Research by King’s College indicates diesel air pollutants can weaken people’s immune systems

Dr Ian Mudway, of King’s College London, has warned that thousands of Londoners may be having their immune system slowly aggravated by the effects of diesel fumes. The very young and very old – and those with existing lung conditions – are particularly vulnerable to being harmed by particulate air pollution. At a meeting of the British Thoracic Society meeting, Dr Mudway said pollution from combusting diesel is also suspected to be gradually attacking some people’s immune system, meaning they will be more likely to suffer illnesses. These impacts may be slow and insidious, only manifesting slowly as we age.  A person’s genetic make-up is a key factor to whether they susceptible to the immune system damage. Research indicates that diesel exhausts including tiny PM2.5 particulates which can get deep into lungs, interact with immune cells in ways that may make the airways more susceptible to infections and allergic reactions.  Dr Mudway said:  “Some people are almost bullet proof, other people will be very sensitive to it.”  Many of the health impacts of air pollution are “sub-clinical”, so do not show up immediately with symptoms. They may, however, be having long term effects. Earlier research in 2010 showed the impact of air pollution in influencing a gene, which resulted in increasing the severity of asthma in children,


Londoners’ immune systems ‘weakened by capital’s toxic air’



Hundreds of thousands of Londoners may be having their immune system slowly aggravated by toxic diesel fumes, a leading expert warned today.

Dr Ian Mudway, of King’s College London, also stressed that young and old – and those with existing lung conditions – are particularly vulnerable to being harmed by filthy air in the capital.

Scientists have made a series of shocking revelations in recent years about the toxic air scandals in London, Paris, Beijing and other capitals, focusing largely on the grim death toll from pollutants which are shortening the lives of millions of people.

But Dr Mudway highlighted at a British Thoracic Society’s meeting in Westminster today that pollution in diesel emissions is also suspected to be gradually attacking some people’s immune system, meaning they will be more likely to suffer illnesses.

“In individuals with pre-existing lung disease the contaminants within the air we breathe can have immediate tangible effects, such as symptomatic ‘flare-ups’ during pollution episodes,” he said.

“But for most of us the effects are more insidious, with the impacts only manifesting slowly as we age.”

Hundreds of thousands of Londoners will be walking around the city unaware that their lungs are being inflamed by toxic pollution, explained Dr Mudway.

A proportion of these individuals risk having their immune system damaged, he added.

Their genetic make-up is likely to be a key factor to whether they are a victim of toxic fumes, with diesel emissions, including tiny PM2.5 particulates which can get deep into lungs, believed to be particularly harmful.

“Some people are almost bullet proof, other people will be very sensitive to it,” he added.

Much of the work highlighted was carried out in London and aimed to identify the most damaging pollutant sources of toxic air.

“The smoking gun points to diesel emissions and further strengthens the arguments to target emissions from these vehicles to improve the respiratory health of Londoners,” said Dr Mudway.

His warning is all the more alarming as hundreds of schools in London are near roads with heavy traffic spewing out fumes as pupils walk to school.

Filthy air levels are higher in central London, with three wealthy areas, Westminster, the City, and Kensington and Chelsea, being the worst blackspots for tiny particulate PM2.5 pollution for five years in a row.

Dr Mudway stressed that many of the health impacts of air pollution are “sub-clinical”, so do not show up immediately with symptoms.

But the death toll from nitrogen dioxide and PM2.5 pollution has been estimated at more than 9,000-a-year in London.

This is not the number of people dying from toxic air but the accumulated total of lost life attributable to it.

Tamzen Isacsson, of the Society of Motor Manufacturers & Traders, stressed the industry was investing billions to engineer the cleanest vehicles in history.

“The latest Euro VI diesel cars are light years away from their older counterparts, with high tech filters capturing 99% of all soot particulates – and the introduction of on road emissions testing from next year will drive even greater advances,” she added.

“The biggest change to air quality will be achieved by encouraging uptake of the latest, lowest emission technologies, regardless of vehicle or fuel type, and ensuring road transport can move smoothly.”


Dr Ian Mudway.


See earlier

Air pollution alters immune function, worsens asthma symptoms

Exposure to dirty air is linked to decreased function of a gene that appears to increase the severity of asthma in children, according to a joint study by researchers at Stanford University and the University of California, Berkeley.

While air pollution is known to be a source of immediate inflammation, this new study provides one of the first pieces of direct evidence that explains how some ambient air pollutants could have long-term effects.

