The short version

Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.

What oxytocin is

A nonapeptide — nine residues, closed into a ring by a single disulfide bond. That bond is what makes it work and what makes it fall apart.

The sequence, and three things it tells you

The FDA substance record gives a systematic name rather than a sequence. Decoded:

Three facts are carried in that one line, and all three matter further down.

The disulfide bridge joins Cys1 to Cys6, closing a six-residue ring and leaving a three-residue tail. This is the bond that fails first in solution, and every degradation product larger than the intact molecule is a disulfide accident.

The C-terminus is amidated — the systematic name ends in glycinamide, not glycine. A preparation that skipped the amidation step is a different and far weaker molecule.

Gln4 and Asn5 are amide side chains, and amides deamidate. Under acid conditions those two positions plus the C-terminal amide are where the molecule comes apart.

What “10 mg” actually contains

Oxytocin acetate is registered as a mono-acetate: one acetic acid equivalent, and the reference-material record states explicitly that the 1067.24 figure “represents the complete salt form, not the free peptide base alone.”

So the peptide fraction of a pure mono-acetate is 1007.19 ÷ 1067.24 = 94.37%, and 10 mg of gross salt is 9.44 mg of peptide. That is the best case — a lyophilisate also carries residual water and counterion beyond stoichiometry.

No source we opened states a peptide-content convention for research-grade oxytocin. Every figure in the reconstitution section assumes 6,000 IU and is therefore a ceiling, not a measurement.

Two residues from vasopressin, and why that is a safety fact

Oxytocin and arginine-vasopressin are both nonapeptides, both with the 1→6 disulfide and the amidated C-terminus, differing at two of nine positions: 3 and 8. Seven residues shared means neither is cleanly selective for its own receptor.

What it is approved for — and the number that should govern everything else

Read directly from the FDA label, the Canadian monograph and the European summary of product characteristics. All three agree.

Approved indications. Antepartum: inducing labour where there is a medical indication, strengthening labour in uterine inertia, and as an adjunct in incomplete or inevitable abortion. Postpartum: producing uterine contraction and controlling bleeding after delivery.

The label restricts elective use in its own words: “Since the available data are inadequate to evaluate the benefits-to-risks considerations, Pitocin is not indicated for elective induction of labor.”

The dose, and the conversion

The conversion from international units to mass comes from two independent regulatory documents on two continents. The European SmPC prints “10 IU (16.7 micrograms)”; a summary of product characteristics published by the Ethiopian regulator states “1 mg of Oxytocin peptide is equivalent to 600 IU.” Both give the same answer:

What that makes a 10 mg vial

Taking 10 mg as net peptide, the vial holds 6,000 IU.

The nasal route, which is where the research doses come from

The behavioural literature standardised on 24 IU sniffed. The historically licensed intranasal dose, recorded in the drug-and-lactation database, was 3 to 4 IU — for promoting milk let-down. The research dose is six to eight times anything ever licensed for that route. The US nasal product has been discontinued; an Australian registration still reads as active, though we could verify only that the entry exists.

Worth noting what the licensed nasal indication actually achieved: one preterm study found a milk-production increase in first-time mothers, and “a larger subsequent trial … found no significant difference versus placebo when mothers received proper lactation support.”

The social literature, and what happened to it

The popular reputation of oxytocin was built on small studies. The large studies that followed did not confirm them. This is the part of the page that matters most, because it is the part the vial is bought for.

Does sniffing it even reach the brain?

Contested, and the honest answer is a little, slowly, and probably not enough to be the whole story.

The evidence for. A 2013 study, read directly: fifteen people, eleven of them dosed, 24 IU intranasal, cerebrospinal fluid sampled once per subject at 45, 60 or 75 minutes. Plasma peaked at 15 minutes. CSF reached significance only at the 75-minute sampling, and there was “no correlation (r < 0.10) between oxytocin plasma and CSF concentrations.” The authors' own caveats: small sample, one timepoint each, lumbar fluid may not reflect what is happening in the ventricles.

The evidence against, and it is a better design. A 2023 study gave intranasal oxytocin with and without a nasal vasoconstrictor — which suppresses absorption into the bloodstream while leaving any direct nose-to-brain route intact. Oxytocin alone raised plasma and produced a robust change in a brain-activity measure. With the vasoconstrictor, blood levels fell and “the majority of neural effects” were abolished with them. The authors conclude the findings “suggest a critical role of peripheral vasculature-mediated routes”, and put blood–brain barrier permeability at under 0.1%.

