Meghan Hodges
Asthma is a complex disease influenced by genetic and environmental factors. Traffic-related air pollution (TRAP) is a significant environmental factor that can trigger asthma attacks and cause the onset of asthma in children and adults. TRAP includes pollutants such as nitrogen dioxide (NO2), ozone (O3), particulate matter (PM), and volatile organic compounds (VOCs) emitted by vehicles, as well as from the wear of brakes and tires, and road surface abrasion. Studies have shown a positive association between TRAP exposure and asthma, with higher risks in urban areas and lower-income communities. Understanding the link between TRAP and asthma is crucial for implementing preventive measures and improving air quality, especially in vulnerable communities.
| Characteristics | Values |
|---|---|
| Traffic-related air pollution (TRAP) | NO2, PM2.5, PM10, nitrogen dioxide, ozone, carbon monoxide, benzene, VOCs, hydrocarbons |
| Percentage of asthma cases due to TRAP | 27-42% in 2000, 18-36% in 2010 |
| Effect of TRAP on asthma risk | Increased risk of asthma among children: PM2.5 (meta-OR = 1.07, 95% CI:1.00-1.13), NO2 (meta-OR = 1.11, 95% CI:1.06-1.17), Benzene (meta-OR: 1.21, 95% CI:1.13-1.29) |
| TRAP exposure near homes and schools | Increased asthma risk: HR 1.51 (95% CI: 1.25-1.82) for homes, HR 1.45 (95% CI: 1.06-1.98) for schools |
| Effect of TRAP on asthma morbidity | Reducing TRAP in Southern California reduced bronchitic episodes in asthmatics by 36-70% |
| Asthma triggers | Cold weather, pet dander, smoke, poor air quality, pollutants, allergens |
| Preventative measures | Close windows and vents in cars, use air conditioning, take outdoor activities indoors or schedule them early in the day, keep quick-relief medicine on hand |
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What You'll Learn
Nitrogen dioxide, ozone, and particulate matter
Ozone (O3) is a major component of smog and is formed from photochemical reactions with pollutants such as volatile organic compounds, carbon monoxide, and nitrogen oxides emitted from vehicles and industry. Ground-level ozone is of particular concern, as it is formed from the reaction of ozone with nitric oxide emitted during fossil fuel combustion. This leads to high concentrations of nitrogen oxides near emission sites and a relative depletion of ozone in these areas.
Particulate matter (PM) refers to inhalable particles composed of sulphate, nitrates, ammonia, sodium chloride, black carbon, mineral dust, or water. PM can vary in size, with PM2.5 and PM10 being the most common in the regulatory framework and relevant for health. Exposure to PM can exacerbate existing asthma, particularly by contributing to oxidative stress and allergic inflammation. Some evidence also suggests that PM may cause new cases of asthma.
The link between these pollutants and asthma has been supported by various studies. For example, the Southern California Children's Health Study investigated the chronic effects of air pollution on respiratory health and found associations between asthma and proximity to major roads and pollutant markers. Another study of two communities in Southern California estimated that reducing nitrogen dioxide and ozone levels to background levels could reduce bronchitic episodes in asthmatics by 36-70%.
While the specific biological pathways remain unclear, it is evident that nitrogen dioxide, ozone, and particulate matter play a significant role in asthma development and exacerbation.
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TRAP exposure and urban areas
Traffic-related air pollution (TRAP) is a significant source of exposure to air pollutants in urban areas. It is a complex mixture of vehicle exhausts, secondary pollutants formed in the atmosphere, evaporative emissions from vehicles, and non-combustion emissions such as road dust and tire wear. TRAP exposure has been linked to a range of adverse health effects, including asthma.
Several studies have found a positive association between TRAP exposure and asthma incidence, particularly in urban areas. For example, a study of ten European cities attributed 14% of childhood asthma cases to exposure to road traffic pollutants. Similarly, in the United States, TRAP was found to be responsible for 27%-42% of childhood asthma cases in 2000 and 18%-36% in 2010, with higher percentages in urban areas.
The Southern California Children's Health Study (CHS) investigated the chronic effects of air pollution on respiratory health. It found a positive association between asthma and residential distance to major roads, suggesting that proximity to traffic contributes to TRAP-related asthma incidence. Furthermore, the CHS study also assessed exposure to traffic-related pollutants at participating schools, indicating that school proximity to traffic may also play a role in asthma development.
Commuting in urban areas is a significant source of TRAP exposure for individuals. Bus commuting, in particular, has been found to contribute significantly to daily exposures of fine particulate matter and other pollutants. For example, a study of three Canadian cities (Toronto, Ottawa, and Vancouver) found that bus commuting accounted for approximately 59-70% of daily exposure to particulate matter (PM2.5).
The health impacts of TRAP exposure are not limited to asthma. It has also been associated with various cardiopulmonary diseases and adverse birth outcomes. The complex mixture of pollutants in TRAP has far-reaching consequences for public health, and it is important to consider both short-term and long-term exposures when assessing health effects.
