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To investigate the link between the risk of bladder cancer and exposure to polycyclic aromatic hydrocarbons (PAH), which are produced during asphalt paving.
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In this article, we are going to have a discussion on the importance of research on bladder cancer and how it’s relevant to asphalt.
Between 1913 and 1999, 7298 men from the historical cohort began working for asphalt-spreading companies in Denmark, Norway, Finland, and Israel.
The bare minimum for inclusion in the cohort was two seasons of work. Personnel files were used to compile the histories of various occupations. A cancer incidence study was conducted using national cancer registries.
The authors calculated benzo(a)pyrene exposures as a marker for 4-6 ring PAHs.
Exposures were reconstructed using data on the evolution of asphalt paving technology used by each company over time, the modeled relationship between production characteristics and exposure levels, and job histories.
The relative risks and 95% confidence intervals were calculated using Poisson regression.
39 of the 48 bladder cancers discovered in asphalt paving workers were exposed for at least 15 years prior to diagnosis. The incidence of bladder cancer was not linked to cumulative PAH exposure.
With a 15-year lag, the association with average exposure became stronger, revealing a twofold increase in relative bladder cancer risk in the two higher exposure categories. There was evidence of an association between exposure and response with lagged averaged exposure.
Risk estimates remained essentially unchanged after being adjusted for age, country, length of employment, and calendar period when re-estimated after excluding non-primary cancers from follow-up.
An earlier sensitivity analysis indicates that the observed exposure-response trends are unlikely to be explained by cigarette smoking confounding.
The authors were unable to account for every possible confounding factor and bias. The findings make it impossible to conclude whether or not PAH exposure and bladder cancer risk among asphalt workers are causally related.
With 273 000 new cases and over 108 000 deaths estimated in 2002. Bladder cancer is now the seventh most common cancer in the world. In developed countries, smoking is the leading risk factor, accounting for approximately 65% of male and 30% of female cases.
Workplace exposure to polycyclic aromatic hydrocarbons (PAH), polychlorinated biphenyls, aromatic amines, formaldehyde, asbestos, and solvents has all been linked to an increased risk of bladder cancer.
It is unclear, however, whether lower PAH exposures (measured in ng/m3 of air), such as those found in the asphalt industry, are also linked to risk.
A recent meta-analysis of 11 case-control studies conducted in six European countries from 1976 to 1996, which included 3346 incident bladder cancer cases and 6840 controls.
discovered that occupational exposure to PAHs increased bladder cancer risk in men by 23% (odds ratio (OR) for highest exposure tertile 1.23, 95% confidence interval (CI) 1.07 to 1.4).5 Men are thought to be 4.3% more likely than women to develop bladder cancer.
asphalt parking lot
The International Agency for Research on Cancer initially assembled the cohort of European asphalt workers to study the risk of lung cancer from bitumen fume exposure.
However, it has evolved into a very rich resource for studying both narrow (such as cancer and bitumen) and broad aetiological questions over time (PAH and lung cancer, cardiorespiratory diseases).
The main findings of the cohort study include increased lung cancer mortality with increasing bitumen fume exposure among asphalt pavers (a subcohort for which the best exposure estimates were available).
positive associations of PAH exposure among asphalt pavers with the risk of death from obstructive lung disease, and ischaemic heart disease, a lack of increased risk for fatal occupational injuries among asphalt workers in the cohort, and an increase in lung cancer mortality with increasing bitumen fume exposure.
We discovered a roughly 2-fold increase in the risk of bladder cancer incidence among asphalt pavers in the highest and lowest PAH exposure groups after allowing for a 15-year lag.
This suggests that exposure to PAH in the asphalt industry may result in bladder cancer. The strength of the association increased after accounting for a latency period, which is consistent with the aetiology of bladder cancer.
This association could be due to the cohort's exposure to causal agents, biases in exposure assessment, confounding by occupational exposures and lifestyle factors, or simply by chance.
Epidemiological studies in other PAH-exposed occupations support our findings. In cohort studies of aluminum smelter workers in Norway and Canada, a significant excess in bladder cancer incidence was found, and this excess incidence increased with cumulative exposure.
The association is typically stronger when the latency is taken into account when constructing an exposure index.
A Canadian case-control study nested in a cohort of aluminum production workers found that cumulative exposure to benzo(a)pyrene lagged by 10 years was the best predisposition factor.
