"In the lecture, the Kandels review Denise Kandel’s earlier work on the gateway hypothesis and on the role of nicotine as a gateway drug, reported in a Science paper in 1975. They also review subsequent studies in which they tested the gateway hypothesis experimentally in a mouse model. In those studies, conducted in collaboration with Amir Levine, Yan You Huang, Bettina Drisaldi, Edmund A Griffin, and others at CUMC, they found that when mice are exposed to nicotine, it alters their brain biochemically and induces activation of a reward-related gene. As a result, nicotine primes the animals’ subsequent response to cocaine, providing a molecular basis for nicotine as a gateway drug for cocaine. Dr. Denise Kandel’s further analysis of 2004 epidemiologic data from a large, longitudinal sample suggested that nicotine also primes human brains to respond to cocaine." ...

The finding of reduced exhaled nitric oxide is an indication that an exposure is causing some sort of inflammatory effect on cells lining the respiratory tract. It doesn't mean anything more or less than that. You can't take two exposures - each of which causes respiratory tract inflammation - and make the statement that the effects of both exposures are equal. Risk posed by an exposure depends on many other factors, including the degree of inflammation induced, the reversibility of the effect, the nature of the exposure, the chronicity of the exposure, etc.

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