Endocrine-Disrupting Chemicals in Human Fetal Growth

Abstract

Fetal growth is regulated by a complex interaction of maternal, placental, and fetal factors. The effects and outcomes that chemicals, widely distributed in the environment, may have on the health status of both the mother and the fetus are not yet well defined. Mainly mixtures of chemical substances are found in the mothers and placenta. Exposure to endocrine-disrupting chemicals (EDCs) can be associated with fetal growth retardation, thyroid dysfunction, and neurological disorders. EDCs mostly interfere with insulin, glucocorticoid, estrogenic, and thyroid pathways, with subsequent effects on normal endocrine and metabolic functions, which cause changes in the epigenome and state of inflammation with life-long effects and consequences. International scientific societies recommend the implementation of research and of all possible preventive measures. This review briefly summarizes all these aspects.

Endocrine-Disrupting Chemicals and Insulin Resistance in Children

“…EDCs can affect both fetal growth and subsequent action over the years, and some EDCs also act on the prenatal period [48].…”

Exploring the Role of Fusobacterium nucleatum in Preterm Birth: A Narrative Review

“…Whether the impact from periodontal infection influences or explicates a direct effect is uncertain but suggests a potentially damaging interaction between periodontitis and preterm delivery (PTD) [23]. From the empirical findings, a clear interest focused on the placental inflammation has emerged [1], [4], [25], [26], [27], [28], [29]. Central relationship between the periodontal disease and preterm birth (PTB) is due to an inflammatory response system responding to signal from bacterial invasion [30], [31].…”

“…Specifically, it has been investigated the role of the Gram-negative periodontal pathogen FN, an opportunistic pathogen agent having a specific role in the pathogenesis of different periodontal conditions, and it is increasingly recognized as an important agent of PTB [42], [50]. FN is credited with the distinction of being the most crucial pathogen implicated in the pathogenesis of periodontitis [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39], [40], [41], [42], [43], counting its systemic effects on immune system [59], [60]. The localized infection and inflammation of the mouse placenta mediated by oral FN colonization have been described previously by several researchers who suggested that the hematogenous transmission of this bacterium had a detrimental effect on pregnancy, producing intrauterine inflammatory response [51].…”

“…It is a Gram-negative, non-spore-forming obligate anaerobe, having a G1C content of 27-28 mol% and a genome size of about 2.4 3 106 bp. It is one of the most common periodontal species associated with periodontitis and it has already been adverted for its power to spread over a periodontal site and establish an efficient systemic inflammatory response [27], [28]. This linkage may be determined by the ability of the pathogen to colonize the placenta, through its ability to adhere and invade the host epithelial and endothelial cells through FadA adhesin, a virulence factor, which may be involved in pathogenesis of intrauterine infection [26], [27], [28], [29], [30].…”

“…It is one of the most common periodontal species associated with periodontitis and it has already been adverted for its power to spread over a periodontal site and establish an efficient systemic inflammatory response [27], [28]. This linkage may be determined by the ability of the pathogen to colonize the placenta, through its ability to adhere and invade the host epithelial and endothelial cells through FadA adhesin, a virulence factor, which may be involved in pathogenesis of intrauterine infection [26], [27], [28], [29], [30]. It has been suggested that the subsequent affection of the placenta may be probably induced through colonization, exciting the premature rupture of fetal membranes, because of the inflammation may assume an unhealthy character, in consequence of the severity of the infection [33], [34], [35].…”