Mortality among residents near cokeworks in Great Britain.
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OBJECTIVES: To investigate whether residents near cokeworks have a higher standardised mortality than those further away, particularly from cardiovascular and respiratory causes, which may be associated with pollution from cokeworks. METHOD: Cross sectional small area study with routinely collected postcoded mortality data and small area census statistics. Populations within 7.5 km of 22 cokeworks in Great Britain, 1981-92. Expected numbers of deaths within 2 and 7.5 km of cokeworks, and in eight distance bands up to 7.5 km of cokeworks, were calculated by indirect standardisation from national rates stratified for age and sex and a small area deprivation index, and adjusted for region. Age groups examined were all ages, 1-14, 15-64, 65-74, > or = 75. Only the 1-14 and 15-44 age groups were examined for asthma mortality. RESULTS: There was a 3% (95% confidence interval (95% CI) 1% to 4%) excess of all deaths within 2 km of cokeworks, and a significant decline in mortality with distance from cokeworks. The excess of deaths within 2 km was slightly higher for females and elderly people, but excesses within 2 km and declines in risk with distance were significant for all adult age groups and both sexes. The size of the excess within 2 km was 5% (95% CI 3% to 7%) for cardiovascular causes, 6% (95% CI 3% to 9%) for ischaemic heart disease, and 2% (95% CI -2% to 6%) for respiratory deaths, with significant declines in risk with distance for all these causes. There was a non-significant 15% (95% CI -1% to 101%) excess in asthma mortality in the 15-44 age group. There were no significant excesses in mortality among children but 95% CIs were wide. Within 2 km of cokeworks, the estimated additional excess all cause mortality for all ages combined related to region and mainly to the greater deprivation of the population over national levels was 12%. CONCLUSIONS: A small excess mortality near cokeworks as found in this study is plausible in the light of current evidence about the health impact of air pollution. However, in this study the effects of pollution from cokeworks, if any, are outweighed by the effects of deprivation on weighed by the effects of deprivation on mortality near cokeworks. It is not possible to confidently exclude socioeconomic confounding or biases resulting from inexact population estimation as explanations for the excess found. (+info)
Proximity to coke works and hospital admissions for respiratory and cardiovascular disease in England and Wales.
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BACKGROUND: The incidence of hospital admissions for respiratory and cardiovascular diseases in areas close to operating coke works in England and Wales was investigated. METHODS: A small area study using distance from source as a proxy for exposure was undertaken in subjects aged 65 or over and children under 5 years within 7.5 km of four coke works (1991 estimated populations 87 760 and 43 932, respectively). The main outcome measures were emergency hospital admissions in 1992/3-1994/5 with a primary diagnosis of coronary heart disease (ICD 410-414), stroke (ICD 431-438), all respiratory diseases (ICD 460-519), chronic obstructive pulmonary disease (ICD 491-492), and asthma (ICD 493) in those aged 65 or over, and all respiratory and asthma admissions in children under 5 years of age. RESULTS: At age 65 or over the combined estimate of relative risk with proximity to coke works (per km) ranged from 0.99 (95% CI 0.90 to 1.09) for chronic obstructive pulmonary disease to 1.03 (95% CI 0.94 to 1.13) for asthma. For children under 5 years the combined estimate of risk was 1.08 (95% CI 0.98 to 1.20) for all respiratory disease and 1.07 (95% CI 0.98 to 1.18) for asthma. There was evidence of significant heterogeneity in risk estimates between coke work groups, especially in children under 5 years (p<0.001 and p=0.004 for respiratory disease and asthma, respectively). For the Teesside coke works in North East England the relative risk with proximity (per km) was 1.09 (95% CI 1.06 to 1.12) for respiratory disease and 1.09 (95% CI 1.04 to 1.15) for asthma. CONCLUSIONS: No evidence overall was found for an association between hospital admissions and living near operational coke works in England and Wales. Trends of a higher risk of hospital admission for respiratory disease and asthma among children with proximity to the Teesside plant require further investigation. (+info)
Biological monitoring the exposure to polycyclic aromatic hydrocarbons of coke oven workers in relation to smoking and genetic polymorphisms for GSTM1 and GSTT1.
