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PubMed2005

Insect GABA receptors: splicing, editing, and targeting by antiparasitics and insecticides.

Ionotropic GABA receptors are abundant in both vertebrate and invertebrate nervous systems, where they mediate rapid, mostly inhibitory synaptic transmission. A GABA-gated chloride channel subunit from Drosophila melanogaster [Resistant to Dieldrin (RDL)] has been cloned, functionally expressed, and found to exhibit many aspects of the pharmacology of native, bicuculline-insensitive insect GABA receptors. RDL is the target of the commercially important insecticide fipronil. A point mutation in the channel-lining region of the RDL molecule is known to underlie most cases of resistance to insecticides acting on GABA receptors. RDL is widely distributed throughout the insect nervous system, but the subunit composition of RDL-containing in native receptors is unknown. It is possible that in some instances, RDL coexpresses with glutamate-gated chloride channel subunits. Other ionotropic receptor subunits (LCCH3 and GRD) form GABA-gated cation channels when heterologously expressed. Interest in RDL as a model ligandgated anion channel has been enhanced by the recent discovery of pre-mRNA A-to-I editing, which, together with alternative splicing, adds to the functional diversity of this GABA receptor subunit.

Alternative Splicing↗

PubMed1961

Multi-resistant Aedes aegypti in Puerto Rico and Virgin Islands.

The Isla Verde, Puerto Rico, laboratory colony, highly resistant to DDT and dieldrin in 1959, became even more so by 1960; resistance to organic phosphates was also greater than before. In laboratory tests Bayer 29493 was best for killing resistant larvae and adults. It is improved with piperonyl butoxide at the ratio of 10:1.

Aedes↗

PubMed1966

Chlorinated hydrocarbon pesticides: degradation by microbes.

In culture, most of the actinomycetes and filamentous fungi tested degraded PCNB; several actinomycetes dechlorinated DDT to DDD, but no microorganism degraded dieldrin. Streptomyces aureofaciens degraded PCNB to pentachloroaniline.

Ascomycota↗

PubMed1995

Organochlorine residues in human breast milk: analysis through a sentinel practice network.

STUDY OBJECTIVE: The study aimed to assess through a sentinel practice network the validity of data on levels of organochlorine residues in human milk along with personal, lifestyle, and exposure variables of breastfeeding women; to compare the results of this new approach with those of the Lower Saxony breast milk surveillance programme; and to test hypotheses on potential determinants of contamination levels. DESIGN: Eligible women were enrolled into this cross sectional study by a network of 51 paediatric practices when bringing their babies for a U3 infant screening examination (4th to 6th week after delivery). Lifestyle and exposure factors were obtained by questionnaire. All milk samples were analysed for hexachlorocyclohexane, hexachlorbenzole, DDT, dieldrin, polychlorinated biphenyls (PCB) and heptachlor; half the samples were also analysed for dioxin. Analytic statistics were computed using polychotomous logistic regression (PLR). SETTING: The study was conducted in Lower Saxony, Germany, from summer 1992 to summer 1993. PARTICIPANTS: Altogether 156 primiparous, breast feeding German women, aged 25-35 years, who had been born and had grown up in West Germany, were studied. MAIN RESULTS: Compared with the regular programme, participants in this study had their milk analysed sooner after delivery and were more likely to have grown up in rural areas, less likely to have been exposed to hazardous substances, less likely to have a diet of health food, and slightly less likely to be a smoker at the time of the study. Breast milk contamination levels were comparable in both studies, and in all but two cases well below the tolerable concentrations established by the Deutsche Forschungsgemeinschaft (German Research Fellowship). After adjustment for potential confounders using polychotomous logistic regression, there were statistically significant positive associations between breast milk contamination and age (PCB, test for trend: p = 0.006), average dietary fat intake per week (dioxin, p = 0.01), and proximity of residence to hazardous sites (dioxin, p < 0.05), and negative associations between residue levels and relative body weight at the time of the study (PCB; p < 0.0001) and difference in body weight (weight minus weight before the pregnancy; PCB, p = 0.0002), respectively. CONCLUSIONS: Sentinel practice networks are a feasible and low-biased approach to population based breast milk studies. The contamination levels and associations found are biologically plausible and comparable with the results of other studies. To reduce organochlorine residue levels in human milk in the short term, breast-feeding women should be advised not to try to reduce their weight until after lactation. Public promotion of a lower dietary fat intake may reduce the lifetime accumulation of organochlorine compounds in the human body fat tissue in the long term, resulting in lower concentrations in breast milk as well.

