PM2.5-bound Polycyclic Aromatic Hydrocarbons Research Articles

Polycyclic aromatic hydrocarbon exposure during pregnancy and changes in umbilical renal function

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants with significant adverse effects on human health, particularly concerning fetal development during pregnancy. This study investigates the relationship between maternal exposure to particulate matter-bound (PM-bound) PAHs and potential alterations in fetal renal function. A cross-sectional investigation was conducted on 450 mother-pair newborns from June 2019 to August 2021. Exposure to PM-bound PAHs was estimated at the residential address using spatiotemporal models based on data from 30 monitoring stations across the study area. Umbilical cord blood samples were collected post-delivery for biochemical analysis of renal function markers, including creatinine (Cr), blood urea nitrogen (BUN), and estimated glomerular filtration rate (eGFR). Multivariable regression models were used to assess the relationship between exposure to each PAHs compound and fetal renal function. Moreover, the mixture effects of exposure to PAHs on fetal renal function were assessed using quantile g-computation analysis. Increased concentrations of various PAH compounds at the residential address correlated with raised levels of umbilical BUN and Cr, suggesting potential renal impairment. Notably, exposure to certain PAHs compounds demonstrated statistically negative significant associations with eGFR levels. An increment of one quartile in exposure to PAHs mixture was correlated with a rise of 1.08 mg/dL (95% CI 0.04, 2.11, p = 0.04) and 0.02 mg/dL (95% CI − 0.00, 0.05, p = 0.05) increase in BUN and Cr, respectively. Moreover, a one-quartile increase in PAHs mixture exposure was associated with − 1.09 mL/min/1.73 m2 (95% CI − 2.03, − 0.14, p = 0.02) decrease in eGFR. These findings highlight the potential impact of PAH exposure on fetal renal function and underscore the importance of considering environmental exposures in assessing neonatal renal health outcomes.

Sources, trigger points, and effect size of associations between PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) and fractional exhaled nitric oxide (FeNO): A panel study with 16 follow-up visits over 4 years

Exposure to fine particulate matter (PM2.5) is a significant concern for respiratory health. However, the sources, trigger points, and effect size of specific associations between PM2.5 components, particularly polycyclic aromatic hydrocarbons (PAHs) and the airway inflammatory marker fractional exhaled nitric oxide (FeNO) have not been fully explored. In this study, 69 healthy college students were enrolled and followed up 16 times from 2014 to 2018. Individual FeNO was measured and ambient air PM2.5 samples were collected for 7 consecutive days before each follow-up. PAHs were quantified using Gas Chromatography-Mass Spectrometry. Linear mixed-effect regression models were employed to evaluate the associations between PM2.5-bound PAHs and FeNO. Additionally, PMF (Positive Matrix Factorization) was utilized to identify sources of PM2.5-bound PAHs and assess their impact on FeNO. Throughout the study, the average (SD) of ΣPAHs concentrations was 78.50 (128.9) ng/m3. PM2.5 and PM2.5-bound PAHs were significantly associated with FeNO at various lag days. Single-day lag analyses revealed maximum effects of PM2.5 on FeNO, with an increase of 7.71% (95% CI: 4.67%, 10.83%) per interquartile range (IQR) (48.10 μg/m3) increase of PM2.5 at lag2, and ΣPAHs showed a maximum elevation in FeNO of 6.40% (95% CI: 2.33%, 10.63%) at lag4 per IQR (57.39 ng/m3) increase. Individual PAHs exhibited diversity peak effects on FeNO at lag3 (6 of 17), lag4 (9 of 17) in the single-day model, and lag0-5 (8 of 17) (from lag0-1 to lag0-6) in the cumulative model. Source apportionment indicated coal combustion as the primary contributor (accounting for 30.7%). However, a maximum effect on FeNO (an increase of 21.57% (95% CI: 13.58%, 30.13%) per IQR increase) was observed with traffic emissions at lag4. The findings imply that strategic regulation of particular sources of PAHs, like traffic emissions, during specific periods could significantly contribute to safeguarding public health.

