It has been suggested for some time that PM2·5 (the smallest type of particulates found in emissions which go unfiltered into the lungs) are associated with increased risk of diabetes; however, nobody really knew how big the effect was.
To really dig down on what was happening, last year scientists took a group of 1,729,108 US veterans and followed them to see what happened over an 8.5-year period, taking note of the all the fine details, where they live and PM2.5 levels.
Diabetes was recorded by using the International Classification of Diseases-9 code, diabetes medication prescription or abnormal blood glucose level tests.
A 10 μg/m3 (micrograms per cubic metre) increase in PM2·5 was associated with increased risk of diabetes and exposure to PM2·5 was associated with increased risk of death. An integrated exposure response function showed that the risk of diabetes increased substantially above 2·4 μg/m3, and then exhibited a more moderate increase at concentrations above 10 μg/m3.
Globally, ambient PM2·5 contributed to about 3.2million incident cases of diabetes, about 8.2million disability adjusted life year (DALYs) caused by diabetes, and 206,105 deaths from diabetes attributable to PM2·5 exposure, especially in low-income and lower-to-middle-income countries.
Importantly, the study shows that substantial risk exists at concentrations well below those outlined in the air quality standards of WHO and national and international regulatory agencies, meaning targets need to tighten even further.
The biological mechanism underpinning the association is based on the premise that pollutants enter the bloodstream where they might interact with tissue components to produce pathological effects. This mechanism is now supported by evidence both in experimental models and humans that inhaled nanoparticles, which when sufficiently small can enter the bloodstream and interact with distant organs—including liver tissue—and exhibit affinity to accumulate at sites of blood vessel (vascular) inflammation.
Both research studies and human evidence suggest that exposure to ambient air pollutants can lead to clinically significant disturbances in oxidative stress, inflammation, cell division and broad metabolic derangements in glucose and insulin homoeostasis. This includes glucose intolerance, decreased insulin sensitivity and impaired secretion, and increased blood lipid concentrations, thus providing biological mechanistic plausibility to the association of PM2·5 exposure and the risk of diabetes.
The global burden of diabetes attributable to PM2·5 air pollution is significant. Reduction in exposure will yield substantial health benefits, but protecting the body from not only breathing particles in, but also providing antioxidant and anti-inflammatory agents must also become a focus until things that contribute to emissions, such as diesel fuels, are faded out.
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