首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 93 毫秒
1.
Two experiments were carried out in order to investigate nicotine intake through passive smoking. In the first study, carboxyhemoglobin (COHb) and serum cotinine were found to increase to a similar extent in seven subjects breathing through the nose only and in another seven subjects breathing through the mouth only during exposure to environmental tobacco smoke. Similarly, no significant difference was found in urinary excretion of nicotine and cotinine over a period of 72 hours, although nicotine and cotinine excretion tended to be slightly higher after inhalation through the nose only. In the second study, nicotine was measured in four subjects who held mainstream or sidestream smoke in the mouth without inhaling. Cotinine levels in serum and amounts of nicotine and cotinine excreted in the urine were low compared with those measured in the breathing study. Nicotine from sidestream smoke, however, is more effectively absorbed by the oral mucosa than nicotine from mainstream smoke. The data suggest that nicotine intake from passive smoking largely takes place in the bronchial tree and that nicotine absorption via the nasal or the oral mucosa is only of minor significance.  相似文献   

2.
Particulate and gaseous emissions from indoor combustion appliances and smoking can elevate the indoor concentrations of various pollutants. Indoor pollutant concentrations resulting from operating one of several combustion appliances, or from sidestream tobacco smoke, were measured in a 27-m3 environmental chamber under varying ventilation rates. The combustion appliances investigated were gas-fired cooking stoves, unvented kerosene-fired space heaters, and unvented natural-gas-fired space heaters. Results showed elevated levels of carbon dioxide, carbon monoxide, nitric oxide, nitrogen dioxide, formaldehyde, and suspended particles from one or more of the pollutant sources investigated. Our findings suggest that, of the sources examined in this study, nitrogen dioxide from combustion appliances and particles from sidestream cigarette smoke are the most serious contaminants of indoor air, if we use existing standards and guidelines as the criteria. An emission rate model was used to quantify the strengths of the pollutant sources, which are reported in terms of the mass of pollutant emitted per energy unit of fuel consumed (in the case of gas and kerosene appliances) and per mass of tobacco combusted (in the case of smoking).  相似文献   

3.
The amount of NO2 and NO produced by the machine smoking of cigarettes was determined for 15 commercial Canadian brands. Average yield of NO was 1.44 μmoles or about 13% of the average reported for American cigarettes. Levels of NO2 were less than 12% of NO and were probably due to the oxidation of NO. In order to assess the contribution of tobacco smoke to levels of NO in ambient air, 5 brands of cigarettes were smoked in 27 cubic meter controlled environment room. Ventilation conditions were either 2.5 or 5.0 air changes per hour (ACH) and each experiment was replicated 3 times for a total of 30 experiments. Ventilation rates of 0.3 and 1.5 ACH were also selected in a second series of experiments in which only one brand of cigarette was smoked. Least squares estimates for the effective ventilation rates were obtained in the usual manner after linearizing the decay portion of the NO time curve. In each of the experiments, the regression explained at least 95% of the variation in the levels of NO with time. Loss of NO due to factors other than ventilation appeared to be constant within experimental error and averaged 2.22 ACH. Equilibrium values for NO were grossly underestimated when results from currently accepted proecedures for smoke analysis were used in modeling the growth and decay of NO. Goodness-of-fit was improved when equilibrium values were estimated based on observed levels in ambient air. This approach may be more suitable for evaluating the potential contribution of cigarette smoke to levels of indoor air pollutants.  相似文献   

4.
It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including α-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16INK4a (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated.  相似文献   

