2008 Articles of the Month
The need for effective asthma management for all children.
Disparities in allergy testing and health outcomes among urban children with asthma
The researchers have found that many children, especially minorities, in urban areas are not receiving treatment for allergies and education on avoidance of household allergens as part of their comprehensive asthma management plans. To be effective, the information on specific allergic reactions in asthmatic children needs to be followed with taking precautions to avoid exposure to those allergens that are found to trigger asthma symptoms.
Jeanette A. Stingone
The Journal of Allergy and Clinical Immunology 122(4):748-753
Asthma has become a widespread disease affecting a significant portion of our children. An effective asthma management plan for each affected child is essential for protecting the child’s health and improving their quality of life. This study shows that many urban children with asthma are not receiving diagnoses or care for allergies that could improve their asthma symptoms.
Background: Previous research has found that treating allergies and reducing exposure to allergens can reduce asthma morbidity.
Objective: We sought to examine whether urban asthmatic children were receiving care for allergies as part of a comprehensive asthma management plan.
Methods: A cross-sectional study, consisting of a parent-reported questionnaire, was conducted in 26 randomly selected New York City public elementary schools during the 2002-2003 school year.
Results: In a sample of 5250 children aged 5 to 12 years, 13.0% were found to have current asthma. The prevalence of allergy diagnosis was 21.0%. Less than half (47.3%) of the subjects with current asthma reported a physician’s diagnosis of allergies.
The frequency of a reported allergy diagnosis varied with race/ethnicity, ranging from 14.4% in Mexican American children to 67.9% in white children. Only 54.9% of asthmatic children with an allergy diagnosis reported allergy testing. Children from lower-/middle-income households and children with public forms of health insurance were the least likely to report testing (adjusted odds ratios, 0.18 and 0.46). Higher frequencies of reported allergy testing were associated with education on allergen avoidance, use of allergy medications, lower exposure to household allergens, and lower prevalence of wheezing.
Conclusions: Many children do not receive comprehensive asthma treatment that includes management of allergies and education on avoidance of household allergens. Lower reported allergy testing might indicate lower access to medical care among middle-income families who are ineligible for public programs but who do not have the income to access higher quality care. Interventions aimed at improving medical care and adherence to treatment guidelines are necessary to decrease asthma morbidity.
Clinical Implications: Successful asthma management includes proper diagnosis of allergies and allergy testing. Allergy testing can be used to tailor allergen avoidance instruction and treatment and to guide patients to reduce exposure to allergens that can trigger asthma exacerbations.
Abstract available at: http://www.jacionline.org/article/S0091-6749(08)01456-5/abstract
Summarizes how aluminum and lead can affect the brain.
Aluminium and lead: molecular mechanisms of brain toxicity
Although the toxic nature of aluminum and lead are still not thoroughly understood, there are several common mechanisms through which these metals harm brain function. Both metals harm the nervous system by impairing cell signaling, neurotransmission, other essential cell functions, and causing oxidative stress, effects which may be interconnected and combine to produce negative health outcomes.
Sandra V. Verstraeten
Patricia I. Oteiza
Archives of Toxicology 2008 Jul 31. [Epub ahead of print]
Aluminum and lead have both emerged as health concerns for children. Aluminum exposure can occur through soil contamination and various industrial processes and products; it is also used in some vaccines as an additional ingredient that is supposed to enhance the vaccine’s effectiveness. It has been proposed that aluminum is associated with Alzheimer’s dementia and Parkinson’s disease.
Lead has been established as a major health concern for children. Lead exposure can occur through lead paint, toys, plastics in which lead is used as an additive, and other sources. Lead poisoning can result in decreased IQ, learning disabilities, behavioral problems, and mental retardation. This study highlights the common mechanisms through which both metals can negatively affect the brain.
The fact that aluminium (Al) and lead (Pb) are both toxic metals to living organisms, including human beings, was discovered a long time ago. Even when Al and Pb can reach and accumulate in almost every organ in the human body, the central nervous system is a particular target of the deleterious effects of both metals. Select human population can be at risk of Al neurotoxicity, and Al is proposed to be involved in the etiology of neurodegenerative diseases. Pb is a widespread environmental hazard, and the neurotoxic effects of Pb are a major public health concern. In spite of the numerous efforts and the accumulating evidence in this area of research, the mechanisms of Al and Pb neurotoxicity are still not completely elucidated. This review will particularly address the involvement of oxidative stress, membrane biophysics alterations, deregulation of cell signaling, and the impairment of neurotransmission as key aspects involved Al and Pb neurotoxicity.
