Secondhand Cigarette Smoke Exposure Research Articles

Risky working conditions and chronic kidney disease

BackgroundIndividuals in the workplace are exposed to various environments, tasks, and schedules. Previous studies have indicated a link between occupational exposures and an increased risk of chronic kidney disease (CKD). However, the social conditions of the work environment may also be a crucial contributing factor to CKD. Furthermore, individuals may encounter multiple occupational-related risk factors simultaneously, underscoring the importance of investigating the joint risk of different working conditions on CKD.MethodsA prospective analysis of 65,069 UK Biobank participants aged 40 to 69 years without CKD at baseline (2006–2010) was performed. A self-administered questionnaire assessed working conditions and a working conditions risk score were developed. Participants who answered “sometimes” or “often” exposure to occupational heat or occupational secondhand cigarette smoke; involved in shift work or heavy workloads (“usually” or “always”), were grouped as high-risk working conditions. Each working condition was scored as 1 if grouped as high-risk, and 0 if not. The working conditions risk score was equal to the sum of these four working conditions. Cox proportional hazard regression models were used to estimate the associations between working conditions and CKD incidence.ResultsThe mean follow-up time was 6.7 years. After adjusting for demographic, lifestyle, and working time factors, the hazard ratios for the development of CKD for heavy workloads, shift work, occupational secondhand cigarette smoke exposure, and occupational heat exposure were 1.24 (95%CI = 1.03, 1.51), 1.33 (95%CI = 1.10, 1.62), 1.13 (95%CI = 1.01, 1.26), 1.11 (95%CI = 0.99, 1.24), respectively. The risk of CKD was found to be significantly associated with an increasing working conditions risk score. Individuals with a working conditions risk score of 4 had an 88.0% (95% CI = 1.05, 3.35) higher risk of developing CKD when compared to those with a working conditions risk score of 0.ConclusionsAdverse working conditions, particularly when considered in combination, can significantly elevate the risk of chronic kidney disease (CKD). These results provide a reference for implementing measures to prevent CKD.

Apelin-Induced Relaxation of Coronary Arteries Is Impaired in a Model of Second-Hand Cigarette Smoke Exposure.

Apelin, an endogenous ligand for APJ receptors, causes nitric oxide (NO)-dependent relaxation of coronary arteries. Little is known about the effects of apelin/APJ receptor signaling in the coronary circulation under pathological conditions. Here, we tested the hypothesis that the vasorelaxing effect of apelin is impaired by cigarette smoke extract (CSE), an established model for second-hand smoke exposure. Isolated rat coronary arteries were treated with 2% CSE for 4 hours. Apelin-induced relaxation of coronary arteries was abolished by CSE exposure, while relaxations to acetylcholine (ACh) (endothelium-dependent relaxation) and to diethyl amine NONOate (NO donor) were similar in control and CSE-treated arteries. Immunoblot analysis demonstrated that apelin increased eNOS ser1177 phosphorylation under control conditions but had no effect after exposure to CSE. Moreover, GRK2 expression was increased in CSE-exposed coronary endothelial cells. Pretreatment with CMPD101, a GRK2 inhibitor, improved the relaxation response to apelin in CSE-exposed coronary arteries. CSE treatment failed to inhibit relaxations evoked by CMF-019, an APJ receptor biased agonist that has little effect on GRK2. In arteries exposed to CSE, apelin impaired the response to ACh but not to diethyl amine NONOate. ACh-induced relaxation was unaffected by CMF-019 in either control or CSE-treated coronary arteries. The results suggest that APJ receptor signaling using the GRK2 pathway contributes to both loss of relaxation to apelin itself and the ability of apelin to inhibit endothelium-dependent relaxation to ACh in CSE-exposed coronary arteries, likely because of impaired production of NO from endothelial cells. These changes in apelin/APJ receptor signaling under pathological conditions (eg, exposure to second-hand smoke) could create an environment that favors increased vasomotor tone in coronary arteries.

Increased Levels of the Acrolein Metabolite 3-Hydroxypropyl Mercapturic Acid in the Urine of e-Cigarette Users.

