Atopy in Danish children and adolescents: results from a longitudinal population study.

BACKGROUND AND OBJECTIVE: Atopy is an objectively measurable trait related to the presence of rhinitis and asthma, but our knowledge about its longitudinal predictors is limited. Data from a 6-year follow-up study of a population sample of children and adolescents (n = 408), aged 7 to 17 years at enrollment, were analyzed to investigate the prevalence and predictors of atopy. METHODS: Case history, including allergic diseases and smoking habits, was obtained by interview and questionnaire. Skin prick test reactivity to common allergens, total serum IgE, airway responsiveness, and pulmonary function were measured using standard techniques. RESULTS: The point prevalence of atopy increased from the first to the second survey, 26% and 44%, respectively; 23% of the participants had a positive skin prick test only at the second survey. Sensitization to house dust mite (HDM) (P < .001), grass (P < .001), dog (P < .001), cat (P < .001), and birch (P = .02) increased significantly in both males and females. No gender differences in the prevalence of positive reactions were found at the first survey, whereas atopy to grass (P = .01) and HDM (P = .02) were more prevalent in males than in females at the second survey. Confining the analysis to participants who were found to be non-atopic at the first survey showed that exposure to maternal smoking (OR 2, CI 1.3 to 3.1; P = .002), increased serum IgE (OR 1.7, CI 1.2 to 2.3; P = .001), new asthma (OR 1.6, CI 1.2 to 2.7; P = .03), and new rhinitis (OR 2.1, CI 1.2 to 3.6; P = .01), but not active smoking, were associated with an increased risk for the presence of a positive skin prick test at the second survey. CONCLUSIONS: This longitudinal population study showed an increase in the point prevalence of atopy in Danish children and adolescents; and, furthermore, that exposure to maternal smoking during childhood, increased serum IgE, and new symptoms of asthma or rhinitis were associated with an increased risk for developing sensitization to common aeroallergens in late adolescence.     

Quantification of atopy and the probability of rhinitis in preschool children: a population-based birth cohort study

BACKGROUND: Atopy quantification using IgE levels/skin test diameter (SPT-MWD) may better predict the expression of rhinitis than using atopy as a dichotomous variable. OBJECTIVE: To investigate the association between the presence, temporal pattern and severity of rhinitis in preschool children and specific IgE levels/SPT-MWDs. METHODS: Children were followed prospectively to age 5 years in a whole-population birth cohort study. We administered questionnaires (n = 815), skin prick tested children (n = 717) and measured specific serum IgE (n = 478) to inhalant and food allergens. Main outcomes were current rhinitis (CR) and current rhinoconjunctivitis (CRC). RESULTS: The prevalence of CR and CRC was 26.1% and 12.1%, respectively. The risk of CR and CRC increased significantly with increasing IgE to grass, mite and cat; CRC was also associated with increasing IgE to dog and peanut. Similarly, increasing SPT-MWDs to inhalant allergens were significantly associated with CR and CRC. This association was also shown for grass within the group of atopic children. Perennial and seasonal rhinitis were associated with increasing IgE/SPT-MWD to mite and grass, respectively. Moderate/severe rhinitis was associated with increasing IgE/SPT-MWD to grass. In a multivariate analysis, increasing levels of IgE/SPT-MWD to grass were the strongest independent predictors of both CR (for IgE: OR 1.42, 95% CI 1.23-1.64, P < 0.001) and CRC (for IgE: 1.51, 1.30-1.76, P < 0.001). CONCLUSION: The probability of CR/CRC increases with increasing specific IgE levels or SPT-MWD. With respect to allergic rhinitis, the absolute levels of specific IgE antibody or the size of SPT wheal offer more information than just the presence/absence of sensitization.     

