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Notes: Background In most epidemiological surveys the estimated prevalence of asthma is based on questionnaire responses, which may depend on the individual's perception as well as medical consulting habits in a given population. Therefore, measurement of bronchial hyper-responsiveness as a key feature of asthma has been suggested as an objective parameter for asthma.Objective The aim of the present study was to validate questionnaire responses on asthma and wheeze against bronchial response to hypertonic saline (HS) (4.5%) in populations previously shown to have a lower prevalence of asthma and allergies: farmers' children and children from anthroposophic families.Methods Children whose parents had completed a written questionnaire in the cross-sectional PARSIFAL-study were drawn from the following four subgroups: ‘farm children’ (n=183), ‘farm reference children’ (n=173), ‘Steiner schoolchildren’ (n=243) and ‘Steiner reference children’ (n=179). Overall, 319 children with wheeze in the last 12 months and 459 children without wheeze in the last 12 months performed an HS challenge.Results Odds ratios, sensitivity, specificity, likelihood ratios and measures of association did not differ significantly between the four subgroups. The correlation between the bronchial response to HS and wheeze and asthma questions was moderate and similar for farm children, farm reference children, Steiner schoolchildren and Steiner reference children (κ for ‘wheeze’: 0.25, 0.33, 0.31, 0.35, respectively, P=0.754, κ for ‘doctor's diagnosis of asthma’: 0.33, 0.19, 0.33, 032, respectively, P=0.499).Conclusion The findings from this study suggest that the reliabilitiy of questionnaire responses on asthma and wheeze is comparable between farmers' children, children raised in families with anthroposophic lifestyle and their respective peers.

Notes: Background Boys have been reported to be more susceptible to childhood wheezing, whereas girls are more susceptible later in life. This difference might be related to both genetic and environmental factors.Objective To investigate the influence of male sex and parental allergic disease on the development of childhood wheezing.Methods Infants (n=4089) born in Stockholm were recruited in a prospective study, BAMSE. Data on parental allergic diseases were obtained from questionnaires answered at the children's birth and on symptoms of wheezing at 1, 2 and 4 years of age. Sensitization to inhalant allergens and lung function was investigated at the age of 4 years.Results Children were classified as having recurrent, transient (n=266), early-onset persistent (n=319) and late-onset wheezing (n=195). Boys were over-represented in all groups of wheezing (odds ratio, OR=1.4–1.5) and both maternal and paternal allergic disease was of importance for the wheezing outcomes. A dominating influence from maternal allergic disease was only seen in children with persistent wheezing. An interaction exceeding additivity was found between male sex and parental allergic disease, particularly in children with persistent wheezing (OR=2.9 and 95% confidence interval, CI 95% 2.1–4.0 for boys with any parental history vs. OR=1.4, CI 95% 1.0–2.1 for girls). Interaction between male sex and parental allergic disease was also observed in children who wheezed at the age of 4 years and were sensitized to inhalant allergens.Conclusion Our data suggest an interaction between male sex and parental allergic disease in childhood wheezing, which may represent a sex-specific genetic influence.

Notes: Seventy similar bungalows constructed between 1968 and 1970 in the same suburban area of Stockholm were investigated regarding the content of house dust mite allergen, absolute indoor humidity, type of ventilation and basement construction. Houses with mechanical exhaust and supply ventilation had an indoor humidity above 7 g/kg less often than houses without this type of ventilation (Odds ratio 0.1, 95% confidence interval 0.0-0.2). Furthermore, only five of the 24 houses with exhaust and supply ventilation contained mattress dust mite allergen concentrations exceeding the median value (98.5 ng/g) compared with 30 of 46 hours which did not have such ventilation (odds ratio =0.1, C.I. 0.0–0.5). Houses with both natural ventilation and crawl space basement harboured significantly less mattress mite allergen than houses having the same type of ventilation, but with a concrete slab basement. In a cold temperate climate, type of building construction and ventilation seem to be important for the occurrence of house dust mite allergens in dwellings. Our results indicate that modern energy-efficient houses should be equipped with mechanical exhaust and supply ventilation to reduce indoor air humidity during the dry winter months and the risk of mite infestation.

