Document 1gEbkXrzDD6zDxZNwaqxd4M15

Occupational and Environmental Medicine Review Papers Short report 289 Vehicle accidents related to sleep: a review Jim Home, Louue Reyner 295 Acquisitionand extinction of somatic symptoms in response to odours: a Pavlovian paradigm relevant to multiple chemical sensitivity O m Van den Bergb, Kris Stegen, llse Van D k t , Catby Rues, Peter Stultns, Paul Eelen, Hendrik Vnrkmanr, Karel P Vande Woestijne, Benoit Nemcry 302 Work characteristicspredict psychiatric disorder: prospectiveresults from the WhitehallII study S A Stansfeld, R Fuhrer, M 1Ship& M G Marmot 308 Incidence of childhood brain and other non-haematopoietic neoplasms near nuclear sites in Scotland, 1975-94L Sbarp, P A M c K i w R ] Black 315 Cohort mortality study of 57 OOO painters and other union members: a 15 year update K y k Steenland, Sue Palu 322 Occupationalrisk factors of lung cancer a hospital based casecontrotstudyJac H J Droste, Jwst 1Wqler, Jan P V i Meerbeeck, Pad A V d e , Marc P van spnmdcr 328 Two year f d o w up of pulmonary function values among welders in New Zealand Riitra Erkinjud-Pekkaneny Tluricr Slam, So0 Cbmg, David Fisbwick Lisa B r h b a w , MOM Kimbell-Dum, Liz mid,Neil Pcorce 334 Chronic rhinitis in workers at risk of reactive airways dysfunction syndromedue to exposureto chlorine Chistopbe Lcroy~],ean-Luc Malo, D& Girard, Jean-Guy I)rrfour,Deny= Guutrin 339 Relation between job strain and myoardial infarction: a casecontrol study Bo Netterstmm, Finn E N i e h , Tage S Kristenscn, Elsa B a d , Iars MsUer 343 Interactions between physical and psychosocial risk factors at work increase the risk of back disorders: an epidemiological approach]Jason Dewmcx, Peter W Buckk, I d G Wonikolis 354 Health effects among workers in sewage treatment plants RamRY- 358 Correction 358 Notice 358 Book reviews .' , 4 . . , , j.. .. rU: i "I Cohort mortality study of 57 000 painters and other union members: a 15 year update Kyle Steenland, Sue Palu National Institute for Occupational Safety and Health OyIOSH), Cincinnati, OH 45208, USA K Steenland S Palu Correspondence to: h4r Kyle Steenland, National Institute for Occupational Safety and Health N O S H ) , Cincinnati,OH 45208, USA. Fax 001 513 841 486. Accepted 23 October 1998 Abstract Objective-To study mortality patterns in the largest existing cohort of painters. Methods-15 years of follow up were added to a study of 42 170 painters and 14 316 non-painters based on union records. There were 23 458 deaths, compared with 5313 in the earlier follow up. Results-Comparisons with the United States population showed significantly increasedrates in painters for lung cancer (standardised mortality ratio ( S M R ) 1.23, 95% confidence interval (95% CI) 1.17 to 1.29), bladder cancer ( S M R 1.23, 95% CI 1.05 to 1.43), liver cancer ( S M R 1.25, 95% CI 1.03 to 1.50),and stomach cancer ( S M R 1.39, 95% CI 1.20 to 1.59). However, in direct comparisons with non-painters only the excesses for lung cancer (SRR 1.23, 95% CI 1.11 to 1.35, increasing to 1.32, 95% CI 16 to 1.93 with 20 years latency) and bladder cancer (SRR 1.77, 95%CI 1.13 to 2.77) were confirmed. Some confounding by smoking may affect these two outcomes, particularly with external referents. Cirrhosis of the liver was increased for both painters and nonpainters (SMRs 1.21, 950/.CI 1.07 to 1.35, and 1.26, 95% CI 1.03 to 1.51, respectively), possibly indicating high alcohol consumption. Suicide ( S M R 1.21, 95% CI 1.05 to 1.38) and homicide ( S M R 1.36,95% CI 1.04 to 1.75) were increased for painters but not for non-painters;neuropsychiatric diseases have been associated with painters in earlier studies. Conclusions--The results suggest modest occupational risks for lung and bladder cancer; these results are consistent with existing publications. The International Agency for Research on Cancer has classified painting as an occupation definitely associated with cancer. (Occup Em.ron Med 1999;56:315-321) Keywords: lung cancer; bladder cancer;painters There are about 700 000 painters in the United States (Rick Hackney, International Brotherhood of Painters and Allied Trades, personal communication). In a 1989 monograph,' the International Agency for Research on Cancer (IARC) determined that painting as an occupation was a definite (class I) cause of cancer. Lung cancer was most strongly and consistently associated with painting, but excesses were also noted for oesophageal, stomach, and bladder cancer. The primary basis for the judgement of the IARC was three large cohort studies of painters, from the United States,' Denmark: and Sweden: although several case-control studies provided supporting evidence.The excess of lung cancer was judged to be about 40% and to be beyond what might be expected due to possible confounding by smoking. Since the IARC review in 1989, there have been a few small cohort studies of painters and many case-control studies of various sites in which positive findings were reported for painters. These studies have tended to support the original findings of excess lung cancer and stomach cancer, to provide additional evidence of excess bladder cancer, excess of haematopoietic cancers (especially myeloma' and nonHodgkin's lymphoma' '), and excess upper respiratory cancer.