Asthma and COPD: Common Genes, Common Environments?

Asthma and COPD show similarities and substantial differences. The

Dutch hypothesis stipulated that asthma and COPD have common genetic
and environmental risk factors (allergens, infections, smoking) in
common, which ultimately lead to clinical disease depending on the
timing and type of environmental exposures (3). Thus a particular
group of shared genetic factors may lead to asthma when combined with
specific environmental factors that are met at a certain stage in
life, whereas combination with other environmental factors, or similar
environmental factors at a different stage in life, this will lead
toward COPD. Multiple genes have been found for asthma and COPD. Next
to genes unique to these diseases, some shared genetic risk factors
exist. Moreover, there are both common host risk factors and
environmental risk factors for asthma and COPD. Here we put forward,
based on the data available, that genes that affect lung development
in utero and lung growth in early childhood in interaction with
environmental detrimental stimuli like smoking and air pollution are
contributing to asthma in childhood and the ultimate development of
COPD. Additional genes and environmental factors then drive specific
immunological mechanisms underlying asthma and others may contribute
to the ultimate development of specific subtypes of COPD, i.e. airway
disease with mucous hypersecretion, small airway disease and
emphysema. The genetic predisposition to the derailment of certain
pathways may further help to define subgroups of asthma and COPD. In
the end this may lead to stratification of patients by their genetic
make-up and open new therapeutic prospects.

Key words: asthma • Dutch hypothesis • COPD • genes • environment