Search

ObjectivesWhile maritime safety generally has improved dramatically over the last century, modern seafarers are still faced with numerous occupational hazards potentially affecting their risk of chronic diseases such as cancer. The aim of this study is to offer updated information on the incidence of specific cancers among both male and female seafarers.MethodsUsing records from the Danish Seafarer Registry, all seafarers employed on Danish ships during 1986–1999 were identified, resulting in a cohort of 33 084 men and 11 209 women. Information on vital status and cancer was linked to each member of the cohort from the Danish Civil Registration System and the Danish Cancer Registry using the unique Danish personal identification number. SIRs were estimated for specific cancers using national rates.ResultsThe overall incidence of cancer was increased for both male and female seafarers (SIR 1.19, 95% CI 1.15 to 1.23, and SIR 1.14, 95% CI 1.07 to 1.22) compared with the general population. This excess was primarily driven by increases in gastrointestinal, respiratory and genitourinary cancers. In addition, male seafarers working in areas with asbestos exposure showed significantly increased risk of mesothelioma. Finally, the male seafarers had an increased risk of lip cancer.ConclusionsThe majority of cancers among seafarers continue to be lifestyle-related. However, occupational exposure to asbestos and ultraviolet radiation seems to affect the cancer pattern among the male seafarers as well.

Objectives To examine mortality patterns and cancer incidence in a pooled cohort of 29 993 US career firefighters employed since 1950 and followed through 2009. Methods Mortality and cancer incidence were evaluated by life table methods with the US population referent. Standardised mortality (SMR) and incidence (SIR) ratios were determined for 92 causes of death and 41 cancer incidence groupings. Analyses focused on 15 outcomes of a priori interest. Sensitivity analyses were conducted to examine the potential for significant bias. Results Person-years at risk totalled 858 938 and 403 152 for mortality and incidence analyses, respectively. All-cause mortality was at expectation (SMR=0.99, 95% CI 0.97 to 1.01, n=12 028). There was excess cancer mortality (SMR=1.14, 95% CI 1.10 to 1.18, n=3285) and incidence (SIR=1.09, 95% CI 1.06 to 1.12, n=4461) comprised mainly of digestive (SMR=1.26, 95% CI 1.18 to 1.34, n=928; SIR=1.17, 95% CI 1.10 to 1.25, n=930) and respiratory (SMR=1.10, 95% CI 1.04 to 1.17, n=1096; SIR=1.16, 95% CI 1.08 to 1.24, n=813) cancers. Consistent with previous reports, modest elevations were observed in several solid cancers; however, evidence of excess lymphatic or haematopoietic cancers was lacking. This study is the first to report excess malignant mesothelioma (SMR=2.00, 95% CI 1.03 to 3.49, n=12; SIR=2.29, 95% CI 1.60 to 3.19, n=35) among US firefighters. Results appeared robust under differing assumptions and analytic techniques. Conclusions Our results provide evidence of a relation between firefighting and cancer. The new finding of excess malignant mesothelioma is noteworthy, given that asbestos exposure is a known hazard of firefighting.

Background: Smoking has been causally associated with increased mortality from several diseases, and has increased considerably in many developing countries in the past few decades. Mortality attributable to smoking in the year 2000 was estimated for adult males and females, including estimates by age and for specific diseases in 14 epidemiological subregions of the world. Methods: Lung cancer mortality was used as an indirect marker of the accumulated hazard of smoking. Never-smoker lung cancer mortality was estimated based on the household use of coal with poor ventilation. Estimates of mortality caused by smoking were made for lung cancer, upper aerodigestive cancer, all other cancers, chronic obstructive pulmonary disease (COPD), other respiratory diseases, cardiovascular diseases, and selected other medical causes. Estimates were limited to ages 30 years and above. Results: In 2000, an estimated 4.83 million premature deaths in the world were attributable to smoking, 2.41 million in developing countries and 2.43 million in industrialised countries. There were 3.84 million male deaths and 1.00 million female deaths attributable to smoking. 2.69 million smoking attributable deaths were between the ages of 30–69 years, and 2.14 million were 70 years of age and above. The leading causes of death from smoking in industrialised regions were cardiovascular diseases (1.02 million deaths), lung cancer (0.52 million deaths), and COPD (0.31 million deaths), and in the developing world cardiovascular diseases (0.67 million deaths), COPD (0.65 million deaths), and lung cancer (0.33 million deaths). The share of male and female deaths and younger and older adult deaths, and of various diseases in total smoking attributable deaths exhibited large inter-regional heterogeneity, especially in the developing world. Conclusions: Smoking was an important cause of global mortality in 2000, affecting a large number of diseases. Age, sex, and disease patterns of smoking-caused mortality varied greatly across regions, due to both historical and current smoking patterns, and the presence of other risk factors that affect background mortality from specific diseases.

