Occupational dust exposure and chronic bronchitis in workers
This review shows the literature and research available in the issue of respiratory diseases and the various occupations. The review shows that there is a pressing need to evaluate and conduct research in the known areas like coal, cement, and pesticides, but alarmingly agriculture and other industries have also to be included.
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Causes of Chronic Bronchitis in Workers
This review shows the literature and research available in the issue of respiratory diseases and the various occupations. The review shows that there is a pressing need to evaluate and conduct research in the known areas like coal, cement, and pesticides, but alarmingly agriculture and other industries have also to be included.
It is not only the factories that are hazardous. There are arguments to show that even farming can cause allergies. Rosenman (2012) in viewing "respiratory hazards that farmers and family members" argues that the grains that can be "contaminated with fungi, bacteria or microbial toxins; pesticides; solvents; gasoline and diesel fuels; and irritant gases such as oxides of nitrogen and ammonia." This may lead to occupational asthma and the allergens in such cases could be grain dust, cow dander, cow urine, egg yolk proteins, alternaria, aspergillus, cladosporium, meal worm, poultry mites, fungi, grain mite, grain weevil and also antibiotics used in feed along with formaldehyde and glutaraldehyde and many types of organic matter. Thus every occupation has its own health hazards. The modern factories and mines have mitigated the hazards with safety practices. (Rosenman, 2012)
There are laws that require adherence to safety practices and in the U.S. The OSHA regulations part: 1910.16, for example, deals with asbestos, tremolite, anthophyllite, and actinolite dust. And the control of exposure of every employee to asbestos, tremolite, anthophyllite, and actinolite dust in every employment and so it has included 'Vinyl chloride.' (United States Department of Labor, 2012) Section 1910.1017 includes 'Acrylonitrile'; Section 1910.1045 'Lead'; Section 1910.1025 includes 'Ethylene oxide' Section 1910.1047 includes 'Methylenedianiline (MDA)'; Section 1910.1050 includes 'Formaldehyde'; Section 1910.1048 includes 'Cadmium'; Section 1910.1027 includes Butadiene (BD), Methylene Chloride, all of which are known disease creators. However the industry wise research on the respiratory system has thrown up results that deal with industries that may be using chemicals not defined in the list. (United States Department of Labor, 2012)
It is true that most factories and workplaces that deal with chemicals and dust entail some of these substances entering the human system through various means. The principal method by which the harmful substances enter human system is through the nasal and oral cavities. Workers tend to inhale dust, fumes and chemicals with which they work and as a result may have contacted diseases, especially of the respiratory system. One of the symptoms that are frequent is chronic asthma, bronchitis, and tracheal infections. There are numerous studies conducted worldwide over this situation and this paper is an attempt at finding the up-to-date findings on this issue. The major industries that are the focal point are the cement industry that is highly polluting, followed by others like the coal, cotton textile, wood, pesticides and other chemical industries. There are many other industries like plastics and construction where materials may cause allergies and respiratory problems.
This paper review the information found so far pertaining to these major industries. Bennett and Bennett (1985) are of the opinion that only recently the occupational airway diseases have received the due attention in the industry, and there is a lack of readily-available data. The interpretation of the data that is available is also scanty and urges that more research be done in the issue. Therefore there has to be further deep research into the issue and more detailed research in various industries conducted.
III. Discussion
The issue of respiratory diseases is important because it leads to greater complications other than asthma or respiratory infections and alterations. For example, Vartiainen; Tuomilehto; Puska, (1996), conducted experiments and epidemiological studies and have proved that there is a link between coronary disease and various infections in different organs, "both viral and bacterial and both acute and chronic." (Vartiainen; Tuomilehto; Puska, 1996) There are even dental infections and infections in the respiratory tract. The chronic respiratory infection leads to coronary disease incidence and mortality and there is a positive association between coronary disease and various infections in different organs especially infections in the respiratory tract. The second importance is that the respiratory diseases may also result in infectious diseases, and this then becomes a pubic hazard. Other than that the workers are themselves in poor health. Owing to all these factors many researchers have gone into the issue of the allergens for various types of pollutants. However the research thus would cover a vast area and vast number of typology and the spectrum is to be shortened. This can be done by concentrating on obvious symptoms and beginning the research from there. Thus a symptom based analysis would be ideal.
