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1.  The indoor environment and inner-city childhood asthma 
Summary
Objective
Exposure to indoor pollutants and allergens has been speculated to cause asthma symptoms and exacerbations and influence the risk of developing asthma. The aim of this article is to review the medical literature regarding the role of the indoor environment on inner-city childhood asthma.
Data sources
A literature search was performed in PubMed. Studies focusing on inner-city indoor allergen, childhood asthma, and environmental controls were included.
Results
The prevalence of asthma in children is increasing especially in inner-city area. Exposure to high levels of indoor allergens and pollutants has been related to asthma development. Studies have shown that mouse, cockroach, pets, dust mite, mold, tobacco smoke, endotoxin and nitrogen dioxide are the important exposures. Recent studies have shown that indoor environmental control is beneficial in reducing asthma morbidity and development.
Conclusions
Inner-city children are exposed to various indoor allergens and pollutants that may lead to asthma development and exacerbation of existing asthma. Multifaceted environmental controls are beneficial in improving asthma symptom and maybe a viable prevention strategy. Further prospective studies of environmental intervention are needed to further identify effective strategies to improve and prevent asthma symptoms in inner-city children.
PMCID: PMC4110514  PMID: 25003723
Indoor environment; allergen; children; asthma; inner-city; air pollution
2.  Childhood asthma and indoor allergens in Native Americans in New York 
Environmental Health  2006;5:22.
Background
The objective of this study was to assess the correlation between childhood asthma and potential risk factors, especially exposure to indoor allergens, in a Native American population.
Methods
A case-control study of St. Regis Mohawk tribe children ages 2–14 years, 25 diagnosed with asthma and 25 controls was conducted. Exposure was assessed based on a personal interview and measurement of mite and cat allergens (Der p 1, Fel d 1) in indoor dust.
Results
A non-significant increased risk of childhood asthma was associated with self-reported family history of asthma, childhood environmental tobacco smoke exposure, and air pollution. There was a significant protective effect of breastfeeding against current asthma in children less than 14 years (5.2 fold lower risk). About 80% of dust mite and 15% of cat allergen samples were above the threshold values for sensitization of 2 and 1 μg/g, respectively. The association between current asthma and exposure to dust mite and cat allergens was positive but not statistically significant.
Conclusion
This research identified several potential indoor and outdoor risk factors for asthma in Mohawks homes, of which avoidance may reduce or delay the development of asthma in susceptible individuals.
doi:10.1186/1476-069X-5-22
PMCID: PMC1552054  PMID: 16859546
3.  Indoor Environmental Exposures and Exacerbation of Asthma: An Update to the 2000 Review by the Institute of Medicine 
Background: Previous research has found relationships between specific indoor environmental exposures and exacerbation of asthma.
Objectives: In this review we provide an updated summary of knowledge from the scientific literature on indoor exposures and exacerbation of asthma.
Methods: Peer-reviewed articles published from 2000 to 2013 on indoor exposures and exacerbation of asthma were identified through PubMed, from reference lists, and from authors’ files. Articles that focused on modifiable indoor exposures in relation to frequency or severity of exacerbation of asthma were selected for review. Research findings were reviewed and summarized with consideration of the strength of the evidence.
Results: Sixty-nine eligible articles were included. Major changed conclusions include a causal relationship with exacerbation for indoor dampness or dampness-related agents (in children); associations with exacerbation for dampness or dampness-related agents (in adults), endotoxin, and environmental tobacco smoke (in preschool children); and limited or suggestive evidence for association with exacerbation for indoor culturable Penicillium or total fungi, nitrogen dioxide, rodents (nonoccupational), feather/down pillows (protective relative to synthetic bedding), and (regardless of specific sensitization) dust mite, cockroach, dog, and dampness-related agents.
Discussion: This review, incorporating evidence reported since 2000, increases the strength of evidence linking many indoor factors to the exacerbation of asthma. Conclusions should be considered provisional until all available evidence is examined more thoroughly.
Conclusion: Multiple indoor exposures, especially dampness-related agents, merit increased attention to prevent exacerbation of asthma, possibly even in nonsensitized individuals. Additional research to establish causality and evaluate interventions is needed for these and other indoor exposures.
Citation: Kanchongkittiphon W, Mendell MJ, Gaffin JM, Wang G, Phipatanakul W. 2015. Indoor environmental exposures and exacerbation of asthma: an update to the 2000 review by the Institute of Medicine. Environ Health Perspect 123:6–20; http://dx.doi.org/10.1289/ehp.1307922
doi:10.1289/ehp.1307922
PMCID: PMC4286274  PMID: 25303775
4.  Environmental tobacco smoke, indoor allergens, and childhood asthma. 
Environmental Health Perspectives  2000;108(Suppl 4):643-651.
Both environmental tobacco smoke and indoor allergens can exacerbate already established childhood albeit primarily through quite disparate mechanisms. In infancy and childhood, environmental tobacco smoke (ETS) exposure is associated with measures of decreased flow in the airways, bronchial hyperresponsiveness, and increased respiratory infections, but the relationship between ETS and allergy is poorly understood. Indoor allergens from dust mite, cockroach, and cat can be associated with asthma exacerbation in children sensitized to the specific allergens. The precise role of either ETS or indoor allergens in the development of asthma is less well understood. The strong and consistent association between ETS and asthma development in young children may relate to both prenatal and postnatal influences on airway caliber or bronchial responsiveness. Dust mite allergen levels predict asthma in children sensitized to dust mite. The tendency to develop specific IgE antibodies to allergens (sensitization) is associated with and may be preceded by the development of a T-helper (Th)2 profile of cytokine release. The importance of either ETS or indoor allergens in the differentiation of T cells into a Th2-type profile of cytokine release or in the localization of immediate-type allergic responses to the lung is unknown. This article evaluates the strength of the evidence that ETS or indoor allergens influence asthma exacerbation and asthma development in children. We also selectively review data for the effectiveness of allergen reduction in reducing asthma symptoms and present a potential research agenda regarding these two broad areas of environmental exposure and their relationship to childhood asthma.
PMCID: PMC1637671  PMID: 10931782
5.  Asthma and other recurrent wheezing disorders in children (chronic) 
Clinical Evidence  2012;2012:0302.
Introduction
Childhood asthma is the most common chronic paediatric illness. There is no cure for asthma but good treatment to palliate symptoms is available. Asthma is more common in children with a personal or family history of atopy, increased severity and frequency of wheezing episodes, and presence of variable airway obstruction or bronchial hyperresponsiveness. Precipitating factors for symptoms and acute episodes include infection, house dust mites, allergens from pet animals, exposure to tobacco smoke, and exercise.
Methods and outcomes
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of single-agent prophylaxis in children taking as-needed inhaled beta2 agonists for asthma? What are the effects of additional prophylactic treatments in childhood asthma inadequately controlled by standard-dose inhaled corticosteroids? We searched: Medline, Embase, The Cochrane Library, and other important databases up to June 2010 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
Results
We found 48 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
Conclusions
In this systematic review we present information relating to the effectiveness and safety of the following interventions: beta2 agonists (long-acting), corticosteroids (inhaled standard or higher doses), leukotriene receptor antagonists (oral), omalizumab, and theophylline (oral).
Key Points
Childhood asthma can be difficult to distinguish from viral wheeze and can affect up to 20% of children.