Adult↗

PubMed2003

Integrative assessment of multiple pesticides as risk factors for non-Hodgkin's lymphoma among men.

BACKGROUND: An increased rate of non-Hodgkin's lymphoma (NHL) has been repeatedly observed among farmers, but identification of specific exposures that explain this observation has proven difficult. METHODS: During the 1980s, the National Cancer Institute conducted three case-control studies of NHL in the midwestern United States. These pooled data were used to examine pesticide exposures in farming as risk factors for NHL in men. The large sample size (n = 3417) allowed analysis of 47 pesticides simultaneously, controlling for potential confounding by other pesticides in the model, and adjusting the estimates based on a prespecified variance to make them more stable. RESULTS: Reported use of several individual pesticides was associated with increased NHL incidence, including organophosphate insecticides coumaphos, diazinon, and fonofos, insecticides chlordane, dieldrin, and copper acetoarsenite, and herbicides atrazine, glyphosate, and sodium chlorate. A subanalysis of these "potentially carcinogenic" pesticides suggested a positive trend of risk with exposure to increasing numbers. CONCLUSION: Consideration of multiple exposures is important in accurately estimating specific effects and in evaluating realistic exposure scenarios.

Adult↗

PubMed1985

Toxicity episodes involving agricultural chemicals and other substances in birds in Victoria, Australia.

A series of case reports detailing observations on toxicity episodes in birds caused by a variety of agricultural chemicals and other substances is presented. These problems arose as a result of ignorance, accident and malicious intent. The episodes involved maldison, monocrotophos, fenitrothion, trichlorofon, dieldrin, chlordane, endrin, metaldehyde, bromadiolone, arsenic, lead and zinc. An unresolved episode where toxicity was implicated is also included.

Animals↗

PubMed1993

Organochlorine and mercury contamination in United Kingdom seals.

In 1988 and 1989 tissue samples were obtained from the grey seal (Halichoerus grypus) population found in the Dee estuary in the north west of England and from harbour seals (Phoca vitulina) from the populations in the Wash and north east Scotland and analysed for mercury and organochlorine compounds. Adult seals from the Dee estuary were highly contaminated with mercury and polychlorinated biphenyls (PCBs), and one animal from the Dee contained traces of dichlorodiphenyltrichloroethane (DDT), suggesting the recent use of this banned pesticide. The levels of hexachlorobenzene in the livers of two Dee seals exceeded those in the blubber, possibly indicating liver malfunction or recent exposure. The same relationship was found for hexachlorobenzene in three specimens from the Wash and, in one of these animals, the liver was also more highly contaminated than the blubber with dieldrin and PCBs. Levels of contamination were lower in seals from the Wash and even lower in animals sampled in Scotland, where only dichlorophenyldichloroethylene, the metabolite of DDT, was routinely detected. The toxicological significance of the results is discussed, particularly in relation to the mortality observed in the seal epizootic of 1988.

Adipose Tissue↗

PubMed2004

Retinal dysplasia in wild otters (Lutra lutra).

Eyes from 88 otters found dead in south-west England between 1990 and 2000, were collected as part of a larger pathological study. Histopathological examination of 131 eyes revealed dysplastic changes such as rosetting and folding in the retinas of 26 of the otters. In the eyes of 42 of the otters there were postmortem and fixation-induced retinal detachment which complicated the differentiation of dysplastic from normal retina, but 11 eyes had folds which probably indicated a dysplastic pathology. The eyes of 18 of the otters had inflammatory or autolytic changes which precluded a definitive evaluation of their dysplastic status. Liver samples from 55 of the otters were analysed for a range of polychlorinated hydrocarbons and for vitamin A. The otters with dysplastic retinas had significantly lower concentrations of vitamin A and higher concentrations of dieldrin than the otters with normal retinas.

Animals↗

PubMed1985

Reconstituted halogenated hydrocarbon pesticide and pollutant mixtures found in human tissues: effects on the immature male Wistar rat after short-term exposure.

