Associated Faculty, NYU Wagner; Associate Professor, NYU School of Medicine
Leonardo Trasande, MD, MPP is an internationally renowned leader in children’s environmental health. His research focuses on identifying the role of environmental exposures in childhood obesity and cardiovascular risks, and documenting the economic costs for policy makers of failing to prevent diseases of environmental origin in children proactively. He also holds appointments in the Wagner School of Public Service and NYU’s College of Global Public Health. He is perhaps best known for a series of studies published in Lancet Diabetes and Endocrinology and the Journal of Clinical Endocrinology and Metabolism that document disease costs due to endocrine disrupting chemicals in the US and Europe of $340 billion and €163 billion annually, respectively.
Dr. Trasande leads one of 35 centers across the country as part of the National Institute of Health’s Environmental Influences on Child Health Outcomes program. He is leveraging the NYU Children’s Health and Environment Study as well as another birth cohort to examine phthalates, bisphenols, organophosphate pesticides and polycyclic aromatic hydrocarbons and their effects on fetal as well as postnatal growth and early cardiovascular and renal risks. These two cohorts are part of a larger initiative nationally to identify preventable and environmental factors that influence child health and disease.
He is Principal Investigator on numerous other NIH-funded projects. These include a study on prenatal and childhood phthalate and bisphenol exposures in Generation R (a Dutch birth cohort) to examine obesity and cardiovascular risks, as well as another project studying the effect of these dietary contaminants in children with chronic kidney disease, with the hypothesis that these exposures create oxidant stress and accelerate disease progression. He is also Principal Investigator for a research project comparing neurodevelopment, cardiometabolic and respiratory profiles of children exposed in utero to the World Trade Center disaster to a comparison group.
He has served as a member of numerous scientific committees and expert panels, including: the American Academy of Pediatrics’ Executive Committee of the Council for Environmental Health; the Science and Technical Advisory Committee for the World Trade Center Health Program; the National Children’s Study Methodological Review Panel of the National Academy of Sciences; the United Nations Environment Programme Steering Committee on a Global Outlook for Chemicals; and the Board of Scientific Counselors for the National Center for Environmental Health at the Centers for Disease Control and Prevention (CDC).
After receiving his bachelor, medical and public policy degrees from Harvard, he completed the Boston Combined Residency in Pediatrics and a legislative fellowship in the Office of Senator Hillary Rodham Clinton. Prior to coming to NYU, he completed fellowship training in environmental pediatrics. For five years he also was a Lead Investigator in one of the original (Vanguard) locations of the National Children's Study, and Deputy Director for the largest (eight location) Study Center spanning a region from upstate New York to central New Jersey.
Increasing evidence from laboratory and human studies shows that synthetic chemicals contribute to disease and dysfunction across the life course. Of particular emerging concern is the disruption of the hormonal process that has been found to be associated with increasing rates of obesity, diabetes, neurodevelopmental disabilities, infertility, and breast and prostate cancers.1 Given the magnitude of human and economic burden associated with these conditions, it might be expected that the passage of bipartisan legislation in both houses of Congress to update the Toxic Substances Control Act (TSCA) for the first time in 40 years would meet with widespread approval by the public health and medical community.
BACKGROUND: Di-2-ethylhexylphthalate (DEHP) is an environmental chemical commonly found in processed foods. Phthalate exposures, in particular to DEHP, have been associated with insulin resistance in adults, but have not been studied in adolescents.
Using cross-sectional data from 766 fasting 12- to 19-year-olds in the 2003-2008 NHANES, we examined associations of phthalate metabolites with continuous and categorical measures of homeostatic model assessment of insulin resistance (HOMA-IR).
Controlling for demographic and behavioral factors, diet, continuous age, BMI category, and urinary creatinine, for each log (roughly threefold) increase in DEHP metabolites, a 0.27 increase (95% confidence interval 0.14-0.40; P < .001) in HOMA-IR was identified. Compared with the first tertile of DEHP metabolite in the study population (14.5% insulin resistant), the third tertile had 21.6% prevalence (95% confidence interval 17.2%-26.0%; P = .02). Associations persisted despite controlling for bisphenol A, another endocrine-disrupting chemical commonly found in foods, and HOMA-IR and insulin resistance were not significantly associated with metabolites of lower molecular weight phthalates commonly found in cosmetics and other personal care products.
Urinary DEHP concentrations were associated with increased insulin resistance in this cross-sectional study of adolescents. This study cannot rule out the possibility that insulin-resistant children ingest food with higher phthalate content, or that insulin-resistant children excrete more DEHP.
In January 1996, Congress passed an appropriations bill amendment prohibiting the US Centers for Disease Control and Prevention (CDC) from using “funds made available for injury prevention … to advocate or promote gun control.” This provision was triggered by evidence linking gun ownership to health harms, created uncertainty among CDC officials and researchers about what could be studied, and led to significant declines in funding. We evaluated the change in the number of publications on firearms in youth compared with research on other leading causes of death before and after the Congressional action. We focused on children and adolescents because they disproportionately experience gun violence and injury.
OBJECTIVES: To assess associations of caesarean section with body mass from birth through adolescence.
