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.