Changes in the levels of ACTH and cortisol after passive exposure to cigarette smoke in smokers and non-smokers

Plasma ACTH and cortisol levels were studied in smokers and non smokers, (exposed or not to smoke of the environment), after passive exposure to cigarette smoking. Non smokers, usually not exposed to smoke, show a rise in both hormones, whereas smokers and non smokers commonly exposed to smoke don't show any change in ACTH and cortisol levels. These data suggest that nicotine acts as an acute stimulus on the hypophysis-adrenal axis even passively inhaled.     

Maternal smoking in pregnancy and sex differences in perinatal death between boys and girls

The sex difference in perinatal mortality in developed countries is largely unexplained. The current study evaluated the differences in the impact of maternal smoking during pregnancy on the risk of perinatal death between males and females. The analysis involved 11,469 and 9,404 newborns derived from two population-based birth cohorts in Northern Finland, for 1966 and 1985-86, respectively. The perinatal mortality rate was 23 per thousand in the 1966 cohort and 9 per thousand in the 1985-86 cohort. The rate ratio (RR) for mortality for males over females is 1.15 and 1.60 in the two cohorts, respectively. Among children whose mothers smoked during pregnancy, the RR was 2.2 (95% CI 1.0, 4.7) for the former cohort and 4.8 (95% CI 1.5, 15.2) for the later cohort; and among the children whose mothers did not smoke the corresponding RR was 1.2 (95% CI 0.9, 1.6) and 1.1 (95% CI 0.6, 1.9). Maternal smoking during pregnancy could be an important determinant accounting for the excess perinatal death for males over females. Our results encourage evaluation of the findings among other populations.     

Estimation of urinary cotinine cut-off points distinguishing non-smokers, passive and active smokers

An objective assessment of exposure to tobacco smoke may be accomplished by means of examining particular biomarkers in body fluids. The most common biomarker of tobacco smoke exposure is urinary, or serum, cotinine. In order to distinguish non-smokers from passive smokers and passive smokers from active smokers, it is necessary to estimate cotinine cut-off points. The objective of this article was to apply statistical distribution of urinary cotinine concentration to estimate cut-off points distinguishing the three above-mentioned groups. The examined group consisted of 327 volunteers (187 women and 140 men) who were ethnically homogenous inhabitants of the same urban agglomeration (Sosnowiec, Poland). The values which enabled differentiation of the examined population into groups and subgroups were as follows: 50 µg l^-1 (differentiation of non-smokers from passive smokers), 170 µg l^-1 (to divide the group of passive smokers into two subgroups: minimally and highly exposed to environmental tobacco smoke), 550 µg l^-1 (differentiation of passive smokers from active smokers), and 2100 µg l^-1 (to divide group of active smokers into two subgroups: minimally and highly exposed to tobacco smoke). The results suggest that statistical distribution of urinary cotinine concentration is useful for estimating urinary cotinine cut-off points and for assessing the smoking status of persons exposed to tobacco smoke.     

Population burden of lung cancer due to environmental tobacco smoke

The population burden of lung cancer due to environmental tobacco smoke is significant because a large fraction of the population is exposed. The risks are, of course, lower than those to smokers themselves; but smoking is self-inflicted, passive smoking is involuntary. Making various assumptions, the proportion of lung cancer cases among non-smokers that could reasonably be attributed to environmental tobacco smoke can be calculated to be about 20–30% in western countries. Thus, non-smokers in the society could benefit considerably from diminishing exposures to other people's smoke.     

Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98

Objective To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease.Design Prospective cohort study covering 39 years.Setting Adult population of California, United States.Participants 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits.Main outcome measures Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking.Results For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98.Conclusions The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.     

Maternal smoking in pregnancy and sex differences in perinatal death between boys and girls

Abstract

The sex difference in perinatal mortality in developed countries is largely unexplained. The current study evaluated the differences in the impact of maternal smoking during pregnancy on the risk of perinatal death between males and females. The analysis involved 11,469 and 9,404 newborns derived from two population‐based birth cohorts in Northern Finland, for 1966 and 1985–86, respectively. The perinatal mortality rate was 23 per thousand in the 1966 cohort and 9 per thousand in the 1985–86 cohort. The rate ratio (RR) for mortality for males over females is 1.15 and 1.60 in the two cohorts, respectively. Among children whose mothers smoked during pregnancy, the RR was 2.2 (95% CI 1.0, 4.7) for the former cohort and 4.8 (95% CI 1.5, 15.2) for the later cohort; and among the children whose mothers did not smoke the corresponding RR was 1.2 (95% CI 0.9, 1.6) and 1.1 (95% CI 0.6, 1.9). Maternal smoking during pregnancy could be an important determinant accounting for the excess perinatal death for males over females. Our results encourage evaluation of the findings among other populations.     

