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A team of researchers, led by Dr. Stephan Schwander, of the University of Medicine and Dentistry of New Jersey - School of Public Health (UMDNJ-SPH), and funded by the National Institute of Environmental Health Sciences, has determined a possible link between exposure to a common component of urban air pollution and a change in the function of important immune cells that protect against the bacteria that cause tuberculosis (Mycobacterium tuberculosis).
Writing in the Journal of Immunology, the scientists describe their findings that exposure to diesel exhaust particles (DEP) suppresses the function of phagocytic immune cells (a type of white blood cells that ingest foreign particles, such as bacteria) on a cellular level. They conclude that this exposure probably causes exposed individuals to be less able to fight off new Mycobacterium tuberculosis infections or to suppress a reactivation of a latent infection by these bacteria.
In laboratory experiments using DEP generated from an automobile diesel engine as model air pollutant particles, and blood samples gathered from 20 healthy individuals, we demonstrated that exposure to DEP makes cells less responsive, says Schwander. The cells, in effect, became desensitized to stimulation with the bacteria that cause TB, he explains. This effect was even greater in cells that had prior exposure to DEP than in those that had concurrent DEP and Mycobacterium tuberculosis exposure.
Tuberculosis is estimated to afflict approximately 8-10 million people and to cause 1.5 million deaths each year worldwide. The incidence of the disease is particularly high in low- and middle-income countries that are experiencing rapid industrial growth and increases in motor vehicle traffic in densely populated urban areas. By the year 2030, scientists estimate that 50 percent of the worlds population will live in urban environments.
Because there is already epidemiological evidence that connects tuberculosis to cigarette smoking and some forms of indoor air pollution, it seemed logical to look at outdoor air pollution for a similar correlation, Schwander adds. The models we used indicated that this may, in fact, be the case. The next step is to see if these results can be confirmed by larger epidemiological studies, conducted in a real world environment.