Zinc chloride (smoke bomb) inhalation lung injury: clinical presentations, high-resolution CT findings, and pulmonary function test results

STUDY OBJECTIVES: Zinc chloride smoke inhalation injury (ZCSII) is uncommon and has been rarely described in previous studies. We hypothesized that structural changes of the lung might correlate with pulmonary function. To answer this question, we correlated findings from high-resolution CT (HRCT) scan and the results of pulmonary function tests (PFTs) in patients with ZCSII. DESIGN: Retrospective cohort study. SETTING: University hospital. PATIENTS: Twenty patients who had been hospitalized with ZCSII-related conditions. MEASUREMENTS: The study included HRCT scan scores (0 to 100), static and dynamic lung volumes, and diffusing capacity of the lung for carbon monoxide (D(LCO)). RESULTS: HRCT scans and PFTs were performed initially after injury (range, 3 to 21 days) in all patients and during the follow-up period (range, 27 to 66 days) in 10 patients. The predominant CT scan findings were patchy or diffuse ground-glass opacities with or without consolidation. The majority of patients showed a significant reduction of FVC, FEV1, total lung capacity, and D(LCO), but normal FEV1/FVC ratio values. Changes of functional parameters correlated well with HRCT scan scores. Substantial improvements in CT scan abnormalities and pulmonary function were observed at follow-up. CONCLUSIONS: The majority of our patients with ZCSII presented with a predominant parenchymal injury of the lung that was consistent with a restrictive type of functional impairment and a reduction in Dlco rather than with obstructive disease. Our results suggest that HRCT scanning and pulmonary function testing may reliably predict the severity of ZCSII.     

Association of tobacco smoke exposure and respiratory syncitial virus infection with airways reactivity in early childhood.

Exposure to infectious agents and environmental tobacco smoke are thought to induce bronchial hyperresponsiveness (BHR). This study was undertaken to determine the effects of passive exposure to tobacco smoke and respiratory syncitial virus (RSV) lower respiratory infection (LRI) during infancy on the occurrence of BHR in the first 2 years of life. Eighty-six cases of documented RSV (mean age, 188 days) and 78 controls (mean age, 162 days) were enrolled from the clinic and in-patient service of a single hospital. None had a history of prior LRI. Subjects were studied at 6-month intervals up to 19 months of age with a standardized respiratory illness and parental smoking questionnaire, partial expiratory flow-volume curves by the "hug" (rapid thoracic compression) technique, and methacholine challenge. Exposure to maternal and paternal cigarette smoking, maternal history of asthma, and mold exposure were associated with decreased levels of length-corrected maximal flow at functional residual capacity (V'(maxFRC)). RSV-LRI was not related to V'(maxFRC). After adjustment of V'(maxFRC) for these factors, V'(maxFRC) was a significantly and positively correlated with a methacholine concentration provoking a 40% fall in V'(maxFRC) (PC40) and negatively correlated with dose-response slope. After adjustment for V'(maxFRC), there were no independent effects of tobacco smoke exposure or RSV-LRI on methacholine responses. These data do not support a role for RSV as a risk factor for airways reactivity in childhood and indicate that exposure to tobacco smoke affects airways reactivity through its effects on airways.     

《天津市控制吸烟条例》实施效果的综合评价

目的 比较《天津市控制吸烟条例》(条例)实施前后连续4年的变化,综合评价控烟的成效.方法 通过天津市发病登记系统收集的心肌梗死(心梗)就诊信息,采用The Survey System进行估算,抽取有代表性的室内场所样本量进行PM_2.5监测和现场观察,以及代表性的人群样本量开展拦截及入户调查.结果 条例实施后医疗卫生、教育和政府机构以及室内候车场所内张贴禁烟标志均有较大程度提高(P< 0.01);条例规定的9类主要公共场所吸烟现象均呈现下降(P< 0.05);全人群“二手烟”暴露率下降26.5%(P< 0.01),室内工作职业人群心梗入院频数随年份出现显著下降趋势(β=-0.061,P=0.00),而同期全人群的心梗就诊例数仍然呈上升趋势(β=0.059,P=0.00).结论 条例的实施对减少吸烟和“二手烟”危害起到促进作用,应广泛宣传控烟带来的健康效益和社会效益,以促进条例的全面落实.     

Establishing smoke-free hospitals in Vietnam: A pilot project

In Vietnam, a pilot ‘smoke-free hospital’ model was implemented in nine hospitals in 2009–2010 to supply lessons learned that would facilitate a replication of this model elsewhere. This study aimed to assess smoking patterns among health professionals and to detect levels of second-hand smoke (SHS) exposure within hospital premises before and after the ‘smoke-free hospital’ model implementation. A pre- and post-intervention cross-sectional study was conducted in nine purposively selected hospitals. Air nicotine levels were measured using passive nicotine monitors; smoking evidence was collected through on-site observations; and smoking patterns were assessed through interviews with health workers. Despite the ‘smoke-free hospital’ intervention, smoking continued among health-care workers who were former smokers. Specifically, self-reported smoking prevalence significantly decreased post-intervention, but the number of daily cigarettes smoked at workplaces among male health workers remained unchanged. Post-intervention, smoking was more likely to take place outside buildings and cafeterias. However, air nicotine levels in the doctors' lounges and in emergency departments did not change post-intervention. Air nicotine levels at other sites decreased minimally. Tailored tobacco cessation programmes, targeting current smokers and mechanisms to enforce non-smoking, should be established to meet requirements of Vietnam's comprehensive National Tobacco Control Law effective in May 2013.     

