Annals of Oncology Advance Access originally published online on August 25, 2006
Annals of Oncology 2007 18(3):431-446; doi:10.1093/annonc/mdl172
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© 2006 European Society for Medical Oncology
reviews |
Occupational exposures to polycyclic aromatic hydrocarbons, and respiratory and urinary tract cancers: a quantitative review to 2005
1 Istituto di Ricerche Farmacologiche ‘Mario Negri’, Milan, Italy
2 International Agency for Research on Cancer, Lyon, France
3 Istituto di Statistica Medica e Biometria, Univesità degli Studi di Milano, Milan, Italy
* Correspondence to: Dr C. Bosetti, Istituto di Ricerche Farmacologiche ‘Mario Negri’, Via Eritrea 62 – 20157 Milan, Italy. Tel: +39-0239014526; Fax: +39-0233200231; E-mail: bosetti{at}marionegri.it
 |
Abstract |
|---|
 Top Abstract introductionpatients and methodsresultsconclusionsAcknowledgementsReferences |
|---|
Background: Exposure to polycyclic aromatic hydrocarbons (PAHs) has been reported in several industries, including those of the aluminum production, coal gasification, coke production, iron and steel foundries, coal tar and related products, carbon black and carbon electrodes production.
Patients and methods: This paper reviews the results from cohort studies conducted on workers exposed to PAHs in these industries, with a focus on cancers of the respiratory and urinary tract.
Results: An excess risk from lung/respiratory cancers was found in most industries, the pooled relative risk (RR) being 2.58 (95% CI 2.28–2.92) for coal gasification, 1.58 (95% CI 1.47–1.69) for coke production, 1.40 (95% CI 1.31–1.49) for iron and steel foundries, 1.51 (95% CI 1.28–1.78) for roofers and 1.30 (95% CI 1.06–1.59) for carbon black production. The evidence for cancers of the bladder and of the urinary system is less consistent, with a significant increased risk only for workers in aluminum production (pooled RR = 1.29, 95% CI 1.12–1.49), coal gasification (pooled RR = 2.39, 95% CI 1.36–4.21), and iron and steel foundries (pooled RR = 1.29, 95% CI 1.06–1.57).
Conclusions: Increased risks from lung and bladder cancers were found in PAH-related occupations. These were modest in most industries, apart from those for coal gasification, and whether they are due at least partially to some bias or confounding remains open to discussion.
Key words: cohort studies, neoplasm, risk, occupational exposure, polycyclic aromatic hydrocarbons, review
|
introduction |
|---|
|
TopAbstractintroductionpatients and methodsresultsconclusionsAcknowledgementsReferences |
|---|
Polycyclic aromatic hydrocarbons (PAHs) are a class of chemicals, characterized by the presence of two or more benzene rings, which derive mainly from the incomplete combustion of organic material. These include hundreds of compounds, among which the best known is benzo[a]pirene, often used as a marker of exposure to PAHs [1].
High exposure to PAH mixtures have been reported, mainly in the past, in several industries and occupations, including aluminum production (mainly when the Södeberg process is used), coal gasification, coke production, iron and steel foundries, diesel engine exhaust, coal tar and related products, carbon black and carbon electrodes production and chimney sweeps.
The epidemiological evidence from workers occupationally exposed to PAHs in various industries and occupations has been reviewed by the International Agency for Research on Cancer (IARC), which classified some of these industries as carcinogenic to humans [2–7], mainly for an increased risk of lung, laryngeal, skin, kidney and urinary bladder cancer. This evidence has been also included in a comprehensive review by Boffetta et al. [8].
This paper reviews the main results from cohort studies conducted on workers from PAH-related occupations, with emphasis on study results reported after the review by Boffetta et al. [8]. Particular attention is given to cancers of the respiratory and urinary tract, since these are the sites most consistently associated with PAH exposures. Skin cancer has not been considered, since ascertainment of incidence or mortality from this neoplasm is problematic. Exposure to diesel engine exhaust in the transport industry and related occupations, which has been related to some excess risk of lung and bladder cancer [8–10], is also not included in the present review, in consideration of the heterogeneous and highly variable working conditions of these groups of workers and the consequent difficulty of obtaining reliable overall risk estimate.
We reviewed, in detail, cohort studies published between 1997 and 2005, while for cohort studies included in the review by Boffetta et al. [8] we summarized only the main results. We also calculated quantitative estimates of the risk of selected cancers based on meta-analyses of results from all available studies.
|
patients and methods |
|---|
|
TopAbstractintroductionpatients and methodsresultsconclusionsAcknowledgementsReferences |
|---|
The studies included in this quantitative review were original cohort investigations published up to December 2005 on workers from selected industries characterized by high exposure to PAHs, and providing information on the risk of lung, bladder and kidney cancers, or more in general of neoplasms of the respiratory and urinary tract. They were identified through searches of the MEDLINE database, using the keywords ‘polycyclic aromatic hydrocarbons, neoplasm, risk, occupational exposure or cohort studies’. Papers were also searched among those quoted in the retrieved studies. A total of 62 papers were identified, including the results of 57 cohort studies, whose main characteristics and results are described in Tables 1–7
.
