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1.  A longitudinal study of adult-onset asthma incidence among HMO members 
Environmental Health  2003;2:10.
Background
HMO databases offer an opportunity for community based epidemiologic studies of asthma incidence, etiology and treatment. The incidence of asthma in HMO populations and the utility of HMO data, including use of computerized algorithms and manual review of medical charts for determining etiologic factors has not been fully explored.
Methods
We identified adult-onset asthma, using computerized record searches in a New England HMO. Monthly, our software applied exclusion and inclusion criteria to identify an "at-risk" population and "potential cases". Electronic and paper medical records from the past year were then reviewed for each potential case. Persons with other respiratory diseases or insignificant treatment for asthma were excluded.
Confirmed adult-onset asthma (AOA) cases were defined as those potential cases with either new-onset asthma or reactivated mild intermittent asthma that had been quiescent for at least one year. We validated the methods by reviewing charts of selected subjects rejected by the algorithm.
Results
The algorithm was 93 to 99.3% sensitive and 99.6% specific. Sixty-three percent (n = 469) of potential cases were confirmed as AOA. Two thirds of confirmed cases were women with an average age of 34.8 (SD 11.8), and 45% had no evidence of previous asthma diagnosis. The annualized monthly rate of AOA ranged from 4.1 to 11.4 per 1000 at-risk members. Physicians most commonly attribute asthma to infection (59%) and allergy (14%). New-onset cases were more likely attributed to infection, while reactivated cases were more associated with allergies. Medical charts included a discussion of work exposures in relation to asthma in only 32 (7%) cases. Twenty-three of these (72%) indicated there was an association between asthma and workplace exposures for an overall rate of work-related asthma of 4.9%.
Conclusion
Computerized HMO records can be successfully used to identify AOA. Manual review of these records is important to confirm case status and is useful in evaluation of provider consideration of etiologies. We demonstrated that clinicians attribute most AOA to infection and tend to ignore the contribution of environmental and occupational exposures.
doi:10.1186/1476-069X-2-10
PMCID: PMC194432  PMID: 12952547
2.  Preterm Birth and Childhood Wheezing Disorders: A Systematic Review and Meta-Analysis 
PLoS Medicine  2014;11(1):e1001596.
In a systematic review and meta-analysis, Jasper Been and colleagues investigate the association between preterm birth and the development of wheezing disorders in childhood.
Please see later in the article for the Editors' Summary
Background
Accumulating evidence implicates early life factors in the aetiology of non-communicable diseases, including asthma/wheezing disorders. We undertook a systematic review investigating risks of asthma/wheezing disorders in children born preterm, including the increasing numbers who, as a result of advances in neonatal care, now survive very preterm birth.
Methods and Findings
Two reviewers independently searched seven online databases for contemporaneous (1 January 1995–23 September 2013) epidemiological studies investigating the association between preterm birth and asthma/wheezing disorders. Additional studies were identified through reference and citation searches, and contacting international experts. Quality appraisal was undertaken using the Effective Public Health Practice Project instrument. We pooled unadjusted and adjusted effect estimates using random-effects meta-analysis, investigated “dose–response” associations, and undertook subgroup, sensitivity, and meta-regression analyses to assess the robustness of associations.
We identified 42 eligible studies from six continents. Twelve were excluded for population overlap, leaving 30 unique studies involving 1,543,639 children. Preterm birth was associated with an increased risk of wheezing disorders in unadjusted (13.7% versus 8.3%; odds ratio [OR] 1.71, 95% CI 1.57–1.87; 26 studies including 1,500,916 children) and adjusted analyses (OR 1.46, 95% CI 1.29–1.65; 17 studies including 874,710 children). The risk was particularly high among children born very preterm (<32 wk gestation; unadjusted: OR 3.00, 95% CI 2.61–3.44; adjusted: OR 2.81, 95% CI 2.55–3.12). Findings were most pronounced for studies with low risk of bias and were consistent across sensitivity analyses. The estimated population-attributable risk of preterm birth for childhood wheezing disorders was ≥3.1%.
Key limitations related to the paucity of data from low- and middle-income countries, and risk of residual confounding.
Conclusions
There is compelling evidence that preterm birth—particularly very preterm birth—increases the risk of asthma. Given the projected global increases in children surviving preterm births, research now needs to focus on understanding underlying mechanisms, and then to translate these insights into the development of preventive interventions.
Review Registration
PROSPERO CRD42013004965
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Most pregnancies last around 40 weeks, but worldwide, more than 11% of babies are born before 37 weeks of gestation (the period during which a baby develops in its mother's womb). Preterm birth is a major cause of infant death—more than 1 million babies die annually from preterm birth complications—and the number of preterm births is increasing globally. Multiple pregnancies, infections, and chronic (long-term) maternal conditions such as diabetes can all cause premature birth, but the cause of many preterm births is unknown. The most obvious immediate complication that is associated with preterm birth is respiratory distress syndrome. This breathing problem, which is more common in early preterm babies than in near-term babies, occurs because the lungs of premature babies are structurally immature and lack pulmonary surfactant, a unique mixture of lipids and proteins that coats the inner lining of the lungs and helps to prevent the collapse of the small air sacs in the lungs that absorb oxygen from the air. Consequently, preterm babies often need help with their breathing and oxygen supplementation.
Why Was This Study Done?
Improvements in the management of prematurity mean that more preterm babies survive today than in the past. However, accumulating evidence suggests that early life events are involved in the subsequent development of non-communicable diseases (non-infectious chronic diseases). Given the increasing burden of preterm birth, a better understanding of the long-term effects of preterm birth is essential. Here, the researchers investigate the risks of asthma and wheezing disorders in children who are born preterm by undertaking a systematic review (a study that uses predefined criteria to identify all the research on a given topic) and a meta-analysis (a statistical method for combining the results of several studies). Asthma is a chronic condition that is caused by inflammation of the airways. In people with asthma, the airways can react very strongly to allergens such as animal fur and to irritants such as cigarette smoke. Exercise, cold air, and infections can also trigger asthma attacks, which can sometimes be fatal. The symptoms of asthma include wheezing (a high-pitched whistling sound during breathing), coughing, chest tightness, and shortness of breath. Asthma cannot be cured, but drugs can relieve its symptoms and prevent acute asthma attacks.