PM2.5-bound polycyclic aromatic hydrocarbons (PAHs): quantification and source prediction studies in the ambient air of automobile workshop using the molecular diagnostic ratio

The presence of polycyclic aromatic hydrocarbons (PAHs) in the atmosphere has been linked to health concerns, including cancer. Automobile workshops are significant contributors to PAH emissions due to their operations. Hence, this investigation aimed to identify and quantify the sources of PM2.5-bound PAHs in the ambient air of automobile workshops in Benin City, Nigeria, using molecular diagnostic ratios. PM2.5 samples were collected from 60 automobiles over 1 year, during the rainy (April to November) and dry (December to March) seasons of 2019. Sample collection utilized a low-volume air sampler with quartz filter paper, and extraction was performed using a 1:1 mixture of acetone and dichloromethane. The analysis involved an HP Agilent Technology 6890 Gas Chromatography (GC) system with a flame ionization detector. The annual average concentrations of PM2.5-bound PAHs in Benin City were 269.87 ± 249.32 ng/m3 (dry season) and 216.30 ± 204.89 ng/m3 (wet season). Molecular diagnostic ratios, such as Fl/(Fl + Py), An/(An + Phe), BaP/(BaP + Chry), BbF/BkF, InP/(InP + BghiP), and BaA/(BaA + Chr), aided in identifying PAH sources. Gasoline combustion, diesel combustion, traffic emissions, and emissions from automobile panel welders were found to be the primary sources of PAHs near vehicle workshops. These findings provide crucial insights for developing effective strategies to reduce emissions and protect public health in the air surrounding automobile workshops in Benin City.

Ambient PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) associated with pro-thrombotic biomarkers among young healthy adults: A 16 times repeated measurements panel study

Studies have shown that the cardio/cerebrovascular toxicity of ambient PM2.5 is related to its bound polycyclic aromatic hydrocarbons (PAHs). Currently, only a few studies have reported the relationship between PM2.5-bound PAHs and promoted blood coagulation and thrombosis, but there isn't a consistent conclusion. Therefore, we conducted a prospective panel study to investigate the association. Thirty-three young healthy adults participated in sixteen repeated visits from 2014 to 2018 in Tianjin, China. During each visit, three pro-thrombotic biomarkers: ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin motif 13), D-dimer and Myeloperoxidase (MPO) were measured. Before each visit, ambient PM2.5 samples were daily collected for one week. Sixteen PAHs were determined using Gas Chromatography-Mass Spectrometer, and the positive matrix factorization (PMF) model was applied to identify the sources. Linear mixed-effects models were fitted to investigate the associations between PM2.5-bound PAHs exposure and the biomarkers. Thirteen time-metrics were defined to identify significant time points of PM2.5-bound PAHs' effects. We observed that the increase of PM2.5-bound PAHs exposure was significantly associated with reduced ADAMTS13, elevated D-dimer and MPO. At lag0, each 5.7 ng/m3 increase in Benzo[j]fluoranthene and per 3.4 ng/m3 increase Dibenz[a,h]anthracene could make a maximum change of −19.08 % in ADAMTS13 and 132.60 % in D-dimer. Additionally, per 16.43 ng/m3 increase in Chrysene could lead to a maximum elevation of 32.14 % in MPO at lag4. The PM2.5-bound PAHs often triggered more significant changes at lag 3,4 and 6. The ambient PM2.5-bound PAHs originated from six sources: coal combustion (43.10 %), biomass combustion (20.77 %), diesel emission (14.78 %), gasoline emission (10.95 %), industrial emission (7.58 %), and cooking emission (2.83 %). The greatest contributors to alterations in ADAMTS13, D-dimer and MPO are industrial emission (−48.43 %), biomass combustion (470.32 %) and diesel emission (13.14 %) at lag4. Our findings indicated that short-term exposure to ambient PM2.5-bound PAHs can induce alterations of pro-thrombotic biomarkers among healthy adults.

Human health risk assessment of PM10-bound heavy metals and PAHs around the Latin America’s Largest opencast coal mine