|
|
|
|
|
|
|
To provide a quantitative overall estimate of the standardized mortality ratios (SMR) or incidence ratios (SIR) for selected cancers in relation to various industries and occupations, the number of cancer deaths/cases observed, and the SMR/SIR were abstracted from each paper. The expected number of deaths/cases in each study was also abstracted or obtained from the ratio of observed deaths/cases over SMR/SIR, and the overall SMR for each neoplasm of interest was calculated as an unweighted ratio of the sum of observed and expected deaths/cases (Table 8). Pooled relative risks (RR) and the corresponding 95% confidence intervals (CI) were also computed as a weighted average of the SMR/SIR, using the inverse of the variance of the logarithm of the SMR/SIR as weight (fixed-effects model [10], Table 8 and Figures 1–7
). Chi-square tests for heterogeneity were used to evaluate the consistency of findings between studies [11].
|
|
|
|
|
|
|
|
For some major industries, the results of the meta-analysis were presented graphically, plotting the SMR/SIR as a black square, whose size was inversely proportional to the variance of the logarithm of the SMR/SIR. For various studies, the 95% CI differed slightly from those published in the original papers because of rounding. For studies which presented results for different categories of workers within the same industry, a single pooled estimate was plotted. Similarly, a single pooled estimate combining studies with less than 10 cancer cases was plotted. Diamonds were used to plot the pooled RR for all studies; their centre represents the RR and their extremes the 95% CI.
|
results |
|---|
|
TopAbstractintroductionpatients and methodsresultsconclusionsAcknowledgementsReferences |
|---|
aluminum production
Table 1 gives information from 15 papers on nine cohorts of aluminum production workers [12–26]. Over the period 1997–2005, five papers were published from Norway [16–18], France [23] and Italy [26]. The data from the three Norwegian studies [16–18] were then included in a subsequent re-analysis [19]. This re-analysis included the results of the cohorts of six aluminum plants from Norway, two of which started to operate before 1920, and the remaining from the period between 1947 and 1958. In total, that study included 11 103 men employed for more than 3 years, and followed-up for cancer incidence between 1953 and 1996. With reference to lung cancer, no excess risk was observed (189 observed cases versus 183.1 expected, corresponding to a SIR of 1.0; 95% CI 0.9–1.2), nor a trend with the cumulative dose of exposure to PAHs. For cancer of the bladder, 130 cases were observed versus 101.7 expected, corresponding to a SIR of 1.3 (95% CI 1.1–1.5). There was also a significant trend in bladder cancer risk in relation to the cumulative dose of PAHs, with a RR of 2 for exposures
2000 µg/m3 for 30 or more years. Thus, this large re-analysis of all the Norwegian studies of aluminum production, including more than 1500 cancer cases and with a long period of follow-up, confirmed an excess risk for cancer of the bladder, but did not show any association for lung cancer. A mortality study conducted by the French National Institute for the Research and Safety [23] updated the data on workers from one of the aluminum reduction plants considered in the paper by Mur et al. [17]. That study included 2133 men employed for at least 1 year between 1950 and 1994, and followed up between 1968 and 1994. Overall, mortality from cancer of the lung was below unity (SMR = 0.6, 95% CI 0.4–1.0, on the basis of 19 observed deaths). There was no excess lung cancer in any of the specific jobs where exposure to PAHs was more likely, nor trends with duration of exposure and time since first exposure. With reference to bladder cancer, the SMR was 1.8, on the basis of seven observed deaths (95% CI 0.7–3.6). Six deaths occurred in jobs with more probable exposure to PAH (SMR = 2.15, 95% CI 0.79–4.68). However, no increase in risk was observed for longer duration of exposure and time since first exposure.
The Italian study [26] was a 10-year mortality update of a cohort of workers from a Prebake aluminum smelter [18], which included 1152 men employed for at least 1 year in the foundry between 1972 and 1980, and followed-up until the end of 2001. No excess mortality was observed for cancer of the lung (11 observed deaths versus 15.8 expected, SMR = 0.7, 95% CI 0.4–1.3), nor of the bladder (three observed deaths versus 3.8 expected, SMR = 0.8, 95% CI 0.3–2.4). Furthermore, no difference in risk was observed when workers were classified in three groups with increasing level of exposure to PAHs.
In eight cohorts of aluminum production workers, 653 lung cancer cases were observed versus 644.9 expected, with a pooled RR of 1.03 (95% CI 0.95–1.11, Table 8). Considering all cancers of the respiratory system, mainly lung cancer, a total of 688 cases were observed compared with 674.1 expected, with a pooled RR of 1.03 (95% CI 0.96–1.11, Table 8 and Figure 1). For bladder cancer, the eight available studies included a total of 196 cases observed versus 155.7 expected, with a pooled RR of 1.29 (95% CI 1.12–1.49, Table 8 and Figure 2). With reference to kidney cancer, the cases observed in four studies were 86 versus 76.7 expected, with a pooled RR of 1.15 (Table 8).
coal gasification
In the past, coal gasification implied high exposures to PAHs, as to other carcinogenic and toxic substances. Five cohort studies are available on exposures occurred in the past (before the 1970s) whose main results are summarized in Table 2 [27–31]. No study on workers employed in this manufacture was published after the review by Boffetta et al. [8].