+" Of note among the recent publications on bladder cancer is a large casecontrol study of bladder cancer among white men (2 100 cases, 116 of whom were painters) in the United States" in which an odds ratio (95% confidence interval (95% CI)) of 1.5 (1.2 to 2.0) was found for painters after adjustment for smoking, and a meta-analysis of 27 case-control studies on bladder cancerI3which found an overall relative risk for bladder cancer of 1.48. There are several known or suspected carcinogens in paint, but known carcinogens have been measured at only a low concentrations or have been present only in certain specialised kinds of painting. Most exposures are airborne, although in some cases dermal exposure may be important. Early in the century, arsenic, a lung carcinogen, was common in paint pigments, but was removed from most paints due to incidents of arsenic poisoning." Turpentine was used before the second world war, and was associated in some reports with kidney dysfunction and contact allergy.'' Tupentine was later replaced by organic solvents, some of which can cause haematopoietic and perhaps liver cancer, and are common in paints. The main solventshave been petroleum solvents, toluene, xylene, ketones, alcohols, esters, and glycol ethers. Benzene, a known leukaemogen, was used in the past,' but has been less common since the 1950s, and often has been present only at low concentrations. Metals in paint pigments include titanium oxide, chromium compounds, and iron compounds; lead was used in the past. Hexavalent chromium is a confirmed lung carcinogen, but airborne concentrations of hexavalent chromium are and have been low for most painters. There is some evidence that lead may also be associated with lung cancer. However, high exposure to airborne lead has not been a t mu316 SteetJOnd, common exposure for most painters, occurring Most union members were from local unions only in construction work in which lead paint (each local union is defined by union members was being removed by blasting. Benzidine and in a small geographical area) composed prim- other aromatic amines, which can cause rily of painters, but the rest were Erom other bladder cancer, have also been present in some local unions composed primarily of other types paints,'*but these are not common or high level of workers. Cohort members were identified exposures. Paint stripping involves exposure to from local unions located in four states (New methylene chloride,15 an animal carcinogen, York, Missouri, California, and Texas). Locals but many painters do not perform this were characterised as mixed local composed operation. Polyurethane paint, again not a primarily of painters, and speciality locals common exposure for most painters, involves composed mainly of other allied trades (note exposure to diisocyanates. There has been an that mixed does not imply a mixture of painters increasing use of water based paints since the and non-painters, but a mixture of different 1960s; these paints contain only small amounts types of painters). The titles of specialty locals of solvents and are thought to be less toxic.'` l6 included automobile, indusmal, Civil, glass, In summary, although there are several sign, paint, carpet, scenic, wood, paper, d q - known carcinogens which have been used by wall, warehouse, and metal workers. The origi- painters, most have been used in specialised nal analysis of this cohort' analysed the data settings or have resulted in only low levels of separately for the mixed and specialty locals. exposure. The organic solvents which have Further discussion with the Painters Union or been commonly used, resultingin higher expo- the present study, however, led to a determina- sures, are not known human carcinogens, tion that the locals entitled industrial, automo- although some have been shown to cause can- bile, sign, and scenic were in fact also primarily cer in animals. Additionalresearch is needed to composed of painters. The industrial painters idenufy the exposures responsible for the painted bridges, painted steel in production