Literature review on asthma

Utilitiesjournals in ncbi databasesmesh databasencbi handbookncbi help manualncbi news & blogpubmedpubmed central (pmc)pubmed clinical queriespubmed healthall literature resources... Toall how tochemicals & bioassaysdna & rnadata & softwaredomains & structuresgenes & expressiongenetics & medicinegenomes & mapshomologyliteratureproteinssequence analysistaxonomytraining & tutorialsvariationabout ncbi accesskeysmy ncbisign in to ncbisign : abstractformatsummarysummary (text)abstractabstract (text)medlinexmlpmid listapplysend tochoose destinationfileclipboardcollectionse-mailordermy bibliographycitation managerformatsummary (text)abstract (text)medlinexmlpmid listcsvcreate file1 selected item: 16194186formatsummarysummary (text)abstractabstract (text)medlinexmlpmid listmesh and other datae-mailsubjectadditional texte-maildidn't get the message? Literature dson g1, eick s, jones information1faculty of health and social work, university of plymouth, plymouth, uk. Ionian@ractaims: this paper reports a review conducted to identify the factors in the indoor environment that have an evidence-based link with the exacerbation or development of asthma and to identify measures that healthcare professionals can promote to reduce exposure to these risk factors in the ound: the indoor environment, particularly at home, has been recognized as a major source of exposure to allergens and toxic chemicals. Exposure to allergens and toxins is thought to exacerbate respiratory conditions, in particular, s: searches were made of health and indoor environment databases, including cochrane library, national health services centre for reviews and assessment reports, british medical journal, cinahl and ovid library, medscape/medline, embase, ingenta, science citation index, web of science. The following keywords were used: allergens, allergen avoidance, asthma, asthma prevention, cat, damp, der p 1, dog, environmental control, house dust mites, indoor air quality, indoor environment, meta analysis, mould, pets, remedial actions, respiratory illnesses and systematic gs: there is evidence of a link between asthma and a small number of indoor environmental factors. There is currently only reasonable evidence for one causative factor for asthma in the indoor environment and that is house dust mite allergen. Although there are many studies of different remedial actions that can be taken in the home, often these give evidence of reduced risk of exposure but not clinical improvement in asthma. Although there is a lack of medical evidence for the reduction of known sensitizers such as mould, this is because of a dearth of research rather than evidence of no sions: there is some evidence of a link between the indoor environment and asthma. Indexed for medline] sharepublication type, mesh terms, substancespublication typereviewmesh termsair pollution, indoor/adverse effects*allergens/immunologyanimalsanimals, domestic/immunologyantigens, dermatophagoides/immunologyasthma/etiology*asthma/immunologybedding and linenscatsdogsecosystemenvironment, controlledenvironmental exposure/prevention & controlfungi/immunologyhousinghumanstobacco smoke pollution/adverse effectssubstancesallergensantigens, dermatophagoidestobacco smoke pollutionlinkout - more resourcesfull text sourceswileyovid technologies, lasthma - genetic allianceasthma - medlineplus health informationindoor air pollution - medlineplus health informationmiscellaneousnci cptac assay portalpubmed commons home. Commentshow to join pubmed commonshow to cite this comment:Ncbi > literature > ncbi web site requires javascript to tionresourcesall resourceschemicals & bioassaysbiosystemspubchem bioassaypubchem compoundpubchem structure searchpubchem substanceall chemicals & bioassays resources... Commentshow to join pubmed commonshow to cite this comment:Ncbi > literature > ly, some studies demonstrated that hmgb1, as proinflammatory mediator belonging to the alarmin family, has a key role in different acute and chronic immune disorders. Asthma is a complex disease characterised by recurrent and reversible airflow obstruction associated to airway hyper-responsiveness and airway literature review aims to analyse advances on hmgb1 role, employment and potential diagnostic application in reviewed experimental studies that investigated the pathogenetic role of hmgb in bronchial airway hyper-responsiveness, inflammation and the correlation between hmgb1 level and asthma. Total of 19 studies assessing the association between hmgb1 and asthma were emerged from this literature review was the confirmation of hmgb-1 involvement in diseases characterised by chronic