Risk Factor For Allergic Sensitization Research Articles

Prevalence and risk factors for allergic sensitization: 3 cross-sectional studies among schoolchildren from 1996 to 2017.

The prevalence of allergic sensitization and allergic diseases has increased for decades in Northern Europe, but recent studies are lacking. We sought to study the prevalence trends of allergic sensitization, associated risk factors, and the association with asthma and allergic rhinitis (AR) among children in Northern Sweden. Three cohorts of children aged 7 to 8 years participated in a skin prick test (SPT) with 10 airborne allergens in 1996, 2006, and 2017, with 2148, 1693, and 1762 participants tested, respectively, representing 87% to 90% of schoolchildren in the catchment communities. Adjusted Poisson regression was used to identify risk factors for allergic sensitization and the association with asthma and AR. The prevalence of any positive SPT response increased from 21% in 1996 to 30% in 2006 and remained at 30% in 2017 (P< .001). Sensitization to cat was the most common for all the years. The risk factor pattern for a positive SPT response was similar in all examinations, with positive and significant associations with a family history of allergy (risk ratio, 1.4-1.5) and negative and significant associations with having a cat at home (risk ratio, 0.7-0.8). The prevalence of physician-diagnosed asthma increased, but the association with allergic sensitization weakened. The opposite trends were found for AR-decreasing prevalence and strengthened association with allergic sensitization. The prevalence of allergic sensitization increased from 1996 to 2006 but plateaued in the next decade, whereas the risk factor pattern remained stable. The diverging trends of associations between allergic sensitization and asthma and AR suggest secular trends in the clinical management of allergic diseases.

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March.

Atopic march refers to the phenomenon wherein the occurrence of asthma and food allergy tends to increase after atopic dermatitis. The mechanism underlying the progression of allergic inflammation from the skin to gastrointestinal (GI) tract and airways has still remained elusive. Impaired skin barrier was proposed as a risk factor for allergic sensitization. Claudin-1 protein forms tight junctions and is highly expressed in the epithelium of the skin, airways, and GI tract, thus, the downregulation of claudin-1 expression level caused by CLDN-1 gene polymorphism can mediate common dysregulation of epithelial barrier function in these organs, potentially leading to allergic sensitization at various sites. Importantly, in patients with atopic dermatitis, asthma, and food allergy, claudin-1 expression level was significantly downregulated in the skin, bronchial and intestinal epithelium, respectively. Knockdown of claudin-1 expression level in mouse models of atopic dermatitis and allergic asthma exacerbated allergic inflammation, proving that downregulation of claudin-1 expression level contributes to the pathogenesis of allergic diseases. Therefore, we hypothesized that the tight junction dysfunction mediated by downregulation of claudin-1 expression level contributes to atopic march. Further validation with clinical data from patients with atopic march or mouse models of atopic march is needed. If this hypothesis can be fully confirmed, impaired claudin-1 expression level may be a risk factor and likely a diagnostic marker for atopic march. Claudin-1 may serve as a valuable target to slowdown or block the progression of atopic march.

