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1.  Long-Term Exposure to Silica Dust and Risk of Total and Cause-Specific Mortality in Chinese Workers: A Cohort Study 
PLoS Medicine  2012;9(4):e1001206.
A retro-prospective cohort study by Weihong Chen and colleagues provides new estimates for the risk of total and cause-specific mortality due to long-term silica dust exposure among Chinese workers.
Human exposure to silica dust is very common in both working and living environments. However, the potential long-term health effects have not been well established across different exposure situations.
Methods and Findings
We studied 74,040 workers who worked at 29 metal mines and pottery factories in China for 1 y or more between January 1, 1960, and December 31, 1974, with follow-up until December 31, 2003 (median follow-up of 33 y). We estimated the cumulative silica dust exposure (CDE) for each worker by linking work history to a job–exposure matrix. We calculated standardized mortality ratios for underlying causes of death based on Chinese national mortality rates. Hazard ratios (HRs) for selected causes of death associated with CDE were estimated using the Cox proportional hazards model. The population attributable risks were estimated based on the prevalence of workers with silica dust exposure and HRs. The number of deaths attributable to silica dust exposure among Chinese workers was then calculated using the population attributable risk and the national mortality rate. We observed 19,516 deaths during 2,306,428 person-years of follow-up. Mortality from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 per 100,000 person-years). We observed significant positive exposure–response relationships between CDE (measured in milligrams/cubic meter–years, i.e., the sum of silica dust concentrations multiplied by the years of silica exposure) and mortality from all causes (HR 1.026, 95% confidence interval 1.023–1.029), respiratory diseases (1.069, 1.064–1.074), respiratory tuberculosis (1.065, 1.059–1.071), and cardiovascular disease (1.031, 1.025–1.036). Significantly elevated standardized mortality ratios were observed for all causes (1.06, 95% confidence interval 1.01–1.11), ischemic heart disease (1.65, 1.35–1.99), and pneumoconiosis (11.01, 7.67–14.95) among workers exposed to respirable silica concentrations equal to or lower than 0.1 mg/m3. After adjustment for potential confounders, including smoking, silica dust exposure accounted for 15.2% of all deaths in this study. We estimated that 4.2% of deaths (231,104 cases) among Chinese workers were attributable to silica dust exposure. The limitations of this study included a lack of data on dietary patterns and leisure time physical activity, possible underestimation of silica dust exposure for individuals who worked at the mines/factories before 1950, and a small number of deaths (4.3%) where the cause of death was based on oral reports from relatives.
Long-term silica dust exposure was associated with substantially increased mortality among Chinese workers. The increased risk was observed not only for deaths due to respiratory diseases and lung cancer, but also for deaths due to cardiovascular disease.
Please see later in the article for the Editors' Summary
Editors' Summary
Walk along most sandy beaches and you will be walking on millions of grains of crystalline silica, one of the commonest minerals on earth and a major ingredient in glass and in ceramic glazes. Silica is also used in the manufacture of building materials, in foundry castings, and for sandblasting, and respirable (breathable) crystalline silica particles are produced during quarrying and mining. Unfortunately, silica dust is not innocuous. Several serious diseases are associated with exposure to this dust, including silicosis (a chronic lung disease characterized by scarring and destruction of lung tissue), lung cancer, and pulmonary tuberculosis (a serious lung infection). Moreover, exposure to silica dust increases the risk of death (mortality). Worryingly, recent reports indicate that in the US and Europe, about 1.7 and 3.0 million people, respectively, are occupationally exposed to silica dust, figures that are dwarfed by the more than 23 million workers who are exposed in China. Occupational silica exposure, therefore, represents an important global public health concern.
Why Was This Study Done?
Although the lung-related adverse health effects of exposure to silica dust have been extensively studied, silica-related health effects may not be limited to these diseases. For example, could silica dust particles increase the risk of cardiovascular disease (diseases that affect the heart and circulation)? Other environmental particulates, such as the products of internal combustion engines, are associated with an increased risk of cardiovascular disease, but no one knows if the same is true for silica dust particles. Moreover, although it is clear that high levels of exposure to silica dust are dangerous, little is known about the adverse health effects of lower exposure levels. In this cohort study, the researchers examined the effect of long-term exposure to silica dust on the risk of all cause and cause-specific mortality in a large group (cohort) of Chinese workers.
What Did the Researchers Do and Find?
The researchers estimated the cumulative silica dust exposure for 74,040 workers at 29 metal mines and pottery factories from 1960 to 2003 from individual work histories and more than four million measurements of workplace dust concentrations, and collected health and mortality data for all the workers. Death from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 deaths per 100,000 person-years), and there was a positive exposure–response relationship between silica dust exposure and death from all causes, respiratory diseases, respiratory tuberculosis, and cardiovascular disease. For example, the hazard ratio for all cause death was 1.026 for every increase in cumulative silica dust exposure of 1 mg/m3-year; a hazard ratio is the incidence of an event in an exposed group divided by its incidence in an unexposed group. Notably, there was significantly increased mortality from all causes, ischemic heart disease, and silicosis among workers exposed to respirable silica concentrations at or below 0.1 mg/m3, the workplace exposure limit for silica dust set by the US Occupational Safety and Health Administration. For example, the standardized mortality ratio (SMR) for silicosis among people exposed to low levels of silica dust was 11.01; an SMR is the ratio of observed deaths in a cohort to expected deaths calculated from recorded deaths in the general population. Finally, the researchers used their data to estimate that, in 2008, 4.2% of deaths among industrial workers in China (231,104 deaths) were attributable to silica dust exposure.
What Do These Findings Mean?
These findings indicate that long-term silica dust exposure is associated with substantially increased mortality among Chinese workers. They confirm that there is an exposure–response relationship between silica dust exposure and a heightened risk of death from respiratory diseases and lung cancer. That is, the risk of death from these diseases increases as exposure to silica dust increases. In addition, they show a significant relationship between silica dust exposure and death from cardiovascular diseases. Importantly, these findings suggest that even levels of silica dust that are considered safe increase the risk of death. The accuracy of these findings may be affected by the accuracy of the silica dust exposure estimates and/or by confounding (other factors shared by the people exposed to silica such as diet may have affected their risk of death). Nevertheless, these findings highlight the need to tighten regulations on workplace dust control in China and elsewhere.
