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.     

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.     

Sidestream tobacco smoke constituents in indoor air modelled in an experimental chamber— Polycyclic aromatic hydrocarbons

Exposure to sidestream tobacco smoke is concerned with constituents in suspension in the indoor atmosphere. The natural dissipation of sidestream tobacco smoke has been investigated in a static atmosphere in a 10 m³ experimental chamber, and the rate of dissipation is expressed as T_0.5, the half-life of residence in the air. Respective T_0.5 of smoke components are calculated from the various sample data points, assuming a kinetic equation of the first-order process. Sidestream smoke has been generated by a smoking machine according to the Coresta standard protocol and then left to age over an 8-hour period, with subsequent sampling at defined time intervals. The experiments have been repeated over five days, and eight data point samples are obtained for each experiment. Besides nicotine, CO, and smoke particulate matter, interest has been focused on polycyclic aromatic hydrocarbons (PAH). The initial concentrations, C₀ for smoke particulate matter and nicotine (gas and particulate phases) are found to be 13.8 mg and 92 μg per cigarette per cubic meter, with T_0.5 being 2.6 and 2.1 hours, respectively. Low molecular-weight PAH have T_0.5 up to 20 hours, explainable only by their high concentrations in the gas phase, while the 3- to 7-ring PAH have T_0.5 of about 2 hours. The contribution of CO to ambient concentration is 91 mg per cigarette per cubic meter. The data can be useful in mathematical modellization studies regarding ventilation or exposure to sidestream smoke.     

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.     

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.     

Evaluation of the mutagenic potential of some compounds using Salmonella typhimurium

The mutagenicity of sodium nitrite, potassium chromate, O-tolidine, and smoke condensate from tobacco was shown on Salmonella typhimurium TA 1535. Sodium nitrite was definitely mutagenic on TA 1535 without S-9 mix. Potassium chromate without S-9 mix was also mutagenic on TA 1535. However, addition of S-9 mix resulted in a complete loss of potassium chromate mutagenicity. O-tolidine with and without S-9 mix elicited a very weak and variable mutagenic effect for strain TA 1535. Smoke condensate from pipe tobacco without S-9 mix elicited a weak mutagenic effect, whereas with S-9 mix it showed no mutagenicity on TA 1535.     

Pollutant emission rates from indoor combustion appliances and sidestream cigarette smoke

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).     

Indoor air exposure to coal and wood combustion emissions associated with a high lung cancer rate in Xuan Wei, China

Residents of Xuan Wei County in China have unusually high lung cancer mortality that cannot be attributed to tobacco use or occupational exposure. They are exposed to smoke from unvented, open pit coal or wood fires (often used for cooking and heating). The variation in lung cancer rates among communes within the county suggests that indoor combustion of smoky coal may be the prime determinant of lung cancer. To characterize the air in Xuan Wei homes, samples of air particles and semivolatile organic compounds were collected from homes located in two communes; one commune has a high rate of lung cancer, and the other has a low rate. Samples collected in the commune where the lung cancer rate is high and where smoky coal is the predominant fuel contained high concentrations of small particles with high organic content; organic extracts of these samples were mutagenic. Samples from homes in the wood-burning commune, which has a low rate of lung cancer, consisted mostly of larger particles of lower organic content and mutagenicity. The smoky coal sample was a mouse skin carcinogen and was a more potent initiator of skin tumors in comparison to the wood or smokeless coal sample.     

The combined effect of uranium and gamma radiation on biological responses and oxidative stress induced in Arabidopsis thaliana

Uranium never occurs as a single pollutant in the environment, but always in combination with other stressors such as ionizing radiation. As effects induced by multiple contaminants can differ markedly from the effects induced by the individual stressors, this multiple pollution context should not be neglected. In this study, effects on growth, nutrient uptake and oxidative stress induced by the single stressors uranium and gamma radiation are compared with the effects induced by the combination of both stressors. By doing this, we aim to better understand the effects induced by the combined stressors but also to get more insight in stressor-specific response mechanisms. Eighteen-day-old Arabidopsis thaliana seedlings were exposed for 3 days to 10 μM uranium and 3.5 Gy gamma radiation. Gamma radiation interfered with uranium uptake, resulting in decreased uranium concentrations in the roots, but with higher transport to the leaves. This resulted in a better root growth but increased leaf lipid peroxidation. For the other endpoints studied, effects under combined exposure were mostly determined by uranium presence and only limited influenced by gamma presence. Furthermore, an important role is suggested for CAT1/2/3 gene expression under uranium and mixed stressor conditions in the leaves.     

Species-Specific Features of Inter- and Intrapopulation Variation in the Level of Chromosome Instability in Rodents

Studies on the common vole Microtus arvalis revealed a distinct cytogenetic response to the influence of ionizing radiation, a wide range of variation in the group average indices of chromosome instability beyond the zone of technogenic impact, and the influence of natural factors (viral infections and fluctuations of population size) on the frequency of chromosome aberrations. In the northern mole vole Ellobius talpinus, neither the mutagenic effect of ionizing radiation nor interpopulation differences in the level of chromosome aberrations in the absence of anthropogenic impact were detected. Variation of genome instability of the rodents is significantly contributed to by species demography and population cycles.     

