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A perspective on the developmental toxicity of inhaled nanoparticles

Hougaard, Karin Sørig, Campagnolo, Luisa, Chavatte-Palmer, Pascale, Tarrade, Anne, Rousseau-Ralliard, Delphine, Valentino, Sarah, Park, Margriet V.D.Z., de Jong, Wim H., Wolterink, Gerrit, Piersma, Aldert H., Ross, Bryony L., Hutchison, Gary R., Hansen, Jitka Stilund, Vogel, Ulla, Jackson, Petra, Slama, Rémy, Pietroiusti, Antonio, Cassee, Flemming R.·2015·Reproductive Toxicology
DOI 10.1016/j.reprotox.2015.05.015
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Fig. 1 Schematic representation of the anatomical characteristics of the different types of placentation in mammals. (A) Pigs and (B) Ruminants (sheep): the placenta is either diffuse (A) or cotyledonary (B), i.e., organized into 70-100 separate entities named placentomes. There is no or very little trophoblastic invasion, respectively. Materno-fetal exchange occurs through 6 cellular layers (maternal endothelium, mesenchyme and epithelium, trophoblast, mesenchyme and fetal vascular endothelium). (C) Primates, rodents and lagomorphs (rabbits): the placenta invades the endometrium and destroys the maternal endothelium, thereby creating lacunae where the trophoblast is in direct contact with the maternal blood. In mice, the trophoblast consists of three cell layers (hemotrichorial placentation) whereas only two trophoblastic cell layers persist at term in primates and lagomorphs (syncytiotrophoblast and cytotrophoblast, the latter being discontinuous in late gestation; hemodichorial placenta). AC: amniotic cavity; AL: allantoic cavity; P: placenta; U: uterus; UC: umbilical cord; YS: yolk sac.
Fig. 1 Schematic representation of the anatomical characteristics of the different types of placentation in mammals. (A) Pigs and (B) Ruminants (sheep): the placenta is either diffuse (A) or cotyledonary (B), i.e., organized into 70-100 separate entities named placentomes. There is no or very little trophoblastic invasion, respectively. Materno-fetal exchange occurs through 6 cellular layers (maternal endothelium, mesenchyme and epithelium, trophoblast, mesenchyme and fetal vascular endothelium). (C) Primates, rodents and lagomorphs (rabbits): the placenta invades the endometrium and destroys the maternal endothelium, thereby creating lacunae where the trophoblast is in direct contact with the maternal blood. In mice, the trophoblast consists of three cell layers (hemotrichorial placentation) whereas only two trophoblastic cell layers persist at term in primates and lagomorphs (syncytiotrophoblast and cytotrophoblast, the latter being discontinuous in late gestation; hemodichorial placenta). AC: amniotic cavity; AL: allantoic cavity; P: placenta; U: uterus; UC: umbilical cord; YS: yolk sac.CC-BY-NC-ND · From the PDF
Fig. 2 Schematic representation of the anatomical and cellular structure of the human placenta. (A) Anchored fetal villi showing the extravillous trophoblast reaching the uterine spiral artery to form plugs in the first trimester. The extravillous trophoblast lines and remodels the uterine spiral artery to allow free flow of maternal blood into the intervillous chamber [193]. (B) Transversal section of the fetal villi illustrating the hemodichorial structure of the human placenta where only two layers (syncytiotrophoblast and the cytotrophoblast) separate maternal and fetal blood in the first and (C) third trimester, where even the cytotrophoblast becomes discontinuous. CT: cytotrophoblast; eEVCT: endovascular extravillous cytotrophoblast; DC: decidual cells; FV: fetal vessel; GC: Giant cells; iEVCT: invasive extravillous cytotrophoblast; IC: intervillous chamber; M: mesenchyme; MSA: maternal spiral artery; pEVCT: proliferative extravillous cytotrophoblast; ST: Syncytiotrophoblast; UV: uterine vein; VCT: villous cytotrophoblast.
Fig. 2 Schematic representation of the anatomical and cellular structure of the human placenta. (A) Anchored fetal villi showing the extravillous trophoblast reaching the uterine spiral artery to form plugs in the first trimester. The extravillous trophoblast lines and remodels the uterine spiral artery to allow free flow of maternal blood into the intervillous chamber [193]. (B) Transversal section of the fetal villi illustrating the hemodichorial structure of the human placenta where only two layers (syncytiotrophoblast and the cytotrophoblast) separate maternal and fetal blood in the first and (C) third trimester, where even the cytotrophoblast becomes discontinuous. CT: cytotrophoblast; eEVCT: endovascular extravillous cytotrophoblast; DC: decidual cells; FV: fetal vessel; GC: Giant cells; iEVCT: invasive extravillous cytotrophoblast; IC: intervillous chamber; M: mesenchyme; MSA: maternal spiral artery; pEVCT: proliferative extravillous cytotrophoblast; ST: Syncytiotrophoblast; UV: uterine vein; VCT: villous cytotrophoblast.CC-BY-NC-ND · From the PDF