Estimation of urinary cotinine cut-off points distinguishing non-smokers,passive and active smokers

Abstract

An objective assessment of exposure to tobacco smoke may be accomplished by means of examining particular biomarkers in body fluids. The most common biomarker of tobacco smoke exposure is urinary, or serum, cotinine. In order to distinguish non-smokers from passive smokers and passive smokers from active smokers, it is necessary to estimate cotinine cut-off points. The objective of this article was to apply statistical distribution of urinary cotinine concentration to estimate cut-off points distinguishing the three above-mentioned groups. The examined group consisted of 327 volunteers (187 women and 140 men) who were ethnically homogenous inhabitants of the same urban agglomeration (Sosnowiec, Poland). The values which enabled differentiation of the examined population into groups and subgroups were as follows: 50 µg l^?1 (differentiation of non-smokers from passive smokers), 170 µg l^?1 (to divide the group of passive smokers into two subgroups: minimally and highly exposed to environmental tobacco smoke), 550 µg l^?1 (differentiation of passive smokers from active smokers), and 2100 µg l^?1 (to divide group of active smokers into two subgroups: minimally and highly exposed to tobacco smoke). The results suggest that statistical distribution of urinary cotinine concentration is useful for estimating urinary cotinine cut-off points and for assessing the smoking status of persons exposed to tobacco smoke.     

Cigarette smoking in male patients with chronic schizophrenia in a Chinese population: prevalence and relationship to clinical phenotypes

The high prevalence of smoking in schizophrenia of European background may be related to smoking's reducing clinical symptoms and medication side effects. Because smoking prevalence and its associations with clinical phenotypes are less well characterized in Chinese than European patients with schizophrenia, we assessed these smoking behaviors using clinician-administered questionnaires and the Fagerstrom Test for Nicotine Dependence (FTND) in 776 Chinese male schizophrenia and 560 control subjects. Patients also were rated on the Positive and Negative Symptom Scale (PANSS), the Simpson and Angus Extrapyramidal Symptom Rating Scale (SAES), and the Abnormal Involuntary Movement Scale (AIMS). We found that the schizophrenia patients had a higher lifetime incidence of smoking (79% vs 63%), were more likely to be heavy smokers (61% vs 31%), and had lower smoking cessation rates (4% vs 9%) (all p<0.0001) than controls. Among the schizophrenia patients smoking prevalence increased with age, with the largest difference from controls in the age cohort of 55-75 years: 75% vs 46% (p<0.0001). Among the schizophrenia smokers 73% started to smoke before the onset of their illness by an average of 7.6 years. The patients with schizophrenia who were current smokers scored significantly lower on the PANSS negative symptom subscore (p<0.005), and on the SAES symptom scale (p<0.04; Bonferroni corrected p>0.05) than the non-smoking patients. These results suggest that Chinese males with schizophrenia smoke more frequently than the general population. Further, smokers with schizophrenia may display fewer negative symptoms and possibly less parkinsonism than non-smokers with schizophrenia.     

Passive smoking at work as a risk factor for coronary heart disease in Chinese women who have never smoked.

OBJECTIVE--To study whether passive smoking at work is a risk factor for coronary heart disease. DESIGN--Case-control study. SETTING--Xi''an, China. SUBJECTS--59 patients with coronary heart disease and 126 controls, all Chinese women with full time jobs, who had never smoked cigarettes. RESULTS--The crude odds ratio for passive smoking from husband was 2.12 (95% confidence interval 1.06 to 4.25) and at work was 2.45 (1.23 to 4.88). The final logistic regression model, with passive smoking from husband and at work as the base, included age, history of hypertension, type A personality, and total cholesterol and high density lipoprotein cholesterol concentrations; the adjusted odds ratios for passive smoking from husband and at work were 1.24 (0.56 to 2.72) and 1.85 (0.86 to 4.00) respectively. For passive smoking at work, statistically significant linear trends of increasing risks (for both crude and adjusted odds ratios) with increasing exposures (amount exposed daily, number of smokers, number of hours exposed daily, and cumulative exposure) were observed. When these exposure variables were analysed as continuous variables, the crude and adjusted odds ratios were also significant. CONCLUSION--Passive smoking at work is a risk factor for coronary heart disease. Urgent public health measures are needed to reduce smoking and to protect non-smokers from passive smoking in China.     