Notes: Background The aetiology of atopic dermatitis (AD) is presumably multi-factorial, with interactions between genetic and environmental factors.Objective To investigate the relation between atopic family history and development of AD up to 4 years.Methods Using annual questionnaires, we studied the cumulative incidence of AD in 0–4-year-olds in a prospective birth cohort of 4089. Atopic diseases in parents and siblings were recorded at birth. The occurrence of serum immunoglobulin E (IgE) antibodies to inhalant and food allergens was analysed in 2614 4-year-olds, and AD was divided into non-IgE-associated and IgE-associated.Results Of the children without atopic parents, 27.1% developed AD; of those with single or double parental atopic history, 37.9% and 50.0%, respectively, did so. The effects of parental history of eczema and of atopic respiratory disease (ARD) did not differ significantly, nor did those of maternal and paternal history. Parental history of ARD increased the risk significantly more for IgE-associated AD than for non-IgE-associated AD (odds ratio (OR) 2.0; 95% confidence interval (CI) 1.5–2.8 vs. OR 1.3; 95% CI 1.0–1.8), whereas the two forms lacked major differences in the effect of parental eczema. A history of eczema in older siblings was a risk indicator for both forms of AD (OR 2.1; 95% CI 1.4–3.3 vs. OR 1.8; 95% CI 1.2–2.6).Conclusions We found no difference between the effects of maternal and paternal atopic history. Parental eczema was a risk factor for AD irrespective of its association with IgE, but parental history of ARD mainly increased the risk of IgE-associated AD.

Notes: Background The relation between socioeconomic status and allergic diseases in childhood is controversial. Some studies have proposed childhood asthma to be more common in families with low socioeconomic status, while sensitization to airborne allergens seems to be more frequent in individuals with higher socioeconomic status in childhood.Objective To assess the relation between socioeconomic status and asthma, rhinitis and sensitization in an unselected prospective birth cohort.Methods Four thousand and eighty-nine families with children born 1994–1996 in predefined areas of Stockholm answered questionnaires on environmental factors, socioeconomic status (parental occupation), and symptoms of allergic disease at birth, 1, 2 and 4 years of age. Blood samples taken at 4 years from 2614 children were analysed for specific IgE to common airborne and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) for various outcomes in relation to socioeconomic status were estimated with a multiple logistic regression model, adjusting for potential confounders such as heredity for allergic diseases, maternal smoking, short duration of breastfeeding and house construction.Results There was a decreasing risk of asthma and rhinitis with increasing socioeconomic status. The OR for asthma was 0.33 (95% CI 0.17–0.66) and for rhinitis 0.50 (0.32–0.79) comparing the highest and the lowest socioeconomic groups, with a tendency to stronger effects in those with heredity for allergic disease. The risk of sensitization to food allergens also decreased with increasing socioeconomic status; OR 0.65 (0.41–1.02) in the highest socioeconomic group (Ptrend=0.03), which was not clearly seen for airborne allergens.Conclusion Asthma, rhinitis and sensitization is more common in lower than in higher socioeconomic groups after adjustment for traditional risk factors. This may be related to additional uncontrolled differences in life style and environmental exposures between the groups, and calls for further studies.

Notes: Introduction There are conflicting data on the association between early exposure to pets and allergic diseases. Bias related to retrospective information on pet ownership has been addressed as a reason for distorted study results.Objective To elucidate how early exposure to cat and dog relates to IgE-sensitization and asthma in children at 2 and 4 years of age, in a prospective birth-cohort study.Methods Four thousand and eighty-nine families with children born 1994–1996 in predefined areas of Stockholm answered questionnaires on environmental factors and symptoms of allergic disease at birth, one, two and four years of age. Dust samples collected from the mothers' beds at birth were analysed for Fel d 1 and Can f 1 in a subgroup of the cohort. Blood samples taken at four years from 2614 children were analysed for allergen-specific IgE to common airborne allergens. Risk associations were calculated with a multiple logistic regression model, with adjustment for potential confounders.Results A correlation was seen between allergen levels and reported exposure to cat and dog. Exposure to cat seemed to increase the risk of cat sensitization, OR (odds ratio) 1.44 (95% confidence interval 1.03–2.01), whereas dog exposure did not have any effect on dog sensitization, OR 1.16 (0.79–1.72). Dog ownership was related to a reduced risk of sensitization to other airborne allergens, OR 0.36 (0.15–0.83), and a similar tendency was seen for cat ownership OR 0.63 (0.37–1.07). Early dog ownership seemed to be associated with a lower risk of asthma, OR 0.50 (0.24–1.03), with no corresponding effect after cat ownership, OR 0.88 (0.56–1.38).Conclusion Early exposure to cat seems to increase the risk of sensitization to cat but not of asthma at 4 years of age. Dog ownership, on the other hand, appears to be associated with lowered risk of sensitization to airborne allergens and asthma. Both aetiological relationships and selection effects have to be considered in the interpretation of these findings.

