Do stroke and hypertension mediate associations between exposure to air pollutants and dementia?

In a recent study published in JAMA Network Open, researchers investigated whether stroke or hypertension modifies or mediates the connection between particulate matter exposure (PM_2.5) within the air and new-onset dementia in america.

Study: Hypertension and Stroke as Mediators of Air Pollution Exposure and Incident Dementia. Image Credit: pikselstock/Shutterstock.com

Background

The cognitive decline amongst individuals with dementia affects their abilities to perform routine activities and increases dependency on others. PM_2.5 exposure has shown constant associations with cardiovascular illness, which can increase dementia risk.

PM_2.5 may mediate the dementia risk through vascular dysfunction; nonetheless, few prior studies have investigated this potential underlying mechanism.

Concerning the study

In the current study, researchers investigated the potential modifying or mediating effects of stroke and hypertension on the link between PM2.5 exposure and new-onset dementia.

The study was conducted as a subset of the Environmental Predictors of Cognitive Health and Aging (EPOCH) study, using biennial survey information obtained from 1998 to 2016 from the Health and Retirement Study (HRS) respondents.

Eligible individuals were aged above 50 with no history of dementia and had adequate data on mediators, exposures, outcomes, and demographics from the Health and Retirement Study.

Individuals with missing information on exposure, primary covariates, or mediators were excluded from the evaluation. The information were analyzed between August and November 2022. The study exposure was PM_2.5 exposure, calculated over the previous ten years for every individual using spatiotemporal models and residential histories.

The models incorporated measurements from america Environmental Protection Agency (US EPA) regulatory networks and various research studies, with over 300 geographical covariates characterizing land cover and usage, transportation, emission sources, vegetation, and population density.

The consequence measure was new-onset dementia, identified using validated algorithms based on informant reports and cognitive testing.

A decomposition-type causal mediation evaluation was performed to quantitatively assess the extent to which stroke and hypertension modified or mediated the link between PM_2.5 and new-onset dementia after adjusting for area-level and individual-level covariates.

Cox proportional hazards modeling and logistic regression modeling were performed to calculate the hazard ratios (HRs) and odds ratios (ORs), respectively.

Covariates included age, gender, body mass index (BMI), race, ethnicity, education, income, smoking status, urbanicity, drinking status, and socioeconomic status.

As well as, the interquartile range (IQR) values were determined. Individuals were identified as hypertensive or having a stroke if the participants themselves or proxies reported a health care provider’s diagnosis of the conditions at follow-up.

Secondary analyses were performed by characterizing PM_2.5 from open fires and agriculture by multiplying PM_2.5 with spatially various fractions of PM_2.5 from each source. 

Sensitivity analyses were also performed by stratifying mediation analyses by age and restricting the evaluation to periods with high-quality PM_2.5 estimates (i.e., from 2006 onward).

Moreover, the analyses were rerun using new-onset stroke because the mediator to make sure temporality between the study exposure and the mediator.

Results

Amongst 27,857 individuals, the researchers found no evidence that stroke or hypertension acted as modifiers or mediators of the connection between PM_2.5 exposure and new-onset dementia.

The mean age of the participants was 61 years; 15,747 were female (57%); 19,249 were non-Hispanic Whites (69%); and 4,105 (15%) were diagnosed with dementia at follow-up (mean duration of 10 years).

Amongst individuals with dementia, 2,204 (54%) were hypertensive at study initiation, and 386 (nine percent) were diagnosed with hypertension at follow-up. 378 individuals (nine percent) had a stroke history at study initiation, while 673 (16%) received a stroke diagnosis at follow-up.

The interquartile range of baseline exposure to PM_2.5 was 11 to fifteen μg per cubic millimeter. Within the adjusted evaluation, increased PM_2.5 exposure (per IQR) was unrelated to increased dementia risk (HR, 1.0).

The team observed positive relationships for stroke and hypertension with new-onset dementia, with HR values of 1.7 and 1.2, respectively, in comparison with individuals freed from hypertension or stroke at follow-up.

Nonetheless, there have been no significant associations between PM_2.5 and stroke (OR per IQR increase in particulate matter exposure, 1.1) and no significant evidence for a relationship between PM_2.5 and hypertension (OR per IQR increase in particulate matter exposure, 1.0).

No evidence was found that stroke or hypertension acted as modifiers or mediators of the link between PM_2.5 exposure and new-onset dementia.

The non-mediated interactions between hypertension and PM_2.5 exposure contributed 39% to the surplus relationship; nonetheless, the findings didn’t attain statistical significance.

The secondary analyses yielded similar results for PM_2.5 exposure from open fires as the overall PM_2.5. Consistent results were obtained within the sensitivity analyses by restricting the comments to younger individuals and periods with high-quality exposure information. As well as, using new-onset stroke because the association mediator also didn’t alter the outcomes.

Conclusion

Overall, the study findings showed that stroke or hypertension didn’t modify or mediate the link between PM_2.5 exposure within the air and incident dementia. Nonetheless, hypertension may increase individual susceptibility to air pollution. Further research should be conducted to explore other modifiers and pathways.