increased cancer risk experienced by painters. factories, or painted on construction sites. The United States cohort study cited by Automobile, sign, and scenic locals were com- IARC is the largest existing cohort of painters, posed of painters who painted automobiles, and is the subject of this paper. The study signs, or special painting jobs. Hence, members population is composed of 56 486 male union of these locals (114029) were added to the members of the International Brotherhood of mixed locals (n=34 141) and these subjects Painters and Allied Trades (IBPAT). This were all considered to be painters. The " -union is composed primarily of paintersyebut remgininp; specialty localq were confirmed t p * - -the members from*the, allied'trades are not- * have-been p h i & nh-painters (xi214 3161. painters. The cohort was-originallyfollowed up Workers in civil locals were government work- to the end of 1979, and included 5313 deaths. ers often driving trucks, workers in glass locals The findings from the original follow up worked manufacturing glass, workers in paint showed significant excesses among the painters locals worked paint manufacturing plants (but compared with the United States population, in fact most of these workers were judged to for lung cancer (standardised mortality ratio have had little potential exposure to paint), ( S M R ) 1.18,95% CI 1.06-1.32) and stomach workers in carpet locals were carpet and rile cancer (1.36, 1.01 to 1BO), and nearly signifi- layers, workers in wood locals were skilled cant excesses for bladder cancer (1.26,0.90 to wood finishers, workers in paper locals were 1.72), kidney cancer (1.41, 0.93 to 2.05), and paper hangers, workers in drywall locals were liver cancer (1.56, 0.95 to 2.41).' Of the drywall finishers, workers in warehouse locals haematopoietic cancers, only leukemias were worked in warehouses in paint manufacturing reported (SMR 1.16 ,95% CI 0.82 to 1.16). In companies or convention halls, whereas work- a direct comparison of union locals composed ers in metal locals worked installing window of painters compared with other trades, lung frames and other finished metal. cancer, bladder cancer, and leukaemia were It is clear, however, that this classification of significantly higher among the painters (SRRs painters and non-painters is not definitive; the 1.46, 2.30, and 2.41). However, in the direct speciality locals are likely to have included a comparison liver, stomach, and kidney cancers few painters, whereas the mixed, industrial, were no longer significantly increased (SRRs automobile, sign, and scenic locals are likely to 1.26, 1.17, and 1.29). likewise have included a few non-painters. We have extended follow up of this cohort by Vital status follow up of this cohort to the an additional 15 years, to the end of 1994,cov- end of 1994 was conducted through the Inter- ering 23 458 deaths, with a goal of evaluating nal Revenue Service, the Health Care Finance whether the observed cancer excesses have Administration, the Post Office, the Social persisted over time. Security Administration Death Tapes, and the National Death Index. Causes of death were Methods obtained directly from death certificates or The cohort is composed of members of the from computerised death certificate data for Painters Union with at least 1 year of union four states (New York, Missouri, California, membership who had been born before 1940 and Texas) and one city (New York City). and were alive at the end of 1975. Members Cause of death information was coded with could have been retired from 1975; retired standard coding conventions in the same way members were kept on the union roster. No for both the observed deaths and the deaths in new union members after 1979 were included the United States comparison population. in the cohort. Cause of death information extended to the t Table 1. Descriprive data for painters and non-painters Painten (n=42170) Na-painters (n=14316) Mean year of birth (range) Mean year of union entry (range) Mean years of follow up after 1975 (range) Vital status as of 12/31/94 (%): Alive Unknown' Deadt Mean year of death (range) 1919 (1865-1941) 1957 (1900-1979) 14 (0-21) 21117 (50) 2794 (7) 18259 (43) 1985 (1975-1995) 1925 (1869-1939) 1962 (1900-1979) 15 (0-21) 90 11 (63) 1058 (7) 4247 (30) 1986 (1975-1995) *Person-time ended at end of last known date alive. t952 Study subjectswere known to have died after the study end date of 12/31/94. end of 1994, the study end date. Race was not known for all cohort members. Death certifi- cate data indicated that the overwhelming majority of union members were white (98%),' and in the analyses all subjectswere