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Background and purpose:We determined the prevalence of physician-diagnosed sleep disorder and its association with tobacco smoke exposure and vitamin D deficiency.MethodsThe National Health and Nutrition Examination Survey (NHANES) of 2011–2012 data base was used for the study. Subjects were asked two questions: “Ever told your doctor you had trouble sleeping?” and “Ever told by doctor have sleep disorder?” The answer “yes” to the second question indicated presence of a doctor-diagnosed sleep disorder (DSD) and “no” indicated its absence. Tobacco smoke exposure was defined by serum cotinine levels while vitamin D levels were measured by serum 25(OH) D. Eight selected variables included in the analyses were BMI, age, gender, smoking exposure, vitamin D levels, income, insurance, and race. Univariate and multivariate analyses were conducted to determine if tobacco smoke exposure and Vitamin D were each predictive of DSD.ResultsOf 5,470 subjected aged 16 to 80+ years about 9% had doctor-diagnosed sleep disorder (DSD). In a multiple regression analysis, active tobacco smoking was predictive of DSD (OR 1.92; 95% CI = 1.38–2.69), while passive smoke exposure was not, even after controlling for all the other significant variables (OR 0.93; 95% CI = 0.57–1.52). The other variables significantly associated with DSD were by order of importance BMI (P < 0.001), Age (P < 0.001) and race (P ≤ 0.001). Vitamin D deficiency was not predictive of DSD.ConclusionThe prevalence of physician-diagnosed DSD was about 9%. Active smoking but not passive smoking as defined by cotinine levels was significantly associated with DSD. Vitamin D was not predictive of DSD. Future studies are therefore needed to demonstrate whether smoking cessation could help reduce DSD.

Objective We explored the association of smoking and GBS colonization among women delivering neonates 35 weeks+. Design Retrospective chart review Setting A large tertiary care inner-city hospital in the southern United States Population/Sample 803 women pregnant women of term or near term neonates Methods The electronic health records of a convenience sample. Main Outcome Measures The outcome variable of interest was maternal GBS colonization. The primary independent variable of interest was tobacco smoking during pregnancy. Results The prevalence of maternal GBS colonization was 32% among the study population. In the univariate analyses, factors associated with maternal GBS colonization were tobacco smoking during pregnancy (P of trend

Background and hypothesisThe role of smoking as a risk factor for group B streptococcal (GBS) colonization in women during pregnancy has not been previously adequately explored. We hypothesized that women of term or near term neonates who smoked during pregnancy were more likely to have GBS colonization than their non-smoking counterparts.MethodsThe electronic health records (EHRs) of a convenience sample of women delivering in an inner-city university tertiary care center were reviewed. The outcome variable of interest was maternal GBS colonization during pregnancy. The primary independent variable of interest was tobacco smoking during pregnancy, determined from the EHRs by the number of cigarettes smoked during gestation. Descriptive statistics were conducted and categorical data were compared by the Fischer's exact test. Multiple logistic regression analysis was further conducted to determine the independent impact of tobacco smoke exposure on GBS colonization.ResultsThe prevalence of maternal GBS colonization was 35% among the study population. In the univariate analyses, factors associated with maternal GBS colonization were tobacco smoking during pregnancy (P of trend ConclusionThe prevalence of GBS colonization in this institution was consistent with recent national rates. Smoking and maternal age were identified as two independent risk factors for GBS colonization during pregnancy. Further studies are needed to confirm these findings.

BackgroundAlthough tobacco smoke has been associated with many infections, little is known of its association with human papillomavirus (HPV) infections among young adult women. The aim of the study was to explore the association of tobacco smoke exposure on HPV infections in young adult women in the United States. It was hypothesized that tobacco smoke exposure (both active and passive) as objectively measured by cotinine levels was associated with increased HPV infection in a national sample of 18 and 26 year-old women in the United States.Study methods and findingsThe NHANES 2007-2012 dataset was used in the analyses. A national representative sample of women 18 to 26 year old (N = 1,414) was included in the study. Infection with any HPV was determined by PCR while tobacco smoke exposure was determined by measuring serum cotinine levels. Women with cotinine levels = 0.05 were considered as exposed. Exposed women were further categorized as passive smokers (cotinine levels 0.05- 10ng/mL). Data were analyzed by descriptive statistics and multiple logistic regression analysis. Exposed women (passive smokers with cotinine levels > = 0.05ng/mL-10ng/mL) were almost 2 times (64% vs 35%) more likely to be infected with any HPV type than their unexposed counterparts (cotinine levels = 10 ng/mL) were more than twice more likely (75%) to be infected with the virus than the unexposed counterparts. The relationship held true even after controlling for various socio-demographics. Indeed in the multiple regression analyses controlling for the various confounders, compared to their unexposed counterparts, women exposed to second hand smoke were more than twice more likely to have HPV infections (OR: 2.45; 95% C.I = 1.34-4.48). When compared to their unexposed counterparts, actively smoking women were more than 3.5 times more likely to be infected with HPV (OR = 3.56; 95% CI 1.23-10.30). Finally, a strong dose-response relationship was further demonstrated with increasing risk of HPV with each quartile of cotinine levels even after controlling for various confounders. The risk of HPV was lowest in the lowest quartile (Referent OR = 1) and increased steadily with each quartile of cotinine levels until the risk was highest among women with cotinine levels in the 4th quartile (OR = 4.16; 95% C.I. = 1.36-12.67).ConclusionBoth passive and active tobacco smoking were strongly associated with any HPV infection in 18 to 26 year old young women with a significant dose-response relationship. Future studies should explore the effect of tobacco smoke exposure among younger women less than 18 years of age.

