焦炉工人血浆BPDE-白蛋白加合物与外周血淋巴细胞DNA损伤水平的相关关系

目的探讨焦炉工人早期生物效应标志物DNA损伤与生物有效剂量标志物苯并(a)芘二氢二醇环氧化物(BPDE)-白蛋白加合物之间的关系。方法选取某焦化厂207名焦炉工人作为接触组,102名非焦炉作业人员为对照组,采用反相高效液相色谱法测定血浆中BPDE-白蛋白加合物浓度,采用彗星实验测定外周血淋巴细胞DNA损伤水平。结果焦炉工人的血浆BPDE-白蛋白加合物浓度和外周血DNA损伤水平明显高于对照组(P<0.01)。使用多元logistic回归分析校正了个体的工龄、吸烟和饮酒状况后,焦炉工人BPDE-白蛋白加合物浓度增高的危险度是对照组的1.72倍(P<0.05),焦炉工人DNA损伤水平增高的危险度是对照组的1.96倍(P<0.05)。BPDE-白蛋白加合物与DNA损伤水平在焦炉工人中存在明显的正相关关系(Spearman偏相关系数=0.235,P<0.01),但在对照组中不存在相关关系(Spearman偏相关系数=0.093,P>0.05)。结论焦炉工人生物有效剂量标志物BPDE-白蛋白加合物和早期生物效应标志物DNA损伤之间存在明显相关。     

焦炉工人血浆BPDE-白蛋白加合物与尿中1-羟基芘浓度的关系

[目的]探讨血浆中苯并(a)芘二氢二醇环氧化物(BPDE)-白蛋白加合物作为焦炉工人多环芳烃长期暴露的生物标志物的可行性及其与尿中1-羟基芘(1-OHP)浓度之间的关系.[方法]采用反相高效液相色谱方法,对焦化厂37名焦炉作业工人(接触组)和47名非焦炉作业人员(对照组)血浆中BPDE-白蛋白加合物和尿中1-羟基芘浓度分别进行测定.[结果]接触组血浆中BPDE-白蛋白加合物和尿中1-羟基芘浓度的中位数分别为42.10fmol/mg白蛋白和5.46 μmol/mol肌酐,均显著高于对照组(14.16fmol/mg白蛋白,2.96 μmol/mol 肌酐,P＜0.01).校正了个体的年龄、吸烟和饮酒状况后,接触组BPDE-白蛋白加合物浓度增高的危险度是对照组的1.79倍(P＜0.05).接触组1-羟基芘浓度增高的危险度是对照组的2.45倍(P＜0.05).并且在所有研究对象中,BPDE-白蛋白加合物与尿中1-羟基芘浓度存在显著的正相关关系(rs=0.349,P＜0.01).[结论]血浆中BPDE-白蛋白加合物与尿中1-羟基芘水平显著相关,BPDE-白蛋白加合物可作为反映多环芳烃较长时期暴露的接触生物标志物.     

尿中2-萘酚作为多环芳烃接触水平的生物监测指标研究

目的 探讨尿中2-萘酚作为焦炉工多环芳烃接触水平生物监测指标的可行性.方法 以某市钢铁炼焦制气厂109名工人和50名本厂机关工作人员为对象,收集周末班后尿20ml,用改良的碱解-高效液相色谱法测定尿中2-萘酚.焦炉作业环境多环芳烃的车间空气监测结果以苯并(a)芘的浓度水平表示.用单因素方差分析、x2检验和spearman 等级相关分析.结果 尿中2-萘酚浓度炉顶工、炉侧工、炉底工和对照组分别为(11.32±4.82)、(9.82±5.11)、(5.24±4.97)和(2.97±2.36)μnol/mol Cr,呈炉顶>炉侧>炉底>对照组的趋势;尿中2-萘酚浓度与多环芳烃接触水平呈正相关关系(r=0.435,P<0.001).结论 焦炉工尿中2-萘酚水平可有效地反映个体短期多环芳烃接触的内剂量水平,可作为焦炉工多环芳烃接触水平的生物监测指标.     

