Columbia University Center for Children's
Environmental Health, New York City

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Principal Investigator: Frederica Perera

Overview	Results
Exposures and Outcomes	Community Partners
Research Projects	Selected Publications

Growth and Development Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes (1998-2008)

Exposure Project: Prenatal and Postnatal Urban Pollutants and Childhood Asthma (1998-2008)

Community Intervention Project: Reduction of Exposure and Risk from Pesticides and Allergens (1998-2008)

Mechanistic Research Project: In Utero Sensitization to Allergens and the Role of Environmental Pollutants in Development of Asthma (2003-2008)

Exposure and Outcomes

Primary Exposures: Urban air pollutants including fine particulates (PM 2.5), PAHs, diesel exhaust, environmental tobacco smoke (ETS), pesticides, pest allergens, endotoxins, lead, and mercury. Psychosocial stressors are also being considered as they can compound the health effects of these exposures.

Primary Outcomes: Asthma, neurocognitive development, cancer risk as evidenced by biomarkers

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Overview

Established in 1998, the Columbia Center for Children’s Environmental Health (CCCEH) conducts community-based research in New York City, Poland, and China to identify and prevent risks of neurodevelopmental impairment and childhood asthma from prenatal and early postnatal exposures to multiple common urban pollutants, to learn how these are contributing to rising rates of asthma, developmental delay and cancer risk and to prevent environmentally related disease in children. This is guided by the notion that relationships between exposures and outcomes can be understood only through a multi-level approach, incorporating molecular, individual and community sources of information on environmental, biological and social risk factors.

The Mothers & Newborns Cohort Study is the Center’s largest study, following over 700 mother-child pairs from predominantly low-income neighborhoods in Northern Manhattan and the South Bronx, through the children’s eighth birthdays. The study examines the respiratory health, cognitive development, and cancer risk in children prenatally exposed to common air pollutants: polycyclic aromatic hydrocarbons (PAHs), fine particulate matter (PM2.5) including diesel exhaust particulates (DEP), environmental tobacco smoke (ETS), pesticides, and home allergens from cockroaches, mice, and dust mites. The Center is conducting molecular epidemiologic cohort studies and laboratory-based research to further understand the development of disease, and investigators employ a unique combination of exposure measurement techniques, including personal air monitors to assess levels of pollutants in pregnant women’s air, and biomarkers in blood. Biomarkers are changes in molecular composition, structure, or function indicating exposure to, susceptibility to, or early damage from pollutants.

The Columbia Center is addressing both the causes of serious health problems in children and the urgent health needs of communities of color. The focus is on moving away from the approach of focusing on main effects of single pollutants to more complex evaluations of the combined effects of pollutants over a range of susceptibilities, within the social context. African-Americans and Latinos in these neighborhoods are at especially high risk for asthma, adverse birth outcomes, impaired development and some types of cancer, and also tend to have disproportionately heavy exposure to environmental pollutants known or suspected of contribute to adverse health outcomes such as lead and urban air pollutants.

An essential component of the Center’s research is community involvement, in which study participants, other local residents, and community organizations function as research partners. Scientists draw on the knowledge of the community to design research projects that address the needs and concerns of community members. The Columbia Center has forged a successful partnership with West Harlem Environmental Action, Inc. (WE ACT ) and nine other community organizations to identify and prevent environmental causes of childhood disease in northern Manhattan and the South Bronx. Through community workshops and newsletters, the Center relays study findings back to neighborhood parents and other primary caretakers of young children who can in turn help to reduce children’s exposure to harmful pollutants that can impede their healthy growth and development. The Center is also conducting home interventions to help families minimize allergens using lower-toxic pest control methods.

The Center is also conducting parallel prospective cohort studies of mothers and children in Poland and China, where coal burning is prevalent, and in downtown Manhattan, to evaluate effects of the World Trade Center destruction in 2001.

