While exposures to urban fine particulate matter (PM2.5) and soot-black carbon (soot-BC) have been associated with asthma exacerbations, there is limited evidence on whether these pollutants are associated with the new development of asthma or allergy among young inner city children. We hypothesized that childhood exposure to PM2.5 and the soot-BC component would be associated with the report of new wheeze and development of seroatopy in an inner city birth cohort.
As part of the research being conducted by the Columbia Center of Children’s Environmental Health (CCCEH) birth cohort study in New York City, two-week integrated residential monitoring of PM2.5, soot-BC (based on a multi-wavelength integrating sphere method), and modified absorption coefficient (Abs*; based on the smoke stain reflectometer) was conducted between October 2005 and May 2011 for 408 children at age 5–6 years old. Residential monitoring was repeated 6 months later (n=262) to capture seasonal variability. New wheeze was identified through the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaires during up to 3 years of follow-up and compared to a reference group that reported never wheeze, remitted wheeze, or persistent wheeze. Specific immunoglobulin (Ig) E against cockroach, mouse, cat, and dust mite and total IgE levels were measured in sera at ages 5 and 7 years.
PM2.5, soot-BC, and Abs* measured at the first visit were correlated moderately with those at the second visit (Pearson r > 0.44). Using logistic regression models, a positive association between PM2.5 and new wheeze was found with adjusted odds ratio [95% confidence intervals] of 1.51 [1.05–2.16] per interquartile range (IQR). Positive but nonsignificant association was found between the development of new wheeze and soot-BC and (OR 1.40 [0.96–2.05]), and Abs* (OR 1.57 [0.91–2.68]); Significantly positive associations were found between air pollutant measurements and new wheeze when restricting to those participants with repeat home indoor measurements 6 months apart. Associations between pollutants and IgE levels were not detected.
Our findings suggest that childhood exposure to indoor air pollution, much of which penetrated readily from outdoor sources, may contribute to the development of wheeze symptoms among children age 5 to 7 years.
indoor air pollution; long-term exposure; PM2.5; black carbon; wheeze; asthma; young children
Differential exposure to combustion by-products and allergens may partially explain the marked disparity in asthma prevalence (3%–18%) among New York City neighborhoods. Subclinical changes in airway inflammation can be measured by fractional exhaled nitric oxide (FeNO). FeNO could be used to test independent effects of these environmental exposures on airway inflammation. Seven and eight year-old children from neighborhoods with lower (range 3–9%, n=119) and higher (range 11–18%, n=121) asthma prevalence participated in an asthma case-control study. During home visits, FeNO was measured, and samples of bed dust (allergens) and air (black carbon) were collected. Neighborhood built-environment characteristics were assessed for the 500m surrounding participants’ homes. Airborne black carbon concentrations in homes correlated with neighborhood asthma prevalence (P<0.001) and neighborhood densities of truck routes (P<0.001) and buildings burning residual oil (P<0.001). FeNO concentrations were higher among asthmatics with compared to asthmatics without frequent wheeze (≥4 times/year) (P=0.002). FeNO concentrations correlated with domestic black carbon among children without seroatopy (P=0.012) and with dust mite allergen among children with seroatopy (P=0.020). The association between airborne black carbon in homes and both neighborhood asthma prevalence and FeNO suggest that further public health interventions on truck emissions standards and residual oil use are warranted.
Asthma; air pollution; airway inflammation; FeNO; residual oil
Background: Urban landscape elements, particularly trees, have the potential to affect airflow, air quality, and production of aeroallergens. Several large-scale urban tree planting projects have sought to promote respiratory health, yet evidence linking tree cover to human health is limited.
Objectives: We sought to investigate the association of tree canopy cover with subsequent development of childhood asthma, wheeze, rhinitis, and allergic sensitization.
Methods: Birth cohort study data were linked to detailed geographic information systems data characterizing 2001 tree canopy coverage based on LiDAR (light detection and ranging) and multispectral imagery within 0.25 km of the prenatal address. A total of 549 Dominican or African-American children born in 1998–2006 had outcome data assessed by validated questionnaire or based on IgE antibody response to specific allergens, including a tree pollen mix.
