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[Effect of the work environment of the coke-processing industry on the respiratory system of coke factory workers].

The influence of the working environment in a coke factory on the respiratory system of workers was examined in 253 workers employed for at least 5 years at coke production in baking ovens, or at coke sorting and processing. They were exposed to high air concentrations of benzo(a)pyrene (BaP) and tar substances as well as other numerous toxic substances e.g. benzene++ derivatives, the level of which however, did not exceed the MAC values. Medical examination comprising the MRC questionnaire and spirometry , using Godart Expirograph, was carried out Among the exposed workers the non-specific chronic respiratory diseases with obstructive symptoms and chronic bronchitis were revealed more often than in the control group such factors as tobacco smoking and the duration of work also had their influence on the frequency of respiratory diseases. The possibility of the impact of high air concentrations of BaP and carbon monoxide cannot be excluded either.

Adult

[Characterization of coke derivate distillation departments in coke plants. Hygienic and ergonomic conditions].

The studies were carried out in three coke plants mostly with the use of individual dosimetric methods but also with the stationary method. They revealed the values 2-5 times exceeding the MAC of the tar substances in the air of all workposts, and benzo(a)pyrene at several posts only. The other toxic substances like benzene homologous and benzologous and dust exceeded the MAC value only incidentally so that the workers of this department were less exposed than the people employed directly at the coke production. The ergonomic examinations did not reveal any excess of energetic expenditure or physiological cost. The results of medical studies will be presented in further papers.

Air Pollutants, Occupational

Is living near a coking works harmful to health? A study of industrial air pollution.

OBJECTIVE: To determine whether there was excess ill health in people living near a coking works, and if so whether it was related to exposure to coking works' emissions. DESIGN: Populations varying in proximity to the coking works were compared with control populations. Health data were correlated with available environmental data. METHODS: Analysis of routinely collected mortality, cancer registration, and birth statistics; community survey using self completed postal questionnaires; retrospective analysis of general practice (GP) records; tests of respiratory function; and analysis of available environmental data. MAIN RESULTS: Study and control populations were comparable in terms of response rates, gender, and most socioeconomic indicators. For adults, age standardised mortality and cancer rates of the population closest to the coking works were comparable with those for the district as a whole. Gender ratios, birthweight, and stillbirth rates were comparable in the study and control populations. For several indicators of respiratory health including cough, sinus trouble, glue ear, and wheeze (but not for asthma and chronic bronchitis) there was a gradient of self reported ill health, with the highest prevalence in areas closest to the works. For example, sinus trouble was reported by 20% of adults and 13% of children in the area closest to the works compared with 13% and 6% respectively in the control area. GP consultations for respiratory disorders increased when pollution (measured by SO2 levels) was high: annual consultation rates per 1000 varied from 752 in the top group of daily pollution levels to 424 in the bottom group. Analysis of locally collected smoke and SO2 data indicated that SO2 concentrations were highest closest to the works and, after closure of the coking works, the number of days on which SO2 and smoke levels exceeded 100 micrograms/m3 and 90 micrograms/m3, respectively, fell steeply. CONCLUSION: Routinely available indicators failed to provide convincing evidence that the coking works had harmed health. Self report and GP consultations indicated that respiratory ill health in the people living close to the works was worse than expected. Some of the excess probably resulted from exposure to coking works emissions. The health effects of relatively low level but intermittently high air pollution from a point source may be subtle, contributing to respiratory morbidity, but not apparent in analysis of routine health indicators.

Adolescent

Evaluation of biomarkers in plasma, blood, and urine samples from coke oven workers: significance of exposure to polycyclic aromatic hydrocarbons.

