Cancer among greenhouse owners and their relatives: results of a pilot study.
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Biomedical subjects
Publications and source records attributed to O Axelson.
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OBJECTIVES: To investigate whether indoor randon or gamma radiation might play a part in myeloid leukaemia as suggested by studies based on crude geographical or geological data for exposure assessment. METHODS: For six months randon and gamma radiation was measured with solid state nuclear track detectors and thermoluminescent dosimeters in dwellings of 44 adult male cases of acute myeloid leukaemia and 211 controls (all subjects deceased). Conditional logistic regression ORs (ORs) and 95% confidence intervals (95% CIs) were estimated for quartiles of radon and gamma radiation and for municipality and dwelling characteristics. RESULTS: The risk of leukaemia was associated with an increasing urbanisation index (p value for trend = 0.008). An increased OR was found among those living in more modern houses (OR 3.0, 95% CI 1.4 to 6.6). Confirming the findings of a previous study in the same area, geological features bore a positive association with myeloid leukemia, even by adjusting for level of urbanisation. Contrary to expectations from the previous study, however, no association appeared between myeloid leukaemia and radon and gamma radiation; for the highest quartiles of exposure, ORs were 0.56 (95% CI 0.2 to 1.4) and 0.52 (95% CI 0.2 to 1.4), respectively. Considering only subjects who had lived > or = 20 years in the monitored home and adjusting for urbanisation, there was still no effect of exposure to radiation. CONCLUSIONS: In view of the limited numbers, the results do not in general refute a possible risk of myeloid leukaemia from exposure to indoor radon or gamma radiation, but decrease the credibility of such a relation in the area studied and also of other studies suggesting an effect without monitoring indoor radiation. Some other fairly strong determinants have appeared--that is, level of urbanisation and living in modern houses--that might need further consideration.
Since the late 1970s several epidemiological studies have appeared linking exposure to phenoxy herbicides or chlorophenols to some malignant tumors. Most of these compounds are contaminated with dioxins and dibenzofurans; for example, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a contaminant of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), a component of Agent Orange which was sprayed in Vietnam during the war. The results of some of the epidemiological studies on cancer risks associated with exposure to these compounds have been manipulated and misinterpreted, particularly by the Australian Royal Commission on the Use and Effects of Chemical Agents on Australian Personnel in Vietnam. Furthermore, a book on Australian war history entitled Medicine at War, commissioned by the Federal Government, reiterates several of these misinterpretations, despite available contrary evaluations from Australian and U.S. authorities. These remarkable and confusing circumstances in the scientific process are considered also in the light of the recent classification of TCDD as carcinogenic to humans, Group 1, by a Working Group at the International Agency for Research on Cancer in Lyon, France.
Immunosuppression, possibly in combination with viruses, could be a main etiologic mechanism for non-Hodgkin's lymphoma (NHL). Chemicals such as phenoxyacetic acids, chlorophenols, dioxins, organic solvents, polychlorinated biphenyls, chlordane, and immunosuppressive drugs have been associated with this disease. Also UV light and blood transfusion have been postulated to be risk factors. Conclusive evidence of a causal association with NHL is not established for all of these exposures, but experimental evidence and clinical observations indicate that all these exposures have in common that they may impair the immune system. Furthermore, acquired and congenital immune deficiency as well as autoimmune disorders increase the risk for NHL. In view of currently available evidence, the first priority for reducing morbidity due to NHL might be to take action against adverse chemical exposures as a measure that is more easily achievable than any other kind of prevention.
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To document the problem of child labor as a health issue, we report here three case-studies in Ecuador: exposure to mercury among gold washers, exposure to organophosphates and carbamates in the fruit-growing industry, and exposure to solvents among shoe cleaners. We measured the relevant biological indicators of exposure (mercury in urine, urinary levels of phenols, and acetylcholine esterase in erythrocytes) among selected samples of 10 children for each working place. In all the case studies, the values of the biological indicators showed elevated exposure to well-known toxicants, which are now rare in developed countries, even among adult workers. The findings meld with a previously reported case study of intoxication from inorganic lead among children employed in the manufacture of roof tiles in Ecuador. This study highlights the need to properly evaluate and control the potential health effects due to exposure to toxic substances among children employed in different occupations in several parts of the world.
