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.     

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.     

Assessing inhalatory and dermal exposures and their resultant health-risks for workers exposed to polycyclic aromatic hydrocarbons (PAHs) contained in oil mists in a fastener manufacturing industry

This study first assessed workers' inhalatory and dermal exposures to polycyclic aromatic hydrocarbons (PAHs) contained in oil mists. Then, their resultant lung cancer and skin cancer risks were estimated. Finally, control strategies were initiated from the health-risk management aspect. All threading workers in a fastener manufacturing plant were included. 16 inhalatory and 88 dermal PAH exposure samples were collected. Results show that the inhalatory gas phase total PAH exposure level (8.60x10(4) ng/m(3)) was much higher than that of particle phase (2.30x10(3) ng/m(3)). Workers' mean inhalatory exposure level (8.83x10(4) ng/m(3)) was lower, but its corresponding 1-sided upper 95% confidence level (UCL(1,95%)=1.02x10(5) ng/m(3)) was higher than the time-weighted average permissible exposure level (PEL-TWA) regulated in Taiwan for PAHs (1.00x10(5) ng/m(3)). The mean whole body total PAHs dermal exposure levels was 5.44x10(6) ng/day and the top five exposed surface areas were lower arm, hand, upper arm, neck, and head/front. The estimated lifetime skin cancer risk (9.72x10(-3)) was lower than that of lung cancer risk (1.64x10(-2)), but both were higher than the significant risk level (10(-3)) defined by the US Supreme Court in 1980. The installation of a local exhaust ventilation system at the threading machine should be considered as the first priority measurement because both lung and skin cancer risks can be reduced simultaneously. If the personal protection equipment would be adopted in the future, both respiratory protection equipment and protective clothing should be used simultaneously.     

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.     

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.     

Pesticide exposure and lung cancer mortality in Leningrad province in Russia

This study was carried out to examine the association between pesticide exposure and lung cancer mortality. We conducted an autopsy based case-control study in Leningrad Province in Russia. A total of 540 lung cancer cases and 582 controls were identified among subjects who had died in the hospitals of the Leningrad province between 1993 and 1998. Using work history records, we assessed exposure to pesticide at the level of industry and job title. Unconditional logistic regression was used to calculate adjusted odds ratio for pesticide exposure and lung cancer mortality. There was no association between ever exposure to pesticide and lung cancer mortality overall (odds ratio=1.06, 95% confidence interval=0.82-1.36) and in both men (odds ratio=1.11, 95% confidence interval=0.84-1.46) and women (odds ratio=0.74, 95% confidence interval=0.37-1.46). We observed no statistically significant odds ratio by duration of pesticide exposure, intensity of pesticide exposure, and cumulative pesticide exposures with lung cancer mortality in both smokers and nonsmokers. Odds ratio also did not differ when the analysis was restricted to individuals who had exposure data with high confidence scores. Our findings suggest no associations between pesticide exposures and mortality of lung cancer in the population of the Leningrad province in Russia that deserves further evaluation.     

Seasonal assessment of environmental tobacco smoke and respirable suspended particle exposures for nonsmokers in Bremen using personal monitoring

