Physical characterization of diesel exhaust particles in exposure chambers

Since the deposition of particulate in the respiratory system is strongly influenced by particle size, a correct assessment of this parameter is important for any inhalation experiment studying the potential health effects of air pollutants. Measuring the distribution of particles according to their aerodynamic diameter and mechanical mobility diameter is crucial in analyzing the deposition of submicron particles in the lower respiratory system. Cascade impactor measurements of diluted diesel exhaust in 12.6 m³ animal exposure chambers in the GMR Biomedical Science Department showed that the mass median aerodynamic diameter of the aerosol was 0.2 μm with 88% of the mass in particles smaller than 1 μm. Diffusion battery measurements showed that the mass median mechanical mobility diameter was about 0.11 μm. Transmission electron micrographs of particles deposited on chamber surfaces revealed both agglomerates and nearly spherical particles. The particles in these chambers are similar in size and shape to diesel particles described elsewhere. The flux of diesel particles to food surfaces was measured. Calculations of the expected daily dose by inhalation and by feeding showed that the “worst case” dose by feeding was only about one-tenth the dose by breathing.     

Pulmonary function testing of animals chronically exposed to diluted diesel exhaust for 267 days

Thw purpose of this work was to assess the potential effect that chronic inhalation of diesel exhaust may have on lung mechanics and lung volumes. Noninvasive pulmonary function tests have been conducted repeatedly on 25 rats exposed to diesel exhaust at a particulate concentration of 1500 μg/m³, for 20 h/day, days/week for 267 days. The same tests were conducted on 25 clean air control animals. When the data is normalized, there are no apparent functionally significant changes occurring in the lungs that may be attributed to the chronic inhalation of diesel exhaust.     

Lymphatic transport of inhaled diesel particles in the lungs of rats and guinea pigs exposed to diluted diesel exhaust

Factors influencing the disposition of the inhaled diesel particles were studied by analyzing the deposition of radioactively labelled diesel particles in the respiratory system, by determining the specific function of alveolar cellular mechanisms in the primary defense against inhaled particles and by identifying the important role of the lymphatic system in the lung clearance of experimental animals exposed to diluted emissions from a diesel engine. Radioactive ¹³¹Barium was used as a tracer of diesel particles and the deposition efficiency was determined to be 15%±6% of the inhaled dose in the Fischer 344 rat strain. The number of cells obtained by bronchial lavage increased significantly after a prolonged exposure to a concentration of 1500 μg/m³ of diesel particles. The increased cell number was more than twofold, contained two distinct cell populations (alveolar macrophages and neutrophils) and represented a reactive mobilization of the defense mechanisms in the organism. Light microscopy studies investigated the role of lymphatic transport of the particulate matter and revealed that the peribrochial and perivascular aggregates of lymphoid tissue contained diesel particles even after short exposure periods at low dose levels. With the increasing burden of particles in the respiratory system, the coloration of hilar and mediastinal lymph nodes continuously changed to gray and finally to dark black, depending upon the dose level and exposure. However, at all exposure levels, most of the diesel particles in the alveoli were phagocytized by an increased alveolar cellular defence and particle-containing macrophages were actively moving towards the mucociliary escalator or towards lymphatic channels leading to peribronchial lymphoid aggregates and bronchial or mediastinal lymph nodes. In the lymph nodes, alveolar macrophages containing diesel particles were found mostly in the afferent subcapsular lymphatic vessels and marginal sinuses. In the later stages, cellular structure disintegrated and large aggregates of particulate matter were dispersed throughout the medullary cords with increasing accumulation towards the hilus. It is concluded that the lymphoid aggregates and lymphatic nodes play an important role in sequestering diesel particles or particle-containing phagocytizing cells and provide a pathway, in addition to the mocociliary clearance for particulate removal from the deep pulmonary region.     

