Alison Lee1, Yueh-Hsiu Mathilda Chiu2, Maria José Rosa3, Calvin Jara3, Robert O Wright4, Brent A Coull5, Rosalind J Wright6. 1. Division of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY. 2. Department of Pediatrics, Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY; Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY. 3. Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY. 4. Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY; Mindich Child Health & Development Institute, Icahn School of Medicine at Mount Sinai, New York, NY. 5. Department of Biostatistics, Harvard School of Public Health, Boston, Mass; Department of Environmental Health, Harvard School of Public Health, Boston, Mass. 6. Department of Pediatrics, Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY; Mindich Child Health & Development Institute, Icahn School of Medicine at Mount Sinai, New York, NY. Electronic address: rosalind.wright@mssm.edu.
Abstract
BACKGROUND: Temporal- and sex-specific effects of perinatal stress have not been examined for childhood asthma. OBJECTIVES: We examined associations between prenatal and/or postnatal stress and children's asthma (n = 765) and effect modification by sex in a prospective cohort study. METHODS: Maternal negative life events were ascertained prenatally and postpartum. Negative life event scores were categorized as 0, 1 to 2, 3 to 4, or 5 or greater to assess exposure-response relationships. We examined effects of prenatal and postnatal stress on children's asthma by age 6 years, modeling each as independent predictors, mutually adjusting for prenatal and postnatal stress, and finally considering interactions between prenatal and postnatal stress. Effect modification by sex was examined in stratified analyses and by fitting interaction terms. RESULTS: When considering stress in each period independently, among boys, a dose-response relationship was evident for each level increase on the ordinal scale prenatally (odds ratio [OR], 1.38; 95% CI, 1.06-1.79; P value for trend = .03) and postnatally (OR, 1.53; 95% CI, 1.16-2.01; P value for trend = .001); among girls, only the postnatal trend was significant (OR, 1.60; 95% CI, 1.14-2.22; P value for trend = .005). Higher stress in both the prenatal and postnatal periods was associated with increased odds of receiving a diagnosis of asthma in girls (OR, 1.37; 95% CI, 0.98-1.91; Pinteraction = .07) but not boys (OR, 1.08; 95% CI, 0.82-1.42; Pinteraction = .61). CONCLUSIONS: Although boys were more vulnerable to stress during the prenatal period, girls were more affected by postnatal stress and cumulative stress across both periods in relation to asthma. Understanding sex and temporal differences in response to early-life stress might provide unique insight into the cause and natural history of asthma.
BACKGROUND: Temporal- and sex-specific effects of perinatal stress have not been examined for childhood asthma. OBJECTIVES: We examined associations between prenatal and/or postnatal stress and children's asthma (n = 765) and effect modification by sex in a prospective cohort study. METHODS: Maternal negative life events were ascertained prenatally and postpartum. Negative life event scores were categorized as 0, 1 to 2, 3 to 4, or 5 or greater to assess exposure-response relationships. We examined effects of prenatal and postnatal stress on children's asthma by age 6 years, modeling each as independent predictors, mutually adjusting for prenatal and postnatal stress, and finally considering interactions between prenatal and postnatal stress. Effect modification by sex was examined in stratified analyses and by fitting interaction terms. RESULTS: When considering stress in each period independently, among boys, a dose-response relationship was evident for each level increase on the ordinal scale prenatally (odds ratio [OR], 1.38; 95% CI, 1.06-1.79; P value for trend = .03) and postnatally (OR, 1.53; 95% CI, 1.16-2.01; P value for trend = .001); among girls, only the postnatal trend was significant (OR, 1.60; 95% CI, 1.14-2.22; P value for trend = .005). Higher stress in both the prenatal and postnatal periods was associated with increased odds of receiving a diagnosis of asthma in girls (OR, 1.37; 95% CI, 0.98-1.91; Pinteraction = .07) but not boys (OR, 1.08; 95% CI, 0.82-1.42; Pinteraction = .61). CONCLUSIONS: Although boys were more vulnerable to stress during the prenatal period, girls were more affected by postnatal stress and cumulative stress across both periods in relation to asthma. Understanding sex and temporal differences in response to early-life stress might provide unique insight into the cause and natural history of asthma.
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