Social Determinants of Smoke Exposure During Pregnancy: Findings From Waves 1 & 2 of the Population Assessment of Tobacco and Health (PATH) Study

Maternal smoking during pregnancy (MSDP) and secondhand smoke (SHS) exposure are associated with a myriad of negative health effects for both mother and child. However, less is known regarding social determinants for SHS exposure, which may differ from those of maternal smoking during pregnancy (MSDP). To identify social determinants for SHS exposure only, MSDP only, and MSDP and SHS exposure, data were obtained from all pregnant women (18–54 years; N = 726) in waves 1 and 2 of the Population Assessment of Tobacco and Health Study (2014–2015). Multiple logistic regressions were conducted using SAS 9.4. Smoke exposure during pregnancy was common; 23.0% reported SHS exposure only, 6.1% reported MSDP only, and 11.8% reported both SHS exposure and MSDP. Results demonstrate that relationships between smoke exposure during pregnancy and social determinants vary by type of exposure. Women at risk for any smoke exposure during pregnancy include those who are unmarried and allow the use of combustible tobacco products within the home. Those who are at higher risk for SHS exposure include those who are younger in age, and those who are earlier in their pregnancy. Those who are at higher risk for maternal smoking include those with fair/poor mental health status and those who believe that others\u27 view tobacco use more positively. These results suggest the need for implementing more comprehensive policies that promote smoke-free environments. Implementing these strategies have the potential to improve maternal and fetal health outcomes associated with tobacco smoke exposure

Environmental tobacco smoke exposure and its health impacts: a review

Worldwide tobacco smoking kills nearly 6 million people each year, including more than600,000 non-smokers who die from smoke exposure. Tobacco smoke is a toxic and carcinogenic mixture of more than 5,000 chemicals. Environmental Tobacco Smoke (ETS), or secondhand smoke, is the combination of side stream smoke, the smoke given off by a burning tobacco product and mainstream smoke, the smoke exhaled by smokers. Exposure to Environmental Tobacco Smoke is detrimental to health which may pose a health risks to nonsmokers. Epidemiological data suggest that exposure to ETS may increase the risk of developing lung cancer, stroke, heart disease, cardiovascular disease, intrauterine growth retardation, predisposition to chronic lung disease, sudden infant death syndrome and is a risk factor for childhood asthma. The human populations most at risk from ETS exposure appear to be neonates, young children, and possibly the fetus while in uterus. The effects of ETS on human health are well-known, passive smoking is harmful to those who breathe the toxins and it is a serious problem for public health. Therefore, the decrease in smoking prevalence could provide substantial health gains in humans. This article reviews information on environmental tobacco smoke (ETS) particles that are of potential interest to scientists and professionals involved in exposure or risk assessment, epidemiology, or tobacco policy and to compile effective ways of reducing exposure in order to contribute to the wellbeing of human.Keywords: Environmental Tobacco Smoke, side stream smoke, main Stream smoke, tobacco

Pulmonary toxicity of chronic exposure to tobacco and biomass smoke in rats

OBJECTIVE: The objective of this study was to examine the separate and combined effects of tobacco and biomass smoke exposure on pulmonary histopathology in rats. INTRODUCTION: In addition to smoking, indoor pollution in developing countries contributes to the development of respiratory diseases. METHODS: Twenty-eight adult rats were divided into four groups as follows: control group (Group I, no exposure to tobacco or biomass smoke), exposed to tobacco smoke (Group II), exposed to biomass smoke (Group III), and combined exposure to tobacco and biomass smoke (Group IV). After six months the rats in all four groups were sacrificed. Lung tissue samples were examined under light microscopy. The severity of pathological changes was scored. RESULTS: Group II differed from Group I in all histopathological alterations except intraparenchymal vascular thrombosis. There was no statistically significant difference in histopathological changes between the subjects exposed exclusively to tobacco smoke (Group II) and those with combined exposure to tobacco and biomass smoke (Group IV). The histopathological changes observed in Group IV were found to be more severe than those in subjects exposed exclusively to biomass smoke (Group III). DISCUSSION: Chronic exposure to tobacco and biomass smoke caused an increase in severity and types of lung injury. CONCLUSION: Exposure to cigarette smoke caused serious damage to the respiratory system, particularly with concomitant exposure to biomass smoke

Children with Special Health Care Need’s Association of Passive Tobacco Smoke Exposure and Dental Caries: 2007 National Survey of Children’s Health