inflammation, especially in pulmonary pathologies. The dominance of th2 response is characteristic of allergic eosinophilic asthma, t2 response characteristic of non allergic eosinophilic asthma, and t17 of neutrophilic asthma. In order to improve knowledge of the disease have been discovered new biomarkers of airway inflammation and respiratory diseases such as asthma, including review aim is to analyse advances on hmgb1 role, employment and potential diagnostic application in asthma. We reviewed experimental studies that investigated the pathogenetic role of hmgb in bronchial airway hyper-responsiveness, inflammation and the correlation between hmgb1 level and sthis literature review has been conducted employing two databases: pubmed and sciencedirect. On these websites we looked for articles from inception through december 2016 using a key term related to asthma: “asthma” and one key term related to hmgb1: “hmgb1”. Determined that the abstracts of those articles whose titles suggested they might have examined the association between asthma and hmgb1 were to be considered. Finally we reviewed and searched references of the selected articles and the ones whose titles suggested that could have considered the association between asthma and hmgb1 in order to identify further studies that met the inclusion criteria. Articles were included in our review according to the following inclusion criteria: english language, publication in peer reviewed journals. Further exclusion criteria were: non-research authors (mc, sq, tc) conducted the initial search and separately reviewed and selected the references based on the inclusion and exclusion obtained from our research of articles includes: study author names, publication dates, study designs (i. The heterogeneity of the studies included in our paper is a limitation of our review since both animals and humans, in vivo and in vitro studies are included; moreover pathogenetic and clinical research are sas resumed in table 1 a total of 19 studies assessing the association between hmgb1 and asthma were s assessing the association between hmgb1 and beincreased levels of hmgb-1 and endogenous secretory rage in induced sputum from asthmatic patients2011x–sputum≫ragespirometryhouhigh mobility group protein b1 (hmgb1) in asthma: comparison of patients with chronic obstructive pulmonary disease and healthy controls2011x–sputum plasma≫–spirometryzhouhmgb1 and rage levels in induced sputum correlate with asthma severity and neutrophil percentage2012x–sputum≫ragespirometryshimthe role of high-mobility group box-1 (hmgb1) in the pathogenesis of asthma2012xxsputum (human) lung tissue, bal (animal)≫il-4, il-5, il-13, and gm-csf–sukkarsoluble rage is deficient in neutrophilic asthma and copd2012x–sputum serum≫rage; saa–leeinhibition of high-mobility group box 1 in lung reduced airway inflammation and remodeling in a mouse model of chronic asthma2013–xmediastinal lymph nodes and lungs tissue bal≫––zhangrecombinant hmgb1 a box protein inhibits th17 responses in mice with neutrophilic asthma by suppressing dendritic cell-mediated th17 polarization2014–xlung tissue≫–whole-body plethysmographyzhanganti-hmgb1 neutralizing antibody ameliorates neutrophilic airway inflammation by suppressing dendritic cell-mediated th17 polarization. Xbone marrowbalflung tissue≫––tangethyl pyruvate decreases airway neutrophil infiltration partly through a high mobility group box 1-dependent mechanism in a chemical-induced murine asthma model2014–xbalflymphnodeslung tissue≫–barometric plethysmographic chambermahigh mobility group box 1: a novel mediator of th2-type response-induced airway inflammation of acute allergic asthma2015–xballung tissue≫il-4, il-5, il-6, il-8, il-17, ifn-γ, gata3measuring airway resistance of lung (rl) and cdyn via mch challengeojohigh-mobility group box 1 promotes extracellular matrix synthesis and wound repair in human bronchial epithelial cells2015x–cell culture–e-cadherin, integrins, extra cellular matrix proteins–yaochicken igy facilitates allergic airway inflammation in a chemical-induced murine asthma model by potentiating il-4 release2015 xlung tissue≫il-4, igy–cupparisputum high mobility group box-1 in asthmatic children: a noninvasive sensitive biomarker reflecting disease status2015x–sputum≫serum total ige levelsspirometryqiaoeffect of different 1,25-(oh)2d3 doses on high mobility group box1 and toll-like receptors 4 expression in lung tissue of asthmatic mice2015–xlung tissue≫hmgb1 and tlr4–liang jphosphatidylinositol 3-kinases pathway mediates lung caspase-1 activation and high mobility group box 1 production in a toluene-diisocyanate induced murine asthma