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Background: Worldwide, lung cancer is the second leading cause of cancer death in women. The present study explored associations between occupational exposures that are prevalent among women, and lung cancer., Methods: Data from 10 case-control studies of lung cancer from Europe, Canada, and New Zealand conducted between 1988 and 2008 were combined. Lifetime occupational history and information on nonoccupational factors including smoking were available for 3040 incident lung cancer cases and 4187 controls. We linked each reported job to the Canadian Job-Exposure Matrix (CANJEM), which provided estimates of probability, intensity, and frequency of exposure to each selected agent in each job. For this analysis, we selected 15 agents (cleaning agents, biocides, cotton dust, synthetic fibers, formaldehyde, cooking fumes, organic solvents, cellulose, polycyclic aromatic hydrocarbons from petroleum, ammonia, metallic dust, alkanes C18+, iron compounds, isopropanol, and calcium carbonate) that had lifetime exposure prevalence of at least 5% in the combined study population. For each agent, we estimated lung cancer risk in each study center for ever-exposure, by duration of exposure, and by cumulative exposure, using separate logistic regression models adjusted for smoking and other covariates. We then estimated the meta-odds ratios using random-effects meta-analysis., Results and Conclusions: None of the agents assessed showed consistent and compelling associations with lung cancer among women. The following agents showed elevated odds ratio in some analyses: metallic dust, iron compounds, isopropanol, and organic solvents. Future research into occupational lung cancer risk factors among women should prioritize these agents., (© 2024 The Authors. American Journal of Industrial Medicine published by Wiley Periodicals LLC.)

Background The value of coronary artery calcium (CAC) in the allocation of PCSK9i (proprotein convertase subtilisin/kexin type 9 inhibitors) among individuals without clinically evident atherosclerotic cardiovascular disease (ASCVD) is unknown for indications that do not require confirmed familial hypercholesterolemia. We aimed to assess the ability of CAC to stratify ASCVD risk under 3 non-familial hypercholesterolemia PCSK9i allocation paradigms. Methods and Results We included participants without clinically evident ASCVD from MESA (Multi-Ethnic Study of Atherosclerosis), CARDIA (Coronary Artery Risk Development in Young Adults) study, DHS (Dallas Heart Study), and HNR (Heinz Nixdorf Recall) study. Three PCSK9i eligibility scenarios were defined: a broad scenario informed only by high low-density lipoprotein cholesterol levels (N=567), a restrictive one combining higher low-density lipoprotein cholesterol levels and presence of ≥2 additional risk factors (N=127), and a high-risk scenario where individuals with subclinical organ damage or high estimated risk would be treated to achieve low-density lipoprotein cholesterol <55 mg/dL (N=471). The high-risk scenario had the highest ASCVD event rates (27.8% at 10 years). CAC=0 was observed in 35% participants in the broad scenario, 25% in the restrictive scenario, and 16% in the high-risk scenario. In all, CAC=0 was associated with the lowest incident ASCVD rates at 5 and 10 years, and CAC burden was independently associated with ASCVD events adjusting for traditional risk factors. Conclusions CAC may be used to refine the allocation of PCSK9i, potentially leading to a more conservative use if CAC=0. The value of CAC testing is greater in scenarios that use low-density lipoprotein cholesterol levels and/or traditional risk factors to define PCSK9i eligibility (CAC=0 present in 1 of 3-4 patients), whereas its prevalence is lower when allocation is informed by presence of noncoronary subclinical organ damage.

