Restaurant smoking restrictions and environmental tobacco smoke exposure

Epididymo-orchitis, an uncommon cause of acute scrotum in prepubertal boys, is infection or inflammation of epididymis and testis. Epididymo-orchitis may be associated with urinary tract infections or reflux of urine predisposed by an underlying vasal anomaly. Two infants with anorectal malformations who presented with acute scrotum are reported. The surgical exploration of the testes showed findings consistent with epididymo-orchitis. Further radiological investigations of urinary tract showed vasal anomalies in both patients. If a patient with anorectal malformation presents with acute scrotum, epididymo-orchitis should be suspected initially. Evaluations should be directed toward defining predisposing vasal anomaly, and appropriate therapeutic measures should be undertaken to prevent recurrences.     

Environmental tobacco smoke and lung cancer

In a case-control study of 1,004 lung cancer cases and 1,004 population controls, all nonsmokers (71 cases, 236 controls) were interviewed for their exposure to environmental tobacco smoke. On the basis of indices of duration, we separated intermediate and high exposures from low or no exposure. The odds ratio for high exposure was 2.09 (95% confidence interval = 1.02-4.28). Exposure from the spouse was only weakly associated with lung cancer risk. We found little association for exposure during childhood. High exposure at the work place showed an odds ratio of 1.91. There was little indication of confounding by dietary habits.     

Misclassification of smoking status and lung cancer risk from environmental tobacco smoke in never-smokers

The aim of this study was to determine the extent to which smokers and smoking quitters differ in habits and risk factors from non-smokers. Subjects comprised 8,109 patients aged 35-67 years having health checks in British primary care. We compared lifestyle and measured cardiovascular risk factors in smokers, former smokers and lifelong abstainers in cross-sectional analyses, and in prospective data in quitters. Results were adjusted for confounding factors. Considering 25 aspects of lifestyle, smokers had significantly worse habits in 20 compared to abstainers, and in 17 compared to former smokers. These included eating more white bread, full cream milk, fried food and meat, and less fruit and vegetables, wholemeal bread and bran cereals. Smokers report drinking more alcohol and taking less exercise. Smokers' mean serum levels were higher for total and low density lipoprotein cholesterol and triglycerides and lower for high density lipoprotein cholesterol. Within five years ex-smokers' data became comparable to lifelong abstainers for most factors, with apparent attenuation over up to 20 years for triglyceride, body mass index and scores for fibre and polyunsaturated fat intake. Smokers who quit after initial examinations had better health profiles even before quitting (p = 0.016) and subsequently made more beneficial health changes (p = 0.039) than continuing smokers. Smoking is associated with relatively poor health choices and risk factor levels. Stopping smoking is associated with a wide range of improved health markers beyond avoidance of tobacco toxicity.     

Respiratory health effects of exposure to environmental tobacco smoke

During the last 25 years, several hundred papers have been published on the respiratory health effects of environmental tobacco smoke (ETS). Various independent assessments have concluded that ETS causes lung cancer in adult nonsmokers and increases the risk of various noncancer effects, principally in children. The effects on children include pneumonia, bronchitis and bronchiolitis in young children; chronic middle ear effusion; increased frequency and severity of attacks among asthmatics; possible induction of asthma in previously asymptomatic individuals; small reductions in lung function; and symptoms of upper respiratory tract irritation. In nonsmoking adults, ETS exposure is associated with irritation of the eyes, nose, and throat, and with wheezing, symptoms of bronchitis, shortness of breath, and decreased lung function. The results of recent studies not only confirm and strengthen the above findings but also provide strong suggestive evidence that ETS causes sinonasal cancer and is a risk factor for sudden infant death syndrome. To mitigate such a preventable environmental health impact, public health measures to reduce involuntary ETS exposure are warranted.     

