Northwest Coalition for
Alternatives to Pesticides
This report is published by the Northwest Coalition for Alternatives to Pesticides. NCAP is a nonprofit, five-state regional organization that promotes sustainable resource manage-ment, prevention of pest problems, use of alternatives to pesticides, and the right to be freefrom pesticide exposure. NCAP strives to substantially reduce or eliminate the use of pesti-cides as a preferred method of pest control in the Northwest and elsewhere.
This report was made possible by the generous support of the Aurora Foundation. It first appeared in the Spring 1996 issue of the Journal of Pesticide Reform and was written byCaroline Cox.
NCAPNorthwest Coalition for Alternatives to PesticidesP.O. Box 1393Eugene, OR 97440Phone: (541) 344-5044Fax: (541) 344-6923e-mail: [email protected] The photograph on the front cover of this report was taken by Lise Beane from the Women’s Community Cancer Project (Boston, Massachusetts). The photograph shows par-ticipants at the Massachusetts Breast Cancer Coalition’s Stop the Epidemic March and Rallyin 1994.
The illustration on page 4 is by Kate Pryka.
Table of Contents
Executive Summary
Chapter 1
Evidence of a Link
Chapter 2
Understanding How DDT Increases Breast Cancer Risk 4
Chapter 3
Policy Recommendations
Chapter 4
Currently Used Pesticides Linked to Breast Cancer
Northwest Coalition forAlternatives to Pesticides Breast cancer is a disease whose frequency has been increasing
in the U.S. for the last forty years. Recent research indicates that
we have an opportunity to prevent some of this disease.

A series of studies has shown that women who have been exposed
to higher levels of the organochlorine insecticide DDT have a risk
of breast cancer that is between two and four times the risk of
cancer in women with lower exposures.

Laboratory studies indicate that DDT and its breakdown products
promote the formation of a hormone, nicknamed “bad” estrogen,
that is linked with breast cancer.

This research gives us the opportunity to set policies that will
reduce our risk of breast cancer:

We need to reduce our exposure to DDT and related chemicals,
and stop using other pesticides that cause breast cancer in
laboratory tests. The herbicide atrazine is particularly important:
it is nearly as potent as the most potent breakdown product of
DDT in promoting formation of the “bad” estrogen, is one of the
most widely used pesticides in the U.S., and has extensively
contaminated U.S. wells and rivers.

We need to support farmers as they develop and implement
successful and cost-effective alternative pest management

Our emphasis must be on preventing breast cancer.
P.O. Box 1393Eugene, OR 97440(541) 344-5044 CHAPTER 1
Cancer is a word that strikes fear in the hearts of most Americans. Most of us have
either struggled with the disease or know and love someone who has. It’s a mysterious disease, and often invisible. It requires treatments that seem worse than the disease itself. It strikes Increase in Breast Cancer
people who are healthy in other ways and often robs them of years of life.
Breast cancer is no different. Over 180,000 U.S. women are diagnosed with breast cancer every year;1 it is the most prevalent cancer in U.S. women.2 Over the last two decades, the incidence of breast cancer has increased at a rate of nearly 2 percent per year.3 (See Figure 1.)In 1940, a women’s lifetime risk of breast cancer was 1 in 16; that figure has now risen to 1 in No one should live in fear. What is needed instead is a good hard look at the causes of breast cancer so that as individuals, as a country, and as a planet we can make changes in ourpersonal habits and in our country’s pesticide policies that will prevent this terrible disease.
This report looks at the evidence scientists have recently collected that indicates pesticidesmay cause breast cancer, and the implications this research has for pesticide policy.
A series of studies completed in the last five years has showed an association between breast cancer risk and a woman’s exposure to organochlorine insecticides. These studies are what’s known as epidemiology. They are not controlled laboratory studies; instead they attempt tocorrelate real-life exposures and cancer risks.
