Advisory Board on Toxic Substances and Worker Health

Recommendations – Adopted at April 18-20, 2017 Meeting

Recommendations

1. Presumptions for Asbestos-related Diseases p. 2

2. Presumptions for Work-Related Asthma p. 6

3. Presumptions for Chronic Obstructive Pulmonary Disease p. 9

4. Revisions of Occupational History Questionnaire p. 13

5. Science and Technical Capacity of EEOICP p. 17

6. Interpretation of the Beryllium Lymphocyte Proliferation Test p. 18

7. Quality Assessment of Contract Medical Consultants p. 19

Attachment 1

Attachment 2
2

Recommendation #1

Presumptions for Asbestos-related Diseases

1. All DOE workers who worked as a maintenance or construction worker at a DOE site for 

250 days or more prior to January 1, 2005 and who are diagnosed 15 years or more after 

the initiation of such work with 1 of 5 asbestos-associated conditions will be presumed to 

have had sufficient asbestos exposure that it was at least as likely as not that asbestos 

exposure was a significant factor in aggravating, contributing to, or causing such 

asbestos-associated conditions. The five asbestos-associated conditions are asbestosis, 

asbestos-related pleural disease, lung cancer, and cancer of ovary and larynx. 

2. All DOE workers who worked as a maintenance or construction worker at a DOE site for 

30 days or more and who are diagnosed 15 years or more after the onset of such work 

with malignant mesothelioma of any bodily site will be presumed to have had sufficient 

asbestos exposure that it was at least as likely as not that asbestos exposure was a 

significant factor in aggravating, contributing to or causing the malignant mesothelioma. 

3. All claims for one of the six asbestos-associated conditions named above that do not meet 

the exposure criteria described in items #1 and #2 above will be referred to an industrial 

hygienist for exposure assessment and to a CMC for evaluation of medical 

documentation and causation. These six conditions are asbestosis, asbestos-related 

pleural disease, malignant mesothelioma, lung cancer, and cancer of ovary and larynx.

4. Chronic obstructive pulmonary disease may have a contribution from asbestos exposure. 

However, claims for this disease should be evaluated as part of a broader set of 

presumptions for chronic obstructive pulmonary disease.

Exposure 

criteria

Asbestosspecific 

Diseases

Mesothelioma

Asbestosspecific 

diseases 

Asbestosis,

Asbestosrelated pleural 

disease

Other Asbestos-related 

Cancers

Lung cancer, 

Cancer of ovary 

and larynx

Duration > 30 days > 250 days > 250 days

Job titles

Maintenance

Construction

Maintenance

Construction

Maintenance

Construction

Calendar 

years

Pre-2005 Pre-2005 Pre-2005

Latency

(minimum)

15 years 15 years 15 years
3

Rationale

The Departments of Labor and Energy recognize that asbestos was used extensively 

throughout the Departments of Energy (DOE) complex. The DOE Former Worker 

Program has documented that 11.9% of 78,894 DOE workers screened between 1998 and 

2016 had chest x-ray evidence of non-malignant asbestos-related lung disease, including 

asbestosis and asbestos-related pleural disease (DOE Former Worker Program Annual 

Report, 2016). The prevalence of non-malignant asbestos-related lung disease varied 

considerably, as low as 4% to 5% at some DOE sites or up to one-quarter to one-third of 

production and construction workers, respectively, at other sites (DOE FWP Report). 

Recent published studies showed excess lung cancer, malignant mesothelioma (an 

asbestos-specific cancer), and asbestosis among DOE construction workers (Dement 

2009; Ringen 2015). Additional published studies at DOE sites show excess lung cancer 

among sub-populations of the work force (Frome 1997; Richardson 1999; Silver 2013; 

Figgs 2013).

Asbestos was used in over 3,000 products during the period when it was commonly 

manufactured in the United States, 1940’s to 1980’s. Some of its uses are wellrecognized, including thermal insulation products, boards, textiles, friction products and 

cement. Other uses are less obvious, including laboratory counter tops, protective pads, 

filters, and others. Due to its frequency and sometimes occult nature of its use, proper 

investigation of a claim for any of the asbestos-related diseases, if consensus exposure 

presumptions are not met, requires a detailed occupational history and evaluation by 

occupational health professionals with substantial knowledge of the asbestos exposure 

and related diseases. 

There is a well-established medical literature documenting non-malignant and malignant 

asbestos-related diseases among construction workers and industrial and commercial 

maintenance workers in the United States. The asbestos-related disease experience 

among such workers at Department of Energy sites, thus, matches a much more 

comprehensive experience with general industry, which provides confidence in setting 

the recommended exposure presumptions based on the broad occupational groups (i.e., 

maintenance and construction) elaborated above. 

Asbestos-related diseases generally increase in frequency with increasing exposure to 

asbestos (Algrante 2016; Markowitz 2016). As such, setting a specific period of 

exposure (e.g., 250 days) is approximate but reasonable for the purpose of setting an 

exposure presumption. It should not be construed as representing a precise limit 

separating those with risk from those without risk. It accords with the underlying 

scientific knowledge and represents a practical element for application of a set of 

presumptions to claims evaluation. Recommending such a time limit should not be 

construed as signifying that asbestos exposure for less than the specified time period is 

without risk. For claims with asbestos exposure less than the recommended period, 

evaluation of a history of asbestos exposure by an industrial hygienist will yield 
4

information about frequency and intensity of exposure, in addition to exposure duration, 

and allow a more informed decision about the claim. 

Malignant mesothelioma is known to occur following relatively brief exposure to 

asbestos, thus permitting the setting of a shorter period of exposure as a presumption of 

significant exposures (i.e., 30 days) (Helsinki 1997; Welch 2007; Markowitz 2015). A 

minimum latency of 15 years for all asbestos-related diseases is supported as a 

presumption by extant medical literature; claims asserting a latency period less than 15 

years can be evaluated on an individual basis.

Setting a calendar year as representative of a specific time demarcation when exposure 

was categorically lowered is inherently problematic. It is highly attractive for assessing 

exposure in claims evaluation but fails to recognize that exposure reduction occurs over 

time, usually a number of years. However, entirely disregarding calendar years in 

assessing exposure for the purpose of establishing presumptions fails to recognize that 

exposure to asbestos has, for many workers, diminished over time. A feasible and 

knowledge-based compromise is to build in a safety margin in setting a calendar time 

element in exposure presumptions. In 1994, OSHA lowered the permissible exposure 

level of asbestos in the workplace. In 1995, DOE issued a new order regarding 

occupational health and safety in the DOE complex. It is reasonable to posit that it 

required a decade of dissemination and diffusion of knowledge, attitudes and practice 

with regard to asbestos use such that exposure to asbestos was decisively diminished 

across the vast majority of workers at DOE facilities. Thus, we recommend 2005 as a 

year to demarcate likely significant asbestos exposure, recognizing that exposures after 

2005 might be significant and will be evaluated by occupational health professionals as 

part of the individual claims evaluation. 

Chronic obstructive pulmonary disease may have a contribution from asbestos exposure 

but is better evaluated in the claims process in accordance with a broader policy that 

addresses the large number of exposures that can aggravate, contribute to, or cause 

chronic obstructive pulmonary disease. 

References

1. Algrante E and Markowitz S. Parenchymal Disease Related to Asbestos. Chapter 16; pp. 

157-170. In Newman Taylor A, Cullinan P, Blanc P, Pickering A. (Eds). Parkes' 

Occupational Lung Disorder, Fourth Edition. CRC Press, 547 pages, 2016.

2. Dement JM, Ringen K, Welch LS, Bingham E, Quinn P. Mortality of older construction 

and craft workers employed at Department of Energy (DOE) nuclear sites. Am J Ind 

Med. 2009 Sep;52 (9):671-82.

