This study investigates PM2.5-bound PAHs for rural sites (Dacheng and Fangyuan) positioned close to heavy air-polluting industries in Changhua County, central Taiwan. A total of 113 PM2.5 samples with 22 PAHs collected from 2014 to 2015 were analyzed, and Positive Matrix Factorization (PMF) and diagnostic ratios of PAHs were applied to quantify potential PAH sources. The influences of local and regional sources were also explored using the conditional probability function (CPF) and potential source contribution function (PSCF) with PMF-modeled results, respectively. Annual mean concentrations of total PAHs were 2.91 ± 1.34 and 3.04 ± 1.40 ng/m3 for Dacheng and Fangyuan, respectively, and their corresponding BaPeq were measured at 0.534 ± 0.255 and 0.563 ± 0.273 ng/m3 in concentration. Seasonal variations with higher PAHs found for the winter than for the spring and summer were observed for both sites. The lifetime excess cancer risk (ECR) from inhalation exposure to PAHs was recorded as 4.7 × 10−5 overall. Potential sources of PM2.5-bound PAHs include unburned petroleum and traffic emissions (42%), steel industry and coal combustion (31%), and petroleum and oil burning (27%), and unburned petroleum and traffic emission could contribute the highest ECR (2.4 × 10−5). The CPF results show that directional apportionment patterns were consistent with the actual locations of local PAH sources. The PSCF results indicate that mainly northeastern regions of China have contributed elevated PM2.5-bound PAHs from long-range transports.

Sediment samples (n = 20) were collected from Yangtze River Estuary (YRE) and the adjacent East China Sea (ECS) inner shelf to explore spatial and temporal distributions, environmental fate, sources and potential health risk of polybrominated diphenyl ethers (PBDEs). Concentrations of BDE-209 and total 7 PBDEs (without BDE-209; ∑7PBDEs) ranged from 62.3 to 1758 pg g−1 and from 36.9 to 233.6 pg g−1 dry weight, respectively; both of the highest values occurred near the city of Wenzhou. Concentrations of BDE-209 and ∑7PBDEs both indicated a decreasing trend from inshore areas toward outer shelf. Significantly positive linear correlations were only observed between logBDE-183 concentrations and TOC/grain size (r2 = 0.6734 and 0.5977 for TOC and grain size, respectively) as well as BDE-209 and TOC/grain size (r2 = 0.4137 and 0.5332 for TOC and grain size, respectively) in the north of 28°N, indicating that YR had significant influence on the distribution of higher brominated congeners only in the north part. Depth profiles of PBDEs in a sediment core P01 (n = 1, m = 11) collected from YRE showed that the input of BDE-209 gradually increased from 1930 to 2010, while the levels of ∑7PBDEs peaked in 1986 and obviously decreased in recent years. Partial Least-Squares Regression (PLSR) revealed that PBDEs in the coastal ECS were mainly from direct discharge of local anthropogenic activities (80.7%), followed by surface runoff of contaminated soils (15.1%), microbial degradation after sedimentation (2.6%) and photodegradation during atmospheric transportation (1.6%). The cancer risk of human exposure to BDE-209 at the 95% confidence level was 3.09 × 10−7, 1.67 × 10−7 and 8.86 × 10−7 for children, teens and adults, respectively, significantly lower than the threshold level (10−6). Hazard index (HI) calculated for non-cancer risk was also far less than 1 for the three groups, suggesting no non-cancer risk.

This work characterizes levels of polycyclic aromatic hydrocarbons (PAHs) in indoor and outdoor air of preschool environments, and assesses the respective risks for 3–5-years old children. Eighteen gaseous and particulate (PM1 and PM2.5) PAHs were collected indoors and outdoors during 63 days at preschools in Portugal. Gaseous PAHs accounted for 94–98% of total concentration (ΣPAHs). PAHs with 5–6 rings were predominantly found in PM1 (54–74% particulate ΣPAHs). Lighter PAHs originated mainly from indoor sources whereas congeners with 4–6 rings resulted mostly from outdoor emissions penetration (motor vehicle, fuel burning). Total cancer risks of children were negligible according to USEPA, but exceeded (8–13 times) WHO health-based guideline. Carcinogenic risks due to indoor exposure were higher than for outdoors (4–18 times).