The first well-publicized study was done in Israel by two scientists, Jerome Westin and Elihu Richter, at the Hebrew University School of Medicine.5 They were interested in what they call the “Israeli breast-cancer anomaly.” During the late 1970s and early 1980s, Israel’s breast cancer rate, particularly in young women, was much higher than that of other coun-tries. While data from most countries showed there was a strong association between the amount of fat in a typical diet and the incidence of breast cancer among young women, data from Israel indicated there was about twice as much breast cancer as might be expected from atypical Israeli diet. Remarkably, this high rate of breast cancer dropped significantly between Source: Adamson, R.H. 1993. Statement before the Subcommittee on Health and 1976 and 1986, a time when breast cancer rates were rising in most other countries.
the Environment, Committee on Energy and Commerce. U.S. House of Westin and Richter looked at a number of the factors that are usually associated with Representatives. Washington, D.C. (Oct. 21.) breast cancer risk and found that they had changed during this period of time, but in such away that the changes should have resulted in more breast cancer, not less.
Then they looked at levels of three organochlorine insecticides in milk: DDE (a major metabolite of DDT), lindane, and α-HCH (α−hexachlorocyclohexane, a chemical relative oflindane also known as α−benzene hexachloride). In the mid-1970s, Israeli milk had some ofthe highest levels of these insecticides in the world; mean levels were 5 to 100 times greaterthan those found in U.S. milk at the time. Israeli women also had higher levels of theseinsecticides in their breast milk. In 1978, “public outcry followed by the threat of SupremeCourt action resulted in the banning first of alpha-BHC, then of lindane, from the cowshed.”Contamination levels in cow and breast milk dropped precipitously (up to 98 percent) by1980. Westin and Richter believed that the drop in breast cancer resulted from this decline.
A 1990 study from Finland also showed a relationship between organochlorine insecticides and breast cancer. Dr. Mussalo-Rauhamaa and his co-workers found that tissue from 40breast cancer patients had higher levels of the organochlorine insecticide β-HCH than tissuefrom women without breast cancer. DDD and DDT levels did not differ.6 In 1992, Frank Falck, a doctor at the University of Michigan, and his co-workers com- pleted a pilot study of the relationship between pesticides and breast cancer in the U.S.2 Thestudy looked at the levels of six organochlorine compounds in breast fat tissue taken fromwomen who were undergoing surgical biopsies of suspected breast cancer or mastectomies.
Levels in 20 women who were diagnosed with breast cancer were compared with levels in 20women who were diagnosed with benign breast disease.
The study found that average concentrations of DDE and DDT were from 50 to 60 percent higher (almost 1900 parts per billion (ppb) compared to about 1200 ppb) in womenwho had breast cancer. They calculated that a 10 ppb increase in the DDE concentration ofbreast fat corresponded to a 1 percent increase in breast cancer risk.
One of Falck’s co-workers, Mary Wolff from New York’s Mount Sinai School of Medi- cine, went on to lead a more in-depth study of the relationship suggested by the Falck study.7From over 14,000 participants in a women’s health study conducted by New York University,they selected 53 who had been diagnosed with breast cancer within six months of joining thestudy. (The study enrolled women between 1985 and 1991.) They used blood samples thathad been frozen and stored since the beginning of the study and compared organochlorinelevels in the blood of these 53 women to those of 173 study participants who did not developbreast cancer.
The results of the study supported the results of the Falck study: DDE levels were about 35 percent higher in women who were later diagnosed with breast cancer. Wolff calculated thateach 0.1 ppb increase in DDE levels in blood resulted in a 0.9 percent increase in breastcancer risk. Blood levels of DDT-related compounds are about 200 times less than levels infat tissues because they are stored most readily in fat tissue.8 This means these results aresimilar to those of the Falck study.7 Wolff also collaborated on a larger study that was completed in 1994.9 Led by Nancy Kreiger from the Kaiser Foundation Research Institute in California, the study made use of acollection of over 50,000 frozen blood samples that had been collected by the Kaiser PermanenteMedical Care Program as part of in-depth health examinations between 1964 and 1969.
