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Nevertheless, in utero cigarette smoke exposure was correlated with impaired Th1 responses to polyclonal stimulation and augmented Th2 differentiation along with enhanced Th2-type cytokine production, a known contributors to allergic inflammation [73,77]

These risk patterns were consistent between sexes and across histological types, and were not explained by the type of cigarettes smoked, levels of inhalation or cholesterol and beta-carotene intake

Similarly, BS 44/25 means particles passing through mesh 44 but retained on mesh 52

Both deliver a very mild draw with minimal tobacco intensity

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