Results: Tree canopy coverage did not significantly predict outcomes at 5 years of age, but was positively associated with asthma and allergic sensitization at 7 years. Adjusted risk ratios (RRs) per standard deviation of tree canopy coverage were 1.17 for asthma (95% CI: 1.02, 1.33), 1.20 for any specific allergic sensitization (95% CI: 1.05, 1.37), and 1.43 for tree pollen allergic sensitization (95% CI: 1.19, 1.72).
Conclusions: Results did not support the hypothesized protective association of urban tree canopy coverage with asthma or allergy-related outcomes. Tree canopy cover near the prenatal address was associated with higher prevalence of allergic sensitization to tree pollen. Information was not available on sensitization to specific tree species or individual pollen exposures, and results may not be generalizable to other populations or geographic areas.
aeroallergen; allergic sensitivity; asthma; built environment; childhood disease; environmental agents; epidemiology; pollen; urban life
Allergy; bed bug; Cimex lectularius; IgE
Exposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAHs), can induce asthma. However, the effects of early repeated PAH exposure over time on different asthma phenotypes have not been examined.
To assess associations between repeated PAH exposure, measured from prenatal personal and residential indoor monitors in children's homes, and asthma in an inner-city cohort.
Prenatal exposure was assessed by personal air monitoring during 48 hours and exposure at 5 to 6 years of age by 2-week residential monitoring in the Columbia Center for Children's Environmental Health cohort. PAH was dichotomized into pyrene (representative semivolatile PAH) and the sum of 8 nonvolatile PAHs. High exposure to each was defined as measures above the median at both repeated time points. Asthma and wheeze were determined by validated questionnaires at ages 5 to 6 years. Children with specific IgE levels greater than 0.35 IU/mL to any of 5 indoor allergens were considered seroatopic.
Among all 354 children, repeated high exposure to pyrene was associated with asthma (odds ratio [OR], 1.90; 95% confidence interval [CI], 1.13-3.20). Among 242 nonatopic children, but not those sensitized to indoor allergens (n = 87) or with elevated total IgE levels (n = 171), high pyrene levels were associated positively with asthma (OR, 2.89; 95% CI, 1.77-5.69), asthma medication use (OR, 2.28; 95% CI, 1.13-4.59), and emergency department visits for asthma (OR, 2.43; 95% CI, 1.20-4.91). Associations between the levels of the 8 nonvolatile PAHs and asthma were not observed, even when stratifying by seroatopy.
Nonatopic children may be more susceptible to the respiratory consequences of early pyrene exposures.
Exposures to ambient air traffic-related pollutants and their sources have been associated with respiratory and asthma morbidity in children. However, longitudinal investigation of the effects of traffic-related exposures during early childhood is limited. We examined associations of residential proximity and density of traffic and stationary sources of air pollution with wheeze, asthma, and immunoglobulin (Ig) E among New York City children between birth and age 5 years.
Subjects included 593 Dominican and African American participants from the Columbia Center for Children’s Environmental Health cohort. Prenatally, through age 5 years, residential and respiratory health data were collected every 3-6 months. At ages 2, 3, and 5 years, serum IgE was measured. Spatial data on the proximity and density of roadways and built environment were collected for a 250 meter buffer around subjects’ homes. Associations of wheeze, asthma, total IgE, and allergen-specific IgE with prenatal, earlier childhood, and concurrent exposures to air pollution sources were analyzed using generalized estimating equations or logistic regression. In repeated measures analyses, concurrent residential density of four-way intersections was associated significantly with wheeze (odds ratio: 1.26; 95% confidence interval [CI]: 1.01, 1.57). Age 1 exposures also were associated with wheeze at subsequent ages. Concurrent proximity to highway was associated more strongly with total IgE (ratio of the geometric mean levels: 1.25; 95% CI: 1.09, 1.42) than were prenatal or earlier childhood exposures. Positive associations also were observed between percent commercial building area and asthma, wheeze, and IgE and between proximity to stationary sources of air pollution and asthma.
Longitudinal investigation suggests that among Dominican and African American children living in Northern Manhattan and South Bronx during ages 0 to 5 years, residence in neighborhoods with high density of traffic and industrial facilities may contribute to chronic respiratory morbidity, and concurrent, prenatal, and earlier childhood exposures may be important. These findings may have broad implications for other urban populations that commonly have high asthma prevalence and exposure to a high density of traffic and stationary air pollution sources.
