Risk of asbestosis, mesothelioma, other lung disease or death among motor vehicle mechanics: a 45-year Danish cohort study

Thorax ◽  
2021 ◽  
pp. thoraxjnl-2020-215041
Author(s):  
Reimar Wernich Thomsen ◽  
Anders Hammerich Riis ◽  
Esben Meulengracht Flachs ◽  
David H Garabrant ◽  
Jens Peter Ellekilde Bonde ◽  
...  

IntroductionThe risk of asbestosis, malignant mesothelioma and lung cancer among motor vehicle mechanics is of concern because of potential exposure to chrysotile asbestos during brake, clutch and gasket repair and maintenance. Asbestos has also been used in insulation and exhaust systems.MethodsWe examined the long-term risk of incident mesothelioma, lung cancer, asbestosis and other lung diseases and mortality due to mesothelioma, lung cancer, asbestosis and other lung diseases in a nationwide cohort of all men registered as motor vehicle mechanics since 1970 in Denmark. This was compared with the corresponding risk in a cohort of male workers matched 10:1 by age and calendar year, with similar socioeconomic status (instrument makers, dairymen, upholsterers, glaziers, butchers, bakers, drivers, farmers and workers in the food industry, trade or public services).ResultsOur study included 138 559 motor vehicle mechanics (median age 24 years; median follow-up 20 years (maximum 45 years)) and 1 385 590 comparison workers (median age 25 years; median follow-up 19 years (maximum 45 years)). Compared with other workers, vehicle mechanics had a lower risk of morbidity due to mesothelioma/pleural cancer (n=47 cases) (age-adjusted and calendar-year-adjusted HR=0.74 (95% CI 0.55 to 0.99)), a slightly increased risk of lung cancer (HR=1.09 (95% CI 1.03 to 1.14)), increased risk of asbestosis (HR=1.50 (95% CI 1.10 to 2.03)) and a chronic obstructive pulmonary disease risk close to unity (HR=1.02 (95% CI 0.99 to 1.05)). Corresponding HRs for mortality were 0.86 (95% CI 0.64 to 1.15) for mesothelioma/pleural cancer, 1.06 (95% CI 1.01 to 1.12) for lung cancer, 1.79 (95% CI 1.10 to 2.92) for asbestosis, 1.06 (95% CI 0.86 to 1.30) for other lung diseases caused by external agents and 1.00 (95% CI 0.98 to 1.01) for death due to all causes.ConclusionsWe found that the risk of asbestosis was increased among vehicle mechanics. The risk of malignant mesothelioma/pleural cancers was not increased among vehicle mechanics.

2021 ◽  
Vol 12 ◽  
pp. 204062232110159
Author(s):  
Jung Eun Yoo ◽  
Dahye Kim ◽  
Hayoung Choi ◽  
Young Ae Kang ◽  
Kyungdo Han ◽  
...  

Background: The aim of this study was to investigate whether physical activity, sarcopenia, and anemia are associated an with increased risk of tuberculosis (TB) among the older population. Methods: We included 1,245,640 66-year-old subjects who participated in the National Screening Program for Transitional Ages for Koreans from 2009 to 2014. At baseline, we assessed common health problems in the older population, including anemia and sarcopenia. The subjects’ performance in the timed up-and-go (TUG) test was used to predict sarcopenia. The incidence of TB was determined using claims data from the National Health Insurance Service database. Results: The median follow-up duration was 6.4 years. There was a significant association between the severity of anemia and TB incidence, with an adjusted hazard ratio (aHR) of 1.28 [95% confidence interval (CI), 1.20–1.36] for mild anemia and 1.69 (95% CI, 1.51–1.88) for moderate to severe anemia. Compared with those who had normal TUG times, participants with slow TUG times (⩾15 s) had a significantly increased risk of TB (aHR 1.19, 95% CI, 1.07–1.33). On the other hand, both irregular (aHR 0.88, 95% CI 0.83–0.93) and regular (aHR 0.84, 95% CI, 0.78–0.92) physical activity reduced the risk of TB. Male sex, lower income, alcohol consumption, smoking, diabetes, and asthma/chronic obstructive pulmonary disease increased the risk of TB. Conclusion: The risk of TB among older adults increased with worsening anemia, sarcopenia, and physical inactivity. Physicians should be aware of those modifiable predictors for TB among the older population.