Put the numbers end to end: roughly 40 µg into the nose, about 2% absorbed, under 0.1% of that crossing into the brain, into a system that clears it in 3 to 20 minutes. Anyone claiming a large, durable central effect from a sniff is claiming something the pharmacokinetics make difficult.

The founding finding, and its replication

The 2005 trust-game experiment is where “the trust hormone” comes from. In 2020 it was subjected to a Registered Report — design and analysis locked before data collection — at over 95% statistical power, and deliberately reproducing the original's minimal-social-contact condition, which earlier replications had left out.

And the 2026 sequel, which is not a simple story

That exploratory signal was then tested properly: pre-registered, n = 359 primary and 578 pooled, 24 IU, double-blind. Oxytocin increased money transferred by 15.1% — €8.29 against €7.20, P = 0.0066; pooled, 16.9% at P = 0.0004.

But the moderator did not behave as advertised. The paper reports “no interaction between OT and dispositional trust within low-trust participants”, with the effect “nearly constant” across trust disposition — so the hypothesis that prompted the study was not the thing that came out of it. The same authors state that up to 90% of reported oxytocin interaction effects may be false positives.

Holding both honestly. The 2020 report killed the general claim at above 95% power. The 2026 study found a real, pre-registered, adequately powered effect in one laboratory economic game measuring money handed to a stranger, while failing to reproduce its own hypothesised moderator. That is not a finding that oxytocin makes people trusting, confident or better at relationships. The authors' own framing — an effect resembling “analgesic effects in pain patients” — is a claim about a deficit state, not an enhancement.

The statistical foundation of the whole field

A second review found something more diagnostic still: statistical power was “critically low and unrelated to the rate of significant results”, and significance was “unrelated to sample size.”

That pattern is the signature. In a healthy literature, larger studies find real effects more often than small ones. Here they did not — which is what you see when results are being selected rather than discovered.

Publication bias, documented by confession

One laboratory opened its own file drawer and published the contents: eight experiments between 2009 and 2014, 453 participants, 13 dependent variables, 25 paradigms — yielding five publications, of which one reported a negative result. In the authors' words, results “were too often not those expected” and their published output became “less and less representative of our actual findings.”

What did not survive

Autism — the clearest test anyone has run

If the social hypothesis were right anywhere, this is where it should have shown. It was funded properly, powered properly, and run for six months.

The trial is SOARS-B, published in the New England Journal of Medicine in 2021 and read directly. 290 children randomised, ages 3 to 17, 24 weeks, escalating to a target of 48 IU a day with permitted escalation to 80 IU. Primary endpoint: the Aberrant Behavior Checklist modified Social Withdrawal subscale, 13 items scored 0 to 39.

Both groups improved by about the same amount. The drug contributed 0.2 points on a 39-point scale. Every secondary endpoint was null: social motivation 0.9 (95% CI −1.0 to 2.9), sociability 0.6 (−1.8 to 3.1), abbreviated IQ 0.1 (−2.9 to 3.0).

The counter-argument, and why the arithmetic defeats it

A 2024 meta-analysis of 12 randomised trials in 498 patients found no overall effect on social impairment but a significant high-dose subgroup: at 48 IU a day, a standardised mean difference of −1.13 (95% CI −1.55 to −0.70). Its own authors caveat that the dose-response analysis “does not allow firm conclusions to be drawn.”

SOARS-B's target dose was 48 IU a day, with escalation to 80. It ran for 24 weeks in 290 children and found nothing. A very large subgroup effect in a pooled analysis, sitting beside a null from a single trial at the same dose — larger than most of the studies in the pool, and independently funded — is far more likely to reflect small-study bias in the pool than a real dose threshold.

What is actually known about harm

Two different risk profiles live under one name, and conflating them is how people get this wrong in both directions.

There is no boxed warning — and that is not reassurance

Checked on five approved US labels. None carries a boxed warning. What gets described as one is the elective-induction restriction, which sits in the label body.