3. DOE Former Worker Grogram Annual Report, 2016. 

(https://energy.gov/sites/prod/files/2016/09/f33/2015-FWP-Annual-Report.pdf).

4. Figgs LW. Lung cancer mortality among uranium gaseous diffusion plant workers: a 

cohort study 1952-2004. Int J Occup Environ Med. 2013 4(3):128-40.

5. Frome EL, Cragle DL, Watkins JP, Wing S, Shy CM, Tankersley WG, West CM. A 

mortality study of employees of the nuclear industry in Oak Ridge, Tennessee. Radiat 

Res. 1997 148(1):64-80.
5

6. Helsinki Consensus Report. Asbestos, asbestosis, and cancer: The Helsinki criteria for 

diagnosis and attribution. Scand J Work Env Health; 23: 311-316, 1997.

7. IARC (International Agency for Research on Cancer). IARC Monographs on the 

Evaluation of Carcinogenic Risks to Humans, Volume 100c: Arsenic, Metals, Fibres and 

Dusts. 2012. Lyon, France: International Agency for Research on Cancer.

8. Markowitz SB. Asbestos-Related Lung Cancer and Malignant Mesothelioma of the Pleura: 

Selected Current Issues. Sem Resp Crit Care Med 2015: 36(3):334-346.

9. Markowitz S. Cancer of the Respiratory Tract Due to Asbestos and Zeolites. Chapter 22; 

pp. 259-276. In Newman Taylor A, Cullinan P, Blanc P, Pickering A. (Eds). Parkes' 

Occupational Lung Disorder, Fourth Edition. CRC Press, 547 pages, 2016.

10. National Toxicology Program (NTP). 2014. Report on Carcinogens, Thirteenth 

Edition. Research Triangle Park, NC: U.S. Department of Health and Human Services, 

Public Health Service. http://ntp.niehs.nih.gov/pubhealth/roc/roc13/.

11. Richardson DB, Wing S. Radiation and mortality of workers at Oak Ridge National 

Laboratory: positive associations for doses received at older ages. Environ Health 

Perspect. 1999 Aug; 107(8): 649–656. 

12. Ringen K, Dement J, Welch L, Bingham E, Quinn P, Chen A, Haas S. Mortality of older 

construction and craft workers employed at department of energy (DOE) nuclear sites: 

follow-up through 2011. Am J Ind Med. 2015 Feb;58(2):152-67.

13. Silver SR, Bertke SJ, Hein MJ, Daniels RD, Fleming DA, Anderson JL, Pinney SM, 

Hornung RW, Tseng CU. Mortality and ionising radiation exposures among workers 

employed at the Fernald Feed Materials Production Center (1951–1985). Occup Environ 

Med. 2013 70(7): 453–463.

14. Welch LS. Asbestos exposure causes mesothelioma, but not this asbestos exposure: an 

amicus brief to the Michigan Supreme Court. Int J Occup Environ Health. 2007 JulSep;13(3):318-27.
6

Recommendation #2

Presumptions for Work-Related Asthma 

1. DOL should use the generally accepted unifying term, work-related asthma (WRA) for 

claims evaluation and decision-making. Work-related asthma includes: a) occupational 

asthma (OA), or new onset asthma that is initiated by an occupational agent, and b) workexacerbated asthma (WEA), which is established asthma that is worsened by workplace 

exposures. The recognition of both forms of work-related asthma should be 

communicated to claimants, their physicians and consulting IH’s and CMC’s.

2. Medical criteria for the diagnosis of asthma: The diagnosis of asthma by a treating or 

evaluating physician should be sufficient for the recognition that the claimant has asthma. 

Bronchodilator reversibility of FEV1 and/or a positive methacholine challenge test may 

be helpful but should not be required to accept the diagnosis of asthma, which is made by 

a health care provider.

3. Work-related asthma, whether OA or WEA, is defined as the presence of medicallydiagnosed asthma that is associated with worsening of any one or more of the following 

in relation to work: asthma-related symptoms, asthma medication usage or asthma-related 

health care utilization temporally related to work, or change in peak expiratory flows 

associated with work. Such a history should be documented by a treating or evaluating 

health care provider, or addressed by a CMC if consulted in a claim evaluation. 

 

4. The same criteria for WRA should be used in evaluating asthma claims whether the claim 

is made contemporaneous with the period of DOE employment or after the end of that 

period of employment. A specific triggering event causing onset of WRA may occur but 

is not typical or necessary. Inciting exposures such as dusts, fumes, heat or cold or others 

should be specifically identified when possible, but should not be required for the 

diagnosis of WRA.

Rationale

Work-related asthma induced or exacerbated by inhaled toxicants in the workplace is 

common in the United States, associated with up to 25% of adult asthma (Tarlo 2008; 

Henneberger, 2011). Occupational asthma in previously health workers is known to be 

caused by over 400 specific workplace agents with additional agents being reported 

annually (Friedman-Jimenez 2015). Dusts, gases, vapors, and fumes in general can 

worsen pre-existing asthma or asthma that otherwise has developed among workers 

(Henneberger, 2011). 

Due to variation in diagnostic criteria, clinical management, and terminology, the chief 

professional organizations of pulmonary physicians in the United States, the American 

Thoracic Society and the American College of Chest Physicians, periodically issue 

consensus statements to promote clarity, uniformity, and quality in the recognition and 

care of workers with work-related asthma (Tarlo 2008; Henneberger, 2011). The criteria 
7

contained in the above recommendation reflect the most recent statements. Specifically, 

the American Thoracic Society wrote in 2011 that work-exacerbated asthmas is “preexisting or concurrent asthma” in which “the exacerbation of asthma was temporally 

associated with work, based either on self-reports of symptoms or medication use relative 

to work, or on more objective indicators like work-related patterns of serial PEFR” and 

when “conditions exist at work that can exacerbate asthma” (Henneberger, 2011). 

Occupational asthma is asthma induced by airborne sensitizers or irritants at work (Tarlo 

2008; Henneberger, 2011).

Asthma, which is marked by chronic airway inflammation, is defined by the “history of 

respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that 

vary over time and in intensity, together with variable expiratory airflow limitation” 

(Global Initiative for Asthma 2016). The diagnosis of asthma is complicated by the fact 

that the patient is often already on asthma medications when an evaluating, treating, or 

consulting physician first sees the patient. The disease is also variable, so that negative 

tests cannot rule out the disease when it is inactive. Objective pulmonary function tests 

may not provide typical patterns that reflect asthma, since physicians (and patients) are 

often reluctant to stop asthma treatment prior to testing. Therefore, the clinical history 

and presentation may effectively become the sole basis for diagnosis and represents a 

fully accepted method in clinical medicine.

Likewise, objective pulmonary function testing that demonstrates airway reversibility in 

relation to workplace agents, though helpful, is not an absolute requirement for the 

diagnosis of work-related asthma (Tarlo 2008). Key to the diagnosis of work-related 

asthma is the temporal relation between workplace exposures and asthma activity, 

whether identified by symptoms, medication usage, or visits to health care providers. Any 

of these measures may suffice as demonstration of the work-elatedness of asthma. 

Notably, there are patients in whom even these measures are not definitive, as workrelated asthma can have delayed symptoms that may not be easily related to exposures at 

work.

References

1. Friedman-Jimenez G, Harrison D, Luo H. Occupational asthma and work-exacerbated 

asthma. Semin Respir Crit Care Med. 2015 Jun;36(3):388-407.

2. Henneberger PK, Redlich CA, Callahan DB, Harber P, Lemiere C, Martin J, Tarlo SM, et 

al. An official American Thoracic Society Statement: work-exacerbated asthma. Am J 

Respir Crit Care Med. 2011; 184:368–378.