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Occupational exposure to polycyclic aromatic hydrocarbons (PAH) increases the risk of developing lung cancer. Human exposure is often demonstrated by increased internal levels of PAH metabolites and of markers for early biological effects, like DNA adducts and cytogenetic aberrations. OBJECTIVE: This study aimed to assess whether the current exposure to PAH of coke oven workers in a Dutch plant induced biological effects, and to determine if these effects are influenced by tobacco smoking and by genetic polymorphisms for the glutathione S-transferase genes GSTM1 and GSTT1. METHODS: Urinary 1-hydroxypyrene (1-OHpyr) levels were used to monitor the internal dose, while the internal effective dose was assessed by monitoring PAH-DNA adducts, DNA strand breaks (Comet assay), sister-chromatid exchanges (SCE) and cells with a high frequency of SCE (HFC) in lymphocytes together with micronuclei (MN) in exfoliated urothelial cells. RESULTS: Occupational exposure to PAH resulted in statistically significant increased 1-OHpyr levels (P<0.001), but it did not cause a significant induction of SCE, HFC, MN, DNA strand breaks or DNA adducts. Smoking caused a significant increase of 1-OHpyr (P<0.05), SCE (P<0.001), HFC (P<0.001) and DNA adducts (P<0.05), but not of MN or DNA strand breaks. Following correction for the smoking-related effects, no occupational induction of the effect biomarkers could be discerned. Multi-variate analysis did not show a significant influence of GSTM1 and GSTT1 polymorphisms on any biomarker. Also no significant interactions were observed between the various biomarkers. CONCLUSION: This study shows that in the examined plant, the occupational exposure to PAH does not result in measurable early biological effects (+info)
Urinary 1-hydroxypyrene in coke oven workers relative to exposure, alcohol consumption, and metabolic enzymes.
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OBJECTIVES: To investigate the influence of personal lifestyle--such as smoking and alcohol consumption-on urinary 1-hydroxypyrene (1-OHP) concentrations in coke oven workers exposed to polycyclic aromatic hydrocarbons (PAHs) and to evaluate the association of 1-OHP concentrations with the genetic polymorphism of several metabolic enzymes including cytochrome P-450 (CYP) 1A1 and glutathione S-tranferases (GSTs). METHODS: The study population contained 162 coke oven workers and 58 controls employed at the largest iron and steel factory in China. Personal data were collected at the interview. 1-OHP in urine was measured with high performance liquid chromatography with fluorescence detection. Genetic polymorphisms were identified by the polymerase chain reaction (PCR) method. RESULTS: A positive association between excretion of urinary 1-OHP and the levels of exposure to PAHs was confirmed. Those people who consumed >or=50 g/day ethanol had significantly higher 1-OHP excretion than did other coke oven workers (p<0.01). No significant difference in urinary 1-OHP was found between smokers and non-smokers, in both controls and exposed subjects. The variant homozygotes at exon 7 of the CYP1A1 gene had significantly higher urinary 1-OHP concentrations than other CYP1A1 genotypes among the exposed workers (p=0.03). There was less association between the concentrations of 1-OHP and the GSTM1, GSTP1, or GSTT1 polymorphism. CONCLUSIONS: The present study confirmed that urinary 1-OHP is a good biomarker for exposure to PAHs. Alcohol consumption affected urinary 1-OHP excretion. The variant genotypes of the CYP1A1 gene may result in the enhancement of PAH metabolites. It is helpful to understand the role of individual susceptibility on metabolism of carcinogens. These findings suggest that the modulating effect of individual lifestyle factors or genetic nature should be considered in future studies on occupational exposure to PAHs and in evaluating the health risk from harmful chemicals. (+info)
The effect of relevant genotypes on PAH exposure-related biomarkers.
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Polycyclic aromatic hydrocarbons (PAHs) in coke oven emissions cause a cancer risk to humans. In a comprehensive biomonitoring study among Estonian coke oven workers, we looked at the effect of genetic polymorphisms in metabolic enzymes on urinary mutagenicity, 1-hydroxypyrene (1-OHP) concentration in urine, and aromatic DNA adducts in white blood cells (WBCs). Coke oven workers were sampled twice (samplings I and II), and controls only once at the time of sampling I. Urinary mutagenicity was measured using the Ames test. CYP1A1, microsomal epoxide hydrolase (mEH), and glutathione S-transferase (GST) genotypes were analyzed by polymerase chain reaction (PCR). Urinary mutagenicity did not differ between exposed and controls, but those coke oven workers who were smokers had significantly higher (P=0.0002) mutagenic activity in urine than nonsmokers. Urinary mutagenicity was moderately correlated to levels of 1-OHP and aromatic DNA adducts, the P values ranging from 0.0005 to 0.002. Carriers of a variant allele in exon 4 of mEH (Arg139) had elevated urinary mutagenicity (sampling I). In addition, urine mutagenicity of persons with predicted high mEH activity was significantly higher. Smoking habit did not explain the differences observed in urinary mutagenicity between mEH phenotype or genotype subgroups. Variation in exon 3 of mEH (His113) was related to a significantly (P=0.01) higher 1-OHP concentration in exposed workers (sampling II). Workers from sampling I who had an Arg139 variation in mEH had lower levels of adducts in lymphocytes (P=0.01) than others, while airborne benzo[a]pyrene (B[a]P) and His113 variation affected interactively on adduct levels. Our study shows that a comprehensive assessment of exposure is essential for elucidation of PAH exposure at a workplace. Even at high exposures metabolic polymorphisms seem to have some effect on biomarker levels, and should be assessed in biomonitoring studies. (+info)
Cross sectional study on lung function of coke oven workers: a lung function surveillance system from 1978 to 1990.
