Air Pollution Implicated as a Contributing Cause of Numerous Age-Related Conditions
A compelling range of evidence links greater particulate air pollution to a greater incidence of age-related disease and mortality. The primary mechanism is considered to be induction of chronic inflammation via the interaction of particulates with lung tissue. Constant, unresolved inflammatory signaling is disruptive to cell and tissue function throughout the body, accelerating the onset and progression of all of the most common disabling and ultimately fatal age-related conditions.
Growing evidence suggests that exposure to fine particulate matter (PM2.5) may reduce life expectancy; however, the causal pathways of PM2.5 exposure affecting life expectancy remain unknown. Here, we assess the causal effects of genetically predicted PM2.5 concentration on common chronic diseases and longevity using a Mendelian randomization (MR) statistical framework based on large-scale genome-wide association studies (GWAS) employing a total of more than 400,000 participants.
After adjusting for other types of air pollution and smoking, we find significant causal relationships between PM2.5 concentration and angina pectoris, hypercholesterolaemia, and hypothyroidism, but no causal relationship with longevity. Mediation analysis shows that although the association between PM2.5 concentration and longevity is not significant, PM2.5 exposure indirectly affects longevity via diastolic blood pressure (DBP), hypertension, angina pectoris, hypercholesterolaemia and Alzheimer's disease, with a mediated proportion of 31.5%, 70.9%, 2.5%, 100%, and 24.7%, respectively. Our findings indicate that public health policies to control air pollution may help improve life expectancy.