Objectives: Despite data linking smoking to increased risk of fetal morbidity and mortality, 11% of pregnant women continue to smoke or use alternative nicotine products. Studies confirm that nicotine exposure during pregnancy increases the incidence of birth defects; however, little research has focused on specific anatomic areas based on timing of exposure. We aim to determine critical in utero and postnatal periods of nicotine exposure that affect craniofacial development, specifically palate growth. Malformation of the palatal structures can result in numerous complications including facial growth disturbance, or impeding airway function. We hypothesized that both in utero and postnatal nicotine exposure will alter palate development.
Materials And Methods: We administered pregnant C57BL6 mice water supplemented with 100 μg/mL nicotine during early pregnancy, throughout pregnancy, during pregnancy and lactation, or lactation only. Postnatal day 15 pups underwent micro-computed tomography (μCT) analyses specific to the palate.
Results: Resultant pups revealed significant differences in body weight from lactation-only nicotine exposure, and μCT investigation revealed several dimensions affected by lactation-only nicotine exposure, including palate width, palate and cranial base lengths, and mid-palatal suture width.
Conclusions: These results demonstrate the direct effects of nicotine on the developing palate beyond simple tobacco use. Nicotine exposure through tobacco alternatives, cessation methods, and electronic nicotine delivery systems (ENDS) may disrupt normal growth and development of the palate during development and the postnatal periods of breastfeeding. Due to the recent dramatic increase in the use of ENDS, future research will focus specifically on this nicotine delivery method.
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http://dx.doi.org/10.1111/ocr.12844 | DOI Listing |
Oncogene
January 2025
Department of Pathology, University of California, San Diego, La Jolla, USA.
Smoking plays an underappreciated role in breast cancer progression, increasing recurrence and mortality in patients. Here, we show that S100A8/A9 innate immune signaling is a molecular mechanism that identifies smoking-related breast cancers and underlies their enhanced malignancy. In contrast to acute exposure, chronic nicotine increased tumorigenicity and reprogrammed breast cancer cells to express innate immune response genes.
View Article and Find Full Text PDFToxics
January 2025
École de Psychoéducation, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Secondhand smoke affects nearly 40% of children worldwide, leading to serious health and behavioral problems. Being neurotoxic, it poses potential risks for child health and learning. In Cuba, there is limited research on the association of secondhand smoke with children's brain health, especially in vulnerable populations like young children at home.
View Article and Find Full Text PDFFront Oncol
January 2025
Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Schleswig-Holstein, Kiel, Germany.
Introduction: Several aspects of the involvement of HPV in the pathogenesis of HPV-associated diseases remain poorly understood including mechanistic aspects of infection and the question of why the majority of HPV-positive HNSCC-patients are non-smokers, whereas HPV-negatives are smokers. Our previous research, based on 1,100 patient samples, hypothesized an explanation for this phenomenon: Smoking induces upregulation of a mucosal protective protein (SLPI), which competes with HPV for binding to Annexin A2 (AnxA2), pivotal for HPV cell entry. Here we investigate the mechanistic aspects of our hypothesis using transfection assays.
View Article and Find Full Text PDFFront Microbiol
January 2025
Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Background: Perinatal nicotine exposure (PNE) induces pulmonary dysplasia in offspring and it increases the risk of respiratory diseases both in offspring and across generations. The maternal gut microbiota and its metabolites, such as short-chain fatty acids (SCFAs), can regulate fetal lung development and are susceptible to nicotine exposure. Therefore, modulation of PNE-induced changes in maternal gut microbiota and SCFAs may prevent the occurrence of pulmonary dysplasia in offspring.
View Article and Find Full Text PDFJAMA Netw Open
January 2025
Herbert Wertheim School of Public Health and Human Longevity Science, University of California, San Diego.
Importance: The degree that in-home cannabis smoking can be detected in the urine of resident children is unclear.
Objective: Test association of in-home cannabis smoking with urinary cannabinoids in children living at home.
Design, Setting, And Participants: This cross-sectional study used baseline data from Project Fresh Air, a 2012-2016 randomized clinical trial to reduce fine particulate matter levels.
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