**2. Epidemiology**

Some anatomical and physiological characteristics of the infant and young child's airways predispose to the development of processes that lead to the narrowing or bronchial obstruc‐ tion, manifested by common symptoms, such as coughing, dyspnoea and noisy or wheezing breathing.

The *narrower airway calibre* is a basic fact, which contributes to the obstruction due to the inflammation of the mucosa, the smooth muscle constriction or the increased secretion of tracheobronchial mucus glands.

Infant *physiological increase of vagal tone*, which continues during the first years of life, as Montgomery and Tepper [18] demonstrated by methacholine inhalation, is known. Patholog‐ ically, bronchial hyperresponsiveness (BHR) is a key element in the pathogenesis of asthma. Having certain anomalies in the protein chain of the beta-receptors of the smooth muscle, such as the substitution of glycine for arginine at position 16 and glutamate for glutamine at position 27, is a characteristic of individuals with atopic predisposition. But in non-predisposed subjects, BHR is usually secondary to the inflammatory reaction that occurs in various circumstances in the bronchial mucosa.

Regarding bronchopulmonary infectious pathology, it is the well-known *immaturity of the immune system*, which in some children continues for several years (infant transient immuno‐ deficiency), facilitating the development of bronchial inflammation processes.

It is not always easy to establish the true diagnosis of asthma in early life, as the evolution of symptoms over the years will confirm the diagnosis by excluding other possible causes of dyspnoea or wheezing, supported by immuno-allergological and respiratory function studies.

In line with these concepts, Martinez et al. [16] distinguish the different phenotypes of the bronchospastic pathology in preschool children, identifying asthma and transient bronchitis (wheezy bronchitis) that encompass various processes suffered by a group of children who, after preschool age, do not show no broncholability, all a consequence of the predisposing factors cited above. However, it is not always easy to determine the phenotype of a particular patient, and in the course of time, as they evolve, the criteria may even have to be modified. Hence, the need to pay attention to the characteristics of the symptoms and their evolution, in addition to a number of circumstances, such as the suffering from other allergic processes by the same child (eczema, allergies to milk proteins), a precocious start of symptoms, or the existence of similar pathologies among siblings, parents or other close relatives, or environ‐ mental pollutants, climate, etc. The lack of a family history in approximately 20% of cases adds another obstacle to the diagnosis.

In most children, asthma begins in the first 5 years of life. A study in Spain in 1982 showed that in 76% of asthmatic children, the process had started before 4 years of age. Several studies indicate that between 15 and 35% of preschool children have had an episode of respiratory distress, with or without wheezing or other breathing noises; however, 60–65% of these children would not suffer crises after the third year. The high diagnostic confusion in this group of children with 'transient bronchitis' comes not only from symptomatic similarity but also from the terminology that has been used to label the process. The appearance of these temporary symptoms can be due to various causes, such as viral infections (respiratory syncytial virus (RSV), parainfluenza, influenza), causing bronchiolitis, which may recur, even more in immunodeficient children. Other possible causes can also be household pollutants (tobacco smoke, cleaning chemicals or industrial products) or weather changes (sudden cooling), among other.
