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BACKGROUND: Ambient air pollution exposure has been associated with childhood asthma, but previous studies have primarily focused on prevalence of asthma and asthma-related outcomes and urban traffic-related exposures. OBJECTIVE: We examined nationwide associations between pre- and postnatal exposure to ambient air pollution components and asthma incidence in children age 0–19 y. METHODS: Asthma incidence was identified from hospital admission, emergency room, and outpatient contacts among all live-born singletons born in Denmark between 1998 and 2016. We linked registry data with monthly mean concentrations of particulate matter (PM) with aerodynamic diameter ≤2.5 μm (PM2.5) and PM with aerodynamic diameter ≤10 μm (PM10), nitrogen dioxide (NO2), nitrogen oxides, elemental carbon, and organic carbon (OC), sulfur dioxide, ozone, sulfate, nitrate, ammonium, secondary organic aerosols, and sea salt. Associations were estimated with Cox proportional hazard models using fixed prenatal exposure means and time-varying postnatal exposures. RESULTS: Of the 1,060,154 children included, 6.1% had asthma during the mean follow-up period of 8.8 y. The risk of asthma increased with increasing prenatal exposure to all pollutants except for O3 and sea salt. We also observed increased risk after restriction to asthma after age 4 y, after additional adjustment for area-specific socioeconomic status, and for postnatal exposure to most pollutants. The hazard ratio (HR) associated with an interquartile range increase of 2.4 and 8.7 µg/m³ in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for PM2.5 and 1.04 (95% CI: 1.02, 1.05) for NO2, respectively. This association with PM2.5 was stable after adjustment for NO2, whereas it attenuated for NO2 to 1.01 (95% CI: 0.99, 1.03) after adjustment for PM2.5. For a 0.5-µg/m³ increase in prenatal OC exposure, for which biomass is an important source, the HR was 1.08 (95% CI: 1.06, 1.10), irrespective of adjustment for PM2.5. DISCUSSION: These findings suggest that early-life exposure to ambient air pollution from multiple sources contributes to asthma development. [ABSTRACT FROM AUTHOR]

The authors comment on a study that demonstrated a developmental version of the U.S. Environmental Protection Agency's Environmental Benefits Mapping and Analysis Program-Community Edition that is said to represent an important advance in the agency's capability for cost-benefit analyses of cumulative risks. They discuss the results of quantifying changes in concentrations of air pollutants and associated changes in pediatric emergency department visits for asthma in Atlanta, Georgia.

BACKGROUND: While various policies have been implemented globally to mitigate climate change and reduce exposure to toxic air pollutants, policy assessments have considered few if any of the benefits to children. OBJECTIVE: To comprehensively assess the co-benefits of climate change mitigation to children, we expanded the suite of adverse health outcomes in the U.S. Environmental Protection Agency's Benefits Mapping and Analysis Program (BenMAP) to include additional outcomes associated with prenatal and childhood exposure to ambient fine particulate matter (PM2.5). We applied this newly expanded program to an assessment of the U.S. Regional Greenhouse Gas Initiative (RGGI), the United States' first regional market-based regulatory program designed to reduce greenhouse gas emissions from the electric power sector within the Northeast. METHODS: We used calculated changes in ambient PM2.5 concentrations for the period 2009-2014, with newly incorporated concentration-response (C-R) functions to quantify changes in the incidence of preterm birth (PTB), term low birth weight (TLBW), autism spectrum disorder (ASD), and asthma. These outcomes are causally or likely to be causally related to PM2.5 exposure. Cost per case estimates were incorporated to monetize those changes in incidence. RESULTS: The estimated avoided cases of adverse child health outcomes included 537 asthma cases, 112 preterm births, 98 cases of ASD, and 56 cases of TLBW, with an associated avoided cost estimate ranging from $191 to $350 million. In a previous analysis of health benefits of RGGI, the only benefits accruing to children were limited to prevented cases of infant mortality and respiratory illnesses, with a monetized impact of $8.1 million-only 2-4% of the new results attributable to RGGI. CONCLUSION: The results of this innovative analysis indicate that RGGI has provided substantial child health benefits beyond those initially considered. Moreover, those health benefits had significant estimated economic value. [ABSTRACT FROM AUTHOR]

BACKGROUND: Long-term exposure to ambient air pollution can lead to adverse health effects in children; however, underlying biological mechanisms are not fully understood. OBJECTIVES: We evaluated the effect of air pollution exposure during different time periods on mRNA expression as well as circulating levels of inflammatory cytokines in children. METHODS: We measured a panel of 10 inflammatory markers in peripheral blood samples from 670 8-y-old children in the Barn/Child, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) birth cohort. Outdoor concentrations of nitrogen dioxide (NO2) and particulate matter (PM) with aerodynamic diameter <10 μm (PM10) from road traffic were estimated for residential, daycare, and school addresses using dispersion modeling. Time-weighted average exposures during infancy and at biosampling were linked to serum cytokine levels using linear regression analysis. Furthermore, gene expression data from 16-year-olds in BAMSE (n=238) were used to evaluate links between air pollution exposure and expression of genes coding for the studied inflammatory markers. RESULTS: A 10 μg=m³ increase of NO2 exposure during infancy was associated with a 13.6% (95% confidence interval (CI): 0.8; 28.1%) increase in interleukin-6 (IL-6) levels, as well as with a 27.8% (95% CI: 4.6, 56.2%) increase in IL-10 levels, the latter limited to children with asthma. However, no clear associations were observed for current exposure. Results were similar using PM10, which showed a high correlation with NO2. The functional analysis identified several differentially expressed genes in response to air pollution exposure during infancy, including IL10, IL13, and TNF. CONCLUSION: Our results indicate alterations in systemic inflammatory markers in 8-y-old children in relation to early-life exposure to traffic-related air pollution. [ABSTRACT FROM AUTHOR]

BACKGROUND: The relation between traffic-related air pollution (TRAP) exposure and the incidence of asthma/allergy in preschool children has been widely studied, but results remain heterogeneous, possibly due to differences in methodology and susceptibility to TRAP. OBJECTIVES: We aimed to study the relation of early TRAP exposure with the development of respiratory/allergic symptoms and asthma during preschool years, and to investigate parental allergy, "stressful" family events, and sex as possible effect modifiers. METHODS: We examined data of 2,015 children from the PARIS birth cohort followed up with repeated questionnaires completed by parents until age 4 years. TRAP exposure in each child's first year of life was estimated by nitrogen oxides (NOx) air dispersion modeling, taking into account both home and day care locations. Association between TRAP exposure and patterns of wheezing, dry night cough, and rhinitis symptoms was studied using multinomial logistic regression models adjusted for potential confounders. Effect modification by parental history of allergy, stressful family events, and sex was investigated. RESULTS: An interquartile range (26 μg/m3) increase in NO[sub x] levels was associated with an increased odds ratio (OR) of persistent wheezing at 4 years (adjusted OR = 1.27; 95% confidence interval: 1.09, 1.47). TRAP exposure was positively associated with persistent wheeze, dry cough, and rhinitis symptoms among children with a parental allergy, those experiencing stressful family events, and boys, but not in children whose parents did not have allergies or experience stressful events, or in girls (all interaction p-values < 0.2). CONCLUSIONS: This study supports the hypothesis that not all preschool children are equal regarding TRAP health effects. Parental history of allergy, stressful family events, and male sex may increase their susceptibility to adverse respiratory effects of early TRAP exposure. CITATION: Rancière F, Bougas N, Viola M, Momas I. 2017. Early exposure to traffic-related air pollution, respiratory symptoms at 4 years of age, and potential effect modification by parental allergy, stressful family events, and sex: a prospective follow-up study of the PARIS birth cohort. Environ Health Perspect 125:737-745; http://dx.doi.org/10.1289/EHP239 [ABSTRACT FROM AUTHOR]

