asbestosis by chest radiography is best guided by standardized methods such as the classification of the International Labour Organisation (ILO) and its modifications. Standard films must always be used. For research and screening purposes, radiological findings of small opacities, grade 1/0, are usually regarded as an early stage of asbestosis. (p.312) Fischer et al reported that the concentration of asbestos fibres in lung tissue is the result of: the intensity and duration of exposure; geometry, type, and bio persistence of fibres; inhalation, elimination, and retention of fibres; and individual factors such as existing lesions, smoking, breathing frequency and volume, and work environment. Light or electron microscopical lung-dust analysis with counts of asbestos bodies or asbestos fibres, are often conducted in order to quantify the actual pulmonary burden. The concentrations of asbestos fibres in the air are reported as fibres in a millilitre (mL) i.e. fibre/mL. Inhalation exposure is generally regarded as cumulative and is expressed as concentration of fibres over time i.e. fibre/mL-years, noting that some asbestos fibres may be removed by mucociliary clearance or macrophages, while others may be retained in the lungs for extended periods. Therefore, to calculate asbestos exposure as cumulative fibre exposure of fibre/mL-year, duration of exposure (measured in years) is multiplied by the average air concentration for the period of exposure (measured in fibre/mL). The Agency for Toxic Substances and Disease Registry (ATSDR) reported that observations of asbestos-related diseases in groups of workers with cumulative exposures ranging from 5 to 1200 fibre/mL-years, resulting from 40 years of occupational exposure to air concentrations of 0.125 to 30 fibre/mL, have been shown. For the presence of pleural plaques, the ATSDR reported that an increased incidence of pleural plaques has been noted at relatively low cumulative exposure levels of approximately 0.12 fibre/mL-years. Ehrlich et al studied the long-term radiological effects of short-term exposure to amosite asbestos among a subset of 386 factory workers from an original cohort of
Summary of Council’s View On the basis of its evaluation of the studies discussed above, the Council considered that the presence of either asbestos bodies or pleural plaques (and diffuse pleural thickening) were indicative of prior asbestos exposure. However, the Council did not find evidence that the presence of either of these markers alone, without a stated asbestos exposure level and duration, and suitable lag period, would indicate that the disease asbestosis was also present. The Council recommends that the RMA considers whether diffuse pleural thickening should be specifically included in the SoPs regime as a compensable disease, possibly by recognising it as a separate disease. New Information on the Relationship between Pleural Plaques and / or Asbestos Bodies and Fibrosing Interstitial Lung Disease and Asbestosis The Council noted there is new information available on the relationship between pleural plaques, asbestos bodies, and asbestosis (see Appendix A. Table A4) and in relation to diffuse pleural thickening (see Appendix A. Table A5). Comparison of the Statements of Principles, Duration of Exposure is used as a Measure of Dose, with the Literature on a Threshold of Asbestos Concentrations In previous RMA reviews in 1996, and 2005 the required of asbestos exposure associated with producing FILD or Asbestosis expressed as days was reduced, and exposure expressed as days changed to hours of exposure. In the SoPs for Asbestosis for 1996 the minimum period of exposure to asbestos fibres was changed from 500 days (RH and BoP) to 200 days (RH) and 365 days (BoP). The rationale for the change was the 500 days minimum period of exposure was derived from occupational studies (15 studies/reviews, particularly studies of Wittenoom mine workers and insulators by de Klerk et al and Cookson et al) and the dose was lowered to account for naval personnel who are often on board ship for 24 hours per day, seven days per week.
