Occupational exposure to pesticides and bile tract carcinoma in men: results from a European multicenter case-control study.

OBJECTIVES: To estimate the associations between occupational exposure to pesticides and extrahepatic biliary tract carcinoma in men, a population-based case-control study was carried out. METHODS: Cases (n = 104), aged 35-70, diagnosed in 1995-1997, were sampled by active reporting systems from hospitals. Controls (n = 1,401) were a random sample of the general male population. Information on occupation and confounding factors was obtained by questionnaires. Exposures were quantified with respect to time, application methods, and use of personal protective equipment. Intensity was evaluated by using a published algorithm which weighted the exposure assigned according to the use of personal protective equipment and mode of application. Logistic regression analyses were conducted adjusted for gallstones, age, and country. RESULTS: Being ever exposed to pesticides resulted in an odds ratio (OR) of 1.0 [95%-confidence interval (CI) 0.6-1.6]. A modestly elevated risk was found for backpack mounted sprayers OR = 1.4 [95% CI 0.7-2.6] and vine farmers OR = 2.5 [95% CI 0.9-7.2]. Using time periods and exposure frequency as intensity measure, no elevated risks were found. The only exception was year of maximum exposure which yielded an OR of 1.6 [95% CI 0.7-3.5]. However, no clear trend was observed in this analysis. CONCLUSIONS: This study does not rule out that pesticide exposure represents an occupational risk factor for extrahepatic biliary tract carcinoma, but no indication of a strong association was observed. Some modes of exposure were weakly, albeit not significantly associated with carcinoma risk. The observed estimates of effects may be influenced by a lack of precise exposure assessment. Different chemical compositions of pesticides were utilized during a long time span of pesticide exposure, and it should be considered that the exposure is assessed with substantial uncertainty that could non-differential and bias results toward the null.

The growing incidence of cancer: role of lifestyle and screening detection (Review).

The increasing incidence of a variety of cancers after the Second World War confronts scientists with the question of their origin. In Western countries, expansion and ageing of the population, as well as progress in cancer detection using new diagnostic and screening tests cannot fully account for the observed growing incidence of cancer. Our hypothesis is that environmental factors play a more important role in cancer genesis than it is usually agreed: i) over the last 2-3 decades, alcohol consumption and tobacco smoking in men have significantly decreased; ii) obesity is increasing in many countries, but the growing incidence of cancer also concerns cancers not related to obesity nor to other lifestyle-related factors; iii) there is evidence that the environment has changed over the same time scale as the recent rise in cancer incidence, and that this change included the accumulation of many new carcinogenic factors in the environment; iv) genetic susceptibility to cancer due to genetic polymorphism cannot have changed over one generation and actually favours the role of exogenous factors through gene-environment interactions; v) age is not the unique factor to be considered since the rising incidence of cancers is seen across all age categories, including children; vi) the fetus is specifically vulnerable to exogenous factors. A fetal exposure during a critical window period may explain why current epidemiological studies may be negative in adults. We therefore propose that the involuntary exposure to many carcinogens in the environment contributes to the rising trend in cancer incidence.

Lifestyle-related factors and environmental agents causing cancer: an overview.

The increasing incidence of a variety of cancers after the Second World War confronts scientists with the question of their origin. In Western countries, expansion and ageing of the population as well as progress in cancer detection using new diagnostic and screening tests cannot fully account for the observed growing incidence of cancer. Our hypothesis is that environmental factors play a more important role in cancer genesis than it is usually agreed. (1) Over the last 2-3 decades, alcohol consumption and tobacco smoking in men have significantly decreased in Western Europe and North America. (2) Obesity is increasing in many countries, but the growing incidence of cancer also concerns cancers not related to obesity nor to other known lifestyle-related factors. (3) There is evidence that the environment has changed over the time period preceding the recent rise in cancer incidence, and that this change, still continuing, included the accumulation of many new carcinogenic factors in the environment. (4) Genetic susceptibility to cancer due to genetic polymorphism cannot have changed over one generation and actually favours the role of exogenous factors through gene-environment interactions. (5) Age is not the unique factor to be considered since the rising incidence of cancers is seen across all age categories, including children, and adolescents. (6) The fetus is specifically vulnerable to exogenous factors. A fetal exposure during a critical time window may explain why current epidemiological studies may still be negative in adults. We therefore propose that the involuntary exposure to many carcinogens in the environment, including microorganisms (viruses, bacteria and parasites), radiations (radioactivity, UV and pulsed electromagnetic fields) and many xenochemicals, may account for the recent growing incidence of cancer and therefore that the risk attributable to environmental carcinogen may be far higher than it is usually agreed. Of major concern are: outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons; indoor air pollution by environmental tobacco smoke, formaldehyde and volatile organic compounds such as benzene and 1,3 butadiene, which may particularly affect children and food contamination by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins and other organochlorines. In addition, carcinogenic metals and metalloids, pharmaceutical medicines and some ingredients and contaminants in cosmetics may be involved. Although the risk fraction attributable to environmental factors is still unknown, this long list of carcinogenic and especially mutagenic factors supports our working hypothesis according to which numerous cancers may in fact be caused by the recent modification of our environment.