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AIMS: To determine the association between lung function of coke oven workers and exposure to coke oven emissions. METHODS: Lung function data and detailed work histories for workers in recovery coke ovens of a steelworks were extracted from a lung function surveillance system. Multiple regressions were employed to determine significant predictors for lung function indices. The first sets of lung function tests for 613 new starters were pooled to assess the selection bias. The last sets of lung function tests for 834 subjects with one or more year of coke oven history were pooled to assess determinants of lung function. RESULTS: Selection bias associated with the recruitment process was not observed among the exposure groups. For subjects with a history of one or more years of coke oven work, each year of working in the most exposed "operation" position was associated with reductions in FEV(1) of around 9 ml (p = 0.006, 95% CI: 3 ml to 16 ml) and in FVC of around 12 ml (p = 0.002, 95% CI: 4 ml to 19 ml). Negative effects of smoking on lung function were also observed. CONCLUSIONS: Exposure to coke oven emissions was found to be associated with lower FEV(1) and FVC. Effects of work exposure on lung function are similar to those found in other studies. (+info)
Lymphohaematopoietic system cancer incidence in an urban area near a coke oven plant: an ecological investigation.
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AIMS: To evaluate the incidence risk of lymphohaematopoietic cancers for the 1986-94 period in Cornigliano, a district of Genoa (Italy), where a coke oven is located a few hundred metres from the residential area. METHODS: The whole of Genoa and one of its 25 districts (Rivarolo) were selected as controls. The trend of risk around the coke oven was evaluated via Stone's method, while the geographic pattern of such risks across the Cornigliano district was evaluated by computing full Bayes estimates of standardised incidence ratio (FBE-SIR). RESULTS: In males, elevated relative risks (RR) were observed for all lymphohaematopoietic cancers (RR 1.7 v Rivarolo and 1.6 v Genoa), for NHL (RR 2.4 v Rivarolo and 1.7 v Genoa), and for leukaemia (RR 2.4 v Rivarolo and 1.9 v Genoa). In females, statistically non-significant RR were observed. In males no excess of risk was found close to the coke oven. In females, a rising risk for NHL was observed approaching the plant, although statistical significance was not reached, while the risk for leukaemia was not evaluable due to the small number of cases. Analysis of the geographic pattern of risk suggested the presence of a cluster of NHL in both sexes in the eastern part of the district, where a foundry had been operational until the early 1980s. A cluster of leukaemia cases was observed in males in a northern part of the area, where no major sources of benzene seemed to be present. CONCLUSIONS: The estimated risks seem to be slightly or not at all related to the distance from the coke oven. The statistically significant higher risks observed in males for NHL and leukaemia, and the clusters of leukaemia in males and of NHL in both sexes deserve further investigations in order to trace the exposures associated with such risks. (+info)
Association of HSP70 and genotoxic damage in lymphocytes of workers exposed to coke-oven emission.
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Heat shock proteins (Hsps) have been reported to protect cells, tissues, and organisms against damage from a wide variety of stressful stimuli. Whether they protect against deoxyribonucleic acid (DNA) damage in individuals exposed to environmental stresses and chemical carcinogens is unknown. In the study, we investigated the association between Hsp70 levels (the most abundant mammalian Hsp) and genotoxic damage in lymphocytes of workers exposed to coke-oven emission using Western dot blot and 2 DNA damage assays, the comet assay and the micronucleus test. The data show that there is a significant increase in Hsp70 levels, DNA damage score, and micronucleus rates in lymphocytes of workers exposed to coke-oven emission as compared with the control subjects. Furthermore, there was a significant negative correlation of Hsp70 levels with DNA damage scores in the comet assay (r = -0.663, P < 0.01) and with micronucleus rates (r = -0.461, P < 0.01) in the exposed group. In the control group, there was also a light negative correlation between Hsp70 with DNA damage and micronuclei rate (r = -0.236 and r = 0.242, respectively), but it did not reach a statistically significant level (P > 0.05). Our results show that individuals who had high Hsp70 levels generally showed lower genotoxic damage than others. These results suggest a role of Hsp70 in the protection of DNA from genotoxic damage induced by coke-oven emission. (+info)