cancer which may be due to some action of the fibrosis itself, but in this study this excess risk may also be due to an underestimate of asbestos exposure. New Information on the Levels of Asbestos Exposure Associated with Asbestosis in the Sound Medical-Scientific Evidence The Council noted there is new information available on the levels of asbestos exposure associated with asbestosis. The Council considered that some of the most important relevant new studies are by Harries, and van Oyen et al. An example of actual military data are studies by Harries, which were conducted in the British Naval Dockyards and provide information regarding asbestos fibre concentrations and exposure of naval personnel in the UK. There are others from, for example, the USA. Furthermore, the study by van Oyen et al is an example of a job-exposure matrix using TWA for occupational asbestos exposure in Australia (see New Information section from [93] and Appendix A. Table A4). Summary of Council’s View The Council’s attempt to compare a cumulative period of hours (from the SoPs) with fibre/mL-years (from the literature) did not reveal any relevant SMSE which could allow definite conclusions about the asbestos duration of exposure factors in Australian military personnel. The relevant SMSE in the information available to the Council was sufficient to show a dose of 25 does cause FILD and Asbestosis [67]-[80]. However, there were also studies that demonstrated the development of asbestosis occurring below this level at between 2-15 fibre/mL-years. , , , Additionally, the Council notes that fibre type should be considered along with estimates of the concentration of fibres, as there are data suggesting differences in rates of development of asbestosis depending on fibre type. The Council believes that the SoPs should ideally use historical measurements from military work environments to determine the relevant dose as well as a cumulative period of time. If these data are not available, then those doses from comparable environments (for example the building of Royal Australian Navy ships) in the
the exposure by occupation exposure times. When exposure was expressed as no asbestosis was found at autopsy when exposure was <2 fibre/mL-years, even after 31-45 years of residence time. In the group exposed to >2-5 fibre/mL-years asbestosis was found (4 deaths). If a threshold dose for asbestosis does exist it is at approximately 2 fibre/mL if off-shift exposure is ignored. No threshold demonstrated. Hein et al (2007) RMA ID: 067597 Follow-up of Chrysotile Textile Workers: Cohort Mortality and 3072 textile plant workers (59% men) 36=asbestosis deaths (1960- 2001) No smoking history Carolina chrysotile asbestos textile plant Small amounts of crocidolite from South Africa Cumulative exposure: N=3072; Median=5.5 fibre/mL-year Fibre concentration method used: statistical modelling of nearly 6000 industrial hygiene samples taken over the period and analysed using Phase Duration of employment: N=3072; median=1.1 years Mortality study of chrysotile exposure and cause of death as indicated within the National Death Index 36 asbestosis deaths (US expected deaths = 0.15; SMR=232.5; 95%CI: 162.8, 321.9; p<0.01) Carolina expected deaths =0.33; SMR=108.2, 95%CI: 75.8, 149.8). Asbestos exposure producing pneumoconiosis seen at 3-<16 fibre/mL-years years Response
Contrast Microscopy. Specific job matrix used to calculate job exposure. Each day in the work history was assigned an exposure level based on the job exposure matrix and cumulative exposure was defined as the sum of the assigned exposure concentrations over all days worked. Mortality analysis (observed pneumoconiosis and other respiratory diseases deaths=85, asbestosis=42) showed increasing trends in pneumoconiosis SMRs with increasing cumulative exposure were observed overall from 3-<16 (SMR 2.43; (1.33-4.08). Asbestosis mortality (observed deaths=62) showed statistically significant interaction between cumulative exposure and age category was observed (p=0.026). Author’s conclusion: association between estimated chrysotile exposure and mortality from asbestosis observed in previous updates of this cohort were confirmed with the addition of 11 years of follow-up. Cumulative exposure was positively and years
significantly associated with asbestosis mortality. Modelled exposure-response relationship showed no threshold for development of asbestosis. Ehrlich et al (1992) RMA ID: 034901 Long Term Radiological Effects of Short Term Exposure to Amosite Asbestos Among Factory Workers Subset of 386 factory workers (100% men) with less than one year of exposure and low cumulative exposure (<25 fibre/mL-year) 238 had serial X-rays Smoking history available Amosite asbestos factory (Imported from South Africa; very small amounts of chrysotile used at one time) Also residential exposure 5 -120 (>5µm long) Cumulative exposure: n=386; Median=25.1 (range=0.1 Exposure concentration: M=51.8 (SD=25) fibre/mL Fibre concentration method used: Membrane Filter Method (1968 and 1971). Average fibre counts for each job title were estimated from measurements carried out at two other plants operated by the company after 1954; one in Tyler, Texas and another in Port Allegheny, Pennsylvania. Duration of exposure: Median=0.5;6 months years Radiological study reporting effect of short term amosite exposure producing parenchymal and pleural abnormalities. Parenchymal abnormality (profusion >1/0 ) >20 years from first employment by cumulative exposure (fibre/mL-year): <5 fibre/mL-year: n=85,10(12%)= abnormal 5.1-25 n=87, 12(14%)= abnormal 25.1-125 n=119, 30(25%)= abnormal >125 n=49,29(59%)= abnormal Asbestos exposure producing parenchymal abnormality seen at <5 fibre/mL-years year:
