Published online: January 23, 2020
Air pollution levels remain dangerously high in many parts of the world, despite strict emissions guidelines. The World Health Organisation estimates that 7 million people worldwide die each year as a result of exposure to airborne particulates, and many of these deaths are linked to respiratory infections, such as pneumonia. Air pollution levels are highest in low and middle-income countries, where the incidence of invasive pneumococcal disease is also high. Streptococcus pneumoniae is the most common cause of pneumonia worldwide, with mortality rates of over 20% in patients with accompanying septicaemia. In the majority of healthy people, this bacterium can harmlessly colonise the back of the nose and throat without causing any symptoms. However, if the bacterium is able to gain access to normally sterile sites such as the lungs, blood and meninges, it has the potential to cause life-threatening disease such as pneumonia, septicaemia and meningitis. Little is known about the conditions that allow this switch from harmless commensal to a potentially life-threatening pathogen, however exposure to high levels of pollution is a known risk factor.
This study, published by Shears et al. in The Journal of Allergy & Clinical Immunology (JACI) demonstrates a clear link between daily inhaled exposure to diesel exhaust particles (DEP), a major component of airborne traffic-related pollution, and susceptibility to pneumococcal pneumonia and sepsis. Shears et al. demonstrate, using a combination of mouse models and lab-based assays with human cells, that exposure to DEP disrupts the delicate balance between S. pneumoniae and the host in the respiratory tract, promoting an environment permissive of bacterial dissemination to the lungs.
The authors found that following exposure to DEP, airway macrophages, which are key cells for controlling bacterial infections and removing debris from the body, become congested with DEP, reducing their ability to kill the pneumococcus. The authors also show that pneumococci are transported from the nasopharynx to the lungs following adherence to DEP and are able to utilise DEP as a source of metabolites, which may promote survival within the airways. These factors allow the bacterium to invade the lungs, and cause significant inflammation, which eventually leads to bacterial translocation into blood, thereby causing severe disease.
This study provides compelling evidence that exposure to particulate pollutants such as DEP can alter the relationship between the host and pneumococcus, tipping the balance towards invasive pathogenicity. Given that 91% of the world’s population inhabit areas where the air pollution exceeds World Health Organisation guideline limits, this study suggests that reducing the amount of airborne pollution has the potential to reduce the global burden of pneumococcal disease significantly.
The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.