Cancer incidence near municipal solid waste incinerators in Great Britain. Part 2: histopathological and case-note review of primary liver cancer cases.
We reported previously a 37% excess risk of liver cancer within 1 km of municipal incinerators. Of 119/235 (51%) cases reviewed, primary liver cancer was confirmed in 66 (55%) with 21 (18%) definite secondary cancers. The proportions of true primaries ranging between 55% and 82% (i.e. excluding secondary cancers) give revised estimates of between 0.53 and 0.78 excess cases per 10(5) per year within 1 km. (+info)
Polychlorinated dibenzo-p-dioxin and dibenzofuran concentrations in the serum samples of workers at continuously burning municipal waste incinerators in Japan.
OBJECTIVES: To find whether concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in serum increased in workers at municipal incinerators that burn continuously. METHODS: 30 Workers employed at three municipal waste incineration plants (incinerator workers) and 30 control workers were studied. The incinerator workers had worn dust masks or airline masks during the periodic repair work inside the incinerators. Previous job, dietary habit, smoking habit, distance from residence to the incineration plant, and body weight and height were obtained from a questionnaire survey. Concentrations of PCDDs/PCDFs were measured in the serum of the workers and the dust deposited in the plants. The influence of various factors on serum concentrations of PCDDs/PCDFs was examined by multiple regression analysis. RESULTS: Dust analysis showed the greatest amount of octachlorodibenzo-p-dioxin (OCDD), followed by 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD), 1,2,3,4,6,7,8-heptachlorodibenzofuran (HpCDF), and octachlorodibenzofuran (OCDF). The toxicity equivalents (TEQs) of PCDDs and PCDFs in the deposited dust were 4.8, 1.0, and 6.4 ng TEQs/g, respectively, for plants A, B, and C. The mean serum TEQs of PCDDs and PCDFs in the incinerator workers and control workers were 19.2 and 22.9 pg TEQs/g lipid, respectively, for area A, 28.8 and 24.5 pg TEQs/g lipid for area B, and 23.4 and 23.6 pg TEQs/g lipid for area C. No significant differences were found between the incinerator workers and the controls for TEQs of PCDDs and PCDFs separately, and TEQs of PCDDs and PCDFs together. However, the serum 1,2,3,4,6,7,8-HpCDF concentration was significantly higher in the incinerator workers than in the controls for all the three areas. When the exposure index to 1,2,3,4,6,7,8-HpCDF is defined as the product of the concentration of 1,2,3,4,6,7,8-HpCDF in the deposited dust and duration of employment, the concentration of 1,2,3,4,6,7,8-HpCDF in serum increased as the exposure index increased. Multivariate analysis suggested that the serum concentration of HpCDF increased with duration of employment at the incineration plants and OCDF increased with employment of > or = 21 years. The other significant variables (p < 0.01 or p < 0.001) were area for hexachlorodibenzo-p-dioxin (HxCDD) and tetrachlorodibenzofuran (TCDF), Brinkman index for HpCDD, and body mass index (BMI) for tetrachlorodibenzo-p-dioxin (TCDD), HpCDD, and TEQs of PCDDs. CONCLUSION: The serum TEQs of PCDDs and PCDFs was not significantly higher among the incinerator workers, but the serum concentration of 1,2,3,4,6,7,8-HpCDF was. This suggests that the incinerator workers had inhaled dust containing PCDDs and PCDFs while working in plants equipped with incinerators that burn continuously. (+info)
Childhood cancers, birthplaces, incinerators and landfill sites.
BACKGROUND: In all, 70 municipal incinerators, 307 hospital incinerators and 460 toxic-waste landfill sites in Great Britain were examined for evidence of effluents causing childhood cancers. Municipal incinerators had previously shown significant excesses of adult cancers within 7.5 and 3.0 km. The relative risks for adults had been marginal and an analysis of childhood cancers seemed to offer a more sensitive approach. METHODS: A newly developed technique of analysis compares distances from suspect sources to the birth addresses and to the death addresses of cancer-children who had moved house. A localized hazard, effective at only one of these times, must be preferentially associated with the corresponding address. This creates an asymmetry of migrations towards or away from age-restricted effective sources. RESULTS: The child-cancer/leukaemia data showed no systematic migration-asymmetries around toxic-waste landfill sites; but showed highly significant excesses of migrations away from birthplaces close to municipal incinerators. Relative risks within 5.0 km of these sites were about 2:1. Hospital incinerators gave analogous results. The ratios greatly exceed findings around 'non-combustion' urban sites. CONCLUSIONS: Because of their locations, the specific effects of the municipal incinerators could not be separated clearly from those of adjacent industrial sources of combustion-effluents. Both were probably carcinogenic. Landfill waste sites showed no such effect. (+info)
Air quality in postunification Erfurt, East Germany: associating changes in pollutant concentrations with changes in emissions.