Additional Information
Please access these websites via the online version of this summary at
The American Lung Association provides information on silicosis
The US Centers for Disease Control and Prevention provides information on silica in the workplace, including links to relevant US National Institute for Occupational Health and Safety publications, and information on silicosis and other pneumoconioses
The US Occupational Safety and Health Administration also has detailed information on occupational exposure to crystalline silica
What does silicosis mean to you is a video provided by the US Mine Safety and Health Administration that includes personal experiences of silicosis; Dont let silica dust you is a video produced by the Association of Occupational and Environmental Clinics that identifies ways to reduce silica dust exposure in the workplace
The MedlinePlus encyclopedia has a page on silicosis (in English and Spanish)
The International Labour Organization provides information on health surveillance for those exposed to respirable crystalline silica
The World Health Organization has published a report about the health effects of crystalline silica and quartz
PMCID: PMC3328438  PMID: 22529751
2.  Small animals in the study of pathological effects of asbestos 
The main pathological effects attributed to asbestos are carcinogenesis and fibrogenesis. Statistical studies have shown that asbestos workers may expect a higher morbidity not only from cancer of the lung and mesothelioma but also from cancer at other sites. Carcinomas have been reported in animals following the injection of asbestos, but the production of carcinomas by inhaled asbestos is less easy to demonstrate; most examples of experimental carcinogenesis with asbestos have been produced in rats. Rats and man react differently to asbestos in that rats do not produce asbestos bodies.
The fibrosis that follows inhalation of asbestos has been frequently described, but studies with specific pathogen free animals have shown that, like the fibrosis that may follow the inhalation of silica dust, gross fibrosis involving the production of abnormal amount of collagen probably requires the intervention of infection as well as asbestos.
Because of the difficulties encountered in the direct investigation of carcinogenesis and fibrogenesis resulting from the inhalation of asbestos, attention has been directed to the mechanisms by which the lung is able to protect itself against these fibrous dusts. While non-fibrous dusts and short fibers can be ingested by macrophages and removed via the bronchus, the long fibers that may also reach the alveolar regions may not be removed by this mechanism. The probability that a fiber may reach the alveoli depends largely on the fiber diameter and only to a small extent on the fiber length, so that, for example, fibers 100 μm long may reach the alveoli of a guinea pig. These long fibers may become coated with a ferroprotein derived from hemoglobin to form an asbestos body and, after morphological changes, the asbestos body may be broken up, the fragments ingested by macrophages and dissolved. The lung is thus cleared of asbestos. In the guinea pig lung, consolidated areas from which the asbestos has disappeared shows signs of return to normal.
This clearance mechanism is inhibited by other factors: quartz dust may almost completely inhibit asbestos body formation; tobacco smoke has a considerable effect, and even very heavy loads of carbon may act similarly.
The normal lung appears able to efficiently eliminate small loads of both nonfibrous and fibrous dust, including the carcinogenic asbestos fibers. The capacity is not unlimited, however, and when the load is heavy there is a much greater probability that fibers will not be detoxicated. In addition, other factors such as silica dust and tobacco smoke may remove the protective mechanism in the lungs.
PMCID: PMC1475401  PMID: 4377872
3.  Enhancement of nitric oxide production by pulmonary cells following silica exposure. 
Environmental Health Perspectives  1998;106(Suppl 5):1165-1169.
In vivo exposure of rat lungs to crystalline silica either by intratracheal instillation or by inhalation results in an increase in mRNA levels for inducible nitric oxide synthase (iNOS) in bronchoalveolar lavage cells (BALC), elevated nitric oxide (.NO) production by BALC, and an increase in .NO-dependent chemiluminescence (CL) from alveolar macrophages (AM). Induction of iNOS message occurs in both AM and polymorphonuclear leukocytes (PMN) harvested from silica-exposed lungs but is not significantly elevated in lavaged lung tissue. In vitro exposure of AM to silica does not stimulate .NO production or enhance iNOS message. However, treatment of naive AM with conditioned media from BALC harvested from silica-exposed rats does increase iNOS message and .NO production by these AM. The potency of this conditioned medium is dependent on interaction between AM and PMN. In the rat model, a relationship exists between the ability of various dusts to cause PMN recruitment or protein leakage into the alveolar space and the induction of iNOS message in BALC, i.e., silica > coal mine dust > carbonyl iron > titanium dioxide. Similarly, a comparison of BALC from a healthy volunteer, a silica-exposed coal miner with a normal chest radiograph, and a silica-exposed coal miner with an abnormal chest radiograph shows a correlation between pathology and both the level of iNOS message in BALC and the magnitude of .NO-dependent CL from AM. These data suggest that .NO may play a role in silicosis and that human pulmonary phagocytes exhibit enhanced .NO production in response to an inflammatory insult.
PMCID: PMC1533358  PMID: 9788892
4.  Pulmonary Fibrosis and Encephalopathy Associated with the Inhalation of Aluminium Dust 
The clinical, radiographic, pathological, and environmental features of a case of extensive aluminium fibrosis of the lungs are reported in a man of 49 years of age who had worked for 13½ years in the ball-mill room of an aluminium powder factory.
It is noteworthy that his symptoms were referable to the central nervous system, and that he died from terminal broncho-pneumonia following rapidly progressive encephalopathy, associated with epileptiform attacks. He had no presenting pulmonary symptoms, and ϰ-ray examination of the chest showed only slight abnormalities. Radiographic examination of the chests of 53 other workers in the same factory, and clinical examination with lung function tests of 23 of them revealed no other definite cases of aluminium fibrosis of the lung, nor any other cases with neurological signs and symptoms.
