Air Pollution: Asthma's Worst Enemy

Air pollution is a major concern for people with asthma, especially children. Research has shown that air pollution can increase the risk of a child developing asthma and can also trigger asthma attacks in those who already have the condition. Climate change is also worsening the situation, with higher temperatures leading to more ground-level ozone pollution, a powerful lung irritant. Furthermore, wildfires produce smoke containing particle pollution that can reach deep into the lungs and enter the bloodstream, causing asthma attacks. Young children are particularly vulnerable to air pollution due to their developing lungs and the fact that they spend more time outdoors. Evidence suggests that air pollutants suppress genes that regulate the immune system, leading to an increased prevalence of asthma. Various pollutants, including ozone, nitrogen dioxide, and sulfur dioxide, can irritate the airways, causing swelling and breathing difficulties. As a result, understanding the impact of pollution on asthma is crucial for developing preventative treatments and safeguarding public health.

Children with asthma are vulnerable to air pollution

Secondly, certain pollutants can suppress genes that regulate the immune system's ability to differentiate allergens from dangerous foreign substances, such as viruses or bacteria. This suppression leads to an inflammatory response, even when the substance is not harmful, which can trigger asthma symptoms. Air pollution can also increase the risk of developing asthma in children who do not already have it. Long-term exposure to air pollution, particularly from burning fossil fuels, has been linked to a higher risk of asthma development.

Furthermore, children with specific gene variations, such as Glutathione S-Transferase Mu 1 (GSTM1) null genotypes, are at an increased risk of developing asthma when exposed to ozone (O3). Ozone is a powerful lung irritant that can trigger asthma attacks and is more prevalent due to higher temperatures caused by climate change. Wildfires, which are also more frequent due to climate change, produce smoke containing particle pollution that can reach deep into children's lungs and trigger asthma attacks.

Additionally, socioeconomic factors play a role in children's susceptibility to air pollution. Children from lower socioeconomic backgrounds may have greater exposure to outdoor air pollution due to neighborhood characteristics, such as increased levels of crime, less green space, or poor food access. Dietary factors also contribute, as a diet low in fruits and vegetables and antioxidants can increase vulnerability to the adverse effects of air pollution.

Understanding these factors is crucial for developing preventative treatments for asthma and safeguarding children's health in a changing climate. Local governments can play a role by issuing smog alerts on high-pollution days, and parents can take precautions to minimize their child's exposure to air pollution during these times.

Ozone exposure and asthma

Ozone is a gas that is helpful in the upper atmosphere but becomes a problem when found in the troposphere, where it can adversely affect the human respiratory and cardiovascular systems. Ground-level ozone is created by chemical reactions between fuel emissions, volatile organic compounds (VOCs), heat, and sunlight. It is most common in cities with more cars and greater use of fossil fuels, and in the summer when there is more sunlight, heat, and low winds.

Ground-level ozone is a major component of "smog" and is associated with worsening respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD). Ozone is very irritating to the lungs and airways, causing inflammation and airway hyperresponsiveness. It can also cause the muscles in the airways to constrict, trapping air in the alveoli, which leads to wheezing and shortness of breath. This can be particularly dangerous for people with asthma, and even low levels of ozone exposure have been associated with respiratory changes and other health outcomes in people with asthma, even when they use asthma therapies such as inhalers.

Several studies have found that ozone exposure is linked to an increased risk of asthma attacks in children. One study found that when the maximum daily 8-hour sliding average ozone concentration was higher than 80 μg/m3, there was an increased risk of asthma attacks, with the effect being more significant when the concentration was above 100 μg/m3. Another study of children with asthma attacks from the First Affiliated Hospital of Xiamen University found that increasing ozone levels, even at low concentrations, were associated with acute asthma attacks.

The effects of ozone exposure can be influenced by individual factors such as genetics and nutrient intake. People with certain genetic characteristics, such as the Glutathione S-Transferase Mu 1 (GSTM1) null genotype, are at an increased risk of developing asthma when exposed to ozone. Additionally, people with reduced intake of certain nutrients, such as vitamins C and E, are also at greater risk from ozone exposure.

Wildfires and asthma attacks

Wildfires are unplanned fires that burn in natural areas such as forests. They are often caused by lightning, but human activities such as burning debris, fireworks, unattended campfires, or discarded cigarettes can also cause them. The risk of wildfires increases in dry, windy conditions with little rain. Wildfire smoke contains pollutants that can have adverse health effects, especially on respiratory health. People with asthma are particularly vulnerable to the effects of wildfire smoke, which can irritate the eyes, nose, throat, and lungs. The inhalation of smoke can cause lung irritation, inflammation, coughing, wheezing, and shortness of breath, triggering asthma attacks.

