Estrone (E1) Unit Converter
Estrone (E1) Unit Converter
Convert oestrone between pg/mL, ng/L and pmol/L — and see the point the number exists to make: after the menopause, oestrone made in fat from androstenedione is the dominant oestrogen, which is why a postmenopausal oestradiol can be unmeasurable while the oestrone is substantial.
Estrone (E1) converter
Mass ⇄ molarOestrone 100 pg/mL
The conversion, and the two units that are the same number
pg/mL = pmol/L ÷ 3.69864
because 3.69864 = 1 pg/mL (10⁻⁹ g/L) ÷ 270.37 g/mol, the molecular weight of oestrone
- MW 270.37
- oestrone (E1), C₁₈H₂₂O₂ — the aromatic A-ring of the oestrogens with a ketone at C17 where oestradiol has a hydroxyl. That single difference is what interconverts them
- pg/mL = ng/L
- identical concentrations. An oestrone of 100 pg/mL is 100 ng/L, and if two reports disagree it is not the units
- 3.70 for E1, 3.67 for E2
- oestrone and oestradiol have almost the same molecular weight — 270.37 against 272.38 — so their conversion factors are nearly identical. Using one for the other introduces an error under 1%, which is the one confusion between these two analytes that does not matter. Every other confusion between them does
- 17β-hydroxysteroid dehydrogenase
- interconverts oestrone and oestradiol reversibly. Oestrone is the more abundant and the less potent of the two; it functions largely as a circulating reservoir that tissues convert to oestradiol locally
- aromatase in adipose tissue
- converts androstenedione to oestrone. This is the dominant route of oestrogen production once the ovaries have stopped, which is why postmenopausal oestrone concentration tracks body fat and why aromatase inhibitors work where they do
Worked example
Oestrone 100 pg/mL
100 pg/mL = 100 ng/L — identical, and that is the whole of that conversion
100 × 3.69864 = 370 pmol/L (369.9 before rounding)
In a premenopausal woman that is mid-interval: Mayo's 17–200 pg/mL is 63–740 pmol/L
In a postmenopausal woman the same result is well above the 7–40 pg/mL band (26–148 pmol/L) — the usual explanations being oestrogen replacement or a high fat mass driving adipose aromatase, not ovarian activity
And the comparison that makes the page: that postmenopausal woman's oestradiol may be under 30 pg/mL and often close to the detection limit of the assay, while her oestrone is 100. After the menopause E1 exceeds E2, and reading the low oestradiol as "no oestrogen" is a mistake
Oestrone and oestradiol across a lifetime
| Setting | Dominant oestrogen | Main source | What the pair looks like |
|---|---|---|---|
| Premenopausal, cycling | Oestradiol (E2) | Granulosa cells of the developing follicle, under FSH drive | E2 varies several-fold across the cycle and exceeds E1 for most of it, peaking pre-ovulation |
| Pregnancy | Oestriol (E3), then E2 | Placenta, using foetal adrenal precursors | All three rise enormously; E3 is the one that is screened on |
| Postmenopausal | Oestrone (E1) | Aromatisation of adrenal and ovarian stromal androstenedione in adipose tissue, and to a lesser extent muscle, skin and bone | E2 falls to the bottom of, or below, the assay’s range while E1 persists at tens of pg/mL. E1 exceeds E2, reversing the premenopausal relationship |
| Postmenopausal with obesity | Oestrone, more so | More adipose tissue means more aromatase | Higher E1 for the same androstenedione — the mechanism behind the association between obesity and oestrogen-receptor-positive endometrial and breast cancer after the menopause |
| On an aromatase inhibitor | Neither — both suppressed | The enzyme converting androstenedione to oestrone and testosterone to oestradiol is blocked | E1 and E2 both fall to very low concentrations; ultrasensitive assays are needed to confirm adequate suppression |
| Adult male | Oestradiol, marginally | Aromatisation of testosterone and androstenedione in fat, brain, bone and testis | Both low; the ratio to testosterone is what matters in gynaecomastia |
Mayo Clinic Laboratories reference values, oestrone by LC-MS/MS
| Group | pg/mL | pmol/L |
|---|---|---|
| Female, premenopausal | 17–200 | 63–740 |
| Female, postmenopausal | 7–40 | 26–148 |
| Adult male | 10–60 | 37–222 |
| Female, Tanner stage I | Undetectable–29 | Undetectable–107 |
| Female, Tanner stage V | 17–200 | 63–740 |
| Male, Tanner stage I | Undetectable–16 | Undetectable–59 |
| Male, Tanner stage V | 10–60 | 37–222 |
When an oestrone is actually worth measuring
| Question | Does E1 help? | Better or additional test |
|---|---|---|
| Is this woman ovulating? Where is she in her cycle? | No | Oestradiol, LH, and a mid-luteal progesterone |
| Has she gone through the menopause? | Rarely needed | FSH with oestradiol, in the right clinical context; the diagnosis is usually clinical |
| Is aromatase inhibition complete in a woman on an aromatase inhibitor? | Yes — E1 is the more abundant oestrogen in that population and is often the more measurable of the two | An ultrasensitive mass spectrometry E1 and E2 together |
| Why does this man have gynaecomastia? | Sometimes, as part of an oestrogen/androgen assessment | Oestradiol, testosterone, LH, hCG, and liver function |
| Is this postmenopausal woman getting oestrogen from somewhere? | Yes — including undisclosed or topical oestrogen, and adipose production | E1 with E2; oral preparations give a characteristically E1-dominant profile |
| Is a child in precocious puberty? | Occasionally, as part of an ultrasensitive oestrogen panel | Ultrasensitive oestradiol, LH, FSH and bone age |
The oestrogen that takes over when the ovaries stop
Oestrone is reported in picograms per millilitre, in nanograms per litre and in picomoles per litre. The first two are numerically identical, and the molar conversion runs through oestrone’s molecular weight of 270.37: one picogram per millilitre is 3.69864 picomoles per litre, so 100 pg/mL is 370 pmol/L. Because oestradiol’s molecular weight of 272.38 is almost the same, its factor of 3.67 is almost the same too — which means that mixing up the two conversion factors is harmless, and mixing up the two analytes is not.
