Air Pollution And Allergies: Is There A Link?

Air pollution is a mixture of gases and particles that can be harmful to human health and the environment. It has been on the rise due to increased urbanization and industrialization, and is a major factor associated with the development of chronic allergic respiratory diseases. In fact, air pollution alone causes allergic rhinitis in 40% of the world population.

Airborne allergens are a major trigger for allergies. Pollutants such as ozone, nitrogen dioxide, and particulate matter produced by traffic and industrial activities can irritate the lungs, aggravate asthma, and make it difficult to breathe. Long-term exposure to air pollution can permanently scar lung tissue and lead to serious tissue damage or even death.

Additionally, air pollution can facilitate the penetration and access of inhaled allergens to the immune system, promoting airway sensitization and inflammation. This interaction between air pollution and allergens can enhance immunoglobulin E-mediated responses and increase the prevalence of allergic respiratory diseases, especially in urban areas.

Therefore, it is crucial to monitor and improve indoor and outdoor air quality to reduce exposure to allergens and irritants, especially for individuals with allergies and asthma.

Air pollution and allergic rhinitis

Air pollution has been on the rise due to increased urbanization and industrialization, and it is a significant factor contributing to the development of chronic allergic respiratory diseases. Allergic rhinitis (AR) is a non-communicable, IgE-mediated inflammatory disease caused by type 1 hypersensitivity reactions induced by allergen exposure. AR affects 10-30% of adults in the US and Europe and up to 40% of children, and it is often ignored, misdiagnosed, or underestimated. The condition has substantial socioeconomic impacts and affects sleep quality, productivity, and overall quality of life.

Air Pollution and AR Prevalence

The rise in air pollution, particularly from traffic diesel exhaust particles (DEP), has been linked to the increasing prevalence of allergic diseases, including AR. DEP, a solid agglomeration of carbonaceous material with volatile organic and sulfurous compounds, is emitted directly by diesel engine fuel combustion. DEP can induce an allergic response even in individuals without previous sensitization.

Mechanisms of Diesel Exhaust Particles and AR

DEP acts as an adjuvant, enhancing the immune response to aeroallergens associated with AR through various mechanisms:

• DEP enhances IgE production when co-administered with allergens.
• DEP enhances basophil activation and the release of IL-4 and IL-8, contributing to lung inflammation.
• DEP can promote de novo mucosal IgE response to an allergen, suggesting an adjuvant role in enhancing IgE response.
• DEP upregulates the expression of co-stimulatory molecules (HLA-DR and CD86) in nasal epithelial cells, contributing to enhanced allergic reactions.
• DEP increases the expression of IL-6 and IL-8 in nasal fibroblasts, aggravating nasal inflammation.
• DEP disrupts tight junctions in the nasal epithelial barrier, increasing paracellular allergen invasion.
• DEP triggers signalling pathways that lead to an enhanced inflammatory response through reactive oxygen species (ROS) generation, exacerbating AR symptoms.

Recent Studies and Treatments

Several studies have investigated the mechanisms and efficacy of medications in alleviating AR symptoms aggravated by air pollution. Fexofenadine hydrochloride is the only medication verified to alleviate AR symptoms during pollen and DEP co-exposure. Other studies have found that co-exposure to allergens and air pollutants, including DEP, ozone, nitrogen dioxide, and oil fly ash, exacerbates AR symptoms and induces changes in the allergic immune response.

Management of AR Exacerbated by Air Pollution

The first-line treatment for AR includes corticosteroids and allergen avoidance. With increasing levels of air pollution, allergen and pollutant co-exposure may need to be considered when assessing and managing AR. Education to improve awareness of air pollution and its impact on AR may be advisable, along with recommendations to avoid peak commuting hours and peak pollen seasons.

Air pollution, particularly DEP, plays a significant role in the symptom exacerbation and rising prevalence of AR. The interaction between environmental exposures and the genetic landscape of allergic disease development is critical to formulating future therapeutic modalities and management strategies for AR.

Air pollution and asthma

Air pollution can cause asthma and worsen symptoms in those already diagnosed with the condition. It can also lead to increased hospital visits and even early death.

