Pediatric Inner-City Environmental Exposures at School and Home and Asthma Study
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
TISSUE(S): Urine
DISEASE(S): Asthma
PROVIDER: ST001048 | MetabolomicsWorkbench |
REPOSITORIES: MetabolomicsWorkbench
Dataset's files
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Project description:BackgroundIn the United States, asthma is the most common chronic disease of childhood across all socioeconomic classes and is the most frequent cause of hospitalization among children. Asthma exacerbations have been associated with exposure to residential indoor environmental stressors such as allergens and air pollutants as well as numerous additional factors. Simulation modeling is a valuable tool that can be used to evaluate interventions for complex multifactorial diseases such as asthma but in spite of its flexibility and applicability, modeling applications in either environmental exposures or asthma have been limited to date.MethodsWe designed a discrete event simulation model to study the effect of environmental factors on asthma exacerbations in school-age children living in low-income multi-family housing. Model outcomes include asthma symptoms, medication use, hospitalizations, and emergency room visits. Environmental factors were linked to percent predicted forced expiratory volume in 1 second (FEV1%), which in turn was linked to risk equations for each outcome. Exposures affecting FEV1% included indoor and outdoor sources of NO2 and PM2.5, cockroach allergen, and dampness as a proxy for mold.ResultsModel design parameters and equations are described in detail. We evaluated the model by simulating 50,000 children over 10 years and showed that pollutant concentrations and health outcome rates are comparable to values reported in the literature. In an application example, we simulated what would happen if the kitchen and bathroom exhaust fans were improved for the entire cohort, and showed reductions in pollutant concentrations and healthcare utilization rates.ConclusionsWe describe the design and evaluation of a discrete event simulation model of pediatric asthma for children living in low-income multi-family housing. Our model simulates the effect of environmental factors (combustion pollutants and allergens), medication compliance, seasonality, and medical history on asthma outcomes (symptom-days, medication use, hospitalizations, and emergency room visits). The model can be used to evaluate building interventions and green building construction practices on pollutant concentrations, energy savings, and asthma healthcare utilization costs, and demonstrates the value of a simulation approach for studying complex diseases such as asthma.
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Project description:Environmental exposures interplay with human host factors to promote the development and progression of allergic diseases. The worldwide prevalence of allergic disease is rising as a result of complex gene-environment interactions that shape the immune system and host response. Research shows an association between the rise of allergic diseases and increasingly modern Westernized lifestyles, which are characterized by increased urbanization, time spent indoors, and antibiotic usage. These environmental changes result in increased exposure to air and traffic pollution, fungi, infectious agents, tobacco smoke, and other early-life and lifelong risk factors for the development and exacerbation of asthma and allergic diseases. It is increasingly recognized that the timing, load, and route of allergen exposure affect allergic disease phenotypes and development. Still, our ability to prevent allergic diseases is hindered by gaps in understanding of the underlying mechanisms and interaction of environmental, viral, and allergen exposures with immune pathways that impact disease development. This Review highlights epidemiologic and mechanistic evidence linking environmental exposures to the development and exacerbation of allergic airway responses.
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Project description:The seminal vesicles are an integral part of the male accessory gland system, and are responsible for producing a complex array of bioactive moieties that support gamete function and promote reproductive success. However, despite their physiological significance, the biology of the seminal vesicles remains poorly defined. Here, we exploit an established reproductive toxicant model, where mice were administered acrylamide (25 mg/kg bw/day) or control each morning for 5 consecutive days prior to collecting seminal vesicle tissue 72 h following the final injection, to complete the first proteomic assessment of mouse seminal vesicles. A total of 5,013 proteins were identified in the core seminal vesicle proteome with bioinformatics analysis of identifying cell proliferation, transcript/protein production and cellular death and survival pathways as prominent biological processes. Comparison of our acrylamide to control seminal vesicle proteome revealed 311 differentially regulated (-1.5 ≤ FC ≥ 1.5, p ≤ 0.05, 205 up-regulated, 106 down-regulated) proteins with immunoblotting analysis confirming proteomic data. Pathways that initiate protein synthesis to promote cellular survival were prominent amongst the dysregulated cellular pathways and RICTOR (Z-score = -3.64, p = 6.69E-07) was a top-ranked upstream driver. Oxidative stress was implicated as a contributor to protein changes with acrylamide leading to a significant increase in 8-OHdG in epithelial cells (5-fold increase, p = 0.016). Direct effects of acrylamide on seminal vesicle function were observed through a reduction in seminal vesicle secretion weight and overall protein content. Together these finding support the emerging concept that in addition to sperm, paternal exposures exert significant influence on the seminal vesicles, and identify new pathways to develop targeted interventions with which to manipulate fertility and reproductive outcomes.