尿中萘及其代谢产物作为焦炉工生物监测指标的研究

目的　探讨尿中萘及其代谢产物作为焦炉工生物监测指标的可行性。方法　在某焦化厂随机选取 2 8名焦炉工人和 2 2名对照个体 ,统一收集工作周末班后 2h尿 ,并使用调查表收集一般情况。采用顶空固相微提取结合气相色谱 -质谱联机方法 ,同时测定尿中萘和芘的水平 ,采用酶水解结合气相色谱 -质谱联机方法 ,同时测定样品中 1-萘酚、 2 -萘酚和 1-羟基芘的水平。使用多元线性回归分析不同工种和吸烟量对尿中这 5种多环芳烃生物标志物浓度的影响。结果　尿中萘、 1-萘酚、 2 -萘酚和 1-羟基芘的浓度呈炉顶工 >炉侧和炉底工 >对照个体的趋势 ,其中尿中 1-萘酚和 1-羟基芘的水平受工种的影响大于2 -萘酚 ;不同暴露水平组中 ,吸烟个体尿中 1-萘酚、 2 -萘酚和 1-羟基芘的浓度均大于不吸烟者 ,但吸烟对 2 -萘酚的影响最大。结论　尿中 1-萘酚和 2 -萘酚浓度均能够有效地反映个体短期多环芳烃暴露的内剂量水平 ,可用于焦炉工的生物监测。     

焦炉工多环芳烃接触与尿1-羟基芘及血清肿瘤坏死因子-α的关系

目的 探讨焦炉工外接触等级与尿中1-羟基芘物质的量浓度的关系,同时研究血清肿瘤坏死因子-α(TNF-α)水平能否作为焦炉工多环芳烃(PAH)的接触评价指标以及TNF-α与1-羟基芘物质的量浓度的关系.方法 以某焦化厂86名生产工人和35名对照者为研究对象,采集血清和班后尿,并收集个人信息,检测血清中TNF-α水平,用高效液相色谱法测定尿中1-羟基芘.结果 焦炉工尿1-羟基芘物质的量浓度(4.78±2.09)μmol/mol Cr显著高于对照组[(2.12±1.81)μmol/mol Cr,P＜0.001],并呈炉顶＞炉侧＞炉底＞对照组的趋势.与外接触呈显著相关性(r=0.727,P＜0.001);在同样外接触条件下,吸烟量显著影响尿中1-羟基芘的水平(P＜0.05);焦炉工血清中TNF-α水平(30.1±2.0)μg/L明显高于对照人群[(17.7±1.8)μg/L,P＜0.001];焦炉工尿1-羟基芘水平与血清中TNF-α呈弱相关(r=0.316,P＜0.001).结论 焦炉工尿中1-羟基芘水平与外接触等级存在良好的剂量-效应关系,可反映PAH接触个体的内剂量水平;焦炉工人血清TNF-α有可能作为PAH接触评价的参数.     

焦炉作业工人淋巴细胞诱变剂的敏感性研究

目的 研究焦炉作业工人外周血淋巴细胞对诱变剂博来霉素(bleomycin,BLM)损伤的敏感性.方法 以94名焦炉作业工人(暴露组)和64名选矿工人(对照组)作为研究对象.收集班后尿,测定尿中1-羟基芘水平反映多环芳烃暴露内剂量.肘静脉血分离淋巴细胞,体外培养20 h后,用8 μg/ml BLM处理30 min,彗星试验评价细胞DNA损伤水平.BLM处理前后DNA损伤的差即为个体对诱变剂的敏感性.结果 两组研究对象在年龄、性别、吸烟饮酒状况等方面差异均无统计学意义.焦炉工尿中1-羟基芘水平(9.0 μg/L,95%CI:6.8～11.7)显著高于对照(1.5 μg/L,95%CI:1.3～1.7)(t=-9.317,P＜0.01).对照组诱变剂敏感性为14.9(95%CI:13.7～16.3),焦炉工为17.7(95%CI:16.3～19.3),差异有统计学意义(t=-2.583,P=0.01).进一步按焦炉工尿1-羟基芘水平几何均数(9.0 μg/L)分层,发现高1-羟基芘水平组焦炉工对BLM的敏感性显著高于低1-羟基芘水平组(F=4.001,P=0.05).对照人群中吸烟者对BLM造成的损伤更为敏感.未发现年龄、饮酒、焦炉作业工龄、外暴露等级等因素对BLM敏感性有显著影响.结论 焦炉逸散物的暴露能够增加外周血淋巴细胞对BLM损伤的敏感程度,可能是焦炉作业工人中肿瘤高发的一个原因.     

