Danger Dust Disease




Crystalline Silica Dust                      
            
Can Kill You In More Ways Than You Know

                            Are You Aware?   
                                             

Silica exposure can cause autoimmune diseases such as lupus, scleroderma, and vasculitis. 
It can also cause silicosis, kidney disease, lung cancer, tuberculosis, and other airways diseases. 
Environmental exposure to silica can occur in workers and bystanders in many industries,
including agriculture construction, and potters. 

Sclero.org


What is Crystalline Silica Dust ?               

Image result for crystalline silica dust
Silica is a natural substance found in most rocks, sand and clay and in products such as bricks and concrete. In the workplace these materials create dust when they are cut, sanded down etc. Some of this dust may be fine enough to reach deep inside the lung, this is known as respirable crystalline silica (RCS) and can cause harm to health.


Silica is synonymous with silicon dioxide (SiO2). Silicon and oxygen are the two most abundant elements in the earth’s crust. Silica is commonly found in nature as sand. Silica exists in many different forms that can be crystalline as well as non-crystalline (amorphous).

Crystalline silica is hard, chemically inert and has a high melting point. These are valued/important properties in various industrial uses.
Quartz is the most common form of crystalline silica and is the second most common mineral on the earth’s surface. It is found in almost every type of rock i.e. igneous, metamorphic and sedimentary. Since it is so abundant, quartz is present in nearly all mining operations
.
Cristobalite is scarce in nature. Some volcanic rocks and meteorites may contain small amounts of it. Cristobalite may also form when quartz is heated at high temperatures starting at 450°C. This is especially true during production and use of refractory materials and/or during calcination of silica (between 800 and 1110°C). As a result, there is a likelihood of exposure to cristobalite in occupational settings
.
Tridymite is also a scarce mineral that is only found in nature in volcanic rocks and meteorites. Tridymite, however, differs from cristobalite in that it is not stable during quartz and refractory materials heating processes at conventional process temperatures. As a result, exposures are very unlikely to occur in occupational or other settings.

Types Of Dust

Fibrogenic dust, such as free crystalline silica (FCS) or asbestos, is biologically toxic and, if retained in the lungs, 
can form scar tissue and impair the lungs' ability to function properly.

Nuisance dust, or inert dust, can be defined as dust that contains less than 1% quartz. Because of its low content of silicates, 
nuisance dust has a long history of having little adverse effect on the lungs. Any reaction that may occur from nuisance dust is potentially reversible. 
However, excessive concentrations of nuisance dust in the workplace may reduce visibility (e.g., iron oxide), may cause unpleasant deposits in eyes, cars, 
and nasal passages (e.g., portland cement dust), and may cause injury to the skin or mucous membranes by chemical or mechanical action.

From an occupational health point of view, dust is classified by size into three primary categories:
Respirable Dust
Inhalable Dust
Total Dust
Respirable Dust

Respirable dust refers to those dust particles that are small enough to penetrate the nose and upper respiratory system and deep into the lungs.
Particles that penetrate deep into the respiratory system are generally beyond the body's natural clearance mechanisms of cilia and mucous and are 
more likely to be retained.


 Silica Dust Can Trigger Autoimmune Diseases
What is an Autoimmune Disease?

An autoimmune disease develops when your immune system, which defends your body against disease, decides your healthy cells are foreign. As a result, your immune system attacks healthy cells. Depending on the type, an autoimmune disease can affect one or many different types of body tissue. It can also cause abnormal organ growth and changes in organ function.

There are as many as 80 types of autoimmune diseases. Many of them have similar symptoms, which makes them very difficult to diagnose. It’s also possible to have more than one at the same time. Autoimmune diseases usually fluctuate between periods of remission (little or no symptoms) and flare-ups (worsening symptoms). Currently, treatment for autoimmune diseases focuses on relieving symptoms because there is no curative therapy.

Autoimmune Disease
Autoimmune disease is not an exaggerated response to foreign matter. This syndrome occurs when foreign chemicals modify tissues or immune cells, affecting the regulation of immune response such as the production of antibodies and inflammatory response. The result is an immune response against our own tissues, tissue damage and disease. The mechanisms which allow this to occur in the body are complex, but there are genetic and environmental factors which affect an individuals susceptibility to autoimmune disease. Exposure to sulfa, penicillin, vinyl chloride, gold salts, silica, mercury, methyl dopa, and other compounds can induce this response by the immune system. Systemic lupus and rheumatoid arthritis are two autoimmune diseases. It should be noted that viral, hormonal, and emotional factors can also contribute to the development of autoimmune disease.

http://extoxnet.orst.edu/faqs/senspop/immune.htm



How Does Silica Trigger Autoimmune Disease ? 
                           Silica can trigger autoimmune diseases via production of autoantibodies 




We describe a case of pulmonary silicosis complicated by microscopic polyangiitis.
   We report a case of pulmonary silicosis with P-ANCA associated microscopic polyangiitis. 
   Our case is unique in that both diagnoses are definitively proven histologically. 

