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1.  New Books 
PMCID: PMC2430264
7.  The Beat 
Environmental Health Perspectives  2008;116(6):A244-A245.
PMCID: PMC2430258
9.  Food Additives and Hyperactivity 
Environmental Health Perspectives  2008;116(6):A240-A241.
PMCID: PMC2430256  PMID: 18560504
12.  Perfluoroalkane Acids and Fetal Growth 
PMCID: PMC2430253  PMID: 18560501
18.  ERRATA 
PMCID: PMC2430247
19.  Carcinogenicity of Aspartame in Rats Not Proven 
Environmental Health Perspectives  2008;116(6):A239-A240.
PMCID: PMC2430246  PMID: 18560494
21.  EHP Papers of the Year, 2008 
PMCID: PMC2430244
22.  Genetics of Hemostasis: Differential Effects of Heritability and Household Components Influencing Lipid Concentrations and Clotting Factor Levels in 282 Pediatric Stroke Families 
Environmental Health Perspectives  2008;116(6):839-843.
The identification of heritable and environmental factors possibly influencing a condition at risk should be a prerequisite for the search for the proportion of variance attributable for shared environmental effects (c2) modulating the risk of disease. Such epidemiologic approaches in families with a first acute ischemic stroke during early childhood are lacking.
Our goal was to estimate the phenotypic variation within lipid concentrations and coagulation factor levels and to estimate the proportions attributable to heritability (h2r) and c2 in pediatric stroke families.
Blood samples were collected from 1,002 individuals from 282 white stroke pedigrees. We estimated h2r and c2 for lipoprotein (a) [Lp(a)], cholesterol, high-density lipoprotein, low-density lipoprotein (LDL), fibrinogen, factor (F) II, FV, FVIIIC, von Willebrand factor (vWF), antithrombin, protein C, protein S, plasminogen, protein Z, total tissue factor pathway inhibitor (TFPI), prothrombin fragment F1.2, and D-dimer, using the variance component method in sequential oligogenetic linkage analysis routines.
When incorporating h2r and c2 in one model adjusted for age, blood group, sex, smoking, and hormonal contraceptives, significant h2r estimates were found for Lp(a), LDL, fibrinogen, protein C, and protein Z. In addition to the significant h2r estimates, c2 showed a significant effect on phenotypic variation for fibrinogen, protein C, and protein Z. A significant c2 effect was found for cholesterol, and plasma levels of FII, FV, vWF, antithrombin, protein S, plasminogen, and TFPI, ranging from 9.3% to 33.2%.
Our research stresses the importance of research on the genetic variability and lifestyle modifications of risk factors associated with pediatric stroke.
PMCID: PMC2430243  PMID: 18560491
heritability; household; lifestyle; pediatric stroke; smoking
23.  Air Pollution, Airway Inflammation, and Lung Function in a Cohort Study of Mexico City Schoolchildren 
Environmental Health Perspectives  2008;116(6):832-838.
The biological mechanisms involved in inflammatory response to air pollution are not clearly understood.
In this study we assessed the association of short-term air pollutant exposure with inflammatory markers and lung function.
We studied a cohort of 158 asthmatic and 50 nonasthmatic school-age children, followed an average of 22 weeks. We conducted spirometric tests, measurements of fractional exhaled nitric oxide (FeNO), interleukin-8 (IL-8) in nasal lavage, and pH of exhaled breath condensate every 15 days during follow-up. Data were analyzed using linear mixed-effects models.
An increase of 17.5 μg/m3 in the 8-hr moving average of PM2.5 levels (interquartile range) was associated with a 1.08-ppb increase in FeNO [95% confidence interval (CI), 1.01–1.16] and a 1.07-pg/mL increase in IL-8 (95% CI 0.98–1.19) in asthmatic children and a 1.16 pg/ml increase in IL-8 (95% CI, 1.00–1.36) in nonasthmatic children. The 5-day accumulated average of exposure to particulate matter < 2.5 μm in aerodynamic diamter (PM2.5) was significantly inversely associated with forced expiratory volume in 1 sec (FEV1) (p = 0.048) and forced vital capacity (FVC) (p = 0.012) in asthmatic children and with FVC (p = 0.021) in nonasthmatic children. FeNO and FEV1 were inversely associated (p = 0.005) in asthmatic children.