What Did the Researchers Do and Find?
The researchers identified 30 studies undertaken between 1995 and the present (a time span chosen to allow for recent changes in the management of prematurity) that investigated the association between preterm birth and asthma/wheezing disorders in more than 1.5 million children. Across the studies, 13.7% of preterm babies developed asthma/wheezing disorders during childhood, compared to only 8.3% of babies born at term. Thus, the risk of preterm babies developing asthma or a wheezing disorder during childhood was 1.71 times higher than the risk of term babies developing these conditions (an unadjusted odds ratio [OR] of 1.71). In analyses that allowed for confounding factors—other factors that affect the risk of developing asthma/wheezing disorders such as maternal smoking—the risk of preterm babies developing asthma or a wheezing disorder during childhood was 1.46 times higher than that of babies born at term (an adjusted OR of 1.46). Notably, compared to children born at term, children born very early (before 32 weeks of gestation) had about three times the risk of developing asthma/wheezing disorders in unadjusted and adjusted analyses. Finally, the population-attributable risk of preterm birth for childhood wheezing disorders was more than 3.1%. That is, if no preterm births had occurred, there would have been more than a 3.1% reduction in childhood wheezing disorders.
What Do These Findings Mean?
These findings strongly suggest that preterm birth increases the risk of asthma and wheezing disorders during childhood and that the risk of asthma/wheezing disorders increases as the degree of prematurity increases. The accuracy of these findings may be affected, however, by residual confounding. That is, preterm children may share other, unknown characteristics that increase their risk of developing asthma/wheezing disorders. Moreover, the generalizability of these findings is limited by the lack of data from low- and middle-income countries. However, given the projected global increases in children surviving preterm births, these findings highlight the need to undertake research into the mechanisms underlying the association between preterm birth and asthma/wheezing disorders and the need to develop appropriate preventative and therapeutic measures.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001596.
The March of Dimes, a nonprofit organization for pregnancy and baby health, provides information on preterm birth (in English and Spanish)
Nemours, another nonprofit organization for child health, also provides information (in English and Spanish) on premature babies and on asthma (including personal stories)
The UK National Health Service Choices website provides information about premature labor and birth and a real story about having a preterm baby; it provides information about asthma in children (including real stories)
The MedlinePlus Encyclopedia has pages on preterm birth, asthma, asthma in children, and wheezing (in English and Spanish); MedlinePlus provides links to further information on premature birth, asthma, and asthma in children (in English and Spanish)
doi:10.1371/journal.pmed.1001596
PMCID: PMC3904844  PMID: 24492409
3.  Molecular epidemiology of respiratory viruses in virus-induced asthma 
Acute respiratory illness (ARI) due to various viruses is not only the most common cause of upper respiratory infection in humans but is also a major cause of morbidity and mortality, leading to diseases such as bronchiolitis and pneumonia. Previous studies have shown that respiratory syncytial virus (RSV), human rhinovirus (HRV), human metapneumovirus (HMPV), human parainfluenza virus (HPIV), and human enterovirus infections may be associated with virus-induced asthma. For example, it has been suggested that HRV infection is detected in the acute exacerbation of asthma and infection is prolonged. Thus it is believed that the main etiological cause of asthma is ARI viruses. Furthermore, the number of asthma patients in most industrial countries has greatly increased, resulting in a morbidity rate of around 10-15% of the population. However, the relationships between viral infections, host immune response, and host factors in the pathophysiology of asthma remain unclear. To gain a better understanding of the epidemiology of virus-induced asthma, it is important to assess both the characteristics of the viruses and the host defense mechanisms. Molecular epidemiology enables us to understand the pathogenesis of microorganisms by identifying specific pathways, molecules, and genes that influence the risk of developing a disease. However, the epidemiology of various respiratory viruses associated with virus-induced asthma is not fully understood. Therefore, in this article, we review molecular epidemiological studies of RSV, HRV, HPIV, and HMPV infection associated with virus-induced asthma.
doi:10.3389/fmicb.2013.00278
PMCID: PMC3771312  PMID: 24062735
molecular epidemiology; virus-induced asthma; respiratory syncytial virus; human rhinovirus; human metapneumovirus; respiratory viruses
4.  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
5.  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
6.  Asthma in children and adolescents in Brazil: contribution of the International Study of Asthma and Allergies in Childhood (ISAAC)  
Revista Paulista de Pediatria  2014;32(1):114-125.
Objective:
To assess asthma among Brazilian pediatric population applying the International Study of Asthma and Allergies in Childhood (ISAAC), an internationally standardized and validated protocol.
Data sources:
ISAAC was conceived to maximize the value of epidemiologic studies on asthma and allergic diseases, establishing a standardized method (self-applicable written questionnaire and/or video questionnaire) capable to facilitate the international collaboration. Designed to be carried out in three successive and dependent phases, the ISAAC gathered a casuistic hitherto unimaginable in the world and in Brazil. This review included data gathered from ISAAC official Brazilian centers and others who used this method.
Data synthesis:
At the end of the first phase, it has been documented that the prevalence of asthma among Brazilian schoolchildren was the eighth among all centers participating all over the world. Few centers participated in the second phase and investigated possible etiological factors, especially those suggested by the first phase, and brought forth many conjectures. The third phase, repeated seven years later, assessed the evolutionary trend of asthma and allergic diseases prevalence in centers that participated simultaneously in phases I and III and in other centers not involved in phase I.
Conclusions:
In Brazil, the ISAAC study showed that asthma is a disease of high prevalence and impact in children and adolescents and should be seen as a Public Health problem. Important regional variations, not well understood yet, and several risk factors were found, which makes us wonder: is there only one or many asthmas in Brazil?
doi:10.1590/S0103-05822014000100018
PMCID: PMC4182995  PMID: 24676199
asthma; epidemiology; child; adolescent; risk factors
7.  Asthma and Farm Exposures in a Cohort of Rural Iowa Children 
Environmental Health Perspectives  2004;113(3):350-356.
