From December 21, 2005
Study Indicates
Pesticides May Effect Pre-pubescent Breast Development
(Beyond Pesticides, December 21, 2005) A recent study
led by Elizabeth Guillette and published in Environmental Health
Perspectives indicates that pesticides, such as those that effect
the endocrine system, may be having more of an effect on breast development
in young girls before age ten than previously thought.
The study examined precocious puberty (early development of initial breast and pubic hair development) in 50 healthy young girls ages eight to ten with no signs of birth defects or tumors living in two agricultural regions in the Yaqui Valley of Sonora, Mexico – one with little to no pesticide exposure and one with pesticide exposure. The study found a distinct difference between the populations. Research showed a poorly defined relationship between the breast size and mammary gland development of the population of young girls exposed to agricultural pesticides and a robust positive relationship between breast size and mammary size among the unexposed population.
Among the girls exhibiting breast development and exposed to pesticides, palpable mammary tissue development was lacking in 12 of the 27 pubescent girls. Comparitively, non of the pubescent lesser-exposed girls exhibiting breast development lacked palpable mammary tissue.
The authors hypothesize “that an altered relationship between breast size, fat deposition, and mammary tissue development could result from in utero and/or childhood exposures to estrogenic or anti-androgenic chemicals as has been reported in studies of laboratory rodents.”
The age at which females exhibit breast development has been declining in some human populations over the past fifty years. The reasons around which confound scientists. The process and timing of puberty is made up of complex interactions between neural and sex hormones. Many factors may influence the process including genetic makeup, nutritional and lifestyle factors, and possible cumulative exposure to environmental estrogens beginning in the fetus and continuing until adulthood.
The authors were careful to account for these factors in monitoring the studied populations of the two regions. Lifestyle factors are essentially the same between the populations. Prior dietary studies determine that the types of food and amount served are similar in the two areas with continual exposure through ingestion of pesticide residues on purchased foods. Both also have limited exposure to plastics, makeup and treated wood furniture that may off-gas. Prior cord blood studies in 1990 from infants born in the agricultural towns two years prior to the birth of the girls participating in the study indicated trans-placental transfer of high levels of organochlorines such as Lindane and DDT metabolites.
The standard measure to determine the staging of puberty and breast development, known as the Tanner scale, primarily involves visual scaling. In this landmark study, the authors analyzed morphometric data including breast size, mammary gland development and fat deposition of breast tissue. Results of the study indicated that using the additional variables shows distinct differences between the populations while the method of visual staging alone would show no difference. The data suggest that more in depth studies are required in order to understand the environmental influences on this increasing phenomenon.
The authors note that, “The role of endocrine disrupting chemicals (EDCs) on the puberty continuum has received limited attention but several reviews suggest a need for more research. The exposure of laboratory animals and wildlife to EDCs is known to alter the ratio of female to male hormones that play a dominant role in sexual development. Exposure to some estrogen mimics or anti-androgens can delay puberty in female rodents, whereas experimental exposure to low doses of estrogenic Bisphenol A, found in some plastics, speeds growth and puberty in rats.”