Traffic; Asthma; IgE; Geographic information systems; Air pollution
Rationale: IgE antibodies to the mammalian oligosaccharide galactose-α-1,3-galactose (α-gal) are common in the southeastern United States. These antibodies, which are induced by ectoparasitic ticks, can give rise to positive skin tests or serum assays with cat extract.
Objectives: To evaluate the relationship between IgE antibodies to α-gal and asthma, and compare this with the relationship between asthma and IgE antibodies to Fel d 1 and other protein allergens.
Methods: Patients being investigated for recurrent anaphylaxis, angioedema, or acute urticaria underwent spirometry, exhaled nitric oxide, questionnaires, and serum IgE antibody assays. The results were compared with control subjects and cohorts from the emergency department in Virginia (n = 130), northern Sweden (n = 963), and rural Kenya (n = 131).
Measurements and Main Results: Patients in Virginia with high-titer IgE antibodies to α-gal had normal lung function, low levels of exhaled nitric oxide, and low prevalence of asthma symptoms. Among patients in the emergency department and children in Kenya, there was no association between IgE antibodies to α-gal and asthma (odds ratios, 1.04 and 0.75, respectively). In Sweden, IgE antibodies to cat were closely correlated with IgE antibodies to Fel d 1 (r = 0.83) and to asthma (P < 0.001).
Conclusions: These results provide a model of an ectoparasite-induced specific IgE response that can increase total serum IgE without creating a risk for asthma, and further evidence that the main allergens that are causally related to asthma are those that are inhaled.
α-gal; red meat allergy; ticks; total serum IgE; ectoparasite
Background: Recent cross-sectional studies suggest a link between butylbenzyl phthalate (BBzP) in house dust and childhood eczema.
Objectives: We aimed to evaluate whether concentrations of monobenzyl phthalate (MBzP), the main BBzP metabolite in urine, during pregnancy are associated prospectively with eczema in young children, and whether this association varies by the child’s sensitization to indoor allergens or serological evidence of any allergies.
Methods: MBzP was measured in spot urine samples during the third trimester of pregnancy from 407 African-American and Dominican women residing in New York City in 1999–2006. Repeated questionnaires asked mothers whether their doctor ever said their child had eczema. Child blood samples at 24, 36, and 60 months of age were analyzed for total, anti-cockroach, dust mite, and mouse IgE. Relative risks (RR) were estimated with multivariable modified Poisson regression. Analyses included a multinomial logistic regression model for early- and late-onset eczema versus no eczema through 60 months of age.
Results: MBzP was detected in > 99% of samples (geometric mean = 13.6; interquartile range: 5.7–31.1 ng/mL). By 24 months, 30% of children developed eczema, with the proportion higher among African Americans (48%) than among Dominicans (21%) (p < 0.001). An interquartile range increase in log MBzP concentration was associated positively with early-onset eczema (RR = 1.52 for eczema by 24 months; 95% confidence interval: 1.21, 1.91, p = 0.0003, n = 113 reporting eczema/376 total sample), adjusting for urine specific gravity, sex, and race/ethnicity. MBzP was not associated with allergic sensitization, nor did seroatopy modify consistently the MBzP and eczema association.
Conclusions: Prenatal exposure to BBzP may influence the risk of developing eczema in early childhood.
butylbenzyl phthalate; eczema; plasticizers
Asthma prevalence varies widely among neighborhoods within New York City. Exposure to mouse and cockroach allergens has been suggested as a cause.
To test the hypotheses that children living in high asthma prevalence neighborhoods (HAPN) would have higher concentrations of cockroach and mouse allergens in their homes than children in low asthma prevalence neighborhoods (LAPN), and that these exposures would be related to sensitization and asthma.
In the NYC Neighborhood Asthma and Allergy Study, a case-control study of asthma, 7–8 year old children from HAPN (n=120) and LAPN (n=119) were recruited through the same middle-income health insurance plan. Children were classified as asthma cases (n=128) or non-asthma controls (n=111) based on reported symptoms or medication use. Allergens were measured in bed dust.
HAPN homes had higher Bla g 2 (P=0.001), Mus m 1 (P=0.003) and Fel d 1 (P=0.003) and lower Der f 1 (P=0.001) than LAPN homes. Sensitization to indoor allergens was associated with asthma, but relevant allergens differed between LAPN and HAPN. Sensitization to cockroach was more common among HAPN than LAPN children (23.7% vs. 10.8%, P=0.011). Increasing allergen exposure was associated with increased probability of sensitization (IgE) to cockroach (P<0.001), dust mite (P=0.009) and cat (P=0.001), but not mouse (P=0.58) or dog (P=0.85).