model2015–xlung tissuelymph node cellsbal≫serum igebarometric plethysmo-graphic chamberliang yhmgb1 binding to receptor for advanced glycation end products enhances inflammatory responses of human bronchial epithelial cells by activating p38 mapk and erk1/22015x–primary culture of human bronchial epithelial cells≫tnf-a, tslp, mmp-9, vegf–shimeosinophils modulate cd4(+) t cell responses via high mobility group box-1 in the pathogenesis of asthma2015–xlung tissue≫il-4 and il-5–houhmgb1 contributes to allergen-induced airway remodeling in a murine model of chronic asthma by modulating airway inflammation and activating lung fibroblasts2015–xbalflung tissue≫ifn-γ, il-5, il-4, il-13, il-1β, tnf-α, vegf, active-tgf-β1, mmp-9–ullahreceptor for advanced glycation end products and its ligand high-mobility group box-1 mediate allergic airway sensitization and airway inflammation2014–xlung tissue≫tlr4-rage–. Were the first to test the level of hmgb1 and of the endogenous secretory receptor for advanced glycation end products (esrage) in sputum of asthmatic patient. In 2011 they dosed hmgb-1 and esrage levels in induced sputum of 44 asthmatic patients (before any asthma treatment) and 15 normal controls (japanese, non-smokers subjects, with no history of respiratory infection for minimum of 4 weeks before the study). Hmgb-1 sputum levels were significantly augmented in asthmatic patients than in controls, and there was an accordance between hmgb-1 level and the severity of disease. Esrage levels in induced sputum from asthmatic subjects were considerably higher than those in healthy ones, with no significant differences in esrage levels between the mild persistent and the severe asthmatic patients [13]. Hmgb1 levels in induced sputum were higher in patients with all severities of asthma and in those with copd than healthy subjects. Plasma and sputum hmgb1 levels were higher in patients with severe asthma than in patients with mild one. There were no significant variation in sputum hmgb1 levels between subjects with mild asthma and controls and between mild asthma and moderate asthma. Plasma hmgb1 levels were noticeably higher in patients with moderate asthma than in those with mild asthma. Serum and sputum hmgb1 levels of copd patients were significantly augmented than levels in asthmatic ones. The differences of plasma and sputum hmgb1 levels were not significant between patients with non eosinophilic asthma and eosinophilic asthma patients. They enrolled subjects using inhaled corticosteroids (ics) reporting increased hmgb1 in the airways in stable copd and in asthmatic sputum.

Moreover, they dosed systemic levels of soluble rage (srage) in a separate group of asthmatic (n = 5101) and copd (n = 534) patients. Subjects with neutrophilic asthma or copd had no levels of lung srage, while levels of srage in non-neutrophilic asthma/copd were almost the same to those in controls. Systemic srage was significantly decreased in patients affected by neutrophilic asthma or copd compared to those which haven’t airway neutrophilia. This study confirmed that sputum hmgb1 expression was higher in asthmatics than in healthy controls; sputum hmgb1 expression was significantly higher in subjects with sputum eosinophilia than in subjects without sputum eosinophilia. In induced sputum samples of asthma group was detected an augmented presence of neutrophils, hmgb1 and rage levels. In severe asthmatics, the percentage of neutrophils and hmgb1 levels were noticeably higher than in mild and moderate asthmatic patients. They showed that sputum hmgb1 levels were significantly augmented in patients with asthma compared to healthy ones. Particularly, patients with severe asthma presented higher sputum hmgb1 levels than patients with mild asthma and than moderate asthmatic ones. In addition, total serum ige levels in the asthmatic group were noticeably elevated than those in the control group and positively correlated to sputum hmgb1. Created an animal model of asthma (mice) to analyse lung tissue and bronchoalveolar lavage (bal) fluid after an intraperitoneal injection of neutralizing antibodies. They observed that rage and tlr2 expression on the cd11b−cd11c+ cells (dendritic cells) augmented importantly in asthmatic animals compared with control ones and these changes were incredibly attenuated by the injection of hmgb1 neutralizing antibodies [16]. In 2013 created a animal model (mice) of chronic asthma in order to demonstrate that the inhibition of hmgb1 expression decreased airway inflammation, mucus generation, and collagen production in lung tissues. They used groups of 10 mice: a control, an asthmatic and 1,25-(oh)2d3 low, middle, high