Asthmatic Parents Research Articles

Comparative Dynamic Pulmonary Function Tests Between Apparently Healthy Young Adult Offspring of Asthmatic and Non-asthmatic Parents: A Pilot Study.

Background While the hereditary component of asthma has been established, its influence on early respiratory function changes in otherwise healthy offspring remains to be explored. Dynamic lung function tests assess airflow in and out of the lungs, providing valuable insights into respiratory health and detecting potential airflow limitations. This study aimed to compare the dynamic lung functions between offspring of asthmatic and non-asthmatic parents. Methodology A case-control design was employed comprising 30 cases (offspring of asthmatic parents) and 30 controls (offspring of non-asthmatic parents). Lung function parameters including forced vital capacity (FVC), forced expiratory volume in one second (FEV1), FEV1/FVC ratio, forced expiratory flow between 25% and 75% of the FVC (FEF 25-75%), and maximum mid-expiratory flow at 50% of the FVC (Vmax 50%) were measured. Statistical analysis was conducted to compare the parameters between cases and controls using the unpaired t-test. Results The mean age of controls was 20.46 ± 2.82 years and the cases was 19.83 ± 1.41 years. The study revealed that cases exhibited lower FEV1 and Vmax 50% values compared to controls, indicating potential airflow limitations and altered mid-exhalation flow rates in the offspring of asthmatic parents. While trends were observed in FVC, FEV1/FVC ratio, and FEF 25-75%, these differences were not statistically significant. Conclusions The findings suggest a potential association between parental asthma and altered lung function parameters, specifically in FEV1 and Vmax 50%, among their offspring. These early respiratory function changes underscore the potential impact of hereditary factors on lung health. Healthcare professionals should take parental asthma into account when evaluating lung functions. This may lead to earlier detection and intervention. Further investigation is warranted to elucidate the underlying mechanisms and long-term implications of these findings.

Asthma and selective migration from farming environments in a three-generation cohort study.

Individuals raised on a farm appear to have less asthma than individual raised elsewhere. However, selective migration might contribute to this as may also the suggested protection from farm environment. This study investigated if parents with asthma are less likely to raise their children on a farm. This study involved three generations: 6045 participants in ECRHS/RHINE cohorts (born 1945-1973, denoted G1), their 10,121 parents (denoted G0) and their 8260 offspring participating in RHINESSA (born 1963-1998, denoted G2). G2-offspring provided information on parents not participating in ECRHS/RHINE. Asthma status and place of upbringing for all three generations were reported in questionnaires by G1 in 2010-2012 and by G2 in 2013-2016. Binary regressions with farm upbringing as outcome were performed to explore associations between parental asthma and offspring farm upbringing in G0-G1 and G1-G2. Having at least one parent with asthma was not associated with offspring farm upbringing, either in G1-G2 (RR 1.11, 95% CI 0.81-1.52) or in G0-G1 (RR 0.99, 0.85-1.15). G1 parents with asthma born in a city tended to move and raise their G2 offspring on a farm (RR 2.00, 1.12-3.55), while G1 parents with asthma born on a farm were less likely to raise their G2 offspring on a farm (RR 0.34, 0.11-1.06). This pattern was not observed in analyses of G0-G1. This study suggests that the protective effect from farm upbringing on subsequent asthma development could not be explained by selective migration. Intriguingly, asthmatic parents appeared to change environment when having children.

