Approaches to estimating and addressing the risk to children from fossil fuel combustion have been fragmented, tending to focus either on the toxic air emissions or on climate change. Yet developing ...children, and especially poor children, now bear a disproportionate burden of disease from both environmental pollution and climate change due to fossil fuel combustion.
This commentary summarizes the robust scientific evidence regarding the multiple current and projected health impacts of fossil fuel combustion on the young to make the case for a holistic, child-centered energy and climate policy that addresses the full array of physical and psychosocial stressors resulting from fossil fuel pollution.
The data summarized here show that by sharply reducing our dependence on fossil fuels we would achieve highly significant health and economic benefits for our children and their future. These benefits would occur immediately and also play out over the life course and potentially across generations.
Going beyond the powerful scientific and economic arguments for urgent action to reduce the burning of fossil fuels is the strong moral imperative to protect our most vulnerable populations. Citation: Perera FP. 2017. Multiple threats to child health from fossil fuel combustion: impacts of air pollution and climate change. Environ Health Perspect 125:141-148; http://dx.doi.org/10.1289/EHP299.
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DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
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 theBdnfgene in the hippocampus and blood of BALB/c mice and that these changes are consistent withBDNFchanges in the cord blood of humans exposed to high maternal BPA levels in utero. Our data suggest thatBDNFDNA methylation in the blood may be used as a predictor of brainBDNFDNA methylation and gene expression as well as behavioral vulnerability induced by early-life environmental exposure. BecauseBDNFexpression 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.
Polycyclic aromatic hydrocarbons are widespread urban air pollutants from combustion of fossil fuel and other organic material shown previously to be neurotoxic.
In a prospective cohort study, we ...evaluated the relationship between Attention Deficit Hyperactivity Disorder behavior problems and prenatal polycyclic aromatic hydrocarbon exposure, adjusting for postnatal exposure.
Children of nonsmoking African-American and Dominican women in New York City were followed from in utero to 9 years. Prenatal polycyclic aromatic hydrocarbon exposure was estimated by levels of polycyclic aromatic hydrocarbon- DNA adducts in maternal and cord blood collected at delivery. Postnatal exposure was estimated by the concentration of urinary polycyclic aromatic hydrocarbon metabolites at ages 3 or 5. Attention Deficit Hyperactivity Disorder behavior problems were assessed using the Child Behavior Checklist and the Conners Parent Rating Scale- Revised.
High prenatal adduct exposure, measured by elevated maternal adducts was significantly associated with all Conners Parent Rating Scale-Revised subscales when the raw scores were analyzed continuously (N = 233). After dichotomizing at the threshold for moderately to markedly atypical symptoms, high maternal adducts were significantly associated with the Conners Parent Rating Scale-Revised DSM-IV Inattentive (OR = 5.06, 95% CI 1.43, 17.93) and DSM-IV Total (OR = 3.37, 95% CI 1.10, 10.34) subscales. High maternal adducts were positivity associated with the DSM-oriented Attention Deficit/Hyperactivity Problems scale on the Child Behavior Checklist, albeit not significant. In the smaller sample with cord adducts, the associations between outcomes and high cord adduct exposure were not statistically significant (N = 162).
The results suggest that exposure to polycyclic aromatic hydrocarbons encountered in New York City air may play a role in childhood Attention Deficit Hyperactivity Disorder behavior problems.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Background: Airborne polycyclic aromatic hydrocarbons (PAH) are widespread urban air pollutants from fossil fuel burning and other combustion sources. We previously reported that a broad spectrum of ...combustion-related DNA adducts in cord blood was associated with attention problems at 6—7 years of age in the Columbia Center for Children's Environmental Health (CCCEH) longitudinal cohort study. Objectives: We evaluated the relationship between behavioral problems and two different measures of prenatal exposure—both specific to PAH—in the same cohort. Methods: Children of nonsmoking African-American and Dominican women in New York City (NYC) were followed from in utero to 6-7 years. Prenatal PAH exposure was estimated by personal air monitoring of the mothers during pregnancy as well as by the measurement of DNA adducts specific to benzoapyrene (BaP), a representative PAH, in maternal and cord blood. At 6-7 years of age, child behavior was assessed using the Child Behavior Checklist (CBCL) (n = 253). Generalized linear models were used to test the association between prenatal PAH exposure and behavioral outcomes. Results: In multivariate analyses, high prenatal PAH exposure, whether characterized by personal air monitoring (greater than the median of 2.27 ng/m³) or maternal and cord adducts (detectable or higher), was positively associated with symptoms of Anxious/Depressed and Attention Problems (p ≤ 0.05). Conclusion: These results provide additional evidence that environmental levels of PAH encountered in NYC air can adversely affect child behavior.