Facteurs environnementaux favorisant le développement d’un asthme

The prevalence of asthma has increased rapidly since the early 1970s, and only changes in exposure to environmental factors; which go together with changes in lifestyle, are likely to explain such a rapid increase. Exposure to allergens is a risk factor for allergic sensitization, and allergic sensitization is a risk factor for allergic asthma. However, apart from indoor mold exposure as a risk factor for childhood asthma, there is insufficient evidence to conclude that the associations between allergen exposure and asthma development are causal. A new challenge for research is to analyze the huge amount of data derived from the metagenomic characterization of the environmental and human microbiome, to understand the role of interactions between viruses, bacteria and allergens in the development of asthma. It is recognized that prenatal and postnatal exposure to air pollution and maternal smoking increase the risk of developing asthma in children. In adults, the data are scarce and the results remain controversial as regards these exposures and asthma incidence. Further research is needed to appraise the effect of exposure to phenols, phthalates and perfluorinated compounds, which are widespread in the environment and may be associated with asthma, especially in children. Frequent use of chemicals for home cleaning especially in the form of sprays -which is a common practice at the population level- is a risk factor for the development of adult asthma. The domestic use of cleaning products might also be a risk factor for asthma in children exposed at home. The chemicals involved in these relationships are still to be identified. Occupational asthma is a major phenotype of adult asthma. A significant part of these asthma cases might relate to occupational exposure to cleaning products. While there is evidence of associations between diet during pregnancy or during childhood and the risk of developing asthma in children, the data in adults are insufficient. Beyond genetic factors, body composition is influenced by dietary choices and physical activity. Further research is needed to clarify the complex interplay between these nutritional factors and asthma development. The new challenge for research is to decipher the role of all the environmental factors to which the individual is exposed since conception ("exposome") in the development of asthma, using a holistic approach.

Tobacco smoke as a risk factor for allergic sensitization in adults: Conclusions of a systematic review and meta-analysis

Tobacco smoke as a risk factor for allergic sensitization in adults: Conclusions of a systematic review and meta-analysis

Implant allergy.

Osteosynthesis materials or artificial joint replacement make part of clinical routine. In case of complaints mostly mechanical causes or infections are found. Metals like nickel, chromium and cobalt or bone cement components like acrylates and gentamicine may however potentially cause intolerance reactions to implants. Correspondingly, eczema, delayed wound/bone healing, recurrent effusion, pain or implant loosening have been described as manifestation of implant allergy. In contrast to the high incidence of cutaneous metal allergy, allergies associated with implants are rare. Diagnosis of metal implant allergy is based on excluding differential diagnoses – in particular infection – and on a combined approach of allergological diagnostics by patch test and histopathology of periimplant tissue. Risk factors for allergic sensitization to implants or triggering periimplant allergic reactions in the case of preexisting cutaneous metal allergy are unknown. Despite the risk of developing complications being unclear, titanium-based osteosynthesis materials are recommended for metal-allergic patients and the use of metal-metal couplings in arthroplasty is rather not recommended for such patients. If a regular, potentially applicable CoCr-polyethylene articulation is preferred, the patient has to be well informed and has to give his written consent.

Early oral exposure to house dust mite allergen through breast milk: A potential risk factor for allergic sensitization and respiratory allergies in children

Early oral exposure to house dust mite allergen through breast milk: A potential risk factor for allergic sensitization and respiratory allergies in children

Study of risk factors for atopic sensitization, asthma, and bronchial hyperresponsiveness in animal laboratory workers.

The aim of this estudy was to investigate the influence of allergen exposure levels and other risk factors for allergic sensitization, asthma, and bronchial hyperresponsiveness (BHR) in workers exposed to laboratory animals. This was a cross-sectional study performed at two universities, 123 workplaces with 737 subjects. Dust samples were collected from laboratories and animal facilities housing rats, mice, guinea pigs, rabbits, or hamsters and analyzed by enzyme-linked immunosorbent assay (ELISA) to measure allergen concentrations. We also sampled workplaces without animals. Asthma was defined by both symptoms and BHR to mannitol. The concentrations of allergens were tested for association with a skin prick test, respiratory symptoms, spirometry data, and BHR. This multivariate analysis was performed by using Poisson regression to estimate the relative risk (RR) for the exposed group. Our sample comprised students and workers, with 336 subjects in the nonexposed group and 401 subjects in the exposed group. Sixty-nine subjects (17%) had positive results in the skin prick test for animal allergens in the exposed group; in the nonexposed group, 10 subjects had positive results (3%) (p<0.001). Exposure to laboratory animals over 2.8 years was associated with atopic sensitization (RR=1.85; 95% confidence interval: 1.09-3.15; p=0.02). Allergen concentration was not associated with sensitization, asthma, or BHR. Exposure to laboratory animals was associated with atopic sensitization. However, we did not find a cutoff allergen concentration that increased the risk for sensitization. Duration of exposure seems to be more relevant to sensitization than concentration of allergens in dust.

