Effects of Maternal Inflammation and Exposure to Cigarette Smoke on Birth Weight and Delivery of Preterm Babies in a Cohort of Indigenous Australian Women

Abstract

Sudden infant death syndrome (SIDS), neonatal deaths, and deaths from infection are higher among Indigenous Australians. This study aimed to determine the effects of inflammatory responses and exposure to cigarette smoke, two important factors associated with sudden death in infancy, on preterm birth, and birth weight in a cohort of Indigenous mothers. Indigenous Australian women (n = 131) were recruited as part of a longitudinal study while attending antenatal care clinics during pregnancy; blood samples were collected up to three times in pregnancy. Serum cotinine, indicating exposure to cigarette smoke, was detected in 50.4% of mothers. Compared with non-Indigenous women, the cohort had 10 times the prevalence of antibodies to Helicobacter pylori (33 vs. 3%). Levels of immunoglobulin G, antibodies to H. pylori, and C-reactive protein (CRP) were all inversely correlated with gestational age (P < 0.05). CRP levels were positively associated with maternal body mass index (BMI; ρ = 0.449, P = 0.001). The effects of cigarette smoke (cotinine) and inflammation (CRP) were assessed in relation to risk factors for SIDS: gestational age at delivery and birth weight. Serum cotinine levels were negatively associated with birth weight (ρ = −0.37, P < 0.001), this correlation held true for both male (ρ = −0.39, P = 0.002) and female (ρ = −0.30, P = 0.017) infants. Cotinine was negatively associated with gestational age at delivery (ρ = −0.199, P = 0.023). When assessed by fetal sex, this was significant only for males (ρ = −0.327, P = 0.011). CRP was negatively associated with gestational age at delivery for female infants (ρ = −0.46, P < 0.001). In contrast, maternal BMI was significantly correlated with birth weight. These data highlight the importance of putting programs in place to reduce cigarette smoke exposure in pregnancy and to treat women with chronic infections such as H. pylori to improve pregnancy outcomes and decrease risk factors for sudden death in infancy.

Associations between repeated ultrasound measures of fetal growth and biomarkers of maternal oxidative stress and inflammation in pregnancy

“…26,27 Two small studies (N ≤ 200) with repeated measures of CRP did not analyze associations by trimester, but also observed inverse associations with birthweight. 6,13 Our studies are somewhat consistent with these findings, although we observed null associations with CRP measured at ~10 weeks gestation, and the most precise effect estimates with levels measured at Few studies have examined cytokines in relation to birthweight or fetal growth, 8,10 and to our knowledge none has done so with repeated biomarkers or ultrasound measurements. Our largely null findings for inflammatory cytokines suggest these markers may not be useful in the study of fetal growth.…”

“…5 Studies in humans, however, are limited by the availability of biomarker measurements from single time points during gestation or the use of birthweight alone as a proxy for growth. [6][7][8][9][10][11][12][13][14] In this study, we sought to address whether maternal inflammation and oxidative stress biomarker concentrations measured longitudinally across pregnancy were associated with repeated ultrasound as well as delivery measures of fetal growth. Additionally, we examined whether associations between biomarkers and growth differed depending on when they were measured during pregnancy, what parameter was used to assess growth (eg, weight or head circumference), and sex of the fetus.…”

Maternal Smoking During Pregnancy and Offspring Birth Weight: A Genetically-Informed Approach Comparing Multiple Raters

“…This response could alter signal transduction pathways, damage macro-molecules, produce vasoactive compounds (e.g., isoprostanes), alter both placental morphology (e.g., placental calcification) and blood flow, and contribute to intrauterine growth retardation and low birth weight (Hutter et al 2010; Stone et al 2014). Additional evidence suggests the possibility of inflammatory pathways (Lin et al 2014; Pringle et al 2015) and epigenetic modifications (Knopik et al 2012), but the mechanisms by which these effects are transmitted is poorly understood. Considerably more research, particularly prospective, genetically informed, and carefully designed animal and human studies that can address critical/sensitive periods of exposure, measurements or biomarkers of exposure effects (e.g., placental tissue) and longitudinal course of disease and behavior is needed to begin to disentangle the likely complex nature of this association.…”

Influence of maternal adiposity, preterm birth and birth weight centiles on early childhood obesity in an Indigenous Australian pregnancy-through-to-early-childhood cohort study

“…48 Identification of early-life risk factors for developing obesity in Indigenous Australian children is therefore essential for the development of public health interventions and policy to reduce childhood obesity in this high-risk population group. Although there have been previous descriptive reports from the Gomeroi gaaynggal cohort outlining the various maternal determinants of pregnancy outcomes, including inflammation, cigarette smoke exposure and pre-pregnancy BMI, 49,50 none have reported on the associations between maternal adiposity, preterm birth or birth weight and early childhood weight status, as has been examined in the current study. This study demonstrates in an Australian Indigenous population cohort, that being born preterm is associated with an increase in BMI in early childhood (mean age 23.4 months) placing these preterm infants on a trajectory for an increased risk of metabolic disease in later life.…”