Asthma prevalence and risk factors in early childhood at Northern Portugal

Asthma is the commonest and most important chronic non-infectious disease in childhood and it has become more prevalent in recent years. There is a shortage of studies in relation to early childhood and so, as part of the INAIRCHILD project, this cross-sectional study aimed to assess the prevalence of asthma and its associated risk factors, namely demographic, environmental, psychosocial and clinical factors for infants and preschoolers living in Northern Portugal. Data concerning asthma prevalence were collected through questionnaires based on those from the International Study of Asthma and Allergies in Childhood (ISAAC-derived), the questionnaires were distributed to 1042 children attending the 17 nurseries involved in the INAIRCHILD project (10 in urban and suburban context, and 7 in rural context). The response rate was 48%. Prevalence of asthma based on symptomatology and odds ratio was calculated. Around 52% of the studied children presented at least one of the respiratory symptoms investigated (wheeze, dyspnea and cough) in the absence of upper respiratory infections. The prevalence of asthma was 10.7%, comparable to the figures for Portuguese schoolchildren (6–7 years old) reported by the national Directorate-General of Health, thus showing that an early diagnosis might be possible and helpful for the mitigation of childhood asthma. Environmental context (urban, suburban or rural), gender and family asthma history showed clear associations with asthma prevalence, namely non-rural location, male gender, and having an asthmatic parent were found to be risk factors.

Sex-Based Differences in Asthma among Preschool and School-Aged Children in Korea.

The purpose of this study was to explore risk factors related to asthma prevalence among preschool and school-aged children using a representative national dataset from the Korea National Health and Nutrition Examination Survey (KNHANES) conducted from 2009–2011. We evaluated the demographic information, health status, household environment, socioeconomic status, and parents’ health status of 3,542 children aged 4–12 years. A sex-stratified multivariate logistic regression was used to obtain adjusted prevalence odds ratios (ORs) and 95% confidence intervals after accounting for primary sample units, stratification, and sample weights. The sex-specific asthma prevalence in the 4- to 12-year-old children was 7.39% in boys and 6.27% in girls. Boys and girls with comorbid atopic dermatitis were more likely to have asthma than those without atopic dermatitis (boys: OR = 2.20, p = 0.0071; girls: OR = 2.33, p = 0.0031). Boys and girls with ≥1 asthmatic parent were more likely to have asthma than those without asthmatic parents (boys: OR = 3.90, p = 0.0006; girls: OR = 3.65, p = 0.0138). As girls got older, the prevalence of asthma decreased (OR = 0.90, p = 0.0408). Girls residing in rural areas were 60% less likely to have asthma than those residing in urban areas (p = 0.0309). Boys with ≥5 family members were more likely to have asthma than those with ≤3 family members (OR = 2.45, p = 0.0323). The factors related to asthma prevalence may differ depending on sex in preschool and school-aged children. By understanding the characteristics of sex-based differences in asthma, individualized asthma management plans may be established clinically.

IL10 Family Member Genes IL19 and IL20 Are Associated With Recurrent Wheeze After Respiratory Syncytial Virus Bronchiolitis

Mechanisms underlying the increased risk of recurrent wheeze after respiratory syncytial virus lower respiratory tract infection (RSV LRTI) are unclear. Specifically, information about genetic determinants of recurrent wheeze after RSV LRTI is limited. We performed a candidate gene association study to identify genetic determinants of recurrent wheeze after RSV LRTI. We investigated 346 single nucleotide polymorphisms (SNPs) in 220 candidate genes in 166 Dutch infants hospitalized for RSV LRTI. Logistic regression analysis was used to study associations between genotypes and haplotypes and recurrent wheeze after RSV LRTI. We found associations with recurrent wheeze for SNPs in IL19, IL20, MUC5AC, TNFRSF1B, C3, CTLA4, CXCL9, IL4R, and IL7 genes. Haplotype analysis of the combined IL19/IL20 genotyped polymorphisms demonstrated an inverse association between the TGG haplotype and recurrent wheeze after RSV LRTI. IL19 and IL20 genes were notably associated with recurrent wheeze in infants without asthmatic parents. The association of IL20 SNP rs2981573 with recurrent wheeze was confirmed in a healthy birth cohort. We concluded that genetic variation in adaptive immunity genes and particularly in IL19/IL20 genes associates with the development of recurrent wheeze after RSV LRTI, suggesting a role for these IL10 family members in the etiology of airway disease during infancy.

