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17.4.2 Activational Toxicity
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Estrogenic Pharmaceuticals. Administration of estrogenic pharmaceuticals to children or adults can result in a variety of abnormalities associated largely with secondary sex characteristics that are reversible upon cessation of drug treatment. Gynecomastia, the development of breast tissue in males, is often the consequence of perturbations in the normal androgen/estrogen ratio. As discussed earlier in this chapter, prolonged administration of drugs with estrogenic or antiandrogenic activity can cause gynecomastia. Gynecomastia had been reported in the medical literature
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INCIDENTS OF ENDOCRINE TOXICITY
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to occur as a result of frequent intercourse when an estrogen-containing cream was used as a vaginal lubricant and among morticans who applied estrogen-containing skin creams to corpses without the use of gloves. Similar to gynecomastia in adult males, activational toxicity from estrogenic drugs has been reported to cause pseudoprecocious puberty in children. Pseudoprecocious puberty is characterized by the development of some indicators of puberty (pubic or facial hair, morphological changes in sex organs, breast development, etc.) in preadolescent individuals. An outbreak of pseudoprecocious puberty was reported among a group of children ranging in age from 4 months to 2 years of age following application of a skin cream to treat dermatitis. Symptoms included pigmentation of the nipples, breast development, the presence of pubic hair, and vaginal discharge and bleeding among the females. Breast development also was reported in prepubertal boys following use of an estrogen-containing hair cream. These reports highlight the fact that dermal exposure can be adequate to attain a suf cient dose of endocrine-active compound to elicit adverse responses. In all of these cases the symptoms of endocrine toxicity resolved following cessation of exposure to the causative agent.
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Environmental Estrogens. Thelarche is de ned as the development of breast tissue in preadolescent females (typically <8 years of age). Since 1979 physicians have monitored an epidemic level of thelarche on the island of Puerto Rico. The cause of thelarche in Puerto Rico is not known; however, evidence strongly implicates exposure to endocrine-disrupting agents. Analyses of blood samples from thelarche and nonthelarche children for environmental chemicals with known estrogenic activity revealed that 68% of the thelarche children contained signi cantly high levels of several types of phthalate esters. Only a single nonthelarche child contained a signi cant amount of phthalate ester and only one type of phthalate ester was found in this individual. Phthalate esters are used as plasticizers and are ubiquitous environmental contaminants. They have been shown to cause a variety of endocrine-related effects in animal models and some phthalate esters have been shown to be estrogenic in vitro. The association between phthalate ester exposure and the high incidence of thelarche in Puerto Rico does not establish causality but has generated concern that environmental agents are responsible for this condition. Kepone (chlordecone) is an organochlorine insecticide (Figure 17.5) that was manufactured in Hopewell, Virginia, from the mid-1960s to 1975. In 1975 the Center for Disease Control determined that employees of the manufacturing facility and other residents of Hopewell, totaling over 200 individuals, had been signi cantly contaminated with this insecticide. Exposed individuals reported a variety of symptoms. Foremost, among the symptoms of Kepone sickness were neurological disorders presenting as tremors, weight loss, and nervousness. However, subsequent evaluations revealed that males exposed to Kepone also experienced testicular dysfunction that was characteristic of estrogen exposure. Later laboratory studies demonstrated that Kepone was an estrogen receptor agonist, which could explain its adverse effects on the male reproductive system.
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Hypothyroidism
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Hypothyroidism describes the clinical state arising from a de ciency in thyroid hormone. Toxicity resulting in hypothyroidism is manifested at several organ systems as
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ENDOCRINE SYSTEM
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Table 17.4 Clinical Manifestations of Hypothyroidism Organ System Skin Cardiovascular Respiratory Digestive Muscle Nervous Manifestation Puffy appearance, dry, course, yellow-tinted skin brittle nails, wound healing slowed, hair loss Enlarged heart, changes in electrocardiographs Maximal breathing capacity reduced, obstructive sleep apnea, uid accumulation in the pleural cavity Reduced appetite with modest weight gain Stiffness, aching Slowing of intellectual functions, lethargy, headaches
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described in Table 17.4, and individual effects may be misdiagnosed as organ-speci c toxicity. Hypothyroidism can result from various causes other than chemical toxicity including diseases of the hypothalamic pituitary thyroidal axis, iodine de ciency, and heritable defects in thyroid hormone production. Chemical agents that have historically been recognized for their ability to cause hypothyroidism include phenylbutazone, resorcinol, lithium, and para-aminosalicylic acid. Disruptions in thyroid hormone levels can occur through chemical-induced increases in the metabolic inactivation and elimination of the hormone. Chemicals that are capable of increasing the metabolic clearance of thyroid hormone include the polycyclic halogenated hydrocarbons (i.e., dioxins, furans, polychlorinated biphenyls, polybrominated biphenyls). A study reported in the New England Journal of Medicine suggested that environmental or occupational exposure to such chemicals can result in hypothyroidism in humans. The study consisted of a comparison of thyroid status in workers who were occupationally exposed to polybrominated biphenyls as compared to workers who were not exposed to any polyhalogenated hydrocarbons. Four of 35 exposed workers and none of 89 unexposed workers exhibited signs of hypothyroidism that included increased plasma levels of thyrotropin and decreased plasma levels of thyroxine. Thyrotropin is secreted by the pituitary gland and stimulates the thyroid gland to produce thyroxine (see Figure 17.1). The increase in thyrotropin and decrease in thyroxine is consistent with hypothyroidism caused by increased clearance of the thyroxine. As discussed earlier in this chapter, perinatal exposure to PBBs during the Michigan milk contamination also produced symptoms characteristics of hypothyroidism.
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