5.
The average particulate environmental tobacco smoke (ETS) exposure of never and current smokers and the average lung cancer mortality rate for current smokers is estimated from empirical data. These estimates are used in a linear downward extrapolation of the lung cancer risk/mg of particulate ETS exposure for current smokers to calculate the average lung cancer risk for never smokers and the number of never smoker lung cancer deaths (LCD) in the U.S. in 1980 from exposure to particulate ETS. The estimated average daily inhaled particulate ETS exposure for never smokers is 0.62 mg/day for men and 0.28 mg/day for women. The average never smoker is estimated to retain 11% of the inhaled exposure, for a daily retained exposure of 0.07 mg for men and 0.03 mg for women. Other estimates are: a daily retained exposure for current smokers of 310 mg for men and 249 mg for women, a smoking-attributable lung cancer risk for current smokers in 1980 of 284 LCD/100,000 men and 121 LCD/100,000 women, and an annual retained-exposure lung cancer risk for never smokers of 0.64 LCD/100,000 men and 0.015 LCD/100,000 women. These risks and exposures estimate 12 lung cancer deaths among never smokers from exposure to particulate ETS: 8 among the 11.96 million male never smokers and 4 among the 28.85 million female never smokers in the U.S. in 1980. Conversely, between 655 and 3,610 never smoker lung cancer deaths are estimated from methods based on the average lung cancer risk observed in epidemiological studies of exposure to ETS. Three possible reasons for the discrepancy between the exposure and risk-based estimates are discussed: the excess risks observed in epidemiological studies are due to bias, the relationship between exposure and risk is supralinear, or sidestream tobacco smoke is substantially more carcinogenic than an equivalent exposure to mainstream smoke.  相似文献   

6.
One hundred and ninety-four randomly selected nonsmoking subjects collected air samples in their breathing zone by wearing personal monitors for 24 h. The study was centered in Hong Kong, and comprised housewives in one group, primarily for assessing exposures in the home, and office workers in a second group to assess the contribution of the workplace to overall exposure. Samples collected were analysed for respirable suspended particles (RSP), nicotine, 3-ethenylpyridine, and environmental tobacco smoke (ETS) particles using ultraviolet absorbance (UVPM), fluorescence (FPM), and solanesol measurements (SolPM). Saliva cotinine analyses were also undertaken to confirm the nonsmoking status of the subjects and to investigate their correlation with ETS exposure measurements. Approximately 6% of the subjects in Hong Kong misclassified their nonsmoking status. Median time-weighted average (TWA) RSP concentrations varied from 43 to 54 μg m−3 with no significant differences detected between any of the groups investigated. Office workers who lived and worked with smokers were exposed to 2.6 μg m−3 ETS particles (SolPM) and 0.44 μg m−3 nicotine, based on median TWA concentrations. Median concentrations of ETS particles and nicotine were below the limits of quantification for housewives living with smokers and were not significantly different from those for housewives living with nonsmokers. It would therefore be unreliable in Hong Kong to use a smoking spouse as a marker for assessing health risks related to ETS exposure. The office workers in this study were significantly more exposed to ETS than housewives from either smoking or nonsmoking homes, and the workplace was estimated to contribute over 33% of the annual exposure to ETS particles and nicotine. Exposure estimates suggest that the most highly exposed office workers in this study receive between 11 and 50 cigarette equivalents per year, based upon upper decile levels for ETS particles and nicotine, respectively.  相似文献   

7.
BackgroundShort telomeres are associated with chronic disease and early mortality. Recent studies in adults suggest an association between telomere length and exposure to particulate matter, and that ethnicity may modify the relationship. However associations in children are unknown.ObjectivesWe examined associations between air pollution and telomere length in an ethnically diverse group of children exposed to high levels of traffic derived pollutants, particularly diesel exhaust, and to environmental tobacco smoke.MethodsOral DNA from 333 children (8–9 years) participating in a study on air quality and respiratory health in 23 inner city London schools was analysed for relative telomere length using monochrome multiplex qPCR. Annual, weekly and daily exposures to nitrogen oxides and particulate matter were obtained from urban dispersion models (2008–10) and tobacco smoke by urinary cotinine. Ethnicity was assessed by self-report and continental ancestry by analysis of 28 random genomic markers. We used linear mixed effects models to examine associations with telomere length.ResultsTelomere length increased with increasing annual exposure to NOx (model coefficient 0.003, [0.001, 0.005], p < 0.001), NO2 (0.009 [0.004, 0.015], p < 0.001), PM2.5 (0.041, [0.020, 0.063], p < 0.001) and PM10 (0.096, [0.044, 0.149], p < 0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p < 0.001)ConclusionsPollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms.  相似文献   

