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Toxicology Reflections

Cardiovascular Disease in Humans as a Result of Exposure to Polycyclic Aromatic Hydrocarbons (PAHs): Is There a Risk?

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Author –

        Polycyclic aromatic hydrocarbons (PAHs) are organic compounds with two or more benzene rings (Meador 2010). This group includes about 100 compounds (Neff, 1979). However, thousands of variants are possible when other chemical groups are attached or when a carbon atom is replaced with nitrogen, sulfur or oxygen atoms (Pereira et al. 2009). PAHs are formed during the incomplete combustion of organic matter and fossil fuels (Environmental Canada 1994, Meador 2010).

Humans can be exposed to PAHs through different routes that include ingestion of contaminated food, dermal absorption (Suzuki and Yoshinaga 2007, Varlet et al. 2007, Li et al. 2008), and inhalation of contaminated particles (Environmental Canada 1994). Cigarette smoke has been shown to be an important source of exposure to PAHs in smokers. The concentration of benzo[a]pyrene can range from 0.5 to 7.8 µg/100 cigarette (Environmental Canada 1994). Traditionally, the major concern associated with PAH exposure to humans is carcinogenicity (Baars 2002, Laffon et al. 2006). However, adverse effects on human health can also include non-carcinogenic effects (Burstyn et al. 2005, Xu et al. 2010). In animals, it has been demonstrated that PAHs are able to alter endocrine function (Gentes et al. 2007), suppress the immune system (Trust et al. 1994, Kaminski et al. 2008), cause hemolytic anemia (Troisi et al. 2007), initiate the development of atherosclerotic plaque (Penn and Snyder 1988), elevate blood pressure (Sasser et al.1989), among other pathologies.

Evidence of cardiovascular disease has been documented in humans exposed to PAHs (Burstyn et al. 2005, Everett et al. 2010, Xu et al. 2010). In particular, elevated risk of cardiovascular disease has been demonstrated in occupational exposure to PAHs (revised by Burstyn et al. 2005), resulting in an increased risk of death from complications related to cardiovascular disease (Evanoff et al 1993).Studies investigating employees involved in asphalt paving demonstrated that exposure to benzo[a]pyrene and other PAHs is associated with fatal ischemic heart disease in an exposure-response relationship.The highest relative risk for fatal ischemic heart disease was observed with benzo[a]pyrene exposures of 273 ng/mor higher (Burstyn et al. 2005).

The biological mechanisms of cardiovascular disease associated to PAHs exposure are unclear. However, studies suggest that the mechanism involved in the pathogenesis and development of atherosclerotic plaques are similar or associated with the mechanisms involved in the carcinogenic and mutagenic properties of PAHs (Benditt and Benditt 1973, Albert et al. 1977,). It has been demonstrated that atherosclerotic plaques tend to be monoclonal, suggesting that mutation may be the mechanism for plaque development (Benditt and Benditt 1973). However, some uncertainties related to this possible mechanism remain, once it was verified that mosaic phenotypes in arteries as a consequence of injuries could also result in monoclonal atherosclerotic plaques, without involvement of somatic mutation by PAHs (Benditt and Benditt 1973, Murry et al. 1997).

Additionally, evidence suggests that oxidative stress could also result in the development of cardiovascular disease by causing inflammation, which has been recognized as an important factor in the development of atherosclerosis and cardiovascular disease (Kunzli and Tager 2005, Ridker 2009). Increased levels of inflammatory biomarkers are recognized as important predictors of cardiovascular disease, independent of smoking habits and previous incidence of cardiovascular disease (Danesh et al. 2000, Curb et al. 2003). More specifically, the C-reactive protein is the most studied of inflammatory biomarkers and its ability to predict cardiovascular disease has been confirmed. However, C-reactive protein levels are also associated with diabetes, hypertension, and obesity (Ridker, 2009). Everett et al. (2010) demonstrated that biomarkers of exposure to PAHs in humans were significantly associated with inflammatory biomarkers, indicating that oxidative stress resulting from exposure to PAHs could be a possible mechanism of cardiovascular disease in humans. The urinary PAH biomarker 2-hydroxyphenanthrene at concentration above 148 ng/g creatinine had an odds ratio of 3.17 for elevated cardiovascular disease when compared to urinary concentration below 48 ng/g creatinine. On the other hand, Clark III et al. (2012) did not observe a relationship between exposure to PAHs and biomarkers of cardiovascular disease, such as fibrinogen, homocysteine, and white blood cell count. Both papers analyzed a large scale population sample, and they also adjusted the models for age, race/ethnicity, body mass, and smoking habit. Everett et al. (2010) adjusted the models for presence of diabetes, blood pressure and physical activities. Variables such as age, body mass, smoking habits, blood pressure, etc. can increase the uncertainty of either the biomarker or the exposure to PAHs. This could directly influence the incidence of cardiovascular disease or result in a predisposition to cardiovascular disease unrelated to exposure to PAHs. The difference in results between these studies might be due to differences in the biomarkers that were chosen in each study.