Purpose: The purpose of this study was to determine a relationship between passive tobacco smoke exposure (secondhand and third hand tobacco smoke exposure) and dental caries in Children with Special Health Care Needs (CSHCN) ages 0-17 years. Method: This study used data from the 2007 National Survey of Children’s Health involving 17,901 CSHCN. Telephone survey data were used to determine recent caries experience and passive tobacco smoke exposure (secondhand and third hand tobacco smoke exposure). Recent caries was defined as a positive response to if CSHCN had “decayed teeth or cavities within the past 6 months.” Passive smoke was defined as a positive response to if someone in the household used cigarettes, cigars, or pipe tobacco. Results: A statistically significant relationship was determined between passive tobacco smoke exposure and recent caries in CSHCN (adjusted odds ratio: 1.23 (95% CI: 1.02, 1.50; p-value= 0.0352). Conclusion: A positive independent association of passive tobacco smoke exposure and dental caries was determined in Children with Special Health Care Needs (CSHCN)

Association between exposure to environmental tobacco smoke and biomarkers of oxidative stress among patients hospitalised with acute myocardial infarction

Objective To determine whether exposure to environmental tobacco smoke was associated with oxidative stress among patients hospitalised for acute myocardial infarction.<p></p> Design An existing cohort study of 1,261 patients hospitalised for acute myocardial infarction.<p></p> Setting Nine acute hospitals in Scotland.<p></p> Participants Sixty never smokers who had been exposed to environmental tobacco smoke (admission serum cotinine ≥3.0 ng/mL) were compared with 60 never smokers who had not (admission serum cotinine ≤0.1 ng/mL).<p></p> Intervention None.<p></p> Main outcome measures Three biomarkers of oxidative stress (protein carbonyl, malondialdehyde (MDA) and oxidised low-density lipoprotein (ox-LDL)) were measured on admission blood samples and adjusted for potential confounders.<p></p> Results After adjusting for baseline differences in age, sex and socioeconomic status, exposure to environmental tobacco smoke was associated with serum concentrations of both protein carbonyl (beta coefficient 7.96, 95% CI 0.76, 15.17, p = 0.031) and MDA (beta coefficient 10.57, 95% CI 4.32, 16.81, p = 0.001) but not ox-LDL (beta coefficient 2.14, 95% CI −8.94, 13.21, p = 0.703).<p></p> Conclusions Exposure to environmental tobacco smoke was associated with increased oxidative stress. Further studies are requires to explore the role of oxidative stress in the association between environmental tobacco smoke and myocardial infarction.<p></p&gt

Tobacco Smoke Mediated Induction of Sinonasal Microbial Biofilms

Cigarette smokers and those exposed to second hand smoke are more susceptible to life threatening infection than non-smokers. While much is known about the devastating effect tobacco exposure has on the human body, less is known about the effect of tobacco smoke on the commensal and commonly found pathogenic bacteria of the human respiratory tract, or human respiratory tract microbiome. Chronic rhinosinusitis (CRS) is a common medical complaint, affecting 16% of the US population with an estimated aggregated cost of $6 billion annually. Epidemiologic studies demonstrate a correlation between tobacco smoke exposure and rhinosinusitis. Although a common cause of CRS has not been defined, bacterial presence within the nasal and paranasal sinuses is assumed to be contributory. Here we demonstrate that repetitive tobacco smoke exposure induces biofilm formation in a diverse set of bacteria isolated from the sinonasal cavities of patients with CRS. Additionally, bacteria isolated from patients with tobacco smoke exposure demonstrate robust in vitro biofilm formation when challenged with tobacco smoke compared to those isolated from smoke naïve patients. Lastly, bacteria from smoke exposed patients can revert to a non-biofilm phenotype when grown in the absence of tobacco smoke. These observations support the hypothesis that tobacco exposure induces sinonasal biofilm formation, thereby contributing to the conversion of a transient and medically treatable infection to a persistent and therapeutically recalcitrant condition

Exposure to Tobacco Smoke and Markers of Subclinical Atherosclerosis in Children and Adolescents. The STRIP Study.

