Public health is threatened by air pollution and high temperature, especially in urban areas and areas impacted by climate change. Well-designed urban forms have co-benefits on promoting human health and mediating atmospheric environment-related threats (e.g., high temperature and air pollution). Previous studies overlooked these mediating effects of urban form on suicide mortality. This study used partial least squares modeling and countywide data in Taiwan to identify the crucial influences and pathways of urban environment, socioeconomic status, and diseases on suicide mortality. The model considered the impact of the characteristics of urban form (i.e., urban development intensity, land mix, and urban sprawl), urban industrial status (i.e., industrial level), urban greening (i.e., green coverage), disease (i.e., important diseases morbidity of human immunodeficiency virus [HIV], cerebrovascular disease [CVD], chronic liver disease and cirrhosis [CLDC], nephritis, nephrotic syndrome and nephrosis [NNSN], malignant tumor [MT]), socioeconomic status (i.e., income level and aging population rate), and the atmospheric environment (i.e., air pollution and high temperature) on suicide mortality. Optimizing land mix and minimizing urban development intensity and urban sprawl have been found to reduce suicide mortality. The mediating effect of urban form on suicide mortality originated from air pollution and high temperature, and mediating air pollution was greater than high temperature. Furthermore, industrial level, important diseases (HIV, CVD, CLDC, NNSN, and MT) morbidity, an aging population rate, air pollution, and high temperature were associated with an increase in suicide mortality, whereas green coverage and income level were associated with a reduction in suicide rates. The findings demonstrate that appropriate urban policy and urban planning may lower suicide mortality, be useful strategies for suicide prevention, and be a foundation for building a healthy city. Moreover, this study provides clarity on the complex relationship of suicide and the urban environment while identifying crucial factors.

The short-term alteration of peripheral cytokines may be an early adverse health effect of PM₂.₅ exposure and may be further associated with cardiovascular disease. We conducted a randomized, double-blind crossover trial using true or sham air filtration among 54 healthy college students in Beijing to investigate the potential benefits of short-term indoor air filtration and the adverse health effects of time-weighted personal PM₂.₅ exposure through inflammatory cytokines. The participants randomly received true or sham air filtration intervention for a week, and the treatment was changed after a two-week washout period. Peripheral blood samples were collected after each intervention period to measure 38 inflammatory cytokines. A linear mixed-effects model was applied to estimate the impacts of air purification or a 10 μg/m³ PM₂.₅ exposure increase on cytokines. Lag effects of PM₂.₅ exposure were analyzed using single-day and moving average lag models. Air filtration reduced indoor and time-weighted average personal PM₂.₅ concentrations by 69.0% (from 33.6 to 10.4 μg/m³) and 40.3% (from 40.6 to 24.3 μg/m³), respectively. We observed a significant association of PM₂.₅ exposure with growth-regulated alpha protein (GRO-α) of −11.3% (95%CI: 17.0%, −5.4%). In the lag models, significant associations between personal PM₂.₅ exposure and interleukin-1 receptor antagonist (IL-1Ra), monocyte chemotactic protein (MCP-1), and eotaxin were obtained at lag0, while associations with cytokines including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein-1β (MIP-1β), IL-4, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) were noted at relatively long lagged exposure windows (lag5-lag6). No significant alteration in cytokines was observed under true air filtration intervention. Our study indicates the effectiveness of air filtration on indoor PM₂.₅ reduction. PM₂.₅ exposure may decrease GRO-α levels and change different cytokine levels time-varyingly. Further study is still needed to explore the mechanisms of PM₂.₅ exposure on the inflammatory response.