Overall, 188 deaths from lung cancer were reported in the five cohorts of coal gasification workers, compared with 87.7 expected, with a pooled RR of 2.29 (95% CI 1.98–2.64, Table 8). Considering all cancers of the respiratory system, 251 deaths were observed versus 104.7 expected (pooled RR = 2.58, 95% CI 2.28–2.92, Table 8 and Figure 3). All the estimates were significantly above unity, although a certain degree of heterogeneity was found. The number of deaths observed from cancer of the bladder in the two cohorts were 12 versus 5.0 expected, corresponding to a pooled RR of 2.39 (95% CI 1.36–4.21); 18 deaths from all cancers of the urinary system were recorded, versus 6.0 expected (pooled RR = 3.27, 95% CI 2.06–5.19, Table 8).
coke production
With reference to coke production, there are 10 cohorts of workers [32–41] (Table 3), among which only a small Norwegian investigation [41] was published after the review by Boffetta et al. [8]. That study was based on a cohort of 888 workers of one coking plant that operated between 1964 and 1988, followed-up for incidence of cancer and other diseases until 1993. No excess was observed for cancer of the lung (seven observed cases versus 8.5 expected, SIR = 0.82) and of the bladder (two observed cases versus 2.4 expected, SIR = 0.82). However, an excess risk was observed in relation to the cumulative dose of PAHs (SIR = 3.60 for 150 µg/m3 year of PAH in the overall cohort, and 4.82 for 15 years of latency). The result of this small study, with a short period of follow-up, should however be interpreted with caution.
Overall, in 10 cohort studies 762 cases of lung cancer were observed, compared with 512.1 expected, with a pooled RR of 1.58 (95% CI 1.47–1.69, Table 8 and Figure 4). A considerable heterogeneity of risk estimates across various studies was, however, observed, particularly between the four larger studies [20–23], which gave RRs of 2.0, 1.2, 1.1 and 2.6, respectively. Some studies reported some excess risk for other neoplasms, such as laryngeal, liver, prostate or kidney cancers, but overall data do not provide a consistent evidence of any excess of risk. Likewise, for cancer of the bladder, no evidence of an increased risk was observed in any of the studies.
iron and steel foundries
Iron and steel foundry workers are another important group of workers exposed to considerable levels of PAHs, mainly in the past. The main results of 10 cohort studies on these workers are shown in Table 4 [42–53]. After the review by Boffetta et al. [8], a mortality study of a cohort of 4288 men and 609 women from a French stainless and alloyed steel plant was published [51]. Workers were employed between the beginning of 1968 and the end of 1991, and were followed-up to the end of 1992. No excess mortality from lung cancer was reported in the overall cohort (SMR = 1.2, 95% CI 0.9–1.6, on the basis of 54 observed deaths). The SMR of bladder cancer was 1.7 (95% CI 0.8–3.2) on the basis of 10 observed deaths. In a case–control analysis of lung cancer nested in the cohort, a RR of 1.9 (95% CI 1.0–3.7) was reported for exposure to PAHs, with a significant trend with duration and cumulative dose of exposure [51].
Ten cohort studies available on workers in iron and steel foundries included a total of 975 lung cancer cases observed compared with 703.7 expected, with a pooled RR of 1.40 (95% CI 1.32–1.49, Table 8). Considering all respiratory neoplasms, there were 1004 observed cases versus 726.0 expected, with a pooled RR of 1.40 (95% CI 1.31–1.49, Table 8 and Figure 5). Cancers of the bladder were 99 versus 83.0 expected based on seven studies, with a pooled RR of 1.29 (95% CI 1.06–1.57, Table 8 and Figure 6). A significant heterogeneity between studies was observed, mainly due to a small cohort, which reported a SMR of 9 [25]. For kidney cancer, 40 cases were observed versus 31.0 expected (pooled RR = 1.30, 95% CI 0.95–1.77, Table 8).
bitumen fumes, coal tar and related products
In relation to coal tar and related products, there were 11 cohorts of workers, three of tar distillation [54–56], two of shale oil extraction [57, 58], two of creosote [59, 60], two of roofers [56, 61] and two of asphalt workers [62, 63] (Table 5).
A mortality study of a cohort of 907 tar distillers and 899 roofers employed in a Dutch industry [56] was published after the review by Boffetta et al. [8]. Workers were employed for at least 6 months between 1947 and 1980, and were followed-up until the beginning of 1988. A non-significant excess mortality from lung cancer was reported for tar distillers, with a total of 48 observed deaths versus 40.6 expected, corresponding to a SMR of 1.2 (95% CI 0.9–1.6). For cancer of the bladder, the SMR was of 0.5 (95% CI 0.06–1.87), on the basis of two observed deaths versus 3.6 expected.
A retrospective cohort study of workers of creosote-based wood treatments [60] was published after the review by Boffetta et al. [8]. This included over 2000 individuals who were employed at 11 wood-treating plants in the USA between 1979 and 1999, followed-up for mortality up to 2001. A modest excess risk for lung cancer mortality was observed (SMR = 1.3, 95% CI 0.9–1.8, based on 38 deaths observed). The SMR for laryngeal cancer was 1.6 (95% CI 0.2–6.6), based on two deaths observed. No deaths from cancer of the bladder and other urinary organs were found, and three deaths were observed from kidney cancer (SMR = 1.9, 95% CI 0.4–5.5). Similar findings were found among hourly employees. Analyses by length of employment and latency among hourly employees showed no clear pattern for both respiratory tract and kidney cancers.
With reference to roofers, in the study by Swaen et al. [56] there were 39 deaths from lung cancer compared with 29.7 expected, corresponding to a non-significant SMR of 1.3 (95% CI 0.9–1.8). The SMR for bladder cancer was close to unity (SMR = 1.1, 95% CI 0.2–3.4), with three observed deaths versus 2.6 expected.