人群锰接触水平的早期生物标志物探索

目的 通过研究工人锰接触水平与生物材料中锰浓度的关系,探索人群接触锰的早期生物标志物.方法 用个体空气采样器采集空气锰,确定时间加权平均暴露剂量,按照不同接触剂量把工人分为对照组、低锰接触组、高锰接触组,测定各组工人发、尿、血清、血细胞及唾液中锰浓度,分析锰接触剂量与生物材料中锰浓度的关系和工龄与生物材料中锰浓度的关系.结果 高锰接触组唾液锰为32.17μg/L,发锰为37.39 mg/kg,尿锰为2.50 μg/L,血清锰为29.61 μg/,血细胞锰为14.49μg/L,均明显高于对照组(分别为10.40μg/L、1.60 mg/kg、0.77μg/L、10.30 μg/L、4.56 μg/L),差异均有统计学意义(P<0.01).唾液锰水平与工人当前锰接触剂量呈明显的正相关(r=0.649,P<0.01),与工人接触锰的工龄呈明显的正相关(r=0.404,P<0.01),与工人锰总接触量之间呈明显的正相关(r=0.342,P<0.01);唾液锰水平与血细胞锰、血清锰水平呈明显的正相关(r值分别为0.359,0.303,均P<0.01).结论 唾液锰可作为人群锰当前接触和历史接触的生物标志物.     

焦炉作业工人尿中1-羟基芘水平检测及其临床意义

目的 探讨焦炉作业工人尿中1-羟基芘水平及其临床意义.方法 将煤化工厂147名焦炉作业工人分为焦油组(接触焦油作业工人)60人和焦炉烟尘组(接触焦炉烟尘作业工人)87人,另选择79名非焦炉作业工人为对照组,采用高效液相色谱紫外检测方法对作业工人尿中1-羟基芘含量进行分析.结果 焦油组和焦炉烟尘组尿中1-羟基芘水平分别为(2.20±0.49)和(1.92±0.59)μg/L,明显高于对照组[(0.59±0.40)μg/L],差异有统计学意义(P＜0.01);焦油组尿中1-羟基芘水平明显高于焦炉烟尘组,差异有统计学意义(P＜0.01).焦油组与焦油烟尘组作业工人尿中1-羟基芘水平不受工龄、性别和吸烟等因素的影响.结论 焦炉作业工人尿中1-羟基芘水平明显增高,以接触者尿中1-羟基芘水平作为评价人体接触多环芳烃指标,可以较好地反映近期接触水平.     

焦炉工人周围血细胞p16基因甲基化研究

目的分析焦炉工人周围血细胞中p16基因启动子区CpG岛异常甲基化状态,寻找焦炉工人肺癌辅助筛查的生物标志物。方法以74名男性焦炉工人为接触组,以47名供水厂男性职工为对照组。采集2组人员的班后尿,用高效液相色谱法检测其内暴露指标1-羟基芘(1-OH-Py)的水平;同时采集晨起空腹肘静脉血,分离周围血单个核细胞,用彗星实验检测DNA损伤情况;并提取基因组DNA,用甲基化特异性聚合酶链反应技术检测p16基因启动子区CpG岛甲基化发生情况。结果接触组尿1-OH-Py水平[(0.46±0.12)μmol/mol Cr]和DNA拖尾的Olive尾距[(0.41±0.25)μm]高于对照组[(0.17±0.06)μmol/mol Cr、(0.32±0.12)μm],差异有统计学意义(P<0.05)。接触组p16基因的异常甲基化的检出率(36.49%)高于对照组(4.26%),差异有统计学意义(P<0.01);并且p16基因的异常甲基化检出率随着尿1-OH-Py的水平升高逐渐增加,差异有统计学意义(P<0.01)。结论周围血p16基因异常甲基化可能是焦炉工人肺癌早期筛查有效的生物标志物。     

