The effect of nicotine content of cigarettes on fetal growth was studied. From April 1985 to April 1987, 86% of all pregnant women in two well-defined geographical areas responded to a questionnaire on social conditions and lifestyle factors in pregnancy. After excluding multiple births and women who gave birth after elective caesarean section, 10,485 pregnant women were available for the study. Results showed that not only smoking, but also nicotine content in cigarettes was related to reduced fetal growth as measured by birthweight, birth length, and head circumference. The timing of smoking during pregnancy played a role. Smoking before pregnancy or smoking early in pregnancy was not related to fetal growth, nor were the partners' smoking habits. The study corroborates the hypothesis that smoking reduces fetal growth and points to nicotine as one of the potential causal factors.
In 1992, British American Tobacco had its Canadian affiliate, Imperial Tobacco Canada, destroy internal research documents that could expose the company to liability or embarrassment. Sixty of these destroyed documents were subsequently uncovered in British American Tobacco's files.
Legal counsel for Imperial Tobacco Canada provided a list of 60 destroyed documents to British American Tobacco. Information in this list was used to search for copies of the documents in British American Tobacco files released through court disclosure. We reviewed and summarized this information.
Imperial Tobacco destroyed documents that included evidence from scientific reviews prepared by British American Tobacco's researchers, as well as 47 original research studies, 35 of which examined the biological activity and carcinogenicity of tobacco smoke. The documents also describe British American Tobacco research on cigarette modifications and toxic emissions, including the ways in which consumers adapted their smoking behaviour in response to these modifications. The documents also depict a comprehensive research program on the pharmacology of nicotine and the central role of nicotine in smoking behaviour. British American Tobacco scientists noted that ".. the present scale of the tobacco industry is largely dependent on the intensity and nature of the pharmacological action of nicotine," and that "... should nicotine become less attractive to smokers, the future of the tobacco industry would become less secure."
The scientific evidence contained in the documents destroyed by Imperial Tobacco demonstrates that British American Tobacco had collected evidence that cigarette smoke was carcinogenic and addictive. The evidence that Imperial Tobacco sought to destroy had important implications for government regulation of tobacco.
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While many studies report determinants of adolescent cigarette smoking, few identify risk factors for nicotine dependence (ND). This study distinguished between risk factors for three hallmarks of ND including cravings, withdrawal symptoms and tolerance.
A total of 319 novice smokers were followed every 3 months from first puff on a cigarette until the end of secondary school. Outcomes included time to first report of cravings, withdrawal symptoms and tolerance.
Female sex, inhalation, smoking a whole cigarette, weekly smoking, daily smoking and alcohol use each independently increased the incidence of the onset of cravings. Inhalation, weekly smoking, daily smoking and alcohol use predicted the onset of withdrawal symptoms. Withdrawal symptoms, smoking a whole cigarette, monthly smoking, daily smoking and friends and siblings smoking increased the incidence of the onset of tolerance. None of parental education, impulsivity, novelty seeking, self-esteem, depression, stress, parental smoking, physical activity, or participation in sports teams was associated with the outcomes.
The hallmarks of early ND are related to intensity and frequency of cigarette use. Avoidance of daily smoking may be particularly important in preventing the onset of ND symptoms and sustained smoking.
To examine the dimensionality of sensations experienced during initial tobacco smoking.
Cross-sectional survey.
Thirteen secondary schools located in British Columbia, Canada.
Data from 1187 adolescents who responded 'yes' to the question: 'Have you ever tried cigarette smoking, even one or two puffs?'.
Participants answered questions about their demographic characteristics, tobacco smoking history and sensations experienced during their initial smoking episodes.
The sensations appear to represent the following three separate but modestly correlated dimensions: a pleasant dimension defined by feeling good and relaxed; an unpleasant dimension defined by coughing, feeling sick and nervous; and a 'buzz' dimension defined by feeling high and dizzy. The three factors made statistically significant contributions to the prediction of transition to regular smoking (defined as having smoked at least 100 cigarettes in one's life-time) after adjusting for age, sex and age at first puff.
The results suggest that three relatively distinct physiological systems appear to explain the relationship between initial smoking sensations and probability of becoming a regular smoker. Researchers examining sensations experienced during initial tobacco smoking episodes should consider using a three-dimensional profile of symptoms composed of pleasant, unpleasant and buzz dimensions.