Farm environment in childhood prevents the development of allergies

BACKGROUND: A protective effect of infections in early life might explain the firmly reported finding of an inverse association between atopic disorders and large sibships. OBJECTIVE: To study the effect of childhood farm, rural non-farm and urban environment, as well as family size and other factors on the occurrence of asthma, wheezing and atopic disorders up to young adulthood. METHODS: Data on lifetime prevalence of physician-diagnosed asthma, allergic rhinitis and/or allergic conjunctivitis, atopic dermatitis, as well as self-reported episodic wheezing from 10 667 Finnish first-year university students aged 18-24 years were collected by a postal questionnaire. Associations of lifetime prevalence of the diseases with living on a farm, in a rural non-farm and urban environment during childhood were estimated by logistic regression analysis. Adjustment was made for potential confounding by gender, parental atopy, parental education, number of older siblings, day care outside the home and passive smoking. RESULTS: The childhood farm environment independently reduced the risk for physician-diagnosed allergic rhinitis and/or allergic conjunctivitis (adjusted odds ratio 0.63, 95% CI 0.50-0.79, P < 0.001), and for diagnosed asthma and episodic wheezing analysed together (OR 0.71, 95% CI 0.54-0.93, P < 0.05), but not for atopic dermatitis during lifetime. Urban childhood environment did not show independent increased risk when compared with rural non-farm residence. The inverse association of sibship size with the occurrence of allergic rhinitis and/or allergic conjunctivitis was found among subjects with one (OR 0.86, 95% CI 0.77-0.96, P < 0.01) or at least four older siblings (OR 0.47, 95% CI 0.26-0.84, P < 0.05). CONCLUSION: Childhood farm environment seems to have a protective effect against allergic rhinitis and/or conjunctivitis, and more weakly against asthma and wheezing irrespective of family size. Environmental exposure to immune modulating agents, such as environmental mycobacteria and actinomycetes, favouring manifestation of a nonatopic phenotype could explain the finding.     

Rhinitis in pre-school children: prevalence, association with allergic diseases and risk factors

BACKGROUND: The aim of our study was to assess the prevalence of rhinitis, sneezing, runny or blocked nose apart from colds in a pre-school children population and to evaluate the risk factors and relationship with allergic diseases and sensitization. METHODS: Eighteen nursery schools were randomly selected. The International Study of Asthma and Allergies in Childhood (ISAAC) written questionnaire (WQ) was distributed and filled by parents of pre-school children (3-5 years). The allergic sensitization to common aeroallergens and foods was evaluated by skin prick test (SPT). chi2 tests were used to compare proportions between rhinitic and non-rhinitic children. RESULTS: One thousand four hundred and two (92%) valuable questionnaires were returned. Prevalence of rhinitis in the last 12 months was 16.8%. Rhinitic children compared to non-rhinitic children presented a significant increase of diagnosed asthma (20.8% vs. 6.2%, P<0.001), lifetime wheezing (43.2% vs. 21.6%, P<0.001), wheezing in the last 12 months (25.0% vs. 9.4%, P<0.001), atopic dermatitis (22.9% vs. 13.9%, P<0.001) and allergic sensitization (29.9% vs. 13.7%, P<0.001). Sensitization to grass pollen and house dust mites were significant risk factors for rhinitis (P<0.01). A family history of atopy, having pets at home, male gender and greater age were significant risk factors for rhinitis, but not smoking exposure, sharing a bedroom or breastfeeding. CONCLUSIONS: In pre-school children rhinitis has a strong association with wheezing symptoms, asthma and atopic dermatitis. Allergic sensitization is a risk factor for rhinitis and should be evaluated even in pre-school children.     

Defining childhood atopic phenotypes to investigate the association of atopic sensitization with allergic disease

AIMS: Although atopic sensitization is common in childhood, its relationship to clinical allergic disease remains incompletely understood. We therefore sought to explore this relationship by defining sensitization based atopic phenotypes. METHODS: Children were recruited at birth (n = 1456) and reviewed at 1, 2, 4 and 10 years. Skin prick testing (SPT) to common allergens was done at 4 (n = 980) and 10 years (n = 1036) with lung function (n = 981), bronchial challenge (n = 784) and serum IgE (n = 953) testing at 10. Atopic phenotypes were defined, by sensitization pattern, for children with SPT at both 4 and 10 years (n = 823). RESULTS: Of phenotyped children, 68.0% were never atopic, 4.3% early childhood atopic (only atopic at age 4), 16.5% chronic childhood atopics (at 4 and 10 years) and 11.2% delayed childhood atopics (only at 10). Never atopics showed small but identifiable prevalence of allergic diseases such as asthma, eczema and rhinitis. Amongst allergen-sensitized subjects, aeroallergen predominated over food sensitization throughout childhood. Chronic childhood atopics showed highest prevalence of lifetime plus persistent wheeze, eczema and rhinitis, increased prevalence of aeroallergen sensitization, some evidence of persistent food sensitization, significantly greater cord IgE than never atopics (P = 0.006), plus higher total IgE (P < 0.001) and bronchial hyper-responsiveness (P < 0.001) at 10 years than other phenotypes. CONCLUSION: A proportion of childhood eczema, rhinitis and asthma is nonatopic. The commonest childhood pattern of atopy is chronic sensitization, associated with early, persisting and clinically significant allergic disease. The currently accepted childhood 'Allergic March' may oversimplify the natural history of childhood atopy and allergic disease.     

