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Title: Polycyclic aromatic hydrocarbons and fatal ischemic heart disease

Abstract

Several toxicologic and epidemiologic studies have produced evidence that occupational exposure to polycyclic aromatic hydrocarbons (PAH) is a risk factor for ischemic heart disease (IHD). However, a clear exposure-response relation has not been demonstrated. We studied a relation between exposure to PAH and mortality from IHD (418 cases) in a cohort of 12,367 male asphalt workers from Denmark, Finland, France, Germany, Israel, The Netherlands and Norway. Exposures to benzo(a)pyrene were assessed quantitatively using measurement-driven exposure models. Exposure to coal tar was assessed in a semiquantitative manner on the basis of information supplied by company representatives. We carried out sensitivity analyses to assess potential confounding by tobacco smoking. Both cumulative and average exposure indices for benzo(a)pyrene were positively associated with mortality from IHD. The highest relative risk for fatal IHD was observed for average benzo(a)pyrene exposures of 273 ng/m{sup 3} or higher, for which the relative risk was 1.64(95% confidence interval = 1.13-2.38). Similar results were obtained for coal tar exposure. Sensitivity analysis indicated that even in a realistic scenario of confounding by smoking, we would observe approximately 20% to 40% excess risk in IHD in the highest PAH-exposure categories. Our results lend support to the hypothesis that occupational PAH exposuremore » causes fatal IHD and demonstrate a consistent exposure-response relation for this association.« less

Authors:
; ; ; ; ; ; ; ; ; ; ; ; ; ; ;  [1]
  1. International Agency for Research on Cancer, Lyon (France)
Publication Date:
OSTI Identifier:
20681262
Resource Type:
Journal Article
Resource Relation:
Journal Name: Epidemiology; Journal Volume: 16; Journal Issue: 6
Country of Publication:
United States
Language:
English
Subject:
01 COAL, LIGNITE, AND PEAT; OCCUPATIONAL EXPOSURE; POLYCYCLIC AROMATIC HYDROCARBONS; COAL TAR; ASPHALTS; HEART; CARDIOVASCULAR DISEASES; HEALTH HAZARDS; BENZOPYRENE; MORTALITY