Population exposure to airborne thorium at the high natural radiation areas in India

High natural radiation areas in the coastal and peninsular India were studied for airborne thorium and resultant population exposure due to inhalation. Four locations covering three states viz., Ayiramthengu and Neendakara in Kerala, Kudiraimozhi in Tamil Nadu and Bhimilipatnam in Andhra Pradesh were investigated. External gamma radiation fields 1 m above the monazite ore bodies ranged from 200 to 3000 nGy h^-1. Soil samples showed ²³²Th specific activity varying from 0·1 to 1·5 Bq g^-1 with surface alpha activity in the range of 1·0–12·5 Bq cm^-2. Suspended particulates in the samples ranged from 60–140 μg m^-3 with ²³²Th showing a wider variation of <0·03–0·3 mBq m^-3. There was poor correlation between suspended particulates and long-lived alpha airborne activity . The resuspension factors for ²³²Th were in the range of 1·5×10^-8–7·9×10^-7 cm^-1. Higher resuspension was correlated with dry sand dunes. The upper limits for Committed Effective Dose (CED) due to inhalation of airborne ²³²Th at the respective high natural radiation areas were estimated to range from 50±30 to 300±130 μSv (5–30 mrem) per year per adult member of public assuming an activity median aerodynamic diameter of 1 μm for the airborne particulates.     

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.     

A study of diesel emissions on Drosophila

A sex-linked recessive lethal test was performed on male fruit flies of the species Drosophila melanogaster, (Oregon-R strain), exposed to an approximate five-fold dilution of exhaust from a diesel engine. The eight hour exposure was achieved by drawing diluted diesel exhaust from a three cubic meter stainless steel exposure chamber housing laboratory animals through a two liter reaction flask modified for use with Drosophila. A preconditioned sampling bag was used to collect the emissions after passing through the exposure chamber containing the flies. Results of analyses performed on the diesel exhaust mixture showed the following: carbon dioxide—0.17%, carbon monoxide—12.2 ppm, hydrocarbons—11.6 ppm, nitrogen oxide—3.8 ppm, nitrogen dioxide—2.9 ppm, sulphur dioxide—1.0 ppm, and particulates—2.18 mg/m³. Two broods of the F₂ generation were investigated for the occurrence of recessive lethal events. These broods approximated the developing gametogenic stages of mature sperm (P₁ matings on days 2 and 3 postexposure) and spermatocytes (P₁ matings on days 8 and 9). Additionally, the F₃ generation was evaluated for the occurrence of mosaic recessive lethal events which might escape detection in the F₂ generation. An equal number of F₂ and F₃ flies for both broods served as concurrent controls. Results indicate that, under the conditions tested, the diesel exhaust did not increase the mutation frequency of the exposed flies (F₂ rate = 0.30%, F₃ rate = 0%) when compared to the concurrent controls (F₂ rate = 0.37%, F₃ rate = 0.15%).     

Experimental measurements of aerosol concentrations in offices

A new automated version of the piezoelectric microbalance measures the mass concentration of airborne particles smaller than a preselected aerodynamic cutoff diameter. It is designed for near-real-time, unattended, round-the-clock measurements of nearly any aerosol environment inhabited by humans. The instrument uses an electrostatic precipitator to deposit particles with greater than 95% efficiency onto a piezoelectric quartz crystal sensor which is able to detect a deposit of 0.005 μg. The precipitator and sensor are nearly identical to those in the portable instrument reported previously. Measurements comparing within ± 15% with gravimetrically measured filter samples are documented for a wide variety of aerosols in the 50 μg/m³ to 5.5 mg/m³ range. The instrument measures particles from 10 μm down to 0.01 μm in diameter, including submicron combustion smokes and metallic fumes. The piezoelectric microbalance technique senses the mass concentration of the aerosol, rather than light scattering properties as is done by photometers and nephelometers. The piezobalance, with 1 L/min sample flow, is more sensitive than any other mass-sensing instrument, making it especially suited for low concentration indoor measurements, even below 50 μg/m³. An automatic piezobalance recently measured respirable aerosol mass concentrations in several offices. Each measurement was the average concentration during a 30-min period. The 24-h/day measurements continued for several days. Especially interesting is the diurnal pattern, both for offices with and without smokers. The effect of a single nearby smoker was clearly illustrated when the smoker was absent one day in the middle of a week. Normal daytime peak concentrations in that office reached 80–110 μg/m³ with a smoker present, but only 50–60 μg/m³ when the smoker was absent. Curious smokers who briefly stopped byt o see the instrument caused single half-hour averages to triple, to values as high as 294 μg/m³ in one office.     

