Exposure to second-hand tobacco smoke and respiratory symptoms in non-smoking adults: cross-sectional data from the general population of Telemark, Norway.

BACKGROUND: In Norway, data on the association between second-hand tobacco smoke (SHS) exposure at home and respiratory symptoms in adults are limited. METHODS: We assessed the association between self-reported exposure to SHS and the prevalence of respiratory symptoms among never-smokers aged 16 to 50 years from the general population who were included in a cross-sectional population-based study in Telemark County, Norway. Logistic regression analysis was used to estimate the odds ratios of symptoms among 8850 never-smokers who provided an affirmative response to questions regarding SHS; 504 (5.7%) of these reported that they lived in a home with daily or occasional indoor smoking. RESULTS: Productive cough and nocturnal dyspnoea were statistically associated with daily SHS exposure (ORs 1.5 [95% CI 1.04-2.0] and 1.8 [1.2-2.7], respectively). In analyses stratified by gender, nocturnal dyspnoea was associated with SHS among women (OR 1.8 [1.1-3.1]), but not among men (OR 0.93 [0.49-1.8]). Symptoms were not associated with occasional SHS exposure in the entire group, but infrequent exposure among men only was associated with increased prevalence of chronic cough; (OR 1.6; [1.04-2.6]) and was negatively associated with wheeze; (OR 0.44 [0.21-0.92)]. CONCLUSIONS: Daily SHS exposure in private homes was associated with productive cough and nocturnal dyspnoea. Our results suggest that preventive measures may be needed to reduce the respiratory effects of SHS at home. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02073708 Registered February 27. 2014.

Effect of Lung Transplantation on Health-Related Quality of Life in the Era of the Lung Allocation Score: A U.S. Prospective Cohort Study.

Under the U.S. Lung Allocation Score (LAS) system, older and sicker patients are prioritized for lung transplantation (LT). The impact of these changes on health-related quality of life (HRQL) after transplant has not been determined. In a single-center prospective cohort study from 2010 to 2016, we assessed HRQL before and repeatedly after LT for up to 3 years using the SF12-Physical and Mental Health, the respiratory-specific Airway Questionnaire 20-Revised, and the Euroqol 5D/Visual Analog Scale utility measures by multivariate linear mixed models jointly modeled with death. We also tested changes in LT-Valued Life Activities disability, BMI, allograft function, and 6-min walk test exercise capacity as predictors of HRQL change. Among 211 initial participants (92% of those eligible), LT improved HRQL by all 5 measures (p < 0.05) and all but SF12-Mental Health improved by threefold or greater than the minimally clinically important difference. Compared to younger participants, those aged ≥65 improved less in SF12-Physical and Mental Health (p < 0.01). Improvements in disability accounted for much of the HRQL improvement. In the LAS era, LT affords meaningful and durable HRQL improvements, mediated by amelioration of disability. Identifying factors limiting HRQL improvement in selected subgroups, especially those aged ≥65, are needed to maximize the net benefits of LT.

Outbreak of autoimmune disease in silicosis linked to artificial stone.

BACKGROUND: There is a well-established association between inhalational exposure to silica and autoimmune disease. We recently observed an outbreak of silica-related autoimmune disease among synthetic stone construction workers with silicosis referred for lung transplantation assessment. AIMS: To characterize the rheumatologic complications in silicosis within these highly exposed, clinically well-characterized patients. METHODS: We systematically reviewed data from all cases of silicosis due to synthetic stone dust referred to our pulmonary institute for lung transplant assessment, which represents the national centre for all such referrals. In addition to silicosis-specific data, we extracted data relevant to the clinical and serological manifestations of autoimmune diseases present in these patients. RESULTS: Of 40 patients in our advanced silicosis national data, we identified nine (23%) with findings consistent with various autoimmune diseases. Among these nine, three also had findings consistent with pulmonary alveolar proteinosis. Based on an expected autoimmune disease prevalence of 3% (based on the upper-end estimate for this group of diseases in European international data), the proportion of disease in our group represents a >7-fold excess (prevalence ratio 7.5; 99% confidence interval 2.6-16.7). CONCLUSIONS: These cases underscore the strong link between silicosis and multiple distinct syndromes of autoimmune diseases. Vigilance is warranted for the recognition of autoimmune complications in persons with known silicosis; so too is consideration of the occupational exposure history in persons presenting with manifestations of autoimmune disease.