Occupational exposure of nonsmoking nightclub musicians to environmental tobacco smoke

This study assessed environmental tobacco smoke (ETS) exposures of nonsmoking musicians in nightclub environments using total suspended particulate (TSP), the ultraviolet absorbing fraction of TSP (UVPM), gaseous nicotine, saliva nicotine, saliva cotinine, and perceived smokiness as exposure/dose indicators. Measured exposures were as high or higher than those of other occupational groups studied. TSP ranged from 110 to 1714 micrograms/m3 (mean 502, SD 390 micrograms/m3). UVPM (mean 221, SD 95 micrograms/m3) was associated with gaseous and saliva nicotine concentrations. Paired-sample variation was much higher for TSP than for UVPM. Correlation of TSP with UVPM, gaseous nicotine, and saliva nicotine was poor. Paired-sample gaseous nicotine results were similar, with exposures of 28.0 to 50.0 micrograms/m3 (mean 37.1, SD 6.9 micrograms/m3), and were high compared with previous studies. These results suggested that nightclub musicians may be exposed to higher concentrations of ETS than some other occupational groups. Saliva nicotine results were consistent with those previously reported with regard to the range of values, large variation observed, and increase in saliva nicotine levels observable after only a few hours of exposure. Saliva nicotine results could not be correlated with other measures of exposure and did not appear to be a reliable biological indicator of absorbed dose. Saliva cotinine levels were comparable to other occupational groups studied, but were lower than previous findings for bartenders and waitresses. Levels ranged from 1.7 to 5.0 ng/mL (mean 3.4, SD 0.9 ng/mL), and increased with number of exposures during the workweek, but did not correlate with other ETS indicators.     

The carcinogenicity of environmental tobacco smoke

Male strain A/J mice were exposed for 6 h a day, 5 days a week to environmental tobacco smoke (ETS) generated from Kentucky 1R4F reference cigarettes. Chamber concentrations were 87 mg/m3 of total suspended particulate matter (TSP), 246 p.p.m. of CO and 16 mg/m3 of nicotine. After 5 months, 33% of the ETS exposed and 11% of the control animals had one or several lung tumors; the difference was statistically not significant. A second group of animals exposed for 5 months to ETS was allowed to recover for another 4 months in filtered air. When they were killed, 85% of the ETS animals had lung tumors (average number per lung: 1.4 +/- 0.2), whereas in the control group 38% had lung tumors (average number of lung tumors in all animals 0.5 +/- 0.2). The differences in tumor incidence and multiplicity were statistically significant. More than 80% of all tumors were adenomas, the rest adenocarcinomas. When animals were pretreated with a carcinogen, lung tumor multiplicity was lower in the ETS exposed animals after 5 months compared with controls injected with a carcinogen and kept in air. However, after an additional 4 month recovery period in air, lung tumor multiplicities were the same in ETS plus carcinogen exposed mice as in carcinogen-treated air-exposed controls. Histopathologic and morphometric analysis of the lung tissue failed to reveal any differences between ETS exposed and control animals. However, immediately after ETS exposure, immunohistochemistry revealed increased staining for CYP1A1 in airway epithelia and lung parenchyma; following recovery in air, the staining disappeared again. Analysis of cell kinetics showed an initial burst of increased DNA synthesis in the epithelial cells of the airways and a smaller early positive response in the parenchyma. Feeding of butylated hydroxytoluene during ETS exposure did not modulate lung tumor development. It was concluded that ETS is a pulmonary carcinogen in strain A/J mice.     

An isolated rat lung perfusion system for use in tobacco smoke studies

An isolated rat lung perfusion system has been developed for use in tobacco smoke studies. The lungs are ventilated by means of subatmospheric (negative) pressure produced through operation of an artificial thorax. The system enables standard respiratory conditions to be employed and so eliminates variations in animal breathing characteristics. The various tests of viability which have been carried out have shown that the preparations are viable for periods of at least 1 hr. It was also demonstrated that transfer of 14C-nicotine from smoke to perfusate was rapid and linear over the period of smoke exposure and that first-pass metabolism of nicotine was of little significance.     

What are the determinants of children''s exposure to environmental tobacco smoke at home?

