Idiomas:
The source document for this Digest states:
Analysis of the human data by itself, while generating concerns, has so far failed to provide firm evidence of direct causal associations between low-level (i.e., levels measured in the general population) exposure to chemicals with EDCs and adverse health outcomes. It is difficult to compare and integrate results from diverse human studies, because data are often collected at different time periods, using different experimental designs and under different exposure conditions. Often exposure data are completely lacking. Of particular concern is the lack of exposure data during critical periods of development that influence later functioning in adult life. Furthermore, the concentrations and potencies of endogenous hormones and phytoestrogens are generally higher than those of exogenous chemicals. Despite these difficulties, exposure to EDCs has been suggested to play a role in adverse health outcomes, and concerns remain. The following examples illustrate the effects of EDCs on humans.
Source & ©:
IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
The source document for this Digest states:
A number of studies report a decline (since the 1930s) in human sperm quality in several countries. There clearly are important variations in sperm count, both within and between countries, but there are no firm data that directly addressed the possible cause and effect relationship between declining sperm quality and exposure to EDCs. Studies to date have been retrospective. Several meta-analyses of existing studies reached different conclusions, and the issue remains controversial. Even if there has been deterioration in semen quality, this would not necessarily be due to endocrine disruption. Available human and experimental animal studies demonstrate that high-level exposure to certain environmental chemicals can impair fertility and increase the rate of spontaneous abortion, but the relationship to endocrine disruption remains speculative. Declining sex ratios (fewer males) have been recorded in a number of regions and countries, and there is evidence that unidentified external influences are associated with such changes, but the mechanism(s) is unknown. Temporal increases in the frequency of development abnormalities of the male reproductive tract, particularly cryptorchidism and hypospadias, have been reported, but the role of exposure to EDCs is unclear. Experimental data show that a number of chemicals can disrupt development of the male reproductive tract via endocrine mechanisms.
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
| For details on: | See IPCS assessment: |
| Assessment of testis function and the the evidence for temporal / geographical trends in sperm quality |
5.1.2.1, 5.1.2.2, page 52 |
| Genetic and ethnic factors that may influence sperm quality and may bias interpretation of studies on trends |
5.1.2.3, page 55 |
| Diethylstilbestrol and certain agricultural chemicals that may affect sperm quality |
5.1.2.4, page 56 |
For further details on semen quality and testis function in
humans, see IPCS
| For details on: | See IPCS assessment: |
| Time to pregnancy and the ability to conceive a child (fecundity) can be used to show temporal and geographical trends |
5.1.3.1, page 57 |
| Human fecundity and fertility that may be reduced in some occupational groups after exposure to man-made chemicals |
5.1.3.2, page 57 |
| Rapid assessment through continuous breeding to identify effects of chemical exposure on fertility |
5.1.3.3, page 58 |
| Some of the known causes of spontaneous abortion (chromosomal and uterine abnormalities) |
5.1.4.1, page 58 |
| Pesticides that may cause spontaneous abortion |
5.1.4.2, page 59 |
| Hexachlorobenzene and ketoconazole and early pregnancy loss |
5.1.4.3, page 59 |
| For details on: | See IPCS assessment: |
| Variation in sex ratios (proportions of males born) between and within different countries |
5.1.5.1, page 59 |
| Medical, occupational and environmental exposure to chemicals such as DBCP and TCDD that may influence the sex ratio |
5.1.5.2, page 60 |
| External factors that may influence the sex ratio |
5.1.5.3, page 61 |
| For details on: | See IPCS assessment: |
| Development of the male reproductive tract |
5.1.6.1, page 61 |
| Research protocols that can detect effects of chemicals on male development |
5.1.6.2, page 61 |
| Exposure to estrogenic and anti-androgenic chemicals during critical periods of development that have adverse effects in laboratory animals |
5.1.6.3, page 62 |
| Risk factors for male reproductive abnormalities such as cryptorchidism and hypospadias |
5.1.6.4.1, page 62 |
| Variations in rates of hypospadias and cryptorchidism around the world |
5.1.6.4.2, page 62 |
| Pesticides and phytoestrogens that may lead to male reproductive tract abnormalities |
5.1.6.4.3, page 64 |
| Laboratory animal studies demonstrating that exposure to estrogens during development can result in cryptorchidism and hypospadias |
5.1.6.4.4, page 65 |
| Estrogen, prolactin and pesticide influences on development of the prostate gland |
5.1.6.5.2, page 65 5.1.6.5.1, page 65 5.1.6.5.3, page 65 |
| Whether low-dose exposure to Diethylstilbestrol and Bisphenol A during development can cause alterations in the developing male reproductive tract |
5.1.6.5.4, page 66 |
The source document for this Digest states:
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
For further details on endometriosis in humans,
see IPCS
| For details on: | See IPCS assessment: |
| The effects of estrogen and progesterone on endometriosis |
5.1.7.1, page 66 |
| Chemical contaminants like PCBs and dioxins that have been implicated in endometriosis |
5.1.7.2, page 66 |
| Dioxins that have been suggested to contribute to development of endometriosis in monkeys |
5.1.7.3, page 67 |
The source document for this Digest states:
Concerns have been raised about the influence of EDCs on the timing of puberty, but the possible mechanisms of action and role of other factors such as nutrition need to be clarified.
