Susceptibility to chlordecone-carbon tetrachloride induced hepatotoxicity and lethality is both age and sex dependent. (1/39)The present paper examines the susceptibility to chlordecone (Kepone, CD) and carbon tetrachloride across different ages (35, 45, and 63-days-old) in male and female Sprague-Dawley rats using different lengths of time on a CD diet (10 ppm). The principal findings are that the hepatotoxicity and mortality associated with CD-CCl4 interaction is highly age-dependent for both sexes. There was marked hepatotoxicity occurring in both sexes as they reached 45 days-of-age and females were considerably more susceptible than males to both CD-CCl4-induced hepatotoxicity and lethality. While 63-day-old females are more susceptible to the CD-CCl4 interaction than their male counterparts, the magnitude of the sex difference is diminished from that observed in 45-day-old rats. These findings challenge the hypothesis of Mehendale (1990, Med. Hypotheses 33, 289-299) that chlordecone (CD) pretreatment eliminates the well-established sex difference in CCl4-treated rats. In contrast to the CD-CCl4 findings, the sex difference in CCl4-induced hepatotoxicity was not age-dependent and was consistent over the three ages studied. The findings that CD-CCl4 interaction is highly age-dependent (within the 3 ages tested) but that CCl4-induced hepatotoxicity is not, suggest that the CD-CCl4 interaction acts via a mechanism that does not primarily involve CCl4 potentiation. (+info)
Examination of selected food additives and organochlorine food contaminants for androgenic activity in vitro. (2/39)In order to produce a reporter gene assay for androgenic chemicals, a constitutive expression vector coding for the human androgen receptor and a reporter construct containing the firefly luciferase coding sequence under transcriptional control of the androgen responsive MMTV promoter were cotransfected into the androgen-insensitive human PC-3 prostate carcinoma cell line and stable transfectants selected. One colony of transfectants, PC-3 LUCAR+, was characterized further. 5alpha-Dihydrotestosterone (DHT) enhanced luciferase activity in a linear fashion for up to 3 days of culture. The Kd for DHT activation was within the range of 25.0-60.0 pM (r2 values >0.95). Flutamide competitively inhibited DHT activation (mean Ki value of 0.89 microM). Progesterone, estradiol, dexamethasone, and hydrocortisone were weak agonists (100-fold less effective than DHT) and diethylstilbestrol was without effect. The effects of organochlorine food contaminants (0, 0.1, 1.0, and 10.0 microM) on luciferase activity in PC-3 LUCAR+ cells were determined after exposure to the chemical for 18 h in the presence and absence of DHT (50 pM). 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE) induced luciferase activity in the absence of DHT (100 microM p,p'-DDE equivalent to 50 pM DHT), but in the presence of DHT (50 pM), p,p'-DDE acted antagonistically. 2,3,7,8-Tetrachlorodibenzo-p-dioxin, kepone, butylated hydroxyanisole, and butylated hydroxytoluene all partially inhibited activation by DHT (50 pM) but alone had little or no effect. Toxaphene at 10 microM induced luciferase activity in the absence of DHT but decreased cell viability. Alpha- and delta-Hexachlorocyclohexanes (HCH) at 10 microM antagonized the DHT effect, but beta-HCH and gamma-HCH mirex, photomirex, oxychlordane, cis- and trans-nonachlor were without effect. Thus, of the chemicals tested, some interact with the human androgen receptor in vitro as agonists, others as antagonists, and some as partial agonists/antagonists. (+info)
Salmonid sexual development is not consistently altered by embryonic exposure to endocrine-active chemicals. (3/39)Fish sexual development is sensitive to exogenous hormone manipulation, and salmonids have been used extensively as environmental sentinels and models for biomedical research. We simulated maternal transfer of contaminants by microinjecting rainbow trout (Oncorhynchus mykiss) and chinook salmon (Oncorhynchus tshawytscha) embryos. Fish were reared for 6 months and sexed, and gonads were removed for histology and measurement of in vitro steroid production. Analysis of fat samples showed that dichlorodiphenylethylene (DDE) levels, o, p'M-DDE