**4. Discussion**

When the responses to the administered questionnaires were reviewed, a significantly higher number of health illnesses were identified among asphalt workers, particularly respiratory diseases. They were identified in both smokers and non-smokers and therefore, they are likely attributed to exposure to bitumen fumes, where inhalation is the primary modality through which asphalt workers were exposed to it. Prior studies such as conducted by (Gamble et al.,1999) [22] align with our observation and indicate significant positive relationship between exposure to bitumen fumes and respiratory diseases.

It was also noted that mechanics that work in asphalt plants are at higher risk to develop respiratory disease [22], which could be attributed to the impact of PAHs they were exposed.

In our study, we noted changes in some of the hematological parameters such as increase in the number of lymphocytes, which aligns with the study published by (Tompa et al) [23] where may attributed this increase to the harmful effects of PAHs.

In addition, the subjects in our study group had significantly higher HCT and MCHC levels compared to the control group, which is likely due to exposure to PAHs. These findings are in alignment with the study conducted by (Wang et al) [24] which showed significantly higher hemoglobin levels with some atypical appearance of the red blood cells, which were attributed to exposure to PAHs.

We also noted higher hemoglobin levels among smokers in both groups, which is a compensatory mechanism that occurs due to decrease in the oxygen level and increase carbon monoxide levels due to smoking [25–27].

We also noted significantly higher AST level between the study and control groups, in contrast to the findings of (Atasoy et al) [28]. The contradictory observations between these two studies could be explained by difference in the type of asphalt used, or the method of use and the extend and level of exposure to PAHs.

In our study, we noted relationship between exposure to PAHs by inhaling bitumen fumes from working closely with asphalt and detection of BPDE-DNA adducts (P = 0.001). On the other hand, (Pavanello et al). demonstrated significant relationship between chronic inhalation of high levels of PAHs and detection of BPDE-DNA adducts [29].

Interestingly, although smoking has somewhat similar effect on DNA as exposure to B[a]P, this study showed no correlation between smoking and the levels of BPDE-DNA adducts (p = 0.43). These findings are in agreement with those of (Pavanello et al) [29] and (van Schooten et al) [30]. However, other studies found significant correlation between the levels of BPDE-DNA adducts and smoking in subjects with occupational exposure PAHs where exposure to tobacco products and PAHs acted synergistically to form BPDE-DNA adducts as reported by (Rojas et al) [31]. These discrepancy between these findings could be explained by interindividual factor variability and route of exposure to PAHs which can play a major role in formation of BPDE-DNA adducts.

Statistically, there was no significant difference in the adducts concentrations between the younger and older age groups (χ2 test, p = 0.18). On the other hand, age did not significantly correlate with the presence of BPDE-DNA adducts among subjects in the study group (p = 0.18). These results are in agreement of those reported by (McClean et al) [32]. and is likely due to the similar metabolic and excretion ability in both age groups.

Given the known carcinogenic effect of B[a]P [8], the presence of BPDE-DNA adducts when measured in the WBC using ELISA technique correlates of the risk of development of B[a]P-induced diseases such as lung cancer [33]. Therefore,

**83**

**Author details**

Razan Zohairee

Damascus, Syria

Department of Toxicology and Pharmacology, Damascus Univresity,

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*Address all correspondence to: rita.joo@hotmail.com

provided the original work is properly cited.

*Detection of Benzo[a]Pyrene Diol Epoxide-DNA Adducts in White Blood Cells of Asphalt Plant…*

Our results suggests that importance of measurement of BPDE-DNA adducts and its role as potential biomarker for exposure to PAHs. As it involves the DNA, it could be a surrogate marker to assess the risk for development of cancer [35, 36].

AST levels and some vital blood parameters can be considered warning indicators for rapid diagnosis of exposure for the asphalt workers. Our results highlight that importance of measurement of BPDE-DNA adducts and its role as potential biomarker for exposure to PAHs and being considered a biomarker for unrepaired

As it involves the DNA, it could be a surrogate marker to assess the risk for

Prof. Marouf Alkayer, Professor of Analytical Chemistry at Faculty of Pharmacy

BPDE-DNA adducts can serve as a useful biomarker to assess prior exposure to

*DOI: http://dx.doi.org/10.5772/intechopen.96437*

**5. Conclusions**

DNA damage.

development of cancer.

**Acknowledgements**

**Conflict of interest**

at Tishreen University in Syria.

The authors declare no conflict of interest.

PAHs and could potentially determine cancer risk [34].

*Detection of Benzo[a]Pyrene Diol Epoxide-DNA Adducts in White Blood Cells of Asphalt Plant… DOI: http://dx.doi.org/10.5772/intechopen.96437*

BPDE-DNA adducts can serve as a useful biomarker to assess prior exposure to PAHs and could potentially determine cancer risk [34].

Our results suggests that importance of measurement of BPDE-DNA adducts and its role as potential biomarker for exposure to PAHs. As it involves the DNA, it could be a surrogate marker to assess the risk for development of cancer [35, 36].