焦炉工尿1-羟基芘与血清癌胚抗原、神经元特异性烯醇化酶关系

目的 验证焦炉工尿1-羟基芘(1-OHPyr)与血清癌胚抗原(CEA)、神经元特异性烯醇化酶(NSE)的关系,探讨CEA和NSE作为焦炉工健康损害的早期效应指标.方法 用职业流行病学现况调查方法,对81名焦炉作业组工人、56名非焦炉作业组工人及77名正常对照组人群采用酶解-高效液相色谱法测定尿1-OHPyr水平,采用定量测定试剂盒(化学发光法)检测血清CEA、NSE水平.结果 焦炉作业组、非焦炉作业组、对照组人群血清中NSE水平分别为(1.56±0.18)、(1.17±0.08)和(0.95±0.12) μg/L,组间比较,差异有统计学意义(P＜0.05);3组人群血清中CEA水平比较,差异无统计学意义(P＞0.05);3组人群尿1-OHPyr质量浓度分别为(3.04±1.79)、(1.94±1.09)和(0.18±0.10) μg/L,组间比较,差异有统计学意义(P＜0.05).尿1-OHPyr水平与血清NSE水平成正相关关系(相关系数=0.386,P＜0.05).结论 煤焦沥青接触者尿1-OHPyr水平和血清NSE水平升高,尿1-OHPyr水平与血清中NSE水平成正相关,血清NSE水平可作为焦炉工健康损害的早期效应标志物及职业损伤的筛检指标.     

尿1—羟基芘作为焦炉工人接触多环芳烃的生物监测指标

对焦炉作业环境中多环芳烃（ＰＡＨｓ）浓度、作业人工接触ＰＡＨｓ的量、尿１－羟基芘（１－ＯＨ芘）排出水平的调查结果表明，焦炉工人尿１－ＯＨ芘排出水平与接触ＰＡＨｓ量呈正相关，吸烟对尿１－ＯＨ比测定影响不明显。因此，尿１－ＯＨ芘可望作评价焦炉工人接触ＰＡＨｓ的生物监测指标。     

1-Hydroxypyrene concentrations in first morning voids and 24-h composite urine: intra- and inter-individual comparisons

Urinary 1-hydroxypyrene (1-OHP) has been suggested as an exposure biomarker for polycyclic aromatic hydrocarbons (PAHs). However, it remains unknown whether a first morning urine sample can be used to reflect average exposure. In this paper, we examine intra-individual differences and inter-individual associations between first morning voids and 24-h composite urine samples. The analysis was performed using data collected from 100 adults who had a wide range of PAH exposure due to differences in their occupation, e.g., coke oven workers vs. non-coke oven workers. For each subject, all the urine voids within each of two 24-h measurement periods were collected. Results showed a significant (40% to 62%) intra-individual difference between first morning voids and 24-h urinary 1-OHP concentrations (in ng/ml urine). Creatinine adjustments of 1-OHP concentrations (in micromol/mol urinary creatinine) reduced the intra-individual difference by approximately 10%. Across all the subjects, a high overall correlation (r=0.76) was observed between first morning and 24-h average 1-OHP concentrations. Work environment and sampling season were found to significantly affect the relationship between first morning and 24-h 1-OHP concentrations. An increase of 1 ng/ml of first morning urinary 1-OHP predicted an increase of 0.5 and 0.25 ng/ml of 24-h urinary 1-OHP for coke oven workers and non-coke oven workers, respectively. Data collected in a winter season showed a higher correlation between first morning and 24-h concentrations than data collected in a fall season. Creatinine adjustments did not significantly improve overall correlations between first morning void and 24-h measurements, but increased total variances for 24-h urines explained by first morning urines in coke workers.     

尿中1-羟基芘作为焦炉工多环芳烃暴露生物监测指标的研究

目的探讨焦炉工外暴露等级与尿中1-羟基芘(1-OHPy)浓度的关系。方法以某焦化厂120名生产工人和30名非接触者为研究对象,收集班后6h尿,并收集个人信息,用高效液相法测定尿中1-羟基芘。结果尿中1-羟基芘浓度呈炉顶>炉侧>炉底>对照组的趋势。与外暴露呈显著相关性(r=0.653,P<0.01),同样外暴露条件下,吸烟者尿中1-羟基芘显著高于未吸烟者(P<0.05)。结论焦炉工尿中1-羟基芘水平与外暴露等级存在明显的相关性,可反映多环芳烃暴露个体的内剂量水平。     

Biomarkers for exposure to ambient air pollution--comparison of carcinogen-DNA adduct levels with other exposure markers and markers for oxidative stress