and p,o, p'-DDE isomers, were elevated 6 months after treatment. A preliminary study showed an increased ratio of males to females after treatment with 80 mg/kg and 160 mg/kg of the xenoestrogen o,o, p'-DDE. One fish treated with 160 mg/kg o,o, p'-DDE had gonads with cells typical of both males and females. A follow-up study, using more fish and excluding the highly toxic 160 mg/kg o,o, p'-DDE dose, showed no effect on sex ratio or gonadal histology. Embryonic exposure of monosex male trout, monosex female trout, and mixed sex salmon to o, o, p'-DDE, p,o, p'-DDE, mixtures of DDE isomers, and octylphenol failed to alter sexual development. We observed no treatment-dependent changes in in vitro gonadal steroid production in any experiments. Trout exposed in ovo and reared to maturity spawned successfully. These results suggest that mortality attributable to the xenoestrogens o,o, p'-DDE, chlordecone, and octylphenol, and the antiandrogen p,o, p'-DDE, is likely to occur before the appearance of subtle changes in sexual development. Because trout appeared to be sensitive to endocrine disruption, we cannot dismiss the threat of heavily contaminated sites or complex mixtures to normal sexual development of salmonids or other aquatic organisms. (+info)
Estrogenic effects of organochlorine pesticides on uterine leiomyoma cells in vitro. (4/39)Although benign, uterine leiomyomas occur with high frequency and significant morbidity in reproductive-age women, and they present a significant health problem. Leiomyomas develop in the uterine myometrium and are sensitive to ovarian hormones, making them potential target sites for endocrine disruptors. Here we utilize cell lines derived from rat uterine leiomyomas to determine if a panel of 7 organochlorine pesticides have potential agonist activity in myometrial cells using cellular and molecular in vitro assays. The organochlorine pesticides investigated have been previously characterized as having agonist activity in other hormonally responsive tissues, but their effects have not been studied in uterine myometrial cells. In Eker rat leiomyoma-derived cells, HPTE, kepone, and the alpha isomer of endosulfan stimulated proliferation, an effect dampened by the antiestrogen ICI 182,780. In addition, these compounds stimulated transcription of the vitellogenin estrogen-response element via the ER in a transcriptional reporter gene assay and induced the expression of an endogenous estrogen-responsive gene, the progesterone receptor (PR). This contrasted with the agonist profile of methoxychlor, dieldrin, toxaphene, and endosulfan-beta. These compounds, unable to stimulate proliferation of uterine leiomyoma cells, did exhibit agonistic activity in these cells at the transcriptional level in the estrogen-sensitive reporter gene assay, and they were also able to upregulate PR message. These data demonstrate that organochlorine pesticides act as estrogen receptor agonists in Eker rat uterine myometrial cells, and they indicate a need for further investigation of the potential tissue-specific agonist activity of these pesticides and their role in the pathogenesis of uterine leiomyoma. (+info)
Methoxychlor may cause ovarian follicular atresia and proliferation of the ovarian epithelium in the mouse. (5/39)Methoxychlor (MXC) is currently used to protect agricultural products from insects. Previous studies show that MXC adversely affects the ovary, but the target cells were not revealed by those studies. Therefore, the purpose of this study was to test the hypothesis that MXC induces ovarian changes by adversely affecting the antral follicles and the ovarian surface epithelium in the mouse. To test this hypothesis, cycling female CD-1 mice (39 days) were dosed with MXC (8, 16, or 32 mg/kg/day), kepone (KPN, 8 mg/kg/day, positive control), or sesame oil (vehicle control) via intraperitoneal injection for 10 or 20 days. Estrous cyclicity was evaluated daily via vaginal lavage. After dosing, ovaries were collected for histological evaluation of follicle numbers, atresia, and surface epithelial height. The results indicate that at the 20-day time point, MXC (32 mg/kg) and KPN (8 mg/kg) increased the percentage of atretic antral follicles (n= 4-9,p