   Exposure to silica should be considered in the history of patients with autoimmune diseases. 
   Furthermore patients with pulmonary silicosis may develop ANCA-associated vasculitis 
   in extrapulmonary sites.  
                                                  
                                                                                                               http://journal.publications.chestnet.org/article.aspx?articleid=1213693


Silica Exposure and Systemic Vasculitis

Work in Department of Energy (DOE) facilities has exposed workers to multiple toxic agents leading to acute and chronic diseases. Many exposures were common to numerous work sites. Exposure to crystalline silica was primarily restricted to a few facilities. I present the case of a 63-year-old male who worked in DOE facilities for 30 years as a weapons testing technician. In addition to silica, other workplace exposures included beryllium, various solvents and heavy metals, depleted uranium, and ionizing radiation. In 1989 a painful macular skin lesion was biopsied and diagnosed as leukocytoclastic vasculitis. By 1992 he developed gross hematuria and dyspnea. Blood laboratory results revealed a serum creatinine concentration of 2.1 mg/dL, ethrythrocyte sedimentation rate of 61 mm/hr, negative cANCA (antineutrophil cytoplasmic antibody cytoplasmic pattern), positive pANCA (ANCA perinuclear pattern), and antiglomerular basement membrane negative. Renal biopsy showed proliferative (crescentric) and necrotizing glomerulonephritis. The patient's diagnoses included microscopic polyangiitis, systemic necrotizing vasculitis, leukocytoclastic vasculitis, and glomerulonephritis. Environmental triggers are thought to play a role in the development of an idiopathic expression of systemic autoimmune disease. Crystalline silica exposure has been linked to rheumatoid arthritis, scleroderma, systemic lupus erythematosus, rapidly progressive glomerulonephritis and some of the small vessel vasculitides. DOE workers are currently able to apply for compensation under the federal Energy Employees Occupational Illness Compensation Program (EEOICP). However, the only diseases covered by EEOICP are cancers related to radiation exposure, chronic beryllium disease, and chronic silicosis.

Discover the world's research
https://www.researchgate.net/publication/8583405_Silica_Exposure_and_Systemic_Vasculitis


Occupational and environmental exposures and risk of systemic lupus erythematosus: silica, sunlight, solvents


Graphic

Conclusions. This study supports the role of specific occupational and non-occupational exposures in the development of SLE.
http://rheumatology.oxfordjournals.org/content/early/2010/07/30/rheumatology.keq214.full








Chemical Reaction

The environmental exposure that has one of the best-studied 
connections with lupus is silica, a mineral that people can be 
exposed to in mining and glass production. 
“Silica is one of the strongest known risk factors for the development of lupus,” says Frederick W. Miller, M.D., Ph.D., 
chief of the Environmental Autoimmunity Group at the 
NIH’s National Institute of Environmental Health Sciences (NIEHS). 
The problem seems to lie in the fine dust from rock or sand, 
or in products such as pottery, ceramics, or tile dust, 
according to Christine G. Parks, M.S.P.H., Ph.D., 
a research fellow in the Epidemiology Branch of the NIEHS.

The increased lupus risk is between two- and fivefold in those 
who have been exposed to silica at work, says Miller, 
who collaborated with Gourley on a review of environmental factors in lupus. Most of the risk noted in studies has been from occupational, 
not occasional, exposures—miners and farmers who were 
regularly exposed to silica dust on the job.



Pulmonary silicosis and systemic lupus erythematosus in men: a report of two cases.

Abstract

We report two cases of coexistence of pulmonary silicosis and systemic lupus erythematosus (SLE). The patients are two men with SLE exposed to silica for 20 years. The hypothesis that silica exposure is linked to a wide variety of known or suspected autoimmune diseases, including SLE, has been discussed in the last decade but few cases of pulmonary silicosis and SLE were reported. Our purpose was to bring attention to the increasing evidence that silica may also cause or stimulate SLE, and to suggest that the researchers look for occupational exposure, mainly in male SLE patients.
PMID:
 
11858360
[PubMed - indexed for MEDLINE]         https://www.ncbi.nlm.nih.gov/pubmed/11858360 

Silica exposure and altered regulation of autoimmunity

Patients with pneumoconiosis suffer not only with respiratory complications such as chronic bronchitis, emphysema and lung fibrosis, but also from autoimmune disorders in the case of silicosis patients and malignant tumors such as pleural mesothelioma and lung cancer in the case of asbestosis patients. The typical autoimmune disorders complicated with silicosis include rheumatoid arthritis (well known as Caplan syndrome) [56], systemic lupus erythematosus (SLE) [78], systemic sclerosis (SSc) [910], and anti-neutrophil cytoplasmic antibody (ANCA)-related vasculitis [1114].

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4166593/

Image result for tungsten carbide blades and hard metal disease


Hard Metal Disease

A Tungsten Carbide and Cobalt Pulmonary Disease
Workers who are exposed to the powdered forms of tungsten carbide and cobalt (<10mm) are more susceptible to the disease because of the dust and aerosol particles in the air (2, 5). Occupational exposure to potentially dangerous substances is often of great concern to government organizations and university-based hospitals. The Center for Disease Control released an article in 1992 about a 35-year-old industrial plant worker who had been exposed to aerosolized tungsten carbide and cobalt powder
http://faculty.virginia.edu/metals/cases/moyer1.html

Hard metal disease: eight workers with interstitial lung fibrosis due to cobalt exposure.