Oestrone and oestradiol are interconverted reversibly by 17β-hydroxysteroid dehydrogenase, and they differ by a single functional group: a ketone at C17 in oestrone where oestradiol has a hydroxyl. Oestradiol is several times the more potent at the oestrogen receptor and is the oestrogen that matters in a cycling woman, where granulosa cells under FSH drive make it directly and its concentration swings several-fold across the cycle. Oestrone in that setting is largely a circulating reservoir that tissues convert to oestradiol locally, and measuring it adds little.
After the menopause the relationship reverses, and that reversal is the substance of this page. The ovarian follicles that made oestradiol are gone, but the adrenal cortex and the ovarian stroma continue to secrete androstenedione, and aromatase in adipose tissue — with smaller contributions from muscle, skin, bone and brain — converts it to oestrone. Oestrone therefore becomes the dominant circulating oestrogen, and a postmenopausal woman can have an oestradiol at or below the detection limit of the assay while carrying an oestrone of several tens of picograms per millilitre. Reading that unmeasurable oestradiol as “no oestrogen” is wrong: the source has moved from the gonad to the fat, and the amount produced now scales with fat mass. That is the mechanism behind the association between obesity and oestrogen-receptor-positive endometrial and postmenopausal breast cancer, and it is why aromatase inhibitors, which block precisely this conversion, are effective in exactly this population.
Practically, then, oestrone is the better measurement whenever the ovary is not the source. It is used to confirm adequate suppression on an aromatase inhibitor, where both oestrogens must be measured by an ultrasensitive mass spectrometry method; it helps in assessing oestrogen excess in men with gynaecomastia; and it identifies exogenous oestrogen exposure, since oral preparations undergo first-pass conversion in the gut wall and liver and produce a characteristically oestrone-dominant profile that transdermal preparations do not. For a cycling premenopausal woman, oestradiol with the day of the cycle attached remains the measurement that answers the question.
Frequently asked questions
How do you convert oestrone from pg/mL to pmol/L?
Multiply by 3.69864, which is one picogram per millilitre divided by oestrone’s molecular weight of 270.37 g/mol. So 100 pg/mL is 370 pmol/L, and dividing by the same factor takes a pmol/L result back to pg/mL. Picograms per millilitre and nanograms per litre are numerically identical, so no conversion is needed between those two.
What is the difference between estrone and estradiol?
They are the two main non-pregnancy oestrogens and differ by a single functional group — a ketone at C17 in oestrone where oestradiol has a hydroxyl — with 17β-hydroxysteroid dehydrogenase interconverting them. Oestradiol is several times more potent at the oestrogen receptor and is the oestrogen of the reproductive years, made by the developing follicle. Oestrone is weaker, more abundant after the menopause, and made largely by aromatisation of androstenedione in adipose tissue. Their molecular weights are almost identical, so their unit conversion factors are nearly the same, but they are not interchangeable results.
Why is my oestradiol very low but my oestrone normal after the menopause?
Because that is the expected postmenopausal pattern. The ovarian follicles that made oestradiol have gone, so oestradiol falls to the bottom of the assay’s range. Meanwhile the adrenal glands and the ovarian stroma continue to make androstenedione, and aromatase in fat converts it to oestrone — which then becomes the dominant circulating oestrogen. A very low oestradiol after the menopause does not mean no oestrogen exposure; it means the source has moved from the ovary to adipose tissue, and how much is produced depends partly on how much adipose tissue there is.
Does obesity raise oestrone?
Yes, and the mechanism is direct: adipose tissue is where most postmenopausal aromatase activity lives, so more fat means more conversion of androstenedione to oestrone. The effect is much more pronounced after the menopause, when adipose aromatisation is the main remaining route of oestrogen production rather than a minor one. This is the accepted explanation for the association between obesity and oestrogen-receptor-positive endometrial cancer and postmenopausal breast cancer.
Why is oestrone measured on aromatase inhibitor treatment?
Because it is the oestrogen that population makes most of, and because the purpose of the drug is to stop it being made. Aromatase inhibitors block the conversion of androstenedione to oestrone and of testosterone to oestradiol, and confirming adequate suppression means measuring concentrations far below the usual reference intervals — which requires an ultrasensitive mass spectrometry assay for both oestrogens, since routine immunoassays are unreliable at that level.
Related calculators
References
- Mayo Clinic Laboratories. Test ID: E1 — Estrone, Serum. Liquid chromatography-tandem mass spectrometry. Reference values: adult males 10–60 pg/mL; premenopausal females 17–200 pg/mL; postmenopausal females 7–40 pg/mL.
- Simpson ER. Sources of estrogen and their importance. J Steroid Biochem Mol Biol. 2003;86(3–5):225–230. doi:10.1016/S0960-0760(03)00360-1
- Rosner W, Hankinson SE, Sluss PM, Vesper HW, Wierman ME. Challenges to the measurement of estradiol: an Endocrine Society position statement. J Clin Endocrinol Metab. 2013;98(4):1376–1387. doi:10.1210/jc.2012-3780
- Key TJ, Appleby PN, Reeves GK, et al. Body mass index, serum sex hormones, and breast cancer risk in postmenopausal women. J Natl Cancer Inst. 2003;95(16):1218–1226. doi:10.1093/jnci/djg022
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.