Editors and affiliations. Gerba 6 O. Mayer 9 D.
Gunther 1. Tucson USA 2. Paron USA 4. Xalapa, Veracruz Mexico 5. Amsterdam The Netherlands 6.
Tucson USA 7. Bayreuth Germany 8. Getzville USA 9. Global hypomethylation of genomic DNA can lead to genomic instability and structural abnormalities in chromosomes, which is also a common phenotype of cancer and aging [ 47 , 48 ]. Together, these show that the balance of DNA methylation is crucial for human genetic stability and individual health.
Address correspondence to A. These conditions and properties favor the production of specific congeners; thus, there are different relative proportions of congeners within given industrial mixtures. When exercising the power of approval under the first paragraph, the Minister may prescribe any condition, restriction or prohibition the Minister considers necessary and modify the measures submitted or their implementation schedule. The Government must make the report public within 30 days after receiving it. The combined antiandrogenic effects of five commonly used pesticides.
In the dynamic model, epigenetic modification is reversible, thus making the epigenome persistently vulnerable. The proportion of stem cells contributes to epigenetic vulnerability of the organism, indicating that the gradual decline of overall epigenome stability with development may arise from, at least in part, the decrease of stem cell proportion in tissues and organs [ 46 ].
The epigenome, especially DNA methylation patterns in mammals including humans, is overall established in gametogenesis and early embryogenesis. The plasticity of the epigenome also contributes to the generation of cells with a broad developmental potential [ 18 ]. In this regard, epigenetic reprogramming in germ cells and the preimplantation embryo is particularly important for early embryonic and placental development [ 51 ]. This leads to a speculation that perturbations of the epigenome in early developmental stages contribute to abnormal fetal and placental development [ 52 ].
The epigenetic dysregulation triggered by environmental cues during these sensitive periods of individual development can persist across the life course leading to altered disease susceptibility and even phenotypic changes later in life [ 13 , 14 ]. Studies have confirmed the developmental plasticity by which a specific genotype can give rise to a range of phenotypes in response to persistent environmental conditions during development [ 53 , 54 , 55 ]. DOHaD phenomenon also describes the relationship between early environmental cues and later-life risk of abnormal metabolism and other diseases, where epigenetic mechanisms could be the bridge connecting these factors [ 56 , 57 , 58 ].
The timing of an intervention is the key to epigenetic alteration in response to environmental pollutants such as endocrine-disrupting chemicals and heavy metal or bioactive food components. For instance, our recent studies showed that prenatal phytochemicals may affect epigenetic patterns more profoundly than the same exposure in postnatal or adulthood [ 59 ]. Likewise, the time windows of the intervention are particularly important for the efficacy of epigenetic perturbation to prevent individual abnormal development [ 60 ].
The concept of developmental programming emphasizes that during sensitive windows of vulnerability, environmental intervention may result in functional dysregulation of gene expression and disease pathogenesis in later life [ 61 ]. Early-life development, in particular during embryogenesis, has been shown to play an important role in the initiation and development of many chronic metabolic diseases as well as cancers, and epigenetic mechanisms have been suggested to be involved in these processes [ 35 ].
The general epigenome, including DNA methylation and histone modifications, is established in the early embryo and the germ cells and has been thought to maintain a very stable modification status throughout the life course. An expanding body of evidence has confirmed that environmental stimuli such as climatic factors and environmental toxicants, occurring especially during prenatal and early postnatal life, may alter epigenetic programming leading to altered disease susceptibility or irreversible phenotypic changes in the offspring [ 62 ].
Among these risk factors, prenatal exposure to environmental contaminants attracts more attention and has been repeatedly found to be associated with aberrant epigenetic modification of regulatory sequences in susceptible genes [ 63 , 64 ]. Here, we review several prenatal environmental pollutants in different categories and their potential impacts on embryonic and postnatal development through epigenetic regulation.
Ambient air pollution includes particulate matter PM of various sizes and composition, as well as gaseous pollutants [ 65 ]. Early-life exposure to air pollution, especially during gestation, is a major health threat to pregnant women [ 66 ] and the developing fetus as well as the children. Air pollution has been shown to associate with various allergic complications both in short-term and long-term influence [ 67 , 68 , 69 ] as it can cross the placenta [ 15 , 70 , 71 ].
Although the specific molecular mechanisms underlying the effect of air pollution are not fully understood, epigenetic modifications are believed to be one of the key contributors that may link air pollution exposure to a range of adverse health outcomes [ 15 , 72 ]. Janssen et al. In addition, maternal exposure to particles also targets miRNAs. Maternal tobacco smoke is a personalized form of air pollution for the mother herself and fetus [ 73 ]. Although smoking is controllable, more than half of female smokers continue to smoke after pregnancy [ 81 ]. Maternal tobacco smoking has been also linked to dysregulated expression of miRNAs.
Maccani et al. Interestingly, the impact of prenatal cigarette smoke on DNA methylation may be gender-specific. It was shown that the male fetus is more susceptible to maternal smoking than the female [ ], and the alteration of DNA methylation in the differentially methylated region DMR of the IGF2 gene was more notable among newborn boys than girls [ ], whereas Bouwland-Both reported an adverse result [ ]. Moreover, a study has shown that maternal smoking showed a much stronger impact on offspring methylation intensity than paternal smoking [ 15 ] Table 1.
Polycyclic aromatic hydrocarbons PAHs are aromatic hydrocarbons with two or more fused benzene rings [ ]. They are mainly formed during incomplete combustion of fossil fuel, domestic wood, and other organic materials that are widely distributed in the air [ ].
PAHs are persistent organic pollutants POPs that have detrimental biological effects such as genotoxicity and carcinogenicity [ , ]. Some PAHs resemble steroid hormones and are lipid soluble, thereby resulting in accumulation in adipose tissue. These PAHs can even transfer across the placental barrier and the fetal blood-brain barrier. There is increasing evidence that prenatal exposure to PAHs results in multiple adverse effects on embryonic development [ , , ].
Prenatal exposure to traffic-related PAHs was also shown to be linked with hypermethylation of the acyl-CoA synthetase long-chain family member 3 ACSL3 gene, which impacts asthma pathogenesis in umbilical cord blood of newborns [ ] Table 1. Pregnant women living near major roads may be easily affected by traffic-related air pollution and have been reported to show decreased DNA methylation in the long interspersed nuclear element 1 LINE-1 gene in placenta tissue [ ]. Aberrant DNA methylation patterns have been found in mitochondria-related and antioxidant defense-related genes of neonates who were prenatally exposed to NO 2 [ ].
of Environmental Contamination and Toxicology. Continuation of Residue Reviews Part of the Reviews of Environmental Contamination and Toxicology book series (RECT, volume ). Download book PDF · Download book EPUB. Reviews of Environmental Contamination and Toxicology. Continuation of Residue Reviews. Editors; (view affiliations). David M. Whitacre; George W. Ware .
In utero exposure to diesel exhaust has been associated with altered methylation of genes that are implicated in cardiovascular-related diseases and substance metabolism [ ] Table 1. Endocrine-disrupting chemicals EDCs are a class of chemical compounds widespread in the environment [ ].