Smoking Habits of Men Employed in Industry,and Mortality

A study of the relation between smoking habits and lung cancer in male industrial workers over a period of three years has confirmed the earlier findings in doctors that the death-rate from lung cancer correlates closely with the number of cigarettes smoked. Of 54,460 men studied 68.7% were current cigarette smokers. The annual mortality rate from lung cancer was 0.33 per thousand in non-smokers and ex-smokers, and 1.2 per thousand for all cigarette smokers, and higher in heavy smokers.Heavy cigarette smokers who retained the cigarette in the mouth between puffs (“drooping” cigarette habit) had an annual mortality rate of 4.1 per thousand.The mortality from coronary thrombosis in smokers was nearly three times that in non-smokers. A mortality gradient with rising consumption of cigarettes was observed.Some correlation between smoking and cancer of other sites and from non-neoplastic lung disease was observed in older men, but no correlation was found with other cardiovascular diseases and cerebrovascular diseases.     

Trends in mortality among California physicians after giving up smoking: 1950-79.

A study was conducted to assess how lung cancer and other mortality trends among California physicians had been influenced by the high proportion who had given up smoking since 1950. Several sample surveys indicated that the proportion of California physicians who currently smoked cigarettes had declined dramatically from about 53% in 1950 to about 10% in 1980. During the same period the proportion of other American men who smoked cigarettes had declined only modestly, from about 53% to 38%. Using the 1950 American Medical Directory a cohort of 10 130 California male physicians was established and followed up for mortality till the end of 1979, during which time 5090 died. The information from follow up and death certification was exceptionally good. The standardised mortality ratio for lung cancer among California male physicians relative to American white men declined from 62 in 1950-9 to 30 in 1970-9. The corresponding decline in standardised mortality ratio was from 100 to 63 for other smoking related cancer, from 106 to 71 for ischaemic heart disease, and from 62 to 35 for bronchitis, emphysema, and asthma. The standardised mortality ratio remained relatively constant for other causes of death not strongly related to smoking. The overall ratio declined in all age groups at a rate of about 1% a year. The total death rate among all physicians converged towards the rate among non-smoking physicians. By the end of the study period physicians had a cancer rate and total death rate similar to or less than those among typical United States non-smokers. This "natural experiment" shows that lung cancer became relatively less common on substantial elimination of the primary causal factor, cigarette smoking. Other smoking related diseases also became relatively less common, though factors other than cigarette smoking may have contributed to this change.     

Passive cigarette smoking increases isoprostane formation

Passive smoking has been demonstrated to exert a variety of deleterious effects eventually resulting in vascular damage. Isoprostanes, a reliable marker of in vivo oxidation injury, have been shown to increase in active cigarette smoking. Data for passive smoking are lacking. We were examining the isoprostane 8-epi-PGF2alpha in 12 smokers and non-smokers exposed daily to passive cigarette smoke for 12 days. Plasma samples stored at liquid nitrogen from people having been examined earlier were used. Prevalues of 8-epi-PGF2alpha are higher in cigarette smokers. Exposure to passive smoking causes a significant increase in 8-epi-PGF2alpha in non-smokers, while in smokers there is only a trendwise increase. After repeated passive smoke exposure, 8-epi-PGF2alpha in non-smokers approaches the respective values of smokers. There is a significant correlation of 8-epi-PGF2alpha to the thromboxane (plasma, serum, conversion from exogenous precursor, 11-dehydro-TXB2) parameters (MDA, HHT- conversion) examined in these patients before. The findings document a significant temporary increase in in vivo oxidation injury due to passive smoke favouring development and/or progression of vascular disease.     

Cigarette tar yields in relation to mortality from lung cancer in the cancer prevention study II prospective cohort, 1982-8