2021-05-31 | PXD021998 | Pride
Project description:A common explanation for the origins and rising prevalence of asthma is that they involve complex interactions between hereditary predispositions and environmental exposures that are incompletely understood. Yet, emerging evidence substantiates the paradigm that environmental exposures prenatally and during very early childhood induce epigenetic alterations that affect the expression of asthma genes and, thereby, asthma itself. Here, we review much of the key evidence supporting this paradigm. First, we describe evidence that the prenatal and early postnatal periods are key time windows of susceptibility to environmental exposures that may trigger asthma. Second, we explain how environmental epigenetic regulation may explain the immunopathology underlying asthma. Third, we outline specific evidence that environmental exposures induce epigenetic regulation, both from animal models and robust human epidemiological research. Finally, we review some emerging topics, including the importance of coexposures, population divergence, and how epigenetic regulation may change over time. Despite all the inherent complexity, great progress has been made toward understanding what we still consider reversible asthma risk factors. These, in time, may impact patient care.
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Project description:BackgroundRain and flooding from Hurricane Katrina resulted in widespread growth of mold and bacteria and production of allergens in New Orleans, Louisiana, which may have led to increased exposures and morbidity in children with asthma.ObjectivesThe goal of the Head-off Environmental Asthma in Louisiana (HEAL) study was to characterize post-Katrina exposures to mold and allergens in children with asthma.MethodsThe homes of 182 children with asthma in New Orleans and surrounding parishes were evaluated by visual inspection, temperature and moisture measurements, and air and dust sampling. Air was collected using vacuum-pump spore traps and analyzed for > 30 mold taxa using bright field microscopy. Dust was collected from the children's beds and bedroom floors and analyzed for mouse (Mus m 1), dust mite (Der p 1), cockroach (Bla g 1), and mold (Alternaria mix) allergens using ELISA.ResultsMore than half (62%) of the children were living in homes that had been damaged by rain, flooding, or both. Geometric mean indoor and outdoor airborne mold levels were 501 and 3,958 spores/m3, respectively. Alternaria antigen was detected in dust from 98% of homes, with 58% having concentrations > 10 µg/g. Mus m 1, Der p 1, and Bla g 1 were detected in 60%, 35%, and 20% of homes, respectively, at low mean concentrations.ConclusionsExcept for Alternaria antigen in dust, concentrations of airborne mold (ratio of indoor to outdoor mold) and dust allergens in the homes of HEAL children were lower than measurements found in other studies, possibly because of extensive post-Katrina mold remediation and renovations, or because children moved into cleaner homes upon returning to New Orleans.
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Project description:BackgroundHome-based interventions to improve indoor air quality have demonstrated benefits for asthma morbidity, yet little is known about the effect of environmental interventions in the school setting.ObjectiveWe piloted the feasibility and effectiveness of a classroom-based air cleaner intervention to reduce particulate pollutants in classrooms of children with asthma.MethodsIn this pilot randomized controlled trial, we assessed the effect of air cleaners on indoor air particulate pollutant concentrations in 18 classrooms (9 control, 9 intervention) in 3 urban elementary schools. We enrolled 25 children with asthma (13 control, 12 intervention) aged 6 to 10 years. Classroom air pollutant measurements and spirometry were completed once before and twice after randomization. Asthma symptoms were surveyed every 3 months.ResultsBaseline classroom levels of fine particulate matter (particulate matter with diameter of <2.5 μm [PM2.5]) and black carbon (BC) were 6.3 and 0.41 μg/m3, respectively. When comparing the intervention to the control group, classroom PM2.5 levels were reduced by 49% and 42% and BC levels were reduced by 58% and 55% in the first and second follow-up periods, respectively (P < .05 for all comparisons). When comparing the children randomized to intervention and control classrooms, there was a modest improvement in peak flow, but no significant changes in forced expiratory volume in 1 second (FEV1) and asthma symptoms.ConclusionsIn this pilot study, a classroom-based air cleaner intervention led to significant reductions in PM2.5 and BC. Future large-scale studies should comprehensively evaluate the effect of school-based environmental interventions on pediatric asthma morbidity.
| S-EPMC5222771 | biostudies-literature
Project description:Relative to research on effects of environmental exposures on exacerbation of existing asthma, little research on incident asthma and environmental exposures has been conducted. However, this research is needed to better devise strategies for the prevention of asthma. The U.S. Environmental Protection Agency (EPA) and National Institute of Environmental Health Sciences held a conference in October 2004 to collaboratively discuss a future research agenda in this area. The first three articles in this mini-monograph summarize the discussion on potential putative environmental exposure; they include an overview of asthma and conclusions of the workshop participants with respect to public health actions that could currently be applied to the problem and research needs to better understand and control the induction and incidence of asthma, the potential role of indoor/outdoor air pollutants in the induction of asthma), and biologics in the induction of asthma. Susceptibility is a key concept in the U.S. EPA "Asthma Research Strategy" document and is associated with the U.S. EPA framework of protecting vulnerable populations from potentially harmful environmental exposures. Genetics, age, and lifestyle (obesity, diet) are major susceptibility factors in the induction of asthma and can interact with environmental exposures either synergistically or antagonistically. Therefore, in this fourth and last article we consider a number of "susceptibility factors" that potentially influence the asthmatic response to environmental exposures and propose a framework for developing research hypotheses regarding the effects of environmental exposures on asthma incidence and induction.