Increase in sensitization to common airborne allergens among adults - two population-based studies 15years apart.

BackgroundStudies on time trends of allergic sensitization among adults are rare. The aim of the study was to compare the prevalence of allergic sensitization to common airborne allergens among adults 15 years apart and to identify risk factors for allergic sensitization.MethodsClinical examinations including skin prick test (SPT) and structured interviews were performed in two random population samples in 1994 and 2009. Furthermore, specific IgE was analyzed in 2009. SPT data were available for 483 subjects in 1994 and for 463 subjects in 2009 in ages 20–60 years. Specific IgE was analyzed in 692 subjects in ages 20–79 years.ResultsSensitization to cat (16% to 26%, p < 0.001), dog (13% to 25%, p < 0.001), birch (13% to 18%, p = 0.031) and timothy (12% to 21%, p < 0.001), based on SPT, increased significantly from 1994 to 2009. Sensitization to any positive SPT increased from 35% to 39%, p = 0.13.The proportion of having ≥3 positive SPT reactions increased from 40% to 56%, p = 0.002. The sensitization pattern yielded similar results based on specific IgE. Risk factors for allergic sensitization were having a family history of allergy (OR 3.1, 95% CI 2.0-4.8 for any positive SPT; OR 2.7, 95% CI 1.8-4.0 for any elevated IgE) and urban living (OR 1.7, 95% CI 1.0-2.7; OR 1.5, 95% CI 1.0-2.4).ConclusionsThe prevalence of allergic sensitization to major airborne allergens as well as multi-sensitization increased significantly between the study years. Young age, a family history of allergy and urban living were significant risk factors for allergic sensitization.

Mouse allergen skin sensitization in asthmatic children of suburban, rural, and inner-city populations

Mouse allergen (MA) exposure is a well-known risk factor for allergic sensitization and is implicated in the pathogenesis of pediatric asthma. Although previous studies report high prevalence of MA sensitization in inner-city asthmatic children, no data exist on its comparison with either suburban or rural children with asthma. We did a retrospective cohort study by chart review of all children (≤18 years of age) who underwent allergy testing during a 6-month period in a tertiary care referral center. Patients were divided geographically into suburban, rural, and inner-city groups based on their zip codes. MA was tested using the standard allergy test panel by skin prick/puncture. Positive skin test reactivity was defined as wheal diameter ≥3 mm and erythema ≥5 mm. A total of 989 patients underwent allergy testing and 349 children were tested for MA with the overall positivity rate of 18.6% (65/349). In children with asthma (mean age, 12.8 years; SD ± 3.19) who had MA testing (n = 166), the rate of positive skin test reactivity was 18% (n = 30). Inner-city asthmatic children had significantly greater MA sensitization compared with either suburban or rural children. MA sensitization is highly prevalent among children with asthma, especially in inner-city populations but also among suburban and rural children. Although most allergists do not routinely test for MA sensitization during the initial evaluation, it may be useful to include it in the allergy testing for children with asthma.

