Tobacco smoking consequences

Evidence from the tobacco industry documents, from research studies that measure free-base directly in tobacco smoke particulate, and from examination of smokeless tobacco products, all show that the level of free-base nicotine as delivered to the tobacco user is a critical variable in the acceptance of tobacco products and their continued use. The physiological impact of the rapid delivery of nicotine in the free-base form is a critical determinant of continued nicotine-seeking behavior, with the unintended consequences of exposure to the other toxic components of tobacco smoke and smokeless tobacco. Evaluating total delivered nicotine alone is not sufficient to characterize product differences. To fully understand the influence nicotine has on the allure of these products, both total and free-nicotine levels must be measured. A comprehensive understanding of nicotine delivery is needed to help find effective means for breaking its addictive nature and, ultimately, in reducing the morbidity and mortality associated with tobacco use. The levels of free-base nicotine must be included as part of any effort to achieve a better understanding of how tobacco products themselves influence their continued use. 

Polycyclic aromatic hydrocarbons (PAHs) represent a class of compounds that contain two or more fused benzene rings. They are environmental pollutants and the most ubiquitous, benzo[a]pyrene (B[a]P), has been upgraded by the International Agency for Research on Cancer to a Group 1 or known human carcinogen [1]. PAHs are products of fossil fuel combustion they are a component of fine particulate matter (size 2.5pm) and as a consequence contaminate the air we breathe, the soil and water supply, and enter the food chain [2, 3]. They are also introduced artificially into smoked, cured, and barbecued food [4, 5], Finally, they are present as a complex mixture in tobacco smoke and second-hand smoke, and are suspect causative agents in human lung cancer [6]. 

I look at many possible causes of fetal damage in this book, but give particular emphasis to man-made environmental toxins, be they chemical pollutants in our air, water, and land, or substances in the consumer marketplace, legal and otherwise. The effects of these toxins are often connected to more than one type of fetal damage. Prenatal exposure to lead, for example, is connected to postnatal occurrences of lower IQ, ADHD, and schizophrenia, usually in different individuals. Prenatal exposure to tobacco smoke, as another example, is connected to a host of effects with adverse postnatal consequences as well. The effects of both sorts of toxins can also be related to other fetal impacts, which in turn are often connected to important social... 

The most common consequence of maternal tobacco smoking during pregnancy is fetal hypoxia. But the metabolites of tobacco smoke also have an impact on fetal development.32 In general, the consequences of maternal tobacco smoking include... 

Nearly all of the metals and isotopes found in tobacco that transfer to tobacco smoke are a consequence of the use of metals found naturally in the soil (some radionuclides in the soil from nuclear reactions and reactors in the area), use of fertilizer containing metals, or agrochemicals applied to the... 

Bonham AC, Chen CY, Mutoh T, load JP (2001) Lung C-flber CNS reflex Role in the respiratory consequences of extended environmental tobacco smoke exposure in young guinea pigs. Environ Health Perspect 109(Suppl 4) 573-578... 

Toxins, either inhaled or ingested, can also reach the fetus. Large molecules in tobacco smoke damage the placenta, and this hampers the ability to convey nntrients from the mother to the baby. As a consequence, babies bom to smokers, or to nonsmokers living in polluted air, are on average, a half-pound lighter than babies bom to mothers breathing nonpolluted air. 

Commonly used drugs, dietary constituents and food additives may be electroactive and consequently are potential sources of interference when biological samples are analysed. Quinine may originate from tonic water, for example, caffeine from coffee and cafifeinated soft drinks and some proprietary stimulants, nicotine and cotinine from tobacco smoke, chloroquine and related compounds from malaria prophylaxis, and pholcodine and other opiate analogues from cold cures. Many such compounds and their metabolites will show an EC response at carbon electrodes under appropriate conditions and can be sources of confusion if unrecognised. 

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