Elevated Respiratory Infection Risk in Pediatric Populations Associated With Ambient Air Pollution

Air pollution exposure, both before and after birth, significantly escalates the risk of respiratory infections in children. | Image Credit: Wimon - stock.adobe.com

Both prenatal and postnatal air pollution exposure is a major risk factor for respiratory infections in children, highlighting an urgent need for further investigation into the complex interplay of pollutants and environmental factors to safeguard vulnerable pediatric populations, according to a study published in Frontiers in Public Health.1

Air pollution causes profound health impacts, making it one of the leading causes of morbidity and mortality. The World Health Organization associates it with 7 million premature deaths annually.2 Contaminants in the atmosphere, like dust, fumes, gas, mist, odor, smoke, or vapor, can endanger human health.3 Since the main pathway of air pollution exposure occurs through breathing, the respiratory tract faces a heightened risk of damage.

Children are more likely to develop respiratory-related conditions from air pollution compared with adults because of their immature immune systems, which ultimately makes them a more vulnerable population.1 Air pollution develops asthma among children, but researchers understand less of the connection between air pollution and respiratory infections.

Researchers conducted a comprehensive literature review that included studies from January 2000 to December 2024. The study's primary end point was to synthesize current knowledge on the potential association between air pollution and respiratory infections in children to highlight existing knowledge gaps.

The air pollutants with the most significant adverse health impacts include particulate matter, nitrogen oxides (NO and NO2), ground-level ozone, sulfur dioxide, and carbon monoxide. Particulate matter originates in diverse settings, including fuel combustion, industrial activities, wildfires, wood burning, gravel pits, agricultural operations, and dusty roads. Common components of particulate matter include sodium chloride, elemental carbon, trace metals, and minerals. Ultrafine particles, despite their small mass, can significantly boost respiratory and systemic damage due to their high toxicity and content of transition metals and organic compounds.

Air quality assessors often evaluate through the Air Quality Index (AQI), a standardized scale derived from the measurements of air concentrations of major pollutants. When the AQI is below 50, researchers consider it safe, whereas they deem values above 100 unhealthy, especially for vulnerable populations.

Various factors influence the risk of respiratory infections, including site of deposition, penetration capacity, bioavailability, and the long residence time of pollutants in the air. Air pollutants exhibit specific toxic properties like promoting oxidative stress, inducing inflammatory responses, deregulating the immune system, and causing genetic alterations. Despite the available data, researchers do not know if the concentrations of pollutants that cause tissue damage in experimental settings represent real-world exposures in humans.

Reactive oxygen species, including oxygen and hydroxyl radicals, hydrogen peroxide, and singlet oxygen, cause oxidative stress. When reactive oxygen species levels become too high, they can oxidize DNA, proteins, and lipids, leading to genomic instability, impaired protein function, and cellular harm or death. Rising pollutant levels intensify reactive oxygen species production, surpassing antioxidant defenses and resulting in oxidative stress and tissue damage. Oxidative stress from air pollution causes mucus hypersecretion, damages lung macrophages and bronchial epithelial cells, inactivates antiproteases, and leads to bronchial wall edema and bronchoconstriction in the respiratory tract.

Oxidative stress and direct exposure to air pollutants can lead to severe inflammation and dysregulate antimicrobial and antiviral immunity in the respiratory tract, increasing the risk of overall infections. Particulate matter exposure triggers inflammation and drives inflammatory cells into respiratory tissues. Similarly, NO2 affects both inflammation and immunity. Notably, NO2 exposure during pregnancy is linked to DNA methylation of mitochondria-related genes and altered antioxidant defense gene expression in offspring.

All pediatric age groups saw more upper and lower respiratory infections, with infants, toddlers, and preschoolers being most susceptible. Both short- and long-term exposure to air pollution correlated with these increases, and prenatal exposure was specifically linked to higher rates of respiratory infections after birth.

Air pollutants, especially particulate matter, can enter the fetal circulatory system. Researchers found some amounts in fetal tissues as early as the first and second trimesters of pregnancy. Pollutants often interrupt normal lung development, which ultimately increases susceptibility to infections through oxidative stress, impaired placental function, and epigenetic modifications.

Lungs become more susceptible to infections due to significant structural and functional changes caused by early life exposure, both prenatally and postnatally. Prior long-term research included in the review demonstrated lasting lung damage from prenatal exposure, evidenced by impaired lung function in children up to age 9.

Air pollution, even with short exposure, can greatly raise the risk of respiratory infections. Extended exposure has a strong connection to increased respiratory infections, leading to higher child mortality rates from lower respiratory tract infections in areas with poor air quality. A review highlighted this, finding over 690,000 deaths in children under 5 due to particulate matter, predominantly in low and middle-income nations.

Some reviewed studies limit the overall research because they did not adequately control for confounding factors and relied on indirect measures of exposure, the authors noted. Most research occurred in high-income or upper-middle-income countries, where pollution levels and population characteristics differ from those in low-income countries, which limits the generalizability of the findings. Lastly, exposure and outcome assessments carry a high risk of bias, and similar issues arise in studies of postnatal air pollution exposure.

“Addressing these knowledge gaps and implementing evidence-based policies will be crucial in developing more targeted, effective, and sustainable approaches to protecting children from the harmful effects of air pollution,” the authors concluded.

References

1. Esposito S, Fainardi V, Titolo A, et al. How air pollution fuels respiratory infections in children: current insights. Front Public Health. 2025;13:1-9. doi:10.3389/fpubh.2025.1567206
2. Air Pollution. World Health Organization. Accessed July 10, 2025. https://www.who.int/health-topics/air-pollution#tab=tab_2
3. Air quality, energy and health. World Health Organization. Accessed July 10, 2025. https://www.who.int/teams/environment-climate-change-and-health/air-quality-energy-and-health/health-impacts