The results of a large cohort study on asphalt workers were recently published [63]. The study was conducted in seven European countries and Israel, and was coordinated by the IARC. It included a total of 79 822 workers, of whom 29 820 were asphalt workers exposed to bitumen fumes, 32 245 constructors not exposed to bitumen fumes, and 17 757 other workers not classifiable as bitumen workers. The workers had been employed for the first time in a variable period between 1913 and 1999. The mean duration of follow-up (which started at variable times in various countries) was 16.7 years, ranging from 11.7 years in France and Germany to 21.9 years in Norway. Overall, in the asphalt workers there were 795 lung cancer deaths observed versus 742.4 expected, corresponding to a SMR of 1.1 (95% CI 1.0–1.2). The SMR for cancer of the lung was higher in the asphalt workers exposed to bitumen (SMR = 1.2, on the basis of 330 observed deaths), than in building or ground constructors (SMR = 1.0, on the basis of 249 observed deaths) and in other workers (SMR = 1.0, on the basis of 216 observed deaths). No excess risk was observed for laryngeal cancer (SMR = 1.0, on the basis of 42 deaths). For bladder cancer, there were 104 deaths observed versus 104.0 expected (SMR = 1.0, 95% CI 0.8–1.2). Similarly, no excess mortality from kidney cancer was found in asphalt workers (SMR = 0.8 95% CI 0.7–1.0, on the basis of 80 deaths observed). The results of this large study suggest, therefore, that asphalt workers had no excess of mortality from cancer of the respiratory and urinary tract.
A subsequent analysis of the same cohort of asphalt workers, based on a semi-quantitative job-exposure matrix [64], reported no excess mortality from lung cancer in workers exposed to bitumen fumes (SMR = 1.1), as well as in those exposed to coal tar (SMR = 1.1). Conversely, an excess mortality from lung cancer was found in workers exposed to diesel exhaust (SMR = 1.31).
Overall, the pooled RR for lung cancer was 1.21 (95% CI 0.95–1.55) in workers of tar distillation, 1.14 (95% CI 0.85–1.51) in those exposed to creosote, 1.51 (95% CI 1.28–1.78) in roofers and 1.14 (95% CI 1.07–1.22) in asphalt workers (Table 8). With reference to bladder cancer, the pooled RR was 1.82 (95% CI 0.76–4.37) in workers of tar distillation, 1.57 (95% CI 0.96–2.56) in roofers and 1.02 (95% CI 0.85–1.23) in asphalt workers (Table 8).
carbon black manufacture
Three papers are available on two cohorts of carbon black production workers [65–67] (Table 6). A US study did not show any significant excess mortality from cancers of the respiratory system [65]. Conversely, an excess mortality from lung and bladder cancer was reported in an English study [66], and was confirmed in a recent update of the same cohort [67]. The excess of mortality from lung cancer seemed limited, however, to two of the five plants considered [67]. Moreover, no relation was found with time since first employment, and internal analyses did not evidence any association with cumulative dose of exposure to carbon black.
Altogether, the data from two cohort studies of carbon black production reported 95 deaths from lung cancer versus 78.4 expected (SMR = 1.30, 95% CI 1.06–1.59, Table 8). However, the results from these two cohorts were not consistent.
carbon and graphite electrode manufacture
The main results from seven cohort studies that reported mortality in carbon electrode workers are given in Table 7 [68–73]. After the revision by Boffetta et al. [8], a historical cohort study was conducted on 1006 male workers employed for at least 1 year between 1945 and 1971 in an Italian plant, and followed-up for mortality between 1955 and 1996 [71]. With reference to specific cancer sites, 34 deaths from lung cancer were reported compared with 44.2 expected (SMR = 0.8, 95% CI 0.5–1.1), and seven deaths from bladder cancer compared to 6.7 expected (SMR = 1.0, 95% CI 0.4–2.1). Analyses of mortality by time since first employment showed a higher risk, although not significant, of lung cancer in subjects with 20 years since first employment. The risk, however, was inversely related to the duration of employment.
A small cohort from Japan [72] was based on 322 male workers employed for more than 5 years in a man-made graphite electrode manufacturing plant in the period 1951–1974, and followed-up for mortality up to 1988. In that cohort, nine deaths from lung cancer were observed compared with 3.4 expected, corresponding to a SMR of 2.6 (95% CI 1.2–5.0). The excess risk was found in separate sub-period analysis. No deaths from bladder cancer were observed, and therefore no excess risk for any other neoplasm.
Another cohort study was conducted on 1291 males employed between 1950 and 1989 in a graphite electrode production plant of Val Camonica, northern Italy, and followed-up until the end of 1997 [73]. The Italian population was used as reference for the period 1950–1989 and the Lombardy population was used for the period 1990–1997. That study did not report any excess of mortality from cancer of the lung (SMR = 1.0) or of the bladder (SMR = 1.1). Analyses stratified by age at death, time since first employment and duration of employment did not show any consistent pattern either for lung or for bladder cancer.
The data of a retrospective cohort from China are also available [74]. That cohort included 6635 male workers employed for more than 15 years during the period 1970–1985 in seven factories, including the carbon plants and the pot room and carbon department in an aluminum reduction plant. An excess mortality from lung cancer was observed (50 deaths observed versus 23.1 expected, SMR = 2.16) with stronger excess in the highly exposed group (SMR = 4.3, based on 26 deaths observed). This data, however, included workers of carbon product manufacturing, along with those of other activities in the aluminum production, and cannot thus be included in a quantitative review of workers of carbon electrodes.