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Asthma risk and traffic-related pollution near homes and schools
Asthma is the most common non-communicable disease among children, affecting approximately 14% of children worldwide and nearly 5 million children in the United States alone. It is a leading chronic airway disease among children in the United States, and the rates have increased significantly in developed countries over the past several decades.
Several studies have found a positive correlation between traffic-related air pollution (TRAP) and the onset of childhood asthma. In a study of ten European cities, 14% of the cases of incident asthma in children and 15% of all exacerbations of childhood asthma were attributed to exposure to pollutants related to road traffic. The risk of developing asthma increases with modelled traffic-related pollution exposure from roadways near homes and schools. Ambient NO2 measured at a central site in each community was also associated with an increased risk of asthma.
The Southern California Children's Health Study (CHS) investigated the chronic effects of air pollution on respiratory health. The study found associations between asthma and residential distance to major roads and measured pollutant markers for intracommunity variation in exposure to traffic. Exposure to traffic-related pollutants has been estimated at participating schools and residences. NO2, ozone (O3), and particulate matter have been continuously measured during the lifetime of most study participants at a location in each community representative of exposure in the neighbourhoods where children live.
The results of these studies indicate that children exposed to higher levels of traffic-related air pollution at school and home are at an increased risk of developing asthma. Almost 10% of public schools in California are located within 150m of roadways with more than 25,000 vehicles daily. Urban minority children of low socioeconomic status endure disproportionately high asthma morbidity.
While the home environment has been extensively studied, many studies do not account for residential mobility or daily activity patterns, such as time spent at school. Physical education and other exercises at school may increase the ventilation rate and dose of pollutants to the lungs, thereby increasing the risk associated with exposure.
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Outdoor air pollution and asthma
Outdoor air pollution has been associated with adverse respiratory effects in children with asthma. Urbanisation is a significant contributor to asthma, and this may be due in part to increased outdoor air pollution. Notably, a study of ten European cities found that 14% of childhood asthma cases and 15% of all exacerbations of childhood asthma were attributed to exposure to pollutants related to road traffic.
Traffic and power generation are the main sources of urban air pollution. Several studies have found a link between outdoor air pollution and the onset of asthma, with one study suggesting that 27%–42% of childhood asthma cases in 2000 were due to traffic-related air pollution (TRAP). TRAP exposure, especially in urban areas, has a significant effect on disease morbidity.
The Southern California Children's Health Study (CHS) investigated the chronic effects of air pollution on respiratory health, finding associations between asthma and residential distance to major roads. Exposure to traffic-related pollutants has been estimated at participating schools and residences. The CHS study also found that asthma risk increased with modelled traffic-related pollution exposure from roadways near homes and schools. Ambient NO2 measured at a central site in each community was also associated with an increased risk of asthma.
Several pollutants have been linked to new-onset asthma, including particulate matter (PM), ozone (O3), nitrogen dioxide (NO2), and sulphur dioxide (SO2). These pollutants likely cause oxidative injury to the airways, leading to inflammation, remodelling, and an increased risk of sensitisation. However, it is important to note that not all studies support a causal link between air pollution and asthma.
Further research is needed to fully understand the mechanisms by which air pollution exposure exacerbates asthma and triggers asthma exacerbations.
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Air pollution and asthma in vulnerable groups
Asthma is a chronic respiratory disease characterised by variable airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Evidence suggests that air pollution negatively impacts asthma outcomes in both adult and paediatric populations. People with asthma are particularly vulnerable to the effects of air pollution, which can irritate the airways and trigger asthma attacks.
Traffic-related air pollution (TRAP) is a significant contributor to the onset of childhood asthma, with 27-42% of cases attributed to TRAP in 2000 and 18-36% in 2010. Urban areas and communities with lower median incomes tend to be more affected by TRAP, and studies have found a positive association between modelled traffic-related pollution exposure and asthma risk. Children living near busy roadways are more vulnerable to TRAP, and their risk of developing asthma increases with greater exposure to traffic-related pollution from nearby roads, schools, and homes.
Several pollutants have been linked to new-onset asthma, including nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and particulate matter (PM). Exposure to high levels of these pollutants can cause oxidative injury to the airways, leading to inflammation and increased risk of sensitisation. Ozone, a common air pollutant, is particularly irritating to the lungs and airways, triggering asthma symptoms. African American adolescents have been found to be more vulnerable to the effects of ozone, experiencing respiratory changes even with low-level exposure.
Indoor air pollution can also exacerbate asthma symptoms. Sources of indoor air pollution include indoor moulds, allergens, and volatile organic compounds (VOCs). Outdoor pollutants can migrate indoors, and indoor triggers can further worsen asthma.
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Frequently asked questions
Traffic and power generation are the main sources of urban air pollution. Exposure to air pollution can cause exacerbations of pre-existing asthma and can also cause new-onset asthma.
Pollutants irritate the airways, causing them to swell and tighten, which leads to breathing problems. Pollutants can also make children more susceptible to upper respiratory infections, which can trigger asthma symptoms.
Traffic-related air pollution (TRAP) is believed to be a major cause of new-onset asthma in children and adults. TRAP includes pollutants such as ozone, particulate matter, carbon oxide, nitrogen oxide, and hydrocarbons.
