Organochlorine compounds in mother and fetus during labor

Polishuk, Z; D, Wassermann; Wassermann, M.; Cucos, Simi; Ron, M.

doi:10.1016/0013-9351(77)90104-9

Cited by 64 publications

(25 citation statements)

References 6 publications

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“…The minimum value of 0.13 would lend support to the common assumption that placental storage of PCBs is relatively low. On the other hand, the ratios calculated for Polishuk et al ( 1977 ) and Rogan et al ( 1986 ) suggest that PCBs accumulate in the placental tissue. Table 2 and Figure 1 illustrate the wide range of reported placental concentrations of PCBs.…”

Section: Discussionmentioning

confidence: 94%

“…The``unexposed population'' studied by Bosse et al (1996) yielded higher concentrations than the population studied by Schlebusch et al (1994 ) , which resided in a highly polluted industrial area in the former German Democratic Republic. Polishuk et al ( 1977 ) , Rogan et al (1986 ), and Bosse et al (1996 ) report placental concentrations ( range: 800 ±5027 ng /g fat ) that are 1.24 times higher than 8 of the 10 breast milk concentrations when compared on a lipid basis. Assuming a placental weight of 550 g ( Diamant et al, 1982 ) , a fat content of 1.25% (Table 1) , and an average PCB concentration in placental fat of 1000 ng /g fat, a placenta would contain about 6.9 g PCB.…”

Section: Discussionmentioning

confidence: 96%

“…Methods utilized by the reviewed studies include packed column gas chromatography (PCGC ) ( Kodama and Ota, 1980;Jacobson et al, 1984;Rogan et al, 1986;Krauthacker, 1992, Czaja et al, 1998 ) and congener -specific or capillary column gas chromatography (CCGC ) ( Polishuk et al, 1977;Janousek et al, 1994;Schlebusch et al, 1994;Bosse et al, 1996;Dewailly et al, 1996;KoopmanEsseboom et al, 1996;Kostyniak et al, 1999;Kivirianta et al, 1998;Lanting et al, 1998a,b;Laden et al, 1999 Table 1. We numerically equated specific gravity with density since the maximum density of water, the reference substance, is 1 g/ ml (Diem, 1962 ).…”

Section: Methodsmentioning

confidence: 99%

“…Human PCB exposure can occur through environmental accidents, dietary intake, and in utero to unborn children (Rappolt and Hale, 1968;Polishuk et al, 1977;Brown et al, 1994;Guo et al, 1994;Stewart et al, 1999 ). PCBs accumulate in adipose tissue, blood lipids, and breast milk, and evidence indicates that this class of xenobiotics travels with the lipid components of blood ( VLDL, LDL, HDL, and chylomicron remnants ) and likely gains access to the many tissue compartments of the human body by utilizing the lipoprotein lipase mechanism ( Spindler-Vomachka et al, 1984;Gallenberg and Vodicnik, 1987;Soues et al, 1989;Borlakoglu et al, 1990a,b;Laden et al, 1999 ).…”

Section: Introductionmentioning

confidence: 99%

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PCB exposure in utero and via breast milk. A review

Dekoning

Karmaus

2000

J Expo Sci Environ Epidemiol

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A review of the literature was conducted to investigate the importance to offspring of in utero and breast milk polychlorinated biphenyl ( PCB ) exposure. All reports that we could identify ( n = 25 ) were included, representing 16 study populations. Tissue -specific PCB concentrations in human placenta, breast milk, maternal blood and cord blood were compared to determine accumulation ratios between tissue compartments. On a lipid basis, the highest concentration of PCB in placenta ( 5027 ng / g fat ) was 2.8 times higher than the highest concentration of PCB in breast milk ( 1770 ng / g fat ) . While there are limitations with regard to quantitation methods and statistical methods utilized by the reviewed studies, our results suggest that PCBs may be capable of crossing the placenta to a greater extent than previously believed. Future studies of PCB body burden in the perinatal period should include placenta, breast milk, maternal and cord blood specimens. In order to compare PCB concentrations in various tissues and with other studies, concentrations should be determined on a lipid basis.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 96%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

PCB exposure in utero and via breast milk. A review

Dekoning

Karmaus

2000

J Expo Sci Environ Epidemiol

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“…Specifically, lindane concentrations in extracted lipids of uteri of pregnant women at term were 2.0 ppm, threefold higher (0.67 ppm) than in adipose tissue and fivefold higher (0.40 ppm) than in maternal blood, showing a significant shift in the distribution of lindane from blood and adipose lipids to uterine lipids during pregnancy (Polishuk et al, 1977). Although limited, these findings indicate that the uterine tissue concentrations of lindane increase during pregnancy, and that concentrations of lindane in blood lipids likely underestimate lipid concentrations in uterus during pregnancy.…”