Regular monotherapy with inhaled corticosteroids improves symptoms, reduces exacerbations, and improves physiological outcomes in children with asthma symptoms requiring regular short-acting beta2 agonist treatment. Their effect on final adult height is minimal and when prescribed within recommended doses have an excellent safety record. Regular monotherapy with other treatments is not superior to low-dose inhaled corticosteroids.
Leukotriene receptor antagonists may have a role as first-line prophylaxis in very young children.
There is consensus that long-acting beta2 agonists should not be used for first-line prophylaxis. CAUTION: Monotherapy with long-acting beta2 agonists does not reduce asthma exacerbations but may increase the chance of severe asthma episodes.
Theophylline was used as first-line prevention before the introduction of inhaled corticosteroids. Although there is weak evidence that theophylline is superior to placebo, theophylline should no longer be used as first-line prophylaxis in childhood asthma because of clear evidence of the efficacy and safety of inhaled corticosteroids. Theophylline has serious adverse effects (cardiac arrhythmia, convulsions) if therapeutic blood concentrations are exceeded.
When low-dose inhaled corticosteroids fail to control asthma, most older children will respond to one of the add-on options available, which include addition of long-acting beta2 agonists, addition of leukotriene receptor antagonists, addition of theophylline, or increased dose of inhaled corticosteroid. However, we don't know for certain how effective these additional treatments are because we found no/limited RCT evidence of benefit compared with adding placebo/no additional treatments. Addition of long-acting beta2 agonists may reduce symptoms and improve physiological measures compared with increased dose of corticosteroids in older children. Long-acting beta2 agonists are not currently licensed for use in children under 5 years of age.Consensus suggests that younger children are likely to benefit from addition of leukotriene receptor antagonists. Although there is weak evidence that addition of theophylline to inhaled corticosteroids does improve symptom control and reduce exacerbations, theophylline should only be added to inhaled corticosteroids in children aged over 5 years when the addition of long-acting beta2 agonists and leukotriene receptor antagonists have both been unsuccessful.
Omalizumab may be indicated in the secondary care setting for older children (aged over 5 years) with poorly controlled allergic asthma despite use of intermediate- and high-dose inhaled corticosteroids once the diagnosis is confirmed and compliance and psychological issues are addressed. However, we need more data to draw firm conclusions.
PMCID: PMC3285219  PMID: 22305975
6.  Environmental risk factors of childhood asthma in urban centers. 
Environmental Health Perspectives  1995;103(Suppl 6):59-62.
Asthma morbidity and mortality are disproportionately high in urban centers, and minority children are especially vulnerable. Factors that contribute to this dilemma include inadequate preventive medical care for asthma management, inadequate asthma knowledge and management skills among children and their families, psychosocial factors, and environmental exposure to allergens or irritants. Living in substandard housing often constitutes excess exposure to indoor allergens and pollutants. Allergens associated with dust mites (DM) and cockroaches (CR) are probably important in both onset and worsening of asthma symptoms for children who are chronically exposed to these agents. Young children spend a great deal of time on or near the floor where these allergens are concentrated in dust. Of children (2 to 10 years of age) living in metropolitan Washington, DC, 60% were found to be sensitive to CR and 72% were allergic to DM. Exposure to tobacco smoke contributes to onset of asthma earlier in life and is a risk factor for asthma morbidity. Since disparity of asthma mortality and morbidity among minority children in urban centers is closely linked to socioeconomic status and poverty, measures to reduce exposure to environmental allergens and irritants and to eliminate barriers to access to health care are likely to have a major positive impact. Interventions for children in urban centers must focus on prevention of asthma symptoms and promotion of wellness.
PMCID: PMC1518936  PMID: 8549491
7.  Childhood asthma. 
Environmental Health Perspectives  1999;107(Suppl 3):421-429.
Asthma prevalence in children has increased 58% since 1980. Mortality has increased by 78%. The burden of the disease is most acute in urban areas and racial/ethnic minority populations. Hospitalization and morbidity rates for nonwhites are more than twice those for whites. Asthma is characterized by recurrent wheezing, breathlessness, chest tightness, and coughing. Research in the past decade has revealed the importance of inflammation of the airways in asthma and clinical treatment to reduce chronic inflammation. Asthma is associated with production of IgE to common environmental allergens including house dust mite, animal dander, cockroach, fungal spores, and pollens. Some interventions to reduce symptoms through control of dust mite and animal dander have had positive results. Control of symptoms through interventions to reduce exposures to cockroach antigen has not been reported. Studies illustrating causal effects between outdoor air pollution and asthma prevalence are scant. Increases in asthma prevalence have occurred at the same time as general improvements in air quality. However, air quality appears to exacerbate symptoms in the child who already has the disease. Decreased pulmonary function has been associated with exposure to particulates and bronchial hyperresponsiveness to smoke, SO(2) and NO(2). Symptoms have been correlated with increased levels of respirable particulates, ozone, and SO(2). Interventions that reduce the negative outcomes in asthma associated with outdoor environmental factors have not been reported. Control of asthma in children will entail the collaborative efforts of patients, family, clinical professionals, and school personnel, as well as community-wide environmental control measures and conducive national and local policies based on sound research.
Images
PMCID: PMC1566232  PMID: 10423388
8.  Environmental Issues in Managing Asthma 
Respiratory care  2008;53(5):602-617.
Management of asthma requires attention to environmental exposures both indoors and outdoors. Americans spend most of their time indoors, where they have a greater ability to modify their environment. The indoor environment contains both pollutants (eg, particulate matter, nitrogen dioxide, secondhand smoke, and ozone) and allergens from furred pets, dust mites, cockroaches, rodents, and molds. Indoor particulate matter consists of particles generated from indoor sources such as cooking and cleaning activities, and particles that penetrate from the outdoors. Nitrogen dioxide sources include gas stoves, furnaces, and fireplaces. Indoor particulate matter and nitrogen dioxide are linked to asthma morbidity. The indoor ozone concentration is mainly influenced by the outdoor ozone concentration. The health effects of indoor ozone exposure have not been well studied. In contrast, there is substantial evidence of detrimental health effects from secondhand smoke. Guideline recommendations are not specific for optimizing indoor air quality. The 2007 National Asthma Education and Prevention Program asthma guidelines recommend eliminating indoor smoking and improving the ventilation. Though the guidelines state that there is insufficient evidence to recommend air cleaners, air cleaners and reducing activities that generate indoor pollutants may be sound practical approaches for improving the health of individuals with asthma. The guidelines are more specific about allergen avoidance; they recommend identifying allergens to which the individual is immunoglobin E sensitized and employing a multifaceted, comprehensive strategy to reduce exposure. Outdoor air pollutants that impact asthma include particulate matter, ozone, nitrogen dioxide, and sulfur dioxide, and guidelines recommend that individuals with asthma avoid exertion outdoors when these pollutants are elevated. Outdoor allergens include tree, grass, and weed pollens, which vary in concentration by season. Recommendations to reduce exposure include staying indoors, keeping windows and doors closed, using air conditioning and perhaps high-efficiency particulate arrestor (HEPA) air filters, and thorough daily washing to remove allergens from one’s person.
PMCID: PMC2396450  PMID: 18426614
asthma; pollutants; particulate matter; nitrogen dioxide; sulfur dioxide; secondhand smoke; ozone; allergens
9.  A systematic review of associations between environmental exposures and development of asthma in children aged up to 9 years 
BMJ Open  2014;4(11):e006554.
