An approach to estimating the environmental burden of cancer from known and probable carcinogens: application to Ontario, Canada.

BACKGROUND: Quantifying the potential cancer cases associated with environmental carcinogen exposure can help inform efforts to improve population health. This study developed an approach to estimate the environmental burden of cancer and applied it to Ontario, Canada. The purpose was to identify environmental carcinogens with the greatest impact on cancer burden to support evidence-based decision making. METHODS: We conducted a probabilistic assessment of the environmental burden of cancer in Ontario. We selected 23 carcinogens that we defined as "environmental" (e.g., pollutants) and were relevant to the province, based on select classifications provided by the International Agency for Research on Cancer. We evaluated population exposure to the carcinogens through inhalation of indoor/outdoor air; ingestion of food, water, and dust; and exposure to radiation. We obtained or calculated concentration-response functions relating carcinogen exposure and the risk of developing cancer. Using both human health risk assessment and population attributable fraction models in a Monte Carlo simulation, we estimated the annual cancer cases associated with each environmental carcinogen, reporting the simulation summary (e.g., mean and percentiles). RESULTS: We estimated between 3540 and 6510 annual cancer cases attributable to exposure to 23 environmental carcinogens in Ontario. Three carcinogens were responsible for over 90% of the environmental burden of cancer: solar ultraviolet (UV) radiation, radon in homes, and fine particulate matter (PM2.5) in outdoor air. Eight other carcinogens had an estimated mean burden of at least 10 annual cancer cases: acrylamide, arsenic, asbestos, chromium, diesel engine exhaust particulate matter, dioxins, formaldehyde, and second-hand smoke. The remaining 12 carcinogens had an estimated mean burden of less than 10 annual cancer cases in Ontario. CONCLUSIONS: We found the environmental burden of cancer in Ontario to fall between previously estimated burdens of alcohol and tobacco use. These results allow for a comparative assessment across carcinogens and offer insights into strategies to reduce the environmental burden of cancer. Our analysis could be adopted by other jurisdictions and repeated in the future for Ontario to track progress in reducing cancer burden, assess newly classified environmental carcinogens, and identify top burden contributors.

Atopic dermatitis: Interaction between genetic variants of GSTP1, TNF, TLR2, and TLR4 and air pollution in early life.

BACKGROUND: Associations between traffic-related air pollution (TRAP) and childhood atopic dermatitis (AD) remain inconsistent, possibly due to unexplored gene-environment interactions. The aim of this study was to examine whether a potential effect of TRAP on AD prevalence in children is modified by selected single nucleotide polymorphisms (SNPs) related to oxidative stress and inflammation. METHODS: Doctor-diagnosed AD up to age 2 years and at 7-8 years, as well as AD symptoms up to age 2 years, was assessed using parental-reported questionnaires in six birth cohorts (N = 5685). Associations of nitrogen dioxide (NO2 ) estimated at the home address of each child at birth and nine SNPs within the GSTP1, TNF, TLR2, or TLR4 genes with AD were examined. Weighted genetic risk scores (GRS) were calculated from the above SNPs and used to estimate combined marginal genetic effects of oxidative stress and inflammation on AD and its interaction with TRAP. RESULTS: GRS was associated with childhood AD and modified the association between NO2 and doctor-diagnosed AD up to the age of 2 years (P(interaction) = .029). This interaction was mainly driven by a higher susceptibility to air pollution in TNF rs1800629 minor allele (A) carriers. TRAP was not associated with the prevalence of AD in the general population. CONCLUSIONS: The marginal genetic association of a weighted GRS from GSTP1, TNF, TLR2, and TLR4SNPs and its interaction with air pollution supports the role of oxidative stress and inflammation in AD.

Genome-Wide Interaction Analysis of Air Pollution Exposure and Childhood Asthma with Functional Follow-up.