DESIGN: Longitudinal birth cohort study, following subjects up to 15 years of age.
SETTING AND PARTICIPANTS: Children born in 1991-1992 in Avon, UK who participated in the Avon Longitudinal Study of Parents and Children (ALSPAC) (n=10 219).
OUTCOME MEASURES: Primary outcome: standardized measures of body mass (weight-for length z-scores at 6 weeks, 10 and 20 months; and body mass index (BMI) z-scores at 38 months, 7, 9, 11 and 15 years). Secondary outcome: categorical overweight or obese (BMI 85th percentile) for age and gender, at 38 months, 7, 9, 11 and 15 years.
RESULTS: Of the 10 219 children, 926 (9.06%) were delivered by caesarean section. Those born by caesarean had lower-birth weights than those born vaginally (-46.1 g, 95% confidence interval(CI): 14.6-77.6 g; P=0.004). In mixed multivariable models adjusting for birth weight, gender, parental body mass, family sociodemographics, gestational factors and infant feeding patterns, caesarean delivery was consistently associated with increased adiposity, starting at 6 weeks (+0.11 s.d. units, 95% CI: 0.03-0.18; P=0.005), through age 15 (BMI z-score increment+0.10 s.d. units, 95% CI: 0.001-0.198; P=0.042). By age 11 caesarean-delivered children had 1.83 times the odds of overweight or obesity (95% CI: 1.24-2.70; P=0.002). When the sample was stratified by maternal pre-pregnancy weight, the association among children born of overweight/obese mothers was strong and long-lasting. In contrast, evidence of an association among children born of normal-weight mothers was weak.
CONCLUSION: Caesarean delivery is associated with increased body mass in childhood and adolescence. Research is needed to further characterize the association in children of normal weight women. Additional work is also needed to understand the mechanism underlying the association, which may involve relatively enduring changes in the intestinal microbiome.
Background: Phthalates have antiandrogenic effects and may disrupt lipid and carbohydrate metabolism. Racial/ethnic subpopulations have been documented to have varying urinary phthalate concentrations and prevalences of childhood obesity.
Objective: We examined associations between urinary phthalate metabolites and body mass outcomes in a nationally representative sample of U.S. children and adolescents.
Methods: We performed stratified and whole-sample cross-sectional analyses of 2,884 children 6–19 years of age who participated in the 2003–2008 National Health and Nutrition Examination Survey. Multivariable linear and logistic analyses of body mass index z-score, overweight, and obesity were performed against molar concentrations of low-molecular-weight (LMW), high-molecular-weight (HMW), and di-2-ethylhexylphthalate (DEHP) metabolites, controlling for sex, television watching, caregiver education, caloric intake, poverty–income ratio, race/ethnicity, serum cotinine, and age group. We used sensitivity analysis to examine robustness of results to removing sample weighting, normalizing phthalate concentrations for molecular weight, and examining different dietary intake covariates.
Results: In stratified, multivariable models, each log unit (roughly 3-fold) increase in LMW metabolites was associated with 21% and 22% increases in odds (95% CI: 1.05–1.39 and 1.07–1.39, respectively) of overweight and obesity, and a 0.090-SD unit increase in BMI z-score (95% CI: 0.003–0.18), among non-Hispanic blacks. Significant associations were not identified in any other racial/ethnic subgroup or in the study sample as a whole after controlling for potential confounders, associations were not significant for HMW or DEHP metabolites, and results did not change substantially with sensitivity analysis.
Conclusions: We identified a race/ethnicity–specific association of phthalates with childhood obesity in a nationally representative sample. Further study is needed to corroborate the association and evaluate genetic/epigenomic predisposition and/or increased phthalate exposure as possible explanations for differences among racial/ethnic subgroups.
Bisphenol A (BPA), a manufactured chemical, is found in canned food, polycarbonate-bottled liquids, and other consumer products. In adults, elevated urinary BPA concentrations are associated with obesity and incident coronary artery disease. BPA exposure is plausibly linked to childhood obesity, but evidence is lacking to date.
To examine associations between urinary BPA concentration and body mass outcomes in children.
DESIGN, SETTING, AND PARTICIPANTS:
Cross-sectional analysis of a nationally representative subsample of 2838 participants aged 6 through 19 years randomly selected for measurement of urinary BPA concentration in the 2003-2008 National Health and Nutrition Examination Surveys.
MAIN OUTCOME MEASURES:
Body mass index (BMI), converted to sex- and age-standardized z scores and used to classify participants as overweight (BMI ≥85th percentile for age/sex) or obese (BMI ≥95th percentile).