OBJECTIVE: The aim was to assess the significance of two biomarkers; antibody to benzo(a)pyrene DNA adducts and concentration of hydroxyethylvaline haemoglobin adducts in samples from a well studied group of coke oven workers. As a measure of exposure we have used 1-hydroxypyrene in urine. METHODS: Urine and blood samples were collected from coke oven workers and a control group. Samples from coke oven plant workers were collected in January and June. 1-Hydroxypyrene was measured in urine by high performance liquid chromatography (HPLC), antibodies to benzo(a)pyrene DNA adducts were measured by ELISA and hydroxyethylvaline haemoglobin adducts were measured by gas chromatography-mass spectrometry (GC-MS). RESULTS: Mean urinary 1-hydroxypyrene in samples from coke oven workers varied from 1.11 to 5.53 umol/mol creatinine and 0.14 umol/mol creatinine in the control group. Workers at the top side had the highest values of urinary 1-hydroxypyrene. Antibody to benzo(a)pyrene DNA adducts did not correlate with either 1-hydroxypyrene nor length of work at the coke oven plant. But antibody concentration in samples collected in January was predictive of the concentration in samples collected in June. A small non-significant increase in hydroxyethylvaline haemoglobin adducts was found in samples from coke oven workers relative to the control group when comparing smokers and nonsmokers separately. CONCLUSION: 1-Hydroxypyrene correlates well with exposure groups based on job description. Antibodies to benzo(a)-pyrene DNA adducts was related to people and not exposure. Work at a coke oven plant might lead to increased hydroxyethylvaline haemoglobin adducts.

Adult

[Effect of new technologies in the coke industry on aromatic polycyclic hydrocarbon concentrations in the ambient air].

Concentractions of aerosols, amount of polycyclic hydrocarbons, in terms of soluble in benzene fraction and benzo(a)pyrene concentration were determined in coking plant air. Air was sampled on the roofs of modern coke batteries and on old-type batteries prior to, and following, modernization and major reapir. Aerosols were determined by passing 10--100 m3 of air through a 26 X 18.5 cm filter. After a weight determination of aerosol content the filter was subjected to benzene extraction and aromatic polycyclic hydrocarbons were isolated from the extract, using thin-layer chromatography. Quantitative determination of these hydrocarbons was done using ultraviolet spectrophotometry. Results of determinations on work-posts in modern and old-type coke batteries prior to, and following, modernization were comapred. Average concentrations of aerosols in the air, amounts of polycyclic hydrocarbons soluble in benzene and concentration of benzo(a)pyrene determined on the roofs of old coke batteries before modernization were as follows: 11.26 mg/m3, 6.37 ug/m3 and 112.28 mg/m3, and after modernization: 0.88 mg/m3, 0.25 mg/m3 and 1.29 ug/m3, respectively. On the roofs of modern high chamber coke batteries average concentrations of aerosols, polycyclic hydrocarbons--benzo(a)pyrene amounts were: 4.21 mg/m3, 0.79 mg/m3 and 5.72 ug/m3, respectively. The results clearly demonstrate that work conditions in modernized coking plants are much better than those in old non-modernized coking plants.

Air Pollutants

Mortality of coke plant workers in The Netherlands.

During the production of coke, large quantities of coke oven gas are emitted. People who work on the top or on the sides of coke ovens are exposed to this oven gas, which contains a range of carcinogenic chemicals. To investigate the cancer risks under these work conditions, a retrospective study was undertaken. In total 11,399 former workers were enrolled in the study. Of these, 5639 had worked in the coke plant for at least six months between 1945 and 1969. The other 5740 had worked in another plant during the same period and formed a non-exposed group for comparison. The study group was followed up until 1984 for mortality. The causes of death were obtained from the Central Bureau of Statistics. Among the coke oven workers significantly higher death rates were found for lung cancer and non-malignant respiratory disease. Mortality in the byproduct section was similar to that expected. Among workers in the tar distillery the rate for lung cancer was higher than expected. The risk for gastric cancer and non-malignant respiratory disease among the workers of the coke shipping department was increased but the SMRs did not reach statistical significance. No data were collected about individual smoking habits or socioeconomic state of the study subjects and the possibility that the risk found could be attributed to these factors cannot be ruled out. It has been stated by other investigators, however, that the effect of not controlling for smoking tends to be modest.

Coke

Determination of benzo[a]pyrene diol epoxide-DNA adducts in white blood cell DNA from coke-oven workers: the impact of smoking.