Objective To assess the risk of lung cancer in smokers of medium tar filter cigarettes compared with smokers of low tar and very low tar filter cigarettes.Design Analysis of the association between the tar rating of the brand of cigarette smoked in 1982 and mortality from lung cancer over the next six years. Multivariate proportional hazards analyses used to assess hazard ratios, with adjustment for age at enrolment, race, educational level, marital status, blue collar employment, occupational exposure to asbestos, intake of vegetables, citrus fruits, and vitamins, and, in analyses of current and former smokers, for age when they started to smoke and number of cigarettes smoked per day.Setting Cancer prevention study II (CPS-II).Participants 364 239 men and 576 535 women, aged ≥ 30 years, who had either never smoked, were former smokers, or were currently smoking a specific brand of cigarette when they were enrolled in the cancer prevention study.Main outcome measure Death from primary cancer of the lung among participants who had never smoked, former smokers, smokers of very low tar (≤ 7 mg tar/cigarette) filter, low tar (8-14 mg) filter, high tar (≥ 22 mg) non-filter brands and medium tar conventional filter brands (15-21 mg).Results Irrespective of the tar level of their current brand, all current smokers had a far greater risk of lung cancer than people who had stopped smoking or had never smoked. Compared with smokers of medium tar (15-21 mg) filter cigarettes, risk was higher among men and women who smoked high tar (≥ 22 mg) non-filter brands (hazard ratio 1.44, 95% confidence interval 1.20 to 1.73, and 1.64, 1.26 to 2.15, respectively). There was no difference in risk among men who smoked brands rated as very low tar (1.17, 0.95 to 1.45) or low tar (1.02, 0.90 to 1.16) compared with those who smoked medium tar brands. The same was seen for women (0.98, 0.80 to 1.21, and 0.95, 0.82 to 1.11, respectively).Conclusion The increase in lung cancer risk is similar in people who smoke medium tar cigarettes (15-21 mg), low tar cigarettes (8-14 mg), or very low tar cigarettes (≤ 7 mg). Men and women who smoke non-filtered cigarettes with tar ratings ≥ 22 mg have an even higher risk of lung cancer.     

Smoking and the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers.

OBJECTIVE--To investigate the effects of exposure to tobacco smoke and of parental consumption of alcohol and illegal drugs as risk factors for the sudden infant death syndrome after a national risk reduction campaign which included advice on prenatal and postnatal avoidance of tobacco smoke. DESIGN--Two year population based case-control study. Parental interviews were conducted for each infant who died and four controls matched for age and date of interview. SETTING--Three regions in England with a total population of 17 million people. SUBJECTS--195 babies who died and 780 matched controls. RESULTS--More index than control mothers (62.6% v 25.1%) smoked during pregnancy (multivariate odds ratio = 2.10; 95% confidence interval 1.24 to 3.54). Paternal smoking had an additional independent effect when other factors were controlled for (2.50; 1.48 to 4.22). The risk of death rose with increasing postnatal exposure to tobacco smoke, which had an additive effect among those also exposed to maternal smoking during pregnancy (2.93; 1.56 to 5.48). The population attributable risk was over 61%, which implies that the numbers of deaths from the syndrome could be reduced by almost two third if parents did not smoke. Alcohol use was higher among index than control mothers but was strongly correlated with smoking and on multivariate analysis was not found to have any additional independent effect. Illegal drug use was more common among the index parents, and paternal use of illegal drugs remained significant in the multivariate model (4.68; 1.56 to 14.05). CONCLUSIONS--This study confirms the increased risk of the sudden infant death syndrome associated with maternal smoking during pregnancy and shows evidence that household exposure to tobacco smoke has an independent additive effect. Parental drug misuse has an additional small but significant effect.     

Excess smoking in malignant-phase hypertension

The smoking habits of 82 patients with malignant-phase hypertension were compared with those of subjects in three control groups matched for age and sex. Sixty-seven (82%) of the patients with malignant-phase hypertension were smokers compared with 41 (50%) and 71 (43%) of the patients in two control groups with non-malignant hypertension, and 43 people (52%) in a general population survey. The excess of smokers in the malignant-phase group was significant for men and women, together and separately, for cigarette smoking alone, and for all forms of smoking. There were no significant differences between the control groups. The chance of a hypertensive patient who smoked having the malignant phase was five times that of a hypertensive patient who did not. Twelve patients in the malignant-phase group had never smoked. All were alive three and a half years on average after presentation (range 11 months to seven years). Twenty-four (36%) of the smokers with malignant-phase hypertension died during the same period. The mortality rate was significantly higher among patients with renal failure, as was the prevalence of smoking. Eighteen patients with malignant-phase hypertension had a serum creatinine concentration higher than 250 μmol/l (2·8 mg/100 ml); 17 were smokers and one an ex-smoker. Eleven of these 18 patients died.It is concluded that hypertensive patients who smoke are much more likely to develop the malignant phase than those who do not, and that once the condition has developed it follows a particularly lethal course in smokers.     

