Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis.

In an attempt to explain the much greater risk of respiratory cancer at the same cumulative exposure in asbestos textile workers in Charleston, South Carolina, than in Quebec miners and millers, both exposed to chrysotile from the same source, 161 lung tissue samples taken at necropsy from dead cohort members were analysed by transmission electron microscopy. Altogether 1828 chrysotile and 3270 tremolite fibres were identified; in both cohorts tremolite predominated and fibre dimensions were closely similar. Lung fibre concentrations were analysed statistically (a) in 32 paired subjects matched for duration of employment and time from last employment to death and (b) in 136 subjects stratified by the same time variables. Both analyses indicated that the Quebec/Charleston ratios for chrysotile fibre concentration in lung tissue were even higher than the corresponding ratios of estimated exposure intensity (mpcf). After allowance for the fact that regression analyses suggested that the proportion of tremolite in dust was probably 2.5 times higher in Thetford Mines, Quebec, than in Charleston, the results from both matched pair and stratification analyses of tremolite fibre concentrations in lung were almost the same as for chrysotile. It is concluded that neither fibre dimensional differences nor errors in estimation of exposure can explain the higher risks of lung cancer observed in asbestos textile workers. The possible co-carcinogenic role of mineral oil used in the past in asbestos textile plants to control dust provides an alternative hypothesis deserving consideration.     

Dust exposure and lung cancer in Quebec chrysotile miners and millers

A large cohort of men born between 1891 and 1920 and employed for at least a month in the chrysotile producing industry of Quebec has been under study since 1966. These men were followed from first employment (the earliest in 1904) to 1992, by which time over 8000 had died, 657 from lung cancer. The current study is of 488 cases of lung cancer formerly employed at three places, viz. a major complex, here called Company 3, in the region of Thetford Mines (243 cases), the mine and mill in the town of Asbestos (206) and a small asbestos-products factory in the same town (39). For each case, four referents were sought by random selection from among survivors to a greater age, after matching on place of employment, age of starting work, smoking habit and date of birth. This process was highly successful, although six cases had less than four referents. For each man (the 488 cases with 1941 referents) and for each calendar year of employment, we obtained the fraction of the year worked at various levels of intensity, assessed in 13 ‘dust categories’ of mpcf (million particles per cubic foot). We then calculated how many years each man spent at these various levels; these years, adjusted for the length of the working week (66 h until 1937; 48h 1938–1949; and 40h 1950–1985), were accumulated up to ten years before the death of the case. The men were classified according as they were non-or ex-smokers, or smokers, of cigarettes. For each man at Company 3 and one referent for each, his years of work in a central area of five mines and in a peripheral area of ten mines were differentiated; contamination of the chrysotile by fibrous tremolite was known to be much greater in the central than in the peripheral area. Case-referent comparisons, within place of employment, were made by conditional logistic regression. As anticipated from earlier subject-years analyses, lung cancer risks were found to be negligible for years worked in dust categories 1 and 2 (averaging 0.5 and 2 mpcf), regardless of place; as the upper limit of category 1 is considerably higher than permitted nowadays, the lung cancer risk from exposure to chrysotile at permitted levels can be taken as extremely small. Patterns of exposure-response for higher categories were irregular. At Company 3, some risks appeared elevated for years spent in the higher dust categories: 3–4, 5–7, 8–10 and 11–13, with averages around 9, 20, 36 and 92 mpcf, respectively. For categories 3–4 and 8–10, the odds ratios were high for some or all work in the central area, but minimal for years spent in the peripheral area only. Odds ratios were fairly low for cigarette smokers who worked in categories 5–7 and also for years spent in the highest categories (11–13). At the mine and mill in Asbestos, all risks were low except for years worked by non-and ex-smokers in categories 7–13 (ca. 40 mpcf). There were no increased risks at the factory. It was known from the subject-years analyses that most of the excess had occurred at Company 3, but it is now clear that for all practical purposes it was confined to the central area there, probably due largely to fibrous tremolite and in dust conditions of at least dust category 3. The average of this category was 7 mpcf or very roughly 24 fibres/ml, about two orders of magnitude higher than today's hygiene standards.     

