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Grain Dusts Grain dust, a complex and variable mixture of particles from plants, insects, soil, microorganisms, and other sources, produces a number of responses within the respiratory tract. These range from an acute inflammatory response (manifest as nasal stuffiness, rhinnorhea, sore throat, and acute bronchitis) to asthma, chronic obstructive pulmonary disease (including bronchitis and airways obstruction), and rarely, when grain has spoiled, hypersensitivity pneumonitis. An acute febrile response, the toxic organic dust syndrome (TODS), may occur with heavy exposure. Most of these responses are common among grain handlers who work with grain regularly, such as grain elevator workers or grain transporters; dusts are especially prevalent when grain is being moved. Farmers, who inhale grain dusts sporadically, appear to be affected less frequently and severely. Diagnosis, treatment and prevention of these respiratory responses depend on linking an individual's symptoms to the specific occupational exposure. Reduction of the exposure is crucial, and can be accomplished by good husbandry and housekeeping, good design and ventilation of storage structures, or removal of a grain handler to a less dusty work place. Early recognition of airways obstruction through medical surveillance will help prevent chronic respiratory illness among grain handlers. I. GRAIN DUSTS IN AGRICULTURE Dusts from grain consist of a complex mixture of organic and inorganic particles from sources as diverse as leaves, soil, and insect parts. (See Fig. 1) The mixture varies with the type of grain, where it is grown, growing conditions, and methods of harvest, storage, and processing. Most grain dust particles are biologically active vegetable dusts, and a significant amount are respirable (less than 10E-6m in diameter). Dusts of certain grains such as durum wheat and barley are reported to be more irritating than others. Adverse health effects also increase as moisture content and spoilage increase. The bulk of particles are from fruits of grasses such as wheat, legumes such as soybeans, or oil seeds such as rape seed. Bits of leaves and stems also may be present. Nonplant contaminants are numerous. Animal material (bits of insects, rodents, or birds, or their excreta), mites, chemical residues (pesticides used to grow or later treat the grain), and inorganic matter (soil including silica particles) all may be intermixed in small quantities. A variety of fungi and bacteria, their spores, and their by-products also pose a respiratory hazard. Species of microorganisms vary with regional climate and change from harvest through storage. In North America major fungi are Penicillium and Aspergillus species; thermophilic actinomycetes increase in wet and overheated grain. Many of the components of grain dust are capable of affecting the respiratory tract individually; together, they produce a heterogeneous array of biological effects as outlined in Section 11. Who is exposed to grain dust, and when? Anyone involved in production, storage, transportation, or processing of grain can suffer the effects of regular inhalation of grain dusts. Exposure starts with farmers and farm workers who grow, harvest, sometimes store, and then transport grain to local storage facilities. These farmers are exposed to grain dust sporadically. Exposure extends far beyond the farm to workers in feed mills, grain elevators, and grain transportation industries. (See Fig. 2) These workers, who are routinely exposed to grain dust, suffer from respiratory responses more commonly and severely than do farmers. Small grain elevator agents and workers store and clean grain, and may grind and mix it into animal feed. Other workers load and transport it by truck or rail to larger elevators, where it is handled by additional workers, and eventually to terminal elevators at harbors or milling centers that store millions of bushels of grain. Grain is then prepared by dock workers and longshoremen for transport abroad, or is processed by millworkers in feed, flour, or seed mills. This unit covers effects of grain dust inhalation detected among this great variety of agricultural workers, concentrating on the grain handlers who work with grain on a daily basis. Occupational asthma from processed grains is well documented, but effects of flour dust and other processed grain products among bakers and food handlers are not discussed here. Exposure to grain dusts can occur at any stage of the above process. Clouds of grain dusts are most evident whenever grain is moved, and especially heavy exposures among any grain handlers occur during dumping and loading grain.