Epidemiologic studies of farm children are of international interest because farm children are less often atopic, have less allergic disease, and often have less asthma than do nonfarm children—findings consistent with the hygiene hypothesis. We studied a cohort of rural Iowa children to determine the association between farm and other environmental risk factors with four asthma outcomes: doctor-diagnosed asthma, doctor-diagnosed asthma/medication for wheeze, current wheeze, and cough with exercise. Doctor-diagnosed asthma prevalence was 12%, but at least one of these four health outcomes was found in more than a third of the cohort. Multivariable models of the four health outcomes found independent associations between male sex (three asthma outcomes), age (three asthma outcomes), a personal history of allergies (four asthma outcomes), family history of allergic disease (two asthma outcomes), premature birth (one asthma outcome), early respiratory infection (three asthma outcomes), high-risk birth (two asthma outcomes), and farm exposure to raising swine and adding antibiotics to feed (two asthma outcomes). The high prevalence of rural childhood asthma and asthma symptoms underscores the need for asthma screening programs and improved asthma diagnosis and treatment. The high prevalence of asthma health outcomes among farm children living on farms that raise swine (44.1%, p = 0.01) and raise swine and add antibiotics to feed (55.8%, p = 0.013), despite lower rates of atopy and personal histories of allergy, suggests the need for awareness and prevention measures and more population-based studies to further assess environmental and genetic determinants of asthma among farm children.
doi:10.1289/ehp.7240
PMCID: PMC1253764  PMID: 15743727
agricultural occupational exposures; ammonia; animal feeding operations; asthma; asthma diagnosis and treatment; asthma health care policy; asthma school screening; asthma underdiagnosis; asthma undertreatment; children; chronic wheeze; cough with exercise; farming; genetic selection; hydrogen sulfide; hygiene hypothesis; odor; rural
8.  Postmenopausal hormone therapy and asthma onset in the E3N cohort 
Thorax  2010;65(4):292-297.
Background
Epidemiological studies have suggested that female hormones might play a role in asthma and that menopausal hormone therapy (MHT or HRT) might increase the risk of asthma in postmenopausal women. The only prospective study addressing this issue reports an increase in the risk of developing asthma which was similar for estrogen alone and estrogen/progestagen treatment.
Methods
The association between the use of different types of MHT and the risk of asthma onset in postmenopausal women was investigated prospectively from 1990 to 2002 by biennial questionnaire as part of the French E3N cohort study. Asthma onset was considered to be the time of medical diagnosis of asthma cases occurring during the follow up of women who were asthma free at baseline. Cox proportional hazards models were used, adjusting for potential confounding factors.
Results
Among 57,664 women free of asthma at menopause 569 incident cases of asthma were identified during 495,448 years of follow-up. MHT was related to an increased risk of asthma onset (HR= 1.20, 95% CI 0.98–1.46) among recent users. The increase in risk of asthma onset was only significant among women reporting the use of estrogen alone (HR= 1.54, 95% CI 1.13–2.09).particularly in never smokers (HR= 1.80 95% CI 1.15–2.80) and women reporting allergic disease prior to asthma onset (HR= 1.86 95% CI 1.18–2.93). A small increase in the risk of asthma onset associated with the use of estrogen/progestagen was also observed in these subgroups.
Conclusion
Postmenopausal use of estrogen alone was associated with an increased rate of newly diagnosed asthma in menopausal women.
doi:10.1136/thx.2009.116079
PMCID: PMC2962872  PMID: 20142267
Asthma; Epidemiology; Menopausal hormone therapy (MHT); Hormone replacement therapy (HRT); Asthma; chemically induced; epidemiology; Body Mass Index; Drug Combinations; Estrogen Replacement Therapy; adverse effects; utilization; Estrogens; adverse effects; Female; France; epidemiology; Humans; Middle Aged; Postmenopause; Progesterone; adverse effects; Prospective Studies; Risk Factors
9.  Bakery flour dust exposure causes non-allergic inflammation and enhances allergic airway inflammation in mice 
Background
Baker’s asthma is one of the most commonly reported occupational lung diseases in countries where fresh bread is baked daily in large quantities, and is characterized by rhinitis, bronchial hyperresponsiveness, and reversible airflow obstruction. Epidemiological studies have identified pre-existing atopy as an important risk factor for developing baker’s asthma, yet the etiology and pathogenesis of baker’s asthma remain poorly understood.
Objective
We sought to develop a mouse model of baker’s asthma that could be used to characterize the development and progression of baker’s asthma.
Methods
We were unable to sensitize mice to bakery flour dust or flour dust extract. We assessed total inflammatory cells, cellular differential, total serum IgE and the pro-inflammatory cytokine response to oropharyngeally instilled bakery flour dust or flour dust extract by itself or in the context of OVA sensitization and challenge.
Results
Both bakery flour dust and flour dust extract consistently elicited a neutrophilic inflammation in a tlr4-independent manner; suggesting that endotoxin is not playing a role in the inflammatory response to flour dust. Moreover, bakery flour dust and dust extract significantly enhance the inflammatory response in OVA sensitized and challenged mice.
Conclusions
Bakery flour dust and flour dust extract are strongly pro-inflammatory and can cause non-allergic airway inflammation and can enhance allergen-mediated airway inflammation.
doi:10.1111/j.1365-2222.2008.03038.x
PMCID: PMC4278578  PMID: 18564331
LPS; endotoxin; toll-like receptor 4; occupational airways disease; baker’s asthma; flour dust; allergic asthma
10.  Sensitisation to airborne moulds and severity of asthma: cross sectional study from European Community respiratory health survey 
BMJ : British Medical Journal  2002;325(7361):411.
Objective
To assess whether the severity of asthma is associated with sensitisation to airborne moulds rather than to other seasonal or perennial allergens.
Design
Multicentre epidemiological survey in 30 centres.
Setting
European Community respiratory health survey.
Participants
1132 adults aged 20-44 years with current asthma and with skin prick test results.
Main outcome measure
Severity of asthma according to score based on forced expiratory volume in one second, number of asthma attacks, hospital admissions for breathing problems, and use of corticosteroids in past 12 months.