Background: There is limited knowledge about mortality risk in persons with increased haemoglobin A 1c (HbA 1c ) levels below the diabetes threshold. Moreover, little is known about how associations between increased HbA 1c and mortality depend on the length of follow-up. Therefore, we studied associations between HbA 1c and mortality over long-term follow-up in persons with and without known diabetes., Methods: We used data from two German population-based cohort studies: KORA S4 Study (Southern Germany, n = 1458, baseline visits in 1999 to 2001, baseline age 55 to 74 years, mortality follow-up 16.8 years) and Heinz Nixdorf Recall (HNR) Study (Ruhr area, n = 4613, baseline visits in 2000 to 2003, baseline age 45 to 75 years, mortality follow-up 17.8 years). Adjusted log-linear models were fitted to estimate relative risks (RRs) with 95% confidence intervals (CI)., Results: In both cohorts, participants with HbA 1c 39 to 41 mmol/mol (5.7%-5.9%) and HbA 1c 42 to 46 mmol/mol (6.0% to 6.4%) did not have a larger overall mortality risk than participants with HbA 1c  < 39 mmol/mol (5.7%): the corresponding adjusted RRs were 1.00 (95% CI: 0.83-1.21) and 1.01 (0.80-1.27) in KORA and 0.99 (0.82-1.21) and 0.83 (0.65-1.07) in the HNR Study. For the pooled cohorts, the RR for HbA 1c 39 to 46 mmol/mol (5.7%-6.4%) was 0.96 (0.85-1.07). Associations between newly detected diabetes (HbA 1c  ≥ 6.5%) and mortality were weak after 4 and 8 years of follow-up, but were stronger after 12 years of follow-up, whereas associations between previously known diabetes (baseline) and mortality decreased., Conclusions: HbA 1c -defined pre-diabetes is not associated with overall mortality. For newly detected and previously known diabetes, mortality risks vary with length of follow-up., (© 2020 John Wiley & Sons Ltd.)

The prospective randomized Positron Emission Tomography (PET)-Guided Therapy of Aggressive Non-Hodgkin Lymphomas (PETAL) trial was designed to test the ability of interim PET (iPET) to direct therapy. As reported previously, outcome remained unaffected by iPET-based treatment changes. In this subgroup analysis, we studied the prognostic value of baseline total metabolic tumor volume (TMTV) and iPET response in 76 patients with T-cell lymphoma. TMTV was measured using the 41% maximum standardized uptake value (SUV 41max ) and SUV 4 thresholding methods. Interim PET was performed after two treatment cycles and evaluated using the ΔSUV max approach and the Deauville scale. Because of significant differences in outcome, patients with anaplastic lymphoma kinase (ALK)-positive lymphoma were analyzed separately from patients with ALK-negative lymphoma. In the latter, TMTV was statistically significantly correlated with progression-free survival, with thresholds best dichotomizing the population, of 232 cm 3 using SUV 41max and 460 cm 3 using SUV 4 . For iPET response, the respective thresholds were 46.9% SUV max reduction and Deauville score 1-4 vs 5. The proportion of poor prognosis patients was 46% and 29% for TMTV by SUV 41max and SUV 4 , and 29% and 25% for iPET response by ΔSUV max and Deauville, respectively. At diagnosis, the hazard ratio (95% confidence interval) for poor prognosis vs good prognosis patients according to TMTV was 2.291 (1.135-4.624) for SUV 41max and 3.206 (1.524-6.743) for SUV 4 . At iPET, it was 3.910 (1.891-8.087) for ΔSUV max and 4.371 (2.079-9.187) for Deauville. On multivariable analysis, only TMTV and iPET response independently predicted survival. Patients with high baseline TMTV and poor iPET response (22% of the population) invariably progressed or died within the first year (hazard ratio, 9.031 [3.651-22.336]). Due to small numbers and events, PET did not predict survival in ALK-positive lymphoma. Baseline TMTV and iPET response are promising tools to select patients with ALK-negative T-cell lymphoma for early allogeneic transplantation or innovative therapies., (© 2019 John Wiley & Sons, Ltd.)

Electroconvulsive therapy (ECT) is the treatment of choice for severe and treatment-resistant depression; disorder severity and unfavorable treatment outcomes are shown to be influenced by an increased genetic burden for major depression (MD). Here, we tested whether ECT assignment and response/nonresponse are associated with an increased genetic burden for major depression (MD) using polygenic risk score (PRS), which summarize the contribution of disease-related common risk variants. Fifty-one psychiatric inpatients suffering from a major depressive episode underwent ECT. MD-PRS were calculated for these inpatients and a separate population-based sample (n = 3,547 healthy; n = 426 self-reported depression) based on summary statistics from the Psychiatric Genomics Consortium MDD-working group (Cases: n = 59,851; Controls: n = 113,154). MD-PRS explained a significant proportion of disease status between ECT patients and healthy controls (p = .022, R 2 = 1.173%); patients showed higher MD-PRS. MD-PRS in population-based depression self-reporters were intermediate between ECT patients and controls (n.s.). Significant associations between MD-PRS and ECT response (50% reduction in Hamilton depression rating scale scores) were not observed. Our findings indicate that ECT cohorts show an increased genetic burden for MD and are consistent with the hypothesis that treatment-resistant MD patients represent a subgroup with an increased genetic risk for MD. Larger samples are needed to better substantiate these findings., (© 2018 The Authors. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics published by Wiley Periodicals, Inc.)