In a Swedish cohort of workers (n = 6,454) from seven aluminum foundries and three secondary aluminum (scrap) smelters there was no overall excess risk of cancer among male or female workers less than 85 years of age (males: 325 observed cases, standardized incidence ratio (SIR) 1.02, 95% confidence interval (CI) 0.91-1.13; females: 22 cases, SIR = 0.95, 95% CI = 0.60-1.44). In male workers, however, significantly elevated risk estimates were observed for cancer of the lung (51 cases; SIR = 1.49, 95% CI = 1.11-1.96), anorectal cancer (33 cases; SIR 2.13, 95% CI = 1.47-2.99), and sinonasal cancer (4 cases; SIR = 4.70, 95% CI = 1.28-12.01). There was no increase of urinary bladder or liver cancer. Lung cancer risks were highest in workers with a short duration of employment (< 5 years) suggesting determinants of risk related to socioeconomic factors rather than the occupational environment under study, but there were also indications of a lung cancer hazard from sand casting of aluminum for 10 years or more (SIR = 2.10, 95% CI = 1.01-3.87). The increase in anorectal cancer could not be etiologically related to occupational determinants of risk. Sand casting of aluminum aside, the cancer risk in secondary aluminum smelting seems to be lower than in primary aluminum smelting and in iron and steel founding, respectively.
Despite the considerable efforts and funds devoted to cancer research over several decades, cancer still remains a mainly lethal disease. Cancer incidence and mortality have not declined at the same rate as other major causes of death, indicating that primary prevention remains a most valuable approach to decrease mortality. There is general agreement that environmental exposures are variously involved in the causation of the majority of cancer cases and that at least half of all cancers could be avoided by applying existing etiologic knowledge. There is disagreement, however, regarding the proportion of cancer risks attributable to specific etiological factors, including diet, occupation and pollution. Estimates of attributable risks are largely based today on unverified assumptions and the calculation of attributable risks involves taking very unequal evidence of various types of factors and treating them equally. Effective primary prevention resulting in a reduction of cancer risk can be obtained by: (i) a reduction in the number of carcinogens to which humans are exposed; or (ii) a reduction of the exposure levels to carcinogens. Exposure levels that could be seen as sufficiently low when based on single agents, may actually not be safe in the context of the many other concomitant carcinogenic and mutagenic exposures. The list of human carcinogens and of their target organs might be quite different if: (i) epidemiological data were available for a larger proportion of human exposures for which there is experimental evidence of carcinogenicity; (ii) more attention was paid to epidemiological evidence that is suggestive of an exposure-cancer association, but is less than sufficient, particularly in identifying target organs; and (iii) experimental evidence of carcinogenicity, supported by mechanistic considerations, were more fully accepted as predictions of human risk.
A large epidemiologic study on residential radon exposure and lung cancer has been conducted in Sweden. An attempt is now made to quantify the impact of random error in the exposure assessment on the risk estimate for lung cancer in this study. The study included 1,360 lung cancer cases, diagnosed from 1980 to 1984, and 2,847 population controls. Radon measurements were performed in 8,992 dwellings occupied by the study subjects some time since 1947. Questionnaires provided information on smoking and other risk factors. Imprecision in the retrospective exposure assessment for radon was estimated from a Monte Carlo technique modeling Swedish conditions. Adjusted risk estimates were obtained from regression analyses based on expected values for true time-weighted average residential radon concentration (TWA), conditional on observed TWA. Without adjustment for random error in the TWA estimates, the linear excess relative risk coefficient was 0.10 per 100 Bq m(-3), but an excess relative risk of about 0.15 to 0.20 per 100 Bq m(-3) was suggested following adjustment. The potentially significant consequences of errors in the retrospective radon exposure assessment should be taken into consideration in the risk estimation as well as in comparisons of results of different studies and in future pooled analyses.
