Skip directly to local search Skip directly to A to Z list Skip directly to navigation Skip directly to site content Skip directly to page options
CDC Home

GRAIN DUST (OAT

OSHA comments from the January 19, 1989 Final Rule on Air Contaminants Project extracted from 54FR2332 et. seq. This rule was remanded by the U.S. Circuit Court of Appeals and the limits are not currently in force.

CAS: None; Chemical Formula: None

A decision by the Occupational Safety and Health Review Commission (Secretary of Labor v. Krause Milling Company, OSAHRC Docket No. 78-2307, April 22, 1986) has held that there was no former OSHA PEL for grain dust. Based on the ACGIH recommendation, OSHA proposed to establish a 4 mg/m3 8-hour TWA PEL for dust generated from wheat, oats, and barley, and NIOSH (Ex. 8-47, Table N1) supported the proposal. However, in the final rule the Agency is establishing an 8-hour TWA limit of 10 mg/m3 for these dusts. Grain dust is a complex mixture of husk particles, cellulose hairs and spikes, starch granules, spores of fungi, insect debris, pollens, rat hair, and approximately 5 percent mineral particles. The mean particle size of the airborne dusts may be less than 5 um. A substantial amount of information was submitted to the record addressing the health evidence and feasibility of attaining a 4 mg/m3 TWA limit in the feed industry (Exs. 3-751, 3-752, 3-755, 8-55, 104, 109, 118, 180, 185, and 198; Tr. pp. 6-247 to 6-319). OSHA has carefully reviewed this evidence and has determined that an exposure limit for grain dust is necessary to reduce the significant risk of adverse respiratory effects associated with exposure to this material. OSHA's review of the health evidence, described below, shows that grain workers will experience adverse respiratory symptoms upon exposure to grain dust levels exceeding the current nuisance dust limit of 15 mg/m3 TWA; this observation was not disputed in the record. Respiratory symptoms are also prevalent among grain dust workers exposed to levels below 10 mg/m3 TWA, as total dust, although these symptoms are diminished compared with those associated with exposure to higher dust levels. Because of uncertainties in establishing a clear threshold exposure level for respiratory effects and in determining the feasibility of the proposed 4 mg/m3 limit (see Section VII, Summary Economic Impact and Regulatory Flexibility Analysis), OSHA is establishing a 10 mg/m3 limit as an 8-hour TWA for wheat, oat, and barley dust to reduce the risk of respiratory disease.

The adverse effects of inhaling grain dust have been known for at least two-and-one-half centuries, dating back to Rammazini who, in 1713, described the respiratory hazards associated with exposure to cereal grain dust. More recently, several epidemiological studies conducted over the past few decades (cited by ACGIH 1986/Ex. 1-3 and Rankin et al. 1986) have demonstrated that exposure to grain dust causes "grain fever," wheezing, chest tightness, productive cough, eye and nasal irritation, and symptoms of chronic respiratory disease. Grain dust may also induce asthmatic reactions via an allergic mechanism, particularly in individuals who are predisposed to developing allergies (i.e., atopic individuals). Thus, OSHA believes that the need for an occupational limit on exposure to grain dust is clear.

The basis for OSHA's proposed 4 mg/m3 limit was a NIOSH-sponsored study of grain workers by Rankin et al. (Study of the Prevalence of Chronic, Non-Specific Lung Disease and Related Health Problems in the Grain Handling Industry, DHHS (NIOSH) Pub. No. 86-117, 1986). A 1980 draft of this study by Rankin and do Pico (Ex. 1-1193) formed the basis for the ACGIH-recommended limit of 4 mg/m3 TWA. This study evaluated the health status of 310 grain handlers in Wisconsin and Minnesota. The grain handlers were selected from eight elevator companies, from state grain inspection agencies, and from longshoring companies. Health status was determined by questionnaire and by physical examination, which included an assessment of pulmonary function, immunologic evaluation, blood and urine chemistries, and chest roentgenograms. The comparison group that served as controls consisted of 239 city workers who spent the majority of their workdays outside.

From the questionnaires, Rankin et al. (1986) found that the grain handlers had a higher prevalence of respiratory symptoms than did the city workers. The prevalence of respiratory symptoms was highly significant (Rankin et al. 1986, Table 13), and was independent of smoking status. The symptoms reported by grain handlers represented both acute and chronic airways reactions (occupational asthma and chronic bronchitis). Wheezing and/or chest tightness generally started within two hours of beginning the work shift. Episodes of grain fever occurred infrequently; this was attributed by the workers to improved working conditions over the previous three years. Acute recurrent conjunctivitis and rhinitis were reported to occur among most grain workers.