Median urinary BPA concentration was 2.8 ng/mL (interquartile range, 1.5-5.6). Of the participants, 1047 (34.1% [SE, 1.5%]) were overweight and 590 (17.8% [SE, 1.3%]) were obese. Controlling for race/ethnicity, age, caregiver education, poverty to income ratio, sex, serum cotinine level, caloric intake, television watching, and urinary creatinine level, children in the lowest urinary BPA quartile had a lower estimated prevalence of obesity (10.3% [95% CI, 7.5%-13.1%]) than those in quartiles 2 (20.1% [95% CI, 14.5%-25.6%]), 3 (19.0% [95% CI, 13.7%-24.2%]), and 4 (22.3% [95% CI, 16.6%-27.9%]). Similar patterns of association were found in multivariable analyses examining the association between quartiled urinary BPA concentration and BMI z score and in analyses that examined the logarithm of urinary BPA concentration and the prevalence of obesity. Obesity was not associated with exposure to other environmental phenols commonly used in other consumer products, such as sunscreens and soaps. In stratified analysis, significant associations between urinary BPA concentrations and obesity were found among whites (P < .001) but not among blacks or Hispanics.
Urinary BPA concentration was significantly associated with obesity in this cross-sectional study of children and adolescents. Explanations of the association cannot rule out the possibility that obese children ingest food with higher BPA content or have greater adipose stores of BPA.
To examine the associations of antibiotic exposures during the first 2 years of life and the development of body mass over the first 7 years of life.
Longitudinal birth cohort study.
A total of 11 532 children born at 2500 g in the Avon Longitudinal Study of Parents and Children (ALSPAC), a population-based study of children born in Avon, UK in 1991–1992.
Exposures to antibiotics during three different early-life time windows (
Antibiotic exposure during the earliest time window (
Exposure to antibiotics during the first 6 months of life is associated with consistent increases in body mass from 10 to 38 months. Exposures later in infancy (6–14 months, 15–23 months) are not consistently associated with increased body mass. Although effects of early exposures are modest at the individual level, they could have substantial consequences for population health. Given the prevalence of antibiotic exposures in infants, and in light of the growing concerns about childhood obesity, further studies are needed to isolate effects and define life-course implications for body mass and cardiovascular risks.
The WHO Multiple Exposures Multiple Effects (MEME) framework identifies community contextual variables as central to the study of childhood health. Here we identify multiple domains of neighborhood context, and key variables describing the dimensions of these domains, for use in the National Children's Study (NCS) site in Queens. We test whether the neighborhoods selected for NCS recruitment, are representative of the whole of Queens County, and whether there is sufficient variability across neighborhoods for meaningful studies of contextual variables.
Nine domains (demographic, socioeconomic, households, birth rated, transit, playground/greenspace, safety and social disorder, land use, and pollution sources) and 53 indicator measures of the domains were identified. Geographic information systems were used to create community-level indicators for US Census tracts containing the 18 study neighborhoods in Queens selected for recruitment, using US Census, New York City Vital Statistics, and other sources of community-level information. Mean and inter-quartile range values for each indicator were compared for Tracts in recruitment and non-recruitment neighborhoods in Queens.
Across the nine domains, except in a very few instances, the NCS segment-containing tracts (N = 43) were not statistically different from those 597 populated tracts in Queens not containing portions of NCS segments; variability in most indicators was comparable in tracts containing and not containing segments.
In a diverse urban setting, the NCS segment selection process succeeded in identifying recruitment areas that are, as a whole, representative of Queens County, for a broad range of community-level variables.
The obesity epidemic has transformed children's healthcare, such that diabetes, hypertension and the metabolic syndrome are phrases more commonly used by child health providers than ever before. This article reviews the economic consequences of this epidemic for healthcare delivery systems, both in the short term when obesity has been associated with increased utilization, and in the long term where increased likelihood of adult obesity and cardiovascular disease is well documented. Large investments through research and prevention are needed and are likely to provide strong returns in cost savings, and would optimally emerge through a cooperative effort between private and government payers alike.
To assess the association of the severity of obesity with diagnosis and health education, and to identify any differences within demographic or other subgroups.
Clinician visits for 2-18 year olds from the 2005-2008 National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey were combined. Descriptive, bivariate and multivariate analyses were used to compare diagnosis of obesity and health education (nutrition, exercise and weight reduction) across elevated body mass index (BMI) groups (overweight, obese and extreme or very obese, defined as >120% of the 95th percentile for age and gender), patient socio-demographic characteristics, physician specialty and type of visit (well child visits (WCV) versus non-well child visits (non-WCV).
A total of 17 808 visits had a calculated BMI, of which 5.8% were extremely obese, 13% were obese and 15.2% were overweight, with the highest percentages among older children, blacks and Hispanics. Diagnosis and weight reduction education were higher among children with an extreme BMI. Nutrition and exercise education were not correlated with severity of obesity. Race, ethnicity or gender biases were not identified. Severity of obesity was significantly associated with presentation to a non-WCV rather than a WCV.
Extremely obese children have higher, but still insufficient, rates of diagnosis and health education. Nutrition and exercise education are not prevalent throughout all age groups. Providers may be relying inconsistently and insufficiently on visual cues to drive their obesity prevention practices. Furthermore, lower rates of diagnosis and education at non-WCV may result in a missed opportunity to prevent comorbidities. This is of particular concern as overweight children are less likely to be seen at WCV than non-WCV.International Journal of Obesity advance online publication, 24 January 2012; doi:10.1038/ijo.2012.1.