considered to be white. About 99% of union members were men: and we restricted our analyses to them. Mortality analyses consisted of standard life table analyses comparing the mortality of the painters with that of the population of the United States, after stratification of deaths and person-years at risk by potential confounders (age, calendar time)." Rates were available for 99 different categories of death. The measure of effect was the SMR. Also, standardised rate ratios (SRRs)were calculated for several cancer outcomes in a direct comparison between painters and non-painters through Poisson regression.Analyseswere conducted for several cancer outcomes by time since first in the union (potential latency). No data were available on duration of union membership. Death certificates include information on other causes of death besides underlying cause. We used this additional informationin a multiple cause proportionate mortality analysis of this cohort, in which the observed proportion of deaths with a specific cause mentioned anywhere on the death certificateis compared with the expected proportion based on all United States deaths." Multiple cause of death data were available for 13 928 deaths (62% of all deaths); some computerised data bases-for example, Missouri, New York City for certain years-provided only underlying cause of death, and deaths from these data bases were therefore excluded from multiple cause analy- ses. The lack of multiple cause death on all deaths in the cohort prohibited a cohort analysis with person-time by multiple cause data; instead we conducted a proportional mortality rate (PMR) analysis on those deaths with multiple cause data, assuming the deaths for which we did have multiple cause data were a representative sample of all deaths. Multiple cause analysis is particularly useful in detecting excesses for causes that are not likely to be listed as the underlying causes, such as chronic but not usually fatal conditions. We conducted this analysis to investigate any possible excess of renal disease on the death certificate, because renal disease has been associated with ~olvents,a'~lthough in the one study when data were presented by type of solvent exposure, exposure to solvents in paints was not associated with risk of renal disease." We were also interested in mental disorders, which have sometimes been associated with painters and which are much more common as contributory rather than underlying causes of death." No direct information was available on the smoking habits of study subjects. Indirect information on the smoking habits of painters was available from the 1970s and 1980s from ToMe 2 SMR resulrsfor selected causes Cause Poinrm SMR (95% CI)(obsurvcd) Non-painrm SMR (95% CI)(observed) Pharyngeal cancer Oesophageal cancer Stomach cancer Lung cancer Laryngeal cancer Liver cancer (specified+unspecified)* Bladder cancer Kidney Hodgkin's lymphoma Non-Hodgkin's lymphomat Leukaemia Myeloma Ischaemic heart disease Cardiomyopathy$ Hypertension with heart disease Pneumonia Emphysema Bronchitis Asbestosis Other non-malignant respiratory diseases Liver cirrhosis Alcoholism Suicide Homicide HIV relatea FaUs All cancers All causes 1.15 (0.85 to 1.52)(49) 1.12 (0.92 to 1.35)(110) 1.39 (1.20 to 1.59)(197) 1.23 (1.17 to 1.29)(1746) 0.97 (0.71 to 1.29)(48) 1.25 (1.03 to 1.50)(119) 1.23 (1.05 to 1.43)(166) 1.06 (0.86 to 1.29)(100) 1.30 (0.74 to 2.11)(16) 1.06 (0.89 to 1.25)(137) 0.92 (0.78 to 1.11)(138) 0.97 (0.75 to 1.24)(64) 0.97 (0.95 to 1.00)(5871) 1.17 (0.99 to 1.37)(146) 1.19 (1.01 to 1.39)(160) 1.14 (1.06 to 1.24)(641) 1.13 (0.99 to 1.28)(232) 1.11 (0.82 to 1.47)(49) 4.70 (2.57 to 7.89)(14) 1.07 (0.99 to 1.14)(799) 1.21 (1.07 to 1.35)(303) 1.11 (0.80 to 1.51)(42) 1.21 (1.05 to 1.38)(219) 1.36 (1.04 to 1.75)(62) 1.79 (1.08 to 2.79)(19) 1.18 (0.98 to 1.41)(122) 1.12 (1.09 to 1.15)(4674) 1.04 (1.03 to 1.06)(18 259) 0.45 (0.7 to 0.98)(6) 0.83 (0.54 to 1.22)(25) 1.51 (1.14 to 1.97)(56) 1.02 (0.92 to 1.12)(422) 0.97 (0.53 to 1.62)(14) 0.93 (0.60 to 1.38)(24) 0.74 (0.46 to 1.11)(22) 0.77 (0.48 to 1.18)(21) 0.54 (0.06 to 1.93)(4) 0.95 (0.66 to 1.32)(34) 0.63 (0.40 to 0.94)(24) 0.90 (0.52 to 1.46)(10) 0.92 (0.87 to 0.97)(1297) 1.81 (1.41 to 2.28)(71) 1.40 (1.03 to 1.85)(49) 1.04 (0.86 to 1.25)(113) 0.81 (0.57 to 1.12)(38) 0.89 (0.37 to 1.68)(8) 0.00 (0.0 to 4.55)(0) 0.90 (0.77 to 1.05)(157) 1.26 (1.03 to 1.51)(109) 0.56 (0.24 to 1.09)(8) 1.06 (0.82 to 1.36)(63) 0.90 (0.52 to 1.44)(17) 1.84 (0.84to 3.49)(9) 1.20 (0.79 to 1.74)(27) 0.96 (0.90 to 1.01)(1086) 0.99 (0.96 to 1.02)(4247) 'ICD-9 codes 155.0, 155.1, 155.2, 156 (this category includes cancers of bile duct and gall bladder; about 25% of these cancers involved the extrahepatic biliary tract; none were gall bladder cancers (ICD-9 1560)). tICD-9 codes 200,202. VCD-9 code 425. PCD-9 code 470-479,494499,504,50&5 19. Respiratory infection, emphysema,asthma, bronchitis,and pneumoconioseshave their own categories.This category is primarily chronic obstructive pulmonary disease. WCD-9 4244. 