Eight hard metal workers exposed to cobalt containing dust (four producers of stone-cutting cobalt-diamond wheels and four grinders of hard metal tools) and affected by interstitial lung fibrosis have been examined. A close relationship between cobalt exposure and clinical findings was observed in six patients who were still working. The clinical picture ranged from minor symptoms to manifestations resembling those of hypersensitivity pneumonitis, with fever, weight-loss, non-productive cough and dyspnea. A restrictive impairment of the ventilatory function was prevalent. The chest roentgenogram of one patient showed a diffuse reticular nodular pattern, while the others presented a mild reticular accentuation of the interstitium. In five patients, bioptic specimens of the lung parenchyma showed interstitial collagenic fibrosis with inflammatory cells infiltrating the alveolar septa. An increased number of lymphocytes and polymorphs was reported in the bronchoalveolar lavage (BAL) fluid from seven patients. Giant multinucleated cells were present in the BAL of four subjects while an inversion of the helper-suppressor ratio was evident in those patients who were still exposed to cobalt when BAL was performed. In this study, the causal role of metallic cobalt inhalation in the etiology of the lung disease is examined and discussed.      
https://www.ncbi.nlm.nih.gov/pubmed/7939595


Carbide tips create health problems

Workers who file saw blades or those who machine tools with tungsten carbide (or other "hard metal") tips may be exposed to toxic levels of cadmium, a cancer-causing agent, and cobalt, a suspected cancer-causing agent. Grinding and filing hard metals may produce high levels of exposure to cobalt, and brazing operations may create high exposures to cadmium. Even though employers use local ventilation and wet grinding methods, overexposure still may occur. According to medical studies, toxic effects of exposure may include kidney disease, asthma, anemia, emphysema, and hard metal lung disease with reduced lung function.
http://www.lni.wa.gov/safety/hazardalerts/951a.asp

Image result for silica dust  banners

           Raynaud's Phenomenon

People can also get Raynaud's phenomenon because of certain underlying diseases (e.g. scleroderma, rheumatoid arthritis or lupus) or injuries.                  This form is known as "secondary Raynaud's phenomenon."
Within the workplace, several hazards can cause secondary Raynaud's phenomenon. Exposure to vibration from power tools is by far the greatest concern. Hand-held power tools such as chain saws, jackhammers and pneumatic rock drillers and chippers can cause "hand-arm vibration syndrome." This disorder is also known as "vibration-induced white finger", "hand-arm vibration syndrome (HAVS)", or "Raynaud's phenomenon of occupational origin." Raynaud's phenomenon, however, is only one aspect of the hand-arm vibration syndrome. Vibration also damages nerves, muscles, bones and joints of the hand and arm.
In early years, before the cancer-causing effects of vinyl chloride were known, workers exposed to high levels of this chemical experienced Raynaud's phenomenon. It also caused breakdown of the bones of the fingertips, and other health problems. Raynaud's phenomenon from vinyl chloride is now an unlikely occurrence in Canada since exposure to this chemical is controlled much better than in the past.
Raynaud's phenomenon is also seen in typists and professional pianists from repeated finger stress, as well as in dentists and dental technicians. Frostbite injury with damage to the blood vessels can also cause Raynaud's phenomenon. A single study reports that fish plant workers developed Raynaud's phenomenon after continually chilling and rewarming their hands several times a day over a period of years.
A few studies have suggested that gripping a hand tool too tightly could cause Raynaud's phenomenon. Other isolated studies have identified Raynaud's phenomenon in workers who injured their hands by using them for hammering, or pushing or twisting heavy objects. In these cases, Raynaud's phenomenon was part of a disorder called hypothenar hammer syndrome.
https://www.ccohs.ca/oshanswers/diseases/raynaud.html


Image result for sarcoidosis banner


                          Sarcoidosis

    Taken as a whole, this body of literature on World Trade Center sarcoidosis helps validate the many case series and case reports of the past few decades reporting sarcoidosis occurring after exposure to silica, talc and other inorganic triggers. Along these same lines, a recent case report used x-ray microanalysis to demonstrate that the granulomas in the lungs of a dental surgeon with sarcoidosis contained the same inorganic dust as is used in dental cleaning procedures [13]. In another case report, a young male developed sarcoidosis after exposure to concrete slurry that is used in tunnel excavation [14].

 In 2011, Song and Tang reported follow up exposure, pathology, and clinical data on seven female workers who had been exposed to polyacrylate nanoparticles for 5 to 13 months and were hospitalized with shortness of breath and pleural effusions. Two of these women subsequently died with progressive respiratory failure. Pathology findings included culture-negative foreign-body granulomas along the pleura, as well as progressive pulmonary fibrosis, inflammation, and foreign-body granulomas in the pleura. Nanoparticles found in the patients’ tissue and effusions were the same raw materials that they were exposed to in the plant, particularly silica nanoparticles and nano- and microscale silicates [18]


 


