Studies have linked gaseous air pollutants to multiple health effects via inflammatory pathways. Several major inflammatory biomarkers, including C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have also been considered as predictors of cardiovascular disease. However, there has been no meta-analysis to evaluate the associations between gaseous air pollutants and these typical biomarkers of inflammation to date. To evaluate the overall associations between short-term and long-term exposures to ambient ozone (O₃), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon dioxide (CO) and major inflammatory biomarkers including CRP, fibrinogen, IL-6 and TNF-α. A meta-analysis was conducted for publications from PubMed, Web of Science, Scopus and EMBASE databases up to Feb 1st, 2021. The meta-analysis included 38 studies conducted among 210,438 participants. Generally, we only observed significant positive associations between short-term exposures to gaseous air pollutants and inflammatory biomarkers. For a 10 μg/m³ increase in short-term exposure to O₃, NO₂, and SO₂, there were significant increases of 1.05% (95%CI: 0.09%, 2.02%), 1.60% (95%CI: 0.49%, 2.72%), and 10.44% (95%CI: 4.20%, 17.05%) in CRP, respectively. Meanwhile, a 10 μg/m³ increase in NO₂ was also associated with a 4.85% (95%CI: 1.10%, 8.73%) increase in TNF-α. Long-term exposures to gaseous air pollutants were not statistically associated with these biomarkers, but the study numbers were relatively small. Subgroup analyses found more apparent associations in studies with better study design, higher quality, and smaller sample size. Meanwhile, the associations also varied across studies conducted in different geographical regions. Short-term exposure to gaseous air pollutants is associated with increased levels of circulating inflammatory biomarkers, suggesting that a systemic inflammatory state is activated upon exposure. More studies on long-term exposure to gaseous air pollutants and inflammatory biomarkers are warranted to verify the associations.

Soil application of Zn fertilizer is an effective approach to improve yield and Zn accumulation in wheat grain. However, it remains unclear whether repeated Zn application can result in high accumulation of heavy metals (HMs) in soils and grains and thus represents a potential risk for human consumption. This study aimed to evaluate the health risk assessment of HMs in a wheat production system which had continuously received 8 years of Zn application at varying rates (0, 2.3, 5.7, 11.4, 22.7, 34.1 kg Zn ha⁻¹). The results showed that Zn application significantly increased the soil total Zn concentration without affecting concentrations of As, Pb, Cd, Cu and Cr. Across Zn rates, Zn application increased grain concentrations of Zn, Pb and Cd by 75%, 51% and 14%, respectively, and reduced grain As concentration by 14%. The human health risk assessment revealed that the threshold hazard quotients for the individual HM were below 1, independent of Zn rates. The hazard index (HI) values at Zn rates of 11.4, 22.7 and 34.1 kg Zn ha⁻¹ were significantly greater than that at null Zn treatment. Furthermore, exposures to As, Cu and Zn accounted for 97% of HI at all Zn rates. Analysis of the threshold cancer risk with Pb and As showed that ingestion of wheat grain even from highest Zn application rate wouldn’t bring the lifetime carcinogenic risk. In contrast, long-term Zn application significantly reduced the carcinogenic risk of As by 9.7–26.5%. In conclusion, repeated soil applications of Zn at optimal rate (5.7 kg Zn ha⁻¹) didn’t cause health risk for Zn, Cu, Cd, Pb, Cr, and As, while improving productivity and grain Zn concentration of wheat to meet human recruitment. Our study highlights the importance of appropriate Zn fertilizer management in improving grain quality while reducing HMs risks from human consumption.