Human exposure to genotoxic compounds present in ambient air has been studied using selected biomarkers in nonsmoking Danish bus drivers and postal workers. A large interindividual variation in biomarker levels was observed. Significantly higher levels of bulky carcinogen-DNA adducts (75.42 adducts/10(8) nucleotides) and of 2-amino-apidic semialdehyde (AAS) in plasma proteins (56.7 pmol/mg protein) were observed in bus drivers working in the central part of Copenhagen, Denmark. In contrast, significantly higher levels of AAS in hemoglobin (55.8 pmol/mg protein), malondialdehyde in plasma (0. 96 nmol/ml plasma), and polycyclic aromatic hydrocarbon (PAH)-albumin adduct (3.38 fmol/ microg albumin) were observed in the suburban group. The biomarker levels in postal workers were similar to the levels in suburban bus drivers. In the combined group of bus drivers and postal workers, negative correlations were observed between bulky carcinogen-DNA adduct and PAH-albumin levels (p = 0.005), and between DNA adduct and [gamma]-glutamyl semialdehyde (GGS) in hemoglobin (p = 0.11). Highly significant correlations were found between PAH-albumin adducts and AAS in plasma (p = 0.001) and GGS in hemoglobin (p = 0.001). Significant correlations were also observed between urinary 8-oxo-7, 8-dihydro-2'-deoxyguanosine and AAS in plasma (p = 0.001) and PAH-albumin adducts (p = 0.002). The influence of the glutatione S-transferase (GST) M1 deletion on the correlation between the biomarkers was studied in the combined group. A significant negative correlation was only observed between bulky carcinogen-DNA adducts and PAH-albumin adducts (p = 0.02) and between DNA adduct and urinary mutagenic activity (p = 0.02) in the GSTM1 null group, but not in the workers who were homozygotes or heterozygotes for GSTM1. Our results indicate that some of the selected biomarkers can be used to distinguish between high and low exposure to environmental genotoxins.     

Biological monitoring of polycyclic aromatic hydrocarbon exposure in a highly polluted area of Poland.

Air pollution in Poland and particularly in Silesia is among the worst in Europe. Many coal mines and coke oven plants are located in this area, representing a major source of carcinogenic polycyclic aromatic hydrocarbons (PAHs). We quantitated the PAH exposure level in air samples using personal sampling devices, collected urine samples from the same individuals, and measured 1-hydroxypyrene with high performance liquid chromatography. Samples were collected twice, once in February and once in September. Mean PAH level of samples collected at three different coke oven plants varied from 2.3 micrograms/m3 to 12.3 micrograms/m3; the lowest mean was in September. Mean levels of 0.15 micrograms/m3 (September) and 0.44 micrograms/m3 (February) were noted for the environmentally exposed group. Mean urinary 1-hydroxypyrene varied from 2.45 to 13.48 mumol/mol creatinine at the three coke oven plants. The corresponding variation between the three different environmentally exposed groups in Silesia was 0.41-1.54 mumol/mol creatinine. In the nonindustrialized area, the mean varied from 0.20 to 0.14 mumol/mol creatinine. Seasonal variation was found both at the coke oven plants and in the environmental exposed groups in Silesia. Both PAH levels and 1-hydroxypyrene varied seasonally among coke oven workers and the environmentally exposed group. Our study shows that PAH exposure in the industrialized area of Silesia is high compared to levels in Western Europe. 1-Hydroxypyrene excretion in environmentally exposed individuals in Poland is among the highest in Europe.     

焦炉工外暴露等级与尿中1-羟基芘水平的关系

目的　探讨焦炉工外暴露等级与尿中 1-羟基芘浓度之间的关系。方法　以某焦化厂 30 5名生产工人和 30名非接触者为调查对象 ,统一收集工作周末班后 6h尿 ,并收集个人信息。根据工人的工作岗位将调查对象分为炉顶、炉侧、炉底和对照 4个外暴露等级。采用碱水解 -高效液相色谱法测定尿中1-羟基芘浓度。使用协方差分析和多元线性回归分析暴露等级、吸烟和饮酒等情况对尿中 1-羟基芘浓度的影响。结果　尿中 1-羟基芘的浓度呈炉顶 >炉侧 >炉底 >对照的趋势 ,与外暴露等级之间呈显著相关(Spearman相关系数为 0 5 35 ,P <0 0 1) ;在同样外暴露条件下 ,吸烟量显著影响尿中 1-羟基芘的水平(P <0 0 5 ) ;未发现饮酒对尿中 1-羟基芘水平的显著影响。结论　焦炉工尿中 1-羟基芘水平与外暴露等级之间存在良好的剂量 -效应关系 ,可反映多环芳烃暴露个体的内剂量水平     

