Evidence that Chemicals Cause Breast Cancer

[Guest guest]

Evidence that Chemicals Cause Breast Cancer

JoAnn Guest

Oct 17, 2004 17:41 PDT

--

State of the Evidence:

Evidence that Chemicals Cause Breast Cancer

edited by Nancy Evans

 

© 2003 by The Breast Cancer Fund and Breast Cancer Action

EXECUTIVE SUMMARY

 

Breast cancer rates have been climbing steadily in the United States

and

other industrialized countries since the 1940's. Billions of dollars

have been spent in an effort to stem this unrelenting tide, yet more

than 50 percent of breast cancer cases remain unexplained by the

characteristics and risk factors associated with the disease.

Ionizing radiation is the only proven environmental cause of human

breast cancer. But powerful circumstantial evidence indicates that

some

of the 85,000 synthetic chemicals in use today are responsible for

many

of the unexplained cases of the disease. While scientists have not

yet

developed an ideal method for linking chemical exposures to breast

cancer, several types of research - experimental, body burden and

ecological studies - provide strong evidence of the connection

between

chemicals and breast cancer.

 

Because the types of evidence vary, the strength of the evidence

linking

chemicals and breast cancer also varies. The strongest evidence

linking

chemicals to breast cancer -- based on the fact that lifetime

exposure

to natural estrogens increases the risk of breast cancer -- concerns

natural and synthetic estrogens, including drugs like

diethylstilbestrol

(DES), plastic additives like bisphenol-A (BPA), polyvinyl chloride

(PVC) (found in many consumer products), dieldrin and some

pesticides.

Other synthetic substances strongly linked to breast cancer through

experimental evidence are: organic solvents (used in many

manufacturing

processes, including the manufacture of computer components),

polycyclic

aromatic hydrocarbons (PAHs) (created in soot and fumes from burning

diesel, fuels or cigarettes) and 1,3 butadiene (a by-product of

internal

combustion engines).

 

There are also chemicals for which the evidence indicates a probable

but

less certain link to breast cancer. These chemicals include dioxin

(created when plastics or other materials containing chlorine are

burned), the pesticide DDT (dichloro-diphenyl-trichloroethane) and

its

metabolite, DDE and PCBs (polychlorinated biphenyls), previously

used in

the manufacture of electrical equipment and other industrial and

consumer products.

 

Finally, there is evidence of chemicals that affect how the body

functions in ways that suggest a possible link between these

substances

and breast cancer. These chemicals include the insecticide

heptachlor

and phthalates, used to make plastic soft and flexible.

 

We clearly have major gaps in our current knowledge about the links

between breast cancer and the environment. Therefore, we need to

focus

our research efforts in areas that are most likely to provide useful

information for framing public policies related to chemical

exposures

and our health. The types of research most likely to produce useful

evidence will be those examining: (1) workplace exposures, (2)

household

exposures and (3) breast milk as a marker for human contamination.

 

While we pursue the research that will lead to more definitive

answers,

the existing evidence linking chemicals to breast cancer demands

that we

act now as a society to begin removing many of these substances from

our

environment. Considerable resources are spent encouraging women to

make

changes in their personal lives in an effort to reduce their risk of

breast cancer. But breast cancer is not just a personal tragedy; it

is a

public health crisis that demands action by society as a whole.

 

This crisis must be addressed by beginning now to implement the

precautionary principle. Under this principle, evidence of harm,

rather

than definitive proof of harm, is the trigger for policy action. In

addition, the precautionary principle mandates that the burden of

proof

with regard to chemicals rests with the manufacturers to demonstrate

that the substances are safe, rather than with the public to show

that

they are harmful. Finally, the precautionary principle rests on the

democratic principle that government officials are obligated to

serve

the public's interest in human health and environmental protection.

 

The following 5-point plan will help us reduce the risk of breast

cancer

and ultimately end the epidemic:

 

PHASE OUT TOXIC CHEMICALS that are omnipresent in the lives of so

many

people.

ENACT " SUNSHINE " LAWS AND ENFORCE EXISTING ENVIRONMENTAL PROTECTION

LAWS

to reduce the use of toxics by requiring companies to report how

many

tons of chemicals they use.

PRACTICE HEALTHY PURCHASING, with local, state and federal

governments

leading the way in purchasing environmentally preferable products,

thereby creating an example for individuals to follow.

OFFER CORPORATE INCENTIVES that encourage businesses to eliminate

the

use of harmful chemicals in their products and processes.

MONITOR BREAST MILK, through a comprehensive community program that

identifies the chemicals present in breast milk, establishes links

to

geographic areas and initiates a plan to eliminate these

contaminants.

We ignore at our peril the increasing evidence that chemicals are

contributing to the rising tide of breast cancer. The obligation to

understand this evidence, and begin to address it through the

implementation of public policies that put health first, rests with

all

of us. It is in our power to change the course we are on. Now is the

time.