RATIONALE: The evidence supporting an association between traffic-related air pollution exposure and incident childhood asthma is inconsistent and may depend on genetic factors. OBJECTIVES: To identify gene-environment interaction effects on childhood asthma using genome-wide single-nucleotide polymorphism (SNP) data and air pollution exposure. Identified loci were further analyzed at epigenetic and transcriptomic levels. METHODS: We used land use regression models to estimate individual air pollution exposure (represented by outdoor NO2 levels) at the birth address and performed a genome-wide interaction study for doctors' diagnoses of asthma up to 8 years in three European birth cohorts (n = 1,534) with look-up for interaction in two separate North American cohorts, CHS (Children's Health Study) and CAPPS/SAGE (Canadian Asthma Primary Prevention Study/Study of Asthma, Genetics and Environment) (n = 1,602 and 186 subjects, respectively). We assessed expression quantitative trait locus effects in human lung specimens and blood, as well as associations among air pollution exposure, methylation, and transcriptomic patterns. MEASUREMENTS AND MAIN RESULTS: In the European cohorts, 186 SNPs had an interaction P < 1 × 10-4 and a look-up evaluation of these disclosed 8 SNPs in 4 loci, with an interaction P < 0.05 in the large CHS study, but not in CAPPS/SAGE. Three SNPs within adenylate cyclase 2 (ADCY2) showed the same direction of the interaction effect and were found to influence ADCY2 gene expression in peripheral blood (P = 4.50 × 10-4). One other SNP with P < 0.05 for interaction in CHS, rs686237, strongly influenced UDP-Gal:betaGlcNAc ß-1,4-galactosyltransferase, polypeptide 5 (B4GALT5) expression in lung tissue (P = 1.18 × 10-17). Air pollution exposure was associated with differential discs, large homolog 2 (DLG2) methylation and expression. CONCLUSIONS: Our results indicated that gene-environment interactions are important for asthma development and provided supportive evidence for interaction with air pollution for ADCY2, B4GALT5, and DLG2.

Exploring nighttime road traffic noise: A comprehensive predictive surface for Toronto, Canada.

Road traffic noise can adversely impact the health of city residents, particularly when it occurs at night. The objective of this study was to evaluate nighttime traffic ambient noise in Toronto, Canada using measured and model-estimated noise levels. Road traffic noise was measured at 767 locations over 3 seasonal sampling campaigns between June 2012 and October 2013 to fully capture noise variability in Toronto. Temporal and campaign-specific spatial models, developed using the noise measurements, were used to build a final predictive surface. The surface was capable of estimating noise across the city over a 24-hr time frame. Measured and surface-estimated noise levels were compared with guidelines from the World Health Organization and the Province of Ontario to identify areas where noise may pose a health risk. Measured mean nighttime noise in Toronto exceeded World Health Organization (40 dBA) guidelines and mean daytime noise exceeded provincial (55 dBA) guidelines. The final predictive surface, incorporating spatial variables and daily cycles in noise levels, provides noise estimates geocoded for the entire study area. This tool could be used for epidemiological studies and to inform noise mitigation efforts. Based on surface-estimated noise levels during the quietest time of night (2 a.m.-2:30 a.m.), 100% of Toronto has nighttime noise exceeding 40 dBA (mean = 57 dBA, range = 49-110 dBA). A predictive surface was developed to estimate geocoded noise levels and facilitate further study of noise in Toronto. This tool can be used to assess road traffic noise, particularly at night, as an environmental health hazard.

Childhood allergic rhinitis, traffic-related air pollution, and variability in the GSTP1, TNF, TLR2, and TLR4 genes: results from the TAG Study.