Author(s):  
Yang Li ◽  
Zhengrong Yin ◽  
Jinshuo Fan ◽  
Siyu Zhang ◽  
Weibing Yang

Abstract An increasing number of studies have reported that exosomes released from various cells can serve as mediators of information exchange between different cells. With further exploration of exosome content, a more accurate molecular mechanism involved in the process of cell-to-cell communication has been revealed; specifically, microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) are shuttled by exosomes. In addition, exosomal miRNAs and lncRNAs may play vital roles in the pathogenesis of several respiratory diseases, such as chronic obstructive pulmonary disease (COPD), lung cancer, and asthma. Consequently, exosomal miRNAs and lncRNAs show promise as diagnostic biomarkers and therapeutic targets in several lung diseases. This review will summarize recent knowledge about the roles of exosomal miRNAs and lncRNAs in lung diseases, which has shed light on the discovery of novel diagnostic methods and treatments for these disorders. Because there is almost no published literature about exosomal lncRNAs in COPD, asthma, interstitial lung disease, or tuberculosis, we summarize the roles of exosomal lncRNAs only in lung cancer in the second section. This may inspire some new ideas for researchers who are interested in whether lncRNAs shuttled by exosomes may play roles in other lung diseases.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Claire A Rushton ◽  
Lucy Riley ◽  
Duwarakan K Satchithananda ◽  
Peter W Jones ◽  
Umesh T Kadam

Purpose: Heart failure (HF) carries poor prognosis which changes over time. Chronic obstructive pulmonary disease (COPD) is common in HF and increases risk of mortality but how COPD severity and change influences HF prognosis is unknown. We hypothesised that in the HF general population, comorbidity stratification by increasing severity and longitudinal change would be associated with increased mortality. Methods: We used a case-control study nested within the UK Clinical Practice Research Datalink database (12-year time-period to 2014), of newly diagnosed HF patients aged over 40 years. Using risk set sampling, four controls were matched to cases on calendar and follow-up time. Routinely collected clinical measures of severity and change for COPD were (i) forced expiration volume in 1 second (FEV 1 ) stages, defined by Global Initiatives for Chronic Obstructive Lung Disease (GOLD) guidelines and (ii) prescribed medications in two time-windows covering 1-year prior to the match date. Conditional logistic regression was used to estimate risk ratios (RR) for all-cause mortality adjusted for known confounders. Results: Of the 50,114 HF sample, 5,848 (11.7%) had COPD and of these 62% died during follow-up compared to 52% of patients without COPD. COPD comorbidity risk associated with mortality stratified by GOLD stages was as follows: stage 1; adjusted RR 1.73 (95% CI 1.50-1.99) to stage 4; 3.14 (2.65, 3.73). Estimates for COPD FEV 1 change compared to no COPD were: GOLD stage same or better; 2.15 (1.97, 2.34) and GOLD stage worse; 2.70 (2.30, 3.17). The mortality estimates for medications severity were: inhalers only 1.13 (1.07,1.19), oral steroids; 1.83 (1.69,1.97) and oxygen; 2.94 (2.47, 3.51). The estimates for medications change were: no new steroids or oxygen; 1.22, (1.16, 1.28), new steroids but not oxygen; 1.84, (1.67,1.28) and new on oxygen; 3.41, (2.71,4.29). Conclusions: COPD is an important and common comorbidity in HF. Our results show that worse COPD severity and recent change based on routinely collected clinical data was associated with increased mortality and provides key prognostic information for clinical assessment in practice.