17beta-estradiol is a hormonal regulator of mirex tumor promotion sensitivity in mice. (6/39)Mirex, an organochlorine pesticide, is a potent non-phorbol ester tumor promoter in mouse skin. Previous studies have shown that female mice are 3 times more sensitive to mirex tumor promotion than male mice and that ovariectomized (OVX) female mice are resistant to mirex promotion, suggesting a role for ovarian hormones in mirex promotion. To determine whether the ovarian hormone 17-beta estradiol (E2) is responsible for the sensitivity of female mice to mirex promotion, female mice were initiated with DMBA; 2 weeks later groups of mice were OVX and implants, with or without E2, were surgically implanted subcutaneously. These mice were treated topically twice weekly with mirex for 26 weeks. E2 implanted OVX mice demonstrated high normal physiologic levels of serum E2 throughout the tumor promotion experiment. E2 implants restored by 80% the intact mirex-sensitive phenotype to the OVX mice. Consistent with a role for E2 and ERalpha and ERbeta, treatment of DMBA-initiated female mice with topical ICI 182,780, an estrogen-receptor antagonist, reduced mirex tumor multiplicity by 30%. However, in cells co-transfected with ERalpha or ERbeta and estrogen-responsive promoter reporter, mirex did not stimulate promoter reporter activity, suggesting that the promotion effect of mirex is downstream of ERalpha/beta. Finally, a tumor promotion study was conducted to determine whether E2 implants could increase the sensitivity of male mice to mirex promotion. E2 implants in male mice did increase sensitivity to mirex promotion; however, the implants did not produce the full female sensitivity to mirex tumor promotion. Collectively, these studies indicate that E2 is a major ovarian hormone responsible for mirex tumor promotion sensitivity in female mice. (+info)
Pivotal role of hepatocellular regeneration in the ultimate hepatotoxicity of CCl4 in chlordecone-, mirex-, or phenobarbital-pretreated rats. (7/39)Our earlier histomorphometric and biochemical studies suggested that the progressive phase of the interactive toxicity of chlordecone (CD) + CCl4 involves suppression of hepatocellular regeneration. The objective of the present work was to correlate hepatocellular regeneration with CCl4 (100 microliters/kg)-induced hepatotoxicity in rats maintained for 15 days on a normal (N) diet, relative to the regenerative response in rats maintained on a diet containing either 10 ppm CD, 225 ppm phenobarbital (PB), or 10 ppm mirex (M). Hepatocellular regeneration was assessed by measuring DNA and 3H-thymidine (3H-T) incorporation, followed by autoradiographic analysis of liver sections. Hepatotoxicity was assessed by measuring plasma transaminases (aspartate and alanine) followed by histopathological observations of liver sections for necrotic, swollen, and lipid-laden cells. Lethality studies were also carried out to assess the consequence of hepatotoxicity on animal survival. Dietary 10 ppm CD potentiated the hepatotoxicity of CCl4 to a greater extent than PB or M, as evidenced by elevations in plasma enzymes. Although the serum enzymes were significantly elevated in PB rats in contrast to the slight elevations in N and M rats, they returned to normal levels by 96 hr. However, serum enzyme elevations in CD rats were progressive with time until death of the animals. Actual liver injury by CCl4 was greater in PB- than in CD-pretreated rats, as evidenced by histopathological observations. A 100% mortality occurred in CD-pretreated rats at 60 hr after CCl4 administration, whereas no mortality occurred in either N-, M-, or PB-pretreated rats, indicating recovery from liver injury. Hepatocellular nuclear DNA levels were significantly decreased starting at 6 hr after CCl4 administration to CD-pretreated rats, but not in M- or PB-pretreated rats. 3H-T incorporation into nuclear DNA as well as percentage of labeled cells showed a biphasic increase in N rats: 1 at 1-2 hr, and the other at 36-48 hr after CCl4 administration. However, only 1 peak of 3H-T incorporation at 36-48 hr was observed in the CD + CCl4 combination, which was also significantly lower when compared to that observed after the M or PB + CCl4 combination treatments. These findings suggest that there is recovery in N-, PB-, or M-pretreated rats from CCl4-induced injury by virtue of the stimulated hepatocellular regeneration and tissue repair.(ABSTRACT TRUNCATED AT 400 WORDS) (+info)
