A spatiotemporal case-crossover model of asthma exacerbation in the City of Houston.
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ABSTRACT:
SUBMITTER: Schedler JC
PROVIDER: S-EPMC9286634 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:PurposeThis retrospective study was conducted to estimate the effects of climate factors and air pollution on asthma exacerbations using a case-crossover analysis.MethodsPatients who visited the emergency department (ED) of 2 university hospitals in Chuncheon for asthma exacerbations from January 1, 2006, to December 31, 2011, were enrolled. Daily average data for meteorological factors (temperature, daily temperature range, relative humidity, wind speed, atmospheric pressure, presence of rain, solar irradiation, and presence of fog) and the daily average levels of gaseous air pollutants (SO?, NO?, O?, CO, and PM10) were obtained. A case-crossover analysis was performed using variables about the weather and air pollution at 1-week intervals between cases and controls before and after ED visits.ResultsThere were 660 ED visits by 583 patients with asthma exacerbations. Low relative humidity (lag 1 and 2) and high wind speed (lag 1, 2, and 3) were associated with ED visits for asthma. Fog (lag 2) showed protective effects against asthma exacerbations in Chuncheon (risk increase: -29.4% [95% CI=-46.3% to -7.2%], P=0.013). These relationships were stronger in patients ?19 years old than in those >60 years old. High levels of ambient CO (lag 1, 2, and 3) and NO? (lag 2 and 3) were associated with decreased ED visits for asthma. However, there were no significant relationships among levels of ambient CO or NO? and asthma exacerbations after adjusting for wind speed and relative humidity.ConclusionsHigh wind speed and low humidity were associated with an increased risk of asthma ED visits. Fog was associated with a decreased risk of asthma ED visits after controlling for seasonal variations in weather and air pollution.
| S-EPMC5011051 | biostudies-literature
Project description:BackgroundChildhood asthma morbidity has been associated with short-term air pollution exposure. To date, most investigations have used time-series models, and it is not well understood how exposure misclassification arising from unmeasured spatial variation may impact epidemiological effect estimates. Here, we develop case-crossover models integrating temporal and spatial individual-level exposure information, toward reducing exposure misclassification in estimating associations between air pollution and child asthma exacerbations in New York City (NYC).MethodsAir pollution data included: (a) highly spatially-resolved intra-urban concentration surfaces for ozone and co-pollutants (nitrogen dioxide and fine particulate matter) from the New York City Community Air Survey (NYCCAS), and (b) daily regulatory monitoring data. Case data included citywide hospital records for years 2005-2011 warm-season (June-August) asthma hospitalizations (n=2353) and Emergency Department (ED) visits (n=11,719) among children aged 5-17 years. Case residential locations were geocoded using a multi-step process to maximize positional accuracy and precision in near-residence exposure estimates. We used conditional logistic regression to model associations between ozone and child asthma exacerbations for lag days 0-6, adjusting for co-pollutant and temperature exposures. To evaluate the effect of increased exposure specificity through spatial air pollution information, we sequentially incorporated spatial variation into daily exposure estimates for ozone, temperature, and co-pollutants.ResultsPercent excess risk per 10ppb ozone exposure in spatio-temporal models were significant on lag days 1 through 5, ranging from 6.5 (95% CI: 0.2-13.1) to 13.0 (6.0-20.6) for inpatient hospitalizations, and from 2.9 (95% CI: 0.1-5.7) to 9.4 (6.3-12.7) for ED visits, with strongest associations consistently observed on lag day 2. Spatio-temporal excess risk estimates were consistently but not statistically significantly higher than temporal-only estimates on lag days 0-3.ConclusionIncorporating case-level spatial exposure variation produced small, non-significant increases in excess risk estimates. Our modeling approach enables a refined understanding of potential measurement error in temporal-only versus spatio-temporal air pollution exposure assessments. As ozone generally varies over much larger spatial scales than that observed within NYC, further work is necessary to evaluate potential reductions in exposure misclassification for populations spanning wider geographic areas, and for other pollutants.
