Elijah Watson, PhD

Does exposure to an economic crisis before and just after birth accelerate biological aging decades later? I examine this question in the Cebu Longitudinal Health and Nutrition Survey, a metropolitan Philippine birth cohort of 3,080 children whose mothers' pregnancies, from May 1983 to April 1984, overlapped the political-economic crisis that followed the August 21, 1983 assassination of Benigno Aquino. Political mobilization concentrated in central Cebu City, while market-linked economic vulnerability varied across the urban–rural gradient of 33 barangays. Using a continuous difference-in-differences design, I ask how the urban–rural gradient in health varied with the inflation each child experienced across pregnancy, and I measure epigenetic clocks from DNA methylation at ages 21–22 and 39–40. Exposure left no clear mark at birth and no detectable divergence in epigenetic aging in early adulthood. By ages 39–40, however, greater exposure was associated with faster aging in more urban than in more rural barangays, clearest for the PCPhenoAge clock, with PCGrimAge and DunedinPACE pointing in the same direction but smaller and less precise. The findings suggest that early-life economic crisis may leave epigenetic signatures of faster aging that become detectable only decades later, though the design cannot separate exposure in pregnancy from exposure in early infancy.

As climate change increases exposure to extreme weather, studying its long-term consequences for human capital and health remains challenging. Building on prior work showing that typhoon-related housing damage in the Cebu Longitudinal Health and Nutrition Survey reduced household wealth and educational attainment, I extend the follow-up by nearly two decades to examine whether these early-life disadvantages persist into midlife and are accompanied by lasting biological consequences. Childhood housing damage predicted accelerated biological aging across multiple epigenetic clocks by age 40, higher blood pressure, greater food insecurity, lower household wealth, and a higher likelihood of experiencing housing damage again during Typhoon Odette in 2021. The findings suggest that childhood disaster exposure can leave enduring biological and socioeconomic consequences while reinforcing vulnerability across the life course.

Infectious disease epidemics require rapid population surveillance to identify high-risk communities and guide resources, but volunteer-based antibody surveys can misrepresent infection risk by oversampling ethnic majority, highly educated, and higher-income participants, potentially attenuating or even reversing true social and spatial disparities. Using a 2020 Chicago community antibody survey conducted before vaccine rollout, we estimated neighborhood-level SARS-CoV-2 infection risk with Bayesian multilevel regression and poststratification (MrP), incorporating American Community Survey demographic estimates, uncertainty in antibody test accuracy, and neighborhood racial-economic segregation measured using the Index of Concentration at the Extremes. Whereas unadjusted data suggested little variation in antibody prevalence across these gradients, MrP-adjusted estimates mirrored Chicago’s social and geographic gradients in COVID-19 burden: seroprevalence in the most economically deprived and predominantly Black neighborhoods was more than twice that of the most economically privileged and predominantly White neighborhoods. These findings show that unequal participation can conceal unequal exposure, making selection bias adjustment essential for estimating the social patterning of infection from imperfect crisis data.