Polycyclic Aromatic Hydrocarbons–Aromatic DNA Adducts in Cord Blood and Behavior Scores in New York City Children

Perera, Frederica P.; Wang, Shuang; Vishnevetsky, Julia; Zhang, Bingzhi; Cole, Kathleen J.; Tang, Deliang; Rauh, Virginia; Phillips, David H.

doi:10.1289/ehp.1002705

Cited by 148 publications

(85 citation statements)

References 56 publications

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“…Levels of PAH-DNA adducts in cord blood have been found to be associated with higher symptom scores of anxiety and depression measured at 4.8 years (Perera et al, 2011). In the same cohort, prenatal exposure to benzo[a]pyrene measured from maternal personal air monitoring (at a median level of 2.27 ng/m 3 ), and also cord blood adduct levels, were associated with these effects, as well as attention problems at age 6-7 years .…”

Section: Rationalementioning

confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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Section: Rationalementioning

confidence: 99%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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“…A new hypothesis suggests that a greater susceptibility to air pollutants may be linked with genomic polymorphism [29] and reduced levels of DNA methylation associated with oxidative stress, by altering the expression of genes involved in the methylation process. In the context of potential epigenetic effects of air pollutants, we have to mention observations made recently by Perera et al [30] in the New York City cohort study on fetal growth and healthy development of children. In the latter study, prenatal exposure It is worth mentioning that the observed dose-dependent relationship without threshold was seen between eCO and fetal exposure to PM 2.5 and that the significant portion of the exhaled CO could be attributed to prenatal PM 2.5 exposure.…”

Section: Discussionmentioning

confidence: 99%

Dose-dependent relationship between prenatal exposure to fine particulates and exhaled carbon monoxide in non-asthmatic children. A population-based birth cohort study

Jędrychowski¹,

Maugeri²,

Spengler³

et al. 2013

International Journal of Occupational Medicine and Environmental Health

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Objectives:The main goal of the study was to assess possible association between fetal exposure to fine particulate matter (PM 2.5 ) and exhaled carbon monoxide (eCO) measured in non-asthmatic children. Material and Methods: The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków. Personal samplers of PM 2.5 were used to measure fine particle mass in the fetal period and carbon monoxide (CO) in exhaled breath from a single exhalation effort at the age of 7. In the statistical analysis of the effect of prenatal PM 2.5 exposure on eCO, a set of potential confounders, such as environmental tobacco smoke (ETS), city residence area, sensitization to house dust allergens and the occurrence of respiratory symptoms monitored over the seven-year follow-up was considered. Results: The level of eCO did not correlate with the self-reported ETS exposure recorded over the follow-up, however, there was a positive significant relationship with the prenatal PM 2.5 exposure (non-parametric trend p = 0.042). The eCO mean level was higher in atopic children (geometric mean = 2.06 ppm, 95% CI: 1.58-2.66 ppm) than in non-atopic ones (geometric mean = 1.57 ppm, 95% CI: 1.47-1.73 ppm) and the difference was statistically significant (p = 0.036). As for the respiratory symptoms, eCO values were associated positively only with the cough severity score recorded in the follow-up (nonparametric trend p = 0.057). In the nested multivariable linear regression model, only the effects of prenatal PM 2.5 and cough severity recorded in the follow-up were related to eCO level. The prenatal PM 2.5 exposure represented 5.1%, while children's cough represented only 2.6% of the eCO variability. Conclusion: Our study suggests that elevated eCO in non-asthmatic children may result from oxidative stress experienced in the fetal period and that heme oxygenase (HO) activity in body tissues may be programmed in the fetal period by the exposure to fine particulate matter.

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“…PAHs have been shown to be neurodevelopmental toxicants in experimental studies [19][20][21]. There are 8 human epidemiological studies which have examined an association between exposure to PAHs and children's development [22][23][24][25][26][27], one study has investigated how polymorphism in PAH metabolic genes affects child cognitive development [28], and another one has assessed the combined exposure to environmental tobacco smoke (ETS) and PAH-DNA adducts after the World Trade Center catastrophe and its impact on child development [29] (Table 4).…”

Section: Exposure To Pahs and Children's Neurodevelopmentmentioning

confidence: 99%

“…High PAH levels (above 17.96 ng/m 3 ) were inversely associated with fullscale IQ (p = 0.007) and verbal IQ (p = 0.003) scores [23]. The same cohort was followed to 7-8 years of age [24], adducts were measured in umbilical cord blood. Higher cord PAH-DNA and other bulky aromatic adducts were associated with higher symptom scores of anxious/depressed at 4.8 years and attention problems at 4.8 and 7 years, in children born to nonsmoking women, the women's smoking status was based on cotinine level in cord blood [24].…”

Section: Exposure To Bfrs and Children's Neurodevelopmentmentioning

confidence: 99%

“…The same cohort was followed to 7-8 years of age [24], adducts were measured in umbilical cord blood. Higher cord PAH-DNA and other bulky aromatic adducts were associated with higher symptom scores of anxious/depressed at 4.8 years and attention problems at 4.8 and 7 years, in children born to nonsmoking women, the women's smoking status was based on cotinine level in cord blood [24]. In the study performed in Poland, Kraków higher (> 17.96 ng/m .…”

Section: Exposure To Bfrs and Children's Neurodevelopmentmentioning

confidence: 99%

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Exposure to widespread environmental toxicants and children’s cognitive development and behavioral problems

Jurewicz¹,

Polańska²,

Hanke³

2013

International Journal of Occupational Medicine and Environmental Health

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Nowadays a special attention is focused on prenatal and childhood exposures to a variety of contaminants in the environment, especially toxicants widely present in the environment and their impact on children's health and neurodevelopment. This article aims at evaluating the impact of exposure to several widespread toxicants including: polycyclic aromatic hydrocarbons (PAHs), phthalates, bisphenol A, brominated flame retardants and gas cooking on children's cognitive development and behavioral problems by reviewing most recent published literature. Epidemiological studies focusing on exposure to widespread toxicants and children's development for the last eleven years were identified by a search of the PubMed, Medline, Ebsco and Toxnet literature bases. The combination of following key words was used: 1) referring to the exposure: pregnancy, prenatal exposure, postnatal exposure, gas cooking, exposure to phthalates, bisphenol A, brominated flame retardants, PAHs and 2) referring to outcome: neurodevelopment, neurobehavior, psychomotor development, behavioral problems, cognitive development, mental health, school achievements, learning abilities. The results from the presented studies suggest that there are strong and rather consistent indications that the developing nervous system is particularly vulnerable to insult from low levels of exposure to widespread environmental contaminants such as: phthalates, bisphenol A, brominated flame retardants, polycyclic aromatic hydrocarbons, gas cooking. Considering the suggested health effects, more epidemiologic data is urgently needed and, in the meantime, precautionary policies must be implemented.

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Polycyclic Aromatic Hydrocarbons–Aromatic DNA Adducts in Cord Blood and Behavior Scores in New York City Children

Cited by 148 publications

References 56 publications

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Dose-dependent relationship between prenatal exposure to fine particulates and exhaled carbon monoxide in non-asthmatic children. A population-based birth cohort study

Exposure to widespread environmental toxicants and children’s cognitive development and behavioral problems

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