Risk factors for occupational acute mountain sickness.

BACKGROUND: Studies of occupational acute mountain sickness (AMS) have not focused on the more severe end of the spectrum to date. AIMS: To examine risk factors associated with the development of occupational AMS severe enough to receive treatment in a compression chamber. METHODS: A nested case referent study in a cohort of high-altitude (4000 m) mine workers, comparing cases of severe, chamber-treated AMS to matched referents. Using logistic regression, we tested potential risk factors based on premorbid surveillance examinations, including cigarette smoking (current smoking, smoking intensity and exhaled carbon monoxide [CO]). RESULTS: There were 15 cases and 30 controls. In multivariate analysis including age, sex and place of residence, current smoking was associated with increased risk of severe AMS (odds ratio [OR] 10.0; 95% confidence interval [CI] 1.5-67.4), taking into account any prior, less severe AMS event, which was also a potent risk factor (OR 33.3; 95% CI 2.8-390). Smoking intensity (cigarettes per day) and exhaled CO were also statistically significantly associated with severe AMS. CONCLUSIONS: Cigarette smoking is a strong, previously under-appreciated risk factor for severe AMS. Because this is a modifiable factor, these findings suggest that workplace-based smoking cessation should be tested as an intervention to prevent such morbidity.

Issue 3-The occupational burden of respiratory diseases, an update.

INTRODUCTION AND AIMS: Workplace exposures are widely known to cause specific occupational diseases such as silicosis and asbestosis, but they also can contribute substantially to causation of common respiratory diseases. In 2019, the American Thoracic Society (ATS) and the European Respiratory Society (ERS) published a joint statement on the occupational burden of respiratory diseases. Our aim on this narrative review is to summarise the most recent evidence published after the ATS/ERS statement as well as to provide information on traditional occupational lung diseases that can be useful for clinicians and researchers. RESULTS: Newer publications confirm the findings of the ATS/ERS statement on the role of workplace exposure in contributing to the aetiology of the respiratory diseases considered in this review (asthma, COPD, chronic bronchitis, idiopathic pulmonary fibrosis, hypersensitivity pneumonitis, infectious pneumonia). Except for COPD, chronic bronchitis and infectious pneumonia, the number of publications in the last 5 years for the other diseases is limited. For traditional occupational lung diseases such as silicosis and asbestosis, there are old as well as novel sources of exposure and their burden continues to be relevant, especially in developing countries. CONCLUSIONS: Occupational exposure remains an important risk factor for airways and interstitial lung diseases, causing occupational lung diseases and contributing substantially in the aetiology of common respiratory diseases. This information is critical for public health professionals formulating effective preventive strategies but also for clinicians in patient care. Effective action requires shared knowledge among clinicians, researchers, public health professionals, and policy makers.

A thematic analysis of quality of life in lung transplant: the existing evidence and implications for future directions.

Health-related quality of life (HRQL) has been assessed in various lung transplantation (LT) investigations but never analyzed systematically across multiple studies. We addressed this knowledge gap through a systematic literature review. We searched the PubMed, CINAHL and PsychInfo databases for publications from January 1, 1983 to December 31, 2011. We performed a thematic analysis of published studies of HRQL in LT. Using a comparative, consensus-based approach, we identified themes that consistently emerged from the data, classifying each study according to primary and secondary thematic categories as well as by study design. Of 749 publications initially identified, 73 remained after exclusions. Seven core themes emerged: (1) Determinants of HRQL; (2) Psychosocial factors in HRQL; (3) Pre- and posttransplant HRQL comparisons; (4) Long-term longitudinal HRQL studies; (5) HRQL effects of therapies and interventions; (6) HRQL instrument validation and methodology; (7) HRQL prediction of clinical outcomes. Overall, LT significantly and substantially improves HRQL, predominantly in domains related to physical health and functioning. The existing literature demonstrates substantial heterogeneity in methodology and approach; relatively few studies assessed HRQL longitudinally within the same persons. Opportunity for future study lies in validating existing and potential novel HRQL instruments and further elucidating the determinants of HRQL through longitudinal multidimensional investigation.

