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#566 - Girls Are Reaching Puberty Early, 01-Oct-1997

Many girls in the U.S. are entering puberty much earlier than normal,
according to a recent study reported in the journal PEDIATRICS.[1] And
there is some evidence that exposure to environmental chemicals many be
contributing to the phenomenon.

Current medical texts say that only 1% of girls show signs of puberty,
such as breast development and pubic hair, before the age of 8.[2] But
the PEDIATRICS study found that a substantial proportion of American
girls have one or both of these characteristics at age 7 and that 1% of
all girls now have one or both of them at age 3.

Data for the study were collected by 225 physicians in suburban
practices who recorded the physical growth of 17,077 of their young
female patients, of whom 90.4% were white and 9.6% were African-
American.[1] The authors of the study say their sample of girls was not
selected randomly and therefore may not accurately represent the entire
U.S. population of female children. However, they know of no systematic
bias in their sample and they believe the girls they studied are
typical.

The early onset of puberty was observed in both white and African-
American girls, but with significant differences between them. African-
Americans showed the first signs of sexual maturity about a year
earlier than whites. Previous studies had observed these racial
differences, but no one has provided an explanation for them.[3] (There
is some evidence that these racial differences have developed only
recently. A 1944 study reportedly found no such differences.[4])

The new PEDIATRICS study found that, at age 7, 27.2% of African-
American girls, and 6.7% of white girls had either breast or pubic hair
development; by age 8, 48.3% of African-American girls and 14.7% of
white girls had one or both of these characteristics. The study also
found that 1% of whites and 3% of African-Americans had such
characteristics at age 3.

The study found that the average age for onset of puberty was just
under 9 for African-Americans and was 10 to 10 1/2 for whites. Current
medical texts say puberty begins between the ages of 11 and 12, on
average.

The authors say it is conceivable that their sample might have been
biased by young girls entering puberty whose parents became concerned
and sent them for medical examination. If so, they said, an equivalent
parental concern should produce, in their sample, an excess of 12 year
olds who show no development, but no such excess appeared in the data.

The study found that age of first menstruation has not changed. Average
age of first menstruation in whites is 12.8 years and in African-
Americans is 8 months earlier. This is a pattern that has held steady
for 30 or 40 years, the authors say.

The principal author of the study, Dr. Marcia E. Herman-Giddens told
the NEW YORK TIMES, "The reason I did this study is that in my clinical
practice, I was seeing a lot of young girls coming in with pubic hair
and breast development, and it seemed like there were too many, too
young. But I don't think any of us expected to see such a large
proportion of girls developing this early," she said.[5] Dr. Herman-
Giddens is an adjunct professor of maternal and child health at the
University of North Carolina (Chapel Hill) School of Public Health.

The PEDIATRICS study suggests that environmental chemicals that mimic
estrogens might be involved. The authors point to a small study of 10
girls who entered puberty early as a result of exposure to hair-care
products that had estrogenic properties.[6] They suggest that other
well-known estrogenic chemicals, such as PCBs (polychlorinated
biphenyls) should be studied to see if they are implicated in early-
onset puberty.

As it happens, a very recent preliminary report indicates that PCBs and
DDE (a breakdown product of the pesticide DDT) may indeed be associated
with early sexual development in girls. Both DDE[7] and PCBs[8] are
known to mimic, or interfere with, sex hormones.

According to the British journal NEW SCIENTIST, Dr. Walter Rogan
described preliminary data at a conference on environmental estrogens
in July in Arlington, Va.[9] Rogan is acting clinical director at the
U.S. National Institute of Environmental Health Sciences (NIEHS) in
Research Triangle, North Carolina.

According to NEW SCIENTIST, between 1979 and 1982 Rogan and his
colleagues measured PCBs and DDE in blood and breast milk of hundreds
of pregnant women in North Carolina. They also measured the chemicals
in fetal blood collected from umbilical cords after birth. They then
monitored the physical growth and maturity of 600 of the children of
these women. According to NEW SCIENTIST, girls with the highest pre-
natal exposures to the chemicals entered puberty 11 months earlier than
girls with lower exposures. For boys, exposures to the chemicals before
birth made no apparent difference in sexual development.

Rogan minimizes the importance of his data, but others say his findings
are significant because few studies have ever looked at chemical
effects on the offspring of exposed women, and the women Rogan studied
were exposed to PCBs and DDE from normal diet and environmental
sources, not from industrial accidents of other abnormally high
exposures.

Is there other evidence that estrogen-mimicking chemicals could speed
up the sexual maturation of mammals? At least three laboratory studies
seem relevant here:

** Female rats were fed a diet that contained a phytoestrogen (a
naturally-occurring plant that mimics estrogen). The ovulation of their
offspring was prematurely terminated --a sign that their sexual
development had been speeded up by their mother's diet.[10]

** Exposing immature female mice to high levels of methoxychlor
stimulated them to early sexual maturity.[11] Methoxychlor is currently
used in this country as a substitute for DDT which was banned in the
1970s, partly because of its estrogenic properties. The estrogenic
properties of methoxychlor have become well-established in recent
years, but its use continues.

** Rats treated once with certain PCBs on the second or third day of
life exhibited a permanent alteration in sexual development.
Specifically, young female rats treated once with Monsanto's Arochlor
1221 (a PCB) achieved sexual maturity in 28 days whereas untreated
controls reached sexual maturity in 42 days.[12]

The authors of the PEDIATRICS study wrote, "This study strongly
suggests that earlier puberty is a real phenomenon, and this has
important clinical, educational, and social implications."

As the authors of the pediatrics study hint, the clinical implications
may be serious. The arrival of puberty is driven by naturally-occurring
estrogenic hormones coursing through the blood stream. There is now
considerable evidence that breast cancer is promoted by the presence of
these same naturally-occurring estrogens. Women who go through puberty
early have a longer-than-normal exposure to these estrogens and
therefore may be in greater danger of getting breast cancer.[13,14]

Breast cancer now kills 46,000 American women each year and the number
is steadily rising; the reasons for the rise are poorly understood but
there is widespread agreement that estrogen plays a role in the
disease.[15] In recent years, researchers have hypothesized that
environmental chemicals that mimic estrogens may also promote breast
cancer.[16]

The social implications of early-onset puberty are obvious: young
children with mature bodies must cope with feelings, urges and
differences from their peers that most children are not well-equipped
to handle. For many children, early pubescence may be a significant
burden to bear.

--Peter Montague (National Writers Union, UAW Local 1981/AFL-CIO)

=====

[1] Marcia E. Herman-Giddens and others, "Secondary Sexual
Characteristics and Menses in Young Girls Seen in Office Practice: A
Study from the Pediatric Research in Office Settings Network,"
PEDIATRICS Vol. 99, No. 4 (April 1997), pgs. 505-512.

[2] G. Bacon and others, A PRACTICAL APPROACH TO PEDIATRIC
ENDOCRINOLOGY (Chicago: Year Book Medical Publishers, 1982), pg. 189.
Current ideas about normal age of puberty are derived from studies such
as: W.A. Marshall and J.M. Tanner, "Variations in Pattern of Pubertal
Changes in Girls," ARCHIVES OF DISEASES OF CHILDHOOD Vol. 44 (1969),
pgs. 291-303; Peter A. Lee, "Normal Ages of Pubertal Events Among
American Males and Females," JOURNAL OF ADOLESCENT HEALTH CARE Vol. 1
(1980), pgs. 26-29; Arline B. Nicholson and Charles Hanley, "Indices of
Physiological Maturity: Derivation and Interrelationships," CHILD
DEVELOPMENT Vol. 24, No. 1 March 1953), pgs. 3-38; and Earle L.
Reynolds and janet V. Wines, "Individual Differences in Physical
Changes Associated With Adolescence in Girls," AMERICAN JOURNAL OF
DISEASES OF CHILDREN Vol. 75 (1948), pgs. 329-350.

[3] For example see, William R. Harlan and others, "Secondary sex
characteristics of girls 12 to 17 years of age: The U.S. Health
Examination Survey,"JOURNAL OF PEDIATRICS Vol. 96, No. 6 (June 1980),
pgs. 1074-1078.

[4] See Leona Zacharias and Richard J. Wurtman, "Age at Menarche," NEW
ENGLAND JOURNAL OF MEDICINE Vol. 280, No. 16 (April 17, 1969), pgs.
868- 875, describing results reported in N. Michaelson, "Studies in
physical development of Negroes. IV. Onset of puberty," AMERICAN
JOURNAL OF PHYSICAL ANTHROPOLOGY Vol. 2 (1944), pgs. 151-166.

[5] Susan Gilbert, "Early Puberty Onset Seems Prevalent," NEW YORK
TIMES April 9, 1997, pg. 10.

[6] Chandra M. Tiwary, "Premature sexual development in children
following the use of placenta and/or estrogen containing hair product
(s)," PEDIATRIC RESEARCH Vol. 135 (1994), pg. 108A. Abstract only.

[7] William R. Kelce and others, "Persistent DDT metabolite p,p'-DDE is
a potent androgen receptor antagonist," NATURE Vol. 375 (June 15,
1995), pgs. 581-585.

[8] James D. McKinney and Chris L. Waller, "Polychlorinated Biphenyls
as Hormonally Active Structural Analogues," ENVIRONMENTAL HEALTH
PERSPECTIVES Vol. 102, No. 3 (March 1994), pgs. 290-297.

[9] Nell Boyce, "Growing up too soon," NEW SCIENTIST August 2, 1997,
pg. 5.

[10] Patricia L. Whitten and others, "A Phytoestrogen Diet Induces the
Premature Anovulatory Syndrome in Lactationally Exposed Female Rats,"
BIOLOGY OF REPRODUCTION Vol. 49 (1993), pgs. 1117-1121.

[11] Laura M. Walters and others, "Purified Methoxychlor Stimulates the
Reproductive Tract in Immature Female Mice," REPRODUCTIVE TOXICOLOGY
Vol. 7 (1993), pgs. 599-606.

[12] Ronald J. Gellert, "Uterotrophic Activity of Polychlorinated
Biphenyls (PCB) and Induction of Precocious Reproductive Aging in
Neonatally Treated Rats," ENVIRONMENTAL RESEARCH Vol. 16 (1978), pgs.
123-130.

[13] B.A. Stoll and others, "Does early physical maturity influence
breast cancer risk?" ACTA ONCOLOGICA Vol. 33, No. 2 (1994), pgs. 171-
176.

[14] D. Apter, "Hormonal events during female puberty in relation to
breast cancer risk," EUROPEAN JOURNAL OF CANCER PREVENTION Vol. 5, No.
6 (1996), pgs. 476-482.

[15] Eliot Marshall, "Search for a Killer: Focus Shifts from Fat to
Hormones," SCIENCE Vol. 259 (January 29, 1993), pgs. 618-621.

[16] Devra Lee Davis and H. Leon Bradlow, "Can Environmental Estrogens
Cause Breast Cancer?" SCIENTIFIC AMERICAN Vol. 273, No. 4 (October,
1995), pgs. 166-172.

Descriptor terms: child development; estrogens; hormone disrupters;
endocrine disrupters; hormones; dde; pcbs; african-americans; studies;
pediatrics; ddt; walter rogan; methoxychlor; phytoestrogens; arochlor
1221; breast cancer;