                                                              Occupational Causes of Sarcoidosis

Table 1

Examples of known occupational causes of sarcoidosis and sarcoidosis-like illness
DiseaseExamples or industry or
occupation
Known or suspected agentEvidence
Hypersensitivity pneumonitisAgriculture, metalworking, lifeguards, bird handlers, othersFungal antigens, bacterial antigens, including mycobacterial antigensEpidemiologic, clinical, immunologic, microbiologic, animal models
Chronic beryllium diseaseDefense industries, electronics, alloy manufactureBerylliumEpidemiologic, clinical, immunologic
Granulomatous lung diseaseMining, manufacturing, agriculture, transportationAluminum, barium, cobalt, copper, gold, rare earth metals, titanium, zirconiumEpidemiologic, clinical, immunologic
Nanoparticle-related granulomas, pleural and pulmonary fibrosisManufacturingsilica nanoparticles, carbon nanoparticlesClinical, immunologic, animal models
SilicosisMining, constructionSilicates, talcEpidemiologic, clinical, immunologic
PsittacosisBird handlingBird protein antigens, bacterial antigensEpidemiologic, clinical, microbiologic
Sarcoidosis-like illnessWorld Trade Center emergency response and clean upWorld Trade Center dust (inorganic dust)Epidemiologic
Clinical
SarcoidosisAgricultureMold, bacteria, silicatesEpidemiologic
Wood burningSilicatesEpidemiologic
MiningSilicatesEpidemiologic
TransportationMetal dust, inorganic particulateEpidemiologic
Metal industriesMetal dust, metalworking fluid aerosolsEpidemiologic
Firefighting, emergency responseInorganic dust, fumesEpidemiologic
ConstructionInorganic dustEpidemiologic
Office work (indoor air)Mold, bacteria, other microbial contaminantsEpidemiologic
Immunologic

Key Points

  • Workplace exposures are associated with the development of sarcoidosis
  • Mycobacterial, fungal, and other microbial antigens are targets for the granulomatous immune response
  • Exposures to inorganic particulate matter can promote an inflammatory response leading to granuloma formation
  • Occupational and environmental exposure histories should be carefully considered in patients with sarcoidosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196683/

Association between exposure to crystalline silica and risk of sarcoidosis

In the following case-referent study, a cohort exposed to diatomaceous earth and cristobalite provided an opportunity to evaluate such an exposure with reference to sarcoidosis. 
CONCLUSION: The odds ratios were high (95% confidence interval) and there were some indications of a dose-response relation which will hopefully encourage further studies. To our knowledge this is the first study to indicate a relation between sarcoidosis and exposure to the crystalline silica, cristobalite.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1757515/

Full Text

The Full Text of this article is available as a PDF (92K).




This outbreak of end-stage silicosis leading to lung transplantation 
caused by dust generated through dry cutting of engineered decorative stone 
with very high silica content
Dr Luba Pushnoy
Safety and Health Administration
Bilboa ,January 28, 2015
Comorbidity of artificial stone silicosis and autoimmune rheumatologic diseases

The new silicosis outbreak carries within an outbreak of autoimmune diseases.

It is associated with multiple distinct rheumatologic entities.
Silica associated autoimmune disease does not differ in clinical presentation from non-silica associated disease.

Autoimmune rheumatologic diseases in patients with silicosis referred to lung transplantation center
9 cases of autoimmune rheumatologic disease were observed among a cohort of 42 patients with silicosis 
referred to lung transplantation center over a 10-year period.
1.Four cases with Systemic Sclerosis
2.Two cases with mixed connective tissue disease
3.One case with Rheumatoid Arthritis
4.One case with Sjogren’s syndrome
5.One case of anti JO-1 dermatomyositis

                 Recommendations
Patients with autoimmune rheumatological disease:
a full occupational history addressing potential silica exposure is needed.



Multiple clinical and biological autoimmune manifestations in 50 workers 

after occupational exposure to silica.

Abstract

OBJECTIVES:

A self referred group of four workers from a factory producing scouring powder with a high silica content showed a surprisingly high number of features compatible with a connective tissue disease. Further subjects working at the same factory were subsequently studied to evaluate the relation between this exposure and the development of autoimmune processes.

METHODS:

A total of 50 subjects (44 women, six men; mean (SD) age 43.7 (5.5) years; mean duration of employment 6.1 years) underwent a prospective study including clinical history and physical examination, an immunobiological study, HLA typing, radiological and functional oesophageal and respiratory examination, ophthalmological examination, and isotopic testing of salivary glands.

RESULTS:

Symptoms of a systemic illness were present in 32 (64%) subjects: six with Sjögren's syndrome; five with the criteria for systemic sclerosis; three with systemic lupus erythematosus (SLE); five with an 'overlap syndrome'; and 13 with undifferentiated findings not meeting the criteria for a defined disease. Antinuclear antibodies were present in 36 (72%) subjects; four had antibodies to native DNA, including two subjects with SLE, one with systemic sclerosis associated with secondary Sjögren's syndrome, and one with overlap syndrome. Anticentromere antibodies were not detected. The frequency of HLA-DR3 was increased in the clinically affected subjects, but did not reach statistical significance.

CONCLUSIONS:

This descriptive study emphasises the high probability of workers occupationally exposed to silica developing a multiple spectrum of clinical and serological autoimmune manifestations.

Comment in

PMID:
 
8394065
 
PMCID:
 
PMC1005094
[PubMed - indexed for MEDLINE] 
Free PMC Article

https://www.ncbi.nlm.nih.gov/pubmed/8394065


Bramwell B: Diffuse scleroderma: its frequency and occurrence in stonemasons; its treatment by fibrinolysisin: elevations of temperature due to fibrinolysin injectionsEdinburg Med J 1914, 12:387.Google Scholar


                                    Silica-induced scleroderma.

