The Impact of Ultrafine Particles on Human Health

Ultrafine particles

Introduction to Ultrafine Particles

In the realm of air pollution, there is an ongoing concern about the harmful effects of various particulate matter on human health. Over the years, researchers have extensively studied the impact of different types of particles on the respiratory system and their potential role in causing diseases. One particular group that has emerged as a topic of interest is ultrafine particles.

Ultrafine particles, also known as nanoparticles, are defined as particles with a diameter less than 100 nanometers. These are incredibly small compared to the cellular structures of the lungs, which raises concerns about their ability to penetrate deep into the respiratory system and potentially cause adverse health effects. In this article, we will explore the characteristics of these, their sources, and their potential impact on human health.

Characteristics of Ultrafine Particles

Ultrafine particles are polydispersed, meaning they come in a range of sizes. While particles with diameters ranging from 90 nm to 110 nm are commonly categorized as ultrafine, there is no clear cut-off point for their adverse effects. These are significantly smaller than the cellular structures in the lungs, allowing them to easily penetrate deep into the respiratory system.

To visualize the size difference, imagine comparing ultrafine particles with a bronchial epithelium. Even particles as small as 0.1 μm (100 nm) are barely visible in comparison. This small size and ability to reach the deepest parts of the lungs make these a potential health hazard.

Sources of Ultrafine Particles

Ultrafine particles can be found in various environmental settings, particularly in urban areas where particulate air pollution is prevalent. Diesel exhaust particles, for example, can serve as an example of fine particles in the form of singlet particles with a size of 10-20 nm. However, these often form aggregates with other substances such as sulphates, metals, and hydrocarbons.

While diesel soot particles are a common source of ultrafine particles in urban air, it is important to note that there are other potential sources as well. For experimental purposes, researchers often use standard fine particles like titanium dioxide and carbon black to study their toxicological effects.

Moreover, these particles also have industrial applications, such as ultrafine carbon black. This suggests the possibility of occupational exposure to these particles, although the extent of the risk to workers has not yet been fully assessed.

Particles in Ambient Air

Ultrafine particles are a significant component of particulate air pollution, which is often measured using the PM10 sampling convention. PM10 refers to the mass of particles collected with a 50% efficiency for particles with an aerodynamic diameter of 10 μm. It closely corresponds to the fraction of inhaled particles that penetrates beyond the larynx to the airways.

While these contribute modestly to the mass of particulate air pollution, they are the predominant particle size by number in urban PM10. Their small size allows them to exist as both singlet particles and aggregates in the air. High power transmission electron microscopic images of PM10 particles collected from urban areas often reveal aggregates comprising chains and clumps of ultrafine particles.

Health Effects Associated with PM10

Increases in PM10 pollution have been associated with a range of adverse health effects. These effects have been extensively documented and include increased use of medication for asthma, asthma attacks in patients with pre-existing asthma, attacks of chronic obstructive pulmonary disease (COPD), admission to hospitals for cardiovascular causes, and even deaths from heart attacks, strokes, and respiratory causes.

While the components of PM10 are not highly toxic on their own, attention has shifted towards identifying the components that are most likely to have toxic potential. Ultrafine particles have been identified as potential mediators of some of the toxicity of PM10 based on toxicological findings and some epidemiological data.

Susceptibility to PM10 Effects

Interestingly, the acute adverse health effects of PM10 are primarily observed in susceptible subgroups, rather than in normal healthy individuals. This observation suggests that there may be factors of susceptibility in these subgroups that contribute to a heightened response to ultrafine particles.

For instance, patients with asthma, COPD, and cardiovascular disease exhibit a greater response to these particles, potentially due to pre-existing inflammation in their lungs. The presence of inflammation or other factors of susceptibility in these individuals may prime their lungs to hyperrespond to ultrafine particles, leading to adverse health effects.

It is important to note that there may also be chronic effects of exposure to PM10 that can affect normal individuals. However, studying these effects proves challenging. While concentrations of these particles were not measured in previous studies on PM10 effects, it remains a hypothetical possibility that they play a role in these chronic health effects.

Deposition of Ultrafine Particles

When considering the deposition of these particles, it is essential to account for their existence as both singlet particles and aggregates. The deposition characteristics of aggregates can vary depending on their compactness. More open aggregates with chains and extensions tend to have greater aerodynamic resistance and a smaller aerodynamic diameter.

Studies have shown that singlet particles with aerodynamic diameters as small as 10 nm readily deposit in the airways and centriacinar regions of the lung. Furthermore, pathological changes in the lungs, such as airway narrowing found in conditions like COPD and asthma, can increase the efficiency of deposition. This may contribute to the heightened susceptibility of individuals with these respiratory conditions to the effects of ultrafine particles.

However, further studies are needed to understand the sites of deposition of the various components of the urban aerosol and the potential differences in the lung’s response to singlet particles versus aggregates.

Evidence of Toxicity

While there is limited direct evidence on the effects of ultrafine particles on human health, toxicological studies with surrogate particles provide valuable insights. These studies, often conducted with carbon black and titanium dioxide particles, consistently demonstrate greater inflammatory effects of fine particles compared to larger ones of the same material.

In human studies, a decrement in evening peak flow in asthmatic patients was found to be associated with the fine component of airborne particles during episodes of severe air pollution. This association suggests a potential role for ultrafine particles in exacerbating respiratory symptoms in susceptible individuals.

Animal studies have also shown that exposure to high concentrations of fine particles can lead to pulmonary overload, characterized by the accumulation of particles in the lungs, inflammation, proliferation, fibrosis, and even tumor production. Even low toxicity particles like carbon black and titanium dioxide can cause overload pathology in rats when exposed at high concentrations.

Phagocytosis and Inflammation

Phagocytosis, the process by which alveolar macrophages clear particles from the lungs, plays a crucial role in the response to inhaled toxins. Studies have shown that these can impair the phagocytic ability of macrophages, inhibiting their ability to clear particles effectively.

The mechanism behind this impairment of phagocytosis may involve cell-to-cell contact rather than soluble mediators. The increased oxidative stress from the large surface area of fine particles is believed to contribute to this effect. Decreased phagocytosis allows for enhanced interaction between ultrafine particles and the epithelium, leading to the release of pro-inflammatory cytokines by macrophages and chemokines by the epithelium.

Oxidative Stress and Calcium

Ultrafine particles have also been linked to oxidative stress and changes in calcium levels in macrophages and epithelial cells. Studies have shown that exposure to ultrafine carbon black increases oxidative stress and pro-inflammatory effects in rats. Furthermore, these particles have been found to increase the resting cytosolic calcium concentration in human monocytic cell lines.

These cellular events, including cytokine and chemokine gene transcription, are likely driven by oxidative stress and calcium changes. The large surface area of these, contributes to oxidative stress, while the amplification of the calcium signaling pathway may enhance the pro-inflammatory effects of these particles.


In conclusion, ultrafine particles represent a unique class of particles with the potential to cause adverse health effects. Their small size allows them to penetrate deep into the respiratory system, posing a risk to human health. While there is still much to learn about the specific mechanisms of particle toxicity, evidence from toxicological studies and limited human studies suggest that these can induce inflammation and exacerbate respiratory symptoms, particularly in susceptible individuals.

Further research is needed to fully understand the role of these in the adverse health effects of particulate air pollution. This includes investigating the specific sites of deposition, the chronic effects of exposure, and the potential risks associated with occupational exposure to these particles. By continuing to expand our knowledge in this area, we can better protect public health and develop effective strategies for mitigating the impact of ultrafine particles on human well-being.