Steroid Phobia among Parents of Asthmatic Children: Myths and Truth.

Asthma is one of the most common chronic diseases of childhood. Inhaled corticosteroids (ICS) are the recommended controller drug for asthma treatment. The aim of our study was to determine concerns and fears of parents of children with asthma towards the use of ICS. One hundred parents of asthmatic children were interviewed using structural questionnaire. Airway inflammation was reported by only 6% of interviewed parents, whereas airway narrowing was addressed by 34%. Interesting data, 71% of parents were concerned with the role of steroids in asthma treatment, but more than half (53%) of them addressed fears from side effects. Apparent gaps were found in knowledge of parents of asthmatic children about ICS as controller asthma medication. So, physician and health providers should explain to asthmatic parents that airway inflammation is the core for asthma management. This may remove fears about ICS and thus improve adherence to treatment.

Mannose‐binding lectin cord blood levels and respiratory symptoms during infancy: a prospective birth cohort study

Respiratory infections cause considerable morbidity during infancy. The impact of innate immunity mechanisms, such as mannose‐binding lectin (MBL), on respiratory symptoms remains unclear. The aims of this study were to investigate whether cord blood MBL levels are associated with respiratory symptoms during infancy and to determine the relative contribution of MBL when compared with known risk factors. This is a prospective birth cohort study including 185 healthy term infants. MBL was measured in cord blood and categorized into tertiles. Frequency and severity of respiratory symptoms were assessed weekly until age one. Association with MBL levels was analysed using multivariable random effects Poisson regression. We observed a trend towards an increased incidence rate of severe respiratory symptoms in infants in the low MBL tertile when compared with infants in the middle MBL tertile [incidence rate ratio (IRR) = 1.59; 95% confidence interval (CI): 0.95–2.66; p = 0.076]. Surprisingly, infants in the high MBL tertile suffered significantly more from severe and total respiratory symptoms than infants in the middle MBL tertile (IRR = 1.97; 95% CI: 1.20–3.25; p = 0.008). This association was pronounced in infants of parents with asthma (IRR = 3.64; 95% CI: 1.47–9.02; p = 0.005). The relative risk associated with high MBL was similar to the risk associated with well‐known risk factors such as maternal smoking or childcare. In conclusion the association between low MBL levels and increased susceptibility to common respiratory infections during infancy was weaker than that previously reported. Instead, high cord blood MBL levels may represent a so far unrecognized risk factor for respiratory morbidity in infants of asthmatic parents.

Biology, Social Environment, and Health: How Family History and Social Conditions Affect Adult Asthma*

Objective. We examine how multiple measures of both biological (family history of asthma) and social risk factors (home environment quality, socioeconomic status, and demographic characteristics) influence asthma risk among U.S. adults.Method. Using logistic regression models, we analyze data from a sample of 6,337 adults from the 2003–2004 National Asthma Survey.Results. Prevalence rates of current asthma are four times higher among adults with a family history of asthma, and the odds of having asthma are influenced most strongly by having asthmatic parents or grandparents (and, to a lesser extent, asthmatic siblings). We also find that social factors, especially characteristics of the home environment, significantly increase the odds of suffering from asthma as an adult.Conclusion. Our results show that all measures of family history are strongly linked to adult asthma prevalence, even when social factors are controlled. Social factors are also important, but very little of this is as a mediating influence that links family history and adult asthma; rather, family and social conditions have mostly independent effects.