8.
Due to the relatively high activity concentrations of (210)Po and (210)Pb that are found in tobacco and its products, cigarette smoking highly increases the internal intake of both radionuclides and their concentrations in the lung tissues. That might contribute significantly to an increase in the internal radiation dose and in the number of instances of lung cancer observed among smokers. Samples of most frequently smoked fine and popular brands of cigarettes were collected from those available on the Egyptian market. (210)Po activity concentrations were measured by alpha spectrometry, using surface barrier detectors, following the radiochemical separation of polonium. Samples of fresh tobacco, wrapping paper, fresh filters, ash and post-smoking filters were spiked with (208)Po for chemical recovery calculation. The samples were dissolved using mineral acids (HNO(3), HCl and HF). Polonium was spontaneously plated-out on stainless steel disks from diluted HCl solution. The (210)Po activity concentration in smoke was estimated on the basis of its activity in fresh tobacco and wrapping paper, fresh filter, ash and post-smoking filters. The percentages of (210)Po activity concentrations that were recovered from the cigarette tobacco to ash, post-smoking filters, and smokes were assessed. The results of this work indicate that the average (range) activity concentration of (210)Po in cigarette tobacco was 16.6 (9.7-22.5) mBq/cigarette. The average percentages of (210)Po content in fresh tobacco plus wrapping paper that were recovered by post-smoking filters, ash and smoke were 4.6, 20.7 and 74.7, respectively. Cigarette smokers, who are smoking one pack (20 cigarettes) per day, are inhaling on average 123 mBq/d of (210)Po and (210)Pb each. The annual effective doses were calculated on the basis of (210)Po and (210)Pb intake with the cigarette smoke. The mean values of the annual effective dose for smokers (one pack per day) were estimated to be 193 and 251 microSv from (210)Po and (210)Pb, respectively.  相似文献   

9.
A complete assessment of the health effects of diesel emissions must take into account the possible chemical transformations (and associated biological impacts) of particulate organic matter (POM) due to reactions with the many gaseous copollutants which have now been unambiguously demonstrated to be present in atmospheres burdened by photochemical air pollution. These copollutants include the “trace” species, nitric (HNO3) and nitrous (HONO) acids, the nitrate radical (NO3), formaldehyde (H2CO) and formic acid (HCOOH), as well as the criteria pollutants, ozone (O3) and nitrogen dioxide (NO2). Techniques for establishing the atmospheric concentrations of the trace pollutants (and their spatial and temporal variations) are briefly described, and we present results of investigations into the reactions of polycyclic aromatic hydrocarbons (PAH) coated on filters and exposed to ambient concentrations of O3 and NO2. Environmental health implications of these results are discussed and include the potential for sampling “artifacts” and their possible effects on the correlation (or lack thereof) between ambient PAH levels and urban lung cancer rates, as well as the problems associated with understanding the appropriate POM “dose” to be employed in animal testing and assessments of impacts on human health.  相似文献   