                                                 In a survey done in East Germany between 1981 and 1988, we found that 
                                            93 of 120 male scleroderma patients had long-term exposure to silica dust. 
We describe our findings in 12 patients with scleroderma and silicosis. The exposure time to silica dust was between 3 and 34 years; the interval between the beginning of exposure and the onset of scleroderma averaged 27.3 years (range 9 to 40 years). Antinuclear antibodies in titers between 80 and 10,240 with nucleolar and/or speckled patterns were found in 10 patients, antibodies against double-stranded DNA in three, 
Scl-70 (topoisomerase I) in three, and anticentromere antibodies in five. The following markers of collagen metabolism were increased in serum: beta-galactosidase in 12 patients, laminin peptide-P1 in 10 patients, N-terminal procollagen type III peptide in 10, and urinary sialic acid excretion 
in 7. We propose that crystalline particles of silica less than 5 microns may be phagocytosed by macrophages and release lymphokines and monokines, which activate fibroblasts and enhance their collagen and glycosaminoglycan synthesis.
 In addition, silica may act as an adjuvant to increase immune reactivity.



Study confirms link between silica exposure and rheumatoid arthritis

A large Swedish population based study of silica exposure and its relation to rheumatoid arthritis (RA) will help our understanding of the disease process, say its authors. The results confirm those of previous smaller and less well controlled studies suggesting that silica exposure is a risk factor for RA.
Conclusions: Silica exposure is associated with increased risk of developing rheumatoid arthritis. This association is not explained by smoking habits.

http://oem.bmj.com/content/62/6/380.full



Occupational textile dust exposure linked to rheumatoid arthritis
The unique shape of textile fibres gives them the capacity to penetrate deep into the lung, where they could prompt an inflammatory response.Another potential explanation could lie in the toxins produced by certain types of bacteria that can be found in textile dust. These toxins may cause respiratory disease in textile workers by generating an inflammatory response in the lungs.
"From a public health perspective, our results imply that efforts should be considered to reduce the incidence of rheumatoid arthritis 
by reducing occupational exposure to textile dust," they conclude.                                                                                                   alehttps://www.eurekrt.org/pub_releases/2016-01/b-otd011216.php 


The Case for Rheumatoid Arthritis

In this context, silica, asbestos, silicone, or nanoparticles not only generate various immunological alterations but are also extensively in contact with people. They may be mediators together with the genetic background in the mechanism that leads to autoimmune diseases such as the case of RA. 
Furthermore, these compounds are derived from the same chemical group. All of them contain silicon, which is one of the most common elements on earth, and despite their similarities, it is very rare for them to be seen as group. 
The epidemiological evidence and experimental approach have revealed the role of these compounds in autoimmunity, especially in RA, and their potential in the activation of the cellular recruitment, Th1-Treg misbalance, inflammasome activation, cytokine production, or ROS release. 
All these responses have been related to autoimmune diseases for years.

https://www.hindawi.com/journals/arthritis/2012/604187/


Silica exposure and rheumatoid arthritis: 
                            A follow up study of granite workers 1940-81.

Klockars M1, Koskela RS, Järvinen E, Kolari PJ, Rossi A.
Author information
Abstract
The incidence and prevalence of subjects awarded disability pensions and the prevalence of subjects receiving free medicines because of rheumatoid arthritis were studied in a Finnish cohort of 1026 granite workers hired between 1940 and 1971 and followed up until 31 December 1981. The incidence of awards of disability pensions because of rheumatoid arthritis during 1969-81, the prevalence of rheumatoid arthritis on 31 December 1981, and the prevalence of subjects receiving free medicines for rheumatoid arthritis at the end of 1981 were significantly higher among the granite workers than in the general male population of the same age. Retrospective analysis of the records of all patients with rheumatoid arthritis in the cohort showed a predominance of a severe, serologically positive and erosive form of rheumatoid arthritis, usually with an age at onset of 50 or over. The possible aetiological or pathophysiological role of granite dust in rheumatoid arthritis may be based on the effects of quartz on the immune system.

PMID: 2823951 PMCID: PMC1246155
[PubMed - indexed for MEDLINE] Free PMC Article
https://www.ncbi.nlm.nih.gov/pubmed/2823951



Caplan's Syndrome

Rheumatoid pneumoconiosis (Caplan's syndrome) with a classical presentation.

[Article in English, Portuguese]

Abstract

Although rare, rheumatoid pneumoconiosis, also known as Caplan's syndrome, can occur in workers exposed to silica, as well as in patients with silicosis, coal workers' pneumoconiosis or asbestosis. Prevalence is higher among patients with silicosis, despite the fact that it was originally described in coal workers with pneumoconiosis. The classical finding that defines this syndrome is that of rheumatoid nodules in the lungs, regardless of whether there are small rounded opacities suggestive of pneumoconiosis or large opacities consistent with massive pulmonary fibrosis, with or without clinical rheumatoid arthritis. We describe the case of a female patient with rheumatoid arthritis, diagnosed 34 years after 7 years of occupational exposure to silica at a porcelain plant. A chest X-ray showed circular opacities of 1-5 cm in diameter, bilaterally distributed at the periphery of the lungs. A CT-guided thoracic punch biopsy of one of those nodules revealed that it was rheumatoid nodule surrounded by a palisade of macrophages, which is typical of Caplan's syndrome. Aspects of diagnosis, classification and occurrence of this syndrome are discussed, emphasizing the importance of the occupational anamnesis of patients with rheumatoid arthritis and lung opacities on chest X-rays.
PMID:
 