In the United States it has been observed that urinary metabolites of PAHs were significantly associated with self-reported cardiovascular disease for two of the eight PAH metabolites studied (Xu et al. 2010). This research adjusted the results for potential confounding factors, which included demographic characteristics, smoking habit, alcohol consumption, blood pressure, plasma cholesterol, and high-density lipoprotein (HDL). However, diet, exercise activities, and genetic characteristics, which are known predisposing factors for cardiovascular disease were not included in the study. Another important limitation in this study was that the PAH metabolites analyzed were urinary monohydroxy because these metabolites reflect recent exposure to PAHs and might not be representative of chronic exposure scenarios that are of greatest interest. In addition, the urinary metabolites better represent PAHs congeners with 2-3 rings that are mainly excreted in the urine, while  that more potent PAHs with four or more rings are excreted primarily in feces and might not be accurately considered (Ramesh et al. 2004 cited by Everett al. 2010). Xu et al. (2010) observed that different exposure categories, such as age, had a significant effect on the estimated risk of exposure, however, cross-sectional assumptions for different exposure categories is very limited.

According to the class materials and the information provided above, cardiovascular disease resulting from exposure to PAHs should be considered a risk to human health. Exposure to PAHs has the probability to cause significant injury (cardiovascular disease as mentioned), as well as the potential severity can include death. It was stated in class that to be considered a risk, there must be an identified source of hazard, a receptor, and an exposure pathway. PAHs are widespread contaminants with environmental concentrations that are greater in industrialized centres with large population sizes (Environment Canada, 2007). Moreover, it has been observed by Everett et al. (2010) that 16.2% of the sampled US population showed elevated concentrations of PAH metabolites in urine, indicative of elevated levels of exposure to the population.

In conclusion, it has been demonstrated in numerous studies that there is a significant correlation between exposure to PAHs and incidence of cardiovascular disease in humans. However, there are still numerous deficiencies in our understanding of this disease that must be identified in order to accurately characterize and quantify the risk of exposure to PAHs in humans. There is currently limited information on the potential of PAHs to cause cardiovascular disease in low dose exposure. There is limited information on the association of background exposure to PAHs and cardiovascular disease. As mentioned in class, if the mechanism of cardiovascular disease development involves damage to the DNA, as a carcinogenic process, it could not be considered background, since any level of exposure could theoretically cause damage and result in disease. It is necessary to conduct additional studies to better understand the effects and risk of chronic exposure to PAHs in people, such as occupational exposure over a lifetime. Moreover, it would be of significant value to determine the potency of PAHs with a greater number of rings to cause incidence of cardiovascular disease. It would also be important to determine if an increased exposure to PAHs results in an increased risk of other inflammatory diseases and vice-versa.

REFERENCE

 

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  5. Clark III JD, Serdar B, Lee DJ, Arheart K, Wilkinson JD, Fleming LE (2012). Exposure to polycyclic aromatic hydrocarbons and serum inflammatory markers of cardiovascular disease. Environmental Research, 117:132–137
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  27. Varlet V, Serot T, Monteau F, Le Bizec B, Prost C (2007) Determination of PAH profiles by GC–MS/MS in salmon processed by four cold-smoking techniques. Food Additives and Contaminantes, 24:744–57.
  28. Xu X, Cook RL, Ilacqua VA, Kan H,Talbott EO, Kearney (2010). Studying associations between urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and cardiovascular diseases in the United States. Science of the Total Environment, 408:943–4948.
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10 thoughts on “Cardiovascular Disease in Humans as a Result of Exposure to Polycyclic Aromatic Hydrocarbons (PAHs): Is There a Risk?

  1. Another possible mechanism explaining PAH induced cardiovascular disease involves the aryl hydrocarbon receptor. There are studies that use aryl hydrocarbon receptor knockout mice to show its connection with cardiovascular development and blood pressure regulation (Zhang, 2011). Stimulation of this receptor may over-activate the renin-angiotensin system which would increase blood pressure and inflammation. Our lab is investigating this hypothesis using benzo[a]pyrene in rats.

