Breast Cancer and POPs

Persistent organic pollutants (POPs) are a class of synthetic, lipophilic, bioaccumulative compounds, many of which were first introduced during the post WWII industrial boom. Most notable among these older POPs are dichlorodiphenyl trichloroethane (DDT) and polychlorinated biphenyls (PCBs), which were banned in the 1970s in the U.S. due to concerns over widespread human exposures and potential adverse health effects in wildlife and humans.

Because of their persistent and bioaccumulative nature, however, exposure to these compounds continues decades later with detectable levels prevalent in human tissue today. Polybrominated diphenyl ethers (PBDEs) are a newer class of POPs, introduced into the marketplace in the late 1970s as flame retardant additives to consumer and building products.  Owing to their similar molecular structure and toxicological properties to PCBs, in combination with the ubiquity of exposure, it appears PBDEs are poised to become the PCBs of the 21st century. In response to recent regulatory action that banned the use of two of the three primary commercial PBDE formulations in the U.S., replacement brominated flame retardants (BFRs) have recently emerged and are in widespread use. 

Interest in the role of POPs in breast cancer etiology stems largely from the well-documented endocrine disrupting properties of these compounds.

The public is under the general impression that the real increase in cancer rates is due to smoking.

Is it because people are living longer that they’re getting more cancers? The answer to that is no, because when we talk about cancer incidence rates, we adjust them to reflect the increasing longevity of the population.

Can genetics be the possible reason for this major increase in cancer? Not at all. There’s no chance whatsoever that the genetics of human populations has changed in the last 40-50 years. It takes tens of thousands of years for genetic effects in the general population to change. So one can exclude genetics and sharply limit the role of smoking.

What about fatty diet? There’s really little evidence that fat is a risk factor for cancer. For instance, if you look at Mediterranean countries, they have extremely high fat consumption, particularly olive oil, which can be as high as 40 percent of the diet. But the rates of cancers, particularly reproductive cancers, are low. However, you find strong relationships between the consumption of animal and dairy fats and some cancers. But that’s a reflection of the fact that these are highly contaminated with a wide range of industrial, chemical, and petrochemical carcinogens.

There has been a massive escalation in the incidence of cancer that cannot be explained away on the basis of smoking, longevity, genetics, or a fatty diet.

What are the rationales of National Cancer Institute and the American Cancer Society on the causes and prevention of cancer?

First of all, they try to explain away cancer by what’s called, “blame the victim.” If you get cancer, it’s your fault. You smoke too much. It’s a fatty diet.” Or they claim it’s because people are spending too much time in the sun. They parallel this emphasis on blame the victim by ignoring, to all intents and purposes, a vast body of scientific information on avoidable causes or risk factors of cancer.

The cancer establishment is fixated on what’s called, “damage control”-the screening, diagnosis, and treatment of cancer, as opposed to prevention.

The Chronicle of Philanthropy, the leading American charity watchdog stated, “The American Cancer Society is more interested in accumulating wealth than saving lives.”

Let’s understand something about screening. Screening is the key strategy of medicine, government, big business and all the breast cancer (prostate cancer) organizations.

Does screening save lives?

Screening for breast cancer with mammography is widely encouraged by governmental programs in both the European Union (EU) and the United States under the assumption that the screening programs save lives. In the case of breast cancer, an analysis of randomized trials with some 247?000 women aged 40–74 years showed that for every 1000 women who participated in screening, 3.9 diagnosed with breast cancer died, compared with 5.0 among those who did not participate. The follow-up time ranged between 5.8 and 20.2 years. Thus, the absolute risk reduction was on the order of one in 1000. The authors of a recent review of six trials involving half a million women estimated the absolute risk reduction to be approximately one in 2000. Note that this benefit relates to fewer breast cancer deaths; no reduction in mortality from all cancers or other causes was found. Whether the potential of screening to reduce breast cancer mortality outweighs the harms of overdiagnosis and overtreatment is still under discussion.

What are the conflicts of interest between NCI, the American Cancer Society, and industry ?

The conflicts of interest extend particularly to the mammography industry-the machine and film industry. We have excellent data showing that pre-menopausal mammography is not only ineffective, but is also dangerous for a variety of reasons, including the high doses of radiation. Two films of a breast in a pre-menopausal woman gives that woman about 500 times the dose of a chest X-ray. If a pre-menopausal woman gets a mammography every year over a ten-year period, the dosages of radiation can well amount to about ten rads (a rad is a “radiation absorbed dose,”) a measure of radiation exposure.