3. Jajosky RA, Harrison R, Reinisch F, Flattery J, Chan J, Tumpowsky C, Davis L, et al. 

Surveillance of work-related asthma in selected U.S. states using surveillance guidelines 

for state health departments – California, Massachusetts, Michigan, and New Jersey, 

1993–1995. MMWR. 1999; 48:1–20. 

4. Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 

2016. Available from: www.ginasthma.org.
8

5. Tarlo SM, Balmes J, Balkissoon R, Beach J, Beckett W, Bernstein D, Blanc PD, Brooks 

SM, Cowl CT, Daroowalla F, Harber P, Lemiere C, Liss GM, Pacheco KA, Redlich CA, 

Rowe B, Heitzer J. Diagnosis and management of work-related asthma: American 

College Of Chest Physicians Consensus Statement. Chest. 2008 Sep;134(3 Suppl):1S41S. 
9

Recommendation #3

Presumptions for Chronic Obstructive Pulmonary Disease 

The Advisory Board recommends that the Energy Employees Occupational Illness 

Compensation Program (EEOICP) revise its exposure presumptions that are used to adjudicate 

claims for chronic obstructive pulmonary disease (COPD). We recommend that EEOICP replace 

the presumptions it has established in DEEOIC Bulletin 16-02 with the following alternative 

presumptions:

1. Any claimant with a physician’s diagnosis of COPD who worked in any covered facility 

either:

(a) In any of the labor categories in Attachment 1 

 (which should be expanded to include all construction and maintenance 

job titles),

 Or

(b) Who reported exposure to vapors, gases, dusts, and fumes (VGDF) with 

relevant tasks on the Occupational History Questionnaire for a period, 

which, in aggregate, totals at least five years, 

is presumed to have experienced sufficient exposure to toxic agents to aggravate, 

contribute to, or cause COPD. 

2. In addition, claims examiners should not deny claims for COPD if the worker had fewer 

than 5 years of exposure; for example, a claimant who has experienced high intensity 

exposures to VGDFs for a period < 5 years during work in a covered facility would have 

an equivalent exposure. Claims that do not meet the requirements set forth here but do 

have reported exposure to VGDF should be sent for industrial hygienist and/or CMC 

review under the policy established in Bulletin 16-03. 

Rationale

Scientific Background

Substantial medical literature has investigated the etiology of COPD among general 

populations in the U.S., Italy, New Zealand, Poland, Australia, Spain, and elsewhere 

(reviewed in ATS Statement, 2003; ATS Statement, 2010 (1,2)). 

In 2003 the American Thoracic Society, which is the preeminent respiratory disease 

organization in the United States, published a consensus statement that concluded that 

occupational exposures were responsible for a substantial fraction of COPD in the United 

States. Another review from the American Thoracic Society published in 2010, “An 

Official American Thoracic Society Public Policy Statement: Novel Risk Factors and The 

Global Burden of Chronic Obstructive Pulmonary Disease,” further concluded that there 

is a very strong and well accepted causal relationship between occupational exposures to 

vapors, gases, dusts and fumes (VGDF) and COPD (ATS Statement, 2010, page 704). 
10

This document also identified some specific agents that are part of the overall 

occupational exposures to vapors gases dust and fumes. Table 5 in this paper lists some 

studies that have identified specific agents, including asbestos and quartz (i.e., crystalline 

silica).

Other primary research studies have defined the causative occupational exposures as a 

combined exposure VGDF. These large studies of varying study designs have 

consistently shown that occupational exposures defined as “gases, dusts, vapors, and 

fumes” increase the risk of COPD. A dose-response relationship has been seen (7,8), and 

the effect is observed among both smokers and non-smokers (4,5). The effect of smoking 

and occupational exposures appears to be additive. Two recent studies by Dement et al 

evaluated COPD and occupational risks in DOE facilities specifically and found that 

VGDF significantly increased the risk for COPD (9),and that VGDF exposure predicted 

accelerated loss of lung function over time (10).

There is a strong biological basis for causation of COPD by VDGF, as described by 

Eisner (2010) (1). Exposure of mice to particulates leads to an inflammatory response in

the airways within 24 hours of exposure. Particulate exposure increases activity of 

fibroblasts with deposition of fibronectin, and chronic exposure in rats led to clear 

fibrosis. Human epithelial cells exposed to particulates express inflammatory cytokines, 

and alveolar macrophages release TNF alpha and IL-1 after exposure, as well as releasing 

reactive oxygen species; all these agents are known to cause inflammation. Long-term 

exposure to particulates leads to airway remodeling and chronic inflammation, both 

hallmarks of COPD.

COPD is caused by cumulative exposure, as demonstrated by the presence of a doseresponse in population-based studies. This fact means that any and all exposures to 

VGDF contribute and aggravate dust-induced COPD. Therefore, it is reasonable that 

exposures outside the DOE complex could be considered when determining if a minimal 

length of exposure has occurred to meet a presumption as part of an individualized 

industrial hygiene review (see #2 above). 

Attributes of Exposure

Covered exposures: The following specific exposures should be presumptive, because 

they impose a risk for COPD that is as great as the risk found by DEEOIC in Bulletin 16-

02 to be presumptive for asbestos: Asbestos; silica; cement dust; engine exhausts; acids 

and caustics; welding, thermal cutting, soldering, brazing; metal cutting and grinding; 

machining aerosols; isocyanates, organic solvents, wood dust, molds and spores; and 

particulates not otherwise regulated (PNOR1). In addition, the scientific evidence 

supports the conclusion that exposures to vapors, gases, dusts, and fumes (VGDF) as a 

broad category increases the risk of COPD. 

 

1

PNOR includes all mineral and inorganic “inert or nuisance dusts” without specific individual U.S. Occupational 

Safety and Health Administration Permissible Exposure Limits (PEL). See OSHA. Chemical Sampling Information: 

Particulates Not Otherwise Regulated (Total Dust) Washington, DC. 2015; NIOSH Pocket Guide to Chemical

Hazards: Particulates not Otherwise Regulated. Atlanta, GA, 2015.
11

Relevant Job Categories: Research supports the presumptions that the labor categories 

listed in Attachment 1 have had significant exposure to VGDF. In Dement’s study at 

DOE facilities published in 2015, which includes these labor categories, only 1.4% of 

COPD cases and 2.5% of controls reported no VGDF exposures (see Supplemental 

Materials, Table IV-S.) However, Attachment 1 is not inclusive, for there are many other 

labor categories in the DOL atomic weapons complex that have had significant exposure 

to VGDF as well. The committee recommends that Attachment 1 be expanded by adding 

“all construction and maintenance workers.” In addition, the Advisory Board separately 

recommends changes to the occupational history questionnaire to better assess each 

individual worker’s exposure to VGDF. If a worker reports exposure to VGDF on the 

OHQ that is substantiated with description of relevant tasks, and additionally meets other 

requirements recommended in this presumption, his/her exposure should be considered to 

aggravate, contribute to, or cause COPD. 

Timing of exposure: Because VGDF exposures continue to take place at DOE sites and 

many of them are unregulated, it should be presumed that reported exposures to toxic 

substances that cause, contribute to or aggravate COPD at any period of employment 

covered by EEOICPA, up to the present time, are contributory exposures. 

Duration of exposure: Based on the evidence presented in the Dement 2015 study, a 

duration of 5 years of reported exposures to VGDF can be presumed to aggravate, 

contribute to, or cause COPD.

Time since last exposure: The committee does not recommend specifying any time 

limit between last exposure and clinical recognition of COPD. COPD is a slowly 

progressive disease, and individuals are often not diagnosed until the disease is advanced, 

or an intervening infection makes the diagnosis more apparent. Since it would not be 

possible to determine in retrospect when a case of COPD could have been first 

diagnosed, and since VDGF is a contributory cause to COPD, it is reasonable to assume 

that VGDF contributed to any diagnosed case of COPD even if the disease is diagnosed 

after the worker has left employment.

