Exposure duration and cerebral amyloidosis in the olfactory cortex of World Trade Center responders: A positron emission tomography and magnetic resonance imaging study.

Background: Amyloid-β proteins, a hallmark of Alzheimer's disease, are believed to play an adaptive role in the cerebral immune response.

Objective: Amyloid is believed to play a role in cerebral immune response and could play a similar role in response to air pollution exposures. In the present study, we examined whether WTC exposure duration was associated with cerebral amyloidosis in WTC responders.

Methods: WTC responders (aged 44-65 years) who varied in exposure duration but did not use personalized protective equipment were assessed using positron-emission tomography with [F]-Florbetaben. The outcome was the cortical [F]-Florbetaben burden, measured using regional standardized uptake value ratios (SUVRs) in 34 Desikan-Killiany regions of interest. Spearman's and generalized linear models were used to estimate correlations between WTC exposure duration and cortical [F]-Florbetaben SUVR. Cognitive and behavioral symptoms were measured. Magnetic resonance imaging was used to measure cortical thickness and diffusivity.

Results: The mean age of imaged responders was 56 years old. WTC exposure duration was associated with olfactory [F]-Florbetaben SUVR (Spearman's  = 0.43, p = 0.011), which was in turn associated with elevated [F]-Florbetaben SUVR in ventral regions ( = 0.41, p = 0.016). Cortical [F]-Florbetaben in ventral regions was associated with reduced response speed ( = -0.72, p < 0.001), was co-located with cortical diffusivity across regions in the parietal and frontal lobes and reduced cortical thickness in the isthmus cingulate ( = -0.53, p = 0.001).

Conclusions: Low-grade amyloidosis in the olfactory and frontal lobes was associated with WTC exposure duration. Future work should examine whether low-grade amyloidosis is correlated with the location or distribution of neurofibrillary tangles in WTC responders.