Impact of cigarette smoking on Volatile Organic Compound (VOC) blood levels in the U.S. Population: NHANES 2003–2004

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.     

Volatile organic compounds concentrations in residential indoor and outdoor and its personal exposure in Korea

To date, personal volatile organic compounds (VOCs) exposure and residential indoor and outdoor VOCs levels have not been characterized in Korea. In this study, residential indoor and outdoor VOCs concentrations were measured and compared simultaneously with the personal exposure for each of 30 participants in a medium city, Asan, and in a metropolitan city, Seoul. Factors that influence personal VOCs exposures were assessed in relation to house characteristics and time activity information. All VOC concentrations were measured using passive samplers during a 24-h period and analyzed using GC-MS. Ten target VOCs were benzene, trichloroethylene, toluene, o-xylene, p-xylene, ethylbenzene, MIBK, n-octane, styrene, and 1,2-dichlorobenzene. Residential indoor and outdoor VOCs concentrations measured in Seoul were significantly higher than those in Asan. Indoor/outdoor (I/O) ratios for all target compounds ranged from 0.94 to 1.51 and I/O ratios of Asan were a little higher than those of Seoul. Results indicate that time activity information can be used to predict personal exposures, although such predictions will result in an over estimation compared to measured exposures. Factors which influence the indoor VOCs level and its personal exposure in relation to house characteristics included house age, indoor smoking, and house type.     

Preliminary measurements of aromatic VOCs in public transportation modes in Guangzhou,China

This study examined the exposure level of aromatic volatile organic compounds (VOCs) in public transportation modes in Guangzhou, China. A total of 40 VOC samples were conducted in four popular public commuting modes (subway, taxis, non-air-conditioned buses and air-conditioned buses) while traversing in urban areas of Guangzhou. Traffic-related VOCs (benzene, toluene, ethylbenzene, m/p-xylene and o-xylene) were collected on adsorbent tubes and analyzed by thermal desorption (TD) and gas chromatography/mass-selective detector (GC/MSD) technique. The results indicate that commuter exposure to VOCs is greatly influenced by the choice of public transport. For the benzene measured, the mean exposure level in taxis (33.6 microg/m(3)) was the highest and was followed by air-conditioned buses (13.5 microg/m(3)) and non-air-conditioned buses (11.3 microg/m(3)). The exposure level in the subway (7.6 microg/m(3)) is clearly lower than that in roadway transports. The inter-microenvironment variations of other target compounds were similar to that of benzene. The target VOCs were well correlated to each other in all the measured transports. The concentration profile of the measured transport was also investigated and was found to be similar to each other. Based on the experiment results, the average B/T/E/X found in this study was about (1.0/4.3/0.7/1.4). In this study, the VOC levels measured in evening peak hours were only slightly higher than those in afternoon non-peak hours. This is due to the insignificant change of traffic volume on the measured routes between these two set times. The out-dated vehicle emission controls and slow-moving traffic conditions may be the major reasons leading elevated in-vehicle exposure level in some public commuting journeys.     

Contribution of tobacco smoke to environmental benzene exposure in Germany

The concentrations of environmental tobacco smoke (ETS) constituents including benzene were measured in the living rooms of 10 nonsmoking households and 20 households with at least one smoker situated in the city and suburbs of Munich. In the city, the median benzene levels during the evening, when all household members were at home, were 8.1 and 10.4 μg/m³ in nonsmoking and smoking homes, respectively. The corresponding levels of 3.5 and 4.6 μg/m³ were considerably lower in the suburbs. Median time-integrated 1-week benzene concentrations in the city were 10.6 μg/m³ in nonsmoking homes and 13.1 μg/m³ in smoking homes. In the suburbs, the corresponding values were 3.2 and 5.6 μg/m³. While the benzene concentrations in nonsmoking homes located in the city were significantly higher (p < 0.05) than in suburban nonsmoking households, no difference was found between smoking and nonsmoking households located either in the city or in the suburbs. Individual exposures to benzene and to specific markers for tobacco smoke of all household members (82 nonsmokers and 32 smokers) were determined by questionnaire, personal monitoring, and biomonitoring. Within the city, the benzene exposure determined by personal samplers was 11.8 μg/m³ for nonsmokers living in nonsmoking homes and 13.3 μg/m³ for nonsmokers in smoking homes. The corresponding values for nonsmokers living in the suburbs were 5.9 and 6.9 μg/m³, respectively. Neither difference was statistically significant. Nonsmokers living in nonsmoking households in the city had significantly higher exposure to benzene compared to their counterparts living in the suburbs (personal samplers: 11.8 vs 5.9 μg/m³, p < 0.001; benzene in exhalate: 2.4 vs. 1.1 μg/m³, p < 0.05; trans,trans-muconic acid excretion in urine: 92 vs. 54 μg/g creatinine, p < 0.05). Nonsmokers from all households with smokers were significantly more exposed to benzene than nonsmokers living in the nonsmoking households (personal samplers: 13.2 vs. 7.0 μg/m³, p < 0.05; benzene in exhalate: 2.6 vs. 1.8 μg/m³, p < 0.01; trans,trans-muconic acid excretion in urine: 73 vs. 62 μg/g creatinine), but the contribution of ETS to the total benzene exposure was relatively low compared to that from other sources. Analysis of variance showed that at most 15% of the benzene exposure of nonsmokers living in smoking homes was attributable to ETS. For nonsmokers living in nonsmoking households benzene exposure from ETS was insignificant.     

