s/r home  | issues  | authors  | 7-8 contents
Generations: Reproductive & Developmental
Effects of Organochlorines
by Eric Weltman, The Greens/Green Party USA
Chlorine's most troubling legacy may be the diminished capacity of humans and other species to reproduce. New evidence links organochlorines to decreased sperm count in males, birth defects, the increase in testicular cancer, and other reproductive and development effects.
Startling signs of the problem include:
- The occurrence of ectopic pregnancies (where gestation occurs outside the uterus) increased 400 percent in the US between 1970 and 1987.
- A 1992 study published in the British Medical Journal found that men in western countries today have sperm counts less than half as high as their grandfathers had at the same age.
- The occurrence of cancer of the testicles has increased 3 to 4 times during the past 40 years.
- Various birth defects of the male reproductive system have increased two to four times in this period, including undescended testicles. 
In addition, some scientists believe that the stunning rise in breast cancer incidence may be linked to the same behavior of organochlorines in the body that causes reproductive disorders.
Until recently, government regulators and scientists were preoccupied with the cancer-causing effects of toxic chemicals. Given this focus, other effects—on the immune, reproductive, and nervous systems, for example—have never been studied for most chemicals. In fact, the effects on human reproduction have been estimated for just one percent of the chemicals in commercial use in the United States. 
However, convincing evidence linking reproductive and developmental health effects to organochlorines has emerged from wildlife, human, and laboratory studies. In wildlife, epidemics of reproductive, developmental, and immunological impairment among birds, fish, marine mammals, and reptiles in the Great Lakes, the Baltic Sea, the Wadden Sea, the St. Lawrence River, and the US Pacific Coast have been attributed to organochlorines in the food chain. 
Perhaps the earliest and best known example was the devastating reproductive problems of our national bird, the bald eagle. In the 1960s, the organochlorine pesticide DDT was found to cause eagle eggs to have thin shells and thus crack easily.
Despite the ban on DDT, however, the problem has continued. A recent report by Dr. Theo Colborn, of the World Wildlife Fund, and her colleagues, described the inability of bald eagles in Washington to reproduce after feeding on local fish. The eagles contained up to 10 times as much of the organochlorines DDT, PCBs and chlordane as would allow them to reproduce successfully. As these chemicals have been banned for about 20 years in the US, their presence demonstrates the ability of toxics produced elsewhere to be transported through the atmosphere. 
In the Great Lakes, 14 species of fish, birds, and wildlife near the top of the food chain are experiencing population declines, attributed to reproductive and developmental disorders associated with organochlorine exposure. For example, male herring gulls on Lake Ontario, exposed to DDT and other organochlorines, were found with female sex organs. When gulls eggs were injected with DDT in the laboratory, the male offspring had female sex organs, strengthening the causal link with organochlorines. 
In 1984, a Florida biologist found that in Lake Apopka, 90 percent of the alligator eggs suddenly failed to hatch. The few males that did hatch had phalluses so tiny they were useless for reproduction. Yet, in another nearby lake, the alligators were normal. Researchers concluded that the difference was caused by a 1980 spill of DDE, the breakdown product of DDT, which contaminated the marshland near the Lake Apopka alligators' nests.
The Florida researchers tested their theory by taking alligator eggs from the uncontaminated lake and painting them with DDE. The eggs were maintained in conditions that would normally produce males. Despite this, some of the DDE-painted eggs became females, while other hatched as sexually-abnormal males. 
There is also evidence linking organochlorines with health effects in humans, including testicular cancer, lowered sperm count and birth defects. Farmworkers in the US, England, Wales, Austria, and Sweden have up to a six-fold elevated risk of testicular cancer, according to several studies. Pesticide exposure has been suggested as an important factor. In addition, the risk of testicular cancer among military dogs exposed to Agent Orange in Vietnam is 80% greater than among military dogs that served in the continental US or other parts of Asia. 
New evidence links organochlorines to decreased sperm count in males, birth defects, the increase in testicular cancer, and other reproductive & development effects.
Organochlorines may also be a factor in decreased sperm count in humans. In 1977, male workers at an Occidental Chemical factory making the organochlorine pesticide dibromochloropropane (DBCP) noticed that none of their wives had had any children since the men had begun working with the chemical. Tests revealed that the majority of the men had zero or severely reduced sperm counts, but no other noticeable health effects.  Men with low sperm counts have been found to have significantly higher concentrations of a number of organochlorines in their semen. 
Another study links organochlorines with developmental problems in human infants. The study followed women who, for at least six years preceding their pregnancy, ate 2 to 3 fish a month from Lake Michigan (which is heavily contaminated with organochlorines). Their offspring were found to have lower birth weight, smaller skull circumference and cognitive, motor, and behavioral deficits at birth compared with those whose mothers did not eat fish. 
