Abstract
Research suggests that human brain health is harmed by chronic exposure to neurotoxic atmospheric pollutants, probably as a result of neuroinflammatory responses. Previous studies correlated chronic air pollution exposure to children’s neurodevelopment and to neurodegeneration in the elderly, without using explicit, focussed cognitive tasks. Although vaccination studies show that acute inflammation can impact attention and social cognition a few hours after vaccination, whether exposure to air pollution could cause similar cognitive dysfunction is unknown. Using an atmospheric chamber, we exposed 81 young healthy adults to diluted diesel exhaust (or clean air) for one hour before completing a facial identification task either immediately or after a four-hour delay period. In the face task, participants made speeded identifications of the gender of a briefly presented target face in the presence of simultaneously presented distractor face (2-face trials) or a scrambled image distractor (1-face trial). Response times (RT) for 2-face trials preceded by a 2-face trial (repeat sequences) versus a 1-face trial (non-repeat sequence) were compared to index reactive attention. Poor control over reactive attention is associated with large differences is such tasks. A significant interaction between sequence type and pollution group was identified, such that reactive attention (non-repeat minus repeated sequences) was 22ms greater for the delayed-diesel compared to the delayed-clean air group, indicating that the former had less efficient adaptive cognitive control. Reactive attention was unaffected by diesel exposure when tested immediately after exposure; response accuracy was similar for all groups arguing against the possibility that speed-accuracy trade-offs could explain the results. These findings provide the first direct experimental evidence that short, city street comparable (8.89μg/m3 PM2.5; 206ppb NO2) diesel exposure can negatively impact attentional executive functioning several hours later. Finding delayed rather than immediate effects support the possibility that such effects stem from neuroimmune, rather than respiratory, responses.