Prenatal Exposure to Polycyclic Aromatic Hydrocarbons, Benzo[
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            ]pyrene–DNA Adducts, and Genomic DNA Methylation in Cord Blood

Herbstman, Julie B.; Tang, Deliang; Zhu, Deguang; Qu, Lirong; Sjödin, Andreas; Li, Zheng; Camann, David; Perera, Frederica P.

doi:10.1289/ehp.1104056

Cited by 223 publications

(158 citation statements)

References 33 publications

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“…4 Prenatal exposure to PAH, through the mother's exposure, was also suggested to alter global DNA-methylation, which has been associated with increased cancer risk. 11 Diesel technology has improved over the last two decades, resulting in lower emissions. However, this improvement mainly concerns trucks and buses; non-road applications (e.g., ships or heavy duty equipment used in mines and construction) are still largely uncontrolled.…”

Section: What's New?mentioning

confidence: 99%

Parental occupational exposure to engine exhausts and childhood brain tumors

Peters

Glass

Reid

et al. 2012

Intl Journal of Cancer

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Childhood brain tumors (CBT) are the leading cause of cancer death in children; their risk factors are still largely unknown. Since most CBTs are diagnosed before five years of age, prenatal exposure and early postnatal factors may be involved in their etiology. We investigated the association between CBT and parental occupational exposure to engine exhausts in an Australian population-based case-control study. Parents of 306 cases and 950 controls completed detailed occupational histories. Odds ratios (OR) and 95% confidence intervals (CI) were estimated for both maternal and paternal exposure in key time periods. Increased risks were observed for maternal exposure to diesel exhaust any time before the child's birth (OR 2.03, 95% CI 1.09-3.81) and paternal exposure around the time of the child's conception (OR 1.62, 95% CI 1.12-2.34). No clear associations with other engine exhausts were found. Our results suggest that parental occupational exposure to diesel exhaust may increase the risk of CBT. Malignant brain tumors are the leading cause of cancer mortality in children. 1,2 Despite decades of research, risk factors for childhood brain tumors (CBT) are largely unknown. Associations with some genetic syndromes and ionizing radiation have been established, but these account for only a small percentage of cases. 1-3 Since most CBT occur before five years of age, prenatal exposure and early postnatal factors may be involved in their etiology.Paternal employment in industries involving exposures to polycyclic aromatic hydrocarbons (PAH) was first suggested as a risk factor for CBT in 1974 and has been observed in several studies since. 1,4,5 PAH are formed during incomplete burning of organic substances (e.g. fuel or tobacco). Few studies have assessed maternal exposures. There is some evidence for genetic and epigenetic mechanisms following preconceptional and in utero exposures. 1,6 We investigated the association between CBT and parental occupational exposure to engine exhausts in our nation-wide Australian case-control study of CBT (Aus-CBT). Material and Methods Study populationIncident cases (aged 0-14 years) were identified through all ten pediatric oncology centers in Australia. Patients were diagnosed between 2005 and 2010. Three controls, frequency matched by age, sex and state of residence, were recruited for each brain tumor case. The control group consisted of two subgroups. The first group of controls was recruited specifically for the Aus-CBT study, by random digit dialing, in 2007-2010. The second set comprised controls from the Australian childhood acute lymphoblastic leukemia (Aus-ALL) study, 7 to increase statistical power at no additional cost. These controls were selected in 2005-2006 by the same method. Written informed consent was obtained from all parents and Ethics approval was granted by all participating hospitals.We were notified of 794 CBT cases, of whom 64 were ineligible (36 with no English-speaking parent, 23 non-residents and five with no biological parent available). Of the 730 el...

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Section: What's New?mentioning

confidence: 99%

Parental occupational exposure to engine exhausts and childhood brain tumors

Peters

Glass

Reid

et al. 2012

Intl Journal of Cancer

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“…Peripheral biomarkers may be of particular relevance for psychiatric disorders because, unlike the brain, tissues such as blood, saliva, or buccal cells are easily accessible in living patients. Several ubiquitous environmental exposures known to affect brain development (e.g., prenatal stress, famine, pollution/toxins) have been associated with epigenetic variation in human peripheral tissues (7)(8)(9)(10)(11). In addition, there is evidence for DNA methylation changes in the peripheral blood of psychiatric patients (12)(13)(14).…”

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confidence: 99%

DNA methylation of BDNF as a biomarker of early-life adversity

Kundaković

Gudsnuk

Herbstman

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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244

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Early-life adversity increases the risk for psychopathology in later life. The underlying mechanism(s) is unknown, but epigenetic variation represents a plausible candidate. Early-life exposures can disrupt epigenetic programming in the brain, with lasting consequences for gene expression and behavior. This evidence is primarily derived from animal studies, with limited study in humans due to inaccessibility of the target brain tissue. In humans, although there is evidence for DNA methylation changes in the peripheral blood of psychiatric patients, a fundamental question remains as to whether epigenetic markers in the blood can predict epigenetic changes occurring in the brain. We used in utero bisphenol A (BPA) exposure as a model environmental exposure shown to disrupt neurodevelopment and exert long-term effects on behavior in animals and humans. We show that prenatal BPA induces lasting DNA methylation changes in the transcriptionally relevant region of the Bdnf gene in the hippocampus and blood of BALB/c mice and that these changes are consistent with BDNF changes in the cord blood of humans exposed to high maternal BPA levels in utero. Our data suggest that BDNF DNA methylation in the blood may be used as a predictor of brain BDNF DNA methylation and gene expression as well as behavioral vulnerability induced by early-life environmental exposure. Because BDNF expression and DNA methylation are altered in several psychiatric disorders that are associated with early-life adversity, including depression, schizophrenia, bipolar disorder, and autism, BDNF DNA methylation in the blood may represent a novel biomarker for the early detection of psychopathology.epigenetics | biomarker | BDNF | bisphenol A | early life

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“…10,24 A possible epigenetic mechanism is suggested by the observation that prenatal PAH exposure resulted in global hypomethylation in umbilical cord blood cells. 46 This alteration persisted in offspring up to 3 years of age. Whether these epigenetic modifications contribute to disease risk later in life, or whether they are simply good markers of prenatal exposure, requires further investigation.…”

Section: -16mentioning

confidence: 90%