OBJECTIVE The objective of this study was to assess the efficacy of pantoprazole in infants with gastroesophageal reflux disease (GERD). MATERIALS AND METHODS Infants ages 1 through 11 months with GERD symptoms after 2 weeks of conservative treatment received open-label (OL) pantoprazole 1.2 mg x kg(-1) x day(-1) for 4 weeks followed by a 4-week randomized, double-blind (DB), placebo-controlled, withdrawal phase. The primary endpoint was withdrawal due to lack of efficacy in the DB phase. Mean weekly GERD symptom scores (WGSSs) were calculated from daily assessments of 5 GERD symptoms. Safety was assessed. RESULTS One hundred twenty-eight patients entered OL treatment, and 106 made up the DB modified intent-to-treat population. Mean age was 5.1 months (82% full-term, 64% male). One third of patients had a GERD diagnostic test before OL study entry. WGSSs at week 4 were similar between groups. WGSSs decreased significantly from baseline during OL therapy (P < 0.001), when all patients received pantoprazole. The decrease in WGSSs was maintained during the DB phase in both treatment groups. There was no difference in withdrawal rates due to lack of efficacy (pantoprazole 6/52; placebo 6/54) or time to withdrawal during the DB phase. The greatest between-group difference in WGSS was slightly worse with placebo at week 5 (P = 0.09), mainly due to episodes of arching back (P = 0.028). No between-group differences in adverse event frequency were noted. Serious adverse events in 8 patients were considered unrelated to treatment. CONCLUSIONS Pantoprazole significantly improved GERD symptom scores and was well tolerated. However, during the DB treatment phase, there were no significant differences noted between pantoprazole and placebo in withdrawal rates due to lack of efficacy.

BACKGROUND AND OBJECTIVES Use of health services in rural communities has not been well studied. We explored how black and white children used health services in a rural Mississippi community. METHODS Data were prospectively collected for 396 children attending a private practice to determine if race was associated with the use of health services in this community. RESULTS White children made more sick contacts than black children (P < 0.001). Black children (36%) were more likely to be treated in the emergency room than white children (24%; P = 0.013). There was no black-white difference in the hospitalization rates, although white children were more likely to undergo ear-nose-throat (ENT) surgery for pressure equalizing tube (PET) placement, and/or tonsillectomy and adenoidectomy (T and A; P < 0.001). Even after controlling for various confounders, the frequency of all physician sick contacts was twice as high for white children than for black children (RR = 2.17; 95% C.I. = 1.32-3.58). CONCLUSION Overall, black children used disproportionately fewer health services than their white counterparts, but used significantly higher emergency room services. Private insurance coverage was the single most significant variable that accounted for the black-white differential use of the emergency room.

BACKGROUND AND OBJECTIVES. Environmental tobacco smoke (ETS) exposure is probably one of the most important public health hazards in our community. Our aim with this article is to (1) review the prevalence of ETS exposure in the United States and how this prevalence is often measured in practice and (2) summarize current thinking concerning the mechanism by which this exposure may cause infections in young children.METHODS. We conducted a Medline search to obtain data published mainly in peer-reviewed journals.RESULTS. There is still a very high prevalence of ETS exposure among US children ranging from 35% to 80% depending on the method of measurement used and the population studied. The mechanism by which ETS may be related to these infections is not entirely clear but may be through suppression or modulation of the immune system, enhancement of bacterial adherence factors, or impairment of the mucociliary apparatus of the respiratory tract, or possibly through enhancement of toxicity of low levels of certain toxins that are not easily detected by conventional means.CONCLUSIONS. The prevalence of ETS exposure in the United States is still very high, and its role in causing infections in children is no longer in doubt even if still poorly understood. Research, therefore, should continue to focus on the various mechanisms of causation of these infections and how to best reduce the exposure levels.

Because passive smoke exposure has not been previously linked to diarrhea diseases in children, it was hypothesized that very young children exposed to environmental tobacco smoke (ETS) exposure at home would also be more likely to develop infectious gastroenteritis (GE) than their unexposed counterparts. During 1-year period, 260 children 36 months and younger were prospectively followed up in a private pediatric practice in a southern community in the United States. Multiple logistic regression analysis showed that ETS was strongly predictive of acute GE in the univariate analysis ( P = .003). Even after controlling for the various confounders, ETS exposure was still significantly associated with acute GE (relative risk = 2.55; 95% CI = 1.26-5.18). It is speculated that, similar to acute respiratory infections, the same mechanisms may explain why ETS may also be associated with acute infectious GE.

BREASTFEEDING: PREDICTORS, ATTITUDES AND PRACTICES AMONG CAUCASIAN (C) AND AFRICAN AMERICAN (AA) WOMEN IN RURAL MISSISSIPPI. 795