Abstract
Objective: Asthma is a syndrome encompassing several phenotypes. Few data exist on the relation of maternal stress in job and private life to the risk of offspring asthma. We aim to examine the association between job stress, negative life events and offspring early-onset transient, early-onset persistent and late-onset asthma.
Methods: A population-based cohort study, which comprised 547,533 liveborn singletons during 1997–2008. We assessed job control and demand based on gender-specific job exposure matrix. We determined negative life events (i.e., death, life-threatening illness, suicide attempt, or alcohol or drug abuse of close family members from one year before or during pregnancy) and asthma using data from Danish national registers. Prevalence ratios (PRs) of each asthma phenotype were estimated using log-binomial models.
Results: Prenatal exposure to negative life events was associated with moderately increased risk of early-onset transient asthma (PR=1.03, 95% CI: 1.00–1.07) and early-onset persistent asthma (PR=1.03, 95% CI: 0.99–1.08), but not late-onset asthma (PR=0.98, 95% CI: 0.91–1.04) among children with no parental atopic history. Among children born to parents without atopic disorders and whose mothers with higher job control (score in the 2nd or highest tertile), maternal exposure to higher job demand (score in the 2nd or highest tertile) was associated with decreased risk of all three asthma phenotypes; the point estimate of PR ranged from 0.77 to 0.94. These later associations were attenuated and not significant for children born to parents with atopic disorders.
Conclusions: Negative life events and job stress may influence offspring asthma phenotypes via different mechanisms.
Footnotes
Cite this article as: European Respiratory Journal 2018 52: Suppl. 62, OA335.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2018