dose group. There was a higher expression of hmgb1 and tlr4 mrnas in the lungs of asthmatic group than in control one. The expression of hmgb1 and tlr4 mrnas in 1,25-(oh)2d3 low and middle dose groups was considerably lower than the asthma group and higher than the control one; the high dose group had an augmented expression of hmgb1 and tlr4 mrnas compared to the asthmatic group [22]. In 2014, made a toluene-2,4-diisocyanate (tdi)-induced murine asthma model, dominated by granulocytic inflammation and explored the role of ethyl pyruvate (ep) on this model. Levels of hmgb1 were significantly higher in tdi induced murine asthma model and ep treatment down-regulated hmgb1 in a dose-dependent manner [23]. Thanks to their previous observation in a murine model of neutrophilic asthma of positive correlation between the increase in hmgb1 expression and th17-mediated airway inflammation, speculated that hmgb1 promoted the production of th17 polarization-related factors, and that hmgb1 blocking inhibited the th17 response. They used a tdi-induced asthmatic murine model, measured levels of ifng, il-4, il-5, il-13, il-17a and tnf-a in supernatants of cultured lymphocytes and accomplished pulmonary histopathological examination. In 2015, using a tdi-induced murine asthma model, demonstrated that caspase-1 activation and hmgb1 production was mediated by phosphatidylinositol 3-kinases (pi3ks); this study also assessed the role of ly294002 a specific inhibitor of pi3k. Level serum ige was significantly increased in tdi-induced murine asthma model, as well as il-4 in supernatant of cultured lymphocytes, the number of inflammatory cells and the protein level of hmgb1 in bal fluid and lung tissue. In tdi-induced murine asthma model, caspase-1 was activated after tdi exposure; after ly294002 adminstration was found abnormal distribution of cleaved caspase-1 but not procaspase-1, so the role of this specific inhibitor was established in the cleavage process of caspase-1 rather than increasing its protein expression. Reported that levels of hmgb1 in balf and lung tissue of asthmatic mice were significantly augmented than controls. Elaborated a mice model of chronic asthma (which have a considerably high hmgb1 expression) in order to consider the effects of hmgb1 on airway responsiveness and re-modeling. Thus, an increase of hmgb1 has been linked to many inflammatory diseases such as allergic asthma, diabetes, atherosclerosis and heart failure [35]. And extracellular hmgb-1 main rmore, recent researches have clarified the role of the immune system thanks to the analysis of two characteristic cytokines, il-4 and il-13, secreted by t helper type 2 cells (th2), basophils and mastocytes typical of allergic immunity, leading to pathological conditions such as asthma and allergy. It has been observed that il-4, il-13 and stat6 are fundamental in the progression of airway hyper-responsiveness, inflammation, as well as mucus production in th2 asthma. Consequently, it was reported that il-4/stat-6 pathway is involved in asthma pathogenesis because stat-6 activation lead to the differentiation of naïve t-cells into th2 effector cells, and it regulates the production of th2 chemokine induced by il-4 and il-13 [38, 39]. Emerged from this literature review was the confirmation of hmgb-1 involvement in diseases characterised by chronic inflammation, especially in pulmonary pathologies. In a previous literature review we demonstrated how hmgb-1 levels were augmented in different tissues of smokers and copd patients [8]. Furthermore asthmatic population have augmented levels of the protein in serum too compared to normal subjects. On the other hand animals studies also demonstrated that treating asthma with drugs known to lower hmgb-1 levels or with anti-hmgb-1 antibodies ameliorate animals condition and decrease in situ inflammatory markers. Bronchostenosis mechanism, fundamental in the asthmatic disease, could be sustained and modulated by this alarmin. Data obtained and collected in this review indicate that hmgb1 is a potential therapeutic target of allergic asthma, nevertheless it is difficult to detect its levels, because it is a nuclear protein. And molecular use cookies to improve your experience with our information about our cookie maltreatment is a common problem with known adverse consequences, yet its contributions to the development and course of pediatric asthma are only poorly review first describes possible pathways connecting child maltreatment to pediatric asthma, including aspects of the physical home environment, health behaviors and disease management, and psychological consequences of child maltreatment.

