Evaluating Beryllium Exposure Data
Referencing: Chronic Beryllium Disease and Sensitization at a Beryllium Processing Facility
We read with great interest "Chronic Beryllium Disease and Sensitization at a Beryllium Processing Facility" (Rosenman et al. 2005). We wish to offer some observations that will broaden the context in which this article is understood.
I agree with the statement by Rosenman et al. (2005) that a limitation of the study is the uncertainty of the exposure estimates. In addition, many statements appear to be unsupported by the data provided. For example, the statement that "most time-weighted averages were below the [Occupational Safety and Health Administration] OSHA (2005) standard of 2 µg/m3" (Rosenman et al. 2005) is unsupported by the data in the tables. Table 11 demonstrates that > 91% of the cohort had average daily weighted average (DWA) exposures > 2 µg/m3. Table 12 presents only the highest exposures and shows 56% of the cohort members having exposures > 2 µg/m3 and all but two cohort members exposed to > 0.2 µg/m3. Rosenman et al. (2005) did not explain how the average exposures of the cohort exceed 2 µg/m3 at a rate greater than the peak exposures. This same mysterious artifact of average exposures exceeding peak exposures is also present in Tables 9 and 10. The exposure-estimating process used by these authors could have introduced an erroneous bias in the data set, which causes me to question the "Discussion" and the conclusions drawn from the data.
One point, unstated by Rosenman et al. (2005), is that the DWA represented the daily exposure based on data averaged over 3 months. This is not the same as taking a single 8-hr air sample on 1 day because the 3-month averaging of the task data does not reveal the daily up and down variation in the individual task sample results. The National Institute for Occupational Safety and Health (NIOSH) has found DWAs not comparable to the lapel sampling method used by OSHA to determine compliance with its permissible exposure limit (PEL) or other 8-hr occupational exposure limits (OELs) (Donaldson and Stringer 1976). In addition, the average exposures presented by Rosenman et al. (2005) in their tables are the result of a second averaging by whole year and finally a third averaging by years of work. Such triple averaging further reduces the standard deviation in the data set, which results in a failure to identify the true high and low ranges of daily exposure. The American Industrial Hygiene Association (AIHA) exposure assessment guide (Mulhausen and Damiano 1998) cautions against ignoring air sample results that comprise the upper tail of an individual's exposure distribution, especially when comparing it to PELs and OELs.
The flame spectroscopy method of chemical analysis of beryllium used by Rosenman et al. (2005) during the data-collection period of this study had a detection limit of 0.1 µg/filter that translates to < 0.1 µg/m3 for any lower value. Therefore, Rosenman et al. (2005) cannot make any statements about exposures lower than this value.
Rosenman et al.'s (2005) description of missing and estimated data, the illogical peak versus average data results, the triple averaged DWA exposure estimates, and the limit of analytical detection of the sampling method all combine to make it likely that virtually all members of the study population experienced multiple days of exposure > 2 µg/m3, and hence the study cannot sustain conclusions about the degree of risk associated with lower levels of exposure. This conclusion is supported by the observation that the rates of chronic beryllium disease (CBD) and sensitization were constant across all the categories of exposure used by Rosenman et al. (2005).
Rosenman et al. (2005) made no recommendations regarding how to protect beryllium workers. We cannot change the past, but we can learn from it and change the future. There are two successful models of beryllium safety: one demonstrates effectiveness in preventing clinical CBD (Johnson et al. 2001), and one demonstrates prevention of beryllium sensitization (BeS) using the beryllium blood lymphocyte proliferation test as an index of BeS (Cummings K, unpublished data). Common to both models are a) organization and cleanliness of the workplace; b) control of the upper range of air level exposure using engineering and respiratory protection; c) control of beryllium migration from the work process to the worker, the work area, and outside the facility; d) detailed training of workers; and e) management and worker commitment to effective program implementation. In the facility studied by Rosenman et al. (2005), it is not clear that any of the above elements of a beryllium safety management plan were consistently accomplished. Although this is understandable, given prevalent scientific opinion at the time, going forward we should make every effort to effectively disseminate these demonstrated beryllium safety principles to the companies and workers using beryllium.
The author is employed by Brush Wellman Inc., a manufacturer of beryllium-containing products.
Marc Kolanz
Brush Wellman, Inc.
Cleveland, Ohio
E-mail: marc_kolanz@brushwellman.com
References
Donaldson HM, Stringer WT 1976. Beryllium Sampling Methods: Comparison of Personal Sample Collection Methods with the AEC Sample Collection Method as Used for One Year in a Beryllium Production Facility. Cincinatti, OH: National Institute for Occupational Safety and Health, Division of Surveillance, Hazard Evaluations and Field Studies.
Johnson JS, Foote K, McClean M, Cogbill G. 2001. Beryllium Exposure Control Program at the Cardiff Atomic Weapons Establishment in the United Kingdom. Appl Occup Environ Hyg 16(5):619-630.
Mulhausen JR, Damiano J, eds. 1998. A Strategy for Assessing and Managing Occupational Exposures. 2nd ed. Fairfax, VA:American Industrial Hygiene Association.
Rosenman K, Hertzberg V, Rice C, Reilly MJ, Aronchick J, Parker JE, et al. 2005. Chronic beryllium disease and sensitization at a beryllium processing facility. Environ Health Perspect 113:1366-1372.
Beryllium Exposure Data: Rosenman et al. Respond
We thank Kolanz for his careful reading of our article (Rosenman et al. 2005). An erratum correcting the problem he noted appears on page A214.