This study assessed the impact on air quality and health risk by long-range transported (LRT) PM2.5-10- and PM2.5-bound metals and PAHs in Taipei City, Taiwan. Several methods with receptor aerosol measurements were used to quantify the effect of LRT. The hybrid single particle lagrangian integrated trajectory model (HYSPLIT) was used in conjunction with the potential source contribution function (PSCF) to distinguish the LRT aerosols. By using a general linear model (GLM) with a marginal mean and positive matrix fraction (PMF), this study also evaluated the annual increased level of LRT (AIRLRT) for each source contribution to the concentration and the resultant health risk of particle-bound metals and polycyclic aromatic hydrocarbons (PAHs). The LRT influenced fine-sized metals and PAHs rather than coarse-sized ones. We found that the level of PM2.5-bound toxic metals (Pb, Cd, and As) and PAHs (Benzo[a]pyrene and dibenzo[a,e]pyrene) could increase by 90% under the influence of LRT in 2014, while an AIRLRT value of 25% for the PM2.5 mass concentration was observed. Overall, the excess cancer risk (ECR) resulting from PM2.5-bound metal and PAH exposures was 6.40 × 10−5 in relation to coal combustions (20.7%), traffic-related emissions (59.7%) and re-suspended aerosols (19.6%). Among these contributors, LRT-related metals and PAHs in PM2.5 accounted for 51% of the total ECR.

In China, the huge amounts of energy consumption caused severe carcinogenic polycyclic aromatic hydrocarbon (PAHs) concentration in the soil and ambient air. This paper summarized that the references published in 2008–2018 and suggested that biomass, coal and vehicular emissions were categorized as major sources of PAHs in China. In 2016, the emitted PAHs in China due to the incomplete combustion of fuel was about 32720 tonnes, and the contribution of the emission sources was the sequence: biomass combustion > residential coal combustion > vehicle > coke production > refine oil > power plant > natural gas combustion. The total amount of PAHs emission in China at 2016 was significantly decreased due to the decrease of the proportion of crop resides burning (indoor and open burning).The geographical distribution of PAHs concentration demonstrated that PAHs concentration in the urban soil is 0.092–4.733 μg/g. At 2008–2012, the serious PAHs concentration in the urban soil occurred in the eastern China, which was shifted to western China after 2012.The concentration of particulate and gaseous PAHs in China is 1–151 ng/m3 and 1.08–217 ng/m3, respectively. The concentration of particle-bound PAHs in the southwest and eastern region are lower than that in north and central region of China. The incremental lifetime cancer risk (ILCR) analysis demonstrates that ILCR in the soil and ambient air in China is below the acceptable cancer risk level of 10−6 recommended by US Environmental Protection Agency (EPA), which mean that there is a low potential PAHs carcinogenic risk for the soil and ambient air in China.

DCOIT (4,5-dichloro-2-n-octyl-4-isothiazolin-3-one) is the main component of SeaNine-211, a new antifouling agent that replaces tributyltin to prevent the growth of undesirable organisms on ships. There have been some studies on the toxicity of DCOIT, but the mechanism of DCOIT’s toxicity to crustaceans still requires elucidation. This study examined the chronic toxicity (4 weeks) of 0, 3, 15, and 30 μg/L DCOIT to the Pacific white shrimp (Litopenaeus vannamei) from the aspects of growth and physiological and histological changes in the hepatopancreas and gills. A transcriptomic analysis was performed on the hepatopancreas to reveal the underlying mechanism of DCOIT in shrimp. The exposure to 30 μg/L DCOIT significantly reduced the survival and weight gain of L. vannamei. High Na⁺/K⁺-ATPase activity and melanin deposition were found in the gills after 4 weeks of 15 μg/L or 30 μg/L DCOIT exposure. The highest concentration of DCOIT (30 μg/L) induced changes in hepatopancreatic morphology and metabolism, including high anaerobic respiration and the accumulation of triglycerides. Compared with the exposure to 3 μg/L DCOIT, shrimp exposed to 15 μg/L DCOIT showed more differentially expressed genes (DEGs) than those in the control, and these DEGs were involved in biological processes such as starch and sucrose metabolism and choline metabolism in cancer. The findings of this study indicate that L. vannamei is sensitive to the antifouling agent DCOIT and that DCOIT can induce altered gene expression at a concentration of 15 μg/L and can interfere with shrimp metabolism, growth and survival at 30 μg/L.

