Global Asbestos Disaster Furuya, Sugio; Chimed-Ochir, Odgerel; Takahashi, Ken ...
International journal of environmental research and public health,
05/2018, Volume:
15, Issue:
5
Journal Article
Peer reviewed
Open access
: Asbestos has been used for thousands of years but only at a large industrial scale for about 100⁻150 years. The first identified disease was asbestosis, a type of incurable pneumoconiosis caused by ...asbestos dust and fibres. The latest estimate of global number of asbestosis deaths from the Global Burden of Disease estimate 2016 is 3495. Asbestos-caused cancer was identified in the late 1930's but despite today's overwhelming evidence of the strong carcinogenicity of all asbestos types, including chrysotile, it is still widely used globally. Various estimates have been made over time including those of World Health Organization and International Labour Organization: 107,000⁻112,000 deaths. Present estimates are much higher.
: This article summarizes the special edition of this Journal related to asbestos and key aspects of the past and present of the asbestos problem globally. The objective is to collect and provide the latest evidence of the magnitude of asbestos-related diseases and to provide the present best data for revitalizing the International Labor Organization/World Health Organization Joint Program on Asbestos-related Diseases.
: Documentation on asbestos-related diseases, their recognition, reporting, compensation and prevention efforts were examined, in particular from the regulatory and prevention point of view. Estimated global numbers of incidence and mortality of asbestos-related diseases were examined.
: Asbestos causes an estimated 255,000 deaths (243,223⁻260,029) annually according to latest knowledge, of which work-related exposures are responsible for 233,000 deaths (222,322⁻242,802). In the European Union, United States of America and in other high income economies (World Health Organization regional classification) the direct costs for sickness, early retirement and death, including production losses, have been estimated to be very high; in the Western European countries and European Union, and equivalent of 0.70% of the Gross Domestic Product or 114 × 10⁸ United States Dollars. Intangible costs could be much higher. When applying the Value of Statistical Life of 4 million EUR per cancer death used by the European Commission, we arrived at 410 × 10⁸ United States Dollars loss related to occupational cancer and 340 × 10⁸ related to asbestos exposure at work, while the human suffering and loss of life is impossible to quantify. The numbers and costs are increasing practically in every country and region in the world. Asbestos has been banned in 55 countries but is used widely today; some 2,030,000 tons consumed annually according to the latest available consumption data. Every 20 tons of asbestos produced and consumed kills a person somewhere in the world. Buying 1 kg of asbestos powder, e.g., in Asia, costs 0.38 United States Dollars, and 20 tons would cost in such retail market 7600 United States Dollars.
: Present efforts to eliminate this man-made problem, in fact an epidemiological disaster, and preventing exposures leading to it are insufficient in most countries in the world. Applying programs and policies, such as those for the elimination of all kind of asbestos use-that is banning of new asbestos use and tight control and management of existing structures containing asbestos-need revision and resources. The International Labor Organization/World Health Organization Joint Program for the Elimination of Asbestos-Related Diseases needs to be revitalized. Exposure limits do not protect properly against cancer but for asbestos removal and equivalent exposure elimination work, we propose a limit value of 1000 fibres/m³.
Asbestos causes asbestosis and malignancies by molecular mechanisms that are not fully understood. The modes of action underlying asbestosis, lung cancer, and mesothelioma appear to differ depending ...on the fiber type, lung clearance, and genetics. After reviewing the key pathologic changes following asbestos exposure, we examine recently identified pathogenic pathways, with a focus on oxidative stress. Alveolar epithelial cell apoptosis, which is an important early event in asbestosis, is mediated by mitochondria- and p53-regulated death pathways and may be modulated by the endoplasmic reticulum. We review mitochondrial DNA (mtDNA)-damage and -repair mechanisms, focusing on 8-oxoguanine DNA glycosylase, as well as cross talk between reactive oxygen species production, mtDNA damage, p53, OGG1, and mitochondrial aconitase. These new insights into the molecular basis of asbestos-induced lung diseases may foster the development of novel therapeutic targets for managing degenerative diseases (e.g., asbestosis and idiopathic pulmonary fibrosis), tumors, and aging, for which effective management is lacking.