References

1. Eisner MD, Anthonisen N, Coultas D, Kuenzli N, Perez-Padilla R, Postma D, et al. An 

official American Thoracic Society public policy statement: Novel risk factors and the 

global burden of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 

2010 Sep 1;182(5):693-718.

2. Balmes J, Becklake M, Blanc P, Henneberger P, Kreiss K, Mapp C, et al. American 

Thoracic Society Statement: Occupational contribution to the burden of airway disease.

Am J Respir Crit Care Med 2003 Mar 1;167(5):787-97.

3. Balmes JR. Occupational contribution to the burden of chronic obstructive pulmonary 

disease. J Occup Environ Med 2005 Feb;47(2):154-60.

4. Blanc PD, Iribarren C, Trupin L, Earnest G, Katz PP, Balmes J, et al. Occupational 

exposures and the risk of COPD: dusty trades revisited. Thorax 2009 Jan;64(1):6-12
12

5. Dement JM, Welch L, Ringen K, Bingham E, Quinn P. Airways obstruction among older 

construction and trade workers at Department of Energy nuclear sites. Am J Ind Med 

2010 Mar;53(3):224-40.

6. Bergdahl IA, Toren K, Eriksson K, Hedlund U, Nilsson T, Flodin R, et al. Increased 

mortality in COPD among construction workers exposed to inorganic dust. Eur Respir J 

2004 Mar;23(3):402-6.

7. Weinmann S, Vollmer WM, Breen V, Heumann M, Hnizdo E, Villnave J, et al. COPD 

and occupational exposures: a case-control study. J Occup Environ Med 2008 

May;50(5):561-9.

8. Mehta AJ, Miedinger D, Keidel D, Bettschart R, Bircher A, Bridevaux PO, et al. 

Occupational exposure to dusts, gases, and fumes and incidence of chronic obstructive 

pulmonary disease in the Swiss Cohort Study on Air Pollution and Lung and Heart 

Diseases in Adults. Am J Respir Crit Care Med 2012 Jun 15;185(12):1292-300.

9. Dement J, Welch L, Ringen K, Quinn P, Chen A, Haas, S. A case-control study of 

airways obstruction among construction workers. Am J Ind Med 2015 58:1083-1097.

10. Dement J, Welch L, Ringen K, Cranford K, Quinn P. Longitudinal decline in lung 

function in older construction workers. Occ Env Med 2017 published on-line May 17
13

Recommendation #4

Revisions of Occupational History Questionnaire

A. The Advisory Board recommends expanding the current list of hazards, exposures, and 

materials on the current Occupational History Questionnaire (OHQ) to include the list of 

hazards and/or materials used by the Building Trades National Medical Screening Program 

(BTMed). 

1. For each exposure reported, the worker should be asked to describe how he/she was 

exposed to each material with an emphasis on describing the tasks associated with the 

exposure; this would be captured using free text. The worker would also be asked to 

rate the frequency of exposure to each hazard, using the scale from BTMed. In 

addition, we suggest adding a box next to each exposure on the list, asking if the 

worker used the material directly or was exposed as a bystander. 

The current version of the OHQ asks about specific exposures that could be 

expanded with the text box and assessment of exposure frequency.

2. The list of hazards should include asbestos; silica; cement dust; engine exhausts; 

acids and caustics; welding, thermal cutting, soldering, brazing; metal cutting and 

grinding; machining aerosols; isocyanates, organic solvents, wood dust, molds and 

spores. Each of these has been shown to cause chronic obstructive pulmonary disease 

(COPD) and other health conditions.

The Advisory Board also recommends adding to the OHQ the list of tasks that is currently 

used in the exposure assessment by BTMed.

 Rationale 

The goal of this recommendation is to expand the amount of information on specific 

hazards and materials available to the claims examiner, the consulting industrial 

hygienist, and the medical consultant. To determine if a disease is related to exposures 

one generally need to know whether an exposure occurred and to be able to assess 

duration and intensity in a qualitative way. The worker’s description of hazards and 

associated tasks is widely considered the most important part of any occupational 

medicine consultation, and needs to be included in the OHQ. 

A primary goal of the OHQ is to identify hazardous exposures for a specific worker, so 

that information can be used in a causation determination. A worker may not know the 

names of all the materials he/she used, but will know the tasks she/he performed. Task 

alone, even without the names of the associated hazards can give the industrial hygienist 

a good sense of what exposures occurred, and what additional questions need to be asked 

in the document acquisition request or directly from the worker. 

EEOICP Bulletin 16 – 03 describes a new process, the direct disease link work process 

(DDLWP), to link medical conditions to specific tasks. The guidance document states 

that “Data supplied by an employee or survivor in an occupational history or other 
14

personal statements can be accepted as reliable when sufficient detail or other 

information is provided that documents the scope and type of work performed.” The 

subcommittee believes that the OHQ, if revised as recommended, would meet this 

standard.

As additional support for these recommendations, the Board notes that Bulletin 16 – 03 

states “the CE needs to carefully compare what job tasks the employee actually 

performed” when using the DDLWP. It also states “To obtain a causation opinion, the 

CE prepares a summary of the employment that specifically references how much time 

the employee spent working on one or more DDLWP and describes the work.” Given 

that the current OHQ does not collect information on tasks, nor on length of time 

performing any specific task or operation, it is important to revise the OHQ to allow the 

claims examiner to effectively utilize the DDLWP.

The Board discussed the feasibility of creating a list of tasks for production workers 

similar to what BTMed uses for construction workers but felt that would be almost 

impossible given the wide range of tasks over the years in the DOE complex. The 

alternative, of getting a more detailed occupational history from each worker, will 

provide the comparable information.

B. The Advisory Board recommends adding a specific question to the OHQ regarding vapors, 

gases, dusts and fumes (VGDF). We suggest adding:

1. The question: “Have you been exposed to vapors, gases, dusts and fumes in your 

work at DOE?”

2. If the answer to (a) is “yes”, the worker should be asked about frequency of exposure 

to VGDF overall using the scale above.

3. If the answer to (a) is “yes” the worker is then asked “Have you already reported all 

exposures to vapors, gases, dust and fumes in your answers above?” If not, he/she 

should be asked to describe additional tasks and materials associated with exposure, 

to VGDF, the frequency using the scale recommended above under recommendation 

(1), the assessment whether the exposure was through direct use or as a bystander, 

and an assessment of the number of years of exposure.

Rationale 

Substantial medical literature has investigated the etiology of COPD among general 

populations in the U.S., Italy, New Zealand, Poland, Australia, Spain, and elsewhere (see 

reviews in ATS Statement, 2003; ATS Statement, 2010 (1;2)). 

In 2003 the American Thoracic Society, which is the preeminent respiratory disease 

organization in the United States, published the enclosed paper concluding that 

occupational exposures were responsible for a substantial fraction of COPD in the United 

States. Another paper from the American Thoracic Society published in 2010, with 
15

Eisner as the lead author and the title “An Official American Thoracic Society Public 

Policy Statement: Novel Risk Factors and The Global Burden of Chronic Obstructive 

Pulmonary Disease,” describes that there is a very strong and well accepted relationship 

between occupational exposures and COPD; see the section starting on page 704. This 

document describes that it is a strong causal relationship and describes other literature 

that has identified some specific agents that are part of the overall occupational exposures 

to vapors gases dust and fumes. Table 5 in this paper lists some studies that have 

identified specific agents, including asbestos and quartz; quartz is another name for as 

crystalline silica.

Other primary research studies have defined the causative occupational exposures as a 

combined exposure to vapors, gases, dusts and fumes (VGDF). These large studies of 

varying study designs have consistently shown that occupational exposures defined as 

“gases, dusts, vapors, and fumes” increase the risk of COPD. A dose-response 

relationship has been seen (7;8), and the effect is observed among both smokers and nonsmokers (4;5). The effect of smoking and occupational exposures appears to be additive. 

