Twenty-two of 83 silicotic sandblasters in the New Orleans area had complicating mycobacterial infections: 10 with Mycobacterium tuberculosis, 9 with M. kansasii, and 3 with M. intracellulare. The place of residence was related to the variety of atypical infection. The mean age of the patients was 44 years and the average exposure to silica was less than 10 years. Sputum conversion occurred in all 18 patients with positive cultures, but 8 died in respiratory failure secondary to progressive silicosis. The roentgenographic features of the disease were often atypical: Lower lobe involvement occurred in 6 patients, hilar adenopathy without calcification in 8, and diffuse filling of air spaces in 5. Pulmonary function studies usually showed a mixed pattern of obstruction and restriction associated with impaired gas transfer. Pulmonary function often declined over relatively short intervals of time with corresponding adverse chest roentgenographic alterations.

BACKGROUND:A previously published cohort study of some 2670 employees of the North American sand industry, followed through 1994, provided strong evidence of a causal relationship between quartz exposure and death from both silicosis and lung cancer, after allowance for cigarette smoking and in the absence of known occupational carcinogens. Unexpectedly, a significant excess mortality from chronic non-malignant renal disease [observed 16; expected 7.6; standardized mortality ratio (SMR) 212] was also found, whereas deaths from renal cancer at this stage were close to expectation (observed 6; expected 5.2).OBJECTIVES:Our primary aim was to discover whether death from chronic renal disease was related to the estimated intensity of crystalline silica exposure. A further aim was to determine whether or not our previous estimates of lung cancer and silicosis risk were confirmed by mortality in the cohort 6 years later.METHODS:With help from the US National Death Index, surviving members of the cohort, with the exception of employees of a small plant in Canada, were traced through 2000. The cause of death was determined for all who had died, for comparison against National and State mortality rates. Nested case-referent analyses were then undertaken, as previously, of deaths from lung cancer and silicosis, plus end-stage renal disease and kidney cancer, in relation to quantitative re-estimates of quartz exposure.RESULTS:The total number of deaths through 1994 was 990; there were 231 additional deaths during the period 1995-2000. The SMRs were significantly higher in the later than the earlier period, mainly due to a relative increase in heart disease and external causes. The updated odds ratios for lung cancer and silicosis were almost identical to those published previously, with lung cancer risk again related to average silica concentration and cumulative exposure, but not to length of employment. In contrast, risks of neither end-stage renal disease nor renal cancer were related to cumulative exposure, although now based on 19 cases (SMR 239), and 10 cases (SMR 202), respectively, in fact, opposite trends were apparent for both diseases. However, because of the small numbers there was only limited power to assess the statistical significance of these trends or of any separate relationship with the duration or intensity of exposure.CONCLUSIONS:Our findings support a causal relationship between lung cancer and quartz exposure after allowance for cigarette smoking, in the absence of other known carcinogens, but failed to find similar evidence to explain the excess mortality from either chronic renal disease or kidney cancer.

The potential of chronic or acute irritant gas exposures to cause asthma or a variant condition, reactive airways dysfunction syndrome (RADS) was investigated by observing asthma incidence in a large working population, using person-years at risk (P-YR) to compute relative rates (RR). Health data came from employee examinations at 62 pulp and paper plants. The 39122 workers who denied asthma beginning before the observation period included: 19326 denying irritant exposures, with no gassing exposures; 19349 with self-reported irritant exposures, and no gassing; and 447 with documented gassings. Asthma was defined as self-reported asthma beginning after the start of observation. P-YR accrued from September 29, 1986, for the nonexposed and exposed workers, and from date of first gassing for gassed workers, and ended with disease onset in any who developed asthma. RR of asthma with 95% confidence intervals (CI95) were calculated for the exposed and gassed groups, relative to the nonexposed. Exposed (nongassed) workers had an elevated asthma rate, RR=1.48, CI95=1.17-1.86, after adjustment for effects of gender and number of examinations. The rate in gassed workers was not significantly elevated: RR=1.95, CI95=0.75-5.08. Of the five asthma cases occurring after gassings, none conformed to diagnostic criteria for RADS. Chronic exposures were associated with increased rate of asthma onset, which must be interpreted with caution because self-reported data defined both exposure category and disease. Documented gassings were not associated with significantly increased rate, and none of 447 gassed persons developed RADS.

