In the present study the prevalence of current wheezing based on the corresponding ISAAC core question "Has your child had wheezing or whistling in the chest in the past 12 months?" was 9.3% among the 6–12-year-old children in the metropolitan area. Physician-diagnosed asthma had a 6.5 % of prevalence (Tables 1 & 2). Union of these two sets of students defined a cumulative asthma prevalence at 12.6 % (Table 2). Hungary participated with two centers in the phase three study of ISAAC in 2003, but none represented the capital. A survey (ISAAC ID 047002) covering schools of two cities from the southeastern lowland of Hungary involved solely the 13–14 age group. Out of the 2899 students who had completed the written questionnaire 204 (7.1 %) reported wheeze in the previous year (6). The other study (ISAAC ID 047001) indicated a 6.6% and 5 % prevalence of current wheeze in the 6 -7-year-old and 13–14-year-old group respectively (6). The overall higher prevalence of the contemporary sampling frame's current wheezing can be either due to the urban environment or a gradually increasing prevalence in the fifteen-year timeframe.
From a Central European perspective, the prevalence of asthma shows heterogeneity. Aberle et al. reported 7.9% of current wheezing and 4.1% of diagnosed asthma among 10–11-year-old students in neighboring Croatia (7). Their survey provided evidence that more boys (63.2%) had asthma. The gender-specific relations are consistent with our results. However, the geographical features of the investigated area resembled Hungary, the level of urbanization did not approximate Budapest, which can explain the higher prevalence in our settings. Results of the Croatian study are more comparable with and more congruent to the former ISAAC surveys conducted in Hungary (ISAAC ID 047001 & 047002) (6).
An almost population-wide screening of primary school students was carried out in Tyrol, Austria (8). The mean age of the participants was 8.4 years (SD ± 1.2). Besides the current wheezing, defined by the ISAAC manual, they used an extended definition for asthma by massing subjects with current wheeze or use of an asthma spray ever or recurrent wheezy bronchitis or a doctor diagnosis. 10.3 % of the total study population had current wheezing, which is 1 % higher than in our subjects. Doctor-diagnosed asthma was at 3.4 %. Based on their residence, Tyrolean students were sub-classified into farm children, rural children and Innsbruck-town children, and their exposure to particular agents (e.g. hay-loft, animal shed or farm milk). They found living on a farm as protective but only for those with regular exposure to farming agents. In our study, children commuting from the suburbs had a lower risk of asthma. With no history of exposure to particular agents 21.3 % of Innsbruck-town children fulfilled the extended criteria of asthma. This is 1.70 times higher than our cumulative asthma results, which can be due to either the regional differences or the different sampling protocol.
In a study from Romania, asthma-like symptoms (dominantly dry cough) were reported among 20% of the participating students (9). 48% of the subjects were exposed to environmental tobacco smoke, one of the expected triggers responsible for the high rate of symptoms.
Out of our participants, 9.65% (n = 370) shared their home with a smoker relative (Additional file 1), which is a remarkable difference compared to the Romanian data. Sixty-eight (18.15%) out of them fit into the CA group and verified tobacco exposure as a major risk factor for asthma (Fig. 3). Indoor tobacco fume also impacts other respiratory outcomes in children, including pneumonia, night cough and croup (10).
Increasing evidence has confirmed mould as another predisposing factor in children (11–15). Visible mould can be a source of fungal spores and other volatile organic compounds. These viable and non-viable particles are sufficient enough to increase the risk of asthma (13). In our sample, mouldy surfaces doubled the chance of asthma development (Fig. 3). Fagbule and Ekanem found that mould was only harmful in the bedroom, and on the contrary, it had a somehow protective effect elsewhere at home (16). The authors noticed that children could also benefit from indoor plants (16). Our study also revealed this favorable correlation between the presence of plants in the bedroom and asthma prevalence (Fig. 3). It is challenging to explain this phenomenon because potted plants' soil could serve as an origin for fungal and other biological agents.
