Cadmium-linked inflammation mechanism is described, offering a potential therapy to limit lung injury and death caused by lower respiratory tract infections.

Cadmium is a toxic heavy metal that is ubiquitous in the environment due to its widespread industrial use. It is known to cause lung damage and increase the risk of lung cancer, but recently, researchers have found that it may also be a culprit in increasing the severity and mortality of lung infections. In this article, we will explore the mechanisms by which cadmium-induced inflammation can worsen lung infections, the factors that make certain populations more susceptible to this harm, and potential interventions that could mitigate the effects of cadmium on the respiratory system.


Lung infections are a leading cause of death worldwide, with over 1.4 million deaths a year caused by lower respiratory tract infections, including bacterial pneumonia. Heavy metals in the environment, such as cadmium, have been linked to an increased risk of death from flu and pneumonia and double the risk of lung disease, especially in communities like North Birmingham, Alabama, which have a history of housing people who worked in mines, coke plants, and heavy industries. Scientists from the University of Alabama at Birmingham have discovered a vital mechanism of cadmium-linked inflammation that increases the severity and mortality of lung infections. The community in North Birmingham is regarded as a National Priorities List area by the US Environmental Protection Agency due to pollution caused by heavy metals like cadmium in the soil and air. The researchers found that this pollution often causes tiny particulate matter less than 2.5 microns in size, which is linked to respiratory infections. The team used a mouse model to describe how cadmium, or Streptococcus pneumoniae infection, impairs the activation of PPAR-gamma in macrophages recruited to the lungs. The researchers found that the experimental drug BVD-523, which is an inhibitor for extracellular signal-regulated kinase (ERK), was successful in protecting mice from lung injury after being exposed to cadmium or infection. The scientists also found that human subjects living in industrial North Birmingham had increased cadmium levels in their lung fluids and showed PPAR-gamma inhibition. Identifying modifiable risk factors that increase individuals’ likelihood of severe pneumonia is an unmet need. Therefore, the researchers suggest that regulating PPAR-gamma in monocyte-derived macrophages may be a novel target to protect against the severity of lower respiratory tract infections secondary to lung injury caused by air pollution.


In conclusion, cadmium-induced inflammation plays a significant role in worsening the severity and mortality of lung infections. With the increasing levels of cadmium in the environment due to various human activities, it is essential to explore and understand the critical mechanisms through which cadmium exposure affects the immune response to infections. This article sheds light on the potential underlying mechanisms of cadmium-induced inflammation and emphasizes the importance of limiting cadmium exposure to reduce the risk of severe lung infections. Therefore, further studies are necessary to identify novel therapeutic strategies to treat and prevent the adverse effects of cadmium exposure on lung health.