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
| For details on: | See IPCS assessment: |
| Whether environmental chemicals can induce precocious puberty |
5.1.8.1, page 68 |
| Whether environmental chemicals can cause polycystic ovarian syndrome that prevents release of eggs from the ovary |
5.1.8.2, page 68 |
| The effects of DDT and oral contraceptives that shorten the duration of lactation |
5.1.8.3, page 69 |
The source document for this Digest states:
Data from human and experimental animal studies clearly indicate that exposure (particularly prenatal exposure) to certain EDCs (e.g., PCBs) can have adverse effects on neurological development, neuroendocrine function, and behavior. Some of these effects appear to result from altered thyroid or neurotransmitter function, but in most instances endocrine mechanisms have not been demonstrated. Similar effects can also result from exposure to chemicals that induce developmental neurotoxicity but have no known endocrine action.
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
For further details on impaired neurobehavioral
development in humans, see IPCS
| For details on: | See IPCS assessment: |
| PCBs that have a negative impact on neurobehavioral development |
5.2.2.1.1, page 70 |
| Reduced thyroid activity in newborns exposed to background environmental levels of PCBs/PHAHs |
5.2.2.1.2, page 71 |
| Neurological effects in adults after PHAH exposure, including impaired memory and dullness |
5.2.2.1.2, page 71 |
| Effects of prenatal exposure to estrogens (such as DES) and androgens on sexual behavioral in girls and boys |
5.2.2.2.1, page 71 |
| Effects of prenatal and early postnatal exposure to PCBs, PCDFs and DDE on neurobehavior |
5.2.2.3.1, page 72 |
| Studies on sex-dependent behavior and sexual behavior after exposure to EDCs during development |
5.2.3.1.1, page 72 5.2.3.1.2, page 72 |
| Studies on sex-dependent and sexual behavior after exposure to EDCs in juvenile or adult life |
5.2.3.1.1, page 72 5.2.3.1.2, page 73 |
| EDCs exerting neurobehavioral effects via thyroid hormone-dependent processes |
5.2.4, page 73 |
The source document for this Digest states:
Source & ©:
IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
For further details on
disturbed immune function
in humans, see IPCS
| For details on: | See IPCS assessment: |
| The structure and function of the immune system |
5.3.1.1, page 75 |
| Chemical-induced toxicity due to EDCs or non-EDCs that can target the immune system |
5.3.1.2, page 75. |
| Diethylstilbestrol, one of the few compounds that can cause immune alterations in humans via a proven endocrine-disrupting mechanism |
5.3.2.1, page 76. |
| Accidental exposure to TCDD, PCBs and PCDFs and immune alterations in humans |
5.3.2.2.1, page 76 |
| Occupational exposure studies on PCBs, PCDFs and PCDDs showing few immune changes in humans |
5.3.2.2.2, page 77 |
| Population exposure to background levels of PCBs/dioxins and immune changes |
5.3.2.2.3, page 77 |
| Immune alterations in laboratory animals following prenatal exposure to diethylstilbestrol |
5.3.3.1, page 77 |
| TCDD and related compounds that cause immune alterations, particularly of thymus–dependent type |
5.3.3.2, page 77 |
The source document for this Digest states:
Temporal increases in the incidence of certain cancers listed below in hormonally sensitive tissues in many parts of the industrialized world are often cited as evidence that widespread exposure of the general population to EDCs has had adverse impacts on human health. These increases cannot be adequately explained by improved diagnostic techniques, and it has been argued that these trends coincide roughly with the increased use and release of industrial chemicals into the environment.
