REF-1458 · Bentur et al., 2014 · Chest · Paper · PubMed

How much CO does one hookah session put in the blood?

In 47 young adults, COHb rose from 2.0% to 17.6% after 30 min indoors; passive sitters 0.8% to 1.2%. A marker, no exercise tested. From the abstract.

Main caveat: Abstract only; the unclear ">25%" and ">40%" figures could not be checked against the paper.
limited, mixed evidenceMeasured on non-athletes and recreational people

Bentur and colleagues (Haifa, Israel) measured what a single indoor group water-pipe session does to people smoking it and to people sitting with them. Sixty-two volunteers aged 24.9 ± 6.2 years took part: 47 active and 15 passive. COHb in active smokers went from 2.0% ± 2.9% to 17.6% ± 8.8% after 30 min (P < .00001).

The abstract then says "six subjects (12.7%) had a >25% increase, and two subjects (4.2%) had a >40% increase". Plasma nicotine rose from 1.2 ± 4.3 to 18.8 ± 13.9 ng/mL (P < .0001), and plasma cotinine and urinary nicotine and cotinine rose too.

Five exhaled-breath cytokines fell, endothelial function did not change, and the session "was associated with adverse cardiorespiratory changes" that the abstract does not itemise. In passive smokers COHb rose from 0.8% ± 0.25% to 1.2% ± 0.8% (P = .003), as did respiratory rate. The authors call for action to limit water-pipe smoking in coffee shops.

Our reading: a large average COHb rise in one sitting, with a wide spread between people; no cigarette arm in this study, no exercise, no later measurement.

Protocol

Participants: n = 62 volunteers, 47 active and 15 passive, aged 24.9 ± 6.2 years. Sex, usual smoking and baseline fitness are not in the abstract.
Exposure: 30 min of indoor group water-pipe smoking, active or passive.
Outcomes, before and after: COHb, nicotine, cotinine, complete blood count, cardiorespiratory parameters; exhaled breath condensate cytokines and endothelial function (EndoPat device, Itamar Medical) in active smokers only.
Funding and interests: PubMed lists non-US government support; the record names no funder and holds no conflict statement.

Key Results

OutcomeBeforeAfterP
COHb, active (%)2.0 ± 2.917.6 ± 8.8<.00001
Plasma nicotine, active (ng/mL)1.2 ± 4.318.8 ± 13.9<.0001
COHb, passive (%)0.8 ± 0.251.2 ± 0.8.003
As printed, active smokers: "six subjects (12.7%) had a >25% increase, and two subjects (4.2%) had a >40% increase". The abstract does not say whether this means a COHb level above 25% and 40%, a rise of that many percentage points, or a relative rise. A relative rise is unlikely to be meant, since the mean rose about eightfold (our inference), but do not quote these as "COHb above 25%".
Other changes: exhaled breath IL-4, IL-5, IL-10, IL-17 and γ-interferon decreased; endothelial function did not change; respiratory rate rose in passive smokers.
Numbers that do not add up: the conclusion says nicotine rose "18-fold", while 1.2 to 18.8 ng/mL is about 16-fold (our arithmetic); the means may come from different calculations.

Mechanisms

Measured: COHb and nicotine before and after one session.
Authors' interpretation: one session has adverse cardiorespiratory health effects, and the minor changes in passive smokers suggest they too may be affected.
Inference: CO bound to haemoglobin carries no oxygen, and whole-body VO2max is delivery-limited (PHYS-09, established), so a COHb at this level would be expected to cost exercise capacity while it lasts. No exercise was measured here; for exercise after a hookah see REF-1468, for CO and threshold work REF-1459.

Practical Application

How much CO does one hookah session put in the blood? In 47 young adults, COHb rose from 2.0% to 17.6% after 30 min indoors; passive sitters 0.8% to 1.2%. A marker, no exercise tested. From the abstract.
Reading a morning after: this paper measured only straight after the session; for the time course see exhaled CO at 10 h in REF-1460. Not from this paper; the base's own practice: any advice to move a key session after a hookah is practice, not this paper's finding.
Safety: not from this paper; the base's own practice: dizziness, chest pain or palpitations go to a doctor (PHYS-12), and after a hookah a headache, nausea or confusion should be treated as possible CO exposure, not trained through.
What it does not show: any effect on performance; any comparison with a cigarette (no cigarette arm); how long COHb stays up; anything in trained athletes.

Limitations

Abstract only; the unclear ">25%" and ">40%" figures could not be checked against the paper.
Exposure marker, not performance: no exercise test.
Uncontrolled before-and-after; passive smokers are a small comparison group (n = 15) and were not the same people.
Who was measured: young volunteers, not athletes; sex and usual use not given.
Single time point after the session; the wide SD (17.6% ± 8.8%) means the average hides large differences between people.
Baseline: a baseline SD above its mean for COHb (2.0% ± 2.9%) and nicotine (1.2 ± 4.3) suggests some participants arrived with recent exposure (our inference).
Funding and interests: non-US government support per PubMed; no statement in the record.
How this entry was checked and changed
Why this level

(from the abstract) — an uncontrolled pre-post study (rubric B) with a serious limitation beyond its design: the main outcome is an exposure marker, not performance, and nothing was measured during exercise