Chest wall shrapnel-induced beryllium-sensitization and associated pulmonary disease.

Chronic beryllium disease (CBD) is an exposure-related granulomatous disease mimicking sarcoidosis. Beryllium exposure-associated disease occurs mainly via inhalation, but skin may also be a source of sensitization. A 65-year-old male with a history of war-related shrapnel wounds was initially diagnosed with pulmonary sarcoidosis. Twenty years later, the possibility of a metal-related etiology for the lung disease was raised. A beryllium lymphocyte proliferation test, elemental analysis of removed shrapnel, and genetic studies were consistent with a diagnosis of CBD. This case demonstrates that retained beryllium-containing foreign bodies can be linked to a pathophysiologic response in the lung consistent with CBD.

Survival following lung transplantation for silicosis and other occupational lung diseases.

BACKGROUND: Information is scant assessing outcomes in lung transplantation (LT) in advanced occupational lung diseases (OLD). AIMS: To analyse survival after LT for OLD. METHODS: Using data from the US Organ Procurement and Transplantation Network Registry (OPTN-R), we identified subjects aged ≥ 18 years transplanted for OLD from 2005 to 2010. OPTN-R selected referents of corresponding age, sex and body mass index (BMI) who underwent LT for other diagnoses were also identified. Post-LT survival time was estimated with Cox proportional hazard models. Baseline age, BMI, forced expiratory volume in 1 s, creatinine, lung allocation score, donor age, donor lung ischaemic time and transplant type (single versus bilateral) were included as covariates. Time-dependent covariates were used to model differences in relative risk over time. RESULTS: Thirty-seven males underwent LT for silicosis (n = 19) or other OLD (n = 18) during the analytic period (0.5% of all LTs). For non-silicotic OLD, 6-month and 1- and 3-year survival estimates were 66, 55 and 55%, compared with the silicotic group (86, 86 and 76%) and referent group (89, 84 and 67%). During the first year post-transplant, those with OLD (silicosis and others combined) manifested an overall 2-fold increased mortality risk [hazard ratio (HR) 2.3, 95% CI 1.3-4.4; P < 0.05] compared to referents. In stratified analysis, this increased risk of death was restricted to those with non-silicotic OLD (HR 3.1, 95% CI 1.5-6.6; P < 0.01). Poorer survival was limited to the first year post-LT. CONCLUSIONS: Subjects undergoing LT for OLD other than silicosis may be at increased risk of death in the first year post-transplantation.

The impact of pretransplant mechanical ventilation on short- and long-term survival after lung transplantation.

Lung transplantation in mechanically ventilated (MV) patients has been associated with decreased posttransplant survival. Under the Lung Allocation Score (LAS) system, patients at greatest risk of death on the waiting list, particularly those requiring MV, are prioritized for lung allocation. We evaluated whether pretransplant MV is associated with poorer posttransplant survival in the LAS era. Using a national registry, we analyzed all adults undergoing lung transplantation in the United States from 2005 to 2010. Propensity scoring identified nonventilated matched referents for 419 subjects requiring MV at the time of transplantation. Survival was evaluated using Kaplan-Meier methods. Risk of death was estimated by hazard ratios employing time-dependent covariates. We found that pretransplant MV was associated with decreased overall survival after lung transplantation. In the first 6 months posttransplant, ventilated subjects had a twofold higher risk of death compared to nonventilated subjects. However, after 6 months posttransplant, survival did not differ by MV status. We also found that pretransplant MV was not associated with decreased survival in noncystic fibrosis obstructive lung diseases. These results suggest that under the LAS, pretransplant MV is associated with poorer short-term survival posttransplant. Notably, the increased risk of death appears to be strongest the early posttransplant period and limited to certain pretransplant diagnoses.

Comparison of cardiac and pulmonary-specific quality-of-life measures in pulmonary arterial hypertension.

