Obstructive Lung Disease Linked to Occupational Exposures in Malawian Tobacco Farmers.

Nicotine and pesticide exposure in agricultural settings have been linked to the development of chronic respiratory disease in workers. However, this has not been extensively studied in Africa. The aim of this study was therefore to determine the prevalence of obstructive lung disease and its relationship to concurrent nicotine and pesticide exposure among small-scale tobacco farmers in Malawi. For this purpose, sociodemographic characteristics, occupational and environmental exposures were evaluated in relation to work-related respiratory symptoms and lung function impairment. A cross-sectional study was conducted enrolling 279 workers in flue-cured tobacco farms in Zomba, Malawi. The study instruments used for assessing the health outcomes were a standardised European Community Respiratory Health Survey II (ECRHS) questionnaire and Spirometry testing. The questionnaires were aimed at collecting relevant data on sociodemographic factors and self-reported respiratory health outcomes. Data were also collected on potential pesticide and nicotine exposures. Spirometry was done to evaluate objective respiratory impairment in accordance with American Thoracic Society guidelines. The mean age of participants was 38 years with 68% being male. The prevalence of work-related ocular nasal symptoms, chronic bronchitis, and work-related chest symptoms was 20%, 17%, and 29%, respectively. Airflow limitation (FEV1/FVC <70%) was found in 8% of workers. Self-reported exposure to pesticides varied from 72%- to 83%, whilst the prevalence of recent green tobacco sickness was 26%. Tasks linked to nicotine exposure, such as sowing (OR: 2.5; CI 1.1-5.7) and harvesting (OR: 2.6; CI 1.4-5.1), were significantly associated with work-related chest symptoms. Pesticide application (OR:1.96; CI 1.0-3.7) was associated with an increased risk of work-related oculonasal symptoms. Duration of pesticide exposure was also associated with obstructive impairment FEV1/FVC

Dietary phenotype and advanced glycation end-products predict WTC-obstructive airways disease: a longitudinal observational study.

BACKGROUND: Diet is a modifier of metabolic syndrome which in turn is associated with World Trade Center obstructive airways disease (WTC-OAD). We have designed this study to (1) assess the dietary phenotype (food types, physical activity, and dietary habits) of the Fire Department of New York (FDNY) WTC-Health Program (WTC-HP) cohort and (2) quantify the association of dietary quality and its advanced glycation end product (AGE) content with the development of WTC-OAD. METHODS: WTC-OAD, defined as developing WTC-Lung Injury (WTC-LI; FEV1 < LLN) and/or airway hyperreactivity (AHR; positive methacholine and/or positive bronchodilator response). Rapid Eating and Activity Assessment for Participants-Short Version (REAP-S) deployed on 3/1/2018 in the WTC-HP annual monitoring assessment. Clinical and REAP-S data of consented subjects was extracted (7/17/2019). Diet quality [low-(15-19), moderate-(20-29), and high-(30-39)] and AGE content per REAP-S questionnaire were assessed for association with WTC-OAD. Regression models adjusted for smoking, hyperglycemia, hypertension, age on 9/11, WTC-exposure, BMI, and job description. RESULTS: N = 9508 completed the annual questionnaire, while N = 4015 completed REAP-S and had spirometry. WTC-OAD developed in N = 921, while N = 3094 never developed WTC-OAD. Low- and moderate-dietary quality, eating more (processed meats, fried foods, sugary drinks), fewer (vegetables, whole-grains),and having a diet abundant in AGEs were significantly associated with WTC-OAD. Smoking was not a significant risk factor of WTC-OAD. CONCLUSIONS: REAP-S was successfully implemented in the FDNY WTC-HP monitoring questionnaire and produced valuable dietary phenotyping. Our observational study has identified low dietary quality and AGE abundant dietary habits as risk factors for pulmonary disease in the context of WTC-exposure. Dietary phenotyping, not only focuses our metabolomic/biomarker profiling but also further informs future dietary interventions that may positively impact particulate matter associated lung disease.