for ≥20 years, no cumulative exposure threshold for parenchymal and pleural fibrosis detected, and parenchymal and pleural progression were still detectable >20 years after the end of exposure. Exposure for ≥1 month was sufficient to produce radiological signs of parenchymal and pleural fibrosis. Those in the lowest cumulative exposure stratum <5 were found to have high rates of abnormality. Increase in risk of parenchymal abnormality of 6-7% for each fibre/ml-years. Larson et al (2010) RMA ID: 067598 Vermiculite Worker Mortality: Estimated Effects of Occupational Exposure to Libby Amphibole 1862 mine and process workers 69=asbestosis deaths No smoking history Vermiculite mining and processing operation (tremolite and actinolite, winchite and richterite) Cumulative exposure: N=1862; Median=4.3 Cumulative exposure Fibre concentration method used: Historical air sampling data were used to estimate the average Duration of exposure: N=1862; Median=0.8 (25th-75th percentile 0.1-4.1 years) Retrospective cohort mortality study Significantly elevated SMR for deaths from asbestosis =69 (expected=0.5; SMR=142.8; 95%CI:111.1,180.8) Asbestos exposure producing asbestosis seen at 8.6 to <44.0 fibre/mL- years years
factors used to convert between the two and 8 hr TWAs calculated. 3rd quartile. Cumulative fibre exposure (20 year lag) showed statistically significant risk from 8.6 to <44.0 fibre/mL-year (n=25; RR=8.0, 95%CI: 3.2, 19.5) and ≥44.0 fibre/mL-year (n= 32, RR= 11.8, 95%CI: 4.9, 28.7) Authors conclusion: statistically significant association from 8.6 fibre/mL- year for deaths from asbestosis with significantly elevated SMR=142.8 for asbestosis. et al (1997) RMA ID: 026469 Exposure and Mineralogical Correlates of Pulmonary Fibrosis in Chrysotile Asbestos Workers 54 asbestos workers necropsy reports (lung tissue for 39 workers) (44=men, 10=women) 34 controls necropsy reports (lung tissue for 31 workers) Chrysotile asbestos textile Raw asbestos predominantly from Quebec with small amounts from BC and Zimbabwe; small amounts of crocidolite Cumulative exposure: N=54; Median=30.2 fibre/mL-year Men had larger cumulative exposures than women 34.6 and 25.6 Exposure assessment method used (published previously): Linear statistical models for reconstructing historic dust exposure levels, taking into account textile Duration of employment: N=54; range=0.1- >27.3 Latency: Median=30.0 Case- control study examining relationship between chrysotile exposure and pulmonary fibrosis in a South Carolina textile plant Asbestosis was usually present in asbestos textile workers with >20 cumulative exposure Asbestos exposure producing asbestosis seen at 10-20
(22=men, 12=women) Fibre counts performed on 39 former textile workers and 31 controls. NB: small numbers Incomplete smoking history available yarn woven but never carded, spun or twisted. median fibre/mL-year respectively processes, dust control measures, and job were developed. Estimates used 5,952 industrial hygiene samples from 1930-1975. Individual exposure data were not available for each worker in the cohort; estimates of exposure by job category at the plant were required. Both the exposure zone concept and the uniform task concept were used to develop exposure models which used historic plant production, control, and Median fibrosis scores were greater in the asbestos workers than in the control population for all levels of exposure significant (p< 0.001) for exposure 7.2-36.5 Chrysotile median 37.6 & tremolite median 5.0 asbestos fibre x106 dry lung p<0.05 36.6-109.5 Chrysotile median 30.8 & Tremolite median 6.4 asbestos fibre x106 dry lung p<0.05 109.5-370 Chrysotile median 104.5 & Tremolite median 27.8 asbestos fibre x106 dry lung p<0.05 Not significant for fibre-years. Author’s conclusion: Both cumulative exposures to asbestos and lung fibre burden were strongly correlated with severity of asbestosis. Lack of year year
exposure data to estimate exposure by job and calendar period. Cumulative lifetime TWA exposure for each worker was calculated by multiplying estimates of exposure for each job held by the time spent in each job and was expressed as fibre-year. statistical power in the study was largely due to the small number of cases with low and intermediate levels of exposure, making it not possible to detect a threshold dose for the development of asbestosis. Asbestosis of grade 2 severity or more was consistently found in workers with lifetime cumulative exposures in excess of 20 fibre/mL-year and in three cases with exposures ranging from 10-20 Authors’ conclusion: histologic asbestosis was usually detectable with exposures of >20 fibre/mL-year and a few cases were found with estimated cumulative exposures of 10-20 fibre/mL-year. McDonald et al (2004) Cited by: Antao et al (2012) RMA ID: 068460 Mortality in a Cohort of Vermiculite Miners Exposed to 406 mine workers (100% men) with net service of at Vermiculite mine/mill Exposure Concentration: M=18 concentration method used: Standard Optical Duration of exposure: M=9 years Cohort mortality study reporting deaths in vermiculite miners from Libby, Montana Asbestos exposure producing respiratory year
