The termed asthma is an umbrella word for multiple diseases
with common symptoms. Asthma has been broadly classified as
two major sets of symptoms: T helper cell high (Th2-high)
and T helper cell low (non-Th2). Th2-high is associated with
early-childhood allergies to common pollutants such as pet
dander, tree pollens, or mold. In contrast, non-TH2 is not
related to an allergic response. The non-Th2 type, marked
explicitly by being non-allergy-related, is far less
understood than the TH-2 type and could transform into
severe or difficult to treat type. Asthma afflicts more than
300 million people worldwide. The most severe manifestation,
known as non-Th2, or non-atopic childhood asthma, represents
the majority of the cases, greater than 85%, particularly in
low-income countries. Yet, whether non-Th2 is a distinct
disease (or endotype) or simply a unique set of symptoms (or
phenotype) remains unknown. 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. Studies show that
nearly 50% of the children whose asthma is poorly controlled
are expected to emerge as severe adult cases. Yet, a
one-size-fits-all treatment approach, currently the norm for
asthma, is ineffective. 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. Now, for the first time, an epidemiological study
has shown that not only is non-Th2 a distinct disease, its
likely inducer is early childhood exposure to airborne
Benzo[a]pyrene, a byproduct of fossil fuel combustion. This
study is the first to demonstrate air pollution as a driver
of the most challenging type of asthma, the severe subtype
which is non-responsive to current therapies. |