The minister responsible for consumer protection, Paul Magnette, will not authorise the marketing in Belgium of mobile phones intended for children. “With this type of phone children can actually be exposed to mechanical dangers or the risks of radiation. In fact scientists all recognise that it is necessary to limit children’s exposure to cumulative amounts of radiation, even if not much is yet known about how sensitive they are to radio waves.”
Archive for the ‘Children’ Category
Belgian minister says no to cell phones for children.
Tuesday, February 10th, 2009Prenatal Phenol and Phthalate Exposures and Birth Outcomes
Monday, February 9th, 2009Prenatal Phenol and Phthalate Exposures and Birth Outcomes
Mary S. Wolff,1 Stephanie M. Engel,1 Gertrud S. Berkowitz,1 Xiaoyun Ye,2 Manori J. Silva,2 Chenbo Zhu,1 James Wetmur,3 and Antonia M. Calafat2
1Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York, New York, USA; 2National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA; 3Department of Microbiology and Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, New York, USA
Abstract
Background: Many phthalates and phenols are hormonally active and are suspected to alter the course of development.
Objective: We investigated prenatal exposures to phthalate and phenol metabolites and their associations with body size measures of the infants at birth.
Methods: We measured 5 phenol and 10 phthalate urinary metabolites in a multiethnic cohort of 404 women in New York City during their third trimester of pregnancy and recorded size of infants at birth.
Results: Median urinary concentrations were > 10 µg/L for 2 of 5 phenols and 6 of 10 phthalate monoester metabolites. Concentrations of low-molecular-weight phthalate monoesters (low-MWP) were approximately 5-fold greater than those of high-molecular-weight metabolites. Low-MWP metabolites had a positive association with gestational age [0.97 day gestational age per ln-biomarker ; 95% confidence interval (CI) , 0.07–1.9 days, multivariate adjusted] and with head circumference. Higher prenatal exposures to 2,5-dichlorophenol (2,5-DCP) predicted lower birth weight in boys (–210 g average birth weight difference between the third tertile and first tertile of 2,5-DCP ; 95% CI, 71–348 g) . Higher maternal benzophenone-3 (BP3) concentrations were associated with a similar decrease in birth weight among girls but with greater birth weight in boys.
Conclusions: We observed a range of phthalate and phenol exposures during pregnancy in our population, but few were associated with birth size. The association of 2,5-DCP and BP3 with reduced or increased birth weight could be important in very early or small-size births. In addition, positive associations of urinary metabolites with some outcomes may be attributable partly to unresolved confounding with maternal anthropometric factors.
Key words: 2 , 5-DCP, birth length, birth weight, BMI , creatinine, phenols, phthalates, pregnancy, urinary biomarker. Environ Health Perspect 116:1092–1097 (2008) . doi:10.1289/ehp.11007 available via http://dx.doi.org/ [Online 20 March 2008]
The attribution of urban and suburban children’s exposure to synthetic pyrethroid insecticides: a longitudinal assessment.
Tuesday, February 3rd, 2009The attribution of urban and suburban children’s exposure to synthetic pyrethroid insecticides: a longitudinal assessment.
Lu C, Barr DB, Pearson MA, Walker LA, Bravo R.
aDepartment of Environmental and Occupational Health, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA.
J Expo Sci Environ Epidemiol. 2008 Sep 3.
Despite the widespread use of synthetic pyrethroid insecticides that led to common exposure in the population, very few studies have been conducted to quantitatively assess human, particularly, children’s, long-term exposures to pyrethroid insecticides.
The objective of the Children Pesticide Exposure Study – Washington (CPES-WA) was to establish the longitudinal exposure profiles for pyrethroid insecticides in a cohort of children living in an urban
and suburban community using urinary pyrethroid metabolites as exposure biomarkers.
The results from this analysis will allow us to examine potential risk factors in relation to the elevated pyrethroid insecticide exposure in children. A total of 23 children, aged 3-11 years, who only consumed conventional diets were enrolled in this 1-year study. We provided organic food items to children for 5 consecutive days in the summer and fall sampling seasons. We measured urinary metabolites for the synthetic pyrethroid insecticides in urine samples that were collected twice daily during each of the four sampling seasons. 3-phenoxybenzoic acid was frequently detected in the urine samples with mean and median daily volume-weighted average levels of 1.5 and 1.2 mug/l, followed by trans-2,2-(dichloro)-2-dimethylvinylcyclopropane carboxylic acid (1.4 and 1.0 mug/l) and cis-2,2-(dichloro)-2-dimethylvinylcyclopropane carboxylic acid (0.5 mug/l, and non-detected). When we took into account season, age, sex, diet, and self-reported residential use of pyrethroid insecticides in a linear mixed-effects model, the results suggested that the combination of the use of pyrethroid insecticides in the household, dietary intake, and seasonal differences play a significant role in predicting children’s exposure to synthetic pyrethroid insecticides. We found CPES-WA children were continuously exposed to pyrethroid insecticides through their diets all year long, and this chronic exposure pattern was periodically modified by episodes of relatively high exposures from residential uses.