 

TABLE OF CONTENTS

Introduction

 

 

The Purpose of This Paper

 

Why Chemicals?

Types of Evidence: A Primer

Evidence that Chemicals Cause Breast Cancer

 

Evidence Indicating a Probable Link Between Chemicals and Breast

Cancer

http://www.breastcancerfund.org/environment_evidence_main.htm

---

NEW

EVIDENCE THAT DIOXIN CAUSES HUMAN CANCERS

 

--

 

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=================================================================

DIOXIN PART 3: NEW EVIDENCE THAT DIOXIN

CAUSES HUMAN CANCERS AND OTHER DISEASES

 

 

 

Two recent studies, published in 1988 and 1989, have indicated a

connection between exposure to dioxin and development of cancers

in humans.

 

Earlier studies had shown little evidence linking human cancers to

dioxins, but these earlier studies have now been

challenged by U.S. government officials as fraudulent. (See RHWN

#171.) One of the recent studies also reveals a connection

 

between dioxin exposure and a variety of non-cancer health

effects, including heart attacks (among men), and digestive

diseases, cirrhosis of the liver, gall bladder and biliary tract

diseases, and genitourinary diseases (among women).

 

 

 

Seveso, Italy

 

On July 10, 1976, an industrial disaster occurred at a chemical

plant operated by the pharmaceutical giant, Hoffman-La Roche, in

the town of Meda, Italy. A visible chemical cloud containing

dioxin (2,3,7,8-TCDD and other dioxins) spread over several

square miles of populated countryside; most heavily hit was the

community of Seveso. More than 200,000 people aged 20 to 74 lived

in towns near the accident. Nearly 31,000 people aged 20 to 74

lived in zones contaminated to some degree by the accident and

about 200 individuals had such high exposures that they developed

chloracne, an acne condition known to be caused by exposure to

dioxins.

 

 

 

A team of Italian physicians and researchers has been studying

health conditions, including death certificates, of 30,703 people

aged 20 to 74 living in areas termed " exposed, " comparing

people's experience there against a larger population of 167,391

individuals aged 20 to 74 living nearby in non-exposed areas. A

recent report in the AMERICAN JOURNAL OF EPIDEMIOLOGY [1] reveals

several elevated disease rates among the exposed group.

 

 

 

The report covers the decade 1976 to 1986, which is a short

period in which to find cancer occurrences. All cancers exhibit a

" latency period " (or delay period) between the time a

cancer-causing exposure occurs and a cancer actually develops;

the latency period varies from 7 to 40 or 50 years.

 

Thus a study of cancers occurring 10 years after an exposure to

cancer-causing

chemicals could only reveal the earliest evidence of cancers and

should be understood to be preliminary in nature.

 

 

 

The results of the study are reported for people living in three

areas, labeled zones A, B and R. Zone A is closest to the

accident site and zone R extends several miles distant; zone B is

between the two. The assumption is that people's exposure varied

with distance from the accident.

 

 

 

In zone A, women had elevated cancers of the gall bladder and

 

biliary tract. They also had elevated occurrences of circulatory

 

diseases and of chronic rheumatic heart disease. Men in zone A

 

had elevated occurrence of cerebrovascular disease (such as

 

stroke). In zone B, men had elevated melanomas (serious skin

 

cancers) and cancers of the lining of the chest cavity (pleura);

 

women in zone B had elevated incidence of soft tissue sarcomas.

 

In zone R, men had elevated incidence of cancers of the lining of

 

the chest cavity (pleura), and they had increased incidence of

 

all blood diseases, and of cerebrovascular disease; women in zone

 

R had increased incidence of cancer of the uterus, as well as

 

hypertensive vascular disease.

 

 

 

The results reported above are averages for the entire decade. In

the case of cancers, which would only begin to occur after a

latency period, the timeperiod of interest is the second five

years of the decade, and, accordingly, the Italian researchers

reported results for each half of the decade.

 

 

 

During the second half of the decade: In zone A there were no

 

elevated cancer levels. In zone B, men showed elevated incidence

 

of cancers of the lung, cancers of the lining of the chest cavity

 

(pleura), serious skin cancers (melanoma), Hodgkin's disease

 

(cancer of the lymph nodes), and leukemia. In zone B, women

 

showed increased incidence of soft tissue sarcomas and of the

 

thyroid gland. In zone R, men showed elevated incidence of

 

leukemia, and women showed elevated incidence of cancer of the

 

brain. It is perhaps relevant to note that two previous studies

 

have implicated brain cancer with exposure to dioxins in weed

 

killers. [2, 3]

 

 

 

This study of the people exposed to dioxin during the Seveso

 

accident does not prove that dioxin exposure caused the cancers

 

or the other serious ailments from which these people suffer in

 

abnormally high numbers (mainly diseases of the heart, blood, and

 

arteries).