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.     

Cancer mortality in the meat and delicatessen departments of supermarkets (1950–2006)

Meat cutters and meat wrappers in the meat department of supermarkets are exposed to oncogenic viruses present in raw meat from cattle, pigs, sheep, and poultry, and their products (unpasteurized milk and raw eggs). Up to the mid 1970s, meat wrappers were also exposed to carcinogens present in fumes emitted from the machine used to wrap meat. Because of this we studied cancer mortality in a cohort of 10,701 workers in the meat and delicatessen departments of supermarkets, and we report here the findings after the third follow-up. Standardized mortality ratios (SMR) were estimated in the cohort as a whole and in race/sex subgroups, using the US population for comparison. Study subjects were followed up from January 1950 to December 2006.Significantly increased SMRs of 1.3 (95% CI, 1.2–1.5), and 2.7 (95% CI, 1.2–5.3) were recorded for cancers of the lung, and tonsils/oropharynx, respectively, in the entire cohort, affecting nearly all race/sex subgroups. SMRs of 4.6 (95% CI, 1.0–13.6) for cancer of the floor of the mouth, and 2.8 (95% CI, 1.3–5.3) for cancer of the gall bladder and biliary tract were recorded only in White male meatcutters. Significantly decreased SMRs were observed for a few cancers.It is not known if the observed excess of cancers is a result of occupational exposures. However, substantial evidence points to fumes from the wrapping machine as a possible candidate for explaining the excess in female meat wrappers. Nested case–control studies that can examine risks from occupational exposures in greater detail, and adequately control for confounding factors are now needed, to permit specifically investigate the role of the oncogenic viruses, fumes and non-occupational risk factors in the occurrence of these cancers. The findings are important, not only occupationally but also because the general population may also experience these exposures, albeit to a lesser degree.     

Using the Q10 model to simulate E. coli survival in cowpats on grazing lands

Microbiological quality of surface waters can be affected by microbial load in runoff from grazing lands. This effect, with other factors, depends on the survival of microorganisms in animal waste deposited on pastures. Since temperature is a leading environmental parameter affecting survival, it indirectly impacts water microbial quality. The Q₁₀ model is widely used to predict the effect of temperature on rates of biological processes, including survival. Objectives of this work were to (i) evaluate the applicability of the Q₁₀ model to Escherichia coli inactivation in bovine manure deposited on grazing land (i.e., cowpats) and (ii) identify explanatory variables for the previously reported E. coli survival dynamics in cowpats. Data utilized in this study include published results on E. coli concentrations in natural and repacked cowpats from research conducted the U.S. (Virginia and Maryland), New Zealand, and the United Kingdom. Inspection of the datasets led to conceptualizing E. coli survival (in cowpats) as a two-stage process, in which the initial stage was due to growth, inactivation or stationary state of the population and the second stage was the approximately first-order inactivation. Applying the Q₁₀ model to these datasets showed a remarkable similarity in inactivation rates, using the thermal time. The reference inactivation rate constant of 0.042 (thermal days)^− 1 at 20 °C gave a good approximation (R² = 0.88) of all inactivation stage data with Q₁₀ = 1.48. The reference inactivation rate constants in individual studies were no different from the one obtained by pooling all data (P < 0.05). The rate of logarithm of the E. coli concentration change during the first stage depended on temperature. Duration of the first stage, prior to the first-order inactivation stage and the initial concentration of E. coli in cowpats, could not be predicted from available data. Diet and age are probable factors affecting these two parameters however, until their environmental and management predictors are known, microbial water quality modeling must treat them as a stochastic source of uncertainty in simulation results.     

Exposure to multiple sources of polycyclic aromatic hydrocarbons and breast cancer incidence

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.     

Preliminary indoor radon risk assessment at the Poços de Caldas Plateau,MG-Brazil

This paper aims to present an assessment of the environmental radiological exposure at a Brazilian area of high natural radiation and discusses the indoor radon exposure risk. A survey of inhabitant exposures arising from the inhalation of radon progeny and external gamma exposure was conducted in urban and rural areas of the Po?os de Caldas Plateau, which is recognized worldwide as a high natural radiation region. The results of this survey indicated that highest radiation exposure was restricted to the rural area of Po?os de Caldas. The radiation exposure in urban locations was quite similar to the values observed in normal background areas in some Brazilian counties. By the application of a constant relative risk model, an additional 20% in the lifetime risk of lung cancer mortality due to the exposure to radon progeny was estimated at Po?os de Caldas. It was also estimated that 16% of all lung cancer deaths at Po?os de Caldas county could be attributable to radon exposure.     

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.     

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.     

Air pollution,ethnicity and telomere length in east London schoolchildren: An observational study

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 NO_x (model coefficient 0.003, [0.001, 0.005], p < 0.001), NO₂ (0.009 [0.004, 0.015], p < 0.001), PM_2.5 (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.