Introduction
Both genes and the environment shape human health and disease. Although
IgE-mediated allergic diseases (atopic diseases) have a genetic
component and are more prevalent in individuals with a family history of
allergic disease, the observed rapid increases in allergic diseases
suggest that environmental factors are the predominant driving forces
behind these increases rather than genetic
alterations.1, 2 Common atopic diseases include atopic
dermatitis, food allergy, allergic rhinitis, and allergic asthma. Human
diets and lifestyle have undergone major alterations. The exposome,
which is the sum total of all the exposures of an individual in a
lifetime, has undergone major shifts in the last few decades, affecting
human health and disease.
A number of factors have been implicated in the increased prevalence of
allergic diseases. Predominant among them are increased exposure to
pollutants and decreased exposure to microbes and parasitic infections.
Air pollution has increased significantly in the last few decades. The
hygiene hypothesis suggests that increased hygiene and lack of exposure
to microbes and parasitic infections at an early age prevents the
necessary stimulus to train the developing immune system to develop
tolerogenic responses. Lifestyle factors, such as increased time spent
indoors, use of antibiotics, and consumption of processed foods and
decreased exposure to farm animals and pets, limit exposure to
environmental allergens, infectious parasitic worms, and microbes. The
lack of exposure to these factors is thought to prevent proper education
and training of the immune system. Other factors that are also
associated with increased risk of allergic diseases are Caesarian birth,
birth order, tobacco smoke exposure and psychosomatic factors.
Increased human population, pollution, and rapid industrialization have
affected our environment bringing about climate change. Climate change
has led to greater variability in temperature, and increases in air
pollution, forest fires, heat waves, droughts, and
floods.3 Thunderstorms during the pollen season have
been linked with increased asthma exacerbations and emergency room
visits.4, 5 During thunderstorms, whole pollen grains
are swept into the clouds where they are broken up into smaller
allergenic pollen fragments and eventually carried back to ground
level.6 Similarly, dust storms and wildfires have been
shown to increase inflammatory responses and asthma
exacerbations.7-9
A number of recent high-throughput “omic” technologies are
accelerating our understanding of allergic diseases and have
revolutionized research. The use of the term “omics” suggests a
comprehensive high-throughput and systematic investigation of biological
parameters. Examples of omic technologies include genomics, epigenomics,
transcriptomics, proteomics, metabolomics, microbiomics, and
exposomics.10 These technologies generate
exponentially growing data sets requiring sophisticated bioinformatics
and computational techniques that can integrate, analyze and interpret
the data to generate hypothesis, which can then be further tested. Of
these, epigenomics has been key in giving us insight to gene-environment
interactions. It has provided us a greater understanding of the
mechanisms by which the environmental factors modulate epigenetic
modifications and expression of genes involved in inflammatory responses
and allergy. Technologies such as bisulfite sequencing, ATAC seq and
cytometry by Time-Of-Flight (EpiTOF) have made it possible to study DNA
methylation and histone modifications, and chromatin accessibility
across the whole genome and at a single cell
level.11-14 Here, we review current knowledge on the
environmental factors that have been shown to affect the development of
allergic diseases and the recent developments in the field.