Congenital cryptorchidism, i.e. failure of the testicular descent to the bottom of the scrotum, is a common birth defect. The evidence from epidemiological, wildlife, and animal studies suggests that exposure to mixtures of endocrine disrupting chemicals during fetal development may play a role in its pathogenesis. We aimed to assess the association between cryptorchidism and prenatal exposure to polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs), and polybrominated diphenyl ethers (PBDEs).
We conducted a case-control study consisting of 44 cryptorchid cases, and 38 controls operated for inguinal hernia, umbilical hernia, or hydrocele at the Turku University Hospital or Rigshospitalet, Copenhagen in 2002-2006. During the operation a subcutaneous adipose tissue biopsy was taken. Samples were analysed for 37 PCBs, 17 PCDD/Fs and 14 PBDEs by gas chromatography-high-resolution mass spectrometry. Chemical concentrations were adjusted for postnatal variation introduced by differences in duration of breastfeeding, age at the operation, and country of origin with a multiple linear regression. Association between adjusted and unadjusted chemical concentrations and the risk of cryptorchidism were analysed with logistic regression to get an estimate for odds ratio (OR) of cryptorchidism per multiplication of chemical concentrations with ca. 2.71 (Napier's constant).
Total-TEq i.e. the WHO-recommended 2,3,7,8-TCDD equivalent quantity of 17 dioxins and 12 dioxin-like PCBs and sum of PCDD/Fs were positively associated with cryptorchidism [OR 3.21 (95% CI 1.29-9.09), OR 3.69 (95% CI 1.45-10.9), respectively], when adjusting for country of origin, the duration the child was breastfed, and age at operation. The association between the sum of PCBs and cryptorchidism was close to significant [OR 1.92 (95% CI 0.98-4.01)], whereas the association between the sum of PBDEs and cryptorchidism was not [OR 0.86 (95% CI 0.47-1.54)]. There were no associations between unadjusted chemical concentrations and the risk of cryptorchidism.
Prenatal exposure to PCDD/Fs and PCDD/F-like PCBs may be associated with increased risk for cryptorchidism. Our finding does not exclude the possibility of an association between the exposure to PBDEs and cryptorchidism.
Cites: Scand J Work Environ Health. 1996 Aug;22(4):267-738881015
In the 1980s and 1990s, the Government of Canada closed and/or issued advisories for a number of shellfish fisheries in coastal areas of British Columbia because of dioxin contamination. Only the direct health risks (i.e., cancer) of consuming contaminated shellfish for the general population were considered by the Government in the formulation of risk management options. A focus on the direct risks does not provide an adequate basis for risk decisions as the countervailing risks which may be created from management measures may easily be overlooked. This study describes the potential health impacts of risk management options for aboriginal coastal peoples in the management of dioxin contamination. Gold River and Powell River in British Columbia, Canada, are the areas of focus. The cancer risks of consuming dioxin contaminated shellfish for these sites are estimated. To assess the countervailing risks of management decisions for comparison, a scenario was developed in which First Nations peoples substitute shellfish with store-bought foods in their diets in the event of a fishery closure or advisory. Increases in mortality due to coronary heart disease are estimated. The results suggest that the health risks of dietary changes among aboriginal peoples may be as significant as those related to eating dioxin contaminated shellfish.
Dioxins and airborne fine particles are both environmental health problems that have been the subject of active public debate. Knowledge on fine particles has increased substantially during the last 10 years, and even the current, lowered levels in the Europe and in the United States appear to be a major public health problem. On the other hand, dioxins are ubiquitous persistent contaminants, some being carcinogens at high doses, and therefore of great concern. Our aim was to (a) quantitatively analyze the two pollutant health risks and (b) study the changes in risk in view of the current and forthcoming EU legislations on pollutants. We performed a comparative risk assessment for both pollutants in the Helsinki metropolitan area (Finland) and estimated the health effects with several scenarios. For primary fine particles: a comparison between the present emission situation for heavy-duty vehicles and the new fine particle emission standards set by the EU. For dioxins: an EU directive that regulates commercial fishing of Baltic salmon and herring that exceed the dioxin concentration limit set for fish meat, and a derogation (= exemption) from the directive for these two species. Both of these two decisions are very topical issues and this study estimates the expected changes in health effects due to these regulations. It was found that the estimated fine particle risk clearly outweighed the estimated dioxin risk. A substantial improvement to public health could be achieved by initiating reductions in emission standards; about 30 avoided premature deaths annually in the study area. In addition, the benefits of fish consumption due to omega-3 exposure were notably higher than the potential dioxin cancer risk. Both regulations were instigated as ways of promoting public health.