Lung function tests showed that exposure to grain dust had a highly significant adverse effect on pulmonary function (Rankin et al. 1986, Table 30). There was, however, no correlation between reduced pulmonary function and job category, length of employment, or place of work. The lung function decrement observed among grain handlers was not related to smoking history alone; grain handlers who were smokers or ex-smokers showed significant declines in pulmonary function when compared to city workers who were smokers or ex-smokers.

Grain workers who reported symptoms had lower values of ventilatory function than did workers without symptoms. The prevalence of chronic bronchitis symptoms with measured airways obstruction was higher in grain workers than in controls, regardless of smoking history. Chronic bronchitis with airways obstruction was also related to length of employment. Rankin et al. (1986) concluded that these findings "suggest that chronic grain dust exposure may result in chronic obstructive pulmonary disease" (p. 26).

Rankin et al.'s (1986) study also included a work-shift study in which 248 grain workers and 192 city workers were sampled for grain dust exposure during a work shift. Symptoms occurring during the shift were recorded and pulmonary function readings were taken before and after the shift. Only 14 percent of grain workers were exposed to an 8-hour TWA level exceeding 5 mg/m3 total grain dust; 7 percent were exposed above 10 mg/m3. Rankin et al. (1986) reported that grain workers showed a significant excess of cough and expectoration during a work shift in which dust concentrations were below 5 mg/m3. At dust levels between 10 and 15 mg/m3, there was a significantly increased prevalence of wheezing and dyspnea during the shift among grain workers as compared with controls (Rankin et al. 1986, Table II-156). Workers with pre-existing airways obstruction experienced significant pre- to post-shift declines in ventilatory function at dust levels below 10 mg/m3. However, the changes observed in pre- to post-shift pulmonary function did not correlate with the presence of symptoms during the shift.

Rankin et al. (1986) also conducted a short-term (three-year) follow-up study of lung function among grain workers. Their results showed no greater declines in FEV or FVC over the three-year period than could be accounted for by age alone. However, there was a significant decline in other measures of lung function (MMF, Vmax50, Vmax75) among both smoking and nonsmoking grain workers. The authors concluded that, although a grain-dust-related decline in these measures was observed, the long-term effects of smoking on lung function were probably greater than those caused by grain dust.

The ACGIH (1986/Ex. 1-3) recommended the 4 mg/m3 TLV based largely on the following conclusion by Rankin et al. (1986):

    The incidence of respiratory symptoms was higher among grain workers exposed to mean total airborne dust (time-weighted average concentration) of 13.9 mg/m3 when compared to grain workers exposed to 4 mg/m3 or less. In the latter group of grain workers the incidence of symptoms was similar to that found among controls (Rankin et al. 1986, p. 51).

This conclusion by Rankin et al. (1986) was derived by correlating the incidence of respiratory symptoms with workers' subjective estimations of dust levels encountered during the work-shift study; workers who judged their dust exposures during the shift to be "more than average" were exposed to mean dust levels of 13.9 + 12 mg/m3 TWA and had significantly higher incidences of respiratory symptoms than did workers who judged their exposures to be "average" (mean TWA dust exposures of 4 + 8.6 mg/m3). From this observation, the ACGIH (1986/Ex. 1-3) interpreted 4 mg/m3 to be a no-observed-effect level.

This interpretation of Rankin et al.'s (1986) results was heavily criticized by rulemaking participants. For example, the National Grain and Feed Association (NGFA) (Ex. 8-55) argued:

    OSHA states that the study found that acute bronchial symptoms did not appear among workers exposed at or below 4 mg/m3. This figure is in fact an average estimated exposure of 4.21 + 8.62 mg/m3 and...was based on workers' arbitrary interpretation[s] of 'average' exposure. The researchers grossly overstated their results by implying that a specific level of 4 mg/m3 was an absolute limit below which the incidence of symptoms among workers was similar to [that among] controls (Ex. 8-55, p. 28).

Although it is true that reliance on employees' subjective impressions of the magnitude of dust exposure during a shift is not as precise as taking quantitative samples of dust exposure, it must be emphasized that Rankin et al. (1986) did find a significant excess of respiratory symptoms among grain workers whose TWA exposures were objectively determined, by air sampling, to be less than or equal to 10 mg/m3 TWA; an excess incidence of wheezing and dyspnea were also reported among grain workers exposed to levels of between 10 and 15 mg/m3 TWA.