The relationship between atopy and non-specific bronchial responsiveness

Atopy is often regarded as a risk factor for the development of asthma, particularly childhood asthma and occupational asthma. This could reflect an association with non-specific bronchial responsiveness (NSBR), though atopy could influence asthma independently. We have evaluated the possible relationship between atopy and NSBR (PD20FEV1 to methacholine) in the siblings of 59 probands with atopic asthma. Thirty-four (58%) were atopic (greater than or equal to 1 prick test with weal diameter greater than or equal to that of a 0.1% histamine control) and 28 (47%) showed NSBR. Atopy and NSBR occurred together more frequently than would be expected by chance (P less than 0.05); both variables being observed in 20 subjects, neither in 17, and only one in 22. A significant association was also noted when atopy was defined by a serum total IgE greater than 150 IU (or greater than 50 IU), but when atopy was defined by other commonly used criteria (greater than or equal to 2 prick tests with weal diameter greater than or equal to histamine control; or weal diameter 2 mm or more greater than a saline control), no significant association was demonstrated. Furthermore, linear logistic regression and multiple regression analyses showed that both the presence and the degree of NSBR were influenced much more by the baseline level of FEV1 than by atopic status. At best, atopy accounted for 10% of the variance of the PD20 measurements. We conclude that atopy is associated with NSBR but not strongly; that the relationship may be readily obscured according to the defining criteria used for atopy; and that atopy should not be used as a marker for NSBR.     

A dual long-term effect of breastfeeding on atopy in relation to heredity in children at 4 years of age

BACKGROUND: The long-term effect of early feeding on atopic sensitization is still unsolved. The aim of this study was to evaluate the long-term effect of breastfeeding on atopy in groups of 4-year-old children stratified by atopic heredity. METHODS: We collected four groups of 4-year-old children from a birth cohort: two groups with differing backgrounds of atopic heredity, all exclusively breast-fed for at least 3 months; and two groups with differing atopic heredity, but all fed with cow's milk-based formula during their first weeks. The data were collected with a questionnaire, skin prick testing, and measurement of serum total and allergen-specific IgE levels. RESULTS: Breastfeeding significantly decreased the risk of allergic rhino-conjunctivitis [odds ratio (OR) 0.41, 95% confidence interval (CI) 0.18-0.95] and sensitization to furred pets, as measured by skin prick results, in children with atopic heredity, whereas in children without atopic heredity, breastfeeding was related to an increased risk of symptomatic atopy (OR 2.57, 95% CI 1.16-5.70), and high serum IgE values. A significant interaction was found between heredity and breastfeeding. CONCLUSIONS: The long-term effect of breastfeeding was dual: in children with atopic heredity, breastfeeding protected against atopy, whereas in children without atopic heredity, it increased the risk of atopy.     

Early childhood environment related to microbial exposure and the occurrence of atopic disease at school age