The study was designed to determine seasonal differences in personal exposures to respirable suspended particles (RSP) and environmental tobacco smoke (ETS) for nonsmokers in Bremen, Germany. The subjects were office workers, either living and working in smoking locations or living and working in nonsmoking locations. One hundred and twenty four randomly selected nonsmoking subjects collected air samples close to their breathing zone by wearing personal monitors for 24 h or, in some cases, for 7-day periods during the winter of 1999. The investigation was repeated in the summer with 126 subjects, comprised of as many of the studied winter population (89 subjects) as possible. Saliva cotinine analyses were undertaken to verify the nonsmoking status of the subjects. Subjects wore one personal monitor while at work and one while away from the workplace on weekdays, and a third monitor at the weekend. Collected air samples were analysed for RSP, nicotine, 3-ethenylpyridine (3-EP) and ETS particles. The latter were estimated using ultraviolet absorbance (UVPM), fluorescence (FPM) and solanesol (SolPM) measurements. ETS exposure was consistently higher in the winter than in the summer, this pattern being particularly evident for subjects both living and working with smokers. The highest median 24-h time weighted average (TWA) concentrations of ETS particles (SolPM, 25 microg m(-3)) and nicotine (1.3 microg m(-3)) were recorded for subjects performing weekday monitoring during the winter. These were significantly higher than equivalent levels of ETS particles (SolPM, 2.4 microg m(-3)) and nicotine (0.26 microg m(-3)) determined during the summer. There were no appreciable differences between winter and summer percent workplace contributions to median TWA ETS particle and nicotine weekday concentrations, the workplace in Bremen, in general, contributing between 35% and 61% of reported median concentrations. Workers, on average, spent one-third of their time at work during a weekday, indicating that concentrations were either comparable or higher in the workplace than in the home and other locations outside the workplace. Median 24-h weekend ETS particle and nicotine concentrations for smoking locations were not significantly different from equivalent weekday levels during the winter, but were significantly lower during the summer. Based upon median 24-h TWA SolPM and nicotine concentrations for the winter, extrapolated to 1 year's ETS exposure, those subjects both living and working in smoking locations (the most highly exposed group) would potentially inhale 13 cigarette equivalents/year (CEs/y). However, based on a similar extrapolation of summer measurements, the same group of subjects would potentially inhale between 1.3 and 1.9 CEs/y. The most highly exposed subjects in this study, based upon 90th percentile concentrations for those both living and working in smoking locations during the winter, would potentially inhale up to 67 CEs/y in the winter and up to 22 CEs/y in the summer. This clearly demonstrates that seasonal effects should be taken into account in the design and interpretation of ETS exposure studies. Air sampling over a 7-day period was shown to be technically feasible, and subsequent RSP, ETS particle and nicotine levels determined by 7-day monitoring were not found to be significantly different from equivalent levels determined by 24-h monitoring. However, the longer sampling period resulted in the collection of an increased quantity of analytes, which improved the limits of quantitation (LOQ) and allowed a more accurate determination of low level ETS exposure. This was reflected by a reduced percentage of data falling below the LOQ for 7-day monitoring compared with 24-h monitoring. The use of a liquid chromatographic method with tandem mass spectrometric detection for saliva cotinine measurement afforded a greatly improved LOQ and greater accuracy at low concentrations compared with the radioimmunoassay (RIA) method used in previous studies by these authors. In this study, 17 subjects out of 180 tested (9.4%) were found to have saliva cotinine levels exceeding the selected threshold of 25 ng ml(-1) used to discriminate between smokers and nonsmokers.     

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.     

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.     

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.     

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.     

Dietary cadmium exposure and kidney stone incidence: A population-based prospective cohort study of men & women

Cadmium exposure is associated with increased urinary calcium excretion. Hypercalciuria is recognised as a major risk factor for kidney stone formation. Increased prevalence of kidney stones among those occupationally exposed to cadmium has previously been suggested. Food is the main source of cadmium exposure in the general population with tobacco representing an important additional source among smokers.We aimed to assess the association between dietary cadmium exposure and kidney stone incidence in two large population-based, prospective cohorts of men (Cohort of Swedish Men; COSM) and women (The Swedish Mammography Cohort; SMC). Those with a history of kidney stones were excluded.At baseline 1997, men (45–79 yrs) and women (48 to 83 yrs), completed a self-administered questionnaire on diet and lifestyle. During 12 years of follow-up, we ascertained 707 cases of kidney stones in men and 290 in women through linkage of the cohorts to the national inpatient and outpatient registers. Individual dietary cadmium exposure was estimated using dietary data and concentrations of cadmium in food. Hazard ratios (HR) were calculated using the Cox proportional hazards regression models with adjustment for other risk factors.Estimated dietary cadmium exposure was not associated with increased kidney stone incidence among men HR 0.97 (95% confidence interval (CI): 0.77–1.23) or women HR 0.99 (95% CI: 0.89–1.43), comparing the highest tertile with the lowest. In conclusion, our results do not support a strong association between dietary cadmium and kidney stone risk at the exposure levels seen in the general population.     

Determination of indoor radon and soil radioactivity levels in Giresun, Turkey

Indoor radon survey and gamma activity measurements in soil samples were carried out in the Giresun province (Northeastern Turkey). The result of analysis of variance showed a relationship between indoor radon and radium content in soil (R(2)=0.54). It was found that indoor radon activity concentration ranged from 52 to 360 Bq m(-3) with an average value of 130 Bq m(-3). A model built by BEIR VI was used to predict the number of lung cancer deaths due to indoor radon exposure. It was found that indoor radon is responsible for 8% of all lung cancer deaths occurring in this province. (137)Cs activity concentration was measured 21 years after the Chernobyl accident. The results showed that (137)Cs activity concentration ranged from 41 to 1304 Bq kg(-1) with an average value of 307 Bq kg(-1). The indoor radon results and the geology of the studied area were discussed. Annual effective doses to the both radionuclides of natural origin and (137)Cs were estimated.     

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.     