PM₂.₅ (particulate matter ≤2.5 μm in aerodynamic diameter) is a major urban air pollutant worldwide. Its effects on the respiratory system of the susceptible population have been less characterized. This study aimed to estimate the association of short-term PM₂.₅ exposure with respiratory outcomes of the retired adults, and to examine whether these associations were stronger among the subjects with GSTT-null genotype. 32 healthy subjects (55–77 years) were recruited for five follow-up examinations. Ambient concentrations of PM₂.₅ were monitored consecutively for 7 days prior to physical examination. Pulmonary outcomes including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV₁), peak expiratory flow (PEF), and fractional exhaled nitric oxide (FeNO), and nasal fluid concentrations of 8-epi-prostaglandin F2 alpha (8-epi-PGF2α), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and IL-1β were measured. A linear mixed-effect model was introduced to evaluate the associations of PM₂.₅ concentrations with respiratory outcomes. Additionally, GSTT1 genotype-based stratification was performed to characterize modification on PM₂.₅-related respiratory outcomes. We found that a 10 μg/m³ increase in PM₂.₅ was associated with decreases of 0.52 L (95% confidence interval [CI]: -1.04, -0.002), 0.64 L (95% CI: -1.13, -0.16), 0.1 (95% CI: -0.23, 0.04) and 2.87 L/s (95% CI: -5.09, -0.64) in FVC, FEV₁, FEV₁/FVC ratio and PEF at lag 2, respectively. Meanwhile, marked increases of 80.82% (95% CI: 5.13%, 156.50%) in IL-8, 77.14% (95% CI: 1.88%, 152.40%) in IL-1β and 67.87% (95% CI: 14.85%, 120.88%) in 8-epi-PGF2α were observed as PM₂.₅ concentration increased by 10 μg/m³ at lag 2. Notably, PM₂.₅-associated decreases in FVC and PEF and increase in FeNO were stronger among the subjects with GSTT1-null genotype. In summary, short-term exposure to PM₂.₅ is associated with nasal inflammation, oxidative stress and lung function reduction in the retired subjects. Lung function reduction and inflammation are stronger among the subjects with GSTT1-null genotype.

Polycyclic Aromatic Hydrocarbons are strongly associated with agricultural, residential, transportation, and industrial activities. This study determined by GC-MS the concentration of 15 PAHs in soil and sediments at different sites from the Awotan-Asunle dumpsite area in the Southwestern region of Nigeria, which is one of the largest dumpsites in Africa. The sources of contamination, toxicity and associated risks for human health were also evaluated. Total PAHs concentrations were from 489 to 5616 μg kg⁻¹, and 642–2159 μg kg⁻¹, for soil and sediment, respectively. For soils, the highest values were observed for indeno[1,2,3-c,d]pyrene, coronene, and phenanthrene, while for sediments, the most abundant species were pyrene, fluoranthene and phenanthrene. Diagnostic ratios were used to determine the sources of PAHs and suggested that the compounds were mainly emitted from non-traffic sources. The total BaP-TEQ and BaP-MEQ for soils did not exceed the value recommended by the Canadian guideline since the country does not present guidelines. The analysis of incremental lifetime cancer risk was high mostly for dermal and ingestion exposures in the population. This study might provide valuable information regarding exposure to PAHs in soils of a Nigerian community.

Two farmed freshwater fish species Nile tilapia (Oreochromis niloticus) and jade perch (Scortum barcoo) were cultured with food waste-based diets and compared with commercial formulated control diet for a period of six months. Sixteen priority polycyclic aromatic hydrocarbons (PAHs) in the diets and cultured fish meat were tested by gas chromatography–mass spectrometry. No significant differences of ∑PAHs were observed between Nile tilapia and jade perch fed with food waste-based diets and control diet (p > 0.05). However, there were significantly higher concentration of ∑PAHs in market fish compared with the same species of fish fed by food waste-based diets (p < 0.05). Thus, the food waste-based diets have a potential to lower the PAH concentrations in farmed fish when compared with market fish. Based on the PAH concentrations, a human health risk assessment was made. The results indicated there were no non-cancer and very low cancer risks of consuming fish cultured with food waste-based diets at the 95th centile (Nile tilapia: hazard index (HI adult) = 0.343 × 10−3, HI children = 0.614 × 10−3 and cancer risk value = 0.943 × 10−6; jade perch: HI adult = 0.456 × 10−3, HI children = 0.814 × 10−3 and cancer risk value = 0.291 × 10−6). In general, the fish fed with food waste-based diets were unlikely to cause adverse health effects, based on the concentrations of PAHs. There is great potential for using food waste-based diets as an alternative to commercial feeds for cultivating freshwater fish.