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Research Projects

Original Projects: 1998-2004

Growth and Development Project: Prenatal and Postnatal Urban Pollutants and their Effects on Fetal Growth and Cognitive Development
Research Results | Abstract | Progress Reports: 2002
Exposure Project: Prenatal and Postnatal Urban Pollutants and Childhood Asthma
Research Results | Abstract | Progress Reports: 2002
Community-Based Intervention: Reducing Risks of Asthma
Research Results | Abstract | Progress Reports: 2002

Current Projects: 2003-2008

Growth and Development Project: Prenatal and Postnatal Urban Pollutants and Neurobehavioral Developmental Outcomes

This community-based participatory research (CBPR) project is examining how prenatal exposure to air pollution, environmental tobacco smoke (ETS) and pesticides may adversely affect fetal growth, increase the risk of neurocognitive delay and impair children's learning ability as they enter school.

This project has several components. First, the project will determine the longer-term health consequences of prenatal exposure to environmental toxicants including PAHs, pesticides and ETS, which researchers have already seen to be detrimental to fetal growth and/or mental development at age two, indicating possible adverse effects on school readiness, neurobehavioral adjustment and ability to learn. Animal data on pesticides and human data on PCBs show that prenatal exposure can have irreversible long-term effects on child development and behavioral adjustment and that prenatal exposure come with greater risk than postnatal exposure. No comparable data is yet available in humans for the pollutants being studied by the Columbia Children's Center.

The cohort of children and families will be followed-up to the time of entry into school. The project is carrying out detailed assessment of neurobehavioral outcomes in over 400 children at age 5 and will determine school performance for 150 children reaching second grade (age 8) during the grant period. Because recent data suggests that social adversity and genetic and nutritional factors can modulate the effects of toxicant exposures, the Columbia Center has added new measures of stressors due to social adversity, including childhood stress levels and observed housing conditions.

A major strength of the Center is its ability to assess both neurodevelopmental and respiratory effects (including wheezing and asthma symptoms) of the same pollutants in the same children. Only a project that can follow the causes, pathways, and outcomes of both respiratory diseases and developmental problems can provide an understanding of the complex interrelationships of these conditions, in a community at high risk for both adverse health outcomes. In addition, studying both asthma and neurobehavioral outcomes in the same cohort is responsive to the needs of policy makers for data on multiple effects of the same pollutants and susceptibility factors that may determine the effects these pollutants have on a particular individual.

Original Funding Period (1998-2004): Abstract | 2002
Current Funding Period (2003-2008): Abstract | 2004 | 2005

Exposure Project: Prenatal and Postnatal Urban Pollutants and Childhood Asthma

The overall aim of this project is to identify risks of childhood asthma from prenatal and postnatal exposure to urban pollutants, including PAHs, ETS and allergens. A goal of the study is to characterize the roles played by environmental exposures in the development of atopy (allergy), persistent wheezing, asthma and/or increased asthma symptoms. Another goal is to determine interactions between environmental exposures and susceptibility factors, before birth and through ages 5-7, to the development of atopy and adverse respiratory outcomes. The research is documenting the biological triggers set in motion by environmental exposures as early as in utero that lead to asthma when children reach five through seven years of age.

The Exposure project is designed to parallel the Growth and Development project, using monitoring and biomarker data on exposures (air pollutants and ETS) and susceptibility factors (social stressors, genetic/metabolic polymorphisms and antioxidant vitamins) of interest to both projects.

This research stems from previous findings of associations between prenatal exposures and possible sensitization in utero, postnatal antigen-specific sensitization (elevated IgE), respiratory symptoms and early diagnosis of asthma by age two. These results indicate that prenatal exposures may be risk factors for irreversible asthma in childhood. This project is evaluating the effects of intrauterine and early childhood exposures on risk of clinically confirmed asthma at ages five through seven, as well as the effects of pest and new pet allergens, endotoxins and mold, and includes a comprehensive assessment of interactions between the contaminants and social, genetic and nutritional susceptibility factors on outcomes at ages five through seven, which includes genotyping and measures of psychosocial stress. This project is also addressing how the timing of exposures to environmental pollutants affects the risk and onset of asthma through school age and whether combined exposures have additive or multiplicative effects.