Studies systematically comparing the performance of health-related quality-of-life (HRQoL) instruments in pulmonary arterial hypertension (PAH) are lacking. We sought to address this by comparing cardiac and respiratory-specific measures of HRQoL in PAH. We prospectively assessed HRQoL in 128 patients with catheterisation-confirmed PAH at baseline and at 6, 12 and post-24 month follow-up visits. Cardiac-specific HRQoL was assessed using the Minnesota Living with Heart Failure Questionnaire (LHFQ); respiratory-specific HRQoL was assessed using the Airways Questionnaire 20 (AQ20); and general health status was assessed using the 36-item Short Form physical component summary (SF-36 PCS). The LHFQ and AQ20 were highly intercorrelated. Both demonstrated strong internal consistency and converged with the SF-36 PCS. Both discriminated patients based on World Health Organization (WHO) functional class, 6-min walking distance (6MWD) and Borg dyspnoea index (BDI), with the exception of a potential floor effect associated with low 6MWD. The LHFQ was more responsive than the AQ20 to changes over time in WHO functional class, 6MWD and BDI. In multivariate analyses, the LHFQ and AQ20 were each longitudinal predictors of general health status, independent of functional class, 6MWD and BDI. In conclusion, both cardiac-specific and respiratory-specific measures appropriately assess HRQoL in most patients with PAH. Overall, the LHFQ demonstrates stronger performance characteristics than the AQ20.

Functional recovery following musculoskeletal injury in hospital workers.

BACKGROUND: Hospital workers are at high risk of work-related musculoskeletal disorders (WRMSDs), but outcomes following such injuries have not been well studied longitudinally. AIMS: To ascertain functional recovery in hospital workers following incident WRMSDs and identify predictors of functional status. METHODS: Cases (incident WRMSD) and matched referents from two hospitals were studied at baseline and at 2 year follow-up for health status [SF-12 physical component summary (PCS)], lost workdays, self-rated work effectiveness and work status change (job change or work cessation). Predictors included WRMSD and baseline demographics, socio-economic status (SES), job-related strain and effort-reward imbalance. Logistic regression analysis tested longitudinal predictors of adverse functional status. RESULTS: The WRMSD-associated risk of poor (lowest quartile) PCS was attenuated from a baseline odds ratio (OR) of 5.2 [95% confidence interval (CI) 3.5-7.5] to a follow-up OR of 1.5 (95% CI 1.0-2.3) and was reduced further in multivariate modelling (OR = 1.4; 95% CI 0.9-2.2). At follow-up, WRMSD status did not predict significantly increased likelihood of lost workdays, decreased effectiveness or work status change. In multivariate modelling, lowest quintile SES predicted poor PCS (OR = 2.0; 95% CI 1.0-4.0) and work status change (OR = 2.5; 95% CI 1.1-5.8). High combined baseline job strain/effort-reward imbalance predicted poor PCS (OR = 1.7; 95% CI 1.1-2.7) and reduced work effectiveness (OR = 2.6; 95% CI 1.6-4.2) at follow-up. CONCLUSIONS: Baseline functional deficits associated with incident WRMSDs were largely resolved by 2 year follow-up. Nonetheless, lower SES and higher combined job strain/effort-reward imbalance predicted adverse outcomes, controlling for WRMSDs.

Occupational exposures and the risk of COPD: dusty trades revisited.

BACKGROUND: The contribution of occupational exposures to chronic obstructive pulmonary disease (COPD) and, in particular, their potential interaction with cigarette smoking remains underappreciated. METHODS: Data from the FLOW study of 1202 subjects with COPD (of which 742 had disease classified as stage II or above by Global Obstructive Lung Disease (GOLD) criteria) and 302 referent subjects matched by age, sex and race recruited from a large managed care organisation were analysed. Occupational exposures were assessed using two methods: self-reported exposure to vapours, gas, dust or fumes on the longest held job (VGDF) and a job exposure matrix (JEM) for probability of exposure based on occupation. Multivariate analysis was used to control for age, sex, race and smoking history. The odds ratio (OR) and adjusted population attributable fraction (PAF) associated with occupational exposure were calculated. RESULTS: VGDF exposure was associated with an increased risk of COPD (OR 2.11; 95% CI 1.59 to 2.82) and a PAF of 31% (95% CI 22% to 39%). The risk associated with high probability of workplace exposure by JEM was similar (OR 2.27; 95% CI 1.46 to 3.52), although the PAF was lower (13%; 95% CI 8% to 18%). These estimates were not substantively different when the analysis was limited to COPD GOLD stage II or above. Joint exposure to both smoking and occupational factors markedly increased the risk of COPD (OR 14.1; 95% CI 9.33 to 21.2). CONCLUSIONS: Workplace exposures are strongly associated with an increased risk of COPD. On a population level, prevention of both smoking and occupational exposure, and especially both together, is needed to prevent the global burden of disease.