2021 ◽  
Vol 15 (10) ◽  
pp. 3473-3475
Author(s):  
U. Sivakumar ◽  
Rinku Garg ◽  
Sunita Nighute

Introduction: PAD was asymptomatic in a large proportion of COPD patients and was associated with more severe lung disease than in COPD subjects without PAD. Materials and Methods: This was a Cross-sectional study conducted at Department of Physiology, Santosh Medical College diagnosed with COPD using Spirometry was recruited for the study with a Sample size of 130 patients. Results: The characteristics of the population for follow-up (n=130) are presented in table 1. The mean Mean±SD was 51.73±6.1 years. The prevalence of never smokers was 21.5%, former smokers were 51.5% and current smokers were 26.9%. In total, 41 out of 130 individuals (31.5%) had PAD based on an ABI of less than 0.6. A statistically significant association was found between COPD and newly diagnosed PAD during follow-up. The association between COPD and incident PAD was stronger (adjusted OR 1.91, 95% CI 1.14–3.21). Stratified analysis by smoking status revealed that the overall association between COPD and newly developed PAD was driven by the ever smoker group. Conclusion: Subjects with COPD have a higher risk of developing PAD. People with both COPD and PAD have a substantially increased risk of death. Consequently, early detection of PAD and preventive actions in people with COPD should receive more attention in clinical respiratory care. Keywords: Peripheral Arterial Disease, Chronic Obstructive Pulmonary Disease, Ankle-brachial index.


Thorax ◽  
2020 ◽  
Vol 75 (6) ◽  
pp. 506-509 ◽  
Author(s):  
Hye Yun Park ◽  
Danbee Kang ◽  
Sun Hye Shin ◽  
Kwang-Ha Yoo ◽  
Chin Kook Rhee ◽  
...  

There has been limited evidence for the association between chronic obstructive pulmonary disease (COPD) and the incidence of lung cancer among never smokers. We aimed to estimate the risk of lung cancer incidence in never smokers with COPD, and to compare it with the risk associated with smoking. This cohort study involved 338 548 subjects, 40 to 84 years of age with no history of lung cancer at baseline, enrolled in the National Health Insurance Service National Sample Cohort. During 2 355 005 person-years of follow-up (median follow-up 7.0 years), 1834 participants developed lung cancer. Compared with never smokers without COPD, the fully-adjusted hazard ratios (95% CI) for lung cancer in never smokers with COPD, ever smokers without COPD, and ever smokers with COPD were 2.67 (2.09 to 3.40), 1.97 (1.75 to 2.21), and 6.19 (5.04 to 7.61), respectively. In this large national cohort study, COPD was also a strong independent risk factor for lung cancer incidence in never smokers, implying that COPD patients are at high risk of lung cancer, irrespective of smoking status.


2019 ◽  
Vol 98 (5) ◽  
pp. 534-540 ◽  
Author(s):  
K. Takeuchi ◽  
K. Matsumoto ◽  
M. Furuta ◽  
S. Fukuyama ◽  
T. Takeshita ◽  
...  

Although they are known to share pathophysiological processes, the relationship between periodontitis and chronic obstructive pulmonary disease (COPD) is not fully understood. The aim of the present study was to test the hypothesis that periodontitis is associated with a greater risk of development of COPD, when smoking is taken into account. The analysis in a 5-y follow-up population-based cohort study was based on 900 community-dwelling Japanese adults (age: 68.8 ± 6.3 [mean ± SD], 46.0% male) without COPD aged 60 or older with at least 1 tooth. Participants were classified into 3 categories according to baseline periodontitis severity (no/mild, moderate, and severe). COPD was spirometrically determined by a fixed ratio of <0.7 for forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) and by FEV1/FVC below the lower limit of normal. Poisson regression was used to calculate the relative risk (RR) of developing COPD according to the severity of periodontitis. The population attributable fraction (PAF) was also calculated. During follow-up, 22 (2.4%) subjects developed COPD. Compared with no/mild periodontitis subjects, a significantly increased risk of COPD occurred among severe periodontitis subjects (RR = 3.55; 95% confidence interval [CI], 1.18 to 10.67), but no significant differences were observed between the no/mild and moderate categories (RR = 1.48; 95% CI, 0.56 to 3.90). After adjustment for potential confounders, including smoking intensity, the relationship between severe periodontitis and risk of COPD remained significant (RR = 3.51; 95% CI, 1.15 to 10.74). Likewise, there was a positive association of periodontitis severity with risk of COPD ( P for trend = 0.043). The PAF for COPD due to periodontitis was 22.6%. These data highlight the potential importance of periodontitis as a risk factor for COPD.