| S-EPMC5552364 | biostudies-literature
Project description:Patients who are prone to exacerbations of asthma experience significant costs in terms of missed work and school, acute care visits, and hospitalizations. Exacerbations are largely driven by environmental exposures including pollutants, stress, and viral and bacterial pathogens. These exposures are most likely to induce acute severe "asthma attacks" in high-risk patients. These personal risk factors for exacerbations can vary with the phenotype of asthma and age of the patient. In children, allergic sensitization is a strong risk factor, especially for those children who develop sensitization early in life. Airway inflammation is an important risk factor, and biomarkers are under evaluation for utility in detecting eosinophilic and type 2 inflammation and neutrophilic inflammation as indicators of risk for recurrent exacerbations. Insights into inflammatory mechanisms have led to new approaches to prevent exacerbations using mAb-based biologics that target specific type 2 pathways. Challenges remain in developing an evidence base to support precision interventions with these effective yet expensive therapies, and in determining whether these treatments will be safe and effective in young children. Unfortunately, there has been less progress in developing treatments for acute exacerbations. Hopefully, greater understanding of mechanisms relating airway viruses, bacteria, mucin production, and neutrophilic inflammatory responses will lead to additional treatment options for patients experiencing acute exacerbations.
| S-EPMC6942520 | biostudies-literature
Project description:BackgroundHuman enterovirus D68 (EV-D68) recently caused an increase in mild-to-severe pediatric respiratory cases in North America and some European countries. Even though few of these children presented with acute paralytic disease, direct causal relationship cannot yet be assumed.ObjectivesThe purposes of this report were to describe the clinical findings of an outbreak of EV-D68 infection in Mexico City and identify the genetic relationship with previously reported strains.Patients/methodsBetween September and December 2014, 126 nasopharyngeal samples (NPS) of hospitalized children <15 years of age with ARI were tested for the presence of respiratory viruses using a multiplex RT-qPCR and EV-D68-specific RT-qPCR. Clinical, epidemiological, and demographic data were collected and associated with symptomatology and viral infections. Phylogenetic analyses were performed using VP1 region.ResultsEnterovirus/rhinovirus infection was detected in 40 patients (31·7%), of which 24 patients were EV-D68-positive. EV-D68 infection prevailed over September and October 2014 and was associated with neutrophilia and lymphopenia, and patients were more likely to develop hypoxemia. Phylogenetic analyses showed that Mexican EV-D68 belongs to the new B1 clade.ConclusionsThis is the first EV-D68 outbreak described in Mexico and occurred few weeks after the United States reported similar infections. Although EV-D68 belongs to new B1 clade, no neurological affection was observed.
| S-EPMC4814865 | biostudies-literature
Project description:BackgroundDespite the substantial role indoor exposure has played in heat wave-related mortality, few epidemiological studies have examined the health effects of exposure to indoor heat. As a result, knowledge gaps regarding indoor heat-health thresholds, vulnerability, and adaptive capacity persist.ObjectiveWe evaluated the role of indoor heat exposure on mortality and morbidity among the elderly (≥65 years of age) in Houston, Texas.MethodsMortality and emergency hospital admission data were obtained through the Texas Department of State Health Services. Summer indoor heat exposure was modeled at the U.S. Census block group (CBG) level using building energy models, outdoor weather data, and building characteristic data. Indoor heat-health associations were examined using time-stratified case-crossover models, controlling for temporal trends and meteorology, and matching on CBG of residence, year, month, and weekday of the adverse health event. Separate models were fitted for three indoor exposure metrics, for individual lag days 0-6, and for 3-d moving averages (lag 0-2). Effect measure modification was explored via stratification on individual- and area-level vulnerability factors.ResultsWe estimated positive associations between short-term changes in indoor heat exposure and cause-specific mortality and morbidity [e.g., circulatory deaths, odds ratio per 5°C increase=1.16 (95% CI: 1.03, 1.30)]. Associations were generally positive for earlier lag periods and weaker across later lag periods. Stratified analyses suggest stronger associations between indoor heat and emergency hospital admissions among African Americans compared with Whites.DiscussionFindings suggest excess mortality among certain elderly populations in Houston who are likely exposed to high indoor heat. We developed a novel methodology to estimate indoor heat exposure that can be adapted to other U.S.LocationsIn locations with high air conditioning prevalence, simplified modeling approaches may adequately account for indoor heat exposure in vulnerable neighborhoods. Accounting for indoor heat exposure may improve the estimation of the total impact of heat on health. https://doi.org/10.1289/EHP6340.