Halogenated hydrocarbon insecticides and polychlorinated biphenyl (PCB) mixtures are routinely detected as residues in human adipose tissue, serum, and milk. Based on average values observed in analytical studies, reconstituted halogenated hydrocarbon pesticide mixtures and PCB mixtures were prepared and administered to immature male Wistar rats. The mixtures were administered at dose levels which approximate the concentrations which would be absorbed by an infant suckling for 180 days (low dose, L), and at three higher dose levels (2 X L, 10 X L, and 100 X L). The pesticide mixture contained isomeric hexachlorocyclohexanes, dieldrin, heptachlor epoxide, oxychlordane, trans-nonachlor, hexachlorobenzene, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane, and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene; the reconstituted PCB mixture contained 13 of the major congeners which have been identified in human milk samples. Administration of the L dose level of the pesticide (0.95 mg/kg), PCB (0.45 mg/kg), and pesticide plus PCB mixture (0.95 + 0.45 mg/kg, respectively) in corn oil on days 1 and 3 did not significantly alter hepatic drug-metabolizing enzyme activities or elicit any observable pathological damage 6 days after the first exposure. In contrast, administration of the higher dose levels of this mixture elicited a dose-dependent induction of several hepatic drug-metabolizing enzymes. Moreover, despite the short duration of exposure to these chemicals, the rats treated with the higher doses (10 X L and 100 X L) of these mixtures exhibited mild alterations in thyroid architecture, changes in hepatocellular nuclei including variations in chromatin distribution, vesiculation of larger nuclei, and frequent appearance of pyknotic shrunken nuclei.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Cyclodiene insecticide resistance: from molecular to population genetics.

This review follows progress in the analysis of cyclodiene insecticide resistance from the initial isolation of the mutant, through cloning of the resistance gene, to an examination of the distribution of resistance alleles in natural populations. Emphasis is given to the use of a resistant Drosophila mutant as an entry point to cloning the associated gamma-aminobutyric acid (GABA) receptor subunit gene, Resistance to dieldrin. Resistance is associated with replacements of a single amino acid (alanine302) in the chloride ion channel pore of the protein. Replacements of alanine302 not only directly affect the drug binding site but also allosterically destabilize the drug preferred conformation of the receptor. Resistance is thus conferred by a unique dual mechanism associated with alanine302, which is the only residue replaced in a wide range of different resistant insects. The underlying mutations appear either to have arisen once, or multiply, depending on the population biology of the pest insect. Although resistance frequencies decline in the absence of selection, resistance alleles can persist at relatively high frequency and may cause problems for compounds to which cross-resistance is observed, such as the novel fipronils.

Animals↗

PubMed1991

Gap junctions in rabbit corneal epithelium: limited permeability and inhibition by cAMP.

Rabbit corneas were mounted in Ussing chambers, and the apical membrane of the superficial cells (SCs) was permeabilized by exposure to digitonin in a Ca(2+)-free Ringer solution. This treatment resulted in the generation of large (60.7 +/- 13.2 microA/cm2, n = 25) Na(+)-dependent tear (T)-to-stroma (S) short-circuit currents (Isc). The Isc was abolished by ouabain and by 1.4 mM Ca2+ and was inhibited by heptanol, 18 alpha-glycyrrhetinic acid, and dieldrin, effects consistent with the notion that corneal transepithelial fluxes include translocations through gap junctions (GJs) before basolateral membrane transport. T-to-S Isc were also generated when T-side Na+ was replaced by K+, eliciting a T-to-S K+ flux via basolateral K+ channels and when, with either Na+ or K+ on the T side, channels were introduced at the apical membrane with amphotericin B. The Isc in all four conditions exhibited similar sensitivity to GJ inhibitors and were inhibited by adenosine 3',5'-cyclic monophosphate (cAMP) elevation. Fluorophotometry combined with SC permeabilization with digitonin demonstrated that the half-time for the SC to sub-SC movement of 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (mol wt 540) exceeded 3 h. These results indicate that junctional communications along the epithelial stratification axis are highly restricted and modulated by cAMP concentration.

Amphotericin B↗

PubMed1996

Upregulation of gap junctional intercellular communication in immortalized gonadotropin-releasing hormone neurons by stimulation of the cyclic AMP pathway.