Objectives
Childhood asthma is a complex condition where many environmental factors are implicated in causation. The aim of this study was to complete a systematic review of the literature describing associations between environmental exposures and the development of asthma in young children.
Setting
A systematic review of the literature up to November 2013 was conducted using key words agreed by the research team. Abstracts were screened and potentially eligible papers reviewed. Papers describing associations between exposures and exacerbation of pre-existing asthma were not included. Papers were placed into the following predefined categories: secondhand smoke (SHS), inhaled chemicals, damp housing/mould, inhaled allergens, air pollution, domestic combustion, dietary exposures, respiratory virus infection and medications.
Participants
Children aged up to 9 years.
Primary outcomes
Diagnosed asthma and wheeze.
Results
14 691 abstracts were identified, 207 papers reviewed and 135 included in the present review of which 15 were systematic reviews, 6 were meta-analyses and 14 were intervention studies. There was consistent evidence linking exposures to SHS, inhaled chemicals, mould, ambient air pollutants, some deficiencies in maternal diet and respiratory viruses to an increased risk for asthma (OR typically increased by 1.5–2.0). There was less consistent evidence linking exposures to pets, breast feeding and infant dietary exposures to asthma risk, and although there were consistent associations between exposures to antibiotics and paracetamol in early life, these associations might reflect reverse causation. There was good evidence that exposures to house dust mites (in isolation) was not associated with asthma risk. Evidence from observational and intervention studies suggest that interactions between exposures were important to asthma causation, where the effect size was typically 1.5–3.0.
Conclusions
There are many publications reporting associations between environmental exposures and modest changes in risk for asthma in young children, and this review highlights the complex interactions between exposures that further increase risk.
doi:10.1136/bmjopen-2014-006554
PMCID: PMC4244417  PMID: 25421340
PAEDIATRICS; PUBLIC HEALTH
10.  Asthma and other wheezing disorders in children 
Clinical Evidence  2006;2006:0302.
Introduction
Asthma is more common in children with a personal or family history of atopy, increased severity and frequency of wheezing episodes, and presence of variable airway obstruction or bronchial hyperresponsiveness. Precipitating factors for symptoms and acute episodes include infection, house dust mites, allergens from pet animals, exposure to tobacco smoke, and anxiety.
Methods and outcomes
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of treatments for acute asthma in children? What are the effects of single-agent prophylaxis in children taking as-needed inhaled beta agonists for asthma? What are the effects of additional prophylactic treatments in childhood asthma inadequately controlled by standard-dose inhaled corticosteroids? What are the effects of treatments and of prophylactic treatments for acute wheezing in infants? We searched: Medline, Embase, The Cochrane Library and other important databases up to October 2005 (BMJ Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
Results
We found 84 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
Conclusions
In this systematic review we present information relating to the effectiveness and safety of the following interventions: beta2 agonists (high-dose nebulised, long-acting [inhaled salmeterol], short-acting [oral salbutamol or by nebuliser, or metered-dose inhaler/spacer versus nebuliser]), corticosteroids (oral prednisolone, systemic, inhaled higher or lower doses [beclometasone]), ipratropium bromide (single or multiple dose inhaled), leukotriene receptor antagonists (oral montelukast), nedocromil (inhaled), oxygen, sodium cromoglycate (inhaled), or theophylline (oral or intravenous).
Key Points
Childhood asthma can be difficult to distinguish from viral wheeze and can affect up to 20% of children.
The consensus is that oxygen, high dose nebulised beta2 agonists and systemic corticosteroids should be used to treat an acute asthma attack. High dose beta2 agonists may be equally effective when given intermittently or continuously via a nebuliser, or from a metered dose inhaler using a spacer, in children with an acute asthma attack.Admission to hospital may be averted by adding ipratropium bromide to beta2 agonists, or by using high dose nebulised or oral corticosteroids.
Prophylactic inhaled corticosteroids improve symptoms and lung function in children with asthma. Their effect on final adult height is unclear. Inhaled nedocromil, inhaled long acting beta2 agonists, oral theophylline and oral leukotriene receptor antagonists are less effective than corticosteroids.Inhaled sodium cromoglycate does not seem to improve symptoms.
CAUTION: Monotherapy with long acting beta2 agonists reduces the frequency of asthma episodes, but may increase the chance of severe asthma episodes and death when those episodes occur. Intravenous theophylline may improve lung function in children with severe asthma, but can cause cardiac arrhythmias and convulsions.
We don't know whether adding higher doses of corticosteroids, long acting beta2 agonists, oral leukotriene receptor antagonists or oral theophylline to standard treatment improves symptoms or lung function in children with uncontrolled asthma.
In infants with acute wheeze, short acting beta2 agonists via a nebuliser or a spacer may improve symptoms, but we don't know whether high dose inhaled or oral corticosteroids or inhaled ipratropium bromide are beneficial.
Oral short acting beta2 agonists and inhaled high dose corticosteroids may prevent or improve wheeze in infants but can cause adverse effects. We don't know whether lower dose inhaled or oral corticosteroids, inhaled ipratropium bromide or inhaled short acting beta2 agonists improve wheezing episodes in infants.
PMCID: PMC2907635
11.  Home Indoor Pollutant Exposures among Inner-City Children With and Without Asthma 
Environmental Health Perspectives  2007;115(11):1665-1669.
Background
Evidence for environmental causes of asthma is limited, especially among African Americans. To look for systematic differences in early life domestic exposures between inner-city preschool children with and without asthma, we performed a study of home indoor air pollutants and allergens.
Methods
Children 2–6 years of age were enrolled in a cohort study in East Baltimore, Maryland. From the child’s bedroom, air was monitored for 3 days for particulate matter ≤ 2.5 and ≤ 10 μm in aerodynamic diameter (PM2.5, PM10), nitrogen dioxide, and ozone. Median baseline values were compared for children with (n = 150) and without (n = 150) asthma. Housing characteristics related to indoor air pollution were assessed by caregiver report and home inspection. In addition, indoor allergen levels were measured in settled dust.
Results
Children were 58% male, 91% African American, and 88% with public health insurance. Housing characteristics related to pollutant exposure and bedroom air pollutant concentrations did not differ significantly between asthmatic and control subjects [median: PM2.5, 28.7 vs. 28.5 μg/m3; PM10, 43.6 vs. 41.4 μg/m3; NO2, 21.6 vs. 20.9 ppb; O3, 1.4 vs. 1.8 ppb; all p > 0.05]. Settled dust allergen levels (cat, dust mite, cockroach, dog, and mouse) were also similar in bedrooms of asthmatic and control children.
Conclusions
Exposures to common home indoor pollutants and allergens are similar for inner-city preschool children with and without asthma. Although these exposures may exacerbate existing asthma, this study does not support a causative role of these factors for risk of developing childhood asthma.
doi:10.1289/ehp.10088
PMCID: PMC2072822  PMID: 18008001
African American; air pollution; allergens; asthma; particulate matter; pediatric; urban
12.  House dust mite barrier bedding for childhood asthma: randomised placebo controlled trial in primary care [ISRCTN63308372] 
BMC Family Practice  2002;3:12.
