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Diseases Caused by Organic Dusts

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Organic Dust and Disease

Dusts of vegetable, animal and microbial origin have always been part of the human environment. When the first aquatic organisms moved to land some 450 million years ago, they soon developed defence systems against the many noxious substances present in the terrestrial environment, most of them of plant origin. Exposures to this environment usually cause no specific problems, even though plants contain a number of extremely toxic substances, particularly those present in or produced by moulds.

During the development of civilization, climatic conditions in some parts of the world necessitated certain activities to be undertaken indoors. Threshing in the Scandinavian countries was performed indoors during the winter, a practice mentioned by chroniclers in antiquity. The enclosure of dusty processes led to disease among the exposed persons, and one of the first published accounts of this is by the Danish bishop Olaus Magnus (1555, as cited by Rask-Andersen 1988). He described a disease among threshers in Scandinavia as follows:

“In separating the grain from the chaff, care must be taken to choose a time when there is a suitable wind which will sweep away the grain dust, so that it will not damage the vital organs of the threshers. This dust is so fine that it will almost unnoticeably penetrate into the mouth and accumulate in the throat. If this is not quickly dealt with by drinking fresh ale, the thresher may never again or only for a short period eat what he has threshed.”

With the introduction of machine processing of organic materials, treatment of large quantities of materials indoors with poor ventilation led to high levels of airborne dust. The descriptions by bishop Olaus Magnus and later by Ramazzini (1713) were followed by several reports on disease and organic dusts in the nineteenth century, particularly among cotton mill workers (Leach 1863; Prausnitz 1936). Later, the specific pulmonary disease common among farmers handling mouldy materials was also described (Campbell 1932).

During recent decades, a large number of reports on disease among persons exposed to organic dusts have been published. Initially, most of these were based on persons seeking medical help. The names of the diseases, when published, were often related to the particular environment where the disease was first recognized, and a bewildering array of names resulted, such as farmer’s lung, mushroom grower’s lung, brown lung and humidifier fever.

With the advent of modern epidemiology, more reliable figures were obtained for the incidence of occupational respiratory diseases related to organic dust (Rylander, Donham and Peterson 1986; Rylander and Peterson 1990). There was also advancement in the understanding of the pathological mechanisms underlying these diseases, particularly the inflammatory response (Henson and Murphy 1989). This paved the way for a more coherent picture of diseases caused by organic dusts (Rylander and Jacobs 1997).

The following will describe the different organic dust environments where disease has been reported, the disease entities themselves, the classical byssinosis disease and specific preventive measures.


Organic dusts are airborne particles of vegetable, animal or microbial origin. Table 1 lists examples of environments, work processes and agents involving the risk of exposure to organic dusts.

Table 1. Examples of sources of hazards of exposure to organic dust


Handling of grain, hay or other crops

Sugar-cane processing




Swine/dairy confinement buildings

Poultry houses and processing plants

Laboratory animals, farm animals and pets


Sewage water and silt

Household garbage



Vegetable fibre processing (cotton, flax, hemp, jute, sisal)


Timber and wood processing


Biotechnology processing


Contaminated water in humidifiers

Microbial growth on structures or in ventilation ducts


It is now understood that the specific agents in the dusts are the major reason why disease develops. Organic dusts contain a multitude of agents with potential biological effects. Some of the major agents are found in table 2.

Table 2. Major agents in organic dusts with potential biological activity

Vegetable agents



Plicatic acid

Alkaloids (e.g., nicotine)


Animal agents



Microbial agents






The relative role of each of these agents, alone or in combination with others, for the development of disease, is mostly unknown. Most of the information available relates to bacterial endotoxins which are present in all organic dusts.

Endotoxins are lipopolysaccharide compounds which are attached to the outer cell surface of Gram-negative bacteria. Endotoxin has a wide variety of biological properties. After inhalation it causes an acute inflammation (Snella and Rylander 1982; Brigham and Meyrick 1986). An influx of neutrophils (leukocytes) into the lung and the airways is the hallmark of this reaction. It is accompanied by activation of other cells and secretion of inflammatory mediators. After repeated exposures, the inflammation decreases (adaptation). The reaction is limited to the airway mucosa, and there is no extensive involvement of the lung parenchyma.