These findings further demonstrate the relevance of exposure and sensitization to cockroach and mouse in an urban community and suggest that cockroach allergen exposure could contribute to the higher asthma prevalence observed in some compared with other NYC neighborhoods.
Asthma; Urban; Cockroach; Mouse; Dust mite; Allergy
To advance asthma cohort research, we need a method that can use longitudinal data, including when collected at irregular intervals, to model multiple phenotypes of wheeze and identify both time-invariant (eg, sex) and time-varying (eg, environmental exposure) risk factors.
To demonstrate the use of latent class growth analysis (LCGA) in defining phenotypes of wheeze and examining the effects of causative factors, using repeated questionnaires in an urban birth cohort study.
We gathered repeat questionnaire data on wheeze from 689 children ages 3 through 108 months (n = 7,048 questionnaires) and used LCGA to identify wheeze phenotypes and model the effects of time-invariant (maternal asthma, ethnicity, prenatal environmental tobacco smoke, and child sex) and time-varying (cold/influenza [flu] season) risk factors on prevalence of wheeze in each phenotype.
LCGA identified four wheezing phenotypes: never/infrequent (47.1%), early-transient (37.5%), early-persistent (7.6%), and late-onset (7.8%). Compared with children in the never/infrequent phenotype, maternal asthma was a risk factor for the other 3 phenotypes; Dominican versus African American ethnicity was a risk factor for the early-transient phenotype; and male sex was a risk factor for the early-persistent phenotype. The prevalence of wheeze was higher during the cold/flu season than otherwise among children in the early-persistent phenotype (P = .08).
This is the first application of LCGA to identify wheeze phenotypes in asthma research. Unlike other methods, this modeling technique can accommodate questionnaire data collected at irregularly spaced age intervals and can simultaneously identify multiple trajectories of health outcomes and associations with time-invariant and time-varying causative factors.
Previously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5 to 6 years, after controlling for current pollution exposure.
Prenatal PAH exposure was measured by personal air monitoring over 48 hrs. ETS exposure, respiratory symptoms and asthma at ages 5–6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap.
A significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p<0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95–4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41–1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5 to 6 years.
Combined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5–6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5 to 6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study.
Prenatal smoke exposure is associated with airway inflammation and asthma in children. It also increases the risk of low birth weight (LBW). LBW is associated with decreased lung function independently of smoking.
To study the independent and joint effects of prenatal smoking and LBW on childhood asthma.
In 1996, all children aged 7 to 8 years in 3 cities in northern Sweden were invited to an International Study of Asthma and Allergy in Childhood questionnaire survey. This study focused on the follow-up of children aged 11 to 12 years, in which 3389 children (96%) participated. A subset of 2121 children underwent skin-prick testing. Self-reported physician-diagnosed asthma has been clinically validated.
Mean birth weight was 3360 g in children exposed to prenatal smoking and 3571 g in nonexposed children (P < .001). The association of prenatal smoking with physician-diagnosed asthma was stronger in LBW children (risk ratio: 8.8 [95% confidence interval: 2.1–38]) than in normal birth weight children (risk ratio: 1.3 [95% confidence interval: 1.0–1.8]). LBW alone was not an independent predictor of asthma. These associations were similar in multivariate analysis, and the interaction term LBW × smoking was highly statistically significant.
There was a strong interaction of LBW and prenatalsmoking on the risk of physician-diagnosed asthma, which has not been demonstrated previously. This was consistently seen with adjustment for known risk factors, including allergic sensitization. Plausibly, airway inflammation from prenatal smoke exposure induces obstructive symptoms more easily in the underdeveloped airways of LBW children.
wheeze; child; prevalence; epidemiology; risk
Objectives and Hypothesis
To determine the feasibility of using a multiple flow offline fractional exhaled nitric oxide (FeNO) collection method in an inner-city cohort and determine this population’s alveolar and conducting airway contributions of NO. We hypothesized that the flow independent NO parameters would be associated differentially with wheeze and seroatopy.