    Zhang, N. (2011). The role of endogenous aryl hydrocarbon receptor signaling in cardiovascular physiology. J Cardiovasc Dis Res, 2(2), 91-95. doi: 10.4103/0975-3583.83033. http://www.sciencedirect.com/science/article/pii/S0975358311220023#

  2. Author –
    It is a very interesting point that you have addressed. I investigated your point in greater detail, and the role of the Aryl Hydrocarbon Receptor (AHR) in heart development and physiology remains contradictory. There is evidence that cardiovascular disease as result of exposure to PAHs might involve the AHR (reviewed by Zhang 2011). However, Incardona et al. (2004 and 2005) also demonstrated that PAHs cause early cardiac dysfunction during key stages of cardiac morphogenesis of fish through an AHR-independent pathway. Also in fish, Huang et al. (2012) showed that Benzo[a]Pyrene (BaP) was capable of inducing cardiovascular developmental defects in zebrafish and alter the expression of multiple genes which have a role in regulating cardiovascular development. They suggested that there is likely to be mechanisms of cardiac toxicity that result from PAH exposure which are not AHR-dependent. For example, they demonstrated that few genes that participate in cell death or survival decision were up-regulated by BaP. It appears that those few genes were comparatively less important than other genes which correlated with proper heart development and cardiotoxicity. However, this data analysis was established by computational analysis and employment of databases. Thus, the less importance attributed to the cell death and survival decision genes in this study might be due to the fact that little research has been done on these genes.

    References
    Huang L, Wang C, Zhang Y, Li J, Zhong Y, Zhou Y, Chen Y, Zuo Z (2012) Benzo[a]pyrene exposure influences the cardiac development and the expression of cardiovascular relative genes in zebrafish (Danio rerio) embryos. Chemosphere, 87: 369–375.

    Incardona JP, Collier TK, Scholz NL (2004) Defects in cardiac function precede morphological abnormalities in fish embryos exposed to polycyclic aromatic hydrocarbons. Toxicology and Applied Pharmacology, 196:191–205.

    Incardona JP, Carls MG, Teraoka H, Sloan CA, Collier TK, Scholz NL (2005) Aryl hydrocarbon receptor-independent toxicity of weathered crude oil during fish development. Environmental Health Perspective, 113:1755–1762.

    Zhang N (2011) The role of endogenous aryl hydrocarbon receptor signaling in cardiovascular physiology. Journal of Cardiovascular Disease Research, 2(2):91-95.

  3. The cardiovascular effects related to PAH exposure are quite interesting. However, I am curious whether there are studies that have investigated the effects of PAH exposure with both cardiovascular and carcinogenic endpoints occurring since carcinogenicity is the major concern. Is it possible to experience both cardiotoxicity and carcinogenic toxicity? There have been other compounds discussed (RE: Triclosan by Ryan) which exhibit multiple endpoints that may or may not be related. I think it might be a worthy investigation to determine if endpoints are determined more by the route of exposure, the variant of PAH, the target organs, or the concentration of PAH exposure.

  4. It would be interesting to compare the relative risk of cardiovascular and carcinogenic endpoints from PAH exposure. Which of these endpoints should drive the decision making process? Carcinogens, like PAHs, are considered to not have a threshold associated with the adverse effect. Therefore, would the exposure associated with an adverse cardiovascular effect be greater than the exposure associated with an acceptable increase in incidence of cancer?

  5. Author –
    I previously discussed the importance of biomarkers for assessing human exposure to PAHs. Today I will go into more detail about those biomarkers and how they can influence the uncertainty of the data.

    As discussed in class, to complete the risk assessment framework it is necessary to characterize the population exposure to a given chemical. Different approaches can be used to measure the exposure (Dor et al. 1999). It is possible to quantify the environmental concentrations of a chemical in contact with the body using, for example, portable sampling devices. Another way to measure the exposure is through quantifying the concentration of the chemical or its metabolites in the body tissues. These indicators are called biological markers and express the overall exposure, which considers all intakes independent of the route of exposure. They can be classified as biomarkers of exposure, effect or susceptibility and can be used to determine a relation between the environmental and body concentration (Dor et al. 1999).