Another specific agent in organic dust is (1→3)-β-D-glucan. This is a polyglucose compound present in the cell wall structure of moulds and some bacteria. It enhances the inflammatory response caused by endotoxin and alters the function of inflammatory cells, particularly macrophages and T-cells (Di Luzio 1985; Fogelmark et al. 1992).

Other specific agents present in organic dusts are proteins, tannins, proteases and other enzymes, and toxins from moulds. Very little data are available on the concentrations of these agents in organic dusts. Several of the specific agents in organic dusts, such as proteins and enzymes, are allergens.


The diseases caused by organic dusts are shown in table 3 with the corresponding International Classification of Disease (ICD) numbers (Rylander and Jacobs 1994).


Table 3. Diseases induced by organic dusts and their ICD codes


Bronchitis and pneumonitis (ICD J40)

Toxic pneumonitis (inhalation fever, organic dust toxic syndrome)

Airways inflammation (mucous membrane inflammation)

Chronic bronchitis (ICD J42)

Hypersensitivity pneumonitis (allergic alveolitis) (ICD J67)

Asthma (ICD J45)

Rhinitis, conjunctivitis



The primary route of exposure for organic dusts is by inhalation, and consequently the effects on the lung have received the major share of attention in research as well as in clinical work. There is, however, a growing body of evidence from published epidemiological studies and case reports as well as anecdotal reports, that systemic effects also occur. The mechanism involved seems to be a local inflammation at the target site, the lung, and a subsequent release of cytokines either with systemic effects (Dunn 1992; Michel et al. 1991) or an effect on the epithelium in the gut (Axmacher et al. 1991). Non-respiratory clinical effects are fever, joint pains, neurosensory effects, skin problems, intestinal disease, fatigue and headache.

The different disease entities as described in table 3 are easy to diagnose in typical cases, and the underlying pathology is distinctly different. In real life, however, a worker who has a disease due to organic dust exposure, often presents a mixture of the different disease entities. One person may have airways inflammation for a number of years, suddenly develop asthma and in addition have symptoms of toxic pneumonitis during a particularly heavy exposure. Another person may have subclinical hypersensitivity pneumonitis with lymphocytosis in the airways and develop toxic pneumonitis during a particularly heavy exposure.

A good example of the mixture of disease entities that may appear is byssinosis. This disease was first described in the cotton mills, but the individual disease entities are also found in other organic dust environments. An overview of the disease follows.


The disease

Byssinosis was first described in the 1800s, and a classic report involving clinical as well as experimental work was given by Prausnitz (1936). He described the symptoms among cotton mill workers as follows:

“After working for years without any appreciable trouble except a little cough, cotton mill workers notice either a sudden aggravation of their cough, which becomes dry and exceedingly irritating¼ These attacks usually occur on Mondays ¼ but gradually the symptoms begin to spread over the ensuing days of the week; in time the difference disappears and they suffer continuously.”

The first epidemiological investigations were performed in England in the 1950s (Schilling et al. 1955; Schilling 1956). The initial diagnosis was based on the appearance of a typical Monday morning chest tightness, diagnosed using a questionnaire (Roach and Schilling 1960). A scheme for grading the severity of byssinosis based on the type and periodicity of symptoms was developed (Mekky, Roach and Schilling 1967; Schilling et al. 1955). Duration of exposure was used as a measure of dose and this was related to the severity of the response. Based on clinical interviews of large numbers of workers, this grading scheme was later modified to more accurately reflect the time intervals for the decrease in FEV1 (Berry et al. 1973).

In one study, a difference in the prevalence of byssinosis in mills processing different types of cotton was found (Jones et al. 1979). Mills using high-quality cotton to produce finer yarns had a lower prevalence of byssinosis than mills producing coarse yarns and using a lower quality of cotton. Thus in addition to exposure intensity and duration, both dose-related variables, the type of dust became an important variable for assessing exposure. Later it was demonstrated that the differences in the response of workers exposed to coarse and medium cottons was dependent not only on the type of cotton but on other variables that affect exposure, including: processing variables such as carding speed, environmental variables such as humidification and ventilation, and manufacturing variables such as different yarn treatments (Berry et al. 1973).