Although we do not currently have any clear explanations for the neurotoxicity of aluminum and lead, there are several common denominators in aluminum and lead toxicities. Efforts to understand and prevent lead exposure and poisoning have received many more resources than similar efforts with aluminum. A greater investment is called for to understand aluminum exposure and method of toxicity so that we can have a better understanding of potential harm from aluminum exposure, if prevention efforts are called for, and if so, what are effective prevention efforts.
Full article available at: http://www.springerlink.com/content/n2577l6701144654/
Heavy Metals, Lead, Lead Poisoning, Neurotoxicants, Toxicology
How high traffic areas influence air quality and health.
Residential Traffic and Children's Respiratory Health
Living near a high traffic area, such as a major thorough thru like a highway, is associated with increased asthma in children. This study illustrates that pollution from a high traffic area can impact children’s health, even in a region considered to have overall good air quality.
Janice J. Kim
Environmental Health Perspectives 116(9):1274-1279
High traffic areas and the resulting exhaust emitted from cars is a significant source of air pollution. Living, working or going to school near a high traffic area has been associated with several health issues, including premature birth, asthma and cardiovascular diseases. This study looks at the influence nearby traffic areas have on children’s respiratory health in a region with good overall air quality.
Background: Living near traffic has been associated with asthma and other respiratory symptoms. Most studies, however, have been conducted in areas with high background levels of ambient air pollution, making it challenging to isolate an independent effect of traffic. Additionally, most investigations have used surrogates of exposure, and few have measured traffic pollutants directly as part of the study.
Objective: We conducted a cross-sectional study of current asthma and other respiratory symptoms in children (n = 1,080) living at varying distances from high-traffic roads in the San Francisco Bay Area, California, a highly urbanized region characterized by good regional air quality due to coastal breezes.
Methods: We obtained health information and home environmental factors by parental questionnaire. We assessed exposure with several measures of residential proximity to traffic calculated using geographic information systems, including traffic within a given radius and distance to major roads. We also measured traffic-related pollutants (nitrogen oxides and nitrogen dioxide) for a subset of households to determine how well traffic metrics correlated with measured traffic pollutants.
Results: Using multivariate logistic regression analyses, we found associations between current asthma and residential proximity to traffic. For several traffic metrics, children whose residences were in the highest quintile of exposure had approximately twice the adjusted odds of current asthma (i.e., asthma episode in the preceeding 12 months) compared with children whose residences were within the lowest quintile. The highest risks were among those living within 75 m of a freeway/highway. Most traffic metrics correlated moderately well with actual pollutant measurements.
Conclusion: Our findings provide evidence that even in an area with good regional air quality, proximity to traffic is associated with adverse respiratory health effects in children.
Full article available at: http://www.ehponline.org/members/2008/10735/10735.html
Air Pollutants, Outdoor Air Quality
How lead exposure and genes play a role in lead poisoning.
Variants in Iron Metabolism Genes Predict Higher Blood Lead Levels in Young Children
Genes that influence how the body handles (metabolizes) iron can also influence how the body processes lead. This study shows certain genetic variations affecting iron metabolism are also associated with increased blood lead levels in children, suggesting there is an increased risk of lead poisoning for some individuals.
Marianne R. Hopkins
Adrienne S. Ettinger
Martha María Téllez-Rojo
Robert O. Wright
Environmental Health Perspectives 116(9):1261-1266
Elevated lead levels in children is an issue of concern because it can cause decreased IQ, learning disabilities, delayed development, and seizures, among other health ailments. Sources of lead in the environment have decreased with the removal of lead-based paint and leaded gasoline from many markets. However, children are still exposed to lead through a variety of sources, including dust and chips from lead-based paint in older homes and other buildings, lead water pipes, and toys. This study explores how genetics combine with environmental exposures to influence lead levels in the body.
Background: Given the association between iron deficiency and lead absorption, we hypothesized that variants in iron metabolism genes would predict higher blood lead levels in young children.
Objective: We examined the association between common missense [[genetic]] variants in the hemochromatosis (HFE) and transferrin (TF) genes and blood lead levels in 422 Mexican children.
Methods: Archived umbilical cord blood samples were genotyped for HFE (H63D and C282Y) and TF (P570S) variants. Blood lead was measured at 24, 30, 36, 42, and 48 months of age. A total of 341 subjects had at least one follow-up blood lead level available and data available on covariates of interest for inclusion in the longitudinal analyses. We used random-effects models to examine the associations between genotype (HFE, TF, and combined HFE + TF) and repeated measures of blood lead, adjusting for maternal blood lead at delivery and child's concurrent anemia status.