Methylazoxymethanol acetate (MAM) is a substance that inhibits migration of neurons in the embryonic brain. After intraperitoneal injection of two different doses of MAM to pregnant rats, microcephaly with or without complete development of the cerebral cortex was observed in every litter. High MAM doses (30 mg/kg) resulted in the lack of superficial layers (II-IV) of the cerebral cortex when the deep layers (V, VI) were seen. The claustrum was present but composed of loosely packed, medium-size, triangular or fusiform neurons with anarchic oriented long axes. After administration of low MAM doses (14 mg/kg) two different parts (medial and lateral) of the insular claustrum were observed. Our results suggest that neurons of the insular claustrum create two different subpopulations of cells, which were similar to that observed in primitive insectivore (e.g., hedgehog), but fuse in development.     

Cancer of the nasal cavity and paranasal sinuses and exposure to environmental tobacco smoke in pet dogs

PURPOSE: To evaluate dynamic MR imaging of the pituitary gland. MATERIAL AND METHODS: 19 patients with suspected mass lesions of the pituitary gland were examined at 1.5 Tesla with dynamic and standard MRI using a Turbo-FLASH sequence (1 image/s for 40 s). RESULTS: In 13/19 patients microadenomas were detected. One of the 13 microadenomas was detected using dynamic imaging and was not seen on standard MRI. The remaining 12 microadenomas were diagnosed with standard MRI. CONCLUSION: Dynamic imaging of the pituitary gland is a time-consuming and costly diagnostic technique. If laboratory results suggest the presence of a microadenoma and conventional MRI is unable to localise it, dynamic imaging should be performed.     

Testosterone worsens endothelial dysfunction associated with hypercholesterolemia and environmental tobacco smoke exposure in male rabbit aorta

OBJECTIVES: To assess the effects of interaction of sex hormones, hypercholesterolemia (HC) and environmental tobacco smoke (ETS) exposure on endothelium-dependent relaxation, we examined vascular reactivity in vitro in an animal model of atherogenesis. BACKGROUND: Animal and human studies indicate the presence of interactions between classic coronary artery disease risk factors and endothelium-dependent relaxation. Sex hormones have also been shown to influence release of endothelium-derived relaxing factor. METHODS: New Zealand White rabbits were randomized to receive either an HC diet (n = 8) or ETS exposure plus HC diet (n = 8). Eight rabbits receiving a normal diet, without exposure to ETS, served as the control group. The HC diet consisted of 3% soybean oil and 0.3% cholesterol by weight over 13 weeks. The source of ETS was sidestream smoke of 4 cigarettes/15 min, 6 h/day, 5 days/week over 10 weeks in a smoking chamber. Rabbits were killed, and fresh aortic rings were harvested and maintained in oxygenated Krebs solution in an organ bath at 37 degrees C. Rings were precontracted with norepinephrine and exposed to acetylcholine in increasing doses, and isometric tension was recorded. Rings were also exposed to physiologic concentrations (1 nmol/liter) of either 17-beta-estradiol, testosterone or progesterone before pre-contraction with norepinephrine and relaxation with acetylcholine. Endothelium-independent relaxation was studied using nitroglycerin. The surface area of the ring covered by lipids was measured by Sudan IV staining. RESULTS: HC and ETS significantly reduced endothelium-dependent relaxation (p = 0.01 and p < 0.0005, respectively) and caused atherogenesis (p < 0.0005 and p = 0.047, respectively) but did not affect endothelium-independent relaxation. Incubation with estradiol and estradiol plus progesterone did not influence endothelium-dependent relaxation. Testosterone reduced endothelium-dependent relaxation (p = 0.049) and augmented the endothelial dysfunction associated with ETS exposure and HC (p = 0.03). CONCLUSIONS: Both HC and ETS are atherogenic and impair endothelial function but do not affect endothelium-independent relaxation. Physiologic levels of estradiol and estradiol plus progesterone do not affect endothelium-dependent relaxation. Physiologic levels of testosterone impair relaxation and augment the endothelial dysfunction associated with ETS exposure and HC.     