As part of a birth cohort study, 9-year-old children (n = 102) of African-American and Dominican mothers living in low-income NYC neighborhoods had FeNO samples collected offline at constant flow rates of 50, 83, and 100 ml/sec. Seroatopy was defined as having measurable (≥0.35 IU/ml) specific IgE to any of the five inhalant indoor allergens tested. Current wheeze (last 12 months) was assessed by ISAAC questionnaire. Bronchial NO flux (JNO) and alveolar NO concentration (Calv) were estimated by the Pietropaoli and Hogman methods.
Valid exhalation flow rates were achieved in 96% of the children. Children with seroatopy (53%) had significantly higher median JNO (522 pl/sec vs. 161 pl/sec, P < 0.001) when compared to non-seroatopic children; however, median Calv was not significantly different between these two groups (5.5 vs. 5.8, P= 0.644). Children with wheeze in the past year (21.6%) had significantly higher median Calv (8.4 ppb vs. 4.9 ppb, P < 0.001), but not JNO (295 pl/sec vs. 165 pl/sec, P = 0.241) when compared with children without wheeze. These associations remained stable after adjustment for known confounders/covariates.
The multiple flow method was easily implemented in this pediatric inner-city cohort. In this study population, alveolar concentration of NO may be a better indicator of current wheeze than single flow FeNO.
asthma; atopy; offline FeNO method; alveolar NO; bronchial flux
Fractional Exhaled Nitric Oxide (FeNO) has been proposed as a biomarker of airway inflammation for cohort studies of asthma.
To assess the association between FeNO and asthma symptoms among seven-year old children living in an inner-city community. To test the association between ETS exposure (previous and current) and FENO among these children.
As part of a longitudinal study of asthma, children recruited in Head Start centers at age 4 years had offline FeNO and lung function testing at age 7 years. Children with allergen specific IgE (≥0.35 IU/ml) at age 7 were considered seroatopic. Environmental tobacco smoke (ETS) exposure at ages 4 and 7 was assessed by questionnaire.
Of 144 participating children, 89 had complete questionnaire data and achieved valid FeNO and lung function tests. Children with reported wheeze in the previous 12 months (n=19) had higher FeNO than those without wheeze (n=70) (geometric means 17.0 vs. 11.0ppb, p=0.005). FeNO remained significantly associated with wheeze (p=0.031), after adjusting for seroatopy and FEV1 in multivariable regression. FeNO at age 7 was positively associated with domestic ETS exposure at age 4 (29%)(β=0.36, p=0.015) but inversely associated with ETS exposure at age 7 (16%) (β= −0.74, p<0.001).
Given its association with current wheeze, independent of seroatopy and lung function, FeNO provides a relevant outcome measure for studies in inner-city communities. While compelling, the positive association between ETS exposure at age 4 and a marker of airway inflammation at age 7 should be confirmed in a larger study.
Exhaled Nitric Oxide; IgE; Inner-city; Wheeze; Environmental Tobacco Smoke
Prior research has linked maternal prenatal and postnatal mental health with the subsequent development of asthma in children. However, this relationship has not been examined in inner-city African Americans and Hispanics, populations at high risk for asthma.
To determine the relationship of maternal demoralization with wheeze, specific wheeze phenotypes, and seroatopy among children living in a low-income, urban community.
African American and Dominican women aged 18 to 35 years residing in New York City (the Bronx and Northern Manhattan) were recruited during pregnancy (n = 279). Maternal demoralization (ie, psychological distress) was measured both prenatally and postnatally by validated questionnaire. Outcomes included wheeze, transient (birth to 2.5 years of age), late onset (3–5 years), and persistent (birth to 5 years of age), evaluated via questionnaire and total and indoor allergen specific IgE (at birth and ages 2, 3, and 5 years). Logistic regression with generalized estimating equations assessed the association of demoralization with wheeze and atopy. Multinomial regression explored associations between demoralization and specific wheeze phenotypes.
Prenatal demoralization significantly predicted overall wheeze (adjusted odds ratio OR, 1.66; 95% confidence interval [CI], 1.29 –2.14), transient wheeze (OR, 2.25; 95% CI, 1.34 –3.76), and persistent wheeze (OR, 2.69; 95% CI, 1.52– 4.77). No association was found between demoralization and IgE after adjustment (total IgE: OR, 1.04; 95% CI, 0.74 –1.45; any specific IgE: OR, 0.96; 95% CI, 0.57–1.60).
