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Maternal tobacco smoking and lung epithelium-specific proteins in amniotic fluid
C Hermans1, V Libotte, M Robin
1Industrial Toxicology and Occupational Medicine Unit, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium. hermans@toxi.ucl.ac.be
Insights
Maternal smoking during pregnancy did not alter fetal lung development markers in amniotic fluid. Clara cell secretory protein (CC16) and surfactant protein A (SP-A) levels remained unchanged, suggesting no impact on bronchoalveolar epithelium function.
Area of Science:
- Perinatology
- Pulmonology
- Toxicology
Background:
- Clara cell secretory protein (CC16) and surfactant protein A (SP-A) in amniotic fluid (AF) indicate fetal lung maturity.
- In utero tobacco smoke exposure may affect fetal lung development.
Purpose of the Study:
- To evaluate the impact of maternal tobacco smoke exposure on fetal bronchoalveolar epithelium function and maturity.
- To assess CC16 and SP-A levels in amniotic fluid from smoking and nonsmoking mothers.
Main Methods:
- Measured CC16 and SP-A levels in amniotic fluid (AF) from term infants of smoking, smoke-exposed, and nonsmoking mothers.
- Assessed tobacco smoke exposure using questionnaires and cotinine levels in AF and maternal urine.
- Compared AF protein profiles using two-dimensional gel electrophoresis and analyzed correlations with gestational age and other proteins.
Main Results:
- No significant differences in CC16 and SP-A levels were found in AF across the three smoking categories.
- Maternal smoking was not a significant predictor of CC16 or SP-A concentrations in AF.
- SP-A levels correlated with gestational age; CC16 levels correlated with low-molecular-weight proteins, suggesting renal excretion.
Conclusions:
- Maternal smoking during pregnancy does not appear to alter the secretory function of the distal airways and alveolar epithelium at term.
- Fetal lung maturity markers CC16 and SP-A in AF are not significantly affected by in utero tobacco smoke exposure.
- CC16's presence in AF is influenced by both secretion and fetal kidney elimination.
Abstract:
The bronchiolar 16 kD Clara cell secretory protein (CC16) and the alveolar surfactant-associated protein A (SP-A) are secreted in the amniotic fluid (AF), where they reflect the growth and the maturity of the fetal lung. To evaluate the possible effects of in utero tobacco smoke exposure upon infant bronchoalveolar epithelium function and maturity, CC16 and SP-A levels were determined in AF obtained at term (36-41 wk) from 28 nonsmoking, 18 smoke-exposed, and 28 smoking mothers with uncomplicated pregnancies. Tobacco smoke exposure was assessed by questionnaire and the assay in AF and maternal urine of cotinine, a stable nicotine metabolite. The specificity of the changes of CC16 and SP-A concentrations in AF was assessed by comparison with nonpulmonary proteins of high- (albumin and transferrin) or low-molecular weight (beta2-microglobulin, retinol binding protein, cystatin-C). Pulmonary and nonpulmonary AF proteins were also compared by two-dimensional gel electrophoresis between smoking and nonsmoking mothers. The levels of CC16 and SP-A as well as low- and high-molecular-weight proteins were not significantly different between the three smoking categories. The protein pattern of AF, established by two-dimensional gel electrophoresis, did not reveal any quantitative or qualitative difference between nonsmoking (n = 10), smoke-exposed (n = 5), and smoking mothers (n = 5). By multiple regression analysis of possible determinants, tobacco smoke did not emerge as a significant predictor of CC16 and SP-A concentrations in AF. SP-A level was dependent only on gestational age at birth (r2 = 0.1, p = 0.001), whereas CC16 correlated only with the levels of low-molecular weight proteins (r2 = 0.2, p = 0.0001). The latter correlation suggests that CC16 enters AF not only as a result of its secretion at the surface of the respiratory tract but also partly following its elimination by the fetal kidney. This study suggests that maternal smoking during pregnancy is not associated with alterations of the secretory functions of the epithelium of the distal airways and the alveoli at term.