318 Steenland, Palu Toble 3 SMR resultsfor cancers, 2Oyears sincefinrunion membership Cuuse Painten SMR (9S% CI) (observed) Non-painten SMR (95% GI)(observed) Pharyngeal cancer* Oesophageal cancer Stomach cancer Lung cancer Laryngeal cancer Liver cancer (specified+unspecified) Bladder cancer Kidney Hodglun's lymphoma Non-Hodgkin's lymphoma Leukaemia Myeloma All cancers All causes 0.99 (0.67 to 1.40)(31) 1.15 (0.92 to 1.42)(86) 1.46 (1.25 to 1.70)(167) 1.24 (1.18 to 1.31)(1360) 0.92 (0.64 to 1.28)(35) 1.17 (0.95 to 1.44)(90) 1.25 (1.06 to 1.47)(146) 0.97 (0.76 to 1.22)(71) 1.17 (0.56 to 2.15)(10) 1.10 (0.91 to 1.32)(110) 1.11 (0.74 to 1.08)(111) 1.01 (0.76 to 1.32)(54) 1.12 (1.08 to 1.16)(3748) 1.05 (1.03 to 1.07)(15163) 0.37 (0.08 to 1.08)(3) 1.02 (0.62 to 1.58)(20) 1.75 (1.27 to 2.35)(44) 0.96 (0.85 to 1.08)(264) 1.28 (0.60 to 2.24)(12) 1.01 (0.60 to 1.60)(18) 0.84 (0.51 to 1.31)(19) 0.67 (0.34 to 1.17)(12) 0.48 (0.01 to 2.67)(1) 1.07 (0.70 to 1.57)(26) 0.56 (0.31 to 0.92)(15) 0.97 (0.50 to 1.69)(12) 0.99 (0.92 to 1.06)(762) 1.02 (0.98 to 1.06)(3025) 'For ICD codes see footnote to table 2. two large surveys." 22 Confounding by smoking for lung cancer and bladder cancer was assessed indirectly by a method described by Axelson and Steenland.z3This method relies on estimates of smoking prevalence among the exposed cohort and the non-exposed population (actual smoking prevalences being unknown), and assumes known relative risks for specific cancers by smoking habit-for example, current, former, never. Expected rate ratios (RRs) due to differences in smoking habits can then be calculated and compared with observed RRs. In this adjustment we assumed relative risks for lung cancer of 10, 15, and 20 for smoking 4 9 , 20-39, and 2 4 0 cigarettes a day, and a relative risk of 5 for former smokers. Results Table 1 provides some descriptive statistics for painters and non-painters. The non-painters were generally younger and joined the union later. Both painters and non-paintersjoined the union rather late in age (mean age 38 and 37, respectively),implyingthat earlier work in their trade may have been common. We were unable to determine the current vital status of 7%of the cohort. Person-timefor these cohort members ended when they were last known alive, which was generally at the end of the previous follow up in 1979. Cause of death data could not be obtained for 5.1% of the known deaths in the cohort. Assuming that these people are indeed dead, and assuming that their causes of death would be distributed between the specific causes in the same fashion as the deaths with known causes, then our observed SMRs are underestimated by about 5%.The missing causes would not be expected to appreciably affect internal comparisons of painters with non-painters. Table 2 provides selected SMR results for painters and non-painters. Results are presented for causes of death which were of initial interest or of later interest because they showed a significant increase among either painters or non-painters. Among causes of initial interest are not only the suspected cancer sites but other causes of death possibly related to non-occupational risk factors-for example, non-malignant respiratory disease and smoking. The results in table 2 indicate that painters have significant excesses .of lung, stomach, bladder, and liver cancer compared with the United States population. Non-painters also had a significant excess of stomach cancer, but did not show excesses of other cancers. Results for non-cancer outcomes indicated a small excesse of non-malignant respiratory diseases among painters, but not among nonpainters. Asbestosis was significantly increased in painters, but not in non-painters, based on 14 deaths. This excess is not surprising given the inclusion in the cohort of construction painters who were likely to have had exposure to asbestos in the past. However, painters did not show excesses of cancer of the peritoneum (SMR 0.60,95% CI 0.30 to 1.07,ll deaths) or cancer of other parts of the respiratory system (SMR 1.09,95% CI 0.60 to 1.77, 15 deaths), sites where mesotheliomas might be expected. Both painters and non-painters had significant excesses of death from cirrhosis of the liver; the excess was more marked among nonpainters. No corresponding excesses were found for death from