Carcinogen and toxicant uptake by e-cigarette users have not been fully evaluated. In the study reported here, we recruited 30 e-cigarette users, 63 nonsmokers, and 33 cigarette smokers who gave monthly urine samples over a period of 4-6 months. Their product use status was confirmed by measurements of exhaled CO, urinary total nicotine equivalents, cyanoethyl mercapturic acid (CEMA), and total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol. Urinary biomarkers of exposure to the carcinogens acrolein (3-hydroxypropyl mercapturic acid, 3-HPMA), benzene (S-phenyl mercapturic acid, SPMA), acrylonitrile (CEMA), and a combination of crotonaldehyde, methyl vinyl ketone, and methacrolein (3-hydroxy-1-methylpropyl mercapturic acid, HMPMA) were quantified at each visit. Data from subject visits with CEMA > 27 pmol/mL were excluded from the statistical analysis of the results because of possible unreported exposures to volatile combustion products such as secondhand cigarette smoke or marijuana smoke exposure; this left 22 e-cigarette users with 4 or more monthly visits and all 63 nonsmokers. Geometric mean levels of 3-HPMA (1249 versus 679.3 pmol/mL urine) were significantly higher (P = 0.003) in e-cigarette users than in nonsmokers, whereas levels of SPMA, CEMA, and HMPMA did not differ between these two groups. All analytes were significantly higher in cigarette smokers than in either e-cigarette users or nonsmokers. The results of this unique multimonth longitudinal study demonstrate consistent significantly higher uptake of the carcinogen acrolein in e-cigarette users versus nonsmokers, presenting a warning signal regarding e-cigarette use.

Passive exposure to e-cigarette emissions is associated with worsened mental health

BackgroundCigarette smoking, secondhand cigarette smoke (SHS) exposure, and e-cigarette use (“vaping”) are each associated with increased rates of depressive symptoms and other internalizing mental health disorders. The prevalence of vaping has increased greatly, yet the mental health correlates of secondhand exposure to e-cigarette emissions are as yet to be investigated. This study examined the potential adverse mental health outcomes associated with different tobacco exposures (direct and passive), with a particular focus on the mental health correlates of secondhand exposure to e-cigarette emissions.MethodsThe Population Assessment of Tobacco and Health Study data collected from a sample of 16,173 Wave 4 adults were used to test the hypothesis that secondhand e-cigarette emissions exposure is associated with increased odds of internalizing mental health disorders. Individuals were categorized as exclusive cigarette smokers, exclusive e-cigarette users, cigarette and e-cigarette dual users, exclusive noncombustible tobacco users, secondhand smoke exposed non-users, secondhand e-cigarette emissions exposed non-users, and non-users with no current SHS/secondhand e-cigarette aerosol exposure. Adjusted weighted logistic regression analysis was used to investigate the association between exposure type and internalizing problems as assessed by scores on the Global Appraisal of Individual Needs-Short Screener (GAIN-SS), a widely used instrument for assessing mental health problems.ResultsCigarette smokers (AOR = 2.53, 95% CI: 2.19–2.92), e-cigarette users (AOR = 3.14, 2.41–4.09), dual users (AOR = 3.37, 2.85–4.00), noncombustible tobacco users (AOR = 1.48, 1.01–2.17), SHS exposed non-users (AOR = 1.63, 1.37–1.94), and secondhand e-cigarette emissions exposed non-users (AOR = 1.43, 1.03–1.99) were each associated with increased odds of moderate to severe internalizing mental health problems as compared to unexposed non-users. Odds of internalizing problems among SHS and secondhand e-cigarette emissions exposed non-users did not differ (p = 0.46).ConclusionsThis is the first study, to our knowledge, to identify an association between recent secondhand exposure to e-cigarette emissions and mental health problems, and the risk is comparable to that of SHS. Corroboration of this relationship needs further research to explicate directionality and mechanisms underlying this association.

Parental health risk perceptions and preventive measures related to Children\u2019s second-hand cigarette smoke exposure in Malaysia