for the period before1975. Used job descriptions to estimate for each job the duration and the number of spent by workers in different operation locations; the cumulative exposure was then calculated respiratory disease. The all-cause linear model would imply a 14% increase in mortality for mine workers exposed occupationally to 100 fibre/mL-year or about 3.2% for a general population exposed for 50 years to an ambient concentration of 0.1 fibre/mL – not insignificant impact. Rohs et al (2008) RMA ID: 067995 Low-Level Fiber-Induced Radiographic Changes Caused by Libby Vermiculite. A 25-Year Follow-up Study (Chest radiographic changes only) 280 mine workers of the original 513 cohort (94.3% men) 80=pleural changes (68=localised pleural plaques 12=diffuse pleural thickening, 28.7%) 8=Interstitial changes (irregular Vermiculite mine/mill Cumulative exposure: N=280 M=2.48 (SD=4.19; fibre/mL-year Cumulative exposure - Interstitial changes (n=8): M= 11.86 Fibre concentration method used: Membrane filters method since 1972. Cumulative fibre exposure was calculated using the TWA by the number of at the TWA summed overall years according to department. Duration of exposure: N=280 based on hire date Hired on or before 1973 n =186 Hired after 1973 n= 94 Radiographic study reporting vermiculite - induced interstitial change and pleural changes in a cohort of vermiculite workers Significant increase seen in the follow-up in pleural changes: 2.0% in the 1980 study to 28.7% in 2005. Interstitial changes: 0.2% in 1980 to 2.9% in 2005 Asbestos exposure producing interstitial changes seen at 11.37
opacities, profusion of ≥1/0; 2.9%) NB. Small numbers of workers with interstitial changes (n=8) Smoking history available (SD=6.46) fibre/mL-year All 8 with interstitial changes occurred at the 72% or greater maximum cumulative fibre exposure range, 6 occurring at the 90% or greater range. Due to new environmental controls, there was a decrease in fibre exposure after 1973. Therefore, each department was assigned two values, fibre exposures through 1973 and exposures after 1973. Individuals were assigned a cumulative fibre exposure value, which was the summation of estimated fibre exposure by department, based on the years employed between 1963 and 1980. Pleural changes directly related to cumulative fibre exposure, greatest prevalence (54.3%) in the highest exposure quartile fibre/mL-year) of workers Pleural changes can occur at low lifetime cumulative fibre exposure levels as demonstrated by the 12% prevalence within participants and living non participants with <1.92 fibre/ mL-years cumulative fibre exposure, and 20% prevalence within participants with <2.21 fibre/mL-year cumulative exposure 2.9% of participants had interstitial changes and were significantly related to cumulative exposure mean exposure of 11.37 fibre/mL-year Author’s conclusion: exposures to asbestos users of Libby
profusion of ≥1/1 according to American Thoracic Society criteriab) Excluded those with known diseases Aims of study were to clarify group suitable for screening by HRCT Variable asbestos exposure although the main exposure types unclear Smoking history available examinations no case of HRCT asbestosis detected. 60 participants with <25 fibre/mL-year, 2 cases were detected, both having basilar crackles and one having small irregular opacities on X-ray the asbestos exposure level associated with each job was assessed using published airborne measurements available in the French database index was then calculated by summing the values for all job positions held, with reference to the occupational calendar established in the interview, the products of the job exposure level (in fibre/mL) by job duration (in years). Dust measurements relationship for 25-99.9 (OR=3.4; 95% Cl: 0.8, 15.2; p>0.05) and≥100 fibre/mL-year (OR=6.1; 95% Cl: 1.5, 25.9) in comparison with ≤25 fibre/mL-year (Trend test p =0.002) but not with duration of exposure (Trend test p=0.791). Author’s conclusions: significant association between HRCT fibrosis and cumulative asbestos exposure, with a clear relationship. Only 2 cases of HRCT pulmonary fibrosis (2%) among the 112 patients with a cumulative fibre exposure of <25 fibre/mL -years. HRCT can detect early-stage asbestosis in people who have been highly exposed to asbestos and whose X-ray can be considered normal. HRCT screening does not seem warranted for people with low response related response
