Introduction Although studies have examined the association between childhood asthma and parental smoking and secondhand smoke, little research has explored the moderating role of birth weight and prematurity (BWP) status on this association. We examined the association between secondhand smoke exposure, asthma, and asthma severity in children aged six to 17 as well as the modifying effect of BWP on parental smoking and asthma. Methods We used data from 36,954 children from the National Survey of Children's Health 2017-2018. In addition to univariate analysis, adjusted and unadjusted logistic regression models were used to estimate the effect of secondhand smoke on asthma. The interaction term between parental smoking and BWP was tested. Multinomial regression was used to evaluate the association between secondhand smoke on asthma severity. Results About 15.1 % of children had asthma and 15.4% of parents reported smoking. Odds of asthma were higher in children living with an outdoor (AOR, 1.27; 95% CI, 1.06-1.52) and indoor (AOR, 1.46; 95% CI, 1.01-2.11) smoker in the adjusted model. The association of parental smoking with asthma differed by birth weight and premature status. Normal weight children who are premature had the highest odds ratio (AOR, 2.15; 95% CI, 1.2-3.86). In the multinomial model, low birth weight and premature children had higher odds of mild (AOR, 1.90; 95% CI, 1.40-2.56) and moderate/severe (AOR, 1.81; 95% CI, 1.16-2.84) asthma compared to the no asthma group. Conclusion The Association of parental smoking on asthma was modified by BWP. Focused asthma interventions in children should inquire about BWP status as well as parental smoking and household smoke exposure to reduce asthma morbidity and mortality.

Current methods for the risk assessment of environmental exposures commonly involve questionnaires, stationary monitoring, and personal air sampling. However, as these approaches do not capture the body's internal response, they lend minimal understanding to the biologic consequence of exposure. In order to address the unmet need of connecting external exposure measurements with signatures of internal exposure, this thesis examines the overarching hypothesis that transcriptomic changes in the human airway epithelium can serve as indicators of physiologic responses to inhaled pollutants. This is an extension of previous work that has demonstrated an airway ''field of injury'' effect where cigarette smoke exposure alters gene-expression in epithelial cells lining the respiratory tract. Specifically, I examine transcriptomic changes and the biologic responses associated with exposure to the following pollutants: environmental tobacco smoke (Aim 1), household air pollution from smoky coal combustion (Aim 2), and electronic cigarette vapor (Aim 3). First, I performed whole-genome transcriptional profiling of the nasal epithelium in children and adults and detected gene-expression changes associated with exposure to environmental tobacco smoke. Next, I employed similar approaches to detect a signature of coal smoke exposure in the buccal epithelium of healthy, non-smoking females exposed to household air pollution Xuanwei, China. The findings from these studies suggest that upper airway gene-expression can reflect the host response to prolific sources of environmental exposures that are major risk factors for chronic lung disease. Lastly, I examine the cellular and physiologic consequences of electronic cigarette (ECIG) aerosol exposure by analyzing transcriptomic profiles of human bronchial epithelial cells that have either been (1) differentiated and exposed in vitro or (2) acquired via bronchoscopy from the airway epithelium of ECIG users. The studies detailed in this dissertation offer valuable insight that will accelerate the efforts to evaluate the health effects of both well-established and emerging types of inhaled exposures in large-scale population studies. Furthermore, the transcriptomic strategies woven throughout the following chapters push for a novel assessment paradigm that may enable the public health community to rapidly characterize the physiologic host response to inhalation exposures of different sources, and to evaluate the biologic consequences of exposure-reduction initiatives. / 2017-05-01T00:00:00Z