The unification of East and West Germany in 1990 resulted in sharp decreases in emissions of major air pollutants. This change in air quality has provided an opportunity for a natural experiment to evaluate the health impacts of air pollution. We evaluated airborne particle size distribution and gaseous co-pollutant data collected in Erfurt, Germany, throughout the 1990s and assessed the extent to which the observed changes are associated with changes in the two major emission sources: coal burning for power production and residential heating, and motor vehicles. Continuous data for sulfur dioxide, total suspended particulates (TSP), nitric oxide, carbon monoxide, and meteorologic parameters were available for 1990-1999, and size-selective particle number and mass concentration measurements were made during winters of 1991 and 1998. We used hourly profiles of pollutants and linear regression analyses, stratified by year, weekday/weekend, and hour, using NO and SO(2) as markers of traffic- and heating-related combustion sources, respectively, to study the patterns of various particle size fractions. Supplementary data on traffic and heating-related sources were gathered to support hypotheses linking these sources with observed changes in ambient air pollution levels. Substantially decreased (19-91%) concentrations were observed for all pollutants, with the exception of particles in the 0.01-0.03 microm size range (representing the smallest ultrafine particles that were measured). The number concentration for these particles increased by 115% between 1991 and 1998. The ratio of these ultrafine particles to TSP also increased by more than 500%, indicating a dramatic change in the size distribution of airborne particles. Analysis of hourly concentration patterns indicated that in 1991, concentrations of SO(2) and larger particle sizes were related to residential heating with coal. These peaks were no longer evident in 1998 due to decreases in coal consumption and consequent decreased emissions of SO(2) and larger particles. These decreases in coal combustion and the decreased concentrations of SO(2) and particles of larger size classes may have led to decreased particle scavenging and may be partially responsible for the observed increases in ultrafine particles. Traffic-related changes, such as increased numbers of trucks and increased use of diesel vehicles in Erfurt, were also associated with increased number concentrations of ultrafine particles. Morning particle peaks of all sizes were associated with NO and CO (markers for traffic) in both the 1991 and 1998 periods. There were significant differences in the ultrafine particle levels for morning hours between 1991 and 1998, suggesting that traffic was the cause of this increase. (+info)
Justification of measurement of eight congeners levels instead of twenty congeners of dioxins for mass screening of human exposure.
Measurement of blood dioxin levels to monitor human exposure is tedious and expensive work, although high-resolution mass spectrometers equipped with high-resolution gas chromatography are becoming relatively common in Japan. The Ministry of Health and Welfare and the Environmental Agency require measurement of 17 dioxins, seven PCDDs and 10 PCDFs, according to a statement in "Dioxin Measurement Guidelines" published in 1997. Additionally, three coplanar polychlorinated biphenyls, for which TEFs were determined, have been included for measurement ad libitum. Recently, we have examined 316 blood samples from four groups of subjects, living in areas 5 km away from any incinerator (A), within 2 km from incinerators that emitted slightly higher levels of dioxins than the allowed level (higher than 80 ng/Nm3) (B), within 2 km of an incinerator which emitted a high level of dioxin (C), and workers at this incinerator (D), for dioxin levels by measuring 20 congeners, including three coplanar PCBs. The average pg TEQ/g lipid values were 23.8 +/- 12.3, 25.6 +/- 11.6, 39.1 +/- 18.8 and 100.7 +/- 127.4 for A, B, C and D, respectively. It was found that more than 90% of the total TEQs of the subjects in all groups were accounted for by eight congeners, 2,3,7,8-TCDD, 1,2,3,7,8-PeCDD, 1,2,3,6,7,8-HxCDD, 2,3,4,7,8-PeCDF, 3,3',4,4',5-PeCB, 1,2,3,4,7,8-HxCDF, 1,2,3,6,7,8-HxCDF and 2,3,4,6,7,8-HxCDF. This is also the case for a further 30 blood samples that had no connection with incinerators. Further, regression analysis of the 346 samples leads to an equation of y = 1.109x - 1.077, with a correlation coefficient, r = 0.9996. Here, y = total pg TEQ of 20 congeners/g lipid of blood, and x = total pg TEQs of eight congeners/g lipid. Accordingly, we propose that measurement of eight instead of 20 congeners is appropriate to obtain dioxin TEQ values of blood, at low cost, with high accuracy and with high efficiency, in a short time. (+info)
Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.