BACKGROUND: Associations between traffic-related air pollution (TRAP) and allergic rhinitis remain inconsistent, possibly because of unexplored gene-environment interactions. OBJECTIVE: In a pooled analysis of 6 birth cohorts (Ntotal = 15,299), we examined whether TRAP and genetic polymorphisms related to inflammation and oxidative stress predict allergic rhinitis and sensitization. METHODS: Allergic rhinitis was defined with a doctor diagnosis or reported symptoms at age 7 or 8 years. Associations between nitrogen dioxide, particulate matter 2.5 (PM2.5) mass, PM2.5 absorbance, and ozone, estimated for each child at the year of birth, and single nucleotide polymorphisms within the GSTP1, TNF, TLR2, or TLR4 genes with allergic rhinitis and aeroallergen sensitization were examined with logistic regression. Models were stratified by genotype and interaction terms tested for gene-environment associations. RESULTS: Point estimates for associations between nitrogen dioxide, PM2.5 mass, and PM2.5 absorbance with allergic rhinitis were elevated, but only that for PM2.5 mass was statistically significant (1.37 [1.01, 1.86] per 5 µg/m(3)). This result was not robust to single-cohort exclusions. Carriers of at least 1 minor rs1800629 (TNF) or rs1927911 (TLR4) allele were consistently at an increased risk of developing allergic rhinitis (1.19 [1.00, 1.41] and 1.24 [1.01, 1.53], respectively), regardless of TRAP exposure. No evidence of gene-environment interactions was observed. CONCLUSION: The generally null effect of TRAP on allergic rhinitis and aeroallergen sensitization was not modified by the studied variants in the GSTP1, TNF, TLR2, or TLR4 genes. Children carrying a minor rs1800629 (TNF) or rs1927911 (TLR4) allele may be at a higher risk of allergic rhinitis.

Traffic, asthma and genetics: combining international birth cohort data to examine genetics as a mediator of traffic-related air pollution's impact on childhood asthma.

Associations between traffic-related air pollution and incident childhood asthma can be strengthened by analysis of gene-environment interactions, but studies have typically been limited by lack of study power. We combined data from six birth cohorts on: asthma, eczema and allergic rhinitis to 7/8 years, and candidate genes. Individual-level assessment of traffic-related air pollution exposure was estimated using land use regression or dispersion modeling. A total of 11,760 children were included in the Traffic, Asthma and Genetics (TAG) Study; 6.3 % reported physician-diagnosed asthma at school-age, 16.0 % had asthma at anytime during childhood, 14.1 % had allergic rhinitis at school-age, 10.0 % had eczema at school-age and 33.1 % were sensitized to any allergen. For GSTP1 rs1138272, the prevalence of heterozygosity was 16 % (range amongst individual cohorts, 11-17 %) and homozygosity for the minor allele was 1 % (0-2 %). For GSTP1 rs1695, the prevalence of heterozygosity was 45 % (40-48 %) and homozygosity for the minor allele, 12 % (10-12 %). For TNF rs1800629, the prevalence of heterozygosity was 29 % (25-32 %) and homozygosity for the minor allele, 3 % (1-3 %). TAG comprises a rich database, the largest of its kind, for investigating the effect of genotype on the association between air pollution and childhood allergic disease.

Lessons learned from implementing a surge capacity support program for COVID-19 contact management in Ontario.

SETTING: In Ontario, local public health units (PHUs) are responsible for leading case investigations, contact tracing, and follow-up. The workforce capacity and operational requirements needed to maintain this public health strategy during the COVID-19 pandemic were unprecedented. INTERVENTION: Public Health Ontario's Contact Tracing Initiative (CTI) was established to provide a centralized workforce. This program was unique in leveraging existing human resources from federal and provincial government agencies and its targeted focus on initial and follow-up phone calls to high-risk close contacts of COVID-19 cases. By setting criteria for submissions to the program, standardizing scripts, and simplifying the data management process, the CTI was able to support a high volume of calls. OUTCOMES: During its 23 months of operation, the CTI was used by 33 of the 34 PHUs and supported over a million calls to high-risk close contacts. This initiative was able to meet its objectives while adapting to the changing dynamics of the pandemic and the implementation of a new COVID-19 provincial information system. Core strengths of the CTI were timeliness, volume, and efficient use of resources. The CTI was found to be useful for school exposures, providing support when public health measures were lifted, and in supporting PHU's reallocation of resources during the vaccine roll-out. IMPLICATIONS: When considering future use of this model, it is important to take note of the program strengths and limitations to ensure alignment with future needs for surge capacity support. Lessons learned from this initiative could provide practice-relevant knowledge for surge capacity planning.