We subsequently review existing studies, which generally report an association between maltreatment experiences and asthma outcomes in childhood. However, this literature is in its early stages; there are only a handful studies, most of them rely on self-reports of both child maltreatment and asthma history, and none have investigated the physiological underpinnings of this association. Taken together, however, the studies are suggestive of child maltreatment playing a role in pediatric asthma incidence and expression that should be explored ng data are sparse and do not allow for specific conclusions. However, the data are suggestive of child maltreatment influencing asthma risk and morbidity long before the adult years. Future research should focus on understanding how child maltreatment contributes to asthma disease risk and progression in this highly vulnerable oundasthma remains one of the most prevalent chronic health problems facing american youth today. An estimated 14 % of children and adolescents under the age of 18 are diagnosed with asthma at some point in their lives [1]. Asthma has a multifactorial etiology, where genetic liabilities and environmental exposures interact in complex ways to cause reversible airway inflammation and obstruction. Though physical exposures such as viral infection, air pollution, dust mites, and cockroach antigen are known to play significant roles in asthma onset and course [6–8], mounting evidence suggests that features of the social environment do as well. In this regard, social “pollutants” such as childhood poverty, neighborhood violence, and familial stress, independently contribute to pediatric asthma outcomes, and have the potential to amplify effects of the physical environment [9–12]. This growing appreciation for social contributors to pediatric asthma, there is a surprising dearth of studies investigating the influence of child maltreatment history on asthma development and maintenance. Importantly, children and adolescents who experienced child maltreatment are more likely to engage in adverse health behaviors, such as smoking, and more likely to be obese, have greater levels of chronic inflammation, and altered hpa axis profiles [17–20] - all factors known to play a role in asthma onset and course [10, 21–23]. Although long-term adverse physiological consequences of child maltreatment are increasingly being identified, very little is known about the role experiences of child maltreatment play with respect to asthma in particular. Based on what is known about the biological sequelae of child maltreatment and the importance of social contributors to asthma, however, experiences of child maltreatment are likely to play an underappreciated role in pediatric note that existing studies support strong links between psychological stress in general and the incidence and expression of asthma [10, 24, 25]. Nonetheless, child maltreatment represents a particularly salient adverse experience for children, and there are reasons to hypothesize its effects on asthma morbidity will be even more pronounced than other stressors, and also come in many different forms. For these reasons we argue that understanding maltreatment’s asthma-related consequences will provide unique insights relevant to research and practice. In addition, a better understanding of how different types of maltreatment may or may not lead to certain asthma-related outcomes can increase our understanding of the exact situations and pathways through which adverse experiences come to negatively impact review will summarize potential pathways through which child maltreatment could influence pediatric asthma outcomes, including youth’s home environment, psychological well-being, health behaviors, and physiological pathways. Subsequently we will review the existing literature suggesting connections between child maltreatment and pediatric asthma, and discuss limitations as well as suggestions for future ial pathways connecting child maltreatment and pediatric considering the ways in which experiences of child maltreatment may come to impact pediatric asthma, several pathways need to be considered, including indirect effects through the physical home environment youth grow up in, disease management and individual health behaviors, and psychological consequences of maltreatment. Future research should make it a priority to disentangle the precise ways in which these other stressors confound, mediate, and moderate the association between child maltreatment and pediatric asthma. At the end of this section, the biological pathways connecting adverse social experiences to asthma-related outcomes will be reviewed physical home physical home environment children grow up in contributes to pediatric asthma in important ways. Exposure to environmental tobacco smoke, indoor air pollution, and allergen exposure inside the family home are all strongly connected to pediatric asthma outcomes [7, 21, 26–29]. Convincing cross-sectional associations between common allergens, such as cockroach or mouse allergen, and asthma diagnosis as well as asthma symptoms and asthma-related hospitalizations and physician visits have been shown [7, 30]. These findings are further strengthened by reports of interventions designed to reduce allergen burdens inside the homes of youth with asthma resulting in improved