Birth order, atopy, and symptoms of allergy and asthma among inner‐city children attending Head Start in New York City

In past research, children with older siblings were more likely than others to wheeze at age 2 years, but less likely by age 6 years. Higher infection transmission and a down-regulated allergic immune response as a result of these infections, respectively, were suggested as the causes. However, in a study of children aged 0-3 years in a low-income urban community in New York City, USA, with high asthma prevalence, we observed no birth-order effect. To evaluate the association between birth order and atopy and respiratory symptoms in 4-year-old children attending Head Start programs in NYC. Respiratory symptoms were assessed by questionnaire for 1005 children (mean age 4.0 years) living in high asthma prevalence neighbourhoods. Serum was collected from a subgroup of the children (n=494) and specific IgE responses to dust mite, cockroach, mouse, and cat allergens were measured. Prevalence of specific IgE (> or =0.35 IU/mL) did not differ significantly among first (35%), second (35%), and later-born children (28%) (P=0.23). Increasing birth order was associated with increasing prevalence of respiratory symptoms in the prior year, including wheeze (first 20%, second 27%, third or later 35%; P<0.001), being awakened at night by cough (28%, 33%, 38%; P=0.005), emergency department visits (14%, 17%, 21%; P=0.02) and hospitalizations for difficulty breathing (6.1%, 6.6%, 10%; P=0.04). The associations of birth order with respiratory symptoms were statistically significant only for the non-seroatopic children and those without an asthmatic parent. Non-seroatopic children with older siblings were more likely than those without older siblings to have respiratory symptoms at age 4 years. Although the stability of these associations over time remains to be determined, the differences in findings between this study and our previous NYC birth cohort study suggest that patterns of asthma development may vary even among low-income populations within the same city.

Prenatal origins of asthma and allergy.

The prevalence of asthma and related allergic disorders has increased considerably over the last 25 years. Genetic stock has not changed, so environmental factors must have influenced the phenotype. Infants who develop allergy already have an altered immune response at birth. We have investigated the development of immune responses during gestation and the effect of maternal allergen exposure during pregnancy and infant exposure in the first month of life on the development of allergy and disease. There was higher specific peripheral blood mononuclear cell proliferation to house dust mite (P = 0.01) and birch pollen (P = 0.004) in the third trimester compared with the second trimester, with the first positive responses seen at 22 weeks gestation. Maternal exposure to birch pollen after 22 weeks resulted in higher (P = 0.005) infant peripheral blood mononuclear cell responses to birch pollen at birth. Infants born at term, with at least one atopic, asthmatic parent, who developed allergic symptoms and positive skin prick test by one year of age had raised proliferative responses to house dust mites at birth compared to those with no symptoms (P = 0.01). In genetically predisposed individuals, antenatal factors, including maternal and thereby fetal exposure to allergens and maternoplacental-fetal immunological interactions, are active in determining whether an allergic predisposition is manifested as disease.

Chromosome 7p linkage and GPR154 gene association in Italian families with allergic asthma

Several genome scans have reported linkage of markers on chromosome 7p with asthma and related phenotypes in different populations. A fine mapping in Finnish and French-Canadian populations has associated the GPR154 gene (also known as G-protein-coupled receptor for asthma susceptibility, GPRA) with elevated IgE or asthma. To confirm chromosome 7p linkage and candidate gene association in Italian families with atopic asthma. In a two-phase approach, we first performed a linkage analysis of chromosome 7, and then a family-based association study on the GPR154 gene for allergic asthma phenotypes in the Italian population. The screening of 117 families with 19 microsatellite markers showed potential linkage for elevated IgE (P<0.002 at 22 cM from p-ter), asthma (P<0.005 at 44 cM), or atopy (P<0.005 at 54 cM). In the second phase of the present study, candidate gene GPR154, which is located in the phase one-linked region, was investigated in 211 families with seven single nucleotide polymorphisms (SNPs) that tag most haplotype variability, by the pedigree disequilibrium test. Elevated IgE levels were associated with two GPR154 gene SNPs (SNP 546333, P=0.0046; rs740 347, P=0.006), and with haplotypes in the global test (P=0.013). Haplotype analysis performed in nuclear families having at least 1 asthmatic parent showed a significant association with asthma (P=0.0173), atopy (P=0.0058), SPT (P=0.0025), and bronchial hyper reactivity (P=0.0163). These results support a susceptibility locus for asthma and related phenotypes on chromosome 7, and are in agreement with recent reports suggesting that a common susceptibility factor for atopic manifestations in asthma is likely conferred by the locus containing the GPR154 gene.