An international prospective general population-based study of respiratory work disability.

BACKGROUND: Previous cross-sectional studies have shown that job change due to breathing problems at the workplace (respiratory work disability) is common among adults of working age. That research indicated that occupational exposure to gases, dust and fumes was associated with job change due to breathing problems, although causal inferences have been tempered by the cross-sectional nature of previously available data. There is a need for general population-based prospective studies to assess the incidence of respiratory work disability and to delineate better the roles of potential predictors of respiratory work disability. METHODS: A prospective general population cohort study was performed in 25 centres in 11 European countries and one centre in the USA. A longitudinal analysis was undertaken of the European Community Respiratory Health Survey including all participants employed at any point since the baseline survey, 6659 subjects randomly sampled and 779 subjects comprising all subjects reporting physician-diagnosed asthma. The main outcome measure was new-onset respiratory work disability, defined as a reported job change during follow-up attributed to breathing problems. Exposure to dusts (biological or mineral), gases or fumes during follow-up was recorded using a job-exposure matrix. Cox proportional hazard regression modelling was used to analyse such exposure as a predictor of time until job change due to breathing problems. RESULTS: The incidence rate of respiratory work disability was 1.2/1000 person-years of observation in the random sample (95% CI 1.0 to 1.5) and 5.7/1000 person-years in the asthma cohort (95% CI 4.1 to 7.8). In the random population sample, as well as in the asthma cohort, high occupational exposure to biological dust, mineral dust or gases or fumes predicted increased risk of respiratory work disability. In the random sample, sex was not associated with increased risk of work disability while, in the asthma cohort, female sex was associated with an increased disability risk (hazard ratio 2.8, 95% CI 1.3 to 5.9). CONCLUSIONS: Respiratory work disability is common overall. It is associated with workplace exposures that could be controlled through preventive measures.

Occupational exposures and COPD: an ecological analysis of international data.

The occupational contribution to chronic obstructive pulmonary disease (COPD) has yet to be put in a global perspective. In the present study, an ecological approach to this question was used, analysing group-level data from 90 sex-specific strata from 45 sites of the Burden of Obstructive Lung Disease study, the Latin American Project for the Investigation of Obstructive Lung Disease and the European Community Respiratory Health Survey follow-up. These data were used to study the association between occupational exposures and COPD Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II or above. Regression analysis of the sex-specific group-level prevalence rates of COPD at each site against the prevalence of occupational exposure and ever-smoking was performed, taking into account mean smoking pack-yrs and mean age by site, sex, study cohort and sample size. For the entire data set, the prevalence of exposures predicted COPD prevalence (0.8% increase in COPD prevalence per 10% increase in exposure prevalence). By comparison, for every 10% increase in the proportion of the ever-smoking population, the prevalence of COPD GOLD stage II or above increased by 1.3%. Given the observed median population COPD prevalence of 3.4%, the model predicted that a 20% relative reduction in the disease burden (i.e. to a COPD prevalence of 2.7%) could be achieved by a 5.4% reduction in overall smoking rates or an 8.8% reduction in the prevalence of occupational exposures. When the data set was analysed by sex-specific site data, among males, the occupational effect was a 0.8% COPD prevalence increase per 10% change in exposure prevalence; among females, a 1.0% increase in COPD per 10% change in exposure prevalence was observed. Within the limitations of an ecological analysis, these findings support a worldwide association between dusty trades and chronic obstructive pulmonary disease for both females and males, placing this within the context of the dominant role of cigarette smoking in chronic obstructive pulmonary disease causation.