Levels of brominated flame retardants in blood in relation to levels in household air and dust.

Levels of tri- to decabrominated diphenyl ethers (BDEs), 1,2-bis(2,4,6-tribromophenoxy)ethane (BTBPE) and 1,2-bis(pentabromophenyl)ethane (DeBDethane) were determined in air, sedimentary dust and human plasma from five households in Sweden. The levels of the individual BDEs in the plasma samples were in the same order of magnitude as in other studies of the general population in Scandinavia, and varied between non-detectable (<0.41 ng g(-1) l.w.) to 17 ng g(-1) (l.w.). BDE#28 and #47 were present in all air samples, with mean values of 0.015 and 0.12 ng m(-3), respectively, except for one sample where the BDE#47 concentration was below the limit of detection (<0.17 ng m(-3)). BDE#209 was found in one of the five air samples at a concentration of 0.26 ng m(-3). DeBDethane was also detected in one sample, in which the BDE#209 level was below LOD (<0.021 ng m(-3)), at a level of 0.023 ng m(-3). All the target compounds were found in the sedimentary dust samples at levels from 0.51 to 1600 ng g(-1), the highest concentration representing BDE#209. The most abundant components in plasma, air and dust were BDE#47, #99 and #209. In the plasma samples BDE#207 and #206 were also present at similar concentrations as BDE#47. In the sedimentary dust samples, DeBDethane was also among the most abundant BFRs. A positive relationship was found for the sumBDE concentrations in dust and plasma, although the relationship was strongly dependent on one of the five observations. BFR levels in dust and air were not dependent on the house characteristics such as living area, floor material or number of electronic devices.

Exposure to dioxins as a risk factor for soft tissue sarcoma: a population-based case-control study.

In a case-control study including 237 cases with soft tissue sarcoma and 237 controls, previous jobs and exposures to different agents, including pesticides, were assessed. Exposure to phenoxyacetic acids or chlorophenols gave a statistically significant increased rate ratio (RR) of 1.80 [95% confidence interval (CI) = 1.02-3.18] for soft tissue sarcoma. Exposure to phenoxyacetic acids of all types gave a nonsignificantly increased RR of 1.34 (95% CI = 0.70-2.56). During the 1950s, exposure to 2,4,5-trichlorophenoxyacetic acid gave a threefold significantly increased risk. High-grade exposure to chlorophenols, which are also contaminated by dioxins, gave an RR of 5.25 (95% CI = 1.69-16.34). The increased risk was thus attributed to dioxin-contaminated phenoxyacetic acids or chlorophenols that gave an RR of 2.43 (95% CI = 1.30-4.54).

Exposure to phenoxyacetic acids, chlorophenols, or organic solvents in relation to histopathology, stage, and anatomical localization of non-Hodgkin's lymphoma.

Results on 105 cases with histopathologically confirmed non-Hodgkin's lymphoma (NHL) and 335 controls from a previously published case-control study on malignant lymphoma are presented together with some extended analyses. No occupation was a risk factor for NHL. Exposure to phenoxyacetic acids yielded, in the univariate analysis, an odds ratio of 5.5 with a 95% confidence interval of 2.7-11. Most cases and controls were exposed to a commercial mixture of 2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid. Exposure to chlorophenols gave an odds ratio of 4.8 (2.7-8.8) with pentachlorophenol being the most common type. Exposure to organic solvents yielded an odds ratio of 2.4 (1.4-3.9). These results were not significantly changed in the multivariate analysis. Dichlorodiphenyltrichloroethane, asbestos, smoking, and oral snuff were not associated with an increased risk for NHL. The results regarding increased risk for NHL following exposure to phenoxyacetic acids, chlorophenols, or organic solvents were not affected by histopathological type, disease stage, or anatomical site of disease presentation. Median survival was somewhat longer in cases exposed to organic solvents than the rest. This was explained by more prevalent exposure to organic solvents in the group of cases with good prognosis NHL histopathology.