clinical outcomes among these youth [31]. Physical home environment likely presents an important link between child maltreatment, especially neglect, and pediatric asthma. For example, physically unsafe and dilapidated housing conditions may go hand in hand with exposure to mold, house dust, allergens, and phthalates, known contributors to asthma [7, 34–36]. Caregivers may also be less likely to engage in recommended preventive measures to successfully manage their children’s asthma and minimize their children’s symptoms, e. Consequently, neglect in particular may negatively affect asthma management and morbidity by way of inadequate physical home behaviors and asthma nce to a variety of health behaviors is an integral part of successful long-term asthma management, which frequently requires adherence to daily medication. Depending on children’s ages, asthma management can involve considerable involvement on the part of other family members, who help oversee daily behaviors such as proper medication adherence. In addition, certain health behaviors youth may engage in, for example smoking, can have especially detrimental consequences among youth with asthma [41, 42] who are frequently found to be more likely to smoke compared to their healthy peers [43, 44]. Parents of children with maltreatment histories are also more likely to be struggling with mental health and substance abuse problems themselves [47–49], both of which may further signal an inability on the part of parents to be actively involved in their children’s disease management ’s own behaviors may also contribute to worse asthma outcomes. This has the potential to negatively affect both the onset of asthma as well as exaggerate existing asthma [51]. This is of interest as obesity is increasingly being identified as a risk factor for pediatric asthma, especially nonatopic asthma, even though the underlying causes are not yet clearly understood [22, 52]. So might other health practices, including drug use, sleep habits, or dietary intake, but these pathways require further logical sequelae of child re to child maltreatment may further increase individuals’ risk for asthma through negatively impacting their psychological well-being. Several small scale studies have established preliminary connections between emotional states such as depression or anxiety and asthma-related outcomes [53, 54] and documented higher rates of behavioral problems and anxiety disorders among youth with asthma [55]. One longitudinal study, for example, linked greater rates of behavior problems to increased rates of asthma morbidity in the form of more days of wheeze and poorer functional asthma status over the course of a 9 month follow-up period [56]. These associations have been observed across youth exposed to different types of child abuse and neglect and may play an important role in linking child maltreatment to pediatric asthma.

Depression, for example, is associated with altered endocrine and immune functions that are relevant to the course of asthma [60, 61]. Asthma is typically thought to be marked by a shift towards th2-dependent processes, both an early-phase response involving il-4 and il-13 and a late-phase response involving il-5. These bind to mast cells in the airways and, by causing them to degranulate and release histamines and leukotrienes, bring about typical asthma symptoms including smooth muscle constriction, mucus production, and edema. Similarly, il-5 aids the production, maturation, and activation of eosinophils which contribute to airway inflammation and obstruction and are involved in longer-term asthma-related inflammatory le studies have shown that stimulated production of these cytokines increases in response to experiences of stress, e. University examinations [67] and for children with asthma this amplified cytokine production is especially pronounced with family-related stressors, such as conflict in the parent–child relationship or chaos in the household [68]. In addition, recent studies have found that child maltreatment is associated with increased expression of il-6, crp [69, 70], and other nonspecific markers of low-grade inflammation, whose role in asthma is increasingly appreciated. Furthermore, a small number of studies have linked other social stressors to cytokine activity of particular relevance to asthma. For example, among youth with asthma, more chronic family and household stress is associated with increased production of the th2 cytokines il-5 and il-13, and higher eosinophil counts [71]. Similarly, exposure to acute stressful life events in the context of chronic family stress has been linked to greater th2 cytokine production, including levels of il-4, il-5, and ifn-gamma, among youth with asthma [72]. Glucocorticoids are important physiologic regulators of many asthma-related immune functions, and the basis of front-line asthma-control therapies for many patients. If maltreatment reduces the availability of glucocorticoids in the airways, or decreases cellular sensitivity to these molecules, there could be implications for asthma expression and/or management [73, 74]. Consistent with this possibility, one study found that among youth with asthma, experiencing both acute and chronic stress was associated with lower expression of glucocorticoid receptor mrna in leukocytes [75], which could plausibly reduce