Increased gap junctional intercellular communication induced by agents that stimulate the adenylyl cyclase/cAMP pathway was observed in the GnRH-secreting neuronal cell line, GT1-7, and possible underlying mechanisms were examined. A 24-hour treatment of GT1-7 neurons with 100 microM dibutyryl cAMP + 100 microM IBMX or with 2 microM forskolin increased by greater than 2-fold the percentage of cells that were dye coupled, using the noninvasive dye coupling assay, fluorescent recovery after photobleaching (FRAP). Longer treatment times (48 h) and higher concentrations of dibutyryl cAMP (500 microM) did not further increase the percentage of dye-coupled cells, while there was no increase in dye coupling observed between untreated cells and cells treated for 2 h or less. The increase in dye coupling induced by dibutyryl cAMP/IBMX was inhibited by octanol or dieldrin, agents known to block gap junction-mediated intercellular coupling in other cell types. Western blot analysis of total protein or membrane protein-enriched extracts revealed no apparent difference in the cellular levels of connexin 26, a connexin subtype previously shown to be expressed by GT1-7 cells, between untreated cells and cells treated for 24 h with dibutyryl cAMP/IBMX or forskolin. In addition, expression of connexin 32 or 43 protein before or after treatment was not detected. On the other hand, a dramatic increase in both the number of neurites and neurites that immunostained positive for connexin 26 was observed in dibutyryl cAMP/IBMX-treated cells. We hypothesize that the observed increase in dye coupling between GT1-7 neurons following stimulation of the adenylyl cyclase/cAMP pathway results from an augmentation of cell-cell contacts due to an increased number of neurites containing gap junctional plaques, possibly through an effect on cellular differentiation.

1-Methyl-3-isobutylxanthine↗

PubMed1985

Organochlorine pesticide residues in human fat in the United Kingdom 1982-1983.

Between December 1982 and October 1983 samples of human body fat were taken during routine necropsies carried out on 187 persons aged over 5 years and four infants aged under 4 months. Comparison of the results of analysis with those from the previous studies in 1976-1977, and earlier, shows a continuing decline in residues of p,p'-dichlorodiphenyltrichloroethane (p,p'-DDT) and dieldrin (HEOD) and a reduction in the amounts of p,p'-dichlorodiphenyltichloroethane [p,p'-DDE, a metabolite of p,p'-DDT] and hexachlorobenzene. The concentrations of other compounds were similar to those observed in the previous studies. The results show that the amounts of organochlorine pesticides and polychlorobiphenyl compounds contained in human fat samples from residents in the UK compare favourably with data obtained in other countries.

Adipose Tissue↗

PubMed1998

Mouse-specific carcinogens: an assessment of hazard and significance for validation of short-term carcinogenicity bioassays in transgenic mice.

1. The International Conference on the Harmonisation of Technical Requirements for the Registration of Pharmaceuticals for human use (ICH) has agreed that bioassay data from only one species, the rat, supported by appropriate mutagenicity and pharmacokinetic data and also information from new (unvalidated) short term in vivo screening tests for potential carcinogenicity, could be used for the licensing of human medicines. This proposal has been supported by reviews of the utility of testing pharmaceuticals in the mouse which have concluded that the mouse bioassay contributes little to regulatory decisions. The current review was undertaken to identify 'genuine' mouse-specific carcinogens using the Gold Carcinogenicity Potency Database (CPD) for the initial identification of potential mouse-specific carcinogens from published literature. Hazard assessments were completed for these chemicals with particular attention focused on the 'genuine' mouse-specific carcinogens. The significance of such chemicals has been discussed together with consideration of on-going work on the validation of short-term carcinogenicity bioassays using transgenic mice. 2. Seventy-six potential mouse specific carcinogens were identified through the Gold Carcinogenicity Potency Database. Following more detailed consideration a total of ten chemicals were excluded from further consideration (three were multispecies carcinogens, five were considered to be non-carcinogenic in the mouse, and the data for two were uninterpretable). The review focused on the remaining 66 chemicals. There was equivocal evidence of carcinogenicity to the rat for 28 chemicals and inadequate data for a further 23 chemicals. Fifteen 'genuine' mouse-specific carcinogens were identified. These 15 chemicals comprise two genotoxic mouse-specific carcinogens (N-methylolacrylamide (924-42-5), 2,6-Dichloro-p-phenylenediamine (609-20-1); five non-genotoxic mouse-specific carcinogens 2-Aminobiphenyl.HCl (2185-92-4), Captan (133-06-2), Dieldrin (60-57-7), Diethylhexyladipate (103-23-1), and Probenicid (57-66-9); five mouse-specific carcinogens with equivocal evidence of mutagenicity were identified; (2,4-diaminophenol.2HCl (137-09-7), Dipyrone (68-89-3), Ozone (10028-15-6), Vinylidene chloride (75-35-4), and Zearalenone (17924-92-4)), and three mouse-specific carcinogens with inadequate mutagenicity data (Benzaldehyde (100-52-7), Piperonyl sulphoxide (120-62-7), Ripazepam (26308-28-1)). 3. It is suggested that the two genotoxic mouse carcinogens would have been considered as potential carcinogens in the absence of a mouse bioassay. Of the five non-genotoxic mouse-specific carcinogens; three induced tumours in mouse liver only and are considered as being of low potential hazard to human health. The remaining two chemicals would have been missed in the absence of a mouse bioassay (2-aminobiphenyl (2185-92-4) and captan (133-06-2)) and thus are good candidates for evaluation in the short term bioassays in transgenic mice currently being validated. 4. The hardest group of mouse-specific carcinogens to evaluate are those for which there is equivocal or inadequate mutagenicity data. The difficulty in evaluating these particular chemicals emphasises the need for adequate mutagenicity data in addition to adequate carcinogenicity data in order to assess potential hazards to human health. Hazard assessments and a consideration of the potential role for short-term bioassays in transgenic mice for the eight chemicals in this subgroup are presented. 5. A number of general conclusions have been derived from this review. Firstly, there are insufficient published genotoxicity data to allow a full assessment fo mutagenic potential for 57/76 of the potential mouse-specific carcinogens identified from the CPD. This is surprising given the clear value of such data in interpreting bioassay results and the much greater resources required for carcinogenicity bioassays. (ABSTRACT TRUNCATED)