Heavy metals (Cr, Co, Ni, As, Cd, and Pb) can be bound to PM adversely affecting human health. Quantifying the source impacts on heavy metals can provide source-specific estimates of the heavy metal health risk (HMHR) to guide effective development of strategies to reduce such risks from exposure to heavy metals in PM2.5 (particulate matter (PM) with aerodynamic diameter less than or equal to 2.5 μm). In this study, a method combining Multilinear Engine 2 (ME2) and a risk assessment model is developed to more effectively quantify source contributions to HMHR, including heavy metal non-cancer risk (non-HMCR) and cancer risk (HMCR). The combined model (called ME2-HMHR) has two steps: step1, source contributions to heavy metals are estimated by employing the ME2 model; step2, the source contributions in step 1 are introduced into the risk assessment model to calculate the source contributions to HMHR. The approach was applied to Huzou, China and five significant sources were identified. Soil dust is the largest source of non-HMCR. For HMCR, the source contributions of soil dust, coal combustion, cement dust, vehicle, and secondary sources are 1.0 × 10−4, 3.7 × 10−5, 2.7 × 10−6, 1.6 × 10−6 and 1.9 × 10−9, respectively. The soil dust is the largest contributor to HMCR, being driven by the high impact of soil dust on PM2.5 and the abundance of heavy metals in soil dust.

Previous studies of polycyclic aromatic hydrocarbons (PAHs) in particulate matter, soils and livers of wild rats indicated that the city centre of Kumasi, Ghana has been severely polluted with high cancer potency. Cattle urine were therefore collected from Kumasi (urban) and Offinso (rural), Ghana: to determine concentrations of urinary PAH metabolites (OH-PAHs); and find their association with sex; and to estimate exposure of cattle to PAHs from the different sites. From the results, geometric mean concentrations (adjusted by specific gravity), GMSG, showed that 2-OHNaphthalene (2-OHNap) was the most abundant OH-PAH in cattle urine from all study sites, and naphthalene-containing-mothballs might have contributed significantly to the levels. There was no significant difference between urinary OH-PAHs concentrations in cattle from urban and rural sites except for 2-OHPhe and 4-OHPhe, and similar to urban areas, rural sites could also be polluted with PAHs. GMSG of 2-OHNap in cattle urine in Kokote (21.9 ± 6.51 ng/mL; a rural area), was significantly higher compared to the other sites followed by Oforikrom (4.15 ± 4.37 ng/mL; urban). The GMSG concentration (ng/mL) of the sum of OH-PAHs decreased in the order, Kokote (44.7) > Oforikrom (7.87) > Saboa (6.98) > Santasi (6.68) > and Twumasen Estate (5.23). The high concentrations of urinary 2-OHNap, 2-3-OHFlu, 2-OHPhe, 3-OHPhe and 4-OHPhe in Kokote indicated high PAHs exposure to cattle in this area or different/specific source of PAHs exposure. GMSG of 2-OHNap was significantly higher in male cattle compared to females while 1-9-OHPhe was significantly higher in females.

Exposure to particulate matter (PM) is associated with various health effects. Physico-chemical properties influence the toxicological impact of PM, nonetheless the mechanisms underlying PM-induced effects are not completely understood.Human bronchial epithelial cells were used to analyse the pathways activated after exposure to summer and winter urban PM and to identify possible markers of exposure.BEAS-2B cells were exposed for 24 h to 10 μg/cm² of winter PM2.5 (wPM) and summer PM10 (sPM) sampled in Milan. A microarray technology was used to profile the cells gene expression. Genes and microRNAs were analyzed by bioinformatics technique to identify pathways involved in cellular responses. Selected genes and pathways were validated at protein level (western blot, membrane protein arrays and ELISA).The molecular networks activated by the two PM evidenced a correlation among oxidative stress, inflammation and DNA damage responses. sPM induced the release of pro-inflammatory mediators, although miR-146a and genes related to inflammation resulted up-regulated by both PM. Moreover both PM affected a set of genes, proteins and miRNAs related to antioxidant responses, cancer development, extracellular matrix remodeling and cytoskeleton organization, while miR-29c, implicated in epigenetic modification, resulted up-regulated only by wPM. sPM effects may be related to biological and inorganic components, while wPM apparently related to the high content of organic compounds.These results may be helpful for the individuation of biomarkers for PM exposure, linked to the specific PM physico-chemical properties.

Although animal data have suggested the carcinogenic activity of trihalomethanes (THMs), there is inconsistent evidence supporting the link between THM exposure and cancers in humans.We investigated the association between specific and total blood THM levels with the risk of total cancer mortality in adults.We analyzed data from the 1999–2004 Third National Health and Nutrition Examination Survey and the Linked Mortality File of the United States. A total of 933 adults (20–59 years of age) with available blood THM levels and no missing data for other variables were included. Four different THM species (chloroform, bromodichloromethane (BDCM), dibromochloromethane (DBCM) and bromoform) were included, and the codes associated with cancer (malignant neoplasm) were C00 through C97, based on the underlying causes of death listed in the International Classification of Disease 10the Revision.Compared with adults in the lowest DBCM, bromoform, and total brominated THM tertiles, those in the highest DBCM, bromoform, and total brominated THM tertiles exhibited adjusted hazard ratios (HR) of total cancer mortality of 4.97 (95% confidence interval (CI) = 1.59–15.50), 4.94 (95% CI = 1.56–15.61), and 3.42 (95% CI = 1.21–15.43) respectively. The risk of total cancer mortality was not associated with increases in blood chloroform and total THM levels.We found that the baseline blood THM species, particularly brominated THMs, were significantly associated with total cancer mortality in adults. Although this study should be confirm by other studies, our findings suggest a possible link between THM exposures and cancer.

