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Abstract
Early life exposure to inorganic arsenic is associated with a wide range of malignant and chronic disease outcomes in humans. Prenatal arsenic exposure may give rise to adverse effects on child health and development as arsenic readily passes through the placenta in human beings. The impact of maternal arsenic exposure on fetal gene expression was conducted in pregnant women living in Southern Thailand. Arsenic exposed newborns had significantly higher levels of arsenic in cord blood, and a set of genes associated with numerous biological pathways, including cell signaling, apoptosis, inflammatory and stress response. A slight increase in promoter methylation of p53 in cord blood lymphocytes which correlated with arsenic accumulation in nails was observed in these exposed newborns. A follow-up study on these exposed children showed a significant increase in oxidative DNA damage, measured as 8-hydroxydeoxyguanosine (8-OHdG) in saliva. In addition, levels of urinary 8-OHdG excretion and salivary hOGG1 expression were significantly decreased in exposed children suggesting a defect in repair of 8-OHdG in arsenic-exposed children. Our study indicates that prenatal arsenic and continued exposure through early childhood can trigger various genetic and epigenetic alterations that may lead to disease development later in life.

AbstractHuman exposure to environmental contaminants such as persistent chlorinated organics, heavy metals, pesticides, phthalates, flame retardants, electronic waste and airborne pollutants around the world, and especially in Southeast Asian regions, are significant and require urgent attention. Given this widespread contamination and abundance of such toxins as persistent organic pollutants (POPs) in the ecosystem, it is unlikely that remediation alone will be sufficient to address the health impacts associated with this exposure. Furthermore, we must assume that the impact on health of some of these contaminants results in populations with extraordinary vulnerabilities to disease risks. Further exacerbating risk; infectious diseases, poverty and malnutrition are common in the Southeast Asian regions of the world. Thus, exploring preventive measures of environmental exposure and disease risk through new paradigms of environmental toxicology, optimal and/or healthful nutrition and health is essential. For example, folic acid supplementation can lower blood arsenic levels, and plant-derived bioactive nutrients can lower cardiovascular and cancer risks linked to pollutant exposure. Data also indicate that diets enriched with bioactive food components such as polyphenols and omega-3 polyunsaturated fatty acids can prevent or decrease toxicant-induced inflammation. Thus, consuming healthy diets that exhibit high levels of antioxidant and anti-inflammatory properties, is a meaningful way to reduce the vulnerability to non-communicable diseases linked to environmental toxic insults. This nutritional paradigm in environmental toxicology requires further study in order to improve our understanding of the relationship between nutrition or other lifestyle modifications and toxicant-induced diseases. Understanding mechanistic relationships between nutritional modulation of environmental toxicants and susceptibility to disease development are important for both cumulative risk assessment and the design and implementation of future public health programs and behavioral interventions.

AbstractInhalable particulate matter (PM) is a health concern, and people living in large cities such as Bangkok are exposed to high concentrations. This exposure has been linked to respiratory and cardiac diseases and cancers of the lung and brain. Throughout 2018, PM was measured in northern Bangkok near a toll road (13.87°N, 100.58°E) covering all three seasons (cool, hot and rainy). PM10 was measured in 24- and 72-h samples. On selected dates aerodynamic size and mass distribution were measured as 3-day samples from a fixed 5th floor inlet. Particle number concentration was measured from the 5th floor inlet and in roadside survey measurements. There was a large fraction of particle number concentration in the sub-micron range, which showed the greatest variability compared with larger fractions. Metals associated with combustion sources were most found on the smaller size fraction of particles, which may have implications for associated adverse health outcomes because of the likely location of aerosol deposition in the distal airways of the lung. PM10 samples varied between 30 and 100 μg m−3, with highest concentrations in the cool season. The largest metal fractions present in the PM10 measurements were calcium, iron and magnesium during the hot season with average airborne concentrations of 13.2, 3.6 and 2.0 μg m−3, respectively. Copper, zinc, arsenic, selenium, molybdenum, cadmium, antimony and lead had large non-crustal sources. Principal component analysis (PCA) identified likely sources of the metals as crustal minerals, tailpipe exhaust and non-combustion traffic. A health risk analysis showed a higher risk of both carcinogenic and non-carcinogenic health effects in the drier seasons than the wet season due to ingestion of nickel, arsenic, cadmium and lead.
Graphical abstract