Exposure to PM2.5 resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.
PMCID: PMC2430242  PMID: 18560490
air pollution; airway inflammation; asthma; epidemiology; lung function; schoolchildren
24.  Association of Environmental Cadmium Exposure with Pediatric Dental Caries 
Environmental Health Perspectives  2008;116(6):821-825.
Although animal experiments have shown that cadmium exposure results in severe dental caries, limited epidemiologic data are available on this issue.
We aimed to examine the relationship between environmental cadmium exposure and dental caries in children 6–12 years of age.
We analyzed cross-sectional data, including urine cadmium concentrations and counts of decayed or filled tooth surfaces, from the Third National Health and Nutrition Examination Survey. We used logistic and zero-inflated negative binomial (ZINB) regression to estimate the association between urine cadmium concentrations and caries experience, adjusting these analyses for potential confounders including environmental tobacco smoke (ETS).
Urine cadmium concentrations ranged from 0.01 to 3.38 ng/mL. Approximately 56% of children had experienced caries in their deciduous teeth, and almost 30% had been affected by caries in their permanent dentition. An interquartile range (IQR) increase in creatinine-corrected cadmium concentrations (0.21 μg/g creatinine) corresponded to a 16% increase in the odds of having experienced caries in deciduous teeth [prevalence odds ratio (OR) = 1.16; 95% confidence interval (CI), 0.96–1.40]. This association was statistically significant in children with low ETS exposure (prevalence OR = 1.30; 95% CI, 1.01–1.67). The results from the ZINB regression indicated that, among children with any caries history in their deciduous teeth, an IQR increase in cadmium was associated with 17% increase in the number of decayed or filled surfaces. We observed no association between cadmium and caries experience in permanent teeth.
Environmental cadmium exposure may be associated with increased risk of dental caries in deciduous teeth of children.
PMCID: PMC2430240  PMID: 18560540
children; dental caries; environmental tobacco smoke; NHANES III; urine cadmium
25.  Meeting Report: Atmospheric Pollution and Human Reproduction 
Environmental Health Perspectives  2008;116(6):791-798.
There is a growing body of epidemiologic literature reporting associations between atmospheric pollutants and reproductive outcomes, particularly birth weight and gestational duration.
The objectives of our international workshop were to discuss the current evidence, to identify the strengths and weaknesses of published epidemiologic studies, and to suggest future directions for research.
Participants identified promising exposure assessment tools, including exposure models with fine spatial and temporal resolution that take into account time–activity patterns. More knowledge on factors correlated with exposure to air pollution, such as other environmental pollutants with similar temporal variations, and assessment of nutritional factors possibly influencing birth outcomes would help evaluate importance of residual confounding. Participants proposed a list of points to report in future publications on this topic to facilitate research syntheses. Nested case–control studies analyzed using two-phase statistical techniques and development of cohorts with extensive information on pregnancy behaviors and biological samples are promising study designs. Issues related to the identification of critical exposure windows and potential biological mechanisms through which air pollutants may lead to intrauterine growth restriction and premature birth were reviewed.
To make progress, this research field needs input from toxicology, exposure assessment, and clinical research, especially to aid in the identification and exposure assessment of feto-toxic agents in ambient air, in the development of early markers of adverse reproductive outcomes, and of relevant biological pathways. In particular, additional research using animal models would help better delineate the biological mechanisms underpinning the associations reported in human studies.
PMCID: PMC2430236  PMID: 18560536
atmospheric pollution; bias; birth weight; environment; exposure assessment; fecundity; geographic information system; intrauterine growth restriction; particulate matter; pregnancy; reproduction; small for gestational age

Results 1-25 (10553)