BackgroundSecondhand smoke (SHS) exposure can affect physical development in children. An understanding of parental risk perception of SHS could guide efforts to develop measures for prevention of SHS exposure among children. This study aimed to assess parental risk perceptions of SHS and action taken by parents to minimise SHS exposure in their children.MethodsThis cross-sectional nationwide study conducted in 2018 recruited convenience sample of 289 parents with children up to age 12 at public areas. Parents were asked to rate the risk level from 1 (no risk) to 5 (extremely high risk) by looking at photographs of an adult smoking in the presence of a child in 8 different situations. The implementation of smoking restriction rules was assessed. Mean scores were calculated with higher scores representing higher risk perception of SHS to child’s health. Linear regression analysis was used to determine factors associated with the level of parental risk perception of SHS exposure to their children’s health.ResultsA total of 246 parents responded. Their mean age was 35 years (SD 6.4). The majority were mothers (75.6%), Malays (72.0%) and had tertiary education level (82.5%), and non-smoker (87.1%). The mean age of respondents’ youngest child was 3 years (SD 3.1). The risk perception level was high [mean scores: 4.11 (SD: 0.82)]. Most parents implemented household (65.0%) and car (68.3%) smoking restriction rules. Lower levels of risk perception were observed among participants who were current smokers (p < 0.001), lived with a smoker (p < 0.001), allowed household smoking with an open window (p = 0.027).ConclusionMost parents perceived that risks of SHS exposure to their children were high but only two-thirds of them had set rules prohibiting smoking. Health policymakers should pay attention to factors associated with lower risk perception among parents.Trial registrationThis study was approved by the Medical Research Ethics Committee, Ministry of Health Malaysia (Registration Number: NMRR-18-3299-44967).

Secondhand smoke exposure, diabetes, and high BMI are risk factors for uterine cervical cancer: a cross-sectional study from the Korea national health and nutrition examination survey (2010\u20132018)

BackgroundHuman papilloma virus infection and tobacco smoking are the major risk factors for cervical cancer. There are limited studies searching other risk factors for cervical cancer and the results are not consistent. This study investigated the relations between cervical cancer and possible risk factors, including secondhand cigarette smoke exposure, diabetes, body mass index (BMI), and work schedule.MethodsIn this cross-sectional study, 29,557 women completed a cervical cancer questionnaire and were selected using 2010–2018 data from the Korea National Health and Nutrition Examination Survey. Details in secondhand smoke exposure, diabetes, BMI, and work schedule were assessed with participants’ health interviews and health-related surveys.ResultsTwo hundred sixty-two women (0.89%) in the sample were diagnosed with cervical cancer. Domestic secondhand smoke exposure, diabetes, and high BMI significantly increased cervical cancer risk. Respective odds ratios and 95% confidence intervals were: 1.547 (1.042–2.297), 2.156 (1.535–3.027), and 1.036 (1.006–1.067). Weekly work hours, and work schedule were not significantly related to cervical cancer incidence.ConclusionAmong Korean women, passive exposure to cigarette smoke at home, diabetes, and high BMI increase risk for cervical cancer.

Cigarette Smoke Exposure, Pediatric Lung Disease, and COVID-19.

The detrimental effects of tobacco exposure on children’s health are well known. Nonetheless, the prevalence of secondhand or direct cigarette smoke exposure (CSE) in the pediatric population has not significantly decreased over time. On the contrary, the rapid incline in use of e-cigarettes among adolescents has evoked public health concerns since increasing cases of vaping-induced acute lung injury have highlighted the potential harm of these new “smoking” devices. Two pediatric populations are especially vulnerable to the detrimental effects of cigarette smoke. The first group is former premature infants whose risk is elevated both due to their prematurity as well as other risk factors such as oxygen and mechanical ventilation to which they are disproportionately exposed. The second group is children and adolescents with chronic respiratory diseases, in particular asthma and other wheezing disorders. Coronavirus disease 2019 (COVID-19) is a spectrum of diseases caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that has spread worldwide over the last year. Here, respiratory symptoms ranging from mild to acute respiratory distress syndrome (ARDS) are at the forefront of COVID-19 cases among adults, and cigarette smoking is associated with worse outcomes in this population, and cigarette smoking is associated with worse outcomes in this population. Interestingly, SARS-CoV-2 infection affects children differently in regard to infection susceptibility, disease manifestations, and complications. Although children carry and transmit the virus, the likelihood of symptomatic infection is low, and the rates of hospitalization and death are even lower when compared to the adult population. However, multisystem inflammatory syndrome is recognized as a serious consequence of SARS-CoV-2 infection in the pediatric population. In addition, recent data demonstrate specific clinical patterns in children infected with SARS-CoV-2 who develop multisystem inflammatory syndrome vs. severe COVID-19. In this review, we highlight the pulmonary effects of CSE in vulnerable pediatric populations in the context of the ongoing SARS-CoV-2 pandemic.

