Sediment samples collected from shelf, slope and interior basin of the northern Gulf of Mexico during 2011–2013, 1–3 years after the Deepwater Horizon (DWH) oil spill, were utilized to characterize PAH pollution history, in this region. Results indicate that the concentrations of surface ΣPAH43 and their accumulation rates vary between 44 and 160 ng g−1 and 6–55 ng cm−2 y−1, respectively. ΣPAH43 concentration profiles, accumulation rates and Δ14C values are significantly altered only for the sediments in the immediate vicinity of the DWH wellhead. This shows that the impact of DWH oil input on deep-sea sediments was generally limited to the area close to the spill site. Further, the PAHs source diagnostic analyses suggest a noticeable change in PAHs composition from higher to lower molecular weight dominance which reflects a change in source of PAHs in the past three years, back to the background composition. Results indicate low to moderate levels of PAH pollution in this region at present, which are unlikely to cause adverse effects on benthic communities.

Cytochrome P450 1A2 (CYP1A2) is an enzyme involved in the metabolic activation of certain carcinogens, and inducible by toxic substrates. To date, few studies have investigated in vivo CYP1A2 induction in humans and its relationship to polycylic aromatic hydrocarbons (PAHs) like benzo(a)pyrene (BaP). Non-smoking healthy male coke-oven workers (n = 30) were recruited as ‘exposure’ group, and non-smoking healthy office workers in the same city (n = 10) were selected as ‘control’ group, to test whether high inhalation exposure to PAHs can induce CYP1A2 activity in human livers. Significantly higher inhalation exposure of PAHs were found among the exposure group compared to the control. Inhalation BaP exposure concentration in the exposure group was more than 30 times higher than the control group (p < 0.001). However, the exposure group did not exhale significant higher levels of ¹³CO2/¹²CO2 in breath samples (p = 0.81), and no significant relationship was found between the inhaled BaP concentration and the ¹³CO2/¹²CO2 ratio (p = 0.91). A significant association was found between the ¹³CO2/¹²CO2 exhalation and dietary BaP intake level. Hepatic CYP1A2 activity/induction level was not effected by inhaled BaP but was altered by ingestion of BaP.

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.

The presence of polycyclic aromatic hydrocarbons (PAHs) in biochars hinders their environmental use. The aim of this study was to determine the freely dissolved (Cfree) PAH content in soil amended with biochar in a long-term (851 days) field experiment. Biochar was added to the soil at a rate of 30 and 45 t/ha. The addition of biochar to the soil resulted in a decrease in Σ13 Cfree PAHs by 25 and 22%, in the soil with the addition of biochar at the rate of 30 and 45 t/ha, respectively. As far as individual PAHs are concerned, in most cases a reduction in Cfree was also observed (from 3.6 to 66%, depending on the biochar rate). During the first 105 days of the experiment, the content of Σ13 Cfree in the biochar-amended soil significantly decreased by 26% (30 t/ha) and 36% (45 t/ha). After this period of time until the end of the experiment, no significant changes in Cfree were observed, regardless of the biochar rate. However, the behavior of individual PAH groups differed depending on the number of rings and experimental treatment. Ultimately, after 851 days of the experiment the content of Σ13 Cfree PAHs was lower by 29% (30 t/ha) and 35% (45 t/ha) compared to the beginning of the study as well as lower by 40% (30 t/ha) and 42% (45 t/ha) than in the control soil. The log KTOC coefficients calculated for the biochar-amended soils were higher immediately after adding biochar and subsequently they gradually decreased, indicating the reduced strength of the interaction between biochar and the studied PAHs. The obtained results show that the addition of biochar to soil does not create a risk in terms of the content of Cfree PAHs.

Recent studies indicate that PAH transformation products such as ketone or quinone-substituted PAHs (OPAHs) are potent aryl hydrocarbon receptor (AhR) activators that elicit toxicological effects independent of those observed for PAHs. Here, we measured eight OPAHs, two sulfur-containing (SPAH), one oxygen-containing (DBF), and one nitrogen-containing (CARB) heterocyclic PAHs (i.e. ΣONS-PAHs = OPAH8 + SPAH + DBF + CARB) in 35 stream sediments collected from a small (∼1303 km²) urban watershed located in south-central Pennsylvania, USA. Combined ΣONS-PAH concentrations ranged from 59 to 1897 μg kg⁻¹ (mean = 568 μg kg⁻¹; median = 425 μg kg⁻¹) and were 2.4 times higher in urban versus rural areas, suggesting that activities taking place on urban land serve as a source of ΣONS-PAHs to sediments. To evaluate urban land use metrics that might explain these data, Spearman rank correlation analyses was used to evaluate the degree of association between ΣONS-PAH concentrations and urban land-use/land-cover metrics along an urban-rural transect at two spatial scales (500-m and 1000-m upstream). Combined ΣONS-PAH concentrations showed highly significant (p < 0.0001) correlations with ΣPAH19, residential and commercial/industrial land use (RESCI), and combined state and local road miles (MILES), suggesting that ΣONS-PAHs originate from similar sources as PAHs. To evaluate OPAH sources, a subset of ΣONS-PAHs for which reference assemblages exist, an average OPAH fractional assemblage for urban sediments was derived using agglomerative hierarchal cluster (AHC) analysis, and compared to published OPAH source profiles. Urban sediments from the Condoguinet Creek (n = 21) showed highly significant correlations with urban particulate matter (X² = 0.05, r = 0.91, p = 0.0047), suggesting that urban particulate matter is an important OPAH source to sediments in this watershed. Results suggest the inclusion of ΣONS-PAH measurements adds value to traditional PAH analyses, and may help elucidate and refine pollutant source identification in urban watersheds.

