Hypothesis: exposure to endocrine-disrupting chemicals may interfere with timing of puberty.
A recent decline in onset of puberty - especially among girls - has been observed, first in the US in the mid-1990s and now also in Europe. The development of breast tissue in girls occurs at a much younger age and the incidence of precocious puberty (PP) is increasing. Genetic factors and increasing prevalence of adiposity may contribute, but environmental factors are also likely to be involved. In particular, the widespread presence of endocrine-disrupting chemicals (EDCs) is suspected to contribute to the trend of earlier pubertal onset. The factors regulating the physiological onset of normal puberty are poorly understood. This hampers investigation of the possible role of environmental influences. There are many types of EDCs. One chemical may have more than one mode of action and the effects may depend on dose and duration of the exposure, as well as the developmental stage of the exposed individual. There may also be a wide range of genetic susceptibility to EDCs. Human exposure scenarios are complex and our knowledge about effects of mixtures of EDCs is limited. Importantly, the consequences of an exposure may not be apparent at the actual time of exposure, but may manifest later in life. Most known EDCs have oestrogenic and/or anti-androgenic actions and only few have androgenic or anti-oestrogenic effects. Thus, it appears plausible that they interfere with normal onset of puberty. The age at menarche has only declined by a few months whereas the age at breast development has declined by 1 year; thus, the time span from initiation of breast development to menarche has increased. This may indicate an oestrogen-like effect without concomitant central activation of the hypothalamic-pituitary axis. The effects may differ between boys and girls, as there are sex differences in age at onset of puberty, hormonal profiles and prevalence of precocius puberty.
Mouritsen
A
A
Department of Growth and Reproduction, University of Copenhagen, Rigshospitalet, Copenhagen, Denmark. akm@dadlnet.dk
Aksglaede
L
L
Sørensen
K
K
Mogensen
S Sloth
SS
Leffers
H
H
Main
K M
KM
Frederiksen
H
H
Andersson
A-M
AM
Skakkebaek
N E
NE
Juul
A
A
D000726:Androgen Antagonists / Q000494:pharmacology; D044383:Black People; D002648:Child; D052244:Endocrine Disruptors / Q000633:toxicity*; D004785:Environmental Pollutants; D004967:Estrogens / Q000494:pharmacology; D005060:Europe / Q000453:epidemiology; D005260:Female; D006801:Humans; D008297:Male; D008572:Menarche / Q000187:drug effects / Q000502:physiology; D009749:Nutrition Surveys; D011627:Puberty / Q000187:drug effects* / Q000502:physiology*; D011628:Puberty, Delayed / Q000209:etiology; D011629:Puberty, Precocious / Q000139:chemically induced / Q000453:epidemiology; D012741:Sexual Maturation / Q000187:drug effects / Q000502:physiology; D014481:United States / Q000453:epidemiology; D044465:White People; D001741:Black or African American
D000726:Androgen Antagonists; D052244:Endocrine Disruptors; D004785:Environmental Pollutants; D004967:Estrogens