Obese Asthmatic Children Research Articles

Greater susceptibility of girls to airborne Benzo[a]pyrene for obesity-associated childhood asthma

BackgroundSexually dimorphic risk of obesity-associated asthma is posited to accelerate around puberty. Yet, the role of air pollution on the lean and obese asthmatic children has never been examined. ObjectiveTo compare whether a unit exposure to airborne benzo[a]pyrene (B[a]P) is associated with altered risks of asthma across the overweight/obese (OV/OB) control, lean asthmatic, and OV/OB asthmatic children, respectively, compared to the lean controls, before and after adjusting for oxidant stress markers (i.e. 15‑F2t‑IsoP, 8‑oxo‑dG, and Carbonyl). MethodsAsthmatic and healthy control children, recruited from polluted urban and rural areas, were matched to ambient concentration of B[a]P. A unit increase in B[a]P and multinomial logistic regression on OV/OB control, lean asthmatic, and OV/OB asthma were compared across the sex- and age-groups. ResultsThe median B[a]P was associated with a linear increase among the female children, according to OV/OB and asthma, respectively, and together, compared to the lean control girls (p = 0.001). While B[a]P was associated with positive relationship with 15‑F2t‑IsoP level among the OV/OB boys, the same exposure-outcome association was inverse among the OV/OB girls. One natural log-unit increase in ambient B[a]P was associated with 10.5-times greater odds (95% CI, 2.6–39.6; p = 0.001) the adolescent OV/OB boys, compared to the unit odds among the lean controls. In contrast, the adolescent OV/OB girls were associated with highest adjusted odds of the asthma (aOR = 15.4; 95% CI, 2.9–29.1; p < 0.001) compared to the lean control girls. An adjustment for 15‑F2t‑IsoP, and Carbonyls was associated with greater odds of asthma per unit exposure for the adolescent OV/OB girls (aOR = 16.2; 95% CI, 1.4–181.8; p = 0.024). ConclusionsB[a]P exposure was associated with a leap in the odds of asthma among the OV/OB adolescents, particularly the girls, after adjusting for 15‑F2t‑IsoP and Carbonyls.

Biomarkers of airway and systemic inflammation in obese asthmatic paediatric patients

BackgroundIt is thought that airway inflammation is more common in obese asthmatic patients because inflammation is harder to control and does not respond well to glucocorticoid treatment. ObjectiveThis study's aim was to investigate the effect of obesity on airway and systemic inflammation in children with asthma and to identify the biomarkers that play a role in this inflammation. MethodsThe study included patients aged 6–16 years who were diagnosed with asthma in the paediatric allergy outpatient clinic of Bagcilar Training and Research Hospital in Turkey. Complete blood count parameters were compared between three groups: obese asthmatic (n=43), obese non-asthmatic (n=45), and non-obese non-asthmatic (control group, n=30). Levels of high-sensitive CRP (hs-CRP), neutrophil gelatinase-associated lipocalin (NGAL), osteopontin (OPN), and matrix metalloproteinase-9 (MMP-9), and 25(OH)-vitamin D were compared between the groups. ResultsNo statistically significant differences were observed in 25(OH)-vitamin D, NGAL, OPN, hs-CRP, and MMP-9 levels between groups. There was a statistically significant negative correlation between FEV1/FVC and NGAL and MMP-9. ConclusionThis is the first study to investigate levels of hs-CRP, NGAL, OPN, MMP-9, and 25(OH)-vitamin D in obese asthmatic children. Larger studies with sputum and BAL examinations are required to determine the potential of biomarkers for identifying inflammation in obese asthmatic children.

