Air Pollution And Asthma: What's The Link?

Asthma is a condition affecting the airways, causing symptoms such as wheezing, coughing, and difficulty breathing. While the causes of asthma are not fully understood, air pollution is believed to be a significant factor. Research has shown that air pollution can worsen asthma symptoms and increase the risk of developing the condition. Poor air quality can trigger asthma flare-ups, as pollutants irritate the airways, causing them to swell and tighten, and leading to breathing problems. This is particularly true for children with asthma, who are especially vulnerable to air pollution. Various studies have found links between specific air pollutants and asthma attacks in children, especially in low-income urban areas.

Outdoor air pollution

Ground-level ozone, a common air pollutant, is a significant trigger for asthma attacks. Studies have found that increased ozone concentrations are associated with decreased lung function, even at low levels, and when asthma is being treated with medication. Ozone exposure can also increase the levels of fatty substances in the blood and cause oxidative stress, leading to airway inflammation, airway hyperreactivity (AHR), and lung injury. Other pollutants, such as SO2, can act as adjuvants, affecting the production of cytokines in airway epithelial cells, which promote T-helper responses and contribute to asthma development.

Particulate matter, such as PM10-2.5 and PM2.5, is another outdoor air pollutant linked to asthma. Exposure to these fine particles in the air has been associated with an increased risk of developing persistent wheezing and asthma, especially in children. This is particularly prevalent in urban areas, where traffic-related air pollution (TRAP) is a significant concern. Children in low-income urban environments are at a higher risk of developing asthma due to their exposure to higher levels of particulate matter and other pollutants.

The impact of outdoor air pollution on asthma is not limited to children. Studies have shown that women are more susceptible to the effects of tobacco smoking, with active and passive smoking linked to the incidence of asthma in adults. Additionally, personal short-term exposure to ozone can increase the risk of asthma exacerbation and hospital admissions, as evidenced by the increase in asthma-related emergency department visits on days with higher pollution levels.

To mitigate the effects of outdoor air pollution on asthma, it is essential to monitor pollution levels and take appropriate precautions. The Environmental Protection Agency (EPA) in the United States provides daily Air Quality Index (AQI) reports, which indicate when people with asthma should limit their time outdoors. Running an air conditioner and reducing outdoor activities on poor air quality days can help minimize exposure. Improving indoor air quality by using air cleaners and venting gas appliances can also reduce the impact of outdoor pollution on asthma.

Indoor air pollution

While outdoor air pollution is often discussed in relation to asthma, indoor air pollution can also negatively affect asthma outcomes. Indoor air pollution can come from various sources, including cigarette smoke, cleaning products, mould, dust mites, and pets.

Cigarette smoke is a complex mixture of over 7000 chemicals, 250 of which are known to be harmful, and 69 of which are known to cause cancer. Tobacco smoking and passive smoking have both been linked to the incidence of asthma in adults, with women appearing to be more susceptible to the effects of tobacco smoke.

Mould is another significant contributor to indoor air pollution. It can worsen lung conditions like asthma and increase the likelihood of infections. Dust mites, which are small insect-like pests, are also common indoor allergens that can aggravate asthma symptoms.

Overall, indoor air pollution can pose a serious health risk, particularly to individuals with asthma. It is important to be aware of potential sources of indoor air pollution and take steps to improve indoor air quality, such as using electric appliances, ensuring proper ventilation, and addressing mould and humidity issues.

Asthma in children

Asthma is a serious and life-threatening chronic respiratory disease that affects over 23 million Americans, including an estimated six million children. Children with asthma are especially vulnerable to air pollution, which can worsen symptoms and trigger asthma attacks.

Several studies have examined the link between air pollution and asthma in children. One study found that children exposed to outdoor coarse particulate matter were more likely to develop asthma. Another study by the EPA and the University of North Carolina investigated the impact of ozone on African American children with moderate-to-severe persistent asthma. The results showed that even low levels of ozone exposure were associated with pulmonary and other health changes, including a decrease in lung function.

Additionally, researchers have hypothesized that younger children may be more susceptible to the effects of air pollution because they typically spend more time outdoors and their respiratory systems are still developing. Air pollution can irritate children's airways, causing swelling and tightness, and making them more prone to upper respiratory infections, which can trigger asthma symptoms.