Congenital fibrosarcoma (CFS) is a rare fibrous tissue malignancy that usually presents in the first few years of life. It is unique among human sarcomas in that it has an excellent prognosis. We describe a temporal clustering of a number of cases of CFS and investigate the possible associated prenatal risk factors. The Pediatric Environmental History, a questionnaire developed in our clinic that is instrumental in determining environmental risk factors for tumor-related disease, was essential in documenting the presence or absence of risk factors considered as human carcinogens. We found a history of exposure to petroleum products in four cases of CFS that occurred at a greater than expected rate in a short time frame-an apparent cancer cluster. We call attention to the possibility that exposure to petroleum products raises the risk of developing CFS. While future studies should focus on systematic investigation of CFS and its underlying mechanisms, this report suggests the need for proactive measures to avoid exposure to solvents and petroleum products during pregnancy.
Lake Chapala is a major source of water for crop irrigation and subsistence fishing for a population of 300,000 people in central Mexico. Economic activities have created increasing pollution and pressure on the whole watershed resources. Previous reports of mercury concentrations detected in fish caught in Lake Chapala have raised concerns about health risks to local families who rely on fish for both their livelihood and traditional diet. Our own data has indicated that 27% of women of childbearing age have elevated hair mercury levels, and multivariable analysis indicated that frequent consumption of carp (i.e., once a week or more) was associated with significantly higher hair mercury concentrations. In this paper we describe a range of environmental health research projects. Our main priorities are to build the necessary capacities to identify sources of water pollution, enhance early detection of environmental hazardous exposures, and deliver feasible health protection measures targeting children and pregnant women. Our projects are led by the Children's Environmental Health Specialty Unit nested in the University of Guadalajara, in collaboration with the Department of Environmental Health of Harvard School of Public Health and Department of Pediatrics of the New York School of Medicine. Our partnership focuses on translation of knowledge, building capacity, advocacy and accountability. Communication will be enhanced among women's advocacy coalitions and the Ministries of Environment and Health. We see this initiative as an important pilot program with potential to be strengthened and replicated regionally and internationally.
There has been little research to date on the linkages between air pollution and infectious respiratory illness in children, and the resulting health care costs. In this study we used data on air pollutants and national hospitalizations to study the relationship between fine particulate air pollution and health care charges and costs for the treatment of bronchiolitis, an acute viral infection of the lungs. We found that as the average exposure to fine particulate matter over the lifetime of an infant increased, so did costs for the child's health care. If the United States were to reduce levels of fine particulate matter to 7 percent below the current annual standard, the nation could save $15 million annually in reduced health care costs from hospitalizations of children with bronchiolitis living in urban areas. These findings reinforce the need for ongoing efforts to reduce levels of air pollutants. They should trigger additional investigation to determine if the current standards for fine-particulate matter are sufficiently protective of children's health.
Acute exposure to outdoor air pollutants has been associated with increased pediatric asthma morbidity. However, the impact of subchronic exposures is largely unknown.
To examine the association between subchronic exposure to 6 outdoor air pollutants (PM2.5, PM10, ozone, nitrogen oxides, sulfur oxides, carbon monoxide) and pediatric asthma hospitalization length of stay, charges, and costs.
We linked pediatric asthma hospitalization discharge data from a nationally representative dataset, the 1999-2007 Nationwide Inpatient Sample, with outdoor air pollution data from the Environmental Protection Agency. Hospitals with no air quality data within 10 miles were excluded. Our predictor was the average concentration of 6 pollutants near the hospital during the month of admission. We conducted bivariate analyses using Spearman correlations and multivariable analyses using Poisson regression for length of stay and linear regression for log-transformed charges and costs, controlling for patient demographics, hospital characteristics, and month of admission.
In unadjusted analyses, all 6 pollutants had minimal correlation with the 3 outcomes ( ρ<0.1, P<0.001). In multivariable analyses, a 1-unit (μg/m) increase in monthly PM2.5 led to a $123 increase in charges (95% confidence interval $40-249) and a $47 increase in costs (95% confidence interval $15-93). No other pollutants were significant predictors of charges or costs or length of stay.
Subchronic PM2.5 exposure is associated with increased costs for pediatric asthma hospitalizations. Policy changes to reduce outdoor subchronic pollutant exposure may lead to improved asthma outcomes and substantial savings in healthcare spending.
The article under evaluation analyzed healthcare utilization data from the German Interview and Examination Survey for Children and Adolescents, a representative cross-sectional survey that quantifies healthcare services and costs by category. The author used widely accepted health economic methods to quantify incremental costs and utilization attributable to elevated BMI in children. There are important limits to consider for policy makers, clinicians and others who may use these data in isolation to quantify economic savings and other benefits to quantify cost-effectiveness and cost-benefit profiles of environmental, dietary, physical activity and/or pharmaceutical interventions to prevent or treat obesity in childhood. Longer term benefits of preventing obesity in childhood must be considered.
Economic analyses are increasingly appearing in the children's environmental-health literature. In this review, an illustrative selection of articles that represent cost analyses, cost-effectiveness analyses, and cost-benefit analyses is analyzed for the relative merits of each approach. Cost analyses remain the dominant approach due to lack of available data. Cost-effectiveness and cost-benefit analyses in this area face challenges presented by estimation of costs of environmental interventions, whose costs are likely to decrease with further technological innovation. Benefits are also more difficult to quantify economically and can only be partially alleviated through willingness-to-pay approaches. Nevertheless, economic analyses in children's environmental health are highly informative and important informants to public-health and policy practice. Further attention and training in their appropriate use are needed.
