Assessment of wood smoke induced pulmonary toxicity in normal- and chronic bronchitis-like bronchial and alveolar lung mucosa models at air-liquid interface.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) has the highest increased risk due to household air pollution arising from biomass fuel burning. However, knowledge on COPD patho-mechanisms is mainly limited to tobacco smoke exposure. In this study, a repeated direct wood smoke (WS) exposure was performed using normal- (bro-ALI) and chronic bronchitis-like bronchial (bro-ALI-CB), and alveolar (alv-ALI) lung mucosa models at air-liquid interface (ALI) to assess broad toxicological end points. METHODS: The bro-ALI and bro-ALI-CB models were developed using human primary bronchial epithelial cells and the alv-ALI model was developed using a representative type-II pneumocyte cell line. The lung models were exposed to WS (10 min/exposure; 5-exposures over 3-days; n = 6-7 independent experiments). Sham exposed samples served as control. WS composition was analyzed following passive sampling. Cytotoxicity, total cellular reactive oxygen species (ROS) and stress responsive NFkB were assessed by flow cytometry. WS exposure induced changes in gene expression were evaluated by RNA-seq (p ≤ 0.01) followed by pathway enrichment analysis. Secreted levels of proinflammatory cytokines were assessed in the basal media. Non-parametric statistical analysis was performed. RESULTS: 147 unique compounds were annotated in WS of which 42 compounds have inhalation toxicity (9 very high). WS exposure resulted in significantly increased ROS in bro-ALI (11.2%) and bro-ALI-CB (25.7%) along with correspondingly increased NFkB levels (bro-ALI: 35.6%; bro-ALI-CB: 18.1%). A total of 1262 (817-up and 445-down), 329 (141-up and 188-down), and 102 (33-up and 69-down) genes were differentially regulated in the WS-exposed bro-ALI, bro-ALI-CB, and alv-ALI models respectively. The enriched pathways included the terms acute phase response, mitochondrial dysfunction, inflammation, oxidative stress, NFkB, ROS, xenobiotic metabolism of AHR, and chronic respiratory disorder. The enrichment of the 'cilium' related genes was predominant in the WS-exposed bro-ALI (180-up and 7-down). The pathways primary ciliary dyskinesia, ciliopathy, and ciliary movement were enriched in both WS-exposed bro-ALI and bro-ALI-CB. Interleukin-6 and tumor necrosis factor-α were reduced (p < 0.05) in WS-exposed bro-ALI and bro-ALI-CB. CONCLUSION: Findings of this study indicate differential response to WS-exposure in different lung regions and in chronic bronchitis, a condition commonly associated with COPD. Further, the data suggests ciliopathy as a candidate pathway in relation to WS-exposure.

Efficacy and Safety of N-Acetylcysteine for Chronic Obstructive Pulmonary Disease and Chronic Bronchitis.

Background: Patients with chronic obstructive pulmonary disease (COPD) and chronic bronchitis are associated with poor clinical outcomes. N-acetylcysteine (NAC) is a widely used therapeutic option for such patients; however, the clinical efficacy of NAC has not been conclusively determined. We hypothesized that high-dose oral NAC can improve the clinical outcomes for patients with concurrent chronic bronchitis and COPD. Objective and Methods. This was a randomized, double-blind, placebo-controlled trial evaluating the efficacy of high-dose NAC for COPD patients with concurrent chronic bronchitis. Study participants were randomized into two groups and administered with NAC (900 mg) twice daily or matching placebo for 3 months. Then, respiratory health status was evaluated using the St. George's Respiratory Questionnaire (SGQR), which was set as the primary end point. Results: A total of 143 COPD patients with chronic bronchitis were screened, and as a result, only 100 patients were enrolled in this study (50 participants were randomized to receive placebo, and others were randomized to receive NAC). After treatment, differences in SGQR scores between the placebo and NAC groups were not significant. Moreover, differences in secondary end points between the two groups after treatment were insignificant. Discussion. High-dose NAC has no marked clinical benefits for COPD patients with concurrent chronic bronchitis.

Urinary metals, arsenic, and polycyclic aromatic hydrocarbon exposure and risk of chronic bronchitis in the US adult population.