BACKGROUND: There is a growing body of evidence that the early childhood environment with respect to day care attendance, older siblings, pet ownership, and early life airway infections may protect from developing atopic disease. Few studies have distinguished between atopic sensitization and symptoms, and none have evaluated independent contributions for all of these different environmental conditions. OBJECTIVE: Examine independent effects on atopic sensitization and symptoms of day care attendance, older siblings, pet ownership, and early infancy's airway disease. METHODS: A cross-sectional survey among 8-13-year-old school children with complete data for 1555 children. RESULTS: After adjustment for confounders, atopic sensitization occurred less frequently in children that had attended a day care centre (OR: 0.73, 95% CI: 0.55-0.98) or had a cat or dog before 2 years of age (OR: 0.78, 95% CI: 0.61-0.99). Having older siblings yielded a nonsignificant trend towards protection (OR: 0.88, 95% CI: 0.70-1.11). For symptoms, there was no relation with having older sibs, day care attendance and pet ownership, although there was a trend towards protection for the combination of atopy and symptoms. In contrast, children with doctors' treated airway disease before age 2, more frequently reported recent symptoms of wheeze, asthma, rhinitis, or dermatitis (all P < 0.05). CONCLUSION: Early life environmental exposure to day care, or pets may protect against atopic sensitization. Protection against symptoms only occurred if atopic sensitization was present as well.     

Higher risk of infantile atopic dermatitis from maternal atopy than from paternal atopy

The risk of infantile atopic dermatitis (AD) posed by maternal atopy and paternal atopy, respectively, were compared in the infants from a birth cohort in whom one of the parents had been designated atopic by skin prick testing. Nineteen with atopic mothers were compared with 20 with atopic fathers. AD, other atopic manifestations and potentially influential factors such as breast-feeding were documented prospectively during the first year in all infants. At 3, 6 and 12 month assessments skin prick sensitivity and total serum IgE concentration were determined. Nine of 19 infants with atopic mothers and two of 20 with atopic fathers had AD (P = 0.023) giving a relative risk of 4.7 (95% confidence interval 2.5 to 9.0). Seven of 19 with atopic mothers and none with atopic fathers had AD with onset before 6 months (P = 0.007). When all types of disease evidence (AD, recurrent wheeze and food reactions) were analysed together no significant difference was apparent between the groups. The two groups were found to be well matched with regard to breast-feeding, time of starting cow's milk, solids and egg, sex, month of birth, parental AD and smoking, race, household pets and neonatal IgE concentration. IgE concentrations at each age and the prevalence of skin prick positivity were similar between the groups. Maternal atopy poses a higher risk for infantile AD and paternal atopy. Whether this may be due to genetic or congenital factors or both is uncertain, but clearly the finding is of relevance in the prediction of allergy in childhood.     

Do parents with an atopic family history adopt a ‘prudent’ lifestyle for their infant? (KOALA Study)

BACKGROUND: Atopic parents may adopt lifestyle characteristics that allegedly protect against atopic disease. If this is true, infants from atopic parents will be characterized by low-risk behaviour. Consequently, aetiologic studies on lifestyle factors and allergic disease in childhood may be biased by confounding by indication. OBJECTIVE: We explored whether the prevalence of 'prudent' lifestyle characteristics differs between atopic and non-atopic families. METHODS: Information about a family history of atopic manifestations and lifestyle characteristics was collected by repeated questionnaires in the Dutch KOALA Birth Cohort Study in 2469 infants from families with divergent lifestyle practices (conventional vs. alternative). RESULTS: In conventional lifestyle families, infants were less often exposed to environmental tobacco smoke when parents were atopic than when they were non-atopic (10.0% vs. 14.7%, P=0.001). In alternative lifestyle families, exposure to smoking was very rare in both groups (1.7% vs. 2.6%). Pets were less often present in families with than without parental atopy (38.8% vs. 51.1%, P=0.008 for conventional lifestyle families; 43.0% vs. 48.4%, P=0.014 for alternative lifestyle families). Infants with atopic siblings had less often been vaccinated according to the standard scheme than infants with non-atopic siblings in conventional lifestyle families (76.6% vs. 85.5%, P<0.001). In alternative lifestyle families, the difference was in the same direction but not statistically significant (30.1% vs. 40.5%, P=0.143). Antibiotic use, breastfeeding and consumption of organic foods were unrelated to a family history of atopic manifestations. CONCLUSION: Some 'prudent' lifestyle characteristics differed between atopic and non-atopic families, depending on whether atopic manifestations were present in parents or older siblings. This has important consequences for the validity in epidemiological studies on the aetiology of allergy in children. Confounding by indication because of a family history of atopic manifestations can best be controlled for by considering atopy in parents and siblings as separate confounders.     