OBJECTIVE—To study the mortality experience of workers at a hydrometallurgical nickel refinery and fertiliser complex in Fort Saskatchewan, Alberta, Canada. METHODS—A total of 1649 male employees of Sherritt International who worked for at least 12 continuous months during the years 1954 to 1978 at the Fort Saskatchewan, Alberta hydrometallurgical nickel refinery and fertiliser complex were followed up for an additional 17 years. Mortality was ascertained from the Canadian mortality data base maintained by Statistics Canada and covered the years 1954-95. Statistics were analysed with Monson's computer program. RESULTS—Total mortality, when compared with the Canadian population, was significantly below expectation. Fewer deaths were found for circulatory disease, ischaemic heart disease, respiratory disease, neoplasms, digestive cancer, and accidents, poisonings, and violence. Among the 718 men in the group exposed to nickel, there were no deaths due to nasal cavity or paranasal sinus cancer. Fewer deaths were found for all causes, circulatory disease, ischaemic heart disease, neoplasms and digestive cancer. Lower death rates were observed than expected for respiratory malignancies and cancer of the bronchus and lung. CONCLUSION—No association was found in this study between exposure to nickel concentrate or metallic nickel in the hydrometallurgical refining process and the subsequent development of respiratory cancer. Keywords: epidemiology; nickel workers; mortality

OBJECTIVE: To update the mortality experience of a cohort of 8508 workers with potential exposure to acrylamide at three plants in the United States from 1984-94. METHODS: Analyses of standardised mortality ratios (SMR) with national and local rates and relative risk (RR) regression modelling were performed to assess site specific cancer risks by demographic and work history factors, and exposure indicators for acrylamide and muriatic acid. RESULTS: For the 1925-94 study period, excess and deficit overall mortality risks were found for cancer sites of interest: brain and other central nervous system (CNS) (SMR 0.65, 95% confidence interval (95% CI) 0.36 to 1.09), thyroid gland (SMR 2.11, 95% CI 0.44 to 6.17), testis and other male genital organs (SMR 0.28, 95% CI 0.01 to 1.59), and cancer of the respiratory system (SMR 1.10, 95% CI 0.99 to 1.22); however, none was significant or associated with exposure to acrylamide. A previously reported excess mortality risk of cancer of the respiratory system at one plant remained increased among workers with potential exposure to muriatic acid (RR 1.50, 95% CI 0.86 to 2.59), but was only slightly increased among workers exposed or unexposed to acrylamide. In an exploratory exposure-response analysis of rectal, oesophageal, pancreatic, and kidney cancer, we found increased SMRs for some categories of exposure to acrylamide, but little evidence of an exposure-response relation. A significant 2.26-fold risk (95% CI 1.03 to 4.29) was found for pancreatic cancer among workers with cumulative exposure to acrylamide > 0.30 mg/m3.years; however, no consistent exposure-response relations were detected with the exposure measures considered when RR regression models were adjusted for time since first exposure to acrylamide. CONCLUSION: The contribution of 1115 additional deaths and nearly 60,000 person-years over the 11 year follow up period corroborate the original cohort study findings of little evidence for a causal relation between exposure to acrylamide and mortality from any cancer sites, including those of initial interest. This is the most definitive study of the human carcinogenic potential of exposure to acrylamide conducted to date.