Exposure to Secondhand Heated-Tobacco-Product Aerosol May Cause Similar Incidence of Asthma Attack and Chest Pain to Secondhand Cigarette Exposure: The JASTIS 2019 Study.

Although secondhand cigarette smoke is known to cause various health consequences, even the short-term effects of exposure to secondhand heated-tobacco-product (HTP) aerosol are unknown. The purpose of this study was to examine short-term symptoms related to secondhand HTP aerosol exposure. An internet-based self-reported questionnaire survey was conducted in 2019 as a part of the Japan Society and New Tobacco Internet Survey (JASTIS) study. In total, 8784 eligible respondents aged 15–73 years were analyzed. We examined the frequency (%) of secondhand combustible cigarette smoke and HTP aerosol exposure, and the exposure-related subjective symptoms (sore throat, cough, asthma attack, chest pain, eye pain, nausea, headache, and other symptoms). Overall, 56.8% of those exposed to secondhand cigarette smoke had any subjective symptoms, compared to 39.5% of those exposed to HTP aerosol. Asthma attack and chest pain were reported more frequently when associated with secondhand HTP exposure (10.9 and 11.8%, respectively) than with secondhand cigarette smoke exposure (8.4 and 9.9%, respectively). Sore throat, cough, eye pain, nausea, and headache were also more frequently reported when associated with secondhand cigarette smoke than with secondhand HTP exposure. This is the first study to examine severe subjective symptoms such as asthma attacks and chest pains, and to suggest that respiratory and cardiovascular abnormalities could be related to secondhand heated-tobacco-product aerosol exposure. Further careful investigations are necessary.

Secondhand Cigarette Smoke Exposure Pattern, Knowledge, Attitude and Perception of Harm amongst Non-Smokers in Sokoto Metropolis, Nigeria

Background: Cigarette smoke contains many carcinogens, and the negative health consequences associated with cigarette smoking are shared and suffered by the passive non-smokers.

In Utero Exposure to Second‐Hand Cigarette Smoke Promotes Epigenetically‐Mediated Cardiac Dysfunction in High‐Fat Fed Male Mice

We investigated whether in utero exposure to second‐hand cigarette smoke (SHS) would adversely affect cardiac structure/function in the exposed offspring fed a high‐fat diet. Pregnant mice (C57B1/6J) were exposed to SHS or air (4 hr/d) from gestational days 6–19. The male offspring (age: 65 days) from the SHS and air exposure groups were fed either normal chow, or high‐fat liquid diet (35% fat; HFD) for 16 weeks (n=12/group). Cardiac function was measured by echocardiography at baseline (30 days) and at the end of pair feeding. Mice were then sacrificed and heart tissue collected for histological and mRNAseq analysis. There was no significant difference in body weight or heart weigh/tibial length between the in utero SHS+HFD and in utero air+HFD treated offspring. However, compared to in utero air+HFD mice, in utero SHS+HFD mice had decreased left ventricular internal diameters and volumes during diastole (3.95±0.09 vs. 4.34±0.24 mm; 67.8±1.5 vs. 85.4±4.4 μl, P&lt;0.05) and systole (2.91±0.07 vs. 3.34±0.15 mm; 32.5±1.9 vs. 46.3±5.1 μl, P&lt;0.05), accompanied by increases in left ventricular wall thickness during diastole (0.72±0.03 vs. 0.66±0.03 mm, P&lt;0.01) and septal thickness during systole (1.2±0.06 vs. 0.99±0.05 mm, P&lt;0.05) and increased fractional shortening. There was also a significant increase in collagen in the hearts of the in utero SHS+HFD mice. These data are consistent with the development of concentric cardiac hypertrophy in in utero SHS+HFD mice. mRNAseq analysis of cardiac tissue revealed 100 up‐regulated and 120 down‐regulated genes in in utero air+HFD vs in utero SHS+HFD. Top Wiki Pathway terms included genes linked to adaptive cardiac hypertrophic responses: adrenergic receptor a1a, MAP2K1, MAP2K3, CDK7, CHUK, PDPK1 and IKBKE, microRNAs in cardiomyocytes, exercise induced changes in circadian rhythm (upregulated BMAL1, downregulated Per2) and signaling via estrogens, TNF alpha and MAP kinases. GO pathways identified included cardiac muscle contraction, protein acetylation and regulation of DNA methylation. We conclude that in utero exposure to SHS produces epigenetically‐regulated differential cardiac responses following challenge with obesogenic high fat diet. (NIH P20 GM103514).Support or Funding InformationNIH P20 GM103514