A recent study published looked at COPD and occupational risks in DOE facilities 

specifically, and found that VGDF significantly increased the risk for COPD (9).

Therefore, it is essential to assess workers’ exposures to VGDF. As noted above, 

research has shown that the question “Have you been exposed to vapors, gases, dusts and 

fumes?” predicts COPD in population-based studies.

COPD is caused by cumulative exposure, as demonstrated by the presence of a doseresponse in population-based studies. This fact means that all on-going exposures to 

VGDF contribute and aggravate dust-induced COPD. 

C. The Board recommends that the version of the OHQ developed in response to these 

recommendations be tested multiple times to determine if it is user friendly and has face 

validity. 

Rationale

The Board understands that these changes would make for a longer questionnaire, but we 

believe adding the worker's description of how they were exposed to materials is essential 

for development of the claim. We understand the Department's concern that workers, 

when presented with a list of hazards, might check off all hazards. Adding a narrative 

description of how the worker was exposed to that hazard would provide validation of the 

exposure, since such a narrative requires knowledge and understanding of tasks. When 

the questionnaire is reviewed by the industrial hygienist, the hygienist will be able to see 

if the narrative is consistent with general IH knowledge about that occupation or specific 

knowledge about the site, and can determine if the OHQ can be used as the basis for 

exposure assessment.
16

References

1. Eisner MD, Anthonisen N, Coultas D, Kuenzli N, Perez-Padilla R, Postma D, et al. 

An official American Thoracic Society public policy statement: Novel risk factors 

and the global burden of chronic obstructive pulmonary disease. Am J Respir Crit 

Care Med 2010 Sep 1;182(5):693-718.

2. Balmes J, Becklake M, Blanc P, Henneberger P, Kreiss K, Mapp C, et al. American 

Thoracic Society Statement: Occupational contribution to the burden of airway 

disease. Am J Respir Crit Care Med 2003 Mar 1;167(5):787-97.

3. Balmes JR. Occupational contribution to the burden of chronic obstructive 

pulmonary disease. J Occup Environ Med 2005 Feb;47(2):154-60.

4. Blanc PD, Iribarren C, Trupin L, Earnest G, Katz PP, Balmes J, et al. Occupational 

exposures and the risk of COPD: dusty trades revisited. Thorax 2009 Jan;64(1):6-12.

5. Dement JM, Welch L, Ringen K, Bingham E, Quinn P. Airways obstruction among 

older construction and trade workers at Department of Energy nuclear sites. Am J 

Ind Med 2010 Mar;53(3):224-40.

6. Bergdahl IA, Toren K, Eriksson K, Hedlund U, Nilsson T, Flodin R, et al. Increased 

mortality in COPD among construction workers exposed to inorganic dust. Eur 

Respir J 2004 Mar;23(3):402-6.

7. Weinmann S, Vollmer WM, Breen V, Heumann M, Hnizdo E, Villnave J, et al. 

COPD and occupational exposures: a case-control study. J Occup Environ Med 2008 

May;50(5):561-9.

8. Mehta AJ, Miedinger D, Keidel D, Bettschart R, Bircher A, Bridevaux PO, et al. 

Occupational exposure to dusts, gases, and fumes and incidence of chronic 

obstructive pulmonary disease in the Swiss Cohort Study on Air Pollution and Lung 

and Heart Diseases in Adults. Am J Respir Crit Care Med 2012 Jun 

15;185(12):1292-300.

9. Dement J, Welch L, Ringen K, Quinn P, Chen A, Haas, S. A case-control study 

of airways obstruction among construction workers. Am J Ind Med 58:1083-1097, 

2015.
17

Recommendation #5

Science and Technical Capacity in EEOICP

The Board recommends that the DEEOICP enhance its scientific and technical capabilities to 

support the development of program policies and procedures, to enhance decision-making on 

individual claims, and to inform its assessment of the merit of the work of its consulting 

physicians and industrial hygienists.

Rationale

The Institute of Medicine’s Review of the DOL Site Exposure Matrices (SEM) in 2013 

made numerous recommendations to improve the SEM. These include 1) making sure 

that the SEM incorporate readily available supplemental data sources into the SEM to 

provide a more complete picture of known exposure-disease links, and 2) forming an 

expert advisory panel to establish explicit causal criteria for use by the EEOICP, design 

and implement a method for reviewing possible exposure-disease links, and identify and 

peer review new exposure-disease links for use in the SEM. 

The Board notes that the EEOICP has ended its contract with the National Library of 

Medicine for the continued updating of the Haz-Map database that is integral to SEM. 

The Board has been asked by EEOICP to provide input into numerous possible exposuredisease links. While the Board will assist in this request to the extent possible, it is noted 

that the Board members have limitations in time to devote to Board activities and has, at 

present, as a Board, no scientific staff or contracted resources to address this request. 

Moreover, evaluating exposure-disease links is an ongoing task for which the EEOICP 

needs permanent capacity to complete.

The Board has observed that numerous current EEOICP policies involving important 

diseases and exposure-disease links, including chronic obstructive lung disease, asbestosrelated diseases, asthma, and others, are not based fully on state-of-the-art scientific 

knowledge.

The Board is willing to assist the Department of Labor in implementing this 

recommendation.
18

Recommendation #6

Interpretation of the Beryllium Lymphocyte Proliferation Test (BeLPT)

The Advisory Board recommends that the finding of two borderline BeLPT tests shall be 

considered the equivalent of one positive BeLPT for the purposes of claims adjudication under 

subpart B and subpart E of EEOICPA.

Rationale

Beryllium sensitization is defined by EEOICPA as a single abnormal BeLPT, which most 

commonly is performed on fresh peripheral blood cells. The BeLPT result is occasionally 

reported as “borderline.” Two “borderline” BeLPT tests have been shown to give about 

the same predictive value for beryllium sensitization as one abnormal (positive) BeLPT 

test (1-2). Thus a person with two ‘borderline” BeLPT tests should be considered 

sensitized to beryllium (BeS), and further BeLPT testing is not indicated. The BeLPT is 

not a perfect test for BeS. False negative and positive BeLPT results can occur for several 

reasons (3). 

References

1. Middleton DC, Fink J, Kowalski PJ, Lewin MD, Sinks T. Optimizing BeLPT criteria 

for beryllium sensitization. Am J Ind Med 2008;51:166-72.

2. Middleton DC, Mayer AS, Lewin MD, Mroz MM, Maier LA. Interpreting borderline 

BeLPT results. Am J Ind Med 2011;54:205-9. PMC4347846:PMC4347846.

3. Occupational Health Best Practices: State of Washington; 2015.
19

Recommendation #7

Quality Assessment of Contract Medical Consultants

We request that the DOL provide the Board with resources to conduct a quality assessment of a 

sample of 50 contract medical consultant (CMC) evaluations that have been associated with 

claim denials. The quality review will assess the nature of the medical information reviewed by 

the CMC, the use of standards of causation, the reasoning of the CMC, the scientific basis for the 

CMC conclusions, among other items. The assessment will likely required contracted services of 

worker-centered occupational physicians who are not associated with the current CMC contract. 

The review may lead to recommendations, including the development of guidance materials.

Rationale

Occupational physician board members reviewed a number of CMC reports together with 

entire claimant records to assess the quality of the medical determinations and identified 

a number of problems, despite the strong credentials of each of the CMCs reviewed. 