(See Fig. 3) In elevators, highest total dust exposures occur during performance of housekeeping and maintenance chores and in towermen working in transfer galleries. How common is exposure to grain dust? Grain dust potentially affects a large population: an estimated half million workers (including farmers) are involved is storage, transportation, and processing of grain. In addition, huge quantities of dust are known to be generated by the grain industry, making the grain industry a major source of industrial pollution: 27 pounds of dust are emitted for every ton of grain handled, resulting in 1.7 million tons of grain dust produced per year. The concentration of particles varies widely, but may reach very high levels. Measurements in elevators have ranged from 0.18 to 781 mg/m3 of total dust, with the respirable range extending up to 76.3 mg/m3. Airborne concentrations of fungal spores often exceed one million spores per cubic meter. Agricultural workers clearly may be exposed to large quantities of dust. The prevalence of resulting respiratory responses is less well defined. Although prevalence of respiratory responses to grain dust varies from study to study, the presence of cough and phlegm, indicators of bronchitis, are consistently high, generally about twice that of nonexposed populations. Studies also find evidence of airways obstruction and chronic lung disease among greater-than-expected numbers of workers. Prevalence rates are thought to be higher than those documented, since studies are completed on "survivor populations", those who have not vacated because of adverse effects of grain dust; this is especially common among those with allergic reactions to grain dust. The variation in prevalence of disease probably stems from the heterogeneous nature of grain dust, as well as from variations in study populations and research techniques. II. RESPIRATORY EFFECTS OF GRAIN DUST INHALATION Grain dust reactions represent multiple and simultaneous potential reactions to multiple causative agents. The many reactions and causative agents may create a complex clinical presentation that at times confounds specific diagnosis, causes physicians to describe health effects in general terms, and makes predictions of future health problems difficult. Further confusing diagnosis is the fact that a single biological response may be caused by different types of grain dust, and a single type of grain dust may cause different types of reactions. In addition, multiple pulmonary responses may occur simultaneously, with involvement of immunological, pharmacological, or physical responses, or a combination of these. Since dust particles range from over 20 microns to less than 5 microns in diameter, they can initiate responses in large and small airways or penetrate the alveoli to initiate biological effects there. Responses may be influenced by smoking history and by length and type of employment in grain handling. Thus, a specific response often cannot be identified with a specific type of grain dust or specific agent within the dust. Although mechanisms of many of the respiratory responses have not been fully defined, a distinct set of acute and chronic health effects have been correlated with occupational handling of grain. The biological responses to grain dust are summarized in Table 1. Links between these responses and specific constituents of grain dust are outlined in Table 2. These tables and the following descriptions concentrate on responses of workers routinely exposed to grain dusts, as opposed to farmers or others exposed occasionally. Inhalation of grain dusts may cause an acute inflammatory reaction of the upper airways, including the nasal mucosa, sinuses, and pharynx, manifest in many cases as nasal stuffiness, sore throat, or rhinnorhea. This nuisance effect of grain dusts is a complaint of nearly all grain workers. Table 1 Biological Effects Effect Prevalence Among Grain Handlers Acute respiratory inflammatory rhinnorhea, sore throat quite common acute bronchitis common Occupational asthma common Chronic obstructive pulmonary chronic bronchitis common airways obstruction occasional to common Toxic organic dust syndrome Hypersensitivity pneumonitis very rare; potentially results
from exposure to spoiled grain
Additional irritant effects: eye irritation extremely common dermatitis occasional to common Deaths from explosions rare PLEASE NOTE: THE FOLLOWING TABLE IS WIDER THAN THE SCREEN. USE THE RIGHT ARROW KEY TO VIEW THE RIGHT SIDE OF THE TABLE. TO
PRINT THE ENTIRE TABLE YOU MUST FIRST EXPORT THE TABLE
AND USE A WORD PROCESSOR OUTSIDE THE RETRIEVAL SYSTEM.