    The widespread use of biomarkers is a consequence of their relative ease of assessment as they generally do not involve invasive techniques and can be used to detect exposure to low environmental concentrations. Effect biomarkers, for example, show the interaction between a given chemical and the body, which helps understand the physiological process that can result in disorder (Dor et al. 1999). As you can see in my first post, biomarkers have been used in different situations to assess PAH exposure. However, their uses are not limited to PAHs metabolites.

    The different characteristics of biomarkers should be checked before their use, such as significance, specificity, existence of a dose-response curve, sample constraints, conservation method, and possibility of controlling contamination (Dor et al. 1999). The choice of the biomarker can directly influence the experimental conclusion. Clark III et al. (2012) did not observe a relationship between exposure to PAHs and biomarkers of cardiovascular disease when using fibrinogen, homocysteine, and white blood cell count. However, Everett et al. (2010) demonstrated that biomarkers of exposure to PAHs were significantly associated with biomarkers of cardiovascular disease in humans (serum C-reactive protein).

    Once in the body, PAHs are oxidized by CYP P450 enzymes into epoxy and hydroxyl derivatives. Subsequently, the hydroxyl groups are conjugated with glucuronic acid or sulfate to be eliminated through urine or feces (Pelkonen and Nebert 1982). Xu et al. (2010) found that urinary monohydroxy can be a good biomarker for assessing human exposure to PAHs. From the eight metabolites studied (metabolites of naphthalene, fluorene, phenanthrene and pyrene) just two showed association with cardiovascular disease: 2-hydroxyphenantrene and 2-hydroxyfluorene. Based on the urine concentration of 2-hydroxyphenantrene they divided the subjects into three groups, and they observed that compared to the lowest tertile the middle and high tertiles had an odds rate of 1.29 and 1.45 of reported cardiovascular disease, respectively.

    Summarizing, biomarkers can be good tools to assess exposure to contaminants such as PAHs. However, there is a large variety of uncertainty related to their use that can include which biomarker is being used, the sampling method, storage techniques and duration, analysis technique, and sensibility. Concomitant diseases (e.g. hepatic disease) might play a role in the uncertainty of assessing biomarker, once these diseases might alter the physiological responses to the stressor. In the case of urinary monohydroxy; kidney disease and filtration rate should not be a considerable interference once the data is corrected for creatinine. Moreover, assumptions related to lifetime exposures should be considered very carefully as monohydroxy has a short half-life, for example the half-life of 1-hydroxypyrene has been reported to be between 4.4 and 35 h, and therefore 1-hydroxypyrene should only be used to assess recent exposure to PAHs (reviewed by Everett et al. 2010).

    References

    Clark III JD, Serdar B, Lee DJ, Arheart K, Wilkinson JD, Fleming LE (2012). Exposure to polycyclic aromatic hydrocarbons and serum inflammatory markers of cardiovascular disease. Environmental Research, 117:132–137

    Dor F, Dab W, Empereur-Bissonnet P,Zmirou D (1999) Validity of biomarkers in environmental health studies: The case of PAHs and Benzene. Critical Reviews in Toxicology, 29(2):129-168.

    Everett CJ, King DE, Player MS, Matheson EM, Post RE, Mainous III AG (2010). Association of urinary polycyclic aromatic hydrocarbons and serum C-reactive protein. Environmental Research, 110:79–82.

    Pelkonen O, Nebert DW (1982) Metabolism of polycyclic aromatic hydrocarbons: etiologic role in carcinogenesis. Pharmacological Reviews, 34:189–222.

    Xu X, Cook RL, Ilacqua VA, Kan H,Talbott EO, Kearney (2010). Studying associations between urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and cardiovascular diseases in the United States. Science of the Total Environment, 408:943–4948.

  6. I thought that the use of biomarkers to identify sources of exposure was interesting. I found a paper http://pubs.acs.org/doi/abs/10.1021/tx300043k which attempting to identify a single pathway of exposure, in this case cigarette smoking. This got me thinking about exposure pathways for PAHs and how they related for risk. Specifically how does the exposure risk for cardiovascular disease compare to the risk to their carcinogenic risks.

  7. Author –
    This week I will discuss with more detail the human exposure to Polycyclic Aromatic Hydrocarbon (PAHs). As discussed in class, to complete the risk assessment framework it is necessary to characterize the population exposure to a given chemical. There are different routes that which humans can be exposed to PAHs, including ingestion of contaminated food, dermal absorption (Suzuki and Yoshinaga 2007, Varlet et al. 2007, Li et al. 2008), and inhalation of contaminated particles (Environmental Canada 1994). Cigarette smoke has been shown to be an important source of exposure to PAHs in smokers. However, in a non-smoker or non-occupational exposed population, the dietary intake is the main route of exposure. Food may be contaminated through particulate deposition or accumulation (e.g. bivalve mollusks) (Falco et al. 2003).

