Objectives: Mortality from respiratory and cardiovascular health conditions contributes largely to the total mortality that has been associated with exposure to PM in epidemiology studies. A mode of action (MoA) for these underlying morbidities has not been established, but it has been proposed that some effects of PM occur through activation of neural reflexes.
Materials And Methods: We critically reviewed the experimental studies of PM (including ambient PM, diesel exhaust particles, concentrated ambient particles, diesel exhaust, and cigarette smoke) and neural reflex activation, and applied the principles of the International Programme on Chemical Safety (IPCS) MoA/human relevance framework to assess whether they support a biologically plausible and human-relevant MoA by which PM could contribute to cardiovascular and respiratory causes of death.
Exposure to inorganic arsenic (iAs) is a significant public health concern with individuals around the globe exposed to harmful levels through contaminated drinking water. Exposure to iAs during pregnancy is of particular concern and has been associated with pregnancy complications and adverse child health later in life. Effects of in utero exposure may be mediated through alterations in key signaling pathways in the placenta that regulate fetal growth and development.
View Article and Find Full Text PDFPrenatal exposure to inorganic arsenic (iAs) has been associated with adverse developmental and reproductive outcomes. These outcomes may be tied to altered functionality of nuclear transcription factors such as the glucocorticoid receptor (GR) in the placenta and associated gene expression. The GR pathway is integral for proper fetal and placental development, and perturbations in this pathway may underlie observed associations between prenatal iAs exposure and adverse birth outcomes.
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