Air pollution and the fetal origin of disease: A systematic review of the molecular signatures of air pollution exposure in human placenta

Abstract

Integration of placental biomarkers in an environmental epidemiological context enables researchers to address fundamental questions essential in unraveling the fetal origin of disease and helps to better define the pregnancy exposome of air pollution.

Environmental exposures and mechanisms in allergy and asthma development

“…TRAP exposure may alter the immune system even before birth. DEPs can cross the placenta and induce oxidative stress pathways in the fetus; thus maternal exposure has the potential for negative health effects to the fetus (148). Offspring of female mice exposed to DEPs in utero and sensitized to OVA postnatally were primed for enhanced allergen-induced bronchoalveolar lavage fluid inflammation, increased Th2 and Th17 cytokines, and elevated AHR compared with unexposed offspring (149)(150)(151).…”

Prenatal exposure of staphylococcal enterotoxin B attenuates the development and function of blood regulatory T cells to repeated staphylococcal enterotoxin B exposure in adult offspring rats

“…Pregnant adverse stimuli, including physicochemical and biological factors during fetal development, may lead to long-term structural and functional effects and form programming/imprinting effects to cause adult diseases [ 16, 17 ]. In a murine model, the addition of microbes to pregnant mice increased the prevalence of certain groups of intestinal innate immune system cells through altering haematopoietic cell development in offspring [ 36 ].…”

“…The developmental origin of health and disease (DOHaD) hypothesis postulates that early life exposures of adverse environmental stimuli can influence disease outcomes throughout the whole lifespan of an organism [ 15 ]. A large amount of epidemiological evidence from humans and animal experimental studies has suggested an association between adverse stimuli during pregnancy and some adult diseases [ 16, 17 ]. Staphylococcus aureus is an important factor leading to adverse pregnancy outcomes and fetal development abnormalities in pregnant women [ 18, 19 ].…”

Translocation of (ultra)fine particles and nanoparticles across the placenta; a systematic review on the evidence of in vitro, ex vivo, and in vivo studies

“…Pregnant women and developing embryos/fetuses comprise a particularly vulnerable population, as nanoparticles (NPs) that infiltrate the bloodstream may reach the placenta and possibly the fetus [ 1 ] . Such in utero exposure may not only influence fetal development and induce adverse pregnancy outcomes, but it can also adversely affect health in later life since the etiology of diseases in adulthood may have a fetal origin [ 2 ], as postulated in the Developmental Origins of Health and Disease hypothesis [ 3 ]. Various epidemiological studies identified associations between prenatal exposure to (ultra)fine particles and adverse health outcomes (i) at birth including an increased risk of low birth weight (< 2500 g) [ 4 , 5 ] and preterm birth (< 37 weeks of gestation) [ 6 , 7 ], and (ii) later in life such as cardiovascular disease [ 8 , 9 ], respiratory problems [ 10 , 11 ], and neurodevelopmental alterations [ 12 , 13 ].…”