Metals, arsenic, and polycyclic aromatic hydrocarbons (PAHs) have all been linked to respiratory diseases. Chronic bronchitis, which is a form of chronic obstructive pulmonary disease (COPD), is a major public health concern and source of morbidity and mortality in the US. The purpose of this study was to analyze the correlation of 14 urinary metals (antimony, barium, cadmium, cesium, cobalt, lead, manganese, mercury, molybdenum, strontium, thallium, tin, tungsten, uranium), seven species of arsenic, and seven forms of polycyclic aromatic hydrocarbon (PAH) concentrations and chronic bronchitis in the US population. A cross-sectional analysis using three datasets from the National Health and Nutrition Examination Survey (NHANES) between 2011 and 2016 in adults, aged 20 years and older. Chronic bronchitis was determined using a self-questionnaire from the NHANES dataset. A specialized weighted complex survey design analysis package was used to analyze NHANES data. Multivariate logistic regression models were used to determine the correlation between urinary metals, arsenic, PAHs, and chronic bronchitis. Models were adjusted for lifestyle and demographic factors. A total of 4186 participants were analyzed; 49.8% were female and 40.5% were non-Hispanic White. All seven types of PAHs showed a positive association with chronic bronchitis (1-hydroxynaphthalene odds ratio (OR): 1.559, 95% confidence interval (CI): 1.271-1.912; 2-hydroxynaphthalene OR: 2.498, 95% CI: 1.524-4.095; 3-hydroxyfluorene OR: 2.752, 95% CI: 2.100-3.608; 2-hydroxyfluorene OR: 3.461, 95% CI: 2.438-4.914; 1-hydroxyphenanthrene OR: 2.442, 95% CI: 1.515-3.937; 1-hydroxypyrene OR: 2.828, 95% CI: 1.728-4.629; 2 & 3-hydroxyphenanthrene OR: 3.690, 95% CI: 2.309-5.896). Of the metals, only urinary cadmium showed a statistically significant positive association (OR: 2.435, 95% CI: 1.401-4.235) with chronic bronchitis. No other metals or arsenic were correlated with chronic bronchitis. Seven forms of urinary PAHs, cadmium, and several demographic factors were associated with chronic bronchitis.

[Preventive and therapeutic effects and mechanism of Xiaoer Feike Granules on chronic bronchitis induced by lipopolysaccharide in rats].

The aim of this paper was to investigate the preventive and therapeutic effects of Xiaoer Feike Granules(XEFK) on chronic bronchitis in rats and its mechanism. Except for 10 rats in the blank group, the remaining 50 of the 60 SD rats were used to establish a model of chronic bronchitis induced by LPS. On the 22 nd day, the model rats were randomly divided into 5 groups according to their body weight, and administrated with purified water, Keteling Capsules 0.11 g·kg~(-1), XEFK 3.2, 1.6 and 0.8 g·kg~(-1)(the dosing concentrations were 0.32, 0.16, 0.08 g·mL~(-1), respectively). These rats took the corresponding drug orally once a day, for consecutive 21 days. The rats were anesthetized 1 hour after the last administration, and the lavage bronchus and alveoli were collected. Then, after the fixation of the smear, neutrophils were counted microscopically, and the contents of glutathione peroxidase(GSH-Px), superoxide dismutase(SOD) and malondialdehyde(MDA) in the bronchoalveolar lavage fluid(BALF) were detected by colorimetric method. Flow cytometry was used to detect the content changes of T cell subsets CD4~+, CD8~+, CD4~+/CD8~(+ )in serum. Hemorheology related indexes were detected by automatic hemorheology. Enzyme-linked immunosorbent assay(ELISA) was used to detect the contents of tumor necrosis factor-α(TNF-α), interleukin-1ß(IL-1ß), IL-2, IL-6 and IL-10 in serum. The expression of TNF-α and IL-10 mRNA in lung was detected by Real-time quantitative PCR(RT-qPCR). HE staining was used to observe the pathological changes in the bronchitis tissues. Compared with the model group, XEFK high and medium dose groups could significantly reduce the contents of neutrophils and MDA in bronchial lavage fluid, and increase the activities of GSH-Px and SOD in BALF, and repair the chronic inflammatory cell infiltration and lymphoid tissue hyperplasia in the bronchial mucosal layer and submucosal layer. The high-dose group could reduce the plasma viscosity of rats, but there was no statistical difference in other hemorheological indexes. CD4~+, CD8~+, CD4~+/CD8~+, IL-2 and IL-10 contents in each dose group were significantly increased, and TNF-α, IL-1ß and IL-6 contents were significantly decreased in serum. Each dose group could significantly down-regulate the expression level of TNF-α mRNA in the lung and increase the expression of IL-10 mRNA. XEFK could reduce lipid peroxidation, increase the content of peripheral blood T cell subsets, regulate the release and secretion of inflammatory factors, and repair the morphological and pathological changes of bronchial tissue. Its mechanism might be related to the improvement of inflammatory response and the enhancement of immune function.

Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models.

The Transient Receptor Potential Ankyrin 1 (TRPA1) cation channel expressed on capsaicin-sensitive afferents, immune and endothelial cells is activated by inflammatory mediators and exogenous irritants, e.g., endotoxins, nicotine, crotonaldehyde and acrolein. We investigated its involvement in acute and chronic pulmonary inflammation using Trpa1 gene-deleted (Trpa1-/-) mice. Acute pneumonitis was evoked by intranasal Escherichia coli endotoxin (lipopolysaccharide: LPS) administration, chronic bronchitis by daily cigarette smoke exposure (CSE) for 4 months. Frequency, peak inspiratory/expiratory flows, minute ventilation determined by unrestrained whole-body plethysmography were significantly greater, while tidal volume, inspiratory/expiratory/relaxation times were smaller in Trpa1-/- mice. LPS-induced bronchial hyperreactivity, myeloperoxidase activity, frequency-decrease were significantly greater in Trpa1-/- mice. CSE significantly decreased tidal volume, minute ventilation, peak inspiratory/expiratory flows in wildtypes, but not in Trpa1-/- mice. CSE remarkably increased the mean linear intercept (histopathology), as an emphysema indicator after 2 months in wildtypes, but only after 4 months in Trpa1-/- mice. Semiquantitative histopathological scores were not different between strains in either models. TRPA1 has a complex role in basal airway function regulation and inflammatory mechanisms. It protects against LPS-induced acute pneumonitis and hyperresponsiveness, but is required for CSE-evoked emphysema and respiratory deterioration. Further research is needed to determine TRPA1 as a potential pharmacological target in the lung.

Exposure of normal and chronic bronchitis-like mucosa models to aerosolized carbon nanoparticles: comparison of pro-inflammatory oxidative stress and tissue injury/repair responses.

Carbon nanoparticles (CNP) are generated by incomplete combustion of diesel engines. Several epidemiological studies associated higher susceptibility to particulate matter related adverse respiratory outcomes with preexisting conditions like chronic bronchitis (CB). Therefore, we compared the effect of CNP exposure on primary bronchial epithelial cells (PBEC) developed in air-liquid interface (ALI) models of normal versus CB-like-mucosa.PBEC cultured at ALI represented normal mucosa (PBEC-ALI). To develop CB-like-mucosa (PBEC-ALI/CB), 1 ng/ml interleukin-13 was added to the basal media of PBEC-ALI culturing. PBEC-ALI and PBEC-ALI/CB were exposed to sham or to aerosolized CNP using XposeALI® system. Protein levels of CXCL-8 and MMP-9 were measured in the basal media using ELISA. Transcript expression of pro-inflammatory (CXCL8, IL6, TNF, NFKB), oxidative stress (HMOX1, SOD3, GSTA1, GPx), tissue injury/repair (MMP9/TIMP1) and bronchial cell type markers (MUC5AC, CC10) were assessed using qRT-PCR.Increased secretion of CXCL-8 and MMP-9 markers was detected 24 h post-exposure in both PBEC-ALI and PBEC-ALI/CB with more pronounced effect in the later. Pro-inflammatory and tissue injury markers were increased at both 6 h and 24 h post-exposure in PBEC-ALI/CB. Oxidative stress markers exhibited similar responses at 6 h and 24 h post-exposure in PBEC-ALI/CB. The club cell specific marker CC10 was increased by 300 fold in PBEC-ALI/CB and 20 fold in PBEC-ALI following CNP exposure.Our data indicates an earlier and stronger reaction of pro-inflammatory, oxidative stress and tissue injury markers in PBEC-ALI/CB models compared to PBEC-ALI models following CNP exposure. The findings may provide insight into the plausible mechanisms of higher susceptibility among predisposed individuals to nanoparticle exposure.

Understanding the importance of key risk factors in predicting chronic bronchitic symptoms using a machine learning approach.