Adverse health effects of airborne toxicants, especially small respirable particles and their associated adsorbed chemicals, are of growing concern to health professionals, governmental agencies, and the general public. Areas rich in petrochemical processing facilities (e.g., eastern Texas and southern California) chronically have poor air quality. Atmospheric releases of products of incomplete combustion (e.g., soot) from these facilities are not subject to rigorous regulatory enforcement. Although soot can include respirable particles and carcinogens, the toxicologic and epidemiologic consequences of exposure to environmentally relevant complex soots have not been well investigated. Here we continue our physico-chemical analysis of butadiene soot and report effects of exposure to this soot on putative targets, normal human bronchial epithelial (NHBE) cells. We examined organic extracts of butadiene soot by gas chromatography-mass spectrometry (GC-MS), probe distillation MS, and liquid chromatography (LC)-MS-MS. Hundreds of aromatic hydrocarbons and polycyclic aromatic hydrocarbons with molecular mass as high as 1,000 atomic mass units were detected, including known and suspected human carcinogens (e.g., benzo(a)pyrene). Butadiene soot particles also had strong, solid-state free-radical character in electron spin resonance analysis. Spin-trapping studies indicated that fresh butadiene soot in a buffered aqueous solution containing dimethylsulfoxide (DMSO) oxidized the DMSO, leading to CH(3)* radical formation. Butadiene soot DMSO extract (BSDE)-exposed NHBE cells displayed extranuclear fluorescence within 4 hr of exposure. BSDE was cytotoxic to > 20% of the cells at 72 hr. Morphologic alterations, including cell swelling and membrane blebbing, were apparent within 24 hr of exposure. These alterations are characteristic of oncosis, an ischemia-induced form of cell death. BSDE treatment also produced significant genotoxicity, as indicated by binucleated cell formation. The combination of moderate cytotoxicity and genotoxicity, as occurred here, can be pro-carcinogenic. (+info)
Biologic effects of oil fly ash.
Epidemiologic studies have demonstrated increased human morbidity and mortality with elevations in the concentration of ambient air particulate matter (PM). Fugitive fly ash from the combustion of oil and residual fuel oil significantly contributes to the ambient air particle burden. Residual oil fly ash (ROFA) is remarkable in the capacity to provoke injury in experimental systems. The unique composition of this emission source particle makes it particularly useful as a surrogate for ambient air PM in studies of biologic effects testing the hypothesis that metals mediate the biologic effects of air pollution particles. A majority of the in vitro and animal model investigations support the postulate that transition metals present in ROFA (especially vanadium) participate in Fenton-like chemical reactions to produce reactive oxygen species. This is associated with tyrosine phosphorylation, nuclear factor kappa B and other transcription factor activation, induction of inflammatory mediator expression, and inflammatory lung injury. It is also evident that vanadium accounts for a significant portion of the biologic activity of ROFA. The extrapolation of this body of investigation on ROFA to the field of ambient air PM is difficult, as particles in numerous environments have such small amounts of vanadium. (+info)
Chronic arsenic poisoning from burning high-arsenic-containing coal in Guizhou, China.
Arsenic is an environmental hazard and the reduction of drinking water arsenic levels is under consideration. People are exposed to arsenic not only through drinking water but also through arsenic-contaminated air and food. Here we report the health effects of arsenic exposure from burning high arsenic-containing coal in Guizhou, China. Coal in this region has undergone mineralization and thus produces high concentrations of arsenic. Coal is burned inside the home in open pits for daily cooking and crop drying, producing a high concentration of arsenic in indoor air. Arsenic in the air coats and permeates food being dried producing high concentrations in food; however, arsenic concentrations in the drinking water are in the normal range. The estimated sources of total arsenic exposure in this area are from arsenic-contaminated food (50-80%), air (10-20%), water (1-5%), and direct contact in coal-mining workers (1%). At least 3,000 patients with arsenic poisoning were found in the Southwest Prefecture of Guizhou, and approximately 200,000 people are at risk for such overexposures. Skin lesions are common, including keratosis of the hands and feet, pigmentation on the trunk, skin ulceration, and skin cancers. Toxicities to internal organs, including lung dysfunction, neuropathy, and nephrotoxicity, are clinically evident. The prevalence of hepatomegaly was 20%, and cirrhosis, ascites, and liver cancer are the most serious outcomes of arsenic poisoning. The Chinese government and international organizations are attempting to improve the house conditions and the coal source, and thereby protect human health in this area. (+info)