19820822
[PubMed - indexed for MEDLINE] 
Free full text
https://www.ncbi.nlm.nih.gov/pubmed/19820822



Caplan's syndrome in marble workers as occupational disease

Rheumatoid pneumoconiosis is an uncommon combination of occupational lung disease caused by exposure to harmful silica dust with rheumatoid inflammation of the joints, rheumatoid arthritis, with an autoimmune background. Until now, the disease was observed mostly among coal and gold miners and granite workers. Written documents on the theme are summarized. This case study outlines the syndrome pathology with typical features presented by the worker, employed for many years in the marble industry. Although in general marble is free of silica, the collection of occupational anamnesis and familiarity with the patient's work conditions and demands gave the authors an opportunity to uncover the exposure source and to determine the most probable diagnosis.
https://www.ncbi.nlm.nih.gov/pubmed/19899255



How can exposure impact your workers’ health?

Crystalline silica is linked to several diseases. These include silicosis (an incurable lung disease), kidney disease, 
chronic obstructive pulmonary disorder (COPD) and lung cancer. Inhaling even a small amount of 
crystalline silica particles drastically increases the risk of developing serious health issues. 
                                                                                                            
Scientific data has linked crystalline silica and lung cancer. 
Both the World Health Organization (WHO) and the National Institute of Health’s (NIH) Toxicology Program 
have classified crystalline silica as a ‘known human carcinogen’. 
OSHA has reviewed more than 50 studies providing evidence of this link. It has found evidence between 
the two in at least ten different industries, prompting the American Cancer Society (ACS) 
to use the same classification as WHO and NIH.

http://www.mohonline.com/silica-exposure-standard-frequently-asked-questions-faq/


Image result for silica dust awareness banner

                             
                                       Silica and Silica Related

The leading silica-related diseases of concern are silicosis, accelerated silicosis, 
acute silicosis (silica-induced alveolar proteinosis), silicotuberculosis, silica-associated lung cancer, 
systemic sclerosis and other silica-related immunopathies, silica related nephropathy, 
and chronic airflow obstruction usually comparable to that seen with smoking
There are a few simple take-home messages from this presentation:
    • Silica exposure is easy to control.
    • Silicosis is easy to prevent.
    • There is no cure for silicosis – treat the complications as they arise.
    • Silica can kill people and can cause many serious diseases besides silicosis.
Text prepared by Tee L. Guidotti and Niels Koehncke ,University of Alberta ,Edmonton, Alberta, Canada                                 25 November 1998
 http://envepi.med.uoeh-u.ac.jp/icoh/SILICA%20Document.html



Goodpasture's Syndrome and Silica: A Case Report and Literature Review


We report a case of Goodpasture's syndrome following chronic low level and an acute, high level of exposure to crystalline silica. A 38-year-old male tilesetter was admitted to the emergency room with dyspnea and respiratory failure. He reported that his symptoms had developed over the previous week after inhaling a large amount of dust while dry-sanding and sweeping a silica-based product used to fill cracks in a cement floor. Over the following days, his pulmonary function declined and he developed acute renal failure.

Construction workers face an increased risk of silica-related disease due to their exposure while using, mixing, cutting, grinding, and sanding concrete and/or silica-based compounds. Over the past decades, techniques like dust suppression and increased use of respirators have lessened health risks to construction workers somewhat; yet, as our case demonstrates, silica exposure remains a pervasive hazard and important cause of disease in exposed persons. This report adds to the body of evidence supporting silica exposure as a causal factor in cases of Goodpasture’s Syndrome.

https://www.hindawi.com/journals/crim/2010/426970/

Goodpasture's Syndrome and p-ANCA Associated Vasculitis in a Patient of Silicosiderosis: An Unusual Association

Crystalline silica has been recognized as both a pneumotoxin and nephrotoxin. Crystalline silica particles are ingested by alveolar macrophages and result in inflammation and activation of fibroblasts [24]. This process is repeated and leads to chronic immune activity and fibrosis. Studies have shown that crystalline silica can be mobilized from the lungs to other organs, including lymph nodes, spleen, and kidney. In silicotic patients, a fourfold increase of silicon concentration was detected in the kidney tissue. Several authors described glomerulonephritis and/or kidney failure in some patients with silicosis [21]. This patient, who was a smoker, worked as an arc welder without any proper safety equipment including respirators or gloves. The details of other environmental exposures during his career as a welder are unknown.
This case reinforces the role of environmental triggers like exposure to silica, metal dust, and tobacco in pathogenesis of Goodpasture's syndrome and p-ANCA associated vasculitis. This case illustrates the complex interrelations of exposure to substances with antigenic properties and immune defects.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202243/




Diagnosis of perinuclear anti-neutrophil cytoplasmic antibody-associated microscopic polyangiitis 
in silicotics: case report

Background
An association between silica exposure and autoimmune diseases including rheumatoid arthritis, 
systemic sclerosis, systemic lupus erythematosus, and anti-neutrophil cytoplasmic autoantibody 
(ANCA)-associated vasculitis has been made.