Australian firefighters' exposure to air toxics during bushfire burns of autumn 2005 and 2006

Bushfire fighting is a hazardous occupation and control strategies are generally in place to minimize the hazards. However, little is known regarding firefighters' exposure to bushfire smoke, which is a complex mixture of toxic gases and particles. In Australia, during the prescribed burning season, firefighters are likely to be exposed on a regular basis to bushfire smoke, but whether these exposures affect health has yet to be determined. There are a number of factors that govern whether exposure to smoke will result in short-term and/or long-term health problems, including the concentrations of air pollutants within the breathing zone of the firefighter, the exposure duration, and health susceptibility of the individual, especially for pre-existing lung or heart disease. This paper presents measurements of firefighters' personal exposure to bushfire smoke, the first step within a risk management framework. It provides crucial information on the magnitude, extent and frequency of personal exposure to bushfire smoke for a range of typical scenarios. It is found that the primary air toxics of concern are carbon monoxide (CO), respirable particles and formaldehyde. Also, work activity is a major factor influencing exposure with exposure standards (both average and short-term limits) likely to be exceeded for activities such as suppression of spot fires, holding the fireline, and patrolling at the edge of a burn area in the urban-rural interface.     

Assessment of air quality in Turin by personal monitoring of nonsmokers for respirable suspended particles and environmental tobacco smoke

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.     

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, R(2), 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.     

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.     

Early wheezing phenotypes and severity of respiratory illness in very early childhood: Study on intrauterine exposure to fine particle matter

The main goal of the paper was to assess the pattern of risk factors having an impact on the onset of early wheezing phenotypes in the birth cohort of 468 two-year olds and to investigate the severity of respiratory illness in the two-year olds in relation to both wheezing phenotypes, environmental tobacco smoke (ETS) and personal PM_2.5 exposure over pregnancy period (fine particulate matter). The secondary goal of the paper was to assess possible association of early persistent wheezing with the length of the baby at birth. Pregnant women were recruited from ambulatory prenatal clinics in the first and second trimester of pregnancy. Only women 18–35 years of age, who claimed to be non-smokers, with singleton pregnancies, without illicit drug use and HIV infection, free from chronic diseases were eligible for the study. In the statistical analysis of respiratory health of children multinomial logistic regression and zero-inflated Poisson regression models were used. Approximately one third of the children in the study sample experienced wheezing in the first 2 years of life and in about two third of cases (67%) the symptom developed already in the first year of life. The early wheezing was easily reversible and in about 70% of infants with wheezing the symptom receded in the second year of life. The adjusted relative risk ratio (RRR) of persistent wheezing increased with maternal atopy (RRR = 3.05; 95%CI: 1.30–7.15), older siblings (RRR = 3.05; 95%CI: 1.67–5.58) and prenatal ETS exposure (RRR = 1.13; 95%CI: 1.04–1.23), but was inversely associated with the length of baby at birth (RRR = 0.88; 95%CI: 0.76–1.01). The adjusted incidence risk ratios (IRR) of coughing, difficult breathing, runny/stuffy nose and pharyngitis/tonsillitis in wheezers were much higher than that observed among non-wheezers and significantly depended on prenatal PM_2.5 exposure, older siblings and maternal atopy. The study shows a clear inverse association between maternal age or maternal education and respiratory illnesses and calls for more research efforts aiming at the explanation of factors hidden behind proxy measures of quality of maternal care of babies. The data support the hypothesis that burden of respiratory symptoms in early childhood and possibly in later life may be programmed already in prenatal period when the respiratory system is completing its growth and maturation.     

Inorganic arsenic in Chinese food and its cancer risk

Even moderate arsenic exposure may lead to health problems, and thus quantifying inorganic arsenic (iAs) exposure from food for different population groups in China is essential. By analyzing the data from the China National Nutrition and Health Survey (CNNHS) and collecting reported values of iAs in major food groups, we developed a framework of calculating average iAs daily intake for different regions of China. Based on this framework, cancer risks from iAs in food was deterministically and probabilistically quantified. The article presents estimates for health risk due to the ingestion of food products contaminated with arsenic. Both per individual and for total population estimates were obtained. For the total population, daily iAs intake is around 42 μg day(-1), and rice is the largest contributor of total iAs intake accounting for about 60%. Incremental lifetime cancer risk from food iAs intake is 106 per 100,000 for adult individuals and the median population cancer risk is 177 per 100,000 varying between regions. Population in the Southern region has a higher cancer risk than that in the Northern region and the total population. Sensitive analysis indicated that cancer slope factor, ingestion rates of rice, aquatic products and iAs concentration in rice were the most relevant variables in the model, as indicated by their higher contribution to variance of the incremental lifetime cancer risk. We conclude that rice may be the largest contributor of iAs through food route for the Chinese people. The population from the South has greater cancer risk than that from the North and the whole population.