Micro-RNAs: Crossroads between the Exposure to Environmental Particulate Pollution and the Obstructive Pulmonary Disease.

Environmental pollution has reached a global echo and represents a serious problem for human health. Air pollution encompasses a set of hazardous substances, such as particulate matter and heavy metals (e.g., cadmium, lead, and arsenic), and has a strong impact on the environment by affecting groundwater, soil, and air. An adaptive response to environmental cues is essential for human survival, which is associated with the induction of adaptive phenotypes. The epigenetic mechanisms regulating the expression patterns of several genes are promising candidates to provide mechanistic and prognostic insights into this. Micro-RNAs (miRNAs) fulfil these features given their ability to respond to environmental factors and their critical role in determining phenotypes. These molecules are present in extracellular fluids, and their expression patterns are organ-, tissue-, or cell-specific. Moreover, the experimental settings for their quantitative and qualitative analysis are robust, standardized, and inexpensive. In this review, we provide an update on the role of miRNAs as suitable tools for understanding the mechanisms behind the physiopathological response to toxicants and the prognostic value of their expression pattern associable with specific exposures. We look at the mechanistic evidence associable to the role of miRNAs in the processes leading to environmental-induced pulmonary disease (i.e., chronic obstructive pulmonary disease).

Characteristics in Stages of Change and Decisional Balance among Smokers: The Burden of Obstructive Lung Diseases (BOLD)-Australia Study.

Smoking cessation remains a health promotion target. Applying the Transtheoretical Model to Australian Burden of Obstructive Lung Diseases (BOLD) data, we examined differences in stages of change (SoC) and readiness to quit decisional behaviours. Factors were identified likely to influence readiness of smokers, ≥40 years old, to quit. Analysis was restricted to current smokers classified to one of three stages: pre-contemplation (PC), contemplation (C) or preparation (P) to quit. Their ability to balance positive and negative consequences was measured using decisional balance. Among 314 smokers, 43.0% females and 60.8% overweight/obese, the distribution of SoC was: 38.1% PC, 38.3% C and 23.5% P. Overweight/obesity was associated with readiness to quit in stages C and P and there were more negative than positive attitudes towards smoking in those stages. Males were significantly heavier smokers in PC and C stages. Females used smoking cessation medication more frequently in PC stage, were more embarrassed about smoking and had greater negative reinforcements from smoking. Age started smoking and factors related to smoking history were associated with readiness to quit and increased the odds of being in stage C or P. An overweight/obese smoker was likely to be contemplating or preparing to quit. In these stages, smokers have more negative attitudes toward smoking. Starting smoking later, taking advice on cessation from health providers and using quit medications indicate increased readiness to quit. Evaluating these factors in smokers and developing cessation gain-framed messages may prove useful to healthcare providers.

Effect of different doses of inhaled ciclesonide on lung function, clinical signs related to airflow limitation and serum cortisol levels in horses with experimentally induced mild to severe airway obstruction.

