Abstract Purpose Survivors of allogeneic hematopoietic stem cell transplantation (allo-HSCT) are at risk for cardiopulmonary adverse events. Data on long-term effects on cardiorespiratory fitness are limited. To address the gap in knowledge, we aimed to determine peak oxygen uptake (V̇O 2 peak) and identify associations between cardiorespiratory fitness and clinical characteristics, self-reported physical activity, cardiac, and pulmonary function. Methods In a nationwide, single-center cross-sectional study, 90 survivors [aged median (range) 35 (17–54) years, 56% females] were examined, 17 (6–26) years after allo-HSCT. Myeloablative conditioning comprised busulfan/cyclophosphamide or cyclophosphamide only. Methods included pulmonary function tests, echocardiography, and cardiopulmonary exercise test. Results Chronic graft-versus-host disease (cGVHD) was found in 31% of the subjects, of whom 40% had bronchiolitis obliterans syndrome (BOS). Seventy-one percent of the survivors did not meet WHO recommendations for physical activity and 42% were overweight. Reduced gas diffusion (DL CO ) and systolic ventricular dysfunction (LVEF) were found in 44% and 31%, respectively. For the group, mean (95% CI), V̇O 2 peak was 36.4 (34.7–38.0) mL/min/kg [89 (85–93)% of predicted]. V̇O 2 peak was low at 43%. Cardiopulmonary factors and deconditioning were equally common limitations for exercise. In a multiple linear regression model, low V̇O 2 peak was associated with low DL CO , low LVEF, BOS, overweight, and inactivity. Conclusion Half of the survivors had reduced cardiorespiratory fitness median 17 years after allo-HSCT. Cardiopulmonary factors and deconditioning were equally common limitations to exercise. We encourage long-term cardiopulmonary monitoring of allo-HSCT survivors and targeted advice on modifiable lifestyle factors.
Exposure to gases and dust may induce airway inflammation. It was hypothesized that heavy construction workers who had been exposed to dust and gases in underground construction work for 1 yr, would have early signs of upper and lower airway inflammation, as compared to outdoor workers. A study group comprising 29 nonsmoking underground concrete workers (mean± sd age 44±12 yrs), and a reference group of 26 outdoor concrete workers (39±12 yrs) were examined by acoustic rhinometry, nasal and exhaled nitric oxide spirometry and a questionnaire on respiratory symptoms. Exposure measurements were carried out. The underground workers had higher exposure to total and respirable dust, α‐quartz and nitrogen dioxide than the references (p<0.001). The occurrence of respiratory symptoms was higher in the underground workers than in the references (p<0.05). Exhaled nitric oxide (NO) (geometric mean±sem) was higher in the underground workers than in the references (8.4±1.09 versus 5.6±1.07 parts per billion (ppb), p=0.001), whereas spirometric values were comparable. The underground workers had smaller nasal cross-sectional area and volume than the references, and more pronounced increases after decongestion (p<0.001). To conclude the exposure in underground construction may cause nasal mucosal swelling and increased levels of exhaled nitric oxide, indicating signs of upper and lower airway inflammation.
Abstract. Objectives. To study the validity of official mortality statistics regarding deaths from pulmonary tuberculosis, and to identify factors contributing to death. Design. A retrospective study. Setting. Cases were enrolled from the data of the Central Bureau of Statistics from where the official mortality statistics are issued, the National Tuberculosis Register and all Autopsy Registers in the region. Subjects. Case and autopsy reports from all patients who died from active pulmonary tuberculosis in two Norwegian counties between 1977 and 1989. Main outcome measures. Patients identified from all three registers with active pulmonary tuberculosis, concomitant diseases/risk‐factors, chest X‐rays, symptoms, number of patients investigated and treated for tuberculosis, duration from hospital admission until start of treatment and/or death. Results. Ninety‐six patients, median age 75 years, died from pulmonary tuberculosis, 51 without treatment. Thirty‐four patients had not been registered at the Central Bureau of Statistics. Thirty‐nine patients had cough on admission. Weight loss and generalized malaise occurred just as frequently. Forty‐two patients had infiltrates on chest X‐ray located elsewhere than in the apical region. In 42 patients, no diagnostic tests for tuberculosis were performed. The median length of stay in hospital was 24 days before death in the untreated group, and 21 days before start of treatment in the treated group. Conclusion. Reliable figures of patients who died from pulmonary tuberculosis could not be obtained from the official statistics because of under‐notification and erroneous codification of diseases. Deaths occurred mainly because the diagnosis was established too late: in half of the patients at autopsy. Eighty‐one patients had concomitant diseases known to lower resistance against tuberculosis. Lack of diagnostic suspicion may have been caused by nonspecific symptoms and atypical chest X‐ray findings.