Estimations of the aluminium contents of the body tissues such as the lungs, brain, liver, and bone are also recorded. When compared with normal values, it was found that the lungs and brain contained about 20 times and the liver 122 times more than normal. As a contribution to the study of the aluminium content of normal tissues, and as a control series for the results given by Tipton, Cook, Steiner, Foland, McDaniel, and Fentress (1957), and Tipton, Cook, Foland, Rittner, Hardwick, and McDaniel (1958, 1959), the aluminium content of eight “normal” brains was estimated and in all cases it was found to be less than 0·6 μg. Al/g. wet weight.
The results of a survey of the dust concentrations in the factory are also given.
The use of aluminium compounds in the experimental production of epilepsy in primates is reviewed, and it is suggested that the neurological signs and symptoms with epileptiform convulsions which occurred in this case might have been related to aluminium intoxication. We hold the view, however, that the interstitial and nodular fibrosis found in the lungs was undoubtedly associated with the inhalation and retention of aluminium dust.
PMCID: PMC1038218  PMID: 13932137
5.  Technogenic Magnetic Particles in Alkaline Dusts from Power and Cement Plants 
Water, Air, and Soil Pollution  2012;224(1):1389.
During this study, we investigated the mineralogical characterization of technogenic magnetic particles (TMPs) contained in alkaline industrial dust and fly ash emitted by coal burning power plants and cement plants. The reaction of tested dust samples varied between values of pH 8 and pH 12. Their magnetic properties were characterized by measurement of magnetic susceptibility (χ), frequency dependence of magnetic susceptibility (χfd), and temperature dependence of magnetic susceptibility. Mineralogical and geochemical analyses included scanning electron microscopy with energy dispersive spectroscopy, microprobe analysis and X-ray diffraction. The TMPs in fly ash from hard coal combustion have the form of typical magnetic spherules with a smooth or corrugated surface as well as a skeletal morphology, composed of iron oxides (magnetite, maghemite, and magnesioferrite) that occurred in the form of incrustation on the surface of mullite, amorphous silica, or aluminosilicate particles. The TMPs observed in fly ash from lignite combustion have a similar morphological form but a different mineralogical composition. Instead of magnetite and magnesioferrite, maghemite and hematite with lower χ values were the prevailing magnetic minerals, which explains the much lower magnetic susceptibility of this kind of ash in comparison with the ash from hard coal combustion, and probably results from the lower temperature of lignite combustion. Morphology and mineralogical composition of TMPs in cement dust is more diverse. The magnetic fraction of cement dust occurs mostly in the form of angular and octahedral grains of a significantly finer granulation (<20 μm); however, spherules are also present. A very characteristic magnetic form for cement dust is calcium ferrite (CaFe3O5). The greatest impact on the magnetic susceptibility of cement dust results from iron-bearing additives (often waste materials from other branches of industry), which should be considered the most dangerous to the environment. Stoichiometric analysis of micro-particles confirmed the presence of heavy metals such as Pb, Mn, Cd, and Zn connected with TMPs, which are carriers of magnetic signals in atmospheric dust. Therefore, in some cases, their presence in topsoil when detected by magnetic measurement can be treated as an indicator of inorganic soil contamination.
PMCID: PMC3543769  PMID: 23325986
Alkaline dusts; Magnetic susceptibility; Technogenic magnetic particles; Iron mineralogy
6.  Respiratory disorders associated with heavy inhalation exposure to dolomite dust 
Although dolomite is classified as a relatively non-toxic, nuisance dust, little information exists as to its potential to produce respiratory disorders following occupational exposure. The purpose of this study was, therefore, to evaluate the possible effects, if any, of heavy inhalation exposure to this chemical on the prevalence of respiratory symptoms, functional impairments and radiographic abnormalities of the lungs.
The study population consisted of a group of 39 exposed subjects engaged in digging and excavating activities that were in operation for building a local dam, as well as 40 healthy non-exposed employees that served as the referent group. Subjects were interviewed and respiratory symptoms questionnaires, as suggested by the American Thoracic Society (ATS), were completed for them. Thereafter, they underwent chest X-ray and lung function tests. Additionally, using routine gravimetric techniques, personal dust monitoring for airborne inhalable and respirable dust was carried out at different dusty work sites. Finally to determine the chemical composition of the dust, it was analyzed by X-ray fluorescence (XRF) technique.
XRF revealed that the major component (50.52%) of the dust was calcium magnesium carbonate, dolomite. Additionally, levels of exposure to inhalable and respirable dust were estimated to be 51.7±24.31 and 23.0±18.11mg/m3, respectively. Statistical analysis of the data showed that symptoms such as regular cough, phlegm, wheezing, productive cough and shortness of breath were significantly (p<0.05) more prevalent among exposed workers. Similarly, the ratio of FEV1/FVC in exposed subjects was significantly different from that of non-exposed individuals. In contrast, no significant abnormalities were observed in the chest radiographs of both groups.
In conclusion, while these data cast doubt on the notion that dolomite is a harmless chemical, they provide evidence in favour of the proposition that exposure to high atmospheric concentrations of this compound is likely to be associated with respiratory symptoms.