Kreiger’s study looked at organochlorine levels in the blood samples of 150 women who werediagnosed with breast cancer following their exam, but before 1991. Each breast cancerpatient was matched with a control patient, a patient not diagnosed with breast cancer, andthe organochlorine levels compared. The study was designed to look for potential differencesbetween racial groups, so equal numbers of white women, black women, and Asian womenwere studied.
Blood levels of DDE were much higher than those measured in the earlier U.S. studies.
These high levels occurred because body burdens were much higher when these samples werecollected (in the late 1960s), since DDT was still being used in the U.S.9 Overall, the studyfound no differences in DDE levels between women who were diagnosed with breast cancerand women who were not. In white women and black women, however, the risk of breastcancer was between 2 and 4 times as great for women who had the highest DDE levels ascompared to women with the lowest DDE levels.10 (It should be noted that the difference wasnot statistically significant.) Asian women typically have very different breast cancer risks thanother ethnic and racial groups; researchers believe that their diets may lower their risk.1 Theincrease in risk in white and black women was about the same size as that measured in theearlier Falck and Wolff studies.9 A recent study from Quebec, Canada, also found a relationship between breast cancer and DDT. Dr. Eric Dewailly and coworkers found that levels of the DDT breakdown productDDE were three times higher in 9 women with hormone responsive breast cancer than in 17women with benign breast disease.11 Overall, how much does DDT exposure increase a women’s risk of breast cancer? The relative risks calculated in these studies for women with the highest DDT exposure arebetween 2 and 10. This means that their risk of breast cancer is between 2 and 10 times therisk faced by a women with low DDT exposure. These risks, when compared to other knownrisk factors for breast cancer, are “among the higher risks for breast cancer observed in theepidemiologic literature.”12 CHAPTER 2
Taken as a whole, these epidemiological studies provide evidence that there is a strong association between a woman’s exposure to certain organochlorine insecticides, particularlyDDT, and her risk of breast cancer. Epidemiology, however, is not able to provide answers toquestions about cause and effect; there is always the possibility that DDT exposure did notcause the increased breast cancer risk. Instead, both high DDT levels and cancer risk might becaused by an unknown or unstudied third factor. Only a controlled experiment is able toestablish a cause. Obviously, a controlled experiment exposing women to organochlorinesintentionally to determine breast cancer risk is out of the question.
So scientists next look to see if there is a realistic mechanism that can explain how DDT might cause breast cancer. If a sound mechanism is documented, the mechanism (togetherwith the association provided by the epidemiology) provides strong support for the hypothesisthat increased DDT exposure causes an increased risk of breast cancer.
When scientists began looking for a mechanism by which exposure to DDT could increase breast cancer risk, the group of hormones known as estrogens seemed a likely place to start.1Estrogens are produced mainly by women’s ovaries and are responsible for the developmentand maintenance of secondary sexual characteristics and behavior. For example, women’smenstrual cycles are regulated by rising and falling levels of several hormones. Estrogens referto a whole family of compounds; one potent estrogen produced by women is called estra-diol.13 Most of the known risk factors for breast cancer involve in one way or another an increase in the amount of estrogen, primarily estradiol, to which a woman is exposed during herlifetime. These include such factors as age (older women, who have had a higher totalexposure to estrogen, have a higher risk of breast cancer than younger women), an early onsetof menstruation (estrogen production begins early), late menopause (estrogen productionends late),1 and long-term use of synthetic estrogens (estrogen replacement therapy).14 Dietshigh in animal fat or alcohol have also been associated with higher risks of breast cancer.1Since fat cells make estrogen,1 and alcohol can increase estrogen production,15 these riskfactors may also be associated with estrogen exposure. Known risk factors that do not appearto be related to estrogen are inheritance of the “breast cancer gene,” a gene that greatlyincreases the risk of breast cancer in young women, and exposure to X-rays or other radia-tion.16 Known risk factors only account for about 30 percent of breast cancer cases,17 so looking at other sources of estrogen exposure seems reasonable.
