in children with variable hair mercury and malnutrition indicators. Methods: An observational cohort study (n = 98) was conducted in native and non-native communities in Madre de Dios, Peru, a region with elevated mercury exposure from artisanal and small-scale gold mining. Adaptive immune responses in young (3–48 months) and older children (4–8 year olds) were evaluated by vaccine type (live attenuated, protein subunits, toxoids) to account for differences in response by antigen, and measured by total IgG concentration and antibody (IgG) concentrations of each EPI vaccine. Mercury was measured from hair samples and malnutrition determined using anthropometry and hemoglobin levels in blood. Generalized linear mixed models were used to evaluate associations with each antibody type. Results: Changes in child antibodies and protection levels were associated with malnutrition indicators, mercury exposure, and their interaction. Malnutrition was associated with decreased measles and diphtheria-specific IgG. A one-unit decrease in hemoglobin was associated with a 0.17 IU/mL (95% CI: 0.04–0.30) decline in measles-specific IgG in younger children and 2.56 (95% CI: 1.01–6.25) higher odds of being unprotected against diphtheria in older children. Associations between mercury exposure and immune responses were also dependent on child age. In younger children, one-unit increase in log₁₀ child hair mercury content was associated with 0.68 IU/mL (95% CI: 0.18–1.17) higher pertussis and 0.79 IU/mL (95% CI: 0.18–1.70) higher diphtheria-specific IgG levels. In older children, child hair mercury content exceeding 1.2 µg/g was associated with 73.7 higher odds (95% CI: 2.7–1984.3) of being a non-responder against measles and hair mercury content exceeding 2.0 µg/g with 0.32 IU/mL (95% CI: 0.10–0.69) lower measles-specific antibodies. Log₁₀ hair mercury significantly interacted with weight-for-height z-score, indicating a multiplicative effect of higher mercury and lower nutrition on measles response. Specifically, among older children with poor nutrition (WHZ = −1), log₁₀ measles antibody is reduced from 1.40 to 0.43 for low (<1.2 µg/g) vs. high mercury exposure, whereas for children with good nutritional status (WHZ = 1), log₁₀ measles antibody is minimally changed for low vs. high mercury exposure (0.72 vs. 0.81, respectively). Conclusions: Child immune response to EPI vaccines may be attenuated in regions with elevated mercury exposure risk and exacerbated by concurrent malnutrition.