alcoholism. Painters, but not non-painters, showed significant excess deaths from suicide and homicide. Multiple cause analyses indicated a deficit of deaths from both acute and chronic renal disease for painters (PMR 0.77, 0.62 to 0.93, 96 deaths, and PMR 0.93, 0.84 to 1.01, 469 deaths, respectively). The corresponding PMRs for non-painters were also not remarkable (PMRs 1.13, 95% CI 0.78 to 1.60, 32 deaths, and PMR 0.93, 95% CI 0.76 to 1.13, 105 deaths for acute and chronic renal disease, respectively). The multiple cause result for painters for other mental disorders (9th revision of the international classification of diseases (ICD-9) 290-302,204-3 19, including dementia, psychoses, delirium, and schizophrenia, was not increased (PMR 0.93, 95% CI 0.84 to 1.02, 397 deaths), as was the case for other diseases of the nervous system and sense organs (ICD-9 320-337, 341-389, including Parkinson's disease, multiple sclerosis, epilepsy, peripheral neuropathies, and disordersof eyes and ears, PMR 0.88,95%CI 0.81 to 0.96, 516 deaths). Table 3 shows analyses of cancer mortality based on data restricted to 3 2 0 years since entering the union (potential latency). These results differed little from the overall results, as 70%of cancer deaths occurred 2 2 0 years after entering the union. i i Table? Poisson regression results comparing painms with non-painrm* Discussion Cause Stomach cancert Lung cancer Liver cancer (specified+unspecified) Bladder cancer Rate ratio (95% Cl) 0.92 (0.68 to 1.25) 1.23 (1.11 to 1.35) 1.36 (0.87 to 2.1 I) 1.77 (1.13 to 2.77) Rare ratio 22Oyan since joining union (95% CI) 0.87 (0.62 KO 1.22) 1.32 (1.16to 1.51) 1.16 (0.69 to 1.93) 1.55 (0.96 to 2.51) Our results show a significant but modest increase in lung (SMR 1.23, 95% CI 1.17 to 1.29) and bladder cancer (1.23, 95% CI 1.05 to 1.50), with an external (United States) comparison population with follow up to the end of 1994. The corresponding SRRs were 1.23 `Age was categorised m 5 year mtervals (c50, 5&54, ...75-80, 380), calendar nme in four mter- vals (1975-1979,198&84~1985-1989,1990-1994). tFor ICD-9 codes see footnote to table 2 (95% CI 1.11 to 1.35) and 1.77 (95% CI 1.13 to 2.77), respectively, with an internal (nonpainter) comparison. These increases, al- Internal comparisons between painters and though relatively small, are consistent with the non-painters were conducted through Poisson publications on painters. regression for cancers which were increased in Analyses of lung cancer SMRs among paintthe external analyses (stomach, lung, liver, and ers by 5-year period showed an increasing bladder). The results are shown in table 4. trend (SMRs of 1.10 (385 deaths), 1.23 (458 Lung and bladder cancer were significantly deaths), 1.23 (476 deaths), and 1.38 (427 increased, whereas liver cancer was non- deaths), for the periods 1975-9, 1980-4, significantly increased. The increase for lung 1985-9, and 1990-4, respectively). The corre- cancer was slight when the analysis was sponding SMRs for bladder cancer were 1.34 restricted to those with 5 2 0 years since first (50 deaths), 1.18 (41 deaths), 1.15 (38 deaths), joining the union (latency). and 1.24 (37 deaths), and for liver cancer they With regard to possible confounding of can- were 1.51 (35 deaths), 1.02 (24 deaths), 1.12 cer SMRS by smoking, two national surveys (28 deaths), and 1.38 (32 dead); neither cancer indicate that painters have smoked more than showed a consistent trend. the general population. Brackbill et d're- By comparison, the earlier findings of ported on a national probability sample of Matanowski et al,' based on the period 1975-9 painters in 1978-90. Among painters in but with fewer union members classified as construction and maintenance (total estimated painters than in the present analysis (33 098 e, at 477 000), 48.9% were current smokers, 42 1701, showed SMRs of 1.18 (326 deaths) 22.9% were former smokers, and 28.2% were for lung cancer, 1.26 (40 deaths) for bladder never smokers. The corresponding figures for cancer, and 1.56 (20 deaths) for liver cancer, all white men in the entire United States popula- slightly higher than our own findings for tion were 36.3%, 26.1%, and 37.6%. Among 1975-9. painters who currently smoke, 32.4% smoked In our own data, direct comparisons (by <20 cigarettes a day, 51.5% smoked 20-39 Poisson regression) of painters to non-painters cigarettes a day, and 16.1% smoked >39 ciga- by period showed SRRS for lung cancer of 1.25 rettes a day. The corresponding figures for the (95% CI 0.97 to 1.62) for 1975-9, and 1.22 entire population of white men were 25.5%, (95% C1 1.08 to 1.38) for 1980-94. The SRRs 53.6%, and 20.9%. for liver cancer