Results
The frequency of sensitisation to moulds (Alternaria alternata or Cladosporium herbarum, or both) increased significantly with increasing asthma severity (odds ratio 2.34 (95% confidence interval 1.56 to 3.52) for either for severe v mild asthma). This association existed in all of the study areas (gathered into regions), although there were differences in the frequency of sensitisation. There was no association between asthma severity and sensitisation to pollens or cats. Sensitisation to Dermatophagoides pteronyssinus was also positively associated with severity. In multivariable logistic regressions including sensitisation to moulds, pollens, D pteronyssinus, and cats simultaneously, the odds ratios for sensitisation to moulds were 1.48 (0.97 to 2.26) for moderate v mild asthma and 2.16 (1.37 to 3.35) for severe v mild asthma (P<0.001 for trend).
Conclusions
Sensitisation to moulds is a powerful risk factor for severe asthma in adults. This should be taken into account in primary prevention, management, and patients' education.
What is already known on this topicSensitisation to moulds is a known risk factor for life threatening exacerbations of asthmaIt is unknown whether such sensitisation is generally associated with severity of asthmaWhat this study addsThe prevalence of sensitisation to moulds (Alternaria alternata or Cladosporium herbarum, or both) increased with increasing severity of asthmaIn this multicentre epidemiological survey, similar patterns of results were observed in various areas of the world
PMCID: PMC119432  PMID: 12193354
11.  The role of ozone exposure in the epidemiology of asthma. 
Environmental Health Perspectives  1993;101(Suppl 4):219-224.
Asthma is a clinical condition characterized by intermittent respiratory symptoms, nonspecific airway hyperresponsiveness, and reversible airway obstruction. Although the pathogenesis of asthma is incompletely understood, it is clear that airway inflammation is a paramount feature of the condition. Because inhalation of ozone by normal, healthy subjects causes increased airway responsiveness and inflammation, it is somewhat surprising that most controlled human exposure studies that have involved asthmatic subjects have not shown them to be especially sensitive to ozone. The acute decrement in lung function that is the end point traditionally used to define sensitivity to ozone in these studies may be due more to neuromuscular mechanisms limiting deep inspiration than to bronchoconstriction. The frequency of asthma attacks following ozone exposures may be a more relevant end point. Epidemiologic studies, rather than controlled human exposure studies, are required to determine whether ozone pollution increases the risk of asthma exacerbations. Asthma affects approximately 10 million people in the United States and, thus, the answer to this question is of considerable public health importance. Both the prevalence and severity of asthma appear to be increasing in many countries. Although increased asthma morbidity and mortality are probably of multifactorial etiology, a contributory role of urban air pollution is plausible. The epidemiologic database to support an association between asthma and ozone exposure is limited, but the results of several studies suggest such an association. Some potential approaches to further investigation of the relationship between asthma and ozone, including those that would link controlled human exposures to population-based studies, are considered.
PMCID: PMC1519718  PMID: 8206036
12.  Risk for Asthma in Offspring of Asthmatic Mothers versus Fathers: A Meta-Analysis 
PLoS ONE  2010;5(4):e10134.
Background
Many human epidemiologic studies demonstrate that maternal asthma confers greater risk of asthma to offspring than does paternal disease. However, a handful have shown the opposite. Given this disparity, a meta-analysis is necessary to determine the veracity and magnitude of the “maternal effect.”
Methodology/Principal Findings
We screened the medical literature from 1966 to 2009 and performed a meta-analysis to compare the effect of maternal asthma vs. paternal asthma on offspring asthma susceptibility. Aggregating data from 33 studies, the odds ratio for asthma in children of asthmatic mothers compared with non-asthmatic mothers was significantly increased at 3.04 (95% confidence interval: 2.59–3.56). The corresponding odds ratio for asthma in children of asthmatic fathers was increased at 2.44 (2.14–2.79). When comparing the odds ratios, maternal asthma conferred greater risk of disease than did paternal asthma (3.04 vs. 2.44, p = 0.037). When analyzing the studies in which asthma was diagnosed by a physician the odds ratios were attenuated and no significant differences were observed (2.85 vs. 2.48, N = 18, p = 0.37). Similarly, no significant differences were observed between maternal and paternal odds ratios when analyzing the studies in which the patient population was 5 years or older (3.15 vs. 2.60, p = 0.14). However, in all cases the trend remained the same, that maternal asthma was a greater risk factor for asthma than paternal.
Conclusions/Significance
The results show that maternal asthma increases offspring disease risk to a greater extent than paternal disease.
doi:10.1371/journal.pone.0010134
PMCID: PMC2853568  PMID: 20405032
13.  Influence of Asthma Epidemiology on the Risk for Other Diseases 
Asthma is a multifactorial chronic disease affecting a significant proportion of people in the United States and worldwide. Numerous laboratory and epidemiological studies have attempted to understand the etiology and underlying mechanisms of asthma and to identify effective therapies. However, the impact of asthma on the risk for other diseases has drawn little attention. This paper discusses the potential effects of asthma as a risk factor for other diseases, explores the potential mechanisms, and reviews the implications of the findings to clinical practice, public health, and research.
doi:10.4168/aair.2012.4.3.122
PMCID: PMC3328728  PMID: 22548204
Asthma; epidemiology; population; chronic diseases; risk; susceptibility
14.  Development of an asthma specific job exposure matrix and its application in the epidemiological study of genetics and environment in asthma (EGEA) 
OBJECTIVES—To develop a method suitable for estimating exposure risks in population studies of asthma from job titles and international codes, by combining a new job exposure matrix (JEM) with the expert judgement approach. The method was applied in the French epidemiological study of the genetics and environment in asthma (EGEA).
METHODS—The JEM contains 22 exposure groups including 18 high risk groups based on known risk factors for occupational asthma, divided into high molecular weight agents, low molecular weight agents, and mixed environments. After applying the JEM to job codes, exposure estimates for each subject were re-evaluated by examining job title texts. Three high risk exposure estimates for asthma were compared: firstly, applying the JEM to original codes (from different coders in each study centre); secondly, applying the JEM to revised codes (from one experienced coder); and thirdly, after reviewing JEM exposure estimates in the light of job title texts.