To determine the trends in incidence of diagnosis of bronchopulmonary dysplasia (BPD) and associated health services use for the neonatal hospitalization of patients with BPD in an era of changing definitions and management.
PATIENTS AND METHODS:
All neonatal hospitalization records available through the Nationwide Inpatient Sample, 1993-2006, were analyzed. Multivariable regression analyses were performed for incidence of BPD diagnosis and associated hospital length of stay and charges. Multiple models were constructed to assess the roles of changes in diagnosis of very low birth weight (VLBW) neonates and different modalities of respiratory support used for treatment.
The absolute incidence of diagnosis of BPD fell 3.3% annually (P = .0009) between 1993 and 2006 coincident with a 3.5-fold increase in the use of noninvasive respiratory support in patients with BPD. When data were controlled for demographic factors, this significant decrease in incidence persisted at a rate of 4.3% annually (P = .0002). All models demonstrated a rise in hospital length of stay and financial charges for the neonatal hospitalization of patients with BPD. The incidence of BPD adjusted for frequency of prolonged mechanical ventilation also decreased but only by 2.8% annually (P = .0075).
The incidence of diagnosis of BPD decreased significantly between 1993 and 2006. In well-controlled models, birth hospitalization charges for these patients rose during the same period. Less invasive ventilatory support may improve respiratory outcomes of VLBW neonates.
Tetraethyl lead was phased out of gasoline in Uganda in 2005. Recent mitigation of an important source of lead exposure suggests examination and re-evaluation of the prevalence of childhood lead poisoning in this country. Ongoing concerns persist about exposure from the Kiteezi landfill in Kampala, the country's capital.
We determined blood lead distributions among Kampala schoolchildren and identified risk factors for elevated blood lead levels (EBLLs; >or= 10 microg/dL). Analytical approach: Using a stratified, cross-sectional design, we obtained blood samples, questionnaire data, and soil and dust samples from the homes and schools of 163 4- to 8-year-old children representing communities with different risks of exposure.
The mean blood lead level (BLL) was 7.15 microg/dL; 20.5% of the children were found to have EBLL. Multivariable analysis found participants whose families owned fewer household items, ate canned food, or used the community water supply as their primary water source to have higher BLLs and likelihood of EBLLs. Distance < 0.5 mi from the landfill was the factor most strongly associated with increments in BLL (5.51 microg/dL, p < 0.0001) and likelihood of EBLL (OR = 4.71, p = 0.0093). Dust/soil lead was not significantly predictive of BLL/EBLL.
Lead poisoning remains highly prevalent among school-age children in Kampala. Confirmatory studies are needed, but further efforts are indicated to limit lead exposure from the landfill, whether through water contamination or through another mechanism. Although African nations are to be lauded for the removal of lead from gasoline, this study serves as a reminder that other sources of exposure to this potent neurotoxicant merit ongoing attention.
Since Mexico's joining the North American Free Trade Agreement (NAFTA) and the Organization for Economic Cooperation and Development (OECD) in 1994, it has witnessed rapid industrialization. A byproduct of this industrialization is increasing population exposure to environmental pollutants, of which some have been associated with childhood disease. We therefore identified and assessed the adequacy of existing international and Mexican governance instruments and policy tools to protect children from environmental hazards.
We first systematically reviewed PubMed, the Mexican legal code and the websites of the United Nations, World Health Organization, NAFTA and OECD as of July 2007 to identify the relevant governance instruments, and analyzed the approach these instruments took to preventing childhood diseases of environmental origin. Secondly, we interviewed a purposive sample of high-level government officials, researchers and non-governmental organization representatives, to identify their opinions and attitudes towards children's environmental health and potential barriers to child-specific protective legislation and implementation.
We identified only one policy tool describing specific measures to reduce developmental neurotoxicity and other children's health effects from lead. Other governance instruments mention children's unique vulnerability to ozone, particulate matter and carbon monoxide, but do not provide further details. Most interviewees were aware of Mexican environmental policy tools addressing children's health needs, but agreed that, with few exceptions, environmental policies do not address the specific health needs of children and pregnant women. Interviewees also cited state centralization of power, communication barriers and political resistance as reasons for the absence of a strong regulatory platform.
The Mexican government has not sufficiently accounted for children's unique vulnerability to environmental contaminants. If regulation and legislation are not updated and implemented to protect children, increases in preventable exposures to toxic chemicals in the environment may ensue.
Elevated concentrations of mercury have been documented in fish in Lake Chapala in central Mexico, an area that is home to a large subsistence fishing community. However, neither the extent of human mercury exposure nor its sources and routes have been elucidated.
Total mercury concentrations were measured in samples of fish from Lake Chapala; in sections of sediment cores from the delta of Rio Lerma, the major tributary to the lake; and in a series of suspended-particle samples collected at sites from the mouth of the Lerma to mid-Lake. A cross-sectional survey of 92 women ranging in age from 18-45 years was conducted in three communities along the Lake to investigate the relationship between fish consumption and hair mercury concentrations among women of child-bearing age.