Never smoker lung cancer risks from exposure to particulate tobacco smoke

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.     

Inhalation of 210Po and 210Pb from cigarette smoking in Poland.

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.     

Polonium-210 budget in cigarettes

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.     

Assessment of arsenic level in the hair of the nonoccupational Egyptian population: pilot study.

Arsenic level of hair samples of apparently healthy Egyptian was measured by means of hydride atomic absorption spectrophotometery. It ranged between 0.04 and 1.04 mg As/kg hair, about 55% of the analysed hair samples were within the range of allowable values (0.08-0.25 mg As/kg hair), but 45% were not. There were no considerable sex-related differences (0.303 and 0.292 mg As/kg hair for males and females, respectively). Different educational levels did not influence it either, when the effect of the age had been excluded. Children and adolescents proved to be more susceptible to arsenic as their mean levels (0.353 microg/g), and were significantly higher than those in the adults (0.233 microg/g). Smoking and some dietary habits had an important role in the elevation of arsenic levels among the nonoccupational Egyptian population: 60% of smokers and 66.7% of indoor passive smokers had arsenic levels >0.25 mg As/kg hair. Arsenic levels were also dependent on the kind of smoking, as hair arsenic of the subject smoking molasses tobacco was found to be significantly higher than that of cigarette smokers (0.459 and 0.209 mg As/kg hair, respectively). The frequency of meat and fish consumption per week was also found to be positively, significantly correlated with arsenic levels. On the other hand, the frequency of consumption of fruits, fresh and cooked vegetables, milk and milk products per week beneficially influenced the arsenic level of the hair samples examined. Arsenic content of the consumed water in Egypt was 0.001 mg/l, which is below the maximum drinking water level allowed by World Health Organisation (WHO). Therefore, the arsenic content of domestic tap water hardly contributed to the arsenic exposure of the Egyptian population in the regions of the study. It is likely that exposure routes by smoking, fish and animal protein consumption are the principal cause of arsenic accumulation in the general Egyptian population.     

Assessment of environmental tobacco smoke and respirable suspended particle exposures for nonsmokers in Hong Kong using personal monitoring

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.     

Environmental and lifestyle factors affect benzene uptake biomonitoring of residents near a petrochemical plant

Background

We monitored urinary benzene excretion to examine factors affecting benzene uptake in a sample of the general population living near a petrochemical plant.

Methods

Our study population included 143 subjects: 33 petrochemical plant workers (W) with low level occupational benzene exposure; 30 residents in a small town 2 km from the plant (2kmR); 26 residents in a second small town located 2 to 4 km from the plant (4kmR); and 54 urban residents 25 km from the plant (25kmR). Exposure to benzene was evaluated by personal air sampling during one work-shift for the W group, and from 8.00 to 20:00 for general population subgroups, and by urinary benzene (BEN-U).

Results

Median airborne benzene exposure was 25, 9, 7 and 6 μg/m³ benzene among the W, 2kmR, 4kmR, and 25kmR subgroups, respectively; the highest level was found among the workers, while there was no significant difference among the other groups. Median BEN-U was 2 to 14-fold higher in smokers compared to non-smokers; among non-smokers BEN-U was the highest in W (median 236 ng/L), and lower in the 2kmR (48 ng/L) and 4kmR (63 ng/L) subgroups than in the 25kmR (120 ng/L) subgroup. A multiple linear regression analysis, explaining up to 73% of BEN-U variability, confirmed that active smoking and airborne benzene most strongly affected BEN-U. Among the non-smoking, non-occupationally exposed study subjects, a positive association was found between BEN-U and the distance of residence from the plant. This association was explained by increased exposure to urban traffic emissions in the study group residing at a greater distance from the plant. Environmental tobacco smoke had a marginally positive role.

Conclusion

Among factors affecting benzene uptake in non-occupationally exposed individuals, urban residence contributes to benzene exposure more than residing in close proximity to a petrochemical plant.     