Low incidence and high remission of allergic sensitization among adults

Prospective studies on the incidence and remission of allergic sensitization among adults are rare. We sought to assess the incidence, remission, risk factors, and prevalence of allergic sensitization in relation to aging over a 10-year period. In 1994, a sample of 664 adults (68% of invited) participated in clinical examinations, including a structured interview and skin prick tests (SPTs). The sample was randomly selected from a large questionnaire survey in Northern Sweden. In 2004, 555 subjects (93% of invited) were re-examined by using the same methods as in 1994. IgE levels were also measured in 2004. In 1994, the prevalence of any positive SPT response was significantly related to age, with the highest prevalence (55%) in subjects aged 20 to 29 years and the lowest prevalence (26%) in subjects aged 50 to 60 years. A similar age-related prevalence was found in 2004, and sensitization to pollen and pets was most common in both years. The results of the SPTs were verified by means of specific IgE measurement. The incidence of any positive SPT response was low. Only 9 subjects had any positive SPT response (ie, a cumulative incidence of 5% over 10 years). Remission was greater (ie, 32% over 10 years). The main risk factors for allergic sensitization were young age and a family history of allergy. Having had furred animals at home during childhood was negatively related to specific IgE levels. The low incidence and high remission in adulthood explain the decreasing prevalence of allergic sensitization by age. Thus the low prevalence of allergic sensitization among the elderly found in cross-sectional studies is an effect of normal aging and not primarily a birth cohort effect.

Association between short sleep duration and the risk of sensitization to food and aero allergens in rural Chinese adolescents

Both long and short sleep duration have been associated with obesity, cardiovascular disease, and diabetes. However, there have been no previous studies investigating the potential relationship between altered sleep duration and allergen sensitization. To explore the association between sleep duration and sensitization to food and aeroallergens. This study includes 1534 rural Chinese adolescent twins aged 12-21 years who completed standard sleep questionnaires and skin prick tests (SPTs) to nine food and five aeroallergens. Total sleep time was defined as the interval from bedtime to wake-up time minus sleep latency. Sensitization was defined as having at least one positive SPT. Compared with individuals with the highest (third) tertile of sleep duration, those who slept less were more likely to be sensitized to any food allergen with odds ratios (ORs) of 1.9 [95% confidence interval (CI): 1.3-2.7] and 1.4 (95% CI: 1.0-1.9) for the first and second tertiles (trend test P(trend)=3×10(-4)), respectively. The corresponding ORs for sensitization to any aeroallergen were 1.5 (95% CI: 1.1-2.0) and 1.3 (95% CI: 1.0-1.7) (P(trend)=8×10(-3)). These associations were independent of percent body fat. In addition, we observed a significant dose-response association between the number of positive SPTs and percentage of shortest sleep duration (first tertile) (P(trend)=1×10(-3)). In this sample of relatively lean rural Chinese adolescents, we found that short sleep duration was associated with increasing risk of sensitization to food and aeroallergens, independent of percent body fat. Longitudinal studies are needed to further determine the temporal and causal relationships. If short sleep duration indeed is one of the risk factors for allergic sensitization, the global burden of allergic diseases could be dramatically reduced by providing appropriate guidance on sleep duration for youth.

Increased Eosinophilic Cationic Protein in Nasal Fluid in Hospitalized Wheezy Infants with RSV Infection

Respiratory syncytial virus (RSV) is a major respiratory pathogen which causes bronchiolitis with dyspnea and wheezing in children less than 2 years old. RSV bronchiolitis in infancy severe enough to cause hospitalization might be a risk factor for allergic sensitization and bronchial asthma in future. However, the pathophysiology behind this development has not been clearly characterized. To evaluate the existence of airway inflammation and characteristic of RSV bronchiolitis, we analyzed and compared the concentrations of eosinophilic cationic protein (ECP) in nasal fluid and plasma. From 69 infants (aged <2 years) hospitalized for possible lower respiratory tract infections including RSV infection, we collected nasal fluid and plasma and determined the ECP concentrations. ECP concentrations in nasal fluid were significantly higher in patients with wheezing and/or bronchial rales than in patients without them (1733 ± 660 ng/mL vs 680 ± 450 ng/mL, p = 0.018), and those of the respiratory syncitial virus-infected group were significantly higher than those of the uninfected group (p = 0.04). Meanwhile, there was no significant difference in plasma ECP levels between patients with wheezing and patients without wheezing, and no significant difference between RSV-infected and other pathogen-infected patients. There were significant correlations between nasal fluid ECP concentrations and both neutrophil and eosinophil counts in the peripheral blood. Nasal fluid ECP concentrations are increased in infants with lower respiratory infections including RSV infection accompanied with wheezing. ECP probably originates from neutrophils as well as eosinophils migrated into airways. The monitoring of ECP concentration in nasal fluid may be useful for evaluating leukocyte (including eosinophils and neutrophils)-mediated airway inflammation during infancy and its severity.