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DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
Background: Polycyclic aromatic hydrocarbons (PAHs) are carcinogenic environmental pollutants generated during incomplete combustion. After exposure and during metabolism, PAHs can form reactive ...epoxides that can covalently bind to DNA. These PAH–DNA adducts are established markers of cancer risk. PAH exposure has been associated with epigenetic alterations, including genomic cytosine methylation. Both global hypomethylation and hypermethylation of specific genes have been associated with cancer and other diseases in humans. Experimental evidence suggests that PAH–DNA adduct formation may preferentially target methylated genomic regions. Early embryonic development may be a particularly susceptible period for PAH exposure, resulting in both increased PAH-DNA adducts and altered DNA methylation. Objective: We explored whether prenatal exposure to PAHs is associated with genomic DNA methylation in cord blood and whether methylation levels are associated with the presence of detectable PAH-DNA adducts. Methods: In a longitudinal cohort study of nonsmoking women in New York City, we measured PAH exposure during pregnancy using personal air monitors, assessed PAH internal dose using prenatal urinary metabolites (in a subset), and quantified benzoa pyrene-DNA adducts and genomic DNA methylation in cord blood DNA among 164 participants. Results: Prenatal PAH exposure was associated with lower global methylation in umbilical cord white blood cells (p * 0.05), but global methylation levels were positively associated with the presence of detectable adducts in cord blood (p = 0.01). Conclusions: These observations suggest that PAH exposure was adequate to alter global methylation in our study population. Additional epidemiologic studies that can measure site-specific cytosine methylation and adduct formation will improve our ability to understand this complex molecular pathway in vivo.
Bisphenol A (BPA) is an estrogenic endocrine disruptor widely used in the production of plastics. Increasing evidence indicates that in utero BPA exposure affects sexual differentiation and behavior; ...however, the mechanisms underlying these effects are unknown. We hypothesized that BPA may disrupt epigenetic programming of gene expression in the brain. Here, we provide evidence that maternal exposure during pregnancy to environmentally relevant doses of BPA (2, 20, and 200 µg/kg/d) in mice induces sex-specific, dose-dependent (linear and curvilinear), and brain region-specific changes in expression of genes encoding estrogen receptors (ERs; ERα and ERβ) and estrogen-related receptor-γ in juvenile offspring. Concomitantly, BPA altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalamus, paralleling changes in estrogen-related receptors. Importantly, changes in ERα and DNMT expression in the cortex (males) and hypothalamus (females) were associated with DNA methylation changes in the ERα gene. BPA exposure induced persistent, largely sex-specific effects on social and anxiety-like behavior, leading to disruption of sexually dimorphic behaviors. Although postnatal maternal care was altered in mothers treated with BPA during pregnancy, the effects of in utero BPA were not found to be mediated by maternal care. However, our data suggest that increased maternal care may partially attenuate the effects of in utero BPA on DNA methylation. Overall, we demonstrate that low-dose prenatal BPA exposure induces lasting epigenetic disruption in the brain that possibly underlie enduring effects of BPA on brain function and behavior, especially regarding sexually dimorphic phenotypes.
This study evaluated the relationship between prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAHs) and child intelligence.
Children of nonsmoking black or Dominican-American women ...residing in New York City were monitored from in utero to 5 years of age, with determination of prenatal PAH exposure through personal air monitoring for the mothers during pregnancy. At 5 years of age, intelligence was assessed for 249 children by using the Wechsler Preschool and Primary Scale of Intelligence-Revised. Multivariate linear regression models were used to estimate and to test the associations between prenatal PAH exposure and IQ.
After adjustment for maternal intelligence, quality of the home caretaking environment, environmental tobacco smoke exposure, and other potentially confounding factors, high PAH levels (above the median of 2.26 ng/m(3)) were inversely associated with full-scale IQ (P = .007) and verbal IQ (P = .003) scores. Children in the high-exposure group had full-scale and verbal IQ scores that were 4.31 and 4.67 points lower, respectively, than those of less-exposed children (<or=2.26 ng/m(3)). The associations between logarithmically transformed, continuous, PAH levels and these IQ measures also were significant (full-scale IQ: beta = -3.00; P = .009; verbal IQ: beta = -3.53; P = .002).
These results provide evidence that environmental PAHs at levels encountered in New York City air can affect children's IQ adversely.
Prenatal exposure to chlorpyrifos (CPF), an organophosphate insecticide, is associated with neurobehavioral deficits in humans and animal models. We investigated associations between CPF exposure and ...brain morphology using magnetic resonance imaging in 40 children, 5.9–11.2 y, selected from a nonclinical, representative community-based cohort. Twenty high-exposure children (upper tertile of CPF concentrations in umbilical cord blood) were compared with 20 low-exposure children on cortical surface features; all participants had minimal prenatal exposure to environmental tobacco smoke and polycyclic aromatic hydrocarbons. High CPF exposure was associated with enlargement of superior temporal, posterior middle temporal, and inferior postcentral gyri bilaterally, and enlarged superior frontal gyrus, gyrus rectus, cuneus, and precuneus along the mesial wall of the right hemisphere. Group differences were derived from exposure effects on underlying white matter. A significant exposure x IQ interaction was derived from CPF disruption of normal IQ associations with surface measures in low-exposure children. In preliminary analyses, high-exposure children did not show expected sex differences in the right inferior parietal lobule and superior marginal gyrus, and displayed reversal of sex differences in the right mesial superior frontal gyrus, consistent with disruption by CPF of normal behavioral sexual dimorphisms reported in animal models. High-exposure children also showed frontal and parietal cortical thinning, and an inverse dose–response relationship between CPF and cortical thickness. This study reports significant associations of prenatal exposure to a widely used environmental neurotoxicant, at standard use levels, with structural changes in the developing human brain.