In this inner-city cohort, prenatal demoralization was associated with transient and persistent wheeze. Understanding how maternal demoralization influences children’s respiratory health may be important for developing effective interventions among disadvantaged populations.
Cat ownership is inversely associated with atopy and asthma in some areas of the world, but the relevance of cat ownership to allergic disease in the inner city is less known.
We sought to evaluate the relationship between cat ownership and the development of early sensitization and wheeze.
By using a prospective birth cohort study, Dominican and African American mothers living in New York City underwent repeated questionnaires about their child from birth to age 5 years. Sera collected from children at ages 2 (n = 323), 3 (n = 336), and 5 (n = 242) years were assayed for anti-cat IgE and anti–Fel d 1 IgG antibodies.
Cat ownership was a significant risk factor for the development of anti-cat IgE by age 2 years (risk ratio [RR], 6.4; 95% CI, 1.9-22) but not for anti-cat IgE development between the ages of 2 and 5 years (RR, 0.88; 95% CI, 0.24-2.3). Current wheeze was significantly more common among those children with anti-cat IgE at ages 3 (RR, 3.5; 95% CI, 2.1-6.0) and 5 (RR, 3.4; 95% CI, 2.3-4.9) years. Cat ownership was inversely associated with current wheeze at age 5 years among children without anti-cat IgE (RR, 0.26; 95% CI, 0.083-0.81). Among children with anti-cat IgE, a similar trend was observed (RR, 0.57; P = .044, Fisher exact test), although one with borderline statistical significance.
Despite a positive association with sensitization, cat ownership in this inner-city cohort was inversely associated with wheeze, potentially suggesting an IgE-independent protective mechanism in this community.
Cat; asthma; allergy; wheeze; inner-city; rhinitis; IgE; IgG; Fel d 1
In 2009, we reported a novel form of delayed anaphylaxis to red meat, which is related to serum IgE antibodies to the oligosaccharide galactose-alpha-1,3-galactose (alpha-gal). Most of these patients had tolerated meat for many years previously. The implication is that some exposure in adult life had stimulated the production of these IgE antibodies.
To investigate possible causes of this IgE antibody response, focusing on evidence related to tick bites, which are common in the region where these reactions occur.
Serum assays were carried out using biotinylated proteins and extracts bound to a streptavidin ImmunoCAP.
Prospective studies on IgE antibodies in three subjects following tick bites showed an increase in IgE to alpha-gal of twenty-fold or greater. Other evidence included i) a strong correlation between histories of tick bites and IgE to alpha-gal (χ2=26.8, p<0.001), ii) evidence that these IgE antibodies are common in areas where the tick Amblyomma americanum is common, and iii) a significant correlation between IgE antibodies to alpha-gal and IgE antibodies to proteins derived from A. americanum (rs=0.75, p<0.001).
The results presented here provide evidence that tick bites are a cause, or possibly the only cause, of IgE specific for alpha-gal in this area of the United States. Both the number of subjects becoming sensitized and the titer of IgE antibodies to alpha-gal are striking. Here we report the first example of a response to an ectoparasite giving rise to an important form of food allergy.
ticks; anaphylaxis; oligosaccharide; alpha-gal; IgE antibody to CCD
Among preschool-age children in New York City neighborhoods with high asthma hospitalization rates, we analyzed the associations of total immunoglobulin E (IgE), specific IgE to common indoor allergens, and allergy symptoms with asthma.
Parents of children in New York City Head Start programs were asked to complete a questionnaire covering demographic factors, health history (including respiratory conditions), lifestyle, and home environment. Children’s serum samples were analyzed for total IgE and specific IgE antibodies to cockroach, dust mite, mouse, and cat allergens by immunoassay. Logistic regression was used to model the association between asthma and IgE, controlling for age, gender, ethnicity/national origin, BMI, parental asthma, smokers in the household, and allergy symptoms (e.g., runny nose, rash).
Among 453 participating children (mean age 4.0 ± 0.5 years), 150 (33%) met our criteria for asthma. In our multivariable logistic regression models, children with asthma were more likely than other children to be sensitized to each allergen, to be sensitized to any of the four allergens (OR=1.6, 95% CI 1.0–2.6), or to be in the highest quartile of total IgE (OR=3.1, 95% CI 1.5–6.4). Allergy symptoms based on questionnaire responses were independently associated with asthma (OR=3.7, 95% CI 2.3–5.9).