One hypothesis as to how organochlorines may cause this vast range of effects focuses on their ability to disrupt the hormone, or endocrine system by mimicking or interfering with reproductive hormones. Hormones act as messengers, sending chemical signals that control the way the entire body grows, is organized, and behaves. Scientists have focused on "xeno-estrogens," chemicals which mimic the female sex hormone estrogen, since most industrial chemical endocrine-disruptors mimic estrogen. For example, the structure of DDT and DDE are quit similar to estrogens. In addition, DDE induces enzymes that break down male hormones. 
Scientists use the tragic experience with DES (diethylstilbestrol), a synthetic estrogen given to pregnant women from 1950 through 1970, as model of the impact of xeno-estrogens. Daughters whose mothers took DES suffer reproductive organ disfunction, abnormal pregnancies, a reduction in fertility, and a rare vaginal cancer. Evidence suggests that the sons are at increased risk of testicular cancer, congenital anomalies of the reproductive system, decreased sperm counts, and reduced fertility. According to Dr. Colborn, the reproductive systems appear to be at particular risk for developmental abnormalities in offspring because of maternal exposure to endocrine-disruptors. 
At least 22 organochlorines or groups of organochlorines are known to mimic or interfere with the body's hormones. The total number of organochlorines that disrupt the endocrine system is in the hundreds. Thousands of other organochlorines have not been tested.  One estimate is that 220 million pounds of pesticides which act as endocrine-disruptors are applied to US crops each year. According to one researcher, "Humans now live in an environment that can be viewed as a virtual sea of oestrogens." (Estrogens & oestrogens are the same.) 
As increased exposure to estrogen is a risk factor for breast cancer, some scientists believe that xeno-estrogens may also be contributing to the rapid increase in breast cancer in the United States.  A 1993 study found that breast cancer in American women is strongly associated with DDE in their blood. It should also be noted that breast cancer in women is associated with an increased likelihood of testicular cancer in their sons. 
The concern over the reproductive and developmental health effects of organochlorines is heightened by several factors. The first is the extreme sensitivity of these end-points to dioxin. The second is that both exposure to organochlorines and their health effects are elevated in the womb and just after birth. The third is that current exposure levels of dioxin may be at or near levels where these effects would be expected to be seen.
According to a review draft of EPA's current dioxin health assessment, reproductive and developmental effects may be occurring at levels lower than originally thought to have an adverse effect on animals.  For example, a single, tiny oral dose (0.064 micrograms per kilogram of body weight) of dioxin on day 15 of pregnancy in rats has no effect on the mother, but increases the likelihood of various reproductive disorders in their male offspring, including undescended testicles, smaller testicles, and reduced sperm count.  The EPA also notes that dioxin can disrupt development at a large number of stages.
Many effects of organochlorines are caused by exposures in the womb, which only become apparent after the offspring mature. Organochlorines are fat-soluble, meaning they are stored in the body's fat. Thus, exposure in the womb can result from any exposure during the mother's lifetime when body fat is mobilized during pregnancy or lactation.  According to the EPA, 4 to 12 percent of the entire amount of dioxin that a person receives in their lifetime could come from breast feeding during the first year of life.  This is of concern as endocrine-disruptors cause particular trouble during the critical period of development before and immediately after birth. 
The EPA has stated in no uncertain terms that the threat is not only real, it is close to, if not already, being realized. According to Lynn Goldman, EPA's Assistant Administrator for Prevention, Pesticides, and Toxics, "We can infer from the data that average everyday exposures [to dioxin] are close to exposures known to cause [non-cancer effects] in laboratory animals." In other words, the time to study has past; the time to act has begun.
1] Rachel's Hazardous Waste News No. 343, June 24, 1993. [RHWN]
2] "The Reproductive Hazards of Industrial Chemicals," Sarah Sexton, The Ecologist, November/December 1993, p. 212.
3] Chlorine, Human Health, and the Environment: The Breast Cancer Warning, Joe Thornton, Greenpeace, October 1993, pp. 42, 43, 45, 48.
4] RHWN No. 365, November 25, 1993.
5] RHWN No. 264, December 18, 1991.
6] "Scientists probe role of estrogen mimics in the environment," Judy Foreman, Boston Globe, January 17, 1994, p. 42.
7] "Development Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans," Theo Colborn, Frederick S. vom Saal, and Ana M. Soto, Environmental Health Perspective, October 1993.
8] Estimate by Richard Wiles, Environmental Working Group, cited in "The Chlorine-Breast Cancer Link," E. Weltman, Multinational Monitor, Jan/Feb 1994, p. 11.
9] RHWN No. 334, April 22, 1993.
10] Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) & Related Compounds: Review Draft, Volume III, EPA, Aug 1994.
11] "Fetal Harm, Not Cancer, Is Called The Primary Threat From Dioxin," Keith Schneider, New York Times, May 11, 1994, p. A1.