Highest concentrations of mercury in fish samples were found in carp (mean 0.87 ppm). Sediment data suggest a pattern of moderate ongoing contamination. Analyses of particles filtered from the water column showed highest concentrations of mercury near the mouth of the Lerma. In the human study, 27.2% of women had >1 ppm hair mercury. On multivariable analysis, carp consumption and consumption of fish purchased or captured from Lake Chapala were both associated with significantly higher mean hair mercury concentrations.
Our preliminary data indicate that, despite a moderate level of contamination in recent sediments and suspended particulate matter, carp in Lake Chapala contain mercury concentrations of concern for local fish consumers. Consumption of carp appears to contribute significantly to body burden in this population. Further studies of the consequences of prenatal exposure for child neurodevelopment are being initiated.
The National Children's Study is a long-term epidemiologic study of 100,000 children from 105 locations across the United States. It will require information on a large number of environmental variables to address its core hypotheses. The resources available to collect actual home and personal exposure samples are limited, with most of the home sampling completed on periodic visits and the personal sampling generally limited to biomonitoring. To fill major data gaps, extant data will be required for each study location. The Queens Vanguard Center has examined the extent of those needs and the types of data that are generally and possibly locally available.
In this review we identify three levels of data--national, state and county--and local data and information sets (levels 1-3, respectively), each with different degrees of availability and completeness, that can be used as a starting point for the extant data collection in each study location over time. We present an example on the use of this tiered approach, to tailor the data needs for Queens County and to provide general guidance for application to other NCS locations.
Preexisting and continually evolving databases are available for use in the NCS to characterize exposure. The three levels of data we identified will be used to test a method for developing exposure indices for segments and homes during the pilot phase of NCS, as outlined in this article.
Most studies of the economic costs of childhood obesity have focused upon hospitalization for comorbidities of obesity, whereas increased expenditures may also be the result of additional outpatient/emergency room visits or prescription drug expenditures. To quantify the magnitude of increased health-care utilization and expenditures among overweight and obese children, we performed descriptive, bivariate, and multivariable analyses on data from 6- to 19-year olds in the 2002-2005 Medical Expenditure Panel Survey (MEPS), a national probability survey of the noninstitutionalized civilian population in the United States. Compared with normal/underweight children, we found that children who were obese during both years of the MEPS had USD194 higher outpatient visit expenditures, USD114 higher prescription drug expenditures, and USD12 higher emergency room expenditures. Children who were overweight during both years, or overweight in one year and obese in the other had USD79 higher outpatient visit expenditures, USD64 higher prescription drug expenditures, and USD25 higher emergency room expenditures than normal/underweight children. Significantly, increased utilization was noted for outpatient visits, prescription drug use, and emergency room visits. Increased costs and utilization were concentrated among adolescents, though 6-11-year-old children who were obese in both years did have more outpatient visits and expenditures than other children. Extrapolated to the nation, elevated BMI in childhood was associated with USD14.1 billion in additional prescription drug, emergency room, and outpatient visit costs annually. Although further research is needed to identify effective interventions, the immediate economic consequences of childhood obesity are much greater than previously realized, and further reinforce efforts to prevent this major comorbidity are needed.
Childhood obesity is increasingly recognized as an epidemic, but the economic consequences have not been well quantified. We evaluated trends in obesity-associated hospitalizations, charges, and costs using 1999-2005 data from a nationally representative sample of admissions to U.S. hospitals. We detected a near-doubling in hospitalizations with a diagnosis of obesity between 1999 and 2005 and an increase in costs from $125.9 million to 237.6 million (in 2005 dollars) between 2001 and 2005. Medicaid appears to bear a large burden of hospitalizations for conditions that occur along with obesity, while private payers pay a greater portion of hospitalization costs to treat obesity itself.
While much attention is focused on national policies intended to protect human health from environmental hazards, states can also prevent environmentally mediated disease through legislation and regulation. However, relatively few analyses have examined the extent to which states protect children from chemical factors in the environment.
Using Lexis Nexis and other secondary sources, we systematically reviewed environmental regulation and legislation in the fifty states and the District of Columbia as of July 2007 intended to protect children against neurodevelopmental disabilities and asthma.
States rarely address children specifically in environmental regulation and legislation, though many state regulations go far to limit children's exposures to environmental hazards. Northeast and Midwest states have implemented model regulation of mercury emissions, and regulations in five states set exposure limits to volatile organic compound emissions that are more stringent than US Environmental Protection Agency standards.
Differences in state environmental regulation and legislation are likely to lead to differences in exposure, and thus to impacts on children's health. The need for further study should not inhibit other states and the federal government from pursuing the model regulation and legislation we identified to prevent diseases of environmental origin in children.
In this review we describe the approach taken by the National Children's Study (NCS), a 21-year prospective study of 100,000 American children, to understanding the role of environmental factors in the development of obesity.