BACKGROUND: Chronic respiratory symptoms involving bronchitis, cough and phlegm in children are underappreciated but pose a significant public health burden. Efforts for prevention and management could be supported by an understanding of the relative importance of determinants, including environmental exposures. Thus, we aim to develop a prediction model for bronchitic symptoms. METHODS: Schoolchildren from the population-based southern California Children's Health Study were visited annually from 2003 to 2012. Bronchitic symptoms over the prior 12 months were assessed by questionnaire. A gradient boosting model was fit using groups of risk factors (including traffic/air pollution exposures) for all children and by asthma status. Training data consisted of one observation per participant in a random study year (for 50% of participants). Validation data consisted of: (1) a random (later) year in the same participants (within-participant); (2) a random year in participants excluded from the training data (across-participant). RESULTS: At baseline, 13.2% of children had asthma and 18.1% reported bronchitic symptoms. Models performed similarly within- and across-participant. Previous year symptoms/medication use provided much of the predictive ability (across-participant area under the receiver operating characteristic curve (AUC): 0.76 vs 0.78 for all risk factors, in all participants). Traffic/air pollution exposures added modestly to prediction as did body mass index percentile, age and parent stress. CONCLUSIONS: Regardless of asthma status, previous symptoms were the most important predictors of current symptoms. Traffic/air pollution variables contribute modest predictive information, but impact large populations. Methods proposed here could be generalized to personalized exacerbation predictions in future longitudinal studies to support targeted prevention efforts.

COPD, airflow limitation and chronic bronchitis in farmers: a systematic review and meta-analysis.

INTRODUCTION: The current definition of chronic obstructive pulmonary disease (COPD) associates persistent airflow limitation and chronic respiratory symptoms. Agricultural work has been associated with an increased risk of developing COPD, but the prevalence and definition of the disease vary greatly between studies. This meta-analysis aimed to assess the association between agricultural work and COPD using the most widely used definitions of the disease. METHODS: Inclusion criteria were: (1) design: cross-sectional or longitudinal, (2) groups: at least one group of farmers and a control group of non-farmers, (3) outcome: prevalence or unadjusted OR of COPD, airflow limitation and/or chronic bronchitis, (4) study subjects: groups of exposed subjects comprising ≥30 individuals and with a mean age ≥40 years and (5) language: English and French language, full-length, original publications in peer-reviewed journals. RESULTS: In total, 22 manuscripts were included in the meta-analysis. Eight studies assessed only the prevalence of airflow limitation, nine assessed only the prevalence of chronic bronchitis and four assessed the prevalence of both these parameters. Only one assessed the prevalence of COPD according to its current definition, and this study also provided the prevalence of airflow limitation. Ten studies showed a positive association between farming exposure and airflow limitation or chronic bronchitis, and 12 showed no association (OR (95% CI)=1.77 (1.50 to 2.08), p<0.001). Cattle, swine, poultry and crop farming were associated with either airflow limitation or chronic bronchitis. CONCLUSION: Although some features of COPD are associated with some agricultural work, well-designed studies with appropriate diagnostic criteria should be conducted to draw strong conclusions about the relationship between COPD and farming.

Quercetin, Kaempferol and Isorhamnetin in Elaeagnus pungens Thunb. Leaf: Pharmacological Activities and Quantitative Determination Studies.

Elaeagnus pungens leaf was documented to be very effective to treat asthma and chronic bronchitis both as traditional Chinese medicine and minority traditional medicine; yet the actual effective components still remain unknown. This work is to investigate the anti-inflammatory, antalgic and antitussive activities of E. pungens leaf, quercetin and kaempferol, and their contents in E. pungens leaf. Pharmacological experiments showed that they could considerably reduce ear-swelling of mouse and relieve writhing reaction of mouse; they could also prevent mouse from coughing significantly. These findings suggested that quercetin and kaempferol are major effective components treating asthma and chronic bronchitis. Quantitative analysis results indicated that the levels of quercetin, kaempferol and isorhamnetin varied greatly in different species of Elaeagnus and in different plant parts: E. pungens leaf is more similar to Elaeagnus umbellate leaf chemically; quercetin level is exceptionally high in Elaeagnus oldhami leaf; E. pungens leaf is a better medical part for treating asthma and chronic bronchitis in comparison with other parts.