BACKGROUND: Inhaled corticosteroids are effective for the treatment of equine asthma but they induce cortisol suppression with potential side effects. OBJECTIVES: To study the efficacy of ciclesonide, an inhaled corticosteroid with an improved safety profile, on lung function, clinical signs related to airway obstruction, and serum cortisol levels in asthmatic horses exposed to a mouldy hay challenge. STUDY DESIGN: Cross-over placebo controlled, blinded, randomised experiment. METHODS: Sixteen horses were enrolled in three subsequent dose-titration studies (8 horses/study) to investigate the effects of inhaled ciclesonide administered for 2 weeks at doses ranging from 450 to 2700 µg twice daily or 3712.5 µg once daily. Systemic dexamethasone (0.066 mg/kg per os) was our positive control. A placebo group was also studied. Lung function and clinical scores were blindly performed before and after 7 and 14 days of treatment. Serum cortisol was measured before and after 3, 5, 7, 10, 14 days of treatment as well as 3 and 7 days post treatment. RESULTS: After 7 days, dexamethasone induced a significant reduction in pulmonary resistance (from 2.5 ± 0.6 at day 0 to 1.1 ± 0.7 cm H2 O/L/s), pulmonary elastance (5.0 ± 2.6 to 1.2 ± 1.0 cm H2 O/L), and of the weighted clinical score (14.8 ± 4.7 to 8.0 ± 4.4). Similarly, ciclesonide 1687.5 µg twice daily significantly improved pulmonary resistance (2.7 ± 1.1 to 1.6 ± 0.8 cm H2 O/L/s), pulmonary elastance (5.2 ± 3.1 to 2.2 ± 1.3 cm H2 O/L), and weighted clinical score (13 ± 2.9 to 10.8 ± 4.2). Serum cortisol suppression (<50 nmol/L) systematically occurred with dexamethasone from day 3 of treatment up to day 3 post treatment, but not with ciclesonide at any tested doses. Placebo did not exert any significant beneficial effect. MAIN LIMITATIONS: Experimentally induced asthma exacerbations in horses might respond differently to treatment than naturally occurring exacerbations. CONCLUSIONS: Inhaled ciclesonide is an effective treatment for horses with equine asthma. Serum cortisol was unaffected by treatment.

Pulmonary Function Impairment From Exposure to Mixed Organic Solvents in Male Shipyard Painters.

OBJECTIVES: This study aimed to examine the effects of chronic exposure to organic solvents on lung function in a shipyard painters. METHODS: Male workers in the shipyard painting department were selected as the organic solvents exposure group. Exposure was classified according to the type of work usually performed, and the cumulative exposure index was obtained using the results of biological monitoring. These were then used to divide the exposure group into low-exposure and high-exposure groups, and the dose-response relationships were examined for decreased lung function. For ventilation indices, we obtained the forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), the FEV1/FVC ratio, and the maximal mid-expiratory flow (MMF) from the forced expiratory flow-volume curve and also calculated these as percentages of the predicted values. RESULTS: FVC and FEV1 showed no significant differences among the control, and low-exposure and high-exposure groups, but FEV1 as a percentage of its predicted value (%FEV1) decreased with increasing exposure at 90.0%, 90.9%, and 90.0% in the control, low-exposure, and high-exposure groups, respectively. MMF% predicted also decreased significantly at 98.5%, 90.1%, and 88.4% in the control, low-exposure, and high-exposure group, respectively, indicating that workers exposed to organic solvents showed obstructive respiratory disease. CONCLUSION: Exposure to organic solvents is associated with obstructive pulmonary dysfunction rather than restrictive pulmonary dysfunction.

A Meta-analysis of Arsenic Exposure and Lung Function: Is There Evidence of Restrictive or Obstructive Lung Disease?

PURPOSE OF REVIEW: Hundreds of millions of people worldwide are exposed to arsenic via contaminated water. The goal of this study was to identify whether arsenic-associated lung function deficits resemble obstructive- or restrictive-like lung disease, in order to help illuminate a mechanistic pathway and identify at-risk populations. RECENT FINDINGS: We recently published a qualitative systematic review outlining the body of research on arsenic and non-malignant respiratory outcomes. Evidence from several populations, at different life stages, and at different levels of exposure showed consistent associations of arsenic exposure with chronic lung disease mortality, respiratory symptoms, and lower lung function levels. The published review, however, only conducted a broad qualitative description of the published studies without considering specific spirometry patterns, without conducting a meta-analysis, and without evaluating the dose-response relationship. We searched PubMed and Embase for studies on environmental arsenic exposure and lung function. We performed a meta-analysis using inverse-variance-weighted random effects models to summarize adjusted effect estimates for arsenic and forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio. Across nine studies, median water arsenic levels ranged from 23 to 860 µg/L. The pooled estimated mean difference (MD) comparing the highest category of arsenic exposure (ranging from > 11 to > 800 µg/L) versus the lowest (ranging from < 10 to < 100 µg/L) for each study for FEV1 was - 42 mL (95% confidence interval (CI) - 70, - 16) and for FVC was - 50 mL (95% CI - 63, - 37). Three studies reported effect estimates for FEV1/FVC, for which there was no evidence of an association; the pooled estimated MD was 0.01 (95% CI - 0.005, 0.024). This review supports that arsenic is associated with restrictive impairments based on inverse associations between arsenic and FEV1 and FVC, but not with FEV1/FVC. Future studies should confirm whether low-level arsenic exposure is a restrictive lung disease risk factor in order to identify at-risk populations in the USA.