OBJECTIVE--This investigation sought to examine whether methods proposed to control the healthy worker survivor effect would influence the shape or magnitude of the dose-response curve for respiratory cancer induced by arsenic. METHODS--Results from an unadjusted analysis are compared with results obtained by applying four different methods for control of the healthy worker survivor effect to data on arsenic exposure and respiratory cancer. The four methods are: exposure lag, adjustment for work status, cohort restriction, and the G null test. RESULTS--Cohort restriction gave erratic results depending upon the minimum years of follow up used. Exposure lag substantially increased the rate ratios and a non-linear shape (decreasing slope) compared with an unlagged analysis. Adjusting for work status (currently employed upsilon retired or otherwise not employed) yielded slightly higher rate ratios than an unadjusted analysis, with an overall shape similar to the baseline analysis. Results from the G null test procedure of Robins (1986), although not directly comparable with the baseline analysis, did show an adverse effect of exposure that seemed to reach a maximum when exposure was lagged between 10 and 20 years. CONCLUSIONS--All results confirm an adverse effect of arsenic exposure on respiratory cancer. In these data, it seems that the healthy worker survivor effect was not strong enough to mask the strong effect of arsenic exposure on respiratory cancer. Nevertheless, several methods show a stronger association between arsenic exposure and respiratory cancer after adjustment for the healthy worker survivor effect, suggesting that for weaker causal associations, studies not controlling for this source of bias will have low power to detect results. Although the G methods are theoretically the most unbiased, further work elucidating the validity of the assumptions underlying lagging, adjustment for work status, and the G methods are needed before clear recommendations can be made.

A case-control study of respiratory cancer, nested within a cohort of male woodworkers, was updated in Finland. The update extended the initial follow up of 3805 workers from 19 plants to 7307 workers from 35 plants. Each case of respiratory cancer (n = 136) diagnosed between 1957 and 1982 within the cohort was matched by year of birth with three controls (n = 408) from the cohort. Chemical exposures were assessed for the cases and the controls by a plant and period specific job exposure matrix. An excess of respiratory cancer was associated with phenol. Concomitant exposures to several other agents occurred as well, however, and no exposure-response relation for phenol was seen. An excess risk and an increasing exposure-response relation were found for engine exhaust from petrol and diesel driven factory trucks. The excess risk associated with pesticides was lower than in our previous study, an indication of qualitative and quantitative differences in exposure between the initial and augmented cohorts. Slightly increased risks were found for terpenes and mould spores, which may be due to chance although the contribution of occupational exposure cannot be ruled out. Exposure to wood dust, mainly from pine, spruce and birch, at a level of about 1 mg/m3, was not associated with lung cancer, upper respiratory cancer, or adenocarcinoma of the lung.

Although firefighters have been shown in some studies to suffer chronic respiratory morbidity from their occupational exposures, an increased risk for dying from non-malignant respiratory diseases has not been documented in any previous retrospective cohort mortality study. In order to assess the possibility that an unusually strong "healthy worker effect" among firefighters might mask this increased risk, a mortality analysis of firefighters was carried out in three cities in relation to the United States population and also to a comparison cohort of police officers. The firefighters were employed between 1945 and 1980 and experienced 886 deaths by 1 January 1984; compared with the United States population they had a significantly reduced risk of dying from all causes (SMR = 82, 95% confidence interval, 77-87), and from non-malignant circulatory diseases (SMR = 81, 95% confidence interval 73-89), but no significant difference in risk of non-malignant respiratory diseases (SMR = 88, 95% confidence interval 66-117). Compared with police, the firefighters experienced a trend toward improved mortality outcomes for all causes investigated (SMR = 82), but they had an excess of deaths from non-malignant respiratory diseases (SMR = 141). The results indicate that firefighters are probably at increased risk for dying from non-malignant respiratory diseases; this increased risk may have been missed in previous studies because of the limitations of using a general reference population.