How do these corrected numbers change our results? More chronic beryllium disease (CBD) and sensitization occurred with exposure below the Occupational Safety and Health Administration (OSHA) permissible exposure limit (PEL) of 2 µg/m3 (OSHA 2005) than we previously reported, but no CBD or sensitization was found below the Department of Energy (DOE) guidelines of 0.2 µg/m3 (DOE 1999) or the even more protective level proposed by the American Conference of Governmental Industrial Hygienists (ACGIH 2005) of 0.02 µg/m3. There was an insufficient number of individuals--only three, and they were all normal--to assess the safety of the DOE guidelines or proposed ACGIH level. Our previously reported findings regarding chemical and physical form--that sensitized individuals compared with individuals with CBD had higher exposure to beryllium in a soluble form and to fumes of beryllium (Rosenman et al. 2005)--remain unchanged. However, the mean peak exposure for the sensitized group in our Table 8, the mean nonsoluble exposure for the sensitized group in Table 9, and the mean dust exposure for the sensitized group and mean fume exposure for the CBD group in Table 10 were no longer significantly different, whereas the peak fume exposure for the CBD group was now significantly different in Table 10.
Having acknowledged and corrected the error pointed out by Kolanz, we take strong exception to his statement that "the study cannot sustain conclusions about the degree of risk associated with lower levels of exposure," by which he means less than the OSHA PEL of 2 µg/m3 (OSHA 2005).
One of Kolanz's criticisms of our article (Rosenman et al. 2005) is that the daily weighted average (DWA) represented the daily exposure based on data averaged over 3 months. Breslin and Harris (1958) conducted a time study, which was updated as activities and location changed for each job title. During a 3-month period, three or more samples were collected and standardized to represent the general area where each person worked, and in some cases the breathing zone during work activities. The arithmetic average of the samples for each location/type was then calculated and weighted by time (Breslin and Harris 1958). Use of these summed weighted values, divided by the shift duration, is consistent with the American Industrial Hygiene Association (AIHA) exposure assessment guidance (Mulhausen and Damiano 1998) cited by Kolanz.
We agree with Kolanz's comment about the use of the flame spectroscopy method of chemical analysis and its general limit of detection of 0.1 µg/m3. In the job exposure matrix and task exposure matrix developed to support this project (Chen 2001), no exposure estimate was < 0.1 µg/m3, so this issue would have no effect on our results.
Kolanz also takes exception with our estimates of mean exposures, stating that these values were derived by triple averaging. We derived the mean exposures as follows: for a given worker in a given job in a given year, we multiplied the number of days worked in that year for that worker by our best estimated DWA for that job in that year. We then summed those values over all jobs for that worker to derive that worker's cumulative exposure. Next we divided that worker's cumulative exposure by the total number of days worked in his/her job history to derive that worker's mean exposure. Thus, there is only one averaging on each worker and a subsequent averaging for the population. We used multiple metrics (cumulative, average, peak job, and peak task for total exposure; exposure by chemical form; and exposure by physical form) to characterize not only the central tendencies of the exposures but also their extreme excursions.
We stand by our statement that
The inclusion of genetic data combined with exposure data may better define which individuals in this cohort are at a particularly high risk of development of CBD and/or sensitization and may account for the absence of typical exposure-response seen with other environmental or occupational toxins.
It is also important to note that both peak exposure and the different chemical and physical forms may be important factors in the risk of development of CBD but are not part of the current OSHA standard (OSHA 2005).
Finally, Kolanz states that "Rosenman et al. (2005) made no recommendations regarding how to protect beryllium workers." Clearly, however, our call to lower the allowable standard is a recommendation we put forth to protect beryllium workers. Despite the limitations of deriving historical exposure estimates, our corrected data continue to point to the inadequacy of the current OSHA standard to protect workers from developing chronic beryllium disease.
M.R. has served as an expert witness both for companies and for workers; he evaluates industrial patients with CBD, serves as the director of a beryllium test laboratory, and is a principal investigator with a grant from Los Alamos. The remaining authors declare they have no competing financial interests.
Kenneth Rosenman
Mary Jo Reilly
Michigan State University
East Lansing, Michigan
E-mail: Rosenman@msu.edu
Vicki Hertzberg
Emory University
Atlanta, Georgia
Carol Rice
University of Cincinnati
Cincinnati, Ohio
Milton Rossman
University of Pennsylvania
Philadelphia, Pennsylvania
References
ACGIH. 2005. Annual Reports of the Committees on TLVs and BEIs for Year 2004. Cincinnati, OH: American Conference of Governmental and Industrial Hygienists.
Breslin AJ, Harris WB. 1958. Health Protection in Beryllium Facilities: Summary of Ten Years of Experience. Washington, DC:U.S. Atomic Energy Commission.
Chen MJ. 2001. Development of Beryllium Exposure Metrics for Workers in a Former Beryllium Manufacturing Plant [PhD Thesis]. Cincinnati, OH:University of Cincinnati.
DOE (Department of Energy). 1999. Chronic beryllium disease prevention program: final rule. Fed Reg 64: 68853-68914.
Mulhausen JR, Damiano J, eds. 1998. A Strategy for Assessing and Managing Occupational Exposures. 2nd ed. Fairfax, VA:American Industrial Hygiene Association.
OSHA. 2005. Toxic and Hazardous Substances. 29CFR1910.1000, Table Z-1. Washington, DC: Occupational Safety and Health Administration.
Rosenman K, Hertzberg V, Rice C, Reilly MJ, Aronchick J, Parker JE, et al. 2005. Chronic beryllium disease and sensitization at a beryllium processing facility. Environ Health Perspect 113:1366-1372.