These included failure to examine the entire medical record, resulting in instances in 

which critical information was overlooked that would have substantiated the claim; 

selective reading and citing of the medical literature to challenge the exposure-outcome 

relationship despite the preponderance of the medical evidence supporting the 

relationship; and a general misunderstanding of the level of certainty required for this 

program. Most concerning, the approach in several cases appeared to be more adversarial 

than objective. A more thorough exploration of CMC reports and the complete claimant 

records is needed to establish how widespread the problems may be and to assess the 

quality, objectivity, and consistency of CMC determinations. This work is very 

intensive, since the records themselves may run from many hundreds to several 

thousands of pages, and it needs to be conducted by occupational medicine physicians 

who have a worker-oriented perspective in line with the overall goal of the EEOICP. The 

scope of the task requires contractor support, and we would recommend explicitly 

identifying physicians who are not engaged with the current contractor to ensure 

independence of the assessment. The Association of Occupational and Environmental 

Clinics is a non-profit organization that includes a worker focus and would be able to 

identify appropriate experts for this task.
Attachment 1

Significant VGDF Exposure: Associated Labor Categories and Job Tasks 2

Automotive mechanic; Vehicle mechanic; Vehicle maintenance mechanic

Boilermaker

Carpenter; Drywaller; Plasterer

Demolition technician; Laborer

Electrical mechanic; Electrician; Floor covering worker

Furnace & saw operator; Furnace builder; Furnace operator; Furnace puller; Furnace technician; 

Furnace tender; Furnace unloader

Glazier; Glass installer; Glazer

Grinder operator; Mason (concrete grinding); Tool grinder; Maintenance mechanic (general 

grinding); Welder (general grinding); Machinist (machine grinding)

Insulation worker; Insulation trade worker; Insulator

Ironworker; Ironworker-rigger

Maintenance mechanic; Electrician; Insulator;

Mason; Brick & tile mason; Concrete and terrazzo worker; Bricklayer, Tilesetter

Millwright

Heavy equipment operator; Operating Engineer

Painter

Pipefitter, Plumber steamfitter; Plumber/pipefitter; Plumbing & pipefitting mechanic; Plumbing 

technician, Steamfitter

Roofer

Sheet metal mechanic; Sheet metal fabricator/installer

Welder; Welder burner; Welder mechanic

 

2 Derived from ATSDR document on asbestos exposure, Case Studies in Environmental Medicine, Asbestos 

Toxicity, January 29, 2014.
Attachment 2

Excerpted from:

Dement J, Welch L, Ringen K, Quinn P, Chen A, Haas, S. A case-control study of airways 

obstruction among construction workers. Am J Ind Med 2015 58:1083-1097.

A Case-Control Study of Airways Obstruction among Construction Workers

Supplemental Material

Exposure Assessment Details

Occupational and Exposure History Questionnaire

Based on our experience in the BTMED program telephone interviews have been found to be an 

effective approach to collecting exposure history data. This is consistent with studies that have 

found telephone interviews to be superior to postal surveys for respiratory symptoms and risk 

factors [Brogger et al., 2002]. The telephone questionnaire obtained a lifetime occupational and 

exposure history through the date of the qualifying BTMED examination. Data domains 

included:

1. Industry and jobs held for at least six months with start and stop dates (month and year). 

Jobs within the same industry and occupation were treated as one job. For each job, 

workers were asked to list the products or services produced, job title/position, and usual 

work hours per week.

2. For all construction-related jobs, a qualitative assessment of frequency (none to daily) of 

doing 90 specific construction tasks known to generate VGDF exposures (e.g. cutting 

concrete, insulation installation, wood sanding, etc.). Open-ended questions were 

included to allow workers to report other construction-related tasks that created VGDF 

exposures but were not included in the listed tasks in the questionnaire. 

3. For non-construction jobs, workers were asked “Does/did this job expose you to vapors, 

gases, dusts, and fumes” as this single survey item has been shown to delineate exposures 

associated with COPD risk [Blanc et al., 2005; Quinlan et al., 2009]. For any job with a 

positive response concerning VGDF exposure, workers provided a description of tasks 

resulting in exposures, materials exposed to, and frequency of exposure.

4. A qualitative assessment of exposure frequency (none to daily) for an a priori list of 

other materials associated with respiratory disease in the literature (e.g. coal dust; 

formaldehyde; beryllium; mercury; polyvinyl chloride fumes (heating or cutting PVC); 

isocyanates; pesticides, insecticides, or herbicides; diesel or gasoline engine exhaust; 

grain dusts; and animal feed or fodder). These data were collected for control of potential 

confounding exposures.
5. Use of respiratory protection (always, sometimes, rarely, or never) and engineering 

controls such as wet methods or local exhaust ventilation (always, sometimes, rarely, or 

never) for reported tasks. 

6. An assessment of the frequency of bystander exposures to asbestos, man-made fibers, 

abrasive cutting or grinding of concrete, drywall/plaster dusts, spray painting, 

sandblasting, welding/cutting, and wood dusts.

7. Service in a branch of the military and if their military jobs resulted in exposures to 

VGDF. For any military job with a positive response concerning VGDF exposure, 

workers provided a description of tasks resulting in exposures, materials exposed to, and 

frequency of exposure.

8. Exposures to passive tobacco smoke at home and at work, having a blood relative with 

COPD [Weinmann et al., 2008], and history of pneumonia as a child [Tager et al., 1988]. 

Respiratory history and smoking history were determined using data from each worker’s 

BTMED exam and any missing data from the BTMED exam was collected during the 

interviews. 

The telephone questionnaire was developed and pilot tested in several ways. First, we assembled 

two separate focus groups of 10-15 experienced construction workers from DOE’s Savannah 

River and Oak Ridge sites to review the draft questionnaire for ease of understanding (language 

level), question syntax, and overall questionnaire flow. We also asked focus group participants 

to identify any common VGDF exposures experienced by construction workers not adequately 

addressed in the draft questionnaire. Secondly, the draft questionnaire was pilot tested via 

telephone administration to approximately 25 construction workers identified by BTMED to 

represent the approximate age and experience range of the COPD cases and controls. 

The final telephone questionnaire was administered by four trained interviewers without 

knowledge of case or control status. Cases and controls were randomly assigned to interviewers. 

Study subjects were first sent an invitation letter describing the study followed by telephone 

contact by the assigned interviewer to obtain informed consent and administer the questionnaire. 

A minimum of two telephone contact attempts were made before a second reminder letter was 

sent. Following the second reminder letter at least two additional telephone contact attempts 

were made. Study subjects were classified as ‘failed to contact’ due to bad addresses or 

telephone numbers and ‘failed to respond’ after no response following two letters and at least 

four phone calls. Information about the study was also provided on the BTMED web site and 

included in the BTMED Newsletter.

Cumulative Exposure Indices

Qualitative cumulative exposure indices were assessed for an a priori list of 15 common 

construction-related exposures shown in Table I. The category ‘particulates not otherwise 

regulated’ (PNOR) includes all mineral and inorganic ‘inert or nuisance dusts’ without specific 

individual U.S. Occupational Safety and Health Administration Permissible Exposure Limits 

(PEL) [NIOSH, 2015; OSHA, 2015]. A PNOR exposure index was included to allow generation 
of an overall index for VGDF exposures comparable to those in the published literature. All 

indices were based on task frequency by job, job duration, and usual work schedule from the 

interviews in combination with task exposure intensity scoring by industrial hygienists. 