were 1.30 (95% CI 0.50 to Stellman et d'reported on 1263 male 3.35) for 1975-9 and 1.35 (95% CI 0.82 to painters aged 45-70 in the American Cancer 2.23) for 1980-94. The SRRs for bladder can- Society CPS-11 population, surveyed in 1982. cer were 9.11 (95% CI 1.26 to 66.7) for The percentage of current, former, and never 1975-9, and 1.39 (95% CI 0.87 to 2.22) for cigarette smokers are 35.7%, 39.8%, and 1980-94, with unstable numbers for the 24.5%. The corresponding figures for the 1975-9 period due to too few deaths from entire male survey population were 23.2%, bladder cancer among non-painters. These 43.6%, and 33.2% (estimated from table results indicate that our SRR findings for the VI").Amount smoked among current smokers 1975-9 period (corresponding roughly to the was comparable for painters and the entire results of Matanowski et d)do not differ from population. the period 1980-94 for lung cancer or liver With an indirect adjustment for sm0king,2~ cancer, but numbers are unstable for bladder the data of Brackbill et ul suggest that a lung cancer. cancer RR of 1.14 for painters versus the For lung cancer, smoking differences be- national population would be expected based tween painters and the United States popula- on smoking differences alone. With the data tion may explain part of the lung cancer excess from Stellman et ul,the estimated RR for lung we found for painters, and to a lesser degree cancer due to smoking differences alone would may explain part of the excess SMRs for blad- be 1.16. der cancer, when the external United States Similar adjustments for bladder cancer, comparison group was used. Indirect adjust- much more weakly related to smoking, would ments for smoking suggest that differences in lead to estimated RRs due to confounding by smoking between the painters in large United smoking in the order of 1.05. States surveys, and the overall United States The adjustments apply only to comparisons comparison population, would account for with the national population. Confounding by about a 15% excess for lung cancer, and a 5% smoking would be expected to be less impor- excess for bladder cancer. Hence, neither the tant in internal comparisons between painters lung nor bladder cancer excess found in this and non-painters (both groups being blue col- study is likely to be fully explained by smoking, lar workers), who would be expected to share in the light of this adjustment. However, we do similar smoking habits. not have direct smoking data on our cohort, 320 stemland, Palu limiting the usefulness of this kind of indirect adjustment. Such confoundingby smoking is less likely to have an effect on internal comparisons (SRRs) between painters and non-painters, as both are blue collar workers likely to share similar smoking habits. For example, the lung cancer RR of 1.323 comparing painters with non- painters (both with 20 years potential latency) is unlikely to be explained by confounding by smoking. The data for other diseases highly related to smoking do not show strong consistently high risks for painters compared with the United States population, also arguing against con- founding by smoking. Oesophageal cancer, laryngeal cancer, emphysema, bronchitis, and other non-malignant respiratory disease (pri- marily chronic obstructive pulmonary disease (COPD)) are all known to have a relative risk of the order of 10 for smokers versus non- smokers, and would be expected to be increased in our SMR analyses if painters smoked much more heavily than the United States population; the RRs for these outcomes were 1.12, 0.97, 1.13, 1.11, and 1.07 respec- tively. These results suggest that if there is a confoundingeffect by s m o b g , it is not severe. The lung cancer excess among painters could also be partly attributable to the use of spackling compounds which formerly con- tained asbestos, although the level of past exposure to respirable asbestos for painters is not known. The SMR for asbestosis was significantly increased (SMR 4.70). However, only 14 deaths were found due to asbestosis among the 18 989 deaths of painters, which does not indicate widespread exposure to high levels of asbestos. Furthermore, there were no excesses of cancer in sites likely to include mesothelioma (peritoneum, other parts of the respiratory system), another disease caused almost exclusively by asbestos. A nested case-control study of New York painters and non-painters within our cohort was conducted by other investigators in the early 1980~,b~a' sed on the earlier follow up of this cohort. This study was based on interviews (primarily with next of kin for cases) collected by posted questionnaires, and was adjusted