Occupational exposures to solvents and metals are associated with fixed airflow obstruction.

Objectives This study investigated the associations between occupational exposures to solvents and metals and fixed airflow obstruction (AO) using post-bronchodilator spirometry. Methods We included 1335 participants from the 2002-2008 follow-up of the Tasmanian Longitudinal Health Study. Ever-exposure and cumulative exposure-unit (EU) years were calculated using the ALOHA plus job exposure matrix (JEM). Fixed AO was defined as post-bronchodilator forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) <0.7 and FEV 1/FVC

Astragalin Inhibits Allergic Inflammation and Airway Thickening in Ovalbumin-Challenged Mice.

Lung inflammation and oxidative stress are the major contributors to the development of obstructive pulmonary diseases. Macrophages are involved in pulmonary inflammation and alveolar damage in emphysema. Astragalin is an anti-inflammatory flavonoid present in persimmon leaves and green tea seeds. This study elucidated that astragalin inhibited inflammatory cell infiltration induced by 20 µM H2O2 and blocked airway thickening and alveolar emphysema induced by 20 µg of ovalbumin (OVA) in mice. OVA induced mouse pulmonary MCP-1, and H2O2 enhanced the expression of MCP-1/ICAM-1/αv integrin in bronchial airway epithelial BEAS-2B cells. Such induction was inhibited by supplying 10-20 mg/kg of astragalin to OVA-challenged mice and 1-20 µM astragalin to oxidant-stimulated cells. Oral administration of 20 mg/kg of astragalin reduced the induction of F4/80/CD68/CD11b in airways of mice challenged with OVA. Additionally, emphysema tissue damage was observed in OVA-exposed alveoli. Mast cell recruitment in the airway subepithelium was blocked by supplementing astragalin to OVA-challenged mice. Orally treating 20 mg/kg of astragalin reduced α-SMA induction in inflammation-occurring airways and appeared to reverse airway thickening and constriction induced by an OVA episode. These results revealed that astragalin may improve airway thickening and alveolar destruction with blockade of allergic inflammation in airways. Therefore, astragalin may be a therapeutic agent antagonizing asthma and obstructive pulmonary diseases.

Inhaled silica-coated TiO2 nanoparticles induced airway irritation, airflow limitation and inflammation in mice.

The wide use of nanotechnology is here to stay. However, the knowledge on the health effects of different engineered nanomaterials (ENMs) is lacking. In this study, irritation and inflammation potential of commercially available silica-coated TiO2 ENMs (10 × 40 nm, rutile) were studied. Single exposure (30 min) at mass concentrations 5, 10, 20 and 30 mg/m(3), and repeated exposure (altogether 16 h, 1 h/day, 4 days/week for 4 weeks) at mass concentration of 30 mg/m(3) to silica-coated TiO2 induced first phase of pulmonary irritation (P1), which was seen as rapid, shallow breathing. During repeated exposures, P1 effect was partly evolved into more intense pulmonary irritation. Also sensory irritation was observed at the beginning of both single and repeated exposure periods, and the effect intensified during repeated exposures. Airflow limitation started to develop during repeated exposures. Repeated exposure to silica-coated TiO2 ENMs induced also pulmonary inflammation: inflammatory cells infiltrated in peribronchial and perivascular areas of the lungs, neutrophils were found in BAL fluids, and the number of CD3 and CD4 positive T cells increased significantly. In line with these results, pulmonary mRNA expression of chemokines CXCL1, CXCL5 and CXCL9 was enhanced. Also expression of mRNA levels of proinflammatory cytokines TNF-α and IL-6 was elevated after repeated exposures. Taken together, these results indicated that silica-coated TiO2 ENMs induce pulmonary and sensory irritation after single and repeated exposure, and airflow limitation and pulmonary inflammation after repeated exposure.