PMCID: PMC3482327  PMID: 23115717
Dolomite dust; Occupational exposure; Respiratory symptoms; Functional impairments of the lungs
7.  Experimental approaches and analytical technique for determining heavy metals in fallen dust at ferrosilicon production factory in Edfu, Aswan, Egypt 
In this study aimed to evaluate the pollution extent of metals and nonmetals inside and outside the ferrosilicon production factory in Edfu, Aswan, Egypt, raw materials (quartz, cokes, iron oxides), ferrosilicon alloy, silica fume, dust and suspended dust (at different sites) samples were collected from the factory, and fallen dust samples were collected from outside the factory, horizontally (at different sites and different distance and directions) and vertically (at different floors in the selected buildings). Gravimetric methods, X-ray fluorescence (XRF), flame photometer, wide range carbon determinator and atomic absorption spectroscopy tools were used for elements determination. The results indicating that the fallen dust and its element contents on southern factory walls being higher than those on eastern factory walls may be due to the nature of the dusts and effects of wind force and wind direction. Fallen dust levels in different regions outside the factory were found to be affected by the distance, direction and floors. The nature of dust samples was affected by gravity and the suspended dust in different factory units depended on the work capacity and method of handling materials by personnel in different production units. Silica fume was a complicated problem, had dangerous effect against the workers’ health, and was characterized by high concentrations of SiO2 (90.6%~93.6%) and heavy metals (Mn, 420.6×10−6~520.3×10−6; Fe, 2354×10−6~2685×10−6; Co, 80.7×10−6~101.6×10−6 and Ni, 5.3×10−6~6.05×10−6). The TSP (Total Suspended Particulate) levels in all factory units were higher than the recommended air quality value (70 μg/m3) under Egyptian law. The effect of ferrosilicon factory fallen dust on the surrounding regions decreased with increasing distance between the factory and these regions. The suspended dust samples in the factory units and their components greatly exceeded national and international standards, so health and environmental criteria must be enforced on these units.
PMCID: PMC1389849  PMID: 16052701
Air pollution; Dust; Heavy metals; Fallen dust
8.  Respiratory diseases in hard metal workers: an occupational hygiene study in a factory. 
A hygiene study of a hard metal factory was conducted from 1981 to 1984. All workers exposed to hard metal were medically examined and their exposure to cobalt measured. Eighteen employees had occupational asthma related to exposure to hard metal, a prevalence rate of 5.6%. Nine had a positive bronchial provocation test to cobalt and reactions of the immediate, late, or dual type were elicited. Exposure measurements suggest that asthma may be caused by cobalt at a mean time weighted average concentration below 0.05 mg/m3. Only two of the nine individuals with cobalt asthma had a positive patch test to cobalt. Chest radiographs of three workers showed diffuse shadows of category 1 or over. X ray microanalysis of lung biopsy specimens from two of these three workers showed the presence of tungsten, titanium, cobalt, nickel, and some minerals. One of the two was diagnosed as having pneumoconiosis due to exposure to silica in a steel industry and the other was suspected of having pulmonary fibrosis caused by dust generated from the carborundum wheels used to grind hard metal. There were no cases with interstitial pneumonitis in the factory.
PMCID: PMC1007687  PMID: 3718895
9.  Iron homeostasis and oxidative stress in idiopathic pulmonary alveolar proteinosis: a case-control study 
Respiratory Research  2008;9(1):10.
Lung injury caused by both inhaled dusts and infectious agents depends on increased availability of iron and metal-catalyzed oxidative stress. Because inhaled particles, such as silica, and certain infections can cause secondary pulmonary alveolar proteinosis (PAP), we tested the hypothesis that idiopathic PAP is associated with an altered iron homeostasis in the human lung.
Healthy volunteers (n = 20) and patients with idiopathic PAP (n = 20) underwent bronchoalveolar lavage and measurements were made of total protein, iron, tranferrin, transferrin receptor, lactoferrin, and ferritin. Histochemical staining for iron and ferritin was done in the cell pellets from control subjects and PAP patients, and in lung specimens of patients without cardiopulmonary disease and with PAP. Lavage concentrations of urate, glutathione, and ascorbate were also measured as indices of oxidative stress.
Lavage concentrations of iron, transferrin, transferrin receptor, lactoferrin, and ferritin were significantly elevated in PAP patients relative to healthy volunteers. The cells of PAP patients had accumulated significant iron and ferritin, as well as considerable amounts of extracellular ferritin. Immunohistochemistry for ferritin in lung tissue revealed comparable amounts of this metal-storage protein in the lower respiratory tract of PAP patients both intracellularly and extracellularly. Lavage concentrations of ascorbate, glutathione, and urate were significantly lower in the lavage fluid of the PAP patients.
Iron homeostasis is altered in the lungs of patients with idiopathic PAP, as large amounts of catalytically-active iron and low molecular weight anti-oxidant depletion are present. These findings suggest a metal-catalyzed oxidative stress in the maintenance of this disease.
PMCID: PMC2265287  PMID: 18215276
10.  Classification of progressive massive fibrosis of coalminers by type of radiographic appearance. 
In a pilot study the chest radiographic appearances of 112 coalminers who developed progressive massive fibrosis (PMF) over an 11 year period have been classified into six types based on the appearances of the large radiographic opacities. The most common type of PMF was one or more large shadows of homogeneous radiodensity. Less common types included markedly rounded shadows usually less than 3 cm in diameter, non-homogeneous shadows appearing to consist of conglomerations of small rounded opacities, and condensations of linear or streaky shadows. Good reproducibility by one reader between two readings were obtained. The lifetime exposures to mixed respirable coal mine dust, and to its quartz component, of these 112 men were compared with those of control subjects matched for age and starting category of simple pneumoconiosis but without PMF. Overall, the men with PMF had been exposed to more mixed dust than controls, confirming that one of the reasons some men with simple pneumoconiosis develop PMF is that they have inhaled more dust than others. Eleven of the 112 cases had large opacities that were not homogeneous and appeared to consist of conglomerations of "r" type small rounded opacities. The average quartz exposures of these men were much higher than in control subjects, suggesting that in this type of PMF quartz was an important causative factor.
PMCID: PMC1069354  PMID: 6743580
11.  Hut lung: a domestically acquired pneumoconiosis of mixed aetiology in rural women. 
Thorax  1991;46(5):334-340.