Background: Measurement of serum cotinine, a major metabolite of nicotine, provides a valid marker for quantifying exposure to tobacco smoke. Exposure to tobacco smoke causes vascular damage by multiple mechanisms, and it has been acknowledged as a risk factor for atherosclerosis. Multifactorial atherosclerosis begins in childhood, but the relationship between exposure to tobacco smoke and arterial changes related to early atherosclerosis have not been studied in children. Aims: The aim of the present study was to evaluate exposure to tobacco smoke with a biomarker, serum cotinine concentration, and its associations with markers of subclinical atherosclerosis and lipid profile in school-aged children and adolescents. Subjects and Methods: Serum cotinine concentration was measured using a gas chromatographic method annually between the ages 8 and 13 years in 538-625 children participating since infancy in a randomized, prospective atherosclerosis prevention trial STRIP (Special Turku coronary Risk factor Intervention Project). Conventional atherosclerosis risk factors were measured repeatedly. Vascular ultrasound studies were performed among 402 healthy 11-year-old children and among 494 adolescents aged 13 years. Results: According to serum cotinine measurements, a notable number of the school aged children and adolescents were exposed to tobacco smoke, but the exposure levels were only moderate. Exposure to tobacco smoke was associated with decreased endothelial function as measured with flow-mediated dilation of the brachial artery, decreased elasticity of the aorta, and increased carotid and aortic intima-media thickness. Longitudinal exposure to tobacco smoke was also related with increased apolipoprotein B and triglyceride levels in 13-year-old adolescents, whose body mass index and nutrient intakes did not differ. Conclusions: These findings suggest that exposure to tobacco smoke in childhood may play a significant role in the development of early atherosclerosis. Key Words: arterial elasticity, atherosclerosis, children, cotinine, endothelial function, environmental tobacco smoke, intima-media thickness, risk factors, ultrasoundSiirretty Doriast

The Effect of Bans and Taxes on Passive Smoking

This paper evaluates the effect of smoking bans in public places on the exposure to tobacco smoke of non-smokers and contrasts it with the effect of excise taxes. Exploiting data on cotinine - a metabolite of nicotine - as well as state and time variation in anti-smoking policies across US states, we show that smoking bans in public places can perversely increase the exposure of non-smokers to tobacco smoke by displacing smokers to private places where they contaminate non-smokers, and in particular young children. In contrast, we find that higher taxes are an efficient way to decrease exposure to tobacco smoke, especially for those most exposed. We supplement this analysis by showing that bans have little effect on smoking cessation, and present evidence of displacement from public places using data on time use.smoking, taxes, bans

A case control study to determine the association between Perthes’ disease and the recalled use of tobacco during pregnancy, and biological markers of current tobacco smoke exposure

Aims: It is well established that there is a strong association between Perthes’ disease and worsening socioeconomic deprivation. It has been suggested that the primary determinant driving this association is exposure to tobacco smoke. This study aimed to examine this hypothesis. Patients and Methods: A hospital case-control study (n = 149/146) examined the association between tobacco smoke exposure and Perthes’ disease, adjusting for area-level socioeconomic deprivation. Tobacco smoke exposure was assessed by parental questionnaire of smoking habits during pregnancy, and by quantitative assay of current exposure using the urinary cotinine-creatinine ratio, which is a widely used and validated measure of tobacco smoke exposure. Results: The odds of Perthes’ disease significantly increased with reported in utero exposure after adjustment for socioeconomic deprivation (maternal smoking odds ratio (OR) 2.06, 95% confidence interval (CI) 1.17 to 3.63; paternal smoking OR 2.09, 95% CI 1.26 to 3.46). The cotinine-creatinine ratio was significantly greater in cases, OR 1.63 (95% CI 1.09 to 2.43), suggesting a greater ‘dose’ of current tobacco exposure. Conclusion: An association exists between tobacco smoke exposure and Perthes’ disease but we remain unable to disentangle the association with socioeconomic deprivation

A prospective cohort study of biomarkers of prenatal tobacco smoke exposure: the correlation between serum and meconium and their association with infant birth weight

<p>Abstract</p> <p>Background</p> <p>The evaluation of infant meconium as a cumulative matrix of prenatal toxicant exposure requires comparison to established biomarkers of prenatal exposure.</p> <p>Methods</p> <p>We calculated the frequency of detection and concentration of tobacco smoke metabolites measured in meconium (nicotine, cotinine, and trans-3'-hydroxycotinine concentrations) and three serial serum cotinine concentrations taken during the latter two-thirds of pregnancy among 337 mother-infant dyads. We estimated the duration and intensity of prenatal tobacco smoke exposure using serial serum cotinine concentrations and calculated geometric mean meconium tobacco smoke metabolite concentrations according to prenatal exposure. We also compared the estimated associations between these prenatal biomarkers and infant birth weight using linear regression.</p> <p>Results</p> <p>We detected nicotine (80%), cotinine (69%), and trans-3'-hydroxycotinine (57%) in most meconium samples. Meconium tobacco smoke metabolite concentrations were positively associated with serum cotinine concentrations and increased with the number of serum cotinine measurements consistent with secondhand or active tobacco smoke exposure. Like serum cotinine, meconium tobacco smoke metabolites were inversely associated with birth weight.</p> <p>Conclusions</p> <p>Meconium is a useful biological matrix for measuring prenatal tobacco smoke exposure and could be used in epidemiological studies that enroll women and infants at birth. Meconium holds promise as a biological matrix for measuring the intensity and duration of environmental toxicant exposure and future studies should validate the utility of meconium using other environmental toxicants.</p