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CHILDREN'S ENVIRONMENTAL HEALTH ARTICLE
OF THE MONTH
Welcome to the Children’s Environmental Health Article of the Month! The Article of the Month is a communication tool geared toward increasing communication both within and outside of the field of children’s environmental health. The Article of the Month is designed to highlight the science-base of current children’s environmental health issues, clearly translating scientific findings to families, educators, health care professionals and many more.
JUNE 2008
Topic
How air quality during pregnancy can influence the health of children.
Title
Prenatal Exposure to Wood Fuel Smoke and Low Birth Weight
Conclusion
Cooking with wood fuel during pregnancy, a potentially modifiable exposure, was associated with low birth weight and marginally lower mean birth weight compared with using natural gas as a fuel.
Author(s)
Amna R. Siddiqui
Ellen B. Gold
Xiaowei Yang
Kiyoung Lee
Kenneth H. Brown
Zulfiqar A. Bhutta
Citation
Environmental Health Perspectives 116(4):543-549
Context
A child’s first environment, the womb, is influenced by the mother’s surroundings. One factor during pregnancy that can impact a baby’s health is air quality. One cause of poor air quality, tobacco smoke, has been a leading cause of low birth weight for infants. Low birth weight is tied to a range of ailments impacting a child’s development, including high mortality rates, impaired growth and chronic disease. There are many potential sources of poor air quality beyond tobacco smoke. Wood is used as a primary fuel source in many parts of the world, often for cooking, releasing wood smoke into the surrounding environment. This study further strengthens evidence that an expectant mother’s exposure to wood smoke is associated with low birth weight.
Abstract
Background: Maternal exposure to wood fuel smoke may lead to impaired fetal growth due to hypoxia and or oxidative stress from smoke constituents such as carbon monoxide and particulate matter.
Objectives: We studied the risk of low birth weight (LBW) and reduced mean birth weight in relation to reported use of wood for cooking during the prenatal period, compared with natural gas (NG).
Methods: We studied a historical cohort of women who had a singleton live birth in the years 2000–2002, from a semirural area of Pakistan. Infant's birth weight was obtained from records, and prenatal records had data for maternal body mass index and parity [[the number of times a woman has given birth]]. Cooking habits, daytime sleep habits, and type of fuel used during the pregnancies in 2000–2002 were ascertained by a survey done in 2004–2005. We performed multiple linear and logistic regression modeling using propensity scores to adjust for confounding variables.
Results: Unadjusted mean (± SD) birth weight was 2.78 ± 0.45 kg [[kilograms]] in wood users, and 2.84 ± 0.43 kg (p < 0.06) in NG users. Infants born to wood users averaged 82 g [[grams]] lighter than infants born to NG users when weight was adjusted for confounders (p < 0.07). The rate of LBW (< 2,500 g) was 22.7% among wood users compared with 15.0% in NG users (p < 0.01), for an adjusted relative risk of 1.64 (95% confidence interval, 1.10–2.34). The population attributable risk for LBW explained by wood use was estimated to be 24%.
Conclusion: Cooking with wood fuel during pregnancy, a potentially modifiable exposure, was associated with LBW and marginally lower mean birth weight compared with using NG.
Web link
Full article available at http://www.ehponline.org/members/2008/10782/10782.html
Keywords
Air Pollutants, Low Birth Weight, Prenatal Exposures
MAY 2008
Topic
How diet can impact the amount of pesticides children take into their bodies.
Title
Dietary Intake and Its Contribution to Longitudinal Organophosphorus Pesticide Exposure in Urban/Suburban Children
Author(s)
Chensheng Lu
Dana B. Barr
Melanie A. Pearson
Lance A. Waller
Citation
Environmental Health Perspectives 116(4):537-542
Context
Modern agriculture often relies on pesticides to control unwanted insects, competing plants, and other organisms that can reduce the yield of a crop. The use of pesticides on crops leaves pesticide residues on food, which children and adults take into their bodies when they eat. However, organic crops are grown using little or no chemicals. This study shows that children’s exposure to a particular class of pesticides, organophosphates, can be greatly reduced by changing their diet to organic fruits and vegetables.
Abstract
Background: The widespread use of organophosphorus (OP) pesticides has led to frequent exposure in adults and children. Because such exposure may cause adverse health effects, particularly in children, the sources and patterns of exposure need to be studied further.
Objectives: We assessed young urban/suburban children's longitudinal exposure to OP pesticides in the Children's Pesticide Exposure Study (CPES) conducted in the greater Seattle, Washington, area, and used a novel study design that allowed us to determine the contribution of dietary intake to the overall OP pesticide exposure.
Methods: Twenty-three children 3–11 years of age who consumed only conventional diets were recruited for this 1-year study conducted in 2003–2004. Children switched to organic diets for 5 consecutive days in the summer and fall sampling seasons. We measured specific urinary metabolites for malathion, chlorpyrifos, and other OP pesticides in urine samples collected twice daily for a period of 7, 12, or 15 consecutive days during each of the four seasons.
Results: By substituting organic fresh fruits and vegetables for corresponding conventional food items, the median urinary metabolite concentrations were reduced to nondetected or close to nondetected levels for malathion and chlorpyrifos at the end of the 5-day organic diet intervention period in both summer and fall seasons. We also observed a seasonal effect on the OP urinary metabolite concentrations, and this seasonality corresponds to the consumption of fresh produce throughout the year.
Conclusions: The findings from this study demonstrate that dietary intake of OP pesticides represents the major source of exposure in young children.