Animals↗

PubMedDate not supplied

Selecting high-priority hazardous chemicals for tri-national control: a maximum-utility method applied to Mexico.

The dispersion of persistent, bioaccumulative toxic chemicals poses risks to human health and the integrity of the ecosystem on a continental scale. Mexico, the United States, and Canada sought to add two pollutants to an existing list of four subject to North American Regional Action Plans (chlordane, DDT, mercury, PCBs). Mexican negotiators used results from an internal selection process, applying 14 criteria in five categories-physicochemical, health-endpoint, data quality/quantity, exposure potential, and control feasibility-to a baseline group of over 4,700 substances. Using policy analysis by the multiattribute maximum-utility method, progressive application of criteria and weighting algorithms acted like successive filters to identify priority lists of 15 and 7 substances/substance groups for Mexico. The 15 are: 1) benzo-a-pyrene (1 other PAHs); 2) cadmium; 3) heptachlor; 4) hexachlorobenzene; 5) lead; 6) lindane (+ other HCH isomers); 7) 2,3, 7,8-tetrachlorodibenzo-p-dioxin (&plus other PCDDs); 8) aldrin; 9) arsenic; 10) chromium; 11) carbon tetrachloride; 12) 3-3'-dichlorobenzidine; 13) dieldrin; 14) nickel; and 15) toxaphene. The first seven are the priority list of seven.

Algorithms↗

PubMedDate not supplied

Inadvertent exposure to xenoestrogens in children.

This article reviews previous studies and presents new data on pesticide exposure in order to provide some indications of the extent and significance of childhood exposure to xenoestrogens, including pesticides, epoxy resins, and polycarbonates. After more than four decades of pesticide use, little is known about their adverse effects on health. There is a need to address the potential risks associated with the current contamination of water, soils, and foods in many agricultural areas. In southeastern Spain, along the Mediterranean coast, extensive areas alongside residential zones are devoted to intensive farming in plastic greenhouses, with the use of large amounts of pesticides. Human tissue samples have been investigated for pesticide residues. Samples of fat from children living in farm areas contained a total of 14 pesticides, including lindane, HCH, heptachlor, aldrin, dieldrin, endrin, endosulfan, o,p'-DDE, and o,p'-DDD, among others. Of the 113 samples studied, 43 were positive for one or more pesticides, some of which have estrogenic activity. The number of new substances that mimic the action of endogenous estrogens is increasing rapidly. These endocrine-disrupting chemicals are not restricted to pesticides. Several different compounds used in the food industry, in plasticizers, and in dental restorations are also estrogenic. The few studies that have investigated their effects in humans all indicate that concerns are warranted. If there is indeed an association between zexposure to substances with hormone-disruptive activity and certain disorders of sexual maturation, the incidence of such disorders should be greater in areas where exposure to agents with this activity is high. We used a spatial ecological design to search for variations in orchidopexy rates and to analyze relationships between these differences and geographical variations in exposure to pesticides. Our results are compatible with a hypothetical association between exposure to hormone-disruptive chemicals and the induction of cryptorchidism. Several methodological limitations in the study design make it necessary to evaluate the results with caution. In conclusion, a closer scrutiny is required to determine whether epoxy resins and polycarbonates contribute, together with estrogenic pesticides, to the exposure of human consumers, especially children, to xenoestrogens.