Work-related spirometric restriction in flavoring manufacturing workers.

BACKGROUND: Flavoring-exposed workers are at risk for occupational lung disease. METHODS: We examined serial spirometries from corporate medical surveillance of flavoring production workers to assess abnormality compared to the U.S. population; mean decline in forced expiratory volume in one second (FEV1) and forced vital capacity (FVC); and excessive declines in FEV1. RESULTS: Of 106 workers, 30 had spirometric restriction, 3 had obstruction, 1 had both, and 13 (of 70, 19%) had excessive declines in FEV1. The adjusted prevalence of restriction was 3.7 times expected. Employees with higher potential for flavorings exposure had 3.0 times and 2.4 times greater average annual declines in FEV1 and FVC respectively, and had 5.8 times higher odds of having excessive FEV1 declines than employees with lower potential for exposure. CONCLUSION: Exposure-related spirometric abnormalities consistent with a restrictive process evolved during employment, suggesting that exposures in flavoring production are associated with a range of pathophysiology.

Obstructive pulmonary function impairment among Korean male workers exposed to organic solvents, iron oxide dust, and welding fumes.

We evaluated spirometric obstructive pulmonary function impairment among workers who were occupationally exposed to organic solvents, iron oxide dust, or welding fumes. Data were collected from records of periodic health examinations of workers. In total, 448 Korean male workers were enrolled and classified into three exposure groups: exposure to organic solvents, iron oxide dust, or welding fumes. Logistic regression analysis was performed to evaluate the association between occupational exposure and pulmonary function. Compared to exposure to organic solvents, exposure to iron oxide dust was significantly associated with obstructive pulmonary function impairment (odds ratio [OR], 9.61; 95% confidence interval [CI], 2.20-41.97). The group exposed to welding fumes did not show a significantly higher OR compare to those exposed to organic solvents (OR, 2.83; 95% CI, 0.74-10.8). These results suggest that exposure to iron oxide dust has a greater association with obstructive pulmonary function impairment than exposure to organic solvents or welding fumes.

Glucagon-like peptide-1 (GLP-1) reduces mortality and improves lung function in a model of experimental obstructive lung disease in female mice.

The incretin hormone glucagon-like peptide-1 (GLP-1) is an important insulin secretagogue and GLP-1 analogs are used for the treatment of type 2 diabetes. GLP-1 displays antiinflammatory and surfactant-releasing effects. Thus, we hypothesize that treatment with GLP-1 analogs will improve pulmonary function in a mouse model of obstructive lung disease. Female mice were sensitized with injected ovalbumin and treated with GLP-1 receptor (GLP-1R) agonists. Exacerbation was induced with inhalations of ovalbumin and lipopolysaccharide. Lung function was evaluated with a measurement of enhanced pause in a whole-body plethysmograph. mRNA levels of GLP-1R, surfactants (SFTPs), and a number of inflammatory markers were measured. GLP-1R was highly expressed in lung tissue. Mice treated with GLP-1R agonists had a noticeably better clinical appearance than the control group. Enhanced pause increased dramatically at day 17 in all control mice, but the increase was significantly less in the groups of GLP-1R agonist-treated mice (P < .001). Survival proportions were significantly increased in GLP-1R agonist-treated mice (P < .01). SFTPB and SFTPA were down-regulated and the expression of inflammatory cytokines were increased in mice with obstructive lung disease, but levels were largely unaffected by GLP-1R agonist treatment. These results show that GLP-1R agonists have potential therapeutic potential in the treatment of obstructive pulmonary diseases, such as chronic obstructive pulmonary disease, by decreasing the severity of acute exacerbations. The mechanism of action does not seem to be the modulation of inflammation and SFTP expression.

