Allocating anthropogenic pollutant emissions over space: application to ozone pollution management.

An inventory of volatile organic compound (VOC) and nitrogen oxides (NOx) emissions is an important tool for the management of ground-level ozone pollution. This paper has two broad aims: it illustrates the potential of a geographic information system (GIS) for enhancing an existing spatially-aggregated, anthropogenic emissions inventory (EI) for Tucson, AZ, and it discusses the ozone-specific management implications of the resulting spatially-disaggregated EI. The main GIS-related methods include calculating emissions for specific features, spatially disaggregating region-wide emissions totals for area sources, and adding emissions from various point sources. In addition, temporal allocation factors enable the addition of a multi-temporal component to the inventory. The resulting inventory reveals that on-road motor vehicles account for approximately 50% of VOC and NOx emissions annually. On-road motor vehicles and residential wood combustion are the largest VOC sources in the summer and winter months, respectively. On-road motor vehicles are always the largest NOx sources. The most noticeable weekday vs. weekend VOC emissions differences are triggered by increased residential wood combustion and increased lawn and garden equipment use on weekends. Concerning the EI's uncertainties and errors, on-road mobile, construction equipment, and lawn and garden equipment are identified as sources in the most need of further investigation. Overall, the EIs spatial component increases its utility as a management tool, which might involve visualization-driven analyses and air quality modeling.

Integrating remote sensing and local vegetation information for a high-resolution biogenic emissions inventory--application to an urbanized, semiarid region.

This paper presents a methodology for the development of a high-resolution (30-m), standardized biogenic volatile organic compound (BVOC) emissions inventory and a subsequent application of the methodology to Tucson, AZ. The region's heterogeneous vegetation cover cannot be modeled accurately with low-resolution (e.g., 1-km) land cover and vegetation information. Instead, local vegetation data are used in conjunction with multispectral satellite data to generate a detailed vegetation-based land-cover database of the region. A high-resolution emissions inventory is assembled by associating the vegetation data with appropriate emissions factors. The inventory reveals a substantial variation in BVOC emissions across the region, resulting from the region's diversity of both native and exotic vegetation. The importance of BVOC emissions from forest lands, desert lands, and the urban forest changes according to regional, metropolitan, and urban scales. Within the entire Tucson region, the average isoprene, monoterpene, and OVOC fluxes observed were 454, 248, and 91 micrograms/m2/hr, respectively, with forest and desert lands emitting nearly all of the BVOCs. Within the metropolitan area, which does not include the forest lands, the average fluxes were 323, 181, and 70 micrograms/m2/hr, respectively. Within the urban area, the average fluxes were 801, 100, and 100 micrograms/m2/hr, respectively, with exotic trees such as eucalyptus, pine, and palm emitting most of the urban BVOCs. The methods presented in this paper can be modified to create detailed, standardized BVOC emissions inventories for other regions, especially those with spatially complex vegetation patterns.

Progression of asbestos effects: a prospective longitudinal study of chest radiographs and lung function.

From an original prospective cohort of 244 current and ex-workers in two asbestos cement plants, longitudinal radiographic data covering ten years were available for 165 and lung function data covering about six years for 150. Estimates of average and cumulative dust exposure were available for each participant, all men. Radiographic progression (onset or worsening) was assessed by comparing earliest and latest films side by side. Annual changes in lung function were computed by fitting regression lines to all the data points. Small opacities (ILO category 1/0 or higher) were found in 16% of initial films, and progression of small opacities occurred in 13% of film pairs. Average and cumulative dust exposure were each significant determinants of the initial presence of small opacities, and were determinants of the progression of both parenchymal and pleural abnormalities. There was greater likelihood of progression if an abnormality was initially present, and a greater likelihood of progression in the plant that had systematic use of some crocidolite. Initial levels of lung function were related to smoking, exposure to dust, and initial radiographic status. Mean annual declines in lung function were modest (FVC-0.017 l/y, FEV1-0.020 l/y) and were related to smoking but not exposure to dust, initial radiographic status, or radiographic progression. Both plants used mainly chrysotile asbestos and exposure levels declined severalfold after 1960. Our findings suggest a waning effect of the larger remote dust exposures on recent annual change in lung function. This accords with human and experimental pathology data showing the relatively low resistance of chrysotile fibres to chemical alteration and clearance.

A comparative study of three methods for analysing longitudinal pulmonary function data.

We compare three methods of longitudinal analysis of pulmonary function data. Our data set is taken from a study of exposure to toluene diisocyanate (TDI) vapours in a new manufacturing plant. The first two methods are a two-stage weighted regression method and maximum likelihood estimation via the EM algorithm, and these give very similar results. The third method, regression with an autoregressive error structure, was not successfully implemented, and in our view needs better documentation.