CDC42-related genes are upregulated in helper T cells from obese asthmatic children

Pediatric obesity-related asthma is more severe and less responsive to medications than asthma in normal-weight children. Obese asthmatic children have nonatopic TH1-polarized systemic inflammation that correlates with pulmonary function deficits, but the pathways underlying TH1-polarized inflammation are not well understood. We compared the CD4+ T-cell transcriptome in obese children with asthma with that in normal-weight children with asthma to identify key differentially expressed genes associated with TH1-polarized inflammation. CD4+ T-cell transcriptome-wide differential gene expression was compared between 21 obese and 21 normal-weight children by using directional RNA sequencing. High-confidence differentially expressed genes were verified in the first cohort and validated in a second cohort of 20 children (10 obese and 10 normal-weight children) by using quantitative RT-PCR. Transcriptome-wide differential gene expression among obese asthmatic children was enriched for genes, including VAV2, DOCK5, PAK3, PLD1, CDC42EP4, and CDC42PBB, which are associated with CDC42, a small guanosine triphosphate protein linked to T-cell activation. Upregulation of MLK3 and PLD1, genes downstream of CDC42 in the mitogen-activated protein kinase and mammalian target of rapamycinpathways and the inverse correlation of CDC42EP4 and DOCK5 transcript counts with FEV1/FVC ratio together support a role of CDC42 in the TH1 polarization and pulmonary function deficits found in patients with obesity-related asthma. Our study identifies the CDC42 pathway as a novel target that is upregulated in TH cells of obese asthmatic children, suggesting its role in nonatopic TH1-polarized systemic inflammation and pulmonary function deficits found in patients with pediatric obesity-related asthma.

The effect of obesity, weight gain, and weight loss on asthma inception and control.

There is ample and growing evidence that obesity increases the risk of asthma and morbidity from asthma. Here, we review recent clinical evidence supporting a causal link between obesity and asthma, and the mechanisms that may lead to 'obese asthma'. Although in some children obesity and asthma simply co-occur, those with 'obese asthma' have increased asthma severity, lower quality of life, and reduced medication response. Underlying mechanistic pathways may include anatomical changes of the airways such as obstruction and dysanapsis, systemic inflammation, production of adipokines, impaired glucose-insulin metabolism, altered nutrient levels, genetic and epigenetic changes, and alterations in the airway and/or gut microbiome. A few small studies have shown that weight loss interventions may lead to improvements in asthma outcomes, but thus far research on therapeutic interventions for these children has been limited. Obesity increases the risk of asthma - and worsens asthma severity or control - via multiple mechanisms. 'Obese asthma' is a complex, multifactorial phenotype in children. Obesity and its complications must be managed as part of the treatment of asthma in obese children.

Serum resistin as an asthma marker and predictor of inhaled corticosteroid response in bronchial asthma in children

Adipokines are factors produced by adipose tissue, that may be proinflammatory (such as leptin and resistin) or anti-inflammatory (such as adiponectin). Effects of these adipokines on the lungs have the potential to evoke or exacerbate asthma. AimOur aim was to assess if serum resistin level is changed in obese and non obese asthmatic children and if it can predict their responsiveness to inhaled glucocorticoids. MethodsSerum levels of resistin, were measured in 60 asthmatic children (30 obese and 30 non obese asthmatic children), and in 30 age and sex matched healthy controls. The measurements were repeated in all asthmatics after 8weeks of treatment with inhaled corticosteroids. ResultsSerum resistin levels were found to be significantly elevated in all asthmatic children than control group and it was significantly elevated in obese children, compared with asthmatic non obese and control children 35±0.2ng/mL vs 20±0.25 vs 10±0.11ng/mL respectively (F<0.005). There was negative correlation between asthma severity as detected by FEV1 and serum resistin levels. Serum resistin levels in all asthmatic children had no correlation with duration of asthma in years. Serum resistin level was significantly reduced in all asthmatic children after inhaled corticosteroids for 8weeks. Also asthmatic children with good response to inhaled corticosteroids had high initial resistin levels compared to corticosteroids non-responder. ConclusionsFrom these results we can conclude that resistin can be considered as a marker of asthma and its severity and high resistin levels can predict favourable anti-inflammatory effect of inhaled glucocorticoids suggesting that resistin may be a marker of steroid-sensitive genotype in asthma in children.