Fig. 3 Mechanistic pathways in developmental toxicity of NP. NP may potentially affect embryonic/fetal development via direct as well as indirect mechanisms. Indirect effects may arise if inhaled NP deposit in the maternal alveoli and here generate reactive oxygen species, in amounts that results in oxidative stress, and inflammation. The inflamed lung tissue may then release inflammatory mediators, such as cytokines and acute phase proteins, to the blood stream, to be transported to organs and tissues with relevance for pregnancy and development (uterus, placenta, fetus), as well as maternal neuro-endocrine and immune circuits. Here the biologically active mediators may trigger a range of responses which in turn may interfere with development. If NP translocate from the alveoli to the maternal blood stream, they may reach the placenta and be taken by the placental cells. Particle induced generation of ROS and inflammation has been proposed to interfere with placental vascularization. If NP passes the placenta, they may exert toxicity directly through generation of ROS and inflammation in fetal tissue. Especially tubular NP have furthermore been proposed to interfere directly with cellular and extracellular constituents and thereby alter vital cellular processes. Finally, toxicity may occur due to the action of released chemical constituents or functionalizations of the NP or contaminants, such as metal catalysts used during manufacture. These may increase generation of ROS, and affect the placenta and the fetus.
Fig. 3 Mechanistic pathways in developmental toxicity of NP. NP may potentially affect embryonic/fetal development via direct as well as indirect mechanisms. Indirect effects may arise if inhaled NP deposit in the maternal alveoli and here generate reactive oxygen species, in amounts that results in oxidative stress, and inflammation. The inflamed lung tissue may then release inflammatory mediators, such as cytokines and acute phase proteins, to the blood stream, to be transported to organs and tissues with relevance for pregnancy and development (uterus, placenta, fetus), as well as maternal neuro-endocrine and immune circuits. Here the biologically active mediators may trigger a range of responses which in turn may interfere with development. If NP translocate from the alveoli to the maternal blood stream, they may reach the placenta and be taken by the placental cells. Particle induced generation of ROS and inflammation has been proposed to interfere with placental vascularization. If NP passes the placenta, they may exert toxicity directly through generation of ROS and inflammation in fetal tissue. Especially tubular NP have furthermore been proposed to interfere directly with cellular and extracellular constituents and thereby alter vital cellular processes. Finally, toxicity may occur due to the action of released chemical constituents or functionalizations of the NP or contaminants, such as metal catalysts used during manufacture. These may increase generation of ROS, and affect the placenta and the fetus.CC-BY-NC-ND · From the PDF

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Cited by

Sorted by citations

Metadata

Authors
Hougaard, K. S., Campagnolo, L., Chavatte-Palmer, P., Tarrade, A., Rousseau-Ralliard, D., Valentino, S., Park, M. V. D. Z., de Jong, W. H., Wolterink, G., Piersma, A. H., Ross, B. L., Hutchison, G. R., Hansen, J. S., Vogel, U., Jackson, P., Slama, R., Pietroiusti, A., & Cassee, F. R.
Venue
Reproductive Toxicology
Publisher
Elsevier BV
Published
2015-08
Volume
56
Pages
118-140
ISSN
0890-6238
DOI
10.1016/j.reprotox.2015.05.015
Cited by
171
References
10
Language
en
Licence
Funders
  • Risks of Nanotechnology Knowledge and Information Center
  • Italian Ministry of Health and COST Action MODENA (LC, AP)
  • FP7 (310584)
  • MARINA (263215)
  • Danish Center for Nanosafety
  • European Research Council (311765)

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