Tobacco Control Policies and Sudden Infant Death Syndrome in Developed Nations

This paper estimates the effects of higher cigarette prices and smoke‐free policies on the prevalence of Sudden Infant Death Syndrome (SIDS). Using a panel of developed countries over a 20 year period, we find that higher cigarette prices are associated with reductions in the prevalence of SIDS. However, we find no evidence that smoke‐free policies are associated with declines in SIDS.     

Airway inflammation and remodeling of cigarette smoking exposure ovalbumin-induced asthma is alleviated by CpG oligodeoxynucleotides via affecting dendritic cell-mediated Th17 polarization

Cigarette smoking (CS) is common in asthma, aggravating inflammatory reactions. However, the current treatment strategies for asthma are still not effective enough, and novel therapeutic approaches are required for CS-induced asthmatic disorders. We here investigated the ability of CpG oligodeoxynucleotides (CpG-ODNs) to inhibit airway inflammation and remodeling in ovalbumin (OVA)-associated asthma in mice exposed to chronic CS, revealing potential mechanistic insights. Lung tissue specimens were histologically analyzed. Th1/Th2/Th17 associated cytokines in serum, bronchoalveolar lavage fluid (BALF), and lung specimens were quantitated by ELISA, qRT-PCR and immunoblot. Parameters of bone marrow-derived dendritic cells (BMDCs) functions were evaluated as well. The results showed that BALB/c mice after CS and OVA treatments developed an asthmatic phenotype with airway inflammation involving both eosinophils and neutrophils, goblet cell metaplasia, airway remodeling, and elevated OVA-specific serum IgE, serum IL-17A, and BALF Th17/Th2 associated cytokines. CpG-ODNs and budesonide were found to synergistically inhibit inflammatory cell recruitment in the lung, airway remodeling, IgE synthesis, and Th17/Th2 associated cytokines. Mechanistically, CpG-ODNs and budesonide acted synergistically on BMDCs via downregulation of TSLP receptor (TSLPR) and IL-23 production, and subsequently contributed to dampen Th17/Th2 polarization in CS-associated asthma. In conclusion, combined administration of CpG-ODNs and budesonide, in a synergistic manner, inhibits airway inflammation, and tissue remodeling mediated by BMDCs by regulating IL-23 secretion and blocking TSLP signaling, which subsequently contribute to alleviate Th17/Th2 imbalance in CS-associated asthma.     

Cigarette smoke disrupts the integrity of airway adherens junctions through the aberrant interaction of p120‐catenin with the cytoplasmic tail of MUC1

Adherens junctions (AJs) containing epithelial cadherin (E‐cad) bound to p120‐catenin (p120ctn) and β‐catenin (β‐ctn) play a crucial role in regulating cell–cell adhesion. Cigarette smoke abrogates cell–cell adhesion between epithelial cells by disrupting E‐cad, a hallmark of epithelial–mesenchymal transition (EMT), yet the underlying mechanism remains unknown. We used an organotypic culture of primary human bronchial epithelial (HBE) cells treated with smoke‐concentrated medium (Smk) to establish an essential role for the interaction between p120ctn and the cytoplasmic tail of MUC1 (MUC1‐CT) in regulating E‐cad disruption. Within the first 4 h of smoke exposure, apical MUC1‐CT repositioned to the basolateral membrane of pseudo‐stratified HBE cells, where it interacted with p120ctn. A time‐dependent increase in MUC1‐CT/p120ctn complexes occurred in conjunction with a time‐dependent dissociation of p120ctn/E‐cad/β‐ctn complexes, as well as the coordinated degradation of p120ctn and E‐cad. Interestingly, Smk induced a similar interaction between MUC1‐CT and β‐ctn, but this occurred 44 h after MUC1‐CT's initial interaction with p120ctn, and well after the AJs were destroyed. Blocking MUC1‐CT's interaction with p120ctn using a MUC1‐CT dominant‐negative peptide, PMIP, successfully abolished Smk's disruptive effects on AJs and recovered apical‐basolateral polarity of HBE cells. The MUC1‐CT/p120ctn interaction was highly dependent on EGFR/Src/Jnk‐mediated tyrosine phosphorylation (TyrP) of MUC1‐CT. Accordingly, EGFR, Src or Jnk inhibitors (AG1478, PP2, SP600125, respectively) abrogated Smk‐induced MUC1‐CT‐TyrP, MUC1‐CT/p120ctn interaction, AJ disruption, and loss of cellular polarity. Our work identified MUC1‐CT and p120ctn as important regulators of epithelial polarity and cell‐cell adhesion during a smoke‐induced EMT‐like process. Novel therapeutics designed to inhibit MUC1‐CT/p120ctn complex formation may prevent EMT in the smoker's airway. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.