Vitamin D Levels of Asthmatic Children with and Without Obesity

Objective: Asthma and obesity are important public health problems that affect millions of people in the world. Recently it has been shown that vitamin D may affect the prevalence of allergic disease and obesity. In this study, we evaluated the correlations between vitamin D, asthma, obesity and severity of asthma. Materials and Methods: One hundred and nineteen subjects were included in the study. The study population consisted of four ageand sex-matched groups: Obese asthmatic children as group 1 (n:34), non-obese asthmatic children as group 2 (n:28), obese nonasthmatic children as group 3 (n:30) and non-obese non-asthmatic children as group 4 (n:27). Results: There was no significant difference in serum vitamin D levels between groups. Also there was no difference between groups when we compared the serum vitamin D levels according to the severity of asthma. Conclusion: There was no correlation between levels of serum vitamin D and presence of asthma and obesity.

Impaired glucose metabolism and bronchial hyperresponsiveness in obese prepubertal asthmatic children.

The prevalence of asthma and obesity has risen in parallel over the last decades, but the exact mechanisms linking these two diseases still remain unclear. The aim of the present study was to investigate the associations between bronchial hyperresponsiveness (BHR), impaired glucose metabolism, obesity, and asthma in prepubertal children. A total of 71 prepubertal children were included in the study and divided in four groups according to the presence of asthma and their Body Mass Index (BMI): Group 1-Healthy Controls (HC), Group 2-Non Obese Asthmatics (NOA), Group 3-Obese Non Asthmatics (ONA), Group 4-Obese Asthmatics (OA) Αll children underwent spirometry and bronchial hyperresponsiveness testing by using the cumulative Provoking Dose of mannitol (PD15, primary study variable); homeostasis model assessment-estimated insulin resistance (HOMA-IR) index was calculated in order to evaluate insulin resistance. Obese children also underwent an oral glucose tolerance testing (OGTT). A statistically significant difference in bronchial hyperreactivity (mean ± SD) was detected in the group of obese asthmatic children who had lower values ​​of PD15 , (174.16 ± 126.42) as compared to normal weight asthmatic children (453.93 ± 110.27), (P < 0.001). Moreover, obese asthmatic children with confirmed insulin resistance (HOMA-IR ≥2.5), had significantly lower PD15 values (89.05 ± 42.75) as ​​compared to those with HOMA-IR <2.5 (259.27 ± 125.75), (P = 0.006). Finally, obese asthmatic children with impaired OGTT had likewise significantly lower PD15 (81.02 ± 42.16) measurements as compared to children with normal OGTT (267.3 ± 112.62), (P = 0.001). Our findings suggest that obesity per se does not correlate to airway hyperreactivity unless it is accompanied by glucose intolerance and insulin resistance. Pediatr Pulmonol. 2017;52:160-166. © 2016 Wiley Periodicals, Inc.

Vitamin D and pulmonary function in obese asthmatic children.

Asthma-related morbidity is higher among children with vitamin D deficiency and obesity, morbidities that frequently co-exist among minority children. However, the effect of co-existent obesity and vitamin D deficiency on pulmonary function is poorly understood. We compared percent-predicted values of pulmonary function across vitamin D categories among 72 obese and 71 normal-weight Hispanic and African-American children with asthma recruited at an urban children's hospital. Serum cytokines associated with Th1 and Th2 inflammation and 25-hydroxyvitamin D (25-OHD) were quantified in fasting serum. 25-OHD levels ≥30 ng/ml were categorized as sufficient, <30 and ≥20 ng/ml as insufficient, and <20 ng/ml as deficient. The role of inflammation was investigated by regression analysis. Vitamin D deficiency was present in 50% of children and did not differ by obese status. Forced Expiratory Volume in the first second (84.5 ± 9.4 vs. 94.8 ± 8.4, P < 0.001), and Functional Residual Capacity (67.5 ± 20.1 vs. 79.3 ± 19, P = 0.01) were lower among vitamin D deficient obese asthmatics than their sufficient counterparts, and Total Lung Capacity was lower than their insufficient counterparts (86.9 ± 14.3 vs. 96.6 ± 10, P = 0.01); similar associations were not observed in normal-weight asthmatics and were not influenced by systemic inflammation. No association between Th1 and Th2 inflammatory measures, vitamin D deficiency, and pulmonary function tests was found. Vitamin D deficiency was associated with pulmonary function deficits among obese children, but not among normal-weight children with asthma, an association that was independent of Th1 and Th2 serum inflammatory measures. Vitamin D deficiency may be one potential mechanism underlying the obese-asthma phenotype. Pediatr Pulmonol. 2016;51:1276-1283. © 2016 Wiley Periodicals, Inc.