atmospheric measurements were available for the period before 1960. Sullivan (2007) RMA ID: 045641 Vermiculite, Respiratory Disease, and Asbestos Exposure In Libby, Montana: Update of a Cohort Mortality Study 1672 mine and mill workers (all men) 40=asbestosis deaths 22=asbestosis deaths Followed May 1982-Dec 2002 No smoking history Vermiculite mine/mill Miners, millers and processors Cumulative exposure: N=1672; Median=8.7 fibre/mL-year All deaths: n=767; Median= 21.0 fibre/mL-year Asbestosis: n=40; Median=228.4 fibre/mL-year (worked <1year =36.2 fibre/mL-year and worked ≥1 year =244.8 fibre/mL-year Fibre concentration method used: Job-exposure matrix exposure index available for this and previous studies of Libby workers is based on fibre count data obtained using Optical Phase Contrast Microscopy of all asbestiform fibres, of which 6% were estimated to be tremolite Duration of exposure: N=1672; M=4.0 (range=1day -43.1) years Asbestosis deaths: n=40 (5.3% of cohort); mean duration of employment in those with asbestosis M=14.6 years Historical cohort mortality reporting vermiculite exposure Based on 22 asbestosis deaths SMR increased with increasing cumulative exposure: <0-49.9 fibre/mL-year exposure (SMR=37.3; 95% Cl:7.5, 122.3); SMR for respiratory death was 1.9 for CFE < 3.5 fibre/mL-year 50.0-249.9 (SMR =212.6; 95%CI: 91.6, 433.2) and ≥250 fibre/mL-year (SMR=749.1; 95% Cl: 373.0, 1367.8) allowing for a 15-year exposure lag More likely than expected to die from asbestosis with employment duration Asbestos exposure producing asbestosis seen at ≥50
<15 months (SMR=38.2; 95% Cl: 7.7, 125.1), 15 months to 9.9 years (SMR=236.0; 95%CI: 107.8, 461.1) and employment duration ≥10 years (SMR=628.6; 95%CI: 301.1, 1185.1) Author’s conclusion: SRR was statistically significant asbestosis increased across categories of exposure duration (≥15 months) and over increasing categories of cumulative exposure from ≥50 fibre/mL-year asbestosis. Note levels of likely exposure were high in this mill. Berry et al (1979) Cited by: Becklake (1991) RMA ID: 000429 Asbestosis: a study of relationships in an asbestos textile factory 379 textile factory workers (100% men) with >10 years’ service 58 =possible asbestosis (34 = certified as asbestosis) Diagnosis and examination by Chrysotile and crocidolite asbestos textile factory first employed after 1950 cumulative exposure: (n=197) M=84 fibre/mL-year Concentration of exposure: M=5.0 fibre/mL Fibre concentration method used: For each job description a dust level was calculated for each year by taking the average of the levels Duration of exposure: M=20.1 Group first employed after 1950 (n=197) the average follow-up since first Morbidity study reporting asbestos exposure producing asbestosis and crepitation’s For possible and certified asbestosis the 1% prevalence are estimated at 55 fibre/mL-year and 72 fibre/mL-year. Asbestos exposure producing asbestosis seen 84 response
no dust measurements For 1933-45 the concentrations were to be 1.5 times those in 1951 and for as 1-25 times the 1951 values. Seidman et al (1986) RMA ID: 020152 Mortality Experience of Amosite Asbestos Factory Workers: Relationships 5 to 40 Years After Onset of Short-Term Work Exposures 820 asbestos factory workers (100% men) 31=asbestosis deaths No smoking history Amosite asbestos factory Concentration of exposure: Median=50 fibre/mL Fibre concentration method used: There were no direct fibre count measurements or exposures in this plant. Average fibre counts for each job title were estimated from measurements carried out at two other plants operated by the company after 1954; one in Tyler, Duration of exposure: N=820; month to years n=384:<6 n=241:6-24 n=195:24+ months Mortality study after short-term work exposure The lower the cumulative exposure dose, the longer it took for adverse mortality experience to become evident and also the smaller the magnitude of that adverse mortality. Workers exposure to <25 fibre/mL-year cumulative exposure observed and expected deaths from 5 to 40 elapsed years since onset work were: 109 men exposed to 6.0 -11.9 fibre/mL-year (asbestosis deaths=1; Asbestos exposure producing asbestosis seen at 100 Dose-
Smoking history available be accurate to a factor of 3-5. Eighteen-year cumulative exposures were calculated by summing annual exposures during the 18 year from first exposure Silica exposure not assessed (also can produce interstitial opacities on chest radiographs) test (X2) =24.4; p<0.001) Risk of small irregular opacities category >1/2 was seen fibre/mL-year (All men n=11; RR=2.19;Trend test (X2) =18.0; p<0.001) Risk of bilateral pleural thickening (grade A) was seen at >200 fibre/mL-year (All men n =40; RR=1.44;Trend test (X2) =4.34; p=0.04) Risk of bilateral pleural thickening (grade B) was seen at >200 fibre/mL-year (All men n =23; RR=1.38;Trend test (X2) =2.36; p=0.12) Author’s conclusion: 20 years from 1st exposure mortality rates were elevated. Men leaving asbestos exposure had a risk of radiographic progression similar to men continuing in exposure and men with abnormal