A cohort of 1020 rotogravure printers exposed to toluene and employed for a minimum period of three months in eight plants during 1925-85 was studied. Air levels of toluene were available since 1943 in one plant and since 1969 in most. Based on these measurements and on present concentrations of toluene in blood and subcutaneous fat, the yearly average air levels in each plant were estimated. They reached a maximum of about 450 ppm in the 1940s and 1950s but were only about 30 ppm by the mid-1980s. Exposure to benzene had occurred up to the beginning of the 1960s. Compared with regional rates, total mortality did not increase during the observation period 1952-86 (129 observed deaths v 125 expected; SMR = 1.03). There was no increase in mortality from non-malignant diseases of the lungs, nervous system, or gastrointestinal and urinary tracts. There was no overall excess of tumours 1958-85 (68 v 54, SMR = 1.26; 95% confidence interval, CI = 0.95-1.7). Among the specific cancers, only those of the respiratory tract were significantly increased (16 v 9; SMR = 1.76, CI = 1.03-2.9). Statistical significance was not attained, however, when only subjects with an exposure period of at least five years and a latency period of at least 10 years were considered. Further, there were no dose response relations with cumulated toluene dose (ppm years). There were no significant increases of tumours at other sites, including leukaemias/lymphomas/myelomas.

Commentary on the paper by Laakkonen et al (see page726) Organic dusts are complex mixtures derived from vegetable and animal sources, often contaminated with endotoxins. Exposures to these dusts have been shown to affect development of respiratory diseases such as asthma, allergic alveolitis, byssinosis, chronic bronchitis, and emphysema.1 Organic dusts occur in a range of occupations including agricultural work; the textile industry, especially cotton processing; flour milling and bakeries; and the wood industry, particularly sawmills, carpentry, and wood processing. Many of these occupations, particularly agricultural work, also have the potential for concurrent exposure to other substances that affect respiratory health, for example metals, gases, fibres, and chemicals.2 In contrast to non-malignant disease, the relationship between organic dusts and cancer appears to be more complex. In a Finnish record linkage study, Laakonen et al 3 identify elevated risks for nasal and lung cancer associated with wood dust and for laryngeal cancer associated with grain milling. They use the Finnish national job-exposure matrix (FINJEM) and occupations …

A national cohort based on the census at 9 November 1970 and the death registration files from 1970 to 1980 was analysed to see if skilled Danish bakers had an excess of respiratory cancer. The group of skilled bakers was divided into occupational subgroups to try to narrow down the possible causes of cancer. Significant excess mortality was found among skilled bakers in retail bakeries, skilled bakers in hotels and restaurants, and independent bakers. To adjust for confounding factors, the SMR was calculated with control groups of equal social status and smoking habits. With all skilled workers as the reference group, skilled bakers in retail bakeries still had an excess, but now insignificant, risk but skilled bakers in hotels and restaurants had a significant excess risk. Compared with all self employed people in urban occupations in which an average of six or fewer workers were employed as a referent group, independent bakers had an insignificant excess risk. Suspected carcinogens in bakeries include polycyclic aromatic hydrocarbons (PAH), reaction products of PAH, free radicals, n-nitrosodimethylamine, aflatoxin, sterigmatocystin, and zeralenone.

A cohort of 3805 men who had worked for at least one year in the particleboard, plywood, sawmill, or formaldehyde glue industries between 1944 and 1965 was followed up until 1981. From within the cohort the 57 patients with verified "respiratory" cancer (ICD 7 codes: 160-162.1, 141, 143-8) were defined as "cases," and 171 men without respiratory cancer from within the cohort were matched on birth year and used as controls. The comparison of exposures was carried out according to work histories and job exposure matrices for each plant. The odds ratio for exposure to wood dust was 1.03 (32 exposed cases) without provision for any latent period, and 0.97 (27 exposed cases) when provision for a minimum latent period of ten years was applied. The odds ratios were 1.60 and 1.68, respectively, when smoking was controlled by stratification. These results did not differ significantly from unity. The estimated average level of exposure to wood dust among the exposed was 1-2 mg/m3 and the mean duration of exposure about ten years. Significantly (one sided test, 5% level) raised odds ratios were observed for exposure to pesticides and phenol. No single pesticide could be identified as "causative" because of frequent multiple exposures. The raised odds ratios for phenol were partly explained by smoking and exposure to pesticides which confounded the observed associations for phenol exposure. Exposure to terpenes and other heating products of coniferous woods was significantly associated with a risk of respiratory cancer when the duration of exposure exceeded five years.

