Otitis media incidence and risk factors in a population-based birth cohort

Otitis media is the main reason young children receive antibiotics and is the leading reason for physician visits. OBJECTIVE: To characterize the incidence, recurrence and risk factors for otitis media in a population-based birth cohort. METHODS: All children born in southwestern British Columbia during 1999 to 2000 were followed until the age of three years. Otitis media was defined using The International Classification of Diseases, Ninth Revision coding of physician visits, and linked with antibiotic prescription data. Information on sex, birth weight, gestational age, Aboriginal status, maternal age, older siblings, maternal smoking during pregnancy, breastfeeding initiation, neighbourhood income, female education and rural residence were obtained from vital statistics, birth hospitalizations, perinatal registry and census data.RESULTS: Complete risk factor information was available for 50,474 children (86% of all births). Nearly one-half of the children (48.6%) had one or more physician visits for otitis media during follow-up, and 3952 children (7.8%) met the definition for recurrent otitis media. Of the children with at least three visits during follow-up (n=7571), 73% had their initial visit during the first year of life. Aboriginal status, maternal age younger than 20 years, male sex and older siblings were the strongest risk factors identified in the adjusted conditional logistic regression models. DISCUSSION: The present study established a population-based birth cohort by linking multiple administrative databases to characterize the incidence of and risk factors for otitis media. Although the incidence of otitis media is generally low in southwestern British Columbia, important risk factors continue to be young maternal age, mothers who smoke during pregnancy and children with Aboriginal ancestry

Air pollution and respiratory infections during early childhood: an analysis of 10 European birth cohorts within the ESCAPE Project

Background: Few studies have investigated traffic-related air pollution as a risk factor for respiratory infections during early childhood. Objectives: We aimed to investigate the association between air pollution and pneumonia, croup, and otitis media in 10 European birth cohorts—BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), MAAS (United Kingdom), PIAMA (the Netherlands), and four INMA cohorts (Spain)—and to derive combined effect estimates using meta-analysis. Methods: Parent report of physician-diagnosed pneumonia, otitis media, and croup during early childhood were assessed in relation to annual average pollutant levels [nitrogen dioxide (NO2), nitrogen oxide (NOx), particulate matter ≤ 2.5 μm (PM2.5), PM2.5 absorbance, PM10, PM2.5–10 (coarse PM)], which were estimated using land use regression models and assigned to children based on their residential address at birth. Identical protocols were used to develop regression models for each study area as part of the ESCAPE project. Logistic regression was used to calculate adjusted effect estimates for each study, and random-effects meta-analysis was used to calculate combined estimates. Results: For pneumonia, combined adjusted odds ratios (ORs) were elevated and statistically significant for all pollutants except PM2.5 (e.g., OR = 1.30; 95% CI: 1.02, 1.65 per 10-μg/m3 increase in NO2 and OR = 1.76; 95% CI: 1.00, 3.09 per 10-μg/m3 PM10). For otitis media and croup, results were generally null across all analyses except for NO2 and otitis media (OR = 1.09; 95% CI: 1.02, 1.16 per 10-μg/m3). Conclusion: Our meta-analysis of 10 European birth cohorts within the ESCAPE project found consistent evidence for an association between air pollution and pneumonia in early childhood, and some evidence for an association with otitis media.The research leading to these results was funded by the European Community’s Seventh Framework Program (FP7/2007–2011) under grant 211250. The BAMSE study was supported by the Swedish Research Council FORMAS (for Environment, Agricultural Sciences and Spatial Planning), the Stockholm County Council, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Swedish Environmental Protection Agency. The GINIplus study was supported for the first 3 years by the Federal Ministry for Education, Science, Research and Technology, Germany (interventional arm) and Helmholtz Zentrum München, Germany (former GSF; National Research Center for Environment and Health) (observational arm). The LISAplus study was supported by grants from the Federal Ministry for Education, Science, Research and Technology, Germany; Helmholtz Zentrum München, Germany (former GSF); Helmholtz Centre for Environmental Research–UFZ, Germany; Marien-Hospital Wesel, Germany; and Pediatric Practice, Bad Honnef, Germany. The PIAMA study is supported by The Netherlands Organization for Health Research and Development; The Netherlands Organization for Scientific Research; The Netherlands Asthma Fund; The Netherlands Ministry of Spatial Planning, Housing, and the Environment; and The Netherlands Ministry of Health, Welfare, and Sport. MAAS was supported by an Asthma UK Grant (04/014); the JP Moulton Charitable Foundation, UK; and the James Trust and Medical Research Council, UK (G0601361). INMA was funded by grants from the Spanish Ministry of Health-Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FISPI041436, FIS-PI081151, FIS-PI042018, FIS-PI09/02311, FIS-PI06/0867, FIS-PS09/00090, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314, and 09/02647); Generalitat de Catalunya-CIRIT, Spain (1999SGR 00241); Conselleria de Sanitat Generalitat Valenciana, Spain; Universidad de Oviedo, Obra social Cajastur, Spain; Department of Health of the Basque Government, Spain (2005111093 and 2009111069); Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001), Spain; and Fundación Roger Torné, Spain. GASPII was funded by The Italian Ministry of Health (ex art.12 D.Lgs 502/92, 2001