Background: Although pesticide use is widespread, the possible effect of early-life exposure to organophosphate (OP) on pediatric respiratory health is not well described. Objectives: We investigated the relationship between early-life exposure to OPs and respiratory outcomes. Methods: Participants included 359 mothers and children from the CHAMACOS birth cohort. Dialkyl phosphate (DAP) metabolites of OP pesticides, specifically diethyl (DE) and dimethyl (DM) phosphate metabolites, were measured in urine from mothers twice during pregnancy (mean = 13 and 26 weeks gestation) and from children five times during childhood (0.5–5 years). Childhood DAP concentrations were estimated by the area under curve (AUC). Mothers reported their child’s respiratory symptoms at 5 and 7 years of age. We used generalized estimating equations (GEE) to examine associations of prenatal and childhood DAP concentrations with repeated measures of respiratory symptoms and exercise-induced coughing at 5 and 7 years of age, adjusting for child’s sex and age, maternal smoking during pregnancy, secondhand tobacco smoke, season of birth, PM2.5, breastfeeding, mold and cockroaches in home, and distance from highway. Results: Higher prenatal DAP concentrations, particularly DE, were nonsignificantly associated with respiratory symptoms in the previous 12 months at 5 or 7 years of age [adjusted odds ratio (aOR) per 10-fold increase = 1.44; 95% CI: 0.98, 2.12]. This association was strongest with total DAP and DE from the second half of pregnancy (aOR per 10-fold increase = 1.77; 95% CI: 1.06, 2.95; and 1.61; 95% CI: 1.08, 2.39, respectively). Childhood DAP, DE, and DM concentrations were associated with respiratory symptoms and exercise-induced coughing in the previous 12 months at 5 or 7 years of age (total DAPs: aOR per 10-fold increase = 2.53; 95% CI: 1.32, 4.86; and aOR = 5.40; 95% CI: 2.10, 13.91, respectively). Conclusions: Early-life exposure to OP pesticides was associated with respiratory symptoms consistent with possible asthma in childhood. [ABSTRACT FROM AUTHOR]

Background: Studies suggest that phthalate exposures may adversely affect child respiratory health. Objectives: We evaluated associations between asthma diagnosed in children between 5 and 11 years of age and prenatal exposures to butylbenzyl phthalate (BBzP), di-n-butyl phthalate (DnBP), di(2-ethylhexyl) phthalate (DEHP), and diethyl phthalate (DEP). Methods: Phthalate metabolites were measured in spot urine collected from 300 pregnant inner-city women. Children were examined by an allergist or pulmonologist based on the first parental report of wheeze, other respiratory symptoms, and/or use of asthma rescue/controller medication in the preceding 12 months on repeat follow-up questionnaires. Standardized diagnostic criteria were used to classify these children as either having or not having current asthma at the time of the physician examination. Children without any report of wheeze or the other asthma-like symptoms were classified as nonasthmatics at the time of the last negative questionnaire. Modified Poisson regression analyses were used to estimate relative risks (RR) controlling for specific gravity and potential confounders. Results: Of 300 children, 154 (51%) were examined by a physician because of reports of wheeze, other asthma-like symptoms, and/or medication use; 94 were diagnosed with current asthma and 60 without current asthma. The remaining 146 children were classified as nonasthmatic. Compared with levels in nonasthmatics, prenatal metabolites of BBzP and DnBP were associated with a history of asthma-like symptoms (p < 0.05) and with the diagnosis of current asthma: RR = 1.17 (95% CI: 1.01, 1.35) and RR = 1.25 (95% CI: 1.04, 1.51) per natural log-unit increase, respectively. Risk of current asthma was > 70% higher among children with maternal prenatal BBzP and DnBP metabolite concentrations in the third versus the first tertile. Conclusion: Prenatal exposure to BBzP and DnBP may increase the risk of asthma among inner-city children. However, because this is the first such finding, results require replication. [ABSTRACT FROM AUTHOR]

BACKGROUND: Genetics may partially explain observed heterogeneity in associations between traffic-related air pollution and incident asthma. OBJECTIVE: Our aim was to investigate the impact of gene variants associated with oxidative stress and inflammation on associations between air pollution and incident childhood asthma. METHODS: Traffic-related air pollution, asthma, wheeze, gene variant, and potential confounder data were pooled across six birth cohorts. Parents reported physician-diagnosed asthma and wheeze from birth to 7-8 years of age (confirmed by pediatric allergist in two cohorts). Individual estimates of annual average air pollution [nitrogen dioxide (NO2), particulate matter ≤ 2.5 μm (PM2.5), PM2.5 absorbance, ozone] were assigned to each child's birth address using land use regression, atmospheric modeling, and ambient monitoring data. Effect modification by variants in GSTP1 (rs1138272/Ala114Val and rs1695/IIe105Val) and TNF (rs1800629/G-308A) was investigated. RESULTS: Data on asthma, wheeze, potential confounders, at least one SNP of interest, and NO2 were available for 5,115 children. GSTP1 rs1138272 and TNF rs1800629 SNPs were associated with asthma and wheeze, respectively. In relation to air pollution exposure, children with one or more GSTP1 rs1138272 minor allele were at increased risk of current asthma [odds ratio (OR) = 2.59; 95% CI: 1.43, 4.68 per 10 μg/m3 NO2] and ever asthma (OR = 1.64; 95% CI: 1.06, 2.53) compared with homozygous major allele carriers (OR = 0.95; 95% CI: 0.68, 1.32 for current and OR = 1.20; 95% CI: 0.98, 1.48 for ever asthma; Bonferroni-corrected interaction p = 0.04 and 0.01, respectively). Similarly, for GSTP1 rs1695, associations between NO2 and current and ever asthma had ORs of 1.43 (95% CI: 1.03, 1.98) and 1.36 (95% CI: 1.08, 1.70), respectively, for minor allele carriers compared with ORs of 0.82 (95% CI: 0.52, 1.32) and 1.12 (95% CI: 0.84, 1.49) for homozygous major allele carriers (Bonferroni-corrected interaction p-values 0.48 and 0.09). There were no clear differences by TNF genotype. CONCLUSIONS: Children carrying GSTP1 rs1138272 or rs1695 minor alleles may constitute a susceptible population at increased risk of asthma associated with air pollution. [ABSTRACT FROM AUTHOR]

Background: Perfluorinated compounds (PFCs) are ubiquitous pollutants. Experimental data suggest that they may be associated with adverse health outcomes, including asthma. However, there is little supporting epidemiological evidence. Methods: A total of 231 asthmatic children and 225 nonasthmatic controls, all from northern Taiwan, were recruited in the Genetic and Biomarkers study for Childhood Asthma. Structure questionnaires were administered by face-to-face interview. Serum concentrations of 11 PFCs and levels of immunological markers were also measured. Associations of PFC quartiles with concentrations of immunological markers and asthma outcomes were estimated using multivariable regression models. Results: Nine PFCs were detectable in most children (≥ 84.4%), of which perfluorooctane sulfonate (PFOS) was the most abundant (median serum concentrations of 33.9 ng/mL in asthmatics and 28.9 ng/mL in controls). Adjusted odds ratios for asthma among those with the highest versus lowest quartile of PFC exposure ranged from 1.81 (95% CI: 1.02, 3.23) for the perfluorododecanoic acid (PFDoA) to 4.05 (95% CI: 2.21, 7.42) for perfluorooctanic acid (PFOA). PFOS, PFOA, and subsets of the other PFCs were positively associated with serum IgE concentrations, absolute eosinophil counts (AEC), eosinophilic cationic protein (ECP) concentrations, and asthma severity scores among asthmatics. Conclusions: This study suggests an association between PFC exposure and juvenile asthma. Because of widespread exposure to these chemicals, these findings may be of potential public health concern. [ABSTRACT FROM AUTHOR]