The human body encounters a number of chemical exposures on a daily basis, which may have short- or long-term health implications. Previously it has been demonstrated that the entire respiratory tract of an individual reacts to exposures like tobacco smoke in a similar manner, and that common molecular changes can be measured in airway epithelium. I propose that cataloguing the exposure of airway epithelial cells to tobacco cigarette (TCIG) smoke and its constituents, electronic cigarette (ECIG) aerosol and other drugs and small molecules can significantly increase the understanding of chemical exposure and identify common gene expression alterations. First, I determined the molecular impact of ECIG aerosol exposure on human airway epithelium in vitro, including alterations in genes related to xenobiotic metabolism, oxidative stress, and ciliated cells. These changes were generally less pronounced than the effects of TCIG exposure, and were more pronounced in ECIG products containing nicotine than those without nicotine. Furthermore, gene expression differences observed in vitro were concordant with differences observed in airway epithelium collected from ECIG users. Second, I examined the impact of TCIG exposure and TCIG constituents on premalignant airway cells, to better understand the progression or regression of precancerous lesions. These data could also identify the constituents of TCIGs and the precancerous mutations that increase the risk for malignancy. Third, in an effort to build a high-throughput methodology for chemical exposures, I exposed primary lung cell lines to small molecule therapeutics and identified lung-specific and lung cell-type-specific effects of exposure, suggesting that profiling additional cell lines would further inform airway gene expression in response to exposure and that organ-specific exposure profiling may provide valuable insight into drug discovery for common diseases. Overall, transcriptomic profiles from the airway epithelium reflect exposure to various inhaled and chemical perturbations. These gene expression profiles indicate common changes across a multitude of airway exposures as well as unique alterations specific to a given perturbation. Gene expression profiling can therefore be used to detail the potential response to a compendium of chemical exposures including those that are either well-established or potential risk factors for chronic lung diseases. / 2019-07-09T00:00:00Z

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Background: Early Childhood Caries (ECC) is one of the most common chronic illnesses among young children, affecting around 23% of children 2-5 years old, leading to pain, discomfort, and poor quality of life. It is a multi-factorial disease that develops through the combined effects of bacteria, tooth morphology, fermentable carbohydrates, time, and various social factors. Several studies have investigated the associations between dental caries and non-traditional factors acquired during the first years of life including; mode of delivery, breastfeeding, and Environmental Tobacco Smoke (ETS). However, the literature on these associations has been inconsistent. Objective: To investigate the unadjusted and adjusted associations between the presence of Early Childhood Caries (ECC) and Severe-ECC (S-ECC), and three non-traditional factors: breastfeeding, mode of delivery, and ETS, among children 1-5 years old. Methods: A cross-sectional design was employed, and a sample of 112 caregiver/ child dyads was recruited from the ongoing flow of patients at Temple University Maurice H. Kornberg School of Dentistry (TUKSoD). After consent, subjects completed a questionnaire and received a standard intra-oral examination and the American Academy of Pediatric Dentistry (AAPD) Caries-risk Assessment Tool (CAT) by a student doctor. The study was approved by the Temple University Institutional Review Board (Protocol # 23885). Chi-square tests, two-sample t-tests and bivariate logistic regressions were used to assess the unadjusted associations. Two multivariable logistic models were developed for ECC and S-ECC and included demographics, overall CRA, and the three non-traditional risk factors. Results: The prevalence of ECC and S-ECC were 61% and 30%, respectively. The following variables were significant in the unadjusted analysis for both ECC and S-ECC: child’s age, maternal educational attainment, overall AAPD CAT classification, sugary snacks per day, presence of plaque on child’s teeth and ETS. Exposure to ETS was associated with an increased adjusted odds ratio for ECC (aOR=5.39 [95% CI: 1.14-25.33], P=0.033), but not for S-ECC. Furthermore, C-section birth was associated with a decreased adjusted odds ratio for both ECC and S-ECC, respectively (ECC: aOR=0.132 [95% CI: 0.02-0.72], P=0.02; S-ECC: aOR=0.141 [95% CI: 0.026-0.748], P=0.021). With inclusion of the AAPD CAT, demographics, and the three non-traditional factors, the overall model accuracy at predicting ECC was 82.2%. Conclusions and Clinical Relevance: In this study of urban, predominantly African American, and low income children, ECC was found associated with two non-traditional factors, ETS and mode of delivery, suggesting that including them in CRA may improve prediction of future dental caries, and aid in the prevention and treatment of disease. Results from this study support the notion that ECC is a multi-factorial disease, and highlights the importance of adopting oral health education among caregivers. / Clinical Research and Translational Medicine