Radiation from routine pre-menopausal mammography reaches reasonably close to the kind of dosage that women got in Hiroshima and Nagasaki outside of the major epicenter where the atom bomb was exploded. Nevertheless, a radiologist will tell women, when asked if there’s any problem with the radiation, “Well my dear,” and they’ll call them by their first name, “not at all. It’s just the same as spending a few days in Denver or taking a transatlantic flight.” This is deception and manipulation.

If we can’t explain this major epidemic of cancer on the basis of smoking, increased longevity, genetics, or a fatty diet, then what are the reasons for it?

They fall into three general categories. The first relates to consumer products. By consumer products, I mean things you can buy in a store which include food, cosmetics and toiletries, and household products. In all of these areas, the consumer, once given the information on which of these pose cancer risks, could boycott them and shop for safer products.

Typically, any organization considered “charitable” is viewed almost as a sacred cow largely immune from careful scrutiny by researchers, the media, and the public. With their well-funded public relations funding, the larger charities have been able to create an atmosphere in which questioning the activities, expenditures, and objectives of a charity is interpreted as an attack on charitable activities themselves.

 

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Benzene may seem innocuous – it is clear, colorless, and has a slightly sweet odor. But it’s one bad actor.

It’s a carcinogen, and you don’t want to be breathing it. Traditionally, people have thought of industrial facilities as the main threat. Data from the U.S. Environmental Protection Agency shows that the top major emitters in Pennsylvania and New Jersey are the refineries in South Philadelphia and Paulsboro.

 

New research out of Emory University in Atlanta suggests that how close you live to one of these facilities may affect your chances of getting a particular kind of cancer, non-Hodgkin’s lymphoma. But the qualifier is that the EPA and the Emory study looked only at major stationary sources. The big “wow” is that, in Philadelphia, the refinery isn’t the biggest source of benzene overall.

 

It’s traffic. An EPA assessment of Philadelphia’s air toxics, based on 2005 data, the latest available, shows that the area with the highest risk of cancer from benzene exposure is roughly along the Vine Street Expressway, near the Schuylkill Expressway. Overall, only about 7 percent of the city’s benzene comes from “major risks,” such as the refinery. Traffic accounts for more than triple that – 26 percent, the largest piece of the city’s benzene pie.

 

To Joseph O. Minott, head of the Clean Air Council in Philadelphia, this means “it really makes sense in urban areas to promote alternatives to the automobile, such as public transit, walking, and biking.” Other sources of benzene include the airport, construction equipment, and gas stations. About 22 percent of the benzene in the city blows in from somewhere else.

 

Beyond that, cigarettes are considered the dominant lifestyle-related source of benzene exposure. In the human body, benzene causes cells to not work correctly. It can lead to anemia and damage the immune system, says the Centers for Disease Control and Prevention. Non-Hodgkin’s lymphoma, which the Emory study tracked, starts in the immune system. The National Cancer Institute estimates it will kill nearly 20,000 Americans this year.

 

Since the 1970s, diagnoses have increased by 3 to 4 percent a year. Researchers think part of the increase is due to things such as changes in the classification system, better diagnoses, and increases of HIV, which also attacks the immune system. But that would account for only half the additional cases, they say. The other half? Increased diagnoses also appear to parallel expanded industrial production, which has prompted suspicion of occupational exposures. The Emory study was one of the first to look at the risk for people who, while they may not work at a facility, live near it. This matters. EPA statistics show that nearly 3,000 people live within a mile of the Philadelphia refinery – most of them white, most with no more than a high school diploma. Fewer than half the households have incomes topping $25,000 a year. In a recent study in the journal Cancer, the Emory researchers found that a person’s risk for the disease falls a third of a percent for every mile between the home and a major facility.

 

This doesn’t necessarily mean you should move. Christopher Flowers, an epidemiologist at Emory who led the study, said the risk is based on mean distance calculations, and there’s no way people could be sure that in moving away from one site, they’re not moving toward another. Plus, the study pointed simply to an association, not a cause. Many other factors could also increase your risk of lymphomas. But, Flowers said, “it is something provocative that merits further exploration.”