Abstract Body: Background: Misalignment between internal circadian timing and environmental time cues, such as light, has been associated with poor cardiometabolic health. We examined whether artificial light at night (ALAN) was associated with higher asleep blood pressure (BP) and lower melatonin levels in a sample of Black adults.

Methods
Normotensive Black adults were recruited from a parent study examining circadian contribution to BP. Participants wore the Philips Respironics Actiwatch 2 for seven consecutive days and during the first 24 hours, they also completed 24-hour ambulatory BP monitoring (ABPM) using the SpaceLabs 90227 device. Saliva was collected hourly during a 30-hour constant routine protocol, one of the gold standard methods to assess circadian amplitude in humans. Radioimmunoassay (RIA) was performed to quantify salivary melatonin. Pearson correlations were performed to examine the associations between 1) ALAN exposure duration and asleep BP and 2) salivary melatonin amplitude and asleep BP.

Results
Nine participants with complete data from the parent study were included in the analyses, including 5 women (56%) and 4 men (44%) with a mean age of 39.67 ± 15.11 years. Actigraphy revealed a mean sleep duration of 393.44 ± 77.11 minutes (6.56 hours), mean wake after sleep onset (WASO) of 69.42 ± 78.40 minutes and mean white light exposure equivalent to 713.58 ± 1890.25 lux during the sleep period of ABPM. There was no significant correlation between ALAN exposure duration and asleep systolic BP or diastolic BP, r(7) = .56, p = 0.12; r(7) = .45, p = .23. RIA is ongoing and analyses to determine whether there is a correlation between salivary melatonin amplitude and asleep BP will be presented at the meeting.

Conclusions
Preliminary findings suggest that ALAN is not correlated with asleep BP in normotensive Black adults; however, our interpretation is limited by small sample size. Given the existing literature demonstrating a relationship between ALAN and asleep BP in other populations, it is possible that this relationship exists in Black adults. Participants exhibited suboptimal sleep, which may have also contributed to their elevated asleep BP. Findings from the salivary melatonin data will provide helpful insights into a potential circadian mechanism underlying elevated asleep BP. Our study is one of few examining the impact of an environmental determinant of circadian health on cardiovascular health in Black adults.