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  I've heard that girls are reaching puberty early, but this is
  ridiculous.  I entered puberty at age 10; most of my friends, age 11.
  That was in the 1950's.  Now, some girls are entering at age 3!  Will my
  daughter's grandchildren (if they are allowed to be conceived and
  carried to term) be born into puberty?  ...Bunny Snow
  =======================Electronic Edition========================
  .                                                               .
  .           RACHEL'S ENVIRONMENT & HEALTH WEEKLY #566           .
  .                     ---October 2, 1997---                     .
  .                          HEADLINES:                           .
  .               GIRLS ARE REACHING PUBERTY EARLY                .
  .                          ==========                           .
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  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
  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.
  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.
  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,"
  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;
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                                          --Peter Montague, Editor