Useful and extraneous variability in longitudinal assessment of lung function.

Longitudinal measurement is increasingly used to quantify the effects of recent and ongoing influences on lung function, whether treatments of groups of patients, or exposures of working or community populations. The variability in an estimate, eg, mean annual change in FEV1, comes from two sources; variability from true differences in annual change among individuals (called signal), and variability from measurement error (called noise). Signal is useful variability, potentially relatable to explanatory variables, and noise is extraneous. Assuming the variance of true differences remains constant, any increase in noise produces a calculable fall in the proportion of signal in the total observation, which fall we term "signal decay". This is not a function of the number of individuals, which influences rather the statistical power to determine that observed differences are not likely from chance alone. Imprecision in the estimation of individuals' rates of change is a major source of signal decay. Within practical limits, this can be compensated for by increasing the length of the study. Higher rates of subject attrition cause signal decay, in addition to loss of statistical power and susceptibility to survivor bias. Increasing the frequency of testing, within a study of constant length, has little effect on signal and noise, but interval testing protects against secular bias and minimizes data loss from subject attrition.

Major mishaps among mobile offshore drilling units, 1955-1981: time trends and fatalities.

Major mishaps among mobile offshore drilling units worldwide from 1955-1981 were identified from industry and government sources. Based on annual numbers of rigs in service and typical staffing patterns, annual mishap rates and fatality rates for rig types and mishap categories were computed. While the frequency of major mishaps has increased in recent years, the mishap rate per 100 rig-years of service has remained stable. The overall stability obscures the fact that jack-up rigs have had an increasing mishap rate while the rate for other rig types combined has gradually declined. Although the fatal mishap rate has also remained constant, the annual fatality rate per 100 000 full time equivalent (FTE) workers has risen sharply. This can be attributed to increasing numbers of lives lost in environmental mishaps while deaths from operational mishaps have declined. There were 344 fatalities during the 27-year period. Although an average of some 13 deaths per year worldwide appears minimal, the relatively small size of the workforce gives this number significance particularly when it is noted that 'occupational' fatalities, those occurring in the course of routine operations, are not included. The overall fatality rate secondary to major mishaps was 84.3 per 100 000 FTE worker-years.

Risk of chronic obstructive pulmonary disease. Collaborative assessment of the validity of the Tecumseh index of risk.

Predictors of chronic obstructive pulmonary disease (COPD) have been identified in the prospective epidemiologic study of the population of Tecumseh, Michigan. Risk of developing COPD within 10 yr can be estimated from a profile that includes as risk factors age, sex, cigarette smoking habits, and forced expiratory volume in one second (FEV1). The index of risk placed 63% of male incidence cases and 64% of female incidence cases in the top 10% of the risk distribution and 81% of male and 86% of female COPD cases in the top 20% of the risk distribution for Tecumseh. The validity of the Tecumseh index of risk for other populations was determined in a collaborative investigation of data collected in longitudinal epidemiologic studies in Baltimore, Boston, Framingham, Louisiana, Staveley, and Tucson. The extent to which the risk model fitted these data sets was assessed by comparing predicted (or expected) onsets of COPD in each population with observations made in each study. The predictors of COPD identified in Tecumseh were shown to be the most important risk factors in the other populations as well. The goodness-of-fit of the index was satisfactory overall. In all populations, a high risk score was associated with an increased incidence of COPD, thus confirming the predictive ability of the risk index. The Tecumseh index of risk provides a practical method for developing a risk profile from answers to standard questions and simple tests of lung function. Risks are greatest for heavy cigarette smokers with reduced lung function, lower in smokers who stop smoking or reduce their cigarette consumption, and lowest of all in nonsmokers with above average lung function.(ABSTRACT TRUNCATED AT 250 WORDS)

Radiographic evidence of asbestos effects in American marine engineers.

Marine engineers undergoing routine annual chest roentgenography showed an unusual prevalence of pleural abnormalities including plaques suggestive of past asbestos exposure. A pilot survey, and a subsequent comprehensive study of the films of more than 5,000 men, showed an overall prevalence of 12% with pleural abnormality (typical calcification or plaque, or diffuse thickening). Prevalence of films classifiable for pneumoconiotic small opacities was negligible--1.2% in the pilot study. Prevalences of pleural abnormality were significantly higher among men with longer union membership, after controlling for age. Older merchant ships contain substantial amounts of asbestos-containing thermal insulation. Marine engineers often remove and reapply insulation, operations known to produce high airborne fiber concentrations. These roentgenographic survey results indicate significant past asbestos exposures of ships' engineering department personnel.

