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Introduction The study focused on the influence of tar concentrations, smoking regimen, and smoking behavior, on benzo[a]pyrene (B[a]P) emission from cigarette mainstream smoke and related health hazards to determine the key factors influencing B[a]P reduction and protection of the smoker’s health. Methods A locally popular brand of cigarettes in Beijing was selected with tar concentrations of 1, 3, 5, 8, 10, and 11 mg/cigarette. Two different machine smoking regimens, the Canada Intense (HCI) regimen and the International Organization for Standardization (ISO) regimen, were adopted to collect the cigarette mainstream smoke. The B[a]P emission concentrations were then measured by gas chromatography and mass spectrum. Results The average B[a]P emission was 8.14–17.6 ng/cigarette for the HCI regimen and 0.92–3.46 ng/cigarette for the ISO regimen. As expected, the tar concentrations and B[a]P emissions exhibited a positive relation in both the HCI and ISO regimens, the cancer risk and non-cancer risk increased with an increase in tar concentrations for both the ISO and HCI regimens, and the smoking behavior also affected the B[a]P emissions with a tendency of VB (ventilation blocking) > HVB (half ventilation blocking) > DP (deep puff), under the same smoking regimen. Under the same conditions, the cancer risk and non-cancer risk in men were 1.19 and 1.11 times, respectively, higher than in women. Conclusions The smoking regimen influences the B[a]P emission relatively more than the cigarette tar concentration and smoking behavior. The cancer risk and non-cancer risk are higher in men than in women that possibly due to longer smoking duration and greater smoking intensity.

To study whether the urinary 1-hydroxypyrene (1-OHP) could be the biomarker of atmospheric PAHs, a small-scale pilot study was carried out on the relation of 1-OHP vs PAHs with the traffic policemen in Beijing of smokers and nonsmokers to be subgroups in both the exposure and control groups. Both the PAHs and 1-OHP were analyzed with high performance liquid chromatography (HPLC). The ambient concentrations of PAHs were different at the different sites (the average sum of PAHs (TPAH) were 12.36, 16.27, 18.37 ng/m3 at the suburban residential, police station and high traffic area, respectively.), but considerably lower than the personal-exposure concentrations (the average TPAH were 65.84 and 47.28 ng/m3 for patrol cars and inspection station, respectively). Pyrene was correlated well with BaP and the summed PAHs (TPAH), with the correlation coefficients ( R) of 0.79, 0.87 for ambient level and 0.92, 0.96 for personal exposure, respectively. The average of 1-hydroxypyrene of smokers and nonsmokers were 0.39, 0.15 μmol/mol creatinine in control group and 0.57, 0.33 μmol/mol creatinine in exposure group, respectively. The better correlation of pyrene to BaP and TPAH especially for personal exposure samples indicated that the probability of urinary 1-hydroxypyrene, the metabolite of pyrene, to be the biomarker of total PAH. Nonsmokers in the exposure and control groups had indistinguishable levels of 1-OHP, presumably because the ambient levels of pyrene were so similar (the average were 3.25, 3.20 ng/m3 at the police station and high traffic area, respectively.). Smokers in the control group had significantly higher 1-OHP than that of the nonsmokers, but showed indistinguishable differences in the exposure group. These results suggested that urinary 1-OHP could be a biomarker of PAHs only when the level of PAHs was at a relatively higher level. Smoking as an important influencing factor need to be controlled carefully. [ABSTRACT FROM AUTHOR]