A form of pneumoconiosis in rural African women termed "Transkei silicosis" has been thought to be due to silica particles inhaled while they are hand grinding maize between rocks. Twenty five women were studied who were considered to have this condition according to the following criteria: rural domicile, radiographic and lung biopsy evidence of pneumoconiosis, no exposure to mining or industry and no evidence of active tuberculosis. They were assessed for radiological, pathological, physiological and bronchoalveolar lavage fluid features. Potential aetiological factors were assessed by determining levels of exposure to respirable quartz and non-quartz containing dusts and smoke in rural dwellings during maize grinding and cooking. Most of the women were symptomless. Radiological findings ranged from a miliary pattern to extensive fibrosis resembling progressive massive fibrosis. Histological features included simple "anthracosis" in 12, anthracosis with macules in six, and mixed dust fibrosis in seven. Cell numbers and their proportions in lavage fluid were normal. More than 60% of macrophages were heavily laden with inorganic inclusions. Respirable quartz concentrations and calculated cumulative time weighted exposures were below those recommended for industry during grinding with sandstone (100% quartz) and they were even lower during grinding with dolerite containing no quartz despite the presence of an appreciable amount of quartz in the ground maize. Total respirable dust and smoke concentrations were greater than the recommended safe levels. Three women had no exposure to maize grinding. It is concluded that the inhalation of non-quartz containing dust and smoke from biomass fuelled fires is more important in the aetiology of this condition than exposure to quartz dust. The term "hut lung" may be more appropriate.
PMCID: PMC463130  PMID: 2068688
12.  Respiratory disease in cork workers (`suberosis') 1 
Thorax  1973;28(4):409-423.
Pimentel, J. Cortez, and Avila, Ramiro (1973).Thorax, 28, 409-423. Respiratory disease in cork workers (`suberosis'). A clinical, immunological, and histological study of 63 workers in the cork industry with bronchopulmonary manifestations is described. From this study, it was possible to recognize three types of reaction to the inhalation of cork dust: asthma-like syndromes, extrinsic allergic alveolitis, and chronic bronchitis with bronchiectasis. The place of histological (lung biopsy and scalene node biopsy) and immunological methods in the diagnosis of these different forms of the disease is evaluated. The high incidence of precipitins to Penicillium frequentans is stressed because the antigens produced by this fungus seem to be more pathogenic than those produced by the mouldy cork itself. The histological studies have demonstrated extrapulmonary foci of disease and have also revealed for the first time, abnormalities in the lungs of symptomless subjects. Pathological changes present in the lungs of patients with the chronic form of extrinsic allergic alveolitis, long after removal from exposure to cork dust, are also described. The experimental material of Horta and Cancella (1956) is reviewed in the light of present knowledge, and the similarity between the lesions produced in animals and those found in cork workers is noted. Finally, especial importance is attached to the finding of cork dust within the lesions, the technique for its identification and staining being described.
PMCID: PMC470051  PMID: 4200382
13.  Measuring Dust Exposure with the Thermal Precipitator in Collieries and Foundries 
The standard thermal precipitator has been modified for field surveys of airborne dust exposure so as to make it more portable. A microprojector is used when assessing the samples and for coal-mine dusts the counts are restricted to the range 0·5 to 5 microns.
In industrial environments the dust concentration appears to vary with a standard deviation of more than 50% of the mean. Part of this variability is due to errors of the thermal precipitator. The standard error of a count of a sample is about 10% to 15% in practical work and the combined effect of this and other errors is that the standard error of a single result is about 15%. However, in practice this can be neglected since the dust concentration itself is so variable. A more important source of error is the bias, due to overlapping among the particles on the cover glasses. The count may give a serious underestimate of the number of airborne particles if high sample densities are used.
The product of average concentration and duration of exposure is probably a good index of the dose of dust retained in a man's lungs. The duration of exposure is measured by a simple time study made at the same time as the concentration is measured.
Samples are taken near workers chosen at random to give unbiased estimates of the dust exposure. Ideally successive samples are taken alongside different workers. However, in a survey at a colliery it was not possible to do this and each day had to be spent with one collier. The mean dust exposure of the coal-getters was 2,860 particle-hours per shift, of those on stone work 2,250 particle-hours per shift, and the remainder had a mean dust exposure of 1,010 particle-hours per shift.
In a survey at a steel works successive samples could be taken alongside different workers. It was found that the dustiness was unrelated to the apparently dusty processes and as the dust was very fine it was suspected that it was the normal atmospheric pollution of the neighbourhood. This was confirmed by samples taken outside.
The cost of such surveys is found to lie between £1 and £2 per sample taken and consequently alternative instruments are being developed which can run unattended for long periods. In future research studies respiratory ventilation as well as dust exposure may be measured over many years, which, combined with periodic medical examinations, would enable the relation between dust exposure and its effects on the men to be determined.
PMCID: PMC1037902  PMID: 13651553
14.  Health effects of coal mining and combustion: carcinogens and cofactors. 
Some polynuclear aromatics (PNA) have been found to be potent carcinogens for all tissues and organs of experimental animals that have been exposed to them, but different dose levels are needed for these effects. They have been known for decades to cause cancer at the site of application but also at certain sites distant from the area of contact. Although some hydrocarbons are potent and complete carcinogens, the majority of related hydrocarbons was originally found to be inactive. Since they generally appear together, it was important to know more about their interaction, particularly whether they would synergize, or antagonize. The polycyclic hydrocarbons have been studied by subcutaneous injection, where they prove very potent carcinogens. They are also very active on the skin of mice where they produce cancer on prolonged application. Inhalation studies, require larger doses yielded negative results until particulate matter was introduced which facilitated the development of lung tumors. Although iron oxide dust was used initially, other dusts were also capable of enhancing the response of the tissue to benzo(a)pyrene carcinogenesis. This point is of importance, particularly since the inhalation of PNA in situations of air pollution or coal mining involves particulates, although of a different type. Soot is not a homogenous substance and several factors determine its properties. Soots will lose some of the absorbed chemicals during their residence in air, but they retain their PNAs for long periods of time when they reach the soil. The carcinogenicity of PNAs in the adsorbed state may be completely absent, depending on particle size of the soot and availability of eluting capability of the tissues or cells in contact with the soot. Whenever the carcinogenic polynuclear aromatics can be eluted they will be active in producing cancer if their residence is adequate. There seems to be no reason to assume that a large increase in coal combustion in the future will by necessity lead to greater risks of cancer to the coal miners or the general urban dweller, because activities to be started now can take into consideration the requirements necessary for control of air pollution in mines as well as in cities. If new uses of coal will be developed, it will be a completely different situation, and statements about the carcinogenic risk from coal utilization do not apply there. Although some of the same carcinogenic PNAs are involved in the health hazards from those processes, other carcinogens and also cocarcinogens will be present, and the exposed workers will not have the apparent benefits of adsorption of PNAs on soot.