Original Funding Period (1998-2004): Abstract | 2002
Current Funding Period (2003-2008): Abstract | 2004 | 2005

Community Intervention Project: Reduction of Exposure and Risk from Pesticides and Allergens

This project, taking place in 300 apartments in both East Harlem and Brooklyn, seeks to provide data to show that building-wide Integrated Pest Management (IPM) is cost-effective over the long term and should be implemented at the citywide or even nationwide level of public housing maintenance. IPM is a pest control strategy that uses a variety of methods including sealing cracks and crevices, and only uses pesticides as a last resort and even then looks to use low-toxicity chemicals. This builds on the results of the pilot project which showed that IPM reduced cockroach populations in East Harlem housing at the three-month follow-up. This project will determine (1) how long IPM keeps pest levels reduced, (2) how long the physical repairs, sealing and caulking last before degrading, and (3) what type of maintenance schedule is necessary to maintain IPM.

Phase 2 of the project is studying 200 apartments in New York City Housing Authority buildings with problems such as mold and peeling paint. 100 of the apartments receive a standard inspection and maintenance for one year, and the other 100 are receiving enhanced inspection and remediation, along with tenant education. The effect of the intervention is being assessed by factors including pest populations, allergen levels, residence pesticide use and the health outcomes of residents with asthma. In addition, educational materials about ETS, pesticides and other environmental threats to children’s health (the Center’s Healthy Home, Healthy Child campaign) will be provided.

The project aims to determine the intervention’s long-term effect on family health, the best time interval for reporting the intervention and whether IPM can be a cost-effective alternative to aerosol pesticide application.

Original Funding Period (1998-2004): Abstract | 2002
Current Funding Period (2003-2008): Abstract | 2004 | 2005

Mechanistic Research Project: In Utero Sensitization to Allergens and the Role of Environmental Pollutants in Development of Asthma

To complement the exposure and asthma project, this research project is investigating the biological mechanisms through which prenatal exposure to major classes of pollutants being studied by the Columbia Children’s Center might increase the risk of asthma. This project was developed from earlier findings that in utero antigen-specific sensitization as well as elevated immunoglobulin E (IgE) antibody levels at age two and respiratory symptoms related to asthma are common in this cohort, and that prenatal exposure to PAHs, a major component of DEP, is associated with elevated IgE levels and respiratory symptoms at age two. IgE is a one of at least five kinds of immunoglobulins produced by the immune system and the main one which is involved in allergic reactions.

Using a mouse model, this project seeks: (1) to determine if in utero sensitization occurs to inhaled mold and cockroach allergens, (2) to determine whether in utero sensitization increases the risk for subsequent airway hyperreactivity and antigen-induced inflammation, and (3) to determine whether pollutants common in the northern Manhattan environment alter the risk for antigen-specific sensitization to these substances.

The aim is that this mouse model for prenatal sensitization to mold and cockroach allergens will lead to a better understanding of the individual and combined effects of urban environmental exposures on the development of asthma and mechanisms through which these effects are mediated. This could contribute to the development of better strategies for asthma prevention.

Current Funding Period (2003-2008): Abstract | 2004 | 2005

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Selected Results

Exposure

All of the pregnant women in the study and their babies had substantial and variable exposure to multiple toxic pollutants that are harmful to fetal growth and child development, such as airborne polycyclic aromatic hydrocarbons (PAHs). 43% had prenatal ETS exposure, verified by plasma levels of cotinine, a nicotine metabolite.

Common exposures include airborne PAHs from vehicular traffic, which are associated with levels of vehicle exhaust including indoor polycyclic aromatic hydrocarbons (PAHs). Outdoor diesel exhaust particle (DEP) levels are significantly associated with nearby traffic density.

