Meghan Hodges
The environment has the potential to affect our DNA and gene expression. Gene expression refers to the way genes function, and can be altered by environmental factors such as food, drugs, light, temperature, and exposure to toxins or pollutants. Pollution is one of the most obvious and severe negative environmental factors, and air pollution in particular is estimated to contribute to approximately seven million early deaths every year worldwide. Recent studies have shown that exposure to air pollution can affect DNA methylation, a biological process in which genes are organized into different chemical groups, and that these changes might in turn influence inflammation, disease development, and exacerbation risk.
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What You'll Learn
Air pollution and DNA methylation
Air pollution is a well-known health hazard, contributing to millions of early deaths and lost life years annually. It is associated with various diseases, including cardiovascular disease, metabolic disorders, and lung pathologies such as asthma and chronic obstructive pulmonary disease (COPD). Emerging evidence suggests that air pollution exposure may also alter epigenetic marks, particularly DNA methylation (DNAm).
DNA methylation refers to the attachment of methyl groups to DNA, typically at the fifth carbon of cytosines, resulting in the formation of 5-methylcytosine (5-mC). This process can be influenced by environmental factors, including air pollution. Studies have found that exposure to air pollutants like particulate matter (PM), black carbon (BC), ozone (O3), and nitrogen oxides (NOx) can lead to changes in DNA methylation patterns, usually resulting in lowered methylation levels.
The complex composition of air pollution makes understanding its specific mechanisms challenging. However, it is believed that air pollution-induced reactive oxygen species (ROS) may increase the oxidation of 5-mC to 5-hydroxymethylcytosine (5-hmC). Additionally, air pollution can decrease global 5-mC generation by reducing DNA methyltransferase (DNMT) expression. These alterations in DNA methylation may have downstream effects on gene expression and cellular functions, contributing to the development and exacerbation of various diseases.
Traffic-related air pollution (TRAP) has been a particular focus of research. Studies have shown that exposure to TRAP is associated with methylation changes in dozens of genes related to cardiometabolic health. In a randomized trial, participants exposed to traffic-related air pollution exhibited methylation changes in 68 CpG loci, with 49 hypermethylated and 19 hypomethylated sites. These loci were linked to pathways involved in cardiovascular signaling, cytokine signaling, immune response, nervous system signaling, and metabolism.
While the exact mechanisms remain to be fully elucidated, the available evidence suggests that air pollution exposure can influence DNA methylation patterns, potentially impacting human health and disease development. Further research is needed to comprehensively understand the complex interplay between air pollution and DNA methylation, as well as the resulting health implications.
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Particulate matter and DNA damage
The environment has the potential to affect our DNA. Gene expression can be altered by environmental factors such as food, drugs, light, temperature, and exposure to toxins or pollutants. These changes can range from small to significant, with certain genes in our system being turned on or off when they are supposed to be in the opposite state. These alterations in gene expression can be passed on from parent to child.
Particulate matter (PM) is a component of air pollution that includes PM10, PM2.5, and ultra-fine PM0.1 particles. Exposure to PM is associated with pulmonary and cardiovascular diseases and cancer. The mechanisms of PM-induced health effects are believed to involve inflammation and oxidative stress. Oxidative stress may arise from the direct generation of reactive oxygen species (ROS) from the surface of particles, soluble compounds such as transition metals or organic compounds, altered function of mitochondria or NADPH-oxidase, and the activation of inflammatory cells capable of generating ROS and reactive nitrogen species.
Oxidative stress-induced DNA damage appears to be an important mechanism of action of urban particulate air pollution. In vitro tests have shown that organic extracts of urban air particles induced cancer in animals and mutagenic effects in bacteria, plants, and mammalian in vitro cells. However, there are few studies on the in vitro evaluation of the cytogenetic and genotoxic effects of fine PM on human lymphocytes.
PM2.5 levels, size, and chemical composition vary depending on local emissions and orographic conformation. The early effects of PM2.5 human exposure are not clearly understood, but the adverse effects of PM on humans depend on its physical characteristics and chemical composition. At the cellular level, PM can induce oxidative stress as a result of cell homeostasis disruption.
In summary, particulate matter air pollution is associated with increased risks of human mortality and morbidity, including cancer and cardiopulmonary diseases. The mechanisms by which PM induces these health effects involve inflammation and oxidative stress, which can lead to DNA damage. However, the specific effects of PM on human health depend on the characteristics and composition of the particulate matter.
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Oxidative stress and inflammation
Oxidative stress is a situation in the cell where the redox balance is shifted towards a pro-oxidant state compared to an antioxidant state. This shift can occur due to increased production of oxidant species or decreased levels of free radical scavengers (e.g. ascorbate or glutathione) or antioxidant enzymes (e.g. catalase, superoxide dismutase, or glutathione peroxidase). The lung lining fluid, which acts as the first antioxidant defence barrier, protects epithelial cells from oxidant injury caused by inhalation.
There are several pathways through which oxidative stress and inflammation are influenced by genetics. One prominent pathway is the Nrf2/ARE (nuclear factor erythroid 2-related factor 2/antioxidant response element) pathway. Under typical conditions, Nrf2 is sequestered in the cytoplasm by Keap1 (Kelch-like ECH-associated protein 1). However, when exposed to oxidative stress, Nrf2 separates from Keap1 and moves into the nucleus, where it forms complexes with other transcription factors. These complexes bind to the ARE in gene promoters, activating the expression of genes involved in cellular defence against oxidative stress and inflammation. Additionally, the NF-κB signalling pathway is activated in response to oxidative stress, regulating cellular proliferation and apoptosis in inflammatory states.