Acceleration of autoimmunity by organochlorine pesticides in (NZB x NZW)F1 mice. (8/39)Systemic lupus erythematosus (SLE) is an autoimmune disorder that affects women more frequently than men. In the (NZB times NZW)F1 mouse, a murine SLE model, the presence or absence of estrogen markedly influences the rate of progression of disease. Three organochlorine pesticides with estrogenic effects were administered chronically to ovariectomized female (NZB times NZW)F1 mice, and we measured the time to development of renal disease, the principal clinical manifestation of lupus in this model. Treatment with chlordecone, methoxychlor, or o,p -dichlorodiphenyltrichloroethane (o,p -DDT) significantly decreased the time to onset of renal impairment, as did treatment with 17ss-estradiol used as a positive control. In an expanded study of chlordecone, we found a dose-related early appearance of elevated anti-double-strand DNA autoantibody titers that corresponded with subsequent development of glomerulonephritis. Immunohistofluorescence confirmed early deposition of immune complexes in kidneys of mice treated with chlordecone. These observations are consistent with an effect of these organochlorine pesticides to accelerate the natural course of SLE in the (NZB times NZW)F1 mouse. Although we originally hypothesized that the effect on progression of autoimmunity was due to estrogenic properties of the pesticides, autoimmune effects and estrogenicity, assessed through measurement of uterine hypertrophy, were not well correlated. This may indicate that uterine hypertrophy is a poor indicator of comparative estrogenic effects of organochlorine pesticides on the immune system, or that the pesticides are influencing autoimmunity through a mode of action unrelated to their estrogenicity. (+info)
Chlordecone is a synthetic chlorinated hydrocarbon insecticide that was widely used in the past for agricultural purposes, particularly in banana plantations. It has been banned in many countries due to its persistence in the environment and its potential negative effects on human health.
Chlordecone is classified as a possible human carcinogen by the International Agency for Research on Cancer (IARC). Exposure to this chemical can occur through contaminated food, water, or air, and it has been linked to various health problems, including neurological effects, endocrine disruption, and an increased risk of certain cancers.
In the medical field, chlordecone exposure is often evaluated in patients who have been exposed to this chemical through environmental contamination or occupational exposure. Medical professionals may use various tests, such as blood or urine tests, to measure the levels of chlordecone in a patient's body and assess any potential health risks.
Mirex is not typically defined in a medical context as it is not a medical term. However, Mirex is a chemical compound that was previously used as an insecticide and flame retardant. It is a colorless solid with a weak chemical odor and is highly stable, which led to its use in various applications.
In the medical field, Mirex may be mentioned in relation to environmental health or toxicology due to its potential harmful effects on human health. Exposure to Mirex can occur through contaminated food, water, or air, and it has been linked to several adverse health outcomes, including neurological damage, reproductive problems, and cancer. However, the use of Mirex as an insecticide has been banned in many countries due to its environmental and health hazards.
Insecticides are substances or mixtures of substances intended for preventing, destroying, or mitigating any pest, including insects, arachnids, or other related pests. They can be chemical or biological agents that disrupt the growth, development, or behavior of these organisms, leading to their death or incapacitation. Insecticides are widely used in agriculture, public health, and residential settings for pest control. However, they must be used with caution due to potential risks to non-target organisms and the environment.
