Use of a robotic sampling platform to assess young children's exposure to indoor bioaerosols.

UNLABELLED: Indoor exposures to allergens, mold spores, and endotoxin have been suggested as etiological agents of asthma; therefore, accurate determination of those exposures, especially in young children (6-36 months), is important for understanding the development of asthma. Because use of personal sampling equipment in this population is difficult, and in children <1 year of age impossible, we developed a personal sampling surrogate: the Pretoddler Inhalable Particulate Environmental Robotic (PIPER) sampler to better estimate their exposures. During sampling, PIPER simulates the activity patterns, speed of motion, and the height of the breathing zones of young children, and mechanically resuspends the deposited dust just as a young child does during running and crawling. The concentrations of allergens, mold spores, and endotoxin measured by PIPER were compared to those measured using traditional stationary air sampling method in 75 homes in central New Jersey, United States. Endotoxin was detected in all homes with median concentrations of 1.0 and 0.55 EU/m(3) for PIPER and stationary sampler, respectively. The difference in median concentrations obtained using the two methods was statistically significant for homes with carpeted floors (P = 0.0001) in the heating season. For such homes, the average ratio of endotoxin concentration measured by PIPER to the stationary sampler was 2.96 (95% CI 2.29-3.63). Fungal spores were detected in all homes, with median fungal concentrations of 316 and 380 spores/m(3) for PIPER and stationary sampler, respectively. For fungi, the difference between the two sampling methods was not statistically significant. For both sampling methods, the total airborne mold levels were statistically significantly higher in the non-heating season than in the heating season. Allergens were detected in ~15% of investigated homes. The data indicate that the traditional stationary air-sampling methods may substantially underestimate personal exposures to endotoxin, especially due to resuspension of dust from carpeted floor surfaces. A personal sampling surrogate, such as PIPER, is a feasible approach to estimate personal exposures in young children. PIPER should be seriously considered as the sampling platform for future exposure studies in young children. PRACTICAL IMPLICATIONS: This study investigated potential indoor bioaerosol exposure of young children using a Pretoddler Inhalable Particulate Environmental Robotic (PIPER) sampler platform. The results show that the traditional stationary air-sampling methods can substantially underestimate personal exposures to resuspended material, and that a personal sampling surrogate, such as PIPER, offers a feasible surrogate for measuring personal inhalation exposures of young children.

A pilot study of children's exposure to CCA-treated wood from playground equipment.

Arsenic from chromated copper arsenate (CCA)-treated wood, widely used in playgrounds and other outdoor equipment, can persist as surface residues on wood. This raises concerns about possible health risks associated with children playing on CCA-treated playgrounds. In a Pilot Study, 11 children (13-71 months) in homes with and without CCA-treated playgrounds were evaluated with post-exposure hand rinses and urine for total arsenic. Samples of wood, soil, and mulch, as well as synthetic wipes, were sampled for total arsenic. In non-CCA-treated playgrounds vs. CCA-treated playgrounds, respectively, wood arsenic was <2.0 mg/kg vs. mean arsenic 2370 mg/kg (range 1440-3270 mg/kg); soil arsenic was <3.0 mg/kg vs. mean arsenic of 19 mg/kg (range 4.0-42 mg/kg); mulch arsenic at one non-CCA-treated playground was 0.4 mg/kg vs. two CCA-treated playgrounds of 0.6 and 69 mg/kg. The arsenic removed using a synthetic wipe at non-CCA-treated playgrounds was <0.5 microg, while mean arsenic from CCA-treated wood was 117 microg (range 1.0-313). The arsenic mass from hand rinses for children who played at non-CCA-treated playgrounds was <0.2 microg, while mean arsenic mass was 0.6 microg (range <0.2-1.9) at CCA-treated playgrounds. Mean urinary total arsenic levels were 13.6 pg/ml (range 7.2-23.1 pg/ml) for all children evaluated, but there was no association between access to CCA-playgrounds and urinary arsenic levels. Arsenic speciation was not performed. This preliminary Pilot Study of CCA-treated wood playgrounds observed dislodgeable arsenic on 11 children's hands after brief periods of play exposure. Future efforts should increase the number of children and the play exposure periods, and incorporate speciation in order to discriminate between various sources of arsenic.

Initial results of environmental monitoring in the Texas Rio Grande Valley.