In seven cohort studies on workers of carbon electrode manufacture, 97 cancers of the lung were observed versus 101.6 expected (pooled RR = 1.00, 95% CI 0.82–1.23, Table 8); for all respiratory cancers, 126 cancers were reported versus 135.7 expected (pooled RR = 0.97, 95% CI 0.81–1.15, Table 8 and Figure 7). Observed deaths were 16 for bladder cancer versus 13.0 expected (pooled RR = 1.35, 95% CI 0.83–2.20) and 20 versus 17.3 (pooled RR = 1.29, 95% CI 0.85–1.95) for all urinary tract cancers (Table 8).
chimney sweeps
Relatively few epidemiological studies have been conducted to quantify cancer risk among chimney sweeps. The largest cohort from Sweden [75], as well as a few other small cohorts, reported an excess risk from lung cancer [76–78]. No cohort study on chimney sweeps has been published since the review by Boffetta et al. [8].
|
conclusions |
|---|
|
TopAbstractintroductionpatients and methodsresultsconclusionsAcknowledgementsReferences |
|---|
The epidemiological data available on aluminum production workers, including more than 650 cancers of the lung and approximately 200 cancers of the bladder, indicate that there is no excess risk for cancer of the lung, but a modest excess risk for cancer of the bladder. The cause–effect inference, however, remains unclear, giving the small excess risk and the limited data on dose- and duration-risk relation [79].
There is definite epidemiological evidence that coal gasification workers had high risks of respiratory and probably urinary neoplasms. Although these workers were mainly exposed to PAHs from coal tar, they may have been exposed to other contaminants, including heavy metals, silica and aromatic amines. Moreover, it is difficult to extrapolate indications from this kind of highly toxic production until 30–40 years ago.
Data also indicate an excess risk for lung cancer, but not for other neoplasms, in workers of coke production, mainly of coke oven. For this group of workers, there are also quantitative exposure-risk estimates, which suggest a dose–response relation with the cumulative dose of PAHs [1, 40]. A meta-analyses of 10 studies estimated a RR of 1.17 for an a priori defined unit of 100 µg/m3 year of benzo[a]pyrene [80]. However, the comparability and validity of unit exposure measurements in various studies and populations remain open to discussion. In fact, only for a few cohorts a direct estimate of exposure was available. This criticism also applies to other industries and occupations considered in that meta-analysis, for which data are in any case more limited and inadequate for any inference of dose- and duration-relations.
Iron and steel foundry workers had an excess risk of cancers of the respiratory tract, particularly until the early 1970s, with a significant dose–risk relation [81]. Those workers, however, were exposed to various other known or potential carcinogenic substances, including several heavy metals, crystalline silica and asbestos. Therefore, it is questionable if the increased risk for respiratory cancers observed in these industries can be related to PAH exposure. The risk of bladder cancer was significantly increased in some studies, but there is no consistent epidemiological evidence on an excess risk.
Data on workers exposed to bitumen fumes, coal tar and related products are limited and do not suggest any increased risk for both respiratory and urinary tract cancers, with the exception of a modest excess risk for lung cancer in roofers. Similarly, data are too limited to draw any conclusion on the association between exposure to carbon black and cancer of the respiratory and urinary tract. Along this line, Monograph no. 93 of the IARC concluded that the epidemiological studies of carbon black provided inadequate evidence of carcinogenity [82, 83].
No excess risk was observed for cancer of the respiratory and urinary system among carbon electrode workers [84].
For some cancer sites and industries, including mainly lung and respiratory tract cancer for coal gasification and coke production workers, the results from various studies were significantly heterogeneous. This probably reflects variable exposure patterns across different cohort and time periods, and indicates that due caution is required to generalize these estimates.
Thus, the epidemiological evidence available to date confirms the existence of some excess risk for cancer of the lung in several PAH-related industries, with the exception of the aluminum and carbon electrode manufactures. The evidence for cancer of the bladder and of the urinary system is less consistent, with a modest increase in risk only for workers of aluminum production, coal gasification, iron and steel foundries. The excess risks observed were, however, modest for most industries (apart from coal gasification, which had an over two-fold increased risk), and whether such excesses are real or due at least partially to some bias or confounding cannot be completely ruled out. In particular, workers from the industries and occupations considered may have been exposed to other occupational carcinogens, as well as to tobacco smoking, which was not allowed for in most of the cohort studies considered.
|
Acknowledgements |
|---|
|
TopAbstractintroductionpatients and methodsresultsconclusionsAcknowledgementsReferences |
|---|
This work was conducted with the contribution of the Italian Association for Cancer Research and the Italian League Against Cancer. The authors thank Mr M. Plummer from IARC for providing the R function to plot the graphs, and Mrs I. Garimoldi for editorial assistance.
Received for publication February 9, 2006. Revision received April 21, 2006. Accepted for publication June 13, 2006.
|
References |
|---|
|
TopAbstractintroductionpatients and methodsresultsconclusionsAcknowledgementsReferences |
|---|
1. Bostrom CE, Gerde P, Hanberg A, et al. (2002) Cancer risk assessment, indicators, and guidelines for polycyclic aromatic hydrocarbons in the ambient air. Environ Health Perspect 110:451–488.
2. International Agency for Research on Cancer. IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, vol. 32: Polynuclear aromatic compounds, Part 1, Chemical environmental and experimental data. Lyon: International Agency for Research on Cancer 1984.
3. International Agency for Research on Cancer. IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, vol. 33: Polynuclear aromatic compounds, Part 2, Carbon blacks, mineral oils and some nitroarenes. Lyon: International Agency for Research on Cancer 1984.
4. International Agency for Research on Cancer. IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, vol. 34: Polynuclear aromatic compounds, Part 3, Industrial exposures in aluminum production, coal gasification, coke production, and iron and steel founding. Lyon: International Agency for Research on Cancer 1984.