Conclusion
Exposure to silica dust was likely one of the cause of p-ANCA-associated MPA. Possible pathogenic mechanisms of autoimmune diseases 
in silicotics and emphasis of the necessity for early diagnosis are discussed.
ANCA-associated MPA, which is one of the most common ANCA-associated vasculitides 
involving both the lung and kidney, was previously diagnosed in a patient with silicosis . 
Therefore, in cases of silicosis with presenting symptoms of hemoptysis, hematuria, proteinuria, or renal failure, 
an early assessment for autoimmune disease, including ANCA-associated MPA, should be carefully considered 
to prevent end organ damage.

http://aoemj.biomedcentral.com/articles/10.1186/s40557-016-0108-1


Kidney Disease and Silicosis

 
This study confirms previous case reports and epidemiologic studies of end-stage renal disease 
that found an association between kidney disease and exposure to silica. 
The epidemiologic data are conflicting on the mechanism by which silica causes kidney disease and are compatible with silica being able to cause kidney disease 
by both an autoimmune and direct nephrotoxic effect. 
Chronic kidney disease should be considered as a complication of 

silicosis.https://www.karger.com/Article/Pdf/45624

One agent, many diseases: exposure-response data and comparative risks of different outcomes following silica exposure.

Evidence in recent years indicates that silica causes lung cancer, and probably renal disease, in addition to its well-known relationship to silicosis. There is also suggestive evidence that silica can cause arthritis and other auto-immune diseases. Silica has, therefore, joined a handful of other toxic exposures such as tobacco smoke, dioxin, and asbestos which cause multiple serious diseases.

CONCLUSIONS:

Keeping in mind that the usual OSHA acceptable excess risk of serious disease or death for workers is 0.1%, it is clear that the current standard is far from sufficiently protective of workers' health. Perhaps surprisingly, kidney disease emerges as perhaps a higher risk than either mortality from silicosis or lung cancer, although the data are based on fewer studies.
https://www.ncbi.nlm.nih.gov/pubmed/15940719

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  TAKE-HOME MESSAGE 

● Kidneys are particularly susceptible to the toxic effects of heavy metals, organic solvents and silica.
 
● It is important to identify occupation related renal diseases in order to provide ideal preventive protection to exposed workers
● Silica exposure is associated with excess mortality from acute renal disease and can also be associated with an increased risk of end-stage renal disease.
 
● Silica exposure has been linked to several multisystem autoimmune diseases.
 
● The main goal at all stages follows the basic principle of removing the source of exposure in order to minimize the disease progression.

Reviews of exposure-related renal disease, such as the present article, highlight the importance of a thorough 
occupational history in all patients with renal disease, with particular emphasis on exposure to silica, heavy metals, and sol

http://www.theijoem.com/ijoem/index.php/ijoem/article/viewFile/45/93                                                                                                                  

Study of kidney dysfunction in non-silicotic Egyptian workers.

The corresponding analytes could have potential value as indicators of renal function before the kidney is irreversibly injured and, thus could be suitable as monitoring tools for at-risk persons exposed to silica. Researches should assess whether the current occupational standards for silica adequately protect workers from renal disease or this established standard needs to be revised.
https://www.ncbi.nlm.nih.gov/pubmed/20851677



                                              Glomerulonephritis

Therefore silica seems to cause glomerulonephritis by disrupting the immune response. 
Including this case mentioned above, we have experienced 10 cases of MPO-ANCA-associated glomerulonephritis, 
at least 3 cases out of which had suffered from silicosis in the past (30%) . 
These results indicate that silicosis should be considered a relevant pathogen of 
MPO-ANCA-associated glomerulonephritis beyond the race.

https://www.jstage.jst.go.jp/article/jpnjnephrol1959/43/4/43_4_351/_article


Further evidence of human silica nephrotoxicity in occupationally exposed workers.

It has previously been shown that granite workers with heavy exposure to silica had glomerular and proximal tubular dysfunction evidenced by increased urinary excretions of albumin, alpha-1-microglobulin (AMG), and beta-N-acetyl-glucosaminidase (NAG). The investigation was replicated in another group of granite workers to further elucidate the exposure effect relation. The urinary excretion of albumin, alpha-1-microglobulin (AMG), beta-2-microglobulin (BMG), and beta-N-acetyl-glucosaminidase (NAG) was determined in two groups of granite workers with low and high exposure to silica. Low molecular weight proteinuria and enzymuria were significantly correlated with duration of exposure in the high but not the low exposure group. These increases were most pronounced in those with 10 or more years of heavy exposure, and in those with radiological evidence of pulmonary fibrosis, particularly those with rounded small opacities denoting classical silicosis. These results provide further evidence that prolonged and heavy exposure to silica is associated with nephrotoxic effects in granite workers.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1035520/





INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

    CONCISE INTERNATIONAL CHEMICAL ASSESSMENT DOCUMENT NO. 24




    CRYSTALLINE SILICA, QUARTZ


    INTER-ORGANIZATION PROGRAMME FOR THE SOUND MANAGEMENT OF CHEMICALS
    A cooperative agreement among UNEP, ILO, FAO, WHO, UNIDO, UNITAR and
    OECD

World Health Organization
    Geneva, 2000

         The International Programme on Chemical Safety (IPCS),
    established in 1980, is a joint venture of the United Nations
    Environment Programme (UNEP), the International Labour Organization
    (ILO), and the World Health Organization (WHO). The overall objectives
    of the IPCS are to establish the scientific basis for assessment of
    the risk to human health and the environment from exposure to
    chemicals, through international peer review processes, as a
    prerequisite for the promotion of chemical safety, and to provide
    technical assistance in strengthening national capacities for the sound management of chemicals
.