Background
The house dust mite is the most important environmental allergen implicated in the aetiology of childhood asthma in the UK. Dust mite barrier bedding is relatively inexpensive, convenient to use, and of proven effectiveness in reducing mattress house dust mite load, but no studies have evaluated its clinical effectiveness in the control of childhood asthma when dispensed in primary care. We therefore aimed to evaluate the effectiveness of house dust mite barrier bedding in children with asthma treated in primary care.
Methods
Pragmatic, randomised, double-blind, placebo controlled trial conducted in eight family practices in England. Forty-seven children aged 5 to 14 years with confirmed house dust mite sensitive asthma were randomised to receive six months treatment with either house dust mite barrier or placebo bedding. Peak expiratory flow was the main outcome measure of interest; secondary outcome measures included asthma symptom scores and asthma medication usage.
Results
No difference was noted in mean monthly peak expiratory flow, asthma symptom score, medication usage or asthma consultations, between children who received active bedding and those who received placebo bedding.
Conclusions
Treating house dust mite sensitive asthmatic children in primary care with house dust mite barrier bedding for six months failed to improve peak expiratory flow. Results strongly suggest that the intervention made no impact upon other clinical features of asthma.
doi:10.1186/1471-2296-3-12
PMCID: PMC116603  PMID: 12079502
13.  Childhood Exposure to Fine Particulate Matter and Black Carbon and the Development of New Wheeze Between Ages 5 and 7 In an Urban Prospective Cohort 
Environment international  2012;45:44-50.
Background
While exposures to urban fine particulate matter (PM2.5) and soot-black carbon (soot-BC) have been associated with asthma exacerbations, there is limited evidence on whether these pollutants are associated with the new development of asthma or allergy among young inner city children. We hypothesized that childhood exposure to PM2.5 and the soot-BC component would be associated with the report of new wheeze and development of seroatopy in an inner city birth cohort.
Methods
As part of the research being conducted by the Columbia Center of Children’s Environmental Health (CCCEH) birth cohort study in New York City, two-week integrated residential monitoring of PM2.5, soot-BC (based on a multi-wavelength integrating sphere method), and modified absorption coefficient (Abs*; based on the smoke stain reflectometer) was conducted between October 2005 and May 2011 for 408 children at age 5–6 years old. Residential monitoring was repeated 6 months later (n=262) to capture seasonal variability. New wheeze was identified through the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaires during up to 3 years of follow-up and compared to a reference group that reported never wheeze, remitted wheeze, or persistent wheeze. Specific immunoglobulin (Ig) E against cockroach, mouse, cat, and dust mite and total IgE levels were measured in sera at ages 5 and 7 years.
Results
PM2.5, soot-BC, and Abs* measured at the first visit were correlated moderately with those at the second visit (Pearson r > 0.44). Using logistic regression models, a positive association between PM2.5 and new wheeze was found with adjusted odds ratio [95% confidence intervals] of 1.51 [1.05–2.16] per interquartile range (IQR). Positive but nonsignificant association was found between the development of new wheeze and soot-BC and (OR 1.40 [0.96–2.05]), and Abs* (OR 1.57 [0.91–2.68]); Significantly positive associations were found between air pollutant measurements and new wheeze when restricting to those participants with repeat home indoor measurements 6 months apart. Associations between pollutants and IgE levels were not detected.
Conclusions
Our findings suggest that childhood exposure to indoor air pollution, much of which penetrated readily from outdoor sources, may contribute to the development of wheeze symptoms among children age 5 to 7 years.
doi:10.1016/j.envint.2012.03.012
PMCID: PMC3366055  PMID: 22572116
indoor air pollution; long-term exposure; PM2.5; black carbon; wheeze; asthma; young children
14.  The Seattle-King County healthy homes project: implementation of a comprehensive approach to improving indoor environmental quality for low-income children with asthma. 
Environmental Health Perspectives  2002;110(Suppl 2):311-322.
Pediatric asthma is a growing public health issue, disproportionately affecting low-income people and people of color. Exposure to indoor asthma triggers plays an important role in the development and exacerbation of asthma. We describe the implementation of the Seattle-King County Healthy Homes Project, a randomized, controlled trial of an outreach/education intervention to improve asthma-related health status by reducing exposure to allergens and irritants in the home. We randomly assigned 274 low-income children with asthma ages 4-12 to either a high- or a low-intensity group. In the high-intensity group, community health workers called Community Home Environmental Specialists (CHES) conducted initial home environmental assessments, provided individualized action plans, and made additional visits over a 12-month period to provide education and social support, encouragement of participant actions, provision of materials to reduce exposures (including bedding encasements), assistance with roach and rodent eradication, and advocacy for improved housing conditions. Members of the low-intensity group received the initial assessment, home action plan, limited education during the assessment visit, and bedding encasements. We describe the recruitment and training of CHES and challenges they faced and explain the assessment and exposure reduction protocols addressing dust mites, mold, tobacco smoke, pets, cockroaches, rodents, dust, moisture, and toxic or hazardous chemicals. We also discuss the gap between the practices recommended in the literature and what is feasible in the home. We accomplished home interventions and participants found the project very useful. The project was limited in resolving structural housing quality issues that contributed to exposure to indoor triggers.
PMCID: PMC1241178  PMID: 11929743
15.  Asthma and the home environment of low-income urban children: Preliminary findings from the seattle-king county healthy homes project 
Objectives
Childhood asthma is a growing public health concern in low-income urban communities. Indoor exposure to asthma triggers has emerged as an important cause of asthma exacerbations. We describe indoor environmental conditions related to asthma triggers among a low-income urban population in Seattle/King County, Washington, as well as caregiver knowledge and resources related to control of these triggers.
Methods
Data are obtained from in-person, structured, closed-end interviews with the caretakers of children aged 4–12 years with persistent asthma living in households with incomes less than 200% of poverty. Additional information is collected during a home inspection. The children and their caregivers are participants in the ongoing Seattle-King County Healthy Homes Project, a randomized controlled trial of an intervention to empower low-income families to reduce exposure to indoor asthma triggers. We report findings on the conditions of the homes prior to this intervention among the first 112 enrolled households.
Results
A smoker was present in 37.5% of homes. Mold was visible in 26.8% of homes, water damage was present in 18.6% of homes, and damp conditions occurred in 64.8% of households, while 39.6% of caregivers were aware that excessive moisture can increase exposures to allergens. Dust-trapping reservoirs were common; 76.8% of children's bedrooms had carpeting. Cockroach infestation in the past 3 months was reported by 23.4% of caregivers, while 57.1% were unaware of the association of roaches and asthma. Only 19.8% of the children had allergy-control mattress covers.
Conclusions
Many low-income urban children with asthma in King County live in indoor environments that place them at substantial risk of ongoing exposure to asthma triggers. Substandard housing and lack of resources often underlie these exposures. Initiatives involving health educators, outreach workers, medical providers, health care insurers, housing agencies, and elected officials are needed to reduce these exposures.
doi:10.1007/BF02350962
PMCID: PMC3456608  PMID: 10741842
Asthma; Child; Indoor Air Pollution; Indoor Environment; Knowledge/Behaviors; Low-Income Populations
16.  Association of Adenotonsillectomy with Asthma Outcomes in Children: A Longitudinal Database Analysis 
PLoS Medicine  2014;11(11):e1001753.
Rakesh Bhattacharjee and colleagues use data from a US private health insurance database to compare asthma severity measures in children one year before and one year after they underwent adenotonsillectomy with asthma measures in those who did not undergo adenotonsillectomy.