10.
The Syracuse, NY, AUDIT (Assessment of Urban Dwellings for Indoor Toxics) study was designed to quantify asthma agent levels in the inner-city homes of a birth cohort whose mothers had a diagnosis of asthma. Risk of exposure to particulate matter (PM), particle number and tobacco smoke was assessed in 103 infants' homes. Repeat measurements were made in 44% of the homes. Infants also were examined on a quarterly basis during the first year of life to monitor their respiratory health and urine cotinine levels. Overall geometric mean (GM) values for PM(2.5) of 21.2 μg/m(3) and for PM(10) of 31.8 μg/m(3) were recorded in homes at visit 1. GM values for PM(2.5) and PM(10) in smoking homes were higher at 26.3 and 37.7 μg/m(3), while values in non-smoking homes were 12.7 and 21.2 μg/m(3) respectively. Fifty-four percent of mothers (55/103) smoked at some point in pregnancy (39% smoked throughout pregnancy). Environmental tobacco smoke (ETS) exposure occurred in 68% of homes during the infants' first year. Significant to this study was the size- and time-resolved monitoring of PM at 140 home visits and the classification of PM count data. PM number counts ranged from continuously low levels (little indoor activity) to continuously high counts (constant indoor activity), and recorded apparent instances of prolonged repeated cigarette smoking. Wheezing in the first year of life was recorded for 38% of the infants (39/103). Adjusted logistic regression modeling demonstrated that elevated levels of indoor PM(2.5) (≥ 15 μg/m(3)) were a significant risk factor for infant wheezing after controlling for infant gender, mothers' age and education level, season of home visit and presence of carpeting (OR 4.21; 95% CI 1.36-13.03; p=0.013). An elevated level of the nicotine metabolite cotinine in infant urine also was associated with infant wheezing after adjusting for infant gender, mothers' age and education level (OR 5.10; 95% CI 0.96-27.24; p=0.057). ETS exposure was pervasive in the AUDIT cohort and a risk for developing infants in this urban population.  相似文献   

11.
Alternative fuels for diesel engine applications are gaining more prominence as they have numerous advantages compared to fossil fuels. They are renewable, biodegradable; provide food and energy security and foreign exchange savings. They address environmental concerns and socio-economic issues as well. Gaseous fuels such as compressed natural gas and hydrogenated compressed natural gas (HCNG) appear more attractive fuels for diesel engine applications operated in dual-fuel mode. Such dual fuel engines can replace considerable amount of liquid-injected pilot fuels by gaseous fuels besides being friendly to the environment. A small quantity of liquid fuel injected towards the end of the compression stroke initiates combustion of the inducted gas in the dual-fuel engines. The main advantage of dual-fuel engines is their lower nitrogen oxides (NOx) and particulate emissions. Hence renewable fuels such as biodiesels and gaseous fuels can be used predominantly for transportation and power generation applications. Gaseous fuels are clean burning and are more economical as well. A suitable carburettor was designed to supply a stoichiometric mixture of air and HCNG to the modified diesel engine operated in dual-fuel mode. The biodiesel used in this study is derived from Honge oil called the Honge oil methyl ester (HOME). This paper presents the performance, combustion and exhaust emission characteristics of a single cylinder, four stroke, direct injection, stationary diesel engine operated on HOME and HCNG in dual-fuel mode. From the results it is observed that HOME–HCNG combination gave lower brake thermal efficiency (BTE) and improved emission levels when compared with diesel/HOME in single fuel operation. Lower smoke and particulate matter were obtained with dual-fuel operation. Comparative measures of BTE, peak pressure, pressure–crank angle variation, smoke opacity, hydrocarbon, carbon monoxide and NOx emissions have been made and analysed.  相似文献   

