Link between asthma symptoms and air pollution is modified by genetic differences

Asthma is a complex disorder that is made up of both heritable genetic factors and environmental exposures. There are a number of genetic mutations that change a single letter in the DNA of a gene, called single nucleotide polymorphisms or SNPs, which have been linked risk for asthma. Many of these SNPs are in genes that are linked inflammation in the airway. One such gene, which is through to play a role in the response to air pollution, is TLR4 (Toll-like receptor 4). A team of researchers from North Carolina recruited people with or without asthma (1741 without asthma, 963 with asthma) for a study working to understand how mutations in genes associated with the TLR4 pathway affect response to air pollution in asthmatics.

To start with, the researchers grouped the participants into 3 categories based on their SNPs in key genes (related to the TLR4 pathway): Predicted to be Hyper-responsive to air pollution, hypo-responsive to air pollution, or neither. They then recorded the frequency and type of symptoms in each participant and measured their distance to the nearest major road (less than 250m or greater then 250 meters). Putting all this data into a statistical model, they found that:

  • There was a trend towards an increased risk for asthma if participants lived near a major road and were in the hyper-responsive to air pollution group. This difference was not quite statistically significant however likely owing to a number of confounding variables.
  • Hypo-responders, those who were less likely to respond to air pollution, had fewer symptom problems including: activity limitations, sleeplessness, and fewer exacerbations.

This data suggests that living near a major road could exacerbate symptoms for people who have asthma and have a genetic profile that makes them more susceptible to reacting to the air pollution. There are a few limitations with this study, namely the small sample size after categorizing people into the three groups. Only 369 people were classified as hyper-responders (13% of the original sample) and fewer still were classified as hypo-responders (132, 4.9% of the original sample). This makes it difficult to assess whether some of the results that showed a trend (risk for asthma, risk for exacerbations) may have been significant with more participants. Additionally, there was no available data on how long any participant lived in the house during the study or how many hours a day they resided beside the major road. These could have significantly influenced the exposure to air pollution and therefore the outcomes measured. Finally, other factors such as noise and loss of sleep from living close to a major road could account for some of the associations and must be taken into account. All in all, this study sheds light on an important problem in our modern society; is our exposure to traffic pollution worsening chronic lung disease in people and can a more careful design of city roads and residential housing remedy this concern?

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