Please see later in the article for the Editors' Summary
Background
Childhood asthma and obstructive sleep apnea (OSA), both disorders of airway inflammation, were associated in recent observational studies. Although childhood OSA is effectively treated by adenotonsillectomy (AT), it remains unclear whether AT also improves childhood asthma. We hypothesized that AT, the first line of therapy for childhood OSA, would be associated with improved asthma outcomes and would reduce the usage of asthma therapies in children.
Methods and Findings
Using the 2003–2010 MarketScan database, we identified 13,506 children with asthma in the United States who underwent AT. Asthma outcomes during 1 y preceding AT were compared to those during 1 y following AT. In addition, 27,012 age-, sex-, and geographically matched children with asthma without AT were included to examine asthma outcomes among children without known adenotonsillar tissue morbidity. Primary outcomes included the occurrence of a diagnostic code for acute asthma exacerbation (AAE) or acute status asthmaticus (ASA). Secondary outcomes included temporal changes in asthma medication prescriptions, the frequency of asthma-related emergency room visits (ARERs), and asthma-related hospitalizations (ARHs). Comparing the year following AT to the year prior, AT was associated with significant reductions in AAE (30.2%; 95% CI: 25.6%–34.3%; p<0.0001), ASA (37.9%; 95% CI: 29.2%–45.6%; p<0.0001), ARERs (25.6%; 95% CI: 16.9%–33.3%; p<0.0001), and ARHs (35.8%; 95% CI: 19.6%–48.7%; p = 0.02). Moreover, AT was associated with significant reductions in most asthma prescription refills, including bronchodilators (16.7%; 95% CI: 16.1%–17.3%; p<0.001), inhaled corticosteroids (21.5%; 95% CI: 20.7%–22.3%; p<0.001), leukotriene receptor antagonists (13.4%; 95% CI: 12.9%–14.0%; p<0.001), and systemic corticosteroids (23.7%; 95% CI: 20.9%–26.5%; p<0.001). In contrast, there were no significant reductions in these outcomes in children with asthma who did not undergo AT over an overlapping follow-up period. Limitations of the MarketScan database include lack of information on race and obesity status. Also, the MarketScan database does not include information on children with public health insurance (i.e., Medicaid) or uninsured children.
Conclusions
In a very large sample of privately insured children, AT was associated with significant improvements in several asthma outcomes. Contingent on validation through prospectively designed clinical trials, this study supports the premise that detection and treatment of adenotonsillar tissue morbidity may serve as an important strategy for improving asthma control.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The global burden of asthma has been rising steadily over the past few decades. Nowadays, about 200–300 million adults and children worldwide are affected by asthma, a chronic condition caused by inflammation of the airways (the tubes that carry air in and out of the lungs). Although asthma can develop at any age, it is often diagnosed in childhood—asthma is one of the commonest chronic diseases in children. In the US, for example, asthma affects around 7.1 million children under the age of 18 years and is the third leading cause of hospitalization of children under the age of 15 years. In people with asthma, the airways can react very strongly to allergens such as animal fur or to irritants such as cigarette smoke. Exercise, cold air, and infections can trigger asthma attacks, which can be fatal. The symptoms of asthma include wheezing, coughing, chest tightness, and shortness of breath. Asthma cannot be cured, but drugs can relieve its symptoms and prevent acute asthma attacks.
Why Was This Study Done?
Recent studies have found an association between severe childhood asthma and obstructive sleep apnea (OSA). In OSA, airway inflammation promotes hypertrophy (excess growth) of the adenoids and the tonsils, immune system tissues in the upper airway. During sleep, the presence of hypertrophic adenotonsillar tissues predisposes the walls of the throat to collapse, which results in apnea—a brief interruption in breathing. People with OSA often snore loudly and frequently wake from deep sleep as they struggle to breathe. Childhood OSA, which affects 2%–3% of children, can be effectively treated by removal of the adenoids and tonsils (adenotonsillectomy). Given the association between childhood OSA and severe asthma and given the involvement of airway inflammation in both conditions, might adenotonsillectomy also improve childhood asthma? Here, the researchers analyze data from the MarketScan database, a large database of US patients with private health insurance, to investigate whether adenotonsillectomy is associated with improvements in asthma outcomes and with reductions in the use of asthma therapies in children.
What Did the Researchers Do and Find?
The researchers used the database to identify 13,506 children with asthma who had undergone adenotonsillectomy and to obtain information about asthma outcomes among these children for the year before and the year after the operation. Because asthma severity tends to decrease with age, the researchers also used the database to identify 27,012 age-, sex-, and geographically matched children with asthma who did not have the operation so that they could examine asthma outcomes over an equivalent two-year period in the absence of complications related to adenotonsillar hypertrophy. Comparing the year after adenotonsillectomy with the year before the operation, adenotonsillectomy was associated with a 30% reduction in acute asthma exacerbations, a 37.9% reduction in acute status asthmaticus (an asthma attack that is unresponsive to the drugs usually used to treat attacks), a 25.6% reduction in asthma-related emergency room visits, and a 35.8% reduction in asthma-related hospitalizations. By contrast, among the control children, there was only a 2% reduction in acute asthma exacerbations and only a 7% reduction in acute status asthmaticus over an equivalent two-year period. Adenotonsillectomy was also associated with significant reductions (changes unlikely to have occurred by chance) in prescription refills for most types of drugs used to treat asthma, whereas there were no significant reductions in prescription refills among children with asthma who had not undergone adenotonsillectomy. The study was limited by the lack of measures of race and obesity, which are both associated with severity of asthma.
What Do These Findings Mean?
These findings show that in a large sample of privately insured children in the US, adenotonsillectomy was associated with significant improvements in several asthma outcomes. These results do not show, however, that adenotonsillectomy caused a reduction in the severity of childhood asthma. It could be that the children who underwent adenotonsillectomy (but not those who did not have the operation) shared another unknown factor that led to improvements in their asthma over time. To prove a causal link, it will be necessary to undertake a randomized controlled trial in which the outcomes of groups of children with asthma who are chosen at random to undergo or not undergo adenotonsillectomy are compared. However, with the proviso that there are some risks associated with adenotonsillectomy, these findings suggest that the detection and treatment of adenotonsillar hypertrophy may help to improve asthma control in children.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001753.
The US Centers for Disease Control and Prevention provides information on asthma, including videos, games, and links to other resources for children with asthma
The American Lung Association provides detailed information about asthma and a fact sheet on asthma in children; it also has information about obstructive sleep apnea
The National Sleep Foundation provides information on snoring and obstructive sleep apnea in children
The UK National Health Service Choices website provides information (including some personal stories) about asthma, about asthma in children, and about obstructive sleep apnea
The “Global Asthma Report 2014” will be available in October 2014
MedlinePlus provides links to further information on asthma, on asthma in children, on sleep apnea, and on tonsils and adenoids (in English and Spanish)
doi:10.1371/journal.pmed.1001753
PMCID: PMC4219664  PMID: 25369282
17.  Tobacco Smoke, Indoor Air Pollution and Tuberculosis: A Systematic Review and Meta-Analysis 
PLoS Medicine  2007;4(1):e20.