This is not to say that estrogen is unhealthy - obviously it is necessary for the normal functioning of women’s bodies. But it does indicate that it may be easy to get too much of agood thing. DDT and related compounds have long been known to have estrogenic effects;the first of these studies was done in the late 1960s.8 Compounds like DDT that haveestrogenic effects but are not made by biological processes are called xenoestrogens. Theestrogenic activity of DDT seemed like a reasonable starting point when looking for a mecha-nism by which DDT exposure might increase breast cancer risk.
Recent research by Leon Bradlow of New York’s Strang-Cornell Cancer Research Labora- tory (together with four co-workers) has documented such a mechanism.18 Bradlow began hisresearch after Wolff completed the 1993 epidemiological study mentioned above. Bradlowwas convinced that DDT could not really increase a woman’s breast cancer risk, and hestudied mechanisms as a way of showing that the epidemiological association must be causedby something else. “I was wrong,” Bradlow said after finishing the study.19 The study looked at two products that can be formed during the breakdown of the common estrogen estradiol. One of these breakdown products (2-hydroxyestrone) has mini-mal estrogenic activity17 and is not toxic to genetic material (genes). The other(16α-hydroxyestrone) is a fully potent estrogen, produces tumors, and is toxic to genes. Thetwo estrogens have been nicknamed “good” and “bad” estrogen in analogy with the “good”and “bad” cholesterols that have received much recent publicity. Women with breast cancerhave nearly five times as much of the “bad” estrogen in their breast tissues as do womenwithout cancer.18 Bradlow’s study showed that o,p’-DDT (a chemical making up about 15 percent of com- mercially-produced DDT8), p,p’-DDE, and o,p’-DDE (both are long-lasting breakdownproducts of DDT) change the way that estrogen is broken down in human cells. In normalcells, there is only a little more “bad” estrogen than there is “good” estrogen. When the DDT-like chemicals were added, the ratio between the two types of estrogen increased, and therewas between 8 and 15 times as much of the “bad” estrogen as there was of the “good”estrogen.18 Additional research has shown that o,p’-DDT also causes certain cells in the mammary glands of adolescent rats to increase in number (proliferate).20 This proliferation “may be acritical factor in chemical carcinogenesis.”20 Four DDT-related compounds, p,p’-DDT (whichmakes up about 85 percent of commercially-produced DDT8), o,p’-DDT, p,p’-DDE, ando,p’-DDE, cause human breast cancer tissue culture cells to proliferate.21 Although there is not yet a scientific consensus,22 these mechanism studies together with the epidemiology studies provide solid evidence that DDT exposure may increase breastcancer risk. This increased risk is an unnecessary risk. It’s time to develop and implementpesticide policies that will prevent our exposure and reduce our risk of breast cancer.
We can significantly reduce our exposure to pesticides linked with breast cancer in three • Stop using DDT. DDT’s uses in the United States were canceled in 1972.23 Since the
amount of DDT used and the amount in American women’s bodies has declined since then,the risk of breast cancer should also be declining. However, DDT is still used outside the U.S.
and residues come to the U.S. on produce, in the blood and tissues of migratory animals, andon contaminated dust particles blown globally by the wind. A recent study of the global distribution of organochlorine insecticides in tree bark found that residues were ubiquitous and not limited to areas where DDT is still being used.24 High concentrations of the DDT breakdown product DDE were found in parts of the midwestern and southwestern U.S.24 There are several steps the U.S. can take to reduce American’s exposure to DDT. The U.S.
needs to strengthen residue standards for DDT and its breakdown products on commoditiesentering the U.S. Because the U.S purchases a large amount of imported food, this willdiscourage its use in other countries. U.S. agricultural aid packages also need to be builtaround nonchemical methods of managing pests.