Background: Urban landscape elements, particularly trees, have the potential to affect airflow, air quality, and production of aeroallergens. Several large-scale urban tree planting projects have sought to promote respiratory health, yet evidence linking tree cover to human health is limited. Objectives: We sought to investigate the association of tree canopy cover with subsequent development of childhood asthma, wheeze, rhinitis, and allergic sensitization. Methods: Birth cohort study data were linked to detailed geographic information systems data characterizing 2001 tree canopy coverage based on LiDAR (light detection and ranging) and multispectral imagery within 0.25 km of the prenatal address. A total of 549 Dominican or African-American children born in 1998-2006 had outcome data assessed by validated questionnaire or based on IgE antibody response to specific allergens, including a tree pollen mix. Results: Tree canopy coverage did not significantly predict outcomes at 5 years of age, but was positively associated with asthma and allergic sensitization at 7 years. Adjusted risk ratios (RRs) per standard deviation of tree canopy coverage were 1.17 for asthma (95% CI: 1.02, 1.33), 1.20 for any specific allergic sensitization (95% CI: 1.05, 1.37), and 1.43 for tree pollen allergic sensitization (95% CI: 1.19, 1.72). Conclusions: Results did not support the hypothesized protective association of urban tree canopy coverage with asthma or allergy-related outcomes. Tree canopy cover near the prenatal address was associated with higher prevalence of allergic sensitization to tree pollen. Information was not available on sensitization to specific tree species or individual pollen exposures, and results may not be generalizable to other populations or geographic area [ABSTRACT FROM AUTHOR]

BACKGROUND: High-molecular-weight phthalates in indoor dust have been associated with asthma in children, but few studies have evaluated phthalate biomarkers in association with respiratory outcomes. OBJECTIVES: We explored the association between urinary concentrations of phthalate metabolites and current asthma. METHODS: In a cross-sectional analysis, 11 metabolites of 8 phthalates [including four metabolites of di(2-ethylhexyl) phthalate] were measured in one first morning void collected from 2001 through 2004 from 623 10-year-old Norwegian children. Logistic regression models controlling for urine specific gravity, sex, parental asthma, and income were used to estimate associations between current asthma and phthalate metabolite concentrations by quartiles or as log10-transformed variables. RESULTS: Current asthma was associated with both mono(carboxyoctyl) phthalate (MCOP) and mono(carboxynonyl) phthalate (MCNP), although the association was limited to those in the highest quartile of these chemicals. The adjusted odds ratio (aOR) for current asthma was 1.9 (95% CI: 1.0, 3.3) for the highest MCOP quartile compared with the lowest quartile, and 1.3 (95% CI: 0.98, 1.7) for an interquartile-range increase. The aOR for current asthma was 2.2 (95% CI: 1.2, 4.0) for the highest MCNP quartile and 1.3 (95% CI: 1.0, 1.7) for an interquartile-range increase. The other phthalate metabolites were not associated with current asthma. CONCLUSIONS: Current asthma was associated with the highest quartiles of MCOP and MCNP, metabolites of two high molecular weight phthalates, diisononyl phthalate and diisodecyl phthalate, respectively. Given the short biological half-life of the phthalates and the cross-sectional design, our findings should be interpreted cautiously. [ABSTRACT FROM AUTHOR]

Background: The emerging consensus that exposure to near-roadway traffic-related pollution causes asthma has implications for compact urban development policies designed to reduce driving and greenhouse gases. Objectives: We estimated the current burden of childhood asthma-related disease attributable to near-roadway and regional air pollution in Los Angeles County (LAC) and the potential health impact of regional pollution reduction associated with changes in population along major traffic corridors. Methods: The burden of asthma attributable to the dual effects of near-roadway and regional air pollution was estimated, using nitrogen dioxide and ozone as markers of urban combustion-related and secondary oxidant pollution, respectively. We also estimated the impact of alternative scenarios that assumed a 20% reduction in regional pollution in combination with a 3.6% reduction or 3.6% increase in the proportion of the total population living near major roads, a proxy for near-roadway exposure. Results: We estimated that 27,100 cases of childhood asthma (8% of total) in LAC were at least partly attributable to pollution associated with residential location within 75 m of a major road. As a result, a substantial proportion of asthma-related morbidity is a consequence of near-roadway pollution, even if symptoms are triggered by other factors. Benefits resulting from a 20% regional pollution reduction varied markedly depending on the associated change in near-roadway proximity. Conclusions: Our findings suggest that there are large and previously unappreciated public health consequences of air pollution in LAC and probably in other metropolitan areas with dense traffic corridors. To maximize health benefits, compact urban development strategies should be coupled with policies to reduce near-roadway pollution exposure. [ABSTRACT FROM AUTHOR]

Background: In the city of New Orleans, Louisiana, and surrounding parishes (NOLA), children with asthma were perilously impacted by Hurricane Katrina as a result of disrupted health care, high home mold and allergen levels, and high stress. Objectives: The Head-off Environmental Asthma in Louisiana (HEAL) study was conducted to examine relationships between the post-Katrina environment and childhood asthma in NOLA and assess a novel asthma counselor intervention that provided case management and guidance for reducing home mold and allergen levels. Methods: Children (4-12 years old) with moderate-to-severe asthma were recruited from NOLA schools. Over 1 year, they received two clinical evaluations, three home environmental evaluations, and the asthma intervention. Quarterly end points included symptom days, medication use, and unscheduled emergency department or clinic visits. A community advisory group was assembled and informed HEAL at all phases. Results: Of the children (n = 182) enrolled in HEAL, 67% were African American, and 25% came from households with annual incomes < $15,000. HEAL children were symptomatic, averaging 6.6 symptom days in the 2 weeks before baseline, and had frequent unscheduled visits to clinics or emergency departments (76% had at least one unscheduled visit in the preceding 3 months). In this report, we describe study design and baseline characteristics of HEAL children. Conclusions: Despite numerous challenges faced by investigators, study staff, and participants, including destroyed infrastructure, disrupted lives, and lost jobs, HEAL was successful in terms of recruitment and retention, the high quality of data collected that will provide insight into asthma-allergen relationships, and the asthma intervention. This success was attributable to using an adaptive approach and refining processes as needed. [ABSTRACT FROM AUTHOR]