| S-EPMC7727721 | biostudies-literature
Project description:Asthmatics are more susceptible to viral infections than healthy individuals and are known to have impaired innate anti-viral defences. Influenza A virus causes significant morbidity and mortality in this population. Immuno-modulatory regulators (IMRs) such as PD-1 are activated on T cells following viral infection as part of normal T cell activation responses, and then subside, but remain elevated in cases of chronic exposure to virus, indicative of T cell exhaustion rather than activation. There is evidence that checkpoint inhibition can enhance anti-viral responses during acute exposure to virus through enhancement of CD8+T cell function. Although elevated PD-1 expression has been described in pulmonary tissues in other chronic lung diseases, the role of IMRs in asthma has been relatively unexplored as the basis for immune dysfunction. We first assessed IMR expression in the peripheral circulation and then quantified changes in IMR expression in lung tissue in response to ex-vivo influenza infection. We found that the PD-1 family members are not significantly altered in the peripheral circulation in individuals with severe asthma but are elevated in pulmonary tissues following ex-vivo influenza infection. We then applied PD-1 Mab inhibitor treatment to bronchial biopsy tissues infected with influenza virus and found that PD-1 inhibition was ineffective in asthmatics, but actually increased infection rates in healthy controls. This study, therefore, suggests that PD-1 therapy would not produce harmful side-effects when applied in people with severe asthma, but could have important, as yet undescribed, negative effects on anti-viral responses in healthy individuals that warrant further investigation.
| S-EPMC9720166 | biostudies-literature
Project description:Asthma is a chronic disease most commonly associated with allergy and type 2 inflammation. However, the mechanisms that link airway inflammation to the structural changes that define asthma are incompletely understood. Using a human model of allergen-induced asthma exacerbation, we compared the lower airway mucosa in allergic asthmatics and allergic non-asthmatic controls using single-cell RNA sequencing. In response to allergen, the asthmatic airway epithelium was highly dynamic and up-regulated genes involved in matrix degradation, mucus metaplasia, and glycolysis while failing to induce injury-repair and antioxidant pathways observed in controls. IL9-expressing pathogenic TH2 cells were specific to asthmatic airways and were only observed after allergen challenge. Additionally, conventional type 2 dendritic cells (DC2 that express CD1C) and CCR2-expressing monocyte-derived cells (MCs) were uniquely enriched in asthmatics after allergen, with up-regulation of genes that sustain type 2 inflammation and promote pathologic airway remodeling. In contrast, allergic controls were enriched for macrophage-like MCs that up-regulated tissue repair programs after allergen challenge, suggesting that these populations may protect against asthmatic airway remodeling. Cellular interaction analyses revealed a TH2-mononuclear phagocyte-basal cell interactome unique to asthmatics. These pathogenic cellular circuits were characterized by type 2 programming of immune and structural cells and additional pathways that may sustain and amplify type 2 signals, including TNF family signaling, altered cellular metabolism, failure to engage antioxidant responses, and loss of growth factor signaling. Our findings therefore suggest that pathogenic effector circuits and the absence of proresolution programs drive structural airway disease in response to type 2 inflammation.