What the label warns about

Administration for induction “should be administered only by the intravenous route and with adequate medical supervision in a hospital.” “Severe water intoxication with convulsions and coma has occurred, associated with a slow oxytocin infusion over a 24-hour period.” Rapid injection produces short-lasting hypotension with flushing and reflex tachycardia. The Canadian monograph adds QT monitoring.

The adverse reaction list — maternal: anaphylaxis, postpartum haemorrhage, cardiac arrhythmia, fatal afibrinogenaemia, subarachnoid haemorrhage, hypertensive episodes, uterine rupture. Fetal and neonatal: bradycardia, arrhythmias, permanent central nervous system damage, fetal death, low Apgar scores, retinal haemorrhage, neonatal seizures.

That list belongs to intravenous obstetric use at term. It is not the risk profile of a sniff — but it is the risk profile of the licensed product, and a page that omits it is not describing the drug.

Water intoxication — the real, documented, mechanistically explained harm

The mechanism is the vasopressin similarity from the top of this page: weak V2 agonism, and an antidiuretic effect stated on the label.

A documented case: a 22-year-old woman on an oxytocin infusion developed generalised tonic-clonic seizures followed by coma eight hours in, from severe hyponatremia with serum sodium below 120 mmol/L. She recovered on hypertonic saline. Exact total dose and incidence data were not in the accessible text.

Two things are both required — the antidiuretic effect and a large hypotonic fluid load. That is why the European SmPC insists on an electrolyte-containing diluent and a fluid balance chart.

What is known about repeated intranasal use in healthy adults

A safety review of 38 randomised controlled trials, 1,529 participants, doses 18 to 40 IU, read directly:

Three serious case reports exist in that whole literature: one of psychotic symptoms with use beyond four weeks, and two of water intoxication — both from excessive fluid intake combined with chronic overuse.

The longest controlled dosing we could find: 40 IU twice daily for 13 weeks in 29 women, and SOARS-B's up to 80 IU a day for 24 weeks in 290 children. So repeated intranasal dosing at that scale has been done under supervision without a safety signal beyond increased appetite, energy and restlessness. That is a real finding — and the same review's authors print the limit of it: safety of “higher-dose, longer-term applications remains unknown.”

Where it stands — approved, and that changes the argument

Every other compound in this library is unapproved somewhere or everywhere. Oxytocin is approved almost everywhere. That makes the position on a research vial harder, not easier.

Canada

Read directly from the Drug Product Database: DIN 00497398, Oxytocin Injection USP, Pfizer Canada ULC, status Marketed, 10 unit/mL, intramuscular and intravenous, prescription, original market date 31 December 1981. A second Canadian product exists under a monograph revised May 2020.

The three Canadian peptide advisories — and why the negatives mean nothing here

Do not over-read that. On every other page in this library a triple negative is worth something. Here it is worth nothing, and for a specific reason: those three documents are advisories about unapproved peptides. Oxytocin is an approved drug with a DIN and a prescription schedule, so it needs no advisory telling anyone it is unauthorised. Absence is not permission. It is a different and stricter category.

United States — and a compounding position that is genuinely unusual

Approved as Pitocin and as generics from at least two manufacturers. We searched the FDA compounding lists and found oxytocin on none of them — not the 503A bulk substances list, not either 503B table, not the nominated-substances list, and not the list of products withdrawn for safety or effectiveness.

The connecting inference in that paragraph is ours. The four list checks and the quoted 503A conditions are direct reads; no FDA document states the reasoning in those words.

One documented quality failure, in a fully regulated market. In August 2017 a US compounder recalled all unexpired lots of oxytocin compounded with Lactated Ringers for sub-potency, citing risk of “a delay in treatment, disruption of clinical care… and worsening of patient's conditions.” Oxytocin potency is a real and failure-prone thing in real supply chains, which the storage section returns to.

Europe

Authorised nationally rather than centrally. A European Medicines Agency listing read directly gives 40 oxytocin products across 18 countries. Oxytocin is WHO-prequalified, and a 2019 WHO, UNFPA and UNICEF joint statement recommends it “should be kept in the cold chain (between 2 and 8 °C) during transportation and storage.”

Sport

Oxytocin does not appear anywhere on the WADA 2026 Prohibited List. We opened the document and searched it. Section S2, which covers peptide hormones and growth factors, names erythropoietins, HIF activators, chorionic gonadotrophin, LH, GnRH and analogues, kisspeptin, corticotrophins, growth hormone and its releasing factors, IGF-1, the fibroblast and hepatocyte growth factors, mechano growth factors, PDGF, thymosin-β4 and VEGF. Oxytocin is in none of those classes. Two independent national anti-doping summaries also contain no mention of it.