Mustard gas exposure and mortality among retired workers at a poisonous gas factory in Japan: a 57-year follow-up cohort study.

OBJECTIVES: Mustard gas (MG) has been the most widely used chemical warfare agent in the past century. However, few but conflicting data exist on the effects of MG exposure on long-term mortality. We investigated MG-related mortality in retired workers at a poisonous gas factory. METHODS: We assessed mortality rates among 2392 male and 1226 female workers, whose vital status could be determined through 31 December 2009, at a poisonous gas factory operating from 1929 to 1945 in Okuno-jima, Japan. The analysis employed standardised mortality ratios (SMRs) calculated using national and prefectural references and a Cox proportional hazard regression model. Applying the Kaplan-Meier method, we compared cumulative death rates in the study cohort stratified by an 'Okuno-jima MG Index' which represented the product of HRs derived for job category and length of service. RESULTS: Among male workers, we found significant excesses in mortality from upper respiratory tract cancer (SMR 3.06), liver cancer (1.67), lung cancer (2.01) and chronic bronchitis/emphysema (4.84) compared with the national population, as well as stomach cancer (1.20) versus the Hiroshima Prefecture population. When stratified into 3 subgroups by the Okuno-jima MG Index, those with a higher Okuno-jima MG Index had significantly higher cumulative rates of death from respiratory cancer and chronic bronchitis/emphysema. CONCLUSIONS: MG exposure significantly increases the long-term risk of death from respiratory cancer and chronic bronchitis/emphysema. The Okuno-jima MG Index may be a useful indicator for estimating cumulative MG exposure.

Chronic bronchitis incidence in the extended cohort of Mayak workers first employed during 1948-1982.

OBJECTIVES: This paper describes findings from the study of chronic bronchitis (CB) incidence after occupational exposure to ionising radiation among workers employed at Russian Mayak Production Association (PA) during 1948 and 1982 and followed up until 2008 based on 'Mayak Worker Dosimetry System 2008'. METHODS: Analyses were based on 2135 verified cases among 21 417 workers. Rate ratios (RR) were estimated by categorical analysis for non-radiation and radiation factors. Excess rate ratios per Gy (ERR/Gy) of external or internal exposures with adjustments via stratification on other factors were calculated. RESULTS: The interesting finding in relation to non-radiation factors was a sharp increase in the RR for CB incidence before 1960, which could be caused by a number of factors. Analyses restricted to the follow-up after 1960 revealed statistically significant associations of the CB incidence and external γ-ray radiation, ERR/Gy=0.14 (95% CI 0.02 to 0.28) having adjusted for sex, attained age, calendar period, plant, smoking status and lung α-particle dose, and internal α-particle radiation, ERR/Gy=1.14 (95% CI 0.41 to 2.18) having adjusted for sex, attained age, calendar period, plant, smoking status and lung γ-ray dose and ERR/Gy=1.19 (95% CI 0.32 to 2.53) having additionally adjusted for pre-employment occupational hazards and smoking index instead of smoking status. CONCLUSIONS: Analyses of CB incidence in the study cohort identified positive significant association with occupational exposure to radiation: however, there are no similar studies of CB incidence in relation to radiation in other cohorts to date with which a meaningful comparison of the results could be made.

A ferret model of COPD-related chronic bronchitis.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the US. The majority of COPD patients have symptoms of chronic bronchitis, which lacks specific therapies. A major impediment to therapeutic development has been the absence of animal models that recapitulate key clinical and pathologic features of human disease. Ferrets are well suited for the investigation of the significance of respiratory diseases, given prior data indicating similarities to human airway physiology and submucosal gland distribution. Here, we exposed ferrets to chronic cigarette smoke and found them to approximate complex clinical features of human COPD. Unlike mice, which develop solely emphysema, smoke-exposed ferrets exhibited markedly higher numbers of early-morning spontaneous coughs and sporadic infectious exacerbations as well as a higher level of airway obstruction accompanied by goblet cell metaplasia/hyperplasia and increased mucus expression in small airways, indicative of chronic bronchitis and bronchiolitis. Overall, we demonstrate the first COPD animal model exhibiting clinical and pathologic features of chronic bronchitis to our knowledge, providing a key advance that will greatly facilitate the preclinical development of novel treatments for this disease.

LC-MS based metabolomics identification of novel biomarkers of tobacco smoke-induced chronic bronchitis.