5. International Agency for Research on Cancer. IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, vol. 35: Polynuclear aromatic compounds, Part 4, Bitumens, coal-tars and derived products, shale-oils and soots. Lyon: International Agency for Research on Cancer 1985.
6. International Agency for Research on Cancer. IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, suppl. 7: Overall evaluations of carcinogenicity: An updating of IARC monographs Volumes 1 to 42. Lyon: International Agency for Research on Cancer 1987.
7. Straif K, Baan R, Grosse Y, et al. (2005) Carcinogenicity of polycyclic aromatic hydrocarbons. Lancet Oncol 6:931–932.[Medline]
8. Boffetta P, Jourenkova N, Gustavsson P. (1997) Cancer risk from occupational and environmental exposure to polycyclic aromatic hydrocarbons. Cancer Causes Control 8:444–472.[CrossRef][Web of Science][Medline]
9. Boffetta P and Silverman DT. (2001) A meta-analysis of bladder cancer and diesel exhaust exposure. Epidemiology 12:125–130.[CrossRef][Web of Science][Medline]
10. International Agency for Research on Cancer. IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans, vol. 46: Diesel and gasoline engine exhausts and some nitroarenes. Lyon: International Agency for Research on Cancer 1989.
11. Greenland S. (1987) Quantitative methods in the review of epidemiologic literature. Epidemiol Rev 9:1–30.[Medline]
12. Jr Milham S. (1979) Mortality in aluminum reduction plant workers. J Occup Med 21:475–480.[Web of Science][Medline]
13. Giovanazzi A and D'Andrea F. (1981) Cause di morte fra i lavoratori di un impianto di riduzione elettrolitica di allumina. Med Lav 4:277–282.
14. Andersen A, Dahlberg BE, Magnus K, Wannag A. (1982) Risk of cancer in the Norwegian aluminum industry. Int J Cancer 29:295–298.[Web of Science][Medline]
15. Ronneberg A and Andersen A. (1995) Mortality and cancer morbidity in workers from an aluminum smelter with prebaked carbon anodes—Part II: Cancer morbidity. Occup Environ Med 52:250–254.
16. Ronneberg A, Haldorsen T, Romundstad P, Andersen A. (1999) Occupational exposure and cancer incidence among workers from an aluminum smelter in western Norway. Scand J Work Environ Health 25:207–214.[Web of Science][Medline]
17. Romundstad P, Haldorsen T, Andersen A. (2000) Cancer incidence and cause specific mortality among workers in two Norwegian aluminum reduction plants. Am J Ind Med 37:175–183.[CrossRef][Web of Science][Medline]
18. Romundstad P, Haldorsen T, Andersen A. (2000) Lung and bladder cancer among workers in a Norwegian aluminum reduction plant. Occup Environ Med 57:495–499.
19. Romundstad P, Andersen A, Haldorsen T. (2000) Cancer incidence among workers in six Norwegian aluminum plants. Scand J Work Environ Health 26:461–469.[Web of Science][Medline]
20. Rockette HE and Arena VC. (1983) Mortality studies of aluminum reduction plant workers: potroom and carbon department. J Occup Med 25:549–557.[Web of Science][Medline]
21. Gibbs GW. (1985) Mortality of aluminum reduction plant workers, 1950 through 1977. J Occup Med 21:761–770.[CrossRef]
22. Mur JM, Moulin JJ, Meyer-Bisch C, et al. (1987) Mortality of aluminum reduction plant workers in France. Int J Epidemiol 16:257–264.
23. Moulin JJ, Clavel T, Buclez B, Laffitte-Rigaud G. (2000) A mortality study among workers in a French aluminum reduction plant. Int Arch Occup Environ Health 73:323–330.[CrossRef][Web of Science][Medline]
24. Spinelli JJ, Band PR, Svirchev LM, Gallagher RP. (1991) Mortality and cancer incidence in aluminum reduction plant workers. J Occup Med 33:1150–1155.[CrossRef][Web of Science][Medline]
25. Carta P, Cocco PL, Fiore C, et al. (1992) Mortalità nei lavoratori della fonderia di alluminio primario di Portovesme in Sardegna. Med Lav 83:530–535.[Medline]
26. Carta P, Aru G, Cadeddu C, et al. (2004) Mortality for pancreatic cancer among aluminum smelter workers in Sardinia, Italy. G Ital Med Lav Ergon 26:83–89.[Medline]
27. Doll R, Vessey MP, Beasley RW, et al. (1972) Mortality of gas-workers—final report of a prospective study. Br J Ind Med 29:394–406.[Web of Science][Medline]
28. Manz A. (1980) Atem- und Harnwege als Lokalisationsstellen berufsbedingter (Teer-) Karzinome bei Kokerei- und Rohrnetzarbeitern. VDI-Berichte 358:227–235.
29. Hansen KS, Viskum S, Pedersen MS. (1986) Dødelighed blandt gasvaerksarbejdere. Ugeskr Laeger 148:610–612.[Medline]
30. Gustavsson P and Reuterwall C. (1990) Mortality and incidence of cancer among Swedish gas workers. Br J Ind Med 47:169–174.[Web of Science][Medline]
31. Berger J and Manz A. (1992) Cancer of the stomach and the colon-rectum among workers in a coke gas plant. Am J Ind Med 22:825–834.[Web of Science][Medline]
32. Reid DD and Buck C. (1956) Cancer in coking plant workers. Br J Ind Med 13:265–269.[Medline]
33. Sakabe H, Tsuchiya K, Takekura N, et al. (1975) Lung cancer among coke oven workers: a report to Labour Standard Bureau, Ministry of Labour, Japan. Ind Health 13:57–68.