Differences in mite specific IgE between asthmatic parents and their offspring are large

RATIONALE: Numerous reports indicate that the incidence of allergies are increasing in modern societies. Questions arise as to whether this is due to improved reporting methods, growing patient awareness, use of better tests, or is actually due to environmental or lifestyle changes. While studying the genetics of asthma, a rather large difference was noted in the levels of specific IgE (s-IgE) to mites in asthmatic parents versus their offspring which is reported herein.

Lung function at age 3 years: effect of pet ownership and exposure to indoor allergens.

To investigate the effect of pet ownership and exposure to indoor allergens on lung function in 3-year-old children. Birth cohort study. Community. Children recruited prenatally and followed prospectively to age 3 years. Specific airway resistance (sRaw) (measured with body plethysmograph) at age 3 years; skin-prick tests; data on cat and dog ownership collected prospectively; allergen levels measured in dust collected from homes (high exposure defined as mite allergens >2 microg/g in mattress, and dog >10 microg/g and cat >8 microg/g allergens on the living room floor). There was no effect of cat or dog ownership at birth or age 3 years on lung function, and no association between lung function and mite, dog, or cat allergen exposure. Sensitized children exposed to high levels of sensitizing allergen had significantly poorer lung function (n = 49, sRaw kiloPascal per second [kPa/s]; geometric mean [GM], 1.20; 95% confidence interval [CI], 1.13-1.28) than children who were not sensitized and not exposed (n = 114; GM, 1.08; 95% CI, 1.04-1.12); not sensitized, but exposed (n = 282; GM, 1.07; 95% CI, 1.05-1.10); or sensitized and not exposed (n = 53; GM, 1.12; 95% CI, 1.06-1.18; P = .005). In a multivariate model, independent significant associates of lung function were maternal and paternal asthma, and the combination of sensitization and exposure to sensitizing allergen, with significant interaction between them. Lung function was substantially worse in sensitized and highly exposed children with both asthmatic parents (GM, 2.23; 95% CI, 1.68-2.97), compared with those with neither (GM, 1.09; 95% CI, 1.04-1.16) or just 1 of these features. Pet ownership, sensitization without exposure, or exposure in nonsensitized individuals have no effect on lung function. However, the combination of specific sensitization and exposure to sensitizing allergen is associated with significantly poorer lung function in early life.

Further support for the association of CCR5 allelic variants with asthma susceptibility.

English and German nuclear families containing multiple asthmatic children and asthmatic parents were analysed to retest a recently reported association between resistance to asthma and the delta32 allele of chemokine receptor 5 (CCR5). Analysis of the families by the transmission-disequilibrium test (TDT) revealed a non-significant trend in the English families that provided marginal confirmation of the association (P < 0.125), but no similar trend was observed in the German families. Case-control comparison of delta32 allele and genotype frequencies in asthmatic vs. non-asthmatic parents revealed a significantly lower frequency of delta32 in asthmatic English parents (P < 0.009) and a similar but non-significant trend in German parents (P < 0.265). Taken together, the pattern of results provides confirmation for the previously observed delta32-asthma association and indicates that susceptibility to asthma may be influenced by CCR5 or another gene in chromosomal region 3p21.