Table A2. Overview of 36 Papers Relevant to Low Level Exposure to Asbestos for Asbestosis (Ordered by Study Type and Date) Original Study Author (RMA ID) or Review of that Study RMA ID Or Review Author (RMA ID) Title Subjects Type of Exposure Level of Exposure (fibre/mL) Duration of Exposure (year) Outcome: Study/Review with asbestos exposure (but with no exposure data that could be compared to the levels in the SoPs), producing Asbestosis; then Other Studies & Reviews Mortality Studies Paris et al (2009) RMA ID: 067601 Pleural Plaques and Asbestosis: and Time-Response Relationships on HRCT Data 5545 retired workers exposure to asbestos (100% men) 882=pleural plaques 375=asbestosis Metal, construction and repairs industry Cumulative Exposure Indexa: M=49.6 (Estimated 80% had high level of exposure) Concentration of exposure (fibre/mL) not reported Duration of exposure: M=27.4 (SD=11.1) years Time since 1st exposure: M=41.9 (SD=8.1) years Morbidity study reporting asbestos exposure producing asbestosis and pleural plaques. Pleural plaques: Overall (n=882) Trend test p<0.0001. High exposure (n=777; 17.5%) OR significant (OR=2.89; 95%CI: 1.51, 5.52; p<0.0001). Asbestosis: Overall (n=375) Trend test p=0.01. High exposure (n=322; 7.3%) OR significant (OR=1.20; 95%CI: 0.62, 2.30; p=0.02). Only cumulative exposure (p<0.0001) or level of exposure (p=0.02) were significantly associated with asbestosis. Both time and dose-response relationships were demonstrated for pleural plaques. Only relationships were shown for asbestosis. Author’s conclusion: Both and response
relationships were demonstrated for pleural plaques, while only dose-response relationships were demonstrated for asbestosis. Reid et al (2005) RMA ID: 037507 The Effect of Asbestosis on Lung Cancer Risk Beyond the Dose Related Effect of Asbestos Alone 1988 (1196 former Wittenoom workers; 792 residents of Wittenoom) cancer prevention program participants 58=lung cancer asbestosis) 1930=non-cases (220=asbestosis) Crocidolite mine/mill Cumulative exposure: Cases (n=58 lung cancer): M=11 (range=2.6-46.5) fibre/mL-year Controls (n=1930 non-cases): M=5 (range=1.8-13.5) fibre/mL-year Concentration of exposure: (n=58 lung cancer): M=12 (range=6.2-40.3) fibre/mL Controls: (n=1930 M=6 (range=2.1-20.3) fibre/mL Duration of exposure (days): (n=58 lung cancer): M=330 (range=118-1048) days Controls(n=1930 non-cases): M=285 (range=106-854) days Morbidity study reporting asbestos exposure producing asbestosis in lung cancer patients. 58 lung cancer cases 21; 36% had radiographic asbestosis compared to 220 (11%) of participants. Radiographic asbestosis (OR=1.94, 95% Cl: 1.09, 3.46) and asbestos exposure (OR=1.21 per fibre/mL-year, 95% Cl: 1.02, 1.42) significantly associated with an increased risk of lung cancer. Intensity of exposure and cumulative exposure were both statistically significant. The interaction between cumulative asbestos exposure and asbestosis was not significant (Hazard Ratio = 0.82, 95% CI: 0.59, 1.13, p = 0.23). Author’s
Selikoff et al (1990) RMA ID: 035792 Asbestotic Radiological Abnormalities Among United States Merchant Marine Seamen 3324 seamen (100% men) 1157 (34.8%)= pneumoconiosis 329 (9.9%) (profusion ≥1/0) 227 (6.8%) (pleural thickening, pleural plaques, with or without calcification) 601 (18.1%) (only radiological change) Merchant marine seamen Not reported Duration of exposure: M=>20 years Morbidity study reporting asbestos exposure producing pneumoconiosis and pleural plaques. Prevalence rate for all radiological asbestos related abnormalities (pleural or parenchymal or both) highest level (38.5%) >40 years from onset of exposure. Authors conclusion: prevalence of asbestotic changes was greater among seamen who had served in the engine department (391/420; 425%) compared with seamen in other departments, including deck (301/820; 36.6%), steward (278/ 981; 28.4%), or with service in multiple departments (167/541; 30.9%) Sluis-Cremer (1989) RMA ID: 035796 Progression of Irregular Opacities in Asbestos Miners 1454 African asbestos mine and mill workers (100% men) (661 discontinued work; 793 continued work) Amphibole mine/mill Mining exposure up to 1st X-ray: exposure after 1st X-Ray: Yes=793; M=38.4 Mining exposure up to 1st X-ray: exposure after 1st X-Ray Yes=793; M=6.7 years Morbidity study reporting asbestos exposure producing asbestosis and pleural plaques. No difference in the frequency of disease incidence or rate of progression between
≤1 to 26.7% in men >15 years of exposure. Authors conclusion: prevalence of pleural abnormality (pleural thickening, calcification, or obliteration of the costophrenic angle) were related to both age and the duration of asbestos exposure. Pleural and parenchymal abnormalities significantly predicted by fibre concentration, after adjusting for age and duration of exposure Mortality Studies Deng et al (2012) RMA ID: 067596 Relationship Between Chrysotile Exposure and Mortality from Lung Cancer and Asbestosis 586 Chinese textile factory workers 226= deaths 37=asbestosis deaths Asbestos chrysotile textile factory Cumulative exposure: N=586; M=126.1 (SD =181.1) Concentration of exposure: M=13.8 (SD=17.3) fibre/mL Duration of exposure: N=586; M=25.4 (SD=8.3) years Mortality study reporting asbestos exposure producing asbestosis. 37=asbestosis deaths 2.39 per 1000 Cumulative asbestos exposure was significantly associated with mortality from asbestosis in all models (p<0.001), except for the additive relative risk model. High estimated cumulative exposures were due to high