Association of wider neck circumference and asthma in obese children

BackgroundObesity is a well-established risk factor for asthma. Previous studies have reported that central obesity is associated with asthma. ObjectiveTo investigate the association between fat distribution, which is determined by anthropometric measures, including neck circumference (NC), and asthma in school-aged children. MethodsChildren diagnosed as having asthma were enrolled along with controls who were admitted to our outpatient department with allergic symptoms, such as rhinitis, urticaria and atopic dermatitis. Anthropometric measures, including height, weight, NC, waist circumference, and hip circumference, were obtained. Skin prick tests, blood eosinophil counts, and serum total IgE level measurements were performed. ResultsA total of 196 children (92 male [46.9%]) were included. Asthma was present in 102 patients (52.1%). Ninety-one of the patients (46.4%) were overweight, and 45 patients (22.9%) were obese. The NC of children with asthma was significantly higher than that of children in the control group. Grades defined according to NC percentiles were also significantly different between groups. In children with asthma, the prevalence of children with an NC higher than the 90th percentile (grade 6) was more frequent when compared with controls. The median NC of obese-overweight children with asthma was significantly higher compared with obese-overweight controls without asthma. Results of multivariable logistic regression analysis revealed that the presence of an NC in the greater than 90th percentile was associated with asthma in obese-overweight children. ConclusionThis study found that NC, which is a simple anthropometric measure, is associated with asthma in obese children.

The lipid profile in obese asthmatic children compared to non-obese asthmatic children

BackgroundA relationship between asthma and obesity has been documented in children and adolescents. An alternate day calorie restriction diet has been reported to improve asthma symptoms by decreasing levels of serum cholesterol and triglycerides, reducing markers of oxidative stress and increasing levels of the antioxidant uric acid. Therefore, to investigate the lipid profile in asthmatic children may be important in asthma control treatment. Materials and methodsOne hundred and sixty newly diagnosed persistent asthmatic children were selected to participate in the study. They were divided into four groups based on their body mass index (BMI): Group I normal weight (BMI=20–24.9kg/m2, n=30); Group II under-weight (BMI<20kg/m2, n=30); Group III overweight (BMI=25–30kg/m2, n=25); and Group IV obese (BMI>30kg/m2, n=25). Fasting blood sugar, fasting insulin, and HbA1c were measured to exclude the possibility of pre-diabetes. Lipid profile measurements included total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), apo-A1, apo-B and triglycerides. ResultsThere were no significant differences in the levels of apo-A1, apo-B, triglycerides, cholesterol and LDL in all four groups. Only the level of HDL was higher in GIV>GIII>GII>GI (75.84±13.95, 68.56±15.28, 64.17±13.93, 63.17±14.34mg/dl, respectively). There were no cases of pre-diabetes in any of the four groups. ConclusionHypercholesterolaemia and hypertriglyceridaemia were not found in any of the persistent asthmatic children, and thus they are not high risk factors for asthma. Similarly, there were no differences in apo-A1 and apo-B between any of the BMI groups. No differences were found in LDL levels, however HDL levels were increased in all four groups, indicating that allergic sensitisation may have occurred. Controlling body weight and restricting calorie intake may be as important as appropriate pharmacological management in controlling asthma.