Previous studies have suggested that a segment of human disease may be attributable to environmental exposures. These may include exposure to chemicals released from a broad range of natural and man-made sources. The purpose of this study was to develop the sampling methodology and prepare a preliminary database on the presence of various organic chemicals in environmental media in two South Texas counties bordered by the Rio Grande River. A third county, located approximately 150 miles north of the Rio Grande River, was also sampled. The South Texas counties were the focus of study due to an increased incidence of anencephalic births in recent years. The environmental media that was sampled included surface water and sediment from the Rio Grande River and irrigation canals, as well as soil from adjacent cropland and pastures. Samples were collected using United States Geological Survey (USGS) quadrangle maps (7.5'; 1:24,000 scale) to identify the area of interest. At least one sampling location was established in each quadrangle. A pond sampler was used for the collection of surface water samples, while soil was collected with a stainless steel trowel. Sediment samples were collected directly in a glass jar. Solid samples were extracted in a soxhlet extractor using methylene chloride. Organic chemicals were concentrated from water samples on a Sep-Pak cartridge and the organics eluted with methanol/acetonitrile. Extracts were analyzed using GC-MS. All of the surface water samples contained aliphatic hydrocarbons and plasticizers, while soil samples contained aliphatics, plasticizers, pesticides, and industrial estrogens. Specific chemicals detected in environmental samples included atrazine and benzene dicarboxylic acid. Contaminant levels in sediments were generally higher than were detected in other media. The results demonstrate the broad variability of contaminant types and concentrations in environmental samples. Although this study presents only a very preliminary characterization of a large area of South Texas, the data indicate a number of pesticides and xenobiotic estrogens that were identified in environmental samples. Additional data providing more details of spatial and temporal distribution of contaminants as well as wildlife studies are needed.

A hospital-based case-control study of stillbirths and environmental exposure to arsenic using an atmospheric dispersion model linked to a geographical information system.

Although adverse reproductive outcomes have been associated with arsenic exposure, the extent and severity of the effects of chronic inhalation of low levels of arsenic on reproduction are not known. We conducted a hospital-based case-control study of stillbirths in a central Texas community that included a facility with more than a 60-year history of producing primarily arsenic-based agricultural products. We collected data on 119 cases and 267 controls randomly selected from healthy live-births at the same hospital and matched for year of birth. We abstracted medical and demographic data for the period January 1, 1983, to December 31, 1993, from hospital records and estimated socioeconomic status by median income from the 1990 Population and Housing Census data. We estimated arsenic exposure levels from airborne emission estimates and an atmospheric dispersion model and linked the results to a geographical information system (GIS) database. Exposure was linked by GIS to residential address at time of delivery. A conditional logistic regression model was fitted including maternal age, race/ethnicity, parity, income group, exposure as a categorical variable, and exposure-race/ethnicity interaction. The prevalence odds ratio observed for Hispanics in the high-exposure group (>100 ng per m3 arsenic) was 8.4, with a 95% confidence interval of 1.4-50.1.

Role of arsenic as a reproductive toxin with particular attention to neural tube defects.

Arsenic has been recognized as a human toxicant for over 2000 years. More recently it has been readily accepted as a human carcinogen. Animal research has demonstrated arsenic's ability to have profound detrimental effects on the developing embryo in avian and mammalian species. This article comprehensively reviews the human and animal literature on the subject of the reproductive toxicity of arsenic. A variety of endpoints are considered, including spontaneous abortion, cardiovascular defects, and arsenic's role in the causation of neural tube defects (NTDs). A summary of the literature that has examined the various postulated mechanisms by which arsenic may produce NTDs is also considered. In addition, a discussion of literature relative to the presence of arsenic in the general environment and in the workplace is presented. This article reaches the conclusion that while further research is clearly needed, particularly on the potential toxicity of organic arsenical compounds, the current literature suggests it may be prudent and appropriate to treat inorganic arsenic as a probable human reproductive toxin.

Interaction between genetic and environmental risk factors for Alzheimer's disease: a reanalysis of case-control studies.

To study the interaction among genetic and environmental risk factors, a reanalysis of case-control studies of Alzheimer's disease (AD) was conducted based on the original data of all studies carried out to January 1, 1990. Seven studies were included in the present analysis, comprising a total of 814 AD patients and 894 control subjects. When comparing those with a positive and negative family history of dementia, similar odds ratio were found for late maternal age [1.7; 95% confidence interval (0.6-4.8) vs. 2.0 (1.1-3.5)], head trauma [1.7 (0.7-4.2) vs. 1.9 (1.1-3.2)], and history of depression [2.0 (0.2-19.8) vs. 2.1 (0.8-1.7)]. This suggests a model in which these risk factors increase the risk for AD independent of family history of dementia. Among those with a positive family history of dementia, the odds ratios for family history of Down's syndrome [4.2 (0.9-20.0)] and of Parkinson's disease [3.3 (0.4-28.2)] tended to be higher than among those with a negative family history of dementia [2.6 (0.8-8.5) and 2.4 (0.8-7.0), respectively]. However, for both disorders the difference in odds ratio was not statistically significant. For history of cigarette smoking, there was no association to AD for those with no first degree relatives with dementia and an inverse relation with AD for those with a positive family history. Although in all analyses, family history of dementia remained significantly associated with AD in the absence of other factors, the odds ratio associated with family history of dementia tended to be lower for those with a positive smoking history, particularly for those with two or more affected relatives. These findings suggest that smoking may interact specifically with a genetically determined process.