cortisol-mediated signaling in these cells. Another study found that among youth with asthma, lower parental support was associated with higher glucocorticoid resistance, as reflected in ex vivo lymphocyte th2 cytokine production, following co-incubation with a mitogen and hydrocortisone [76]. These patterns have not been studied in the context of maltreatment, but if present they could function as a pathway for increasing risk of asthma development or ng studies linking child maltreatment history and pediatric identified seven studies that report on the association of child maltreatment history and pediatric asthma, five of them focusing on cross-sectional associations and two taking advantage of longitudinal follow-up et al. Child and parent-reported history of physical or sexual abuse during the past year was associated with a roughly doubled likelihood of parent-reported current asthma, as well as greater rates of asthma-related health care and medication use after controlling for a number of confounders. In a relatively large cross-sectional study of 6–7 year olds in brazil [78], parent reports of emotional abuse were associated with symptom intensity among children with non-atopic, but not atopic, asthma. By contrast, another cross-sectional study [79] found that among 160 4–6 year olds, parent-reported physical abuse was associated with an increased risk of child asthma. Similarly, in a study of 15 year old swedish adolescents [80], self-reported physical abuse was associated with increased self-reported asthma risk, whereas sexual abuse was not. One possibility is that physical abuse predisposes youth to asthma onset, but does not play a significant role in the course of disease. This study is of interest in that it compared the effects of both self-reported physical and sexual abuse and official reports of maltreatment on self-reported lifetime asthma diagnosis. The authors found no association between self-reported abuse and asthma, but found that an official record of child maltreatment roughly doubled risk of asthma diagnosis. This points to the importance of considering different effects of self-reported versus official maltreatment records, possibly because official records are indicative of younger age at exposure or particularly severe cases of child strongest evidence comes from two studies using longitudinal designs to explore child maltreatment and pediatric asthma associations. Trauma class was unrelated to self-reported asthma history; no cross-sectional associations were found at baseline, or longitudinal associations at a 1 year follow-up or age 25 in this sample. Through that project, they may have received medical, psychological, and/or addictions treatment, which may have reduced the consequences of one study has directly compared the impact of different types of abuse and neglect while also taking advantage of hospital records to evaluate more objective asthma-related outcomes. After controlling for a number of individual, family, and community factors (though not asthma history or severity), reports of child maltreatment were associated with a 74–100 % greater risk of hospital treatment for asthma. 82] may in part be due to the focus on more severe asthma here (hospitalization for asthma based on medical records). Few studies do not allow detailed conclusions about the extent of asthma-related consequences following experiences of child maltreatment. When taken together, they are, however, suggestive of child maltreatment playing a role in pediatric asthma. Rates of sexual abuse are also lower, requiring larger samples to detect r research is needed to clarify whether different types of maltreatment have different consequences for asthma, both in terms of its development and expression. Nonetheless, the details of the links between child maltreatment and pediatric asthma have yet to be understood in all their tions of research to noted above, there are several limitations to the existing studies in this area of research that complicate the interpretation of their findings. With regard to the overall association between child maltreatment and pediatric asthma, three important methodological issues arise. First, five out of the seven studies investigating the influence of child maltreatment on pediatric asthma outcomes rely solely on cross-sectional data. These designs prohibit conclusions about the direction of causality, and raise questions about whether the observed associations are reflective of maltreatment’s effects on asthma, or an alternative scenario involving reverse causality and/or third variables. For example, as described in more detail in the next sections, it is possible that asthma elicits harsh parenting, or that some of the reported associations have their origin in disadvantaged socioeconomic , a measurement issue for both child maltreatment and asthma is the heavy reliance on self- and caregiver-reports. Not only are there problems with the reliability and accuracy of self- and caregiver-reports of asthma and maltreatment history, but given that in many studies the same individual (either an older child or a caregiver) reports on both, there are additional issues of shared-method variance that may influence , the existing studies do not allow for the separation of effects of child maltreatment from effects of other, co-occurring stressors.