12.
《Environment international》2012,38(8):1321-1328
The impact of cigarette smoking on volatile organic compound (VOC) blood levels is studied using 2003–2004 National Health and Nutrition Examination Survey (NHANES) data. Cigarette smoke exposure is shown to be a predominant source of benzene, toluene, ethylbenzene, xylenes and styrene (BTEXS) measured in blood as determined by (1) differences in central tendency and interquartile VOC blood levels between daily smokers [≥ 1 cigarette per day (CPD)] and less-than-daily smokers, (2) correlation among BTEXS and the 2,5-dimethylfuran (2,5-DMF) smoking biomarker in the blood of daily smokers, and (3) regression modeling of BTEXS blood levels versus categorized CPD. Smoking status was determined by 2,5-DMF blood level using a cutpoint of 0.014 ng/ml estimated by regression modeling of the weighted data and confirmed with receiver operator curve (ROC) analysis. The BTEXS blood levels among daily smokers were moderately-to-strongly correlated with 2,5-DMF blood levels (correlation coefficient, r, ranging from 0.46 to 0.92). Linear regression of the geometric mean BTEXS blood levels versus categorized CPD showed clear dose–response relationship (correlation of determination, R2, ranging from 0.81 to 0.98). Furthermore, the pattern of VOCs in blood of smokers is similar to that reported in mainstream cigarette smoke. These results show that cigarette smoking is a primary source of benzene, toluene and styrene and an important source of ethylbenzene and xylene exposure for the U.S. population, as well as the necessity of determining smoking status and factors affecting dose (e.g., CPD, time since last cigarette) in assessments involving BTEXS exposure.  相似文献   

13.
This review summarizes the published literature on the presence of polycyclic aromatic hydrocarbons (PAH) in indoor air, settled house dust, and food, and highlights geographical and temporal trends in indoor PAH contamination. In both indoor air and dust, ΣPAH concentrations in North America have decreased over the past 30 years with a halving time of 6.7 ± 1.9 years in indoor air and 5.0 ± 2.3 years in indoor dust. In contrast, indoor PAH concentrations in Asia have remained steady. Concentrations of ΣPAH in indoor air are significantly (p < 0.01) higher in Asia than North America. In studies recording both vapor and particulate phases, the global average concentration in indoor air of ΣPAH excluding naphthalene is between 7 and 14,300 ng/m3. Over a similar period, the average ΣPAH concentration in house dust ranges between 127 to 115,817 ng/g. Indoor/outdoor ratios of atmospheric concentrations of ΣPAH have declined globally with a half-life of 6.3 ± 2.3 years. While indoor/outdoor ratios for benzo[a]pyrene toxicity equivalents (BaPeq) declined in North America with a half-life of 12.2 ± 3.2 years, no significant decline was observed when data from all regions were considered. Comparison of the global database, revealed that I/O ratios for ΣPAH (average = 4.3 ± 1.3), exceeded significantly those of BaPeq (average = 1.7 ± 0.4) in the same samples. The significant decline in global I/O ratios suggests that indoor sources of PAH have been controlled more effectively than outdoor sources. Moreover, the significantly higher I/O ratios for ΣPAH compared to BaPeq, imply that indoor sources of PAH emit proportionally more of the less carcinogenic PAH than outdoor sources. Dietary exposure to PAH ranges from 137 to 55,000 ng/day. Definitive spatiotemporal trends in dietary exposure were precluded due to relatively small number of relevant studies. However, although reported in only one study, PAH concentrations in Chinese diets exceeded those in diet from other parts of the world, a pattern consistent with the spatial trends observed for concentrations of PAH in indoor air. Evaluation of human exposure to ΣPAH via inhalation, dust and diet ingestion, suggests that while intake via diet and inhalation exceeds that via dust ingestion; all three pathways contribute and merit continued assessment.  相似文献   

14.
Efforts to reduce the energy needs to heat or cool dwellings have the potential to create new health hazards. Increases in indoor levels of radon and its progeny from the reduction in air exchange rates add a substantial radioactive burden to the general population. Other indoor pollutants reaching critical concentrations in homes with low air exchange rates are CO and NO2 from unvented combustion in gas stoves and heaters, tobacco smoke, and asbestos fibers. In addition, insulation materials and certain types of furniture may contribute the toxicant formaldehyde diffusing from foam injected walls or chipboard. Risk estimations using linear dose-response relationships show risk factors per kWh saved which are orders of magnitude greater than for a kWh produced by large power plants using coal, oil, gas, or uranium.  相似文献   

