**1. Introduction**

Epidemiological studies from around the world indicate that particulate matter poses a serious health threat to public health [1]. Air pollution with suspended particles and gaseous substances is assumed to be a possible risk factor for bronchial asthma [2–4]. Bronchial asthma (BA) is one of the most common chronic noncommunicable diseases in children and adults, characterized by variable respiratory symptoms and airflow limitation [5]. The global prevalence of physician-diagnosed asthma in adults is 4.3% (95% CI: 4.2%, 4.4%), with large differences between

countries [6]. Asthma is a heterogeneous disease with different underlying disease processes. Recognizable clusters of demographic, clinical, and/or pathophysiological characteristics are often called as asthma phenotypes [4]. Some of the most common are allergic and non-allergic asthma, differing in the presence of atopy, the type of airway inflammation, responses to inhaled corticosteroid treatment. Later, the term "endotype" was introduced as a conceptual basis for new ideas about the molecular heterogeneity of bronchial asthma [7], and T2- and non-T2-endotypes have now been described. Meta-analyses, including cohort studies, support the role of fine particles in asthma in children [8–11]. The question of whether the incidence of asthma in adults is associated with exposure to ambient particulate matter (PM) remains open: there are not enough studies, and the available data are contradictory—the relative risks were about 1.0 and, in most studies, did not reach a critical level of statistical significance [12–17]. Besides, adult asthma, unlike asthma in children, is associated with other risk factors and is known for its female predominance, uncommon remission, and unusual mortality [18]. The chapter describes the current literature data, as well as our study on the effect of fine particles in the ambient air on the formation, course, and possible underlying mechanisms of atopic allergic and eosinophilic non-allergic phenotypes of the T2-endotype of bronchial asthma in adults (18–65 years old).

Bronchial asthma is a heterogeneous disease characterized by the chronic inflammation of the airways [6]. The known variants of the combination of demographic, clinical, and/or pathophysiological characteristics are often called "bronchial asthma phenotypes" [6]. Several studies have shown that air pollution with PM increases the risk of bronchial asthma exacerbations and frequency of hospitalizations [2, 3, 19, 20] and worsens the quality of life of patients with asthma [21]. Meanwhile, the role of PM in the onset of bronchial asthma in adults is still open [22].

The earliest study reporting an association between long-term exposure to air pollution and the incidence of bronchial asthma described a cohort of non-smoking Seventh-day Adventists in California, USA [12]. Considering gender, age, education, smoking, and gaseous pollutants (ozone and sulfur dioxide) as confounders, no association was found between new cases of bronchial asthma and PM10 in the ambient air.

A Swiss cohort study with an 11-year follow-up showed that the incidence of bronchial asthma among non-smokers was associated with an increase in PM10 concentrations: hazard ratio 1.30 (95% CI: 1.05, 1.61) per 1 μg/m3 of PM10, not being changed when adjusted by education, occupational exposure, secondhand smoking, asthma or allergies in parents, exposure to other pollutants, proximity to roads with heavy traffic, and functional state of the lungs [13].

A meta-analysis of the incidence of bronchial asthma among the adult population in six prospective cohorts followed up within the ESCAPE study revealed a positive but insignificant relationship between new cases of bronchial asthma and average annual concentrations of PM10 and PM2.5: odds ratio 1.04 (95% CI: 0.88, 1.23) and 1.04 (95% CI: 0.88, 1.23) by 10 μg/m3 PM10 and 5 μg/m3 PM2.5, respectively. The models included PM concentrations, as well as such confounders as gender, age, education, body mass index, smoking, and clinical aspects of BA [14]. Similar results were obtained in a cohort of women living in the USA (follow-up period 2008–2012), where the odds ratio for new cases of bronchial asthma, adjusted by age, education, body mass index, consumption of dietary fiber, smoking, and occupational hazards, was 1.20 (95% CI: 0.99, 1.46) for an increase in PM2.5 concentrations by 3.6 μg/m3 (interquartile range) [15].

#### *Fine Particles in the Ambient Air as a Risk Factor of Bronchial Asthma in Adults DOI: http://dx.doi.org/10.5772/intechopen.112419*

In older age groups, a 2-year increase in PM2.5 by 10 μg/m3 was associated with an increased risk of bronchial asthma by 2.24% (95% CI: 0.93%, 5.38%) in people aged >44 years [16], a 3-year increase in the average annual concentration of PM2.5 by 10 μg/m3 led to an increase in the bronchial asthma incidence by 9% (95% CI: 4%, 14%) among elderly people (65+) [17]. Similar results were reported by [23] for low- and middle-income countries (China, India, Ghana, Mexico, Russia, and South Africa): 5.12% of the asthma cases in the study population over 50 years of age (95% CI: 1.44%, 9.23%) could be attributed to long-term exposure to PM2.5.

The phenotypic heterogeneity of bronchial asthma was investigated by a cluster analysis of well-characterized patients, grouping them into 4–5 phenotypic clusters, considering age, gender, lung function, medical aid need, and body mass index [24, 25]. To date, the T2 and non-T2 asthma endotypes, defined as "a disease subtype that is determined by a separate functional or pathological biological mechanism" [7], have been described. T2-endotype is characterized by a high level of type 2 inflammatory response in the airways [3, 7] and more severe course [6]. The molecular mechanisms of the non-T2-endotype are under investigation [3, 7, 26]. Considering different asthma phenotypes and endotypes when studying health effects of ambient particles was not regarded in previous epidemiological studies, but several authors hypothesized that the bronchial asthma linked to PM might be described as a separate phenotype, and its initial mechanisms could include damage to the airway epithelium, T2- as well as T17-mediated responses [27, 28].

The issue of the relationship between bronchial asthma and separate fractions of PM in the ambient air is insufficiently studied [2, 3]. There are also no convincing data on the effects of ambient particles with different chemical composition or origin. There is some information about the role of the oxidizing potential, which depends on the chemical composition of suspended particles. As discussed above, reactive oxygen species induced by particulate matter are regarded as an important mediator of their toxicity. The oxidation potential of PM2.5 taken from the atmospheric air of Paris was increased in the presence of metals such as copper and zinc, as well as polycyclic aromatic hydrocarbons and soluble organic compounds in PM [29]. The effects of fine particulate matter were enhanced by concomitant exposure to particulate matter and bacterial endotoxins in residential air: for emergency medical visits due to asthma exacerbations in the last 12 months, the odds ratio for comparing the subgroup with high exposures to PM2.5 and endotoxin and the subgroup with low levels of both pollutants was 5.01 (95% CI: 2.54, 9.87) [30]. Similar findings were shown in a recent Japanese study [31]. Combined exposure to PM10 and bacterial endotoxin near livestock farms was associated with the higher prevalence of bronchial asthma [32]. Thus, this line of research also deserves attention.