    Falco et al. (2003)estimated the daily intake of carcinogenic PAHs in different categories of food for children, teenagers, male adults, female adults, and seniors in Catalonia (Spain). Cereals and meat presented the highest levels of total PAHs, 14.5 mg/kg and 13.4 mg/kg respectively. The mean estimated dietary intake of total PAHs for adult male was 8.4 mg/day, followed by adolescents (8.2 mg/day), children (7.4 mg/day), seniors (6.3 mg/day), and female adults (6.3 mg/day). Despite dietary intake might contribute to approximately 70% of the exposure to PAH, to calculate the total daily intake other sources of exposure should be considered, such as inhalation. PAHs emission rate from sources like heavy-duty diesel automobiles can achieve 1000 μg/kg. Automotor vehicles directly contribute to PAH emission through combustion of fuel. Additional emission of PAHs due to abrasion of rubber tires, asphalt road surfaces, and brake linings are also pointed as remarkable source the compounds. However, the quantification of this contribution involves lots of uncertainty related to tires composition, brand and year of fabrication (Ravindra et al. 2008). The risk associated with human exposure to atmospheric PAHs is highest in cities, due the density of population, increasing vehicular traffic, and scarce dispersion of the atmospheric pollutants ( (Environment Canada, 2007). Domestic emissions are also an important source of PAH. It is strongly associated with the burning activity, such as coal, oil, gas and garbage. Authors reported emission factors of 5.3-13.2 mg/kg of BaP in inhaled particles of wood combustion (Ravindra et al. 2008).A study performed in Minnesota, USA, BaP was found in 19% of the household dust sample (reviewed by US EPA 2006).
    As demonstrated above, human PAH exposure varies with different activities and behaviour, type of food ingested, and habitat. On my future posts, I want to discuss in more details the infant and children exposure. It is a very interesting scenario, mostly when it comes to carcinogenic compounds that accumulate throughout life.

    Reference
    Suzuki K, Yoshinaga J (2007) Inhalation and dietary exposure to polycyclic aromatic hydrocarbons and urinary 1-hydroxypyrene in non-smoking university students. International Archives of Occupational Environmental Health, 81:115–21.
    Varlet V, Serot T, Monteau F, Le Bizec B, Prost C (2007) Determination of PAH profiles by GC–MS/MS in salmon processed by four cold-smoking techniques. Food Additives and Contaminantes, 24:744–57.

    Li et al., 2008 Li Z, Sandau CD, Romanoff LC, Caudill SP, Sjodin A, Needham LL (2008) Concentration and profile of 22 urinary polycyclic aromatic hydrocarbon metabolites in the US population. Environ Research, 107:320–31.

    Falco et al. Polycyclic Aromatic Hydrocarbons in Foods: Human Exposure through the Diet in Catalonia, Spain. Journal of Food Protection, Vol. 66, No. 12, 2003, Pages 2325–2331

    Ravindra et al. Atmospheric polycyclic aromatic hydrocarbons: Source attribution, emission factors and regulation. Atmospheric Environment, Volume 42, Issue 13, April 2008, Pages 2895–2921

    Environment Canada (1994) Canadian environmental protect act – Priority substances list assessment report: Polycyclic aromatic hydrocarbons. In: Services MoSa (ed), Ottawa, Ontario

  8. Great outline on the estimated daily intake for PAHs. When I think of PAHs I think of BBQ’d food and construction work (specifically road pavers). Every time you drive by a crew paving a road you just want to hold your breath or turn on your in-car circulation system to prevent the stench of the fresh asphalt from permeating your air space. This basically led me to check out the occupational exposure of construction workers, specifically for asphalt pavers.

    An article found that the dose (measured in the urine) of PAHs in paving workers was significantly higher than the dose measured in millers1. Millers are the workers who break up the old asphalt in preparation for pavers1. Additionally, it found that after the weekend upon their return to work and prior to starting work both the pavers and millers had similar doses1. Interestingly, enough the report also found dermal exposure to contribute more to the urinary concentrations of PAHs than inhalation1. I was wondering if you know any information on occupational exposure and how their exposure may differ from the average person. Also, are their higher TDIs for occupational workers in that industry considering that it is likely that their exposure is higher?