Researchers have linked exposure to dirty air to changes in a gene that, in turn, is connected to more severe asthma symptoms.

The findings, published in the October 2010 issue of the Journal of Allergy and Clinical Immunology, come from a study of 181 children with and without asthma in the California cities of Fresno and Palo Alto.

The researchers found that air pollution exposure suppressed the immune system’s regulatory T cells (Treg), and that the decreased level of Treg function was linked to greater severity of asthma symptoms and lower lung capacity. Treg cells are responsible for putting the brakes on the immune system so that it doesn’t react to non-pathogenic substances in the body that are associated with allergy and asthma. When Treg function is low, the cells fail to block the inflammatory responses that are the hallmark of asthma symptoms.

The findings have potential implications for altered birth outcomes associated with polluted air, much the same as those noted for the effects of cigarette smoke.

“When it came out that cigarettes can cause molecular changes, it meant the possibility that mothers who smoked could affect the DNA of their children during fetal development,” said study lead author Dr. Kari Nadeau, pediatrician at Stanford’s Lucile Packard Children’s Hospital and an assistant professor of allergy and immunology at Stanford’s School of Medicine. “Similarly, these new findings suggest the possibility of an inheritable effect from environmental pollution.”

Seventy-one participants came from the Fresno Asthmatic Children’s Environment Study (FACES), a longitudinal study led by principal investigator Dr. Ira Tager, professor of epidemiology at UC Berkeley’s School of Public Health, and co-principal investigator S. Katharine Hammond, UC Berkeley professor and chair of environmental health sciences. The researchers also recruited 30 children from Fresno who did not have asthma.

“I’m not aware of any other studies that have looked at how chemicals can alter cells so early in the regulatory process, and then connected that effect to clinical symptoms,” said Tager. “There are people who still question the direct link between air pollution and human health, but these findings make the health impact of pollutants harder to deny.”

Fresno was chosen because it is located in California’s Central Valley, where trapped hot air mixes with high traffic and heavy agriculture to create some of the highest levels of air pollution in the country. It is also a region known for its high incidence of asthma: Nearly one in three children there have the condition, earning Fresno the nickname, “The Asthma Capitol of California.”

The researchers compared the participants from Fresno with 80 children, half with asthma and half without, in the relatively low-pollution city of Palo Alto, Calif. The children were matched by age, gender and asthma status, among other variables. The children were tested for breathing function, allergic sensitivity and Treg cells in the blood.

Daily air quality data came from California Air Resources Board monitoring stations. The researchers calculated each child’s annual average exposure to polycyclic aromatic hydrocarbons (PAH), a byproduct of fossil fuel and a major pollutant in vehicle exhaust.

The study found that the annual average exposure to PAH was 7 times greater for the children in Fresno compared with the kids in Palo Alto. Levels of ozone and particulate matter were also significantly higher in Fresno.

Not surprisingly, the study found that the children in Fresno had lower overall levels of Treg function and more severe symptoms of asthma than the children in Palo Alto. For example, the non-asthmatic children in Fresno had Treg function results that were similar to the children with asthma in Palo Alto.

The study authors correlated increased exposure to PAH with methylation of the gene, Forkhead box transcription factor (Foxp3), which triggers Treg cell development. Methylation effectively disables the gene’s function, leading to reduced levels of Treg cells. The connection between Treg function and the severity of asthma symptoms was true for children in both groups.

While previous studies have found associations between pollution – especially motor vehicle exhaust – and an increased risk of developing asthma, few have traced its molecular pathway so completely, the study authors said.

“The link between diesel exhaust and asthma could simply have been that the particulates were irritating the lungs,” said Nadeau. “What we found is that the problems are more systemic. This is one of the few papers to have linked from A to Z the increased exposure to ambient air pollution with suppressed Treg cell levels, changes in a key gene and increased severity of asthma symptoms.”

The researchers noted that Treg cells are important for other autoimmune disorders, so the implications of this study could go beyond asthma.

Other co-authors of the study are Dr. John Balmes, UC Berkeley professor of environmental health sciences; Elizabeth Noth and Boriana Pratt, UC Berkeley researchers at FACES; and Cameron McDonald-Hyman, research assistant at Stanford University’s School of Medicine.

The National Institutes of Health, U.S. Environmental Protection Agency, the American Lung Association and the Mickey Leland National Urban Air Toxics Research Center helped support this research.