Air pollution is the contamination of the air with harmful substances. These can be gases, chemicals, or small particles in the air.

Small airborne particles, found in haze, smoke, soot, and airborne dust, can lead to serious air quality problems. These small airborne particles are called "particulate matter" or PM. The smallest particles (PM2.5) are the most dangerous as they can get deep into the lungs or even into the bloodstream.

People with asthma are at greater risk from breathing in small particles and irritating gases. They can irritate the airways and make asthma worse.

Outdoor Air Pollution

Ozone

Ozone is one of the most common air pollutants. While it helps protect us from UV rays in the upper atmosphere, ozone causes problems when found in the air we breathe. Ground-level ozone is most common in cities where there are more cars and the burning of fossil fuels. It is also more common in the summer when there is more sunlight, heat, and low winds. Ground-level ozone is associated with worsening respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD).

Nitrogen Dioxide

Nitrogen dioxide (NO2) comes from burning fuels and emissions from cars, trucks, and power plants. Breathing in NO2 can cause someone to develop asthma and can worsen lung disease, especially asthma.

Sulfur Dioxide

Sulfur dioxide (SO2) comes from burning fossil fuels, transportation, volcanoes, and industrial processes. It can harm plants and lungs and lead to health problems.

Carbon Monoxide

Carbon monoxide (CO) forms from the incomplete combustion of fuels and wood. It has no smell and can be dangerous when it builds up inside buildings, homes, and cars.

Methane

Methane (CH4) is a gas that is part of air pollution. It mostly comes from animal agriculture and, in subarctic regions, from melting permafrost. It is a major greenhouse gas that is worsening the climate crisis. Methane can turn into ground-level ozone, which is harmful to human health.

Indoor Air Pollution

Tobacco Smoke

Tobacco smoke is a complex mixture containing over 7000 chemicals, at least 250 of which are known to be harmful and at least 69 of which are known to cause cancer. Tobacco smoke increases the risk of developing cardiovascular disease, stroke, COPD, lung cancer, and other cancers. It has an impact on asthma and is a well-known modifiable risk factor for symptom control and exacerbation.

Wood-Burning and Unflued Gas Heaters

Residential heating devices can be a large contributor to ambient PM, especially in rural communities. The majority of these heating sources are old and inefficient, resulting in high levels of PM emissions.

Cooking Behaviors

Most people from low- or middle-income countries use biomass fuel (wood, animal dung, and crop residues) or coal to cook, producing high levels of indoor pollution. Using coal and wood as cooking fuels have been identified as risk factors for asthma.

Molds

Indoor sources of molds may also be a risk factor for asthma. Exposure to increased levels of certain molds can be linked to uncontrolled asthma in males.

Air pollution and anaphylaxis

Air pollution has been identified as a major factor in the development of allergic respiratory diseases, including allergic rhinitis and asthma. These diseases can trigger anaphylaxis, a severe and potentially fatal allergic reaction.

Air pollution can cause an increase in the incidence of allergic diseases, with a variety of air pollutants attracting attention as causative factors. These include ozone, nitrogen dioxide, and particulate matter, which are produced by traffic-related and industrial activities.

Particulate matter, in particular, has been identified as a major contributor to smog and air pollution. It is produced by mechanical processes such as mining and construction, as well as the burning of fossil fuels like coal, natural gas, and petroleum products. Diesel emissions represent the majority of particulate matter in urban air pollution.

The impact of air pollution on allergic diseases has been the subject of epidemiological and toxicological research. Studies have found a causal relationship between air pollution and the exacerbation of asthma and other respiratory diseases. Air pollutants have been shown to affect the balance between antioxidant pathways and airway inflammation, leading to adverse effects on respiratory health.

Additionally, air pollution has been linked to the development of asthma and allergies. Urban air pollution, including gaseous materials and particulate matter, has been identified as an important environmental and extrinsic etiologic agent. Exposure to air pollutants, especially particulate matter and certain gaseous agents, can exacerbate asthma and lead to allergic disorders.

The impact of air pollution on allergic diseases is an area of ongoing research, with a focus on identifying susceptible subpopulations to target therapy and prevention of pollution-induced respiratory diseases.