Notes: Increased concentrations of mast cell tryptase in post mortem blood have frequently been observed in sudden infant deaths but the cause of this has not yet been clarified.〈section xml:id="abs1-2"〉〈title type="main"〉ObjectiveThe aim was to evaluate factors (immunological, morphological and anamnestic data) behind the observed increase in mast cell tryptase in sudden infant deaths with elevated tryptase.〈section xml:id="abs1-3"〉〈title type="main"〉MethodsMast cell tryptase and total immunoglobulin (Ig) E were measured in post mortem sera from 44 infants younger than 1.5 years. Radioallergosorbent tests were performed for possible allergens (mixture for relevant food allergens, Phadiatop and latex). IgG subclasses, IgM, and complement factors (C3, C4 and factor B) were measured with radial immunodiffusion. Mast cells, labelled with antibodies against mast cell tryptase, were counted in the lungs and heart. The circumstances of death and medical history of the deceased infant and family were obtained through police and hospital records.〈section xml:id="abs1-4"〉〈title type="main"〉ResultsIn 40% of the SIDS cases tryptase was elevated (〉10 μg/L). Total IgE in serum was increased in 33% compared with clinical reference values but showed no association with mast cell tryptase. RAST tests were positive in three cases. In one of these cases both tryptase and total IgE were elevated. The only variable that was associated with high tryptase values was prone position at death (P ≤ 0.05 ). Allergy or asthma in the family were alleged in 50% of the cases, but was not associated with elevated tryptase or IgE. Children with elevated total IgE also displayed high concentrations of IgG1 and IgG2. Infants who died in the spring had significantly higher IgE than the others (P ≤ 0.05).〈section xml:id="abs1-5"〉〈title type="main"〉ConclusionThe results do not support the hypothesis that the elevated tryptase concentrations in sudden infant death are caused by allergy. The association between prone position at death and elevated tryptase could hypothetically be explained by mast cell degranulation due to, for example, a hypoxic stimulus in these infants.

Notes: Associations between parental educational level and possible risk factors for atopic disease during the first months of life were explored in a cohort of 4089 neonate children born 1994–96 in Stockholm, Sweden. Reports concerning a number of life style factors during pregnancy and after the baby was born were obtained by questionnaire. There was a strong negative association between duration of education and maternal smoking during pregnancy, parental smoking after the baby was born and keeping of cat and dog (p-trend 〈 0.001), respectively. For example, smoking during pregnancy was reported by 6.7% (95% CI 5.5–7.9) of mothers with college or university degree and by 22.2% (95% CI 20.1–24.5) of those with the shortest education. Indicators of dampness and poor ventilation were also more common in homes of those with the shortest education. The results show that the educational level has an influence on risk factors for development of atopic disease in childhood and indicates a need of deeper understanding of life style in different socioeconomic groups. The data also indicate that various possible confounding factors need to be thoroughly investigated when analysing studies of risk factors for allergic disease in childhood.

Notes: To examine the association between environmental exposure during the first two years of life and development of atopic disease later in child-hood, 115 children sensitized to airborne allergens and 54 non allergic controls were investigated. Fifty-seven of the atopic children were skin prick test (SPT) positive to house dust mites (HDM). Information on exposure was obtained from questionnaires. Parental allergy was a more important risk factor for development of atopy than any of the environmental risk factors. Exposure during the 2 first yr of life to environmental tobacco smoke (ETS) and home dampness was more frequently found among the HDM-sensitized children than among the controls (OR = 2. 8, CI 1. 0-7. 3 and OR = 4. 6, CI 1. 4-15. 0 respectively). A combination of these two factors seemed to be particularly harmful (OR = 8. 7, CI 2. 3-33. 1). Similar but less pronounced effects were seen for children with other allergies. Later in life exposure both to dampness and ETS was of the same magnitude in the atopic children as in the controls. It appears that exposure to environmental factors during the first few years of life may trigger for development of atopic disease and that interactions may be of particular importance.

Notes: This paper argues that with a certain allergen profile of airborne and food allergens and the use of total IgE-antibody levels, combined with the number of allergens positive at test represent a powerful tool to identify allergic disease in childhood. The allergens featured in such a profile will be dependent on the subject's age and geographical location.