**1. Introduction**

Asthma comes from the Greek word for "panting" and has been described as a pathological condition for centuries. It is a chronic inflammatory disorder of the airways in which many immunological cells play a role, including mast cells and eosinophils. In susceptible individ‐ uals, this inflammation causes symptoms which are usually associated with widespread variable airflow obstruction that is often reversible, either spontaneously or with treatment, and causes an associated airway hyperresponsiveness (AHR) to a variety of stimuli. The clinical features of asthma include dyspnea, wheezing and coughing.

During the last forty years there has been an increased understanding of the wide spectrum of this disease and as a result a number of effective treatments have been developed. Despite these advances, however, the mortality continues to increase and approximately 500 Canadi‐ ans and 3500 Americans die each year from asthma. It remains a major cause of morbidity, as the leading cause of school absenteeism and the third leading cause of work absenteeism. The prevalence of asthma in North America has been on a constant rise over the last 25 years and it is estimated that currently over 3 million Canadians and 25 million Americans suffer from asthma. Worldwide the prevalence rates of asthma are rising on average by 50% each decade and developing a better understanding of the risk factors associated with this trend is critical. These may be broadly classified as either host genetic factors or environmental factors (Table 1).

One of the marked risk factors of asthma associated with the westernized lifestyle is our changing diet and/or nutritional status. It has been hypothesized that the significant change in our diet plays a dominant role in the etiology of asthma. Seaton *et al*. have proposed that

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**Table 1.** Risk factors associated with asthma

asthma prevalence has increased in UK because of an alteration in diet associated with industrialization [1]. This has lead to a substantial decline in the consumption of fresh fruits, green vegetables, fish and red meat, and as a result decrease in pulmonary antioxidant defences and an increase in susceptibility to inhaled irritants and allergens [1]. These foods are the main sources of antioxidants, substances that protect cells against the effects of free radicals generated during oxidative stress.

Oxidative stress is important in the pathophysiology of asthma [2] and development of AHR [3]. A large number of epidemiologic studies have reported the protective effects of dietary antioxidants such as micronutrients vitamin A, C, and E, polyphenol, and carotenoids against the development of asthma and decline of lung function. In a study on American children higher levels of antioxidants beta-carotene and Vitamin C, along with antioxidant trace mineral selenium is associated with a lower risk of asthma [4]. Dietary vitamin C intake is positively associated with 1 Second Forced Expiratory Volume (FEV1) in children and adults [5-8] but less frequently with asthma or wheeze in children and adults [4, 9-11]. Dietary vitamin E intake is positively associated with ventilatory function [5, 6, 12] but negatively associated with asthma and wheeze in children [13], adult-onset wheeze [11] and the likelihood of atopic sensitization in adults [14]. Fresh fruits intake is inversely associated with wheeze [15] and chronic lung disease onset [16] and is positively associated with FEV1 [17]. Total fruit and vegetable intake is inversely related to asthma prevalence [18] but not to FEV1 [19] or airway obstruction [20]. Vegetables may protect against chronic bronchitis, asthma [21], and wheeze [22]. Moreover, dietary polyphenols intake are associated with lower disease risk with beneficial clinical outcomes attributed to both the antioxidants and anti-inflammatory properties of polyphenols [23]. Polyphenols consist of a large group of natural antioxidants extracted from plants and flavonoids comprise the most studied group.

In addition to antioxidants, intake of fats, particularly the changing composition of polyunsa‐ turated fatty acids (PUFA) in westernized diets, has been implicated in the etiology of asthma. There has been a reduced intake of saturated fat accompanied by an increase in n-6 PUFA consumption, particularly linoleic acid and arachidonic acid. In addition, there has been a decrease in consumption of n-3 PUFA such as eicosapentaenoic acid (EPA) and docosahexae‐ noic acid (DHA). Thus, it has been postulated that the increased ratio of n-6:n-3 PUFA in diets of industrialized countries may also contributed to the increased asthma incidence.

Ancient Egyptian papyrus writings contain prescriptions for asthma that include several herbs suggesting that naturally occurring bioactive compounds may been used to effectively treat asthma. This chapter summarizes the current knowledge on the effects of dietary compounds and nutrients on allergy and asthma, with a focus on the mechanisms involved, wherever possible.
