Reproductive Effects of Halogenated Aromatic Hydrocarbons on Nonhuman Primates*

Allen, James; Barsotti, D.A.; Lambrecht, Linda K.; Miller, John P.

doi:10.1111/j.1749-6632.1979.tb56623.x

Cited by 126 publications

(29 citation statements)

References 9 publications

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“…The highest relative risk for the offspring of the sawmill cohort was an OR of 5.68 when the interquartile range of exposure during spermatogenesis was used. Organs and tissues that originate from embryonic ectoderm have previously been shown to be targets for toxicity following exposure to dioxin-contaminated halogenated aromatic hydrocarbons (24). Differentiated tissues derived from ectoderm include skin, eyes, conjunctiva, nails, hair, and the central and peripheral nervous systems.…”

Section: Discussionmentioning

confidence: 99%

Reproductive effects of paternal exposure to chlorophenate wood preservatives in the sawmill industry

Dimich‐Ward¹,

Hertzman²,

Teschke³

et al. 1996

Scand J Work Environ Health

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Objectives The purpose of the study was to determine whether paternal occupational exposure to dioxincontaminated chlorophenols is associated with an increased risk of congenital anomalies or other adverse reproductive outcomes in offspring. Methods As a result of a multistep linkage, 19 675 births between 1952 and 1988 were identified as children of a cohort of 9512 fathers who had worked at least one year in British Columbia sawmills where chlorophenate wood preservatives had been used. A nested case-referent analysis was applied, using conditional logistic regression, with five referents matched per case according to year of birth and gender. Chlorophenate exposure was based on expert raters' estimations of hours of exposure applied to specific time windows prior to birth. Results The offspring of male sawmill workers were at increased risk for developing congenital anomalies of the eye, particularly congenital cataracts; elevated risks for developing anencephaly or spina bifida and congenital anomalies of genital organs were shown according to specific windows of exposure. No associations were found for low birthweight, prematurity, stillbirths, or neonatal deaths. C O~C~U S~O~S The study adds further support to the hypothesis of male-mediated developmental toxicity. Paternal exposure to chlorophenates was associated with the development of certain congenital anomalies in offspring.

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Section: Discussionmentioning

confidence: 99%

Reproductive effects of paternal exposure to chlorophenate wood preservatives in the sawmill industry

Dimich‐Ward¹,

Hertzman²,

Teschke³

et al. 1996

Scand J Work Environ Health

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show abstract

“…Animal experimentation has demonstrated that, based on the minimal effective carcinogenic dose, TCDD is the most potent animal carcinogen yet discovered (31). There is mounting experimental evidence suggesting that TCDD may affect human fertility, because it is associated with anovulation and dysfunctional spermatogenesis in primates and other animals (32)(33)(34)(35). Developmental anomalies in infants may arise as a result of exposure via breast milk (36).…”

Section: Discussionmentioning

confidence: 99%

The Drug Salicylamide Is an Antagonist of the Aryl Hydrocarbon Receptor That Inhibits Signal Transduction Induced by 2,3,7,8-Tetrachlorodibenzo- p -dioxin

2004

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ABSTRACT2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant, that has been linked with a variety of deleterious effects on human health, including increased cancer rates and reproductive anomalies. The detrimental effects of TCDD are mediated via the aryl hydrocarbon receptor (AhR), a transcription factor that regulates the expression of the carcinogen-activating enzymes cytochromes P-450 (CYP) 1A1, 1A2, and 1B1. In the present study, we examined the ability of synthetic derivatives of salicylic acid to affect TCDD-stimulated AhRmediated signal transduction in human hepatoma HepG2 cells. Salicylamide (SAL), an analgesic drug, caused a potent and long-lasting inhibition of TCDD-induced CYP enzyme activity. Acetylsalicylic acid (aspirin) and the naturally occurring phytochemical salicylic acid had no effect on CYP activity. SAL inhibited the increase in CYP1A1, -1A2, and -1B1 mRNA levels that occurs on exposure to TCDD. TCDD-induced transcription of these genes was also inhibited by SAL, but not by aspirin or salicylic acid, as demonstrated by luciferase reporter assays. The transcription of the CYP1 family of genes is regulated by the interaction of TCDD-activated AhR with the xenobiotic-responsive element present in the promoter regions of these genes. As shown by electrophoretic mobility shift assay, SAL completely blocked the binding of TCDD-activated AhR to the xenobiotic responsive element. Also, SAL substantially blocked the binding of TCDD to the cytosolic AhR. These results demonstrate that SAL, a commonly used analgesic, is a potent inhibitor of AhR-mediated signal transduction, and may be an effective agent in the prevention of TCDD-associated disease.

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“…Decreases in serum estradiol and progesterone were reported in rhesus monkeys exhibiting reproductive dysfunction, following exposure to 2,3,7,8-TCDD (500 ppt in the diet for 7 months) (52) and polybrominated biphenyls (53). Exposure to Aroclor 1248 at doses of 2.5 and 5.0 ppm in the diet caused prolonged menstrual cycles and decreased peak progesterone levels in female rhesus monkeys (54). Aroclor 1242 caused an increase in basal leutinizing hormone and follicle-stimulating hormone secretion by the pituitary in rats (55 ).…”

Section: Estrogen Receptor-mediated Effectsmentioning

confidence: 99%

Characterization of Potential Endocrine-Related Health Effects at Low-Dose Levels of Exposure to PCBs

Brouwer¹,

Longnecker²,

Birnbaum³

et al. 1999

Environmental Health Perspectives

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This article addresses issues related to the characterization of endocrine-related health effects resulting from low-level exposures to polychlorinated biphenyls (PCBs). It is not intended to be a comprehensive review of the literature but reflects workshop discussions. "The Characterizing the Effects of Endocrine Disruptors on Human Health at Environmental Exposure Levels," workshop provided a forum to discuss the methods and data needed to improve risk assessments of endocrine disruptors. This article contains an overview of endocrine-related (estrogen and thyroid system) interactions and other low-dose effects of PCBs. The data set on endocrine effects includes results obtained from mechanistic methods/ and models (receptor based, metabolism based, and transport protein based), as well as from in vivo models, including studies with experimental animals and wildlife species. Other low-dose effects induced by PCBs, such as neurodevelopmental and reproductive effects and endocrine-sensitive tumors, have been evaluated with respect to a possible causative linkage with PCB-induced alterations in endocrine systems. In addition, studies of low-dose exposure and effects in human populations are presented and critically evaluated. A list of conclusions and recommendations is included.

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Reproductive Effects of Halogenated Aromatic Hydrocarbons on Nonhuman Primates*

Cited by 126 publications

References 9 publications

Reproductive effects of paternal exposure to chlorophenate wood preservatives in the sawmill industry

Reproductive effects of paternal exposure to chlorophenate wood preservatives in the sawmill industry

The Drug Salicylamide Is an Antagonist of the Aryl Hydrocarbon Receptor That Inhibits Signal Transduction Induced by 2,3,7,8-Tetrachlorodibenzo- p -dioxin

Characterization of Potential Endocrine-Related Health Effects at Low-Dose Levels of Exposure to PCBs

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