Maternal smoking increases risk of allergic sensitization and wheezing only in children with allergic predisposition: longitudinal analysis from birth to 10 years

The role of passive smoking for allergies and asthma in children above the age of 3 years remains unclear and possible interactive effects with parental allergies have not been formally evaluated in long-term studies. To examine the interaction of passive smoking and an allergic predisposition regarding allergic sensitization, allergic airway symptoms and respiratory infections during the first 10 years of life. In a prospective multicenter birth cohort study with 1314 recruited children in Germany, we assessed serum immunoglobulin E against common allergens at seven time points, and parental smoking and respiratory symptoms annually by using questionnaires. Longitudinal analyses were performed using generalized estimating equation models (stratified by parental allergy status). During the first 10 years, 18% of the children were exposed to regular maternal smoking since pregnancy, 43% to irregular maternal or only paternal smoking. Among children with two allergic parents, a mother who smoked regularly significantly increased the odds for allergic sensitization (adjusted OR 4.8, 95% CI 1.3-18.2) and wheezing (adjusted OR 5.7, 95% CI 1.7-19.0) in her child compared with children who were never exposed. For those with only one allergic parent, the odds were doubled and also statistically significant, whereas in children without allergic parents maternal smoking had no effects. There was no association of maternal smoking with allergic rhinitis or respiratory infections. Our results suggest that regular maternal smoking is a strong risk factor for allergic sensitization and asthma symptoms during the first 10 years of life, but only in children with allergic parents.

Predicting the development of early skin test sensitization in offspring of parents with asthma

The direct causal relationship between skin sensitization and asthma are controversial until now and remains to be further researched. Our aim is to analyse the role of parental asthma in the development of skin sensitization in offspring. This study was performed among nuclear families (determined by index of asthma patients), and subjects included parents and offspring. Parents were subdivided into four phenotypes on the basis of skin sensitization (SPT+ or SPT-) and asthma status (AST+ or AST-) and offspring were subdivided into three age groups: 3-8, 9-14 and 15-20 years. The main tests included a standard questionnaire and skin prick tests. Offspring's skin sensitization differed among parental phenotypes at all ages (P < 0.05). In the SPT+/AST-, SPT-/AST+ and SPT+/AST+ groups, offspring were significantly more likely to be allergic than the ones in SPT-/AST- group at 3-8 years. Offspring with at least one parent with asthma were significantly more likely to have positive skin prick test response than those with non-asthmatic parents at age 3-8 years and 9-14 years, but not at 15-20 years among offspring with allergic parents. Results were independent of asthma in the children and of the characteristics of atopy in the parents. Parent asthma history is an independent risk factor for allergic sensitization in their offspring in a Chinese population.

Degree and clinical relevance of sensitization to common allergens among adults: a population study in Helsinki, Finland