Furthermore, there is evidence that air pollutants may impact DNA associated with asthma. A study funded by the EPA suggested that air pollutants suppress genes that regulate the immune system's ability to differentiate allergens from dangerous foreign substances. This can lead to an inappropriate inflammatory response, even to harmless substances, which contributes to the development of asthma.

To protect children with asthma from the harmful effects of air pollution, it is recommended to monitor pollution levels and limit their time outdoors when the air quality is poor. Improving indoor air quality by using air cleaners and venting gas appliances can also help reduce children's exposure to pollutants.

Asthma and oxidative stress

Asthma is a chronic inflammatory lung disease that results in airflow limitation, hyperreactivity, and airway remodelling. Oxidative stress is believed to play a role in the development of asthma. Oxidative stress is one of the biological mechanisms proposed to explain the link between outdoor air pollution and asthma.

Oxidative stress is induced by secondary oxidation, which results in airway inflammation, airway hyperreactivity (AHR), and a decrease in lung function in asthmatic adults. It is caused by reactive oxygen species (ROS) that induce epithelial cell inflammation, AHR, and lung injury. ROS are produced by pollutants, such as ozone (O3) and sulphur dioxide (SO2), which can act directly or indirectly by inducing inflammation. O3 is a highly reactive gaseous pollutant that exerts inflammatory effects on the respiratory system.

Oxidative stress is also associated with decreased antioxidant defences, such as superoxide dismutase, catalase, and glutathione. Antioxidants are major defence mechanisms of the cells against oxidative stress. They work to protect cells and tissues against the continuous production of reactive oxygen and nitrogen species during normal metabolism. Asthma is characterised by a loss of antioxidant activity and a disequilibrium of the airway reducing state, which is a determinant of asthma initiation and severity.

According to a hierarchical oxidative stress model, low levels of oxidative stress lead to the activation of the transcription factor nuclear erythroid 2 p45-related factor 2 (Nrf2), which encodes genes responsible for antioxidant and anti-inflammatory functions. At low levels of oxidative stress, antioxidants can restore cellular redox homeostasis. However, when high levels of oxidative stimuli are present, additional intracellular signalling cascades are triggered that are potentially pro-inflammatory.

In bronchial asthma, oxidative stress aggravates airway inflammation by inducing pro-inflammatory mediators, enhancing bronchial hyperresponsiveness, stimulating bronchospasm, and increasing mucin secretion. Higher levels of molecules involved in oxidative stress have been found in biological samples from asthmatic patients compared to non-asthmatic control subjects.

Air pollution and genes

Asthma is a complex disease influenced by both genetic and environmental factors. While there is a well-established link between air pollution and asthma, the specific genes involved in this interaction are not yet fully understood. However, recent studies have shed light on the role of certain genes and their impact on respiratory responses to air pollutants.

Gene-Environment Interactions

The interplay between genes and the environment is crucial in understanding the development of asthma. Genetic predisposition, influenced by family history, plays a significant role in an individual's susceptibility to asthma. Having one parent with asthma doubles the risk, while having two parents with the condition quadruples it. This highlights the importance of genetics in asthma development.

Additionally, environmental factors, such as air pollution, also contribute significantly to asthma. Air pollution encompasses various gaseous pollutants and particulate matter, including ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, and particulate matter like smoke and soot. These pollutants can irritate the airways, particularly in individuals with asthma, exacerbating their symptoms and increasing hospital visits.

Specific Genes and Air Pollutants

While the identification of specific genes involved in the interaction with air pollution has been challenging, some genes have been implicated. For example, the genes GSTM1 and TNF are associated with oxidative stress responses to ozone and environmental tobacco smoke. Additionally, the IL4 gene has been linked to changes in promoter methylation in response to inhaled diesel exhaust particles and allergen exposure.

Epigenetic Modifications

Epigenetic mechanisms, such as DNA methylation, are also believed to play a role in the interaction between air pollution and asthma. These mechanisms regulate gene expression in cells by responding to environmental changes and developmental signals, potentially contributing to the development of asthma. For instance, prenatal exposure to traffic-related air pollution (TRAP) and polycyclic aromatic hydrocarbons (PAHs) has been associated with an increased risk of asthma and allergic sensitization in children.

Future Directions

To further advance our understanding of the complex relationship between air pollution and genes in asthma, several approaches can be considered. These include whole-genome association studies, improved exposure and phenotype assessments, and the investigation of joint interactions with diet and other co-factors that influence individual susceptibility.

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