Serum Lipid Profile and Leptin Levels in Asthmatic Libyan Children

Aim:To study lipid profile and leptin levels in non-obese Libyan children with asthma.. Materials and Methods:70 Libyan children from Pediatrics Department, Faculty of Medicine, Benghazi University, Benghazi, Libya were included for the present study (from 2013 to 2014). Group I formed the normal control group (N: 30 Children) and Group II is 40 Libyan children with asthma. Their age group varied from 4 to 12 years old. Serum lipid profile and leptin were measured by routine standard methods. Results and discussion: The Libyan children with asthma showed an increase in serum total cholesterol, LDL cholesterol, VLDL cholesterol, HDL cholesterol and triglycerides. Serum Leptin levels did not show marked changes between the two groups. The presence of hypercholesterolemia could be a triggering factor for generation of proinflammatory response in these children. Though leptin levels did not show marked response further studies may be necessary to study the role of leptin in obese asthmatic Libyan children.

Asthma and insulin resistance in obese children and adolescents.

Obese children and adolescents have an increased risk for asthma. A few studies have evaluated the association of insulin resistance and asthma in obese pediatric populations. We examined whether there was a relationship between high degrees of insulin resistance and the presence of asthma in obese children and adolescents. A total of 153 patients aged 4-15 years with at or above the 95th percentile BMI for age were prospectively recruited. Assessments included diagnosis of asthma, skin prick test reactivity to common environmental aeroallergens, and HOMA estimated insulin resistance, with the median (2.22) used as a cutoff value to categorize insulin resistance. There were 56 (36.6%) asthmatic and 97 (63.4%) non-asthmatic patients. HOMA values were significantly associated with positive skin tests (p = 0.008) and allergic asthma diagnosis (p = 0.016). Baseline insulin value was significantly associated with the risk of presenting asthma with positive skin testing (odds ratio 1.084, p = 0.037). Differences in age, BMI, and waist circumference were found between the groups of HOMA-IR <2.22 and ≥2.22. Waist circumference (WC) was significantly associated with FVC (p = 0.0001) and FEV1 (p < 0.0003); the greater the WC, the lower FVC and FEV1 values. Insulin resistance is a risk for allergic asthma in obese children and adolescents. Waist circumference was related to CVF and FEV1 impairment.

Diet-Induced Weight Loss in Obese Children With Asthma: A Randomized Controlled Trial

ME Jensen, PG Gibson, CE Collins, JM Hilton, LG Wood. Clin Exp Allergy. 2013;43(7):775–784 The goal of this study was to assess if dietary intervention (DI) can achieve weight loss in obese asthmatic children and if diet-induced weight loss leads to changes in asthma outcomes. The study evaluated 32 obese (BMI z score ≥1.64 SD score) Australian children aged 8 to 17 years, with a physician diagnosis of asthma. Exclusion criteria included unexplained weight change during the past 3 months, inflammatory or endocrine disorders, and respiratory disorders other than asthma. In this 10-week, randomized controlled trial, 32 obese asthmatic children were randomized to …

Asthma and obesity in children: current evidence and potential systems biology approaches.

Both obesity and asthma are highly prevalent, complex diseases modified by multiple factors. Genetic, developmental, lung mechanical, immunological and behavioural factors have all been suggested as playing a causal role between the two entities; however, their complex mechanistic interactions are still poorly understood and evidence of causality in children remains scant. Equally lacking is evidence of effective treatment strategies, despite the fact that imbalances at vulnerable phases in childhood can impact long-term health. This review is targeted at both clinicians frequently faced with the dilemma of how to investigate and treat the obese asthmatic child and researchers interested in the topic. Highlighting the breadth of the spectrum of factors involved, this review collates evidence regarding the investigation and treatment of asthma in obese children, particularly in comparison with current approaches in 'difficult-to-treat' childhood asthma. Finally, the authors propose hypotheses for future research from a systems-based perspective.