Air pollution in opencast coal mine areas is a critical issue, resulting in harmful severe effects on human health. Therefore, it is essential to understand the air pollution factors and to assess the risks to humans. This study evaluated the potential risks (carcinogen and non-carcinogen) of inhalation exposure to PM10-bound heavy metals and Polycyclic Aromatic Hydrocarbons (PAHs) in an open pit mine in northern Colombia. During February-May 2022, PM10 samples were collected at eight sites. Heavy metals (i.e., Al, Cr(VI), Mn, Cu, Zn, As, Pb) and PAHs (thirteen priority PAHs, and one non-priority PAH) levels linked to PM10 were analyzed by X-ray fluorescence and gas chromatography–mass spectrometry, respectively. PM10 concentrations were found to range between 4.70 and 59.90 µg m−3. Out of the three different zones of the study area (i.e., North Zone, South Zone, and Populated Zone), the North Zone recorded the highest daily average concentrations of Cr(VI) (104.16 ng m−3), Mn (28.39 ng m−3), Cu (33.75 ng m−3), Zn (57.99 ng m−3), As (44.92 ng m−3), and Pb (27.13 ng m−3). The fraction of the analyzed heavy metals at all monitoring sites was 82%–89% for Al, followed by Cr(VI) with 3%–6%. Cr(VI) was the major contributor to the carcinogenic risk values, while Cu, Cr(VI), and As were the main drivers for the non-carcinogenic risk. The average cancer risk range for heavy metals was 3.30 × 10–04 –5.47 × 10–04. On the other hand, the cancer risk for PAHs exposure was acceptable. The average incremental lifetime cancer risk (ILCR) values varied between 2.87 × 10–07 and 4.21 × 10–07. Benzo[a]pyrene contributed to 54%–56% of the total risk from inhalation of PM10-bound PAHs, while Indeno[1,2,3-cd]pyrene contributed to 16%–19%. Based on the Monte Carlo sensitivity analysis, exposure to Cr(VI) was the main factor affecting cancer risk in the North, South, and Populated Zones. A suitable risk assessment and management plan requires understanding PM10-bound heavy metals and PAHs concentration levels as well as their potential health risks, mainly in open-cast coal mine zones. Our study found that people living near open-pit mines face potential health risks, so it is crucial to establish policies and regulations to control emission sources.

Pollution characteristics and health risk assessment of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, and halogenated-PAHs in Shanxi, China

Pollution characteristics and health risk assessment of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, and halogenated-PAHs in Shanxi, China

The potential health risk assessment of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) on the human respiratory system within the ambient air of automobile workshops in Benin City, Nigeria

The potential health risk assessment of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) on the human respiratory system within the ambient air of automobile workshops in Benin City, Nigeria

Assessing Lifetime Cancer Risk Associated with Population Exposure to PM-Bound PAHs and Carcinogenic Metals in Three Mid-Latitude Metropolitan Cities.

Lifetime cancer risk characterization of ambient PM-bound carcinogenic metals and polycyclic aromatic hydrocarbons (PAHs) were examined in the cities of Los Angeles (USA), Thessaloniki (Greece) and Milan (Italy), which share similar Mediterranean climates but are different in their urban emission sources and governing air quality regulations. The samples in Milan and Thessaloniki were mostly dominated by biomass burning activities whereas the particles collected in Los Angeles were primary impacted by traffic emissions. We analyzed the ambient PM2.5 mass concentration of Cadmium (Cd), Hexavalent Chromium (Cr(VI)), Nickel (Ni), Lead (Pb), as well as 13 PAH compounds in the PM samples, collected during both cold and warm periods at each location. Pb exhibited the highest annual average concentration in all three cities, followed by Ni, As, Cr(VI), Cd and PAHs, respectively. The cancer risk assessment based on outdoor pollutants was performed based on three different scenarios, with each scenario corresponding to a different level of infiltration of outdoor pollutants into the indoor environment. Thessaloniki exhibited a high risk associated with lifetime inhalation of As, Cr(VI), and PAHs, with values in the range of (0.97-1.57) × 10-6, (1.80-2.91) × 10-6, and (0.77-1.25) × 10-6, respectively. The highest cancer risk values were calculated in Milan, exceeding the US EPA standard by a considerable margin, where the lifetime risk values of exposure to As, Cr(VI), and PAHs were in the range of (1.29-2.08) × 10-6, (6.08-9.82) × 10-6, and (1.10-1.77) × 10-6, respectively. In contrast, the estimated risks associated with PAHs and metals, except Cr(VI), in Los Angeles were extremely lower than the guideline value, even when the infiltration factor was assumed to be at peak. The lifetime cancer risk values associated with As, Cd, Ni, Pb, and PAHs in Los Angeles were in the range of (0.04-0.33) × 10-6. This observation highlights the impact of local air quality measures in improving the air quality and lowering the cancer risks in Los Angeles compared to the other two cities.