Table 2 Biological Effects of Specific Constituents of Grain Dust bacterial and
fungal matter
including animal matter inorganic mat-
grain, spores and by- including ter including
plant matter products mites soil
Acute respiratory throat X ? ש acute bronchitis X Occupational asthma: ש immunological X X X ש nonimmunological X X X Chronic obstructive pulmonary ש chronic bronchitis X ? ? ש airways obstruction X ? Toxic organic dust syndrome (TODS) X X Hypersensitivity pneumonitis (spoil- X ed grain only) Additional irritant effects: ש eye irritation X ש dermatitis X X "Grain asthma", a form of occupational asthma producing bronchoconstriction with cough, wheezing, and dyspnea, may immediately follow exposure, be delayed several hours, include a dual (immediate and delayed) response, or recur successive nights following exposure. The asthmatic reaction may be caused by any number of grain dust components, but the mechanism for producing the response is not always clear. It is now recognized that delayed asthma (IgG-mediated) may be induced in addition to the classical IgE-mediated immediate response, and that asthma also may be induced through physical or pharmacological mechanisms. The prevalence of grain asthma is thought to be artificially low because persons with asthma allergies either do not seek employment as grain handlers or leave this employment rapidly because of an increase in asthmatic symptoms. However, the prevalence of occupational asthma has been reported to be five times that of workers in other professions [50% (grain handlers) rather than 11% (others) among nonsmokers]. Many complaints associated with grain dust fall into the category of chronic obstructive pulmonary disease. Bronchitis, characterized by chronic cough and phlegm production, is the most consistent response induced by grain dust. Chronic exposure to grain dusts is thought to lead to increased bronchial reactivity and chronic bronchitis, either with or without airways obstruction.Loss of lung function is greater among grain handlers than that expected for a comparable group not handling grain, but of the same age. At first airflow obstruction (measured by decreased forced expiratory volumes, or FEV,) is observed during work but is reversible, improving when the grain handler is not at work. With repeated exposure, this obstruction may become chronic. There is also evidence that workers who have an acute response to grain dust (decline in lung function over a work shift) are more likely to have accelerated baseline declines in lung function over time. While bronchitis and airways obstruction are common among nonsmoking grain handlers, these are more common among grain handlers who smoke cigarettes. It is thought that cigarette smoke and grain dust work additively, accelerating changes in the peripheral airways so the respiratory symptoms occur sooner, or at a younger age, and are more frequent and severe. There is some evidence that cigarette smoke and grain dust may act synergistically in decreasing expiratory flow rates. An acute systemic reaction may result from inhalation of grain dusts. The toxic organic dust syndrome (TODS, commonly referred to as "grain fever") is characterized by chills, fever, flushed face, myalgia, and malaise, sometimes with cough, wheezing, and shortness of breath. The illness typically occurs in new workers, or commences following heavy exposure in a worker who has been temporarily removed from grain dust such as on a Monday following vacation. Symptoms typically commence after work, and may last several hours or a few days. Some researchers feel that this is a response to inhalation of endotoxins.'ר A similar syndrome (sometimes called pulmonary mycotoxicosis, atypical farmer's lung, or silo unloader's syndrome) is caused by spoiled grain or silage containing high concentrations of fungal and bacterial spores and by-products, and is seen among farmers. Malaise, myalgia, and chills typically commence a few hours after exposure. This biological response is described in depth in Unit 2. A few cases of hypersensitivity pneumonitis (See Unit 2) have been reported following exposure to moldy or contaminated grain. Grains stored in elevators are commonly fumigated. Fumigants inhaled either during the fumigation process or from residues immediately after grain is removed from storage can be lethal. Respiratory effects of fumigants are discussed in Unit 6. In addition to reactions of the respiratory system, grain dust can produce dermatitis and conjunctivitis among workers. Explosions of high concentrations of grain dusts have killed many grain elevator employees, and continue to pose a potentially severe Diagnosis Because of the complexity of causative agents and potential biological responses, each patient's reaction to grain dust inhalation varies. Diagnosis depends on a thorough occupational history documenting type and time of exposure, and correlating these to onset of symptoms. Workers in grain elevators, feed mills, or grain transportation industries may experience any of the responses listed in Table 2 (excluding hypersensitivity pneumonitis) fairly commonly. Farmers who are not routinely exposed to grain dust might experience acute inflammatory responses or TODS, especially when exposed to massive quantities of bacterial or fungal-laden dusts, such as when shoveling moldy grain or working with spoiled corn silage in an enclosure. (See Fig. 4) Exposure to grain dusts also could trigger asthma or hypersensitivity pneumonitis in a sensitized farmer. Onset of chronic obstructive pulmonary disease in a farmer would probably result from multiple occupational exposures, one of which could be exposure to grain