Altered Cortical Brain Structure and Increased Risk for Disease Seen Decades After Perinatal Exposure to Maternal Smoking: A Study of 9000 Adults in the UK Biobank

Author:

Salminen Lauren E1,Wilcox Rand R2,Zhu Alyssa H1,Riedel Brandalyn C13,Ching Christopher R K1,Rashid Faisal1,Thomopoulos Sophia I1,Saremi Arvin1,Harrison Marc B1,Ragothaman Anjanibhargavi1,Knight Victoria1,Boyle Christina P1,Medland Sarah E4,Thompson Paul M1,Jahanshad Neda1

Affiliation:

1. Imaging Genetics Center, USC Mark and Mary Stevens Neuroimaging and Informatics Institute, Keck School of Medicine of the University of Southern California, Marina del Rey, CA USA

2. Department of Psychology, University of Southern California, Los Angeles, CA, USA

3. Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, USA

4. QIMR Berghofer Medical Research Institute, Brisbane, Australia

Abstract

Abstract Secondhand smoke exposure is a major public health risk that is especially harmful to the developing brain, but it is unclear if early exposure affects brain structure during middle age and older adulthood. Here we analyzed brain MRI data from the UK Biobank in a population-based sample of individuals (ages 44–80) who were exposed (n = 2510) or unexposed (n = 6079) to smoking around birth. We used robust statistical models, including quantile regressions, to test the effect of perinatal smoke exposure (PSE) on cortical surface area (SA), thickness, and subcortical volumes. We hypothesized that PSE would be associated with cortical disruption in primary sensory areas compared to unexposed (PSE−) adults. After adjusting for multiple comparisons, SA was significantly lower in the pericalcarine (PCAL), inferior parietal (IPL), and regions of the temporal and frontal cortex of PSE+ adults; these abnormalities were associated with increased risk for several diseases, including circulatory and endocrine conditions. Sensitivity analyses conducted in a hold-out group of healthy participants (exposed, n = 109, unexposed, n = 315) replicated the effect of PSE on SA in the PCAL and IPL. Collectively our results show a negative, long term effect of PSE on sensory cortices that may increase risk for disease later in life.

Funder

National Institutes of Health

Publisher

Oxford University Press (OUP)

Subject

Cellular and Molecular Neuroscience,Cognitive Neuroscience

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