Future research should be devoted to enhancing our understanding of the complexity of pyrethroid insecticide exposure patterns.Journal of Exposure Science and Environmental Epidemiology advance online publication, 3 September 2008; doi:10.1038/jes.2008.49.
http://www.ncbi.nlm.nih.gov/pubmed/18766203?dopt=AbstractPlus
PMID: 18766203 [PubMed - as supplied by publisher]
Association of environmental toxicants and conduct disorder in U.S. children: NHANES 2001-2004.
Tuesday, February 3rd, 2009Environ Health Perspect. 2008 Jul;116(7):956-62. Links
Association of environmental toxicants and conduct disorder in U.S. children: NHANES 2001-2004.
Braun JM, Froehlich TE, Daniels JL, Dietrich KN, Hornung R, Auinger P, Lanphear BP.
Department of Epidemiology, University of North Carolina Chapel Hill, Chapel Hill, NC 27599-7435, USA. jmbraun@unc.edu
OBJECTIVE: The purpose of this study was to examine the association of tobacco smoke and environmental lead exposure with conduct disorder (CD). METHODS: The National Health and Nutrition Examination Survey (NHANES) 2001-2004 is a nationally representative cross-sectional sample of the noninstitutionalized U.S. population. We examined the association of prenatal tobacco, postnatal tobacco, and environmental lead exposure with CD in children 8-15 years of age (n = 3,081). We measured prenatal tobacco exposure by parent report of cigarette use during pregnancy, and postnatal tobacco using serum cotinine levels. We assessed lead exposure using current blood lead concentration. Parents completed the Diagnostic Interview Schedule for Children to determine whether their children met criteria of the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV ) for CD. RESULTS: Overall, 2.06% of children met DSM-IV criteria for CD in the past year, equivalent to 560,000 U.S. children 8-15 years of age. After adjustment, prenatal tobacco exposure was associated with increased odds for CD [odds ratio (OR) = 3.00; 95% confidence interval (CI), 1.36-6.63]. Increased blood lead levels (fourth vs. first quartile) and serum cotinine levels (fifth vs. first quintile) were associated with an 8.64-fold (95% CI, 1.87-40.04) and 9.15-fold (95% CI, 1.47-6.90) increased odds of meeting DSM-IV CD criteria. Increasing serum cotinine levels and blood lead levels were also associated with increased prevalence of CD symptoms (symptom count ratio, lead: 1.73; 95% CI, 1.23-2.43; symptom count ratio, cotinine: 1.97; 95% CI, 1.15-3.40). CONCLUSIONS: These results suggest that prenatal tobacco exposure and environmental lead exposure contribute substantially to CD in U.S. children.
PMID: 18629321 [PubMed - in process]
PMCID: PMC2453167
Prenatal and Postnatal Exposure to Cell Phone Use and Behavioral Problems in Children.
Tuesday, February 3rd, 2009Preventive Psychiatry E-Newsletter # 337
Prenatal and Postnatal Exposure to Cell Phone Use and Behavioral Problems in Children.
Original Article
Epidemiology. 19(4):523-529, July 2008.
Divan, Hozefa A. a; Kheifets, Leeka a; Obel, Carsten b; Olsen, Jorn a
Abstract:
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 pre-natally, and, to a lesser degree, post-natally, was associated with behavioral difficulties such as emotional and hyperactivity problems around the age of school entry. These associations may be non-causal and may be due to unmeasured confounding. If real, they would be of public health concern given the widespread use of this technology.
(C) 2008 Lippincott Williams & Wilkins, Inc.
Epidemiologic evidence of relationships between reproductive and child health outcomes and environmental chemical contaminants.
Tuesday, February 3rd, 20091: J Toxicol Environ Health B Crit Rev. 2008 May;11(5-6):373-517. Links
Epidemiologic evidence of relationships between reproductive and child health outcomes and environmental chemical contaminants.
Wigle DT, Arbuckle TE, Turner MC, Bérubé A, Yang Q, Liu S, Krewski D.