Urban parks are an important part of the urban ecological environment. The environmental quality of parks is related to human health. To evaluate sources of polycyclic aromatic hydrocarbons (PAHs) in soils of urban parks and their possible health risks, soil samples from 122 parks in Beijing, China, were collected and analyzed. The total content of 16 PAHs between 0.066 and 6.867 mg/kg. Four-ring PAHs were predominant, followed by 5-ring PAHs, while the fraction of 2-ring PAHs was the lowest. The dominant PAHs sources were found to be coal combustion and oil fuels such as gasoline and diesel. A conditional inference tree (CIT) was used to identify the key influencing factors for PAHs. Traffic emissions was the most important factor, followed by coal consumption, as well as the history and location of the park. Incremental lifetime cancer risk (ILCR) for urban park soil in Beijing were low under normal conditions. The soil PAHs exposure pathway risk for both children and adults decreased in the following order: ingestion > dermal contact > inhalation. The risk from soil in parks to children’s health is slightly higher than that of adults, although the health risk due to exposure to PAHs was not extraordinary. Ecosystem risk was negligible.

This study reports a characterization of indoor polycyclic aromatic hydrocarbons (PAHs) associated with dust (dust-PAHs) in household evaporative coolers and their associated health effects. Extensive analysis showed that the indoor dust-PAHs stemmed mostly from pyrogenic sources (vehicular emissions) with mean total concentrations limited between 131 and 429 ng g−1. The distribution pattern of PAHs based on number of rings exhibited the following order of decreasing relative abundance: 4 > 3 > 5 > 6 > 2 rings. Results indicate that the mutagenicity of dust-PAHs exceeded their carcinogenicity, but that the potential carcinogenic effects are still significant. The mean lifetime cancer risk for different age groups for three pathways based on Model 2 (dermal (1.39 × 10−1 to 1.91 × 10−2), ingestion (2.13 × 10−3 to 8.08 × 10−3) and inhalation (1.62 × 10−7 to 4.06 × 10−7)) was 7.4–146 times higher than values predicted by Model 1 (dermal (5.13 × 10−5 to 3.03 × 10−3), ingestion (9.34 × 10−5 to 1.31 × 10−3) and inhalation (7.13 × 10−20 to 1.68 × 10−20)). Hence, exposure to dust-PAHs in household evaporative coolers lead to high risk, especially for children (less than 11 years) (HQ = 2.71 × 10−20 to 54.8 and LTCRs = 7.13 × 10−20 to 1.39 × 10−1). Strategies should be considered to eliminate such pollutants to protect people, especially children, from the non-carcinogenic and carcinogenic effects by changing household evaporative coolers with other cooling systems.

Interactions between the intestine and the liver, the so-called ‘gut-liver axis’, play a crucial role in the onset of hepatic steatosis and non-alcoholic fatty liver disease. However, not much is known about the impact of environmental pollutants on the gut-liver axis and consequent hepatic steatosis. Bisphenol A (BPA), a widely used plasticiser, is an important environmental contaminant that affects gut microbiota. We hypothesised that BPA induces hepatic steatosis by promoting gut microbiota dysbiosis and activating the gut-liver axis. In this study, male CD-1 mice were fed with diet containing BPA (50 μg/kg body weight/day) for 24 weeks. Dietary exposure to BPA increased lipid contents and fat accumulation in the liver. Analysis of 16 S rRNA gene sequencing revealed that the diversity of gut microbiota reduced and the composition of gut microbiota was altered in the BPA-fed mice. Further, the abundance of Proteobacteria, a marker of dysbacteria, increased, whereas the abundance of Akkermansia, a gut microbe associated with increased gut barrier function and reduced inflammation, markedly decreased. Expression levels of intestinal tight junction proteins (zona occludens-1 and occludin) also decreased drastically, leading to increased intestinal permeability and elevated levels of endotoxins. Furthermore, BPA up-regulated the expression of Toll-like receptor 4 (TLR4) and phosphorylation of nuclear factor-kappa B (NF-κB) in the liver and increased the production of inflammatory cytokines, including interleukin-1β, interleukin-18, tumour necrosis factor-α, and interleukin-6. Take together, our work indicated that dietary intake of BPA induced hepatic steatosis, and this was closely related to dysbiosis of gut microbiota, elevated endotoxin levels, and increased liver inflammation through the TLR4/NF-κB pathway.

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.

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.