The literature is controversial on the role of pet allergens in asthma prevalence (17–19). We found that overall pet ownership did not associate with asthma in accordance with current meta-analyses (19); however, pet-specific risks differed. A UK birth cohort showed that early childhood ownership could have a prophylactic effect, but surrounding rabbits or rodents could contribute to non-atopic asthma with a higher-odds (20). Exposure to mouse antigens could associate with wheezing (21). Among the subjects of the current study, a rodent's presence resulted in lower odds of asthma (Fig. 3). Inconsistency might be a result of a non-species-specific investigation. In addition, rodents were subjects of leisure pet ownership in our study, but the exposure to their antigens can also be from pests invading households. Such circumstances may also associate with other pollutive agents and a lower socioeconomic environment. Our observations concluded dog-keeping as a potential risk factor of asthma, but cat-ownership did not (Fig. 3). An explanation could be the so-called cat paradox (20, 22, 23). The increased odds associated with dog ownership argue with the contemporary view (19). The latter statistical relationship seems plausible but might be casual; a more detailed assessment of pet ownership should be conducted in the future.
Outdoor air pollution also plays a role in asthma development. In the current setting, the proximity of any air-polluting factories or heavy vehicle traffic associated with the risk of asthma (Fig. 3). Although numerous reports support these findings, from an environmental health point-of-view the particular composition and concentration of airborne pollutants instead reflect the association (24–27).
The protective effect of suburban living can also be a surrogate reference of this association between air pollution and asthma because exposure to ubiquitous atmospheric agents is suspected to be lower at those sites.
Living in a weedy area is considered a risk factor of asthma development with an OR of 1.3319 (Fig. 3). It is also associated with allergic rhinitis prevalence in the same environment, where common ragweed Ambrosia artemisiifolia is the most widespread cause of allergy-associated symptoms (28). However, a higher level of pollen load showed a non-significant association with allergy risk in Budapest (29). Despite the geographical distance, it is worth noting that 14% of asthmatic children of the 3–11-year-old population sensitized against ragweed in a US-based study (30).
Measurement of physical activity is challenging to carry out: besides the duration and frequency, the intensity is supposed to be a question of interest. Questionnaire-based research is a limiting factor of good quality and comparable data. Our current survey reported a significant association when children realizing vigorous activity more than three times a week were less likely to be in the cumulative asthma group (Table 5). Visual display time as a reference for sedentary lifestyle correlated with the odds ratio of asthma, but the relationship was not statistically significant (Table 5).
The ISAAC Phase Three summarised similar tendencies, but the methodology was different (31). Other studies with different approaches reported an ambiguous correlation between physical activity and asthma prevalence (32–36). We must emphasize that asthma has also been reported as a barrier to physical activity; thus, in the future, we should analyze this relation through an interdisciplinary lens (32). Emerging technologies, including wearable biosensors or smartphone applications, may serve as more accurate physical activity data resources in the future.
Dietary patterns influence the risk of asthma development. A Mediterranean-style diet, rich in fruits, vegetables and whole grains while taking less meat and dairy in, and other plant-based foods have associated with reduced odds for asthma (37–41). A Westernized diet, including a predominant amount of animal products with higher fat intake and lower fibre consumption, is a risk factor of asthma (39). It would be welcome to keep adherence to a healthier diet where it is already historically and geographically predisposed; trends showed an increased prevalence of asthma symptoms in the Mediterranean and Latin-America (39, 42). In the current sampled population, such emblematic meals of urbanized living like fast-food and drinks with artificial additives associated with cumulative asthma (Fig. 4).
Regular consumption of margarine also showed an association with cumulative asthma (Fig. 4). A high rate of fat intake is also attributed to the Westernized diet, but there is more emphasis placed on the composition of fat fractions. According to the lipid hypothesis, an increased intake of polyunsaturated fatty acids (PUFAs) over saturated fat can increase asthma prevalence and allergic sensitization, but controversial results are also available (39, 40, 43, 44). Margarine can serve as a significant source of PUFAs. Therefore, we should be aware of its potential causative role in asthma and atopy development (43, 45–47).
Frequent intake of cereals showed an association with decreased odds of cumulative asthma (Fig. 4). The literature has supported this finding, though the protective mechanism is not completely understood yet (39–41, 44). Our survey did not evaluate prior cereal consumption, although the early introduction of cereal grains into the diet is substantial to avoid sensitization (48).
High energy diet is a predisposing factor of obesity. Obesity is associated with worse asthma control and an increased risk of exacerbations in all ages (39). Besides the fact that obese and overweight children are more likely to have asthma, according to the current view, obesity-related asthma in childhood is a separate entity with a Th1 cell polarization (39, 49, 50). Our observation reinforced the conception of the association between asthma and BMI-for-age percentiles, but the phenotyping of obese asthmatics was beyond our scope (Fig. 5).