Mobile phone use and acoustic neuromas.
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Biomedical subjects
Publications and source records attributed to Lennart Hardell.
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Exposure to polyvinyl chloride (PVC) plastics as a risk factor for testicular cancer was investigated. In total, 981 cases who were 20-75 years old and had reported to the Swedish Cancer Registry during 1993-1997 were included. One matched control from the population registry was used. Exposure was assessed by a questionnaire that was supplemented over the phone. Furthermore, an occupational hygienist qualified all exposures. In all, 791 matched pairs completed the questionnaire. Overall exposure to PVC plastics gave the odds ratio (OR)=1.35, 95% confidence interval (CI)=1.06-1.71, increasing with >10 year latency period to OR=1.45, 95% CI=1.06-1.98. No dose-response relationships were found but rather an inverse relationship with the highest odds ratios in the lowest exposure category. In conclusion, no clear association with testicular cancer and exposure to PVC could be found in our study in contrast to a previous observation.
We analysed the trends in incidence rates of childhood cancer in Sweden. All cases of malignant diseases and benign brain tumours in children, 0-14 years old, reported to the Swedish Cancer Registry 1960 to 1998 were included, n=9298. Cases were classified according to the International Classification of Childhood Cancer. Average annual change in incidence rate was calculated to +1.01%, (95% confidence interval CI=0.80, 1.22). An increase in incidence rate per year was found for leukaemia, +0.85% (95% CI=0.42, 1.28), lymphomas +1.87% (95% CI=1.17, 2.58), CNS (central nervous system) tumours +1.45% (95% CI=1.02, 1.88), sympathetic nervous system tumours +1.61% (95% CI=0.79, 2.44), hepatic tumours +2.62% (95% CI=2.02, 3.21), and germ cell and gonadal tumours +1.21% (95% CI=0.23, 2.19). Of the CNS tumours, significant changes were seen for low-grade glioma/astrocytoma +2.10% (95% CI=1.41, 2.80), benign brain tumours +3.77% (95% CI=2.47, 5.10), and PNET/medulloblastoma +1.96% (95% CI=0.48, 3.46). Changes in diagnostic criteria and better diagnostic tools may have contributed to these results.
OBJECTIVE: To evaluate in a case-control study possible risk of endometrial cancer associated with environmental endocrine disruptors. METHODS: We analyzed the adipose tissue concentrations of polychlorinated biphenyls, hexachlorobenzene (HCB), p,p'-dichlorodiphenyl-dichloroethylene (p,p'-DDE), chlordanes, and polybrominated biphenyls in 76 cases with endometrial cancer and 39 controls with benign endometrial hyperplasia. RESULTS: For the different chemicals, odds ratios (ORs) and 95% confidence intervals (CI) were close to unity taking the median concentration among the controls as cutoff value. However, for p,p'-DDE OR = 1.9, 95% CI = 0.8-4.8 was obtained. Additional estrogen replacement therapy yielded in this category OR = 2.3, 95% CI = 0.6-8.6. CONCLUSION: The results suggest an interaction between p,p'-DDE and estrogen replacement drugs in the etiology of endometrial cancer, although no significant associations were found.
Mycosis fungoides (MF) is a rare disease with an unknown etiology. Its distribution suggests that occupational exposures may play a role. In the present study, we searched for occupational factors associated with MF. A European multicenter case-control study on seven rare cancers, including MF, was conducted from 1995 to 1997. Patients between 35 and 69 years of age diagnosed with MF (n = 134) were identified and their diagnoses were checked by a reference pathologist who classified 83 cases as definitive, 35 cases as possible, and 16 cases as not histologically verified. Of the 118 histologically verified cases, 104 were interviewed, of which 76 were definitive cases. As controls, we selected population controls and colon cancer controls to serve all seven case groups. Altogether, 833 colon cancer controls and 2071 population controls were interviewed. The response rate was 91.5% for cases (76 of the 83 definitive cases), and 66.6% for controls. A high risk of MF for men was observed in the industries of other non-metallic mineral products (Odds Ratio [OR] 5.3, 95% confidence interval [CI] = 1.7-16.2) and of wholesale trade (OR 3.6, 95% CI = 1.3-10.5). A high risk was found for female employees in the sector of pulp paper manufacture (OR 14.4, 95% CI = 2.2-95.1). The male occupations with the highest risks were glass formers, potters, and ceramics workers (OR 17.9, 95% CI = 5.4-59.4) and technical salesmen (OR 8.6, 95% CI = 2.4-30.8). For women, the occupations associated with the highest risks were government executives (OR 4.8, 95% CI = 1.0-22.6) and railway and road vehicles loaders (OR 3.9, 95% CI = 1.0-14.0). The results suggest that some occupational factors are associated with MF. Working as glass formers, pottery, and ceramics workers carried the highest risk, and these findings deserve further attention and replication. Females working in the paper and pulp industries may also be exposed to carcinogens of relevance to MF.
