
That's quite interesting, but the best thing about this study is the methodology. This is the first neuroimaging study I've seen which involved a car. Not a picture of a car. An actual car.
They used PET scanning to measure the binding of nicotine to brain nicotinic acetylcholine receptors (nAChRs), the major target of the drug. They first injected people with a radioactive tracer compound, in this case a nicotine-like molecule which binds to nAChRs. Because nicotine binds to the same target, it displaces the tracer and reduces the radioactive signal from the brain.
Where did the car come in? Well, volunteers were scanned before and after sitting in a car for one hour, next to a smoker who smoked cigarettes over the course of the hour. An average of 3.7 cigarettes to be precise. The windows were closed to keep the car nice and smoky.
The scene was made even more remarkable by the fact that the subject was still being injected with the tracer compound during this period: they were attached to a drip which went through a little gap in the window and outside. Sadly, they don't show us any pictures...

Anyway, they found that secondhand smoking did cause modest but significant binding to the receptors. The graph shows tracer binding in four areas of the brain - the lower the line, the more nicotine. After secondhand smoke, the lines go down.
After sitting in a "placebo car" in which no-one was smoking, however, there was no effect (the empty circles.) Then later on, the participants were able to smoke some cigarettes first-hand: this had a much stronger effect as you'd expect.
The effect of secondhand smoke was pretty large, though. Actual smoking led to nicotine receptor occupancy of about 50%. Secondhand smoke weighed in at about 20%. Interestingly, in the participants who were regular smokers themselves, the secondhand smoke made them report increased cravings for a cigarette - and this correlated with secondhand smoke nicotine binding (though only in one area of the brain.)

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