Alveolar epithelial cell (AEC) apoptosis, arising from mitochondrial dysfunction and mitophagy defects, is important in mediating idiopathic pulmonary fibrosis (IPF). Our group established a role for ...the mitochondrial (mt) DNA base excision repair enzyme, 8-oxoguanine-DNA glycosylase 1 (mtOGG1), in preventing oxidant-induced AEC mtDNA damage and apoptosis and showed that OGG1-deficient mice have increased lung fibrosis. Herein, we determined whether mice overexpressing the mtOGG1 transgene (
) are protected against lung fibrosis and whether AEC mtOGG1 preservation of mtDNA integrity mitigates phosphatase and tensin homolog-induced putative kinase 1 (PINK1) deficiency and apoptosis. Compared with wild type (WT),
mice have diminished asbestos- and bleomycin-induced pulmonary fibrosis that was accompanied by reduced lung and AEC mtDNA damage and apoptosis. Asbestos and H
O
promote the MLE-12 cell PINK1 deficiency, as assessed by reductions in the expression of PINK1 mRNA and mitochondrial protein expression. Compared with WT,
-knockout (
) mice are more susceptible to asbestos-induced lung fibrosis and have increased lung and alveolar type II (AT2) cell mtDNA damage and apoptosis. AT2 cells from
mice and PINK1-silenced (siRNA) MLE-12 cells have increased mtDNA damage that is augmented by oxidative stress. Interestingly, mtOGG1 overexpression attenuates oxidant-induced MLE-12 cell mtDNA damage and apoptosis despite PINK1 silencing. mtDNA damage is increased in the lungs of patients with IPF as compared with controls. Collectively, these findings suggest that mtOGG1 maintenance of AEC mtDNA is crucial for preventing PINK1 deficiency that promotes apoptosis and lung fibrosis. Given the key role of AEC apoptosis in pulmonary fibrosis, strategies aimed at preserving AT2 cell mtDNA integrity may be an innovative target.
Although the use of asbestos has been banned in several industrialized countries, many workers continue to be exposed in asbestos repair and removal work, and asbestos is still widely used in various ...newly industrialized, rapidly developing countries. According to the most recent World Health Organization estimates, more than 107,000 people die each year from asbestos-related lung cancer, mesothelioma, and asbestosis resulting from exposure at work. The asbestos epidemic is far from over. The expert meeting on "asbestos, asbestosis, and cancer" was convened in Helsinki in 1997 and consisted of 19 participants from eight countries. This meeting had the goal to "discuss disorders in association with asbestos and agree upon state of the art criteria for diagnosis and attribution with respect to asbestos". This report summarizes the results of a project, organized by the Finnish Institute of Occupational Health (FIOH), to update the 1997 and 2000 Helsinki criteria documents in view of the new advances in research.
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BFBNIB, NMLJ, NUK, ODKLJ, PNG, UL, UM, UPUK
Asbestos-related diseases are still a major public health problem. The World Health Organization (WHO) has estimated that 107,000 people worldwide die each year from mesothelioma, lung cancer, and ...asbestosis. We review what is known about asbestos use, production, and exposure and asbestos-related diseases in the world today, and we offer predictions for the future. Although worldwide consumption of asbestos has decreased, consumption is increasing in many developing countries. The limited data available suggest that exposures may also be high in developing countries. Mesothelioma is still increasing in most European countries and in Japan but has peaked in the United States and Sweden. Although the epidemic of asbestos-related disease has plateaued or is expected to plateau in most of the developed world, little is known about the epidemic in developing countries. It is obvious that increased asbestos use by these countries will result in an increase in asbestos-related diseases in the future.
Background
Silicosis is a fibrotic lung disease caused by exposure to respirable crystalline silica. Historically, silicosis was common among miners and other professions in the 20th century, and in ...recent decades has re‐emerged in coal mining and appeared in new workplaces, including the manufacture of distressed jeans and artificial stone countertops.
Methods
Physician billing data for the province of Ontario between 1992 and 2019 were analyzed across six time‐periods (1993−1995, 1996−2000, 2001−2005, 2006−2010, 2011−2015, and 2016−2019). The case definition was two or more billing records within 24 months with a silicosis diagnosis code (ICD‐9 502, ICD‐10 J62). Cases from 1993 to 1995 were excluded as prevalent cases. Crude incidence rates per 100,000 persons were calculated by time‐period, age, sex, and region. Analyses were repeated in parallel for pulmonary fibrosis (PF) (ICD‐9 515, ICD‐10 J84) and asbestosis (ICD‐9 501; ICD‐10 J61).
Results
From 1996 to 2019, 444 cases of silicosis, 2719 cases of asbestosis and 59,228 cases of PF were identified. Silicosis rates decreased from 0.42 cases per 100,000 in 1996−2000 to 0.06 per 100,000 people in 2016−2019. A similar trend was observed for asbestosis (1.66 to 0.51 per 100,000 persons) but the incidence rate of PF increased from 11.6 to 33.9 per 100,000 persons. Incidence rates for all outcomes were higher among men and older adults.