Disease clusters in occupational medicine: a protocol for their investigation in the workplace.

Disease clusters have been an important source of epidemiologic and medical information in the history of occupational medicine. Many accepted disease-exposure linkages were first observed and investigated as disease clusters in the workplace setting. Recent interest in disease cluster methodology has focused on traditional environmental settings. There has been very little work on a similar methodology for the investigation of disease clusters in the workplace, despite the many advantages of workplace cluster investigations for recognizing new etiologic associations. In this paper, a protocol is proposed and discussed which can be implemented in both acute and chronic disease cluster outbreaks in the workplace, where no obvious previously recognized cause is identified. A standardized approach to occupational disease cluster investigation will lead to increased efficiency, decreased social-political tensions, and a greater yield of scientific information.

Disease clusters: a central and ongoing role in occupational health.

To review and evaluate whether the investigation of disease clusters continues to play an important role in establishing disease-toxin connections in the workplace, 87 original disease cluster reports were identified that established disease-toxin connections in occupational medicine (from 1775 to 1990). Four advantages of the workplace with regard to cluster discovery and investigation were identified: natural denominator boundaries, shared exposures, the ability to form intermediate hypotheses, and the possibility of locating comparable populations in which to study these hypotheses. Because new products, intermediate products, and procedures are introduced into working environments faster than epidemiologic and toxicologic studies can be designed to evaluate their potential risks, disease cluster investigations will remain central to the understanding of disease, and to protecting workers.

Familial aggregation of Alzheimer's disease and related disorders: a collaborative re-analysis of case-control studies.

Case-control studies of Alzheimer's disease were re-analysed to examine the association of Alzheimer's disease with family history in first degree relatives of dementia, Down's syndrome and Parkinson's disease. Overall, the relative risk of Alzheimer's disease for those with at least one first degree relative with dementia was 3.5 (95% confidence interval 2.6-4.6). Stratification according to age of onset of Alzheimer's disease showed that the relative risk decreased with increasing onset age. However, among patients with an onset of disease after 80 years, there were still significantly more subjects with one or more first degree relatives with dementia as compared to controls (relative risk 2.6; 95% confidence interval 1.3-5.2). The relative risk of Alzheimer's disease was significantly lower in patients who had one first degree relative with dementia (relative risk 2.6; 95% confidence interval 2.0-3.5) as compared to those who had two or more affected relatives (relative risk 7.5; 95% confidence interval 3.3-16.7). Furthermore, the re-analysis showed a significant association between Alzheimer's disease and family history of Down's syndrome (relative risk 2.7; 95% confidence interval 1.2-5.7), which was strongest in those patients who had a positive family history of dementia. The relative risk of Alzheimer's disease for those with a positive family history of Parkinson's disease was 2.4 (95% confidence interval 1.0-5.8).

Chrysotile asbestos and health in Zimbabwe: II. Health status survey of active miners and millers.

As part of the effort to establish industrial practice and public policy regarding asbestos in Zimbabwe, we have conducted a cross-sectional study of the chrysotile mines and mills. A stratified random sample of workers with greater than 10 years of exposure has been evaluated by spirometry, chest radiographs, and employment history. The latter was converted to quantitative estimates of exposure dose, using a matrix based on measured and reconstructed fiber levels for each job and facility during the years of work. Based on these data, a clear dose-response between asbestos exposure and functional loss has been demonstrated, with mean losses from predicted of about 400-600 cc in vital capacity in the 10% of the population with heaviest exposures. Low-grade parenchymal radiographic abnormalities (ILO grade greater than or equal to 1/0) were evident in 8.7% of the total study group and were almost 10 times more common in those with more than 100 fibers/cc.years cumulative exposure than in those with 16 fibers/cc.years or less. Pleural disease was relatively rare, occurring in just under 10% of the study group, and was unrelated to exposure dose. Overall, these findings are compatible with results of similar studies in Quebec and Swaziland and suggest that similar control strategies are probably indicated.

Liver injury in workers exposed to dimethylformamide.

