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Lindane and Women

Lindane Modification and Uterine Muscle

Pesticides and Breast Cancer Risk, An Evaluation of Lindane (PDF Format)

Breast Cancer

Lindane: Linked to breast and other cancers, has been identified as an endocrine disruptor - a chemical which mimics the female hormone estrogen and causes cancer. Such chemicals have also been linked to fertility problems. bbc

The United Nations is currently considering the elimination or
reduction of twelve of some of the most damaging chemicals that are
Persistent Organic Pollutants (POP) through the formulation of an
international, legally binding treaty. Nine of the POP chemicals under
consideration are pesticides that have been extensively used in both
developed and developing countries. Although many countries have banned
these chemicals, they remain stockpiled, are produced or used illegally, or,
because of lengthy half-lives, they continue to exist in soil, or other
environmental media. In Geneva, this paper instructed both government
delegates and public interest groups about how these chemicals are
particularly injurious to women's bodies.)
Persistent Organic Pollutants & Reproductive Health

TYPE OF TEST : TDLo - Lowest published toxic dose
SPECIES OBSERVED : Human - woman
DOSE : 5 mL/kg
SEX/DURATION : female 18 week(s) after conception
TOXIC EFFECTS : Reproductive - Effects on Embryo or Fetus - fetal death 
REFERENCE : JRPMAP Journal of Reproductive Medicine. (2 Jacklynn Ct., St. Louis, MO 63132) V.3- 1969- Volume(issue)/page/year: 37,992,1993

GEDRI Project: 06915-04

Lindane Modification and Uterine Muscle

The hypothesis of this proposal is that lindane inhibition of gap junctional communication relaxes uterine muscle and interferes with parturition. Additionally, mechanisms of lindane modification of Ca2+ homeostasis will be investigated. Should the gap junction hypothesis be shown to be untenable, the Ca2+ experiments may provide the basis for the alternate hypothesis that lindane-induced changes in Ca2+ homeostasis initiate relaxation of the uterus. The specific aims of the proposal are to: l) Characterize lindane's effects on parturition in rats; 2) Characterize lindane inhibition of rat uterine contractility in vitro; 3) Evaluate mechanisms whereby lindane inhibits gap junctional communication; 4) Evaluate the relationship between lindane-induced inhibition of gap junctional communication and uterine contractility in vitro; 5) Analyze whether inhibition of gap junctional communication in uterine muscle contributes to lindane's observed effects on parturition; and 6) Investigate mechanisms of lindane-induced Ca2+ release from intracellular stores. Identification of the mechanism of lindane inhibition of gap junctional communication should facilitate understanding of the toxicant effects of this pesticide, not only in the reproductive system, but perhaps in other tissues as well. Furthermore, studies of lindane's mechanism of relaxation of uterine contractility may provide insight for new therapeutic approaches to preterm labor.


Studies have demonstrated that g -HCH accumulates in the fatty tissue of pregnant women and can be transferred to the fetus through the placenta and to neonates through the milk (Siddiqui et al. 1981b). Concentrations of g -HCH in human milk have been shown to be approximately five and seven times greater than concentrations in maternal or umbilical cord blood, respectively (Siddiqui et al. 1981b). Data also exist that suggest that the longer the potential exposure to g -HCH, the higher the concentration of g -HCH in the maternal blood system (Saxena et al. 1981a, 1981b). Older women were found to have higher g -HCH levels in the placenta and umbilical cord blood than younger women (Saxena et al. 1983). During pregnancy, higher levels of g -HCH were reported in the fetal blood tissue, uterine muscle, placenta, and amniotic fluid than in maternal adipose tissue. g -HCH levels increased in maternal blood serum during delivery (Polishuk et al. 1977b; Roncevic et al. 1987; Wasserman et al. 1982). Males exposed to HCH in the environment accumulate g -HCH and other HCH isomers in adipose tissue and to a smaller extent in the testes or semen (Szymczynski and Waliszewski 1981, 1983).

Pregnant and/or lactating women should not be exposed to -f -HCH (Ginsburg et al. 1977; Kramer et al. 1980; Solomon et al. 1977a). In pregnant women, g -HCH crosses the placenta. HCH and Y-HCH body tissue levels have also been associated with premature labor and spontaneous abortions (Rasmussen 1980; Saxena et al. 1980, 1981a, 1981b; Wassermann et al. 1982).

Recognition and Management of Pesticide Poisonings

Also see:

Endocrine Disrupting Chemicals



Dioxin Primer



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