Background
Tobacco smoking, passive smoking, and indoor air pollution from biomass fuels have been implicated as risk factors for tuberculosis (TB) infection, disease, and death. Tobacco smoking and indoor air pollution are persistent or growing exposures in regions where TB poses a major health risk. We undertook a systematic review and meta-analysis to quantitatively assess the association between these exposures and the risk of infection, disease, and death from TB.
Methods and Findings
We conducted a systematic review and meta-analysis of observational studies reporting effect estimates and 95% confidence intervals on how tobacco smoking, passive smoke exposure, and indoor air pollution are associated with TB. We identified 33 papers on tobacco smoking and TB, five papers on passive smoking and TB, and five on indoor air pollution and TB. We found substantial evidence that tobacco smoking is positively associated with TB, regardless of the specific TB outcomes. Compared with people who do not smoke, smokers have an increased risk of having a positive tuberculin skin test, of having active TB, and of dying from TB. Although we also found evidence that passive smoking and indoor air pollution increased the risk of TB disease, these associations are less strongly supported by the available evidence.
Conclusions
There is consistent evidence that tobacco smoking is associated with an increased risk of TB. The finding that passive smoking and biomass fuel combustion also increase TB risk should be substantiated with larger studies in future. TB control programs might benefit from a focus on interventions aimed at reducing tobacco and indoor air pollution exposures, especially among those at high risk for exposure to TB.
Evidence from a number of studies suggest that tobacco smoking, environmental tobacco smoke, and indoor air pollution from biomass fuels is associated with an increased risk of tuberculosis.
Editors' Summary
Background.
Tobacco smoking has been identified by the World Health Organization as one of the leading causes of death worldwide. Smokers are at higher risk than nonsmokers for a very wide variety of illnesses, many of which are life-threatening. Inhaling tobacco smoke, whether this is active (when an individual smokes) or passive (when an individual is exposed to cigarette smoke in their environment) has also been associated with tuberculosis (TB). Many people infected with the TB bacterium never develop disease, but it is thought that people infected with TB who also smoke are far more likely to develop the symptoms of disease, and to have worse outcomes when they do.
Why Was This Study Done?
The researchers were specifically interested in the link between smoking and TB. They wanted to try to work out the overall increase in risk for getting TB in people who smoke, as compared with people who do not smoke. In this study, the researchers wanted to separately study the risks for different types of exposure to smoke, so, for example, what the risks were for people who actively smoke as distinct from people who are exposed to smoke from others. The researchers also wanted to calculate the association between TB and exposure to indoor pollution from burning fuels such as wood and charcoal.
What Did the Researchers Do and Find?
In carrying out this study, the researchers wanted to base their conclusions on all the relevant information that was already available worldwide. Therefore they carried out a systematic review. A systematic review involves setting out the research question that is being asked and then developing a search strategy to find all the meaningful evidence relating to the particular question under study. For this systematic review, the researchers wanted to find all published research in the biomedical literature that looked at human participants and dealt with the association between active smoking, passive smoking, indoor air pollution and TB. Studies were included if they were published in English, Russian, or Chinese, and included enough data for the researchers to calculate a number for the increase in TB risk. The researchers initially found 1,397 research studies but then narrowed that down to 38 that fit their criteria. Then specific pieces of data were extracted from each of those studies and in some cases the researchers combined data to produce overall calculations for the increase in TB risk. Separate assessments were done for different aspects of “TB risk,” namely, TB infection, TB disease, and mortality from TB. The data showed an approximately 2-fold increase in risk of TB infection among smokers as compared with nonsmokers. The researchers found that all studies evaluating the link between smoking and TB disease or TB mortality showed an association, but they did not combine these data together because of wide potential differences between the studies. Finally, all studies looking at passive smoking found an association with TB, as did some of those examining the link with indoor air pollution.
What Do These Findings Mean?
The findings here show that smoking is associated with an increased risk of TB infection, disease, and deaths from TB. The researchers found much more data on the risks for active smoking than on passive smoking or indoor air pollution. Tobacco smoking is increasing in many countries where TB is already a problem. These results therefore suggest that it is important for health policy makers to further develop strategies for controlling tobacco use in order to reduce the impact of TB worldwide.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0040020
The World Health Organization (WHO)'s Tobacco Free Initiative provides resources on research and policy related to tobacco control, its network of initiatives, and other relevant information
WHO also has a tuberculosis minisite
The US National Library of Medicine's MedLinePlus provides a set of links and resources about smoking, including news, overviews, recent research, statistics, and others
The Health Consequences of Smoking: A Report of the Surgeon General provides information on the health consequences of smoking
Tobacco Country Profiles provides information on smoking in different countries
doi:10.1371/journal.pmed.0040020
PMCID: PMC1769410  PMID: 17227135
18.  Endotoxin as a determinant of asthma and wheeze among rural dwelling children and adolescents: A case–control study 
Background
The association between endotoxin exposure and asthma is complex and has been associated with rural living. We examined the relationship between domestic endotoxin and asthma or wheeze among rural school-aged children (6–18 years) and assessed the interaction between endotoxin and other characteristics with these outcomes.
Methods
Between 2005 and 2007 we conducted a case–control study of children 6–18 years in the rural region of Humboldt, Canada. Cases (n = 102) reported doctor-diagnosed asthma or wheeze in the past year. Controls (n = 208) were randomly selected from children without asthma or wheeze. Data were collected to ascertain symptoms, asthma history and indoor environmental exposures (questionnaire), endotoxin (dust collection from the play area floor and child’s mattress), and tobacco smoke exposure (saliva collection). Statistical testing was completed using multiple logistic regression to account for potential confounders and to assess interaction between risk factors. A stratified analysis was also completed to examine the effect of personal history of allergy.
Results
Among children aged 6–12 years, mattress endotoxin concentration (EU/mg) and load (EU/m2) were inversely associated with being a case [odds ratio (OR) = 0.44, 95% confidence interval (CI) = 0.20-0.98; and OR = 0.38, 95% CI = 0.20-0.75, respectively]. These associations were not observed in older children or with play area endotoxin.
Conclusions
Our results suggest that endotoxin exposure might be protective for asthma or wheeze. The protective effect is found in younger school-aged, non-allergic children. These results may help explain the inconsistencies in previous studies and suggest that the protective effects of endotoxin in the prevention of atopy and asthma or wheeze are most effective earlier in life.
doi:10.1186/1471-2466-12-56
PMCID: PMC3545854  PMID: 22966977
Asthma; Children; Endotoxin; Wheeze; Pediatrics; Allergy
19.  Feather bedding and childhood asthma associated with house dust mite sensitisation: a randomised controlled trial 
Archives of Disease in Childhood  2011;96(6):541-547.
Introduction
Observational studies report inverse associations between the use of feather upper bedding (pillow and/or quilt) and asthma symptoms but there is no randomised controlled trial (RCT) evidence assessing the role of feather upper bedding as a secondary prevention measure.
Objective
To determine whether, among children not using feather upper bedding, a new feather pillow and feather quilt reduces asthma severity among house dust mite (HDM) sensitised children with asthma over a 1-year period compared with standard dust mite avoidance advice, and giving children a new mite-occlusive mattress cover.
Design
RCT.
Setting
The Calvary Hospital in the Australian Capital Territory and the Children's Hospital at Westmead, Sydney, New South Wales.
Patients
197 children with HDM sensitisation and moderate to severe asthma.
Intervention
New upper bedding duck feather pillow and quilt and a mite-occlusive mattress cover (feather) versus standard care and a mite-occlusive mattress cover (standard).