Inhalation exposure to flame retardants used as additives to minimize fire risk and plasticizers is ubiquitous in human daily activities, but has not been adequately assessed. To address this research gap, the present study conducted an assessment of human health risk for four age groups through inhalation exposure to size fractionated particle-bound and gaseous halogenated flame retardants (polybrominated diphenyl ethers (PBDEs) and alternative halogenated flame retardants (AHFRs)) and organophosphate esters (OPEs) at indoor and outdoor environments (school, office, and residence) in three districts of a megacity (Guangzhou, China). Results demonstrated that OPEs were the dominant components among all targets. Indoor daily intakes of PBDEs and OPEs were 13–16 times greater than outdoor levels for all age groups. Gaseous OPEs contributed significantly greater than particle-bound compounds to daily intakes of all target compounds. Based on the different life scenarios, hazard quotient (HQ) and incremental life cancer risk (ILCR) from adults exposure to PBDEs and OPEs in indoor and outdoor settings were the greatest, followed by adolescents, children, and seniors. The estimated HQ and ILCR for all age groups both indoors and outdoors were lower than the safe level (HQ = 1 and ILCR = 10−6), indicating that the potential health risk for local residents in Guangzhou via inhalation exposure to atmospheric halogenated flame retardants and OPEs was low.

Atmospheric particulate matter (PM) pollution levels and human health risks resulting from exposure to non-anthropogenic pollution sources, such as coal mine-fires, are serious global issues. The toxicity of PM₁₀-bound metals and polycyclic aromatic hydrocarbons (PAHs) was assessed according to their non-cancer and cancer risks (CRs) at the mine-fire and in an adjacent city area. Health risks were estimated for inhalation, ingestion, and dermal absorption pathways. The non-cancer risks, presented in terms of the hazard index (HI) and hazard quotient (HQ), were found to be significant (>1) at all locations, except in the mining (for HQ-dermal) and city background area (for HQ-ingestion and HQ-dermal) in children and adults, respectively. The total CR was estimated to be highest at the city nearby the mine-fire area (3.31E-02 and 1.93E-02) followed by the mine-fire area (2.66E-02 and 1.71E-02) for children and adults, respectively. The total CR and CR via individual exposure routes were estimated to be in the high risk (10⁻³ ≤ CR < 10⁻¹) category at the mine-fire site and adjacent city area. For all exposures, CR levels were calculated to be higher than the acceptable range (from 1.00E-06 to 1.00E-04), except for the CR-inhalation level at the A5 location. Among all elements, Cd and BaPₑqᵤ were more significant for the CR at the coal mine-fire and the adjacent city area. Hence, this study concluded that non-anthropogenic sources, such as coal mine-fires, could be part for the significant health risk (carcinogenic and non-carcinogenic) levels in the study area.

Concentrations of unsubstituted and methylated polycyclic aromatic hydrocarbons (PAHs and Me-PAHs) were examined in road dusts from some representative areas with different land-use types in northern Vietnam, providing updated information about the occurrence, sources, and risks of these pollutants in Southeast Asian region. The Vietnamese road dusts were contaminated with low to moderate levels of PAHs and Me-PAHs as compared to those from other countries in the world. Concentrations of PAHs and Me-PAHs (Σ34PAHs) decreased in the order: urban (median 1800; range 1100–5500) ≈ industrial (1300; 550–10,000) > suburban (450; 310–1300) ≈ rural road dust (330; 210–2300 ng g⁻¹), suggesting an urban-rural declining trend and effects of urbanization-industrialization processes in PAH emission extent in Vietnam. The profiles and diagnostic ratios of PAHs and Me-PAHs in our samples revealed that these compounds were mainly derived from pyrogenic sources rather than petrogenic sources. Traffic emissions (e.g., vehicle exhaust, tire debris, and possible leaks of fuels, oils, and lubricants) were estimated as principal sources of PAHs and Me-PAHs, especially in the urban and industrial areas. Other pyrogenic sources (e.g., coal, wood, and biomass combustion) were also existed in the industrial, suburban, and rural areas, reflecting PAH origins from thermal industrial processes, open burning of agricultural by-products, and domestic energy utilization. Persons working outdoors and children in the urban and industrial areas were estimated to receive higher intake doses of PAHs and Me-PAHs, which were one to two orders of magnitude higher than those estimated for other groups. Except for potential cancer risk estimated for the occupational groups in the industrial area under the worst exposure scenarios, the non-cancer and cancer risk levels were generally acceptable; however, more comprehensive risk assessment considering other exposure pathways (e.g., inhalation and diet) is needed.