Dust exposure and mortality in an American chrysotile textile plant

Three parallel cohort studies of asbestos factory workers were undertaken to investigate the effects of mineral fibre type and industrial process on malignant mesothelioma, respiratory cancer, and asbestosis. This report describes the mortality of a cohort of 2543 men, defined as all those employed for at least a month from 1938 to 1958 in a textile plant in South Carolina in which chrysotile was the only type of asbestos used. Of these, 863 men (34%) had died before 31 December 1977, one from malignant mesothelioma. Twenty one deaths were ascribed to asbestosis and 66 to cancer of the lung. Compared with the number expected from South Carolina, there was an excess of 30 deaths from respiratory cancer (ICD 160-164) in men 20 or more years after first employment (SMR 199.5). In men employed five years or more, no SMRs for this category rose above 300. Individual exposures were estimated (in mpcf X years) from recorded environmental measurements. Life table analyses and "log-rank" (case-control) analyses both showed a steep linear exposure-response that was some 50-fold greater at similar accumulated dust exposures than in Canadian chrysotile mining and milling. These findings agree closely with those from another study in this plant and confirm that mesothelioma is rarely associated with chrysotile exposure. Cigarette smoking habits did not greatly differ between the textile workers and the Canadian miners and millers. The far greater risk of lung cancer in the textile industry, if not attributable to other identified cocarcinogens, may be related to major differences in the size distribution of fibres in the submicroscopic range which are not detected by the usual fibre or particle counting procedures.     

Dust exposure and mortality in an American chrysotile textile plant.

Three parallel cohort studies of asbestos factory workers were undertaken to investigate the effects of mineral fibre type and industrial process on malignant mesothelioma, respiratory cancer, and asbestosis. This report describes the mortality of a cohort of 2543 men, defined as all those employed for at least a month from 1938 to 1958 in a textile plant in South Carolina in which chrysotile was the only type of asbestos used. Of these, 863 men (34%) had died before 31 December 1977, one from malignant mesothelioma. Twenty one deaths were ascribed to asbestosis and 66 to cancer of the lung. Compared with the number expected from South Carolina, there was an excess of 30 deaths from respiratory cancer (ICD 160-164) in men 20 or more years after first employment (SMR 199.5). In men employed five years or more, no SMRs for this category rose above 300. Individual exposures were estimated (in mpcf X years) from recorded environmental measurements. Life table analyses and "log-rank" (case-control) analyses both showed a steep linear exposure-response that was some 50-fold greater at similar accumulated dust exposures than in Canadian chrysotile mining and milling. These findings agree closely with those from another study in this plant and confirm that mesothelioma is rarely associated with chrysotile exposure. Cigarette smoking habits did not greatly differ between the textile workers and the Canadian miners and millers. The far greater risk of lung cancer in the textile industry, if not attributable to other identified cocarcinogens, may be related to major differences in the size distribution of fibres in the submicroscopic range which are not detected by the usual fibre or particle counting procedures.     

Occupational exposure to textile dust and lung cancer risk: Results from the ICARE Study

Background

To investigate the association of lung cancer with occupational exposure to textile dust and specifically to cotton dust in the population‐based case‐control study ICARE.

Methods

Lifelong occupational history of 2926 cases and 3555 controls was collected using standardized questionnaires, with specific questions for textile dust exposure. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using unconditional logistic regression models controlling for confounding factors including smoking and asbestos exposure.

Results

An inverse association between textile dust exposure and lung cancer was found among workers exposed ≥5% of their work time (OR = 0.80, 95%CI = 0.58‐1.09), more pronounced for distant exposures (40+ years; up to a 56% reduced risk, statistically significant). The OR of lung cancer was significantly decreased among workers exposed to cotton fibers (OR = 0.70, 95%CI = 0.48‐0.97).

Conclusions

Our results provide some evidence of a decreased risk of lung cancer associated with exposure to textile dust, particularly cotton.

     

Nasal cancer in the textile and clothing industries

A case-control study of 160 patients with cancers of the nasal cavity and paranasal sinuses and 290 controls showed an excess risk associated with employment in the textile or clothing industries, with the increase (relative risk [RR] = 2.1) found only among female workers. There was, however, no increasing trend in risk with years of employment or duration since first exposure. Both male and female workers were at an increased risk of adenocarcinoma (RR = 2.5), with further enhancement of risks for those experiencing dusty work conditions. Although aetiological inferences cannot be drawn from this study, the finding of raised risk supports some previous observations and the need for further investigation of the cancer experienced by textile and clothing workers.     

Nasal cancer in the textile and clothing industries.

A case-control study of 160 patients with cancers of the nasal cavity and paranasal sinuses and 290 controls showed an excess risk associated with employment in the textile or clothing industries, with the increase (relative risk [RR] = 2.1) found only among female workers. There was, however, no increasing trend in risk with years of employment or duration since first exposure. Both male and female workers were at an increased risk of adenocarcinoma (RR = 2.5), with further enhancement of risks for those experiencing dusty work conditions. Although aetiological inferences cannot be drawn from this study, the finding of raised risk supports some previous observations and the need for further investigation of the cancer experienced by textile and clothing workers.     

Dust exposure and mortality in chrysotile mining, 1910-75.