Classification exposure error in studies on tobacco smoke in pregnancy and birth weight of newborns]

In this paper, the on-line coupling of solid-phase extraction, based on a restricted-access support with liquid chromatography-mass spectrometry (LC-MS), for the analysis of biological samples is described. The system was tested with cortisol and prednisolone for plasma analysis and arachidonic acid for urine analysis. A precolumn packed with a 25-micron C18 alkyl-diol support is used for direct plasma or urine injection. Using column-switching techniques, the analytes enriched on the precolumn are eluted to the analytical column without transfer loss. An on-line heart-cut technique was employed and only the analyte-containing fraction eluting from the LC column is directed to the MS to protect the LC-MS interface and ion-source from contamination. The whole system is operated in a parallel mode, that is, sample pre-treatment and LC-MS analysis are performed simultaneously to provide the shortest possible analysis time. The only off-line sample pre-treatment step required was centrifugation to remove particulate matter. With the fully automated system, total analysis times of 5 and 9.5 min were achieved for cortisol in serum and arachidonic acid in urine, respectively. Cortisol and related compounds were quantitatively recovered from plasma with a detection limit for prednisolone (direct injection of 100 microliters on restricted-access precolumn) of 2 ng/ml.     

Lifetime exposure to environmental tobacco smoke among urban women: differences by socioeconomic class

This study sought to determine cumulative lifetime exposure to environmental tobacco smoke (ETS) among urban women in relation to sociodemographic factors. In a population survey carried out in Geneva, Switzerland, during 1993-1995, a representative sample of 1,883 women aged 35-74 years answered interview questions on lifetime ETS exposure. Exposed women were defined as those who had spent at least 1 hour daily in a smoky environment during 1 or more years. The prevalence of current ETS exposure was 31.0% among 1,458 never or former smokers. Lifetime prevalence was 58.3% among 1,061 never smokers. The home (42.1%) and the workplace (39.6% of employed women) were the most frequent sources of ETS exposure, leisure time activity being a secondary source. Throughout a lifetime, work accounted for the greatest average intensity of exposure (on average, 19 hours of exposure per week), while the longest duration of exposure (on average, 18 years) was in the home. Cumulative lifetime exposure (intensity (in hours/week) x duration) from all sources combined was 308 hours/week-years, which can correspond to 30.8 hours/week over a period of 10 years or 20.5 hours/week over a period of 15 years. Women from low socioeconomic classes had more intense and longer exposures than women from higher socioeconomic classes, mainly because of work exposure. Both the intensity and the duration of lifetime ETS exposure were greater than previously suspected. Reduction of ETS exposure in the workplace should be a public health priority.     

Mortality studies of machining fluid exposure in the automobile industry. IV: A case-control study of lung cancer

The taxanes represent a new class of clinical chemotherapeutic agents. A series of in vitro studies were independently of each other initiated in two different institutes (Amsterdam and Madison) to test the hypothesis that hyperthermia might enhance the cytotoxicity of taxanes. Clonogenic capacity experiments (Amsterdam) included the exposure of R1- and SW 1573-cells to 1, 4, or 24 h of paclitaxel with heat 43 degrees C x 60 min in the last hour of drug treatment or at 24, 48 as well as 72 h post drug treatment. Survival assay experiments (Madison) included the exposure of L-929-cells to paclitaxel and docetaxel for 24 h with heat 41.8 degrees C x 60 min the first or last hour of drug treatment as well as 24 and 48 h post treatment. No thermal enhancement of cytotoxicity for the taxanes was observed in these human and murine cell lines, with congruent data in both institutes. In addition, high performance liquid chromatography studies at 41.8 degrees C and 43 degrees C demonstrated paclitaxel and docetaxel were heat stable.     

Evidence for an association between environmental tobacco smoke exposure and birthweight: a meta-analysis and new data

Because of the strong association of active smoking with fetal growth retardation, increasing interest has focused on whether there is also an association with exposure to environmental tobacco smoke (ETS). We examined this issue in a retrospective study and by conducting a review of the literature and data pooling. In our study, nonsmoking women with singleton livebirths born in 1986-87 (n = 992) provided information on exposure to ETS for 1 h or more per day and paternal smoking. The risk of low birthweight (LBW, < 2500 g) was not increased in infants of ETS-exposed women, but there was a somewhat increased risk for LBW at term (adjusted odds ratio [OR] 1.8, 95% confidence interval [CI] 0.6, 4.8) and small-for-gestational-age (< 10th percentile of weight; OR = 1.4, 95% CI = 0.8, 2.5). These results were in the range of 16 other studies in the literature that had odds ratios from 1.0 to 2.2. A weighted average of the results of all studies on LBW at term or small-for-gestational-age yielded a pooled estimate of 1.2 [95% CI = 1.1, 1.3] in nonsmoking women. The pooled estimate of mean birthweight indicated a decrement of 28 g with ETS exposure of nonsmoking women [95% CI = -41, -16], with a greater decrement (about 40 g) seen among more homogeneous studies.     