Stop using insecticides related to DDT. Certain insecticides that are chemically related
to DDT are still in widespread use in the U.S. Methoxychlor is used for insect control onfruit and vegetable crops, on shade trees, and in dairy barns.25 Endosulfan is used on vegetablecrops.21 Endosulfan and methoxychlor have both shown estrogenic activity in laboratory testsusing breast cancer cell cultures;20 methoxychlor has also shown a variety of estrogenic effects •Stop using
in laboratory animals.26-28 We need immediate action to end the use of these pesticides in the insecticides
U.S. and abroad. Government policies should cancel uses of these insecticides in the U.S. and related to
reduce legal contamination levels on imported food. These policies need to be coupled withworldwide educational programs that give farmers the tools they need to successfully use more sustainable pest management practices.
Stop using other pesticides linked with breast cancer. Sixteen currently-used pesticides
have been linked with breast cancer in laboratory tests. (See pp. 10-11 for a complete list.)Most compelling are the triazine herbicides, some of the most commonly used herbicides inthe U.S. Atrazine is used on corn, sugar cane, and sorghum. Simazine is used on corn, citrus •Stop using
orchards, and nut orchards. Cyanazine is used on corn and cotton.29 While triazine herbicidesdo not appear to be estrogenic,21 all three of these herbicides have been shown to cause mammary tumors in female rats;29 atrazine has also caused mammary tumors in male rats.30 pesticides
Atrazine was nearly as potent as DDE in promoting the formation of the “bad” estrogen that linked with
is linked to breast cancer. Atrazine in particular, and the other triazines, often contaminate water. Many studies of stream and river water in the Midwest’s corn belt have found atrazinein over 90 percent of the samples analyzed. Atrazine was the second most commonly detected pesticide in the U.S. Environmental Protection Agency’s (EPA’s) national survey of drinkingwater wells.29 When EPA proposed to initiate the process of examining the triazines’ cancer risks to see if more regulatory actions were required (this process is called a Special Review), they received80,000 comments mostly opposing the Special Review.31 Many of these comments were fromfarmers stating that they would suffer economic damages if the use of triazine herbicides werefurther restricted.
EPA now needs to hear from, and take notice of, the millions of women at risk of breast cancer. Alternatives to the use of these herbicides exist and are profitable. The U.S. should notengage in the almost science fiction-like task of weighing a woman’s breast cancer risks against pesticide manufacturers’ profits. We need to stop using these herbicides and support farmers alternatives
who are using the many successful and cost-effective alternatives that are available.
“If reducing avoidable exposures to xenoestrogens made it possible to avert only 20 percent to pesti-
of breast cancers every year,” wrote cancer researchers Devra Lee Davis and H. Leon Bradlow, “at least 36,000 women — and those who care about them — would be spared this difficult •Emphasize
disease, and the public would be spared the burgeoning expenses of treatment and care. Such prevention of
prospects are too tantalizing to ignore.”1 It is rare that we, as a nation, have the ability toprevent a disease. We must seize this opportunity and take the steps necessary to prevent CHAPTER 4
Atrazine is a triazine herbicide used in the production of corn and sorghum.32 Atrazine is
the most heavily-used (total annual use, by weight) pesticide in U.S. agriculture.33 Feeding atrazine to rats caused increases in benign and malignant mammary gland tumors in females.32 Effect of Pesticides on
One study found that it increased the incidence of typically rare benign mammary tumors in "Good" and "Bad" Estrogen
males.30 Atrazine is nearly as potent as the DDT breakdown product DDE in promoting the in Breast Cancer Cells