An increasing incidence of testicular cancer has been reported from several western countries during the last decades. According to current hypothesis testicular cancer is initiated during the foetal period and exposure to endocrine disruptors such as some persistent organic pollutants has been of concern. We have previously reported the results for concentrations of polychlorinated biphenyls (PCBs), p,p'-dichlorodiphenyl-dichloroethylene (pp'-DDE), hexachlorobenzene (HCB) and chlordanes in 58 cases with testicular cancer, 61 age-matched controls and 44 case mothers and 45 control mothers. In that report, significant increase of odds ratio (OR) was found for sum of PCBs, HCB, trans- and cis-nonachlordane in case mothers. These data have now been further analysed for 37 congeners of PCBs. No significant differences were found among cases and controls. However, case mothers had significantly increased concentrations of a number of PCB congeners. A priori decided grouping of PCBs yielded for oestrogenic PCBs OR = 2.4, 95% confidence interval (CI) = 0.95-6.0, enzyme-inducing PCBsOR = 2.6, 95% CI = 1.03-6.5 and toxic equivalents (TEQ) yielded OR = 3.3, 95% CI = 1.3-8.4. These data further elucidate the role of foetal exposure to different PCB congeners in the aetiology of testicular cancer.
STUDY OBJECTIVE: Is there any epidemiologically visible influence on the cancer incidence after the Chernobyl fallout in Sweden? DESIGN: A cohort study was focused on the fallout of caesium-137 in relation to cancer incidence 1988-1996. SETTING: In northern Sweden, affected by the Chernobyl accident in 1986, 450 parishes were categorised by caesium-137 deposition: < 3 (reference), 3-29, 30-39, 40-59, 60-79, and 80-120 kiloBecquerel/m(2). PARTICIPANTS: All people 0-60 years living in these parishes in 1986 to 1987 were identified and enrolled in a cohort of 1 143 182 persons. In the follow up 22 409 incident cancer cases were retrieved in 1988-1996. A further analysis focused on the secular trend. MAIN RESULTS: Taking age and population density as confounding factors, and lung cancer incidence in 1988-1996 and total cancer incidence in 1986-1987 by municipality as proxy confounders for smoking and time trends, respectively, the adjusted relative risks for the deposition categories were 1.00 (reference < 3 kiloBecquerel/m(2)), 1.05, 1.03, 1.08, 1.10, and 1.21. The excess relative risk was 0.11 per 100 kiloBecquerel/m(2) (95% CI 0.03 to 0.20). Considering the secular trend, directly age standardised cancer incidence rate differences per 100 000 person years between 1988 to 1996 and the reference period 1986-1987, were 30.3 (indicating a time trend in the reference category), 36.8, 42.0, 45.8, 50.1, and 56.4. No clear excess occurred for leukaemia or thyroid cancer. CONCLUSIONS: Unless attributable to chance or remaining uncontrolled confounding, a slight exposure related increase in total cancer incidence has occurred in northern Sweden after the Chernobyl accident.