Associations between particulate matter elements and early-life pneumonia in seven birth cohorts: results from the ESCAPE and TRANSPHORM projects

Evidence for a role of long-term particulate matter exposure on acute respiratory infections is growing. However, which components of particulate matter may be causative remains largely unknown. We assessed associations between eight particulate matter elements and early-life pneumonia in seven birth cohort studies (Ntotal = 15,980): BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), INMA (Spain), MAAS (United Kingdom) and PIAMA (The Netherlands). Annual average exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc, each respectively derived from particles with aerodynamic diameters ≤ 10 μm (PM10) and 2.5 μm (PM2.5), were estimated using standardized land use regression models and assigned to birth addresses. Cohort-specific associations between these exposures and parental reports of physician-diagnosed pneumonia between birth and two years were assessed using logistic regression models adjusted for host and environmental covariates and total PM10 or PM2.5 mass. Combined estimates were calculated using random-effects meta-analysis. There was substantial within and between-cohort variability in element concentrations. In the adjusted meta-analysis, pneumonia was weakly associated with zinc derived from PM10 (OR: 1.47 (95% CI: 0.99, 2.18) per 20 ng/m3 increase). No other associations with the other elements were consistently observed. The independent effect of particulate matter mass remained after adjustment for element concentrations. In conclusion, associations between particulate matter mass exposure and pneumonia were not explained by the elements we investigated. Zinc from PM10 was the only element which appeared independently associated with a higher risk of early-life pneumonia. As zinc is primarily attributable to non-tailpipe traffic emissions, these results may suggest a potential adverse effect of non-tailpipe emissions on health.This research received funding from the European Community's Seventh Framework Program (FP7/2007-2011): ESCAPE (grant agreement number: 211250) and TRANSPHORM (ENV.2009.1.2.2.1). The Swedish Research Council FORMAS, the Stockholm County Council, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Swedish Environmental Protection Agency supported BAMSE. The Italian Ministry of Health (ex art.12 D.Lgs 502/92, 2001) supported GASPII. The GINIplus study was supported for the first three years by grants of the Federal Ministry for Education, Science, Research and Technology (grant no. 01 EE 9401-4). The LISAplus study was supported by grants 01 EG 9732 and 01 EG 9705/2 from the Federal Ministry for Education, Science, Research and Technology, by the Federal Ministry for Environment (IUF, FKZ 20462296) and by the Helmholtz Zentrum München, Munich Center of Health. The Netherlands Organization for Health Research and Development, The Netherlands Organization for Scientific Research, The Netherlands Asthma Fund, The Netherlands Ministry of Spatial Planning, Housing, and the Environment and The Netherlands Ministry of Health, Welfare and Sport supported PIAMA. An Asthma UK Grant 04/014, the Moulton Charitable Trust, the James Trust and Microsoft Research supported MAAS. Grants from the Spanish Ministry of Health-Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FISPI041436, FIS-PI081151, FIS-PI042018, FIS-PI09/02311, FIS-PI06/0867, FIS-PS09/00090, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314, and 09/02647), Generalitat de Catalunya-CIRIT 1999SGR 00241, Conselleria de Sanitat Generalitat Valenciana, Universidad de Oviedo, Obra social Cajastur, Department of Health of the Basque Government (2005111093 and 2009111069), Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001) and Fundación Roger Torné supported INMA