Concentrations and determinants of outdoor, indoor and personal nitrogen dioxide in pregnant women from two Spanish birth cohorts

Determinants of outdoor, indoor and personal concentrations of nitrogen dioxide (NO₂) were assessed in a subset of pregnant women of the Spanish INMA (Environment and Childhood) Study. Home indoor and outdoor NO₂ concentrations were measured during 48 h with passive samplers for 50 and 58 women from the INMA cohorts of Valencia and Sabadell, respectively. Women from Sabadell also carried personal NO₂ samplers during the same period. Data on time–activity patterns, socio-economic characteristics, and environmental exposures were obtained through questionnaires. Multiple linear regression models were developed to predict NO₂ levels.In Valencia, median outdoor NO₂ levels (42 µg/m³) were higher than median indoor levels (36 µg/m³). In Sabadell, personal NO₂ showed the highest median levels (40 µg/m³), followed by indoor (32 µg/m³) and outdoor (29 µg/m³) levels. Personal exposure to NO₂ correlated best with the indoor NO₂ levels. Temporal and traffic-related variables were significant predictors for outdoor NO₂ levels. Thirty-two percent of the indoor NO₂ variability in the two cohorts was explained by outdoor NO₂ levels and the use of the gas appliances. The model for personal exposure accounted for 59% of the variance in NO₂ levels in Sabadell with four predictor variables (outdoor and indoor NO₂ levels, time spent in outdoor environments and time exposed to a gas cooker). No significant association was found between personal or indoor NO₂ levels and exposure to environmental tobacco smoke (ETS) at home.Personal NO₂ levels were found to be strongly influenced by indoor NO₂ concentrations. The study supports the use of time–activity patterns along with indoor measurements to predict personal exposure to traffic-related air pollution.     

Indoor climate in low-ventilated day-care institutions

Measurements of indoor atmospheric environment were carried out in a day nursery and a kindergarten, in which natural air infiltration supplied the rooms with only 1–2 m³ fresh air per person and hour under the prescribed occupancy. The exposure situation from the field was duplicated under controlled conditions in a climate chamber. The results indicate unacceptably high concentrations of carbon dioxide, and emphasize the need for more elaborate building design in airtight buildings.     

Facilities for diesel exhaust studies

It is the major intent of this report to examine the animal inhalation facilities at the EPA Health Effects Research Laboratory in Cincinnati, Ohio, associated with the exposure to the exhaust of diesel-powered equipment. The facility serves as a center for toxicologic evaluation, in relevant animal models, of potentially hazardous environmental pollutants from diesel engine exhaust. Briefly, the entire engine exhaust is mixed with filtered and conditioned air in a dilution tube. That diluted exhaust enters a large volume mixing chamber and a portion passes through dynamic flow irradiation chambers (to simulate sunlight) and is then conducted to animal exposure chambers. The system provides nonirradiated exhaust in the same concentration (directly from the mixing chamber) and also filtered, conditioned ambient air for control animal exposure. The major physical components of the diesel emission system include: air purifiers, animal exposure chambers, engine-dynamometers, irradiation chambers, monitoring instrumentation and data acquisition systems.     

Health effects of oxidants

Oxidants of significance to human health include ozone, nitrogen dioxide, and peroxyacetylnitrate. All of these compounds are involved in complex photochemical reactions which makes quantification and prediction of their individual health effects difficult. Ozone causes trauma to lung tissues and interferes with enzyme systems in the lungs and other tissues causing a broad range of symptoms. Measurable health impacts can occur at concentrations as low as 390 μg/m³. Acute effects of ozone exposure are reversible at normal urban concentrations (80–120 μg/m³). A special problem of concern, however, is increased susceptibility to infectious diseases contracted through the lungs. Nitrogen dioxide also causes trauma to lung tissues and interferes with enzyme systems. Measurable impacts can occur at concentrations as low as 100 μg/m³, but recovery is rapid and it is not known whether repeated exposures at this level have cumulative effects or predispose the lungs to permanent damage. Chronic exposure of laboratory animals to higher nitrogen dioxide levels can cause emphysema-like conditions and reduction in resistance to respiratory infection. Epidemiological studies of children in houses with gas stoves confirm the finding of reduced resistance to respiratory infection. The U.S. EPA estimates that health effects may occur in young children exposed to concentrations in excess of 280 to 560 μg/m³ one-hour average. These concentrations occur routinely in houses having gas stoves. Peroxyacetylnitrate is a powerful eye irritant in photochemical smog. Other health effects are similar to those of ozone, but less important because of the relatively low concentrations of this pollutant compared to other oxidants.     