Whitwell, F., Newhouse, Muriel, L., and Bennett, Diane R. (1974). British Journal of Industrial Medicine, 31, 298-303. A study of histological cell types of lung cancer in workers suffering from asbestosis in the United Kingdom. The present study concerns the predominant cell type of lung cancer in workers with certified asbestosis who died of carcinoma of the lung in the United Kingdom between 1962 and 1972. Clinical data, necropsy reports, histological sections, and in some cases paraffin blocks were obtained from the nine pneumoconiosis panels in the country and from hospitals where the patients had been treated. Histological analysis was confined to the 88 male and nine female cases in which adequate postmortem tissue had been obtained. The number of female cases was considered to be too small to be of value as a separate series. Among the males, adenocarcinoma was the commonest type of lung cancer found in 34%. Information about the smoking habits of 69 of the 88 men was obtained; all had smoked at some time. There was little difference between the smoking habits of any group whatever the cell type of carcinoma. The difficulty in finding a comparable series of non-asbestos-exposed individuals is pointed out. It is the usual practice to hold a necropsy on any patient when asbestosis has been certified wherever the place of death. This series therefore has a wider basis of selection than any hospital-based series. Cigarette smoking can exert a carcinogenic effect on different parts of the bronchial tree, producing squamous or oat-celled tumours proximally and adenocarcinoma distally. Asbestos dust lying in distal parts of the lung may exert a co-carcinogenic probably a multiplicative effect with tobacco smoke, producing adenocarcinoma of the distal part of the respiratory tract.

An investigation was carried out to determine the cause of death and the incidence of tumours among 1932 workers in a ferrochromium plant in Sweden. The workers had been exposed mainly to metallic and trivalent chromium (Cr3+); hexavalent chromium (Cr6+) was also present in certain working operations. The population was defined as all men employed at the plant for at least one year during 1930-75, and were classified according to their occupation within the industry. The causes of death were initially obtained from parish registers. For deaths occuring between 1951 and 1975, death certificates were collected from the National Central Bureau of Statistics. Data on the incidence of cancer during 1958-75 were obtained from the Swedish National Cancer Registry. Expected death rates and incidence of tumours were calculated, based on the rates for the county in which the factory was situated. The total number of deaths from tumours was less than expected (69 versus 76·7). Five cases of respiratory cancer were found, against an expected 7·2. Among maintenance workers, an increased death rate from all tumours and an increased number of respiratory tumours were found. Two of the latter were mesotheliomas and could be connected with asbestos exposure. No increase was found for respiratory tumours among the heavily exposed workers at the arc-furnaces; one case of mesothelioma was found in this group.

A previous report analysed the pattern of mortality during the first year of follow up among 9928 patients taking cimetidine who were recruited to a postmarketing drug surveillance study in Glasgow, Nottingham, Oxford, and Portsmouth. A further analysis has now been conducted extending the period of follow up to four years. The 12 month report noted that cimetidine was being given, knowingly or unknowingly, in the late stages of many diseases and also to counter the adverse gastric effects of other drugs used in the treatment of serious disorders. This finding was underlined by a steady fall in the excess death rate among cimetidine users with increasing length of follow up, such that by the fourth year the pattern of observed deaths was not much different from that expected on the basis of national rates. Some excess of observed over expected deaths from gastric cancer, lung cancer, and urinary disorders was still apparent after four years of follow up, but there was no evidence that cimetidine was responsible. Indeed, no fatal disorder emerged as being associated with cimetidine during the follow up period. Deaths from the complications of disease related to gastric acid occurred in only 38 of the 9928 subjects over the four years. These findings provide further evidence of the safety of cimetidine.

