An off patent miracle cancer cure?

The LA Times features a study arising from the Silent Spring institute.

Common chemicals are linked to breast cancer – Los Angeles Times

More than 200 chemicals — many found in urban air and everyday consumer products — cause breast cancer in animal tests, according to a compilation of scientific reports published today.

Writing in a publication of the American Cancer Society, researchers concluded that reducing exposure to the compounds could prevent many women from developing the disease.

The research team from five institutions analyzed a growing body of evidence linking environmental contaminants to breast cancer, the leading killer of U.S. women in their late 30s to early 50s.

Experts say that family history and genes are responsible for a small percentage of breast cancer cases but that environmental or lifestyle factors such as diet are probably involved in the vast majority.

“Overall, exposure to mammary gland carcinogens is widespread,” the researchers wrote in a special supplement to the journal Cancer. “These compounds are widely detected in human tissues and in environments, such as homes, where women spend time.”

The scientists said data were too incomplete to estimate how many breast cancer cases might be linked to chemical exposures.

The resources to come out of this study include two databases, one that summarizes animal mechanistic studies, and one that summarizes human epidemiological studies. It’s a good start and I hope these databases are continually expanded. The study was essentially a big lit review and data organization project.

There are two major issues with the way carcinogenicity is studied. Firstly, animals other than humans are dosed at high levels to test for possible cancer outcomes. This leaves most researchers vulnerable to the charge that these high dose studies do not translate well to humans because the dose-response relationship at ambient levels is not well studied. So, the obvious criticism is that just because cancer endpoints were seen at high levels does not mean that the same thing will happen at low levels. This cuts both ways, though. We’re seeing with bisphenol A that low doses can cause more harm than intermediate doses. Another issue is the additivity of the interactions. Does 1 “dose” of PAH + 1 “dose” of PCB = 2 “doses” of PAH? We’re exposed to a whole host of chemicals all our lives, who knows which ones add, which ones subtract, which ones multiply, etc.

Of course, as with most diseases, some macro variables dominate. For instance, the US has seen 8-9% decline in breast cancer incidence recently due to a decreased use of hormone replacement therapy. So, as with all diseases, taking care of some of these big ticket items is very important. One discouraging story I read today reported on a four percentage point decline in mammograms (70 to 66%) in women age 40 and older. Why? decreased access to health insurance and dropping the ball on promotion.

The depressing fact of the matter is that the boring basics of good preventative healthcare, screening, good lifestyle and diet are the most important factors, and if we take care of these factors, we will make most health issues easier to deal with.

Caveat Emptor: They found a correlation, not a causative mechanism. But Polybrominated Diphenyl Ethers (PBDEs, yum!) have structures that can mimic endocrine hormones. Because hormones signal at very low doses and continuously, our whole toxicological risk testing structure of looking for acute effects at high doses and trying to extrapolate those effects to low doses is flawed for endocrine disrupting compounds. We are finally beginning to see some new research, especially with other toxics such as Bisphenol A, which test for chronic conditions and subtle gene and hormonal signalling effects at low doses. After all, small changes in hormone regulation especially at childbirth and a young age can have very serious effects later on in life.

Inside Bay Area – NEW: Flame retardants linked to thyroid disease in cats

A mysterious epidemic of thyroid disease in cats may be linked to flame retardants common in carpets, foam furniture and mattresses, according to U.S. Environmental Protection Agency researchers, who suggest that scientists have underestimated the damaging health risk the chemicals pose to humans.

The research, published Wednesday in the journal Environmental Science and Technology, does not prove these compounds, known as PBDEs, caused the rash of hyperthyroidism in the nation’s household cats over the past 30 years.

Rather, it lays out a hypothesis, showing that cats are heavily contaminated by these compounds, which leach from household products and are found everywhere, particularly household dust. Cats, meticulous cleaners, ingest PBDE-contaminated dust daily.

The case of fire retardants is especially difficult because they save many lives, so manufacturers can always point to that fact and resist change. The logical fallacy, however is as follows:

1. Fire retardants save lives (therefore good)
2. PBDEs are fire retardants
3. Therefore, PBDEs are good!!

The search for a safer fire retardant needs to continue, and will not happen unless the old ones are under pressure of being phased out.