In the late 1970s, the author and his colleagues published the first scientific evidence of an association between exposure to phenoxyacetic acids and chlorophenols and certain malignant tumors; the study subjects were also exposed to contaminating dioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The results have been corroborated in other studies. Over the years, industry and its allied experts have attacked these studies, but in 1997 IARC classified TCDD as a human carcinogen, Group I. The author and colleagues found an increased risk of non-Hodgkins lymphoma (NHL) for subjects exposed to these chemicals or to some persistent organic pollutants; the increasing incidence in Sweden leveled off in about 1990. The author postulated that the regulation of or ban on these chemicals in Sweden in the 1970s contributed to the now decreasing incidence of NHL. Recent findings of an association between cellular telephones and brain tumors have provoked much unfounded criticism from industry and from the Swedish Radiation Protection Authority. Thus the precautionary principle is prohibited and early warnings of a cancer risk ignored. The experience of cancer risks from certain chlorinated phenols may serve as a model of how the precautionary principle could be used to take early warnings seriously. Unfortunately, the lessons of history seem to go unheeded, as exemplified by the case of cellular telephones.
The authors' case-control study on the possible association between brain tumors and mobile and cordless telephone use included 1,617 patients and 1,617 controls. A questionnaire was answered by 1,429 (88%) cases and 1,470 (91%) controls. Use of analog cellular telephones yielded an odds ratio (OR) for brain tumors of 1.31, 95% confidence interval (CI) = 1.04-1.64, increasing for ipsilateral use to OR = 1.65, 95% CI = 1.19-2.30. The authors found the highest risk for the 20-29-yr age group, with OR = 5.91, 95% CI = 0.63-55 for ipsilateral use of analog phones. The highest risks were associated with >5-year latency period in the 20-29-yr age group for analog phones (OR = 8.17, 95% CI = 0.94-71), and cordless phones (OR = 4.30, 95% CI = 1.22-15).
An increasing incidence of testicular cancer has been reported from several countries in the Western world during the last decades. According to current hypothesis, testicular cancer is initiated during the fetal period, and exposure to endocrine disruptors, i.e., xenoestrogens, has been of concern. In this investigation we studied the concentrations of the sum of 38 polychlorinated biphenyls (PCBs), p,p'-dichlorodiphenyl-dichloroethylene, hexachlorobenzene (HCB), and chlordanes, in 61 cases with testicular cancer and 58 age-matched controls. Furthermore, case and control mothers were also asked to participate, and 44 case mothers and 45 control mothers agreed. They were of similar age. In cases only the concentration on lipid basis of cis-nonachlordane was significantly increased, whereas case mothers showed significantly increased concentrations of the sum of PCBs, HCB, trans- and cis-nonachlordane, and the sum of chlordanes. Among case mothers the sum of PCBs yielded an odds ratio (OR) of 3.8; 95% confidence interval (CI), 1.4-10 was calculated using the median concentration for the control mothers as cutoff value. For HCB, OR = 4.4 (95% CI, 1.7-12); for trans-nonachlordane, OR = 4.1 (95% CI, 1.5-11); for cis-nonachlordane, OR = 3.1 (95% CI, 1.2-7.8); and for sum of chlordanes, OR = 1.9 (95% CI, 0.7-5.0). No consistent different risk pattern was found for seminoma or nonseminoma testicular cancer.
Is the decline of the increasing incidence of non-Hodgkin lymphoma (NHL) in Sweden and other countries a result of cancer preventive measures? The yearly age-standardized incidence of NHL increased significantly in Sweden during 1971-1990, for men an average of 3.2% and for women 3.1%. The corresponding figures for 1991-2000 were -0.8% and -0.2%, respectively. A decline of the increasing incidence has also been seen in other countries, such as the United States, Finland, and Denmark. Immunosuppression is one established risk factor for NHL, possibly with interaction with Epstein-Barr virus. Phenoxyacetic acids and chlorophenols, both pesticides, have been associated with NHL. Use of these chemicals was banned in Sweden in 1977 and 1978, respectively. Also, persistent organic pollutants such as polychlorinated biphenyls, hexachlorobenzene, chlordanes, and dioxins have been shown to increase the risk. Exposure of the whole population occurs predominantly through the food chain. Exposure to such chemicals was highest in the 1960s and 1970s. Because of regulation in the 1970s, exposure has declined substantially in the population. The change in incidence of NHL in Sweden and other countries may serve as a good example of how prohibition and limitation of exposure may be reflected in cancer statistics some decades later.