All pregnant women in the study were also exposed to airborne pesticides during their third trimester of pregnancy, when fetal brain growth is at its peak. In addition, all of the babies in were born with detectable levels of one or more pesticides in cord blood samples.

Exposure to the organophosphate (OP) pesticides chlorpyrifos and diazinon has been markedly reduced as a result of the EPA ban on these chemicals for residential use in 2001 and the levels of these chemicals in prenatal air samples and maternal and cord blood showed significant declines.

Children in the study are commonly exposed in utero to high levels of cockroach and mouse allergens, as evidenced by biomarkers in cord blood. Not surprisingly, allergen levels, pest infestation, and pesticide concentrations were highest in more deteriorated housing conditions.

Growth and Development Project

Prenatal exposure to the pesticides chlorpyrifos and diazinon is associated with reduced birth weight; improved birth outcomes were evident in the cohort after the EPA’s ban of these pesticides for home use in 2000 and 2001.

Prenatal exposure to two household pesticides, chlorpyrifos and diazinon, which transfer readily to the fetus, reduced birth weight by an average of 6.6 ounces, the equivalent of weight reduction seen in babies born to women who smoked. (Whyatt et al., 2004)

Governmental regulation has immediate positive effects on children’s health. The Center’s Mothers & Children Study is the first to show benefits to newborns from the 2000/2001 EPA bans on the home use of the pesticides chlorpyrifos and diazinon. (Whyatt et al., 2004)

Combined exposure to multiple pollutants and psychosocial stressors has multiplicative harmful effects on fetal growth and cognitive development.

Newborns exposed prenatally both to high levels of PAHs (measured by PAH-DNA damage) and ETS had significantly lower birth weight and smaller head circumference than newborns without these combined exposures. (Perera et al, 2004a).

Prenatal exposure to ETS combined with chronic material hardship (unmet basic needs of food, clothing, adequate housing) was associated with significantly higher rates of developmental delay at two years of age compared to children who were prenatally exposed to ETS but whose families did not experience material hardship. This finding suggests that the harmful effects of ETS are exacerbated under conditions of deprivation, with cognitive outcomes similar to those associated with prenatal low-level lead exposure. (Rauh et al., 2004).

Infants with higher prenatal exposure to polycyclic aromatic hydrocarbons are born with genetic damage associated with increased cancer risk.

Approximately 40% of babies in the study were born with genetic damage associated with air pollution that can increase cancer risk. Of particular concern, newborns had higher levels of carcinogen-DNA adducts than mothers per unit of estimated exposure, indicating greater fetal susceptibility and potential risk from these pollutants. (Perera et al., 2004b)

Prenatal exposure to PAHs was associated with an increase in stable chromosomal alterations. This is the first study to show that environmental exposure during pregnancy to such pollutants can cause a low level of chromosomal abnormalities in fetal WBC. Such genetic alterations have been linked in other studies to increased risk of cancer in children and adults. (Bocskay et al, CEBP, 2005).

Prenatal exposure to air pollution, secondhand smoke, and pesticides adversely affects fetal growth, increasing risk of neurocognitive delay and impairing children’s learning ability as they enter school.

High exposure to airborne PAHs from fuel combustion decreased birth weight and head circumference among African-American infants in the study. Previous research shows that lower birth weight, even in the normal range, is associated with adverse effects on health and physical and cognitive development in childhood.

High exposure to the pesticide chlorpyrifos was associated with reduced birth weight and length (regardless of ethnicity), similar to the reductions typically seen in women who smoke during pregnancy.

Exposure to ETS was a risk factor both for lower birth weight and for reduced scores on a standardized test for mental development at age two years. Research shows that lower scores on the mental development test are associated with early school behavior problems, learning disabilities, and lower teachers’ ratings of academic performance. Almost one-third of children in the study who were prenatally exposed to ETS showed cognitive delay at two years of age.

The interactive effects of multiple exposures worsen these adverse fetal growth and postnatal cognitive functioning outcomes.