The most important need in the research is to identify the symptoms that are emanating from industrial pollution. There need to be a common variable or symptomatic indicator. The respiratory tract shows common pathology symptoms and the best and therefore one of the key variables that is used to determine and study the issue of respiratory problems with industrial workers is the subtypes of chronic cough, followed by asthma or chronic obstructive pulmonary disease, also found often with chronic cough, and therefore is an indicator of the presence of the pathology causing environment. (Groneberg; Nowak; Wussow; Fischer, 2006) The chronic cough within the workplace shows that there is an occupational contribution to chronic cough and to the symptom cough in general, and as an occupation-related chronic cough is "defined as a disease state that is characterized by the presence of cough for a period longer than three months per year which is caused by an occupational exposure to an airway irritant." (Groneberg; Nowak; Wussow; Fischer, 2006)
The activation of C-fibre receptors shows that there is evidence to link asthma and rhinitis with obstructive respiratory diseases can occur by work-related airflow limitation on account of inhaling or being exposed to allergens, toxins or organic dusts and can cause occupational asthma and COPD. There have also been studies done on animals and animal models on asthma and models of cough for the same substances identify the allergens, irritants such as TDI or other noxious gases such as NO2, SO2 or ozone and the influence of occupational triggers of cough. The animals used were guinea pigs rats and mice and in them a clearly established neurophysiology of the cough reflex has been found. Taking that as a variable, the analysis can now proceed to the various types of industry and how the issue is studied there. (Groneberg; Nowak; Wussow; Fischer, 2006) For that purpose the first one to be chosen is the cement industry because it visibly pollutes and has been the subject of controversy. The cement dust must be causing respiratory problems, more than any other industry.
Cement Dust
There is evidence as per Groneberg, et al. (2006) that exposure to cement dust resulted chronic cough and chronic phlegm among Portland cement workers. Thus occupational Portland cement dust exposure and respiratory health deterioration has a correlation. This was also found to be the case with the Nigerian cement workers and the test for dust-exposed workers and a comparison of rapid declines in FEV1 showed that not only in the cement factories, but also the construction workers both underground and surface construction had chronic cough. On the other hand a negative finding can also be cited. The issue of cement dust in a Portland cement factory and respiratory disease like chronic obstructive lung disease -- COLD using five hundred men was attempted Vestbo; Rasmussen, (1990) and using the data on hospitalization they established that about 7.8% of the total population were admitted to hospital at least once because of respiratory disease and "4.3% had been admitted because of COLD."
The correlation between the duration of exposure to cement dust up to 30 years did not show the result as must have indicated. Therefore Vestbo and Rasmussen (1990) concluded that "long-term exposure to cement dust does not lead to higher morbidity of severe respiratory disease than other types of blue collar work." (Fell; Thomassen; Kristensen; Egeland; Kongerud, 2003) The healthy worker effect and incomplete exposure information have been problems in former studies regarding the association between exposure to Portland cement dust and respiratory effects. The researchers used the estimation of particle exposure for Norwegian cement plant workers using about a hundred workers the research established that "prevalence of chronic obstructive pulmonary disease was 14.3% in the exposed group and 14.0% among the controls. Their findings do not support the hypothesis that cement dust exposure has a negative impact on lung function or gives an increase in respiratory symptoms" (Fell; Thomassen; Kristensen; Egeland; Kongerud, 2003) Another industry with a potential for respiratory diseases is the coal and gold mine sectors. They have also been researched well.
Coal Dust
It is noted here that Groneberg, et al. (2006) reports that the "relation between chronic cough, coal mining and coal miners' pneumoconiosis was examined in 205 miners with simple CWP and 289 without CWP, as a coincidence of pneumoconiosis and chronic cough was suggested before but had never been proofed." In a study on the cellular actions and interactions of key inflammatory cells and target cells in coal dust toxicity by Schins and Borm (1993) it was found that the inhaled coal dust particles affect non-cellular and cellular sources of ROS in the lung, and may cause damage of lung target cell and also the macromolecules including & alpha;-1-antitrypsin and DNA. There is yet to be established any evidence on the effects on DNA and micro molecules. The coal dust was found to be present in the extracellular matrix, they also have a presence in modifying role of ROS, cytokines, proteases and ant proteases causing tissue damage and remodelling in the respiratory tract. However the inhalation of coal dust causes lung disorders, like pneumoconiosis, progressive massive fibrosis, chronic bronchitis, lung function loss, and emphysema. (Schins, Borm, 1993)
Oxman et al. (1992) studied the lung function, emphysema, chronic bronchitis, or mortality in workers of coal mines and gold mines for dust exposure and one of the outcomes of interest and the research showed that there is a significant association between loss of lung function and cumulative respired dust exposure. For the gold miners, the risk was three times as large as for coal miners and the maximum sufferers were the gold miners. This was due to higher silica content in gold mine dust. The effects were not found to be severe for coal mines.