Bromotrichloromethane is a type of halomethane, which is a class of chemicals containing carbon and halogen atoms. Specifically, bromotrichloromethane is a colorless liquid with the chemical formula CBrCl3. It has been used as a fire extinguishing agent, a refrigerant, and an intermediate in the production of other chemicals.
In medical terms, bromotrichloromethane may be encountered in the context of occupational health and safety or environmental exposure assessment. Exposure to high levels of this chemical can cause irritation to the eyes, skin, and respiratory tract, as well as potential neurological effects such as headache, dizziness, and loss of consciousness. Long-term exposure has been linked to liver and kidney damage in animal studies.
It is important to note that bromotrichloromethane is not used in medical treatments or procedures. Its use in industrial applications has been largely phased out due to its ozone-depleting properties and potential health hazards.
CXCR5 is a type of chemokine receptor that is primarily expressed on the surface of certain immune cells, including B cells and some T cells. It belongs to the family of G protein-coupled receptors (GPCRs) and plays a crucial role in the trafficking and homing of these immune cells to specific tissues in the body.
CXCR5 specifically binds to a chemokine ligand called CXCL13, which is produced by various cell types, including stromal cells in lymphoid organs. The binding of CXCL13 to CXCR5 triggers a signaling cascade that leads to the activation of several downstream signaling pathways, ultimately resulting in the migration and accumulation of immune cells in the vicinity of the CXCL13 source.
In the context of the immune system, CXCR5 is essential for the formation of germinal centers, which are specialized structures within lymphoid organs where B cells undergo activation, proliferation, and differentiation into antibody-secreting plasma cells. The interaction between CXCL13 and CXCR5 helps to recruit B cells and follicular T helper (Tfh) cells to the germinal center, where they can engage in productive interactions that drive humoral immune responses.
Abnormalities in CXCR5 signaling have been implicated in various pathological conditions, including autoimmune diseases, cancer, and infectious diseases. Therefore, understanding the molecular mechanisms underlying CXCR5 function is of great interest for the development of novel therapeutic strategies to target these disorders.
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Acceleration of autoimmunity by organochlorine pesticides: a comparison of splenic B-cell effects of chlordecone and estradiol...
Selective induction of cytochrome P450e by kepone (chlordecone) in primary cultures of adult rat hepatocytes. | Molecular...
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Transformation of the recalcitrant pesticide chlordecone by Desulfovibrio sp.86 with a switch from ring-opening dechlorination...
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Occupational exposure to pesticides and prostate cancer: a systematic review and meta-analysis | Occupational & Environmental...
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François Jacob Institute of biology - Metagenomics of prokaryotes
Struggle against environmental poisoning and police violence in Martinique - Workers World
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Preliminary characterisation of Sargassum storage sites in Martinique | BRGM
- The weakly estrogenic organochlorine pesticide chlordecone can accelerate the development of systemic lupus erythematosus (SLE) in ovariectomized (NZBxNZW)F1 mice, with a shortened time to appearance of autoantibodies and disease similar to that produced by treatment with the sex hormone 17beta-estradiol (E2). (nih.gov)
- To validate the use of measurements of Na+/K+- ATPase in erythrocytes as a marker for the same enzyme in brain, the organochlorine pesticide chlordecone (143500), the organotins triethyltin (997502) and tributyltin (688733), mercuric-chloride (7487947) and methyl-mercury were chosen as chemical probes. (cdc.gov)
- Chlordecone is a pesticide that controls a beetle that destroys banana plants. (workers.org)
- A pesticide linked to cancer - chlordecone - was sprayed on banana crops on the islands for two decades and now nearly all the adult local residents have traces of it in their blood. (berkeley.edu)