Role of TNF- α and its 55 and 75 kDa receptors in bronchial hyperreactivity

The pathophysiological role of the tumour necrosis factor (TNF) system was studied in adults (n=37) and children (n=43) non asthmatic offspring of asthmatic parents with and without bronchial hyperreactivity proved by methacholine airway challenge test. Serum TNF α and its soluble receptors (sTNF-R1 and R2) were determined by enzyme-linked immunosorbent assay (ELISA). Significantly elevated TNF α (adults: mean±SD=5·18±0·87 pg ml−1, children: 5·08±1·78)vs . non-hyperreactives (adults: 4·12±0·43, P<0·0001, children: 3·75±0·68, P=0·0084), sTNF-R1 (adults: 1·44±0·31 ng ml−1, children: 1·30±0·25 vs. adults: 1·21±0·14,P =0·0305, children: 1·13±0·11 ng ml−1,P =0·0042) and sTNF-R2 (adults: 0·85±0·40 ng ml−1, children: 0·70±0·46 vs. adults: 0·56±0·56 P=0·0084, children: 0·33±0·17, P=0·0048) and decreased sTNF-R1/R2 ratio (adults: mean±SD=0·96±0·73, children: 2·85±2·06 vs. adults: 4·82±3·40, P=0·0272, children: 4·42±2·30,P =0·0167) were measured in patients with bronchial hyperreactivity. The provocation doses of methacholine causing a 20% reduction (PD20) in forced expiratory volume in 1 sec (FEV1) were found to be in a significant negative linear correlation with TNF α, sTNF-R1 and R2 levels in hyperreactive adults and with TNFα , sTNF-R2 in hyperreactive children. TNF α correlated significantly with its receptors both in hyperreactive adults and children and with the body mass index (BMI) values of adults. The TNF system may contribute to the pathophysiology of bronchial hyperreactivity. Altered shedding of sTNF-R1 seems to occur in hyperreactive patients.

Family history and the risk of early-onset persistent, early-onset transient, and late-onset asthma.

Family history of asthma and allergies strongly influences asthma risk in children, but the association may differ for early-onset persistent, early-onset transient, and late-onset asthma. We analyzed the relation between family history and these types of asthma using cross-sectional data from a school-based study of 5,046 Southern California children. Parental and/or sibling history of asthma and allergy were generally more strongly associated with early-onset persistent asthma compared with early-onset transient or late-onset asthma. For children with two asthmatic parents relative to those with none, the prevalence ratio for early-onset persistent asthma was 12.1 [95% confidence interval (CI) = 7.91-18.7] compared with 7.51 (95% CI = 2.62-21.5) for early-onset transient asthma and 5.38 (95% CI = 3.40-8.50) for late-onset asthma. Maternal smoking in pregnancy was predominantly related to the risk of early-onset persistent asthma in the presence of parental history of allergy and asthma, and the joint effects were more than additive (interaction contrast ratio = 3.10, 95% CI = 1.45-4.75). Our results confirm earlier data that parental history of asthma and allergy is most strongly associated with early-onset persistent asthma and suggest that among genetically predisposed children, an early-life environmental exposure, maternal smoking during pregnancy, favors the development of early-onset asthma that persists into later early childhood.

Parental history and the risk for childhood asthma. Does mother confer more risk than father?

Although heredity plays a major role in asthma and in other allergic diseases, mechanisms underlying the inheritance of these disorders are poorly understood, as is the relative contribution of maternal and paternal conditions to risk of disease. We investigated doctor-diagnosed maternal and paternal asthma, eczema, and hay fever as cross-sectional predictors of childhood asthma and allergic disease in 306 children with a median age of 3.5 yr from families in which at least one parent had a history of either asthma or other allergic conditions. For both childhood asthma and eczema, the strongest parental predictors were the same conditions in the parents. For asthma in particular, maternal asthma was most strongly associated with asthma in the child over all ages in both univariate (OR = 3.2, 95% CI = 1.5 to 6.7) and multivariable (OR = 4.1, 95% CI = 1.7 to 10.1) models. Paternal asthma was weakly associated with childhood asthma in the univariate model (OR = 1.4, 95% CI = 0.6 to 3.2), but this association increased in magnitude in the multivariable model (OR = 2.7, 95% CI = 1.0 to 7.2). Among the children < 5 yr of age, the risk for childhood asthma associated with maternal asthma (OR = 5.0, 95% CI = 1.7 to 14.9) was greater than the risk associated with paternal asthma (OR = 1.6, 95% CI = 0. 5 to 5.9), whereas both maternal asthma and paternal asthma were associated with similar risks among children >= 5 yr of age (OR = 4. 6, 95% CI = 1.1 to 19.0 and OR = 4.1, 95% CI = 1.0 to 16.0, respectively). The odds of having a child with asthma were three times greater in families with one asthmatic parent and six times greater in families with two asthmatic parents than in families where only one parent had inhalant allergy without asthma; furthermore, inhalant allergy in one parent also conferred additional risk in the presence of asthma in the other parent. Further investigation is needed into the relative importance of genetic factors and in utero and postnatal exposures in determining the differential effects of maternal and paternal asthma on the development of childhood asthma.