    1. McClean M.D., Rinehart R.D., NGO L., Eisen E.A., Kelsey K.T., Wiencke J.K., Herrick R.F. (2004). Urinary 1-Hydroxyopyrene and Polycyclic Aromatic Hydrocarbon Exposure Among Asphalt Paving Workers. Ann. Occup. Hyg. 48: 565 – 578

  9. I feel the same way when I smell that tar/new pavement smell! I do find it really interesting that there are differences in urine concentrations of PAH between paving workers and millers. Do you guys think it has something to do with the weathering, aging, or processing of old asphalt that results in lower exposure for Millers? A report by ATSDR (1995) suggests difference in PAH exposure and effects between coke oven workers and cold-rolling mill workers was exposure to higher levels of sulfur dioxide and carbon monoxide. Thus, it may be that the additional exposure to coke over workers increased the effects of PAH exposure. However, one of the uncertainties noted in the ATSDR report is that smoking habits of subjects was not included as a potential contributor.

    Overall, this is a very interesting and complex topic Carla! I think you have done a great job at tackling this and helping to explain some of the uncertainties and considerations that may need to be included in decision-making!

    Reference:

    [ATSDR] Agency for Toxic Substances and Disease Registry. 1995. Toxicological profile for polycyclic aromatic hydrocarbons. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service. http://www.atsdr.cdc.gov/toxprofiles/tp69.pdf

  10. Author –
    As I mentioned on my previous posts, cardiovascular disease has been documented in humans exposed to PAHs (Burstyn et al. 2005, Everett et al. 2010), in particular, elevated risk of cardiovascular disease has been demonstrated in occupational exposure to PAHs (revised by Burstyn et al. 2005). In this study, the authors adjusted the relative risk accounting to possible sources of uncertainty, e.g. tobacco smoking, once it contributes to mortality from ischemic heart disease. Addressing the issue brought for Breda, when the asphalt paving workers are compared to the general population, the mortality risk from cardiovascular diseases is higher, as result of the occupational exposure; representing an odds ratio of 1.5 (reviewed by Burstyn et al. 2005). The highest relative risk of fatal heart ischemic disease was observed with benzo[a]pyrene exposures of 273 ng/m3 or higher. However, the endpoint of most concern in PAH exposure are the carcinogenic effects. Thus, no threshold should be assumed since any exposure could potentially cause disease.

    In addition to the cardiovascular effects, carcinogenic effects were assessed on the same group of workers analyzed by Burstyn et al. (2005). They did not find indication of association between exposure to PAH and cancers. Burstyn et al. (2007) investigated the association between exposure to PAH during asphalt paving and risk of bladder cancer. They observed an indication of exposure‐response association with lagged averaged exposure, however they were unable to control for all possible sources of uncertainty. Contradictory, other studies have described a risk of cancer among asphalt-exposed workers (Boffetta et al. 1997, Okona-Mensah et al. 2005). It was also demonstrated that a dermatotoxic risk associated with chronic PAHs exposure exists (Eshak et al. 2012).

    I hope I have answered all the questions and concerns addressed.

    Burstyn I, Kromhout H, Partanen T, Svene O, Langard S, Ahrens W, Kauppinen T, Stucker I, Shaham J, Heederik D,Ferro G, Heikkila P, Hooiveld M, Johansen C, Radem BG, Boffetta P (2005). Polycyclic Aromatic Hydrocarbons and Fatal Ischemic Heart Disease. Epidemiology, 16 (6):744-750
    Evanoff BA, Gustavsson P, Hogstedt C (1993) Mortality and incidence of cancer in a cohort of Swedish chimney sweeps: an extended follow up study. British Journal of Industry Medicine 50:450-459
    Bursty et al. Bladder cancer incidence and exposure to polycyclic aromatic hydrocarbons among asphalt pavers. Occup Environ Med. 2007; 64(8): 520–526.
    Boffetta et al. Cancer risk from occupational and environmental exposure to polycyclic aromatic hydrocarbons. Cancer Causes & Control, 8(3):444-472, 1997.
    Okona-Mensah et al. An approach to investigating the importance of high potency polycyclic aromatic hydrocarbons (PAHs) in the induction of lung cancer by air pollution. Food and Chemical Toxicology 43 (7):1103–1116, 2005.
    Eshak et al. Polycyclic Aromatic Hydrocarbons: Role of Apoptosis in Dermatotoxic and Carcinogenic Effect in Asphalt Road Paving Workers. J Clinic Toxicol 2012, 2:5.
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