2010 ◽  
Vol 17 (6) ◽  
pp. 287-294 ◽  
Author(s):  
Shannon L Walker ◽  
David L Saltman ◽  
Rosemary Colucci ◽  
Lesli Martin

OBJECTIVE: To assess awareness among persons at risk for lung cancer, chronic obstructive pulmonary disease (COPD) and sleep apnea regarding symptoms and risk factors of the disease, and their attitudes regarding the disease and toward those who are affected.METHODS: A quantitative hybrid telephone and Internet survey of a representative population of Canadian adults at risk for at least one of the three diseases was conducted. To measure the awareness and attitudes of First Nations, Inuit and Métis people to these diseases, a proportionate number were also surveyed.RESULTS: A total of 3626 individuals were contacted. Of these, 3036 (84%) were eligible to participate. Of those at risk for lung cancer and COPD, 65% and 69%, respectively, were due to tobacco smoke exposure. Among those at risk, 72% believed that they were informed about lung cancer compared with 36% for COPD and 56% for sleep apnea. Most respondents were knowledgeable about the common symptoms of lung cancer, COPD and sleep apnea, but were less aware of the impact lifestyle choices could have on the development of these disorders and the availability of treatment. Most of the participants (77%) believed that smoking was an addiction rather than a habit (19%). There were no significant differences in the awareness of risk factors, symptoms and attitudes toward all three lung diseases between First Nations, Inuit and Métis people and the general population.CONCLUSIONS: Canadians are reasonably aware of risk factors and symptoms for lung cancer and sleep apnea. However, there is poor awareness of COPD as a disease entity. There is a lack of appreciation for the impact lifestyle choices and changes can have on lung diseases.


2015 ◽  
Vol 45 (3) ◽  
pp. 807-827 ◽  
Author(s):  
Silke Meiners ◽  
Oliver Eickelberg ◽  
Melanie Königshoff

Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, “dysregulation of the extracellular matrix”, which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases.


2015 ◽  
Vol 24 (137) ◽  
pp. 428-435 ◽  
Author(s):  
George A. Margaritopoulos ◽  
Eirini Vasarmidi ◽  
Joseph Jacob ◽  
Athol U. Wells ◽  
Katerina M. Antoniou

For many years has been well known that smoking could cause lung damage. Chronic obstructive pulmonary disease and lung cancer have been the two most common smoking-related lung diseases. In the recent years, attention has also focused on the role of smoking in the development of interstitial lung diseases (ILDs). Indeed, there are three diseases, namely respiratory bronchiolitis-associated ILD, desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis, that are currently considered aetiologically linked to smoking and a few others which are more likely to develop in smokers. Here, we aim to focus on the most recent findings regarding the role of smoking in the pathogenesis and clinical behaviour of ILDs.


2015 ◽  
Vol 26 (6) ◽  
pp. 1160-1173 ◽  
Author(s):  
Zhigang Jin ◽  
Jin Wei Chung ◽  
Wenyan Mei ◽  
Stefan Strack ◽  
Chunyan He ◽  
...  

Recent genome-wide association studies reveal that the FAM13A gene is associated with human lung function and a variety of lung diseases, including chronic obstructive pulmonary disease, asthma, lung cancer, and pulmonary fibrosis. The biological functions of Fam13a, however, have not been studied. In an effort to identify novel substrates of B56-containing PP2As, we found that B56-containing PP2As and Akt act antagonistically to control reversible phosphorylation of Fam13a on Ser-322. We show that Ser-322 phosphorylation acts as a molecular switch to control the subcellular distribution of Fam13a. Fam13a shuttles between the nucleus and cytoplasm. When Ser-322 is phosphorylated by Akt, the binding between Fam13a and 14-3-3 is enhanced, leading to cytoplasmic sequestration of Fam13a. B56-containing PP2As dephosphorylate phospho–Ser-322 and promote nuclear localization of Fam13a. We generated Fam13a-knockout mice. Fam13a-mutant mice are viable and healthy, indicating that Fam13a is dispensable for embryonic development and physiological functions in adult animals. Intriguingly, Fam13a has the ability to activate the Wnt pathway. Although Wnt signaling remains largely normal in Fam13a-knockout lungs, depletion of Fam13a in human lung cancer cells causes an obvious reduction in Wnt signaling activity. Our work provides important clues to elucidating the mechanism by which Fam13a may contribute to human lung diseases.


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