PMCID: PMC1638110  PMID: 540618
15.  Baritosis: a benign pneumoconiosis. 
Thorax  1976;31(1):30-39.
Baritosis is one of the benign pneumoconioses in which inhaled particulate matter lies in the lungs for years without producing symptoms, abnormal physical signs, incapacity for work, interference with lung function, or liability to develop pulmonary or bronchial infections or other thoracic disease. Owing to the high radio-opacity of barium, the discrete shadows in the chest radiograph are extremely dense. Even in the most well-marked cases with extreme profusion of the opacities, massive shadows do not occur. When exposure to barium dust ceases the opacities begin slowly to disappear. Nine cases of baritosis occurring in a small factory in which barytes was crushed, graded, and milled are described. Two of the cases occurred after only 18 and 21 month's exposure, and 9 of the 10 men employed for more than one and a half years had baritosis. Five of the affected men examined at intervals since their exposure to barytes ceased in 1964 showed marked clearing of their radiological abnormalities.
PMCID: PMC470358  PMID: 1257935
16.  Dust exposure and impairment of lung function at a small iron foundry in a rapidly developing country 
OBJECTIVES—A cross sectional prospective study was carried out among iron foundry workers (exposed) and soft drink bottling and supply company workers (unexposed) to assess their occupational exposure to ambient respiratory dust in their work environment and its effect on their lung function profile.
PARTICIPANTS—Lung function was measured in 81 exposed and 113 unexposed workers. Personal respirable dust concentrations were measured for all the exposed and the unexposed workers. Information on respiratory signs and symptoms was also collected from the participants.
RESULTS—Among the exposed workers, midexpiratory flow (FEF25-75), forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF), FEV1/FVC, and FEV1/VC ratios were significantly lower whereas the vital capacity (VC) and forced vital capacity (FVC) were non-significantly higher. Job at the iron foundry was a significant predictor of lung function. Exposure to high concentration of respirable dust at the iron foundry was also a significant predictor. Workers working in high exposure areas (general works, furnace, continuous casting areas, and fabrication workshop) had lower lung function values than workers in medium and low exposure areas. Smoking did not enhance the effects of exposure to dust on lung function.
CONCLUSIONS—Exposure to respirable dust was higher among the iron foundry workers; and among these, general, furnace, rolling mill, and fabrication workers had higher exposures to dust than did workers in continuous casting, the mechanical workshop, and the bottling plant. Job type and exposure to dust were significant predictors of lung function. Implementation of industrial hygiene and proper and efficient use of personal protection equipment while at work could help to protect the respiratory health of industrial workers.

Keywords: lung function; dust exposure; foundry; smoking; personal protection
PMCID: PMC1740042  PMID: 11555687
17.  Contribution of reactive oxygen and nitrogen species to particulate-induced lung injury. 
Environmental Health Perspectives  1998;106(Suppl 5):1157-1163.
Recently, a second pathway for the generation of potential oxidants with the reactivity of the hydroxyl radical without the need for metal catalysis has been described. In response to various inflammatory stimuli, lung endothelial, alveolar, and airway epithelial cells, as well as activated alveolar macrophages, produce both nitric oxide (.NO) and superoxide anion radicals (O2.-). .NO regulates pulmonary vascular and airway tone and plays an important role in lung host defense against various bacteria. However, .NO may be cytotoxic by inhibiting critical enzymes such as mitochondrial aconitase and ribonucleotide reductase, by S-nitrosolation of thiol groups, or by binding to their iron-sulfur centers. In addition, .NO reacts with O2.- at a near diffusion-limited rate to form the strong oxidant peroxynitrite (ONOO-), which can nitrate and oxidize key amino acids in various lung proteins such as surfactant protein A, and inhibit their functions. The presence of ONOO- in the lungs of patients with acute respiratory distress syndrome has been demonstrated by measuring levels of nitrotyrosine, the stable product of tyrosine nitration. Various studies have shown that inhalation or intratracheal instillation of various respirable mineral dusts or asbestos fibers increased levels of inducible nitric oxide synthase mRNA. In this presentation, we review the evidence for the upregulation of .NO in the lungs of animals exposed to mineral particulates and assess the contribution of reactive nitrogen species in the pathogenesis of the resultant lung injury.
PMCID: PMC1533367  PMID: 9788891
18.  CD11c+/CD11b+ Cells Are Critical for Organic Dust–Elicited Murine Lung Inflammation 
Organic dust exposure in the agricultural industry results in significant lung disease. Macrophage infiltrates are increased in the lungs after organic dust exposures, yet the phenotype and functional importance of these cells remain unclear. Using an established intranasal inhalation murine model of dust-induced lung inflammation, animals were treated once or daily for 3 weeks with swine confinement organic dust extract (DE). Repetitive DE treatment for 3 weeks resulted in significant increases in CD11c+/CD11b+ macrophages in whole lung–associated tissue. These cells displayed increased costimulatory molecule (CD80 and CD86) expression, enhanced phagocytic ability, and an increased production of IL-6, CXCL1, and CXCL2. Similar findings were observed with the CD11c+/CD11b+ macrophage infiltrate after repetitive exposure to peptidoglycan, a major DE component. To determine the functional importance of macrophages in mediating DE-induced airway inflammation, lung macrophages were selectively depleted using a well-established intranasal clodronate liposome depletion/suicide strategy. First, macrophage depletion by clodronate liposomes resulted in significant reductions in airway neutrophil influx and TNF-α and IL-6 production after a single exposure to DE. In contrast, after repetitive 3-week exposure to DE, airway lavage fluid and lung tissue neutrophils were significantly increased in clodronate liposome–treated mice compared with control mice. A histological examination of lung tissue demonstrated striking increases in alveolar and bronchiolar inflammation, as well as in the size and distribution of cellular aggregates in clodronate–liposome versus saline–liposome groups repetitively exposed to DE. These studies demonstrate that DE elicits activated CD11c+/CD11b+ macrophages in the lung, which play a critical role in regulating the outcome of DE-induced airway inflammation.