Background: Thoracic aortic calcification (TAC) and coronary artery calcification (CAC) are markers of subclinical atherosclerosis and are associated with incident major cardiovascular events. We investigated major determinants for incidence and progression of TAC and the association between TAC and CAC incidence and progression., Methods and Results: In a population-based cohort study, 3270 participants (aged 45-74 years, 53.1% women) received cardiac computed tomography at baseline and after a mean follow-up of 5.1±0.3 years for quantification of calcification of the ascending (ATAC) and descending thoracic aorta (DTAC) and CAC. Multivariable relative risk regression analysis was used to investigate associations of cardiovascular risk factors with incident TAC, of baseline TAC with incident CAC, and of baseline CAC with incident TAC. Of 1243 participants with baseline TAC of 0, 517 (41.6%) revealed incident TAC after 5 years. Incidence of descending TAC was higher (34.5%) than ascending TAC (23.3%). Incident TAC after 5 years was associated with age (relative risk 1.26 [95% CI 1.21-1.33], per 5 years), blood pressure (relative risk 1.06 [95% CI 1.03-1.10], per 10 mm Hg), low-density lipoprotein cholesterol (relative risk 1.08 [95% CI 1.04-1.12], per 20 mg/dL), and smoking (relative risk 1.28 [95% CI 1.07-1.53]). Among the 1185 participants without CAC at baseline, the risk of developing CAC was 28.3% when baseline TAC was present compared with 22.2% among those without baseline TAC (excess risk 6.1% [95% CI 1.2-11.0%]). The point estimate of excess risk for incident CAC was higher for ascending TAC (10.8% [95% CI 4.8-16.7%]) and low for descending TAC (1.8% [95% CI -3.2% to 6.7%]). Excess risk for developing ascending and descending TAC with present baseline CAC was 16.4% (95% CI 12.7-20.0%) and 15.6% (95% CI 10.8-20.4%), respectively., Conclusion: TAC and CAC share similar major determinants for incident calcification. Participants with TAC, especially ascending TAC, are at elevated risk for development of CAC., (© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Aim: The sleep disturbing effect of many drugs is derived from clinical trials with highly selected patient collectives. However, the generalizability of such findings to the general population is questionable. Our aim was to assess the association between intake of drugs labelled as sleep disturbing and self-reported nocturnal sleep disturbances in a population-based study., Methods: We used data of 4221 participants (50.0% male) aged 45 to 75 years from the baseline examination of the Heinz Nixdorf Recall Study in Germany. The interview provided information on difficulties falling asleep, difficulties maintaining sleep and early morning arousal. We used the summary of product characteristics (SPC) for each drug taken and assigned the probability of sleep disturbances. Thereafter, we calculated cumulative probabilities of sleep disturbances per subject to account for polypharmacy. We estimated prevalence ratios (PR) using log Poisson regression models with robust variance., Results: The adjusted PRs of any regular nocturnal sleep disorder per additional sleep disturbing drug were 1.01 (95% confidence interval (CI) 0.97, 1.06) and 1.03 (95% CI 1.00, 1.07) for men and women, respectively. Estimates for each regular nocturnal sleep disturbance were similarly close to 1. PRs for regular nocturnal sleep disturbances did not increase with rising cumulative probability for drug-related sleep disturbances., Conclusions: SPC-based probabilities of drug-related sleep disturbances showed barely any association with self-reported regular nocturnal sleep disturbances. We conclude that SPC-based probability information may lack generalizability to the general population or may be of limited data quality., (© 2016 The British Pharmacological Society.)