The limit, stated plainly. WADA's own Monitoring Program PDF would not open across two routes, so the statement that oxytocin is not monitored rests on two national summaries rather than the primary document. And no source we opened describes a validated test for exogenous oxytocin — which, for an endogenous hormone cleared in minutes, would be analytically difficult. That last point is our reasoning, not a sourced fact.

Reconstitution — and the only compound here where the vial is too strong to measure

Every other page in this library worries about a vial holding too few doses. This one is the reverse, by a factor of thousands.

U-100 syringe, 1 unit = 0.01 mL. All figures assume 10 mg = 6,000 IU of net peptide; if the 10 mg is gross mono-acetate, reduce every IU figure by 5.6%.

3 mL is both the cleanest fill and the largest one possible. One syringe unit is exactly 20 IU, which is two standard ampoules' worth — and the vial itself holds only 3 mL, so nothing larger will physically go in. The smaller fills are listed because they are possible, not because they are better.

Where it stops being measurable

At the 3 mL fill, one syringe mark is 33.3 µg — which is 20 IU, or 20,000 milliunits.

Even at research scale the precision is poor

There is no comfortably legible fill, and that is the honest answer. 3 mL is the most the vial will take, and at 3 mL a 24 IU draw is 1.2 units — between marks. A half-mark misread there is a 42% dose error; at 1 or 2 mL no reading is possible at all. Bigger fills read better on this compound — the reverse of the usual advice, and a consequence of the vial being enormously stronger than anything it would be used for — but the glass runs out of room before the numbers become comfortable. Doses in one vial, for scale: 250 at 24 IU, 125 days at 48 IU a day, and 1,500 to 2,000 at the historically licensed 3–4 IU nasal dose.

Storage — the one compound here whose stability is genuinely well studied

Oxytocin degradation in hot climates is a maternal-mortality problem, so WHO, USP and national regulators have all measured it. This is the best stability evidence in the library, and it points the opposite way to most of these pages.

How it fails

From a 2009 kinetic study, read directly — aqueous oxytocin at 40, 55, 70 and 80 °C across pH 2.0, 4.5, 7.0 and 9.0. Two regimes, split by pH:

At acid pH: deamidation at Gln4, Asn5 and the C-terminal glycinamide — precisely the three amide groups identified at the top of this page. At pH 4.5 and above: disulfide chemistry — trisulfide and tetrasulfide monomers, disulfide-linked dimers and dityrosine-linked aggregates, by thiol–disulfide exchange at the Cys1–Cys6 bridge.

The rates, and they are unusually generous

pH 4.5 is the pH of maximum stability — and it is no accident that the approved label lists the pH as adjusted with acetic acid. Simulated shelf lives from a WHO study: three years at 2–8 °C, one year at 25 °C, six months at 30 °C, and a transport maximum of one week at 40 °C.

The field evidence, which is not theoretical

What that means for a recommended 28 days

This runs opposite to almost every other page here. On most compounds a 28-day in-use limit is argued as a microbiological limit against an unmeasured chemical one. For oxytocin the chemistry is measured, and it is generous: refrigerated aqueous oxytocin loses no measurable activity over four years, with formal cold-chain shelf lives of three to four years. Twenty-eight days sits inside that envelope by a factor of roughly forty.

So the recommended window is a microbiological and handling limit, not a chemical one — governed by preservative status, septum integrity and how many times a needle goes through it. Four qualifications, all load-bearing:

Net position: 28 days is conservative on chemistry and appropriate on microbiology. Refrigerate at 2 to 8 °C, protect from light, do not freeze, and treat heat excursions as the real risk — because with this molecule, uniquely well documented, they demonstrably are.

Questions we actually get

Does it work for bonding, trust or social confidence?

Not as a general claim. The founding trust experiment failed a replication powered above 95%, and a review of the field concludes the evidence “does not provide robust convergent evidence that human trust is reliably associated with OT (or caused by it).” Mean statistical power across 107 studies was 12.2%. The best-powered positive result — 359 people, pre-registered, +15.1% at P = 0.0066 — is real, but it is one laboratory economic game measuring money handed to a stranger, and it failed to reproduce its own hypothesised moderator. That is evidence oxytocin can nudge one behaviour in one task. It is not evidence it improves relationships.