Objectives The aim of this study was to estimate the prevalence of respiratory symptoms and physician-diagnosed asthma and assess the impact of current occupational exposure. Design Cross-sectional analyses of the prevalence of self-reported respiratory health and association with current occupational exposure in a random sample of the general population in Telemark County, Norway. Settings In 2013, a self-administered questionnaire was mailed to a random sample of the general population, aged 16–50, in Telemark, Norway. The overall response rate was 33%, comprising 16 099 responders. Outcome measures The prevalence for respiratory symptoms and asthma, and OR of respiratory symptoms and asthma for occupational groups and exposures were calculated. Occupational exposures were assessed using self-reported exposure and an asthma-specific job-exposure matrix (JEM). Results The prevalence of physician-diagnosed asthma was 11.5%. For the occupational groups, the category with agriculture/fishery workers and craft/related trade workers was associated with wheezing and asthma attack in the past 12 months, showing OR 1.3 (1.1 to 1.6) and 1.9 (1.2 to 2.8), respectively. The group including technicians and associated professionals was also associated with wheezing OR 1.2 (1.0 to 1.3) and asthma attack OR 1.4 (1.1 to 1.9). The JEM data show that exposure to flour was associated with wheezing OR 3.2 (1.4 to 7.3) and woken with dyspnoea OR 3.5 (1.3 to 9.5), whereas exposures to diisocyanates, welding/soldering fumes and exposure to vehicle/motor exhaust were associated with dyspnoea OR 2.9 (1.5 to 5.7), 3.2 (1.6 to 6.4) and 1.4 (1.0 to 1.8), respectively. Conclusions The observed prevalence of physician-diagnosed asthma was 11.5%. The ‘manual’ occupations were associated with respiratory symptoms. Occupational exposure to flour, diisocyanates, welding/soldering fumes and vehicle/motor exhaust was associated with respiratory symptoms in the past 12 months and use of asthma medication. However, prospective data are needed to confirm the observed associations.
A competent assessment of causal relationships in the case of work-related lung disorders depends on correct diagnosis, a detailed occupational history and updated epidemiological knowledge about causal relationships, obtained from the literature. Assessments for purposes of compensation demand, in addition, an explicit choice of methods for calculating causes, before a meaningful attempt can be made to weight the various factors in and outside the working environment. If adequate epidemiological knowledge is available, the causal probability, based on the etiological fraction among the exposed persons (attributable risk) may be a useful tool for apportioning the different causal factors.
The objective of the study was to assess the relationship between breastfeeding and lower respiratory tract infections (LRTIs) during the first year of life, with special reference to maternal smoking. A cohort of 3,754 children born in 1992-1993 in the City of Oslo, Norway was recruited and data were collected at birth, 6 and 12 months of age. Complete information was obtained from 3,238 children (follow-up rate 86%). The main outcome was an episode of a LRTI, such as pneumonia, bronchitis or bronchiolitis, based on a self-administered questionnaire addressed to parents when the child was 6 and 12 months old. The outcome was specified as physician-diagnosed. In logistic regression analysis adjusting for confounding, maternal smoking increased the risk of LRTIs in children breastfed for 0-6 months (odds ratio (AOR) 1.7; 95% confidence interval (95% CI) 1.2-2.4), but not essentially when the child was breastfed for more than 6 months (AOR 1.1; 95% CI 0.7-1.6). Short-term breastfeeding (0-6 months) and no maternal smoking was related to an adjusted AOR of LRTIs of 1.3 (95% CI 1.0-1.7), and short-term breastfeeding combined with maternal smoking was related to an adjusted AOR of 2.2 (95% CI 1.6-3.1), as compared with long-term breastfeeding and no maternal smoking. The present study indicates a protective effect of long-term breastfeeding on the risk of lower respiratory tract infection during the first year of life. The results suggest that the protective effect is strongest in children exposed to environmental tobacco smoke.
Isolated lung cells constitute a valuable system for studying mechanisms involved in chemically induced toxicity in the lung. Different lung cells isolated from various species may be studied. Bronchiolar Clara and alveolar type 2 cells produce important lung-specific proteins, hold a major role in the metabolism of xenobiotics and serve as progenitor cells for other lung cell types. They are possible target cells in lung carcinogenesis. Alveolar macrophages play an important role in lung defence and in inflammatory responses. In the present study we have characterised chemically induced DNA damage, apoptosis, changes in cell cycle progression, transformation and alterations in gene expression in these specific lung cells isolated from rat, rabbit and human. Major differences between the cell types and the various species in the induction of DNA damage by chemicals were found, as measured by the 32P-postlabelling and alkaline filter elution techniques. Benzo(a)pyrene and hydrogen fluoride were found to induce apoptosis in the isolated cells as measured by microscopical analysis and flow cytometry. The function of various important tissue- or cell type specific proteins (CYP 2B1, Clara cell protein) and/or cellular signal transduction pathways constitute important targets that may be affected by exposure to toxic compounds. Using immunological and molecular techniques the differential expression of specific proteins/RNAs and their activity can be studied. Among other proteins, c/ebp is involved in the regulation of transcription at the end of signal pathways. The protein is differentially expressed in rat lung cells and thus could be suitable for studying differential toxic effects in various lung cells. In humans, bronchoalveolar lavage (BAL) fluid from human volunteers can be readily obtained and examined after exposure to different chemical compounds. An increase in the percentage of CD3-positive cells (T-lymphocytes) was found after exposure to hydrogen fluoride. The number of certain cell types and cytokines may be used to estimate the degree of inflammatory reaction. In conclusion, the use of in vitro data including the use of specific, primary human lung cell types may contribute considerably to the quality of risk assessment, together with in vivo data from animals and man.