Background: In 1997 a Working Group of the International Agency for Research on Cancer changed an earlier classification of crystalline silica as a human carcinogen from Group 2A to Group 1, though commenting that the carcinogenicity might vary dth industrial circumstances and depend on additional factors affecting biological activity, including the distribution of its polymorphs,Objective: We aimed to determine whether pure quartz exposure uncomplicated by the presence of other contaminating carcinogens, as experienced by workers in the production of high-grade industrial sand, was causally related to an increased risk of lung cancer.Methods: A cohort of 2670 men employed before 1980 for 3 years or more in one of nine North American sand-producing plants and a large associated office complex was selected for study, Of the cohort, 2644 (99%) were traced through 1994, and certificated cause of death ascertained for 1025 (99%) of the 1039 men known to have died. Standardised mortality ratios (SMRs) were calculated for the main causes of death, using both US and state or provincial male mortality rates for reference,Findings: The main analyses of deaths, 20 or more years after first employment against regional rates, gave the following SMRs: all causes 109, lung cancer 139, other malignancies 98, non-malignant respiratory disease 161, and nephritis/nephrosis 244, There were, in total, 37 deaths from silicosis or silico-tuberculosis, with one or more death at least in all nine production plants, Analyses failed to show any relation between lung cancer risk and duration of employment, The increased SMR for lung cancer was wholly due to high rates in four plants in two states, whereas no increase was found in the remainder of the cohort.Conclusion: In the absence of information on smoking histories and risk in relation to estimated exposure, the increased SMR for lung cancer (139), although statistically significant, cannot be attributed confidently to crystalline silica. An answer to the question of attributability must await the findings of the nested case-control study, in which level of exposure and smoking habits were ascertained for cases and matched controls. The strong indication in this cohort of excess mortality from non-malignant renal disease deserves further investigation. (C) 2001 British Occupational Hygiene Society. Published by Elsevier Science Ltd. All rights reserved.

BACKGROUND Lung cancer and silicosis mortality were examined longitudinally and by a case-referent analysis in a cohort of workers selected from the North American industrial sand industry. Date of hire in the case-referent sub-cohort extended as far back as the second decade of the twentieth century. OBJECTIVE The aim of this study component was to develop estimates of average and cumulative exposure to respirable crystalline silica for the 342 selected cases and referents. METHODS Process and dust control histories were developed for each plant, and quantitative exposure data obtained from each of them and from a trade organization. An algorithm was developed to convert historical exposures reported in particle count concentrations to modern measures of mass concentration of respirable crystalline silica. Personal exposures were adjusted for use of protective equipment based on frequency of use and type of protection. FINDINGS Between 1974 and 1998, a total of 14249 exposure measurements had been taken using a cyclone and membrane filter and gave an overall geometric mean of 42 microg/m3. The only exposure data identified earlier were based on approximately 500 samples collected across the industry between 1947 and 1955 using the Greenburg-Smith impinger, with analysis by microscopy. These data were converted to modern measures using a factor of 1 mppcf = 276 microg/m3 respirable dust and then adjusting for percentage silica. In general, the highest exposures occurred in bagging and bulk-loading operations and the lowest in wet processing of sand. CONCLUSIONS There has been a substantial decline in exposure levels in this industry over time. The decline was rapid between the 1940s and 1970s and current exposures are, on average, less than 50 microg/m3. The use of personal protective equipment was judged to have had little impact on exposure before the 1970s.

Background: A cohort mortality study of 2670 men in nine North American industrial sand plants resulted in 83 deaths from lung cancer 20 or more years after hire (standardized mortality ratio 139) and 37 deaths from silicosis (including seven from silico-tuberculosis). The lung cancer excess was unrelated to duration of employment and not found in all plants. Objectives: The primary aim was to determine whether lung cancer risk among these employees was related to quantitative estimates of crystalline silica exposure, after allowance for cigarette smoking. A secondary aim was to do the same for silicosis mortality, partly as a means of validating the estimated levels of exposure. Methods: A nested case-referent study was undertaken with cases matched with up to two controls on plant, age and date of first employment from men who survived the case. Exposures were estimated by linking work histories to a job-exposure matrix, undertaken separately. Cigarette smoking information was obtained from medical records and other sources, blind as to case-control status. Matched statistical analyses were conducted using conditional logistic regression. Findings: Odds ratios for silicosis mortality were significantly related to cumulative silica exposures and tended to a relationship with category of average crystalline silica concentration, but inconsistently with length of employment. After accounting for a strong effect of cigarette smoking, odds ratios for lung cancer were related to cumulative crystalline silica exposure and to average silica concentration, but not to length of employment. Conclusion: These findings support a causal relationship between lung cancer and quartz exposure after allowance for cigarette smoking, in the absence of cristobalite or other known occupational carcinogens.