Occupational exposures and risk of gastric cancer in a population-based case-control study.

Gastric cancer trends seem to follow improvements in the environment of blue-collar workers, but the etiological role of occupational exposures in gastric carcinogenesis is scantily investigated. The risk of gastric adenocarcinoma in 10 common occupational industries, and particularly the long-term effects of asbestos, organic solvents, impregnating agents, insecticides, and herbicides, were evaluated in a population-based case-control study, including data on most established risk factors. The study base included all individuals of ages 40-79, born in Sweden and living in either of two areas (total population, 1.3 million) with differing gastric cancer incidences, from February 1989 through January 1995. We interviewed 567 cases classified to site (cardia/noncardia) and histological type, and 1,165 population-based controls, frequency-matched for age and sex. Metal workers had a 46% excess gastric cancer risk [adjusted odds ratio (OR), 1.46; 95% confidence interval (CI), 1.10-1.94], increasing to 1.65 (95% CI, 1.17-2.32) for >10 years in the industry. The elevated risk after exposure to herbicides (OR, 1.56; 95% CI, 1.13-2.15) was attributable to phenoxyacetic acids (adjusted OR, 1.70; 95% CI, 1.16-2.48), similarly across tumor subtypes, and not modified by smoking, body mass index, or Helicobacter pylori. The absence of interaction was demonstrated by the pure multiplicative effect found among those exposed to both H. pylori and phenoxyacetic acids (OR, 3.42; 95% CI, 1.41-8.26). Organic solvents, insecticides, impregnating agents, and asbestos were not associated with gastric cancer risk. Employment in the metal industry and exposure to phenoxyacetic acids were both positively and independently associated with gastric cancer risk. The fractions of all gastric cancers attributable to these job-related exposures were small but not negligible (7 and 5%, respectively) in the Swedish population.

How to combine the use of different mobile and cordless telephones in epidemiological studies on brain tumours?

Mobile phone users in epidemiological studies have often used more than one phone model, and sometimes also more than one mobile phone system (analogue and digital systems). Until now, this has not been taken into account in epidemiological studies, mainly because we do not know the possible interaction mechanism(s) and, hence, how to integrate exposure from different phones into one dosimetric measure. In this paper we take a step towards starting a discussion about how to proceed with this important issue and the possible use of parameters such as weighting factors, measured specific absorption rate (SAR) values and integrated specific absorption values are discussed. As a base of this discussion two previously published studies are used, one on mobile phones and cancer and the other one on subjective symptoms.

Use of cellular telephones and brain tumour risk in urban and rural areas.

AIMS: To investigate the association between the use of cellular or cordless telephones and the risk for brain tumours in different geographical areas, urban and rural. METHODS: Patients aged 20-80 years, living in the middle part of Sweden, and diagnosed between 1 January 1997 and 30 June 2000 were included. One control matched for sex and age in five year age groups was selected for each case. Use of different phone types was assessed by a questionnaire. RESULTS: The number of participating cases was 1429; there were 1470 controls. An effect of rural living was most pronounced for digital cellular telephones. Living in rural areas yielded an odds ratio (OR) of 1.4 (95% CI 0.98 to 2.0), increasing to 3.2 (95% CI 1.2 to 8.4) with >5 year latency time for digital phones. The corresponding ORs for living in urban areas were 0.9 (95% CI 0.8 to 1.2) and 0.9 (95% CI 0.6 to 1.4), respectively. This effect was most obvious for malignant brain tumours. CONCLUSION: In future studies, place of residence should be considered in assessment of exposure to microwaves from cellular telephones, although the results in this study must be interpreted with caution due to low numbers in some of the calculations.

The effects of diet and zinc treatment on the fatty acid composition of serum lipids and adipose tissue and on serum lipoproteins in two adolescent patients with acrodermatitis enteropathica.