Main outcome measures
The proportion of children reporting four or more episodes of wheeze in the past year; an episode of speech-limiting wheeze; or one or more episodes of sleep disturbance caused by wheezing; and spirometry with challenge testing. Statistical analysis included multiple logistic and linear regression.
Results
No differences between groups were found for primary end points – frequent wheeze (OR 1.51, 95% CI 0.83 to 2.76, p=0.17), speech-limiting wheeze (OR 0.70, 95% CI 0.32 to 1.48, p=0.35), sleep disturbed because of wheezing (OR 1.17, 95% CI 0.64 to 2.13, p=0.61) or for any secondary end points. Secondary analyses indicated the intervention reduced the risk of sleep being disturbed because of wheezing and severe wheeze to a greater extent for children who slept supine.
Conclusion
No differences in respiratory symptoms or lung function were observed 1 year after children with moderate–severe asthma and HDM sensitisation were given a mite-occlusive mattress cover and then received either feather upper bedding (pillow and quilt) or standard bedding care.
doi:10.1136/adc.2010.189696
PMCID: PMC3093241  PMID: 21451166
20.  The effects of indoor environmental exposures on pediatric asthma: a discrete event simulation model 
Environmental Health  2012;11:66.
Background
In 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.
Methods
We 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.
Results
Model 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.
Conclusions
We 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.
doi:10.1186/1476-069X-11-66
PMCID: PMC3527278  PMID: 22989068
Asthma; Simulation; Indoor; Housing; Air pollution; Lung function; Allergen; Green building
21.  Lung function, asthma symptoms, and quality of life for children in public housing in Boston: a case-series analysis 
Environmental Health  2004;3:13.
Background
Children in urban public housing are at high risk for asthma, given elevated environmental and social exposures and suboptimal medical care. For a multifactorial disease like asthma, design of intervention studies can be influenced by the relative prevalence of key risk factors. To better understand risk factors for asthma morbidity in the context of an environmental intervention study, we conducted a detailed baseline evaluation of 78 children (aged 4–17 years) from three public housing developments in Boston.
Methods
Asthmatic children and their caregivers were recruited between April 2002 and January 2003. We conducted intake interviews that captured a detailed family and medical history, including questions regarding asthma symptom severity, access to health care, medication usage, and psychological stress. Quality of life was evaluated for both the child and caregiver with an asthma-specific scale. Pulmonary function was measured with a portable spirometer, and allergy testing for common indoor and outdoor allergens was conducted with skin testing using the prick puncture method. Exploratory linear and logistic regression models evaluating predictors of respiratory symptoms, quality of life, and pulmonary function were conducted using SAS.
Results
We found high rates of obesity (56%) and allergies to indoor contaminants such as cockroaches (59%) and dust mites (59%). Only 36% of children with persistent asthma reported being prescribed any daily controller medication, and most did not have an asthma action plan or a peak flow meter. One-time lung function measures were poorly correlated with respiratory symptoms or quality of life, which were significantly correlated with each other. In multivariate regression models, household size, body mass index, and environmental tobacco smoke exposure were positively associated with respiratory symptom severity (p < 0.10). Symptom severity was negatively associated with asthma-related quality of life for the child and the caregiver, with caregiver (but not child) quality of life significantly influenced by caregiver stress and whether the child was in the intensive care unit at birth.
Conclusion
Given the elevated prevalence of multiple risk factors, coordinated improvements in the social environment, the built environment, and in medical management would likely yield the greatest health benefits in this high-risk population.
doi:10.1186/1476-069X-3-13
PMCID: PMC544563  PMID: 15585065
22.  Impact of Environmental Controls on Childhood Asthma 
Exposure to allergens early in life can lead to sensitization and the development of childhood asthma. It is thought that increased exposure with the advent of modern housing is likely contributing to the rise in prevalence of childhood asthma during the past few decades. The progression from allergen exposure to sensitization and asthma development has been noted with respect to dust mites, pets, cockroach, mouse, mold, tobacco smoke, endotoxin, and air pollution, although some have found a protective effect with pet and endotoxin exposure. Recent studies have shown that allergen remediation may be beneficial in reducing asthma morbidity and development, although there is also some evidence to the contrary. Examples of allergen remediation that have been studied include the use of dust mite–impermeable covers, high-efficiency particulate air filtration, integrated pest management, home repairs, ventilation improvement, and pet removal. Several multifaceted, randomized controlled trials have shown that reducing multiple early allergen exposures with environmental controls is associated with a decreased risk of asthma.
doi:10.1007/s11882-011-0206-7
PMCID: PMC3166452  PMID: 21710109
Asthma; Asthma prevention; Asthma control; Children; Allergen; House dust mites; Home remediation; Mold; Endotoxin; Integrated pest management; Pollution; Cats; Dogs; Tobacco
23.  Effects of BMI, Fat Mass, and Lean Mass on Asthma in Childhood: A Mendelian Randomization Study 
PLoS Medicine  2014;11(7):e1001669.
In this study, Granell and colleagues used Mendelian randomization to investigate causal effects of BMI, fat mass, and lean mass on current asthma at age 7½ years in the Avon Longitudinal Study of Parents and Children (ALSPAC) and found that higher BMI increases the risk of asthma in mid-childhood.
Please see later in the article for the Editors' Summary
Background
Observational studies have reported associations between body mass index (BMI) and asthma, but confounding and reverse causality remain plausible explanations. We aim to investigate evidence for a causal effect of BMI on asthma using a Mendelian randomization approach.
Methods and Findings
We used Mendelian randomization to investigate causal effects of BMI, fat mass, and lean mass on current asthma at age 7½ y in the Avon Longitudinal Study of Parents and Children (ALSPAC). A weighted allele score based on 32 independent BMI-related single nucleotide polymorphisms (SNPs) was derived from external data, and associations with BMI, fat mass, lean mass, and asthma were estimated. We derived instrumental variable (IV) estimates of causal risk ratios (RRs). 4,835 children had available data on BMI-associated SNPs, asthma, and BMI. The weighted allele score was strongly associated with BMI, fat mass, and lean mass (all p-values<0.001) and with childhood asthma (RR 2.56, 95% CI 1.38–4.76 per unit score, p = 0.003). The estimated causal RR for the effect of BMI on asthma was 1.55 (95% CI 1.16–2.07) per kg/m2, p = 0.003. This effect appeared stronger for non-atopic (1.90, 95% CI 1.19–3.03) than for atopic asthma (1.37, 95% CI 0.89–2.11) though there was little evidence of heterogeneity (p = 0.31). The estimated causal RRs for the effects of fat mass and lean mass on asthma were 1.41 (95% CI 1.11–1.79) per 0.5 kg and 2.25 (95% CI 1.23–4.11) per kg, respectively. The possibility of genetic pleiotropy could not be discounted completely; however, additional IV analyses using FTO variant rs1558902 and the other BMI-related SNPs separately provided similar causal effects with wider confidence intervals. Loss of follow-up was unlikely to bias the estimated effects.