Conclusions
A decreasing incidence of silicosis was observed in this analysis. However, the incidence of PF increased, consistent with findings from other jurisdictions. While cases of silicosis have been recorded among artificial stone workers in Ontario these cases do not seem to have impacted the population rates thus far. Ongoing, periodic surveillance of occupational diseases is helpful for tracking population‐level trends over time.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Uncertainty exists regarding the clinical relevance of exercise training across the range of interstitial lung diseases (ILDs).
To establish the impact of exercise training in patients with ILDs of ...differing aetiology and severity.
142 participants with ILD (61 idiopathic pulmonary fibrosis (IPF), 22 asbestosis, 23 connective tissue disease-related ILD (CTD-ILD) and 36 with other aetiologies) were randomised to either 8 weeks of supervised exercise training or usual care. Six-minute walk distance (6MWD), Chronic Respiratory Disease Questionnaire (CRDQ), St George Respiratory Questionnaire IPF-specific version (SGRQ-I) and modified Medical Research Council dyspnoea score were measured at baseline, 9 weeks and 6 months.
Exercise training significantly increased 6MWD (25 m, 95% CI 2 to 47 m) and health-related quality of life (CRDQ and SGRQ-I) in people with ILD. Larger improvements in 6MWD, CRDQ, SGRQ-I and dyspnoea occurred in asbestosis and IPF compared with CTD-ILD, but with few significant differences between subgroups. Benefits declined at 6 months except in CTD-ILD. Lower baseline 6MWD and worse baseline symptoms were associated with greater benefit in 6MWD and symptoms following training. Greater gains were seen in those whose exercise prescription was successfully progressed according to the protocol. At 6 months, sustained improvements in 6MWD and symptoms were associated with better baseline lung function and less pulmonary hypertension.
Exercise training is effective in patients across the range of ILDs, with clinically meaningful benefits in asbestosis and IPF. Successful exercise progression maximises improvements and sustained treatment effects favour those with milder disease.
Results, ACTRN12611000416998.
Carbon nanotubes have distinctive characteristics, but their needle-like fibre shape has been compared to asbestos, raising concerns that widespread use of carbon nanotubes may lead to mesothelioma, ...cancer of the lining of the lungs caused by exposure to asbestos. Here we show that exposing the mesothelial lining of the body cavity of mice, as a surrogate for the mesothelial lining of the chest cavity, to long multiwalled carbon nanotubes results in asbestos-like, length-dependent, pathogenic behaviour. This includes inflammation and the formation of lesions known as granulomas. This is of considerable importance, because research and business communities continue to invest heavily in carbon nanotubes for a wide range of products under the assumption that they are no more hazardous than graphite. Our results suggest the need for further research and great caution before introducing such products into the market if long-term harm is to be avoided.
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IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
10.
Health risk of chrysotile revisited Bernstein, David; Dunnigan, Jacques; Hesterberg, Thomas ...
Critical reviews in toxicology,
02/2013, Volume:
43, Issue:
2
Journal Article
Peer reviewed
Open access
Abstract
This review provides a basis for substantiating both kinetically and pathologically the differences between chrysotile and amphibole asbestos. Chrysotile, which is rapidly attacked by the ...acid environment of the macrophage, falls apart in the lung into short fibers and particles, while the amphibole asbestos persist creating a response to the fibrous structure of this mineral. Inhalation toxicity studies of chrysotile at non-lung overload conditions demonstrate that the long (>20 µm) fibers are rapidly cleared from the lung, are not translocated to the pleural cavity and do not initiate fibrogenic response. In contrast, long amphibole asbestos fibers persist, are quickly (within 7 d) translocated to the pleural cavity and result in interstitial fibrosis and pleural inflammation. Quantitative reviews of epidemiological studies of mineral fibers have determined the potency of chrysotile and amphibole asbestos for causing lung cancer and mesothelioma in relation to fiber type and have also differentiated between these two minerals. These studies have been reviewed in light of the frequent use of amphibole asbestos. As with other respirable particulates, there is evidence that heavy and prolonged exposure to chrysotile can produce lung cancer. The importance of the present and other similar reviews is that the studies they report show that low exposures to chrysotile do not present a detectable risk to health. Since total dose over time decides the likelihood of disease occurrence and progression, they also suggest that the risk of an adverse outcome may be low with even high exposures experienced over a short duration.
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DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
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