Autor/es reacciones

José Gregorio Soto Campos

Director of the Pneumology and Allergy Clinical Management Unit of the Hospital de Jerez 

It is an interesting and well-designed study on the epidemiological link between postnatal exposure to ozone and asthma in the U.S. This study corroborates what we already knew: there are specific pollutants capable of inducing airway inflammation (ozone, nitrogen dioxide, and particles smaller than 2.5 micrometers), bronchial hyperreactivity (ozone and nitrogen dioxide), and oxidative stress (ozone, nitrogen dioxide, and particles smaller than 2.5 micrometers), which are associated with the onset of exacerbations or even the initiation of asthma – although the mechanisms behind this are not yet clarified.

It has been proposed that exposure to atmospheric pollutants may amplify sensitization to aeroallergens, as there is evidence of this response to ozone, nitrogen dioxide, sulfur dioxide, and diesel combustion particles. Several mechanisms may be involved, including: an increase in allergen deposition in the airway due to particle transport; an increase in epithelial permeability due to oxidative stress; an increase in antigenicity as proteins undergo chemical modifications when exposed to pollutants; or even an adjuvant effect promoted by the action of diesel combustion particles on the human respiratory epithelium.

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