We aimed to assess the prevalence of allergic sensitization and multiple sensitization, risk factors, and the clinical impact of being sensitized in the adult population of Helsinki, Finland. As a part of the FinEsS study, a population-based random sample of 498 adults aged 26-60 years were tested for 15 common aeroallergens with skin prick tests (SPTs) and interviewed on respiratory symptoms and diseases, including respiratory irritants and childhood environment. The prevalence of at least one positive prick test was 46.9%. A large difference by age was found: 56.8% were sensitized among those aged 26-39 years, 49.2% in the age group 40-49 years, and 35.6% in the age group 50-60 years (P<0.001). Sensitization to multiple allergens was common among young subjects with 42% of the sensitized responding to at least four allergens, while this proportion was only 16% of the sensitized among those aged 50-60 years. The prevalence of physician-diagnosed asthma, allergic rhinitis (AR) or conjunctivitis, and wheeze increased significantly with increasing number of positive responses to SPTs. Having a family history of AR or conjunctivitis was a significant risk factor for allergic sensitization and for sensitization to any of the pollens. Further, urban living in childhood yielded an increased risk for pollen sensitization. The prevalence of allergic sensitization was high in the urban adult population of Helsinki. More than half of those aged 26-39 years was sensitized and 24% was sensitized to at least four allergens. Sensitization to multiple allergens was associated with a high prevalence of asthma, AR or conjunctivitis, and wheeze.

Elevated cord serum immunoglobulin e increases the risk of allergic sensitization at age 4 and 10 and asthma at age 10

Purpose Evidence suggests that elevated cord serum immunoglobulin E (CS-IgE) is a risk factor for allergic sensitization in early childhood. Whether CS-IgE is a risk for asthma is controversial. We hypothesize that elevated CS-IgE levels increase the risk of allergic sensitization (positive skin prick test) and asthma at age 10 years. The hypotheses were tested in a 10-year follow-up of a birth cohort. Methods CS-IgE was available for 1358 of 1456 children born between 1989 and 1990 at Isle of Wight, UK. The cohort was evaluated for allergic diseases at ages 1, 2, 4, and 10 years. Outcomes of interest were positive skin prick tests and asthma. Skin prick tests for six allergens were performed on 981 children at age 4 and 1036 at age 10. Asthma was defined based on physician's diagnosis. Exposure was elevated levels of CS-IgE (≥0.5 kU/L). We used logistic regression to estimate the risk of asthma and allergic sensitization for elevated levels of CS-IgE. Results At ages 4 and 10 years, 16.7% and 27.0% of children, respectively, showed allergic sensitization. The risk of allergic sensitization was higher for those with elevated CS-IgE at both age 4 (odds ratio OR = 2.05, 95% confidence interval CI = 1.28–3.30) and age 10 (OR =1.73, 95% CI = 1.13–2.65). The prevalence of asthma was 10.3% at age 1–2, 15.2% at age 4, and 12.8% at age 10. The association of asthma and elevated CS-IgE was not significant at ages 1 to 2 or at 4, but it reached significance at age 10 (OR = 1.66, 95% CI = 1.05–2.62). Conclusion Our findings suggest that elevated CS-IgE is not only a risk factor for allergic sensitization at ages 4 and 10 years, but also a risk factor for asthma at age 10, probably related to late onset of asthma. This study provides further evidence that the susceptibility for asthma in children may be programmed in utero.

Advances in environmental and occupational diseases 2003

The past year has seen a welcome increase in the number of articles published in the Journal on environmental and occupational disorders. Some of the major themes have been risk factors for allergic sensitization, the measurement and containment of domestic allergens (especially cockroach but also house dust mite), and risk factors for occupational allergy and asthma. Some important articles were also presented on mechanisms of occupational and environmental asthma.

Parental asthma as a risk factor for the development of early skin test sensitization in children