RESULTS—The study comprised 173 cases with asthma and 285 controls (age 18-65). Odds ratios (ORs) for asthma for high risk jobs were 1.0 (95% confidence interval (95% CI) 0.6 to 1.7), applying the JEM to original codes; 1.4 (95% CI 0.8 to 2.3), applying the JEM to revised codes; and 1.7 (95% CI 1.1 to 2.7), applying the JEM and subsequently re-evaluating exposure estimates from job title texts. Asthma ORs were 1.4 (95% CI 0.6 to 2.9) for high molecular weight agents, 2.3 (95% CI 1.2 to 4.4) for low molecular weight agents, and 2.1 (95% CI 0.9 to 5.2) for mixed environments.
CONCLUSIONS—This asthma JEM, when enhanced by expert re-evaluation of exposure estimates from job title texts, may be a useful tool in general population studies of asthma. In this study, a 1.7-fold increase in prevalence odds of high risk exposures was found among asthmatic workers compared with controls, with risk magnitude varying for different classes of exposure.


Keywords: job exposure matrix; asthma; occupational exposure; epidemiological methods; case-control
doi:10.1136/oem.57.9.635
PMCID: PMC1740014  PMID: 10935945
15.  Wheezing Rhinovirus Illnesses in Early Life Predict Asthma Development in High-Risk Children 
Rationale: Virus-induced wheezing episodes in infancy often precede the development of asthma. Whether infections with specific viral pathogens confer differential future asthma risk is incompletely understood.
Objectives: To define the relationship between specific viral illnesses and early childhood asthma development.
Methods: A total of 259 children were followed prospectively from birth to 6 years of age. The etiology and timing of specific viral wheezing respiratory illnesses during early childhood were assessed using nasal lavage, culture, and multiplex reverse transcriptase–polymerase chain reaction. The relationships of these virus-specific wheezing illnesses and other risk factors to the development of asthma were analyzed.
Measurements and Main Results: Viral etiologies were identified in 90% of wheezing illnesses. From birth to age 3 years, wheezing with respiratory syncytial virus (RSV) (odds ratio [OR], 2.6), rhinovirus (RV) (OR, 9.8), or both RV and RSV (OR , 10) was associated with increased asthma risk at age 6 years. In Year 1, both RV wheezing (OR, 2.8) and aeroallergen sensitization (OR, 3.6) independently increased asthma risk at age 6 years. By age 3 years, wheezing with RV (OR, 25.6) was more strongly associated with asthma at age 6 years than aeroallergen sensitization (OR, 3.4). Nearly 90% (26 of 30) of children who wheezed with RV in Year 3 had asthma at 6 years of age.
Conclusions: Among outpatient viral wheezing illnesses in infancy and early childhood, those caused by RV infections are the most significant predictors of the subsequent development of asthma at age 6 years in a high-risk birth cohort.
doi:10.1164/rccm.200802-309OC
PMCID: PMC2556448  PMID: 18565953
rhinovirus; respiratory syncytial virus; wheezing; asthma; allergic sensitization
16.  Epidemiological aspects of and risk factors for wheezing in the first year of life*  
Jornal Brasileiro de Pneumologia  2014;40(6):617-625.
OBJECTIVE:
To determine, in a sample of infants, the prevalence of and risk factors for occasional wheezing (OW) and recurrent wheezing-wheezy baby syndrome (WBS).
METHODS:
Parents of infants (12-15 months of age) completed the International Study of Wheezing in Infants questionnaire.
RESULTS:
We included 1,269 infants residing in the city of Blumenau, Brazil. Of those, 715 (56.34%) had a history of wheezing, which was more common among boys. The prevalences of OW and WBS were 27.03% (n = 343) and 29.31% (n = 372), respectively. On average, the first wheezing episode occurred at 5.55 ± 2.87 months of age. Among the 715 infants with a history of wheezing, the first episode occurred within the first six months of life in 479 (66.99%), and 372 (52.03%) had had three or more episodes. Factors associated with wheezing in general were pneumonia; oral corticosteroid use; a cold; attending daycare; having a parent with asthma or allergies; mother working outside the home; male gender; no breastfeeding; and mold. Factors associated with WBS were a cold; physician-diagnosed asthma; ER visits; corticosteroid use; pneumonia; bronchitis; dyspnea; attending daycare; bronchodilator use; having a parent with asthma; no breastfeeding; mother working outside the home; and a dog in the household.
CONCLUSIONS:
The prevalence of wheezing in the studied population was high (56.34%). The etiology was multifactorial, and the risk factors were intrinsic and extrinsic (respiratory tract infections, allergies, attending daycare, and early wheezing). The high prevalence and the intrinsic risk factors indicate the need and the opportunity for epidemiological and genetic studies in this population. In addition, mothers should be encouraged to prolong breastfeeding and to keep infants under six months of age out of daycare.
doi:10.1590/S1806-37132014000600005
PMCID: PMC4301246  PMID: 25610502
Asthma; Prevalence; Risk factors
17.  Plasma antibodies against heat shock protein 70 correlate with the incidence and severity of asthma in a Chinese population 
Respiratory Research  2005;6(1):18.
Background
The heat shock proteins (Hsps) are induced by stresses such as allergic factors and inflammatory responses in bronchi epithelial cells and therefore may be detectable in patients with asthma. However, the etiologic link between anti-Hsps and asthma (its severity and related inflammatory responses such as interleukin-4 and immunoglobulin E) has not been established. We determined whether antibodies against Hsp60 and Hsp70 were present in patients with asthma and evaluated their associations with risk and severity of asthma.
Methods
We determined the levels of anti-Hsp60 and anti-Hsp70 by immunoblot and their associations with risk and symptom severity of asthma in 95 patients with asthma and 99 matched non-symptomatic controls using multivariate logistic regression analysis.
Results
Compared to the controls, asthma patients were more likely to have detectable anti-Hsp60 (17.2% vs 5.1%) and anti-Hsp70 (33.7% vs 8.1%) (p ≤ 0.001). In particular, the presence of anti-Hsp70 was associated with a greater than 2 fold risk for asthma (adjusted OR = 2.21; 95% CI = 1.35~3.59). Furthermore, both anti-Hsp60 and anti-Hsp70 levels were positively correlated with symptom severity (p < 0.05) as well as interleukin-4 and immunoglobulin E (p < 0.05). Individuals with antibodies against anti-Hsp60 and anti-Hsp70 were more likely to have a family history of asthma (p < 0.001) and higher plasma concentrations of total immunoglobulin E (p = 0.001) and interleukin-4 (p < 0.05) than those without antibodies.