34. Davies GM. (1977) A mortality study of coke oven workers in two south Wales integrated steelworks. Br J Ind Med 34:291–297.[Web of Science][Medline]
35. Hurley JF, Archibald RMcL, Collings PL, et al. (1983) The mortality of coke workers in Britain. Am J Ind Med 4:691–704.[Web of Science][Medline]
36. Wu W. (1988) Occupational cancer epidemiology in the People's Republic of China. J Occup Med 30:968–974.[CrossRef][Web of Science][Medline]
37. Swaen GMH, Slangen JJM, Volovics A, et al. (1991) Mortality of coke plant workers in the Netherlands. Br J Ind Med 48:130–135.[Web of Science][Medline]
38. Franco F, Chellini E, Seniori Costantini A, et al. (1993) Mortality in the coke oven plant of Carrara, Italy. Med Lav 84:443–447.[Medline]
39. Chau N, Bertrand JP, Mur JM, et al. (1993) Mortality in retired coke oven plant workers. Br J Ind Med 50:127–135.[Web of Science][Medline]
40. Costantino JP, Redmond CK, Bearden A. (1995) Occupationally related cancer risk among coke oven workers: 30 years of follow-up. J Occup Environ Med 37:597–604.[CrossRef][Web of Science][Medline]
41. Bye T, Romundstad PR, Ronneberg A, Hilt B. (1998) Health survey of former workers in a Norwegian coke plant: Part 2. Cancer incidence and cause specific mortality. Occup Environ Med 55:622–626.
42. Koskela RS, Hernberg S, Kärävä R, et al. (1976) A mortality study of foundry workers. Scand J Work Environ Health 2:73–89.
43. Gibson ES, Martin RH, Lockington JN. (1977) Lung cancer mortality in a steel foundry. J Occup Med 19:807–812.[CrossRef][Web of Science][Medline]
44. Breslin P. (1979) Mortality among foundry men in steel mills. In Lemen R and Dement JM (Eds.). Dusts and Disease(Pathotox Publishers, Park Forest South, IL) pp. 439–447.
45. Decouflé P and Wood DJ. (1979) Mortality patterns among workers in a gray iron foundry. Am J Epidemiol 109:667–675.
46. Andjelkovich DA, Mathew RM, Richardson RB, Levine RJ. (1990) Mortality of iron foundry workers: I. Overall findings. J Occup Med 32:529–540.[CrossRef][Web of Science][Medline]
47. Andjelkovich DA, Mathew RM, Yu RC, et al. (1992) Mortality of iron foundry workers: II. Analysis by work area. J Occup Med 34:391–401.[Web of Science][Medline]
48. Andjelkovich DA, Shy CM, Brown MH, et al. (1994) Mortality of iron foundry workers: III. Lung cancer case-control study. J Occup Med 36:1301–1309.[CrossRef][Web of Science][Medline]
49. Hansen ES. (1991) Cancer mortality among Danish molders. Am J Ind Med 20:401–409.[Web of Science][Medline]
50. Sherson D, Svane O, Lynge E. (1991) Cancer incidence among foundry workers in Denmark. Arch Environ Health 46:75–81.[Web of Science][Medline]
51. Rotimi C, Austin H, Delzell E, et al. (1993) Retrospective follow-up study of foundry and engine plant workers. Am J Ind Med 24:485–498.[Web of Science][Medline]
52. Sorahan T, Faux AM, Cooke MA. (1994) Mortality among a cohort of United Kingdom steel foundry workers with special reference to cancers of the stomach and lung, 1946 –90. Occup Enviran Med 51:316–322.
53. Moulin JJ, Clavel T, Roy D, et al. (2000) Risk of lung cancer in workers producing stainless steel and met allic alloys. Int Arch Occup Environ Health 73:171–180.[CrossRef][Web of Science][Medline]
54. Maclaren WM and Hurley JF. (1987) Mortality of tar distillation workers. Scand J Work Environ Health 13:404–411.[Web of Science][Medline]
55. Moulin JJ, Mur JM, WiId P, et al. (1988) Etude épidémiologique de mortalité parmi les salariés d'une usine de distillation des goudrons de houille. Rev Epidém Santé Publ 36:99–107.
56. Swaen GM and Slangen JM. (1997) Mortality in a group of tar distillery workers and roofers. Int Arch Occup Environ Health 70:133–137.[CrossRef][Web of Science][Medline]
57. Bogovski P. (1981) Historical perspectives of occupational cancer. In Vainio H, Sorsa M, Hemminki K (Eds.). Occupational Cancer and Carcinogenesis(Hemisphere, Washington DC) pp. 921–939.
