Fine particulate matter, i.e. particles with a diameter smaller than 2.5 micrometers (PM2.5), is a global issue in public health. Diesel exhaust particles constitute the main component of PM2.5 and their health effects have been studied for a long time. One health effect that has been identified in recent emerging evidence is that the developing fetus is susceptible to nanoparticle-rich diesel exhaust. In humans, exposure to ambient air pollution during pregnancy has been associated with fetal growth perturbations, childhood asthma, and more. In rodent models, gestational exposure to diesel exhaust has been associated with detrimental effects to several organ systems. Previously, the developmental effects of diesel exhaust particles were primarily attributed to the endocrine disrupting effects of organic chemicals adsorbed to the particles, such as polycyclic aromatic hydrocarbons. Within the past decade, the proposed mechanisms instead involve the toxic properties of the particles themselves.
Ambient PM2.5 contains a large proportion of ultrafine (nano-sized) particles (UFPs) that, due to their small size, have a high physicochemical reactivity and show unique behaviors in vivo. An emerging industry has begun to apply engineering of nanosized particles for applications in a wide range of products, including consumer use. Inhaled nanoparticles, whether ambient or engineered, can reach the alveolar region and extrapulmonary organs. Additionally, the translocation of inhaled nanoparticles across the placenta have been described. Developmental toxicity, following exposure of pregnant animals to nanoparticles (diesel soot, carbon black, etc.), has been observed relative to the offspring’s male reproductive system, the immune system with linkage to asthma susceptibility, the cardiovascular system and the central nervous system. Oxidative stress likely plays an important role in nanoparticle toxicity, as pre-treatment with antioxidants partially suppresses the developmental toxicity of nanoparticles. Some other underlying mechanisms have also been proposed as potentially important in the developmental toxicity of particles, e.g. activation of toll like receptors and interference with cell division. Our understanding of the mechanisms of developmental nanoparticle toxicity should to be broadened and reviewed in detail for better risk assessment and management for protecting the health of expecting mothers and their children.
This Research Topic welcomes studies that increases the knowledge of mechanisms relating to the developmental toxicity of nanoparticles, including both environmental UFPs and engineered nanomaterials. Article types included Original Research (in vitro, ex vivo, in vivo and epidemiological), Reviews, and Methods. These can be related, but not limited, to:
- Use of in vitro or in vivo models for delineation of the molecular mechanisms of developmental nanotoxicology;
- Application of antioxidative compounds in prevention of developmental toxicity of particles;
- Particle kinetics in and between the maternal and fetal compartments ;
- Description of differences in profiles of developmental toxicity depending on route of exposure;
- Identification of the properties associated with developmental toxicity, such as size, shape and composition of particles;
- Modification of developmental toxicity by surface modification of particles;
- Placental toxicity of particles, in vitro, ex vivo, and in vivo.
Fine particulate matter, i.e. particles with a diameter smaller than 2.5 micrometers (PM2.5), is a global issue in public health. Diesel exhaust particles constitute the main component of PM2.5 and their health effects have been studied for a long time. One health effect that has been identified in recent emerging evidence is that the developing fetus is susceptible to nanoparticle-rich diesel exhaust. In humans, exposure to ambient air pollution during pregnancy has been associated with fetal growth perturbations, childhood asthma, and more. In rodent models, gestational exposure to diesel exhaust has been associated with detrimental effects to several organ systems. Previously, the developmental effects of diesel exhaust particles were primarily attributed to the endocrine disrupting effects of organic chemicals adsorbed to the particles, such as polycyclic aromatic hydrocarbons. Within the past decade, the proposed mechanisms instead involve the toxic properties of the particles themselves.
Ambient PM2.5 contains a large proportion of ultrafine (nano-sized) particles (UFPs) that, due to their small size, have a high physicochemical reactivity and show unique behaviors in vivo. An emerging industry has begun to apply engineering of nanosized particles for applications in a wide range of products, including consumer use. Inhaled nanoparticles, whether ambient or engineered, can reach the alveolar region and extrapulmonary organs. Additionally, the translocation of inhaled nanoparticles across the placenta have been described. Developmental toxicity, following exposure of pregnant animals to nanoparticles (diesel soot, carbon black, etc.), has been observed relative to the offspring’s male reproductive system, the immune system with linkage to asthma susceptibility, the cardiovascular system and the central nervous system. Oxidative stress likely plays an important role in nanoparticle toxicity, as pre-treatment with antioxidants partially suppresses the developmental toxicity of nanoparticles. Some other underlying mechanisms have also been proposed as potentially important in the developmental toxicity of particles, e.g. activation of toll like receptors and interference with cell division. Our understanding of the mechanisms of developmental nanoparticle toxicity should to be broadened and reviewed in detail for better risk assessment and management for protecting the health of expecting mothers and their children.
This Research Topic welcomes studies that increases the knowledge of mechanisms relating to the developmental toxicity of nanoparticles, including both environmental UFPs and engineered nanomaterials. Article types included Original Research (in vitro, ex vivo, in vivo and epidemiological), Reviews, and Methods. These can be related, but not limited, to:
- Use of in vitro or in vivo models for delineation of the molecular mechanisms of developmental nanotoxicology;
- Application of antioxidative compounds in prevention of developmental toxicity of particles;
- Particle kinetics in and between the maternal and fetal compartments ;
- Description of differences in profiles of developmental toxicity depending on route of exposure;
- Identification of the properties associated with developmental toxicity, such as size, shape and composition of particles;
- Modification of developmental toxicity by surface modification of particles;
- Placental toxicity of particles, in vitro, ex vivo, and in vivo.