Perinatal exposure to nicotine and implications for subsequent obstructive lung disease.

Many diseases are due to gene-environment or epigenetic-environment interactions resulting in a change in the program that controls tissue structure and function. Changes in the in utero and external environment during perinatal development due to parental smoking, or nicotine exposure, may reduce the capacity of the offspring to protect themselves against environmental stressors. Nicotine is genotoxic and also induces reactive oxygen species [ROS] production. It also reduces the antioxidant capacity of the lung. The lungs of the offspring are therefore developing in an environment of an oxidant-antioxidant imbalance with the concomitant adverse effects of the oxidants and nicotine on cell integrity. Consequently, they are more prone to develop respiratory diseases such as asthma and emphysema later in life. The use of NRT by pregnant or lactating females is therefore not an appropriate strategy to quit smoking.

Hydrogen sulfide and particle matter levels associated with increased dispensing of anti-asthma drugs in Iceland's capital.

BACKGROUND: Air pollutants in Iceland's capital area include hydrogen sulfide (H2S) emissions from geothermal power plants, particle pollution (PM10) and traffic-related pollutants. Respiratory health effects of exposure to PM and traffic pollutants are well documented, yet this is one of the first studies to investigate short-term health effects of ambient H2S exposure. OBJECTIVES: The aim of this study was to investigate the associations between daily ambient levels of H2S, PM10, nitrogen dioxide (NO2) and ozone (O3), and the use of drugs for obstructive pulmonary diseases in adults in Iceland's capital area. METHODS: The study period was 8 March 2006 to 31 December 2009. We used log-linear Poisson generalized additive regression models with cubic splines to estimate relative risks of individually dispensed drugs by air pollution levels. A three-day moving average of the exposure variables gave the best fit to the data. Final models included significant covariates adjusting for climate and influenza epidemics, as well as time-dependent variables. RESULTS: The three-day moving average of H2S and PM10 levels were positively associated with the number of individuals who were dispensed drugs at lag 3-5, corresponding to a 2.0% (95% confidence interval [CI] 0.4, 3.6) and 0.9% (95% CI 0.1, 1.8) per 10 µg/m3 pollutant concentration increase, respectively. CONCLUSION: Our findings indicated that intermittent increases in levels of particle matter from traffic and natural sources and ambient H2S levels were weakly associated with increased dispensing of drugs for obstructive pulmonary disease in Iceland's capital area. These weak associations could be confounded by unevaluated variables hence further studies are needed.

[Pulmonary events induced by non-steroidal anti-inflammatory drugs in patients with sickle cell disease]. / Manifestations respiratoires induites par les anti-inflammatoires non stéroïdiens chez le drépanocytaire.

Painful sickle cell crises are among the principal manifestations of sickle cell disease. Their treatment routinely requires the use of non-steroidal anti-inflammatory drugs (NSAIDS). These drugs also, however, inhibit the cyclooxygenase cycle in arachidonic acid metabolism, promoting the synthesis of leukotrienes, which have bronchoconstrictive effects. This study took place from March through August, 2007, and included 100 patients of both sexes, aged 2 to 59 years, with any sickle cell phenotype (SS, SC, AS, SFA2, or SAFA2) and treated by NSAIDs in the Immunology and Haematology department of the University Hospital of Cocody. We analysed the characteristics of the respiratory events induced by taking NSAIDs to identify potential risk factors for their occurrence. We found that 5% of these patients presented respiratory symptoms linked to NSAIDs. These appeared within 30 minutes of drug intake for 80%; in 60% of these cases, only corticosteroid and antihistamine treatment resolved these symptoms. The occurrence of respiratory events did not differ by sex; however, younger subjects were more exposed to these respiratory events. All patients with family or individual history of atopy-like hypersensitivity type I events presented these respiratory symptoms when taking NSAIDS for sickle-cell crises.