BACKGROUND The role of silicosis as either a necessary or incidental condition in silica associated lung cancer remains unresolved. To address this issue a cohort analysis of dose-response relations for crystalline silica and lung cancer mortality was conducted among diatomaceous earth workers classified according to the presence or absence of radiological silicosis. METHODS Radiological silicosis was determined by median 1980 International Labour Organisation system readings of a panel of three “B” readers for 1809 of 2342 white male workers in a diatomaceous earth facility in California. Standardised mortality ratios (SMR) for lung cancer, based on United States rates for 1942–94, were calculated separately for workers with and without radiological silicosis according to cumulative exposures to respirable crystalline silica (milligrams per cubic meter × years; mg/m3-years) lagged 15 years. RESULTS Eighty one cases of silicosis were identified, including 77 with small opacities of ⩾1/0 and four with large opacities. A slightly larger excess of lung cancer was found among the subjects with silicosis (SMR 1.57, 95% confidence interval (CI) 0.43 to 4.03) than in workers without silicosis (SMR 1.19, 95% CI 0.87 to 1.57). An association between silica exposure and lung cancer risk was detected among those without silicosis; a statistically significant (p = 0.02) increasing trend of lung cancer risk was seen with cumulative exposure, with SMR reaching 2.40 (95% CI 1.24 to 4.20) at the highest exposure level (⩾5.0 mg/m3-years). A similar statistically significant (p = 0.02) dose-response gradient was observed among non-silicotic subjects when follow up was truncated at 15 years after the final negative radiograph (SMR 2.96, 95% CI 1.19 to 6.08 at ⩾5.0 mg/m3-years), indicating that the association among non-silicotic subjects was unlikely to be accounted for by undetected radiological silicosis. CONCLUSIONS The dose-response relation observed between cumulative exposure to respirable crystalline silica and lung cancer mortality among workers without radiological silicosis suggests that silicosis is not a necessary co-condition for silica related lung carcinogenesis. However, the relatively small number of silicosis cases in the cohort and the absence of radiographic data after employment limit interpretations.

There is limited and conflicting evidence regarding the exposure-response relationship between exposure to crystalline silica and silicosis; the level of risk to current workers remains uncertain. We conducted an epidemiologic investigation of 1,809 workers in the diatomaceous earth industry, where exposures to crystalline silica are primarily to the cristobalite form. On the basis of the median of three independent readings, 81 (4.5%) workers were judged to have opacities on chest radiographs (small opacities, profusion >= 1/0, and/or large opacities). Age-adjusted relative risk of opacities increased significantly with cumulative exposure to crystalline silica. The concentration of respirable crystalline silica to which workers were exposed (highly correlated with period of hire) was an important determinant of risk after accounting for cumulative exposure. For workers with an average exposure to crystalline silica of <= 0.50 mg/m3 (or hired >= 1950), the cumulative risk of opacities for a cumulative exposure to crystalline silica of 2.0 mg/m3-yr was approximately 1.1%; for an average exposure > 0.50 mg/m3 (or hired < 1950), the corresponding cumulative risk was 3.7%. These findings indicate an exposure-response relationship between cumulative exposure to crystalline silica and radiographic opacities; moreover, the relationship was substantially steeper among workers exposed at the highest average concentrations of crystalline silica.

We appreciate Dr. Thomas's interest, but we cannot agree that his rule of thumb applies well to the data shown in the figure. Our equations allow upward adjustment of the observed FVC in percent predicted (FVC% PRED) in proportion to the reduction of observed FEV1/FVC. The line added by Dr. Thomas identifies about nine individuals as having FEV1/FVC >0.65 and FVC% PRED ranging from <70%, down to about 45%. No one would doubt that these individuals show restrictive abnormality, but what about the more numerous individuals with mild obstruction just above his line? The mathematical adjustment for obstruction will be small because the obstruction is mild, and their adjusted FVCs will still be below the lower limit of normal (however it is reckoned). Those individuals also show restrictive physiology, since their obstruction does not account for the subnormal FVC. Defining Patients' Abnormal Pulmonary FunctionCHESTVol. 111Issue 4PreviewLefante and colleagues (August 1996)1 are to be commended for demonstrating the correlation between FEV1/FVC and FVC expressed as a percentage of the predicted value (FVC%PRED) in 656 working men with reduced values of FEV1/FVC. The lower the FEV1/FVC, the lower was the FVC%PRED. Full-Text PDF