Children with attention-deficit/hyperactivity disorder (ADHD) have a higher rate of obesity than children without ADHD. Obesity risk alleles may overlap with those relevant for ADHD. We examined whether risk alleles for an increased body mass index (BMI) are associated with ADHD and related quantitative traits (inattention and hyperactivity/impulsivity). We screened 32 obesity risk alleles of single nucleotide polymorphisms (SNPs) in a genome-wide association study (GWAS) for ADHD based on 495 patients and 1,300 population-based controls and performed in silico analyses of the SNPs in an ADHD meta-analysis comprising 2,064 trios, 896 independent cases, and 2,455 controls. In the German sample rs206936 in the NUDT3 gene (nudix; nucleoside diphosphate linked moiety X-type motif 3) was associated with ADHD risk (OR: 1.39; P = 3.4 × 10(-4) ; Pcorr  = 0.01). In the meta-analysis data we found rs6497416 in the intronic region of the GPRC5B gene (G protein-coupled receptor, family C, group 5, member B; P = 7.2 × 10(-4) ; Pcorr  = 0.02) as a risk allele for ADHD. GPRC5B belongs to the metabotropic glutamate receptor family, which has been implicated in the etiology of ADHD. In the German sample rs206936 (NUDT3) and rs10938397 in the glucosamine-6-phosphate deaminase 2 gene (GNPDA2) were associated with inattention, whereas markers in the mitogen-activated protein kinase 5 gene (MAP2K5) and in the cell adhesion molecule 2 gene (CADM2) were associated with hyperactivity. In the meta-analysis data, MAP2K5 was associated with inattention, GPRC5B with hyperactivity/impulsivity and inattention and CADM2 with hyperactivity/impulsivity. Our results justify further research on the elucidation of the common genetic background of ADHD and obesity., (Copyright © 2013 Wiley Periodicals, Inc.)

The heritability of attention deficit hyperactivity disorder (ADHD) is approximately 0.8. Despite several larger scale attempts, genome-wide association studies (GWAS) have not led to the identification of significant results. We performed a GWAS based on 495 German young patients with ADHD (according to DSM-IV criteria; Human660W-Quadv1; Illumina, San Diego, CA) and on 1,300 population-based adult controls (HumanHap550v3; Illumina). Some genes neighboring the single nucleotide polymorphisms (SNPs) with the lowest P-values (best P-value: 8.38 × 10(-7)) have potential relevance for ADHD (e.g., glutamate receptor, metabotropic 5 gene, GRM5). After quality control, the 30 independent SNPs with the lowest P-values (P-values ≤ 7.57 × 10(-5) ) were chosen for confirmation. Genotyping of these SNPs in up to 320 independent German families comprising at least one child with ADHD revealed directionally consistent effect-size point estimates for 19 (10 not consistent) of the SNPs. In silico analyses of the 30 SNPs in the largest meta-analysis so far (2,064 trios, 896 cases, and 2,455 controls) revealed directionally consistent effect-size point estimates for 16 SNPs (11 not consistent). None of the combined analyses revealed a genome-wide significant result. SNPs in previously described autosomal candidate genes did not show significantly lower P-values compared to SNPs within random sets of genes of the same size. We did not find genome-wide significant results in a GWAS of German children with ADHD compared to controls. The second best SNP is located in an intron of GRM5, a gene located within a recently described region with an infrequent copy number variation in patients with ADHD., (Copyright © 2011 Wiley Periodicals, Inc.)

Boron neutron capture therapy (BNCT) provides highly targeted delivery of radiation through the limited spatial distribution of its effects. This translational research/phase I clinical trial investigates whether BNCT might be developed as a treatment option for squamous cell carcinoma of head and neck (SCCHN) relying upon preferential uptake of the two compounds, sodium mercaptoundecahydro-closo-dodecaborate (BSH) or L-para-boronophenylalanine (BPA) in the tumour. Before planned tumour resection, three patients received BSH and three patients received BPA. The (10)B-concentration in tissues and blood was measured with prompt gamma ray spectroscopy. Adverse effects from compounds did not occur. After BPA infusion the (10)B-concentration ratio of tumour/blood was 4.0 +/- 1.7. (10)B-concentration ratios of tumour/normal tissue were 1.3 +/- 0.5 for skin, 2.1 +/- 1.2 for muscle and 1.4 +/- 0.01 for mucosa. After BSH infusion the (10)B-concentration ratio of tumour/blood was 1.2 +/- 0.4. (10)B-concentration ratios of tumour/normal tissue were 3.6 +/- 0.6 for muscle, 2.5 +/- 1.0 for lymph nodes, 1.4 +/- 0.5 for skin and 1.0 +/- 0.3 for mucosa. BPA and BSH deliver (10)B to SCCHN to an extent that might allow effective BNCT treatment. Mucosa and skin are the most relevant organs at risk.