RéSUMé: CONTEXTE: En Ontario, ce sont les bureaux de santé publique qui s'occupent des enquêtes de cas, de la recherche des contacts et des suivis. Pendant la pandémie de COVID-19, les besoins opérationnels et de capacité de la main-d'œuvre à combler pour conserver cette stratégie de santé publique ont atteint une ampleur jamais vue. INTERVENTION: L'Initiative de recherche des contacts dans le cadre de la lutte contre la COVID-19 de Santé publique Ontario a été mise sur pied dans l'objectif de centraliser l'effectif. Mobilisant des ressources humaines d'organisations fédérales et provinciales, ce programme a permis de faire les appels initiaux et de suivi aux contacts étroits de cas de COVID-19 exposés à un risque élevé. Grâce à des critères bien établis pour les soumissions au programme, à l'uniformisation des scripts et à la simplification du processus de gestion des données, un grand volume d'appels a pu être traité. RéSULTATS: Durant les 23 mois de l'Initiative, 33 des 34 bureaux de santé publique y ont eu recours. Ce sont ainsi plus d'un million d'appels à des contacts étroits qui ont pu être faits. L'Initiative a permis d'atteindre les objectifs en s'adaptant au contexte pandémique en constante évolution et de mettre en œuvre un nouveau système de gestion des renseignements provinciaux sur la COVID-19. Ses grandes forces sont la rapidité, le volume et l'efficacité de l'utilisation des ressources. Elle a été particulièrement utile dans les cas d'exposition en milieu scolaire, permettant d'offrir du soutien à la levée des mesures sanitaires et d'aider à la réaffectation des ressources des bureaux de santé publique pendant la campagne de vaccination. CONSéQUENCES: Si l'on envisage de réutiliser ce modèle, il importe de tenir compte des forces et des faiblesses du programme pour qu'il cadre avec les besoins futurs de soutien en matière de capacité de mobilisation. Les leçons tirées de cette initiative pourraient s'avérer pertinentes pour la planification de cette capacité.

Otitis media in infancy and the development of asthma and atopic disease.

Otitis media is a frequent respiratory infection of early childhood and it is important to fully understand the long-term complications and sequelae. Literature examining otitis media in early childhood and subsequent development of atopic disease is sparse despite there being vast literature on the association between respiratory infections and atopic disease. Current data support the hypothesis that otitis media infections in early life, especially frequent or severe infections, influence the developing immune system, resulting in increased risk for asthma. Recent findings have also reported an association between otitis media and eczema. Atopic children and those with a family history of atopy appear to be at greater risk. Future work should investigate the specific mechanisms involved. It is possible that vaccines and preventive strategies aimed at reducing the burden of otitis media could also reduce the burden of childhood asthma and atopic disease.

Residential air pollution and otitis media during the first two years of life.

BACKGROUND: : Otitis media is the leading reason young children receive antibiotics or visit a physician. We evaluated the impact of ambient air pollution on outpatient physician visits for otitis media in a population-based birth cohort. METHODS: : All children born in southwestern British Columbia during 1999-2000 were followed until the age of 2 years. Residential air pollution exposures were estimated for the first 24 months of life by inverse-distance weighting of monitor data (CO, NO, NO2, O3, PM2.5, PM10, SO2), temporally adjusted land-use regression models (NO, NO2, PM2.5, black carbon, woodsmoke), and proximity to roads and point sources. We used generalized estimating equations to longitudinally assess the relationship between physician visits for otitis media (ICD-9) and average pollutant exposure in the 2 months prior to the visit, after adjustment for covariates. RESULTS: : Complete exposure and risk-factor data were available for 45,513 children (76% of all births). A total of 42% of subjects had 1 or more physician visits for otitis media during follow-up. Adjusted estimates for NO, PM2.5, and woodsmoke were consistently elevated (eg, relative risk of 1.10 [95% confidence interval = 1.07-1.12] per interquartile range [IQR] increase in NO; 1.32 [1.27-1.36] per IQR increase in days of woodsmoke exposure). No increased risks were observed for the remaining pollutants (eg, 1.00 [0.98-1.03] per IQR increase in PM10; 0.99 [0.97-1.01] per IQR increase in black carbon). CONCLUSIONS: : Modest but consistent associations were found between some measures of air pollution and otitis media in a large birth cohort exposed to relatively low levels of ambient air pollution.