Airborne particulate matter (PM) was collected in Beijing between 24 February and 12 March 2014 to investigate chemical characteristics and potential industrial sources of aerosols along with health risk of haze events. Results showed secondary inorganic aerosol was the major contributor to PM2.5 during haze days. Utilizing specific elements, including Fe, La, Tl and As, as fingerprinting tracers, four emission sources, namely iron and steel manufacturing, petroleum refining, cement plant, and coal combustion were explicitly identified; their elevated contributions to PM during haze days were also estimated. The average cancer risk from exposure to inhalable PM toxic metals was 1.53 × 10⁻⁴ on haze days, which is one order of magnitude higher than in other developed cities. These findings suggested heavy industries emit large amounts of not only primary PM but also precursor gas pollutants, leading to secondary aerosol formation and harm to human health during haze days.

The distribution, inventory, and potential risk of organochlorine pesticides (OCPs), including Hexachlorocyclohexanes (HCHs) and Dichlorodiphenyltrichloroethanes (DDTs), and their correlation with soil properties and anthropogenic factors were investigated in soils of the Campanian Plain. The total concentrations of HCHs and DDTs ranged from 0.03 to 17.3 ng/g (geometric mean: GM = 0.05 ng/g), and 0.08–1231 ng/g (GM = 14.4 ng/g), respectively. In general, the concentration of OCPs in farmland and orchards was higher than on land used for non-agricultural purposes. There are significant differences in the concentration of OCPs in the soils across the region, more specifically, the Acerra-Marigliano conurbation (AMC) and Sarno River Basin (SRB) are recognized as severely OCP-contaminated areas. The recent application of technical HCHs and DDTs in large quantities appears unlikely in light of the ratio of α-HCH/β-HCH and p,p′-DDT/p,p′-DDE, and the prohibition of the use of these chemicals in Italy nearly forty years ago. The clear correlation between the concentration of DDTs and organic carbon suggests a typical secondary distribution pattern. The mass inventory of OCPs in soils of the Campanian Plain is estimated to have a GM of 17.3 metric tons. There is no clear evidence linking the impact of geographical distribution of OCPs on the incidence of cancer, and the 95% confidence interval of total incremental lifetime cancer risk (TILCR) data falls below the internationally accepted benchmark value of 1 × 10−5.

Pesticide exposure is hypothesized as one of the risk factors for the development of childhood brain tumors (CBT). This hospital-based case–control study evaluated the association of pyrethroid pesticide exposure with the risk for CBT in a children population in East China. In total, 161 CBT cases and 170 controls were recruited from 2 children's medical centers in Shanghai (Xinhua Hospital and Shanghai Children's Medical Center) between September 2012 and June 2015. The cases and controls were matched for age, sex, and province of residence. Pyrethroid pesticide exposure was evaluated by urinalysis of 3 nonspecific metabolites of pyrethroids (cis-DCCA, trans-DCCA, and 3-PBA) using gas chromatography-mass spectrometry (GC-MS) detection and by administering a questionnaire. Unconditional logistic regression showed that trans-DCCA, 3-PBA, and total metabolites (sum of the 3 metabolites) were positively associated with the increased risk of CBT. Children in the highest quartile had a nearly 3-fold increased risk of CBT compared with those in the lowest quartile after adjusting for confounding factors (trans-DCCA, odds ratio (OR) = 2.58, 95% confidence interval (CI), 1.38–4.80, p = 0.003; 3-PBA, OR = 3.26, 95% CI, 1.73–6.14, p < 0.0001; total metabolites, OR = 3.60, 95% CI, 1.87–6.93, p < 0.0001). We also found that exposure to both mosquitocide and cockroach killer was related to the increased risk of CBT (mosquitocide, OR = 1.68, 95% CI, 1.06–2.67, p = 0.027; cockroach killer, OR = 1.83, 95% CI, 1.13–2.95, p = 0.013). These findings indicate that exposure to pyrethroid pesticides might be associated with increased risk of CBT. Prospective cohort studies with larger sample sizes are required to confirm this conclusion.