Introduction: Non-melanoma skin cancer (NMSC), in contrast to skin melanoma (MEL), is considered a negligible health problem because mortality of NMSC is low. The aim of this study was to provide insights into the burden of NMSC and MEL by analysing nationwide skin cancer hospitalization data and data from a dermatologist panel of Germany. We wanted to estimate hospitalization costs due to skin cancer in Germany., Material and Methods: We analysed the most recent nationwide hospitalization data from 2003 and estimated hospitalization costs due to MEL and NMSC. We estimated the annual number of private dermatologist practice visits in Germany due to skin cancer., Results: In 2003, 20 455 melanoma-related and 41 929 NMSC-related hospitalizations occurred in Germany. Age-standardized hospitalization rates for NMSC were 2.5-fold and 1.8-fold higher among men and women than the rates for MEL, respectively. The age-specific proportions of hospitalizations for NMSC in relation to all cancer-related hospitalizations increased within the age range of 65 years and more. Among people aged 90 years and more, 14% of all cancer-related hospitalizations were due to NMSC. Estimated annual hospitalization costs for MEL were euro50 to 60 million, and those for NMSC were euro105 to 130 million. The estimated number of private dermatologist practice visits in Germany 2003 is considerably higher for NMSC than MEL CONCLUSIONS: Analyses of hospitalizations data and data from private dermatologists give NMSC higher public health relevance than can be obtained from consideration of death statistics.

Background: There is some evidence of an elevated risk for testicular cancer among firefighters., Methods: We performed a population-based case-control study including 269 testicular cancer cases and 797 controls matching on age and region with a special focus on occupational exposures. Job tasks were coded according to the International Standard Classification of Occupations (ISCO 68). We used conditional logistic regression to calculate odds ratios (OR)., Results: Three controls (0.4%) and four cases (1.5%) ever worked as firefighters. Firefighters showed an increased odds of testicular cancer in the matched evaluation (OR = 4.3, 95% confidence interval (95% CI) 0.7-30.5). The adjustment for a history of cryptorchidism or family history of testicular cancer did not alter our results., Conclusion: Although the association between firefighting and testicular cancer risk is based on only small numbers of exposed subjects in our study, the finding is consistent with a recent cohort study from New Zealand. Occupational hazards experienced by firefighters may increase the risk of testicular cancer., (Copyright 2003 Wiley-Liss, Inc.)

Background: Numerous studies have been carried out to evaluate the association between lung cancer and occupational asbestos exposure. However, the effects of timing of exposure have not been analyzed thoroughly., Methods: Two German case-control studies with data on occupational asbestos exposure histories have been pooled. Duration of work in potentially asbestos exposed jobs and two derived weighted exposure measures are analyzed together with time since last exposure. A spline function is used to model the effect of time since exposure., Results: The odds ratios (OR) and corresponding 95% confidence intervals were 1.8 (1.2, 2.7) and 2.4 (1.7, 3.4) for subjects having worked for 3 to 7 years and 8 or more years, respectively, in a job with potential asbestos exposure compared to never-exposed. Based on an evaluation of time since last exposure, the OR decreased significantly to about one-half after more than 20 years since exposure ceased. Using a spline function, applied to workers' complete exposure histories, the effect of an increment of exposure is greatest 10-15 years after that exposure was received., Conclusions: In contrast to previous indications, the risk of lung cancer increases soon after asbestos exposure, with its maximum effect from 10 to 15 years after the exposure was received.