9.2.4  Autoimmune-related disease

         In humans, immune activation by occupational exposure to
    respirable quartz may be linked to scleroderma, rheumatoid arthritis,
    polyarthritis, mixed connective tissue disease, systemic lupus
    erythematosus, Sjögren's syndrome, polymyositis, and fibrositis
    (Haustein et al., 1990; Ziegler & Haustein, 1992; Otsuki et al.,
    1998). The cellular mechanism that leads from quartz dust exposure to
    autoimmune diseases is not known (Otsuki et al., 1998; NIOSH,
    forthcoming). One theory is that when respirable silica particles are
    encapsulated by macrophages, fibrogenic proteins and growth factors
    are generated, and ultimately the immune system is activated (Haustein
    et al., 1992; Ziegler & Haustein, 1992; Haustein & Anderegg, 1998).

         Several epidemiological studies have reported statistically
    significant numbers of excess deaths or cases of autoimmune-related
    diseases such as scleroderma (Sluis-Cremer et al., 1985; Steenland &
    Brown, 1995b), rheumatoid arthritis (Sluis-Cremer et al., 1986;
    Klockars et al., 1987), and systemic lupus erythematosus (Steenland &
    Brown, 1995b) in silica-exposed workers.

    9.2.5  Renal disease

         Recent epidemiological studies have found statistically
    significant associations between occupational exposure to crystalline
    silica dust and renal diseases and subclinical renal changes
    (Steenland et al., 1992; Ng et al., 1993; Boujemaa et al., 1994; Hotz
    et al., 1995; Nuyts et al., 1995; Steenland & Brown, 1995b; Steenland
    & Goldsmith, 1995; Calvert et al., 1997).
http://www.inchem.org/documents/cicads/cicads/cicad24.htm#SubSectionNumber:9.2.4


High silica exposure, characterized by many years of exposure more than high intensity, is associated with the onset of ANCA-SVV. 
The importance of silica exposure from agricultural sources has not always been considered and may be a particular concern in the development of this disease, especially in the southeastern United States. 
Risk for disease from silica exposure may still be a possibility many years after exposure has ceased, which emphasizes the need for understanding the role of multiple exposures in inducing autoimmune dysfunction in small-vessel vasculitides, including ANCA-SVV.

http://cjasn.asnjournals.org/content/2/2/290.full


Image result for silica dust banner


Crystalline Silica Dust can cause much more than Silicosis

Microscopic polyangiitis accompanied by pleuritis as the only pulmonary manifestation of occupational silica exposure.

Abstract

A 68-year-old man, who had worked for processing quartz-containing stones for more than 50 years, complained of low-grade fever and arthralgia. Mediastinal lymph nodes were markedly swollen on chest computed tomography. Pathological findings of the lymph node were compatible with silicosis, with a high titer of myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA). During follow-up with prednisolone treatment, pleuritis and uveitis developed as manifestations of vasculitis. Thus, he was diagnosed with MPO-ANCA-associated vasculitis with occupational silica exposure, possibly microscopic polyangiitis (MPA). This case is rare, because pleuritis was the only pulmonary manifestation, without interstitial pneumonia, alveolar hemorrhage or glomerulonephritis.
PMID:
 
20467178
[PubMed - indexed for MEDLINE] 
Free full text

https://www.ncbi.nlm.nih.gov/pubmed/20467178


Kidney disease and arthritis in a cohort study of workers exposed to silica.

These data represent the largest number of kidney disease cases analyzed to date in a cohort with well-defined silica exposure and suggest a causal link between silica and kidney disease. Excess risk of end-stage renal disease due to a lifetime of occupational exposure at currently recommended limits is estimated to be 14%, above a background end-stage renal disease risk of 2%.
https://www.ncbi.nlm.nih.gov/pubmed/11416778/

Image result for Pulmonary Alveolar Proteinosis




Pulmonary Alveolar Proteinosis Associated with Dust Inhalation

Not Secondary but Autoimmune?

Secondary PAP occurs as a consequence of underlying conditions such as hematologic or autoimmune diseases, infections, or exposure to inhaled dusts including silica, titanium, aluminum, cement, and tin 

We know that autoimmune diseases can be associated with occupational exposure. The strongest associations have been reported for silica exposure and rheumatoid arthritis, lupus, scleroderma, and glomerulonephritis. Weaker associations have been found for solvents with scleroderma, undifferentiated connective tissue disease, and multiple sclerosis (13). It is clear that occupational exposure can influence the development of autoimmune disease.

http://www.atsjournals.org/doi/full/10.1164/rccm.200912-1800ED#.WDDrR_tNyLg.facebook




                      

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