formation of the “bad” estrogen, 16α-hydroxyestrone, that has been linked with breast can- Cyanazine is a triazine herbicide used primarily on corn.34 It “ranks in the top five most
commonly used pesticides in U.S. agricultural production.”34 Feeding of cyanazine to rats caused a significant increase in malignant mammary gland tumors in females.32 Cyanazine production in the U.S. will end by December 31, 1999; use will continue for three additional 1,3-Dichloropropene (Telone) is a soil fumigant35 and is one of the top ten pesticides used
in U.S. agriculture.33 It causes mammary tumors in mice and rats.36 Dichlorvos is an organophosphate insecticide used in greenhouses, on fruit and vegetable
crops, on livestock, and as a fumigant. It has been used to make pet flea collars and pest strips.37 Feeding of dichlorvos to rats caused an increase in mammary gland tumors in fe- Source: Bradlow, H.L. et al. 1995. Effects of pesticides on the ratio of 16α/2- hydroxyesterone: A biologic marker of breast cancer risk. Environ. Health Persp. Endosulfan is an insecticide used on a strikingly wide variety of fiber, fruit, and vegetable
crops.39 It is the fifth most commonly detected pesticide on U.S. produce.40 It is estrogenic inlaboratory tests (causes breast cancer cells to increase in number)21 and promotes formation of Endosulfan, atrazine, and DDT all promote the “bad” estrogen linked to increased risk of breast cancer.18 the formation of “bad” estrogen. In thisexperiment, concentrations between 2 and Ethalfluralin is an herbicide used prior to planting in the production of soybeans, dry
beans, and sunflower seeds. Feeding of ethalfluralin to rats caused mammary gland tumors.41 Ethylene oxide is a fumigant and sterilant used to fumigate spices and sterilize cosmetics
and hospital equipment. A study in which female mice inhaled ethylene oxide showed that thefrequency of mammary gland tumors, as well as several other cancers, was increased.42 Etridiazole (Terrazole) is a fungicide. It is applied to soil and is also used to treat seeds.35
Feeding of etriadiazole to rats caused an increase in mammary tumors.36 Methoxychlor is an insecticide closely related to DDT. Production and use in the U.S.
totals about a half million pounds per year; about 60 percent of this is used in agriculture.43Methoxychlor causes breast cancer tissue culture cells to increase in number.21 Oryzalin is a dinitroaniline herbicide. Major uses include turf, almond orchards, and grape
vineyards. Feeding of oryzalin to rats increased the incidence of mammary gland tumors infemales.44 Prometon is a triazine herbicide.35 In feeding studies with rats, it causes mammary tumors
Propazine is a triazine herbicide used prior to planting in the production of sorghum, as
well as after planting in carrots, celery, and fennel. Feeding of propazine to female rats in-creased the incidence of benign and malignant mammary gland tumors.45 Simazine is a triazine herbicide used to kill unwanted plants in corn production; in fruit,
nut, and citrus orchards; and in non-crop areas.32 It is one of the 25 most heavily-used (totalannual use, by weight) agricultural pesticides in the U.S.33 Feeding rats simazine caused anincrease in the incidence of malignant mammary gland tumors in females.32 Terbuthylazine is a triazine herbicide used to kill algae in commercial cooling towers,
ponds, fountains, and aquariums. In female rats, feeding of high doses increased the incidenceof malignant mammary gland tumors.46 Terbutryn is a triazine herbicide used to kill unwanted plants prior to planting of sorghum
and on uncultivated land.35 In a feeding study using rats, terbutryn increased the number ofmalignant mammary gland tumors.47 Tribenuron methyl (Express) is a sulfonylurea herbicide used primarily in wheat and barley
production. Feeding of tribenuron methyl to rats caused an increase in the frequency of malignant mammary gland tumors in females.48 REFERENCES
Davis, D.L. and H.L. Bradlow. 1995. Can environ- distribution of persistent organochlorine compounds.
