THE BLOG

A Prescription For Climate Change Could Reduce Your Health Problems

A study suggests reducing air pollution could lead to a lower rate of infection and help to save costs out of individual wallets and government coffers.

01/26/2018 14:05 EST | Updated 01/26/2018 14:12 EST

Climate change is a big issue in Canada as this country attempts to lead the world in the reduction of chemical emissions known to impact the planet. That being said, proposed and passed legislation at both the national and provincial levels have led to, at times, inflammatory reactions. In essence, despite the good associated with action, some Canadians do not seem to appreciate the benefits at the personal level.

Getty Images/iStockphoto

Soon, this may change thanks to a recent study from a team of researchers in Taiwan. They decided to look at how one aspect of climate change action — air pollution — harms individual health, leading to increased infection and health-care costs. The results reveal the work to reduce chemicals in the air may end up saving people and government money, now.

The study is based on a long history of air pollution studies. For well over six decades, researchers have known particles in the air can lead to troubles in the lungs. As the years have passed, the work has focused on a particular type of molecule in the atmosphere. It's officially known as fine particulate matter less than 2.5 micrometres in diameter, although it's commonly referred to as PM2.5.

As far back as the 1990s, PM2.5 was regarded as a potential threat to long-term health, and prolonged exposure could lead to chronic conditions that may shorten a person's lifespan. Over time, the short-term impact of exposure was also identified when researchers found a direct link between PM2.5 and allergic conditions such as asthma. In these cases, the particles increased the potential for irritation in the lungs, which could lessen the threshold for the trigger response.

This information alone can reveal the importance of improving our air.

Eventually, at least in mice, researchers found great exposure to these particles led to an imbalance in the immune system that could improve the chances for an attack. The same was found for normal levels of air pollution a few years later. The immediate impact of PM2.5 was revealed.

This information alone can reveal the importance of improving our air. Yet, from a population-based perspective, the results may appear not to justify the means. Reducing asthma is valuable, yet may not be worth the costs associated with carbon taxes, reduced fossil-fuel dependence and the shift to environmentally friendly energy production.

But this new Taiwanese study underscores how PM2.5 affects us all. The researchers did this by focusing on the entire immune response, not just the one associated with asthma. The team wanted to determine if each of us can be affected by exposure and, if so, how exactly that happens.

Getty Images/EyeEm

As with any theory, it first had to be tested in the lab. The team used experiments known to mimic the immune response in the lungs in the hopes of finding one marker they could then use in animal and human studies. They actually found two.

The first is known as intercellular adhesion molecule-1, or ICAM-1. It's a major player in inflammation, as it helps to recruit immune cells to an environment under attack. Based on the work in the laboratory environment, exposure to certain types of PM2.5 led to an increase in the production of this molecule suggesting more inflammation would occur.

The other marker is known as interleukin-6, most commonly referred to as IL-6. This is one of the key molecules involved in inflammation and is a regular suspect in chronic inflammatory illnesses. A rise in this molecule means the immune system is going through a fight, even if there is no real enemy.

Reducing exposure could lead to a lower rate of infection and help to save costs out of individual wallets and government coffers.

With the markers in hand, the Taiwanese team next tested their theory with mice to see if the findings held true in living animals. The results revealed the same outcome. While this was enough to show how mammals could be effective, the group they wanted to take this one step further and find out if people affected by PM2.5 had the same issues.

As one of the most common routes of exposure to PM2.5 happens to be cigarette smoke, the team asked current and ex-smokers to offer samples of their blood. Eight such people agreed and, as expected, they had higher levels of ICAM-1 and IL-6 as predicted. As controls, an equal number of non-smokers were tested. Their levels were normal. The team had shown the results from the lab, animals and humans were similar enough to suggest these two molecules were the basis for problems due to exposure.

More from HuffPost Canada:


The results of this study highlight the importance of PM2.5 on our health in the short term. As one example, the increase in inflammation due to exposure can lead to a higher risk for respiratory infection. This can be extremely costly on the health-care system as well as the individual in terms of both health and productivity. Reducing exposure could lead to a lower rate of infection and help to save costs out of individual wallets and government coffers.

The results also offer a glimpse at long-term savings as well. Both ICAM-1 and IL-6 are implicated in chronic diseases such as Type 2 diabetes, cardiac ailments and depression. Lowering the levels of these molecules by preventing PM2.5 exposure may help to keep people healthier longer.

There is little doubt the debate over actions to control air pollution in the context of climate change will continue for years to come. However, thanks in part to this study, a new reason for these efforts can be seen. Granted, the costs of these motions may seem to be a significant burden in the short term. Yet, they may end up being far less costly then the health-care and out-of-pocket dollars needed to treat ailments due to PM2.5 exposure.

Follow HuffPost Canada Blogs on Facebook

Also on HuffPost: