Publications

Over the past 20 years, girls have been reaching puberty at earlier ages, raising questions about the reasons why. Early puberty (mainly menarche) has been found associated with increased risk of breast cancer and other adverse health outcomes or risky behaviors. Besides known factors like diet and obesity, there is concern that exposure to hormonally active chemicals, which has increased, could affect timing of puberty. We have been studying this in the Breast Cancer and the Environment Research Program (BCERP). BCERP includes research collaborations integrated across biologic, epidemiologic, and community outreach projects, funded by the National Institutes of Health (NIH) (see also www.bcerp.org). Our goal in this paper was to examine age at puberty in girls in relation to several classes of chemicals that persist in our environment for years; chemicals like DDT/DDE and other pesticides, PCBs, and PBDEs (a group of fire retardants).  (Close)

The chemicals of interest were measured in the blood samples of more than 600 girls, 6-9 years old, who are participants at two of the BCERP study sites; recruited from Kaiser members in N. CA and school-based in the Cincinnati, Ohio area. The girls were seen once or twice per year, depending on the site, for up to seven years. At these visits, information on many factors was collected from the parents or girls, such as lifestyle factors including diet and physical activity, descriptive characteristics, health history and a variety of possible exposures. A physical exam was also conducted at each visit to measure body size and the stage of puberty (breast and pubic hair development). We use statistical models to compare the ages when the girls first enter puberty in those with higher chemical levels (top 25%) to girls with lower levels (bottom 25%). These models also account for some other factors that could confuse the relationship (like race/ethnicity or household income). Our work was conducted in accordance with the policies of the IRBs at both study sites and the California committee for the protection of human subjects.  (Close)

Generally, we found that girls with higher chemical concentrations in their blood entered puberty at older ages. Median differences in age at puberty were about 5-11 months later in girls with higher versus lower levels of each chemical, taking into account factors like race/ethnicity, site, household income, and caregiver’s education. The associations varied somewhat by the body size (e.g. BMI) of the girl, which is known to be related to pubertal timing. When BMI was taken into account, there was less difference in age at puberty for girls with higher versus lower PCB and pesticide levels, meaning the effect of these chemicals may be on body size or growth. Differences in age at puberty for girls with higher vs. lower PBDEs levels were not changed by accounting for BMI. (Close)

This is the first study we know of that was able to measure the chemicals in young girls mostly before puberty and then follow them for years as they develop. We only studied girls from two areas in the U.S., but they generally represented a variety of race and ethnic groups. Most prior studies measured the chemicals after the study subjects had already reached puberty and many examined menarche, or the age at which periods begin, which is a later stage of puberty than we studied. The results of these few studies were not very consistent, with some finding earlier puberty and others finding later puberty, or no effect, with higher exposures to the chemicals we studied. There was one study with similar design as ours conducted in boys, and they also found delays in age at puberty.2,3 A couple of studies were able to measure the chemicals in the mothers during pregnancy and then re-contacted the offspring later to ask their age at menarche; these reported earlier onset with higher DDE levels (but not PCBS in both studies, nor did they examine PBDEs). Some animal studies have suggested a delay in the onset of puberty in females with exposure either around puberty or during pregnancy. (See discussion in manuscript).  (Close)

Almost all girls had measurable levels of at least some of these chemicals, as is found for the general U.S. population. Our study shows that puberty is delayed among girls with higher blood levels of these chemicals that are considered endocrine disruptors. The difference in age is similar to effects of more well-known predictors of puberty timing, such as BMI and race/ethnicity, although not in the same direction. Finding a delay in puberty in girls with higher chemical exposure does not help explain the general trend of younger age at puberty.  However, it does suggest that exposure to these chemicals, during a stage of rapid growth and hormonally-driven changes, has an effect on the body’s development. These changes may in turn influence later health endpoints or behaviors. Other types of chemicals and lifestyle factors are being examined in this large, multi-site study, providing a wealth of information about puberty and possible relationships to breast cancer (see www.bcerp.org).  (Close)

Because of concerns about the decline in the age at which children are reaching puberty, there has been an upsurge in research on contributing factors in the past decade or so. The epidemic of obesity is thought to explain some of the change, but likely not all of it. Many factors likely interact and may vary by the individual. Some of these other factors include race (younger in Blacks), genetics (mother’s age at development, as well as a variety of susceptibility genes that are only recently being studied), physical activity, stress (father absence for example), whether children were breast-fed or not, and chemical exposures, as we examined.  (Close)

The BCERP includes a prospective study of girls, recruited at ages 6-8 years in 2004-2007, and followed annually to measure onset of pubertal maturation. The study is being conducted at three sites, using similar methods: 1) Kaiser Permanente in the San Francisco Bay Area, 2) Cincinnati Children’s Hospital/University of Cincinnati, Ohio, and 3) Mt. Sinai Medical School, New York, focused in Harlem (see www.bcerp.org). The chemical concentrations were measured at the National Center for Environmental Health of the Centers for Disease Control and Prevention (CDC). There are collaborators from many other institutions, including locally; UC San Francisco, UC Berkeley, UC Davis, Zero Breast Cancer, Impact Assessment, Inc., and the California Department of Public Health. The BCERP was funded primarily by the National Institute of Environmental Health Sciences and the National Cancer Institute.  (Close)

The chemicals we examined are persistent in the environment, even though some of them are no longer used in the U.S. (PCBs and DDT for example). They get into the food chain and can be best avoided by limiting consumption of fat-based animal products, including some fish and meat, as well as dairy. DDT is still used in other countries to a limited extent and thus immigrants may have higher levels. EDCs can be passed on to offspring during pregnancy, as well as through breast-feeding, although breast-feeding is still considered to have many other important benefits to the infant. Many types of PBDE’s have recently been withdrawn from use in manufacturing, but were commonly used in foam furniture and hard-casing plastics (such as for TVs or computers) to meet fire retardation guidelines. These products will remain in general circulation for some time and proper disposal is important. Furniture with exposed foam should be repaired or replaced to avoid exposure. Vacuuming with a HEPA filter could also help reduce exposure from chemicals that accumulate in dust. See 10 quick tips to reduce general exposure and links to resources on this page.  (Close)

All information we collect is kept confidential, or private, according to the law. We use password protection and encryption for data files with any personal information. Personal identifiers (name, address, etc.) were taken off the files used for analysis, and only grouped results are calculated and presented.  All work is conducted under the oversight of the Institutional Review Boards, designed to protect human subjects, at all sites.  (Close)

• Avoid using pesticides in and around the house.
• Choose organic produce when possible or grow your own.
• Choose safer plastics for storing food and beverages, and in children’s toys and other products.: (Recycling #s to avoid–3, 6, 7. #s 1, 2, 4 and 5 are safer.). Or substitute glass, ceramic, cloth, or wood.
• Choose cosmetics and soaps that don’t contain parabens, triclosan, or artificial fragrance. (phthalates)
• Choose furniture or bedding that is not made from polyurethane foam and avoid foam carpet padding (or carpet itself if possible).
• Choose to buy household cleaners that are non-toxic, and don’t have warning labels that say: "Danger" or "Poison" or "Warning". Or make your own less toxic cleaners with vinegar, borax, and lemon juice.
• Avoid air fresheners or scented candles since they may contain formaldehyde and phthalates. Call the manufacturer to check.
• Avoid keeping sales receipts, which may contain BPA, in your pockets, purse or car. Instead store them in a plastic bag.
• Avoid eating the fatty parts of meat or char-grilled (blackened) foods and don’t over-indulge in dairy products.
• Avoid smoking and choose to maintain a smoke-free environment.

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1. Safe Cosmetics:www.safecosmetics.org
2. Seafood consumption: www.seafoodwatch.org; www.epa.gov/ost/fish
3. Organic Foods and Farmer’s markets: www.pcfma.com, www.beyondpesticides.org
4. Alternative cleaning/household products: www.greenguide.org, www.checnet.org
5. Technical information about various products: http://householdproducts.nlm.nih.gov

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