Job loss and fetal growth restriction: identification of critical trimesters of exposure

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Purpose
Previous research suggests that job loss in a household during pregnancy may perturb fetal growth. However, this work often cannot rule out unmeasured confounding due to selection into job loss. Recent work using data on exogenous job loss (due to a plant closure) finds that a father's unexpected job loss during his spouse's pregnancy increases the risk of a low weight birth. Using a unique set of linked registries in Denmark, we build on this work and examine whether associations between a father's unexpected job loss and low birthweight differ by trimester of in utero exposure. We additionally examine trimester-specific associations of job loss with small-for-gestational-age, a proxy for restricted fetal growth, which may cause low birthweight.

Methods
We apply a sibling control design to over 1.4 million live births in Denmark, 1980 to 2017, to examine whether this plausibly exogenous form of job loss corresponds with increased risk of low weight or small-for-gestational-age births, depending on the timing of displacement in the first, second, or third trimester.

Results
Results indicate an elevated risk of low birthweight (OR = 1.80, 95% CI: 1.24, 2.62) and small-for-gestational-age (OR = 1.40, 95% CI: 1.02, 1.93) among gestations exposed to job loss in the second trimester of pregnancy. Sensitivity analyses using continuous outcome measures (e.g., birthweight in grams, birthweight for gestational age percentile) and maternal fixed effects analyses produce substantively similar inference.

Conclusions
Findings support the notion that unexpected job loss may affect fetal growth and that the second trimester in particular appears sensitive to this external stressor.
OriginalsprogEngelsk
TidsskriftAnnals of Epidemiology
Vol/bind76
Sider (fra-til)174-180
Antal sider7
ISSN1047-2797
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
Samantha Gailey received support from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) under Award Number T32HD095134. This project also benefited from support provided by the Minnesota Population Center (P2CHD041023), which also receives funding from NICHD. Tim Bruckner received support from the Council on Research, Computing, and Libraries (CORCL) Single Investigator Award, UC Irvine.

Publisher Copyright:
© 2022 Elsevier Inc.

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