Environmental pollution challenges public health surveillance: the case of mercury exposure and intoxication in Brazil.

Pollution, causing millions of deaths annually, disproportionally affects low- and middle-income countries (LMICs). Mercury ranks among the three main chemicals of major public health concern, and even low levels can cause cardiovascular and nervous outcomes, with children and indigenous populations being especially vulnerable. Nearly 80% of all emissions in South America originate from the Amazon. Brazil, the fifth-largest contributor to global mercury emissions, exemplifies the challenges faced by LMICs in effectively monitoring and addressing mercury exposure/intoxication. Despite having powerful tools such as SINAN (a digital platform for compulsory disease reporting), and Community Health Agents, data reveals significant underreporting, especially in the Amazon. Furthermore, SINAN has important delays in its update: for instance, 196 cases of Munduruku Indigenous people in 2019 have only been included in 2023. In this Personal View, we outline insightful recommendations to enhance public health surveillance and implement enduring, effective strategies to monitor, report and address mercury exposure/intoxication, focusing on the Brazilian Amazon. Although these recommendations are tailored to the challenges of this country, they hold potential for adaptation by other Amazonian countries facing similar issues (high mercury emissions and the presence of vulnerable populations, among others).

Methylmercury neurotoxicity: Beyond the neurocentric view.

Mercury is a highly toxic metal widely used in human activities worldwide, therefore considered a global public health problem. Many cases of mercury intoxication have occurred in history and represent a huge challenge nowadays. Of particular importance is its methylated form, methylmercury (MeHg). This mercurial species induces damage to several organs in the human body, especially to the central nervous system. Neurological impairments such as executive, memory, motor and visual deficits are associated with MeHg neurotoxicity. Molecular mechanisms involved in MeHg-induced neurotoxicity include excitotoxicity due to glutamatergic imbalance, disturbance in calcium homeostasis and oxidative balance, failure in synaptic support, and inflammatory response. Although neurons are largely affected by MeHg intoxication, they only represent half of the brain cells. Glial cells represent roughly 50 % of the brain cells and are key elements in the functioning of the central nervous system. Particularly, astrocytes and microglia are deeply involved in MeHg-induced neurotoxicity, resulting in distinct neurological outcomes depending on the context. In this review, we discuss the main findings on astroglial and microglial involvement as mediators of neuroprotective and neurotoxic responses to MeHg intoxication. The literature shows that these responses depend on chemical and morphophysiological features, thus, we present some insights for future investigations, considering the particularities of the context, including time and dose of exposure, brain region, and species of study.

Revisiting Genetic Influence on Mercury Exposure and Intoxication in Humans: A Scoping Review.

Human intoxication to mercury is a worldwide health problem. In addition to the type and length of exposure, the genetic background plays an important role in mercury poisoning. However, reviews on the genetic influence in mercury toxicity are scarce and not systematic. Therefore, this review aimed to systematically overview the most recent evidence on the genetic influence (using single nucleotide polymorphisms, SNPs) on human mercury poisoning. Three different databases (PubMed/Medline, Web of Science and Scopus) were searched, and 380 studies were found that were published from 2015 to 2022. After applying inclusion/exclusion criteria, 29 studies were selected and data on characteristics (year, country, profile of participants) and results (mercury biomarkers and quantitation, SNPs, main findings) were extracted and analyzed. The largest number of studies was performed in Brazil, mainly involving traditional populations of the Tapajós River basin. Most studies evaluated the influence of the SNPs related to genes of the glutathione system (GST, GPx, etc.), the ATP-binding cassette transporters and the metallothionein proteins. The recent findings regarding other SNPs, such as those of apolipoprotein E and brain-derived neurotrophic factor genes, are also highlighted. The importance of the exposure level is discussed considering the possible biphasic behavior of the genetic modulation phenomena that could explain some SNP associations. Overall, recommendations are provided for future studies based on the analysis obtained in this scoping review.