15.
Exposure to respirable suspended particles (RSP), environmental tobacco smoke (ETS) particles, nicotine, and 3-ethenylpyridine (3-EP) was assessed in Turin for 188 subjects during February and March 1995. Personal monitors were worn over a 24-h period, each subject providing a saliva sample for cotinine analysis both prior to and following the monitoring period. Comprehensive lifestyle questionnaires were also completed before and after the 24-h monitoring period. The study comprised housewives in one group, primarily for assessing exposures in the home, and office workers in a second group to assess exposures in the workplace. A single personal monitor was worn by each participating housewife, while employed subjects wore one monitor at work and a separate monitor at home and elsewhere. Based on median 24-h time-weighted average exposures, the most highly exposed subjects to RSP, ETS particles, nicotine, and 3-EP were office workers living with smokers and employed in locations where smoking was allowed. Annualised exposures for nonsmokers living and working in smoking environments indicate that the home contribution to RSP is between 3 and 4 times that obtained from the workplace. Similarly nicotine and ETS particle contributions from the home are, respectively, 4 and 7 times more than those obtained from the workplace. Subjects living and working with smokers had the highest median saliva cotinine levels of 1.7 ng mL−1. Using a cut off level of 25 ng mL−1, up to 6.5% of subjects were found to have misreported themselves as nonsmokers.  相似文献   

16.
In the second half of 1997, large areas in Southeast Asia were severely affected by a smoke-haze pollution episode caused by the emissions of an estimated 45,600 km2 of vegetation that burnt on the Indonesian islands Kalimantan and Sumatra. To document the impacts of these fires on air quality, data for total suspended particulate matter (TSP) and for particulate matter below or equal to 10 microns in diameter (PM10) from selected sites in Indonesia, Malaysia and Singapore are analysed in this paper. These data are supplemented by meteorological data, satellite images and a summary of related research. TSP was above 2,000 μg m–3 for several days in Indonesian locations close to the most extensive fire activity. In Malaysia and Singapore, ambient particle concentrations increased to several times their average September levels. Characteristically for emissions from vegetation burning, the additional atmospheric particle loading during the smoke-haze episode was predominantly due to an increase of the fraction below or equal to 2.5 microns in diameter (PM2.5). Due to the dominance of respirable particles (PM2.5) in the smoke-haze, air quality reporting based on TSP or PM10 may be inadequate to assess the health risk. Upgrading of PM2.5 monitoring facilities is therefore needed. Reducing the probability of similar smoke-haze events in future would require appropriate fire use and smoke management strategies. Electronic Publication  相似文献   

17.
Chinese hamsters were exposed for eight hours per day to automotive diesel exhaust emissions which were diluted with air (18 to 1) and had a particulate level of 6.4 mg/m3. Pulmonary function measurements were made after six months exposure. Body weight (BW), lung weight (LW), vital capacity (VC), residual volume by water displacement (RVw) and by gas dilution (RVD), alveolar volume (VA), and carbon monoxide transfer factor (DLCO) were measured. LW showed a significant increase in the diesel exposed animals (P < 0.01) while VC, RVW, and DLCO showed decreases (P < 0.01). Static deflation volume-pressure curves showed depressed deflation volumes for diesel exposed animals when volumes were corrected for body weight and even greater depressed volumes when volumes were corrected for lung weight. However, when volumes were expressed as percent vital capacity, the diesel exposed animals had higher lung volumes at 0 and 5 cm H2O. Results of the pathological examination of the lung tissue will be necessary for final analysis of our findings. However, preliminary interpretation indicates possible emphysematous changes which are compatible with the observed decrease in DLCO.  相似文献   