This research has found that combined exposure to multiple pollutants and psychosocial stressors has multiplicative effects on fetal growth and cognitive development. Newborns exposed prenatally both to high levels of PAHs (measured by PAH-DNA damage) and ETS had significantly lower birth weight and smaller head circumference than newborns without these combined exposures.

Similarly, prenatal exposure to ETS combined with chronic material hardship (unmet basic needs of food, clothing, and adequate housing) was associated with significantly higher rates of developmental delay at two years of age than in children who were prenatally exposed to ETS but whose families did not experience material hardship. This finding suggests that the harmful effects of ETS are exacerbated under conditions of deprivation, with cognitive outcomes similar to those associated with prenatal low-level lead exposure.

Prenatal exposure to the organophosphate pesticide chlorpyrifos is associated with delays in psychomotor and cognitive development as well as attentional disorders such as ADHD.

Children prenatally exposed to high levels of chlorpyrifos were significantly more likely than children exposed to low levels to experience delay in both psychomotor and cognitive development at 3 years of age. In addition, highly exposed children were significantly more likely than less exposed children to manifest symptoms of attentional disorders, Attention-deficit/Hyperactivity Disorder (ADHD), and pervasive personality disorder at age 3. Although the EPA banned residential use of chlorpyrifos in 2001, this pesticide is still widely used in agriculture (Rauh et al. 2006).

Exposure Project: Prenatal and Postnatal Urban Pollutants and Childhood Asthma

Prenatal exposure to the air pollutant, pyrene, appears to upregulate antigen-specific IgE production at a young age and may provide clues towards explaining the pathogenesis of asthma in inner city children.

Antibodies against mouse, cockroach and dust mite were detectable in 9.4, 8.7 and 3.6%, respectively, of children in the cohort as early as age 2 years. Increased pyrene exposure was associated with increased anti-mouse and dust mite IgE at age 2 years, but not with allergen-specific cytokine production, cord blood mononuclear cell proliferation or total IgE at birth. In addition, allergen-specific IgE levels greater than 0.35 IU/ml were significantly associated with cough and difficulty breathing at age 2 years (Miller et al., submitted).

Sensitization occurs in utero, children show allergic response to antigens at ages 2 and 3 years, and children living in more deteriorated housing have worse pest infestation and higher allergen levels.

Newborns show a high rate of sensitization to multiple inhalant indoor antigens, especially to cockroach as evidenced by over half of babies in the study being born with an immune response to cockroaches. (Miller et al., 2001)

There is evidence of cockroach, mouse, and rarely dust mite allergy as early as ages 2 and 3 years with 16% of 2-year-olds in the cohort having a positive allergen-specific IgE to at least one antigen. Increased prevalence of respiratory symptoms was observed among children with an increase in any of the three allergen-specific IgE’s measured. (Miller et al., 2004)

Pest infestation, allergen levels, and pesticide use remain higher among women and babies living in the most deteriorated housing. (Whyatt et al., 2002)

Multiple exposures increase respiratory symptoms and probable asthma diagnosis at ages 1 and 2 years.

Combined prenatal exposure to airborne PAHs and postnatal exposure to ETS results in increased respiratory symptoms at 1 year and increased respiratory symptoms and probable asthma diagnosis at 2 years of age. (Miller et al., 2004)

Birth order does not appear to be a risk factor for allergy symptoms and IgE.

Total sera IgE was detectable in 35% of the childrens cord blood and averaged 15 IU/ml, and 21 IU/ml at age 24 and 36 months, respectively. IgE was not significantly different at either age between children with and without older siblings. There were also no consistent associations between birth order and either wheeze, itchy eyes, or eczema at these ages. (Goldstein et al., 2005)

High prenatal exposure to certain PAHs increased the likelihood of children’s allergic response to cockroach, mouse, and dust mite allergens as measured by elevated IgE at two years of age; elevated IgE is an established predictor of asthma risk.