BACKGROUND: Studies of exposure to environmental tobacco smoke (ETS) and risk of spontaneous abortion are limited to a few studies of self-reported exposure, and the results have been inconsistent. The aim of this study was to investigate risk of early spontaneous abortion related to ETS and active smoking as defined by plasma cotinine levels. METHODS: We conducted a population-based case-control study in Uppsala County, Sweden, between January 1996 and December 1998. Cases were 463 women with spontaneous abortion at 6 to 12 completed weeks of gestation, and controls were 864 pregnant women matched to cases according to the week of gestation. Exposure status was defined by plasma cotinine concentrations: nonexposed, 15 ng/mL. Multivariable analysis was used to estimate the relative risk of spontaneous abortion associated with exposure to ETS and active smoking. RESULTS: Nineteen percent of controls and 24% of cases were classified as having been exposed to ETS. Compared with nonexposed women, risk of spontaneous abortion was increased among both ETS-exposed women (adjusted odds ratio = 1.67; 95% confidence interval = 1.17-2.38) and active smokers (2.11; 1.36-3.27). We could not show a differential effect of exposure to ETS or active smoking between normal and abnormal fetal karyotype abortions. CONCLUSIONS: Nonsmoking pregnant women exposed to ETS may be at increased risk of spontaneous abortion. Given the high prevalence of ETS exposure, the public health consequences of passive smoking regarding early fetal loss may be substantial.
Persons who use chewing tobacco and snuff experience an increased risk of oral cancer. Because of the pharmacologic properties of nicotine and other constituents of smokeless tobacco, there is also concern that smokeless tobacco products may lead to cardiovascular diseases as well. The relatively few human population studies to date conflict with respect to whether smokeless tobacco use elevates cardiovascular risk factors or leads to cardiovascular disease or death from cardiovascular causes. Hemoglobin adducts to carcinogens present in smokeless tobacco products are measurable in the blood of smokeless tobacco users, indicating that smokeless-tobacco-related carcinogens circulate throughout the body. This prompts a concern that smokeless tobacco may increase risks of other cancers as well. The evidence to date from epidemiologic studies indicates no relationship between smokeless tobacco and bladder cancer, but there is suggestive evidence linking smokeless tobacco use to prostate cancer risk. Only single studies have been conducted of some cancers, and inconsistencies among studies of the same cancer site have been reported. Molecular epidemiologic studies may help identify markers of malignant transformation in smokeless tobacco users that may help in early intervention to prevent or ameliorate the consequences of oral cancer. Further studies are needed to determine more clearly the cardiovascular and non-oral cancer risks potentially associated with smokeless tobacco use.
Nicotine from maternal smoking during pregnancy can cross the placental barrier, possibly resulting in fetal brain sensitization, as indicated by studies in which prenatal exposure to maternal smoking was associated with an increased risk of tobacco use among adolescent offspring. We investigated whether this association persists beyond adolescence by studying cigarette smoking and the use of snus (Swedish oral moist snuff) among 983 young adults from a prospective cohort study conducted in Stockholm, Sweden, between 2006 and 2010. Self-reported questionnaire data were linked with data from national population-based registers from 1983 onward. Maternal smoking during pregnancy was consistently associated with snus use in offspring (e.g., for lifetime daily snus use, adjusted odds ratio = 2.04, 95% confidence interval: 1.32, 3.16; for use of >3 cans of snus per week vs. less, odds ratio = 3.85, 95% confidence interval: 1.57, 10.15). No association was apparent with offspring's smoking, age at onset of tobacco use, or changes in use between 2006 and 2010. These findings indicate that prenatal exposure to maternal smoking is associated with regular and heavy nicotine intake from smokeless tobacco rather than from smoking. This should be further explored in epidemiologic studies that simultaneously address the roles of genetics and social environments.
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Comment In: Am J Epidemiol. 2014 Jun 15;179(12):1418-2124761006
Comment In: Am J Epidemiol. 2014 Jun 15;179(12):1422-324761007
Men and women are thought to regulate their smoking differently and to differ in their susceptibility to nicotine addiction.
Various measures of smoke exposure were compared between 400 current regular tobacco-dependent (DSM-IV) male and female light (1-15 cigarettes per day) and heavy (>15 cigarettes per day) smokers. Between 2 and 8 PM, blood was collected for nicotine and cotinine analysis, and breath carbon monoxide (CO) was measured. Individuals with genetic variants of the CYP2A6 gene were removed from analysis (n = 25).
No significant difference was found in the number of cigarettes per day or CO levels between the sexes. However, females had significantly lower nicotine levels than males (16.9 +/- 0.6 vs. 21.1 +/- 0.07, p