Does it help anxiety?

Nothing we opened supports it, and it is not an approved indication in any label we read. A preregistered meta-analysis of non-social executive function found no overall effect (g = 0.07, p = 0.30). The anxiety-specific meta-analyses were paywalled, so on this question we have no directly-read evidence either way, and we would rather say that than imply we checked.

Does it help autism?

The largest trial says no. 290 children, 24 weeks, up to 80 IU a day: a difference of −0.2 points, 95% CI −1.5 to 1.0, P = 0.61, every secondary endpoint null, and the low-baseline-oxytocin rescue hypothesis tested and null as well.

Does sniffing it reach the brain?

A little, slowly, and probably not enough. Nasal bioavailability around 2%, blood–brain barrier permeability under 0.1%, plasma half-life 3 to 20 minutes — and when a nasal vasoconstrictor blocked absorption into blood, most of the measurable neural effect went with it, meaning it had been travelling by bloodstream rather than nose-to-brain.

Is it safe?

At intranasal research doses, short-term, in healthy adults, the evidence says yes: 38 randomised trials, 1,529 participants, adverse effects in 18% and all mild, at essentially the placebo rate. Extended in one trial to 80 IU a day for 24 weeks in children without a safety signal beyond appetite, energy and restlessness. The risks are dose- and route-specific — the approved label reports maternal death from water intoxication at 40 to 50 milliunits a minute intravenously with hypotonic fluid loading — and the same safety review states that higher-dose, longer-term safety “remains unknown.”

Is it approved?

The molecule is. This vial is not. DIN 00497398, marketed, prescription-only in Canada since 1981; FDA-approved as Pitocin and generics; forty nationally authorised products across eighteen European countries. All of it for labour induction and postpartum bleeding, by intravenous infusion, in hospital. No label anywhere covers social, behavioural or wellness use.

Is it banned in sport?

No. We opened the WADA 2026 Prohibited List and searched it; oxytocin does not appear, and it falls into none of the peptide-hormone classes named in section S2. Two national anti-doping summaries agree. We could not open WADA's own Monitoring Program document, so the statement that it is not monitored is one step short of a direct read.

Why is the vial so much larger than any dose?

Because 10 mg is a normal size for a research peptide and an extraordinary quantity of oxytocin. The approved dose is nanograms per minute; this vial holds six thousand international units. Nothing about the vial size implies anything about an appropriate quantity — it implies the opposite, and the reconstitution section above works through what that does to a syringe.