An apparent epidemic cluster of toxic liver disease was reexamined among workers exposed to the solvent dimethylformamide. A demographically similar but unexposed group from a preemployment population was used for comparison. Analysis, after data transformation of the liver transaminases, revealed significant differences between the two populations with respect to the serum glutamic pyruvic transaminase and the ratio of serum glutaminic oxaloacetic transaminase to serum glutamic pyruvic transaminase. Thus a value of the ratio of serum glutamic oxaloacetic transaminase to serum glutamic pyruvic transaminase. Thus a value of the ratio less than 1 may be suggestive of toxic liver disease. Medical surveillance of the working population for 14 months revealed no further cases of toxic liver disease. Dimethylformamide was almost certainly the causative agent of the original epidemic. The use of preemployment populations as a source of unexposed subjects in the analysis of occupational clusters is recommended, especially in the scenario of relatively acute, and highly prevalent, occupational diseases.

Occupational risk factors and Alzheimer's disease: a case-control study.

A case-control study was conducted to assess occupational exposure to organic solvents and lead as risk factors for Alzheimer's disease. All case subjects were diagnosed at a Veterans Administration Hospital in Bedford, Massachusetts. Control subjects were selected from Massachusetts voter registration lists and matched by sex, year of birth, and town of residence. Information on occupational history was assessed by mailed questionnaire sent to the spouse or next of kin of the study subject. A total of 98 case and 162 control subjects were included in the matched analysis. No apparent association of increased risk of Alzheimer's disease was observed for ever having occupational exposure to organic solvents or lead.

Liver disease associated with occupational exposure to the solvent dimethylformamide.

STUDY OBJECTIVE: to characterize an outbreak of liver disease among workers in a fabric coating factory; and to determine the outbreak's cause and natural history and strategies for clinical recognition, treatment, and prevention. DESIGN: clinical-epidemiological investigation. SETTING: academic medical center, Occupational Medicine Clinic, and worksite. PATIENTS: fifty-eight of sixty-six workers participated in the study. All had standard liver function tests at least once. Forty-six workers completed a questionnaire; 27 had more extensive clinical evaluation for recognized liver abnormalities. RESULTS: a plant-wide outbreak of liver disease was recognized after a new employee presented with signs and symptoms of hepatitis. Evaluation of the worksite showed that dimethylformamide, a widely used industrial solvent and known hepatotoxin, was being used to coat fabric in poorly ventilated areas without appropriate skin protection. No other major hepatotoxic exposure was identified. Overall, 36 of 58 (62%) workers tested had elevations of either aspartate aminotransferase (AST) or alanine aminotransferase (ALT) levels. Enzyme abnormalities occurred almost exclusively in production workers (35 of 46 were abnormal), whereas only 1 of 12 nonproduction workers showed any elevations in enzyme levels (P less than 0.0001). Serologic tests excluded known infectious causes of hepatitis in all but 2 workers and changes characteristic of toxic liver injury were confirmed by histologic examinations of biopsy specimens from 4 workers. The ratio of AST to ALT levels was one or less in all but 1 worker. After modification of work practices and removal of workers most severely affected from exposure, improvement in liver enzyme abnormalities and symptoms in most patients were seen, although some patients showed persistent elevations of enzyme levels. CONCLUSIONS: an outbreak of toxic liver disease has been associated with exposure to dimethylformamide in the workplace. The diagnosis of toxic liver disease was established by the clinical histories, negative viral serologies, an enzyme pattern of ALT levels being greater than AST levels, epidemiologic data on coworkers, and liver biopsy specimens. The high prevalence of unsuspected liver enzyme abnormalities in these workers suggests that occupational liver disease may occur more frequently than is generally recognized.

Risk factors for Alzheimer's disease: a case-control study.

A case-control study was conducted to assess personal and family medical history and the appearance of Alzheimer's disease. We compared 98 men with clinically diagnosed Alzheimer's disease and 162 controls, matched by sex, year of birth, and town of residence. Family history of dementia and personal history of depression were more frequent in patients. The number of cigarettes smoked was greater in cases.

Accuracy of work history obtained from a spouse.

In an evaluation of the usefulness of collecting work exposure information from wives of workers, 26 husband-wife pairs were interviewed separately about exposure of the husband to organic solvents. There was 58% concordance between the husbands and wives for answers to a simple question regarding solvent exposure. Amplification of these answers through the use of a computerized occupation-exposure linkage system yielded 81% concordance. When the analysis was restricted to those reporting exposure to solvents for more than five years, an 88% concordance was achieved with the linkage system. It was concluded that wives can accurately recall their husbands' work histories with respect to jobs having solvent exposure. The exposure specificity of such histories is significantly enhanced by the use of an occupation-exposure linkage system.

Epidemiologic patterns of frontal and maxillary sinus cancer.

A significant disease in mortality rates for maxillary and frontal sinus cancer was found for older females, particularly in urban areas of New York State, over a 30-year period. A similar observation was made for males residing in rural areas. The decline in female rates might be related to the discontinued use of carcinogenic agents such as Thorotrast, whereas that in males might be related to changes in those industries associated with an increased risk for these cancer sites.