The study was designed to test the hypothesis that the risk of lung cancer from asbestos exposure is confined to persons with radiographic evidence of pulmonary fibrosis. Occupational and smoking histories were obtained from 271 patients with a confirmed diagnosis of primary lung cancer and 678 referents (279 with other respiratory disease and 399 with cardiac disease). Histories were reviewed blind to assess the timing, duration, and probability of exposure to asbestos. To allow for a lag between asbestos exposure and the development of lung cancer, subjects were classified by the time they had spent in an occupation entailing definite or probable exposure more than 15 years before diagnosis. The presence and extent of fibrosis was assessed blindly from chest radiographs by three readers and scored for small opacities with the ILO 1980 International Classification of Radiographs of the Pneumoconioses. 93 (34.3%) cases had worked in an occupation with definite or probable asbestos exposure compared with 176 (25.8%) referents (crude odds ratio for lung cancer 1.49, 95% Cl 1.09-2.04). After adjustment for age, sex, smoking history, and area of referral, the odds ratio (95% Cl) was 2.03 (1.00-4.73) in the subgroup of 211 with a median ILO score for small parenchymal opacities of 1/0 or more, and 1.56 (1.02-2.39) in the 738 with a score of 0/1 or less (ie, those without radiological evidence of pulmonary fibrosis). These results suggest that asbestos is associated with lung cancer even in the absence of radiologically apparent pulmonary fibrosis.

This review updates the published epi- demiological literature since 1986, a year chosen because the International Agency for Research on Cancer (IARC) conducted a thor- ough review of papers published before that date.The IARC working group concluded at that time that the evidence for carcinogenicity of crystalline silica in experimental animals was sufficient, while in man it was limited.'These conclusions led the IARC to classify crystalline silica as 2A -that is, "probably carcinogenic to humans".2The evidence on which these judgements are based was summarised in an editorial published in 1989.3Only brief ref- erence will be made to papers published before that date.For the present review, relevant fac- tors taken into account include: (1) the dis- tinction between silica exposure and silicosis;(2) study design and quality; (3) confounding exposures, including smoking; and (4) de- monstration of dose dependency.Very few studies are available of cohorts, defined by their employment, that have been exposed to crystalline silica but not to other potentially carcinogenic materials.As with most other epidemiological studies which focus on lung cancer as the primary outcome of interest, smoking could rarely be accounted for fully in the reviewed literature.Also, past silica exposure levels could only be approximated or ranked in an ordinal fashion, if exposure was estimated at all.

OBJECTIVETo derive a method of taking into account the effects of obstruction on the FVC, allowing more accurate assessment of other negative ("restrictive") influences.DESIGNIn 656 subjects with airways obstruction, defined as FEV1/FVC of 0.70 or less, regression of FVC was expressed as percentage of predicted value (FVC %PRED) on potential explanatory variables, including FEV1/FVC. The resulting equation was used to adjust FVC %PRED in 530 other obstructed men, to test whether the adjustment resulted in a different relationship of FVC %PRED to body weight.SETTINGA large occupational respiratory surveillance program utilizing rigorously quality-assured and standardized spirometry.SUBJECTSThe study included 5,188 men aged 45 to 65 years who denied fibrogenic dust exposures, including 656 with airways obstruction.RESULTSThere was a significant (p < 0.0001) linear relationship between more severe obstruction (lower FEV1/FVC) and lower FVC %PRED. Depending on which of several predictive equations is used, obstruction explains 15 to 17% of variability in FVC %PRED over the entire range of severity of obstruction. Adjusting for obstruction in the separate group of 530 subjects showed a significantly larger effect of body weight on FVC %PRED.CONCLUSIONA simple equation can be used to discount the negative effects of obstruction on FVC. This allows more accurate clinical interpretation and can be useful in the analysis of epidemiologic data.

It is both an honor and a source of sadness that I present this first Thomas A. Neff Lecture. Tom had the primary attributes of the academic chest physician—he was a fine and dedicated teacher, and a caring, highly competent practitioner of his specialty. I also have it from someone who should know that he was a favorite of the fellows. At a time when specialty medicine needs more Tom Neffs, these skills and personal attributes may become in short supply. Pulmonary medicine will miss Tom!