The relationship between parental and children's serum IgE and asthma.

This paper examines the familial aggregation of physician-diagnosed asthma in relation to the age- and sex-standardized total serum IgE levels of children and their parents in a sample of the general population in Tucson, Arizona, that has been followed in a longitudinal study for over 20 yr. There were 591 nuclear families containing 1,177 children who provided information about the presence or absence of a physician diagnosis of asthma. The serum IgE data were less complete: both parents and one or more of their children in 251 of the nuclear families, containing 468 children, had serum IgE levels measured. There was a very strong tendency for asthmatic patients to have asthmatic children, but only a small part of this appeared to be related to the familial aggregation of total serum IgE. In the absence of an asthmatic parent, there was a slight but significantly higher prevalence of asthma in children of whom both parents had IgE levels in the highest tertile. Very high rates of children's asthma depended on there being an asthmatic parent who also had at least moderate levels of serum IgE. It was also shown that asthmatic children have considerably higher total IgE levels than would be expected on the basis of their parents' IgE levels alone. The data appear compatible with several familial-aggregation hypotheses and a strong environmental influence determining which children are likely to develop asthma. We speculate that the inflammation in the airways of asthmatic patients itself tends to increase the serum IgE level, possibly secondary to mediators that it generates.

Altered T lymphocyte phenotype at birth in babies born to atopic parents

Flow cytometry was used to analyse the cord blood T cells of 33 babies at high risk 'HR' for developing allergy (born to at least one atopic, asthmatic parent), and 10 low risk 'LR' babies (born to non-atopic parents), following normal term deliveries. Significantly lower numbers of CD25+, (activated) T cells (p < 0.005) were seen in the cord blood of the HR babies who had developed both allergic symptoms and positive skin prick tests by one year of age when compared with the LR group. CD45RO+ (memory) T cells were detected in both HR and LR babies with a trend for lower numbers of memory cells to be detected in HR infants who later developed allergic symptoms and/or positive skin prick tests. Significantly lower numbers of CD4+/CD45RO+ were seen in the cord blood of HR babies who developed allergic symptoms compared to HR babies who showed no sign of allergy by one year and to the LR babies (p < 0.05 and p < 0.005). The presence of activated and memory T cells at birth implies intra-uterine priming. The significantly lower numbers of memory T cells in the HR babies suggests a suppression of T cell activation or lack of antigenic priming in this group. This prenatal influence on babies born to atopic parents may have important implications with regard to the mechanisms underlying atopic sensitisation.

Bronchial Response to Methacholine in “Healthy” Children of Asthmatic Parents: Effect of Treatment with Cromolyn Sodium

Cumulative dose response curves to inhaled methacholine were established in 24 "healthy" children of asthmatic parents and 7 healthy children of healthy parents. Atopic children of asthmatic parents demonstrated higher bronchial hyperreactivity (BHR) than nonatopic children. The BHR was about ten times less than in the atopic parents of asthmatic children, indicating marked increase in BHR with age in atopic members of asthmatic families. Six weeks of treatment with cromolyn sodium (disodium cromoglycate) decreased BHR significantly (p less than 0.05) in eight atopic children, while no change occurred in BHR in five nonatopic children.