PMCID: PMC3547108  PMID: 22822029
macrophage; neutrophil; airway inflammation; peptidoglycan; organic dust
19.  Respiratory health effects and exposure to superabsorbent polymer and paper dust - an epidemiological study 
BMC Public Health  2011;11:557.
The primary aim of the present study was to investigate if exposure to dust from absorbent hygiene products containing superabsorbent polymer is related to symptoms from the airways and from the eyes. The secondary aim was to estimate the current exposure to superabsorbent polymer among production and maintenance workers in a plant producing hygiene products.
The cohort comprised 1043 workers of whom 689 were exposed to super absorbent polymer and 804 were exposed to paper dust (overlapping groups). There was 186 workers not exposed to either superabsorbent polymer or to paper dust They were investigated with a comprehensive questionnaire about exposure, asthma, rhinitis and symptoms from eyes and airways. The results were analyzed with logistic regression models adjusting for sex, age, atopy and smoking habits. An aerosol sampler equipped with a polytetrafluoroethylene filter with 1 μm pore size was used for personal samplings in order to measure inhalable dust and superabsorbent polymer.
The prevalence of nasal crusts (OR 1.4, 95% CI 1.01-2.0) and nose-bleeding (OR 1.7, 95% CI 1.2-2.4) was increased among the paper dust exposed workers (adjusted for superabsorbent polymer exposure). There were no significant effects associated with exposure to superabsorbent polymer (adjusted for paper dust exposure). The average exposure to inhalable levels of total dust (paper dust) varied between 0.40 and 1.37 mg/m3. For superabsorbent polymer dust the average exposure varied between 0.02 and 0.81 mg/m3.
In conclusion, our study shows that workers manufacturing diapers in the hygiene industry have an increased prevalence of symptoms from the nose, especially nose-bleeding. There was no relation between exposure to superabsorbent polymer and symptoms from eyes, nose or respiratory tract, but exposure to paper dust was associated with nose-bleeding and nasal crusts. This group of workers had also a considerable exposure to superabsorbent polymer dust.
PMCID: PMC3155498  PMID: 21752269
20.  Protein Kinase C epsilon is Important in Modulating Organic Dust-Induced Airway Inflammation 
Experimental lung research  2012;38(8):383-395.
Organic dust samples from swine confinement facilities elicit pro-inflammatory cytokine/chemokine release from bronchial epithelial cells and monocytes, dependent, in part, upon dust-induced activation of the protein kinase C (PKC) isoform, PKCε. PKCε is also rapidly activated in murine tracheal epithelial cells following in vivo organic dust challenges, yet the functional role of PKCε in modulating dust-induced airway inflammatory outcomes is not defined. Utilizing an established intranasal inhalation animal model, experiments investigated the biologic and physiologic responses following organic dust extract (ODE) treatments in wild-type (WT) and PKCε knock-out (KO) mice. We found that neutrophil influx increased by greater than two-fold in PKCε KO mice following both a one-time challenge and three weeks of daily challenges with ODE as compared to WT mice. Likewise, lung pathology revealed that bronchiolar and alveolar inflammation and lymphoid aggregates were significantly increased in ODE-treated PKCε KO mice. Airway hyper-responsiveness to methacholine increased in PKCε KO + ODE to a greater magnitude than WT + ODE animals. There were no significant differences in cytokine/chemokine release elicited by ODE treatment between groups. However, ODE-induced nitric oxide (NO) production differed in that ODE exposure increased nitrate levels in WT animals but not in PKCε KO mice. Moreover, ODE failed to upregulate NO from ex vivo stimulated PKCε KO lung macrophages. Collectively, these studies demonstrate that PKCε-deficient mice were hypersensitive to organic dust exposure, and suggest that PKCε is important in the normative lung inflammatory response to ODE. Dampening of ODE-induced NO may contribute to these enhanced inflammatory findings.
PMCID: PMC4066446  PMID: 22897707
protein kinase C epsilon; airway inflammation; airway hyper-responsiveness; nitric oxide; neutrophil; lung
21.  Chronic exposure to iron oxide, chromium oxide, and nickel oxide fumes of metal dressers in a steelworks 
Graham Jones, J., and Warner, C. G. (1972).Brit. J. industr. Med.,29, 169-177. Chronic exposure to iron oxide, chromium oxide, and nickel oxide fumes of metal dressers in a steelworks. Occupational and medical histories, smoking habits, respiratory symptoms, chest radiographs, and ventilatory capacities were studied in 14 steelworkers employed as deseamers of steel ingots for periods of up to 16 years. The men were exposed for approximately five hours of each working shift to fume concentrations ranging from 1·3 to 294·1 mg/m3 made up mainly of iron oxide with varying proportions of chromium oxide and nickel oxide.
Four of the men, with 14 to 16 years' exposure, showed radiological evidence of pneumoconiosis classified as ILO categories 2 or 3. Of these, two had pulmonary function within the normal range and two had measurable loss of function, moderate in one case and mild in the other.
Many observers would diagnose these cases as siderosis but the authors consider that this term should be reserved for cases exposed to pure iron compounds. The correct diagnosis is mixed-dust pneumoconiosis and the loss of pulmonary function is caused by the effects of the mixture of metallic oxides. It is probable that inhalation of pure iron oxide does not cause fibrotic pulmonary changes, whereas the inhalation of iron oxide plus certain other substances obviously does.