- Earlier this month judges in Paris dismissed a legal case brought by residents from the French Caribbean islands of Martinique and Guadeloupe over the widespread use of the pesticide chlordecone which has polluted local ecosystems. (mediapart.fr)
- The toxic pesticide chlordecone was used on banana plantations in the French West Indies until 1993 but continued to pollute the waters surrounding the. (sustainablepulse.com)
- Effects of Probiotic Oral Intake on Plasma Chlordecone (Kepone) Concentrations in Individuals Environmentally Exposed to Pesticide in Martinique. (who.int)
- Chlordecone, better known in the United States under the brand name Kepone, is an organochlorine compound and a colourless solid. (wikipedia.org)
- In the U.S., chlordecone, commercialized under the brand name "Kepone", was produced by Allied Signal Company and LifeSciences Product Company in Hopewell, Virginia. (wikipedia.org)
- Chlordecone (also known as Kepone) was used as an insecticide on tobacco, ornamental shrubs, bananas, and citrus trees, and in ant and roach traps. (cdc.gov)
- Selective induction of cytochrome P450e by kepone (chlordecone) in primary cultures of adult rat hepatocytes. (aspetjournals.org)
- Kepone (chlordecone) treatment of the cultures increased P450e mRNA in a dose-dependent manner that disclosed a 10-fold greater potency, compared with cultures exposed to phenobarbital. (aspetjournals.org)
- Kepone, also known as chlordecone, is a toxic, nonbiodegradable insecticide that a chemical plant in Hopewell, Virginia dumped into the James River from 1966 until 1975. (encyclopediavirginia.org)
- https://encyclopediavirginia.org/entries/kepone-chlordecone. (encyclopediavirginia.org)
- In the US a factory producing chlordecone - sold commercially as kepone - was shut down in 1975 after workers fell seriously ill there. (berkeley.edu)
- Chlordecone is a toxic organochlorine insecticide that was used in banana plantations until 1993 in the French West Indies. (ird.fr)
Mirex and Chlordecone16
- What are mirex and chlordecone? (cdc.gov)
- Mirex and chlordecone are two separate but similar chemicals that are manufactured insecticides (insect killing) that are not found naturally in the environment. (cdc.gov)
- Mirex and chlordecone have not been manufactured or used in the United States since the late 1970s. (cdc.gov)
- How can I be exposed to mirex and chlordecone? (cdc.gov)
- The most likely way you could be exposed to very small amounts of mirex and chlordecone is from contaminated food grown or caught near hazardous waste sites. (cdc.gov)
- If you live near a hazardous waste site you might be exposed to mirex and chlordecone from contaminated dirt or if you eat wildlife (fish and game) living near hazardous waste sites. (cdc.gov)
- How can mirex and chlordecone affect my health? (cdc.gov)
- Can mirex and chlordecone cause cancer? (cdc.gov)
- The Department of Health and Human Services considers mirex and chlordecone to be reasonably anticipated to be human carcinogens (causing cancer). (cdc.gov)
- Can I get a medical test to check for mirex and chlordecone? (cdc.gov)
- Mirex and chlordecone can be measured in blood and several other body fluids. (cdc.gov)
- Mirex and chlordecone can be measured in your blood for several years after you have been exposed. (cdc.gov)
- How can I protect myself and my family from mirex and chlordecone? (cdc.gov)
- Most people don't need to take any special steps to avoid mirex and chlordecone in their daily lives. (cdc.gov)
- Children should avoid playing in the dirt near hazardous waste sites to avoid coming in contact with mirex and chlordecone. (cdc.gov)
- Toxicological Profile for Mirex and Chlordecone. (comprehensivephysiology.com)
- Chlordecone reductase homolog HAKRC. (invivogen.com)
- Since 2003, local authorities in the two islands have restricted the cultivation of various food crops because the soil is badly contaminated by chlordecone. (wikipedia.org)
- Thus NIRS could be considered a time- and cost-effective method for characterising soil contamination by chlordecone. (ird.fr)
- Given that Sargassum can accumulate arsenic and chlordecone, it is important to assess the possible impact of its storage on the quality of the environment (water, soil, sediment, etc. (brgm.fr)
