Continuous exposure to pollution may have a direct biological effect on chronic nasal and sinus tissue inflammation, according to researchers at Johns Hopkins, who have finally found molecular evidence of this in their experiments in mice. They published their results in the American Journal of Respiratory Cell and Molecular Biology, and these have wide-ranging implications for individuals living in large cities and industrial areas, especially in developing countries.
“In the US, regulations have kept a lot of air pollution in check, but in places like New Delhi, Cairo, or Beijing, where people heat their houses with wood-burning stoves, and factories release pollutants into the air, our study suggests people are at higher risk of developing chronic sinus problems,” said Murray Ramanathan, MD, associate professor of otolaryngology - head and neck surgery, Johns Hopkins University School of Medicine, Baltimore, MD.
In the United States, over 12% of adults have chronic sinusitis, which is over 29 million people, according to the Centers for Disease Control and Prevention (CDC), and experience congestion, pain, facial pressure, and a stuffy, drippy nose. The social implications of chronic sinonasal disease can include depression, lost productivity, and chronic fatigue.
Although smog, ash, and other particulate matter from industrial smokestacks and other air polluters have been known to increase asthma symptoms, until now, researchers have failed to find evidence that these pollutants have similar damaging effects on the upper respiratory system.
For 6 hours per day, 5 days per week, for 16 weeks, Dr. Ramanathan and colleagues exposed 38 male mice (8-weeks-old) to either filtered air (n=19), or concentrated Baltimore air (n=19) with particles less than or equal to 2.5 micrometers, which were 30% to 60% lower in concentration than average concentrations of similar sized particles in New Delhi, Cairo, and Beijing.
Researchers flushed the noses and sinuses of these animals, and looked for inflammatory and other cells. In the mice that breathed polluted air, they found more white blood cells, including macrophages, neutrophils, and eosinophils, compared with those breathing filtered air.
In addition, they found higher levels of messenger RNA in the nasal fluid of mice breathing polluted air in the genes for interleukin 1b, interleukin 13, oncostatin M, and eotaxin-1, all direct protein biomarkers of inflammation.
Dr. Ramanathan and fellow researchers found 5 to 10 times higher concentrations of inflammatory cytokines in the mice breathing polluted air compared with those breathing filtered air.
“Inflammation that attracts eosinophils is what happens in the lungs of people with asthma; so essentially the chronic exposure to air pollution in mice is leading to a kind of asthma of the nose,” says Dr. Ramanathan.
The nasal epithelium in mice breathing polluted air was 30% to 40% thicker—another inflammatory manifestation—than those breathing filtered air. They also found less claudin-1 and E-cadherin in mice breathing polluted air, and up to 80% less E-cadherin [Query: Is this sentence correct? See original]. Protein serum albumin levels were also much higher in mice breathing polluted air, indicating that the barriers to the nasal passages and sinuses had been breached.
“We’ve identified a lot of evidence that breathing in dirty air directly causes a breakdown in the integrity of the sinus and nasal air passages in mice,” noted Dr. Ramanathan. “Keeping this barrier intact is essential for protecting the cells in the tissues from irritation or infection from other sources, including pollen or germs.”
He added that his team plans to perform further studies of the specific molecular changes that occur when the sinus and nasal barriers are breached because of air pollution, as well as ways to repair them.
The study was funded by grants from the National Institute of Environmental Health Sciences (ES020859 and U01 ES026721) and the Flight Attendant Medical Research Institute.