Combined and interactive effects of multiple environmental exposures also appear to increase children’s risk for asthma. Toddlers who were both prenatally exposed to PAHs and had postnatal exposure to ETS have higher rates of asthma precursor symptoms compared to toddlers who were not similarly exposed.

Community-Based Intervention: Reducing Risks of Asthma

Pest infestation and toxic pesticide use is prevalent in low-income housing.

Baseline measurements showed cockroaches in 77% of apartments and mice in 13%. 15% of residents reported using illegal pesticides to control pests.

Residents living in apartments with higher pest infestation are more likely to have physician diagnosed asthma.

37% of apartments had at least one resident with physician-diagnosed asthma. In senior-citizen buildings, apartments with high allergen levels had 6.6 greater odds of having an asthmatic resident, controlling for smoking, and other potential confounders. In family buildings, apartments with high cockroach allergen levels had 1.7 greater odds of having an asthmatic resident.

Low-toxicity IPM methods are effective at reducing pest infestation by half.

Initial analyses indicate that IPM succeeded in reducing cockroaches compared to control buildings at both 3 and 6 month follow-up. At 3-month follow-up, the number of cockroaches was reduced by 50% in 68% of apartments that received an IPM intervention, and 48% of controls. It appears that the effect of IPM may taper off slightly at 6-month follow-up, but IPM apartments still have greater reductions in cockroaches than control apartments.

Mechanistic Research Project

In utero sensitization to ovalbumin (OVA) occurs in mouse models. Data suggest that a pregnant mouse sensitized to OVA, and probably in the presence of a Th2-polarized state, can transfer an asthma-like phenotype to her offspring.

Offspring of mice sensitized and challenged with ovalbumin (OVA) exhibited increased airway hyperresponsiveness, increased allergic pulmonary inflammation, increased T cell proliferation, and increased levels of OVA-specific IgE compared to offspring of non-treated mice, similar to published reports.

Preliminary results suggest that in utero sensitization to environmental inhaled allergens may occur in the mouse model.

Offspring born to mothers exposed prenatally to the inhaled mold, aspergillus, (dose 12.5 or dose 25), developed increased airway hyperreactivity (AHR) and inflammatory cells in their bronchoalveolar fluid compared to naïve mice.

Fetal dendritic cells are found to be important mediators.

Offspring born to mothers exposed to bone marrow derived dendritic cells were found to have higher levels of total and ovalbumin-specific IgE.

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Community Partners

In collaboration with its Community Advisory Board, the priority for the Columbia Center for Children’s Environmental Health has been communication of study findings back to the communities in which the New York City study cohort of mothers and children reside, in ways that are meaningful and useful in daily life. The CCCEH collaborates with community organizations advocating for increased environmental justice in poorer neighborhoods located in northern Manhattan and the South Bronx. The coalition of eight direct service and environmental health advocacy organizations ensures that results from the scientific research are delivered to these communities in ways that are meaningful and usable in improving daily environmental health at home and in the larger neighborhood.

Community organizations working with the Columbia Center include:
Alianza Dominicana
Best Beginnings
For A Better Bronx
Harlem Dowling - West Side
Heart of Harlem
New York City Department of Education
Northern Manhattan Improvement Corporation
Northern Manhattan Perinatal Partnership
Nos Quedamos/We Stay
St. Mary's Episcopal Church
West Harlem Environmental Action (WE ACT)

The community health education campaign, Healthy Home Healthy Child (HHHC) , was developed by the Columbia Children's Center to share health information and prevention methods for air pollution, cigarette smoke, drugs & alcohol, garbage management, lead poisoning, nutrition and pesticides. The HHHC campaign has served to heighten awareness in the local community regarding health risks of environmental exposures and preventive behaviors to reduce exposures in households.

The Center has produced a series of newsletters for the Mothers and Newborns Study and the HHHC campaign with important information for parents about how to prevent children from being exposed to harmful substances including mercury and some types of pesticides. These newsletters include tips on how to reduce exposure, useful resources, and other important health information.