Exposure and health risk assessment of PM2.5-bound polycyclic aromatic hydrocarbons during winter at residential homes: A case study in four Chinese cities

Residential indoor PM2.5 were concurrently collected in Hong Kong, Guangzhou, Shanghai, and Xi'an during the winter and early spring seasons of 2016–2017, for updating the current knowledge of the spatial variation of indoor air pollution and the potential health risks in China. PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) were characterized, and the associated inhalation cancer risks were assessed by a probabilistic approach. Higher levels of indoor PAHs were identified in Xi'an residences (averaged at 176.27 ng m−3) with those of other cities ranging from 3.07 to 15.85 ng m−3. Traffic-related fuel combustion was identified as a common contributor to indoor PAHs through outdoor infiltration for all investigated cities. Indoor PAHs profiles showed city-specific differences, while distinctions between profiles based on indoor activities or ambient air quality were limited. Similar with the total PAHs concentrations, the estimated toxic equivalencies (TEQ) with reference to benzo[a]pyrene in Xi'an residences (median at 18.05 ng m−3) were above the recommended value of 1 ng m−3 and were magnitudes higher than the other investigated cities with estimated median TEQ ranging from 0.27 to 1.55 ng m−3. Incremental lifetime cancer risk (ILCR) due to PAHs inhalation exposure was identified with a descending order of adult (median at 8.42 × 10−8) > adolescent (2.77 × 10−8) > children (2.20 × 10−8) > senior (1.72 × 10−8) for different age groups. Considering the lifetime exposure-associated cancer risk (LCR), potential risks were identified for residents in Xi'an as an LCR level over 1 × 10−6 was identified for half of the adolescent group (median at 8.96 × 10−7), and exceedances were identified for about 90 % of the groups of adults (10th percentile at 8.29 × 10−7) and seniors (10th percentile at 1.02 × 10−6). The associated LCR estimated for other cities were relatively insignificant.

PM2.5/PM10-bound PAHs in Hotan city: Concentrations, sources, and contribution to ·OH

The air pollution in Hotan, Xinjiang is serious and the high concentration of polycyclic aromatic hydrocarbons (PAHs) cannot be ignored. Studies on the characteristics of PAHs in the region are still limited. In this paper, PM10 and PM2.5 samples were collected from the urban area of Hotan in summer and winter, and the concentrations, sources and contributions to hydroxyl radicals (·OH) of 12 PAHs were analyzed. The mean concentrations of PM2.5/PM10-bound PAHs were much higher in winter (150 ± 38.8 ng/m3 and 156 ± 38.1 ng/m3) than in summer (6.34 ± 6.28 ng/m3 and 7.64 ± 6.75 ng/m3), with greater contributions from medium and high molecular weight PAHs. PAHs are mainly derived from vehicle emissions, coal and biomass combustion, with coal combustion making the largest contribution to ·OH concentrations. The combination of air mass trajectory clustering and potential source contribution factor analysis (PSCF) revealed that long-range transport contributed less to the PAHs content, and local domestic source emissions dominated. Studies have shown a significant positive correlation between PAHs and ·OH concentrations, indicating that PAHs are oxidatively toxic to humans. Controlling PAHs emission in winter in Hotan and reducing the concentration of PAHs in respirable particulate matter will help to reduce the damage to human health.

Toxicological and Mutagenic Effects of Particulate Matter from Domestic Activities.

People spend most of their time indoors, particularly in their houses where daily activities are carried out, enhancing particulate matter (PM) emissions with consequent adverse health impacts. This study intended to appraise the toxicological and mutagenic responses of particulate matter with a diameter less than 10 μm (PM10) released from cooking and ironing activities under different conditions. The cytotoxicity of the PM10 total organic extracts was tested in A549 cells using the WST-8 and the lactate dehydrogenase (LDH) assays, while the interference in cell cycle dynamics and reactive oxygen species (ROS) production was analysed by flow cytometry. The S. typhimurium TA98 and TA100 Ames tester strains with and without metabolic activation were employed to determine the mutagenic potential of the PM10-bound polycyclic aromatic hydrocarbons (PAHs). PM10 organic extracts decreased the metabolic activity of A549 cells; however, no effects in the LDH release were observed. An increase in ROS levels was registered only for cells treated with PM10 at IC20 from steam ironing, in low ventilation conditions, while cell cycle dynamics was only affected by exposure to PM10 at IC20 from frying horse mackerel and grilling boneless pork strips. No mutagenic effects were observed for all the PM10-bound PAHs samples.