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
For further details on
disturbed immune function
in humans, see IPCS
The source document for this Digest states:
Numerous human epidemiological studies and experimental laboratory studies have been conducted to determine whether environmental EDCs may contribute to an increased risk of breast cancer, but the current scientific evidence does not support a direct association between exposure to environmental EDCs and increased risk of breast cancer. However, studies published to date have measured EDC exposure levels in adult women; data on exposures during critical periods of development are lacking. Adult women currently at risk for breast cancer may have been exposed to exogenous EDCs in utero or during infancy, childhood, and adolescence in the mid-twentieth century when contaminant levels of organochlorines were higher.
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
For further details on
incidence of breast cancer
in humans, see IPCS
| For details on: | See IPCS assessment: |
| Factors that may be involved in breast cancer |
5.4.2.1.1, page 79 |
| Phytoestrogens, particularly soy products that may reduce the risk of developing breast cancer |
5.4.2.1.2, page 79 |
| Whether organochlorine compounds such as DDT, PCBs, Dieldrin, HCB, ß-Hexachlorocyclohexane, TCDD and PBBs play a role in breast cancer |
5.4.2.1.3, page 80 |
| Factors such as carcinogenic agents, irradiation and cigarette smoking during prepubertal years that may be related to an increased risk of developing breast cancer at a later date |
5.4.2.1.4, page 83 |
| The influence of synthetic hormones, phytoestrogens and other estrogens on breast cancer in animals |
5.4.2.2.1, page 83 |
| Lack of effect of organochlorine compounds on mammary gland cancer in laboratory animals |
5.4.2.2.2, page 83 |
The source document for this Digest states:
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
| For details on: | See IPCS assessment: |
| Estrogen as a major risk factor for endometrial cancer |
5.4.3.1, page 84 |
| Phytoestrogens such as genistein, diadzein and some environmental chemicals such as methoxychlor, nonylphenol and bisphenol A that have been shown to induce uterotropic response (growth of the uterus) in laboratory animals |
5.4.3.2, page 84 |
The source document for this Digest states:
Temporal increases in the incidence of testicular cancer have been reported in certain countries, but rates vary considerably among countries. The risk started rising around 1910 in Nordic countries, and somewhat earlier in England and Wales, and therefore cannot be attributed solely to chemicals introduced in the mid or late twentieth century. Some evidence suggests that the incidence of cryptorchidism and hypospadias may show similar geographic variations to the incidence of testicular cancer and that these conditions may be developmentally linked. However, EDC exposure data for critical periods are lacking.
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
| For details on: | See IPCS assessment: |
| The increasing incidence of testicular cancer in young men |
5.4.4.1, page 84 |
| Lack of animal models for testicular cancer |
5.4.4.2, page 85 |
The source document for this Digest states:
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
| For details on: | See IPCS assessment: |
| Occupational studies of PCB-exposed workers that have not shown an association between PCBs and prostate cancer |
5.4.5.1, page 85 |
| The hypothesis that consumption of green tea may lower mortality from prostate and breast cancer |
5.4.5.2, page 85 |
The source document for this Digest states:
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
| For details on: | See IPCS assessment: |
| The incidence of thyroid cancer in humans |
5.4.6.1, page 86 |
| The possibility that environmental chemicals such as TCDD, PCBs and PBBs that increase the metabolism of thyroid hormones , and thereby could cause thyroid tumors in laboratory animals |
5.4.6.2, page 86 |
The source document for this Digest states:
Overall, the biological plausibility of possible damage to certain human functions (particularly reproductive and developing systems) from exposure to EDCs seems strong when viewed against the background of known influences of endogenous and exogenous hormones on many of these processes. Furthermore, the evidence of adverse outcomes in wildlife and laboratory animals exposed to EDCs substantiates human concerns. The changes in human health trends in some areas (for some outcomes) are also sufficient to warrant concern and make this area a high research priority, but non-EDC mechanisms also need to be explored.
Source & ©: IPCS "Global Assessment of the state-of-the-science of
Endocrine disruptors
For details on conclusions that can be drawn based on possible EDC
effects on humans, see IPCS
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