Performance of self-reported occupational exposure compared to a job-exposure matrix approach in asthma and chronic rhinitis.

OBJECTIVES: Self-reported exposure to vapours, gas, dust or fumes (VGDF) has been widely used as an occupational exposure metric in epidemiological studies of chronic lung diseases. Our objective was to characterise the performance of VGDF for repeatability, systematic misclassification, and sensitivity and specificity against exposure likelihood by a job-exposure matrix (JEM). METHODS: We analysed data from two interviews, 24 months apart, of adults with asthma and chronic rhinitis. Using distinct job as the unit of analysis, we tested a single response item (exposure to VGDF) against assignment using a JEM. We further analysed VGDF and the JEM among a subset of 199 subjects who reported the same job at both interviews, using logistic regression analysis to test factors associated with VGDF inconsistency and discordance with the JEM. RESULTS: VGDF was reported for 193 (44%) of 436 distinct jobs held by the 348 subjects studied; moderate to high exposure likelihood by JEM was assigned to 120 jobs (28%). The sensitivity and specificity of VGDF against JEM were 71% and 66%, respectively. Among 199 subjects with the same job at both interviews, 32% had a discordant VGDF status (kappa = 0.35). Those with chronic rhinitis without concomitant asthma compared to asthma alone were more likely to have a VGDF report discordant with the JEM (OR 3.6, 95% CI 1.4 to 9.0; p = 0.01). Rhinitis was also associated with reported VGDF in a job classified by the JEM as low exposure (OR 3.9, 95% CI 1.6 to 9.4; p = 0.003). CONCLUSION: The VGDF item is moderately sensitive measured against JEM as a benchmark. The measure is a useful assessment method for epidemiological studies of occupational exposure risk.

Pulmonary toxicity associated with pomalidomide.

Pomalidomide, previously used to treat multiple myeloma, has been reported to cause acute pulmonary toxicity that improves with drug discontinuation. We present a case of delayed pneumonitis with persistent fibrosis associated with pomalidomide. A 61-year-old male treated with pomalidomide and corticosteroids presented with acute on chronic dyspnea, profound hypoxemia, and ground glass opacities on computerized tomographic imaging. Corticosteroid taper and discontinuation of pomalidomide resulted in clinical improvement, but with substantial residual pulmonary fibrosis. Given the temporal improvement, but not resolution, following discontinuation of an agent with an established propensity for lung injury, we attribute this presentation to pomalidomide toxicity.

Occupation in chronic obstructive pulmonary disease and chronic bronchitis: an update.

This review critically evaluates the recent scientific literature relevant to occupational risk factors for chronic obstructive pulmonary disease (COPD) and chronic bronchitis. The 2003 American Thoracic Society statement on the occupational contribution to the burden of airway disease synthesized relevant data on this topic through 1999. Since 2000, 14 separate studies have published values or provide data that allow estimation of the population attributable risk per cent (PAR%) for the proportion of chronic bronchitis or COPD due to work-related factors. Based on data since 2000, the median PAR% value for both chronic bronchitis and COPD is 15%. A number of additional studies have been published that underscore the association between specific occupational exposures and airflow obstruction. In addition, data are emerging that indicate the extent to which COPD is a cause of work disability; limited data raise the possibility that among those with occupational COPD, disability may be even more prominent. This review supports previous analyses concluding that there is a causal association between work-related exposures and COPD.

How much adult asthma can be attributed to occupational factors?

PURPOSE: Many occupational factors can cause asthma or reactivate preexisting disease. We carried out a critical review and synthesis of the available literature to estimate the proportion of adult asthma that is attributable to workplace factors. METHODS: We reviewed published citations from 1966 through May 1999 as well as recent abstracts of studies providing risk estimates for asthma among various occupations. We extracted published attributable risk estimates, derived others from published data, and extrapolated estimates from the incidence rates of occupational asthma. We used a semiquantitative score to rank studies based on their characteristics. RESULTS: We obtained 43 attributable risk estimates from 19 different countries: 23 were published estimates, 8 were derived from published data, and 12 were extrapolated from incidence data. The median value for the attributable risk of occupationally associated asthma was 9%(25th to 75th interquartile range: 5% to 19%). The derived estimates (median attributable risk = 25%) were significantly greater than published values (median = 9%, P = 0.002), whereas the extrapolated estimates were significantly lower (median = 5%, P = 0.04). The 12 highest scored studies based on their characteristics yielded a median risk estimate of 15%. CONCLUSION: Occupational factors are associated with about 1 in 10 cases of adult asthma, including new onset disease and reactivation of preexisting asthma.