Use of urinary cotinine and questionnaires in the evaluation of infant exposure to tobacco smoke in epidemiologic studies

In this study we have investigated whether proteoglycans (aggrecan) are modified by nonenzymatic glycation as in collagen. Purified human aggrecan from osteoarthritic and normal human knee articular cartilage was assayed for pentosidine, a cross-link formed by nonenzymatic glycation, using reverse-phase HPLC. In addition, an in vitro study was done by incubation of purified bovine nasal cartilage aggrecan with ribose. Pentosidine was found in all the purified human aggrecan samples. 2-3% of the total articular cartilage pentosidine was found in aggrecan. Purified link protein also contained penosidine. The in vitro study led to pentosidine formation, but did not appear to increase the molecular size of the aggrecan suggesting that pentosidine was creating intramolecular cross-links. Similar amounts of glycation were found in osteoarthritic and normal cartilage. Like collagen, aggrecan and link proteins are crosslinked by nonenzymatic glycation in normal and osteoarthritic cartilage. Crosslinking could be reproduced, in vitro, by incubating aggrecan with ribose.     

Glutathione S-transferase mu1 and N-acetyltransferase 2 genetic polymorphisms and exposure to tobacco smoke in nonsmoking and smoking lung cancer patients and population controls

We conducted a case-control study to assess the risk of lung cancer in relation to genetic polymorphisms of the detoxifying enzymes glutathione-S-transferase mu1 (GSTM1) and N-acetyl transferase 2 (NAT2), focusing on never-smokers, women, and older people. The study base consisted of persons > or =30 years of age in Stockholm County from 1992 to 1995. We recruited never-smoking lung cancer cases and a sex- and age-matched sample of ever-smoking cases at the three county hospitals mainly responsible for diagnosing and treating lung cancer. A total of 185 cases (25.4% men; 47.6% never-smokers) and 164 frequency-matched population controls (28.7% men; 48.2% never-smokers) supplied blood for genotyping. Detailed information was collected by interview on active and passive smoking, occupations, residences, and diet. The overall odds ratio (OR) for lung cancer associated with the GSTM1 null (GSTM1-) versus GSTM1+ genotype was 0.8 [95% confidence interval (CI), 0.5-1.2], with an OR close to unity among smokers, and lower ORs suggested among never-smokers. For NAT2 slow versus rapid acetylator genotypes, the OR was 1.0 (95% CI, 0.6-1.5) overall, which broke down into an increased risk for slow acetylators among never-smokers but an increased risk for rapid acetylators among smokers. Among never-smokers, a gene interaction was suggested, with combined slow acetylator and GSTM1+ genotype conferring particularly high risk (OR = 3.1; 95% CI, 1.1-8.6), but no clear pattern emerged among smokers. A detailed analysis among smokers showed no interaction between pack-years of smoking and the GSTM1 genotype but suggested a steeper increase in risk with increasing pack-years of smoking exposure for rapid than for slow acetylators. Our results do not support a major role for the GSTM1 genetic polymorphism as a risk factor for lung cancer among smokers or nonsmokers. There was, however, some suggestion that the slow acetylator genotype may confer an increased risk among never-smokers and that the rapid acetylator genotype interacts with pack-year dose to produce a steeper risk gradient among smokers.     