58. Miller BG, Cowie HA, Middleton WG, Seaton A. (1986) Epidemiologic studies of Scottish oil shale workers: III. Causes of death. Am J Ind Med 9:433–446.[Web of Science][Medline]
59. Karlehagen S, Andersen A, Ohlson CG. (1992) Cancer incidence among creosote-exposed workers. Scand J Work Environ Health 18:26–29.[Web of Science][Medline]
60. Wong O and Harris F. (2005) Retrospective cohort mortality study and nested case-control study of workers exposed to creosote at 11 wood-treating plants in the United States. J Occup Environ Med 47:683–697.[CrossRef][Web of Science][Medline]
61. Hammond EC, Selikoff IJ, Lawther PL, Seidman H. (1976) Inhalation of benzpyrene and cancer in man. Ann NY Acad Sci 271:116–124.[Web of Science][Medline]
62. Hansen ES. (1989) Cancer incidence in an occupational cohort exposed to bitumen fumes. Scand J Work Environ Health 15:101–105.[Web of Science][Medline]
63. Boffetta P, Burstyn I, Partanen T, et al. (2003) Cancer mortality among European asphalt workers: an international epidemiological study. I. Results of the analysis based on job titles. Am J Ind Med 43:18–27.[CrossRef][Web of Science][Medline]
64. Boffetta P, Burstyn I, Partanen T, et al. (2003) Cancer mortality among European asphalt workers: an international epidemiological study. II. Exposure to bitumen fume and other agents. Am J Ind Med 43:28–39.[CrossRef][Web of Science][Medline]
65. Robertson JM and Inman KJ. (1996) Mortality in carbon black workers in the United States. J Occup Environ Med 38:569–570.[CrossRef][Web of Science][Medline]
66. Hodgson JT and Jones RD. (1985) A mortality study of carbon black workers employed at five United Kingdom factories between 1947 and 1980. Arch Environ Health 40:261–268.[Web of Science][Medline]
67. Sorahan T, Hamilton L, van Tongeren M, et al. (2001) A cohort mortality study of U.K. carbon black workers, 1951 –1996. Am J Ind Med 39:158–170.[CrossRef][Web of Science][Medline]
68. Teta MJ, Ott MG, Schnatter AR. (1987) Population based mortality surveillance in carbon products manufacturing plants. Br J Ind Med 44:344–350.[Web of Science][Medline]
69. Moulin JJ, Wild P, Mur JM, et al. (1989) Risk of lung, larynx, pharynx and buccal cavity cancers among carbon electrode manufacturing workers. Scand J Work Environ Health 5:30–37.[Medline]
70. Gustavsson P, Bellander T, Johansson L, Salmonsson S. (1995) Surveillance of mortality and cancer incidence among Swedish graphite electrode workers. Environ Res 70:7–10.[Medline]
71. Donato F, Monarca S, Marchionna G, et al. (2000) Mortality from cancer and chronic respiratory diseases among workers who manufacture carbon electrodes. Occup Environ Med 57:484–487.
72. Mori I. (2002) Cancer mortality among man-made graphite electrode manufacturing workers: results of a 38 year follow up. Occup Environ Med 59:473–480.
73. Merlo DF, Garattini S, Gelatti U, et al. (2004) A mortality cohort study among workers in a graphite electrode production plant in Italy. Occup Environ Med 61:e9.
74. Liu N, Wang Z, Dong D, et al. (1997) Cancer mortality among carbon workers in China: retrospective cohort study. J Occup Health 39:325–330.
75. Evanoff BA, Gustavsson P, Hogstedt C. (1993) Mortality and incidence of cancer in a cohort of Swedish chimney sweeps: an extended follow up study. Br J Ind Med 50:450–459.[Web of Science][Medline]
76. Hansen ES, Olsen JH, Tilt B. (1982) Cancer and non-cancer mortality of chimney sweeps in Copenhagen. Int J Epidemiol 11:356–361.
77. Hansen ES. (1983) Mortality from cancer and ischemic heart disease in Danish chimney sweeps: a five-year follow-up. Am J Epidemiol 117:160–164.
78. Letzel S, Weber A, Schaller KH, et al. (1992) Investigations on health hazards of chimney sweeps in Germany: results of a follow-up study. Int Arch Occup Environ Health 64:43–48.[CrossRef][Web of Science][Medline]
79. Tremblay C, Armstrong B, Theriault G, Brodeur J. (1995) Estimation of risk of developing bladder cancer among workers exposed to coal tar pitch volatiles in the primary aluminum industry. Am J Ind Med 27:335–348.[Web of Science][Medline]
80. Armstrong B, Hutchinson E, Unwin J, Fletcher T. (2004) Lung cancer risk after exposure to polycyclic aromatic hydrocarbons: a review and meta-analysis. Environ Health Perspect 112:970–978.[Web of Science][Medline]
81. Xu Z, Brown LM, Pan GW, et al. (1996) Cancer risks among iron and steel workers in Anshan, China, Part II: Case-control studies of lung and stomach cancer. Am J Ind Med 30:7–15.[CrossRef][Web of Science][Medline]
82. Baan R, Straif K, Grosse Y, et al. (2006) WHO International Agency for Research on Cancer Monograph Working Group. Carcinogenicity of carbon black, titanium dioxide, and talc. Lancet Oncol 7:295–296.[CrossRef][Web of Science][Medline]
83. La Vecchia C and Bosetti C. (2003) Cancer risk in carbon electrode workers: An overview of epidemiological evidence. Eur J Cancer Prev 12:431–434.[CrossRef][Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  W. B. GRANT Air Pollution in Relation to U.S. Cancer Mortality Rates: An Ecological Study; Likely Role of Carbonaceous Aerosols and Polycyclic Aromatic Hydrocarbons Anticancer Res, September 1, 2009; 29(9): 3537 - 3545. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M R Sim, A D. Monaco, J L Hoving, E MacFarlane, D McKenzie, G Benke, N de Klerk, and L Fritschi Mortality and cancer incidence in workers in two Australian prebake aluminium smelters Occup. Environ. Med., July 1, 2009; 66(7): 464 - 470. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. Kerr Editor-in- New wave Ann. Onc., January 1, 2008; 19(1): 3 - 4. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||