The next refinement of the relationship between exposure to cotton dust and a response (either symptoms or objective measures of pulmonary function), was the studies from the United States, comparing those who worked in 100% cotton to workers using the same cotton but in a 50:50 blend with synthetics and workers without exposure to cotton (Merchant et al. 1973). Workers exposed to 100% cotton had the highest prevalence of byssinosis independent of cigarette smoking, one of the confounders of exposure to cotton dust. This semiquantitative relationship between dose and response to cotton dust was further refined in a group of textile workers stratified by sex, smoking, work area and mill type. A relationship was observed in each of these categories between dust concentration in the lower dust ranges and byssinosis prevalence and/or change in forced expiratory volume in one second (FEV1).

In later investigations, the FEV1 decrease over the work shift has been used to assess the effects of exposure, and it is also a part of the US Cotton Dust Standard.

Byssinosis was long regarded as a peculiar disease with a mixture of different symptoms and no knowledge of the specific pathology. Some authors suggested that it was an occupational asthma (Bouhuys 1976). A workgroup meeting in 1987 analysed the symptomatology and pathology of the disease (Rylander et al. 1987). It was agreed that the disease comprised several clinical entities, generally related to organic dust exposure.

Toxic pneumonitis may appear the first time an employee works in the mill, particularly when working in the opening, blowing and carding sections (Trice 1940). Although habituation develops, the symptoms may reappear after an unusually heavy exposure later on.

Airways inflammation is the most widespread disease, and it appears at different degrees of severity from light irritation in the nose and airways to severe dry cough and breathing difficulties. The inflammation causes constriction of airways and a reduced FEV1. Airway responsiveness is increased as measured with a methacholine or histamine challenge test. It has been discussed whether airways inflammation should be accepted as a disease entity by itself or whether it merely represents a symptom. As the clinical findings in terms of severe cough with airways narrowing can lead to a decrease in work ability, it is justified to regard it as an occupational disease.

Continued airways inflammation over several years may develop into chronic bronchitis, particularly among heavily exposed workers in the blowing and carding areas. The clinical picture would be one of chronic obstructive pulmonary disease (COPD).

Occupational asthma develops in a small percentage of the workforce, but is usually not diagnosed in cross-sectional studies as the workers are forced to leave work because of the disease. Hypersensitivity pneumonitis has not been detected in any of the epidemiological studies undertaken, nor have there been case reports relating to cotton dust exposure. The absence of hypersensitivity pneumonitis may be due to the relatively low amount of moulds in cotton, as mouldy cotton is not acceptable for processing.

A subjective feeling of chest tightness, most common on Mondays, is the classical symptom of cotton dust exposure (Schilling et al. 1955). It is not, however, a feature unique to cotton dust exposure as it appears also among persons working with other kinds of organic dusts (Donham et al. 1989). Chest tightness develops slowly over a number of years but it can also be induced in previously unexposed persons, provided that the dose level is high (Haglind and Rylander 1984). The presence of chest tightness is not directly related to a decrease in FEV1.

The pathology behind chest tightness has not been explained. It has been suggested that the symptoms are due to an increased adhesiveness of platelets which accumulate in the lung capillaries and increase the pulmonary artery pressure. It is likely that chest tightness involves some kind of cell sensitization, as it takes repeated exposures for the symptom to develop. This hypothesis is supported by results from studies on blood monocytes from cotton workers (Beijer et al. 1990). A higher ability to produce procoagulant factor, indicative of cell sensitization, was found among cotton workers as compared to controls.

The environment

The disease was originally described among workers in cotton, flax and soft hemp mills. In the first phase of cotton treatment within the mills—bale opening, blowing and carding—more than half of the workers may have symptoms of chest tightness and airways inflammation. The incidence decreases as the cotton is processed, reflecting the successive cleaning of the causative agent from the fibre. Byssinosis has been described in all countries where investigations in cotton mills have been performed. Some countries like Australia have, however, unusually low incidence figures (Gun et al. 1983).