Results: Of 422 children genotyped, 17.7, 3.3, and 18.9% carried the HFEH63D, HFEC282Y, and TFP570S [[genetic]] variants, respectively. One percent of children carried both the HFE C282Y and TF P570S variants, and 3% of children carried both the HFE H63D and TF P570S variants. On average, carriers of either the HFE (β = 0.11, p = 0.04) or TF (β = 0.10, p = 0.08) variant had blood lead levels that were 11% and 10% higher, respectively, than wild-type subjects. In models examining the dose effect, subjects carrying both variants (β = 0.41, p = 0.006) had blood lead 50% higher than wild-type subjects and a significantly higher odds of having a blood lead level > 10 µg/dL (odds ratio = 18.3; 95% confidence interval, 1.9–177.1).
Conclusions: Iron metabolism gene variants modify lead metabolism such that HFE variants are associated with increased blood lead levels in young children. The joint presence of variant alleles in the HFE and TF genes showed the greatest effect, suggesting a gene-by-gene-by-environment interaction.
Full article available at: http://www.ehponline.org/members/2008/11233/11233.html
Further discussion of this article is available at: http://www.ehponline.org/docs/2008/116-9/ss.html#meta
Lead, Lead Poisoning
How cell phones may impact the behavior of young children.
Prenatal and Postnatal Exposure to Cell Phone Use and Behavioral Problems in Children
Cell phone exposure, especially prenatal exposure, is associated with behavioral problems in school-aged children. The associated behavioral difficulties include emotional, conduct, hyperactivity and peer problems. These associations highlight the potential affects radiofrequency fields may have on public health.
Hozefa A. Divan
Cell phone technology and use has quickly become widespread. However, despite the commonplace use of cell phones, little is known about the impacts this technology may have on those that are the most vulnerable, children. This study illustrates the need for precaution and further research on radiofrequency fields emitted by cell phones and similar devices.
Background: The World Health Organization has emphasized the need for research into the possible effects of radiofrequency fields in children. We examined the association between prenatal and postnatal exposure to cell phones and behavioral problems in young children.
Methods: Mothers were recruited to the Danish National Birth Cohort early in pregnancy. When the children of those pregnancies reached 7 years of age in 2005 and 2006, mothers were asked to complete a questionnaire regarding the current health and behavioral status of children, as well as past exposure to cell phone use. Mothers evaluated the child’s behavior problems using the Strength and Difficulties Questionnaire.
Results: Mothers of 13,159 children completed the follow-up questionnaire reporting their use of cell phones during pregnancy as well as current cell phone use by the child. Greater odds ratios for behavioral problems were observed for children who had possible prenatal or postnatal exposure to cell phone use. After adjustment for potential confounders, the odds ratio for a higher overall behavioral problems score was 1.80 (95% confidence interval = 1.45–2.23) in children with both prenatal and postnatal exposure to cell phones.
Conclusions: Exposure to cell phones prenatally - and, to a lesser degree, postnatally - was associated with behavioral difficulties such as emotional and hyperactivity problems around the age of school entry. These associations may be noncausal and may be due to unmeasured confounding. If real, they would be of public health concern given the widespread use of this technology.
This preliminary research raises the question of what government policies are or should be in place to assure that children are appropriately and adequately protected from unknown or unstudied hazards of new technologies.
Abstract available at: http://www.epidem.com/pt/re/epidemiology/abstract.00001648-200807000-00001.htm
Electric and Magnetic Fields (EMFs), Prenatal Exposures
How common household materials can affect indoor air quality and children’s health.
Indoor Residential Chemical Emissions as Risk Factors for Respiratory and Allergic Effects in Children: A Review
Evidence shows many residential materials, such as particleboard and plastics, may be decreasing indoor air quality and impacting respiratory health and allergies in children. These common but less recognized risk factors need to be further researched and addressed to aid in the implementation of preventive actions.
Indoor Air 17:259-277
Many infants and children spend the majority of their time indoors. It has been documented that it is not unusual for indoor air to be of poorer quality than outdoor air. Poor air quality and chemical exposures can impact children’s health by causing and/or triggering asthma, respiratory illnesses and allergies. While some sources of poor indoor air quality, such as mold, have been well studied, other elements of our built environment have been given less attention. This study calls for a wider consideration of indoor air quality risk factors and identifies a need for further research.