Background: This study examines the role of occupational factors in the development of diffuse malignant mesothelioma with special emphasis on the dose-response relationship for asbestos and on the exposure to man-made vitreous fibers (MMVFs)., Methods: One hundred and twenty-five male cases, diagnosed by a panel of pathologists, were personally interviewed concerning their occupational and smoking history. The same number of population controls (matched for sex, age and region of residence) underwent similar interviews by trained interviewers. Odds ratios (OR) were calculated for an expert-based exposure index using conditional logistic regression., Results: Exposure to asbestos shows the expected sharp gradient with an OR of about 45 for a cumulative exposure > 1.5 fiber years (arithmetic mean 16 fiber years). A significant OR was calculated even for the lowest exposure category "> 0 - < or = 0.15 fiber years". Although the mean cumulative exposure to MMVF is roughly 10% of the exposure to asbestos, an increased OR is observed in an ever/never evaluation. This observation is heavily hampered by methodical problems. A corresponding case-control study was performed using a lung tissue fiber analysis in addition to interviews. Both interviews and the lung tissue analysis yielded similar OR levels between the reference and the maximum exposure intervals., Conclusions: Despite a possible influence as a result of selection and information bias, our results confirm the previously reported observation of a distinct dose-response relationship even at levels of cumulative exposure below 1 fiber year. Moreover, the study confirms that asbestos is a relevant confounder for MMVF. A causal relationship between exposure to MMVF and mesothelioma could neither be detected nor excluded, as in other studies., (Copyright 2001 Wiley-Liss, Inc.)

Background: The occupational lung cancer risk in manufacturing and repair of shoes was studied by pooling of two major case-control studies from Germany., Methods: Some 4184 incident hospital-based cases of primary lung cancer and 4253 population controls, matched for sex, age, and region of residence were intensively interviewed with respect to their occupational and smoking history. Based on the occupational coding and a free text search, all individuals who had ever worked in shoe manufacturing or repair for at least half a year were identified. Shoemaker-years were calculated as the cumulated duration of working in shoe manufacturing or repair. Odds ratios (OR) and 95% confidence intervals (CI) were calculated via conditional logistic regression. Additional adjustment for smoking and occupational asbestos exposure was used., Results: Seventy-six cases and 42 controls who had ever worked in shoe manufacture or repair (OR = 1.89, 95% CI: 1.29-2.78). After adjustment for smoking, this risk was lowered to 1.69 (95% CI: 1.09-2.62). Further adjustment for asbestos exposure only slightly changed the risk estimates upwards. The smoking adjusted OR in males was 1.50 (95% CI: 0.93-2.41) and 2.91 (95% CI: 0.90-9.44) in females. Logistic regression modeling showed a positive dose-effect relationship between duration of exposure in shoe manufacture and repair and lung cancer risk. The odds ratio for 30 years of exposure varied between 1.98 and 2.24 depending on the model specified., Conclusions: The study demonstrates an increased lung cancer risk for shoemakers and workers in shoe manufacturing. The risk seems to double after being 30 years in these occupations., (Copyright 2000 Wiley-Liss, Inc.)

Background: To investigate the association between lung cancer and occupational exposure to man-made vitreous fibers (MMVF), a pooled analysis of two case-control studies was conducted in the years 1988-1994., Methods: The case series consisted of 3498 males who were histologically or cytologically verified primary lung cancer cases. 3541 male population controls were drawn at random from the general population and matched to cases by sex, age, and place of residence. To examine the relationship between MMVF and lung cancer we asked all study subjects who worked for at least 6 months as construction and installation workers whether they ever installed or removed insulations and what kind of insulation material they used., Results: Some 304 (8.7%) cases and 170 (4.8%) controls reported to have insulated with glass wool or mineral wool mats. Coded as ever/never exposed, the odds ratio was 1.48 (95% CI: 1.17-1.88), adjusted for smoking and asbestos. To be sure to exclude any confounding effect of asbestos, we tried to identify those cases and controls who insulated with glass wool or mineral wool mats only and never reported any asbestos exposure. For this group we calculated an odds ratio of 1.56 (95% CI: 0.92-2.65), after adjustment for smoking. An elevated risk was also estimated on the basis of an expert rating which was done for a subgroup of cases and controls. Ever exposure to MMVF (but not to asbestos) in this subgroup yielded an odds ratio of 1.30 (95% CI: 0.82-2.07)., Conclusions: Our study provides some indication for an excess risk of man-made vitreous fibers. This result also persists after adjustment for smoking and asbestos., (Copyright 2000 Wiley-Liss, Inc.)