Air pollution and eczema

Eczema, also known as atopic dermatitis, is a common skin condition that causes itchiness, rashes, dry patches, and infection. It affects over 31 million Americans and is characterised by flare-ups that can last days or weeks.

Recent studies have suggested that air pollution may increase the risk of developing eczema. Exposure to air pollution can activate the aryl hydrocarbon receptor pathway, promote oxidative stress, impair the skin barrier, and initiate a pro-inflammatory response, all of which are underlying pathologic mechanisms of eczema.

Epidemiological studies have found a positive correlation between air pollution and eczema in both children and adults. However, the results are not entirely consistent, with some studies finding no association. This may be due to varying criteria for the diagnosis and severity of eczema, age of participants, exposure and outcome assessment methods, and other co-occurring climatic factors.

In addition to outdoor air pollution, indoor air pollution has also been linked to eczema. Indoor sources of air pollution include furniture, tobacco smoke, air conditioners, stoves, wall paints, construction materials, clothing, and human body emissions.

Overall, while the comprehensive effects of environmental chemicals as triggers of eczema are still a subject of debate, eliminating exposure to known correlated chemicals might improve eczema symptoms.

Air pollution and conjunctivitis

Air pollution has been associated with an increased risk of conjunctivitis, with nitrogen dioxide (NO2) and ozone (O3) being the most significant contributors. The impact of air pollution on conjunctivitis is higher among females and those under 18 years of age.

Overview

Conjunctivitis is a common eye disease, causing serious health and economic burdens worldwide. It is characterised by inflammation of the conjunctiva, resulting in symptoms like redness, itching, and tearing. While the symptoms are typically mild and self-limiting, they can impact individuals' quality of life, affecting their daily activities, school performance, and work productivity.

Several studies have suggested a link between air pollution and conjunctivitis. A meta-analysis of 12 studies from 10 regions, including 30,103,982 conjunctivitis cases, found positive associations between six common air pollutants and conjunctivitis. The pollutants included carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), particulate matter with diameters less than 2.5 μm (PM2.5) and 10 μm (PM10), and sulfur dioxide (SO2). However, only NO2 and O3 showed statistically significant effects.

Another multi-city study in China, including data from four cities, found that short-term exposure to PM2.5, PM10, NO2, SO2, and O3 was associated with increased conjunctivitis outpatient visits. This study also found that females were more sensitive to air pollutants than males.

A study in South Korea, using public big data, investigated the relationship between weather factors, air quality, and the prevalence of conjunctivitis. It found that carbon monoxide (CO) exposure was the most important air pollutant associated with conjunctivitis, followed by month and province.

Vulnerable Populations

Vulnerable populations who are more susceptible to the effects of air pollution on conjunctivitis include females and individuals under 18 years of age.

A meta-analysis found that PM2.5, NO2, and O3 had a greater impact on conjunctivitis risk in females than in males, and in people under 18 years of age compared to those 18 and older. Another study in Hangzhou, China, also reported that females were more sensitive to air pollutants than males.

Mechanisms

The exact mechanisms underlying the association between air pollution and conjunctivitis are not yet fully understood. However, some studies have proposed the following:

• Particulate matter (PM2.5 and PM10) may cause inflammation of tissue cells and cell death by affecting the adaptability of intraocular epidermal cells.
• NO2 and O3 have strong oxidative stress effects, which may stimulate conjunctival cell inflammation.
• NO2 is an acidic gas that can change the acidic and alkaline environment of the inner epidermal cells of the eyes, disrupting their function and causing inflammation.

Limitations and Further Research

The current evidence has some limitations. Most studies used air pollutant data from fixed environmental monitoring stations rather than individual-level exposures, which may introduce measurement errors. Additionally, there is a lack of studies on the association between certain air pollutants, such as carbon monoxide, and conjunctivitis, which limits the statistical power of the analyses.

Further epidemiological research from more countries and cities is needed to comprehensively understand the effects of air pollution on conjunctivitis and to identify vulnerable subpopulations. Future studies should also explore the underlying mechanisms and the cost-effectiveness of preventive measures to improve air quality and reduce conjunctivitis incidence.

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