Distributions of personal VOC exposures: a population-based analysis

Information regarding the distribution of volatile organic compound (VOC) concentrations and exposures is scarce, and there have been few, if any, studies using population-based samples from which representative estimates can be derived. This study characterizes distributions of personal exposures to ten different VOCs in the U.S. measured in the 1999-2000 National Health and Nutrition Examination Survey (NHANES). Personal VOC exposures were collected for 669 individuals over 2-3 days, and measurements were weighted to derive national-level statistics. Four common exposure sources were identified using factor analyses: gasoline vapor and vehicle exhaust, methyl tert-butyl ether (MBTE) as a gasoline additive, tap water disinfection products, and household cleaning products. Benzene, toluene, ethyl benzene, xylenes chloroform, and tetrachloroethene were fit to log-normal distributions with reasonably good agreement to observations. 1,4-Dichlorobenzene and trichloroethene were fit to Pareto distributions, and MTBE to Weibull distribution, but agreement was poor. However, distributions that attempt to match all of the VOC exposure data can lead to incorrect conclusions regarding the level and frequency of the higher exposures. Maximum Gumbel distributions gave generally good fits to extrema, however, they could not fully represent the highest exposures of the NHANES measurements. The analysis suggests that complete models for the distribution of VOC exposures require an approach that combines standard and extreme value distributions, and that carefully identifies outliers. This is the first study to provide national-level and representative statistics regarding the VOC exposures, and its results have important implications for risk assessment and probabilistic analyses.     

Neurobehavioral performance in adolescents is inversely associated with traffic exposure

On the basis of animal research and epidemiological studies in children and elderly there is a growing concern that traffic exposure may affect the brain. The aim of our study was to investigate the association between traffic exposure and neurobehavioral performance in adolescents. We examined 606 adolescents. To model the exposure, we constructed a traffic exposure factor based on a biomarker of benzene (urinary trans,trans-muconic acid) and the amount of contact with traffic preceding the neurobehavioral examination (using distance-weighted traffic density and time spent in traffic). We used a Bayesian structural equation model to investigate the association between traffic exposure and three neurobehavioral domains: sustained attention, short-term memory, and manual motor speed. A one standard deviation increase in traffic exposure was associated with a 0.26 standard deviation decrease in sustained attention (95% credible interval: − 0.02 to − 0.51), adjusting for gender, age, smoking, passive smoking, level of education of the mother, socioeconomic status, time of the day, and day of the week. The associations between traffic exposure and the other neurobehavioral domains studied had the same direction but did not reach the level of statistical significance. The results remained consistent in the sensitivity analysis excluding smokers and passive smokers. The inverse association between sustained attention and traffic exposure was independent of the blood lead level. Our study in adolescents supports the recent findings in children and elderly suggesting that traffic exposure adversely affects the neurobehavioral function.     

Levels of household particulate matter and environmental tobacco smoke exposure in the first year of life for a cohort at risk for asthma in urban Syracuse, NY

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.     

Determination of aniline and related mono-aromatic amines in indoor air in selected Canadian residences by a modified thermal desorption GC/MS method

A modified thermal desorption method to determine low levels of aniline and other related mono-aromatic amines (MAAs) in residential air is described. The method was successfully applied to the determination of levels of these chemicals in residential air from 69 selected homes in two Canadian regions. Instrument detection limits of between 0.02 and 0.06 ng per thermal desorption tube were achieved for aniline and other MAAs. In the absence of environmental tobacco smoke (ETS) the mean concentrations of aniline in both indoor air and outdoor air were similar, at about 0.01 microgram/m3 after correction with field blanks. There was however a statistically significant difference in aniline concentrations between field blanks and indoor or outdoor air samples. No significant difference of aniline levels in the two study regions was observed. A clear link between aniline concentrations in indoor air and smoking activities inside homes was evident. Analysis of cigarette leaves indicated that aniline was most likely formed due to combustion during smoking. Shoe polishing was identified as another source of aniline in indoor air.     

A quantitative estimate of nonsmokers' lung cancer risk from passive smoking

This work presents a quantitative assessment of nonsmokers' risk of lung cancer from passive smoking. The estimates given should be viewed as preliminary and subject to change as improved research becomes available. It is estimated that U.S. nonsmokers are exposed to from 0 to 14 mg of tobacco tar per day, and that the typical nonsmoker is exposed to 1.4 mg per day. A phenomenological exposure-response relationship is derived, yielding 5 lung cancer deaths per year per 100,000 persons exposed, per mg daily tar exposure. This relationship yields lung cancer mortality rates and mortality ratios for a U.S. cohort which are consistent to within 5% with the results of both of the large prospective epidemiological studies of passive smoking and lung cancer in the United States and Japan. Aggregate exposure to ambient tobacco smoke is estimated to produce about 5000 lung cancer deaths per year in U.S. nonsmokers aged ≥ 35 yr, with an average loss of life expectancy of 17 ± 9 yr per fatality. The estimated risk to the most-exposed passive smokers appears to be comparable to that from pipe and cigar smoking. Mortality from passive smoking is estimated to be about two orders of magnitude higher than that estimated for carcinogens currently regulated as hazardous air pollutants under the federal Clean Air Act.     