Cigarette smoke exposure impairs β-cell function through activation of oxidative stress and ceramide accumulation

ObjectivesEpidemiological studies indicate that first- and second-hand cigarette smoke (CS) exposure are important risk factors for the development of type 2 diabetes (T2D). Additionally, elevated diabetes risk has been reported to occur within a short period of time after smoking cessation, and health risks associated with smoking are increased when combined with obesity. At present, the mechanisms underlying these associations remain incompletely understood. The objective of this study was to test the impact of CS exposure on pancreatic β-cell function using rodent and in vitro models. MethodsBeginning at 8 weeks of age, C57BL/6 J mice were concurrently fed a high-fat diet (HFD) and exposed to CS for 11 weeks, followed by an additional 11 weeks of smoking cessation with continued HFD. Glucose tolerance testing was performed during CS exposure and during the cessation period. Cultured INS-1 β-cells and primary islets were exposed ex vivo to CS extract (CSE), and β-cell function and viability were tested. Since CS increases ceramide accumulation in the lung and these bioactive sphingolipids have been implicated in pancreatic β-cell dysfunction in diabetes, islet and β-cell sphingolipid levels were measured in islets from CS-exposed mice and in CSE-treated islets and INS-1 cells using liquid chromatography-tandem mass spectrometry. ResultsCompared to HFD-fed, ambient air-exposed mice, HFD-fed and CS-exposed mice had reduced weight gain and better glucose tolerance during the active smoking period. Following smoking cessation, CS-mice exhibited rapid weight gain and had accelerated worsening of their glucose tolerance. CS-exposed mice had higher serum proinsulin/insulin ratios, indicative of β-cell dysfunction, significantly lower β-cell mass (p = 0.017), reduced β-cell proliferation (p = 0.006), and increased islet ceramide content compared to non-smoking control mice. Ex vivo exposure of isolated islets to CSE was sufficient to increase islet ceramide levels, which was correlated with reduced insulin gene expression and glucose-stimulated insulin secretion, and increased β-cell oxidative and endoplasmic reticulum (ER) stress. Treatment with the antioxidant N-acetylcysteine markedly attenuated the effects of CSE on ceramide levels, restored β-cell function and survival, and increased cyclin D2 expression, while also reducing activation of β-cell ER and oxidative stress. ConclusionsOur results indicate that CS exposure leads to impaired insulin production, processing, secretion and reduced β-cell viability and proliferation. These effects were linked to increased β-cell oxidative and ER stress and ceramide accumulation. Mice fed HFD continued to experience detrimental effects of CS exposure even during smoking cessation. Elucidation of the mechanisms by which CS exposure impairs β-cell function in synergy with obesity will help design therapeutic and preventive interventions for both active and former smokers.

Pediatric asthma: Principles and treatment.

Approximately one-half of children with asthma present with symptoms before 3 years of age. The typical history describes recurrent episodes of wheezing and/or cough triggered by a viral upper respiratory infection (URI), activity, or changes in weather. When symptoms occur after a viral URI, children with asthma often take longer than the usual week to fully recover from their respiratory symptoms. Wheezing and coughing during exercise or during laughing or crying, and episodes triggered in the absence of infection suggest asthma. A trial of bronchodilator medication should show symptomatic improvement. The goal of asthma therapy is to keep children "symptom free" by preventing chronic symptoms, maintaining lung function, and allowing for normal daily activities. Avoidance of triggers identified by a history, such as second-hand cigarette smoke exposure, and allergens identified by skin-prick testing can significantly reduce symptoms. According to the 2007 National Asthma Education and Prevention Program (NAEPP) report, if impairment symptoms are present for >2 days/week or 2 nights/month, then the disease process is characterized as persistent, and, in all age groups, inhaled corticosteroids (ICS) are recommended as the preferred daily controller therapy. Montelukast is approved for children ages ≥ 12 months and is often used for its ease of daily oral dosing. Long-acting beta-2 adrenergic agonists should only be used in combination with an ICS. For more-severe or difficult-to-control phenotypes, biologic therapy has been developed, which targets the type of inflammation present.