Metaphase analysis, micronuclei assay, and urinary mutagenicity assay of mice exposed to diesel emissions

Female Swiss mice were exposed 8 h/day to diesel exhaust for 1, 3, and 7 weeks. Urine was collected overnight for 4 days prior to sacrifice while the mice continued to be exposed for eight hours during the day. The presence of mutagens was determined by the Ames Salmonella test. One hour prior to sacrifice each mouse received 1 mg/kg colcemide. After sacrifice, the marrow from each femur was obtained. The marrow from one femur was used to prepare slides for metaphase analysis and the other for micronuclei assay. Other mice received IP 50 mg/kg cyclophosphamide 24 h prior to sacrifice or 1 μmole/kg benzo(a)pyrene in each of four daily doses prior to sacrifice and served as positive controls. The Ames Salmonella assay of the unconcentrated urine after 1, 3, and 7 weeks and concentrated urine after 7 weeks exposure to diesel exhaust did not significantly vary from clean air controls. In the micronucleus test, and metaphase analysis, cyclophosphamide produced a strong positive response and the 7 week diesel exposure was not different from clean air controls.     

Genotoxicity of syrian hamster lung cells treated in vivo with diesel exhaust particulates

Polycyclic aromatic hydrocarbons extracted and concentrated from diesel exhaust particulates have been shown to be mutagenic and carcinogenic, but attempts to induce pulmonary tumors through chronic inhalation of diesel exhaust by experimental animals have failed. We have attempted to resolve this incongruity by measuring chromosomal damage in lung tissue of chronically exposed hamsters, using the highly sensitive test for genotoxic chemical agents, sister chromatid exchange (SCE) analysis. To determine the degree of responsiveness of the test system to both diesel exhaust particulates and benzo(a)pyrene (BaP), these agents were instilled intratracheally into anesthetized hamsters as suspensions in 0.25 ml volumes of Hank's balanced salt solution (HBSS). Lung tissues from these animals were subsequently cultured in vitro and chromosomes from the resulting cell divisions were scored for exchanges of chromatin between sister chromatids. Control animals, treated weekly with 0.25 ml of BSS for 10 weeks, showed an average value of 12 SCE's per cell, while animals treated weekly with 200 ng BaP over a 10-week period showed an average of 17 SCE's per cell. HBSS, given as a single treatment, also produced an average of 12 SCE's per cell in control animals, but animals treated with a single instillation of 12.5 μg BaP showed an average SCE value of 19. These data confirmed that the procarcinogen BaP can be metabolically activated by lung cells in vivo and also demonstrated the efficacy of using this technical approach to study the effect of chemical mutagens that enter the lungs. Diesel exhaust particulates, administered in a range from 0 to 20 mg per hamster over a 24 h exposure period, produced a linear SCE dose-response ranging from 12 to 26 SCE's per metaphase. This curve suggested that a concentration of 3 mg of diesel particulates per hamster would not produce a statistically significant increase in SCE's above control values. One group of 8 hamsters, chronically exposed to diesel exhaust particulates for 3 months showed an average of 12 SCE's per cell. This was equivalent to a set of 5 control animals which also showed an average of 12 SCE's per cell. Although the scope of this study was limited, the data demonstrated that diesel exhaust particulates can induce genotoxic damage but a 3-month exposure to 6 mg/m³ of diesel exhaust particulates was insufficient to produce measurable mutagenic changes in lung cells. This negative response is consistent with the results from other studies in which similar exposures failed to produce pulmonary tumors.     

Pulmonary function evaluation of cats after one year of exposure to diesel exhaust

Adult male, inbred, disease-free cats of uniform age and size were exposed eight hours per day, seven days per week to a 1 : 18 dilution of diesel exhaust emissions. After one year of exposure, the animals were removed from the chambers for measurement of lung volumes, forced expiratory flow rates, dynamic compliance and resistance, diffusing capacity, and nitrogen washout. No important changes in pulmonary function were detected with the exception of a decrease in closing volume (P < 0.05). The inability to detect decrements in pulmonary function may have been due to insufficient cocentration of exhaust, insufficient exposure length, or to the use of a species resistant to diesel exhaust. To test these possibilities, the cats are being exposed for an additional year, and another species, hamsters, are being exposed for future testing at exhaust dilutions of 1 : 18 and 1 : 9.     

