Birth Defects Caused by Herbicides, Insecticides, and Industrial Chemicals that Disrupt the Endocrine System
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Birth Defects Caused by Herbicides, Insecticides, and Industrial Chemicals that Disrupt the Endocrine System

The endocrine system is one of three main regulating systems in the body, along with the nervous and immune systems. It consists of various organs known as the endocrine glands and includes the ovaries, the testes, and the adrenal, thyroid and pituitary glands. These glands release hormones, such as estrogen, testosterone or adrenaline, into the bloodstream, which deliver chemical messages to distant cells, to regulate diverse functions including reproduction, development, and metabolism.

Endocrine disruption occurs when a chemical interferes with the function of natural hormones in the body, for example by mimicking a hormone, blocking its effects, or stimulating or inhibiting the endocrine system.

Endocrine disruption leads to carcinogenic, reproductive and developmental effects. Potential reproductive effects include disruption of ovarian function, reduced sperm production, and reduced fertility. Potential developmental effects include low birth weight and birth defects.

In 1995, public and private entities released 60 million pounds of suspected endocrine-disrupting chemicals in the US. Significant sources of exposure are daily exposure to industrial chemicals at work, drinking water; contaminated food (fish, meat, and produce in particular); and, for children pesticide ingestion from lawns and rugs, in addition to traces of endocrine disruptors that are present in plastic toys and metal food cans.

Scientific research confirms that human health is impacted by these herbicides, insecticides, and industrial chemicals.

Dangerous herbicides include 2,4-D, 2,4,5-T, alachlor, amitrole, atrazine, metribuzin, nitrofen, trifluralin, fungicides, benomyl, hexachlorobenzene, mancozeb, maneb, metiram-complex, tributyl tin, zineb, and ziram.

The endocrine disrupting insecticides are HCH, carbaryl, chlordane, dicofol, dieldrin, DDT and metabolites, endosulfan, heptachlor and h-epoxide, lindane 1-HCH, methomyl, methoxychlor, mirex, oxychlordane, parathion, synthetic pyrethroids, toxaphene, and transnonachlor/ The nematocides include aldicarb, and DBCP.

Industrial chemicals to be avoided are: cadmium, dioxin (2,3,7,8-TCDD), lead, mercury, PBBs, chlorinated hydrocarbons, solvents, PCBs, pentachlorophenol (PCP), penta-tononylphenol, phthalates, and styrenes.

The Illinois EPA reports the following as known hormone disruptors: atrazine, chlordanes, chlordecone (kepone), DDD, DDE, DDT, 1,2-dibromo-3-chloropropane, dicofol (kelthane), dieldrin, diethylstilbestrol (DES), dioxins (2,3,7,8-), endosulfans, furans (2,3,7,8-), lindane, methoxychlor, p-nonylphenol, PCBs, toxaphene and tributyl tin.

The history of DES is instructive. From 1945 to 1971, doctors prescribed the drug diethylstilbestrol (DES) to an estimated five million pregnant women in the US. Now recognized as a potent endocrine disruptor capable of distorting fetal development, doctors originally encouraged pregnant women to take DES to prevent miscarriages. In the early-1970's, doctors began to notice reproductive abnormalities in the sons and daughters of DES mothers. Specifically, DES daughters exhibited malformed reproductive organs and reduced fertility, and experienced a high incidence of ectopic pregnancies, miscarriages, and premature births. DES sons suffered from small and undescended testicles, hypospadias, and abnormal semen (Schettler 1996). The DES experience suggests that fetal exposure to endocrine disruptors can cause long-term adverse health effects in humans.

The DES case and research conducted by Theo Colborn, a senior scientist for the World Wildlife Fund, suggest that the embryo is the most sensitive life stage of animals and humans to the hazards posed by endocrine disruptors. Hormones released by the endocrine system play a critical role in embryonic development and early fetal exposure to endocrine disruptors can lead to major structural changes in the genital tract, including abnormal cell growth. These changes typically go unnoticed until maturity, when the effects are often irreversible.

