Glossary

Type a term:

Personal Care Products: Evidence

Hair care products containing hormones induce early puberty.

In a study of young African-American girls aged 1-6 years old, hormones absorbed through the use of hair care products containing estrogen or placental hormones induced early puberty, resulting in breast development and pubic hair growth. Discontinuation of these products led to regression of the premature signs of puberty [Tiwary, 1998].

In a study of hair care product usage by military personnel, researchers found that over a quarter of non-white female enlisted personnel used hair care products that contained estrogenic hormone supplements. Of great concern was the finding that 13.4% of respondents’ young children also used these products [Tiwary and Ward, 2003].

African-American girls have earlier onset of puberty than girls of other ethnic backgrounds.

Although many factors are involved, racial differences in age of sexual development have been reliably documented, with African-American girls showing signs of development significantly earlier than both Hispanic and non-Hispanic Caucasian-American girls [Chumlea et al., 2003]. Earlier puberty is associated with increased risk of breast cancer [Stoll, 1998].

African-American women have increased rates of early-onset breast cancer.

U.S. cancer statistics reveal that although the trend reverses later in life, premenopausal African-American women have a higher incidence of breast cancer than their Caucasian-American age-mates. Although about 20% of breast cancer diagnoses in Caucasian-Americans are made in premenopausal (under age 50) women, between 30-40% of breast cancer diagnoses in African-American women are made in younger women [Newman, 2005].

A number of genetic, lifestyle and environmental factors underlie the observed racial differences in incidence and age-of-onset of breast cancer, many of which may be related to lifespan exposures to estrogens and estrogen-like products [Bernstein et al., 2003]. Of particular concern in the pattern of breast cancer in African-American women is the recognition that younger women are more likely to be diagnosed with more aggressive breast cancers [Winchester et al., 1996].

Phthalates are abundant in our homes and in our bodies.

Studies measuring levels of chemicals in ordinary air and dust from homes found significant levels of several phthalates in both of types of samples [Rudel et al., 2001]. Urine samples taken during a large study examining health status of US citizens ranging in age, racial and ethnic backgrounds, and geographical distributions revealed that there is a broad based and extensive exposure to phthalates [Silva et al., 2004].

Premature breast development has been found in young girls who had unusually high levels of serum phthalates.

A study in Puerto Rico explored blood levels of many contaminants, with the goal of understanding the high incidence of premature breast development among young girls. Although no pesticides were found in the serum samples from any of the girls studied, high levels of phthalates were found in those girls who had early breast development, but not in those with normal timing of sexual maturation [Colon et al., 2000].

Elevated monomethyl phthalate levels are associated with early breast development in young girls.

A recent case-control study examined phthalate levels in apparently healthy girls who went through thelarche (breast development) before the age of 8, as compared with girls who underwent precocious puberty because of abnormalities in their neuroendocrine systems and with girls who were progressing through puberty at normal ages. Increased levels of monomethyl phthalate (MMP) were associated with early thelarche group, but not either of the comparison groups [Chou et al., 2009].

Phthalates are weakly estrogenic in human breast cancer cells, but not in experimental models using lab animals.

Studies examining the effects of various phthalates on cell division rates in human breast cells grown in the lab demonstrated weak effects of some of these phthalates, although others were without effect. Those phthalates that demonstrated weak estrogenic effects exerted additive effects, that is, combining chemicals increased the rate of cell division [Harris et al., 1997]. Despite demonstrated effects of the phthalates on cell division in lab Petri dishes (not in a living animal), tests in which the same compounds were injected into rats did not reveal any estrogenic activity of the chemicals. Scientists have concluded that under normal circumstances, major phthalates are rapidly metabolized, or changed, into forms that are non-estrogenic when they are consumed by or injected into living organisms [Hong et al., 2005]. The same metabolites that are formed following injection into rats are not estrogenic, even in cell proliferation studies in which the cells are grown in the lab [Picard et al., 2001].

Phthalates alter levels of androgens and estrogens in women and may influence breast cancer risk in premenopausal women.

Despite the lack of direct effect of low levels of phthalates on estrogen-mediated activity, phthalates have been shown to have significant effects on hormone secretion in developing male rats, with decreased testosterone secretion resulting in abnormal development of essential male reproductive structures [Fisher, 2004]. Although methods and species are different, low levels of androgens like testosterone have been associated with increased risk for breast cancer in younger, premenopausal women [Wang et al., 2000].

Parabens accumulate in human breast tissue.

Samples of breast tumor tissue that had been removed surgically were examined for the presence of several common parabens. Significant levels of several parabens were found in these breast tissue samples, with the highest concentrations being of methylparaben, the most common paraben used in many cosmetics and personal care products. Parabens detected in the tissues were in the form that has been shown to exert estrogen-like activity in other experiments [Darbre et al., 2004a]. Concerns have been raised that the researchers did not compare levels of parabens in breast tissues from women with cancer with those from women without the disease [Golden and Gandy, 2004]. While a serious issue, the original author points out that without long-term studies and a real understanding of the profiles of women in both groups, the role of parabens in the development of disease would be difficult to understand [Darbre, 2004b]. Instead, the important point is that there are high levels of this class of chemicals found in breast tissue and there is good reason to want to learn more about the possible involvement of these estrogen-mimicking substances on mammary tumor development.

Human breast cancer cells are affected by parabens.

Studies examining the effects of several parabens, including the commonly used methylparaben, benzylparaben and n-butyl parabens, demonstrate that these chemicals are weakly estrogenic. That is, these chemicals bind to the estrogen receptor, change the activity of genes that are normally regulated by estrogens, and induce the proliferation of human breast tumor cells (MCF-7 cells) when the cells were grown in laboratory dishes. [Byford et al., 2002; Darbre et al., 2003].

Parabens are weakly estrogenic when administered topically to rodents.

In studies with young rats and mice, topical and subcutaneous treatments with parabens commonly found in personal care products led to enhanced growth and proliferation of uterine tissue, another organ (like the breast) whose development is regulated in large part by estrogens [Routledge et al., 1998; Darbre et al., 2002, 2003; Hossaini et al, 2000].