Citation Formats

Burstyn, I., Kromhout, H., Partanen, T., Svane, O., Langard, S., Ahrens, W., Kauppinen, T., Stucker, I., Shaham, J., Heederik, D., Ferro, G., Heikkila, P., Hooiveld, M., Johansen, C., Randem, B.G., and Boffetta, P.. Polycyclic aromatic hydrocarbons and fatal ischemic heart disease. United States: N. p., 2005. Web. doi:10.1097/01.ede.0000181310.65043.2f.
Burstyn, I., Kromhout, H., Partanen, T., Svane, O., Langard, S., Ahrens, W., Kauppinen, T., Stucker, I., Shaham, J., Heederik, D., Ferro, G., Heikkila, P., Hooiveld, M., Johansen, C., Randem, B.G., & Boffetta, P.. Polycyclic aromatic hydrocarbons and fatal ischemic heart disease. United States. doi:10.1097/01.ede.0000181310.65043.2f.
Burstyn, I., Kromhout, H., Partanen, T., Svane, O., Langard, S., Ahrens, W., Kauppinen, T., Stucker, I., Shaham, J., Heederik, D., Ferro, G., Heikkila, P., Hooiveld, M., Johansen, C., Randem, B.G., and Boffetta, P.. Tue . "Polycyclic aromatic hydrocarbons and fatal ischemic heart disease". United States. doi:10.1097/01.ede.0000181310.65043.2f.
@article{osti_20681262,
title = {Polycyclic aromatic hydrocarbons and fatal ischemic heart disease},
author = {Burstyn, I. and Kromhout, H. and Partanen, T. and Svane, O. and Langard, S. and Ahrens, W. and Kauppinen, T. and Stucker, I. and Shaham, J. and Heederik, D. and Ferro, G. and Heikkila, P. and Hooiveld, M. and Johansen, C. and Randem, B.G. and Boffetta, P.},
abstractNote = {Several toxicologic and epidemiologic studies have produced evidence that occupational exposure to polycyclic aromatic hydrocarbons (PAH) is a risk factor for ischemic heart disease (IHD). However, a clear exposure-response relation has not been demonstrated. We studied a relation between exposure to PAH and mortality from IHD (418 cases) in a cohort of 12,367 male asphalt workers from Denmark, Finland, France, Germany, Israel, The Netherlands and Norway. Exposures to benzo(a)pyrene were assessed quantitatively using measurement-driven exposure models. Exposure to coal tar was assessed in a semiquantitative manner on the basis of information supplied by company representatives. We carried out sensitivity analyses to assess potential confounding by tobacco smoking. Both cumulative and average exposure indices for benzo(a)pyrene were positively associated with mortality from IHD. The highest relative risk for fatal IHD was observed for average benzo(a)pyrene exposures of 273 ng/m{sup 3} or higher, for which the relative risk was 1.64(95% confidence interval = 1.13-2.38). Similar results were obtained for coal tar exposure. Sensitivity analysis indicated that even in a realistic scenario of confounding by smoking, we would observe approximately 20% to 40% excess risk in IHD in the highest PAH-exposure categories. Our results lend support to the hypothesis that occupational PAH exposure causes fatal IHD and demonstrate a consistent exposure-response relation for this association.},
doi = {10.1097/01.ede.0000181310.65043.2f},
journal = {Epidemiology},
number = 6,
volume = 16,
place = {United States},
year = {Tue Nov 01 00:00:00 EST 2005},
month = {Tue Nov 01 00:00:00 EST 2005}
}
  • Workers in coke oven plants have a higher incidence of lung cancer than the general population. They are exposed to a variety of chemicals, in particular the polycyclic aromatic hydrocarbons (PAH), including benzo(a)pyrene. To evaluate the genotoxic effects of PAH exposure, air samples and urine samples were analyzed for PAH by capillary gas chromatography and high-performance liquid chromatography, respectively. Since benzo(a)pyrene is activated to 7 beta,8 alpha-dihydroxy-(9 alpha,10 alpha)-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDE) and binds to DNA, we have used ultrasensitive enzymatic radioimmunoassay and synchronous fluorescence spectrophotometry to measure BPDE-DNA adducts in lymphocyte DNA. The results show that workers were exposed to highmore » concentrations of atmospheric PAH. However, the mean PAH exposure levels are reduced 60% when the workers wore masks during work. When compared to exposure levels, the urinary excretion of PAH was relatively low. Approximately one-third of the workers had detectable putative BPDE-DNA adducts in lymphocytes by ultrasensitive enzymatic radioimmunoassay, and 10% of the samples had emission peaks at 379 nm by synchronous fluorescence spectrophotometry. The four most positive samples were the same in both of the assays. Antibodies to an epitope(s) on BPDE-DNA were found in the sera of approximately one-third of the workers. Detection of DNA adducts and antibodies to these adducts are internal indicators of exposure to benzo(a)pyrene.« less