18.
Concentration levels of 210Pb and 210Po in dry tobacco leaves in Greece   总被引:1,自引:0,他引:1  
Tobacco leaves are large and have sticky exudates that retain the radon decay products once they deposit on the leaves. The study of 210Po in tobacco is required, because of the cumulative alpha-radiation dose delivered to humans from inhaled 210Po in cigarette smoke. 210Pb is the other element of interest since it is the 210Po precursor in the radioactive decay chain. In the present study, the concentrations of these two radionuclides were determined in tobacco samples from seven regions in Greece. 210Po was determined by alpha spectrometry using a surface barrier detector after radiochemical separation and spontaneous deposition of polonium on a nickel disk. The 210Pb activity in the samples was determined via the 210Po resulting from the decay of 210Pb. The results of the present study indicate that 210Po concentrations ranged from 3.6 to 17.0 mBqg(-1) (average 13.1 mBqg(-1)) of dry tobacco, while 210Pb concentrations ranged from 7.3 to 18.0 mBqg(-1) (average 13.4 mBqg(-1)). The mean value of the annual committed effective dose for smokers (20 cigarettes per day) of Greek tobacco was estimated to be 287 microSv (124 microSv from 210Po and 163 microSv from 210Pb). The inhalation dose for smokers is on average about 12 times higher than for non-smokers living in the mid-latitudes of the northern hemisphere.  相似文献   

19.
The carcinogenic etfect of 210Po and 210Pb with respect to lung cancer is an important problem in many countries with very high cigarette consumption. Poland has one of the highest consumptions of cigarettes in the world. The results of 210Po determination on the 14 most frequently smoked brands of cigarettes which constitute over 70% of the total cigarette consumption in Poland are presented and discussed. Moreover, the polonium content in cigarette smoke was estimated on the basis of its activity in fresh tobaccos, ash, fresh filters and post-smoking filters. The annual effective doses were calculated on the basis of 210Po and 210Pb inhalation with the cigarette smoke. The results of this work indicate that Polish smokers who smoke one pack (20 cigarettes) per day inhale from 20 to 215 mBq of 210Po and 210Pb each. The mean values of the annual effective dose for smokers were estimated to be 35 and 70 microSv from 210Po and 210Pb, respectively. For persons who smoke two packs of cigarettes with higher radionuclide concentrations, the effective dose is much higher (471 microSv yr(-1)) in comparison with the intake in diet. Therefore, cigarettes and the absorption through the respiratory system are the main sources and the principal pathway of 210Po and 210Pb intake of smokers in Poland.  相似文献   

20.
BackgroundDespite studies having consistently linked exposure to single-source polycyclic aromatic hydrocarbons (PAHs) to breast cancer, it is unclear whether single sources or specific groups of PAH sources should be targeted for breast cancer risk reduction.ObjectivesThis study considers the impact on breast cancer incidence from multiple PAH exposure sources in a single model, which better reflects exposure to these complex mixtures.MethodsIn a population-based case-control study conducted on Long Island, New York (N = 1508 breast cancer cases/1556 controls), a Bayesian hierarchical regression approach was used to estimate adjusted posterior means and credible intervals (CrI) for the adjusted odds ratios (ORs) for PAH exposure sources, considered singly and as groups: active smoking; residential environmental tobacco smoke (ETS); indoor and outdoor air pollution; and grilled/smoked meat intake.ResultsMost women were exposed to PAHs from multiple sources, and the most common included active/passive smoking and grilled/smoked food intake. In multiple-PAH source models, breast cancer incidence was associated with residential ETS from a spouse (OR = 1.20, 95%CrI = 1.03, 1.40) and synthetic firelog burning (OR = 1.29, 95%CrI = 1.06, 1.57); these estimates are similar, but slightly attenuated, to those from single-source models. Additionally when we considered PAH exposure groups, the most pronounced significant associations included total indoor sources (active smoking, ETS from spouse, grilled/smoked meat intake, stove/fireplace use, OR = 1.45, 95%CrI = 1.02, 2.04).ConclusionsGroups of PAH sources, particularly indoor sources, were associated with a 30–50% increase in breast cancer incidence. PAH exposure is ubiquitous and a potentially modifiable breast cancer risk factor.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号