Air pollution is a ‘likely contributor’ to the most severe form of asthma, according to a new study published in the journal Environmental Health.
Asthma affects more than 300 million people worldwide, with the most severe asthma, known as non-Th2, representing the majority of the cases, particularly in low-income countries. Yet, whether non-Th2 is a distinct disease or simply a unique set of symptoms remains unknown.
In order to find out the answer to this question, researchers from Lehigh University tested two comparable groups of children from an industrial city, Ostrava, and the surrounding semi-rural area in the Czech Republic.
Ostrova is an industrial city with a high level of coal mining activities.
The researchers found that the levels of Benzo[a]pyrene, an air pollutant that is a byproduct of fossil fuel combustion, were 11-times higher than the recommended air quality standards.
Based on this, the researchers found that not only is non-Th2 a distinct disease, but it is also likely caused by childhood exposure to Benzo[a]pyrene.
They found that not only was elevated exposure to Benzo[a]pyrene associated with correspondingly elevated odds of non-Th2 asthma but it was also associated with depressed systemic oxidant levels.
Hyunok Cho, lead author of the study said: ‘Non-Th2 asthma is associated with very poor prognosis in children and great, life-long suffering due to the absence of effective therapies.
‘There is an urgent need to better understand its mechanistic origin to enable early diagnosis and to stop the progression of the disease before it becomes severe.
‘The primary reason for lack of therapeutic and preventive measures is that no etiologic, or causal, driver has ever been identified for the non-Th2 asthma.
‘The identification of non-Th2 asthma as a distinct disease, with early exposure to Benzo[a]pyrene as a driver, has the potential to impact tens of millions of sufferers, since this would make it possible to intervene before the onset of irreversible respiratory injuries.
‘Contrary to the current body of evidence supporting adult onset of non-atopic asthma, our data suggest for the first time that the lung function deficit and suppressed oxidative stress levels during early childhood are critical sentinel events preceding non-atopic asthma.’
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