Conclusions
These data suggest that anti-Hsp60 and especially anti-Hsp70 correlate with the attacks and severity of asthma. The underlying molecular mechanisms linking antibodies to heat shock proteins and asthma remain to be investigated.
doi:10.1186/1465-9921-6-18
PMCID: PMC549531  PMID: 15710045
18.  Risk factors for oligodendroglial tumors: A pooled international study 
Neuro-Oncology  2010;13(2):242-250.
Oligodendroglial tumors are rare subtypes of brain tumors and are often combined with other glial tumors in epidemiological analyses. However, different demographic associations and clinical characteristics suggest potentially different risk factors. The purpose of this study was to investigate possible risk factors for oligodendroglial tumors (including oligodendroglioma, anaplastic oligodendroglioma, and mixed glioma). Data from 7 case–control studies (5 US and 2 Scandinavian) were pooled. Unconditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for age group, gender, and study site. Data on 617 cases and 1260 controls were available for analyses. Using data from all 7 studies, history of allergies and/or asthma was associated with a decreased risk of anaplastic oligodendroglioma (OR = 0.6; 95% CI: 0.4–0.9), and history of asthma only was associated with a decreased risk of oligodendroglioma (OR = 0.5; 95% CI: 0.3–0.9) and anaplastic oligodendroglioma (OR = 0.3; 95% CI: 0.1–0.9). A family history of brain tumors was associated with an increased risk of anaplastic oligodendroglioma (OR = 2.2; 95% CI: 1.1–4.5). Having had chicken pox was associated with a decreased risk of oligodendroglioma (OR = 0.6; 95% CI: 0.4–0.9) and anaplastic oligodendroglioma (OR = 0.5; 95% CI: 0.3–0.9) in the US studies. Although there is some overlap in risk factors between oligodendroglial tumors and gliomas as a group, it is likely that additional factors specific to oligodendroglial tumors have yet to be identified. Large, multi-institution international studies will be necessary to better characterize these etiological risk factors.
doi:10.1093/neuonc/noq173
PMCID: PMC3064625  PMID: 21149253
anaplastic oligodendroglioma; epidemiology; mixed glioma; oligodendroglioma; risk factors
19.  Evaluation of a possible association of urban air toxics and asthma. 
Environmental Health Perspectives  1995;103(Suppl 6):253-271.
The prevalence of asthma, measured either as the frequency of hospital admissions or number of deaths attributed to asthma, has increased over the last 15 to 20 years. Rapid increases in disease prevalence are more likely to be attributable to environmental than genetic factors. Inferring from past associations between air pollution and asthma, it is feasible that changes in the ambient environment could contribute to this increase in morbidity and mortality. Scientific evaluation of the links between air pollution and the exacerbation of asthma is incomplete, however. Currently, criteria pollutants [SOx, NOx, O3, CO, Pb, particulate matter (PM10)] and other risk factors (exposure to environmental tobacco smoke, volatile organic compounds, etc.) are constantly being evaluated as to their possible contributions to this situation. Data from these studies suggest that increases in respiratory disease are associated with exposures to ambient concentrations of particulate and gaseous pollutants. Similarly, exposure to environmental tobacco smoke, also a mixture of particulate and gaseous air toxics, has been associated with an increase in asthma among children. In addition, current associations of adverse health effects with existing pollution measurements are often noted at concentrations below those that produce effects in controlled animal and human exposures to each pollutant alone. These findings imply that adverse responses are augmented when persons are exposed to irritant mixtures of particles and gases and that current measurements of air pollution are, in part, indirect in that the concentrations of criteria pollutants are acting as surrogates of our exposure to a complex mixture. Other irritant air pollutants, including certain urban air toxics, are associated with asthma in occupational settings and may interact with criteria pollutants in ambient air to exacerbate asthma. An evaluation of dose-response information for urban air toxics and biological feasibility as possible contributors to asthma is therefore needed. However, this evaluation is compounded by a lack of information on the concentrations of these compounds in the ambient air and their effects on asthma morbidity and mortality. Through an initial review of the current toxicological literature, we propose a tentative list of 30 compounds that could have the highest impact on asthma and respiratory health. These compounds were selected based on their ability to induce or exacerbate asthma in occupational and nonoccupational settings, their allergic potential and ability to react with biological macromolecules, and lastly, their ability to irritate the respiratory passages. We recommend better documentation of exposure to these compounds through routine air sampling and evaluation of total exposure and further evaluation of biological mechanisms through laboratory and epidemiological studies directed specifically at the role these substances play in the induction and exacerbation of asthma.
PMCID: PMC1518937  PMID: 8549483
20.  Prevalence of Childhood Asthma in Korea: International Study of Asthma and Allergies in Childhood 
Childhood asthma is a major concern because it leads to more hospital visits and a heavy economic burden. Proper management and prevention strategies for childhood asthma must be based on correct evaluation of prevalence and risk factors for its development. In Korea, nationwide studies were conducted in 1995 and 2000 on students from 68 elementary schools (age, 6-12 years) and junior high schools (age, 12-15 years) by the Korean Academy of Pediatric Allergy and Respiratory Diseases. We used the Korean version of the International Study of Asthma and Allergies in Childhood (ISAAC) written and video questionnaires at the same schools during the same period (October-November). The prevalence of asthma in junior high school children seemed to increase over 5 years. However, in elementary school children, the prevalence of asthma symptoms decreased, although the prevalence of 'diagnosis of asthma, ever' and 'treatment of asthma, last 12 months' increased. In addition, it was found that various factors, such as obesity, passive smoking, dietary habits, raising pets at home, and fever/antibiotic use during infancy were associated with childhood asthma. When prevalence of asthma in Korea was compared with that in different regions, the prevalence changes in the 6-7 years age group did not seem to be consistent between regions, whereas similar trends were observed among children aged 13-14 years. To conduct another epidemiological study to evaluate the time trend over time, a third nationwide survey is planned in 2010, and we anticipate ISAAC Phase 3 will explore recent changes in the prevalence of childhood asthma and assess its risk factors in Korean children. On the basis of accurate data on the current status of childhood asthma in 2010, we will be able to establish proper management strategies.
doi:10.4168/aair.2010.2.2.61
PMCID: PMC2846742  PMID: 20358019
Asthma; child; Korea
21.  Asthma prevalence and risk factors among children and adolescents living around an industrial area: a cross-sectional study 
BMC Public Health  2013;13:1038.