- Chlordecone levels (soil and/or Sargassum ) were also quantified for five of the eight sites in Martinique. (brgm.fr)
- Chlordecone has been found to act as an agonist of the GPER (GPR30), which interacts strongly with the estrogen sex hormone estradiol. (wikipedia.org)
- Chlordecone can accumulate in the liver and the distribution in the human body is regulated by binding of the pollutant or its metabolites to lipoproteins like LDL and HDL. (wikipedia.org)
- The French islands of Martinique and Guadeloupe are heavily contaminated with chlordecone, following years of its massive and unrestricted use on banana plantations. (wikipedia.org)
- This study aimed at assessing the potential of near infrared reflectance spectroscopy (NIRS) for determining chlordecone content in Andosols, Nitisols and Ferralsols from Martinique. (ird.fr)
- The atlas reports that "92% of people tested in Martinique have chlordecone in their body and 19% of children tested exceed the toxic dose. (workers.org)
- Workers in plants that made these chemicals and may have been exposed to high levels of chlordecone over a long period of time (several years) sometimes had harmful effects on the nervous system, skin, liver, and male reproductive system. (cdc.gov)
- Liver cancer has been seen in animals exposed to high doses of mirex or chlordecone. (cdc.gov)
- BACKGROUND: Inhabitants of Guadeloupe are chronically exposed to low dose of chlordecone via local food. (hal.science)
- RESULTS: We derive ERFs for 3 possible effects at chronic low chlordecone dose: cancers, developmental impairment, and hepatotoxicity. (hal.science)
- The differences in effects between chlordecone and E2 indicate that chlordecone is not functioning simply as an estrogen mimic with respect to effects on the immune system. (nih.gov)
- Studies in animals with chlordecone have shown similar effects as those seen in workers. (cdc.gov)
- The effects of chlordecone and E2 treatment on splenic germinal center (GC) and marginal zone B cells were examined. (nih.gov)
- Similarities in the effects of chlordecone and E2 on specific immune functions, such as diminished apoptosis in GC B cells, may provide valuable clues regarding key events in the acceleration of autoimmunity by E2, chlordecone, and other agents. (nih.gov)
- Available knowledges on mode of action and key-event hazards of chlordecone are used to identify effects of chlordecone that could occur at low dose. (hal.science)
- 12 mg kg(-1), nevertheless ca. 80% samples were correctly predicted when the set was divided into three or four classes of chlordecone content. (ird.fr)
- We develop methods for quantifying the health impacts of chlordecone and present the results in 2 articles: 1. (hal.science)
- Chlordecone reduced total B cell and GC B-cell apoptosis without affecting proliferation, another feature shared by E2 treatment. (nih.gov)
- However, chlordecone treatment did not alter the composition of splenic B-cell subsets in marked contrast to the decrease in transitional B cells and increase in marginal zone B cells seen in E2-treated mice. (nih.gov)
- The Food and Drug Administration (FDA) has not found mirex or chlordecone in U.S.-wide studies of food conducted after 1992. (cdc.gov)
- At its second meeting, the Persistent Organic Pollutants Review Committee adopted the risk profile on Chlordecone, on the basis of the draft contained in document UNEP/POPS/POPRC.2/8. (pops.int)
- At its third meeting, the Persistent Organic Pollutants Review Committee adopted the risk management evaluation on chlordecone, on the basis of the draft contained in document UNEP/POPS/POPRC.3/10 and the revision to the risk profile contained in document UNEP/POPS/POPRC.3/20/Add.10. (pops.int)
- In 2009, chlordecone was included in the Stockholm Convention on Persistent Organic Pollutants, which bans its production and use worldwide. (wikipedia.org)
- In recent years there have been marches and protests, mainly in Fort-de-France, Martinique's capital, over the chlordecone poisoning of the environment. (workers.org)
- Chlordecone bioaccumulates in animals by factors up to a million-fold. (wikipedia.org)
- Chlordecone was not federally regulated until after the Hopewell disaster, in which 29 factory workers were hospitalized with various ailments, including neurological. (wikipedia.org)