Science for the People - January/February 2003 - From the Ground Up

From the Ground Up

Science for the People

Dual Studies Show Roundup Herbicide is Hormone Disruptor

Two new studies indicate that Monsanto’s herbicide, Roundup, is a hormone disruptor and is associated with birth defects in humans.

The first study followed Minnesota families applying pesticides to their crops to find whether elevated exposure to pesticides caused birth defects in children. The study found that two kinds of pesticides —fungicides and the herbicide Roundup — were linked to statistically significant increases in birth defects. Roundup was linked to a 3-fold increase in neurodevelopmental (Attention Deficit) disorders.

A recent test tube study reveals that Roundup can severely reduce the ability of mouse cells to produce hormones. Roundup interferes with the fundamental protein called StAR (steroidogenic acute regulatory protein).

The StAR protein is key to the production of testosterone in men (thus controlling male characteristics, including sperm production) but also the production of adrenal hormone (essential for brain development), carbohydrate metabolism (leading to loss or gain of weight), and immune system function. The authors point out that “a disruption of the StAR protein may underlie many of the toxic effects of environmental pollutants.”

Minnesota study: EHP Supplement 3, Vol. 110 (June 2002), pgs. 441-449. StAR study: EHP Vol. 108, No. 8 (August 2000), pgs. 769-776.

Environmental Toxins and Breast Cancer Link Remains Murky

A new study led by Marilie Gammon finds few associations between the risk of breast cancer and serum levels of environmental toxins measured around the time of diagnosis. While that might seem to be good news, the study has severe limitations which undermine the policy implications of its conclusions.

Launched in 1993 as a result of a law mandating the National Cancer Institute to study links between environmental contaminants and breast cancer, the study examined risk of breast cancer as a function of current body burden levels of a series of compounds of traditional, historic concern (DDT, DDE, PCBs, chlordane and dieldrin).

The authors conclude that “it seems unlikely that breast cancer risk is associated with organochlorines when measured close to the time of breast cancer diagnosis.” They imbed this conclusion in a series of cautionary statements, the most important of which is:

“These data do not rule out the possibility, however, that breast cancer risk is elevated by high organochlorine exposures several decades earlier that, through variations in individual metabolism, now measure as low body burden levels. Also, very limited data recently suggest that breast cancer mortality may be associated with some organochlorine compounds. These possibilities require additional research.”

This possibility— that breast cancer risk may be elevated by organochlorine exposures several decades earlier— is the heart of the endocrine disruption hypothesis: exposure during crucial times in development causes developmental errors which (in the case of breast cancer) increase the likelihood of cancer later in life. Hence the results presented by Gammon et al., while potentially reassuring about the impact of current exposures, are very limited in what they tell us about endocrine disruption’s contribution to breast cancer risk, even with respect to the chemicals they studied.

Gammon, MD, et al. Environmental Toxins and Breast Cancer on Long Island. II. Organochlorine Compound Levels in Blood. Cancer Epidemiology Biomarkers & Prevention II: 686-697. 2002.