Analysing the causes of chronic cough: relation to diesel exhaust, ozone, nitrogen oxides, sulphur oxides and other environmental factors

Coughing and mucus secretion are coordinated neuronal reflexes that protect the respiratory tract from noxious exogenous substances under physiological conditions. However, within chronic exposure to noxious substances such as tobacco smoke, urban dust, or occupational factors [1-3], the originally protective mechanisms may lead to a states of chronic distress with hypersecretion and chronic coughing [4-10]. The neurophysiology of the cough reflex and its relation to bronchoconstriction and different forms of adult and pediatric asthma is very complex [11]. However, there is little doubt that chronic cough can be related to the exposure to different environmental air pollutants. Amongst them, pollutants such as diesel exhaust, ozone, nitrogen and sulphur dioxide have all been suggested to participate as main causes or co-factors in the development of chronic cough [12].These suggestions do not only base on epidemiological and clinical observations, but also on the neurophysiological and -anatomical understanding of the cough reflex. In this respect it is generally accepted, that airway pollutant-caused airway irritation leading to chronic cough displays a complex phenomenon involving a variety of reflex mechanisms [13-19].Neurophysiologically, a subgroup of rapidly adapting receptors (RARs) among the three major types of vagal sensory receptors is suggested to act as "cough receptors". Next to these RARs, a further effect by bronchopulmonary C-fibers on the cough reflex has been suggested, and there are data indicating that i.e. ozone, one of the main environmental air pollutants, exerts an influence on vagal-sensory innervation [20-24]. Also, transient receptor potential vanilloid-1 seems to play a role in the mediation of the cough reflext [25,26] and airway nerves and their mediators in general are likely to play an important role in the general pathology of cough and airway inflammation [27-33].In the light of the clinical, epidemiological and experimental data