mental estrogens cause breast cancer? Scientific 25. Swartz, W.J., C.S. Wink, and W.D. Johnson. 1994. Re- Falck, F. et al. 1992. Pesticides and polychlorinated sponse of adult murine uterine epithelium to 50% biphenyl residues in human breast lipids and their methoxychlor. Repr. Toxicol. 8(1):81-87.
relationship to breast cancer. Arch. Env. Health 26. Gray, L.E. 1989. A dose-response analysis of methoxy- chlor-induced alterations of reproductive development Adamson, R. 1993. Statement before the Subcom- and function in the rat. Fund. Appl. Toxicol. 12:92-108.
mittee on Health and the Environment, Committee 27. Swartz, W.J. and M. Corkern. 1992. Effects of methoxy- on Energy and Commerce. U.S. House of Repre- chlor treatment of pregnant mice on female offspring of sentatives. Washington, D.C. (October 21.) Mr.
the treated and subsequent pregnancies. Repr. Toxicol.
Adamson testified as director of the Division of Can- cer Etiology at the National Cancer Institute.
28. vom Saal, F.S. et al. 1995. Estrogenic pesticides: bind- Marshall, E. 1993. Search for a killer: Focus shifts ing relative to estradiol in MCF-7 cells and effects of from fat to hormones. Science 259:616-617.
exposure during fetal life on subsequent territorial be- Westin, J.B. and E. Richter. 1990. The Israeli breast havior in male mice. Toxicol. Lett. 77:343-350.
cancer anomaly. Ann. N.Y. Acad. Sci. (609):269- 29. U.S. EPA. 1994. Atrazine, simazine and cyanazine; No- tice of initiation of special review. Fed. Reg.
Mussalo-Rauhamaa, H. et al. 1990. Occurrence of beta-hexachlorocyclohexane in breast cancer pa- 30. Pintér, A. et al. 1990. Long-term carcinogenicity bioas- say of the herbicide atrazine in F344 rats. Neoplasma Wolff, M.S. 1993. Blood levels of organochlorine residues and risk of breast cancer. J. Nat. Cancer 31. U.S. EPA. Prevention, Pesticides and Toxic Substances.
1995. Questions and answers: Phase-out of cyanazine.
U.S. Dept. of Health and Human Services. Public Health Service. Agency for Toxic Substances and 32. U.S. EPA. 1994. Atrazine, simazine, and cyanazine; Disease Registry. 1994. Toxicological profile for 4,4'- Notice of initiation of special review. Fed. Reg.
DDT, 4,4'-DDE, 4,4'-DDD (update). Atlanta, Georgia.
33. Aspelin, A.L. 1994. Pesticide industry sales and usage: Kreiger, N. et al. 1994. Breast cancer and serum 1992 and 1993 market estimates. U.S. EPA. Office of organochlorines: A prospective study among white, Prevention, Pesticides and Toxic Substances. Office of black, and Asian women. J. Natl. Cancer Inst.
Pesticide Programs. Biological and Economic Analysis 10. Savitz, D.A. 1994. Re: Breast cancer and serum 34. U.S. EPA. Prevention, Pesticides and Toxic Substances.
organochlorines: A prospective study among white, 1995. Questions and answers: Phase-out of cyanazine.
black, and Asian women. J. Natl. Cancer Inst. 86(16): 35. Farm Chemicals Handbook ‘95. 1995. Willoughby, OH: 11. Dewailly, E. et al. 1994. High organochlorine body burden in women with estrogen receptor-positive 36. U.S. EPA. Office of Pesticide Programs. Health Effects breast cancer. J. Natl. Cancer Inst. 86(3):232-234.
Division. 1995. List of chemicals evaluated for carcino- 12. Wolff, M.S. and P.G. Toniolo. 1995. Environmental genic potential. Memo from S.R. Irene, acting director.
organochlorine exposure as a potential etiologic fac- tor in breast cancer. Environ. Health Persp. 103 37. Extension Toxicology Network. Cooperative Extension at Cornell Univ., Michigan State Univ., Oregon State 13. Epps, R.P., and Stewart, S.C. (eds.) 1995. The Univ., and Univ. of California at Davis. 1993. Dichlor- women’s complete health book. Delacorte Press.