DATA SOURCES AND EXTRACTION:
We review the literature with regard to the two core hypotheses in the NCS that relate to environmental origins of obesity and describe strategies that will be used to test each hypothesis.
Although it is clear that obesity in an individual results from an imbalance between energy intake and expenditure, control of the obesity epidemic will require understanding of factors in the modern built environment and chemical exposures that may have the capacity to disrupt the link between energy intake and expenditure. The NCS is the largest prospective birth cohort study ever undertaken in the United States that is explicitly designed to seek information on the environmental causes of pediatric disease.
Through its embrace of the life-course approach to epidemiology, the NCS will be able to study the origins of obesity from preconception through late adolescence, including factors ranging from genetic inheritance to individual behaviors to the social, built, and natural environment and chemical exposures. It will have sufficient statistical power to examine interactions among these multiple influences, including gene-environment and gene-obesity interactions. A major secondary benefit will derive from the banking of specimens for future analysis.
Pediatricians can help limit children's exposures to environmental hazards, but few studies have assessed their comfort with discussing and dealing with environmental health issues. We surveyed the membership of the Minnesota Chapter of the American Academy of Pediatrics to assess pediatricians' attitudes and beliefs about the effect the environment can have on children's health, and to assess their practices in regard to screening for, diagnosing, and treating illnesses related to environmental exposures. Results showed that Minnesota pediatricians agree that children are suffering from preventable illnesses of environmental origin but feel ill-equipped to educate parents about many common exposures and their consequences. Responses also indicated significant demand for education on the subject and for a referral center that can evaluate patients who may be suffering from environmental exposures.
Prospective, multiyear epidemiologic studies have proven to be highly effective in discovering preventable risk factors for chronic disease. Investigations such as the Framingham Heart Study have produced blueprints for disease prevention and saved millions of lives and billions of dollars. To discover preventable environmental risk factors for disease in children, the US Congress directed the National Institute of Child Health and Human Development, through the Children's Health Act of 2000, to conduct the National Children's Study. The National Children's Study is hypothesis-driven and will seek information on environmental risks and individual susceptibility factors for asthma, birth defects, dyslexia, attention-deficit/hyperactivity disorder, autism, schizophrenia, and obesity, as well as for adverse birth outcomes. It will be conducted in a nationally representative, prospective cohort of 100,000 US-born children. Children will be followed from conception to 21 years of age. Environmental exposures (chemical, physical, biological, and psychosocial) will be assessed repeatedly during pregnancy and throughout childhood in children's homes, schools, and communities. Chemical assays will be performed by the Centers for Disease Control and Prevention, and banks of biological and environmental samples will be established for future analyses. Genetic material will be collected on each mother and child and banked to permit study of gene-environment interactions. Recruitment is scheduled to begin in 2007 at 7 Vanguard Sites and will extend to 105 sites across the United States. The National Children's Study will generate multiple satellite studies that explore methodologic issues, etiologic questions, and potential interventions. It will provide training for the next generation of researchers and practitioners in environmental pediatrics and will link to planned and ongoing prospective birth cohort studies in other nations. Data from the National Children's Study will guide development of a comprehensive blueprint for disease prevention in children.
Exposure in prenatal life to methylmercury (MeHg) has become the topic of intense debate in the United States after the Environmental Protection Agency (EPA) announced a proposal in 2004 to reverse strict controls on emissions of mercury from coal-fired power plants that had been in effect for the preceding 15 years. This proposal failed to incorporate any consideration of the health impacts on children that would result from increased mercury emissions. We assessed the impact on children's health of industrial mercury emissions and found that between 316,588 and 637,233 babies are born with mercury-related losses of cognitive function ranging from 0.2 to 5.13 points. We calculated that decreased economic productivity resulting from diminished intelligence over a lifetime results in an aggregate economic cost in each annual birth cohort of $8.7 billion annually (range: $0.7-$13.9 billion, 2000 dollars). $1.3 billion (range: $51 million-$2.0 billion) of this cost is attributable to mercury emitted from American coal-fired power plants. Downward shifts in intellectual quotient (IQ) are also associated with 1566 (range: 115-2675) excess cases of mental retardation (MR defined as IQ < 70) annually. This number accounts for 3.2% (range: 0.2-5.4%) of MR cases in the United States. If the lifetime excess cost of a case of MR (excluding individual productivity losses) is $1,248,648 in 2000 dollars, then the cost of these excess cases of MR is $2.0 billion annually (range: $143 million-$3.3 billion). Preliminary data suggest that more stringent mercury policy options would prevent thousands of cases of MR and billions of dollars over the next 25 years.