Coal and gold mines seem to be the places where all workers and participants are in the risk of pulmonary infections and the study of a large number of workers by Attfield and Hodous (1992) on the issue was conclusive. They published a study of over seven thousand U.S. coal miners and used linear regression analysis to relate estimates of cumulative dust exposure to several pulmonary functions. Using the data from medical examinations as variables for the period 1969 to 1971 and keeping the study to underground airborne dust sampling measurements, they reported that there is no evidence of coal dust causing lung diseases. Further the outcomes were similar to those reported for British coal miners, and this would demonstrate an adverse effect of coal mine dust exposure on pulmonary function to the minimum. These are not conclusive of the issue. Similar conditions exist in the textile industry too.
Cotton Textile
The textile industry has both the cotton and silk industry. In a study with cotton and silk textile workers of Chinese origin, the chronic effects of long-term exposure to cotton dust and endotoxin was studied by Christiani et al. (2003) The study of four hundred Chinese cotton textile workers on a similar number of silk textile workers for a decade showed that the "cumulative incidence of byssinosis and chest tightness was 24% and 23%, respectively, and was significantly more common in smokers than in non-smokers. Alternately with the silk workers, chest tightness was 10%." (Christiani, et al., 2003)
Thus it showed that the chronic bronchitis, cough, and dyspnoea were more with the cotton group than in the silk group. There was a greater risk of exposure to endotoxin and a greater risk for byssinosis. Thus cotton dust is shown to be harmful to human respiratory symptoms. It is also shown that when the workers left off from the place for a long time there is great improvement in health after leaving off the exposure. There are not much relevant studies undertaken in this industry and there is a need to conduct more research in this industry for the effects of the pollutants on the workers. The case of wood industry is equally unsatisfactory.
Wood Dust
Very few results are available for the wood dust research. In a research that focused on occupational and environmental exposures as risk factors for metal dust exposure, Baumgartner; Samet; Coultas, et al. (1999) used wood dust exposure using referral centres where patients came from the selected industries and occupations considered to represent more or less intense exposure. Duration of exposures -- occupational and environmental exposures were stratified by duration of exposure, but results were based on small numbers. The researchers used "multiple logistic regression-adjusted risk estimates for statistically significant occupational exposures" for idiopathic pulmonary fibrosis by duration of exposure. Occupational exposures were researched for cases of idiopathic pulmonary fibrosis -- IPF. Of the two hundred cases that were observed in referral centres between January 1989 and July 1993 it was found that: "farming livestock, hairdressing; metal dust; raising birds, stone cutting/polishing vegetable dust/animal dust and exposure to livestock all resulted in dusty environments." (Baumgartner; Samet; Coultas, et al., 1999) There are other industries that use direct chemicals that could harm people in more than one ways.
IV. Conclusion
The issue of chronic bronchitis in workers of all industry is not a casual analysis. There has been extensive research in some fields while there have been flaws in others. One important fact that emerged in the discussion is that the variable indicator of the working of the pollutant in the respiratory tract causes the chronic cough within the workplace. There is also direct evidence to link asthma and rhinitis with obstructive respiratory diseases caused by work-related airflow limitation and these are common to all industries. With regard to the cement dust, it resulted in chronic cough and chronic phlegm among Portland cement workers. But strangely researchers have not pursued the issue and somehow the literature shows that the respiratory problems are not present in cement factories.
There were researchers like Vestbo and others, who negated the association between exposure to Portland cement dust and respiratory effects. Such exceptions being omitted, the general problems of the exposure to dust and its effects on the respiratory system for other industries have been well documented. Therefore it is stated that though the current reviews are against the hypothesis that cement dust exposure has a negative impact on lung function there may be issues of pneumoconiosis and chronic cough in this industry that has never been documented.
Therefore future researches must concentrate on this possibility. There is evidence to show that the pollution causes inflammatory cells and target cells in coal dust cases, and the coal worker have suffered the lung function, emphysema, chronic bronchitis, and there are mortality in workers of coal mines and gold mines as a result of dust exposure and in most cases there were reported loss of lung function which also spanned the U.S. coal miners and British miners. There are opinions that say coal dust causes respiratory problems and yet again studies that conclude that coal mined are not causing lung diseases. The issue therefore ought to be investigated with more depth.
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