Workers in the aluminum smelting industry had a higher risk of bladder cancer when exposed for more than 10 years (OR 5.9, 95% CI 1.0 to 7.32) and when exposed to "tar asphalt" (OR 3.1, 95% CI 1.2 to 9.7 in lagged analysis), according to a population-based case-control study from Canada.
In France, a hospital-based case-control study with 658 male cases revealed an elevated risk (OR 1.3, 95% CI 1.2 to 9.7) for PAH exposure (adjusted for smoking, coffee consumption, and occupational exposure to aromatic amines) and a significant trend for a dose-response relation.
As a result, our findings may have significant implications for determining the risk of bladder cancer due to air pollution in general.
It should be noted that exposures to PAH in ng/m3 are quite common in urban areas that are polluted by vehicle traffic. This generalizability, however, is compromised by the likelihood that asphalt pavers' dermal route of exposure.
asphalt pavement
We focused on airborne exposures because we lacked estimates of dermal PAH exposure. If exposure from the two routes had a strong correlation, the risk attributed to the airborne route would be exaggerated (though not the risk due to PAH dose).
If exposures from the two routes are not correlated, our airborne exposure may be weakly related to the true dose of PAH, resulting in an attenuation of the risk attributable to airborne exposures.
Because we lacked complete occupational histories, it is possible that some cohort members were occupationally exposed to elements outside of the asphalt industry (such as PAH released during aluminum smelting) that contributed to the development of bladder cancer in the studied population.
If these exposures were linked to exposures acquired while working in the asphalt industry, our estimates of the risk attributable to PAHs could be skewed.
This problem can only be solved by collecting complete occupational histories, including details on jobs outside the paving industry, in a nested case-referent design.
Such data were available for the Danish subcohort, whose pension fund kept track of each member's entire career path. An examination of this group of workers reveals no increase in the prevalence of employment in PAH-exposed professions outside the asphalt sector.
Individual smoking habits and other lifestyle factors (such as diet and exercise) that may have increased the risk of bladder cancer are not well documented.
As a result, these confounding factors cannot be completely eliminated. We specifically demonstrated that average PAH exposure had increased in the past4 and that cigarette smoking was more prevalent.
When a strong effect of smoking is assumed, previous sensitivity analyses, show that differences in cigarette smoking are extremely unlikely to account for even modest exposure-response gradients (RR1.6 in the highest exposure group) seen in this cohort (RR 3–5 for smokers vs never smokers).
Confounding by smoking and other lifestyle factors does not typically result in false-positive results in industry-based studies.
Longer latency periods would have addressed the issue of the biological plausibility of our findings to a greater extent, but such analyses in this relatively young cohort would have been futile because there aren't enough cases in exposed rubrics to account for lags of the order of 30 years.
Exposure may have been classified incorrectly during the exposure assessment. For example, we assumed that benzo(a)pyrene exposures were the same for all coal tar-containing products.
According to an analysis of measurements taken in the French asphalt industry, this assumption is incorrect, but we were unable to find more specific information about the cohort's prior coal tar use.
asphalt paver
The assessment of exposure to diesel exhaust, a source of PAH exposure, was too uncertain to draw valid conclusions.
Furthermore, because the pavers in the study were all exposed to diesel exhaust from passing vehicles or diesel-powered paving equipment, there was little variation in the exposure estimates.
Furthermore, we were unable to fully validate the data collected via company questionnaires, raising the possibility that not all cohort members were correctly classified in terms of the exposure determinants used in the quantitative assessment of benzo(a)pyrene exposure.
The occupational histories of the cohort members may have been extracted incorrectly, resulting in biases of unknown magnitude and direction.
We attempted to address this issue by including in the current analyses only subjects who worked exclusively in paving, one of the study's most easily identifiable groups, and by selecting companies for the study that had precise personnel records36.
Those who changed jobs, on the other hand, were excluded due to this restriction and may have moved on to more or less exposed jobs, though reliable data on this is lacking.
This study's limitation makes predicting the degree of bias impossible, but the results should still be internally consistent for the chosen group.
This precludes a causal interpretation of our findings, but it is worth noting that neither the cumulative nor average exposure index is an ideal proxy for a biologically effective dose.