Most research into effects of residential exposures on respiratory health has focused on allergens, moisture/mold, endotoxin, or combustion products. A growing body of research from outside the US; however, has associated chemical emissions from common indoor materials with risk of asthma, allergies, and pulmonary infections. This review summarizes 21 studies in the epidemiologic literature on associations between indoor residential chemical emissions, or emission-related materials or activities, and respiratory health or allergy in infants or children. Associations, some strong, were reported between many risk factors and respiratory or allergic effects. Risk factors identified most frequently included formaldehyde or particleboard, phthalates or plastic materials, and recent painting. Findings for other risk factors, such as aromatic and aliphatic chemical compounds [[e.g. chemicals found in adhesives, PVC flooring and carpeting]], were limited but suggestive. Elevated risks were also reported for renovation and cleaning activities, new furniture, and carpets or textile wallpaper. Reviewed studies were entirely observational, limited in size, and variable in quality, and specific risk factors identified may only be indicators for correlated, truly causal exposures. Nevertheless, overall evidence suggests a new class of residential risk factors for adverse respiratory effects, ubiquitous in modern residences, and distinct from those currently recognized. It is important to confirm and quantify any risks, to motivate and guide necessary preventive actions.
Practical Implications: Composite wood materials that emit formaldehyde, flexible plastics that emit plasticizers, and new paint have all been associated with increased risks of respiratory and allergic health effects in children. Although causal links have not been documented, and other correlated indoor-related exposures may ultimately be implicated, these findings nevertheless point to a new class of little recognized indoor risk factors for allergic and respiratory disease, distinct from the current set of indoor risk factors. The available evidence thus raises initial questions about many common residential practices: for instance, using pressed wood furnishings in children's bedrooms, repainting infant nurseries, and encasing mattresses and pillows with vinyl for asthmatic children. The findings summarized here suggest a need for substantially increased research to replicate these findings, identify causal factors, and validate preventive strategies.
This review article reinforces the need for a legal framework, standards and enforcement mechanism for indoor air/environmental quality and for commercial/consumer/ construction products commonly used in indoor environments. Parents and other caregivers do not know what constitutes healthy indoor air, nor do they have a right to know in advance of hazards at school or child care, nor do they have recourse or interventions to protecting their children when they suspect or have proof that poor indoor air quality is harming their child.
Federal standards exist for many outdoor air pollutants. But no indoor air/environmental quality standard exists for children at home, at school/child care, or in other indoor environments. Addressing indoor air quality is challenging. The U.S. Environmental Protection Agency has an active and successful indoor environments program, focused on voluntary efforts and market-based approaches. Congress needs to give the agency the legislative authority to set standards and enforce them, as well as promote better product stewardship and more disclosure about products used indoors.
Full article available courtesy of the publisher at: http://www3.interscience.wiley.com/cgi-bin/fulltext/118513148/HTMLSTART
Air Pollutants, Asthma, Indoor Air Quality, Respiratory Diseases
How air quality during pregnancy can influence the health of children.
Prenatal Exposure to Wood Fuel Smoke and Low Birth Weight
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.
Amna R. Siddiqui
Ellen B. Gold
Kenneth H. Brown
Zulfiqar A. Bhutta
Environmental Health Perspectives 116(4):543-549
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.
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.
Full article available at http://www.ehponline.org/members/2008/10782/10782.html
Air Pollutants, Low Birth Weight, Prenatal Exposures
How diet can impact the amount of pesticides children take into their bodies.
Dietary Intake and Its Contribution to Longitudinal Organophosphorus Pesticide Exposure in Urban/Suburban Children
Dana B. Barr
Melanie A. Pearson
Lance A. Waller
Environmental Health Perspectives 116(4):537-542
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.
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.
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?
Full article available at http://www.ehponline.org/members/2008/10912/10912.html
Food Safety & Nutrition, Pesticides
The link between infant lead exposure and the development of Alzheimer’s disease later in life.
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
Md. Riyaz Basha
David P. Cox
Christopher A. McPherson
Deborah C. Rice
Debomoy K. Lahiri
Nasser H. Zawia
Journal of Neuroscience 28(1):3-9
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.
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.
Full article available courtesy of the Journal of Neuroscience at http://www.jneurosci.org/cgi/content/full/28/1/3
Disease Susceptibility, Lead
New environmental health approaches focusing on how substances in the environment, such as pollutants, can interact with genes to influence health and disease.
Environmental Exposures and Gene Regulation in Disease Etiology
Thea M. Edwards
John Peterson Myers
Environmental Health Perspectives 115(9): 1264-1270
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.
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.
Full article available at http://www.ehponline.org/members/2007/9951/9951.html
Chemicals, Disease Susceptibility, Fetal origins of disease