Presence of atopy in first-degree relatives as a predictor of a female proband's depression: results from the Northern Finland 1966 Birth Cohort

BACKGROUND: Recent investigations suggest a common genetic rather than environmental cause to explain the association between IgE-mediated atopic allergies and depression. OBJECTIVE: Taking into account psychosocial confounding factors, we investigated separately and at the epidemiologic level the effects of maternal, paternal, and sibling atopy on the cumulative incidence of a child's depression. METHODS: We used an unselected, genetically homogenous, general population birth cohort of 12,058 live-born children in Finland. The 31-year prospective follow-up included questionnaire information on atopic disorders of the cohort members' parents and siblings. The probands' own atopic conditions were evaluated by means of skin prick tests, and information on lifetime depression diagnoses was gleaned from postal questionnaires and national hospital discharge registers. Potential confounders were mother's parity, father's social class, maternal smoking during pregnancy, proband's regular daily smoking, and proband's dwelling place. Total variable information was available from 4068 cohort members. RESULTS: Among female probands, the presence of atopy in parents was the strongest predictor for lifetime depression (P <.001), and sibling atopy and parental atopy were the strongest predictors for hospital-treated depression (P =.018 and P =.036, respectively). After controlling for confounders, it was noticed that maternal atopy increased a female proband's risk of lifetime depression up to 1.9-fold (odds ratio, 1.9; 95% CI, 1.1-3.0). The corresponding risk increased over 4-fold if parental-maternal atopy was combined with proband's own atopy. CONCLUSIONS: Our findings suggest that maternal inheritance could be a significant causative factor in the association between atopy and depression of female probands.     

Effect of animal contact and microbial exposures on the prevalence of atopy and asthma in urban vs rural children in India.

BACKGROUND: Environmental factors, including microbial exposures and close animal contact, are implicated in the lower prevalence of asthma and allergy in rural vs urban children. OBJECTIVES: To determine (1) the prevalence of asthma, rhinitis, eczema, and atopic sensitization in rural and urban children in India; (2) differences in microbial and animal exposures in these locales; and (3) whether differences in environmental exposures account for the different rates of asthma and atopy in these locales. METHODS: One child from each of 50 urban (Mysore) and 50 rural (Vinobha) households in southern India was randomly selected for data analysis. Allergy, asthma, health, environment, and lifestyle information was obtained using a questionnaire and household inspections. Atopy was determined via skin prick testing for common allergens. Endotoxin content was measured in house dust samples. RESULTS: Children from rural vs urban areas had lower prevalences of self-reported asthma (8% vs 30%; P = .005), rhinitis (22% vs 42%; P = .03), and atopic sensitization (36% vs 58%; P = .03). Higher median dust endotoxin loads were found in rural vs urban households (6.50 x 10(4) EU/m2 vs 1.27 x 10(4) EU/m2; P < .001). In multivariate analysis, close indoor animal contact (adjusted odds ratio [OR] 0.2; 90% confidence interval [CI], 0.05-0.9), outdoor animal contact (OR, 0.3; 90% CI, 0.1-0.8), and exclusive breastfeeding for at least 6 months (OR, 0.2; 90% CI, 0.1-0.5) were associated with lower atopic sensitization; mud flooring was associated with lower self-reported wheezing (OR, 0.1; 90% CI, 0.02-1.0). CONCLUSION: Children in India who live with close animal contact and mud flooring and who were exclusively breastfed in infancy are less likely to develop asthma, rhinitis, and atopic sensitization.     