In two adolescent patients with acrodermatitis enteropathica fatty acid spectra in serum lipids and adipose tissue and serum lipoprotein concentrations were followed for about 7 yr. One patient was treated by diet and iv infusions of high amounts of linoleic acid and later by different doses of zinc. The other boy was given only varying doses of zinc. Extra supply of linoleic acid raised its concentrations in serum triglycerides, cholesterol esters, phospholipids, and adipose tissue lipids from low to normal or high levels. In both patients linoleic acid in serum lipids was sensible to the dose of zinc, decreasing when it was low and increasing when it was high. Serum triglycerides increased when the supply was low and was normalized when high doses were given. High-density lipoprotein cholesterol, however, remained low throughout the study. We conclude that in acrodermatitis enteropathica zinc thus seems to be of importance in regulating linoleic acid and serum lipoprotein metabolism.

Viral infection, atopy and mycosis fungoides: a European multicentre case-control study.

Mycosis fungoides (MF) is a rare disease with an unknown aetiology, although it has been suggested that infections may play a role. The present study investigates whether infections, atopic disorders and some other diseases are risk indicators for MF. A European multicentre case-control study involving seven rare cancers, including MF, was conducted from 1995 to 1998. Patients between 35 and 69 years of age diagnosed with MF (n = 140) were recruited, and the diagnoses were verified by a reference pathologist, who classified 83 cases as definitive and 35 cases as possible; 22 cases were not accepted. Of the 118 accepted cases, 104 patients were interviewed (including 76 definitive cases and 28 possible cases). These 76 definitive cases were used for this study. A common set of controls to serve all case groups were interviewed, representing a total of 4574 controls. The latter included 1008 colon cancer patients and 3566 subjects selected from population registers. Information on infections, skin pathology and clinical history 5 years before the diagnosis of MF was used to estimate odds ratios (ORs) derived from logistic regression-modelling, which included gender, age and country. The highest ORs for MF were found in patients who reported a history of psoriasis 5 years before MF was diagnosed (OR 7.2, 95% CI: 3.6-14.5). Urticaria had an OR of 1.4 (95% CI: 0.6-3.6). Infections and atopic diseases were not closely associated with MF. Some diseases correlated to MF. Whether this has a causal background or reflects early diagnostic uncertainty is not known.

Are alcohol intake and smoking associated with mycosis fungoides? A European multicentre case-control study.

The incidence of mycosis fungoides (MF) is low, and the aetiology of the disease is unknown. The aim of this study was to investigate whether wine consumption protects against the disease and whether smoking constitutes a risk factor. This paper is part of the European Rare Cancers Study that tries to determine the risk factors for seven selective rare cancers, including mycosis fungoides, involved in the development of cancer. A multicentre case-control study was conducted in six European countries. Only incident cases with confirmed histology were included in the analysis which include a total of 76 cases of MF and 2899 controls. Wine intake had no protective effect; on the contrary the consumption of more than 24 g of alcohol per day was associated with a high risk of MF (odds ratio (OR)=3.02, 95% confidence interval (CI), 1.34-6.79), after adjusting for centre, country, age, sex and education. There was a dose-dependent increase in the risk of MF with increased smoking habits, albeit the observed trend was not statistically significant. A combined exposure to high tobacco and alcohol use yielded a significantly increased risk factor for MF (P=0.0073). Alcohol intake was associated with MF.

External radiotherapy prior to thyroid cancer: a case-control study.

PURPOSE: The aim of this investigation was to study previous radiotherapy of malignant diseases as a risk factor for thyroid cancer. METHODS AND MATERIALS: By using the Swedish Cancer Registry all cases of thyroid cancer with another malignant disease at least one year previously and living within the catchment area of our hospital were traced. During 1959-1989 a total of 1056 cases of thyroid cancer were identified. Of these 37 had had another previous malignant disease and they constituted the cases in this study. As controls four persons with at least two malignant diseases, thyroid cancer excluded, were selected for each case from the same cancer registry. RESULTS: Ten (27.0%) of the 37 patients with thyroid cancer as a second tumor had earlier been irradiated with the treatment dose including the thyroid gland as compared with 34 (24.5%) of the 139 control patients. Eight of the ten cases with previous irradiation of the thyroid gland had papillary cancer. The median latency was 13 years. The estimated radiation dose in the thyroid varied between 3 and 40 Gy. External radiotherapy gave a crude odds ratio of 1.1 with 95% confidence interval = 0.5-2.8 for thyroid cancer. The weighted odds ratio was calculated to 2.3 with confidence interval = 0.5-8.9. CONCLUSION: This case-control study gave a non significantly increased odds ratio for thyroid cancer in patients with external radiotherapy including the thyroid gland.