Chronic diseases of environmental origin are a significant and increasing public health problem among the children of New York State, yet few resources exist to address this growing burden. To assess New York State pediatricians self-perceived competency in dealing with common environmental exposures and diseases of environmental origin in children, we assessed their attitudes and beliefs about the role of the environment in children's health. A four-page survey was sent to 1,500 randomly selected members of the New York State American Academy of Pediatrics in February 2004. We obtained a 20.3% response rate after one follow-up mailing; respondents and nonrespondents did not differ in years of licensure or county of residence. Respondents agreed that the role of environment in children's health is significant (mean 4.44 /- 0.72 on 1-5 Likert scale). They voiced high self-efficacy in dealing with lead exposure (mean 4.16-4.24 /- 0.90-1.05), but their confidence in their skills for addressing pesticides, mercury and mold was much lower (means 2.51-3.21 /- 0.90-1.23; p < 0.001). About 93.8% would send patients to a clinic "where pediatricians could refer patients for clinical evaluation and treatment of their environmental health concerns." These findings indicate that New York pediatricians agree that children are suffering preventable illnesses of environmental origin but feel ill-equipped to educate families about common exposures. Significant demand exists for specialized centers of excellence that can evaluate environmental health concerns, and for educational opportunities.
Prospective, multi-year epidemiologic studies such as the Framingham Heart Study and the Nurses' Health Study have proven highly effective in identifying risk factors for chronic illness and in guiding disease prevention. Now, in order to identify environmental risk factors for chronic disease in children, the US Congress authorized a National Children's Study as part of the Children's Health Act of 2000. Enrollment of a nationally representative cohort of 100,000 children will begin in 2008, with follow-up to continue through age 21. Environmental assessment and examination of biomarkers collected at specified intervals during pregnancy and childhood will be a major component of the Study. Recruitment at 105 sites across the United States is planned, and will begin at 7 Vanguard Centers in 2008, including Waukesha County, Wis. The National Children's Study will provide information on preventable risk factors for such chronic diseases as asthma, certain birth defects, neurobehavioral syndromes, and obesity. In addition, the National Children's Study will provide training in pediatric environmental health for the next generation of researchers and practitioners.
Parkinson disease (PD) and Alzheimer disease (AD), the two most common neurodegenerative disorders in American adults, are of purely genetic origin in a minority of cases and appear in most instances to arise through interactions among genetic and environmental factors. In this article we hypothesize that environmental exposures in early life may be of particular etiologic importance and review evidence for the early environmental origins of neurodegeneration. For PD the first recognized environmental cause, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), was identified in epidemiologic studies of drug abusers. Chemicals experimentally linked to PD include the insecticide rotenone and the herbicides paraquat and maneb; interaction has been observed between paraquat and maneb. In epidemiologic studies, manganese has been linked to parkinsonism. In dementia, lead is associated with increased risk in chronically exposed workers. Exposures of children in early life to lead, polychlorinated biphenyls, and methylmercury have been followed by persistent decrements in intelligence that may presage dementia. To discover new environmental causes of AD and PD, and to characterize relevant gene-environment interactions, we recommend that a large, prospective genetic and epidemiologic study be undertaken that will follow thousands of children from conception (or before) to old age. Additional approaches to etiologic discovery include establishing incidence registries for AD and PD, conducting targeted investigations in high-risk populations, and improving testing of the potential neurologic toxicity of chemicals.
Methyl mercury is a developmental neurotoxicant. Exposure results principally from consumption by pregnant women of seafood contaminated by mercury from anthropogenic (70%) and natural (30%) sources. Throughout the 1990s, the U.S. Environmental Protection Agency (EPA) made steady progress in reducing mercury emissions from anthropogenic sources, especially from power plants, which account for 41% of anthropogenic emissions. However, the U.S. EPA recently proposed to slow this progress, citing high costs of pollution abatement. To put into perspective the costs of controlling emissions from American power plants, we have estimated the economic costs of methyl mercury toxicity attributable to mercury from these plants. We used an environmentally attributable fraction model and limited our analysis to the neurodevelopmental impacts--specifically loss of intelligence. Using national blood mercury prevalence data from the Centers for Disease Control and Prevention, we found that between 316,588 and 637,233 children each year have cord blood mercury levels > 5.8 microg/L, a level associated with loss of IQ. The resulting loss of intelligence causes diminished economic productivity that persists over the entire lifetime of these children. This lost productivity is the major cost of methyl mercury toxicity, and it amounts to $8.7 billion annually (range, $2.2-43.8 billion; all costs are in 2000 US$). Of this total, $1.3 billion (range, $0.1-6.5 billion) each year is attributable to mercury emissions from American power plants. This significant toll threatens the economic health and security of the United States and should be considered in the debate on mercury pollution controls.
A growing body of research supports the role of outdoor air pollutants in acutely aggravating chronic diseases in children, and suggests that the pollutants may have a role in the development of these diseases. This article reviews the biologic basis of children's unique vulnerability to highly prevalent outdoor air pollutants, with a special focus on ozone, respirable particulate matter (PM 2.5 [<2.5 microm in diameter] and PM 10 [<10 microm in diameter]), lead, sulfur dioxide, carbon monoxide, and nitrogen oxides. We also summarize understanding regarding health effects and molecular mechanisms of action. Practitioners can significantly reduce morbidity in children and other vulnerable populations by advising families to minimize pollutant exposures to children with asthma, or at a broader level by educating policymakers about the need to act to reduce pollutant emissions. Management of children with asthma must expand beyond preventing exposures to agents that directly cause allergic reactions (and therefore can be diagnosed by means of skin tests) and must focus more attention on agents that cause a broad spectrum of nonspecific, generalized inflammation, such as air pollution.