Among preschool-aged urban children, asthma was associated with total IgE and sensitization to cat, mouse, cockroach, and dust mite allergens. However, allergy symptoms were more prevalent and more strongly associated with asthma than was any allergen-specific IgE; such symptoms may precede elevated specific IgE or represent a different pathway to asthma.
asthma; allergy; IgE; children; Hispanic; indoor allergens
Acetaminophen has been associated with asthma and is in part metabolised via the glutathione pathway. Inner-city minority children have high asthma morbidity and a relatively high frequency of a minor allele variant in the glutathione S transferase Pi gene (GSTP1). We hypothesised that prenatal acetaminophen exposure would predict wheeze at age 5 years in an inner-city minority cohort and examined whether this association was modified by common polymorphisms in genes related to the glutathione pathway.
An ongoing population-based birth cohort study of Dominican Republic and African-American children in New York prospectively assessed the use of analgesics during pregnancy and current wheeze at age 5 years in 301 children. Genotyping was conducted for GST polymorphisms. Binomial regression was used to adjust for potential confounders including postnatal acetaminophen use.
34% of mothers reported acetaminophen use during pregnancy and 27% of children had current wheeze at 5 years. Prenatal exposure to acetaminophen predicted current wheeze (multivariate relative risk 1.71; 95% CI 1.20 to 2.42; p=0.003), and the risk increased monotonically with increasing number of days of prenatal acetaminophen exposure (p trend <0.001). 68% of children had at least one copy of the GSTP1 minor allele (Val). The risk of wheeze was modified by GSTP1 (additive interaction p=0.009) and was observed only among children with the GSTP1 minor allele.
Prenatal exposure to acetaminophen predicted wheeze at age 5 years in an inner-city minority cohort. The risk was modified by a functional polymorphism in GSTP1, suggesting a mechanism involving the glutathione pathway.
Conidia derived from a small number of common fungal genera are widely accepted as the etiological agents responsible for fungal allergic sensitization. The contribution of fungal conidia, spores, airborne hyphae, and subcellular fragments from other uncharacterized fungal genera remains unclear. In this proof-of-concept study, we examined the composition of mycoaerosols that atopic women were exposed and sensitized to in their own indoor environment using the fluorescent halogen immunoassay (fHIA).
Patients and Methods
Mycoaerosols were collected onto mixed cellulose ester protein binding membranes (PBMs) for 30 minutes with volumetric air sampling pumps. The PBMs were laminated with an adhesive cover slip and indirectly immunostained with individual patient serum IgE using the fHIA. Samples were examined using confocal laser scanning microscopy and immunostained particles were expressed as a percentage of total particles.
All air samples contained a broad spectrum of fungal spores, conidia, hyphae, and other fungal particulates. Airborne concentrations varied between individual study participant environments. Positively immunostained conidia belonging to moniliaceous amerospores, Cladosporium, Alternaria, and many unknown species were observed in the majority of air samples. Other fungal genera including Bipolaris, Curvularia, Pithomyces, and Stachybotrys, in addition to, ascospore genera and dematiaceous hyphal fragments released detectable allergen. Twelve percent of all fHIA haloes quantified in the analysis were directed towards fungal particles. No immunostaining was detected to conidia belonging to Epicoccum, Fusarium, and Spegazzinia species.
In addition to characterized fungal aeroallergens, we observed a wider composition of fungi that bound human IgE. Field surveillance studies that utilize immunodiagnostic techniques such as the fHIA will provide further insight into the diversity of fungi that function as aeroallergen sources in individual study participant environments.
allergen; Alternaria; Cladosporium; Conidia; Fungi; Hyphae; Immunoassay; Mold
Time trends for allergic sensitization are poorly known.
To compare the trends in prevalence of allergic sensitization and associated risk factors in children.
Two cohorts of children (age 7–8 years) were invited to skin prick testing (SPT) ten years apart, 1996 and 2006. Participation rate was 2148 (88%) and 1700 (90%), respectively. The methods were identical and ten common airborne allergens were used. An expanded ISAAC-questionnaire about symptoms and possible risk factors for allergic conditions was completed by the parents.