Occupational and environmental determinants of benign thyroid disease and follicular thyroid cancer were evaluated in a series of cases in 1977-1987. Of the cases initially diagnosed as follicular thyroid cancer, only 31 remained after a reclassification, whereas 44 were found to be benign thyroid disease. Both series were compared with 387 randomly selected population controls. Occupational solvent exposure was strongly associated with benign thyroid disease (odds ratio, OR, 2.8; 95% confidence interval, 95% CI, 0.9-9.0 for women and OR 18.9; 95% CI 2.2-161 for men). Eight of the nine men found to have benign disease had been exposed to solvents, and six of them to trichloroethylene. For both types of cases, a private well at the birth address increased the risk, OR 2.0; 95% CI 0.9-4.0 and OR 3.0; 95% CI 1.2-7.2, respectively, whereas the risk was lower for those living in coastal areas. Less fish and shellfish in the diet increased the risk for malignant thyroid disease only. Although based on small numbers, the study indicates etiologic roles of occupational and environmental factors for both conditions studied. The influences of occupation and diet differ, however, for the two outcomes.
Throughout history, there are many illustrations showing more or less rational efforts to avoid disease, but preventive measures have often been, and still are, neglected or even counteracted for economic reasons. Some examples of early preventive actions are given along with illustrations of how the increasing knowledge through epidemiological and other research has created a foundation for adequate decisions to the benefit of health protection, although frequently taken after much discussion and considerable time-lag from the first evidence of a particular health risk. There is also an inherent problem in successful health protection since both public and political support for the issue might get lost along with the scientific activity and knowledge in the field.
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Parkinson's disease (PD) shows a geographical variation. All prescriptions for anti-parkinsonian drugs were recorded for a half-year in a region with low L-dopa consumption. Hospital and outpatient records were studied and physicians were asked to supply details of PD patients in the region, with 147,777 inhabitants. The crude prevalence was 115 PD per 100,000 inhabitants, based on 170 cases. In contrast to other studies we report an age-standardized prevalence, which was 76 per 100,000, using the European Standard Population as reference. The corresponding approximate incidences were 11.0 (crude) and 7.9 (age-standardized) per 100,000 person-years. Male preponderance appeared in all age groups. Mean age at onset was 65.6 years, the highest figure reported. Variation between studies for age at onset, differences in prevalence, and male preponderance suggest environmental risk factors to be of importance for PD.
Of 311 colorectal cancers diagnosed in 1984-86 in the county of Ostergotland, Sweden, 179 were included in a case-control study, and, of these, 70 were investigated using immunohistochemical staining for p53 gene mutations. Alcohol use as well as medication with hydralazine-containing antihypertensive drugs, but not heredity were associated with p53 staining. The study is offered to illustrate the possible value of investigating molecularly defined tumour subtypes in relation to specific risk factors.
To evaluate the possible relation between exposure to organic solvents and the development of multiple sclerosis, we carried out a best-evidence synthesis of the available information. We found 13 studies with varying methodology that included information on solvent exposure. In 10 of the studies, there were indications of an increased risk of multiple sclerosis in relation to solvent exposure. We made three selections of studies for both pooled analyses and meta-analyses. The relative risk point estimates that we obtained varied from 1.7 to 2.6. Our evaluation is consistent with the hypothesis that organic solvents may be a cause of multiple sclerosis.
The incidence of neoplasms in childhood and adolescence in northern and central Sweden before and after the radioactive fallout from the Chernobyl accident was investigated in an ecologic study, 1978 to 1992. The study included all parishes in the six most contaminated counties classified after aerial mapping of ground radiation from 137Cs and investigated 746 cases of neoplasms in ages 0-19 y, diagnosed in the six counties. Incidence and relative risks of neoplasms were compared in areas with high, intermediate, and low contamination after versus before the Chernobyl accident in 1986. A continuous increase of brain tumor incidence in the ages 0-19 y during the period 1978-92 without clear relationship to the Chernobyl fallout was discovered. No clear relationship between the incidence of brain tumor and the exposure to varying levels of radiation from 137Cs was apparent. A somewhat decreased relative risk of acute lymphatic leukemia appeared in areas with increased exposure. Other neoplasms showed no changes in incidence over time or with regard to exposure. Until now, there is no indication that the Chernobyl accident has affected the incidence of childhood and adolescence neoplasms in Sweden, but it is still too early for any final conclusion about the effect of this event.