During wildfire events, people with asthma are advised to stay indoors with windows and doors closed. The use of air conditioning with high-efficiency particulate air (HEPA) filters can help remove smoke particles from the air. It is recommended to avoid physical activity that involves heavy breathing, as it can increase the inhalation of smoke particles. If going outside is necessary, keeping a quick-relief asthma inhaler close by is essential. The U.S. Centers for Disease Control and Prevention (CDC) also suggests wearing a "respirator," a tightly fitting mask approved by the National Institute of Occupational Safety and Health (NIOSH) to filter out smoke particles.

The evidence linking wildfire smoke to respiratory issues is compelling. Studies have shown that emergency department visits for asthma increase during wildfire events. For example, during the Canadian wildfire smoke episodes in the United States in April–August 2023, asthma-associated emergency department visits were 17% higher than expected. These findings highlight the public health concerns associated with wildfire smoke exposure and the need to monitor and reduce exposure for people with asthma.

The impact of wildfire smoke on asthma is influenced by individual factors. Children, older adults, and people with pre-existing respiratory conditions like asthma are among the most vulnerable. Additionally, women and occupationally exposed groups may be at higher risk. The frequency, severity, and duration of wildfires have increased due to climate change and fuel load from modern fire suppression, further exacerbating the health risks associated with wildfire smoke exposure.

The pollutants in wildfire smoke, such as fine particulate matter (PM2.5), can cause lung injury, local and systemic inflammation, airway epithelium compromise, and increased susceptibility to infections. These effects can lead to exacerbations of pre-existing asthma, long-term lung function impairment, and increased all-cause mortality. Wildfire smoke exposure may also be associated with the onset of asthma, especially in vulnerable populations. Overall, the intensification of wildfire activity has significant implications for public health, and understanding the link between wildfire smoke and asthma is crucial for risk mitigation and emergency response planning.

Oxidative stress and asthma

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 and other human diseases such as cancer, cardiovascular disorders, and immunologic diseases.

Oxidative stress results from an imbalance between the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and the capacity of antioxidant defence mechanisms. ROS and RNS include superoxide anion, hydroxyl radical, hypohalite radical, hydrogen peroxide, nitric oxide, peroxynitrite, and nitrite. These molecules play a major role in airway inflammation and are determinants of asthma severity.

Oxidative stress is one of the biological mechanisms proposed to explain the association between outdoor air pollution and asthma. Pollutants such as ozone (O3), nitrogen dioxide (NO2), and sulfur dioxide (SO2) can act directly by producing free ROS and RNS or indirectly by inducing inflammation. O3 exposure, for instance, causes ROS production and changes in the expression of claudins, leading to tight junction barrier permeability and airway hyperreactivity (AHR).

In addition, oxidative stress may contribute to the structural changes in the airways of asthma patients, supporting remodelling processes, decreasing sensitivity to anti-inflammatory and anti-asthmatic treatments, and worsening the clinical course of the disease. It is also associated with decreased antioxidant defences, such as superoxide dismutase, catalase, and glutathione.

The relationship between oxidative stress and asthmatic inflammation is bidirectional, and the contribution of oxidative stress to asthma pathology remains partially controversial. While oxidative stress is commonly observed in asthmatic patients, it is still unclear whether it is a consequence of chronic airway inflammation or a principal contributor to the development of asthma.

Genetic susceptibility to air pollution

Asthma is a genetically complex disease caused by multiple genes and environmental factors that interact with one another. Several studies have shown that air pollution is associated with a range of respiratory effects, including asthma. Genetic susceptibility is likely to play a role in the response to air pollution exposure.

Genes involved in oxidative stress and inflammatory pathways are logical candidates for studying the interaction with air pollutants. The genes most commonly studied in this context are GSTM1, GSTP1, NQO1, and TNF. However, the inconsistency of the results prevents the drawing of firm conclusions.

One of the biological mechanisms proposed to explain the association between outdoor air pollution and asthma is oxidative stress. Pollutants can act directly by producing reactive oxygen species (ROS) and diffusing from the airway surface, or indirectly by inducing inflammation. Ozone (O3) exposure, for instance, causes ROS production and changes in the expression of claudins, leading to airway hyperreactivity (AHR) and lung injury.

Specific polymorphisms in antioxidant enzyme genes, such as the glutathione-S-transferase family, have been associated with differences in susceptibility to the adverse effects of pollutants. Adults and children with the Glutathione S-Transferase Mu 1 (GSTM1) null genotype are more susceptible to ozone, experiencing larger lung function decrements and lower pH in exhaled breath.

Linkage analyses using inbred mice identified chromosomal segments (quantitative trait loci) with genes controlling susceptibility to lung inflammatory (chromosome 17), injury (chromosome 11), and hyperpermeability (chromosome 4) responses to ozone exposure. Similar genetic mechanisms may control pulmonary responses to other pollutants as well.

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