Mothers and Newborns Study: Protecting Your Children from Mercury – What You Can Do – Winter, 2007 (PDF) (4 pp., 392K)
Mothers and Newborns Study: Protecting Your Children from Pesticides – What You Can Do – Spring, 2007 (PDF) (4 pp., 312K)

The HHHC campaign has developed other written materials ("tip sheets") on topics including:

"Healthy Home Healthy Child" (PDF) (2pp., 221K)
"Cigarette Smoke" (PDF) (2pp., 72K)
"Lead Poisoning" (PDF) (2pp., 57K)
"Pesticides" (PDF) (2pp., 145Kb)

Selected Publications

Bocskay KA, Tang D, Orjuela MA, Liu X, Warburton DP, Perera FP. Chromosomal aberrations in cord blood are associated with prenatal exposure to carcinogenic polycyclic aromatic hydrocarbons. Cancer Epidemiology, Biomarkers & Prevention, 2005;14(2):506-11. Abstract | Full-Text (PDF) (7 pp, 122 K) | PubMed

This study suggests that a direct relationship between in utero environmental polycyclic aromatic hydrocarbons (PAHs) exposures and increased risk for childhood cancers may exist. Specifically, chromosomal aberrations, known to be linked with increased cancer risk in adults, were measured among 60 minority newborns from low-income neighborhoods of New York City. A significant association between prenatal PAH exposures measured in air (results of tobacco smoke or vehicle exhausts) and chromosomal aberrations was observed. Such results may influence critical environmental policy initiatives that could ultimately affect the health of children in many low-income urban communities.

Perera FP, Tang D, Tu YH, Cruz LA, Borjas M, Bernert T, Whyatt RM. Biomarkers in maternal and newborn blood indicate heightened fetal susceptibility to procarcinogenic DNA damage. Environmental Health Perspectives 2004;112(10):1133-1136. Abstract | Full-Text (PDF) (7 pp, 122 K) | PubMed

This study assessed fetal versus adult susceptibility to polycyclic aromatic hydrocarbons (PAHs) and environmental tobacco smoke (ETS). The authors observed DNA damage and concluded that a developing fetus is far more susceptible than an adult to the carcinogenic effects of PAHs. Furthermore, it was suggested that the developing fetus has less of an ability to repair damaged DNA as well as a reduced ability to clear ETS elements from their system, thus increasing a fetus’ overall susceptibility to the detrimental effects of these environmental constituents on children’s health.

Perera FP, Rauh V, Whyatt RM, Tsai WY, Tang D, Diaz D, Hoepner L, Barr D, Tu YH, Camann D, Kinney P. Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children. Environmental Health Perspectives 2006;114(8):1287-1292. Abstract | Full-Text (PDF) (7 pp, 122 K) | PubMed

This study focused on the association between prenatal polycyclic aromatic hydrocarbon (PAH) exposure and child mental and psychomotor development. Specifically, high prenatal PAH exposure was found to be directly associated with both lower mental development and overall cognitive developmental delays in children by age 3.

Rauh VA, Garfinkel R, Perera FP, Andrews H, Barr D, Whitehead D, Tang D, Whyatt RM 2006. Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first three years of life among inner-city children. Pediatrics, 2006 Dec;118(6):e1845-59. Epub 2006 Nov 20. Abstract | Full-Text(PDF) (6pp., 124Kb) | PubMed

This report examines cognitive and motor development at 12, 24, and 36 months as a function of chlorpyrifos (CPF) levels in umbilical cord plasma collected from the newborns at delivery. The authors found that children prenatally exposed to high CPF levels were significantly more likely than children exposed to low levels of CPF to experience delay in both psycho-motor and cognitive development at 36 months of age. In addition, highly exposed children were significantly more likely than less exposed children to exhibit symptoms of attentional disorders, ADHD, and pervasive personality disorder at 3 years of age.

Full List of Publications | Publications List from NIEHS PubMed Database