dust/fibre concentrations in the workplace and the longer duration of employment. Estimated risk of asbestosis mortality increased with asbestos cumulative exposure in a convex curve, which tended to be steeper at a low exposure level (<50 fibre/mL-year) than a higher exposure level (>50 fibre/mL-year). Risk of asbestosis mortality rose more sharply than lung cancer mortality at higher exposure levels (>150 fibre/mL-year). Author’s conclusion: study confirmed strong associations between exposure to chrysotile asbestos and lung cancer and asbestosis, in which clear exposure-response relationships were observed. Moolgavkar et al (2010) Cited by Antao et al (2012) RMA ID 068460 Potency Factors for Risk Assessment at Libby, Montana 1662 Libby vermiculite workers (100% men) 117=non-malignant respiratory disease Vermiculite mine/mill Cumulative exposure: N=1662 M=91.4 Worked <1 M=8.5 fibre/mL-year Employment duration: N=1662 M= 3.6 years; Worked <1 year(n=850): 0.27 years. Worked ≥1 Mortality study reporting asbestos exposure producing non-malignant respiratory disease. Risk for non-malignant respiratory disease
Worked ≥1 year: M=178 117 non-malignant respiratory disease cumulative exposure: M=270 Worked <1 year: M=16.1 Worked ≥1 year: M=447 year (n=812): M=7.1 years 117 non-malignant respiratory disease employment duration: 91.4 M= 5.9 years; Worked <1 year (n=48): 0.30 years Worked ≥1 year (n=69): M=9.8 years cumulative exposure of 100 fibre/mL-year: RR=1.14 (95% CI: 1.09, 1.18). Non-malignant respiratory disease (n=117): SMR=2.29 (95% Cl: 1.89, 2.74). respiratory disease for those worked ≥1 year (n=69): SMR=2.62 (95% Cl: 2.04, 3.31). Author’s conclusion: SMRs for non-malignant respiratory disease are significantly elevated in the entire cohort and also in the sub-cohort of workers employed for ≥ 1 Detailed comparison by exposure categories was not possible for respiratory disease. Agency for Toxic Substances and Disease Registry (ATSDR) (2002) Cited by US Department of Health & Human Services, ATSDR & Disease Registry Division of Health Health consultation: mortality in Libby, Montana (1979-1998) 542 subjects 12=asbestosis deaths (1=household contact, 11=former mine employees) Libby, Montana community Not reported Duration of exposure: Former employees died from n=11; M=24.5 (SD=10.7; years Mortality due to asbestosis was significantly elevated over the 20-year period. All asbestosis deaths were associated with the mining and milling facility through either previous employment or as a household contact of a
Assessment & Consultation (2008) RMA ID:067997 former worker. Author’s conclusion: SMR were all statistically significant for asbestosis in all areas of analysis. A mortality for the Libby community revealed significantly elevated SMR for asbestosis (40 to 80 times higher than expected) and lung cancer (20% to 30% higher than expected) Liddell et al (1997) RMA ID: 026465 The 1891-1920 Birth Cohort of Quebec Chrysotile Miners and Millers: Development from 1904 and Mortality to 1992 9780 workers (100% men) 8009=deaths 108= pneumoconiosis deaths Chrysotile mine/mill and asbestos factory Level of exposure: Exposure 300 million particles per cubic foot (mppcf) British Occupational Hygiene Society (1968) suggested an asbestos air concentration of 1 mppcf = 3 fibre/ml (detected by phase contrast microscopy). Therefor the concentration of exposure approximately 300 Duration of employment: >1 month (0.1 years) Mortality study reporting asbestos exposure producing pneumoconiosis. Pneumoconiosis death rates per 100 000 subject-years clearly associated with exposure at the asbestos mine/mill (23=deaths) and Thetford mine-company 3 (53=deaths). Men whose exposures were <300mpcf.y accounted for 30 pneumoconiosis deaths. Exposure <300 mpcf.y has been essentially mild, although there was a small risk of pneumoconiosis mortality. Author’s
mppcf = 900 fibre/mL conclusion: Higher exposures have, led to excesses, increasing with degree of exposure, of mortality from all causes, but such exposures, of at least 300 mpcf.y. Albin et al (1994) RMA ID: 034864 Retention patterns of asbestos fibres in lung tissue among asbestos cement workers 165 Lung tissue analysis (69 Swedish asbestos-cement workers and 96 controls) 2=pulmonary fibrosis deaths chrysotile, tremolite, and crocidolite Concentration of exposure: M=1.7 (median=1.2, range=00-7-3) fibre/mL. For workers performing milling, mixing, sawing, and polishing operations, or sweeping asbestos barn M=>2 fibre/mL Duration of employment: M=18 (median=15) years Mortality study reporting asbestos exposure producing pulmonary fibrosis. Chrysotile relatively rapid removal in lungs, whereas amphiboles (tremolite and crocidolite) displayed a slower removal patterns. Author’s conclusion: Chrysotile retention may be dependent on dose rate, chrysotile and crocidolite retention may be increased by smoking, and chrysotile and tremolite retention may be enhanced by the presence of lung fibrosis. Amandus et al (1987) Antao et al Study reporting asbestos exposure producing respiratory disease. Non-malignant respiratory disease (n=20): SMR=2.43 (95% CI: 1.48, 3.75; p<0.05).