The telephone interviews collected information concerning the frequency of performing a 

specified set of 90 construction-related tasks resulting in exposures to ‘vapors, gases, dusts, and 

fumes’ (VGDF). Task frequency from the questionnaire and assigned exposure days per month 

were as follows:

Worker Reported Task Frequency Description Assigned Days of 

Exposure Per Month

None: Did not perform the task 0

Rarely: Performed the task less than once per month 1

Monthly: Performed task 1-2 times per month 2

Weekly: Performed task weekly or most weeks 10

Daily: Performed task daily or almost every day 20

In addition to collecting information about the frequency of performing tasks, exposure intensity 

for each task reported by workers for jobs held more than six months was scored by three senior 

American Board of Industrial Hygiene (ABIH) certified industrial hygienists, each with 40 or 

more years of experience. Hygienists performed intensity scoring for the 15 a priori agents and 

90 construction tasks in the questionnaire prior to data collection following guidelines proposed 

by Rice and Heineman [2003]. For each agent, exposure intensities were ‘calibrated’ relative to 

NIOSH Recommended Exposure Levels (RELs), ACGIH Threshold Limit Values (TLV), or 

OSHA Permissible Exposure Levels (PELs) (Table 1). Intensity of exposure for each agent/task 

combination was recorded on a four-level ordinal scale. These ordinal categories and assigned 

exposure intensities relative to the reference concentration were as follows: 

Exposure Intensity Category and Description Assigned Exposure 

Intensity Weight 

Relative to 

Reference 

Concentration

None: Not exposed 0

Low: Less than half the reference concentration 0.5

Moderate: More than half but generally not greater than the reference concentration 1.0

High: Generally higher to much higher than the reference concentration 2.0

Explicit standardization rules on exposure intensity have been shown to improve exposure 

ratings [McGuire et al., 1998]. In addition to recording exposure intensity, experience and 

familiarity of the reviewer with the task was ranked on a three-level scale (direct experience, 

indirect experience, or literature reference only) [Rice and Heineman, 2003]. 

For derivation of exposure intensity score consensus among the industrial hygienists, three 

rounds of scoring were used. Any differences among the three hygienists of more than one 

exposure intensity category were noted and hygienists were asked to further document the 

rational for their choice of exposure scale based on direct personal experience or published 

literature. This documentation and rationale was shared among the three hygienists, who were 
allowed to modify their score if they felt appropriate. For tasks where full consensus was not 

achieved, the final intensity score used a weighted average of the industrial hygienists’ scores, 

with greater weight being given to raters most knowledgeable concerning the specific exposure 

and task (i.e. direct experience) [Ramachandran and Vincent, 1999]. Multi-rater kappa statistics 

were used to assess rater agreement [Chen et al., 2005; Fleiss et al., 2003]. 

Cases and controls reported a small number of tasks resulting in VGDF exposures in nonconstruction work and during military service. Many of these tasks were the same or similar to 

already scored construction tasks and were matched to construction tasks for exposure intensity 

assignment where appropriate. All remaining unscored tasks were scored for exposure intensity 

applying the same procedures used for construction tasks by one of the study industrial 

hygienists (JD). Workers also recorded frequency of exposure to a list of agents associated with 

bystander exposures in construction and non-construction work. Bystander exposures are 

typically much less than breathing zone exposures experienced by workers preforming tasks 

[Donovan et al., 2011]; therefore, bystander intensity was assigned a value of 10% (intensity 

weight=0.1) of the reference concentration.

Workers also were asked about the normal or usual number of hours worked each week for all 

jobs held 6 months or more. Cumulative exposure indices were calculated for each exposure 

scenario (i.e. construction, non-construction, military, and bystander) and these were summed to 

arrive at an overall cumulative exposure index for each agent. The following relationship was 

used to generate the cumulative exposure indices by exposure scenario:

Agent Cumulative Exposure Index = ∑ D ∗ ((H)/40) ∗ ((F) ∗ 12)/240) ∗ (I)

N

All Jobs & Tasks

Where:

D = Duration of the job in years

H = Average hours of work per week for each job

F = Frequency (days per month) of performing the task or experiencing the exposure (bystander)

I = Assigned exposure intensity relative to the agent reference concentration (0 to 2.0)

N = Number of jobs and tasks contributing to the exposure index for the agent of concern

For presentation of exposure distributions for cases and controls the cumulative exposure indices 

were categorized using tertile break points for the exposed controls [Hsieh et al., 1991], with 

unexposed subjects placed in a separate category. For regression modeling cumulative exposure 

indices were retained as continuous variables and standardized by dividing each worker’s 

cumulative exposure by a value representing an exposure at the upper 95th percentile of the 

range for all workers. Exposures were thus expressed as a fraction of the upper 95th percentile 

of the exposure distribution which allowed more directed comparison of exposure-response 

patterns across the exposures of a priori interest. Acids and caustics were grouped together as 

these exposures occurred with low frequency and their mode of action (e.g. respiratory irritation) 

is likely similar. 
References

1. Blanc PD, Eisner MD, Balmes JR, Trupin L, Yelin EH, Katz PP. 2005. Exposure to 

vapors, gas, dust, or fumes: Assessment by a single survey item compared to a detailed 

exposure battery and a job exposure matrix. Am J Ind Med 48: 110-117.

2. Brogger J, Bakke P, Eide GE, Gulsvik A. 2002. Comparison of telephone and postal 

survey modes on respiratory symptoms and risk factors. Am J Epidemiol 155: 572-576.

3. Chen B, Zaebst D, Seel L. 2005. A macro to calculate kappa statistics for categorizations 

by multiple raters. SAS Users Group International (SUGI 30) 2005 Philidelphia, Pa.: 

SAS Institute.

4. Donovan EP, Donovan BL, Sahmel J, Scott PK, Paustenbach DJ. 2011. Evaluation of 

bystander exposures to asbestos in occupational settings: A review of the literature and 

application of a simple eddy diffusion model. Crit Rev Toxicol 41: 52-74.

5. Fleiss JL, Levin B, Paik MC. 2003. Statistical Methods for Rates and Proportions. Third 

Edition ed. New York: John Wiley & Sons, Inc.

6. Hsieh CC, Maisonneuve P, Boyle P, Macfarlane GJ, Roberston C. 1991. Analysis of 

quantitative data by quantiles in epidemiologic studies: Classification according to cases, 

noncases, or all subjects? Epidemiology 2: 137-140.

7. McGuire V, Nelson LM, Koepsell TD, Checkoway H, Longstreth WT, Jr. 1998. 

Assessment of occupational exposures in community-based case-control studies. Annu 

Rev Public Health 19: 35-53.

8. NIOSH. 2015. NIOSH Pocket Guide to Chemical Hazards: Particulates not otherwise 

regulated Atlanta, GA.

9. OSHA. 2015. Chemical Sampling Information: Particulates Not Otherwise Regulated 

(Total Dust) Washington, DC.

10. Quinlan PJ, Earnest G, Eisner MD, Yelin EH, Katz PP, Balmes JR, Blanc PD. 2009. 

Performance of self-reported occupational exposure compared to a job-exposure matrix 

approach in asthma and chronic rhinitis. Occup Environ Med 66: 154-160.

11. Ramachandran G, Vincent JH. 1999. A Bayesian approach to retrospective exposure 

assessment. Appl Occup Environ Hyg 14: 547-557.

12. Rice C, Heineman EF. 2003. Application of a method to evaluate the quality of work 

histories and document the exposure assessment process. Am J Ind Med 44: 94-106.

13. Tager IB, Segal MR, Speizer FE, Weiss ST. 1988. The natural history of forced 

expiratory volumes. Effect of cigarette smoking and respiratory symptoms. Am Rev 

Respir Dis 138: 837-849.