Instead, we found associations only with average, not cumulative, exposure indices, which is consistent with the findings of the cohort's lung cancer mortality study.
Positive results with average exposure may be explained by the possibility that average exposures were assessed with greater certainty than cumulative exposure: unlike most industries, asphalt paving makes estimating the duration of employment difficult because it is influenced by weather in a given month and year (for example, paving season ends with the first frost).
While the actual estimation of average exposure required several assumptions that could not be verified, the exposure intensity models that drive average exposure estimates were thought to be reasonably valid and precise for the purposes of this epidemiological study.
Exposures were assessed without regard for a cohort member's health. As a result, we expect exposure misclassification to be non-differential, resulting in attenuated risk estimates (at least in the highest exposure categories), rather than positively biased risk estimates.
We observed a decline in relative risk in the highest, compared to the second-highest, average exposure categories, which is consistent with such a measurement error effect. However, such effects depend on the disease model used and are small, making it unreliable.
Coal tar in asphalt was a significant source of PAH exposure for the cohort in the past; however, the asphalt industry in the countries under study has voluntarily stopped using coal tar. Because of the long latency, the positive impact of this policy on health may not be obvious.
However, even in the absence of coal tar in the asphalt, some asphalt paving processes (such as indoor mastic paving and hot repaving) generate high PAH exposures.4,14 As a result, caution is required to ensure that PAH exposure in the industry remains as low as possible.
Bladder Cancer
We don't know if the secondary bladder cancers were metastatic, de novo (caused by primary cancer treatment), or de novo (caused by PAH exposure). People who survive primary tumors may be more likely to develop secondary tumors as a result of cancer treatment.
There would be a negative relationship between PAH exposure and cancer treatment, potentially leading to confounding by prior cancer treatment if diagnosis and treatment resulted in the termination of employment in asphalt paving.
Given that the time elapsed between the primary tumor and secondary bladder cancer appeared to be in the range of 1-4 years, this is unlikely to have an effect on analyses where exposure was delayed by 15 years.
Even if there is no link between PAH exposure and cancer treatment, prior PAH exposure, and cancer treatment may increase the risk of bladder (secondary) cancer and alter the effect of PAH in people who already have secondary bladder cancer.
If PAH exposure was the root cause of both the primary and secondary tumors, bladder cancer "adjustment" would be inappropriate once the primary tumor was identified.
We would want to rule out bladder cancers that had already spread because the primary research question is whether PAH exposure causes de novo bladder cancers.
If secondary bladder tumors develop as a result of a shared susceptibility with the primary tumor, the underlying susceptibility (genetic, metabolic, or lifestyle) acts as an effect modifier, amplifying the impact of PAH exposure on the risk of bladder cancer through treatment or the primary tumor.
Finally, if a primary tumor is rapidly fatal and conceals a diagnosis of bladder cancer that would have been detected otherwise, underestimating the risk associated with occupational exposure to PAH, a primary tumor unrelated to occupational exposure to PAH may be a competing cause with a secondary tumor.
We investigated the extent to which these mechanisms may have influenced our findings by limiting the population at risk to those with no history of cancer.
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The main reason why the population at risk selection had no effect on the overall findings is most likely due to the small number of non-primary bladder cancers in our study.
One of the study's strengths is that bladder cancer diagnoses were based on histological examinations, which greatly reduced the possibility of outcome misclassification.
Instead of relying solely on mortality statistics, the use of data from countries with excellent cancer incidence data increased the likelihood that bladder cancer was correctly identified.
However, we were unable to account for every possible confounding factor and bias. The findings prevent us from concluding whether PAH exposure and bladder cancer risk among asphalt workers are causally related or not.
The main points
Asphalt paving workers may be at a higher risk of developing bladder cancer.
Polycyclic aromatic hydrocarbons (PAH) exposure may increase the risk of developing bladder cancer at relatively "low" levels of airborne exposure.
The results are difficult to interpret due to their borderline statistical significance, our inability to account for all potential sources of bias and confounding, and the lack of a monotonic exposure-response relationship.
The primary goal of new studies with a specific design should be to characterize the bladder cancer risk of PAH at exposure levels typical of polluted urban environments and "low-exposed" occupational settings.
Making policy recommendations to reduce the risk of bladder cancer from PAH exposure necessitates an accurate quantitative exposure assessment that considers all routes of exposure.
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