We report a further follow-up of a birth cohort of 11 379 workers exposed to chrysotile. The cohort consisted of 10 939 men and 440 women, born 1891-1920, who had worked for at least a month in the mines and mills of Asbestos and Thetford Mines in Quebec. For all subjects, length of service and estimates of accumulated dust exposure were obtained, with a smoking history for the vast majority. Three methods of analysis, two based on the "man-years" methods, the other a "case-and-multiple-controls" approach, gave results consistent with one another and with previous analyses. By the end of 1975, 4463 men and 84 women had died. Among men, the overall excess mortality, 1926-75 was 2% at Asbestos and 10% at Thetford Mines, much the dustier region. The women, mostly employed at Asbestos, had a standardised mortality ratio (SMR) all causes, 1936-75) of 0.90. Analysis of deaths 20 years or more after first employment showed that in men with short service (less than five years) there was no discernible correlation with dust exposure. Among men employed at least 20 years, there were clear excesses in those exposed to the heaviest dust concentrations. Reanalysis in terms of exposure to age 45 showed definite and consistent trends for SMRs for total mortality, for lung cancer, and for pneumoconiosis to be higher the heavier the exposure. The response to increasing dose was effectively linear for lung cancer and for pneumoconiosis. Lung cancer deaths occurred in non-smokers, and showed a greater increase of incidence with increasing exposure than did lung cancer in smokers, but there was insufficient evidence to distinguish between multiplicative and additive risk models. There were no excess deaths from laryngeal cancer, but a clear association with smoking. Ten men and one woman died from pleural mesothelioma. If the only subjects studied had been the 1904 men with at least 20 years' employment in the lower dust concentrations, averaging 6.6 million particles per cubic foot (or about 20 fibres/cc), excess mortality would not have been considered statistically significant, except for pneumoconiosis. The inability of such a large epidemiological survey to detect increased risk at what, today, are considered unacceptable dust concentrations, and the consequent importance of exposure-response models are therefore emphasised.     

Respiratory symptoms and lung function in wool textile workers

Our study investigated a group of 216 wool textile workers (158 women and 58 men). Respiratory symptoms were assessed by questionnaire in wool textile workers and in 130 not exposed (control) workers. Ventilatory capacity was measured in wool workers by recording maximum expiratory flow-volume (MEFV) curves on Monday before and after the work shift. Forced vital capacity (FVC), 1-second forced expiratory volume (FEV₁), and flow rates at 50% and the last 25% of the vital capacity (FEF₅₀, FEF₂₅) were measured on the MEFV curves. Analysis of the data demonstrated a significantly higher prevalence of all chronic respiratory symptoms in wool workers than in controls. being the highest in wool workers for nasal catarrh (M: 63.8%; F: 44.9%) and for sinusitis (M: 62.1%; F: 43.0%). A high prevalence of acute symptoms, associated with the work shift, was also noted in wool workers. Exposure to wool dust caused significant across-shift reductions of ventilatory capacity varying from 1.4% for FEV, to 9.1% for FEF₅₀. Textile workers exposed to wool for > 10 years in the workplace had similar across-shift reductions of ventilatory capacity tests as those with shorter exposures. In a large number of these wool workers, FEF₅₀ and FEF₂₅ were below 70% of predicted normal values. Smokers had acute and chronic lung function changes similar to those of nonsmokers, indicating that smoking did not account for all the respiratory effects seen in wool processing workers. Our data suggest that dust exposures in wool textile mills may be associated with the development of chronic respiratory symptoms and impaired lung function.     

The amphibole hypothesis--a nested case-control study of lung cancer and exposure to chrysotile and amphiboles

This paper describes a case control study investigating separately the lung cancer risk of exposure to chrysotile and to amphiboles. Logistic regression models were used to estimate separate exposure-response curves for the two fibre types, controlling for smoking. In the period longer than 15 years before lung cancer diagnosis, smokers above the 90th percentile of cumulative exposure to either chrysotile (OR = 1.8, 95% CI = 0.6-5.2) or amphibole (OR = 2.3, 95% CI = 0.9-6.2) had a somewhat higher risk than those with lower exposure. The author found suggestive evidence of an association between chrysotile and lung cancer, and especially between amphiboles and lung cancer. In this study, cumulative exposures to amphiboles were on average 40 times lower than cumulative exposures to chrysotile, and the author assumes that the amphibole effect would be much higher if the amphibole level of cumulative exposure were the same as that of chrysotile.     