The association of in-utero exposure to polycyclic aromatic hydrocarbons and umbilical liver enzymes

BackgroundThe adverse health influences of polycyclic aromatic hydrocarbons (PAHs) exposures have been examined in several previous research. However, the evidence on the health influences of PAHs exposure during pregnancy and childhood is scarce, with no study on the infant's liver function. Therefore, in this study, the association of in-utero exposure to particulate matter-bound PAHs (PM-bound PAHs) on the umbilical liver enzymes was investigated. MethodsA total of 450 mother-pair samples were assessed in this cross-sectional study in Sabzevar, Iran (2019–2021). The concentrations of PM-bound PAHs were estimated based on spatiotemporal models at residential addresses. The umbilical cord blood alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) were measured as indicators of infant's liver function. The association of PM-bound PAHs with umbilical liver enzymes was evaluated using multiple linear regression, controlled for relevant covariates. The quantile g-computation (g-comp) was used to investigate the combined impact of the 15 PAHs on liver function biomarkers. ResultsHigher levels of total 4-ring PAHs, Dibenzo[a,h]anthrancene, Anthracene, Pyrene, Benzo[a]anthracene, Phenanthrene, Fluorene, Acenaphthylene and Naphthalene were associated with higher umbilical ALP. An increase in total 5-ring PAHs, Benzo[g,h,i]perylene, Benzo[a]pyrene and Chrysene was associated with higher umbilical AST levels. Each 1 ng/m3 increase in exposure to Benzo[g,h,i]perylene was related with 182.21 U/L (95 % CI: 116.11, 248.31, P < 0.01) increase in umbilical GGT. PAHs mixture exposure was positively associated with higher umbilical AST and ALT, while no significant associations were noted for ALP and GGT. We observed a potentially stronger association for girls compared to boys based on umbilical ALT and AST. However, for GGT and ALP, these associations were stronger for boys compared to girls. ConclusionOverall our findings suggested that exposure to PAHs during pregnancy had adverse effects on infant's liver function.

Investigation of PM2.5-bound Polycyclic aromatic hydrocarbons (PAHs) and their derivatives (nitrated-PAHs and oxygenated-PAHs) in the roadside environment at the eastern coastal region of China: characterization, source identification, and toxicity evaluation

Investigation of PM2.5-bound Polycyclic aromatic hydrocarbons (PAHs) and their derivatives (nitrated-PAHs and oxygenated-PAHs) in the roadside environment at the eastern coastal region of China: characterization, source identification, and toxicity evaluation

Characterization, risk assessment, and source estimation of PM10-bound polycyclic aromatic hydrocarbons during wintertime in the ambient air of Basrah City, Iraq

In this study, the concentration and structure of polycyclic aromatic hydrocarbons (PAHs) associated with the ambient PM10 in Basrah City, Iraq have been investigated for the first time. From December 2021 to February 2022, PM10 samples were collected on quartz fiber filters, extracted using an optimized extraction protocol, and analyzed for the sixteen US EPA priority PAHs. The results indicated that 4- and 5-ring PAHs represent 52% of the total detected PAHs. The most abundant PAHs over the study period were chrysene (1.2 ± 1.5 ng m−3), fluorene (0.9 ± 1.4 ng m−3), and benzo[b]fluoranthene (0.7 ± 0.9 ng m−3). Source identification suggested that PM10-bound PAHs primarily originated from pyrogenic and petrogenic activities in Basrah City. In addition, the cancer risk associated to PAH exposure was assessed based on benzo[a]pyrene equivalent concentration and was found ranging from 0.07 to 6.32 ng m-3; hence, it exceeded the threshold limit of 1.0 ng m−3 established by the European legislation (EU, 2014). Benzo[a]pyrene was determined to be main contributor to total carcinogenic power of the detected PAHs, accounting for 50.3%, followed by dibenz[a,h]anthracene (22.3%). Similarly, benzo[a]pyrene represented a major contributor to PAH associated mutagenicity, accounting for 43.5% of the total.