Regulatory agencies in the Western Hemisphere are currently assessing the potential human health risks of environmental contamination by 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). Some U.S. agencies such as the Environmental Protection Agency (EPA) and Centers for Disease Control (CDC) have assumed that TCDD behaves as a tumor initiator in animals and have used linear low-dose mathematical extrapolation models for estimating any human risk. In contrast, the Ontario Ministry of the Environment, the State Institute of National Health of The Netherlands, and the Federal Environmental Agency of the Federal Republic of Germany have concluded that TCDD does not have initiator activity; these agencies have advocated a risk extrapolation approach which applies a safety factor to a no-observable-effect level. Estimations of the potential risk obtained by these two approaches can differ by three to four orders of magnitude and have a major impact on the allocation of resources within the affected countries. This paper critically reviews the TCDD bacterial, animal, and human data on mutagenesis, carcinogenesis, and tumor promotion and concludes that the scientific evidence does not support risk estimations which are based on TCDD as a tumor initiator. Rather, the animal data overwhelmingly support TCDD as a tumor promoter. Risk estimations which incorporate tumor promotion activity more accurately reflect the scientific understanding of TCDD's mechanism of action and provide better estimates of its risk.
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).
Comment In: J Natl Cancer Inst. 1990 Nov 21;82(22):1785-62231775
Our aim was to assess the mortality of fishermen and fishermen's wives in Finland, presuming that the mortality reflects their high consumption of contaminated fish.
All Finnish fishermen, registered since 1980, were identified from the Professional Fishermen Register (N = 6410), and the fishermen's wives from the national population register (N = 4260). The cohorts were individually linked with cause-of-death data until 2005 at Statistics Finland. The follow-up started in the year after the first registration as a fisherman and at marriage (if later) for the wives. The standardized mortality ratios (SMRs) were calculated based on the national mortality rates. In addition, blood samples and food frequency questionnaire data were collected from a volunteer sample.
The average fish consumption and serum concentrations of fish-derived fatty acids and environmental contaminants were higher among the fishermen and their wives than among the general population from the same region. The fishermen and their wives had lower mortality from all causes (SMR 0.78, 95% confidence interval (CI) 0.73-0.82, and 0.84, 0.76-0.93, respectively), and ischaemic heart diseases (0.73, 0.65-0.81, and 0.65, 0.50-0.83) than the general population. Mortality from cerebrovascular diseases and malignant neoplasms was decreased among the fishermen (0.67, 0.52-0.85, and 0.90, 0.80-1.01), but not among the wives. In addition, the fishermen's mortality from water transport accidents was extremely high (8.31, 5.65-11.79).
The fishermen and their wives had lower mortality from many natural causes. The high intakes of environmental contaminants in fish were not seen as excess mortality.
BACKGROUND: After the 2(nd) World War a long range of chemical agents have been introduced on the market, both in Sweden and most other countries. From the 1950's several pesticides gained increasing use in agriculture and forestry. In the 1970's public concern increased in Sweden especially regarding use of phenoxy herbicides to combat deciduous wood, although statements from different authorities were reassuring of the safety. MATERIALS AND METHODS: At the end of the 1970's the author and his colleagues published the first scientific evidence of an association between exposure to phenoxyacetic acids, chlorophenols and certain malignant tumours, i.e., soft-tissue sarcoma and malignant lymphoma. The study subjects were also exposed to contaminating dioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Later studies showed also an association between certain persistent organic pollutants such as polychlorinated biphenyls and non-Hodgkin lymphoma (NHL) with an interaction with titers of antibodies to Epstein-Barr virus early antigen. These results have been corroborated in other studies. DISCUSSION: Over the years industry and its allied experts have attacked our studies, but in 1997 IARC classified TCDD as a human carcinogen, Group I. The increasing incidence of NHL in Sweden levelled off about 1990. The author postulated that the regulation or ban of the use of chlorophenols, certain phenoxy herbicides and some persistent organic pollutants in Sweden back in the 1970s has contributed to the now decreasing incidence of NHL. Unfounded criticism from industry experts may prohibit the precautionary principle and early warnings of cancer risk can be ignored. Cancer risks by certain chlorinated phenols may serve as a model of how the precautionary principle should be used by taking early warnings seriously.
We investigated whether prenatal exposure from the maternal diet to the toxicants polychlorinated biphenyls (PCBs) and dioxins is associated with the development of immune-related diseases in childhood. Children participating in BraMat, a sub-cohort of the Norwegian Mother and Child Cohort Study (MoBa), were followed in the three first years of life using annual questionnaires (0-3years; n=162, 2-3years; n=180), and blood parameters were examined at three years of age (n=114). The maternal intake of the toxicants was calculated using a validated food frequency questionnaire from MoBa. Maternal exposure to PCBs and dioxins was found to be associated with an increased risk of wheeze and more frequent upper respiratory tract infections. Furthermore, maternal exposure to PCBs and dioxins was found to be associated with reduced antibody response to a measles vaccine. No associations were found between prenatal exposure and immunophenotype data, allergic sensitization and vaccine-induced antibody responses other than measles. Our results suggest that prenatal dietary exposure to PCBs and dioxins may increase the risk of wheeze and the susceptibility to infectious diseases in early childhood.