Background
The exposure to air pollution has negative effects on human health, increasing the risk of respiratory diseases, such as asthma. Few data are yet available on the epidemiology of childhood asthma in some areas of Italy. The aim of the study was to estimate asthma prevalence and related risk factors in children and adolescents residents around the industrial area of Termoli, Molise region, Central-South Italy.
Methods
Prevalence was assessed through the administration of modified ISAAC questionnaires filled out by parents of 89 children and adolescents for the identification of confirmed and probable cases, and by analyzing pediatricians’ databases on drug prescriptions for symptoms control and treatment of assisted population in the study area (n = 1,004), compared to a control area (n = 920) with lower industrialization. The association of asthma with risk factors was evaluated by univariate (Chi-square or Fisher’s Exact test) and regression logistic analysis.
Results
A total of 22 (24.7%) asthmatics were identified, including both confirmed (n = 7; 7.9%) and probable cases (n = 15; 16.8%), most of them (n = 17; 77.3%) resident of Termoli town. All asthma cases were georeferenced based on the residence, however clusters were not found. Using drug prescriptions analysis, a higher prevalence (n = 138; 13.7%) of diagnosed cases was found. Lifetime history of both atopic dermatitis and bronchitis were significantly relateds to asthma cases, as well as an elevated body mass index, whose association is consistent with prevalence data of overweight/obese children living in the study area. Moreover, being resident of the town of Termoli was associated to the occurrence of cases.
Conclusions
Although our data indicated a prevalence concordance with previous national studies in pediatric population, a definitive correlation with environmental industrial factors present in the study area was not established. However, asthma outcome was significantly associated to individuals living in the town of Termoli that, despite the industrial/manufacturing activities, is also subjected to a higher environmental pressure due to the presence of toll road, state highway, railroad, and seaport which may cause air pollution from motor vehicle traffic and increase asthma induction. This study provides hitherto unavailable data on asthma in childhood population living in an industrialized area which was never investigated before, could be part of a systematic review or meta-analysis procedure, might suggest significant findings for larger observational studies, and contribute to complete the frame of disease epidemiology in Italy.
doi:10.1186/1471-2458-13-1038
PMCID: PMC4228310  PMID: 24188412
Childhood asthma; Industrial area; Prevalence; Risk factors; Drug prescription
22.  Comparison of orally exhaled nitric oxide in allergic versus nonallergic rhinitis 
Background:
Fractional exhaled nitric oxide (FeNO), a well-known marker of airway inflammation, is rarely evaluated in rhinitis of different etiology. We aimed to compare the eNO levels in allergic rhinitis (AR) and nonallergic rhinitis (NAR) with/without asthma, as well as the contributing factors that interfere with elevated FeNO.
Methods:
Patients were enrolled based on chronic nasal symptoms. Orally exhaled NO was measured with the single exhalation method at 50 mL/s. All subjects underwent a panel of tests: skin-prick tests, asthma control test, blood sampling, spirometry, and health-related quality-of-life questionnaires.
Results:
The study group consisted of mainly women (130 women/41 men), with a mean age of 32.6 ± 13.2 years. AR was diagnosed in 122 (78.2%), NAR in 34 (21.8%), and 15 subjects were healthy controls. FeNO was insignificantly higher in patients with AR compared with patients with NAR and controls (32.2 parts per billion [ppb] versus 27 and 19.4 ppb), with no difference between genders. NAR + asthma had higher FeNO than those without asthma (40.5 ppb versus 14.9 ppb; p < 0.03), whereas accompanying asthma did not affect FeNO levels in the AR group. AR ± asthma had significantly higher FeNO levels than the NAR-only group (p < 0.01). Among AR + asthma, perennial sensitization caused higher FeNO levels than did seasonal allergens (48.5 ± 33.9 and 19.5 ± 13.6′ p = 0.003), whereas FeNO was significantly higher during the allergen season. Nasally inhaled corticosteroids insignificantly reduced FeNO levels in all groups. Severity and seasonality of rhinitis, asthma, and ocular symptoms, but not gender, age, body mass index, Total IgE, forced expiratory volume in 1 second, and smoking, were associated with FeNO.
Conclusion:
Rhinitis and comorbid asthma are responsible for increased FeNO, irrespective of atopy. However, NAR without asthma may not be considered as a strong risk factor for airway inflammation.
doi:10.2500/ajra.2012.26.3717
PMCID: PMC3906508  PMID: 22487277
Airway inflammation; allergic rhinitis; asthma; atopy; exhaled nitric oxide; inhaled corticosteroids; nonallergic rhinitis
23.  Associations between criteria air pollutants and asthma. 
Environmental Health Perspectives  1995;103(Suppl 6):235-242.