Background: The effect of ambient air pollution on global variations and trends in asthma prevalence is unclear. Objectives: Our goal was to investigate community-level associations between asthma prevalence data from the International Study of Asthma and Allergies in Childhood (ISAAC) and satellite-based estimates of particulate matter with aerodynamic diameter < 2.5 μm (PM2.5) and nitrogen dioxide (NO2), and modelled estimates of ozone. Methods: We assigned satellite-based estimates of PM2.5 and NO2 at a spatial resolution of 0.1° x 0.1° and modeled estimates of ozone at a resolution of 1° x 1° to 183 ISAAC centers. We used center-level prevalence of severe asthma as the outcome and multilevel models to adjust for gross national income (GNI) and center- and country-level sex, climate, and population density. We examined associations (adjusting for GNI) between air pollution and asthma prevalence over time in centers with data from ISAAC Phase One (mid-1900s) and Phase Three (2001-2003). Results: For the 13- to 14-year age group (128 centers in 28 countries), the estimated average within-country change in center-level asthma prevalence per 100 children per 10% increase in center-level PM2.5 and NO2 was -0.043 [95% confidence interval (CI): -0.139, 0.053] and 0.017 (95% CI: -0.030, 0.064) respectively. For ozone the estimated change in prevalence per parts per billion by volume was -0.116 (95% CI: -0.234, 0.001). Equivalent results for the 6- to 7-year age group (83 centers in 20 countries), though slightly different, were not significantly positive. For the 13- to 14-year age group, change in center-level asthma prevalence over time per 100 children per 10% increase in PM2.5 from Phase One to Phase Three was -0.139 (95% CI: -0.347, 0.068). The corresponding association with ozone (per ppbV) was -0.171 (95% CI: -0.275, -0.067). Conclusion: In contrast to reports from within-community studies of individuals exposed to traffic pollution, we did not find evidence of a positive association between ambient air pollution and asthma prevalence as measured at the community level. [ABSTRACT FROM AUTHOR]

Background: Air pollutants have been associated with childhood asthma and wheeze. Epigenetic regulation of nitric oxide synthase—the gene responsible for nitric oxide production—may be affected by air pollutants and contribute to the pathogenesis of asthma and wheeze.Objective: Our goal was to investigate the association between air pollutants, DNA methylation, and respiratory outcomes in children.Methods: Given residential address and buccal sample collection date, we estimated 7-day, 1-month, 6-month, and 1-year cumulative average PM2.5 and PM10 (particulate matter ≤ 2.5 and ≤ 10 µm aerodynamic diameter, respectively) exposures for 940 participants in the Children’s Health Study. Methylation of 12 CpG sites in three NOS (nitric oxide synthase) genes was measured using a bisulfite-polymerase chain reaction Pyrosequencing assay. Beta regression models were used to estimate associations between air pollutants, percent DNA methylation, and respiratory outcomes.Results: A 5-µg/m3 increase in PM2.5 was associated with a 0.20% [95% confidence interval (CI): –0.32, –0.07] to 1.0% (95% CI: –1.61, –0.56) lower DNA methylation at NOS2A position 1, 0.06% (95% CI: –0.18, 0.06) to 0.58% (95% CI: –1.13, –0.02) lower methylation at position 2, and 0.34% (95% CI: –0.57, –0.11) to 0.89% (95% CI: –1.57, –0.21) lower methylation at position 3, depending on the length of exposure and CpG locus. One-year PM2.5 exposure was associated with 0.33% (95% CI: 0.01, 0.65) higher in average DNA methylation of 4 loci in the NOS2A CpG island. A 5-µg/m3 increase in 7-day and 1-year PM2.5 was associated with 0.6% (95% CI: 0.13, 0.99) and 2.8% (95% CI: 1.77, 3.75) higher NOS3 DNA methylation. No associations were observed for NOS1. PM10 showed similar but weaker associations with DNA methylation in these genes.Conclusions: PM2.5 exposure was associated with percent DNA methylation of several CpG loci in NOS genes, suggesting an epigenetic mechanism through which these pollutants may alter production of nitric oxide. [ABSTRACT FROM AUTHOR]

Background: Concerns regarding the health impact of urban air pollution on asthmatic children are pronounced along the U.S.-Mexico border because of rapid population growth near busy border highways and roads.Objectives: We conducted the first binational study of the impacts of air pollution on asthmatic children in Ciudad Juarez, Mexico, and El Paso, Texas, USA, and compared different exposure metrics to assess acute respiratory response.Methods: We recruited 58 asthmatic children from two schools in Ciudad Juarez and two schools in El Paso. A marker of airway inflammation [exhaled nitric oxide (eNO)], respiratory symptom surveys, and pollutant measurements (indoor and outdoor 48-hr size-fractionated particulate mat­ter, 48-hr black carbon, and 96-hr nitrogen dioxide) were collected at each school for 16 weeks. We examined associations between the pollutants and respiratory response using generalized linear mixed models.Results: We observed small but consistent associations between eNO and numerous pollutant metrics, with estimated increases in eNO ranging from 1% to 3% per interquartile range increase in pollutant concentrations. Effect estimates from models using school-based concentrations were generally stronger than corresponding estimates based on concentrations from ambient air monitors. Both traffic-related and non-traffic-related particles were typically more robust predictors of eNO than was nitrogen dioxide, for which associations were highly sensitive to model specification. Associations differed significantly across the four school-based cohorts, consistent with heterogene­ity in pollutant concentrations and cohort characteristics. Models examining respiratory symptoms were consistent with the null.Conclusions: The results indicate adverse effects of air pollution on the subclinical respiratory health of asthmatic children in this region and provide preliminary support for the use of air pollu­tion monitors close to schools to track exposure and potential health risk in this population. [ABSTRACT FROM AUTHOR]

Background: The fractional concentration of nitric oxide in exhaled air (FeNO) potentially detects airway inflammation related to air pollution exposure. Existing studies have not yet provided conclusive evidence on the association of FeNO with traffic-related pollution (TRP). Objectives: We evaluated the association of FeNO with residential TRP exposure in a large cohort of children. Methods: We related FeNO measured on 2,143 children (ages 7-11 years) who participated in the Southern California Children's Health Study (CHS) to five classes of metrics of residential TRP: distances to freeways and major roads; length of all and local roads within circular buffers around the home; traffic densities within buffers; annual average line source dispersion modeled nitrogen oxides (NOx) from freeways and nonfreeway roads; and predicted annual average nitrogen oxide, nitrogen dioxide, and NOx from a model based on intracommunity sampling in the CHS. Results: In children with asthma, length of roads was positively associated with FeNO, with stronger associations in smaller buffers [46.7%; 95% confidence interval (CI), 14.3-88.4], 12.4% (95% CI, -8.8 to 38.4), and 4.1% (95% CI, -14.6 to 26.8) higher FeNO for 100-, 300-, and 1,000-m increases in the length of all roads in 50-, 100-, and 200-m buffers, respectively. Other TRP metrics were not significantly associated with FeNO, even though the study design was powered to detect exposures explaining as little as 0.4% of the variation in natural log-transformed FeNO (R2 = 0.004). Conclusion: Length of road was the only indicator of residential TRP exposure associated with airway inflammation in children with asthma, as measured by FeNO. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level. OBJECTIVE: We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM2.5) air pollution versus the diesel-related carbonaceous fraction of PM2.5 METHODS: Daily 24-hr personal samples of PM2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays. RESULTS: We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03-2.04)], shortness of breath (1.41; 95% CI, 1.01-1.99), and total symptoms (1.30; 95% CI, 1.04-1.62) with an increase in personal EC, but not with personal PM2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants. CONCLUSION: Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel "soot" fraction of PM2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts. [ABSTRACT FROM AUTHOR]