Immunologic aberrations in asbestos cement workers: dissociation from asbestosis.

Immunoregulatory disorders have been implicated in the pathogenesis of asbestosis. We therefore compared the immunologic status of a well-characterized group of 31 current and former asbestos-cement workers with that of a group of 52 healthy controls, after adjustments had been made for the possible confounding effects of age, race, and smoking. The asbestos workers had significantly decreased percentages and numbers of both B and T lymphocytes in peripheral blood and a paradoxical IgG hypergammaglobulinemia. Analysis of T-lymphocyte subpopulations revealed that total T-cell numbers (OKT3+), helper-inducer T-cell numbers (OKT4+), and suppressor-cytotoxic T cell numbers (OKT8+) were decreased by similar proportions. These decreases were negatively correlated with time elapsing since the end of exposure to asbestos. In both workers and controls, lymphocyte proliferative responses to phytohemagglutinin (PHA) were correlated positively with the number of OKT4+ cells and negatively with age and serum IgG levels. When adjustments had been made for these confounding variables, no differences in PHA responses were noted between workers and controls. No relationship was detected in the workers between any of the immunologic aberrations noted and (1) radiographic category of pneumoconiosis, (2) estimates of cumulative asbestos exposure, or (3) abnormalities of pulmonary function. These data suggest that the immunologic perturbations we have noted in asbestos-exposed individuals are epiphenomena, unrelated to the pathogenesis of asbestosis itself.

Humoral immunologic abnormalities in workers exposed to asbestos cement dust.

Serum specimens from 144 workers exposed to asbestos cement dust were examined for the presence of ANA, RF, immunoglobulins, and IC. These immunologic findings were compared with chest radiographic changes. A high percentage of workers had polyclonal hypergammaglobulinemia, and there was a statistically significant association between elevated levels of IgG and IgM and radiographic classification. Although a significant number of workers had an increased prevalence of ANA and elevated levels of IC, there was no correlation between these parameters and chest radiographs. These findings support B cell hyperactivity in workers exposed to asbestos and suggest that autoantibody production and IC are not directly involved in disease pathogenesis.

Effect of atropine on the bronchial response of asthmatic subjects to the inhalation of ultrasonically nebulized distilled water.

To determine whether atropine provides protection against the bronchoconstriction that develops in asthmatic subjects after inhalation of ultrasonically nebulized distilled water, we exposed six asthmatic patients to this stimulus with and without pretreatment with atropine (0.04 mg/kg). The mean FEV1 decreased from 3.32 to 2.39 L (-28%) without and from 3.49 to 3.18 L (-9%) with atropine. This protective effect was statistically significant (p less than 0.05), suggesting that cholinergic pathways are involved in the obstructive response to the inhalation of ultrasonically nebulized distilled water.

Bronchoalveolar lavage cell--lymphocyte interactions in normal nonsmokers and smokers. Analysis with a novel system.

We investigated the ability of smoker and nonsmoker pulmonary alveolar macrophages (AM) to facilitate lymphocyte proliferative responses in a novel system allowing separation of lymphocyte and AM effects. Bronchoalveolar lavage cells (BLC) were obtained from 7 nonsmokers and 5 older smokers and cultured with purified peripheral blood lymphocytes (PL) and the mitogen phytohemagglutinin. Increasing amounts of BLC were added such that BLC/PL ratios were 1:100, 1:10, 1:2, 1:1 of either autologous or homologous PL. Lymphocyte proliferation was dose-related, increasing with 1:100 and 1:10 BLC/PL ratios, and decreasing to or below initial responses with 1:2 or 1:1 ratios. Depletion of T-lymphocytes from BLC demonstrated that these effects were mediated by AM. Phytohemagglutinin (PHA) dose-response curves of nonsmokers obtained using autologous or homologous PL were not different. When BLC from smokers were cultured with autologous PL, lymphocyte proliferative responses were less than those of similar cultures from nonsmokers. However, when similar smoker BLC were cultured with homologous PL from nonsmokers, proliferative responses were not different from those of nonsmokers. Peak proliferative responses of peripheral blood mononuclear cells were not different from maximal proliferative responses of PL-BLC cultures at any PHA dose. These data show that human AM provide dose-related help and suppression of mitogen-induced lymphocyte proliferation similar to that reported with peripheral blood macrophages. Smoker AM facilitated mitogen-driven proliferation of homologous PL in a normal fashion, demonstrating the utility of this culture system in distinguishing lymphocyte effects present in autologous cultures.