Tobacco smoke (TS) is a major causative agent to lead to chronic bronchitis (CB). However the mechanisms of CB induced by TS are unclear. In this report, rats were exposed to different concentrations of TS and the metabolic features of CB were characterized by using a nontargeted metabolic profiling method based on liquid chromatography-mass spectrometry (LC-MS) to detect the altered metabolic patterns in serum from CB rats and investigate the mechanisms of CB. 11 potential biomarkers were identified in serum of rats. Among them, the levels of lysophosphatidylethanolamine (18:1), lysophosphatidic acid (18:1), lysophosphatidylethanolamine (18:0), lysophosphatidylethanolamine (16:0), lysophosphatidylethanolamine (20:4), docosahexaenoic acid, 5-hydroxyindoleacetic acid and 5'-carboxy-γ-tocopherol were higher in TS group compared to control group. Conversely, the levels of 4-imidazolone-5-propionic acid, 12-hydroxyeicosatetraenoic acid and uridine were lower in TS group. The results indicated that the mechanism of CB was related to amino acid metabolism and lipid metabolism, particularly lipid metabolism. In addition, lysophosphatidylethanolamines were proved to be important mediators, which could be used as biomarkers to diagnose CB. These results also suggested that metabolomics was suitable for diagnosing CB and elucidating the possible metabolic pathways of TS-induced CB.

Studies on mitogen-activated protein kinase signaling pathway in the alveolar macrophages of chronic bronchitis rats.

Lipopolysaccharide (LPS), a potent stimulator of inflammatory responses in alveolar macrophages (AMs), activates several intracellular signaling pathways, including mitogen-activated protein kinases (MAPK). In the present study, we investigated the MAPK pathway in AMs of chronic bronchitis (CB) rats. CB was induced by endotracheal instillation of LPS followed by Bacillus Calmette Guerin injection through the caudal vein 1 week later. Specific inhibitors were used and protein phosphorylations were detected by Western blot. We found that Genistein (PTK inhibitor) could inhibit protein kinase C (PKC), phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt or PKB) MAPK signaling pathway with different degrees, LY294002 (PI3K inhibitor) could not only inhibit phospho-PI3K/Akt expression, but also inhibit p38 and c-Jun NH2-terminal kinases (JNK) phosphorylation. Calphostin C (PKC inhibitor) could inhibit phospho-PKC expression and exerted significant effects on extracellular signal-regulated kinases (ERK) phosphorylation, however, it had no impact on p38 and JNK phosphorylation. These results demonstrated that the LPS mediated signaling pathway of MAPK in AMs of CB rats could be described as follows: PTK-PI3K-Akt-JNK/p38 or PTK-PI3K-PKC-ERK, and PI3K may have a negative regulation on the activation of downstream proteins.

[Clinical and pathogenetic features of occupational bronchitis].

With multidimentional correlation analysis, the authors studied clinical and pathogenetic features of occupational bronchitis development. Analysis covered relationships of symptoms and syndromes of the disease, main spirometric signs of bronchial obstruction, presence and character of exogenic risk factors and the patients age. The authors revealed regularities of interrelations of clinical, instrumental and environmental characteristics of dust diseases, their role in unfavorable course and outcomes of occupational bronchitis.

Incidence of chronic bronchitis in a cohort of pulp mill workers with repeated gassings to sulphur dioxide and other irritant gases.

BACKGROUND: Occupational exposure to irritants is associated with chronic bronchitis. The aim of this study was to elucidate whether repeated peak exposures with respiratory symptoms, gassings, to sulphur dioxide (SO2) and other irritant gases could increase the risk of chronic bronchitis. METHODS: The study population comprised 3,060 Swedish pulp mill workers (84% males) from a cohort study, who completed a comprehensive questionnaire with items on chronic bronchitis symptoms, smoking habit, occupational history, and specific exposures, including gassings. 2,037 have worked in sulphite mills. Incidence rates and hazard ratios (HRs) for the observation period, 1970-2000, in relation to exposure and the frequency of repeated gassings to SO2 and other irritant gases were calculated. RESULTS: The incidence rate for chronic bronchitis among workers with repeated gassings was 3.5/1,000 person-years compared with 1.5/1,000 person-years among unexposed workers (HR 2.1, 95% confidence interval (CI) 1.4-3.1). The risk was even higher in the subgroup with frequent gassings (HR 3.2, 95% CI 2.0-5.2), particularly among never-smokers (HR 8.7, 95% CI 3.5-22). CONCLUSIONS: Repeated gassings to irritant gases increased the incidence of chronic bronchitis in our study population during and after work in pulp mills, supporting the hypothesis that occupational exposures to irritants negatively affect the airways. These results underscore the importance of preventive actions in this work environment.