McLaughlin Centre for Population Health Risk Assessment, University of Ottawa, Ottawa, Ontario, Canada. don.wigle@sympatico.ca
This review summarizes the level of epidemiologic evidence for relationships between prenatal and/or early life exposure to environmental chemical contaminants and fetal, child, and adult health. Discussion focuses on fetal loss, intrauterine growth restriction, preterm birth, birth defects, respiratory and other childhood diseases, neuropsychological deficits, premature or delayed sexual maturation, and certain adult cancers linked to fetal or childhood exposures. Environmental exposures considered here include chemical toxicants in air, water, soil/house dust and foods (including human breast milk), and consumer products. Reports reviewed here included original epidemiologic studies (with at least basic descriptions of methods and results), literature reviews, expert group reports, meta-analyses, and pooled analyses. Levels of evidence for causal relationships were categorized as sufficient, limited, or inadequate according to predefined criteria. There was sufficient epidemiological evidence for causal relationships between several adverse pregnancy or child health outcomes and prenatal or childhood exposure to environmental chemical contaminants. These included prenatal high-level methylmercury (CH(3)Hg) exposure (delayed developmental milestones and cognitive, motor, auditory, and visual deficits), high-level prenatal exposure to polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans (PCDFs), and related toxicants (neonatal tooth abnormalities, cognitive and motor deficits), maternal active smoking (delayed conception, preterm birth, fetal growth deficit [FGD] and sudden infant death syndrome [SIDS]) and prenatal environmental tobacco smoke (ETS) exposure (preterm birth), low-level childhood lead exposure (cognitive deficits and renal tubular damage), high-level childhood CH(3)Hg exposure (visual deficits), high-level childhood exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (chloracne), childhood ETS exposure (SIDS, new-onset asthma, increased asthma severity, lung and middle ear infections, and adult breast and lung cancer), childhood exposure to biomass smoke (lung infections), and childhood exposure to outdoor air pollutants (increased asthma severity). Evidence for some proven relationships came from investigation of relatively small numbers of children with high-dose prenatal or early childhood exposures, e.g., CH(3)Hg poisoning episodes in Japan and Iraq. In contrast, consensus on a causal relationship between incident asthma and ETS exposure came only recently after many studies and prolonged debate. There were many relationships supported by limited epidemiologic evidence, ranging from several studies with fairly consistent findings and evidence of dose-response relationships to those where 20 or more studies provided inconsistent or otherwise less than convincing evidence of an association. The latter included childhood cancer and parental or childhood exposures to pesticides. In most cases, relationships supported by inadequate epidemiologic evidence reflect scarcity of evidence as opposed to strong evidence of no effect. This summary points to three main needs: (1) Where relationships between child health and environmental exposures are supported by sufficient evidence of causal relationships, there is a need for (a) policies and programs to minimize population exposures and (b) population-based biomonitoring to track exposure levels, i.e., through ongoing or periodic surveys with measurements of contaminant levels in blood, urine and other samples. (2) For relationships supported by limited evidence, there is a need for targeted research and policy options ranging from ongoing evaluation of evidence to proactive actions. (3) There is a great need for population-based, multidisciplinary and collaborative research on the many relationships supported by inadequate evidence, as these represent major knowledge gaps. Expert groups faced with evaluating epidemiologic evidence of potential causal relationships repeatedly encounter problems in summarizing the available data. A major driver for undertaking such summaries is the need to compensate for the limited sample sizes of individual epidemiologic studies. Sample size limitations are major obstacles to exploration of prenatal, paternal, and childhood exposures during specific time windows, exposure intensity, exposure-exposure or exposure-gene interactions, and relatively rare health outcomes such as childhood cancer. Such research needs call for investments in research infrastructure, including human resources and methods development (standardized protocols, biomarker research, validated exposure metrics, reference analytic laboratories). These are needed to generate research findings that can be compared and subjected to pooled analyses aimed at knowledge synthesis.
PMID: 18470797 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/18470797?dopt=AbstractPlus
Plastics that May Be Harmful to Children and Reproductive Health
Tuesday, February 3rd, 2009This Report on plasticizers makes some strong recommendation for abatement of risk. Dr. Mark Cullen of MCS fame is one of the authors. It’s well worth reading. Jennifer Armstrong, M.D., the president of the American Academy of Environmental Medicine, sent it to us.
Larry Plumlee, M.D.
View Report at Environment and Human Health, Inc.
Summary
The plastics problem is growing in scale and complexity due to a collision of factors, including government neglect of the importance of endocrine disruption; the explosive growth of the U.S. and international plastics industry; the absence of any plastic ingredient and source labeling requirements; nearly complete recycling failure for PVC and polycarbonate plastics; environmental contamination of air, water, soils, oceans, fish and wildlife; nearly universal human exposure to BPA and DEHP from food and beverages in high income nations; the dependence of the plastics industry on petroleum; and government failure to require health and environmental testing prior to chemical production, sale, and disposal. Collectively, these pose a serious challenge to the environment and human health.
Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants.
Wednesday, January 28th, 2009Inhal Toxicol. 2008 Mar;20(5):499-506.
Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants.
Calderón-Garcidueñas L, Villarreal-Calderon R, Valencia-Salazar G, Henríquez-Roldán C, Gutiérrez-Castrellón P, Torres-Jardón R, Osnaya-Brizuela N, Romero L, Torres-Jardón R, Solt A, Reed W.
Instituto Nacional de Pediatría, Mexico City, Mexico.
Mexico City children are chronically exposed to significant concentrations of air pollutants and exhibit chronic respiratory-tract inflammation. Epidemiological, controlled human exposures, laboratory-based animal models, and in vitro/in vivo studies have shown that inflammatory, endothelial dysfunction, and endothelial damage mediators are upregulated upon exposure to particulate matter (PM). Endothelial dysfunction is a critical event in cardiovascular disease. The focus of this work was to investigate whether exposure to ambient air pollution including PM(2.5) produces systemic inflammation and endothelial injury in healthy children. We measured markers of endothelial activation, and inflammatory mediators in 52 children age 8.6+/-0.1 yr, residents of Mexico City (n: 28) or of Polotitlán (n: 24), a city with low levels of pollutants. Mexico City children had significant increases in inflammatory mediators and vasoconstrictors, including tumor necrosis factor (TNF)alpha, prostaglandin (PG) E2, C-reactive protein, interleukin-1beta, and endothelin-1. There was a significant anti-inflammatory response, and a downregulation of vascular adhesion molecule-1, intercellular adhesion molecule-1 and -2, and selectins sE and sL. Results from linear regression found TNF a positively associated with 24- and 48-h cumulative levels of PM(2.5), while the 7-d PM(2.5) value was negatively associated with the numbers of white blood cells in peripheral blood in highly exposed children. Systemic subclinical inflammation, increased endothelin- 1, and significant downregulation of soluble adhesion molecules are seen in Mexico City children. Children chronically exposed to fine PM above the standard could be at risk of developing cardiovascular diseases, atherosclerosis, stroke, and other systemic effects later in life.
PMID: 18368620 [PubMed - in process]
Effect of Honey, Dextromethorphan, and No Treatment on Nocturnal Cough and Sleep Quality
Wednesday, January 28th, 2009http://archpedi.ama-assn.org/cgi/reprint/161/12/1140.pdf
ARTICLE
Effect of Honey, Dextromethorphan, and No Treatment on Nocturnal Cough and Sleep Quality
for Coughing Children and Their Parents
Ian M. Paul, MD, MSc; Jessica Beiler, MPH; Amyee McMonagle, RN; Michele L. Shaffer, PhD; Laura Duda, MD; Cheston M. Berlin Jr, MD
Objectives: To compare the effects of a single nocturnal dose of buckwheat honey or honey-flavored dextromethorphan (DM) with no treatment on nocturnal cough and sleep difficulty associated with childhood upper respiratory tract infections.
Design: A survey was administered to parents on 2 consecutive days, first on the day of presentation when no medication had been given the prior evening and then the next day when honey, honey-flavored DM, or no treatment had been given prior to bedtime according to a partially double-blinded randomization scheme.
Setting: A single, outpatient, general pediatric practice.
Participants: One hundred five children aged 2 to 18 years with upper respiratory tract infections, nocturnal symptoms, and illness duration of 7 days or less.
Intervention: A single dose of buckwheat honey, honeyflavored DM, or no treatment administered 30 minutes prior to bedtime.
Main Outcome Measures: Cough frequency, cough severity, bothersome nature of cough, and child and parent sleep quality.
Results: Significant differences in symptom improvement were detected between treatment groups, with honey consistently scoring the best and no treatment scoring the worst. In paired comparisons, honey was significantly superior to no treatment for cough frequency and the combined score, but DM was not better than no treatment for any outcome. Comparison of honey with DM revealed no significant differences.
Conclusions: In a comparison of honey,DM,and no treatment, parents rated honey most favorably for symptomatic relief of their child’s nocturnal cough and sleep difficulty due to upper respiratory tract infection. Honey may be a preferable treatment for the cough and sleep difficulty associated
with childhood upper respiratory tract infection.
Trial Registration: clinicaltrials.gov
Identifier: NCT00127686.
Arch Pediatr Adolesc Med. 2007;161(12):1140-1146