Background Recent epidemiologic evidence has challenged the paradigm suggesting a direct causal relationship between allergic sensitization and asthma. Objective We sought to investigate the role of a familial predisposition for asthma in the development of atopy in children. Methods Subjects were participants in the Tucson Children's Respiratory Study. Skin tests to aeroallergens were performed in parents and in children at ages 6, 11, and 16 years. Parents were considered asthmatic if they reported physician-confirmed asthma. Parents were divided into 4 phenotypes on the basis of skin sensitization (Skt+ or Skt−) and asthma status (As+ or As−): Skt−/As−, Skt−/As+, Skt+/As−, and Skt+/As+. Results Children's allergic sensitization differed among parental phenotypes at all ages ( P < .0001). Children in the Skt+/As− and Skt+/As+ groups were significantly more likely to be allergic than children in the Skt−/As− group at all ages. Among children with allergic parents, those with at least one parent with asthma were significantly more likely to have positive skin test responses than those with nonasthmatic parents at age 6 years (52.4% vs 37.4%, P < .005) and 11 years (70.1% vs 55.6%, P < .005) but not at age 16 years (82.3% vs 75.1%, P = .180). Results were independent of wheezing in the child and of the characteristics of atopy in parents. The Skt−/As+ group had too few subjects for meaningful comparisons. Conclusion Among children of atopic parents, parental asthma is a risk factor for allergic sensitization in early childhood. The strong association between allergic sensitization and asthma is at least in part explained by an increased susceptibility to allergen sensitization in subjects predisposed to asthma.

Systemic administration of Bordetella pertussis enhances pulmonary sensitization to house dust mite in juvenile rats.

The incidence of allergies and asthma has increased significantly in the past few decades. The objectives of this study were to establish an allergy model in weanling rats to more closely reflect the developing immune system of children, and to determine whether systemic administration of inactivated Bordetella pertussis could enhance pulmonary and systemic immune responses to locally administered house dust mite antigen (HDM). Three-week old female Brown Norway rats were sensitized with 10 micro g HDM intratracheally or intraperitoneally, with or without a simultaneous injection of 10(8) whole killed B. pertussis organisms. Ten days later, all the rats were challenged with 5 micro g HDM via the trachea. Bronchial lymph nodes and bronchoalveolar lavage fluid (BAL) were collected 0, 2, and 4 days post-challenge. Coadministration of pertussis and intratracheal instillation of HDM enhanced HDM-specific lymphoproliferative responses and increased BAL levels of total protein, lactate dehydrogenase, HDM-specific IgE and IgG antibodies, and the number of eosinophils in BAL to the same extent as had occurred in the systemically immunized animals. The data show that intratracheal instillation of HDM induces a mild allergic sensitization in juvenile rats, and that ip injection with B. pertussis enhances this sensitization process to levels seen in animals injected with antigen and B pertussis together. These results suggest that simultaneous exposure to Th2-inducing vaccine components and allergenic proteins may be a risk factor for allergic sensitization and the development of asthma in susceptible individuals.

House dust mite allergen in US beds: Results from the first national survey of lead and allergens in housing

Background: Although exposure to house dust mite allergen is a major risk factor for allergic sensitization and asthma, nationwide estimates of dust mite allergen levels in US homes have not been reported. Objective: The purpose of this study was to estimate the prevalence of dust mite allergen in beds of US homes and to identify predictors of dust mite allergen concentration. Methods: Data were obtained from the first National Survey of Lead and Allergens in Housing, a cross-sectional survey of 831 permanently occupied noninstitutional housing units that permitted resident children. Dust mite allergen concentration (Der f 1 plus Der p 1) was determined from a dust sample collected from a bed. The percentages of homes with concentrations at or greater than detection, 2.0 μg/g bed dust, and 10.0 μg/g bed dust were estimated. Independent predictors of allergen concentration were assessed with multivariable linear regression. Results: The percentages of US homes with dust mite allergen concentrations at or greater than detection, 2.0 μg/g, and 10.0 μg/g were 84.2% (SE, 1.73), 46.2% (SE, 2.0), and 24.2% (SE, 2.1), respectively. Independent predictors of higher levels were older homes, non-West census regions, single-family homes, no resident children, lower household income, heating sources other than forced air, musty or mildew odor, and higher bedroom humidity. Conclusion: Most US homes have detectable levels of dust mite allergen in a bed. Levels previously associated with allergic sensitization and asthma are common in US bedrooms. Predictors can be used to identify conditions under which homes are more likely to have increased dust mite allergen levels. (J Allergy Clin Immunol 2003;111:408-14.)