温石棉与肺癌关系的巢式病例对照研究

目的探讨单纯接触温石棉与肺癌发病的关系。方法按照巢式病例对照的研究方法，从一个追踪了30年接触温石棉的男性固定队列中，收集所有的肺癌患者作为病例组，按1：4的配对比例在该队列中选取非癌症者作为对照组，配对因素为同性别、年龄相差〈5岁、工龄相差〈5年、吸烟情况一致。结果研究队列中收集到40例肺癌病例，发病水平高于全国平均水平[标化死亡比（SMR）=1．77]。肺癌发病密度由高到低的工种分别是原料工（741．5／10万人年）、梳纺工（424．3／10万人年）、编织工（365．0／10万人年）、维修工（285．5／10万人年），与接触温石棉的浓度高低一致。与低浓度接触组比较，高浓度接触组发生肺癌的相对危险度（OR）为3．7，95％可信区间为2．30～8．16，差异有统计学意义（P〈0．01）。结论单纯温石棉接触能增加工人肺癌发病的危险性。     

The combination of effects on lung cancer of cigarette smoking and exposure in quebec chrysotile miners and millers

Although it is well known that both cigarette smoke and microscopic airborne asbestos fibres can cause lung cancer, evidence as to how these two agents combine is nebulous. Many workers have believed in the multiplicative theory, whereby asbestos increases the risk in proportion to the risk from other causes. However, evidence against this theory is mounting: a recent review concluded that the multiplicative hypothesis was untenable, and that the relative risk of lung cancer from asbestos exposure was about twice as high in non-smokers as in smokers, a finding largely independent of type of asbestos fibre. The criteria for entry to the current study were met by 7279 men in the 1891-1920 birth cohort of Quebec chrysotile miners and millers. The data consisted of date of birth, place of employment, smoking habit, asbestos exposure accumulated to age 55 and, for those 5527 who died between 1950 and June 1992, date and cause of death; 533 of the deaths were from lung cancer. For the principal analyses, ex-smokers were excluded from the study cohort, which comprised 5888 men, of whom 473 died of lung cancer. The conventional form of analysis is simply of the double dichotomy: non-smokers of cigarettes, 'unexposed' and exposed; all others, 'unexposed' and exposed. The respective standardized lung cancer mortality ratios (SMRs) were 0.29 and 0.62; and 1.37 and 1.72. Thus, the differences in relative risk, due to exposure, were closely similar, 0.33 and 0.35. On the other hand, the effects of asbestos measured by the corresponding ratios, 2.12 and 1.25, did differ, being 1.7 times as high in non-smokers as in others. The principal analysis was much more penetrating: the method was to fit models to a 'disaggregated' 6 x 10 array, by smoking habit (excluding ex-smokers) and asbestos exposure, of lung cancer SMRs. Both linear and log-linear models were fitted: the former included the additive and linear-multiplicative; the latter embraced the more conventional multiplicative form. The additive model fitted much the best. The fit of each multiplicative model was improved by the introduction of an interaction term that implied a less than multiplicative relationship. Thus smoking and exposure to chrysotile appear to have acted independently in causing lung cancer, with 10 cigarettes a day having an effect roughly equivalent to exposure amounting to 700 million particles per cubic foot x years. The refutation of the multiplicative hypothesis in these data reinforces its inapplicability in general; but the additive hypothesis is not generally applicable either. Indeed, there seems to be no good reason to believe that interactions conform to any simple theory. The implications are important.     

Mortality from lung cancer among workers employed in formaldehyde industries

A historical cohort of 26,561 workers employed in ten facilities was assembled to evaluate cancer risks associated with exposure to formaldehyde. Historical exposures to formaldehyde by job, work area, plant, and calendar time were estimated using monitoring data available from participating plants, comments from long-term workers and company officials, exposure evaluations from walk-through surveys conducted by project industrial hygienists, and results from monitoring specifically performed for this project. A previous report of findings from this study noted a 30% excess mortality from lung cancer among wage workers. The relative risk for lung cancer (whether estimated by SMRs or SRRs) 20 or more years after first exposure did not generally rise with increasing exposure to formaldehyde. Various estimates of exposure were investigated including duration, intensity, peak, cumulative, and average, and by exposures lagged by 5, 10, 20, and 30 years. The excess did not appear to arise gradually, but emerged suddenly among workers whose total cumulative exposure was less than 0.1 ppm-years. Slightly positive, but nonsignificant, exposure-response associations between lung cancer and level of formaldehyde occurred in only a few out of a large number of comparisons (e.g., for persons hired before the start dates for the study and for workers also exposed to particulates). There was a lack of consistency among the various plants for risk of lung cancer, with six plants having elevated SMRs and four plants having deficits. Mortality from lung cancer was more strongly associated with exposure to other substances including phenol, melamine, urea, and wood dust than with exposure to formaldehyde. Workers exposed to formaldehyde without exposure to these substances did not experience an elevated mortality from lung cancer. The risk did not increase with cumulative levels of formaldehyde among those exposed to other substances and there was a slightly negative trend for those exposed to formaldehyde alone. Although some role for formaldehyde, particularly in association with other substances, in the excess of lung cancer seen among these workers cannot be ruled out, these findings suggest that exposure to phenol, melamine, urea, wood dust or other exposures also occurring in the area where these substances were used (i.e., production of resin and molding compounds) may play a more primary role. This association should be further evaluated in other studies that include workers from resin and molding compound operations.