The prevalence of any positive SPT increased from 21% in 1996 to 30% in 2006 (p<0.001). The pattern of sensitization remained similar, and sensitization to cat was most common both years, 13% and 19%, respectively. Sensitization to mites and mould were uncommon in both surveys. A family history of allergy was a significant risk factor for a positive SPT both years (OR 1.7). Factors that in 1996 had a protective effect, i.e. rural living and having several siblings, had lost this effect in 2006. The prevalence of most risk factors remained similar, but respiratory infections and smoking among parents decreased significantly. During the same period there was no significant increase in prevalence of current wheeze (11.9% to 12.4%, n.s.) or symptoms of rhinitis or eczema.
The prevalence of allergic sensitization increased significantly from 1996 to 2006, while no increase in clinical symptoms was found. The parallel decrease in parental smoking and respiratory infections indicate a different influence of environmental factors on allergic sensitization and clinical symptoms, respectively.
allergic sensitization; atopic disease; epidemiology; OLIN; school children; skin prick test
Our work group report details the importance of pest allergen exposure in inner-city asthma. We will focus specifically on mouse and cockroach exposure. We will discuss how exposure to these pests is common in the inner city and what conditions exist in urban areas that might lead to increased exposure. We will discuss how exposure is associated with allergen sensitization and asthma morbidity. Finally, we will discuss different methods of intervention and the effectiveness of these tactics.
Asthma; allergies; environmental allergens; indoor allergens; pest; rodents; inner city; abatement; mouse; cockroach
The relationships between cockroach and mouse allergen exposure, anti-cockroach and anti-mouse IgE, and wheeze, rhinitis, and atopic dermatitis in children as young as age 3 years are of public health importance but have not been thoroughly evaluated.
We hypothesized that inner-city children might have anti-cockroach and anti-mouse IgE by age 3 years, and their presence would be associated with respiratory and atopic symptoms.
Children were followed prospectively from birth through age 3 years (n = 404). Residential levels of cockroach and mouse allergens, sera levels of anti-cockroach and anti-mouse IgE, and parental report of wheeze, rhinitis, and atopic dermatitis were measured.
The odds of early wheeze were significantly higher among children who had IgE to cockroach (odds ratio [OR], 3.3; 95% CI, 1.8-6.2), mouse (OR, 4.6; 95% CI, 2.3-9.0), or both (OR, 9.7; 95% CI, 3.4-27.3). The odds of rhinitis or atopic dermatitis were also higher among children with IgE to cockroach, mouse, or both. Higher IgE class to cockroach and mouse was associated with wheeze and atopic dermatitis (tests for trend, P < .002).
Children age 2 to 3 years who have anti-cockroach and anti-mouse IgE are at increased risk of wheeze and atopy. Moreover, a dose-response relationship was found between higher IgE class and increased prevalence of wheeze, rhinitis, or atopic dermatitis. These findings indicate the importance of reducing exposure to cockroach and mouse allergens for susceptible children.
Cockroach; mouse; allergy; wheeze; inner city; rhinitis; IgE; atopic dermatitis; eczema; asthma; sensitization
Season of birth has been associated with the development of atopy and asthma. Relationships among a particular birth season, maternal allergen exposure during the birth season, and childhood development of allergies to allergens in higher concentration during the birth season may be important.
To investigate the effects of winter birth (January 1 to March 31) and prenatal cockroach and mouse allergens in settled dust on indoor allergen–specific cord blood mononuclear cell (CBMC) proliferation, TH2 production, and cord blood IgE concentration.
As part of an ongoing prospective study, 350 cord blood samples were collected. The CBMCs were cultured with cockroach, dust mite, and mouse protein extracts, and proliferation was measured. Interleukin 5, interferon-γ, and total IgE levels were measured. Home dust samples were analyzed for cockroach and mouse allergens.
An isolated association was observed between winter birth and a greater mean (SD) cockroach interleukin 5 ratio (winter vs nonwinter birth: 26,043 [11,403] vs 11,344 [3,701]; P = .02). Other associations between winter birth and increased CBMC proliferation, T-helper cytokines, or cord blood IgE levels were not detected. Higher mouse allergen levels were associated with decreased mouse-induced proliferation (winter vs nonwinter birth: mean [SD] stimulation index, 1.72 [0.12] vs 2.02 [0.11]; P = 04).
Winter birth and increased cockroach or mouse allergen levels during pregnancy were not consistently abssociated with greater CBMC proliferation, T-helper cytokine production, or cord blood IgE levels. Greater indoor allergen exposure during pregnancy does not seem to affect the development of cockroach or mouse immune responses in utero.