References

1. Pitocin (oxytocin injection, USP) US prescribing information, 2014 and 2021 revisions, plus the DailyMed structured label — read directly. The approved indications, the 0.5–10 mU/min dose ladder, the standard 1,000 mL dilution, the antidiuretic statement, the 40–50 mU/min water-intoxication threshold, the full adverse reaction list, and the checked absence of any boxed warning.
2. Oxytocin Injection USP labels from Fresenius Kabi (rev. Sept 2022) and West-Ward/Hikma (rev. Dec 2018) — read directly. Two further confirmations of no boxed warning, and the “do not permit to freeze” storage instruction.
3. European Summary of Product Characteristics — read directly. The verbatim “10 IU (16.7 micrograms)” conversion, the 1–20 mU/min range, the electrolyte-diluent and fluid-balance requirements, and the 2–8 °C / 4-year storage statement.
4. Summary of product characteristics published by the Ethiopian FDA — read directly. “1 mg of Oxytocin peptide is equivalent to 600 IU”, the second and independent source for the mass conversion, plus the 3–20 minute half-life.
5. Health Canada Drug Product Database — read directly. DIN 00497398, Pfizer Canada ULC, Marketed, 10 unit/mL, prescription, first marketed 31 December 1981. Plus the Fresenius Kabi Canada product monograph, revised 22 May 2020, for the QT monitoring note.
6. FDA UNII record 1JQS135EYN — read directly. The systematic name from which this page's sequence, disulfide bridge and C-terminal amidation were decoded. The decoding is ours.
7. Reference-material record for oxytocin acetate — the mono-acetate MW of 1067.24 and the explicit statement that it “represents the complete salt form, not the free peptide base alone.”
8. IUPHAR/BPS Guide to Pharmacology — oxytocin as a full agonist at the human vasopressin V2 receptor, pKi 5.4–6.8 against vasopressin's 7.9–9.1.
9. Striepens et al., Scientific Reports 2013 — read directly. The CSF-penetration study: 15 subjects, 11 dosed, 24 IU, one CSF sample each, significance only at 75 minutes, and “no correlation (r < 0.10)” between plasma and CSF.
10. “Sniffing oxytocin: nose to brain or nose to blood?”, Molecular Psychiatry 2023 — read directly. The vasoconstrictor design, the abolition of the majority of neural effects, and the “<0.1%” blood–brain barrier figure.
11. Declerck et al., Registered Report, Nature Human Behaviour 2020 — abstract read via the journal's indexed record; publisher full text robots-blocked. The >95%-powered replication and its null result in the minimal-social-contact condition.
12. PNAS 2026, the pre-registered sequel — n = 359, +15.1% at P = 0.0066, pooled 16.9%, and the failure of the dispositional-trust moderator, with the authors' own “up to 90% of reported OT interaction effects may be false positives.”
13. Quintana, the power analysis — 107 studies from 35 meta-analyses, mean power 12.2%, no equivalence in any of the 26 non-significant meta-analyses, no improvement over eight years.
14. Mierop et al., Perspectives on Psychological Science 2020 — power “unrelated to the rate of significant results”, significance “unrelated to sample size.”
15. Lane et al. 2016 — the file-drawer paper. 8 experiments, 453 participants, 13 dependent variables, 25 paradigms, 5 publications, 1 reporting negatives.
16. Sikich et al., SOARS-B, New England Journal of Medicine 2021, NCT01944046 — read directly. 290 children, 24 weeks, up to 80 IU/day, the verbatim primary result, every null secondary, the failed baseline-oxytocin rescue analysis, and the adverse-event profile.
17. MacDonald et al. 2011, the intranasal safety review — read directly. 38 RCTs, 1,529 participants, 18% reporting mild effects, the near one-to-one placebo relationship, the three serious case reports, and the printed caveat that longer-term safety “remains unknown.”
18. Hawe et al., Pharmaceutical Research 2009 — read directly. The degradation chemistry: deamidation at acid pH, thiol–disulfide exchange and dityrosine aggregation above it, and the half-life figures across four temperatures and four pH values.
19. USP and WHO stability sources — the 90.0–110.0% potency specification, the 48-month refrigerated stability, the simulated shelf lives, and the 2016 systematic review finding 36% of 559 samples across 15 countries out of specification.
20. WADA 2026 Prohibited List, effective 1 January 2026 — opened and searched. Oxytocin absent; the section S2 class list quoted here. Plus two national anti-doping summaries, both searched, both silent on oxytocin.
21. FDA compounding documents — the 503A bulk substances page (updated 14 May 2026), both 503B tables, the nominated-substances list, and 21 CFR 216.24 (current 3 Sept 2026). All four read directly, all four checked negatives, plus FDA's own statement of the three alternative 503A conditions.
22. European Medicines Agency listing PSUSA/00002263/202006, dated 11 February 2021 — read directly. 40 oxytocin products across 18 countries. Plus the 2019 WHO/UNFPA/UNICEF joint statement on cold-chain storage.

What we could not check, listed rather than hidden. Twelve documents refused us. The two that cost most: a 2026 Cortex pooled-equivalence replication of the trust finding, blocked across three routes — so its sample size and effect size appear nowhere on this page; and WADA's own Monitoring Program PDF, robots-blocked across two routes, which is why the sport section stops one step short of a direct read. The anxiety and threat-processing meta-analyses were paywalled, which is why the anxiety answer above says we have no directly-read evidence either way rather than implying a negative. The 2005 trust paper itself was not opened; its claim and status here come from the reviews and replications that examine it. Emotion-recognition meta-analyses are cited second-hand and are unverified as to effect size. The Canadian DPD full-listing route returned 403, so we did not enumerate every Canadian oxytocin DIN. The Australian nasal registration was verified only as an existing, active-reading entry — sponsor and indications did not display. And the case report of hyponatremic seizures gave no total dose or incidence figures in its accessible text.