In a study of a cohort of 2498 men and 1032 women employed in the manufacture of mustard gas in Cheshire during the second world war 3354 (95%) individuals were successfully traced for mortality to the end of 1984. Large and highly significant excesses were observed as compared with national death rates for deaths from cancer of the larynx (11 deaths observed, 4.04 expected, p = 0.003), pharynx (15 observed, 2.73 expected, p less than 0.001), and all other buccal cavity and upper respiratory sites combined (lip, tongue, salivary gland, mouth, nose) (12 observed, 4.29 expected, p = 0.002). For lung cancer, a highly significant but more moderate excess was observed (200 observed, 138.39 expected, p less than 0.001). Significant excesses were also observed for deaths from acute and chronic non-malignant respiratory disease (131 observed, 91.87 expected and 185 observed, 116.31 expected, respectively). The risks for cancers of the pharynx and lung were significantly related to duration of employment. None of these results is substantially altered when expected numbers are calculated from Cheshire urban areas rather than national rates, although the relative risks for lung cancer and non-malignant respiratory disease are substantially reduced if rates for Merseyside, the nearest large conurbation, are used. The results provide strong evidence that exposure to mustard gas can cause cancers of the upper respiratory tract and some evidence that it can cause lung cancer and non-malignant respiratory disease.(ABSTRACT TRUNCATED AT 250 WORDS)

In a search for clues to previously industrial carcinogens the occupational and smoking histories of young and middle aged men with different types of cancer were compared. The study population comprised men aged 18-54 and resident in the counties of Cleveland, Humberside, and Cheshire (including the Wirral). From hospital and cancer registration records 2942 members of the study population in whom cancers were diagnosed during the period 1975-80 were identified retrospectively. The occupational and smoking histories of these patients were sought by a postal questionnaire addressed either to the patients themselves or, if they had died, to their next of kin. The overall response rate to the questionnaire was 52.1%. Additionally, limited occupational information was obtained for 89% of cases from their hospital notes. Analysis of these data suggests that no serious bias arose as a consequence of the incomplete response to the questionnaire. This paper concentrates on the results for cancers of the respiratory tract and mesothelioma. Mesothelioma was found to cluster in laggers, electricians, and shipyard workers, and nasal carcinoma in woodworkers. Carcinomas of the larynx and of the bronchus were examined by formal statistical techniques, each being compared with a control group made up of all other cancers combined. Several interesting occupational and industrial associations were shown, in particular, an excess of bronchial carcinoma in the leather industry (RR = 2.6, CI 1.2-6.0), in building labourers (RR = 1.7, CI 1.0-2.9) and other construction workers (RR = 1.8, CI 1.0-3.0), in bakers and pastry cooks (RR = 3.6, CI 1.3-10.4). and in cooks (RR = 2.5, CI 1.2-5.1). In addition, a small cluster of lung tumours was observed in men who had worked as dental mechanics.

A comparative study was conducted to assess empirically the suspected bias associated with occupational health studies based only on information obtainable from employers' records. Standardised mortality ratios were extracted from five occupational cohorts for which extensive follow up had been conducted and were compared with proportional mortality ratios based on deaths known (KTE) and unknown (UTE) to the employer, and on total deaths. For the five cohorts examined the suspected bias for the cause of death categories all cancer, respiratory cancer, heart disease, and accidents was generally found to be minimal unless the number of UTE deaths was in excess of 75%. Furthermore, a strong inverse relationship was observed between the percentage of UTE deaths and the level of agreement between proportional mortality ratios based on KTE deaths and total deaths. In partial support of these findings it was also observed that workers who left the industry in three of the five cohorts subsequently experienced similar overall mortality compared with those who continued employment. These findings should serve as a rough indication of the potential value of estimating disease risks from KTE deaths and serve as a guide for other investigators using limited data.