Parenchymal and airway diseases caused by asbestos.

PURPOSE OF REVIEW: The extensive industrial use of asbestos for many decades has been linked to development of benign and malignant pleuropulmonary disease. This review summarizes newer evidence and ongoing controversies that exist in the literature regarding asbestos-related parenchymal and airway diseases. RECENT FINDINGS: Asbestosis represents a significant respiratory problem despite the improvement in the workplace hygiene and a decrease in use of asbestos. The management of asbestosis remains challenging as currently there is no specific treatment. The role of asbestos exposure alone as a cause of chronic airway obstruction remains uncertain. The relationship between lung cancer and asbestos exposure alone and in combination with smoking has also been investigated. The benefit of screening for asbestos-related pleuropulmonary disease remains uncertain as does the use of computed tomography scanning for the purpose of screening. SUMMARY: Future studies will help clarify the clinical issues and shape screening strategies for asbestos-exposed individuals.

Occupational exposure and pulmonary function of jute mill workers in Sunsari, Nepal.

Most workers of building, pottery, timber, food and mine industries suffer from non-specific lung diseases and ventilatory disorders. There are many such industries operative in Sunsari, Nepal and so far no study has been reported on pulmonary function of jute mill workers of this region, who are also exposed to dust as other workers in similar types of industries. A brief clinical sheet regarding age, occupational particulars, smoking habits and presence or absence of respiratory symptoms was recorded for each worker. Spirometric parameters were recorded using an electronic spirometer. The group consisted of 95 male workers with mean age 28.43 +/- 7.58 yrs, weight 53.77 +/- 8.70 kg and height 164.83 +/- 6.82 cm. The study indicated an overall reduction in FVC, FEV1, PEFR, FEF25-75% and MVV. FEV1/FVC was within the normal range. Further division of workers into smokers and non-smokers, showed comparatively more decline in PEFR, FEF 25.0-75.0% and FEV1/ FVC in smokers. From this study, it can be concluded that exposure of jute dust leads to combined types of spirometric deficit revealing restrictive or obstructive diseases.

Cigarette smoking and diffuse lung disease.

Cigarette smoke, a toxic collection of more than 4000 chemicals generated from combustion of tobacco plant leaves, is known to cause several respiratory ailments, including chronic bronchitis, emphysema and lung cancer, and is associated with an increase in respiratory infections. In addition, cigarette smoking is considered a principal aetiological factor responsible for the development of certain diffuse interstitial and bronchiolar lung diseases, namely respiratory bronchiolitis-interstitial lung disease (RB-ILD), desquamative interstitial pneumonia (DIP) and adult pulmonary Langerhans' cell histiocytosis (PLCH). Although not exclusively seen in cigarette smokers, substantial clinical and epidemiological data support a central role for smoking as the primary causative agent of most RB-ILD, DIP and PLCH. Additional evidence in support of cigarette smoke as a primary aetiological agent in RB-ILD, DIP and PLCH is the observation that smoking cessation may lead to disease improvement, while recurrence of these disorders has been observed to occur in the transplanted lung upon re-exposure to tobacco smoke. Furthermore, histopathological changes of respiratory bronchiolitis, DIP and PLCH (with or without co-existent emphysema) may be found on lung biopsy in the same individual, implicating smoking as a common inciting agent of these diverse lesions. Recent studies also suggest a role for cigarette smoking as a potential co-factor in the development of acute eosinophilic pneumonia, usual interstitial pneumonia and rheumatoid arthritis-associated interstitial lung disease. In the current review, we propose a novel classification that takes into account the complex relationship between cigarette smoking and diffuse lung diseases. Investigation on the role of smoking as a potential causative factor or modifier of these diverse diffuse lung diseases is important, as smoking cessation utilizing state-of-the-art tobacco cessation efforts should be a central part of therapy, while pharmacotherapy with corticosteroids or other immune modifying agents should be reserved for selected patients.