Respiratory diseases such as asthma, wheeze and reduced lung function physically and economically burden many individuals, and have biologic underpinnings to the prenatal and childhood timeframes via fetal programming and epigenetic mechanisms. This dissertation studies risk and preventive factors for respiratory illnesses during three distinct timeframes: the prenatal period, infancy, and childhood/adolescence. By using data that oversampled immigrant Latino families, we were afforded additional opportunities to study race/ethnicity and nativity as a confounder or effect measure modifier, further tailoring our public health message to an important and growing population in our communities.
Our first study used longitudinal data from a population based nested case-control study in Los Angeles to analyze three different maternal stressors as well as paternal support during pregnancy to determine if these stressors carried differential risk of reported lifetime wheeze in the young offspring. We further examined whether Latina ethnicity modified those same associations. The risk of wheeze in the offspring was increased from high levels of pregnancy anxiety (aRR 1.40, 95% CI 1.07, 1.83), negative life events (aRR 1.36, 95% CI 1.06, 1.75), or low paternal support (aRR 1.41, 95% CI 1.02, 1.96). Additionally, the risk of lifetime wheeze was stronger in the offspring of Latina mothers than of White mothers for these same stressors.
Using data from the same sample in the second study, we assessed whether maternal nativity in a Latina population confounded or modified the association between exclusive breastfeeding and asthmatic symptoms. Using cross-sectional data restricted to Latinas, we found a 49% reduction in risk of asthmatic symptoms with >3 months of exclusive breastfeeding (aRR=0.51, 95% CI 0.28, 0.90). Foreign-born Latinas were more likely to initiate and continue breastfeeding for at least three months compared with US-born Latinas. We did not find evidence that maternal nativity confounded or modified the association, but rather predicted the woman’s breastfeeding behavior.
In the third study, using cross-sectional data from the Los Angeles Family and Neighborhood Survey (L.A.FANS-2, 2006/8, n=584), we analyzed whether various psychosocial stressors predicted lung function in youth ages 10-17 after adjusting for air pollution. No consistent results were seen between self-reported psychosocial stressors, caregiver stressors, or negative behaviors and lung function in youth. We observed a suggestion of reduced lung function in males from family fighting (FEV1: -156.2ml, 95% CI -327.8, 15.5), absence of a father in the house (FEV1: -176.2ml, 95% CI -322.7, -29.7) and the summary stress score (FEV1: -45.6ml, 95%CI -97.6, 6.3), which were all stronger in older males ages 15-17. Additionally, feeing unsafe at school was associated with reduced lung function in younger participants ages 10-14 (FEV1: -129.8ml, 95%CI -241.4, -18.2). None of the measures were associated with reduced lung function in females.
In conclusion, prenatal psychosocial stressors and breastfeeding behaviors are potentially modifiable, and are associated with respiratory illnesses. Further work is warranted looking at psychosocial stressors later in youth. Individually tailored messages, particularly to Latinas, who may have stronger effects from prenatal stressors or negative breastfeeding behavior by nativity status, should be a priority towards preventing childhood respiratory illnesses.