No association between immunohistochemical expression of p53, c-erbB-2, Ki-67, estrogen and progesterone receptors in female papillary thyroid cancer and ionizing radiation.

An association has previously been reported between exposure to medical diagnostic ionizing radiation and papillary thyroid cancer in women. To further evaluate potential mechanisms in carcinogenesis, the expression of p53, c-erbB-2, as well as Ki-67, estrogen and progesterone receptors were analyzed by immunohistochemistry in 19 women exposed to X-rays and for comparison in nine women without such reported exposure. They all had papillary thyroid cancer. No difference was found between these groups. The results of this study showed that p53, c-erbB-2, Ki-67, estrogen and progesterone receptors are not involved in papillary thyroid cancer associated with exposure to medical diagnostic ionizing radiation.

Some aspects of the etiology of non-Hodgkin's lymphoma.

In epidemiologic studies, non-Hodgkin's lymphoma (NHL) has been associated with exposure to chemicals such as phenoxyacetic acids; chlorophenols; dioxins; organic solvents including benzene, polychlorinated biphenyls, chlordanes; and immunosuppressive drugs. Experimental evidence and clinical observations indicate that these chemicals may impair the immune system. The risk is increased for NHL in persons with acquired and congenital immune deficiency as well as autoimmune disorders. Also, certain viruses have been suggested to be of etiologic significance for NHL. In some cases of NHL the common mechanism for all these agents and conditions may be immunosuppression, possibly in combination with viruses.

Concentrations of organochlorines related to titers to Epstein-Barr virus early antigen IgG as risk factors for hairy cell leukemia.

Hairy cell leukemia (HCL) is a rare chronic B-cell malignancy that, according to modern classifications, is a subgroup of non-Hodgkin lymphomas (NHLs). A rapid increase in incidence of NHL has been reported in many countries. The reasons for this increase are largely unknown, but exposure to organochlorines has been suggested as a risk factor. Epstein-Barr virus is a human herpesvirus that has been associated with certain subgroups of NHL. In this study, we measured lipid adjusted blood concentrations (in nanogram per gram) of 36 congeners of polychlorinated biphenyls (PCBs), p, p'-dichlorodiphenyldichloroethylene (p,p'-DDE), hexachlorobenzene (HCB), and four subgroups of chlordanes (trans-nonachlor, cis-nonachlor, MC6, and oxychlordane) in incident cases of HCL and controls from the general population. We obtained results on organochlorines and antibodies for 54 cases and 54 controls. Titers of antibodies to the Epstein-Barr early antigen and Epstein-Barr nuclear antigen, measured as P107, were correlated to concentrations of organochlorines to evaluate the possibility of an interaction between these factors in the pathogenesis of HCL. We found no significant difference in lipid-adjusted blood concentrations of total PCBs, p,p'-DDE, HCB, or the sum of the chlordanes between cases and controls. Titers of antibodies to Epstein-Barr early antigen IgG [Greater and equal to] 40 were correlated to an increased risk for HCL. This risk was further increased in those with a level above the median value of p,p'-DDE, HCB, or the sum of the chlordanes, suggesting an interaction between Epstein-Barr virus and a higher concentration of these chemicals. We also found increased risk for the sum of immunotoxic PCB group.

Case-control study on colon cancer regarding previous diseases and drug intake.

Some diseases and drugs have previously been associated with increased risk for colon cancer. A case-control study on colon adenocarcinoma was conducted encompassing 329 cases and 658 controls. History of previous diseases and drug intake was assessed by questionnaire. Appendectomy was associated with a protective effect with odds ratio (OR) 0.5 and 95% confidence interval (CI) 0.2-0.9. Cholecystectomy was associated with increased risk, especially in females, for right sided and transverse colon cancer, OR 1.5 (CI 0.9-2.5) and OR 1.8 (CI 0.8-3.5), respectively. Ulcerative colitis increased the risk, OR 11 (CI 3.5-38). Also hyperplasia of the prostate gland and diabetes in men were related to an increased risk with OR 4.4 (CI 1.5-13) and OR 2.9 (CI 1.4-6.0), respectively. For men and women together diabetes mellitus yielded an increased OR of 1.7 (1.0-3.0). Regarding drugs somewhat increased risks were found for beta-2-stimulating agents, OR 1.9 (CI 0.6-5.4), benzodiazepine, OR 1.7 (CI 0.9-3.3), iron, OR 1.9 (CI 0.5-6.7), and paracetamol, OR 2.5 (0.6-8.5). Increased risks were found for hydralazine in men, OR 2.3 (CI 0.7-7.0), methyldopa in men, OR 4.3 (1.1-18), sulfonylurea, OR 2.9 (CI 1.2-6.7), and verapamil, OR 22 (CI 2.4-480). Somewhat decreased risk was found for indometacin, OR 0.6 (0.2-1.6).