Macrophage activation, age and sex effects of immunometabolism in obese asthma.

Obese asthma is characterised by infiltration of adipose tissue by activated macrophages and mast cells. The aim of this study was to examine the age and sex effects of immunometabolism in obese asthma. Obese and non-obese asthmatic children and adults underwent spirometry, body composition assessment by dual energy X-ray absorptiometry and measurement of serum soluble CD163 (sCD163), tryptase, C-reactive protein (CRP) and other adipocytokines. Plasma CRP (p<0.01) and leptin (p<0.01) were elevated in obese asthmatic adults, and sCD163 (p=0.003) was elevated in obese asthmatic children. We observed significantly higher sCD163 in obese female children compared to obese female adults and male children, and higher CRP in obese female adults compared to obese male children and adults. Serum tryptase concentrations were not significantly different across age groups. sCD163 positively correlated with the proportion of android fat in obese female children (r=0.70, p=0.003) and obese female adults (r=0.65, p=0.003). In obese female children, sCD163 was inversely associated with forced expiratory volume in 1 s % predicted (r=-0.55, p=0.02) and was positively associated with the Asthma Control Questionnaire (r=0.57, p=0.02). Obese children with asthma have sex-specific macrophage activation, which may contribute to worse asthma control and lung function. The heterogeneous systemic inflammatory profile across age and sex suggests the existence of sub-phenotypes in obese asthma at the molecular level.

Characterization of the Immune Inflammatory Profile in Obese Asthmatic Children

Asthma and obesity are two common disorders often associated in children and characterized by an inflammatory status. Growing evidences support a connection between obesity and asthma since weight reduction can improve asthmatic symptoms. In this study, we have enrolled eighty children: 17 non asthmatics and non obese, 19 obese, 28 asthmatics-obese and, 16 asthmatics non-obese, respectively. In all participants, respiratory functional tests and body mass index (BMI) were calculated. Moreover, systemic inflammation of biomarkers such as T helper (h)1-type, Th2-type and T regulatory-type serum cytokines along with major adipokines was determined. Data will show that the association between asthma and obesity leads to a predominant Th1-type response with an increase in pro-inflammatory cytokines. This inflammatory profile in asthmatics-obese children is sustained by elevated serum levels of leptin and visfatin, while adiponectin concentration is rather diminished. Finally, levels of systemic inflammatory biomarkers positively correlate with the increase in BMI values in all population subgroups.

Quality of life among urban children with obesity and asthma.

To investigate quality of life (QoL) among obese asthmatic children and elucidate its association with lung function. Preadolescent inner-city children with obesity, asthma, both, or neither completed the Pediatric Quality of Life 4.0 (PedsQL) and Asthma Quality of Life Questionnaires and spirometry testing. Spirometric indices, composite and individual QoL scores were compared between groups using analysis of variance while proportion of children reporting item-specific impairment were compared by chi-squaretest. The composite QoL scores did not differ between obese asthmatics and the other study groups. FEV1/FVC was the lowest among obese asthmatics but did not correlate with QoL measures. Overall QoL in obese asthmatic preadolescents is well preserved. Since QoL measures did not correlate with spirometric indics, asthma severity may not serve as a surrogate marker of QoL. QoL evaluation should be incorporated in asthma management and early identification of changes may prevent further deterioration.

High expression of Toll-like receptors 2 and 9 and Th1/Th2 cytokines profile in obese asthmatic children.

