Determination of biological exposure limit of damage in red blood cells caused by exposure to polycyclic aromatic hydrocarbons using benchmark dose method in general population
10.3969/j.issn.1006-2483.2023.02.004
- VernacularTitle:多环芳烃暴露致红细胞损伤生物暴露限值基准剂量分析
- Author:
Qingqing WANG
1
;
Jing CUI
1
;
Wenjie PENG
1
;
Ting ZHANG
2
,
3
;
Miao YUAN
1
;
Lin PANG
1
;
Xiaolin ZHOU
2
,
3
;
Hongmei YU
1
,
4
Author Information
1. Department of Health Statistics, School of Public Health, Shanxi Medical University, Taiyuan , Shanxi 030001, China
2. China Institute for Radiation Protection, Taiyuan , Shanxi 030006 , China
3. State Environmental Protection Key Laboratory of Radiation Environment and Health, Taiyuan , Shanxi 030006 , China
4. Shanxi Provincial Key Laboratory of Major Diseases Risk Assessment , Taiyuan , Shanxi 030001, China
- Publication Type:Journal Article
- Keywords:
Polycyclic aromatic hydrocarbon;
Chronical exposure;
Hematological damage;
Benchmark dose;
Biological exposure limitation
- From:
Journal of Public Health and Preventive Medicine
2023;34(2):16-20
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the biological exposure limit of blood system damage caused by long-term exposure to polycyclic aromatic hydrocarbons (PAHs) in non-occupational population by using the benchmark dose method, and to provide relevant reference for further improving the assessment of PAHs-induced health damage effects. Methods Adult residents living in downwind direction of a coke-oven plant in Shanxi Province were selected as the research subjects, and the information collected from baseline was used as the control. The metabolites of PAHs in urine were used as exposure biomarker, and the abnormal rate of red blood cell index was used as response biomarker. The relationship between urinary OH-PAHs and the erythrocyte damage rate was analyzed, and the benchmark dose (BMD) and the lower confidence limitation for the benchmark dose (BMDL) were calculated using Bayesian dose-optimizing software. Results The urinary PAH metabolites were mainly naphthalene and fluorene. The detection concentrations of 2-OHFlu and 1-OHPhe in the final year were higher than those in the baseline (P<0.05). With the increase of exposure years, the abnormal rate of red blood cells in the final year was higher than that in the baseline (P<0.05). In addition, the abnormal rate of red blood cells increased with the increase of the concentrations of five metabolites of PAHs in urine, and the chi-square trend test was significant (P<0.05). The benchmark dose (BMD) of OH-PAHs was 0.67 μmol/mol Cr, 0.82 μmol/mol Cr, 1.40 μmol/mol Cr and 0.78 μmol/mol Cr, respectively. The BMD of 2-OHNap in people with barbecue diet habits was 0.23 μmol/mol Cr. The BMD of 2-OHNap in people without barbecue diet habits was 1.44 μmol/mol Cr. Conclusion There is a dose-response relationship between the concentration of PAHs metabolites in urine and the damage of red blood cells. Long-term exposure to PAHs can lead to hematological damage. It is suggested that targeted public health interventions should be formulated to reduce the exposure of the general population to PAHs.