Conclusions
Higher BMI increases the risk of asthma in mid-childhood. Higher BMI may have contributed to the increase in asthma risk toward the end of the 20th century.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The global burden of asthma, a chronic (long-term) condition caused by inflammation of the airways (the tubes that carry air in and out of the lungs), has been rising steadily over the past few decades. It is estimated that, nowadays, 200–300 million adults and children worldwide are affected by asthma. Although asthma can develop at any age, it is often diagnosed in childhood—asthma is the most common chronic disease in children. In people with asthma, the airways can react very strongly to allergens such as animal fur or to irritants such as cigarette smoke, becoming narrower so that less air can enter the lungs. Exercise, cold air, and infections can also trigger asthma attacks, which can be fatal. The symptoms of asthma include wheezing, coughing, chest tightness, and shortness of breath. Asthma cannot be cured, but drugs can relieve its symptoms and prevent acute asthma attacks.
Why Was This Study Done?
We cannot halt the ongoing rise in global asthma rates without understanding the causes of asthma. Some experts think obesity may be one cause of asthma. Obesity, like asthma, is increasingly common, and observational studies (investigations that ask whether individuals exposed to a suspected risk factor for a condition develop that condition more often than unexposed individuals) in children have reported that body mass index (BMI, an indicator of body fat calculated by dividing a person's weight in kilograms by their height in meters squared) is positively associated with asthma. Observational studies cannot prove that obesity causes asthma because of “confounding.” Overweight children with asthma may share another unknown characteristic (confounder) that actually causes both obesity and asthma. Moreover, children with asthma may be less active than unaffected children, so they become overweight (reverse causality). Here, the researchers use “Mendelian randomization” to assess whether BMI has a causal effect on asthma. In Mendelian randomization, causality is inferred from associations between genetic variants that mimic the effect of a modifiable risk factor and the outcome of interest. Because gene variants are inherited randomly, they are not prone to confounding and are free from reverse causation. So, if a higher BMI leads to asthma, genetic variants associated with increased BMI should be associated with an increased risk of asthma.
What Did the Researchers Do and Find?
The researchers investigated causal effects of BMI, fat mass, and lean mass on current asthma at age 7½ years in 4,835 children enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC, a long-term health project that started in 1991). They calculated an allele score for each child based on 32 BMI-related genetic variants, and estimated associations between this score and BMI, fat mass and lean mass (both measured using a special type of X-ray scanner; in children BMI is not a good indicator of “fatness”), and asthma. They report that the allele score was strongly associated with BMI, fat mass, and lean mass, and with childhood asthma. The estimated causal relative risk (risk ratio) for the effect of BMI on asthma was 1.55 per kg/m2. That is, the relative risk of asthma increased by 55% for every extra unit of BMI. The estimated causal relative risks for the effects of fat mass and lean mass on asthma were 1.41 per 0.5 kg and 2.25 per kg, respectively.
What Do These Findings Mean?
These findings suggest that a higher BMI increases the risk of asthma in mid-childhood and that global increases in BMI toward the end of the 20th century may have contributed to the global increase in asthma that occurred at the same time. It is possible that the observed association between BMI and asthma reported in this study is underpinned by “genetic pleiotropy” (a potential limitation of all Mendelian randomization analyses). That is, some of the genetic variants included in the BMI allele score could conceivably also increase the risk of asthma. Nevertheless, these findings suggest that public health interventions designed to reduce obesity may also help to limit the global rise in asthma.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001669.
The US Centers for Disease Control and Prevention provides information on asthma and on all aspects of overweight and obesity (in English and Spanish)
The World Health Organization provides information on asthma and on obesity (in several languages)
The UK National Health Service Choices website provides information about asthma, about asthma in children, and about obesity (including real stories)
The Global Asthma Report 2011 is available
The Global Initiative for Asthma released its updated Global Strategy for Asthma Management and Prevention on World Asthma Day 2014
Information about the Avon Longitudinal Study of Parents and Children is available
MedlinePlus provides links to further information on obesity in children, on asthma, and on asthma in children (in English and Spanish
Wikipedia has a page on Mendelian randomization (note: Wikipedia is a free online encyclopedia that anyone can edit; available in several languages)
doi:10.1371/journal.pmed.1001669
PMCID: PMC4077660  PMID: 24983943
24.  Seasonal Variation and Environmental Predictors of Exhaled Nitric Oxide in Children with Asthma 
Pediatric pulmonology  2008;43(6):576-583.
Summary
The fraction of exhaled nitric oxide (FeNO), a measure of airway inflammation, shows promise as a noninvasive tool to guide asthma management, but there is a paucity of longitudinal data about seasonal variation and environmental predictors of FeNO in children. The objective of this project was to evaluate how environmental factors affect FeNO concentrations over a 12-month study period among children with doctor diagnosed asthma. We conducted a prospective cohort study of 225 tobacco-smoke exposed children age 6 to 12 years with doctor-diagnosed asthma including measures of FeNO, medication use, settled indoor allergens (dust mite, cat, dog, and cockroach), and tobacco smoke exposure. Baseline geometric mean FeNO was 12.4 ppb (range 1.9 to 60.9 ppb). In multivariable analyses, higher baseline FeNO levels, atopy, and fall season were associated with increased FeNO levels, measured 6 and 12 months after study initiation, whereas inhaled steroid use, summer season, and increasing nicotine exposure were associated with lower FeNO levels. In secondary analyses of allergen sensitization, only sensitization to dust mite and cat were associated with increased FeNO levels. Our data demonstrate that FeNO levels over a year long period reflected baseline FeNO levels, allergen sensitization, season, and inhaled steroid use in children with asthma. These results indicate that FeNO levels are responsive to common environmental triggers as well as therapy for asthma in children. Clinicians and researchers may need to consider an individual’s baseline FeNO levels to manage children with asthma.
doi:10.1002/ppul.20816
PMCID: PMC3483596  PMID: 18429012
allergen; sensitization; tobacco smoke; inhaled corticosteroid
25.  The challenge of preventing environmentally related disease in young children: community-based research in New York City. 
Environmental Health Perspectives  2002;110(2):197-204.
Rates of developmental and respiratory diseases are disproportionately high in underserved, minority populations such as those in New York City's Washington Heights, Harlem, and the South Bronx. Blacks and Latinos in these neighborhoods represent high risk groups for asthma, adverse birth outcomes, impaired development, and some types of cancer. The Columbia Center for Children's Environmental Health in Washington Heights uses molecular epidemiologic methods to study the health effects of urban indoor and outdoor air pollutants on children, prenatally and postnatally, in a cohort of over 500 African-American and Dominican (originally from the Dominican Republic) mothers and newborns. Extensive data are collected to determine exposures to particulate matter < 2.5 microm in aerodynamic diameter (PM(2.5)), polycyclic aromatic hydrocarbons (PAHs), diesel exhaust particulate (DEP), nitrogen oxide, nonpersistent pesticides, home allergens (dust mite, mouse, cockroach), environmental tobacco smoke (ETS), and lead and other metals. Biomarkers, air sampling, and clinical assessments are used to study the effects of these exposures on children's increased risk for allergic sensitization, asthma and other respiratory disorders, impairment of neurocognitive and behavioral development, and potential cancer risk. The center conducts its research and community education in collaboration with 10 community-based health and environmental advocacy organizations. This unique academic-community partnership helps to guide the center's research so that it is most relevant to the context of the low-income, minority neighborhoods in which the cohort resides, and information is delivered back to these communities in meaningful ways. In turn, communities become better equipped to relay environmental health concerns to policy makers. In this paper we describe the center's research and its academic-community partnership and present some preliminary findings.
PMCID: PMC1240736  PMID: 11836150

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