A cohort of 406 men employed before 1963 for at least one year in a vermiculite mine in Montana was followed up until July 1983. The vermiculite ore as fed to the mill contained 4-6% of amphibole fibre in the tremolite series. Vital status was established in all but one of the 406 and death certificates were obtained and coded for 163 of the 165 men who died. Compared with white men in the United States, the cohort experienced excess mortality from all causes (SMR 1.17), respiratory cancer (SMR 2.45), non-malignant respiratory disease (SMR 2.55), and accidents (SMR 2.14). Four deaths were from malignant mesothelioma (proportional mortality 2.4%). Compared with Montana death rates, the SMR for respiratory cancer was somewhat higher (3.03). Man-year analyses of respiratory cancer and estimated cumulative exposure gave a relation that did not depart significantly from linearity. The results of this and case-referent analyses indicate an increased risk of mortality from respiratory cancer in this cohort of about 1% for each fibre year of exposure. In relation to estimated exposure the mortality experienced by the cohort from both lung cancer and mesothelial tumours was higher than in chrysotile mining.

The mortality of nearly 41000 medically qualified men and women in the United Kingdom has been observed for twelve years. During the first 10 years 4597 of the men and 366 of the women died. These deaths have been analyzed in relation to the smoking habits reported by doctors in reply to a questionnaire dispatched to them in 1951 (both sexes) and again in 1957 and 1960. An association with smoking is found in differing degrees in men for seven causes of death and no association was found with the remaining 61% of the death rate and this includes such major causes as other forms of cancer cerebrovascular accidents hypertension myocardial degeneration suicide and accident. A linear rise of death rate was observed from nonsmoker to light medium and heavy smokers which indicates that there is no smoking threshold which must be reached before the death rate from cancer of the lung shows a response. The death rate continues to fall step by step the longer smoking has been given up. Whether smoking acts synergistically with air pollution upon the respiratory tract is not known. Some suggest a reasonable conclusion that cigarette smoking is one of the more important etiological factors in chronic bronchitis in Great Britain and relying on clinical evidence it could be said that possibly chronic bronchitis itself plays a part in producing cancer of the lung. Tobacco and alcohol play some part in the production of cancers of the upper respiratory and digestive tracts. Excess mortality due to coronary disease without hypertension is limited to cigarette smokers which is marked at under age 55 but disappears at over age 75. Evidence supports the claim that cigarette smoking is one of the causes of coronary thrombosis under age 75. Continued smoking may prevent or delay the healing of a chronic gastric ulcer and thereby it may increase the mortality rate. Mortality from alcoholism and cirrhosis of the liver is specially high in heavy smokers. There appears to be no cause of mortality which is lessened by smoking.

Enterline, P., de Coufle, P., and Henderson, V. (1973). British Journal of Industrial Medicine, 30, 162-166. Respiratory cancer in relation to occupational exposures among retired asbestos worker. A cohort of 1 348 men who completed their working lifetime in the asbestos industry and retired with an industry pension during the period 1941-67 was observed through 1969 for deaths. The average length of employment in the asbestos industry for these men was 25 years and all had exposures to asbestos dust. In some instances these exposures were very high and continued for many years. Mortality for this cohort of men after age 65 was 14·7% higher than for the entire population of United States white men living at the same ages and time periods. This excess was due almost entirely to cancer and respiratory disease. The cancer excess was chiefly due to respiratory cancer where mortality was 2·7 times the expected. The respiratory disease excess was entirely due to asbestosis. A time-weighted measure of asbestos dust exposure at the time of retirement was calculated for each man. This was made up of the summed products of dust levels for each job (expressed in mppcf) and years at each level. This measure was directly related to the respiratory cancer excess at ages 65 and over, ranging from 1·7 times expected for men with less than 125 mppcf-years exposure to 5·6 times expected for men with 750 or more mppcf-years exposure. There appeared to be no direct relationship between asbestos dust exposure and respiratory cancer below 125 mppcf-years. Important increments in respiratory cancer mortality apparently occurred somewhere between 100 and 200 mppcf-years exposure. Separation of the effects of time from the effects of average dust level on respiratory cancer mortality showed that the contribution of each was about the same and that a time-weighted measure of asbestos dust appears to be an appropriate method for predicting respiratory cancer effects.