Potential risk factors for Ebstein anomaly, National Birth Defects Prevention Study, 1997-2011.

Ebstein anomaly is a rare congenital heart defect (CHD) that, when severe, requires corrective surgery or other catheter-based intervention in the first year of life. Due to its rarity, risk factors for Ebstein anomaly remain largely unknown. Using national data, we examined 18 potential risk factors for Ebstein anomaly. Using 1997-2011 data from the National Birth Defects Prevention Study, a population-based case-control study, we calculated crude and adjusted odds ratios and 95% confidence intervals for paternal age, maternal socio-demographics, reproductive history, and modifiable risk factors, and infant characteristics reported by mothers of 135 Ebstein anomaly cases and 11,829 controls. Mothers of Ebstein anomaly cases had 4.1 (95% confidence interval: 1.8, 9.5) times the odds of reporting a family history of CHD compared with mothers of controls. Ebstein anomaly was associated with maternal second-hand cigarette smoke exposure at home (odds ratio = 2.2 [95% confidence interval: 1.1, 4.4]), but not maternal cigarette smoking (odds ratio = 1.3 [95% confidence interval: 0.8, 2.1]). Odds were elevated, but the 95% confidence interval included 1.0, for maternal marijuana use (odds ratio = 1.8 [95% confidence interval: 0.9, 3.8]) and paternal age ≥40 years at delivery (odds ratio = 1.9 [95% confidence interval: 1.0, 3.5]). Maternal exposure to second-hand cigarette smoke at home and a family history of CHD were associated with elevated odds of Ebstein anomaly. Genetic analyses could clarify the potential heritability of Ebstein anomaly.

Correction: The Influence of Second-Hand Cigarette Smoke Exposure during Childhood and Active Cigarette Smoking on Crohn's Disease Phenotype Defined by the Montreal Classification Scheme in a Western Cape Population, South Africa.

[This corrects the article DOI: 10.1371/journal.pone.0139597.].

Second hand tobacco smoke adversely affects the bone of immature rats

OBJECTIVES:To evaluate the influence of secondhand cigarette smoke exposure on longitudinal growth of the tibia of growing rats and some parameters of bone quality.METHODS:Forty female rats were randomly divided into four groups: control: rats were sham exposed; 30 days: rats were exposed to tobacco smoke for 30 days; 45 days: rats were exposed to tobacco smoke for 45 days; and 60 days: rats were exposed to tobacco smoke for 60 days. Blood samples were collected to evaluate the levels of cotinine and alkaline phosphatase. Both tibias were dissected and weighed; the lengths were measured, and the bones were then stored in a freezer for analysis of bone mineral content and mechanical resistance (maximal load and stiffness).RESULTS:Exposure of rats to tobacco smoke significantly compromised bone health, suggesting that the harmful effects may be time dependent. Harmful effects on bone growth were detected and were more pronounced at 60-day follow-ups with a 41.8% reduction in alkaline phosphatase levels (p<0.01) and a decrease of 11.25% in tibia length (p<0.001). Furthermore, a 41.5% decrease in bone mineral density was observed (p<0.001), leading to a 42.8% reduction in maximum strength (p<0.001) and a 56.7% reduction in stiffness (p<0.001).CONCLUSION:Second hand cigarette smoke exposure in rats affected bones that were weaker, deforming them and making them osteopenic. Additionally, the long bone was shorter, suggesting interference with growth. Such events seem to be related to time of exposure.