PMCID: PMC1009395  PMID: 5021996
22.  Spectrum of High Resolution Computed Tomography Findings in Occupational Lung Disease: Experience in a Tertiary Care Institute 
To study the spectrum of high resolution computed tomography (HRCT) findings in occupational lung disease in industrial workers and to assess the utility of International classification of HRCT for occupational and environmental respiratory diseases (ICHOERD).
Materials and Methods:
Retrospective analysis of radiological data (radiographs and computed tomography chest scans) gathered over a period of 3 years (January 2010- December 2012) of industrial workers in an organised sector who presented with respiratory complaints. The HRCT findings were evaluated using ICHOERD.
There were 5 females and 114 males in the study, with a mean age of 49 years. These workers were exposed to different harmful agents including silica, asbestos, cotton dust, metal dust, iron oxide, organic dust, rubber fumes, plastic fumes, acid fumes, and oil fumes. There were 10 smokers in the study. The radiograph of chest was normal in 53 patients. 46% of these normal patients (21.8% of total) demonstrated positive findings on HRCT. When the radiograph was abnormal, HRCT provided more accurate information and excluded the other diagnosis. The HRCT findings were appropriately described using the ICHOERD. Bronchiectasis was the most common finding (44.5%) with mild central cylindrical bronchiectasis as the most common pattern. Pleural thickening was seen in 41 patients (34.5%). Enlarged hilar or mediastinal lymphnodes were seen in 10 patients (8.4%) with egg-shell calcification in 1 patient exposed to silica. Bronchogenic carcinoma was seen in 1 patient exposed to asbestos.
Occupational lung disease is a common work related condition in industrial workers even in the organized sector. Though chest radiograph is the primary diagnostic tool, HRCT is the undisputed Gold Standard for evaluation of these patients. Despite the disadvantage of radiation exposure, low dose CT may serve as an important tool for screening and surveillance. The ICHOERD is a powerful and reliable tool not only for diagnosis, but also for quantitative and analytical measurement of disease, thereby contributing to assessing the medical epidemiology of lung disease. It should always be used while evaluating HRCT of a patient with occupational lung disease.
PMCID: PMC3935267  PMID: 24605259
Classification; high resolution computed tomography; ICHOERD; industrial worker; occupational lung disease
23.  Silicosis in a Himalayan village population: role of environmental dust. 
Thorax  1991;46(5):341-343.
The Himalayan villages of Chuchot Shamma and Stok were surveyed because silicosis had been suspected from the radiographs of some of the inhabitants. The villages are agricultural, and Chuchot is exposed to frequent dust storms. Chest radiographs of villagers aged 50-62 were assessed blind by two independent observers using ILO criteria. In Chuchot five of seven men and all of the nine women examined showed varying grades of silicosis, compared with three of 13 men and seven of 11 women in Stok, which lies 300 metres higher and is exposed to fewer dust storms. The difference in prevalence of silicosis between the two villages was significant, as was the differences between men and women. Three patients from the village adjoining Chuchot were later found to have radiological evidence of progressive massive fibrosis. A necropsy on a man in a neighbouring village in the Indus valley showed classical silicosis in a hilar lymph node. Chemical analysis of the inorganic dust in the lung showed that 54.4% was elemental silicon [corrected]. This was similar to the silicon [corrected] content of dust samples collected from houses in Chuchot, which included particles of respirable size. X-ray microanalysis showed that quartz formed 16-21% of the inorganic lung dust. This study suggests that silicosis is common among the older inhabitants of these Himalayan villages. The dust exposure is clearly environmental and not industrial. Further studies are needed to define the extent and severity of silicosis in this community and to examine possible preventive measures.
PMCID: PMC463131  PMID: 2068689
24.  Morphological investigations of fibrogenic action of Estonian oil shale dust. 
A review of morphological investigations carried out to clarify the pathogenicity of industrial dust produced in the mining and processing of Estonian oil shale is given. Histological examination of lungs of workers in the oil shale industry taken at necropsies showed that the inhalation of oil shale dust over a long period (more than 20 years) may cause the development of occupational pneumoconiotic changes in oil shale miners. The pneumoconiotic process develops slowly and is characterized by changes typical of the interstitial form of pneumoconiotic fibrosis in the lungs. Emphysematous changes and chronic bronchitis also occur. The average chemical content of oil shale as well as of samples of oil shale dust generated during mining and sorting procedures is given. The results of experiments in white rats are presented; these studies also indicate a mild fibrogenic action of Estonian oil shale dust.
PMCID: PMC1637705  PMID: 221215
25.  Pulmonary disease from occupational exposure to an artificial aluminium silicate used for cat litter. 
All available workers engaged in bagging an artificial crystalline aluminium silicate--the kiln-dried residue from the calcining and water extraction of alunite (a hydrated sulphate of aluminium and potassium) that is currently classified as a nuisance dust--were studied after a complaint of respiratory and systemic symptoms, including arthritis, by an employee of the factory, who showed physiological and radiographic evidence of diffuse pulmonary fibrosis and in whom lung biopsy showed diffuse fibrosis with granulomas. Inhalation challenge produced a transient decrease in transfer factor and transfer factor standardised for alveolar volume. Twenty-five subjects were known to have been exposed at some time to the dust of alunite-residue. Of the 17 who could be contacted, all agreed to attend for respiratory questionnaire and occupational history, pulmonary function testing (spirometry, lung volumes, gas transfer), and posteroanterior chest radiograph. Six subjects considered that occupational exposure to the dust was responsible for respiratory symptoms. Three subjects had abnormality of the chest radiograph consistent with pulmonary fibrosis. The mean percentage of predicted transfer factor standardised for effective alveolar volume was 71.1% in subjects with abnormal chest radiographs and 86.6% in subjects with normal radiographs (p = 0.10). There was a trend in the correlation between the percentage of predicted transfer factor standardised for effective alveolar volume and total dust exposure (sum of the products of grade of severity of each exposure period and duration of each exposure period in months) (r = 0.40 p = 0.10). This study suggests that there may be a relation between inhalation of the dust of this form of aluminium silicate and pulmonary fibrosis.
PMCID: PMC1008753  PMID: 7448131

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