Although some of the studies reviewed here made an effort to control for some co-occurring stressors e. Second, even though the vast majority of child maltreatment involves cases of neglect, only one existing study examined the influence of neglect on pediatric asthma outcomes. As mentioned at the beginning of this paper, however, there are reasons to believe that due, for example, to influences on the physical home environment, children experiencing neglect may be at an increased risk of worse asthma outcomes. Consequently, it remains unclear whether differential asthma outcomes are a consequence of exposure to child maltreatment or other events included in the summary score, such as the death of a loved one or parental divorce. More detailed information, for example on the timing and duration of exposure, is necessary to better understand the associations between child maltreatment and pediatric s also vary substantially with respect to asthma measurement. Research that considers indicators of asthma-related morbidity, health-care utilization, and functional impairment would provide a more nuanced understanding of how maltreatment relates to the child’s experience of asthma and associated costs for the medical system. Similarly, information regarding asthma management outcomes, such as the number of prescriptions filled and the type of prescriptions (e. It is possible that experiences of child maltreatment during particular developmental windows, such as infancy and early childhood, may have particularly strong and long-lasting effects on pediatric asthma onal important role of socioeconomic role socioeconomic status (ses) may play in the associations between child maltreatment and pediatric asthma also warrants consideration. Previous research has shown that children and adolescents from low ses environments are more likely to suffer from asthma and that growing up in low ses families is associated with many of the same psychological sequelae that have been shown to follow child maltreatment [9]. Most studies evaluating the effect of child maltreatment on pediatric asthma have not evaluated possible interactions with ses, but this should be considered in the future. One study reported that stressful life events (including experiences of abuse) were more common among adolescents living in physical housing conditions marked by cockroaches, insecticides, dampness, and smoking, all of which have the potential to worsen asthma [84]. As children and adolescents from low ses backgrounds are at higher risk for substandard housing, general life stressors and child maltreatment, they may be particularly vulnerable to worse asthma the largely cross-sectional nature of available data, existing studies on the influence of child maltreatment on pediatric asthma also do not allow for careful consideration of issues of reverse causality. Consequently, it is possible that children with chronic health conditions, such as asthma, are exposed to more abusive and neglectful behaviors from their parents, as they may require greater resources in terms of finances, emotional support, and general supervision and attention. These studies clearly suggest that the extent to which chronic health conditions, such as asthma, may increase the risk of child maltreatment experiences needs to be investigated more endations for future on existing research on the impact of child maltreatment on pediatric asthma, there are several recommendations for future research. However, to truly understand the connections between child maltreatment and pediatric asthma, more longitudinal data are , use of more in-depth study designs will be needed to understand whether particular aspects of maltreatment are influential in shaping pediatric asthma outcomes. When focusing on child physical neglect, details on the physical home environment may provide information on how neglect comes to influence pediatric asthma. In short, a more detailed examination of potential moderators and mediators of the association between child maltreatment and asthma is needed. This may also provide insights into potential protective factors which could inform future research and prevention , more work is needed to understand the biological pathways that might connect child maltreatment with asthma outcomes. Hence, nothing is known on direct effects of child maltreatment on lung functioning measures among children and adolescents, or about relevant airway or allergic inflammatory processes typically associated with asthma y, most studies to date do not report on gender effects but it is not clear that they were always examined in detail. At least one study has reported boys to be more likely to report general health and mental health symptoms in response to child abuse than girls [80], suggesting that there may be sex-based differences with respect to pediatric asthma as sionsalthough several studies link experiences of child maltreatment to adult-onset asthma and asthma morbidity among adults [99–101], very little research has investigated these associations among children and adolescents. Existing data are sparse and do not allow for specific conclusions regarding the exact associations between various types of child maltreatment and asthma-related outcomes. More research is needed to understand how child maltreatment contributes to asthma disease risk and progression in this highly vulnerable ledgementsthis manuscript was supported by the national institutes of health (grant hl108723; ec). 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Research and use cookies to improve your experience with our information about our cookie maltreatment is a common problem with known adverse consequences, yet its contributions to the development and course of pediatric asthma are only poorly review first describes possible pathways connecting child maltreatment to pediatric asthma, including aspects of the physical home environment, health behaviors and disease management, and psychological consequences of child maltreatment.