Objective: Our goal was to quantify the short-term effects of particulate matter with aerodynamic diameter = 10 μm (PM10) and nitrogen dioxide (NO2) on respiratory health of asthmatic children from published panel studies, and to investigate the influence of study and population characteristics as effect modifiers. Data extraction: After a systematic literature review, we extracted quantitative estimates of the association of PM10 and/or NO2 with respiratory symptoms and peak expiratory flow (PEF). Combined effect estimates for an increase of 10 μg/m3 were calculated by random effects meta-analysis for all studies and for different strata defined by study characteristics. The effect of publication bias was investigated with Egger's and Begg's tests and "trim-and-fill" analyses. Data synthesis: We identified 36 studies; 14 were part of the European Pollution Effects on Asthmatic Children in Europe (PEACE) study. Adverse associations of PM10 with asthma symptoms were statistically significant [odds ratio (OR) = 1.028; 95% confidence interval (CI), 1.006- 1.051]. There were also associations, although not statistically significant, of PM10 with cough (OR = 1.012; 95% CI, 0.997-1.026) and on PEF (decrease of -0.082 L/min; 95% CI, -0.214 to 0.050). NO2 had statistically significant associations with asthma symptoms in the overall analysis considering all possible lags (OR = 1.031; 95% CI, 1.001-1.062), but not when we evaluated only the 0-1 lag. We found no publication bias, although it appeared when excluding the PEACE studies. When we applied the trim-and-fill method to the data set without the PEACE studies, the results were similar to the overall estimates from all studies. There was an indication for stronger PM10 associations for studies conducted in summer, outside of Europe, with longer lags, and in locations with higher NO2 concentrations. Conclusions: We found clear evidence of effects of PM10 on the occurrence of asthma symptom episodes, and to a lesser extent on cough and PEF. The results for NO2 are more difficult to interpret because they depend on the lag times examined. There was an indication of effect modification by several study conditions. [ABSTRACT FROM AUTHOR]

Objective: Despite multiple published studies regarding the association between formaldehyde exposure and childhood asthma, a consistent association has not been identified. Here we report the results of a systematic review of published literature in order to provide a more comprehensive picture of this relationship. Data sources: After a comprehensive literature search, we identified seven peer-reviewed studies providing quantitative results regarding the association between formaldehyde exposure and asthma in children. Studies were heterogeneous with respect to the definition of asthma (e.g., self-report, physician diagnosis). Most of the studies were cross-sectional. Data extraction: For each study, an odds ratio (OR) and 95% confidence interval (CI) for asthma were either abstracted from published results or calculated based on the data provided. Characteristics regarding the study design and population were also abstracted. Data synthesis: We used fixed- and random-effects models to calculate pooled ORs and 95% CIs; measures of heterogeneity were also calculated. A fixed-effects model produced an OR of 1.03 (95% CI, 1.02-1.04), and random effects model produced an OR of 1.17 (95% CI, 1.01-1.36), both reflecting an increase of 10 μg/m³ of formaldehyde. Both the Q and I³ statistics indicated a moderate amount of heterogeneity. Conclusions: Results indicate a significant positive association between formaldehyde exposure and childhood asthma. Given the largely cross-sectional nature of the studies underlying this metaanalysis, further well-designed prospective epidemiologic studies are needed. [ABSTRACT FROM AUTHOR]

Background: In the past 15 years, asthma prevalence has increased and is disproportionately distributed among children, minorities, and low-income persons. The National Institute of Environmental Health Sciences (NIEHS) Division of Extramural Research and Training developed a framework to measure the scientific and health impacts of its extramural asthma research to improve the scientific basis for reducing the health effects of asthma. Objectives: Here we apply the framework to characterize the NIEHS asthma portfolio's impact in terms of publications, clinical applications of findings, community interventions, and technology developments. Methods: A logic model was tailored to inputs, outputs, and outcomes of the NIEHS asthma portfolio. Data from existing National Institutes of Health (NIH) databases are used, along with publicly available bibliometric data and structured elicitation of expert judgment. Results: NIEHS is the third largest source of asthma-related research grant funding within the NIH between 1975 and 2005, after the National Heart, Lung, and Blood Institute and the National Institute of Allergy and Infectious Diseases. Much of NIEHS-funded asthma research focuses on basic research, but results are often published in journals focused on clinical investigation, increasing the likelihood that the work is moved into practice along the "bench to bedside" continuum. NIEHS support has led to key breakthroughs in scientific research concerning susceptibility to asthma, environmental conditions that heighten asthma symptoms, and cellular mechanisms that may be involved in treating asthma. Conclusions: If gaps and limitations in publicly available data receive adequate attention, further linkages can be demonstrated between research activities and public health improvements. This logic model approach to research impact assessment demonstrates that it is possible to conceptualize program components, mine existing databases, and begin to show longer-term impacts of program results. The next challenges will be to modify current data structures, improve the linkages among relevant databases, incorporate as much electronically available data as possible, and determine how to improve the quality and health impact of the science that we support. [ABSTRACT FROM AUTHOR]

BACKGROUND: Whether there is a causal relation between long-term exposure to traffic and asthma development is so far not clear. This may be explained by inaccurate exposure assessment. OBJECTIVE: We investigated the associations of long-term traffic-related exposures with asthma onset assessed retrospectively and respiratory symptoms in 9- to 10-year-old children. METHODS: We collected information on respiratory outcomes and potential confounding variables by parental questionnaire in 2,871 children in Oslo. Nitrogen dioxide exposure was assessed by the EPISODE dispersion model and assigned at updated individual addresses during lifetime. Distance to major road was assigned at birth address and address by date of questionnaire. Cox proportional hazard regression and logistic regression were used. RESULTS: We did not find positive associations between any long-term traffic-related exposure and onset of doctor-diagnosed asthma. An interquartile range (IQR) increase of NO2 exposure before asthma onset was associated with an adjusted risk ratio of 0.82 [95% confidence interval (CI), 0.67--1.02]. Handling early asthma cases (children < 4 years of age) with recovery during follow-up as noncases gave a less negative association. The associations for late asthma onset (≥ 4 years of age) were positive but not statistically significant. For current symptoms, an IQR increase of previous year's NO2 exposure was associated with adjusted odds ratios of 1.01 (95% CI, 0.83--1.23) for wheeze, 1.10 (95% CI, 0.79--1.51) for severe wheeze, and 1.01 (95% CI, 0.84--1.21) for dry cough. CONCLUSIONS: We were not able to find positive associations of long-term traffic-related exposures with asthma onset or with current respiratory symptoms in 9- to 10-year-old children in Oslo. [ABSTRACT FROM AUTHOR]

BACKGROUND: Little is known about the respiratory effects of short-term exposures to petroleum refinery emissions in young children. This study is an extension of an ecologic study that found an increased rate of hospitalizations for respiratory conditions among children living near petroleum refineries in Montreal (Canada). METHODS: We used a time-stratified case--crossover design to assess the risk of asthma episodes in relation to short-term variations in sulfur dioxide levels among children 2--4 years of age living within 0.5--7.5 km of the refinery stacks. Health data used to measure asthma episodes included emergency department (ED) visits and hospital admissions from 1996 to 2004. We estimated daily levels of SO2 at the residence of children using a) two fixed-site SO2 monitors located near the refineries and b) the AERMOD (American Meteorological Society/Environmental Protection Agency Regulatory Model) atmospheric dispersion model. We used conditional logistic regression to estimate odds ratios associated with an increase in the interquartile range of daily SO2 mean and peak exposures (31.2 ppb for AERMOD peaks). We adjusted for temperature, relative humidity, and regional/urban background air pollutant levels. RESULTS: The risks of asthma ED visits and hospitalizations were more pronounced for same-day (lag 0) SO2 peak levels than for mean levels on the same day, or for other lags: the adjusted odds ratios estimated for same-day SO2 peak levels from AERMOD were 1.10 [95% confidence interval (CI), 1.00--1.22] and 1.42 (95% CI, 1.10--1.82), over the interquartile range, for ED visits and hospital admissions, respectively. CONCLUSIONS: Short-term episodes of increased SO2 exposures from refinery stack emissions were associated with a higher number of asthma episodes in nearby children. [ABSTRACT FROM AUTHOR]