Five-year longitudinal study of workers employed in a new toluene diisocyanate manufacturing plant.

The respiratory health of 277 workers in a new toluene diisocyanate (TDI) manufacturing plant was studied prospectively during 5 yr of exposure. Personal TDI monitors were used to continuously measure peak and 8-h time-weighted average (TWA) concentrations in over 2,000 samples. Longitudinal change in pulmonary function was assessed in 223 men in whom 3 or more data points allowed construction of individual slopes of annual change. Regression of annual change on smoking (pack-years), atopic status, and cumulative TDI exposure dichotomized at 68.2 parts per billion (ppb) months into low and high exposure groups showed significant effects of smoking on spirometric tests and lung volumes. After adjusting for pack-years of smoking, the 74 men in the high cumulative TDI exposure category had significantly larger declines in FEV1, %FEV, and FEF25--75% than did the 149 men in the low category. Annual change in FEV1 was then examined in 6 smoking-exposure categories: in never smokers, average annual decline was 38 ml/yr greater in those with higher cumulative TDI exposure. Current and previous cigarette smokers did not show this effect of cumulative TDI exposure. Analysis of FEV1 change by time above 20 ppb TDI yielded a similar result in never smokers, a 24 ml/yr excess average decline attributable to longer time above 20 ppb. In current cigarette smokers, those with longer time above 20 ppb had excess decline of 18 ml/yr (42 versus 24 ml/yr). our low and high cumulative exposure groups spent 2 and 15%, respectively, of their working time above 5 ppb TDI. The different health effects observed in these groups supports the NIOSH-recommended standard of 5 ppb TDI as an 8-h TWA.

Evidence for histamine-mediated inhibition of monocyte chemotaxis in atopic dermatitis.

Leukocyte chemotaxis was studied in 11 patients with severe childhood onset atopic dermatitis at a time when their disease was relatively quiescent. Pyoderma had been an important complication of the dermatitis in these patients. The chemotactic responsiveness of patient neutrophils and monocytes was on the average not significantly different from that of healthy control subjects, although three patients were identified who had significantly impaired responses. No correlation between IgE levels and leukocyte chemotaxis was observed. Because excessive amounts of histamine have been recovered from the skin of patients with atopic dermatitis, we evaluated the effects of histamine on the chemotactic responsiveness of leukocytes from these patients. Histamine caused a small dose-related increase in chemotaxis of neutrophils from both patients and control subjects (10(-7)M to 10(-5)M histamine). In contrast, histamine had no effect on the chemotaxis of monocytes from control subjects but inhibited the chemotactic responsiveness of monocytes from atopic dermatitis patients. These findings suggest that an abnormal sensitivity of monocytes to histamine is an intrinsic feature of atopic dermatitis that may be detectable when the disease is quiescent. Furthermore, this abnormality may contribute to the impairment of monocyte chemotaxis that has been previously observed in patients with active atopic dermatitis.

Noncomparability of longitudinally and cross-sectionally determined annual change in spirometry.

Annual decline in lung function determined longitudinally is often compared with predicted decline determined cross-sectionally. To test this comparison, spirometric data were collected 5 times over 5 yr from 52 adult male Caucasians. The age regression coefficient for FEV1 and FVC, determined cross-sectionally at each visit, was more than twice the longitudinal annual change computed from the same data as the mean of the slopes of each subject's regression lines. The discrepancy persisted even when the first visit was deleted to reduce learning effects on longitudinal estimates. This discrepancy may be partly explained by the sensitivity of cross-sectional analyses to past noxious influences, whereas longitudinal analyses are sensitive only to influences that continue to affect annual decline during the study period. We also found historical evidence of an increase in height-specific VC, which would artifactually steepen cross-sectionally determined regression lines. Thus, observed longitudinal changes of study cohorts should be compared with control longitudinal data.

Lung function consequences of exposure and hypersensitivity in workers who process green coffee beans.

Three hundred seventy-two workers were examined at two coffee processing plants in New Orleans. Workplace dust concentrations were relatively low, and respiratory symptom prevalences were not different in various areas of the plants. After controlling for other variables, men with lengthy employment and exposure to dust of green (unroasted) coffee had lower mean residual FEV1 values (regression coefficient, -0.011 L/yr employed, p less than 0.05). Similarly, workers with serum IgE antibodies to green coffee beans had lower mean residual FEV1 (-0.244 L, p less than 0.05). Each effect remained significant after controlling for the other. In a subset that included all workers exposed to green coffee, acute changes in expiratory flow rates were not related to differences in exposure. The finding of adverse impacts of exposure and sensitization, in a work force relatively free of overt asthma, has important implications for worker health protection.