Indoor radon exposure and risk of lung cancer: a nested case-control study in Finland

BACKGROUND: Inhaled radon has been shown to cause lung cancer among underground miners exposed to very high radon concentrations, but the results regarding the effects of residential radon have been conflicting. PURPOSE: Our aim was to assess the effect of indoor radon exposure on the risk of lung cancer. METHODS: To investigate this effect, a nested case-control study was conducted in Finland. The subjects of the study were the 1973 lung cancer case patients (excluding patients with cancers of the pleura) diagnosed from January 1, 1986, until March 31, 1992, within a cohort of Finns residing in the same one-family house from January 1, 1967, or earlier, until the end of 1985 and 2885 control subjects identified from the same cohort and matched by age and sex. In September 1992, a letter was sent to all study subjects or proxy respondents explaining the purpose and methods of the study. After giving informed consent, the study participants were asked to fill out a questionnaire on smoking habits, occupational exposures, and other determinants of lung cancer risk and radon exposure. The odds ratio (OR) of lung cancer was estimated from matched and unmatched logistic regression analyses relative to indoor radon concentration assessed by use of a 12-month measurement with a passive alpha track detector. RESULTS. Five hundred seventeen case-control pairs were used in the matched analysis, and 1055 case subjects and 1544 control subjects were used in the unmatched analysis. The OR of lung cancer for indoor radon exposure obtained from matched analysis was 1.01 (95% confidence interval [CI] = 0.94-1.08) per 2.7 pCi/L (100 Bq m-3) after adjustment for the cigarette smoking status, intensity, duration, and age at commencement of smoking by subjects. For indoor radon concentrations 1.4-2.6, 2.7-5.3, 5.4-10.7, and 10.8-34.5 pCi/L (50-99, 100-199, 200-399, and 400-1277 Bq m-3, respectively), the matched ORs were 1.03 (95% CI = 0.84-1.26), 1.00 (95% CI = 0.78-1.29), 0.91 (95% CI = 0.61-1.35), and 1.15 (95% CI = 0.69-1.93), respectively, relative to the concentration below 1.4 pCi/L (0-49 Bq m-3). The unmatched analysis yielded similar results with somewhat smaller CIs. In the analyses stratified by age, sex, smoking status, or histologic type of lung cancer, no statistically significant indications of increased risk of lung cancer related to indoor radon concentration were observed for any of the subgroups. CONCLUSIONS: Our results do not indicate increased risk of lung cancer from indoor radon exposure. IMPLICATION: Indoor radon exposure does not appear to be an important cause of lung cancer.     

Smoking at home: The impact of smoking cessation on nonsmokers' exposure to environmental tobacco smoke.

Nonsmokers who live with smokers are at increased risk for chronic disease. This study evaluated the impact of eliminating smoking in the home on nonsmokers' environmental tobacco smoke (ETS) exposure. Nonsmokers participated in measurements of their ETS exposure before and after the smoker in their home quit smoking. A matched comparison group of nonsmokers from nonsmoking homes was also included. ETS exposure was assessed using passive nicotine monitors, an exposure diary, and a questionnaire. Nonsmokers from smoking homes had significantly higher exposure to ETS than those from nonsmoking homes. There was a 60% reduction in nicotine levels following smoking cessation by the household smoker. However, there were still detectable levels of nicotine measured at posttest. These results have important implications for individual risk reduction and public health policy. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Evaluation of the effect of environmental exposure to tobacco smoke on variability of peak expiratory flow rate in children

A panel study was conducted in autumn (116 children) and repeated in spring (66 children) to test the hypothesis that the individual variability of peak expiratory flow rate (PEFR) depends on the environmental exposure to tobacco smoke (ETS). PEFR was measured twice a day (morning: PEFR-M; evening: PEFR-E), using individual meters at homes, in children exposed (ETS+) and not exposed (ETS-) to tobacco smoke at home. In examined groups the individual variability of PEFR-M was--on average--8.0% (ETS+; autumn), 8.1% (ETS+; spring), 10.5% (ETS-; autumn) and 7.7% (ETS-; spring). The individual variability of PEFR-E was 8.0% (ETS+; autumn), 7.9% (ETS+; spring), 9.5% (ETS-; autumn) and 7.4% (ETS-; spring). The results of multivariate analysis of within- and between-subject variability showed the presence of statistically significant within-subject variability only in ETS+ group (PEFR-M in autumn; PEFR-M and PEFR-E in spring). With all the limitations of a panel study design the findings suggest that environmental exposure to tobacco smoke in children affects the degree of within-subject variability of PEFR in children.