 

Nevertheless, this study confirms that it is

 

definitely misleading and untrue when anyone says there is " no

 

evidence " of cancer or other serious diseases among humans

 

exposed to dioxins. (In addition, an earlier U.S. government

 

study has shown that Vietnam veterans exposed to Agent Orange [a

 

weed killer contaminated with dioxin] suffer from elevated

 

incidence of cancers, liver damage, cardiovascular deterioration,

 

and degeneration of the endocrine system. See RHWN #73.)

 

 

 

Sweden

 

 

 

Phenoxyacetic acids (for example, the weed killers known as

2,4,5-T and 2,4-D) are almost always contaminated with dioxins

during manufacture. During the late 1970s, Swedish researchers

studied workers who had been exposed to phenoxyacetic acids and

found increased incidence of soft tissue sarcomas (rare cancers

of the connective tissues). [4, 5]

 

During the mid'80s, several

additional studies confirmed the relationship between soft tissue

sarcomas and exposure to phenoxy herbicides, while other studies

failed to confirm such a relationship. Now a new study has once

again shown a three-fold increase in soft tissue sarcomas among

workers exposed to phenoxy herbicides. [6] This is the tenth

study that we know of showing a positive relationship between

exposure to phenoxy herbicides and soft tissue sarcomas. [7]

Five studies have failed to confirm such a relationship. [8]

 

 

 

How can one make sense out of conflicting reports, when 10

 

studies show that certain chemicals cause cancer and 5 studies

 

show that those same chemicals do not cause cancer? How can the

 

public know what policies make sense to pursue?

 

 

 

In our experience, people who make money manufacturing, or using,

such chemicals prefer to argue that " we just don't know, " and

" until all the facts are in, we should not make any changes. "

 

Unfortunately, all the facts will never be in. People, including

consumers buying phenoxy herbicides at the lawn-care store and

politicians making laws, will always have to make decisions based

on incomplete information.

 

 

 

From our viewpoint, the key question is this: Is it more

important to protect people and the environment from damage, or

to protect chemicals from regulation, control and outright bans?

 

--Peter Montague

 

===============

 

[1] Pier Alberto Bertazzi and others, " Ten-year Mortality Study

of the Population Involved in the Seveso Incident in 1976, "

AMERICAN JOURNAL OF EPIDEMIOLOGY, Vol. 129 (1989), pgs.

1187-1200.. "

 

 

 

[2] A. Bair and others, " Lung Cancer and Other Causes of Death

 

Among Licensed Pesticide Applicators, " JOURNAL OF THE NATIONAL

 

CANCER INSTITUTE Vol. 71 (1983), pgs. 31-37.

 

 

 

[3] D. Coggon and others, " Mortality of Workers Exposed to

 

2-methyl-4-chlorophenoxy-acetic acid. " SCANDINAVIAN JOURNAL OF

 

WORK, ENVIRONMENT AND HEALTH Vol. 12 (1986), pgs. 448-454.

 

 

 

[4] Olav Axelson and others, " Herbicide Exposure and Cancer

 

Mortality, " SCANDINAVIAN JOURNAL OF WORK, ENVIRONMENT AND HEALTH

 

Vol. 6 (1980), pgs. 73-79.

 

 

 

[5] Lennart Hardell and others, " Malignant Lymphoma and Exposure

 

to Chemicals, Especially Organic Solvents, Chlorophenols, and

 

Phenoxy Acids: A Case-Control Study. " BRITISH JOURNAL OF CANCER

 

Vol. 43 (1981), pgs. 169-176.

 

 

 

[6] Lennart Hardell and others, " The Association Between Soft

 

Tissue Sarcomas and Exposure to Phenoxyacetic Acids--A New

 

Case-referent Study, " CANCER Vol. 62 (1988), pgs. 652-656.

 

 

 

[7] Nine of the studies are listed in footnotes 1 through 9 of

 

the Hardell study we cited in our footnote 6 (above), and the

 

tenth study is the Hardell study itself cited in our footnote 6

 

(above).

 

 

 

[8] The five studies are listed in footnotes 10 through 14 of the

 

Hardell study we cited in our footnote 6 (above).

 

 

 

Descriptor terms: seveso, italy; dioxin; gender; males; females;

 

cancer; gall bladder; gall bladder cancer; circulatory; heart

 

disease; herbicides; agent orange; phenoxyacetic; hodgkin's

 

disease; lung cancer; skin cancer; sarcomas; uterine cancer;

 

leukemia; brain cancer;

 

 

 

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_________________

JoAnn Guest

mrsjo-

www.geocities.com/mrsjoguest/Genes