Evidence synthesis - Evaluating risk communication during extreme weather and climate change: a scoping review. / Synthèse des données probantes - Évaluation de la communication des risques en présence de changements climatiques et de phénomènes météorologiques extrêmes : examen de la portée.

INTRODUCTION: Communicating risk to the public continues to be a challenge for public health practitioners working in the area of climate change. We conducted a scoping literature review on the evaluation of risk communication for extreme weather and climate change to inform local public health messaging, consistent with requirements under the Ontario Public Health Standards (OPHS), which were updated in 2018 to include effective communication regarding climate change and extreme weather. METHODS: Search strategies were developed by library information specialists and used to retrieve peer-reviewed academic and grey literature from bibliographic databases (Medline, Embase, Scopus and CINAHL) and Google country specific searches, respectively. The search strategy was validated through a workshop with experts and community stakeholders, with expertise in environment, health, emergency management and risk communication. RESULTS: A total of 43 articles were included. These articles addressed issues such as: climate change (n = 22), flooding (n = 12), hurricane events (n = 5), extreme heat (n = 2), and wild fires (n = 2). Studies were predominantly from the US (n = 14), Europe (n = 6) and Canada (n = 5). CONCLUSION: To meet the OPHS 2018, public health practitioners need to engage in effective risk communication to motivate local actions that mitigate the effects of extreme weather and climate change. Based on the scoping review, risk communication efforts during short-term extreme weather events appear to be more effective than efforts to communicate risk around climate change. This distinction could highlight a unique opportunity for public health to adapt strategies commonly used for extreme weather to climate change.

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 (N total=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/m(3) 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.

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.

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.

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

BACKGROUND: 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.

Early-life otitis media and incident atopic disease at school age in a birth cohort.

BACKGROUND: Otitis media is a common and costly disease that peaks in early childhood. Recent reviews concluded that the relationship between otitis media and atopy is not well understood, and that further research is warranted. METHODS: Logistic regression was used to analyze data from a German Birth Cohort (n = 1690; born 1997­1999). Parental questionnaires were used to assess children for physician-diagnosed otitis media throughout the first 2 years of life and for incident atopic disease (asthma, allergic rhinitis, and eczema) during the sixth year of life. Odds ratios were adjusted for gender, older siblings, city, parental education, breast-feeding, and daycare. Parallel analyses were completed for the full birth cohort and for a population subset with atopic mothers. RESULTS: The adjusted odds of asthma were elevated for children with early-life otitis media, but were statistically significant only for those children with at least 3 episodes (adjusted odds ratio: 4.26 [95% confidence interval: 1.34­13.6]). Associations between early-life otitis media and allergic rhinitis were largely inconsistent. There was a positive association between early-life otitis media and late-onset allergic eczema (≥2 episodes: 2.68 [1.35­5.33], ≥3 episodes: 3.84 [1.80­8.18]). Similar results were found for the maternal atopy subgroup but with greater effect estimates. CONCLUSIONS: Children diagnosed with otitis media during infancy were at greater risk for developing late-onset allergic eczema and asthma during school age, and associations were stronger for frequent otitis. These results indicate that frequent otitis media during infancy may predispose children to atopic disease in later life.