8-Hydroxydeoxyguanosine in DNA from leukocytes of healthy adults: relationship with cigarette smoking, environmental tobacco smoke, alcohol and coffee consumption

8-Hydroxydeoxyguanosine (8-OHdG) has been widely used as a biomarker of oxidative DNA damage in both animal and human studies. However, controversial data exist on the relationship between 8-OHdG formation and age, sex and tobacco smoking in humans, while few or no data are available on other exposures such as environmental tobacco smoke, alcohol, coffee and tea consumption. We investigated the level of 8-OHdG in DNA from peripheral leukocytes among 102 healthy adults living in Brescia province, North Italy, aged 25-45 (mean: 35.2 years), of which 51 were males. 8-OHdG levels expressed as a ratio to total deoxyguanosine (8-OHdG/106 dG) in DNA showed wide interindividual variation, the highest value (63.8) being 6. 2-fold greater than the lowest (10.3). Current smokers showed lower mean 8-OHdG values than subjects who never smoked (29.3 and 34.0, respectively, p<0.05), and an inverse relationship was found between 8-OHdG and lifetime smoking, which was independent of age, sex and body mass index. An inverse relationship was also found with coffee drinking while no association was observed with alcohol and tea consumption, exposure to environmental tobacco smoke and use of vitamins in all subjects, and with use of oral contraceptives in females. The inverse relationship between smoking status and 8-OHdG levels could be explained by the presence of efficient repair processes for the oxidative damage induced by smoking. In this study, the smokers were relatively young (77% were less than 40 years) and only 7% smoked 30 or more cigarettes a day. In conclusion, it would appear that 8-OHdG levels in leukocytes may not provide a sensitive marker of exposure to tobacco smoking.     

Delay and probability discounting as related to different stages of adolescent smoking and non-smoking

This study examined relations between different patterns of adolescent cigarette smoking and discounting of monetary rewards due to delay (delay discounting) and probabilistic uncertainty (probability discounting). The study also examined the relation between smoking and the number of peer friends who smoke and level of parent education. Participants were 55 adolescents (28 females) between 14 and 16 years of age who were categorized according to the following patterns of smoking behavior: "never smokers" (n=19; 10 females) who had not tried even one cigarette; "triers" (n=17; 9 females) who had recently tried cigarettes for the first time; and "current smokers" (n=19; 9 females) who smoked a minimum of one cigarette every week for at least 6 months prior to data collection. It was hypothesized that current smokers would discount more than those who had never smoked. No specific hypotheses were made for participants only trying cigarettes. Unexpectedly, results indicated no differences in discounting between the current smokers and never smokers. However, the trier group discounted probabilistic rewards significantly more than the never- and current-smoker groups. Also, triers and current smokers both reported having more friends who smoked than never smokers, and fathers of never smokers had significantly more education than fathers of either triers or current smokers. These results suggest that impulsive discounting may be more related to adolescents trying cigarettes than to their becoming regular smokers, whereas number of peer friends who smoke and parent level of education seem to differentiate between those who have smoked to some extent (triers and current smokers) and those who have not even tried cigarettes (never smokers).     

Carbon monoxide yield of cigarettes and its relation to cardiorespiratory disease.

Estimates of the carbon monoxide yield of their cigarettes have been obtained for 4910 smokers (68% of all smokers) in the Whitehall study of men aged 40 to 64. In the 10 years after examination 635 men died. When men smoking cigarettes with high carbon monoxide yield were compared with those smoking cigarettes with a low yield, and after adjusting for age, employment grade, amount smoked, and tar yield, the risk of death was 32% lower for coronary heart disease, 49% higher for lung cancer, and 10% lower for total mortality; these differences were not statistically significant. Among men who said that they inhaled the risk of fatal coronary heart disease was 51% lower in the high carbon monoxide group (p less than 0.01), while the risk of lung cancer was 75% higher. These results provide no evidence that a smoker can reduce his risk of death by smoking a brand with a low carbon monoxide yield; he might even increase it. The complex interactions between characteristics of the smoker, smoking behaviour, constituents of tobacco smoke, and health are again demonstrated.     

Characteristics and consequences of passive smoking

Summary The consequences of passive smoking are well documented regarding the risk of lung cancer, obstructive ventilatory trouble, ischemic cardiopathy, infant disease of the respiratory ducts and of foetus growth delay caused by smoking during pregnancy. If the potential risk is much lower than the risk induced by active smoking, very few people can avoid exposure to smoke because of the large amount of active smokers in the French population. Rather than the characteristics of the emitting source and the particularities of smoking (speed and inhalation), it is mostly the ventilation of rooms where non-smokers are exposed to the smoker's smoke that constitutes the significant point. The consequences of environmental smoking on health would justify to take statutory decisions protecting the rights of the smokers. This is in accordance with the resolution passed by the European Community's Council and the Secretaries of Health of the member countries. More precisely, non smoking rules in closed rooms open to the public should be enforced, particularly in schools, hospitals and finally at the workplace.