Explore the vast range of titles available.

Few studies have investigated traffic-related air pollution as a risk factor for respiratory infections during early childhood. 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. 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. 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). 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.

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.

Genetics may partially explain observed heterogeneity in associations between traffic-related air pollution and incident asthma. 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. 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. 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. Children carrying GSTP1 rs1138272 or rs1695 minor alleles may constitute a susceptible population at increased risk of asthma associated with air pollution.

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, SO3), 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, PM, 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.

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.

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 rs 1138272, the prevalence of heterozygosity was 16 % (range amongst individual cohorts, 11–17 %) and homozygosity for the minor allele was 1 % (0–2 %). For GSTP1 rsl695, the prevalence of heterozygosity was 45 % (40–48 %) and homozygosity for the minor alíele, 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.

CITATION: MacIntyre EA, Brauer M, Melen E, Bauer CP, Bauer M, Berdel D, Bergstrom A, Brunekreef B, Chan-Yeung M, Klumper C, Fuertes E, Gehring U, Gref A, Heinrich J, Herbarth O, Kerkhof M, Koppelman GH, Kozyrskyj AL, Pershagen G, Postma DS, Thiering E, Tiesler CM, Carlsten C, TAG Study Group. 2014. GSTP1 and TNF gene variants and associations between air pollution and incident childhood asthma: the traffic, asthma and genetics (TAG) Study. Environ Health Perspect 122:418-424; http://dx.doi.org/10.1289/ehp.1307459

Background Contact tracing is an important tool in slowing the spread of infectious disease and preventing illness. People may face barriers to contact tracing adherence, depending on various personal and contextual characteristics. Thus, we examined a large-scale COVID-19 contact tracing initiative and compared adherence across several socio-demographic and exposure characteristics. Methods We analyzed data for 130,255 participants in Ontario’s COVID-19 contact tracing initiative from September 2020 to December 2021. During contact follow-up calls, callers recorded whether contacts reported self-isolating and whether they completed follow-up. We performed unadjusted and adjusted logistic regressions to estimate the odds ratios (OR) and 95% confidence intervals (CI) of self-isolating and of completing follow-up, according to contacts’ age group, neighbourhood material resources, COVID-19 wave, exposure setting, region, and preferred language. Results In the adjusted analyses, odds of completing follow-up decreased as neighbourhood-level material resources decreased, with OR = 0.57 (95% CI: 0.54–0.60) comparing highest resource areas to lowest. Compared to COVID-19 contacts living in the Greater Toronto Area, other Ontario regions had higher odds of completing follow-up, with ORs ranging from 1.19 (95% CI: 1.14–1.24) to OR = 1.91 (95% CI: 1.78–2.04). Contacts whose preferred languages were not English had lower odds of self-isolating (OR = 0.57, 95% CI: 0.38–0.84). The 0–4 and 5–11 year old age groups had lower odds of self-isolating than 20–29 year olds, with respective ORs of 0.60 (95% CI: 0.48–0.75) and 0.57 (95% CI: 0.48–0.67). Conclusions In preparing for future pandemics, contact tracing programs may benefit from prioritizing additional supports for those who live in areas with fewer material resources, have language preferences other than English, and live in large metropolitan centres.

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 (PM 2.5 ) 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.

Background: During the 2023 wildfire season, Ontario, Canada, had unprecedented wildfire smoke, but the health impact on the population is unknown. We aimed to quantify the acute impact of the wildfire smoke on respiratory and cardiovascular outcomes across Ontario. Methods: We conducted a quasi-experimental study by leveraging the timing of 2 consecutive wildfire smoke episodes in June 2023. Heavy wildfire smoke blanketed much of Ontario on 2 occasions, in early June and again in late June, causing severely degraded daily air quality. Following the epidemiologic triangulation framework, we collected health data on emergency department visits for 4 outcomes (asthma-related causes, other respiratory causes, ischemic heart disease, and non-cardiorespiratory causes) from Ontario's real-time syndromic surveillance system and the National Ambulatory Care Reporting System. We also employed different epidemiologic methodologies, including interrupted time-series and case-crossover analyses. Results: After the initial heavy wildfire smoke in early June 2023, daily asthma-related visits increased substantially across Ontario, peaking at a 23.6% increase (95% confidence interval 13.2%-34.9%) at a 1-day lag and lasting up to a lag of 5 days after the start of the smoke episode. The later episode of heavy smoke, despite causing higher exposures, had a reduced effect on asthma-related visits. We did not detect any effect on other outcomes in either episode. These findings were consistent across different methodologies and data sources. Post hoc analysis revealed that asthmarelated visits were briefly elevated after the wildfire smoke among children (40% higher), but we observed a more sustained effect among adults (48% higher, lasting 1 week). Interpretation: The 2023 wildfires substantially increased asthma-related emergency department visits in Ontario, with age and timing of exposure being important factors influencing the impact. As wildfires emerge as one of the fastest-growing environmental risk factors globally, future research should identify and evaluate measures to effectively mitigate the acute health impacts of wildfire smoke.