Radionuclides in cigarettes may lead to carcinogenesis via p16 inactivation

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 p16^INK4a (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.     

Effect of cigarette smoking on residential NO2 levels

Two studies evaluating the levels and sources of nitrogen dioxide in approximately 90 employee homes in the Richmond area with continuous sampling during the weeks of August 5, 1980, and February 9, 1981, were performed using samplers in the living room, bedroom, kitchen, and outdoors. Additional data were collected concerning appliance usage, heating/cooling plant, ventilation and cigarette smoking. Results were analyzed using BMDP routines. The largest contributor to NO₂ concentration was found to be gas-fired kitchen appliances. The mean kitchen level for homes with gas appliances during the winter study was 188 μg/m³. Excluding participants with gas kitchens, incremental influence due to cigarette smoking was detected. The 7-day, 3-room average level of NO₂ in the homes of nonsmokers and smokers without gas-fired appliances was 12 and 15 μg/m³, respectively, in the summer. The corresponding winter values were 19 and 22 μg/m³. Furthermore, the individual levels of NO₂ in the homes of smokers were generally below both the adjacent outdoor level and the National Ambient Air Quality Standard limit for annual exposure.     

Tobacco smoke increases the risk of otitis media among Greenlandic Inuit children while exposure to organochlorines remain insignificant

BackgroundPrenatal exposure to environmental levels of organochlorines (OCs) has been demonstrated to have immunotoxic effects in humans. We investigated the relationship between prenatal exposure to OCs and the occurrence of otitis media (OM) among Inuit children in Greenland.MethodsWe estimated the concentration of 14 PCB congeners and 11 pesticides in maternal and cord blood samples and in breast milk in a population-based cohort of 400 mother–child pairs. At follow-up, we examined the children's ears and used their medical records to assess the OM occurrence and severity. Multivariate regression analyses were used with adjustments for passive smoking, crowding, dietary habits, parent's educational level, breast feeding and the use of child-care.ResultsThe children were 4–10 years of age at follow-up and 223 (85%) participated. We found no association between prenatal OC exposure and the development of OM. Factors associated with the child's hazard of OM during the first 4 years of life were: mother's history of OM (HR 1.70, 95% CI 1.11–2.59, p = 0.01); mother's smoking habits: current (HR 2.47, 95% CI 1.45–4.21, p < 0.01) and previous (HR 2.00, 95% CI 1.19–3.36, p < 0.01); number of smokers in the home (HR 1.17, 95% CI 1.05–1.31, p < 0.01). After adjustment mothers' smoking habits remained significant.ConclusionWe found no relationship between high levels of prenatal exposure of OCs and occurrence of OM. Passive smoking was found as the strongest environmental risk factor for the development of OM.Interventions to reduce passive smoke in children's environment are needed.     

Urinary methyl tert-butyl ether and benzene as biomarkers of exposure to urban traffic

Methyl tert-butyl ether (MTBE) and benzene are added to gasoline to improve the combustion process and are found in the urban environment as a consequence of vehicular traffic. Herein we evaluate urinary MTBE (MTBE-U) and benzene (BEN-U) as biomarkers of exposure to urban traffic. Milan urban policemen (130 total) were investigated in May, July, October, and December for a total of 171 work shifts. Personal exposure to airborne benzene and carbon monoxide (CO), and atmospheric data, were measured during the work shift, while personal characteristics were collected by a questionnaire. A time/activity diary was completed by each subject during the work shift. Spot urine samples were obtained for the determination of MTBE-U and BEN-U. Median personal exposure to CO and airborne benzene were 3.3 mg/m(3) and 9.6 μg/m(3), respectively; median urinary levels in end-of-shift (ES) samples were 147 ng/L (MTBE-U) and 207 ng/L (BEN-U). The time spent on traffic duty at crossing was about 40% of work time. Multiple linear regression models, taking into account within-subject correlations, were applied to investigate the role of urban pollution, atmospheric conditions, job variables and personal characteristics on the level of biomarkers. MTBE-U was influenced by the month of sampling and positively correlated to the time spent in traffic guarding, CO exposure and atmospheric pressure, while negatively correlated to wind speed (R(2) for total model 0.63, P<0.001). BEN-U was influenced by the month and smoking habit, and positively correlated to urinary creatinine; moreover, an interaction between CO and smoking was found (R(2)=0.62, P<0.001). These results suggest that MTBE-U is a reliable marker for assessing urban traffic exposure, while BEN-U is determined mainly by personal characteristics.     

A study of the growth and decay of cigarette smoke NOx in ambient air under controlled conditions

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.