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Project description:In the last decade, more than half of U.S. children were born to working mothers and 65% of working men and women were of reproductive age. In 2004 more than 28 million women age 18-44 were employed full time. This implies the need for clinicians to possess an awareness about the impact of work on the health of their patients and their future offspring. Most chemicals in the workplace have not been evaluated for reproductive toxicity, and where exposure limits do exist, they were generally not designed to mitigate reproductive risk. Therefore, many toxicants with unambiguous reproductive and developmental effects are still in regular commercial or therapeutic use and thus present exposure potential to workers. Examples of these include heavy metals, (lead, cadmium), organic solvents (glycol ethers, percholoroethylene), pesticides and herbicides (ethylene dibromide) and sterilants, anesthetic gases and anti-cancer drugs used in healthcare. Surprisingly, many of these reproductive toxicants are well represented in traditional employment sectors of women, such as healthcare and cosmetology. Environmental exposures also figure prominently in evaluating a woman's health risk and that to a pregnancy. Food and water quality and pesticide and solvent usage are increasingly topics raised by women and men contemplating pregnancy. The microenvironment of a woman, such as her choices of hobbies and leisure time activities also come into play. Caregivers must be aware of their patients' potential environmental and workplace exposures and weigh any risk of exposure in the context of the time-dependent window of reproductive susceptibility. This will allow informed decision-making about the need for changes in behavior, diet, hobbies or the need for added protections on the job or alternative duty assignment. Examples of such environmental and occupational history elements will be presented together with counseling strategies for the clinician.
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Project description:ObjectiveTo complete a systematic review of the literature describing associations between all environmental exposures and asthma symptoms and exacerbations in children up to mean age of 9 years.DesignSystematic review.SettingReference lists of identified studies and reviews were searched for all articles published until November 2013 in electronic databases (MEDLINE, EMBASE, CINAHL, Cochrane Controls Trials Register).ParticipantsStudies were selected which examined a link between exposure to environmental factors and asthma symptoms and exacerbations where the study participants were children with a mean age of ≤9 years.Primary and secondary outcome measuresIndices of asthma symptoms, control and exacerbations.ResultsA total of 27 studies were identified including eight where inhaled allergens and four where environmental tobacco smoke (ETS) were the exposures of interest. There was evidence that exposure to allergen, ETS, poor air quality and unflued heaters had a modest magnitude of effect (ORs between 2 and 3). There was also evidence of interactions observed between exposures such as allergen and ETS.ConclusionsExposure to inhaled allergens, ETS, unflued heaters and poor air quality has an important effect on exacerbations in young children with asthma and should be minimised or, ideally, avoided. Better understanding of the effect of exposure to damp housing, air conditioning and dietary factors plus interactions between environmental exposures associated with exacerbations is required.
| S-EPMC3927936 | biostudies-literature
Project description:BackgroundThe indoor home environment plays a crucial role in determining the outcome of respiratory diseases, including asthma. Researchers, clinicians, and patients would benefit from self-reported questionnaires to assess indoor home environmental exposures that may impact on respiratory health.ObjectiveTo review self-reported instruments for assessing indoor home environmental exposures in asthma patients and to characterise their content, development, and psychometric properties.DesignA scoping review was conducted with content assessment.MethodsA literature search was conducted in Embase and PubMed using the key words housing quality, questionnaire and asthma and their index terms, covering articles published in English between January 2000 to July 2023. Articles in which questionnaires or single item questions were used to assess indoor home environmental exposures in asthma patients in middle- and high-income countries were included. We excluded articles in which the questionnaire required an interviewer or onsite observations and those conducted in low-income countries.ResultsWe screened 1584 articles to identify 44 studies containing self-reported questionnaires measuring indoor home environmental exposures. 36 studies (82%) were cross sectional, 35 (80%) had a sample size of greater than 1000 participants, and 29 (66%) were conducted in children. Most studies (86%, n = 38) had binary (yes/no) or multiple-choice responses. 25 studies (57%) included a recall period of 12 months. 32 studies (73%) had a response rate of greater than 50%. Dampness, biological exposures (e.g. mould), and second-hand tobacco smoke were the most assessed indoor home environmental exposures. Childhood asthma (54%, n = 24) and asthma symptoms (36%, n = 16) were the most examined asthma related outcomes. The exposure most associated with adverse asthma outcomes was exposure to damp (79%, n = 35). 13 studies (29%) had developed a self-reported instrument by adapting questions from previous studies and almost all instruments (n = 42 studies, 95%) had not been validated.ConclusionsThe scoping review did not identify a comprehensive, validated self-reported questionnaire for assessing indoor home environmental exposures in patients with asthma. There is need to develop and validate a robust but pragmatic self-reported instrument, incorporating the findings from this review.
| S-EPMC11494864 | biostudies-literature