for smoking.Painters and non-painters had similar smokinghabits. A risk Of lung cancer was found for being a painter, after adjustment for smoking, which increased for painters who reportedly did not wear respiratory protection. Limitations of these results include a low response rate and the reliability of detailed work history data collected by posted question- naires from next of kin. Our data also indicated a modest but significant increase in liver cancer in painters compared with the United States population (SMR 1.25); non-painters did not show such an increase. However, the importance of this finding is lessened because painters did not show an increase in liver cancer in a direct comparison with non-painters, especially in the comparison with 3 2 0 years latency where an effect would be most likely. Also, both painters and non-painters had excesses of cir- rhosis, which is associated both with liver cancer and alcohol consumption. Although cirrhosis could conceivably be related to exposure to solvents among painters, the fact that non-painters had a significant increase in cirrhosis compared with the United States population lessens the probability that the excess of cirrhosis among painters is due to an occupational exposure. Stomach cancer was in excess for both painters and non-painters, compared with the United States population. However, painters did not have an excess of stomach cancer when compared directly with non-painters. The excess of stomach cancer versus the United States population for both painters and nonpainters may be due to non-occupational risk factors-such as diet. Both painters and non-painters had excesses of death from falls compared with the United States population. It is likely that both these excesses are partly due to occupational factors, given that working in high places is common for both groups. Painters had modest but significantlyhigher rates of suicide and homicide than the United States population, but non-painters did not. We have no explanation why this should be, but solvent exposure could possibly play a part. Such an interpretation is speculative. For suicide, there is some published evidence that painters have an increased rate of neuropsychiamc disorders.z5 In summary, the modest excesses of lung and bladder cancers that we have found among painters are consistent with an occupational aetiology and are consistent with the scientific literature. Confounding by smokingmay play a part in these excesses, particularly for lung cancer which is highly related to smoking, but any such confounding is unlikely to completely explain these findings. The main weaknesses in our data are the lack of detailed work history and the lack of any specific exposure information; the agents responsible for the cancer excesses found here are unknown (see introduction on this point). 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S a n d 3 Wrk Enwimn Healrh 1990;16:182-8. Vancouver style All manuscripts submitted to Occup E n v i m Med should conform to the uniform requirements for manuscripts submitted to biomedical journals (known as the Vancouver style.) Occup Emiron Med, together with many other international biomedical journals, has agreed to accept articles prepared in accordance with the Vancouver style. The style (described in full in the JAW4 [11) is intended to standardise requirementsfor authors, and is the same as in this issue. References should be numbered consecutively in the order in which they are first mentioned in the text by Arabic numerals on the line in square brackets on each occasion the reference is cited (Manson[l] confirmed other reports[2][3][4][5]). In future references to papers submitted to Clccup Environ Med should include: the names of all authors if there are three or less or, if there are more, the first three followed by et d,the.title of journal articlesor book chapters; the titles of journals abbreviated according to the style of Index Medicus; and the first and final page numbers of the article or chapter.Titles not in Index Medicus should be given in full. Examples of common forms of references are: I International Committee of Medical Journal Editors. Uniform requirements for manuscripts submitted to biomed journals.3 A M A 1993;269:2282-6. 2 Soter NA, Wasserman SI, Austen KF. Cold urticaria: release into the circulation of hisanaine and eosinophil chemotactic factor of anaphylaxis during cold challenge. N E n d 3Med 1976;294687-90. 3 Weinstein L,Swam MN. Pathogenic properties of invad- ing micro-organisms.In: Sodeman WA Jr, Sodeman WA, eds. Pathok~gicphyswbgy, mechanisms of disease. 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