There is now uniform evidence that bacterial endotoxins are the causative agent for toxic pneumonitis and airways inflammation (Castellan et al. 1987; Pernis et al. 1961; Rylander, Haglind and Lundholm 1985; Rylander and Haglind 1986; Herbert et al. 1992; Sigsgaard et al. 1992). Dose-response relationships have been described and the typical symptoms have been induced by inhalation of purified endotoxin (Rylander et al. 1989; Michel et al. 1995). Although this does not exclude the possibility that other agents could contribute to the pathogenesis, endotoxins can serve as markers for disease risk. It is unlikely that endotoxins are related to the development of occupational asthma, but they could act as an adjuvant for potential allergens in cotton dust.

The case

The diagnosis of byssinosis is classically made using questionnaires with the specific question “Does your chest feel tight, and if so, on which day of the week?”. Persons with Monday morning chest tightness are classified as byssinotics according to a scheme suggested by Schilling (1956). Spirometry can be performed, and, according to the different combinations of chest tightness and decrease in FEV1, the diagnostic scheme illustrated in table 4 has evolved.


Table 4. Diagnostic criteria for byssinosis


Grade ½.          Chest tightness on the first day of some working weeks

Grade 1.          Chest tightness on the first day of every working week

Grade 2.          Chest tightness on the first and other days of the working week

Grade 3.          Grade 2 symptoms accompanied by evidence of permanent incapacity in the form of diminished effort intolerance and/or reduced ventilatory capacity




Treatment in the light stages of byssinosis is symptomatic, and most of the workers learn to live with the slight chest tightness and bronchoconstriction that they experience on Mondays or when cleaning machinery or carrying out similar tasks with a higher than normal exposure. More advanced stages of airways inflammation or regular chest tightness several days of the week require transfer to less dusty operations. The presence of occupational asthma mostly requires work change.


Prevention in general is dealt with in detail elsewhere in the Encyclopaedia. The basic principles for prevention in terms of product substitute, exposure limitation, worker protection and screening for disease apply also for cotton dust exposure.

Regarding product substitutes, it has been suggested that cotton with a low level of bacterial contamination be used. An inverse proof of this concept is found in reports from 1863 where the change to dirty cotton provoked an increase in the prevalence of symptoms among the exposed workers (Leach 1863). There is also the possibility of changing to other fibres, particularly synthetic fibres, although this is not always feasible from a product point of view. There is at present no production-applied technique to decrease the endotoxin content of cotton fibres.

Regarding dust reduction, successful programmes have been implemented in the United States and elsewhere (Jacobs 1987). Such programmes are expensive, and the costs for highly efficient dust removal may be prohibitive for developing countries (Corn 1987).

Regarding exposure control, the level of dust is not a sufficiently precise measure of exposure risk. Depending on the degree of contamination with Gram-negative bacteria and thus endotoxin, a given dust level may or may not be associated with a risk. For endotoxins, no official guidelines have been established. It has been suggested that a level of 200 ng/m3 is the threshold for toxic pneumonitis, 100 to 200 ng/m3 for acute airways constriction over the workshift and 10 ng/m3 for airways inflammation (Rylander and Jacobs 1997).

Knowledge about the risk factors and the consequences of exposure are important for prevention. The information basis has expanded rapidly during recent years, but much of it is not yet present in textbooks or other easily available sources. A further problem is that symptoms and findings in respiratory diseases induced by organic dust are non-specific and occur normally in the population. They may thus not be correctly diagnosed in the early stages.

Proper dissemination of knowledge concerning the effects of cotton and other organic dusts requires the establishment of appropriate training programmes. These should be directed not only towards workers with potential exposure but also towards employers and health personnel, particularly occupational health inspectors and engineers. Information must include source identification, symptoms and disease description, and methods of protection. An informed worker can more readily recognize work-related symptoms and communicate more effectively to a health care provider. Regarding health surveillance and screening, questionnaires are a major instrument to be used. Several versions of questionnaires specifically designed for diagnosing diseases induced by organic dust have been reported in the literature (Rylander, Peterson and Donham 1990; Schwartz et al. 1995). Lung function testing is also a useful tool for surveillance and diagnosis. Measurements of airway responsiveness have been found to be useful (Rylander and Bergström 1993; Carvalheiro et al. 1995). Other diagnostic tools such as measurements of inflammatory mediators or cell activity are still in the research phase.



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