Background: Although in several epidemiological studies exposure to diesel motor emissions (DME) shows an elevated lung cancer risk, it is still controversial whether DME is a human carcinogen., Methods: In a pooled analysis of two case-control studies on lung cancer in Germany a total of 3498 male cases with histologically or cytologically ascertained lung cancer and 3541 male population controls were included. Information about lifelong occupational and smoking history was obtained by questionnaire. Drivers of lorries, buses, taxies, diesel locomotives and forklift trucks, bulldozers, graders, excavators, and tractors, were considered as exposed to DME and their cumulative exposure was estimated. All odds ratios were adjusted for smoking and asbestos exposure., Results: The evaluation of lung cancer risk for all jobs with DME-exposure combined showed an odds ratio of OR=1.43 (95%-CI: 1.23-1.67). Most pronounced was the increase in lung cancer risk in heavy equipment operators (OR=2. 31 95%-CI: 1.44-3.70). The risk of tractor drivers increased with length of employment and reached statistical significance for exposures longer than 30 years (OR=6.81, 95%-CI: 1.17-39.51). The group of professional drivers (e.g., trucks, buses, and taxies), showed an increased risk only in West Germany (OR=1.44, 95%-CI: 1. 18-1.76), but not in East Germany (OR=0.83, 95%-CI: 0.60-1.14). DME-exposure in other traffic related jobs (e.g., diesel engine locomotive drivers, switchmen, forklift operators) was associated with an odds ratio of OR=1.53 (95%-CI: 1.04-2.24)., Conclusions: The study provides further evidence that occupational exposure to diesel motor emissions is associated with an increased lung cancer risk., (Copyright 1999 Wiley-Liss, Inc.)

Background: To investigate the association between lung cancer and occupational factors in women., Methods: Six hundred eighty-six women with lung cancer and 712 controls matched for age and region were interviewed to gather occupational histories and information about other risk factors and confounders. Odds ratios (OR) and 95%-confidence intervals (CI) were calculated., Results: There were 11 cases and 2 controls who reported occupational asbestos exposure. Significantly elevated risks (P < 0.05, smoking-adjusted), were observed in the following industries: chemical, oil (OR 3.7), pottery, glass (OR 2.5), engine, vehicle building (OR 2.2), paper, wood, print (OR 1.9), cleaning service, hairdressing, housekeeping, waste disposal (OR 1.5); and occupations: assemblers, unskilled metal workers (OR 2.5), stock clerks, etc. (OR 1.6), restaurant owners and hoteliers (OR 2.7), as well as waitresses and travel attendants (OR 2.6)., Conclusions: The study provides evidence that both occupations previously observed as hazardous in males, and occupations of particular significance for women only, play a role in the risk of lung cancer in women.

Background: In studies in men, risk estimates on occupation and bladder cancer are distorted by about 10% when not adjusting for smoking. We examined the degree to which occupational risk estimates for bladder cancer in women are confounded by smoking, and the degree of residual confounding by inadequate control of this effect., Methods: Primary data of 11 case-control studies on occupation and bladder cancer from Denmark, France, Germany, Greece, Italy, and Spain were pooled. Information for smoking and lifetime occupational history for 700 female cases and 2,425 female controls ages 30-79 was abstracted and recoded. Logistic regression was used to calculate odds ratios (OR) by occupation, applying five models which differed in their degree of adjustment for smoking., Results: In major occupational groups, risk estimates were distorted by less than 10% when not adjusting for smoking. A statistically significant excess risk for bladder cancer was found in 13 specific occupations and industries. In most occupations, adjustment for smoking led the ORs towards the null value, but all statistically significant associations were maintained after adjustment. In three occupations (lathe operators, field crop workers, and wood manufacturers), a statistically significant excess risk was masked when not adjusting for smoking. In six occupations, estimates were distorted by more than 10% (-22% up to +40%). In occupations where smoking acted as a positive confounder, the proportion of confounding removed using a dichotomous smoking variable (ever/never) was around 60%. In one occupation (buyers), controlling for smoking status (ever, never) led to over-adjustment, because the percentage of smokers was high but the quantity smoked was low.