Effects of dog ownership and genotype on immune development and atopy in infancy

BACKGROUND: Exposure to furred pets might confer protection against the development of allergic sensitization through a mechanism that is incompletely understood. OBJECTIVE: The objective of this study was to determine the effects of pet exposure and genotype on immunologic development and the incidence of atopic markers and diseases in the first year of life. METHODS: Pet exposure in the home was compared with cytokine secretion patterns (mitogen-stimulated mononuclear cells at birth and age 1 year) and indicators of atopy (allergen-specific and total IgE, eosinophilia, food allergy, atopic dermatitis) in 285 infants. Interactions with genotype at the CD14 locus were also evaluated in the data analyses. RESULTS: Exposure to dogs was associated with reduced allergen sensitization (19% vs 33%, P =.020) and atopic dermatitis (30% vs 51%, P <.001). The risk for atopic dermatitis was further influenced by genotype at the CD14 locus (P =.006), even after adjusting for exposure to dogs (P =.003). Furthermore, infants with the genotype -159TT were less likely to develop atopic dermatitis if they were exposed to a dog (5% vs 43%, P =.04). Last, dog exposure was associated with increased IL-10 (117 vs 79 pg/mL, P =.002) and IL-13 (280 vs 226 pg/mL, P =.013) responses at age 1 year. CONCLUSIONS: Having a dog in infancy is associated with higher IL-10 and IL-13 cytokine secretion profiles and reduced allergic sensitization and atopic dermatitis. These findings suggest that postnatal exposure to dogs can influence immune development in a genotype-specific fashion and thereby attenuate the development of atopy in at-risk children.     

Atopy and new-onset asthma in young Danish farmers and CD14, TLR2, and TLR4 genetic polymorphisms: a nested case-control study

BACKGROUND: Evidence exists that exposure to high levels of microbial agents such as endotoxin in the farm environment decreases the risk of atopic sensitization. Genetic variation in innate immunity genes may modulate the response to microbial agents and thus influence susceptibility to asthma and atopy. OBJECTIVE: To study potential associations between single nucleotide polymorphisms (SNPs) in CD14, Toll-like receptor 2 (TLR2), and TLR4 genes, and atopy and new-onset asthma in young farmers. METHODS: A nested case-control study was conducted within a cohort of 1901 young Danish farmers. We genotyped 100 new-onset asthma cases and 88 control subjects for three CD14 SNPs, three TLR2 SNPs, and two TLR4 SNPs. Atopy at baseline (defined as a positive skin prick test to one or more common inhalant allergens) was found in 17 asthma cases (17.0%) and in 17 controls (19.3%). RESULTS: The CD14/-260T allele was significantly associated with less atopy [odds ratio (OR) 0.39; 95% confidence interval (CI) 0.21-0.72, additive genetic model], whereas the CD14/-651T allele was positively associated with atopy (OR 2.53; 95% CI 1.33-4.80). Similar results were obtained by haplotype analysis. Stratified analysis by farm childhood showed stronger effects of both CD14 SNPs on atopy among farmers who were born and raised on a farm, although no significant interaction was found. No associations between CD14, TLR2, or TLR4 genotypes and new-onset asthma were found. CONCLUSION: The CD14/-260 and CD14/-651 promoter polymorphisms are associated with atopy prevalence among young adults exposed to farm environments.     

New pregnancies and loss of allergy

BACKGROUND: Inverse associations between allergic disease and sibship have been consistently described and are frequently explained by purported lower rates of early infection among children from small families. Alternative explanations include the possibility that pregnancy itself determines maternal atopic status. OBJECTIVE: To test the hypothesis that atopy defined by skin prick test (SPT) declines with increasing numbers of pregnancies. METHODS: At enrollment to a birth cohort, mothers were skin prick tested to three common allergens. Seven years later these women underwent a second SPT and provided information on their reproductive histories. At both visits, information on allergic disease was also sought. RESULTS: Twenty five (15%) women who were initially atopic were no longer so at the second visit; loss of hayfever symptoms was reported by 33 (29%) women. Women with higher numbers of intervening pregnancies were more likely to 'lose' their atopy (P=0.05) and symptoms of hayfever (P=0.02); this was not true for asthma. The findings could not be accounted for by maternal age. CONCLUSION: Successive pregnancies may in part determine a mother's atopic state. Since maternal atopy is a risk factor for childhood atopic disease, this process may affect the atopic state of successive children. These findings suggest an alternative explanation for the sibship effect in allergic disease.     