Genetics play a crucial role in governing susceptibility to oxidative stress. The oxidative burden in the body is regulated by the balance between pro-oxidant genes, which orchestrate processes that produce oxidant species, and antioxidant genes. Functional polymorphisms that influence inflammation and oxidative stress may act as heritable markers associated with other allelic variants, predisposing individuals to oxidative stress and inflammation. For example, the CYP1A1 subfamily of Cytochrome P450 (CYP) enzymes is involved in metabolising various substances within the human body, including toxins and drugs. However, CYP1A1's metabolic activity can also lead to the generation of reactive oxygen species (ROS) as byproducts, particularly when dealing with certain procarcinogens like polycyclic aromatic hydrocarbons (PAHs) found in environmental pollutants and food contaminants.
Oxidative stress has gained significant attention due to its association with the onset and progression of various diseases, including cancer, diabetes, metabolic disorders, atherosclerosis, and cardiovascular diseases. Elevated levels of ROS can trigger fundamental changes at the cellular level, resulting in chronic inflammation, DNA damage, and disruptions in cell signalling pathways. These alterations can contribute to the pathogenesis of different diseases. For instance, in cardiovascular diseases like atherosclerosis, oxidative stress contributes to the formation of arterial plaques. Similarly, in diabetes, oxidative stress is implicated in insulin resistance and pancreatic beta-cell dysfunction.
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Gene expression and environmental factors
Environmental factors such as light, temperature, food, drugs, and exposure to toxins or pollutants can alter gene expression. While the DNA gene sequences are not affected by the environment, the way genes function can be. For instance, air pollution can induce reactive oxygen species (ROS) that may increase the oxidation of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC). This can lead to a decrease in the global generation of 5-mC due to reduced DNA methyltransferase (DNMT) expression.
Several studies have found that air pollution exposure is associated with a range of respiratory effects and an increased risk of developing lung diseases, including lung cancer, asthma, and chronic obstructive pulmonary disease (COPD). For example, a study of 63 steel-foundry workers in Brescia, Italy, who were exposed to particulate matter under normal factory conditions, found significant changes in the methylation of four genes that may suppress tumors. Another study by Baccarelli showed that elderly people in Boston had DNA damage from breathing in particulate matter.
The effects of air pollution on DNA methylation have been observed across the human lifespan, and interventions such as exercise and B vitamins have been proposed to reduce the impact on DNA methylation and health. Additionally, recent evidence suggests that epigenetic alterations can occur throughout the lifespan, influencing gene expression in different ways. For example, a recent animal study found that exposure to diesel exhaust induced hypermethylation of the IFN-γ promoter and hypomethylation of IL-4 in CD4+ T cells among mice sensitized to the fungus allergen Aspergillus fumigatus.
The role of gene-by-gene interactions and epigenetic mechanisms needs to be considered along with gene-by-environment interactions to fully understand how the environment alters gene expression.
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Epigenetic alterations and disease risk
Air pollution is a serious threat to human health and is a major cause of many diseases, including cardiovascular disease, metabolic disorders, respiratory issues, lung pathologies, and asthma. It has been estimated that air pollution exposure contributes to approximately seven million premature deaths annually worldwide, along with more than 3% of disability-adjusted life years lost.
Several components of traffic-related air pollution (TRAP), such as particulate matter (PM), black carbon (BC), ozone (O3), nitrogen oxides (NOx), and polyaromatic hydrocarbons (PAHs), have been linked to changes in DNA methylation (DNAm), typically lowering it after exposure. These epigenetic alterations can impact gene expression and increase the predisposition to various diseases. For instance, exposure to PM2.5 has been found to alter epigenetic age, a marker of mortality and disease risk, and promote circadian rhythm disruption and metabolic dysfunction.
While the connection between environmental exposure and disease risk due to epigenetic modifications is well-established, the specific signaling pathways connecting pollutants to the epigenome remain unclear. However, understanding these epigenetic alterations caused by specific pollutants may lead to the development of biomarkers to assess disease risk associated with air pollution. These biomarkers could be used to predict and assess the risk factors for the development and progression of diseases influenced by air pollution.
Moreover, epigenetic modifications can be transmitted across generations, indicating that environmental influences experienced by one generation may persist beyond the second generation. This raises concerns about the long-term health implications of air pollution exposure, not only for those directly exposed but also for subsequent generations.
Further research is needed to identify more robust epigenetic marks associated with specific diseases induced by particular pollutants. By enhancing our understanding of the epigenetic alterations caused by air pollution, we may be able to develop preventive and remedial strategies to reduce morbidity and improve health outcomes in polluted environments.
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Frequently asked questions
Pollution is the introduction of harmful substances or products into the environment that can have negative effects on living things and the environment.
Pollution can affect the genome by altering gene expression. Gene expression is the way genes function, and it can be altered by environmental factors such as food, drugs, toxins, and pollutants. These changes can be slight and might not have any noticeable effects, but they can also be dramatic. For example, certain important genes within our DNA could be turned on or off at the wrong times. These alterations in gene expression can be passed on from parent to child.
Air pollution exposure is estimated to contribute to approximately seven million early deaths every year worldwide. Air pollution has been shown to lower DNA methylation (DNAm) and influence inflammation, disease development, and exacerbation risk. Several traffic-related air pollution (TRAP) components, including particulate matter (PM), black carbon (BC), and nitrogen oxides (NOx), have been associated with changes in DNAm.
Air pollution has numerous harmful health effects and contributes to the development and morbidity of cardiovascular disease, metabolic disorders, and a number of lung pathologies, including asthma and chronic obstructive pulmonary disease (COPD). Air pollution exposure has also been linked to increased rates of cancer, respiratory diseases, and heart problems.