The evidence that asthma is increasing in prevalence is becoming increasingly compelling. This trend has been demonstrated not only in the United States, but also in the United Kingdom, New Zealand, Australia, and several other Western countries. In the United States, the increase is largest in the group under 18 years of age. There is mounting evidence that certain environmental air pollutants are involved in exacerbating asthma. This is based primarily on epidemiologic studies and more recent clinical studies. The U.S. Clean Air Act of 1970 provides special consideration to the class of outdoor air pollutants referred to as criteria pollutants, including O3, sulfur dioxide (SO2), particulate matter (PM), NOx, CO, and Pb. Standards for these pollutants are set by the U.S. Environmental Protection Agency with particular concern for populations at risk. Current evidence suggests that asthmatics are more sensitive to the effects of O3, SO2, PM, and NO2, and are therefore at risk. High SO2 and particulate concentrations have been associated with short-term increases in morbidity and mortality in the general population during dramatic air pollution episodes in the past. Controlled exposure studies have clearly shown that asthmatics are sensitive to low levels of SO2. Exercising asthmatics exposed to SO2 develop bronchoconstriction within minutes, even at levels of 0.25 ppm. Responses are modified by air temperature, humidity, and exercise level. Recent epidemiologic studies have suggested that exposure to PM is strongly associated with morbidity and mortality in the general population and that hospital admissions for bronchitis and asthma were associated with PM10 levels. In controlled clinical studies, asthmatics appear to be no more reactive to aerosols than healthy subjects. Consequently, it is difficult to attribute the increased mortality observed in epidemiologic studies to specific effects demonstrated in controlled human studies. Epidemiologic studies of hospital admissions for asthma have implicated O3 as contributing to the exacerbation of asthma; however, most study designs could not separate the O3 effects from the concomitant effects of acid aerosols and SO2. Controlled human clinical studies have suggested that asthmatics have similar changes in spirometry and airway reactivity in response to O3 exposure compared to healthy adults. However, a possible role of O3 in worsening atopic asthma has recently been suggested in studies combining allergen challenge following exposure to O3. Attempts at identification of factors that predispose asthmatics to responsiveness to NO2 has produced inconsistent results and requires further investigation. In summary, asthmatics have been shown to be a sensitive subpopulation relative to several of the criteria pollutants. Further research linking epidemiologic, clinical, and toxicologic approaches is required to better understand and characterize the risk of exposing asthmatics to these pollutants.
PMCID: PMC1518942  PMID: 8549479
24.  Asthma and allergies in Jamaican children aged 2–17 years: a cross-sectional prevalence survey 
BMJ Open  2012;2(4):e001132.
Objective
To determine the prevalence and severity of asthma and allergies as well as risk factors for asthma among Jamaican children aged 2–17 years.
Design
A cross-sectional, community-based prevalence survey using the International Study of Asthma and Allergies in Childhood questionnaire. The authors selected a representative sample of 2017 children using stratified, multistage cluster sampling design using enumeration districts as primary sampling units.
Setting
Jamaica, a Caribbean island with a total population of approximately 2.6 million, geographically divided into 14 parishes.
Participants
Children aged 2–17 years, who were resident in private households. Institutionalised children such as those in boarding schools and hospitals were excluded from the survey.
Primary and secondary outcome measures
The prevalence and severity of asthma and allergy symptoms, doctor-diagnosed asthma and risk factors for asthma.
Results
Almost a fifth (19.6%) of Jamaican children aged 2–17 years had current wheeze, while 16.7% had self-reported doctor-diagnosed asthma. Both were more common among males than among females. The prevalence of rhinitis, hay fever and eczema among children was 24.5%, 25% and 17.3%, respectively. Current wheeze was more common among children with rhinitis in the last 12 months (44.3% vs 12.6%, p<0.001), hay fever (36.8% vs 13.8%, p<0.001) and eczema (34.1% vs 16.4%, p<0.001). Independent risk factors for current wheeze (ORs, 95% CI) were chest infections in the first year of life 4.83 (3.00 to 7.77), parental asthma 4.19 (2.8 to 6.08), rhinitis in the last 12 months 6.92 (5.16 to 9.29), hay fever 4.82 (3.62 to 6.41), moulds in the home 2.25 (1.16 to 4.45), cat in the home 2.44 (1.66 to 3.58) and dog in the home 1.81 (1.18 to 2.78).
Conclusions
The prevalence of asthma and allergies in Jamaican children is high. Significant risk factors for asthma include chest infections in the first year of life, a history of asthma in the family, allergies, moulds and pets in the home.
Article summary
Article focus
The prevalence of asthma and allergies in both developed and developing countries is continuing to rise.
In some Caribbean countries, asthma is a public health problem associated with high economic costs.
This study determined the prevalence of asthma, allergy symptoms and associated risk factors.
Key messages
We demonstrated that the prevalence of asthma and allergy symptoms among Jamaican children aged 2–17 years is high.
Both the prevalence and severity of asthma symptoms are comparable to that reported among children in high-income countries.
Current wheeze and doctor-diagnosed asthma were more common in males and in children with allergies.
A history of asthma in the family, chest infections in the first year of life, allergies, exposure to moulds and pets in the home were associated with significant risk for asthma.
Identifying children at high risk for asthma and controlling modifiable risk factors is important in reducing the prevalence and morbidity related to asthma.
Strengths and limitations of this study
This is the first national study on asthma and allergies in Jamaica using a nationally representative sample of children with a response rate of 80%.
We used a modified ISAAC protocol in which sampling was done by household rather than by school. Using a population-based sampling strategy; we sampled one child and one adult per household. This approach enabled us to obtain national prevalence estimates for both adults and children in one survey at a reduced cost.
Limitations of this study include the fact that the prevalence of asthma and allergies was based solely on self-reports, no objective measures were done. Also in younger children, caregivers responded to questionnaires.
doi:10.1136/bmjopen-2012-001132
PMCID: PMC3400072  PMID: 22798254
25.  The impact of food allergy on asthma 
Food allergy is a potentially severe immune response to a food or food additive. Although a majority of children will outgrow their food allergies, some may have lifelong issues. Food allergies and other atopic conditions, such as asthma, are increasing in prevalence in Western countries. As such, it is not uncommon to note the co-existence of food allergy and asthma in the same patient. As part of the atopic march, many food allergic patients may develop asthma later in life. Each can adversely affect the other. Food allergic patients with asthma have a higher risk of developing life-threatening food-induced reactions. Although food allergy is not typically an etiology of asthma, an asthmatic patient with food allergy may have higher rates of morbidity and mortality associated with the asthma. Asthma is rarely a manifestation of food allergy alone, but the symptoms can be seen with allergic reactions to foods. There may be evidence to suggest that early childhood environmental factors, such as the mother’s and child’s diets, factor in the development of asthma; however, the evidence continues to be conflicting. All food allergic patients and their families should be counseled on the management of food allergy and the risk of developing co-morbid asthma.
PMCID: PMC3047906  PMID: 21437041
food allergy; diagnosis; treatment; asthma

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