Sensitization to Alternaria and Cladosporium by the age of 4 years

Of 1218 children born on the Isle of Wight in 1989/90, and followed for atopy at age 4 years, 981 were skin-prick tested witha battery of allergens. Of these 61 (6%) reacted positively to Alternaria alternata and Cladosporium herbarum (47 to Alternaria, 21 to Cladosporium and seven to both). Twenty-four (39%) were asymptomatic (latent atopy) of which 12 had a single positive reaction either to Alternaria or Cladosporium. Asthma was the most common disease in children sensitized to moulds, Alternaria sensitization correlated positively with clinical diagnosis of asthma (P < 0.01), eczema (P <0.001) and rhinitis (P <0.05), Likewise, Cladosporium sensitivity correlated with a diagnoses of asthma, eczema and rhinitis (all P <0.05). Age of the house correlated with reported damp and lack of central heating (both P <0.001), but not with sensitization to moulds. An association between the presence of damp or age of the house and mould allergy was confounded by 21 children moving house in the first 4 years. Exposure to pets, passive tobacco smoking and season of birth had no bearing on mould sensitivity. At 4 years of age Alternaria and Cladosporium were the third most common causes of sensitization, i.e. after house dust mite and grass pollen.     

The association between mother and child MTHFR C677T polymorphisms, dietary folate intake and childhood atopy in a population-based, longitudinal birth cohort

Background A recent study suggested a link between folate metabolism and atopy, based on a positive association between a common polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene and allergic sensitization in Danish adults. Objective We investigated the associations between MTHFR C677T and allergy or atopy in a large, population‐based birth cohort of children and their mothers, the Avon Longitudinal Study of Parents and Children (ALSPAC). We also looked for evidence of a pre‐natal effect of maternal folate metabolism on subsequent atopic disease in the offspring. Methods Mothers were recruited in pregnancy and the children followed from birth. Atopy in the child was assessed at 7–8 years of age by skin prick tests to common allergens. Asthma was defined as a physician diagnosis and current symptoms at 71/2 years of age. Asthma and allergy status of the mothers were obtained from self‐completion questionnaires. Results Data on MTHFR C677T genotype and allergy were available for 5364 children and on allergy and/or asthma for 7356 mothers. In children, the prevalence of atopy was 20.0% and asthma 10.0% whereas in mothers, the prevalence of self‐reported allergy was 42.7% and asthma 11.5%. Atopy in the child was associated with male gender (P<0.001), less tobacco smoke exposure and higher maternal education. MTHFR C677T genotype was not associated with social factors or dietary folate intake. We found no evidence of associations between the MTHFR C677T variant allele and atopy, allergy or asthma in mothers or children. There was no evidence to support an effect of maternal MTHFR C677T genotype on atopy in the offspring. Conclusion The results of this study do not support the hypothesis that impaired folate metabolism is associated with allergy in adults or children in this population.     

Relationship between atopic status and nasal interleukin 10 and 11 levels in infants with respiratory syncytial virus bronchiolitis.

BACKGROUND: Interleukin 10 (IL-10) and IL-11 are known to have anti-inflammatory activities, and they have been implicated in the pathogenesis of respiratory syncytial virus (RSV) infection. OBJECTIVES: To determine IL-10, IL-11, and myeloperoxidase levels in nasal secretions of infants with acute RSV bronchiolitis and to investigate whether there are any differences in these levels in patients with vs without atopy. METHODS: We measured IL-10, IL-11, and myeloperoxidase levels in nasal secretions of 44 infants (20 were atopic) with acute RSV bronchiolitis. The nasal secretion samples were obtained from patients at hospital admission and were stored immediately at -70 degrees C until analysis. Atopy was defined as having at least 1 positive skin prick test reaction to common allergens, a history of atopic dermatitis, or a high serum IgE level compared with age-matched controls. RESULTS: Levels of IL-10, IL-11, and myeloperoxidase increased significantly in samples from infants with acute RSV bronchiolitis. Levels of IL-10 and IL-11 were significantly lower in patients with vs without atopy (P < .05). Myeloperoxidase levels showed no significant difference in patients with vs without atopy (P = .18). Patients with severe symptoms tended to have lower IL-10 levels (P = .09), but no relationship was shown between symptom severity and IL-11 levels. Nasal myeloperoxidase levels were significantly higher in patients with severe symptoms (P < .05). CONCLUSIONS: Production of IL-10 and IL-11 was significantly lower in patients with vs without atopy during acute RSV bronchiolitis. The airway inflammation induced by RSV infection may be different in patients with vs without atopy, and this is associated with lower induction of these immunoregulatory cytokines in children with atopy.