BACKGROUND: Air pollution is associated with respiratory symptoms, lung function decrements, and hospitalizations. However, there is little information about the influence of air pollution on lung injury. OBJECTIVE: In this study we investigated acute effects of air pollution on pulmonary function and airway oxidative stress and inflammation in asthmatic children. METHODS: We studied 182 children with asthma, 9--14 years of age, for 4 weeks. Daily ambient concentrations of sulfur dioxide, nitrogen dioxide, ozone, and particulate matter ≤ 2.5 µm in aerodynamic diameter (PM2.5) were monitored from two stations. Once a week we measured spirometry and fractional exhaled nitric oxide (FeNO), and determined thiobarbituric acid reactive substances (TBARS) and 8-isoprostane--two oxidative stress markers--and interleukin-6 (IL-6) in breath condensate. We tested associations using mixed-effects regression models, adjusting for confounding variables. RESULTS: Interquartile-range increases in 3-day average SO2 (5.4 ppb), NO2 (6.8 ppb), and PM2.5 (5.4 µg/m3) were associated with decreases in forced expiratory flow between 25% and 75% of forced vital capacity, with changes being --3.1% [95% confidence interval (CI), --5.8 to --0.3], --2.8% (95% CI, --4.8 to --0.8), and --3.0% (95% CI, --4.7 to --1.2), respectively. SO2, NO2, and PM2.5 were associated with increases in TBARS, with changes being 36.2% (95% CI, 15.7 to 57.2), 21.8% (95% CI, 8.2 to 36.0), and 24.8% (95% CI, 10.8 to 39.4), respectively. Risk estimates appear to be larger in children not taking corticosteroids than in children taking corticosteroids. O3 (5.3 ppb) was not associated with health end points. FeNO, 8-isoprostane, and IL-6 were not associated with air pollutants. CONCLUSION: Air pollution may increase airway oxidative stress and decrease small airway function of asthmatic children. Inhaled corticosteroids may reduce oxidative stress and improve airway function. [ABSTRACT FROM AUTHOR]

BACKGROUND: The association between chronic exposure to air pollution and adverse health outcomes has not been well studied. OBJECTIVE: This project investigated the impact of chronic exposure to high ozone levels on childhood asthma admissions in New York State. METHODS: We followed a birth cohort born in New York State during 1995--1999 to first asthma admission or until 31 December 2000. We identified births and asthma admissions through the New York State Integrated Child Health Information System and linked these data with ambient ozone data (8-hr maximum) from the New York State Department of Environmental Conservation. We defined chronic ozone exposure using three indicators: mean concentration during the followup period, mean concentration during the ozone season, and proportion of follow-up days with ozone levels > 70 ppb. We performed logistic regression analysis to adjust for child's age, sex, birth weight, and gestational age; maternal race/ethnicity, age, education, insurance status, smoking during pregnancy, and poverty level; and geographic region, temperature, and copollutants. RESULTS: Asthma admissions were significantly associated with increased ozone levels for all chronic exposure indicators (odds ratios, 1.16--1.68), with a positive dose--response relationship. We found stronger associations among younger children, low sociodemographic groups, and New York City residents as effect modifiers. CONCLUSION: Chronic exposure to ambient ozone may increase the risk of asthma admissions among children. Younger children and those in low socioeconomic groups have a greater risk of asthma than do other children at the same ozone level. [ABSTRACT FROM AUTHOR]

BACKGROUND: Despite extensive evidence that air pollution affects childhood asthma, state-level and national-level tracking of asthma outcomes in relation to air pollution is limited. OBJECTIVES: Our goals were to evaluate the feasibility of linking the 2001 California Health Interview Survey (CHIS), air monitoring, and traffic data; estimate associations between traffic density (TD) or outdoor air pollutant concentrations and childhood asthma morbidity; and evaluate the usefulness of such databases, linkages, and analyses to Environmental Public Health Tracking (EPHT). METHODS: We estimated TD within 500 feet of residential cross-streets of respondents and annual average pollutant concentrations based on monitoring station measurements. We used logistic regression to examine associations with reported asthma symptoms and emergency department (ED) visits/hospitalizations. RESULTS: Assignment of TD and air pollution exposures for cross-streets was successful for 82% of children with asthma in Los Angeles and San Diego, California, Counties. Children with asthma living in high ozone areas and areas with high concentrations of particulate matter < 10 µm in aerodynamic diameter experienced symptoms more frequently, and those living close to heavy traffic reported more ED visits/hospitalizations. The advantages of the CHIS for asthma EPHT include a large and representative sample, biennial data collection, and ascertainment of important sociodemographic and residential address information. Disadvantages are its cross-sectional design, reliance on parental reports of diagnoses and symptoms, and lack of information on some potential confounders. CONCLUSIONS: Despite limitations, the CHIS provides a useful framework for examining air pollution and childhood asthma morbidity in support of EPHT, especially because later surveys address some noted gaps. We plan to employ CHIS 2003 and 2005 data and novel exposure assessment methods to re-examine the questions raised here. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

BACKGROUND: Asthma is the most important chronic disease of childhood. The U.S. Environmental Protection Agency has concluded that children with asthma continue to be susceptible to ozone-associated adverse effects on their disease. OBJECTIVES: This study was designed to evaluate time trends in associations between declining warm-season O3 concentrations and hospitalization for asthma in children. METHODS: We undertook an ecologic study of hospital discharges for asthma during the high O3 seasons in California's South Coast Air Basin (SoCAB) in children who ranged in age from birth to 19 years from 1983 to 2000. We used standard association and causal statistical analysis methods. Hospital discharge data were obtained from the State of California; air pollution data were obtained from the California Air Resources Board, and demographic data from the 1980, 1990, and 2000 U.S. Census. SoCAB was divided into 195 spatial grids, and quarterly average O3, sulfur dioxide, particulate matter with aerodynamic diameter ≤ 10 µm, nitrogen dioxide, and carbon monoxide were assigned to each unit for 3-month periods along with demographic variables. RESULTS: O3 was the only pollutant associated with increased hospital admissions over the study period. Inclusion of a variety of demographic and weather variables accounted for all of the non-O3 temporal changes in hospitalizations. We found a time-independent, constant effect of ambient levels of O3 and quarterly hospital discharge rates for asthma. We estimate that the average effect of a 10-ppb mean increase in any given mean quarterly 1-hr maximum O3 over the 18-year median of 87.7 ppb was a 4.6% increase in the same quarterly outcome. CONCLUSIONS: Our data indicate that at current levels of O3 experienced in Southern California, O3 contributes to an increased risk of hospitalization for children with asthma. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent studies indicate that the composition of fine particulate matter [PM≤2.5 μm in aerodynamic diameter (PM2.5)] is associated with increased hospitalizations for cardiovascular and respiratory diseases. The metal composition of PM2.5 influences allergic and/or inflammatory reactions, and ambient zinc contributes to worsening pulmonary function in susceptible adults. However, information is limited concerning associations between ambient air zinc levels and health care utilization for asthma, especially among children. OBJECTIVE: We aimed to investigate the relationship between outdoor ambient air PM2.5 zinc levels and urgent health care utilization for children living in an urban area. METHODS: We used a time-series study to estimate the association of ambient air PM2.5 zinc levels with hospital admissions and emergency department (ED) utilization by children in Baltimore, Maryland, controlling for time trends. We used data from daily discharge administrative claims of ED and hospital utilization for asthma in children, 0-17 years of age for Greater Baltimore from June 2002 through November 2002. We collected ambient air PM2.5 metal concentration data, determined by X-ray fluorescence spectroscopy, during the U.S. Environmental Protection Agency-sponsored Baltimore Supersite project. RESULTS: Previous-day medium levels of zinc (8.63-20.76 ng/m³) are associated with risks of pediatric asthma exacerbations that are 1.23 (95% confidence interval, 1.07-1.41) times higher than those with previous-day low levels of zinc (< 8.63 ng/m³) after accounting for time-varying potential confounders. CONCLUSION: Results suggest that high ambient air PM2.5 zinc levels are associated with an increase in ED visits/hospital admissions for asthma on the following day among children living in an urban area. [ABSTRACT FROM AUTHOR]