Smoking-Related Interstitial Lung Disease in a Non-Smoker

SESSION TITLE: Fellow Case Report Poster - Diffuse Lung Disease I SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Pulmonary Langerhans cell histiocytosis (PLCH) is an uncommon diffuse cystic lung disease that occurs almost exclusively in young adult smokers. We present a case of PLCH in a non-smoker. CASE PRESENTATION: A 23-year-old male presented with acute onset of sharp, left-sided chest pain and shortness of breath. His past medical history was significant for two episodes of left-sided pneumothoraces, which were managed with chest tube placement. He did not have a history of current or prior cigarette smoking. He did not have a significant second-hand cigarette smoke exposure. On presentation, his vitals were stable. Physical examination revealed decreased breath sounds on the left side of the chest. Chest X-ray showed left-sided pneumothorax and bilateral diffuse interstitial infiltrates. He was treated with chest tube placement. CT of the chest revealed bilateral, multiple thick and thin walled cysts in the upper and middle lung fields with relative sparing of the bases. Video-assisted thoracoscopic lung biopsy (VATS) was obtained and mechanical pleurodesis was performed to treat his recurrent pneumothorax. Immunohistochemical staining for S-100 protein was positive in the Langerhans cells, consistent with PLCH. DISCUSSION: PLCH is a rare interstitial lung disease characterized by infiltration and proliferation of Langerhans cells. It occurs mostly in young adults, 20-40 years of age. Cigarette smoking is considered to be the inciting factor. There are no direct experimental data that support the role of cigarette smoke in the pathogenesis of PLCH. But, there are several observational studies, suggesting that the disease may be causally related to smoking. A history of current or previous cigarette smoking is identified in up to 97 percent of patients. PLCH has also been described in association with malignancy especially bronchogenic carcinoma and Hodgkin’s lymphoma. It is extremely rare in non-smokers and the etiology remains unknown. CONCLUSIONS: The overwhelming majority of adult patients with PLCH smoke cigarettes or were exposed to substantial second-hand smoke. PLCH has been described under the spectrum of smoking-related interstitial lung diseases. PLCH in non-smokers is not well studied. Reference #1: Suri H, Yi E, Nowakowski G, et al. Pulmonary langerhans cell histiocytosis. Orphanet J Rare Dis. 2012; 7: 16. doi: 10.1186/1750-1172-7-16 PMCID: PMC3342091 Reference #2: Abbott G, et al. Pulmonary Langerhans cell Histiocytosis1. Archives of the AFIP. DOI: http://dx.doi.org/10.1148/rg.243045005 DISCLOSURE: The following authors have nothing to disclose: Sathish Kumar Krishnan, Kumar Shah, Gurminder Dhillon No Product/Research Disclosure Information

Comparative Analysis of Lipid Extracts and Imaging Mass Spectrometry for Evaluating Cerebral White Matter Biochemical Pathology in an Experimental Second-Hand Cigarette Smoke Exposure Model.

BackgroundWhite matter injury and degeneration are common features of developmental and aging-associated diseases, yet their pathobiological bases are poorly understood. However, recent advances in Matrix-Assisted Laser Desorption Ionization (MALDI) instruments and chemistry have provided critical tools for myelin-lipid analytical research.DesignThis study characterizes Cigarette Smoke (CS) exposure effects on frontal lobe lipid ion profiles in adult male A/J mice that had been exposed to air for 8 weeks (A8), CS for 4 (CS4) or 8 weeks (CS8), or CS8 followed by 2 weeks recovery (CS8+R). MALDI data acquired by analysis of lipid extracts plated onto a ground steel target (high through-put) were compared with Imaging Mass Spectrometry (IMS).ResultsMALDI-time-of-flight (TOF) detected 120 lipid ions with m/z’s of 600 to 1300 (phospholipids and sulfatides) in samples plated onto the steel target or analyzed by IMS, but just 25 ions (18%) were detected by both methods. IMS more effectively detected ions in the highest m/z range, whereas the extracts had abundant middle-range m/z ions. The experimental groups were better discriminated by PCA and R-generated heat map hierarchical clustering of IMS data than lipid extract data. On the other hand, both methods clearly delineated the CS4, CS8 and CS8+R experimental groups from control.ConclusionsMALDI analysis of brain lipid extracts plated onto a ground steel target for high through-put studies, or imaged directly in tissue can be used to assess biochemical pathology of white matter neurodegeneration and responses to treatment.

The Influence of Second-Hand Cigarette Smoke Exposure during Childhood and Active Cigarette Smoking on Crohn's Disease Phenotype Defined by the Montreal Classification Scheme in a Western Cape Population, South Africa.