We have undertaken a study among coke-oven workers to test the feasibility of an enzyme-linked immunosorbent assay with anti-trans-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene- DNA antibodies for monitoring occupational exposure to polycyclic aromatic hydrocarbons (PAH). Coke-oven workers are occupationally exposed to relatively high levels of PAH and are at increased risk for lung cancer. Three blood samples were collected from each of the 56 coke-oven workers exposed to PAH and 44 unexposed workers employed in a steel-rolling factory of the same plant. In addition, PAH levels were measured in ambient air by personal sampling, and the excretion of 1-hydroxypyrene in urine was also measured on 3 consecutive working days. All participants were interviewed regarding working conditions, personal hygiene, and smoking habits. The results showed that the coke-oven workers were exposed to substantial concentrations of atmospheric PAH (1-186 micrograms/m3), including benzo[a]pyrene (0.1-7.8 micrograms/m3) and pyrene (0.6-23.6 micrograms/m3). Both benzo[a]pyrene and pyrene were shown to be representative for the whole group of PAH. Forty-seven percent of the coke-oven workers had detectable levels of PAH-DNA adducts in their white blood cells, compared with 30% of the controls. In both groups, smokers had significantly higher levels of PAH-DNA adducts than did nonsmokers. At one site, we found the correlation positive between DNA adducts and the duration of exposure (r = .47, P = .005). Generally, the correlation was not significant between PAH-DNA adducts in blood and the concentration of PAH in the air and 1-hydroxypyrene in urine.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide

Lymphocyte sister chromatid exchange (SCE) frequencies in coke oven workers.

Lymphocyte sister chromatid exchange (SCE) frequencies were determined for 12 long-term coke oven workers and 12 other age-matched steelworkers with no coke oven work exposure. All study participants were nonsmokers. The exposed group had a mean of 28.9 years' exposure to the coke oven emissions. SCE frequencies for the exposed individuals ranged from 7.97 to 11.20 SCEs per cell while the control individuals ranged from 6.73 to 10.60 SCEs per cell. The mean SCE frequency for the exposed group was 9.54 +/- SD 1.15 SCEs per cell, and was 14% higher than the 8.35 +/- SD 1.09 SCEs per cell of the control group (p = .016). The long-term exposure to coke oven emissions experienced by the coke oven workers may be the explanation for this small difference.

Adult

Mortality due to respiratory cancers in the coke oven plants of the Lorraine coalmining industry (Houillères du Bassin de Lorraine).

The main activity of the Houillères du Bassin de Lorraine (Lorraine Collieries), employing 23,000 operatives and executives, is coalmining. The coke production is carried out by two coke oven plants with a workforce of respectively 747 and 552 workers. The coal coking process entails the emission of noxious products such as polycyclic aromatic hydrocarbons (PAH) from the ovens. The influence of occupational exposure on mortality due to respiratory cancers, and particularly to lung and upper respiratory and alimentary tracts cancer, was investigated among a cohort of 534 male workers from the two coke oven plants who had retired from work between 1963 and 1982. The job history of each subject has been precisely reconstructed by indicating the duration of exposure on the ovens, close to the ovens, and in maintenance occupations. The cohort mortality has been analysed according to the method of indirect standardisation with reference to the French male population and by a case-control study concerning the consumption of tobacco per cohort. The mortality due to lung cancer is 2.51 times higher than expected. This excess of mortality differs, but not significantly, between the two coke oven plants (standardised mortality ratio equals 3.05 and 1.75 respectively). It is not significantly higher among subjects exposed for more than five years, directly exposed on the ovens or working near the ovens or at maintenance occupations on the ovens (SMR = 2.78), than among those exposed for less than five years (SMR = 2.35) or those not exposed at all. Even taking into account the excess of mortality due to lung cancers in the Moselle district (1.6 time that of France), the excess of lung cancers does not seem to be explained by the regional factor, or by tobacco and alcohol consumption. Although no significant relation was offered between lung cancer and the duration of exposure to PAH, even when taking smoking habits into account, the carcinogenic role of occupational nuisances cannot be excluded.

Age Factors

Anti-benzo[a]pyrene diolepoxide--DNA adduct levels in peripheral mononuclear cells from coke oven workers and the enhancing effect of smoking.

The level of (+/-)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE) bound to DNA of lymphocytes plus monocytes in 39 coke oven workers exposed to polycyclic aromatic hydrocarbons (PAH) and 39 non-exposed persons (controls) were investigated, each of the groups consisting of smokers and non-smokers. The adduct level was measured by an improved HPLC/fluorescence method (Rojas, M., Alexandrov, K., van Schooten, F. J., Hillebrand, M., Kriek, E. and Bartsch, H., Carcinogenesis, 15, 557-560, 1994) through the release of the corresponding benzo[a]pyrene (B[a]P) tetrols. The anti-BPDE-DNA adduct was detected in 51% of coke oven workers exposed to PAH and in 18% of the non-exposed (control) subjects. The mean level of anti-BPDE-DNA adducts/10(8) nucleotides in coke oven workers (15.7 +/- 37.8) was approximately 8 times higher than in non-exposed subjects (2.0 +/- 8.7). The interindividual variation of adduct levels was approximately 100-fold in coke oven workers and approximately 50-fold in controls respectively. Smokers in the exposed group had 3.5 times more DNA adducts than non-smokers. With the exception of one non-smoker with very high adduct levels (52.8 adducts/10(8)), the control subjects showed the presence of barely detectable adducts in only 16% of the samples examined. The increased in vivo formation in some smokers and high variability of anti-BPDE-DNA adducts in coke oven workers suggests variations in genetically controlled activation/inactivation reactions of PAH metabolism.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide

Chromosomal aberrations and sister-chromatid exchanges in lymphocytes from coke oven workers.

To test whether coke oven workers, an occupational group known to be at increased cancer risk, manifest increased peripheral blood chromosomal aberration frequencies, we obtained samples from a group of 30 steelworker volunteers, who had worked several years at coke oven jobs. Exposure estimates were made using measurements of work place atmospheric coal tar pitch volatiles and work histories. No statistically significant positive regression of chromosomal aberrations on exposure estimates was found. The data from the coke oven workers were also compared with the obtained concurrently and employing precisely the same laboratory protocol from a group of male Brookhaven National Laboratory employees. The coke oven workers as a group were found to have statistically significantly elevated frequencies of chromatid aberrations and of sister-chromatid exchanges.

Aneuploidy

Cancer experience among coke by-product workers.

This paper presents the site-specific cancer mortality, 1953-1966, for men employed in by-product coke plants in Allegheny County, Pa. Approximate relative risks, which take into account race, age, and calendar years of follow-up, have been calculated for various work areas of the coke plant. The major findings are: 1. As indicated previously by Lloyd and Redmond, men with five or more years at the coke ovens have an excess risk of dying from lung cancer and kidney cancer. 2. Cancers of the digestive system are significantly elevated in nonoven workers. Cancers of two sites, the colon and pancreas, account for the total excess in cancers of the digestive system. 3. Cancers of the buccal cavity and pharynx appear high in nonoven workers, although the number of deaths involved is small. These observations clearly indicate the need to consider nonoven as well as oven workers when evaluating cancer hazards in the coke plant.

Age Factors

Evaluation of exposure to polycyclic aromatic hydrocarbons in a coke production and a graphite electrode manufacturing plant: assessment of urinary excretion of 1-hydroxypyrene as a biological indicator of exposure.

OBJECTIVES: Characterisation of the airborne concentration of 13 polycyclic aromatic hydrocarbons (PAHs) at various workplaces in a graphite electrode and a coke production plant. Validation of the urinary excretion of 1-hydroxypyrene (hydroxypyrene) as a biological marker of exposure to PAH. DESIGN: Cross sectional study of workers exposed to PAHs (106 in the graphite electrode producing plant and 16 in the coke works). METHODS: Personal air sampling during at least six hours per workshift using a glass fibre filter and a Chromosorb 102 solid sorbent tube and analysis of PAHs by high performance liquid chromatography (HPLC) and spectrofluorometric detection (SFD). Collection of spot urine samples before and after the shift and analysis of 1-hydroxypyrene by HPLC and SFD. RESULTS: The workers most exposed to PAHs were those occupied at the topside area of the coke oven plant and those working in the blending and impregnation areas of the graphite electrode producing plant (mean airborne concentration of total PAHs: 199 and 223 micrograms/m3 respectively). Except for naphthalene and perylene, the relative proportion of the different PAHs did not differ between the plants. Pyrene concentration in air was highly correlated with the total airborne PAH concentration (r = 0.83, p < 0.0001) and the correlation coefficients between hydroxypyrene concentration in postshift urine samples and pyrene or total PAHs in air were 0.67 (p < 0.0001) and 0.72 (p < 0.0001) respectively. Excretion of hydroxypyrene doubled when the exposure to pyrene in air increased 10-fold. The half life for the urinary excretion of hydroxypyrene was around 18 hours (95% confidence interval 16.1-19.8). Smoking habits only explained 2.3% of the variance in hydroxypyrene excretion compared with 45% for the pyrene concentration in air. CONCLUSION: The determination of the urinary excretion of hydroxypyrene in postshift urine samples can be used as a suitable biomarker to assess individual exposure to PAHs in coke ovens and in graphite electrode manufacturing plants.

Air Pollutants, Occupational