Metaanalysis of 4 Swedish case-control studies on exposure to pesticides as risk-factor for soft-tissue sarcoma including the relation to tumor-localization and histopathological type.

In four previous case-control studies we have shown an association between exposure to phenoxyacetic acids or chlorophenols and soft-tissue sarcoma (STS). These chemicals are contaminated by dioxins and dibenzofurans, some of which are known carcinogens in experimental animals. In a meta-analysis of our four studies we studied such exposure including the relation to tumour localization and histopathological type of STS. In total 434 histopathologically verified STS cases and 948 controls were included. Anatomical tumour localization was assessed by scrutinizing medical records for all cases. In the analysis stratification was made for age, vital status and study. Significantly increased risks were obtained for exposure to phenoxyacetic acids and chlorophenols, odds ratios 2.7 and 3.3, 95% confidence intervals 1.9-4.7 and 1.8-6.1, respectively. The increased risk was independent of histopathological subtype and anatomical site although especially high odds ratios were obtained for body sites close to areas where dermal contact may occur in sprayers. Phenoxyacetic acids and chlorophenols with their contaminating dioxins and dibenzofurans should be regarded as carcinogenic for STS regardless of tumour localization and histopathological type.

Colon-cancer and dietary habits - a case-control study.

The importance of dietary factors in colon carcinogenesis was analyzed as part of a case-control study from Northern Sweden encompassing 312 cases and 623 controls. Data on 28 different food items, each divided into consumption before and after the age of 25, were collected by a food frequency questionnaire. Mantel-Haenszel odds ratios (MH-ORs) were calculated for various food items and nutritients and are given in parentheses where A represents consumption before and B after the age of 25. Reduced MH-ORs were seen for daily cheese intake (A=0.64, B=0.41) and also for intake of crisp bread, boiled and fried fish although not significantly. A non-significantly decreased risk was seen for fibre-rich food. When food items were grouped with regard to their content of certain nutrients, decreased risks were associated with food rich in selenium (A=0.74, B=0.82). Also food rich in vitamin C gave a reduced MH-OR but only for intake before the age of 25 (A=0.75, B=1.09). For daily consumption of 2 or more cups of tea a reduced MH-OR of 0.61 was seen. Frequent intake of smoked food gave increased MH-ORs for both age groups (A=1.52, B=1.36) whereas high fat intake was not identified as a risk factor for colon cancer. Intake of alcohol or coffee was not associated with colon cancer risk in this study.

Case-control study on risk factors for testicular cancer.

Occupational exposures were assessed in a case-control study on testicular cancer using self administered questionnaires. Answers were obtained for 148 (91%) cases and 314 (87%) controls. Of the cases 101 had seminoma and 47 had embryonal testicular cancer. Occupational plastics work yielded odds ratio (OR) 2.9 with 95% confidence interval (CI) 1.3-6.5. Increased risk was found for embryonal cancer regarding farming (OR 3.1; CI 1.03-9.1) and contact with farm animals (OR 3.3; CI 1.00-10.9), but not for seminoma. For all testicular cancer exposure to insects repellents, mostly containing N,N-diethyl-m-toluamide (DEET) gave OR 1.7; CI 1.03-2.8, with a dose-response effect. Somewhat increased risks were found for amateur radio operators (OR 2.2; CI 0.7-6.6), work with radar equipment (OR 2.0; CI 0.3-14.2) and engineers in electronics and telecommunication industry (OR 2.3; CI 0.8-6.7) based on few exposed subjects, however. Video display unit work gave OR 1.5; CI 0.98-2.3 and for exposure 480 working days (median number) the risk increased further to OR 1.8; CI 1.1-3.2. Because of low numbers of exposed subjects in some calculations some of these results might be spurious and need to be further studied.