[The role of genetic factors in the development of chronic dust bronchitis in workers of coal mining enterprises of Kuzbass].

The distribution of genotypes of HP, GC, EsD, AsP and polymorphisms GSTT1 (GST-theta1) and GSTM1 (GST-micro1) and NOS3 (polymorphism VNTR4) in miners with chronic dust bronchitis, and in those without this occupational disease has been studied The carriers of genotypes of genotypes EsD 1-2, AsP bb were shown to be more prone to develop chronic dust bronchitis. Endogenous factors of resistance to the disease are the genotypes GC 1-1, EsD 1-1, AsP bc.

Agricultural exposures and chronic bronchitis: findings from the AGRICAN (AGRIculture and CANcer) cohort.

PURPOSE: Livestock farming has been recognized as a risk factor for chronic bronchitis (CB). The role of crop farming, however, has been less studied. We sought to assess the role of a large range of farming activities on the risk of CB in the French agricultural cohort AGRICAN (AGRIculture and CANcer). METHODS: Data on respiratory health and farming activities were collected by questionnaire from 2005 to 2007. Associations between farming activities and self-reported doctor's diagnosis of CB were estimated by a logistic regression adjusted for confounders. RESULTS: CB was reported by 1207 farmers (8.4%). Two farming activities were associated with CB: cattle raising (odds ratio [OR] 1.24, 95% confidence interval 1.03-1.48), and potato production (OR 1.33, 95% confidence interval 1.13-1.57). Associations were more pronounced in small-scale cattle raising and in large-scale potato production, in particular among the longest exposed workers (≥20 years). Pesticide poisoning and exposure to pesticides in potato farmers were significantly associated with CB risk (OR 1.64 and OR 1.63, respectively). CONCLUSIONS: This analysis suggests that other agricultural settings not previously reported, such as potato production, may be a risk factor for CB. The nature and circumstances of exposure to hazardous agents need to be further explored.

[Lipid metabolism in occupational chronic bronchitis associated with diabetes mellitus].

The study of 311 patients with chronic occupational bronchitis associated with diabetes mellitus (or diabetes-free) revealed lipid metabolism disorders presenting with overweight, obesity, dyslipoproteinemia. Diabetes mellitus addition to chronic bronchitis increased frequency of lipid metabolism disorders and higher values of lipid state. The revealed lipid metabolism disorders were more marked in the females.

Exposure to outdoor air pollution and chronic bronchitis in adults: a case-control study.

BACKGROUND: Although Lebanon is a highly polluted country, so far no study has specifically been designed to assess the association between outdoor air pollution and chronic bronchitis in this country. OBJECTIVE: To assess the association between exposure to outdoor air pollution and chronic bronchitis in Lebanon. METHODS: A pilot case-control study was conducted in two tertiary care hospitals. Cases consisted of patients diagnosed with chronic bronchitis by a pulmonologist and those epidemiologically confirmed. Controls included individuals free of any respiratory signs or symptoms. After obtaining informed consent, a standardized questionnaire was administered. RESULTS: Bivariate, stratified (over smoking status and gender) and multivariate analyses revealed that passive smoking at home (ORa: 2.56, 95% CI: 1.73-3.80) and at work (ORa: 1.89, 95% CI: 1.13-3.17); older age (ORa: 1.75, 95% CI: 1.55-2.39); lower education (ORa: 1.44, 95% CI: 1.21-1.72); living close to a busy road (ORa: 1.95, 95% CI: 1.31-2.89) and to a local power plant (ORa: 1.62, 95% CI: 1.07-2.45); and heating home by hot air conditioning (ORa: 1.85, 95% CI: 1.00-3.43) were moderately associated with chronic bronchitis; an inverse association was found with heating home electrically (ORa: 0.58, 95% CI: 0.39-0.85). A positive dose-effect relationship was observed in those living close to a busy road and to a local diesel exhaust source. CONCLUSION: Chronic bronchitis is associated with outdoor air pollution.