  • The {sup 32}P-postlabeling assay, thin-layer chromatography, and reverse-phase high-pressure liquid chromatography (HPLC) were used to separate DNA adducts formed from 10 polycyclic aromatic hydrocarbons (PAHs) and 6 nitrated polycyclic aromatic hydrocarbons (NO{sub 2}-PAHs). The PAHs included benzo[j]fluoranthene, benzo[k]fluoranthene, indeno[1,2,3-cd]pyrene, benzo[a]pyrene, chrysene, 6-methylchrysene, 5-methylchrysene, and benz[a]anthracene. The NO{sub 2}-PAHs included 1-nitropyrene, 2-nitrofluoranthene, 3-nitrofluoranthene, 1,6-dinitropyrene, 1,3-dinitropyrene, and 1,8-dinitropyrene. Separation of seven of the major PAH-DNA adducts was achieved by an initial PAH HPLC gradient system. The major NO{sub 2}-PAH-DNA adducts were not all separated from each other using the initial PAH HPLC gradient but were clearly separated from the PAH-DNA adducts. Amore » second NO{sub 2}-PAH HPLC gradient system was developed to separate NO{sub 2}-PAH-DNA adducts following one-dimensional TLC and HPLC analysis. HPLC profiles of NO{sub 2}-PAH-DNA adducts were compared using both adduct enhancement versions of the {sup 32}P-postlabeling assay to evaluate the use of this technique on HPLC to screen for the presence of NO{sub 2}-PAH-DNA adducts. To demonstrate the application of these separation methods to a complex mixture of DNA adducts, the chromatographic mobilities of the {sup 32}P-postlabeled DNA adduct standards (PAHs and NO{sub 2}-PAHs) were compared with those produced by a complex mixture of polycyclic organic matter (POM) extracted from diesel emission particles. The diesel-derived adducts did not elute with the identical retention time of any of the PAH or NO{sub 2}-PAH standards used in this study. HPLC analyses of the NO{sub 2}-PAH-derived adducts (butanol extracted) revealed the presence of multiple DNA adducts.« less
  • Photoinduced toxicity of polycyclic aromatic hydrocarbons (PAHs) occurs via photosensitization reactions (e.g., generation of singlet-state oxygen) and by photomodification (photooxidation and/or photolysis) of the chemicals to more toxic species. The quantitative structure-activity relationship (QSAR) described in the companion paper predicted, in theory, that photosensitization and photomodification additively contribute to toxicity. To substantiate this QSAR modeling exercise it was necessary to show that toxicity can be described by empirically derived parameters. The toxicity of 16 PAHs to the duckweed Lemna gibba was measured as inhibition of leaf production in simulated solar radiation (a light source with a spectrum similar to thatmore » of sunlight). A predictive model for toxicity was generated based on the theoretical model developed in the companion paper. The photophysical descriptors required of each PAH for modeling were efficiency of photon absorbance, relative uptake, quantum yield for triplet-state formation, and the rate of photomodification. The photomodification rates of the PAHs showed a moderate correlation to toxicity, whereas a derived photosensitization factor (PSF; based on absorbance, triplet-state quantum yield, and uptake) for each PAH showed only a weak, complex correlation to toxicity. However, summing the rate of photomodification and the PSF resulted in a strong correlation to toxicity that had predictive value. When the PSF and a derived photomodification factor (PMF; based on the photomodification rate and toxicity of the photomodified PAHs) were summed, an excellent explanatory model of toxicity was produced, substantiating the additive contributions of the two factors.« less
  • Supercritical fluid extraction (SFE) with CO/sub 2/ is a rapid alternative to liquid solvent extraction for the recovery of organic air pollutants collected on polyurethane foam (PUF) sorbent plugs. Quantitative recovery (> 95%) of polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs) ranging from naphthalene to perylene, several heteroatom-containing PAHs, and n-alkanes ranging from C/sub 12/ to C/sub 24/ was achieved with 10-20 min extractions. Class-selective extraction of n-alkanes versus PAHs resulted from the sequential extraction of the same PUF plug at 80 and 380 atm. Directly coupled SFE with gas chromatography (SFE-GC) allowed a PUF sample to be analyzed inmore » < 1 hr including sample collection, extraction, analyte concentration, and GC separation. The application of SFE and coupled SFE-GC for the extraction and analysis of organic air pollutants that have been collected on PUF is demonstrated for cigarette smoke, diesel exhaust, and roofing tar volatiles.« less
  • Noninvasive tests have greatly improved in their ability to diagnose coronary artery disease. In addition, new testing modalities have been added to the authors armamentarium. However, no test is clearly superior to all others in every clinical circumstance. Moreover, none have been shown to provide sensitivities and specificities consistently above 90%. Therefore, their use for diagnostic purposes in populations with a lower prevalence of disease is only of moderate value. Conversely, for the assessment of the functional significance of coronary artery disease or prognosis in patients with ischemic heart disease, the addition of noninvasive imaging modalities to exercise testing ismore » of high value.« less