GSTP1 and TNF Gene Variants and Associations between Air Pollution and Incident Childhood Asthma: The Traffic, Asthma and Genetics (TAG) Study

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.Medicine, Department ofPopulation and Public Health (SPPH), School ofNon UBCMedicine, Faculty ofReviewedFacult

Air pollution and respiratory infections during early childhood: an analysis of 10 European birth cohorts within the ESCAPE Project

Background: Few studies have investigated traffic-related air pollution as a risk factor for respiratory infections during early childhood. Objectives: We aimed to investigate the association between air pollution and pneumonia, croup, and otitis media in 10 European birth cohorts—BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), MAAS (United Kingdom), PIAMA (the Netherlands), and four INMA cohorts (Spain)—and to derive combined effect estimates using meta-analysis. Methods: Parent report of physician-diagnosed pneumonia, otitis media, and croup during early childhood were assessed in relation to annual average pollutant levels [nitrogen dioxide (NO2), nitrogen oxide (NOx), particulate matter ≤ 2.5 μm (PM2.5), PM2.5 absorbance, PM10, PM2.5–10 (coarse PM)], which were estimated using land use regression models and assigned to children based on their residential address at birth. Identical protocols were used to develop regression models for each study area as part of the ESCAPE project. Logistic regression was used to calculate adjusted effect estimates for each study, and random-effects meta-analysis was used to calculate combined estimates. Results: For pneumonia, combined adjusted odds ratios (ORs) were elevated and statistically significant for all pollutants except PM2.5 (e.g., OR = 1.30; 95% CI: 1.02, 1.65 per 10-μg/m3 increase in NO2 and OR = 1.76; 95% CI: 1.00, 3.09 per 10-μg/m3 PM10). For otitis media and croup, results were generally null across all analyses except for NO2 and otitis media (OR = 1.09; 95% CI: 1.02, 1.16 per 10-μg/m3). Conclusion: Our meta-analysis of 10 European birth cohorts within the ESCAPE project found consistent evidence for an association between air pollution and pneumonia in early childhood, and some evidence for an association with otitis media.The research leading to these results was funded by the European Community’s Seventh Framework Program (FP7/2007–2011) under grant 211250. The BAMSE study was supported by the Swedish Research Council FORMAS (for Environment, Agricultural Sciences and Spatial Planning), the Stockholm County Council, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Swedish Environmental Protection Agency. The GINIplus study was supported for the first 3 years by the Federal Ministry for Education, Science, Research and Technology, Germany (interventional arm) and Helmholtz Zentrum München, Germany (former GSF; National Research Center for Environment and Health) (observational arm). The LISAplus study was supported by grants from the Federal Ministry for Education, Science, Research and Technology, Germany; Helmholtz Zentrum München, Germany (former GSF); Helmholtz Centre for Environmental Research–UFZ, Germany; Marien-Hospital Wesel, Germany; and Pediatric Practice, Bad Honnef, Germany. The PIAMA study is supported by The Netherlands Organization for Health Research and Development; The Netherlands Organization for Scientific Research; The Netherlands Asthma Fund; The Netherlands Ministry of Spatial Planning, Housing, and the Environment; and The Netherlands Ministry of Health, Welfare, and Sport. MAAS was supported by an Asthma UK Grant (04/014); the JP Moulton Charitable Foundation, UK; and the James Trust and Medical Research Council, UK (G0601361). INMA was funded by grants from the Spanish Ministry of Health-Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FISPI041436, FIS-PI081151, FIS-PI042018, FIS-PI09/02311, FIS-PI06/0867, FIS-PS09/00090, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314, and 09/02647); Generalitat de Catalunya-CIRIT, Spain (1999SGR 00241); Conselleria de Sanitat Generalitat Valenciana, Spain; Universidad de Oviedo, Obra social Cajastur, Spain; Department of Health of the Basque Government, Spain (2005111093 and 2009111069); Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001), Spain; and Fundación Roger Torné, Spain. GASPII was funded by The Italian Ministry of Health (ex art.12 D.Lgs 502/92, 2001