Gaseous and particulate polycyclic aromatic hydrocarbons (PAHs) and size-segregated particulate matter (PM) in indoor air and outdoor air, along with personal exposure, were monitored in rural households of Northern China. The daily average concentrations of 28 species were 1310 ± 811, 738 ± 321, 465 ± 247, and 655 ± 250 ng/m3 in kitchen air, bedroom air, and outdoor air, and for personal exposure, respectively. PAHs tended to occur in the particulate phase with increasing molecular weight. Absorption by particulate organic carbon was dominant in the gas-particle partitioning process. The daily averaged concentrations of PM2.5 and PM1.0 were 104 ± 39.5 and 88.4 ± 39.3 μg/m3 in kitchen air, 79.0 ± 63.2 and 65.7 ± 57.5 μg/m3 in bedroom air, 52.9 ± 16.5 and 41.5 ± 12.5 μg/m3 in outdoor air, and 71.7 ± 30.8 and 61.5 ± 28.4 μg/m3 for personal exposure, respectively. The non-priority components contributed 5.5 ± 2.8% to the total PAHs, while their fraction of carcinogenic risk reached 85.6 ± 6.9%. The mean cancer risk posed to rural residents via inhalation exposure to PAHs exceeded the current acceptable threshold of 1.0 × 10−6 and the national average estimated in China. The personal exposure levels of PAHs and PM in households using clean energy were lower than those in households using traditional biomass by 30.0%, 29.4%, and 38.5% for PAH28, PM2.5, and PM1.0, respectively. However, the cancer risk of personal inhalation exposure to PAH28 from using liquid petroleum gas (LPG) was higher than that from using firewood, implying the adoption of LPG may not effectively reduce the cancer risk despite the decreasing exposure levels of PAH28 and PM with respect to the use of firewood. Cooking individuals suffered higher exposure levels of PAH28 and PM1.0 compared with non-cooking individuals, and the cancer risk of personal inhalation exposure to PAH28 for cooking individuals was 1.7 times that for non-cooking individuals. Cooking was a critical factor that affected the personal exposure levels of the local male and female residents.

Heavy metals in the topsoil affected adversely human health through inhalation, ingestion and dermal contact. The health risk assessment, which are quantified from soil heavy metals sources under different land use, can provide an important reference basis for preventing and controlling the soil heavy metals pollution from the source. In this study, simple statistical analysis and Positive Matrix Factorization (PMF) were used to quantify sources of soil heavy metals; then a health risk assessment (HRA) model combined with PMF was proposed to assess quantificationally the human health risk (including non-cancer risk and cancer risk) from sources under residential-land, forest-land and farm land. Xiang River New District (XRNQ) was chosen as the example and four significant sources were quantitatively analyzed in the study. For cancer risk, industrial discharge was the largest source and accounted for about 69.6%, 69.7%, 56.5% for adults under residential-land, forest-land and farm-land, respectively. For non-cancer risk, industrial discharge was still the largest significant source under residential-land and forest-land and accounted for about 41.7%, 39.2% for adult, respectively; while agricultural activities accounted for about 51.8% for adult under farm-land. The risk trend of children, including cancer risk and non-cancer risk, was similar with adults. However, the non-cancer risk areas of adults affected by industrial discharge was higher than that of children, while the cancer risk areas of adults were on the contrary. The new exploration was useful to assess health risk quantification from sources under different land use, thus providing certain reference in preventing and controlling the pollution from the source for local authorities effectively.