Normative spirometric values were derived from 5,042 white (of mainly European ancestry) and black (of mainly African ancestry) men and women paper plant workers who are never-smokers, with no respiratory symptoms or diagnoses and no history of occupational exposure to fibrogenic dusts or irritant chemicals. This cohort was selected from a much larger population under long-term respiratory surveillance (n > 50,000 at 50 plants). Standardized equipment, procedures, and data reduction methods complied with ATS recommendations. Data were collected by the medical departments of the participating companies as part of their routine health surveillance, and the graphic and numeric test results were transmitted to the Tulane University Section of Environmental Medicine for centralized quality assurance, interpretation, and archiving. The large numbers allow derivation of gender- and race-specific reference values. Lower limits of normal were derived and depend upon residual variation and any changes in variation with age. The results indicate that polynomial regression equations provide a significantly better fit than linear regressions with breakpoints. In addition to being more biologically plausible, the polynomial model more closely matches observed longitudinal changes in lung function with age. The age range of the cohort, 18 to 65, provides a regression that more closely matches the observed values in this range, because it does not include "supernormal" elderly survivors, which can lessen the slope of the regression and artifactually increase the predicted values of 50 to 65 yr olds. The regression equations derived for black men and women do not support the use of a single race adjustment (0.85 or 0.88) for all age, sex, height, and spirometric test parameter combinations. These race- and gender-specific regression equations, with their respective lower limits of normal, should improve the detection and quantification of adverse health effects in working individuals and populations.

American Journal of Industrial MedicineVolume 25, Issue 4 p. 609-610 Letter to the Editor Potency versus importance in fiber pathogenicity Dr. Janet M. Hughes PhD, Corresponding Author Dr. Janet M. Hughes PhD Department of Biostatistics and Epidemiology, Tulane Medical Center, New Orleans, LouisianaTulane University Medical Center, 1430 Tulane Avenue, SL-57, New Orleans, LA 70122Search for more papers by this authorHans Weill MD, Hans Weill MD Department of Medicine, Tulane Medical Center, New Orleans, LouisianaSearch for more papers by this author Dr. Janet M. Hughes PhD, Corresponding Author Dr. Janet M. Hughes PhD Department of Biostatistics and Epidemiology, Tulane Medical Center, New Orleans, LouisianaTulane University Medical Center, 1430 Tulane Avenue, SL-57, New Orleans, LA 70122Search for more papers by this authorHans Weill MD, Hans Weill MD Department of Medicine, Tulane Medical Center, New Orleans, LouisianaSearch for more papers by this author First published: April 1994 https://doi.org/10.1002/ajim.4700250416Citations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume25, Issue4April 1994Pages 609-610 RelatedInformation

In this report of a 5-yr longitudinal study of workers employed at six cotton textile mills, exposure and across-shift FEV1 change were evaluated as possible predictors of the annual change in FEV1 for yarn manufacturing workers. A total of 611 workers had three repeatable spirometric tests, over at least 3 yr, and at least one (average of three) across-shift test, while always working the same shift. The "same shift" criterion controlled for the effect of diurnal variation. Average exposure was determined from measures of lint-free elutriated cotton dust in combination with job histories. This study found a significant association between the acute and chronic effects of cotton dust exposure. Both exposure and across-shift change proved to be significant predictors of annual change, and excess annual declines in FEV1 were predicted even for exposures of 200 micrograms/m3 and across-shift drops in FEV1 of 200 ml. These results suggest that, to prevent dust-related chronic decline in lung function, current smokers should be excluded from yarn manufacturing work and exposures should be reduced below 200 micrograms/m3, to approximately 100 micrograms/m3.

A survey of workers in seven man made mineral fibre (MMMF) production plants, the subject of a previous report, was conducted, with other blue collar workers serving as regional comparisons. Based on the median reading of chest radiographs by five readers, a low prevalence of small opacities, all at the 1/0 and 1/1 profusion levels, was again found: for workers with MMMFs, 23/1435 (1.6%); for comparison workers, 2/305 (0.7%). Spirometric measurements indicated generally healthy populations, and were not related to presence of opacities. Ninety three per cent (21/23) of MMMF workers with opacities worked at the two plants with the highest exposures to fine fibres, resulting in a dose-response relation across plants. For one location, the prevalences of opacities for the MMMF and comparison workers were not significantly different (5.9% (13/220) v 3.1% (2/65)). No comparison x ray films were obtained for the MMMF plant with the highest prevalence (6.6%), so a second phase of the study was conducted, with pre-employment films from these two plants. On this second reading, the prevalence of opacities was lower; there were no significant differences between the two groups of films, and no relation between opacities and exposure indices. There was considerable inter and intrareader variability. These results indicate no adverse clinical, functional or radiographic signs of effects of exposure to MMMFs in these workers.