Perfluoroalkyl substances (PFAS) were among various persistent organic pollutants suspected to have been released during the collapse of the World Trade Center (WTC) on 9/11. Evidence on the ...association between prenatal PFAS exposure and child neurodevelopment is limited and inconsistent. This study evaluated the association between prenatal PFAS exposure and child cognitive outcomes measured at 5 different time points in a population prenatally exposed to the WTC disaster. The study population included 302 pregnant women in the Columbia University WTC birth cohort enrolled between December 13, 2001 and June 26, 2002 at three hospitals located near the WTC site: Beth Israel, St. Vincent’s, and New York University Downtown. We evaluated the association between prenatal exposure to four PFAS (perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorohexanesulfonic acid (PFHxS), perfluorononanoic acid (PFNA)) and child neurodevelopment measured using the Bayley Scales of Infant Development (BSID-II) at approximately 1, 2 and 3 years of age and using The Wechsler Preschool and Primary Scale of Intelligence (WPPSI) at approximately 4 and 6 years of age. Geometric mean (range) concentrations of PFAS were 6.03 (1.05, 33.7), 2.31 (0.18, 8.14), 0.43 (<LOQ, 10.3) and 0.67 (<LOQ, 15.8) ng/mL for PFOS, PFOA, PFNA and PFHxS, respectively. Several PFAS were associated with increases in cognitive outcomes in females and overall (males and females combined). Child sex modified the association between PFOS and the mental development index measured using BSID-II, with the observed relationship being positive for females and negative for males. Through principal component analyses, we observed a negative relationship between PFNA and the psychomotor development index measured using BSID-II and the verbal IQ measured using WPPSI. Our results suggest a sex- and compound-specific relationship between prenatal PFAS exposures and childhood neurodevelopment.
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•Perfluoralkyl substances (PFAS) are widespread environmental toxicants.•PFAS cross the placenta, exposing the fetus during vulnerable developmental periods.•Findings on prenatal PFAS exposure and child neurodevelopment are inconsistent.•We found sex- and compound-specific trends for this relationship.
Main Findings: We found sex- and compound-specific relationships between prenatal PFAS exposures and childhood neurodevelopment.
Bisphenol A (BPA) is a ubiquitous endocrine disrupting compound. Several experimental and epidemiological studies suggest that gestational BPA exposure can lead to neurodevelopmental and behavioral ...problems in early-life, but results have been inconsistent. We previously reported that prenatal BPA exposure may affect child behavior and differently among boys and girls at ages 3–5 years.
We investigated the association of prenatal and early childhood BPA exposure with behavioral outcomes in 7–9 year old minority children and hypothesized that we would observe the same sex-specific pattern observed at earlier ages.
African-American and Dominican women enrolled in an inner-city prospective cohort study and their children were followed from mother’s pregnancy through children’s age 7–9 years. Women during the third trimester of pregnancy and children at ages 3 and 5 years provided spot urine samples. BPA exposure was categorized by tertiles of BPA urinary concentrations. The Child Behavioral Checklist (CBCL) was administered at ages 7 and 9 to assess multiple child behavior domains. Associations between behavior and prenatal (maternal) BPA concentrations and behavior and postnatal (child) BPA concentration were assessed via Poisson regression in models stratified by sex. These models accounted for potential confounders including prenatal or postnatal urinary BPA concentrations, child age at CBCL assessment, ethnicity, gestational age, maternal intelligence, maternal education and demoralization, quality of child’s home environment, prenatal environmental tobacco smoke exposure, and prenatal mono-n-butyl phthalate concentration.
The direction of the associations differed between boys and girls. Among boys (n=115), high prenatal BPA concentration (upper tertile vs. lower two tertiles) was associated with increased internalizing (β=0.41, p<0.0001) and externalizing composite scores (β=0.40, p<0.0001) and with their corresponding individual syndrome scales. There was a general decrease in scores among girls that was significant for the internalizing composite score (β=−0.17, p=0.04) (n=135). After accounting for possible selection bias, the results remained consistent for boys. Conversely, high postnatal BPA concentration was associated with increased behaviors on both the internalizing composite (β=0.30, p=0.0002) and externalizing composite scores (β=0.33, p<0.0001) and individual subscores in girls but fewer symptoms in boys. These results remained significant in girls after accounting for selection bias.
These results suggest BPA exposure may affect childhood behavioral outcomes in a sex-specific manner and differently depending on timing of exposure.
•We assessed sex-specific associations between bisphenol A (BPA) and child behavior.•We measured BPA in maternal urine during pregnancy and in child urine at ages 3–5.•We administered the CBCL at ages 7 and 9 years to assess behavioral symptoms.•Boys with high prenatal BPA had increased internalizing and externalizing problems.•Associations of postnatal BPA with behavior differed from those of prenatal BPA.
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