Section: Discussionmentioning

confidence: 92%

Phospholipase-Mediated Inhibition of Spontaneous Oscillatory Uterine Contractions by Lindane in Vitro,

Wang

Loch‐Caruso

2002

Toxicology and Applied Pharmacology

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Although regulation of uterine contractility is fundamental for parturition, mechanisms by which toxicants modify uterine muscle contractions remain poorly understood. In a previous cumulative concentration-response study, 10 μM lindane (γ-hexachlorocyclohexane) reduced contraction force and 30 μM lindane abolished contractions in Gestation Day 10 rat uterine strips when lindane was added to muscle baths at 10-min intervals. Other studies showed that brief (<10 min) exposures to 10-100 μM lindane inhibit gap junctions and activate phospholipase pathways in rat myometrial cells in culture. Consequently, lindane was used as a prototype toxicant with known uterine activity to investigate the hypothesis that activation of a specific phospholipase pathway provides a mechanistic link between inhibition of uterine contraction and inhibition of myometrial gap junctions. Uterine tissue and cells were pretreated with phospholipase pathway inhibitors to evaluate the role of phospholipase pathways in lindane's actions in the uterus. Concentrations of inhibitors were selected based on previous reports of effective concentrations for the enzyme activity and on pilot toxicity studies of the inhibitors on uterine contraction and gap junction communication. To monitor uterine contractions, longitudinal uterine strips were excised from Gestation Day 10 rats and suspended in isometric muscle baths, consistent with previous experiments. Exposure in vitro for 60 min to 10-50 μM lindane, an effective concentration range for the uterine responses of interest, revealed that 30 μM lindane rapidly abolished contractions. Subsequently, uterine strips were pretreated with phospholipase pathway inhibitors and then challenged with 30 μM lindane, the lindane concentration that elicited maximal inhibition of uterine contraction. Pretreatment with 20-50 μM of the phosphatidylinositol-specific phospholipase C inhibitor 1-O-octadecyl-2-O-methyl-sn -glycerol-3-phosphorylcholine (ET-18-OCH 3 ) reversed lindane-induced inhibition of spontaneous uterine contractions. Gap junction intercellular communication was monitored by injecting the fluorescent dye Lucifer yellow into rat myometrial cells grown in culture and assessing dye transfer to adjacent cells using epifluorescence microscopy. Similar to uterine contraction, pretreatment of cell cultures with phospholipase C inhibitors (30 μM ET-18-OCH 3 , 50 μM tricyclodecan-p-yl-xanthogenate · K [D609] or 50 μM tricyclodecan-p-yl-xanthogenate · K or 2-nitro-4-carboxyphenyl-N,Ndophenylcarbamate [NCDC]) partially reversed inhibition of dye transfer by 100 μM lindane, a 4To whom correspondence and reprint requests should be addressed at 1420 Washington Heights, Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI 48109-2029. Fax: (734) lindane concentration previously shown to abolish myometrial Lucifer yellow dye transfer under similar culture conditions. In contrast, pretreatment with 20 μM of bromoenol lactone (BEL) to inhibit the calcium-i...

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Susceptibility of Children to Environmental Xenobiotics

Woolf¹,

Sandel²

2009

General, Applied and Systems Toxicology

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The growth of interest in paediatric environmental health reflects a widespread recognition that the impact of the environment on children's health is of major importance for this and succeeding generations. Children have a greater vulnerability to the adverse health effects of many environmental toxicants and xenobiotics than do adults, by virtue of their smaller size, increased weight‐adjusted intake of toxicants, developmental differences in body systems and functions, overall physiological and toxicodynamic differences, and differences in the environments they inhabit, the air they breathe, the foods they eat and the behaviours they display every day. The overall impact of such adverse effects of the environment, manifested by subsequent poorer health and the need for costly healthcare services, is amplified by the longer lifespans of children and is associated with intergenerational transmission of harmful effects, to the detriment of mankind. Conversely there is also great potential for averting such harmful effects by improving the quality of the environment and sparing children the consequences of such exposures.

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Organochlorine compounds in mother and fetus during labor

Cited by 64 publications

References 6 publications

PCB exposure in utero and via breast milk. A review

PCB exposure in utero and via breast milk. A review

Phospholipase-Mediated Inhibition of Spontaneous Oscillatory Uterine Contractions by Lindane in Vitro,

Susceptibility of Children to Environmental Xenobiotics

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