Endocrine disruption may occur at extremely minute chemical doses, even at levels 100 times lower than those associated with appreciable cancer risks (Mitchell 1997). Frederick vom Saal , a biologist at the University of Missouri, argues that endocrine disruptors defy the dose-response paradigms applied to toxic and carcinogenic chemicals: the response function is shaped like an upside-down U (Lutz 1996).

The EPA has banned in the U.S. the use of the following chemicals suspected of endocrine disruption: PCBs, chlordane, DDT, aldrin, dieldrin, endrin, heptachlor, kepone, toxaphene, and 2,4,5-T.

But true to EPA bias that chemicals are safe, until proven otherwise, the EPA's official position is that "with few exceptions (e.g., DES, dioxin, DDT/DDE), a causal relationship between exposure to a specific environmental agent and an adverse effect on human health operating via an endocrine disruption mechanism has not been established." US Environmental Protection Agency, Special Report on Environmental Endocrine Disruption: An Effects Assessment and Analysis, Prepared for the Risk Assessment Forum, US Environmental Protection Agency, Washington, DC., February 1997.

The developmental effects of toxic exposures to these chemicals include fetal death, altered growth, and both structural and functional birth defects.

Structural developmental defects are deformities that are visible, or detectable by physical examination or autopsy. Functional developmental defects occur when organs that may appear normal nonetheless work abnormally, such as reduced IQ.

Congenital anomalies are abnormalities present at birth. There are over 200 separate congenital anomalies, ranging from purely cosmetic to generally fatal. Some defects can be corrected with surgery and rehabilitation early in life, while others cause permanent disability.

According to US health statistics, congenital anomalies are the leading reported cause of infant mortality. The National Center for Health Statistics (NCHS) reports that in 1991 congenital anomalies caused 21 percent of infant deaths. Infant deaths due to congenital anomalies account for over five percent of all potential life years lost before age 65, according to Waitzman, Scheffler and Romano (1996). These figures are significant given the extremely low incidence of birth defects.

Congenital anomalies remain a leading cause of death throughout childhood, accounting for 13 percent of deaths between ages one and four years, and five percent of deaths at ages five to fourteen

In addition to premature mortality, congenital anomalies cause early death and permanent disability, resulting in higher medical expenses, and the cost of special education and rehabilitation. These financial costs are accompanied by the pain and suffering of the individual and his or her family.

The median birth weight in the US has been quite constant in recent years, at 7 pounds, 7 ounces or about 3375 grams (US DOC 1995, Table No. 96). Infants weighing less than 2500 g (5 lbs., 8 oz., about 75 percent of the median) at birth have low birth weight. The low birth weight class includes newborns weighing less than 1500 g (very low birth weight), which in turn includes those weighing less than 1000 g (extremely low birth weight).

Low birth weight is more common than congenital anomalies. Seven percent of live births in 1991 were infants with low birth weight. The condition occurs more frequently among infants born to mothers who are African-American, or have low income and education. For example, black mothers are 2.3 times as likely as white mothers to give birth to a low birth weight infant.

Infant mortality ratios for low birth weight are larger than for some congenital anomalies. Low birth weight infants are 19 times more likely to die before their first birthday than are infants weighing 2500 g or more at birth. This excess mortality is highly concentrated among infants with very low birth weight. Newborns weighing between 1500 g and 2499 g are 5.7 times more likely than heavier newborns to die within a year, but very low birth weight infants are 78.5 times more likely to die. Although fewer than 20 percent of low birth weight infants weigh less than 1500 g at birth, this group accounts for over 75 percent of deaths among low birth weight infants.

Low birth weight often is associated with short gestation, which itself is a significant risk factor for infant mortality, with a mortality ratio of 12.8. Disorders related to short gestation and low birth weight are the fourth leading cause of infant mortality, after congenital anomalies, sudden infant death syndrome, and respiratory distress syndrome (US DOC 1995, Table No. 122). Low birth weight appears to exert a substantial influence on infant mortality independently of effects of short gestation. Among newborns with a gestational age of less than 37 weeks, for example, those weighing less than 2500 g at birth face a risk of infant mortality 10.2 times larger than their heavier counterparts.