Development of a personal exposure monitor for two sizes of inhalable particulates

Measurement of personal exposure to ambient level particulate concentrations is often extremely difficult because of a lack of personal exposure monitors capable of collecting measurable quantities within a meaningful sampling period. A new personal exposure monitor for two fractions of inhalable particulates (i.e., the 3–15 μm aerodynamic diameter and the < 3 μm or respirable fraction) has been developed and characterized. This monitor is capable of collecting a sample of each fraction that is quantifiable with ambient concentrations of inhalable/respirable particulates as low as 25 μg/m³ in a 24-h sampling period. Wind tunnel tests have been made on the particulate personal exposure monitor to determine sampling efficiency as a function of relative wind speed and orientation with respect to the sampler.     

Diesel soot: Mutation measurements in bacterial and human cells

Both hot pipe and dilution chamber samples of the exhaust from a diesel (Oldsmobile 350) engine have been collected, extracted with methylene chloride and those extracts have been tested for mutagenicity in forward mutation assays in human lymphoblasts and S. typhimurium. In the absence of a metabolic activation system, the extract was significantly mutagenic to the bacteria in the range of 0 to 30 μg/ml, but introduced no mutations in human cells at concentrations up to 200 μg/ml under the same conditions of assay medium. However, when assayed in the presence of a postmitochondrial supernatant derived from rat liver, the the soot extracts were significantly mutagenic to both bacteria and human cells in the range of 50–100 μg/ml. Fractionation of the soot extract on the basis of polarity by sequential elution from a silicic acid column permitted concentration of the mutagenic activity in the alkane/toluene eluate, as determined by bacterial assays. Preliminary characterization of this fraction and preliminary studies of pure compounds leads us to suspect the alkyl substituted phenanthrenes as representing at least a significant fraction of the mutagenic activity of this alkane/toluene eluate.     

Application of a “closed-can” technique for measuring radon exhalation from mine samples of Punjab, Pakistan

Using the closed-can technique, radon exhalation rate measurements have been carried out for shale and coal samples collected from various mines located in the Chakwal and Makarwal areas of Pakistan. For the two areas, the measured average values of the exhalation rates from shale are 1.45±0.13 and 0.67±0.25 Bq m⁻² h⁻¹ and for coal are 1.0±0.03 and 0.65±0.32 Bq m⁻² h⁻¹, respectively. These values are much lower than the measured exhalation rates from alum-shale-based Nordic concrete which has values in the 50–200 Bq m⁻² h⁻¹ range. The lower values of the measured exhalation rates from the shale and coal deposits in the Chakwal and Makarwal areas are indicative of their lower uranium contents and mine workers in these areas do not face any abnormal health hazard due to radon since the exhalation rates have been found to be on the low side.     

Investigation of volatile organic compounds and phthalates present in the cabin air of used private cars

The presence of selected volatile organic compounds (VOCs) including aromatic, aliphatic compounds and low molecular weight carbonyls, and a target set of phthalates were investigated in the interior of 23 used private cars during the summer and winter. VOC concentrations often exceeded levels typically found in residential indoor air, e.g. benzene concentrations reached values of up to 149.1 µg m^− 3. Overall concentrations were 40% higher in summer, with temperatures inside the cars reaching up to 70 °C. The most frequently detected phthalates were di-n-butyl-phthalate and bis-(2-ethylhexyl) phthalate in concentrations ranging from 196 to 3656 ng m^− 3.     

The influence of ventilation on indoor/outdoor air contaminants in an office building

The air quality in a newly built preschool was investigated in a longitudinal study. Typical air contaminants emanating from building materials were determined, their variation over time (0–18 months) was measured, and the influence of the ventilation system (81%–91% recirculation of return air) on contaminant concentrations was studied. Volatile organic compounds were sampled by adsorption on porous polymer, analysed by a GC/FID system, and identified by MS. A spatial build-up in concentration (ppb or μg/m³ levels) is evident for all the organic compounds, as well as for CO₂, from the outdoor air, through the ventilation system, and through the rooms to the exhaust air. The longitudinal comparison over time shows that all the organic compounds decline in concentration mainly within the first 6 months of occupancy: 1-butanol 4–14 times, toluene and pentanal + hexanal 2–4 times, while formaldehyde remained at a constant low level of 90 ppb (110 μg/m³). It is difficult to believe that the problems of poor air quality in 100 preschools in Stockholm are caused by the organic compounds alone unless interactions occur. A preschool building needs to be gassed off during the first 6 months after its construction with no recirculation of return air allowed (outdoor air rate approx 4–5 ach). During at least 1–2 additional years, it is desired that the recirculation rate of return air is restricted, perhaps to 50%.     

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.