The NGFA also criticized the Rankin et al. (1986) study for failing to address potential biases in the design and administration of the health questionnaire (Ex. 8-55, p. 25). In Appendix C of its submission, the NGFA cites a discussion of questionnaire biases by Gamble and Battigelli (in Patty's Industrial Hygiene and Toxicology, 3rd rev. ed., vol. 1, pp. 129-32, Clayton and Clayton 1981) and states that questionnaires provide a large source of error that must be guarded against," particularly when the questionnaire is self-administered (Ex. 8-55, Appendix C, pp. 3-4). OSHA believes that, although such biases are possible, Rankin et al. (1986) took measures to reduce such biases. First, their study population derives from many workplaces, including eight grain elevators, state grain inspection agencies, and longshoring companies; it thus appears unlikely that the overall results obtained from the questionnaires would be substantially biased as a result of employee dissatisfaction with the working conditions of a particular worksite. Second, Rankin et al. (1986) did rely on trained interviewers to review all questionnaires for completeness and to assist in the completion of a questionnaire when necessary. The use of trained interviewers, according to Gamble and Battigelli (Ex. 8-55, Appendix C, p. 3), may correct such biases. In addition, Rankin et al. (1986) found a correlation between symptoms reported on questionnaires and exposure levels, which suggests that the questionnaire results were not heavily biased.

Despite some of the criticisms of the Rankin et al. (1986) study, these authors' results are consistent with some other published studies of grain workers. Dr. Roy Buchan, Chief of the Occupational Health and Safety Section, College of Veterinary Medicine and Biomedical Sciences at Colorado State University, performed a study of the general health of 31 grain handlers (submitted as part of Ex. 3-751). A total of 204 personal TWA dust samples were taken, of which only six exceeded 10 mg/m3. Dr. Buchan found that neither age of facility, smoking history, nor past exposure to grain dust had any significant effect on symptom responses. There was a statistically significant association between grain dust exposure levels and symptom responses. The reported symptoms included nasal and throat irritation, chest discomfort, and phlegm production. Dr. Buchan concluded that, "although the association was mathematically weak but statistically significant, it would rationally be expected that symptom severity would become more pronounced as dust concentrations increase, since dust exposures in this investigation were surprisingly low (mean = 0.7 mg/m3 TWA)." In a larger study of 390 Canadian grain workers, Cotton , Graham, Li et al. (1983, submitted as part of Ex. 3-751) also reported a significant excess incidence of respiratory symptoms among grain workers despite total dust concentrations generally below 10 mg/m3.

Although these studies show a consistent pattern of increased prevalence of respiratory symptoms among grain handlers exposed below 10 mg/m3, the association between low-level exposure to grain dust and the development of chronic pulmonary disease remains open to interpretation. Several studies, including Rankin et al. (1986), Chan-Yeung, Giclas, and Henson (1980/Ex. 1-474), and Broder, Corey, Davies et al. (1985, as cited in Ex. 3-751) have generally not found decrements in pulmonary function associated with long-term exposure to grain dust. In addition, chest roentgenograms have found no evidence of lung scarring or fibrosis (Rankin et al. 1986) among grain handlers. However, symptoms of chronic bronchitis have been frequently noted among grain handlers, including those who have never smoked (Rankin et al. 1986; Cotton, Graham, Li et al. 1983). According to Cotton et al. (1983, as cited in Ex. 3-751, p. 139), "The significance of the increase in chronic bronchitis and cough in workers and wheezing in nonsmoking workers in terms of eventual respiratory disability remains uncertain but the nuisance and discomfort of these symptoms for workers must also be considered."

Because of the conflicting evidence for an association between exposure to grain dust and the development of chronic lung damage, the NGFA (Exs. 8-55 and 180) and the American Feed Industry Association (AFIA) (Ex. 185) take the position that grain dust has been shown to be a nuisance dust. For example, in its posthearing brief, the AFIA stated:

    [F]eed industry workers are generally healthy, and experience no unique adverse health effects resulting from current levels of grain dust exposure. Therefore, setting a PEL for grain dust is unwarranted and unnecessary. The studies relied on by OSHA...fail to show that grain dust, at current levels, is a "harmful physical agent"....Granted, grain dust may have some effect on some individuals' health; however, nothing in the record demonstrates that these effects, at typical current levels, are anything more than reversible and non-serious (Ex. 180, p. 14).
OSHA does not concur with this view. In the studies described above, as well as in others in the record, grain workers have consistently reported an excess prevalence of respiratory symptoms, including chronic bronchitis, at low levels of exposure to grain dust. OSHA believes that these symptoms, even in the absence of definitive evidence of irreversible lung damage, constitute material impairment of health and interfere with the well-being of workers. This was attested to at the informal hearing by Deborah Berkowitz, Director of Safety and Health for the Food and Allied Trades Department, AFL-CIO:

    I want to make it clear that study after study documents a very real acute hazard to grain workers. Living with chronic bronchitis is not a hazard that should go unchecked. In fact, study after study point to the possibility of very real long-term damage from chronic cumulative effects of exposure to grain dust. But even without the possibility of long-term disability, acute hazards clearly pose significant risk[s] to workers (Tr. pp. 6-306 to 6-307)

OSHA concludes that employees are placed at significant risk of respiratory symptoms, including chronic bronchitis, as a result of exposure to grain dust. It is clear that such symptoms occur at grain dust levels exceeding OSHA's former limit for dusts and particulates (15 mg/m3 TWA); in addition, workers have reported symptoms of wheezing and dyspnea upon exposure to dust levels between 10 and 15 mg/m3 TWA. Increases in respiratory symptoms have also been reported to occur among grain workers exposed generally to less than 10 mg/m3, although symptoms are diminished at these lower levels. At this time, it is difficult to identify the threshold at which adverse respiratory effects are likely to occur. This uncertainty is reflected in a posthearing submission by the NGFA (Ex. 118) in which Dr. George Bardwell of the University of Denver performed a statistical analysis of the FEV measurements reported by Chan-Yeung, Giclas, and Henson (1980/Ex. 1-474) in grain workers. Dr. Bardwell estimated that the threshold for reduced FEV is 6.41 mg/m3, with a 95-percent confidence interval of between 0 and 24.4 mg/m3.

In addition, considerable information was entered into the record addressing the technological feasibility of achieving the proposed 4 mg/m3 grain dust PEL (Exs. 3-751, 3-752, 3-755, 8-55, 109, 118, 180, 185, and 198). These data are conflicting, particularly with regard to smaller grain elevators. In light of these uncertainties, OSHA is establishing a 10 mg/m3 8-hour TWA limit for grain dust, measured as total dust. OSHA finds that establishing this limit will substantially reduce the risk of adverse respiratory effects that occur at higher levels of exposure. OSHA has also concluded that a 10 mg/m3 TWA limit is technologically feasible (see Section VII).

The American Feed Industry Association (Ex. 185) objected to OSHA's inclusion of oat and barley dust in the definition of grain dust, stating that the studies relied on by OSHA in the NPRM pertaining to oat and barley dust (Darke, Knowelden, Lacey, and Ward 1976; Cockcroft et al. 1983) were not relevant to addressing the effects of exposure to oat and barley dust at levels below 15 mg/m3. However, Rankin et al. (1986) reported in their study, which involved exposure to much lower levels of grain dust, that the types of dust most likely to bring on or aggravate symptoms of cough and/or expectoration were durum wheat and barley, followed by spring wheat, rye, and oat. Least likely were corn, soybean, sunflower, and others. In addition, Mr. George Talley and Mr. Michael Garcia, industrial hygienists at Los Alamos National Laboratory, commented that, according to their personal experience, barley beards are more irritating than wheat dust (Ex. 3-1095). Therefore, OSHA finds that there is sufficient evidence to include oat and barley in the definition of grain dust.

At the informal hearing, Ms. Berkowitz raised the question as to whether OSHA intended to apply the grain dust limit to flour mills and bakeries (Tr. 6-310). To support this position, she submitted several reports describing asthma occurring among bakers; bakers' asthma has been attributed to flour dust exposure (Ex. 3-751). As with all other substances included in this rulemaking, OSHA intends the new limit for grain dust to apply to all workplaces, including flour mills and bakeries where there is the potential for exposure to grain dust.

In the final rule, OSHA is establishing an 8-hour TWA limit of 10 mg/m3 for grain dust, measured as total dust. Grain dusts other than oat, wheat, and barley are regulated under OSHA's generic "particulates not otherwise regulated" PEL of 15 mg/m3 (total particulate) and 5 mg/m3 (respirable fraction). The Agency concludes that this limit will substantially reduce the significant risk of acute and chronic respiratory symptoms and disease associated with exposure to grain dust at the levels formerly permitted by the absence of an OSHA limit. The Agency has determined that the respiratory effects caused by exposure to grain dust represent material impairments of health.

 

 
Contact Us:
USA.gov: The U.S. Government's Official Web PortalDepartment of Health and Human Services
Centers for Disease Control and Prevention   1600 Clifton Rd. Atlanta, GA 30333, USA
800-CDC-INFO (800-232-4636) TTY: (888) 232-6348 - Contact CDC–INFO