Adipose Tissue↗

PubMed2002

Gene induction studies and toxicity of chemical mixtures.

As part of its mixtures program, the Agency for Toxic Substances and Disease Registry (ATSDR) supports in vitro and limited in vivo toxicity testing to further our understanding of the toxicity and health effects of chemical mixtures. There are increasing concerns that environmental chemicals adversely affect the health of humans and wildlife. These concerns have been augmented by the realization that exposure to chemicals often occurs to mixtures of these chemicals that may exhibit complex synergistic or antagonistic interactions. To address such concerns, we have conducted two studies with techniques that are being used increasingly in experimental toxicology. In the first study, six organochlorine pesticides (4,4 -DDT, 4,4 -DDD, 4,4 -DDE, aldrin, dieldrin, or endrin) were selected from the ATSDR Comprehensive Environmental Response, Compensation and Liability Act of 1980 (or Superfund) priority list and tested for their ability to modulate transcriptional activation of an estrogen-responsive reporter gene in transfected HeLa cells. In these assays, HeLa cells cotransfected with an expression vector encoding estrogen receptor and an estrogen-responsive chloramphenicol acetyltransferase (CAT) reporter plasmid were dosed with and without selected environmental chemicals either individually or in defined combinations. Estradiol consistently elicited 10- to 23-fold dose-dependent inductions in this assay. By contrast, all six of the organochlorine pesticides showed no detectable dose-related response when tested either individually or in binary combinations. Thus, these chemicals as binary mixtures do not exhibit any additional estrogenicity at the levels tested in these assays. In the second study, arsenic [As(V)], cadmium [Cd(II)], chromium [Cr(III, VI)], and lead [Pb(II)] were tested in a commercially developed assay system, CAT-Tox (L), to identify metal-responsive promoters and to determine whether the pattern of gene expression changed with a mixture of these metals. This assay employs a battery of recombinant HepG2 cell lines to test the transcriptional activation capacity of xenobiotics in any of 13 different signal-transduction pathways. Singly, As(V), Cd(II), Cr(III, VI), and Pb(II) produced complex induction profiles in these assays. However, no evidence of synergistic activity was detected with a mixture of Cd(II), Cr(III), and Pb(II). These results have shown metal activation of gene expression through several previously unreported signal-transduction pathways and thus suggest new directions for future studies into their biochemical mechanisms of toxicity. In conclusion, the (italic)in vitro(/italic) methods used in these studies provide insights into complex interactions that occur in cellular systems and could be used to identify biomarkers of exposure to other environmental chemical mixtures.

Biomarkers↗

PubMed1994

Human milk as a bioindicator for body burden of PCDDs, PCDFs, organochlorine pesticides, and PCBs.

In the State Laboratory of North Rhine-Westphalia for Food, Pharmaceutical and Environmental Chemistry (Chemisches Landesuntersuchungsamt), more than 600 individual human milk samples have been analyzed for polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), and more than 1400 individual milk samples have been analyzed for organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) since 1984. All samples were collected on a voluntary basis from nursing mothers mostly living in North Rhine Westphalia, a federal state in Germany. The samples analyzed so far show a typical pattern of PCDDs and PCDFs. Out of the 210 possible congeners, only those with 2,3,7,8-chlorine substitution were found. While OCDD normally shows the highest concentration, the levels of the other dioxin congeners decrease with decreasing number of chlorine atoms. A different pattern was found for PCDFs. Within this group 2,3,4,7,8-P5CDF is the most abundant congener, followed by the hexachlorodibenzofurans. The mean level of tetrachlorodibenzodioxin (TCDD) was found to be of 3.2 pg/g on a fat basis and for total PCDDs and PCDFs, calculated as I-TEq (NATO/CMMS), 29.3 pg/g on a fat basis. The investigations of the past 2 years have revealed somewhat lower levels compared to former years. This might be an indication that the efforts undertaken to minimize dioxin emissions and to shut down known sources have already had an effect on the body burden of humans. Although mostly banned for a considerable period of time now, some lipophilic persistent pesticides such as DDT, dieldrin, hexachlorobenzene (HCB), and hexachlorocyclohexanes (HCH) can still be found in human milk.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzofurans↗