| S-EPMC10440046 | biostudies-literature
Project description:BackgroundWe describe this case of a young gentleman presenting with acute dyspnoea on a background history of known, long-standing asthma. His dramatic presentation, notable for profound hypoxia and cyanosis, led to an unexpected additional diagnosis of type one congenital methaemoglobinaemia.Case presentationA 26-year-old Irish gentleman was transferred urgently to the emergency department resuscitation room with marked cyanosis and tachypnoea. His oxygen saturation was 70% on 100% high flow oxygen. His arterial blood gas (On Fi02 90%) demonstrated a PaO2 = 76.8 kPa, SpO2 = 99%, pCO2 = 3 kPa and pH = 7.51. A saturation gap was evident and on further analysing the arterial blood gas, the methaemoglobin level was noted to be 28%. No contributing drugs were identified. Our patient was diagnosed with type one congenital methaemoglobinaemia. He recovered well from this admission, however, has had recurrent presentations to hospital since with high methaemoglobin levels noted on each occasion.DiscussionCongenital methemoglobinemia is a rare, often overlooked differential diagnosis in patients presenting with cyanosis and dyspnoea. This is the only case, to our knowledge, of a patient with both asthma and congenital methaemoglobinaemia. Congenital methaemoglobinaemia was first described in 1943 by Dr Deeny who described two siblings as suffering from 'Familial Idiopathic Methaemoglobinaemia'. The case we present is the first reported Irish case of congenital methaemoglobinaemia, we are aware of, since 1943.Current treatment strategies include high-flow oxygen, methylene blue infusion (contraindicated in glucose-6-phosphate-dehydrogenase deficiency) and red cell exchange transfusions in the emergency setting whilst oral ascorbic acid and riboflavin are preventative.
| S-EPMC6938945 | biostudies-literature
Project description:BackgroundPost-hospital syndrome refers to the period of generalized risk of adverse health outcomes among patients who are recently discharged from hospital. This period is associated with a short-term increased risk of readmission which may not be related to the original condition. While the majority of studies of post-hospital syndrome have focused on all-cause readmissions, whether and to what extent such a phenomenon exists within discrete medical conditions is not yet known.ObjectiveTo investigate whether the risk of admission due to asthma is increased in individuals who are discharged following any-cause hospital admission.MethodsUsing administrative health data for the period 1997 to 2007 from the province of British Columbia, Canada, we created a cohort of adults with asthma. Using a case-crossover design, we assessed the association between discharge from a hospital (exposure) within 30 days before an asthma-related hospitalization (the outcome), using two 30-day control periods within the same subject. Conditional logistic regression was performed to calculate the relative risk (RR) of the outcome in association with exposure. We performed several sensitivity and subgroup analyses.ResultsThe final cohort included 3,852 patients experiencing 6,333 instances of the outcome. Mean age at the time of the outcome was 43.7 (SD 14.2), 69.0% of such outcomes belonged to females. The RR of the outcome within the next 30 days of a previous any-cause discharge was 1.40 (95% CI 1.22 - 1.59). However, the association was mainly caused by discharge from asthma-related admission [RR?=?1.99 (95% CI 1.65 - 2.39)]. The RR associated with non-asthma-related discharge was 0.88 (95% CI 0.74 - 1.04) and was not statistically significant. Similar results were obtained in a range of sensitivity analyses.DiscussionOur results indicate that in patients with asthma, the 30-day risk of asthma-related admission is increased after an episode of asthma-related hospitalization, but not after an episode of non-asthma-related hospitalization.
| S-EPMC3880050 | biostudies-literature
Project description:Asthma exacerbation (AE) usually denotes worsening of asthma symptoms that requires intense management to prevent further deterioration. AE has been reported to correlate with clinical and demographic factors, such as race, gender, and treatment compliance as well as environmental factors, such as viral infection, smoking, and air pollution. In addition, recent observations suggest that there are likely to be genetic factors specific to AE. Understanding genetic factors specific to AE is essential to develop therapy tailored for exacerbation-prone asthma. Here, we summarize the results of studies involving genetic risk factors for AE. To simplify and enhance understanding, we reviewed the studies according to the following categories: hypothesis-driven approaches, hypothesis-free approaches, gene-environment interactions, and pharmacogenetics.
| S-EPMC5352570 | biostudies-literature