Low birth weight is less closely linked to mortality and disability throughout life than are congenital anomalies. But some low birth weight survivors experience continued disadvantages, ranging from greater morbidity (Lewit et al. 1995) to greater chances of preschool developmental delays, enrollment in special education, and grade repetition (Chaikind and Corman 1991, Corman and Chaikind 1993). Persons of low birth weight and their families may experience significant financial and nonfinancial burdens during the first year of life as well as in later years.

Observed adverse effects in aquatic life and wildlife exposed to endocrine disruptors include abnormal thyroid function and low birth weight. Scientists know that the thyroid gland and the hormones it produces contribute to body growth. In fish having a bony skeleton (teleosts), for example, skeletal growth is "particularly sensitive to the state of the thyroid gland" (US EPA 1997). Targeted scientific research indicates possible links between pesticide exposure and reduced birth weight in various fish and bird species, and between PCB exposure and reduced birth weight in monkeys and rats (Schettler et al. 1996).

Two scientific studies suggest a potential link between maternal exposure to endocrine disruptors and an increased incidence of low birth weight in humans. The first study examined mothers living in Michigan who ate two or three meals of Great Lakes fish a month in the six years prior to pregnancy (Jacobson et al. 1984). Great Lakes fish in the 1970s and early-1980s contained significant levels of PCBs and other contaminants currently suspected of endocrine disruption. Since PCBs bioaccumulate in human body fat, the mothers unknowingly passed the harmful contaminants on to their babies through the placenta during pregnancy and through breast milk during infancy. Jacobson et al. observed evidence of a direct correlation between maternal fish consumption and birth weight: the higher the mother's consumption of Lake Michigan fish, the lower the infants birth weight. The study found that exposed infants weighed 190 g to 250 g less than normal infants at birth, and had a gestational age six to 12 days shorter than that of normal infants.

The second study examined women employed by either of two capacitor manufacturing facilities in New York between the years 1946 and 1975 (Taylor et al. 1989). Employees worked with PCBs in the manufacturing process and regularly experienced air and/or dermal contact exposures. Taylor et al. observed small decreases in birth weight in relation to increasing levels of PCB exposure. The authors note, however, that while these results may suggest a causal link between maternal PCB exposure and reduced birth weight, the exposed infants investigated in this study had a healthy mean birth weight of 3,300 g.

In light of the reproductive effects of endocrine disruptors affect males and females in different ways.

Health effects observed in males during recent years, which are believed to be be linked to endocrine disruptors, include: cryptorchidism (undescended testicles), decreased sperm count, reductions in sperm motility (forward motion of the sperm) and morphology (percentage of sperm having a normal shape), hypospadia (abnormal urethral opening), and shortened penis size (US EPA 1997). Great Britain, for example, has reported a doubling of both cryptorchidism and hypospadia among males between 1970 and 1987 (Burger 1996).

Reductions in sperm count present the greatest threat to male reproductive health. Canadian doctors consider sperm counts of 30 million/mL to 100 million/mL as normal, with most men producing about three milliliters of seminal fluid per ejaculation (Nichols 1996). Danish scientists who have analyzed 61 sperm count studies published between 1938 and 1991 (Carlsen et al. 1992) have found a significant decrease in mean sperm count, from 113 million/mL in 1940 to 66 million/mL in 1990. In addition they found a decrease in seminal volume, from 3.40 mL to 2.75 mL per ejaculation (Auger et al. 1995; Irvine et al. 1996). The EPA's position is that a causal link between the possible reduction in sperm counts and environmental endocrine disruptors has not been established.

Health effects observed in females during recent years, which are believed to be linked to environmental endocrine disruptors, include: reduced fertility, irregular menstrual cycles, altered ovarian function, endometriosis (reproductive disease leading to pelvic and menstrual discomfort, and infertility), and complicated pregnancies (e.g., miscarriage) (US EPA, 1997). The US, for example, reported a 400 percent increase in ectopic pregnancies (formed in the fallopian tubes) among women between 1970 and 1987 (Burger, 1996). Aside from the work on DES, however, only a limited number of endocrine disruption studies evaluate reproductive function in females.

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