Polycyclic aromatic hydrocarbons (PAHs) were studied in 230 daily fine particulate matter (PM2.5) samples collected in four seasons at urban and suburban sites of Shanghai, China. This study focused on the emission sources of PAHs and its dynamic results under different weather conditions and pollution levels and also emphasized on the spatial sources of PM2.5 and PAHs at a regional level. Annual concentrations of PM2.5 and 16 EPA priority PAHs were 53 μg/m3 and 6.9 ng/m3, respectively, with highest levels in winter. Positive matrix factorization (PMF) modeling identified four sources of PAHs: coal combustion, traffic, volatilization and biomass combustion, and coking, with contributions of 34.9%, 27.5%, 21.1% and 16.5%, respectively. The contribution of traffic, a local-indicative source, increased from 17.4% to 28.7% when wind speed changed from >2m/s to <2m/s, and increased from 18.3% to 31.3% when daily PAH concentrations changed from below to above the annual mean values. This indicated that local sources may have larger contributions under stagnant weather when poorer dispersion conditions and lower wind speed led to the accumulation of local-emitted pollutants. The trajectory clustering and potential source contribution function (PSCF) and concentration weighted trajectory (CWT) models showed clearly that air parcels moved from west had highest concentrations of PM2.5, total PAHs and high molecular weight (HMW) PAHs. While small differences were found among all five clusters in low molecular weight (LMW) PAHs. Sector analyses determined that regional transport source contributed 39.8% to annual PM2.5 and 52.5% to PAHs, mainly from western regions and varying with seasons. This work may make contribution to a better understanding and control of the increasingly severe air pollution in China as well as other developing Asian countries.

In August 2009, a blowout of the Montara H1 well 260 km off the northwest coast of Australia resulted in the uncontrolled release of about 4.7 M L of light crude oil and gaseous hydrocarbons into the Timor Sea. Over the 74 day period of the spill, the oil remained offshore and did not result in shoreline incidents on the Australia mainland. At various times slicks were sighted over a 90,000 km² area, forming a layer of oil which was tracked by airplanes and satellites but the slicks typically remained within 35 km of the well head platform and were treated with 183,000 L of dispersants. The shelf area where the spill occurred is shallow (100–200 m) and includes off shore emergent reefs and cays and submerged banks and shoals. This study describes the increased inputs of oil to the system and assesses the environmental impact. Concentrations of hydrocarbon in the sediment at the time of survey were very low (total aromatic hydrocarbons (PAHs) ranged from 0.04 to 31 ng g⁻¹) and were orders of magnitude lower than concentrations at which biological effects would be expected.

Increasing anthropogenic activities in the Arctic represent an enhanced threat for oil pollution in a marine environment that is already at risk from climate warming. In particular, this applies to species with free-living pelagic larvae that aggregate in surface waters and under the sea ice where hydrocarbons are likely to remain for extended periods of time due to low temperatures. We exposed the positively buoyant eggs of polar cod (Boreogadus saida), an arctic keystone species, to realistic concentrations of a crude oil water-soluble fraction (WSF), mimicking exposure of eggs aggregating under the ice to oil WSF leaking from brine channels following encapsulation in ice. Total hydrocarbon and polycyclic aromatic hydrocarbon levels were in the ng/L range, with most exposure concentrations below the limits of detection throughout the experiment for all treatments. The proportion of viable, free-swimming larvae decreased significantly with dose and showed increases in the incidence and severity of spine curvature, yolk sac alterations and a reduction in spine length. These effects are expected to compromise the motility, feeding capacity, and predator avoidance during critical early life stages for this important species. Our results imply that the viability and fitness of polar cod early life stages is significantly reduced when exposed to extremely low and environmentally realistic levels of aqueous hydrocarbons, which may have important implications for arctic food web dynamics and ecosystem functioning.

Polycyclic aromatic hydrocarbons (PAHs) were assessed spatially and temporally within and adjacent to a former coking and steel manufacturing facility in Sydney, Nova Scotia, Canada. Concentrations of PAHs were measured in surface soils, marine and estuary sediments prior to and during remediation of the Sydney Tar Ponds (STPs) site which was contaminated by nearly a century of coking and steel production. Previous studies identified PAHs in surficial marine sediments within Sydney Harbour, which were considered to be derived from STP discharges. Numerous PAH fingerprint techniques (diagnostic ratios, principal component analysis, quantitative and qualitative analysis) were applied to soil and sediment samples from the STPs and surrounding area to identify common source apportionment of PAHs. Results indicate coal combustion (from historical residential, commercial and industrial uses) and coal handling (from historic on-site stockpiling and current coal transfer and shipment facilities) are likely the principal source of PAHs found in urban soils and marine sediments, consistent with current and historical activities near these sites. However, PAH fingerprints associated with STP sediments correlated poorly with those of urban soils and marine sediments, but were similar to coal tar, historically consistent with by-products produced by the former coking operations. This study suggests PAH contamination of Sydney Harbour sediments and urban soils is largely unrelated to historic coking operations or recent remediation of the STPs site, but rather a legacy of extensive use of coal for a variety of activities.

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).