There is plenty of evidence for particulate air pollution to have a negative effect on long-term health, particularly those derived from Asian populations that are exposed to more coal and wood smoke than tends to be the case in the US and Western Europe.
While the relative importance of the various mechanisms involved are up for debate, the most plausible are those involving raised inflammation as a result of interactions between particles and lung tissue. The chronic inflammation of aging drives near all age-related conditions, and more inflammation means more dysfunction.
Image credit: Janak Bhatta/Wikepedia/CC BY-SA 4.0
As researchers note here, not all particulate air pollution is equal. It is reasonable to expect some types of particle to be worse than others, and that is what is found by mining data on health and pollution in a region of the US. This is focused on the Northeast, and one might consider comparing this with another interesting analysis of long-term US data on health and air pollution, that one covering the Puget Sound region. Both studies focused on the link to age-related neurodegeneration, a set of conditions strongly correlated with inflammation.
Long-term effects of PM2.5 components on incident dementia in the northeastern United States
Fine particulate matter (PM2.5) is an important air pollutant worldwide. Exposure to PM2.5 has been associated with adverse health effects, including cardiovascular disease, respiratory disease, lung cancer, and premature mortality. Several studies also suggest that long-term PM2.5 exposure is a risk factor for neurodegenerative diseases. Studies suggest that PM2.5 has the potential to induce dementia through biological mechanisms such as systemic inflammation, oxidative stress, and neuroinflammation. In addition, some evidence indicates that PM2.5 can exacerbate or accelerate existing diseases via these biological pathways.
A growing body of epidemiological evidence suggests that particulate air pollution contributes to dementia, including several longitudinal studies conducted in the United States and around the world. The majority of these studies found positive associations between PM2.5 and dementia. A systematic review and meta-analysis also concluded that exposure to PM2.5 is associated with a 16% higher risk of dementia per 10 μg/m3 increase in PM2.5 concentration.
However, previous studies have almost exclusively focused on the effects of PM2.5 mass concentrations. As a complex mixture, the toxic effects of PM2.5 may be determined primarily by its chemical components. PM2.5 components, such as organic matter (OM), inorganic nitrate (NO3-), inorganic sulfate (SO42-), black carbon (BC), soil particles (SOILs), and sea salt (SS), emitted from specific sources, have different physicochemical and toxicological characteristics, resulting in various health effects. To fill these knowledge gaps, we conducted a population-based cohort study of the Medicare dataset and a well-validated high-resolution (1 km × 1 km) PM2.5 components dataset from 2000-2017. The latter includes data on OM, NO3-, SO42-, BC, SOILs, and SS in the northeastern United States, where better exposure estimates exist.
We identified dementia diagnoses from patients' hospital and medical insurance records and carried out Cox proportional hazards regression to investigate their association with PM2.5 components. Among ∼2 million participants, 15.1% developed dementia. From the single-pollutant models, hazard ratios per interquartile range increase were 1.10 for black carbon, 1.08 for inorganic nitrate, 1.03 for organic matter, 1.13 for sulfate, 1.07 for soil particles, and 1.04 for sea salt. Increase in exposure to black carbon and sulfate per interquartile range had the strongest associations with dementia incidence.
Source: Fight Aging!