Stress During Pregnancy Linked to Higher Risk for Asthma in Offspring

Laurie Barclay, MD

March 18, 2010

March 18, 2010 — Maternal stress during pregnancy is linked to a higher risk for asthma in the offspring, according to the results of a prospective study reported online March 18 in the American Journal of Respiratory and Critical Care Medicine.

"This is the first study in humans to show that increased stress experienced during pregnancy in these urban, largely minority women, is associated with different patterns of cord blood cytokine production to various environmental stimuli, relative to babies born to lower-stressed mothers," lead author Rosalind Wright, MD, MPH, associate physician at Brigham and Women's Hospital in Boston, Massachusetts, said in a news release.

In the Urban Environment and Childhood Asthma Study, the investigators evaluated associations among prenatal maternal stress and cord blood mononuclear cell (CBMC) cytokine responses among 557 families in Boston; Baltimore, Maryland; New York City; St. Louis, Missouri, and other cities. Each child had a parent with history of asthma or allergy.

Prenatal maternal stress was defined as financial hardship, Difficult Life Circumstances (a 26-item survey to assess particular life stressors occurring within the previous 6 months; eg, domestic violence), community violence, and/or stressful neighborhood/block and housing conditions. A composite cumulative stress indicator was created using factor analysis to produce latent variables representing 3 contexts (individual stressors, housing and neighborhood problems).

CBMCs were incubated with innate stimuli (lipopolysaccharide, Poly I:C, CpG, peptidoglycan [PG]), adaptive stimuli (tetanus, dust mite, cockroach), respiratory syncytial virus, phytohemagglutinin, or medium alone. Multiplex enzyme-linked immunosorbent assays were used to measure cytokines. After adjustment for sociodemographic factors, parity, season of birth, maternal asthma and steroid use, prenatal smoking, and birth weight for gestational age, associations among increasing cumulative stress and cytokine responses were evaluated with linear regression.

Among the study cohort, 71% of mothers were black and 19% were Latino, and 69% had an income less than $15,000. Mothers with the highest cumulative stress tended to be older and were more likely to have asthma and to deliver lower–birth weight infants. Higher levels of prenatal stress were associated with increased interleukin 8 production after microbial stimuli (CpG, PIC, PG) and increased tumor necrosis factor-alpha production to microbial stimuli (CpG, PIC). In the adaptive panel, higher stress was related to higher interleukin 13 levels after dust mite stimulation and lower levels of phytohemagglutinin-induced gamma-interferon.

"The cytokine patterns seen in the higher stress groups, which are an indication of how the child's immune system is functioning at birth, may be a marker of increased risk for developing asthma and allergy as they get older," Dr. Wright said. "For example, while the debate continues as to whether primary sensitization to allergens begins before birth, these findings suggest the possibility that prenatal stress may enhance the neonates' response to inhalant antigens, specifically those antigens that the fetus is likely to encounter more directly in utero, like dust mite."

On the basis of these findings, the study authors concluded that prenatal stress was associated with altered innate and adaptive immune responses in CBMCs, and that stress-induced perinatal immunomodulation may affect the expression of allergic disease in these children.

"The current findings suggest that psychological stress is involved in programming of the infant immune response and that this influence begins during pregnancy," said Dr. Wright. "As these infants mature, we will learn how these factors manifest later in terms of the development of asthma and allergy."

Limitations of this study include the possibility that some relationships were observed by chance because of multiple comparisons, in addition to variability and noise in the cytokine assays.

Federal funds from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, and from the National Center for Research Resources, National Institutes of Health, supported this study and Dr. Wright.

Am J Respir Crit Care Med. Published online March 18, 2010.

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