BackgroundSmoking may worsen the disease outcomes in patients with Crohn’s disease (CD), however the effect of exposure to second-hand cigarette smoke during childhood is unclear. In South Africa, no such literature exists. The aim of this study was to investigate whether disease phenotype, at time of diagnosis of CD, was associated with exposure to second-hand cigarette during childhood and active cigarette smoking habits.MethodsA cross sectional examination of all consecutive CD patients seen during the period September 2011-January 2013 at 2 large inflammatory bowel disease centers in the Western Cape, South Africa was performed. Data were collected via review of patient case notes, interviewer-administered questionnaire and clinical examination by the attending gastroenterologist. Disease phenotype (behavior and location) was evaluated at time of diagnosis, according to the Montreal Classification scheme. In addition, disease behavior was stratified as ‘complicated’ or ‘uncomplicated’, using predefined definitions. Passive cigarette smoke exposure was evaluated during 3 age intervals: 0–5, 6–10, and 11–18 years.ResultsOne hundred and ninety four CD patients were identified. Cigarette smoking during the 6 months prior to, or at time of diagnosis was significantly associated with ileo-colonic (L3) disease (RRR = 3.63; 95%CI, 1.32–9.98, p = 0.012) and ileal (L1) disease (RRR = 3.54; 95%CI, 1.06–11.83, p = 0.040) compared with colonic disease. In smokers, childhood passive cigarette smoke exposure during the 0–5 years age interval was significantly associated with ileo-colonic CD location (RRR = 21.3; 95%CI, 1.16–391.55, p = 0.040). No significant association between smoking habits and disease behavior at diagnosis, whether defined by the Montreal scheme, or stratified as ‘complicated’ vs ‘uncomplicated’, was observed.ConclusionSmoking habits were associated with ileo-colonic (L3) and ileal (L1) disease at time of diagnosis in a South African cohort.

Protection of Cigarette Smoke‐Induced Lung Fibrosis in Guinea Pigs by Inhalation of Aerosolic All‐Trans Retinoic Acid

We reported earlier that both mainstream (MS) and secondhand (SH) cigarette smoke exposure to guinea pigs caused lung injury with accumulation of amorphous granular materials in alveolar space and an increase in the levels of retinol. We previously reported that the accumulation of retinol in lung was associated with a decrease in the levels of retinoic acid implying an abnormality in lung retinoid metabolism and signaling. The objective of the present study was to demonstrate whether the lung injury is due to fibrosis and whether inhalation of aerosolic all-trans retinoic acid (ATRA) immediately after smoke exposure can protect against smoke-induced lung fibrosis. Six weeks old male guinea pig were exposed twice daily for 6 weeks to MS or SH smoke from 3 1R3F cigarettes. The sham control group (SC) received a treatment identical to smoke-exposed groups but in the absence of cigarettes. Four animals from each group received daily either aerosolic ATRA (2.78mM) or vehicle twice for 20 min/day after smoke exposure. Morphological analysis of lungs showed deleterious alterations in the lungs of both MS and SH groups and accumulation of severe trichrome-positive (blue dye) materials in throughout the region of lung in comparison to the normal. ATRA treatment showed significant protection against lung damage; however the protection was more evident in MS than SH groups. The mechanism by which ATRA aerosol protects cigarette smoke-induced lung fibrosis is under investigation. (Supported by NIH grant: 1R03HL095419-01A1).

The association between childhood environmental exposures and the subsequent development of Crohn's disease in the Western Cape, South Africa.

BackgroundEnvironmental factors during childhood are thought to play a role in the aetiolgy of Crohn's Disease (CD). However the association between age at time of exposure and the subsequent development of CD in South Africa is unknown.MethodsA case control study of all consecutive CD patients seen at 2 large inflammatory bowel disease (IBD) referral centers in the Western Cape, South Africa between September 2011 and January 2013 was performed. Numerous environmental exposures during 3 age intervals; 0–5, 6–10 and 11–18 years were extracted using an investigator administered questionnaire. An agreement analysis was performed to determine the reliability of questionnaire data for all the relevant variables.ResultsThis study included 194 CD patients and 213 controls. On multiple logistic regression analysis, a number of childhood environmental exposures during the 3 age interval were significantly associated with the risk of developing CD. During the age interval 6–10 years, never having had consumed unpasteurized milk (OR = 5.84; 95% CI, 2.73–13.53) and never having a donkey, horse, sheep or cow on the property (OR = 2.48; 95% CI, 1.09–5.98) significantly increased the risk of developing future CD. During the age interval 11–18 years, an independent risk-association was identified for; never having consumed unpasteurized milk (OR = 2.60; 95% CI, 1.17–6.10) and second-hand cigarette smoke exposure (OR = 1.93; 95% CI, 1.13–3.35).ConclusionThis study demonstrates that both limited microbial exposures and exposure to second-hand cigarette smoke during childhood is associated with future development of CD.