Albumin adducts of electrophilic benzene metabolites in benzene-exposed and control workers

BACKGROUND: Metabolism of benzene produces reactive electrophiles, including benzene oxide (BO), 1,4-benzoquinone (1,4-BQ), and 1,2-benzoquinone (1,2-BQ), that are capable of reacting with blood proteins to produce adducts. OBJECTIVES: The main purpose of this study was to characterize relationships between levels of albumin adducts of these electrophiles in blood and the corresponding benzene exposures in benzene-exposed and control workers, after adjusting for important covariates. Because second blood samples were obtained from a subset of exposed workers, we also desired to estimate within-person and between-person variance components for the three adducts. METHODS: We measured albumin adducts and benzene exposures in 250 benzene-exposed workers (exposure range, 0.26-54.5 ppm) and 140 control workers (exposure range < 0.01-0.53 ppm) from Tianjin, China. Separate multiple linear regression models were fitted to the logged adduct levels for workers exposed to benzene < 1 ppm and > or =1 ppm. Mixed-effects models were used to estimate within-person and between-person variance components of adduct levels. RESULTS: We observed nonlinear (hockey-stick shaped) exposure-adduct relationships in log-scale, with inflection points between about 0.5 and 5 ppm. These inflection points represent air concentrations at which benzene contributed marginally to background adducts derived from smoking and from dietary and endogenous sources. Adduct levels were significantly affected by the blood-collection medium (serum or plasma containing either heparin or EDTA), smoking, age, and body mass index. When model predictions of adduct levels were plotted versus benzene exposure > or =1 ppm, we observed marked downward concavity, particularly for adducts of the benzoquinones. The between-person variance component of adduct levels increased in the order 1,2-BQ < 1,4-BQ < BO, whereas the within-person variance components of the three adducts followed the reverse order. CONCLUSIONS: Although albumin adducts of BO and the benzoquinones reflect exposures to benzene > or = 1 ppm, they would not be useful biomarkers of exposure at ambient levels of benzene, which tend to be < 0.01 ppm, or in those working populations where exposures are consistently < 1 ppm. The concavity of exposure-adduct relationships is consistent with saturable metabolism of benzene at air concentrations > 1 ppm. The surprisingly large effect of the blood-collection medium on adduct levels, particularly those of the benzoquinones, should be further investigated.     

DNA adduct formation of benzo[a]pyrene in white blood cells of workers exposed to polycyclic aromatic hydrocarbons

The major DNA adducts of anti-benzo[a]pyrene diolepoxide (BPDE) were determined by high performance liquid chromatography with fluorescence detection (HPLC-FLD) in white blood cells (WBC) of workers exposed to benzo[a]pyrene (B[a]P). In addition, ambient concentrations of B[a]P at the workplace were determined by personal air sampling. Workers in a refractory setting were examined before (n=26) and 3 months after (n = 33) changing the production material (binding pitch). Furthermore, 9 coke oven workers were examined. The change in the production process in the refractory setting led to a decrease in the median of ambient B[a]P concentrations (0.14 to <0.07 microg/m3). The median of BPDE-DNA adduct levels in WBC also decreased from 0.9 adducts/10(8) nucleotides before changing the production material to <0.5 adducts/10(8) nucleotides 3 months afterwards. The B[a]P concentrations at the workplace for the coke oven workers were found to be significantly higher than in the refractory setting. However, BPDE-DNA adduct concentrations in coke oven workers and refractory setting workers showed no significant difference, which was probably due to the low number of studied subjects in the coke-oven setting. No significant differences could be observed for BPDE-DNA adduct levels between current smokers (n=21) and non-smokers (n=14; p = 0.93) from both plants. In addition, no correlation between B[a]P concentrations in the air and DNA adduct levels in refractory workers and in coke oven workers could be found (r = -0.03, p = 0.87). Because of the missing correlation between personal air sampling and BPDE-DNA adduct levels in WBC, the results may indicate that their formation is either influenced by other routes of exposure to B[a]P (e.g., skin absorption, dietary habits) or interindividual differences in their formation and repair.