PM2.5-bound PAHs near a typical industrial park: Determining health risks associated with specific industrial sources

Source-specific potential health risk was proposed as an effective index for determining priority control sources of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) near an industrial park. However, industry-specific emission profiles were limited. In this study, 60 emission source samples from 13 industries and 139 p.m.2.5 samples near an industrial park were collected from 2020 to 2021. The PAH profiles of 12 industrial emission sources were constructed to address the difficulty of source apportionment refined to industrial categories. A diagnostic ratio method and a positive matrix factorization method (PMF) were used to qualitatively and quantitatively determine the emission sources of 16 p.m.2.5-bound PAHs. The incremental lifetime carcinogenic risk (ILCR) of PAH inhalation exposure for the local population was attributed to sources by a PMF-ILCR model. The results show that the local PAH pollution seriously exceeded (86.3% sampling days) the standard (GB3095-2012). The concentration of PAHs was 33.6 ± 32.6 ng/m3 and showed a seasonal trend of “heating season > autumn > spring”. There were five main sources of PM2.5-bound PAHs near the industrial park: heavy oil combustion (29.8%), coal and natural gas combustion (28.0%), vehicle emissions (19.9%), steel industry emissions (19.4%) and tar volatilization (2.9%). There is potential carcinogenic risk to both children (3.1 × 10−6) and adults (1.2 × 10−5). The mass contribution of each source to ambient PAHs is not equivalent to its contribution to potential health risk. The risks of PM2.5-bound PAHs almost all correspond to vehicle emissions (46.3%), heavy oil combustion (25.9%) and steel industrial sources (24.9%).

Effects of COVID-19 Control Measures on the Concentration and Composition of PM2.5-Bound Polycyclic Aromatic Hydrocarbons in Shanghai

In order to explore the effects of COVID-19 control measures on the concentration and composition of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs), and to better understand the sources of PM2.5-bound PAHs, PM2.5, samples were collected at two sites in urban and suburban areas of Shanghai before the lockdown, during the lockdown, after the lockdown in 2020, and during the same periods in 2019. The mass concentrations of 21 individual PAHs were determined via GC-MS analysis. While the COVID-19 control measures significantly reduced the absolute concentration of PM2.5-bound PAHs, they had no significant effect on their relative abundances, indicating that the significantly reduced traffic emission may not originally be the major source of PAHs in Shanghai. The differences in the composition of PM2.5-bound PAHs at three different lockdown-related periods may be caused by the gas-particle distribution of semi-volatile PAHs. The similarity in the composition of PM2.5-bound PAHs in different functional areas and different periods brings more uncertainties to the identification of PAH sources using the diagnostic ratios. During the lockdown period, the toxic equivalent concentration of PM2.5-bound PAHs in Shanghai was estimated to decrease by about 1/4, which still exhibits substantial carcinogenic risk upon exposure via inhalation.

Optimization of Cancer Risk Assessment Models for PM2.5-Bound PAHs: Application in Jingzhong, Shanxi, China.

The accurate evaluation of the carcinogenic risk of PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) is crucial because of the teratogenic, carcinogenic, and mutagenic effects of PAHs. The best model out of six models was selected across three highly used categories in recent years, including the USEPA-recommended inhalation risk (Model I), inhalation carcinogen unit risk (Models IIA-IID), and three exposure pathways (inhalation, dermal, and oral) (Model III). Model I was found to be superior to the other models, and its predicted risk values were in accordance with the thresholds of PM2.5 and benzo[a]pyrene in ambient-air-quality standards. Models IIA and III overestimated the risk of cancer compared to the actual cancer incidence in the local population. Model IID can replace Models IIB and IIC as these models exhibited no statistically significant differences between each other. Furthermore, the exposure parameters were optimized for Model I and significant differences were observed with respect to country and age. However, the gender difference was not statistically significant. In conclusion, Model I is recommended as the more suitable model, but in assessing cancer risk in the future, the exposure parameters must be appropriate for each country.

PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) from the atmosphere of Xi'an, China: Seasonal variation, sources, and health risk assessments

Ambient air samples of fine particulate matter (PM2.5) were collected in a main urban area of Xi'an, Guanzhong Plain, whose contents including organic carbon (OC), elemental carbon (EC) and eight carbon components were measured by thermo-optical analysis. Polycyclic aromatic hydrocarbons (PAHs) were determined by high-performance liquid chromatography. As a result, OC and EC accounted for 74.5% of PM2.5 in winter. During winter, light-molecular-weight PAHs (with 2 and 3 benzene rings) concentration predominated in the atmosphere. Molecular diagnostic ratios were calculated to distinguish between different sources of carbon components and PAHs, which revealed natural dust, fossil fuels combustion, and traffic emissions (diesel and gasoline emissions) were the major source contributors. Health risk assessment of PAHs indicated the non-carcinogenic risk values were far lower than 1 for all populations. Some carcinogenic risk values induced by PM2.5-bound PAHs were higher than 10−6, which means that there was a certain potential carcinogenic risk in carcinogenic PAHs. High exposure pollutants (acenaphthylene, benzo(b) fluoranthene, naphthalene and chrysene) were observed with potential in vitro oxidative and inflammatory responses. The results showed that long-term exposure to the environment with PAHs pollutants could cause sustained immune and respiratory system damage to the human body. Air quality management should be carried out to improve ambient air quality and reduce health hazards.

Deposition effect of inhaled particles in the human: Accurate health risks of personal exposure to PAHs and their derivatives from residential solid fuel combustion

The drastic household clean heating renovation has been undertaken in rural northern China since 2017. A method incorporating the deposition efficiency of particulate matters (PMs) in the human respiratory tract is firstly introduced into the personal exposure (PE) study which is more accurately assess the health risks of homemakers inhaling PM-bound four subclasses polycyclic aromatic hydrocarbons (PAHs) emitted from different solid fuels (i.e., biomass, raw coal chunk, and clean coal). Homemakers using clean coal show the lowest exposure levels of all PAH subclasses (parent, alkylated, oxygenated, and nitro PAHs) and total quantified PAHs (ΣPAHs). Remarkable reductions of 93.9% and 89.0% on ΣPAHs in PE PM2.5 are observed with the substitutions of the raw coal chunk and biomass fuel by the clean coal, respectively. 86.8–96.8% of ΣPAHs are inhaled by the human body, while approximately 22.4–44.8% are deposited in the respiratory tract. The deposition concentrations (DC) of ΣPAHs in the biomass and raw coal chunk groups are 12 and 5 times the clean coal group, respectively. PAHs in coarse mode PE particles with an aerodynamic size between 2.5 and 100 μm mostly deposit in the head airway (HA) (98%). Moreover, the PAHs in fine particles (i.e., with aerodynamic size less than 2.5 μm) mainly deposit in the alveolar region (AR), accounting for 20–70% of ΣPAHs. Replacing biomass and raw coal chunk with clean coal reduced incremental lifetime cancer risks (ILCR) by 91% and 92%, respectively. This study improves the understanding of the PM-bound PAHs deposition in the human respiratory system and contributes to the promotion of domestic energy transition in rural northern China.

Associations of personal PM2.5 and PM2.5-Bound polycyclic aromatic hydrocarbons exposure with blood lipid profiles: A panel study from middle-aged Chinese adults

Adverse effects of fine particulate matter (particulate matter ≤2.5 μm aerodynamic diameter, PM2.5) and PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) on blood lipid profiles remain uncertain. We designed a panel study with repeated measures. In this panel study, we enrolled 215 adult residents who participated in two study periods from the Wuhan-Zhuhai cohort. Personal 24-h PM2.5, sixteen kinds of 24-h PM2.5-bound PAHs, and blood lipid profiles were repeatedly measured across two study periods. We observed that an interquartile-range increase in four-ring or five-ring PAHs was linked with a 0.112 and 0.108 mmol/l increase in triglyceride, respectively in single-constituent models. These associations remained robust in both constituent-PM2.5 joint models and single-constituent residual models. Additionally, we observed that the significant relationships of four/five-ring PAHs with triglycerides were stronger among females, non-smokers, and participants without hypertension and diabetes. Bayesian kernel machine regression models further revealed that combining sixteen kinds of PM2.5-bound PAHs as a mixture of pollutants could result in a cumulative toxic effect on total cholesterol and triglycerides. No significant relationships were observed between personal PM2.5 exposure and blood lipid changes. Our findings suggest that exposure to PM2.5-bound PAHs may adversely affect lipid metabolism, which provides new evidence for formulating pollution abatement strategies for cardiovascular health.