Exposure to chemical mixtures in Mexican children: high-risk scenarios

Abstract

In developing countries, the management of environmental toxicants is inadequate, thus, humans may be exposed to levels higher than normal levels (background levels). Therefore, the aim of this study was to evaluate the exposure level of Mexican children to dichlorodiphenyltrichloroethane (DDT), dichlorodiphenyldichloroethylene (DDE), lead, and polycyclic aromatic hydrocarbons [using 1-hydroxypyrene (1-OHP) as exposure biomarker] and to assess the percentage of children exposed to these four compounds at concentrations higher than normal in each community studied. We performed random sampling in eight communities in Mexico (five communities in Chiapas State and three communities in San Luis Potosi State). DDT and DDE were analyzed by gas chromatography/mass spectrometry, the quantification of lead in blood was performed using atomic absorption spectrophotometry, and 1-OHP analyses were performed using HPLC with a fluorescence detector. Elevated DDT, DDE, and 1-OHP levels were found in children living in the indigenous communities of Chiapas State, while higher blood lead levels were found in two communities in San Luis Potosí. Approximately 30 % of children living in Chiapas were exposed to all four compounds at concentrations above the guidelines for each compound, whereas 48 % of children studied were exposed to all four contaminants at concentrations higher than normal in a community in San Luis Potosí State. As expected, our results showed that in hot spots, children are exposed to levels higher than normal. Therefore, child environmental health programs are urgently needed.

Rapid analysis of persistent organic pollutants by solid phase microextraction in serum samples

“…On the other hand, in agreement to environmental and human exposure values to POPs [36,[42][43][44], the detection and quantification limits found in this work are acceptable for biomonitoring. The simplicity and sensitivity of this technique allows it to be applied in biomonitoring programs in order to assess the presence of POPs mixtures in children and the general population, particularly at polluted sites, many of which exist in developing countries due to an extensive use of these compounds.…”

“…Children are potentially at a higher risk than adults [42]. In common risk scenarios in Mexico [43][44][45], children are one of the most susceptible populations, and the issue of health effects from exposure to mixtures of pollutants is a public health issue in those sites.…”

DDE and PCB 153 independently induce aryl hydrocarbon receptor (AhR) expression in peripheral blood mononuclear cells

“…It is important to remember that humans are usually exposed to complex chemical mixtures rather than to individual compounds (Domínguez-Cortinas et al, 2013;Perez-Maldonado et al, 2004Orta-Garcia et al, 2014;Trejo-Acevedo et al, 2012). Moreover, it was noted that populations are exposed to proinflammatory compounds (as DDE and PCB153) and compounds such as PAHs, PCBs, and TCCD (AhR agonists) simultaneously (Costilla-Salazar et al, 2011;Martínez-Salinas et al, 2011;PerezMaldonado et al, 2013;Trejo-Acevedo et al, 2012).…”

Environmental exposure to arsenic and chromium in children is associated with kidney injury molecule-1

“…Water supply for about 75% of the total population relies on groundwater abstraction, which is heavily contaminated with arsenic and fluoride, particularly in the north-central region of Mexico (CONAGUA, 2010;Armienta and Segovia, 2008). In San Luis Potosi, a central-north state in Mexico, the risk of exposure to heavy metals such as arsenic, cadmium, chromium and lead is high as a result of mining and industrial activities (Calderon et al, 2001;Carrizales et al, 2006;Dominguez-Cortinas et al, 2013;Trejo-Acevedo et al, 2009). In animal models, these kidney toxicants have been shown to target predominantly the proximal tubule causing reactive oxygen species generation followed by endoplasmic reticulum stress and mitochondrial damage, culminating in cellular necrosis/apoptosis (Barbier et al, 2005;Sabolic, 2006).…”