Measurement of environmental tobacco smoke exposure among adults with asthma.

Because the morbidity and mortality from adult asthma have been increasing, the identification of modifiable environmental exposures that exacerbate asthma has become a priority. Limited evidence suggests that exposure to environmental tobacco smoke (ETS) may adversely affect adults with asthma. To study the effects of ETS better, we developed a survey instrument to measure ETS exposure in a cohort of adults with asthma living in northern California, where public indoor smoking is limited. To validate this survey instrument, we used a passive badge monitor that measures actual exposure to ambient nicotine, a direct and specific measure of ETS. In this validation study, we recruited 50 subjects from an ongoing longitudinal asthma cohort study who had a positive screening question for ETS exposure or potential exposure. Each subject wore a passive nicotine badge monitor for 7 days. After the personal monitoring period, we readministered the ETS exposure survey instrument. Based on the survey, self-reported total ETS exposure duration ranged from 0 to 70 hr during the previous 7 days. Based on the upper-range boundary, bars or nightclubs (55 hr) and the home (50 hr) were the sites associated with greatest maximal self-reported exposure. As measured by the personal nicotine badge monitors, the overall median 7-day nicotine concentration was 0.03 microg/m(3) (25th-75th interquartile range 0-3.69 microg/m(3)). Measured nicotine concentrations were highest among persons who reported home exposure (median 0.61 microg/m(3)), followed by work exposure (0.03 microg/m(3)), other (outdoor) exposure (0.025 microg/m(3)), and no exposure (0 microg/m(3); p = 0.03). The Spearman rank correlation coefficient between self-reported ETS exposure duration and directly measured personal nicotine concentration during the same 7-day period was 0.47, supporting the survey's validity (p = 0.0006). Compared to persons with no measured exposure, lower-level [odds ratio (OR) 1.9; 95% confidence interval (CI), 0.4-8.8] and higher-level ETS exposures (OR 6.8; 95% CI, 1.4-32.3) were associated with increased risk of respiratory symptoms. A brief, validated survey instrument can be used to assess ETS exposure among adults with asthma, even with low levels of exposure. This instrument could be a valuable tool for studying the effect of ETS exposure on adult asthma health outcomes.

Human pulmonary responses to experimental inhalation of high concentration fine and ultrafine magnesium oxide particles.

Exposure to air polluted with particles less than 2.5 micron in size is associated epidemiologically with adverse cardiopulmonary health consequences in humans. The goal of this study was to characterize human pulmonary responses to controlled experimental high-dose exposure to fine and ultrafine magnesium oxide particles. We quantified bronchoalveolar lavage (BAL) cell and cytokine concentrations, pulmonary function, and peripheral blood neutrophil concentrations in six healthy volunteers 18 to 20 hr after inhalation of fine and ultrafine magnesium oxide particles produced from a furnace system model. We compared postexposure studies with control studies from the same six subjects. Mean +/- standard deviation (SD) cumulative magnesium dose was 4,138 +/- 2,163 min x mg/m3. By weight, 28% of fume particles were ultrafine (<0.1 micron in diameter) and over 98% of fume particles were fine (<2.5 micron in diameter). There were no significant differences in BAL inflammatory cell concentrations, BAL interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor, pulmonary function, or peripheral blood neutrophil concentrations postexposure compared with control. Our findings suggest that high-dose fine and ultrafine magnesium oxide particle exposure does not produce a measurable pulmonary inflammatory response. These findings are in marked contrast with the well-described pulmonary inflammatory response following zinc oxide particle inhalation. We conclude that fine and ultrafine particle inhalation does not result in toxicity in a generic manner independent of particle composition. Our findings support the concept that particle chemical composition, in addition to particle size, is an important determinant of respiratory effects.