14. Colditz, G.A. et al. 1995. The use of estrogens and 38. U.S. Dept. of Health and Human Services. Public Health progestins and the risk of breast cancer in postm- Service. Agency for Toxic Substances and Disease Reg- istry. 1995. Toxicological profile for dichlorvos. (Aug.) 39. U.S. Dept. of Health and Human Services. Public Health 15. Drinking raises breast cancer risk. 1993. Environ.
Service. Agency for Toxic Substances and Disease Reg- istry. 1993. Toxicological profile for endosulfan. (April.) 16. Pollner, F. 1993. Focus: A holistic approach to breast 40. U.S. Food and Drug Administration. 1995. Pesticide pro- cancer research. Environ. Health. Persp. 101(2): gram residue monitoring: 1994. J. AOAC Intern.
17. Davis, D.L. et al. 1993. Medical hypothesis: 41. U.S. EPA. Prevention, Pesticides and Toxic Substances.
Xenoestrogens as preventable causes of breast can- R.E.D. facts: Ethalfluralin. Washington, D.C. (Jan.) cer. Environ. Health Persp. 101(5): 372-377.
42. U.S. Dept. of Health and Human Services. Public Health 18. Bradlow, H.L. et al. 1995. Effects of pesticides on Service. Agency for Toxic Substances and Disease Reg- the ratio of 16α/2-hydroxyesterone; A biologic marker istry. 1990. Toxicological profile for ethylene oxide.
of breast cancer risk. Environ. Health Persp. 103 43. U.S. Dept. of Health and Human Services. Public Health 19. “Pesticides tied to breast cancer.” 1994. The Regis- Service. Agency for Toxic Substances and Disease Reg- istry. 1994. Toxicological profile for methoxychlor. (May.) 20. Brown, N.M. and C.A. Lamartiniere. 1995.
44. U.S. EPA. Prevention, Pesticides and Toxic Substances.
Xenoestrogens alter mammary gland differentiation 1994. Reregistration eligibility decision: Oryzalin. Wash- and cell proliferation in the rat. Environ. Health.
45. Extension Toxicology Network. Cooperative Extension 21. Soto, A. et al. 1995. The E-SCREEN assay as a at Cornell Univ., Michigan State Univ., Oregon State tool to identify estrogens: An update of estrogenic Univ., and Univ. of California at Davis. 1993. Propazine.
environmental pollutants. Environ. Health Persp.
46. U.S. EPA. Prevention, Pesticides and Toxic Substances.
22. Safe, S.H. 1995. Environmental and dietary estro- 1995. Reregistration eligibility decision: Terbuthylazine.
gens and human health: Is there a problem? Environ.
47. U.S. EPA. Office of Pesticides and Toxic Substances.
23. U.S. EPA. 1990. Suspended, canceled, and re- 1986. Guidance for the reregistration of pesticide prod- stricted pesticides. Washington, D.C. (February.) ucts containing terbutryn as the active ingredient.
24. Simonich, S.L. and Hites, R.A. et al. 1995. Global 48. U.S. EPA. Office of Pesticides and Toxic Substances.
1989. Pesticide fact sheet: Tribenuron methyl (#219).
Washington, D.C. (June 30.)

Source: http://www.wolf.sk/dok/pesticidy/bcancerreport.pdf


Field testing of a fish bioconcentration model proposed for risk assessment of human pharmaceutical residues in aquatic environments Jeffrey N. Brown†, Nicklas Paxéus*, Lars Förlin‡ and D.G. Joakim Larsson† † Institute for Neuroscience and Physiology, the Sahlgrenska Academy at Göteborg University, Sweden. * Environmental Chemistry, Gryaa


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