14. Weinmann S, Vollmer WM, Breen V, Heumann M, Hnizdo E, Villnave J, Doney B, 

Graziani M, McBurnie MA, Buist AS. 2008. COPD and occupational exposures: A casecontrol study. J Occup Environ Med 50: 561-569.
Table I-S: COPD Cases and Controls by DOE Site

DOE Site Description1 Cases

(n=834)

Controls

(n=1243)

Total

(n=2077)

Brookhaven National Laboratory 19 29 48

Fernald Feed Materials Production Center (FMPC) 137 183 320

General Electric Company, Cincinnati 23 39 62

Hanford 167 224 391

Idaho National Engineering and Environmental 

Laboratory

55 66

121

Kansas City Plant 37 53 90

Mallinckrodt Chemical/Weldon Spring 10 14 24

Oak Ridge (All Sites) 114 195 309

Paducah Gaseous Diffusion Plant 44 58 102

Portsmouth Gaseous Diffusion Plant 54 92 146

Rocky Flats Plant 62 101 163

Savannah River Site 112 189 301

 

1 Case and control distribution by site not significantly different, Chi-Square=7.47, p=0.76

Table II-S: COPD Cases and Controls by Trade or Job Category

Trade Group or Job1 Cases

(n=834)

Controls

(n=1243)

Total

(n=2077)

Asbestos Worker or Insulator 25 37 62

Boilermaker 16 27 43

Carpenter 55 77 132

Cement Mason/Brick Mason/Plasterer 23 12 35

Electrician 128 226 354

Ironworker 50 64 114

Laborer 115 152 267

Mechanical Trades 7 8 15

Millwright 14 19 33

Operating Engineer 53 81 134

Painter 29 30 59

Plumber, Steamfitters, Pipefitter 130 200 330

Roofer 13 9 22

Sheet Metal Worker 45 82 127

Sprinkler Fitter 8 8 16

Teamster 32 34 66

All Other Construction and Non-Construction 91 177 268

 

1 Case and control distribution by trade significantly different, Chi-Square= 33.09, p=0.033
Table III-S: Exposure Intensity Scoring Results

Agent or Exposure Multi-Rater 

Kappa

Asbestos 0.71

Silica 0.66

Cement Dust 0.82

Man-Made-Mineral-Fibers 0.67

Engine Exhausts (Diesel or Gasoline) 0.71

Acids 0.49

Caustics 0.58

Welding, Thermal Cutting, Soldering, or Brazing 0.80

Metal Cutting, Grinding, and Machining Aerosol 0.80

Paint-Related Aerosol 0.78

Isocyanates 0.66

Organic Solvents 0.69

Wood Dust 0.70

Molds and Spores 0.78

Particulates not otherwise regulated (PNOR) 0.41
Table IV-S: Cumulative Exposure Index Distributions for COPD Cases and Controls

Cumulative Exposure Index

Cases or 

Controls

Mean 

(Std Err)

No Reported 

Exposure1

Number (%) of Workers by Tertile2

Tertile #1

Low

Tertile #2

Medium

Tertile #3

High

Asbestos Cases 39.3(1.3) 41 (4.9) 240 (28.8) 222 (26.2) 331 (39.7)

Controls 31.1 (1.0) 81 (6.5) 383 (30.8) 395 (31.8) 384 (30.9)

Silica Cases 45.7 (1.4) 35 (4.2) 236 (28.3) 240 (28.3) 323 (38.7)

Controls 38.1 (1.0) 71 (5.7) 388 (31.2) 396 (31.9) 388 (31.2)

Cement Dust Cases 32.1 (1.1) 48 (5.8) 261 (31.3) 226 (27.1) 299 (35.9)

Controls 27.9 (0.8) 103 (8.3) 398 (32.0) 365 (29.4) 377 (30.3)

Man-Made-Mineral-Fibers Cases 17.9 (0.7) 68 (8.2) 233 (27.9) 232 (27.8) 301 (36.1)

Controls 16.4 (0.6) 115 (9.3) 374 (30.1) 382 (30.7) 372 (29.9)

Engine Exhausts (Diesel or Gasoline) Cases 10.5 (0.5) 136 (16.3) 171 (20.5) 239 (28.7) 288 (34.5)

Controls 8.1 (0.4) 236 (19.0) 331 (26.6) 343 (27.6) 333 (26.8)

Acids and Caustics Cases 0.9 (0.1) 689 (82.6) 46 (5.5) 43 (5.2) 56 (6.7)

Controls 0.7 (0.1) 1082 (87.1) 53 (4.3) 53 (4.3) 55 (4.4)

Welding, Thermal Cutting, Soldering, or Brazing Cases 17.3 (0.8) 42 (5.0) 259 (31.1) 247 (29.6) 286 (34.3)

Controls 15.5 (0.6) 78 (6.3) 384 (30.9) 396 (31.9) 385 (31.0)

Metal Cutting, Grinding, and Machining Aerosol Cases 39.9 (1.7) 103 (12.4) 227 (27.2) 225 (27.0) 279 (33.5)

Controls 36.3 (1.4) 165 (13.3) 357 (28.7) 364 (29.3) 357 (28.7)

Paint-Related Aerosols Cases 6.0 (0.3) 128 (15.4) 229 (27.4) 225 (27.0) 252 (30.2)

Controls 5.6 (0.2) 209 (16.8) 340 (27.4) 352 (28.3) 342 (27.5)

Isocyanates Cases 1.3 (0.1) 625 (74.9) 57 (6.8) 64 (7.7) 88 (10.6)

Controls 1.0 (0.1) 985 (79.2) 85 (6.8) 87 (7.0) 86 (6.9)

Organic Solvents Cases 28.1 (1.0) 38 (4.6) 249 (29.9) 219 (26.3) 328 (39.3)

Controls 23.4 (0.8) 84 (6.8) 382 (30.7) 394 (31.7) 383 (30.8)

Wood Dust Cases 5.0 (0.2) 74 (8.9) 224 (26.9) 240 (28.8) 296 (35.5)

Controls 4.4 (0.2) 129 (10.4) 363 (29.2) 383 (30.8) 368 (29.6)

Molds and Spores Cases 14.2 (0.6) 137 (16.4) 193 (23.1) 222 (26.6) 282 (33.8)

Controls 12.1 (0.4) 237 (19.1) 332 (26.7) 338 (27.2) 336 (27.0)

Particulates not otherwise regulated (PNOR) Cases 89.4 (2.7) 28 (3.4) 232 (27.8) 237 (28.4) 337 (40.4)

Controls 74.2 (2.0) 67 (5.4) 389 (31.3) 398 (32.0) 389 (31.3)

ALL VGDF Cases 367.0 (11.2) 12 (1.4) 237 (28.4) 249 (29.9) 336 (40.3)

Controls 310.4 (8.3) 31 (2.5) 398 (32.0) 410 (33.0) 404 (32.5)

1 Number and percent of workers not reporting exposures included in the cumulative index.

2 Tertile cut points were based on the distribution of exposures for exposed controls. The percent ( ) represents the percent of the total distribution of exposures, 

including workers with no reported exposure.
Table V-S: Assessment of Cigarette Smoking and Exposure Interactions

Cumulative Exposure Index RERI1

(95% CI)

Asbestos 1.03 (0.95-1.11)

Silica 1.03 (0.95-1.12)

Cement Dust 1.01 (0.95-1.09)

Man-Made-Mineral-Fibers 1.00 (0.94-1.08)

Engine Exhausts 1.01 (0.92-1.10)

Acids and Caustics 1.06 (0.99-1.16)

Welding, Thermal Cutting, Soldering, Brazing 1.01 (0.95-1.09)

Metal Cutting, Grinding, and Machining Aerosol 0.99 (0.93-1.06)

Paint-Related Aerosols 1.02 (0.96-1.09)

Isocyanates 1.01 (0.95-1.10)

Organic Solvents 1.02 (0.95-1.10)

Wood Dust 1.05 (0.98-1.13)

Molds and Spores 1.07 (1.00-1.16)

Particulates not otherwise regulated (PNOR) 1.03 (0.96-1.12)

All VGDF 1.03 (0.95-1.12)

1 Relative excess risk due to interaction (RERI) based on a linear odds-ratio model. RERI represents the increased 

risk for a 10% increase in cumulative VGDF exposure and 10 pack-years of smoking compared to the sum of risks 

for smoking and VGDF exposure. Likelihood-based 95% confidence estimates for each RERI are shown.