In a recent article published in the British Medical Journal (BMJ), researchers at Harvard T.H. Chan School of Public Health presented the findings of a systematic review and meta-analysis that showed a link between air pollutants, especially particulate matter 2.5 (PM2.5) and clinical dementia. PM2.5 are fine air particles/droplets two and one-half microns or less in width.
Study: Ambient air pollution and clinical dementia: systematic review and meta-analysis. Image Credit: fran_kie / Shutterstock
Background
Over 57 million people globally are living with dementia. Estimates suggest an uncontrollable surge in dementia cases worldwide, with numbers expected to rise to 153 million by 2050. There is enough evidence that nearly 40% of these cases arise due to potentially modifiable risk factors, such as long-term exposure to ambient air pollution.
Indeed, it is a hugely important health topic and a research priority. Accordingly, in the past decade, studies evaluating the association between ambient air pollution and dementia have increased substantially. However, they used varying approaches to quantify the associations between long-term exposure to air pollutants and the rise in dementia cases.
Overall, there remains a scarcity of systematic reviews that could provide actionable results that regulatory agencies and clinicians could use to guide patients and the public regarding dementia risk due to rising air pollution.
About the study
In the present study, researchers scanned more than 2,080 studies from databases, such as PubMed, Web of Science, and EMBASE, from their launch till July 2022. All these studies considered air pollutants and alternatives of traffic pollution that met the United States Environmental Protection Agency criteria, had adult (≥18 years) participants, and performed a longitudinal follow-up. More importantly, these studies averaged exposure to these air pollutants over a year to show a relationship between ambient air pollutants and clinical dementia.
Further, two independent authors assessed the risk of potential bias in included environmental studies utilizing the Risk of Bias In Non-randomised Studies of Exposures (ROBINS-E) tool, which addresses these biases more intensively than prior approaches, which might impact the interpretation of final results.
Another distinguishing feature of this meta-analysis was that it used active case ascertainment. This method allowed screening of the whole study population for dementia among those who did not have this condition at baseline. Finally, the team used Knapp-Hartung standard errors to do a meta-analysis when a minimum of three studies for a given air pollutant used similar approaches.
Study findings
The team identified 51 studies that examined the relationship between ambient air pollution and dementia, all of which were published in the past decade. However, they used only 16 in the meta-analyses after screening via the ROBINS-E tool. Of 14 studies on PM2.5, seven used active case ascertainment, and seven, six, and one were from North America, Europe, and Hong Kong, respectively.
The researchers found adequate evidence of the relationship between PM2.5 and clinical dementia, even in regions where annual exposure was far below the current European Union regulations' annual standard of 12μg/m3. Every 2 to 3 μg/m3 upsurge in average yearly exposure to PM2.5 increased the risk of developing dementia by 17%, especially among the studies using active case ascertainment.
Based on the studies with active case ascertainment, the researchers derived the best estimates. Accordingly, the best estimate for the effect of a 2 μg/m3 higher concentration of PM2.5 was a hazard ratio (HR) of 1.42. However, given time trend biases, a more conservative estimate was 1.17. The confidence limits were too wide for both estimates. Thus, these findings need to be interpreted with caution.
Further, the authors found evidence of the relationship between dementia and nitrogen oxide (NOx) and nitrogen dioxide (NO2) levels, though data was limited. They determined a 5% and 2% rise in risk for every 10 μg/m3 increase in yearly exposure to NO2, respectively.
Furthermore, the authors noted that air pollution's projected relationship with dementia risk was relatively lower compared to other risk factors, e.g., smoking. However, since more people get exposed to air pollution, its repercussions on human health could be considerable at the mass scale.
Conclusions
The current review findings suggested that exposure to ambient PM2.5 increased dementia rate, and likely NO2 and NOx; however, data for the latter is limited. Nevertheless, these results strengthen the evidence that air pollution is one of the most important modifiable risk factors for clinical dementia. Thus, mitigation efforts to decrease exposure to air pollution might help reduce the burden of dementia. For this, clinicians need to communicate measures that patients could take to reduce their exposure on a personal level. However, more importantly, regulatory agencies should take steps at the policy level for the best outcomes.
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