In a case-control study, 839 male hospital-based cases of primary lung cancer and the same number of population-based controls--matched by sex, age, and region of residence--were personally interviewed for their job and smoking histories. The study allows to quantify occupational asbestos exposure that was thought to be a welding-associated risk: 6% of cases and 2% of controls were classified into the occupational category "welders or burners# (odds ratio [OR] = 2.65). This OR was reduced to 1.93 (95% confidence limit [CL]: 1.03-3.61) after adjustment for smoking and asbestos. In contrast, a history of welding in general for at least a half-year is 28% among cases and 23% among controls, yielding an OR of 1.25 (95% CL: 0.94-1.65) after adjustment for both confounders. The OR of welding for more than 6,000 hr is 1.45 (95% CL = 1.04-2.02), reduced to 1.10 after adjustment for smoking and asbestos. Oxyacetylene welding for more than 6,000 hr lifelong is associated with an OR of 1.86 (95% CL = 1.01-3.43) reduced to 1.46 (n.s.) after adjustment for smoking and asbestos. The risk of oxyacetylene welding seems to be highest for oat cell carcinoma with an adjusted OR for ever-exposure of 1.46 (95% CL = 0.69-3.10). Therefore, the present study supports the hypothesis that some, but not all, of the excess risk of welders observed in the literature may be due to a history of cigarette smoking and occupational asbestos exposure. The elevated risk for the subgroup of employees in the aircraft industry reported for the midterm evaluation of the study still prevails, though no longer statistically significant. However, employees in this industry who ever welded show an OR of 2.29 (95% CL = 1.19-4.42) after adjustment for smoking and asbestos.

In a hospital-based case-control study, 391 male cases or primary lung cancer and the same number of controls--matched by sex, age, and region--were personally interviewed for their job and smoking histories. The data reported reflect the midpoint of a study aiming at a total of 1,000 cases. One objective of the study was to assess confounding by asbestos exposure in what was thought to be a welding-associated risk. While the odds ratios (OR) increased steeply with cumulative exposure to tobacco smoke and were raised also for lifelong asbestos exposure of over 4,100 working hours (OR = 1.91), the effect of welding exposure was reduced after adjustment for smoking and exposure to asbestos. Furthermore, no consistent dose-response relationship could be shown in relation to welding hours. Therefore the present study supports the hypothesis that some, if not all, of the excess risk of welders observed in the literature may be due to the exposure to asbestos. The finding that the subgroup of employees in the aircraft industry showed an increased odds ratio of 2.14 after adjustment for smoking and exposure to asbestos deserves further attention. This suggests the need for further research on the role of berryllium-containing alloys, which has been suggested by other authors.

A hospital-based case-control study of laryngeal cancer was conducted in Bremen in 1986 and 1987 with 100 prevalent male laryngeal cancer patients and 100 male hospital controls with diseases not considered to be related to smoking, alcohol, or occupational exposures, who were frequency matched by age. The odds ratio for heavy smoking (more than 30 pack-years) reached a value of 3.5 (95% confidence limits (CL) 1.1, 7.9). Ex-smokers showed a significant decrease in risk; this reached the level of those who had never smoked about 15 years after smoking cessation. For daily consumers of alcohol an odds ratio of 3.2 (95% CL 1.4, 7.5) was observed. Among the 17 occupations in which at least ten subjects had worked, excess risks were observed for stock keeping and transportation workers, and for leather and textile workers. The odds ratio was significantly increased for the latter (p less than 0.05). Among all those persons ever employed in a priori defined-risk occupations, an odds ratio of 2.74 (95% CL 1.23, 6.06) was observed. Considering responses to an exposure check-list, no increased risks could be shown for exposure to asbestos, coal tar, or welding fumes. On the other hand, excess risks were observed for exposures to diesel oil, gasoline, and mineral oil, controlling for smoking and alcohol. The findings in occupational and exposure subgroups were based on small numbers of cases and controls and, consequently, were subject to large sampling errors. Many of the results are consistent, however, with occupational risk factors reported from other studies.