dust. Diagnostic tests for occupational asthma include pulmonary function tests, in particular assessment of FEV(1) or peak flow rates before and after work. Skin tests usually are not useful; reactions to grain dust usually cannot be linked to a specific dust component. Diagnosis of chronic obstructive pulmonary disease is dependent on assessment of respiratory symptoms, lung function (typically, an obstructive pattern is detected), and chest radiographs. Chest radiographs typically reveal nonspecific signs of airways obstruction, and are useful for excluding other pulmonary diseases. The importance of monitoring grain industry and agricultural workers for early onset of chronic obstructive pulmonary disease cannot be overemphasized. Spirometry should be performed annually to document changes in lung function, especially when workers are symptomatic. Diagnosis of TODS or "grain fever," which is common among grain industry workers, depends on presentation with appropriate symptoms and signs following a known exposure to grain dust. Individuals usually lack serum precipitins to antigens of spoiled grain, have normal pulmonary functions, and usually have a clear chest radiograph. A similar syndrome seen among farmers is characterized by massive exposure to bacterial.and fungal-laden dusts from spoiled grain or silage. Diagnosis of hypersensitivity pneumonitis and distinctions of acute hypersensitivity pneumonitis and TODS are described in depth in Unit 2. Treatment The major thrust of any treatment program among both grain industry workers and farmers should be to control exposure sources. This is critical to prevent repeated episodes of acute responses, and (in the case of chronic obstructive pulmonary disease and hypersensitivity pneumonitis) to prevent permanent damage, disability, and possibly death. Grain industry workers with occupational asthma, progressive chronic obstructive pulmonary disease, or hypersensitivity pneumonitis should be relocated to low or no-exposure areas. Farmers with these illnesses often can alter work practices to prevent exposure; treatment procedures and the dramatic steps taken by some farmers with hypersensitivity pneumonitis are outlined in Unit 2. Use of personal protective equipment, medical surveillance, and other preventive steps are discussed in the following section. No specific treatment is required for either acute inflammatory responses or TODS. Both are self-limiting. Medication for patients with occupational asthma is similar to that for other asthmatics, but should be combined with job changes to reduce exposure to grain dusts. Desensitization is not helpful. Both smoking cessation and decreased exposure are critical to patients with chronic obstructive pulmonary disease; bronchodilators or antibiotics should be given as indicated. III. PREVENTION OF GRAIN DUST INDUCED ILLNESS As with any occupational disease, prevention rests primarily on reducing exposure to the source of illness. Because of the threat of grain dust explosions, attempts to reduce dust levels in grain elevators have been made since the turn of the century. More recent controls on the farm include structural improvements such as combines or tractor cabs with filtered air. In newer grain elevators, totally enclosed conveyor belts, dust collectors, and good ventilation systems have greatly reduced dust. These improvements are lacking on older farm equipment and in older or smaller rural elevators. Adding them, while desirable, is both costly and difficult. Thus, farmers and other grain handlers should be taught the hazards of grain dust inhalation, and techniques for decreasing these hazards based on good husbandry techniques in growing, harvesting, and storing the grain, and on good housekeeping and work practices in elevators. Complete drying of grain is crucial to reduce spoilage and resulting bacterial and fungal spores and toxins. Fumigating the grain also will help. Grain placed in storage should always be top quality, with insect and animal contamination kept to a minimum. When grain dust levels are above 10 mg/m3, or when workers are especially sensitive, personal protective equipment (a certified dust mask, see Unit 9) should be used. Because exposure to grain dust cannot be fully controlled, medical
surveillance must be a second major component of any preventive program. New
workers of a grain handling business should have a preemployment examination
that includes an occupational and medical history, physical examination, and
spirometry. Anyone who demonstrates respiratory symptoms or disease, pulmonary
function abnormalities, or evidence of airways obstruction should ideally be
placed in a job where less exposure to dusts will occur. Regular medical
workups, which include lung function tests performed as close as possible to the
place of employment, will allow detection of developing airflow obstruction
while it is still reversible. Inquiries should be made into the cause of
absenteeism and complaint of respiratory or other grain dust-related symptoms.
Workers who develop airflow obstruction or significant respiratory symptoms
should transfer to low dust jobs. Reduction of dust inhalation through use of a
respirator may be possible for some workers. Because of the apparent additive
effect of smoking and grain dust, smoking cessation programs should be
recommended for anyone in regular contact with grain dust. Medical evaluation
also should address nonrespiratory effects of grain dust exposure, such as skin
rash and eye irritation. תתתתתתתתתתתתתתתתתתתתThe National Dairy Database (1992)תתתתתתתתתתתתתתתתתתתת תתתתתתתתתתתתתתתתתתתתת\NDB\OCCSAFE\TEXT2\OF200600.TXTתתתתתתתתתתתתתתתתתתתתתת %f TITLE;GRAIN DUSTS |