BACKGROUND: Glutathione S-transferase P1 (GSTP1) plays a role in a spectrum of respiratory diseases; however, the effects of sequence variation across the entire locus in asthma pathogenesis have yet to be determined. OBJECTIVES: This study was designed to investigate whether sequence variations in the GSTP1 coding and promoter regions are associated with asthma and wheezing outcomes and to determine whether variants affect susceptibility to maternal smoking. METHODS: Four haplotype tagging SNPs were selected that accounted for 83% of the common haplotypic variation in GSTP1. The associations of GSTP1 variants with asthma and wheezing were assessed among white children in the Children's Health Study (CHS). RESULTS: The Ile105Val allele and a SNP in the upstream promoter region (SNP1: rs6591255, putative transcription factor 1 binding site) were associated with asthma and wheezing outcomes, an association observed in two cohorts of the CHS recruited in different years. Haplotypes that included both the promoter SNP (i.e., rs6591255) and the 105 Val variant were associated with an increased risk for asthma in non-Hispanic whites. Using SNP- and haplotype-based approaches, the effect of maternal smoking on wheezing was largest in children with the Ile105Val allele. CONCLUSIONS: Variants in both the promoter and coding regions of the GSTP1 locus may contribute to the occurrence of childhood asthma and wheezing and may increase susceptibility to adverse effects of tobacco-smoke exposure. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent studies have identified associations between the concentration of phthalates in indoor dust and allergic symptoms in the airways, nose, and skin. OBJECTIVES: Our goal was to investigate the associations between allergic symptoms in children and the concentration of phthalate esters in settled dust collected from children's homes in Sofia and Burgas, Bulgaria. METHODS: Dust samples from the child's bedroom were collected. A total of 102 children (2-7 years of age) had symptoms of wheezing, rhinitis, and/or eczema in preceding 12 months (cases), and 82 were nonsymptomatic (controls). The dust samples were analyzed for their content of dimethyl phthalate (DMP), diethyl phthalate (DEP), di-n-butyl phthalate (DnBP), butyl benzyl phthalate (BBzP), di(2-ethylhexyl) phthalate (DEHP), and di-n-octyl phthalate (DnOP). RESULTS: A higher concentration of DEHP was found in homes of case children than in those of controls (1.24 vs. 0.86 mg/g dust). The concentration of DEHP was significantly associated with wheezing in the preceding 12 months (p = 0.035) as reported by parents. We found a dose-response relationship between DEHP concentration and case status and between DEHP concentration and wheezing in the preceding 12 months. CONCLUSIONS: This study shows an association between concentration of DEHP in indoor dust and wheezing among preschool children in Bulgaria. [ABSTRACT FROM AUTHOR]

OBJECTIVES: We assessed whether any household dust reduction intervention has the effect of increasing or decreasing the development or severity of atopic disease. DATA SOURCES: Electronic searches on household intervention and atopic disease were conducted in January 2007 in EMBASE, MEDLINE, and the Cochrane Central Register of Controlled Trials. No date or language restriction was placed on the literature search. DATA EXTRACTION: We included randomized controlled trials comparing asthma outcomes in a household intervention group with either placebo intervention or no intervention. DATA SYSNTHESIS: Fourteen studies met the inclusion criteria. Eight recruited antenatally and measured development of atopic disease. Six recruited known atopic individuals and measured disease status change. Meta-analyses on the prevention studies found that the interventions made no difference to the onset of wheeze but made a significant reduction in physician-diagnosed asthma. Metaanalysis of lung function outcomes indicated no improvement due to the interventions but found a reduction in symptom days. Qualitatively, health care was used less in those receiving interventions. However, in one study that compared intervention, placebo, and control arms, the reduction in heath care use was similar in the placebo and intervention arms. CONCLUSIONS: This review suggests that there is not sufficient evidence to suggest implementing hygiene measures in an attempt to improve outcomes in existing atopic disease, but interventions from birth in those at high risk of atopy are useful in preventing diagnosed asthma but not parental-reported wheeze. [ABSTRACT FROM AUTHOR]

BACKGROUND: Polymorphisms in the proinflammatory cytokine genes tumor necrosis factor-α (TNF) and lymphotoxin-α (LTA, also called TNF-α) have been associated with asthma and atopy in some studies. Parental smoking is a consistent risk factor for childhood asthma. Secondhand smoke and ozone both stimulate TNF production. OBJECTIVES: Our goal was to investigate whether genetic variation in TNF and LTA is associated with asthma and atopy and whether the association is modified by parental smoking in a Mexican population with high ozone exposure. METHODS: We genotyped six tagging single nucleotide polymorphisms (SNPs) in TNF and LTA, including functional variants, in 596 nuclear families consisting of asthmatics 4-17 years of age and their parents in Mexico City. Atopy was determined by skin prick tests. RESULTS: The A allele of the TNF-308 SNP was associated with increased risk of asthma [relative risk (RR) = 1.54; 95% confidence interval (CI), 1.04-2.28], especially among children of nonsmoking parents (RR = 2.06; 95% CI, 1.19-3.55; p for interaction = 0.09). Similarly, the A allele of the TNF-238 SNP was associated with increased asthma risk among children of nonsmoking parents (RR = 2.21; 95% CI, 1.14-4.30; p for interaction = 0.01). LTA SNPs were not associated with asthma. Haplotype analyses reflected the single SNP findings in magnitude and direction. TNF and LTA SNPs were not associated with the degree of atopy. CONCLUSIONS: Our results suggest that genetic variation in TNF may contribute to childhood asthma and that associations may be modified by parental smoking. [ABSTRACT FROM AUTHOR]