Policy implications
This study reinforces the need for child-focused pesticide regulatory policies. It illustrates that caregivers with the resources, interest and ability to provide organic foods for their children can measurably decrease their child's exposure to potentially harmful pesticides. But all children deserve this additional measure of protection. Our pesticide regulations are capable of doing so (such as by further lowering acceptable pesticide residue levels on foods, eliminating neurotoxic pesticides from food use, etc.). Specifically, the article underscores the importance of maintaining and expanding the Food Quality Protection Act -- legislation adopted in 1996 which began the process of assuring that children and other vulnerable populations are adequately considered and protected in pesticide regulation.
The study also raises the question of exposures through foods provided in institutional settings (schools, hospitals, etc.) and through programs such as the Federal Special Supplemental Nutrition Program for Women, Infants, and Children (WIC).
An additional question raised by this study's authors is that the level of children's exposure to pesticides in their diet may be associated with the foods country of origin -- are imported foods adequately checked to assure that they meet U.S. standards?
Web link
Full article available at http://www.ehponline.org/members/2008/10912/10912.html
Keywords
Food Safety & Nutrition, Pesticides
APRIL 2008
Topic
The link between infant lead exposure and the development of Alzheimer’s disease later in life.
Title
Alzheimer’s Disease (AD)-Like Pathology in Aged Monkeys after Infantile Exposure to Environmental Metal Lead (Pb): Evidence for a Developmental Origin and Environmental Link for AD
Author(s)
Jinfang Wu
Md. Riyaz Basha
Brian Brock
David P. Cox
Fernando Cardozo-Pelaez
Christopher A. McPherson
Jean Harry
Deborah C. Rice
Bryan Maloney
Demao Chen
Debomoy K. Lahiri
Nasser H. Zawia
Citation
Journal of Neuroscience 28(1):3-9
Context
Alzheimer’s disease commonly occurs in older adults causing deterioration of the brain leading to dementia and death. Building on evidence that exposure to particular substances early in life can influence the adult onset of disease, the authors explore the long-term impacts of lead exposure in infants in relation to Alzheimer’s disease. Using animal models to follow subjects from exposure through maturity, the researchers find early lead exposure increases the expression of Alzheimer’s disease-related genes later in life, illustrating the role environmental and genetic factors may both play together in the disease.
Abstract
The sporadic nature of Alzheimer's disease (AD) argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and the period of their action are unknown. Recent studies in rodents have shown that exposure to lead (Pb) during brain development predetermined the expression and regulation of the amyloid precursor protein (APP) and its amyloidogenic β-amyloid (Aβ) product in old age. Here, we report that the expression of AD-related genes [APP, BACE1 (β-site APP cleaving enzyme 1)] as well as their transcriptional regulator (Sp1) were elevated in aged (23-year-old) monkeys exposed to Pb as infants. Furthermore, developmental exposure to Pb altered the levels, characteristics, and intracellular distribution of Aβ staining and amyloid plaques in the frontal association cortex. These latent effects were accompanied by a decrease in DNA methyltransferase activity and higher levels of oxidative damage to DNA, indicating that epigenetic imprinting in early life influenced the expression of AD-related genes and promoted DNA damage and pathogenesis. These data suggest that AD pathogenesis is influenced by early life exposures and argue for both an environmental trigger and a developmental origin of AD.
Web link
Full article available courtesy of the Journal of Neuroscience at http://www.jneurosci.org/cgi/content/full/28/1/3
Keywords
Disease Susceptibility, Lead
MARCH 2008
Topic
New environmental health approaches focusing on how substances in the environment, such as pollutants, can interact with genes to influence health and disease.
Title
Environmental Exposures and Gene Regulation in Disease Etiology
Author(s)
Thea M. Edwards
John Peterson Myers
Citation
Environmental Health Perspectives 115(9): 1264-1270
Context
Environmental factors, especially contaminants, have been increasingly shown to influence human health. Endocrine (hormone) disruption is an example of how chemicals in the environment can affect the body, influencing development, growth, maturation, and reproduction by mimicking hormones or interacting with hormone receptors. The ability of environmental factors to alter gene expression and regulation is explored in this article.
Abstract
Objective: Health or disease is shaped for all individuals by interactions between their genes and environment. Exactly how the environment changes gene expression and how this can lead to disease are being explored in a fruitful new approach to environmental health research, representative studies of which are reviewed here.
Data sources: We searched Web of Science and references of relevant publications to understand the diversity of gene regulatory mechanisms affected by environmental exposures with disease implications.
Data synthesis: Pharmaceuticals, pesticides, air pollutants, industrial chemicals, heavy metals, hormones, nutrition, and behavior can change gene expression through a broad array of gene regulatory mechanisms. Mechanisms include regulation of gene translocation, histone modifications, DNA methylation, DNA repair, transcription, RNA stability, alternative RNA splicing, protein degradation, gene copy number, and transposon activation. Furthermore, chemically induced changes in gene regulation are associated with serious and complex human diseases, including cancer, diabetes and obesity, infertility, respiratory diseases, allergies, and neurodegenerative disorders such as Parkinson and Alzheimer diseases. One of the best-studied areas of gene regulation is epigenetics, especially DNA methylation. Our examples of environmentally induced changes in DNA methylation are presented in the context of early development, when methylation patterns are initially laid down. This approach highlights the potential role for altered DNA methylation in fetal origins of adult disease and inheritance of acquired genetic change.
Conclusions: The reviewed studies indicate that genetic predisposition for disease is best predicted in the context of environmental exposures. Second, the genetic mechanisms investigated in these studies offer new avenues for risk assessment research. Finally, we are likely to witness dramatic improvements in human health, and reductions in medical costs, if environmental pollution is decreased.
Web link
Full article available at http://www.ehponline.org/members/2007/9951/9951.html
Keywords
Chemicals, Disease Susceptibility, Fetal origins of disease