Asthma is a common pulmonary disease with chronic inflammation of the airways, and obesity is a chronic state of low-grade inflammation. Toll-like receptors (TLRs) are involved in the innate immune response. This study was designed to analyze whether obesity has an effect on the immune response of patients with asthma. We included obese asthmatic, obese, asthmatic, and healthy children. Biochemical and anthropometric analyses were performed. Interleukin (IL)-2, interferon (IFN) gamma, IL-4, IL-10, IL-1beta, and tumor necrosis factor alpha were measured. Peripheral blood mononuclear cells were analyzed by immunostaining with anti-TLR2 and anti-TLR9 antibodies. The data were expressed as means ± SEM or medians and percentiles. Kruskal-Wallis test and Dunn's multiple comparison test were applied. Asthmatic patients, both obese and nonobese, exhibited a mild asthma phenotype; none had infectious process, exacerbation, or acute symptoms during the 30 days before the inclusion in the study. The IL-2 and IFN-gamma levels in the obese asthmatic group were lower than in the other three groups. IL-4 levels in the obese asthmatic group were almost equal to those of the asthmatic group and more than in the other two groups, without significant difference. There were higher levels of TLR2 and TLR9 in obese asthmatic patients than in the other three groups. There is a decrease in Th1 cytokines in obese asthmatic patients, and we only found a trend to an increased Th2 profile. Patients studied do not appear to fit into any of the endotypes described until now. This is the first study showing the high expression of TLR2 and TLR9 in obese asthmatic patients. It is necessary to study other cytokines in obese asthmatic patients to see if it is possible to fit them into any of the already described endotypes or if it is a distinct endotype.

Obesity and Asthma in Children: Current and Future Therapeutic Options

With the childhood prevalence of obesity and asthma increasing, it is important for pediatric professionals to appreciate that obesity modifies the diagnosis and management of asthma. These disease modifications present challenges to clinical management, including decreased responsiveness to controller therapy and decreased quality of life compared with normal-weight asthmatic children. While consensus guidelines do not currently suggest specific changes in asthma management for obese patients, management of some patients may be improved with consideration of the latest evidence. This article briefly summarizes what is known regarding the complex relationship between obesity and asthma in children, and discusses practical issues associated with the diagnosis and effective clinical management of asthma in obese children. On average, obese patients with asthma do not respond as well to inhaled corticosteroid therapy. Management approaches including weight loss and routine exercise are safe, and may improve important asthma outcomes. Asthma providers should learn to facilitate weight loss for their obese patients. In addition, pharmacologic interventions for weight loss in obese asthma, though not currently recommended, may soon be considered.

Polycyclic aromatic hydrocarbon exposure, obesity and childhood asthma in an urban cohort

BackgroundExposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAHs) from traffic emissions and other combustion sources, and childhood obesity, have been implicated as risk factors for developing asthma. However, the interaction between these two on asthma among young urban children has not been studied previously. MethodsExposure to early childhood PAHs was measured by two week residential indoor monitoring at age 5–6 years in the Columbia Center for Children's Environmental Health birth cohort (n=311). Semivolatile [e.g., methylphenanthrenes] and nonvolatile [e.g., benzo(a)pyrene] PAHs were monitored. Obesity at age 5 was defined as a body mass index (BMI) greater than or equal to the 95th percentile of the year 2000 age- and sex-specific growth charts (Center for Disease Control). Current asthma and recent wheeze at ages 5 and 7 were determined by validated questionnaires. Data were analyzed using a modified Poisson regression in generalized estimating equations (GEE) to estimate relative risks (RR), after adjusting for potential covariates. ResultsNeither PAH concentrations or obesity had a main effect on asthma or recent wheeze. In models stratified by presence/absence of obesity, a significant positive association was observed between an interquartile range (IQR) increase in natural log-transformed 1-methylphenanthrene (RR [95% CI]: 2.62 [1.17–5.88] with IQRln=0.76), and 9-methylphenanthrene (2.92 [1.09–7.82] with IQRln=0.73) concentrations and asthma in obese children (n=63). No association in non-obese (n=248) children was observed at age 5 (Pinteraction<0.03). Similar associations were observed for 3-methylphenanthrene, 9-methylphenanthrene, and 3,6-dimethylphenanthrene at age 7. ConclusionsObese young children may be more likely to develop asthma in association with greater exposure to PAHs, and methylphenanthrenes in particular, than non-obese children.