Perfluoroalkyl substances and ovarian hormone concentrations in naturally cycling women.
OBJECTIVE
To examine associations between environmental exposure to perfluoroalkyl substances (PFASs) and ovarian hormone concentrations in naturally cycling women.


METHODS
E2 and P were measured in saliva samples collected daily for a single menstrual cycle and concentrations of PFASs (including perfluoroctane sulfonate [PFOS] and perfluoroctanoic acid) were measured in serum samples collected during the same cycle.


METHODS
Not applicable.


METHODS
A total of 178 healthy, naturally cycling women, aged 25-35 years.


METHODS
None.


METHODS
Mean follicular E2 (cycle days -7 to -1, where 0 is the day of ovulation); mean luteal P (cycle days +2 to 10).


RESULTS
Among nulliparous, but not parous women, PFOS concentrations were inversely associated with E2 (β = -0.025, 95% CI -0.043, -0.007) and P (β = -0.027, 95% CI -0.048, -0.007). Similar, but weaker results were observed for perfluorooctanesulfonic acid. No associations were observed between other PFASs (including perfluoroctanoic acid) and ovarian steroid concentrations, nor were any associations noted in parous women.


CONCLUSIONS
Our results demonstrate that PFOS and perfluorooctanesulfonic acid may be associated with decreased production of E2 and P in reproductive age women. These results suggest a possible mechanism by which PFASs affect women's health, and underscore the importance of parity in research on PFASs and women's reproductive health.
Department of Obstetrics and Gynecology, University of Rochester School of Medicine and Dentistry, Rochester, New York. Electronic address: Emily_barrett@urmc.rochester.edu.
Emily S
ES
Barrett
Department of Biostatistics and Computational Biology, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Chongshu
C
Chen
Department of Biostatistics and Computational Biology, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Sally W
SW
Thurston
Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway.
Line Småstuen
LS
Haug
Division of Environmental Medicine, Norwegian Institute of Public Health, Oslo, Norway.
Azemira
A
Sabaredzovic
The Cancer Center, Oslo University Hospital, Oslo, Norway.
Frøydis Nyborg
FN
Fjeldheim
The Cancer Center, Oslo University Hospital, Oslo, Norway.
Hanne
H
Frydenberg
Department of Human Evolutionary Biology, Harvard University, Cambridge, Massachusetts.
Susan F
SF
Lipson
Department of Human Evolutionary Biology, Harvard University, Cambridge, Massachusetts.
Peter T
PT
Ellison
The Cancer Center, Oslo University Hospital, Oslo, Norway; Institute of Community Medicine, UiT, The Arctic University of Norway, Tromsø, Norway.
Inger
I
Thune
D000328:Adult; D017738:Alkanesulfonic Acids / Q000097:blood; D015415:Biomarkers / Q000378:metabolism; D052244:Endocrine Disruptors / Q000009:adverse effects / Q000097:blood*; D004781:Environmental Exposure; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D005466:Fluorocarbons / Q000009:adverse effects / Q000097:blood*; D006801:Humans; D008597:Menstrual Cycle / Q000097:blood* / Q000187:drug effects; D010053:Ovary / Q000187:drug effects / Q000378:metabolism*; D010298:Parity; D011374:Progesterone / Q000378:metabolism*; D018570:Risk Assessment; D012463:Saliva / Q000378:metabolism*; D013997:Time Factors
D017738:Alkanesulfonic Acids; D015415:Biomarkers; D052244:Endocrine Disruptors; D005466:Fluorocarbons; D011374:Progesterone; D004958:Estradiol; C076994:perfluorooctane sulfonic acid
E(2); PFOS; Perfluoroalkyl substances; endocrine disruptors; progesterone