BACKGROUND AND OBJECTIVES: Early-life exposure to environmental tobacco smoke (ETS) can result in developmental delay as well as childhood asthma and increased risk of cancer. The high cost of childhood asthma related to ETS exposure has been widely recognized; however, the economic impact of ETS-related developmental delay has been less well understood. METHODS AND RESULTS: The Columbia Center for Children's Environmental Health (CCCEH) has reported adverse effects of prenatal ETS exposure on child development in a cohort of minority women and children in New York City (odds ratio of developmental delay = 2.36; 95% confidence interval 1.22–4.58). Using the environmentally attributable fraction (EAF) approach, we estimated the annual cost of one aspect of ETS-related developmental delay: Early Intervention Services. The estimated cost of these services per year due to ETS exposure is > $50 million per year for New York City Medicaid births and $99 million per year for all New York City births. CONCLUSION: The high annual cost of just one aspect of developmental delay due to prenatal exposure to ETS provides further impetus for increased prevention efforts such as educational programs to promote smoke-free homes, additional cigarette taxes, and subsidizing of smoking cessation programs. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Home dampness and the presence of mold and allergens have been associated with asthma morbidity. We examined changes in asthma morbidity in children as a result of home remediation aimed at moisture sources. DESIGN: In this prospective, randomized controlled trial, symptomatic, asthmatic children (n = 62), 2–17 years of age, living in a home with indoor mold, received an asthma intervention including an action plan, education, and individualized problem solving. The remediation group also received household repairs, including reduction of water infiltration, removal of water-damaged building materials, and heating/ventilation/air-conditioning alterations. The control group received only home cleaning information. We measured children's total and allergen-specific serum immunoglobulin E, peripheral blood eosinophil counts, and urinary cotinine. Environmental dust samples were analyzed for dust mite, cockroach, rodent urinary protein, endotoxin, and fungi. The follow-up period was 1 year. RESULTS: Children in both groups showed improvement in asthma symptomatic days during the preremediation portion of the study. The remediation group had a significant decrease in symptom days (p = 0.003, as randomized; p = 0.004, intent to treat) after remodeling, whereas these parameters in the control group did not significantly change. In the postremediation period, the remediation group had a lower rate of exacerbations compared with control asthmatics (as treated: 1 of 29 vs. 11 of 33, respectively, p = 0. 003; intent to treat: 28.1% and 10.0%, respectively, p = 0.11). CONCLUSION: Construction remediation aimed at the root cause of moisture sources and combined with a medical/behavioral intervention significantly reduces symptom days and health care use for asthmatic children who live in homes with a documented mold problem. [ABSTRACT FROM AUTHOR]

This mini-monograph was developed to highlight the experiences of the National Institute of Environmental Health Sciences (NIEHS)/U.S. Environmental Protection Agency (EPA) Centers for Children's Environmental Health and Disease Prevention Research, focusing particularly on several areas of interest for the National Children's Study. These include general methodologic issues for conducting longitudinal birth cohort studies and community-based participatory research and for measuring air pollution exposures, pesticide exposures, asthma, and neurobehavioral toxicity. Rather than a detailed description of the studies in each of the centers, this series of articles is intended to provide information on the practicalities of conducting such intensive studies and the lessons learned. This explication of lessons learned provides an outstanding opportunity for the planners of the National Children's Study to draw on past experiences that provide information on what has and has not worked when studying diverse multiracial and multiethnic groups of children with unique urban and rural exposures. The Children's Centers have addressed and overcome many hurdles in their efforts to understand the link between environmental exposures and health outcomes as well as interactions between exposures and a variety of social and cultural factors. Some of the major lessons learned include the critical importance of long-term studies for assessing the full range of developmental consequences of environmental exposures, recognition of the unique challenges presented at different life stages for both outcome and exposure measurement, and the importance of ethical issues that must be dealt with in a changing medical and legal environment. It is hoped that these articles will be of value to others who are embarking on studies of children's environmental health. [ABSTRACT FROM AUTHOR]

The National Children's Study will address, among other illnesses, the environmental causes of both incident asthma and exacerbations of asthma in children. Seven of the Centers for Children's Environmental Health and Disease Prevention Research (Children's Centers), funded by the National Institute of Environmental Health Sciences and the U.S. Environmental Protection Agency, conducted studies relating to asthma. The design of these studies was diverse and included cohorts, longitudinal studies of older children, and intervention trials involving asthmatic children. In addition to the general lessons provided regarding the conduct of clinical studies in both urban and rural populations, these studies provide important lessons regarding the successful conduct of community research addressing asthma. They demonstrate that it is necessary and feasible to conduct repeated evaluation of environmental exposures in the home to address environmental exposures relevant to asthma. The time and staff required were usually underestimated by the investigators, but through resourceful efforts, the studies were completed with a remarkably high completion rate. The definition of asthma and assessment of disease severity proved to be complex and required a combination of questionnaires, pulmonary function tests, and biologic samples for markers of immune response and disease activity. The definition of asthma was particularly problematic in younger children, who may exhibit typical asthma symptoms sporadically with respiratory infections without developing chronic asthma. Medications confounded the definition of asthma disease activity, and must be repeatedly and systematically estimated. Despite these many challenges, the Children's Centers successfully conducted long-term studies of asthma. [ABSTRACT FROM AUTHOR]

Outdoor carbon monoxide comes mainly from vehicular emissions, and high concentrations occur in areas with heavy traffic congestion. CO binds to hemoglobin, forming carboxyhemoglobin (COHb), and reduces oxygen delivery. We investigated the link between the adverse effects of CO on the respiratory system using COHb as a marker for chronic CO exposure. We examined the relationship between acute respiratory infections (ARIs) and COHb concentrations in school-age children living in urban and suburban areas of Quito, Ecuador. We selected three schools located in areas with different traffic intensities and enrolled 960 children. To adjust for potential confounders we conducted a detailed survey. In a random subsample of 295 children, we determined that average COHb concentrations were significantly higher in children attending schools in areas with high and moderate traffic, compared with the low-traffic area. The percentage of children with COHb concentrations above the safe level of 2.5% were 1, 43, and 92% in low-, moderate-, and high-traffic areas, respectively. Children with COHb above the safe level are 3.25 [95% confidence interval (CI), 1.65-6.38] times more likely to have ARI than children with COHb < 2.5%. Furthermore, with each percent increase in COHb above the safety level, children are 1.15 (95% CI, 1.03-1.28) times more likely to have an additional case of ARI. Our findings provide strong evidence of the relation between CO exposure and susceptibility to respiratory infections. [ABSTRACT FROM AUTHOR]

Global phthalate ester production has increased from very low levels at the end of' World War H to approximately 3.5 million metric tons/year. The aim of the present study was to investigate potential associations between persistent allergic symptoms in children, which have increased markedly in developed countries over the past three decades, and the concentration of phthalates in dust collected from their homes. This investigation is a case-control study nested within a cohort of' 10,852 children. From the cohort, we selected 198 cases with persistent allergic symptoms and 202 controls without allergic symptoms. A clinical and a technical team investigated each child and her or his environment. We found higher median concentrations of butyl benzyl phthalate (BBzP) in dust among cases than among controls (0.15 vs. 0.12 μg/g dust). Analyzing the case group by symptoms showed that BBzP was associated with rhinitis (p = 0.00 1) and eczema (p = 0.001), whereas di(2-ethylhexyl) phthalate (DEHP) was associated with asthma (p = 0.022). Furthermore, dose-response relationships for these associations are supported by trend analyses. This study shows that phthalates, within the range of what is normally found in indoor environments, are associated with allergic symptoms in children. We believe that the different associations of symptoms for the three major phthalates-BBzP, DEI-IP, and di-n-butyl phthalate-can be explained by a combination of chemical physical properties and toxicologic potential. Given the phthalate exposures of children worldwide, the results from this study of Swedish children have global implications. [ABSTRACT FROM AUTHOR]

The article discusses a meeting by the President's Task Force on Environment Health Risks and Safety Risks to Children to renew its commitment in the U.S. on October 14, 2015. Topics include identifying priority risks and issues that can be addressed by interagency efforts, developing strategies to protect children's health, and communicating information to decision makers to protect children's environmental health and safety. Gins McCarthy and Sylvia Matthews Burwell organized the meeting.

The article presents information on social impact bonds (SIBs), that will support efforts to reduce emergency department visits and hospital stays related to asthma in Fresno, California. As part of a pilot program, 200 local children with asthma will begin preventive care early in 2013; and the researchers will match each child's diagnosis and treatment costs, and provide them with an idea of savings that could come from preventive care.

The article presents information on a study conducted on asthma among children living near major roadways in Los Angeles County, which concluded that reducing regional pollution by 20 percent would result in fewer cases of bronchitis among children with asthma.