We included in a case-control study on brain tumours and mobile and cordless telephones 1,617 patients aged 20-80 years of both sexes diagnosed during January 1, 1997 to June 30, 2000. They were alive at the study time and had histopathology verified brain tumour. One matched control to each case was selected from the Swedish Population Register. The study area was the Uppsala-Orebro, Stockholm, Linköping and Göteborg medical regions of Sweden. Exposure was assessed by a questionnaire that was answered by 1,429 (88%) cases and 1,470 (91%) controls. In total use of analogue cellular telephones gave an increased risk with odds ratio (OR)=1.3, 95% confidence interval (CI)=1.04-1.6, whereas digital and cordless phones did not overall increase the risk significantly. Ipsilateral use of analogue phones gave OR=1.7, 95% CI=1.2-2.3, digital phones OR=1.3, 95% CI=1.02-1.8 and cordless phones OR=1.2, 95% CI=0.9-1.6. The risk for ipsilateral use was significantly increased for astrocytoma for all studied phone types, analogue phones OR=1.8,95% CI=1.1-3.2, digital phones OR=1.8, 95% CI=1.1-2.8, cordless phones OR=1.8, 95% CI=1.1-2.9. Use of a telephone on the opposite side of the brain was not associated with a significantly increased risk for brain tumours. Regarding anatomical area of the tumour and exposure to microwaves, the risk was increased for tumours located in the temporal area on the same side of the brain that was used during phone calls, significantly so for analogue cellular telephones OR=2.3, 95% CI=1.2-4.1. For acoustic neurinoma OR=4.4, 95% CI=2.1-9.2 was calculated among analogue cellular telephone users. When duration of use was analysed as a continuous variable in the total material, the risk increased per year for analogue phones with OR=1.04, 95% CI=1.01-1.08. For astrocytoma and ipsilateral use the trend was for analogue phones OR=1.10, 95% CI=1.02-1.19, digital phones OR=1.11, 95% CI=1.01-1.22, and cordless phones OR=1.09, 95% CI=1.01-1.19. There was a tendency of a shorter tumour induction period for ipsilateral exposure to microwaves than for contralateral, which may indicate a tumour promotor effect.
Two Swedish epidemiological studies have shown an association between the use of mobile telephones, mainly of the analogue type, and brain tumours. These findings have been corroborated in a Finnish study. Supportive evidence has also come from studies in USA, but these investigations, as well as a Danish study, are inconclusive due to e.g., few exposed subjects, short latency periods and methodological shortcomings. The Swedish Radiation Protection Authority (SSI) engaged two epidemiologists from a private company to conduct a review of the literature. They claimed that use of mobile telephones is not associated with increased risk for brain tumours. Their conclusion was, however, based on an unbalanced view of current literature in favour of studies showing no association. These circumstances are further explored in this communication.
During a 1-yr period, a 50-yr-old man had developed 6 basal cell skin cancer lesions on his scalp and face, 5 of which were localized on the right side of his head. The man had used an analog cellular telephone during 1987-1992; after 1992, he used a digital cellular telephone. In addition, he had used a cordless telephone since 1997. He always placed a phone on his right ear during phone calls. The right side of this individual's head contained 5 of the 6 tumors that eventually developed.
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The concentration of certain persistent organic pollutants was determined in a family including both parents and one son with neurological impairment suggested to be Attention Deficit-Hyperactivity Disorder (ADHD). For comparison control subjects from other ongoing studies were used. They were of the same sex and age group as the respective family member. For polychlorinated biphenyls, hexachlorobenzene, and chlordanes similar results were found in the study groups. The concentration of DDE, the main metabolite of DDT, was increased in the mother, 782 ng/g lipid, compared with mean 403, median 259 (range 51-1354) for the female controls. Also, the son had an increased concentration of 259 ng/g lipid, compared with mean 104, median 72 (range 46-349) for controls. A low concentration was found in the father, 127 ng/g lipid. As a child and as a teenager to the age of 17, the mother was exposed to DDT in her home environment. We discuss the potential of fetal and breast-feeding exposure of the son. Neurodevelopmental impairment has been reported for dioxins and PCBs, but DDT seems to have been less investigated in this respect.