for >1 is enough for "ascertainment" of asbestosis (i.e. >5.0 fibre/mL-year). Estimates of cumulative asbestos exposures required for induction of asbestosis have diminished during the years. The threshold cumulative dose of asbestos necessary for clinical manifestations of asbestosis 20-200 fibre/mL-year with a few cases of 2-20 US Department of Health and Services, ATSDR & Disease Registry Division of Health Assessment & Consultation (2008) RMA ID: 067997 Summary Report. Exposure to Vermiculite From Libby, Montana, at 28 Processing Sites in the United States 28 sites - 3 groups who experienced the most significant exposure to asbestos former employees at exfoliation facilities, household contacts of these former employees, and some community members sites that exfoliated Vermiculite from Libby: Not reported Not reported Report. Author’s conclusion: Fibre levels inside the exfoliation facilities ranged from below detection levels fibre/mL. Before 1980, measured fibre levels ranged from 1-10 fibre/mL, which is above the current acceptable level of 0.1 fibre/mL for occupational exposure to asbestos. Libby indicated airborne fibre levels were as high as 245 fibre/mL in an unloading area. sampling results indicated airborne fibre
Agency for Toxic (2001) RMA ID: 035227 Toxicological Profile for Asbestos Not reported Not reported Level of exposure: 10 fibre are typically in a cubic metre (fibre/m3) of rural outdoor air. There is 1 million cm3 (or 1 million mL) in a cubic metre so there would be 0.00001 fibre/mL of asbestos in rural air. Air in the city is 10 fold higher. Close to asbestos mines or factories levels reach 10,000 fibre/m3 i.e. 0.01 fibre/mL. Not reported Report. Author’s conclusion: asbestosis at prolonged exposures of 5-20 fibre/mL corresponds to cumulative exposures of 50-200 fibre/mL-year for a 10 year exposure. Chronic exposure significantly increases asbestosis mortality rates in exposed workers with cumulative exposure of 32-1271 fibre/mL-year. Cases of asbestosis with very high asbestos air fibre and shorter latent periods (5-6 years) compared with latency of 10-20 years from studies of workers more recently exposed to lower fibre concentrations. Exposure durations (median 6-12 months) at 5-100 fibre/mL associated with pulmonary fibrosis. Burdorf & Swuste (1999) Roggli et al (2010) RMA ID: 067548 An Expert System for the Evaluation Of Historical Asbestos Exposure as Diagnostic Not reported Not reported Not reported Not reported Historical Review. Author’s conclusion: a life time risk of asbestosis of 2 per 1000 cases at 4.5 fibre/mL-year. Evidence of direct exposure to asbestos amounting to, or
sufficient to induce asbestos-related disease. Anonymous (1997) RMA ID: 026517 Asbestos, Asbestosis, and Cancer: the Helsinki Criteria for Diagnosis and Attribution Not reported Not reported For clinical purposes, the following are recommended to identify persons with a high probability of exposure to asbestos dust at work: > 0.1 million amphibole fibres (>5 μm) per gram of dry lung tissue or over I million amphibole fibres (>1 μm ) per gram of dry lung tissue; or over 1000 asbestos bodies per gram of dry tissue (100 asbestos bodies per gram of wet tissue) or over 1 asbestos body per mL of bronchoalveolar lavage fluid, as measured by light microscopy Not reported Report.Author’s conclusion: asbestosis generally associated high exposure levels with radiological signs of parenchymal fibrosis. Mild fibrosis may occur at lower exposure levels, and detectable parenchymal fibrosis may not been seen on X-rays. HRCT can confirm radiological findings of asbestosis and show early changes not seen on chest X-rays. Cumulative exposure, on a probability basis, should be considered the main criterion for the attribution of a substantial contribution by asbestos to lung cancer risk. RR is roughly doubled for exposed to asbestos fibres at a cumulative exposure of 25 fibre-years or with an equivalent occupational history, at which level asbestosis may or may not be present or
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