Recently, health damage to children exposed to synthetic polyurethane (PU) running tracks has aroused social panic in China. Some possible toxic volatiles may be responsible for these damages. However, the exact cause remains unclear. We have detected a low concentration of sulfur dioxide (SO₂; 1.80–3.30 mg/m³) on the surface of the PU running track. Surprisingly, we found that SO₂ was generated from the PU running track, and even such a low concentration of SO₂ could induce severe lung inflammation with hemorrhage, inflammatory cell infiltration, and inflammatory factor secretion in mice after 2-week exposure. Prolonged exposure (5 weeks) to the SO₂ caused chronic pulmonary inflammation and pulmonary fibrosis in the mice. Peripheral hemogram results showed that platelet concentration increased significantly in the SO₂ group compared to that in the control group, and the proportion of blood neutrophils and monocytes among total leukocytes was more imbalanced in the SO₂ group (16.6%) than in the control group (8.0%). Further histopathology results of sternal marrow demonstrated that hematopoietic hyperplasia was severely suppressed with increased reticular stroma and adipocytes under SO₂ exposure. These data indicate that a low concentration of SO₂ generated spontaneously from PU running track outdoors as a secondary product is still harmful to health, as it impairs the respiratory system, hematopoiesis, and immunologic function. This indicates that the low-concentration SO₂ could be a major cause of diseases induced by air pollution, such as chronic obstructive pulmonary disease.

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.

The effect of ambient air pollution exposure on childhood hypertension has emerged as a concern in China, and previous studies suggested pet ownership is associated with lower blood pressure (BP). However, limited information exists on the interactive effects pet ownership and air pollution exposure has on hypertension. We investigated the interactions between exposure to pet ownership and air pollutants on hypertension in Chinese children. 9354 students in twenty-four elementary and middle schools (aged 5–17 years) in Northeastern China were evaluated during 2012–2013. Four-year average concentrations of particulate matter with aerodynamic diameter of ≤10 μm (PM10), SO2, NO2, and O3, were collected in the 24 districts from 2009 to 2012. Hypertension was defined as average diastolic or systolic BP (three time measurements) in the 95th percentile or higher based on height, age, and sex. To examine effects, two-level regression analysis was used, controlling covariates. Consistent interactions between exposure to pet and air pollutants were observed. Compared to children exposed to pet, those not exposed exhibited consistently stronger effects of air pollution. The highest odds ratios (ORs) per 30.6 μg/m3 increase in PM10 were 1.79 (95%confidence interval [95%CI]: 1.29–2.50) in children without current pet exposure compared to 1.24 (95%CI: 0.85–1.82) in children with current pet exposure. As for BP, only O3 had an interaction for all exposure to pet ownership types, and showed lower BP in children exposed to pet. The increases in mean diastolic BP per 46.3 μg/m3 increase in O3 were 0.60 mmHg (95%CI: 0.21, 0.48) in children without pet exposure in utero compared with 0.34 mmHg (95%CI: 0.21, 0.48) in their counterparts. When stratified by age, pet exposure was more protective among younger children. In conclusion, in this large population-based cohort, pet ownership is associated with smaller associations between air pollution and hypertension in children, suggesting pet ownership reduces susceptibility to the health effects of pollutants.

Even though the Amazon region is widely studied, there is still a gap regarding Cr exposure and its risk to human health. The objectives of this study were to 1) determine Cr concentrations in seven chemical fractions and 6 particle sizes in Amazon soils, 2) quantify hexavalent Cr (CrVI) concentrations using an alkaline extraction, 3) determine the oral and lung bioaccessible Cr, and 4) assess Cr exposure risks based on total and bioaccessible Cr in soils. The total Cr in both A (0–20 cm) and B (80–100 cm) horizons was high at 2346 and 1864 mg kg⁻¹. However, sequential extraction indicated that available Cr fraction was low compared to total Cr, with Cr in the residual fraction being the highest (74–76%). There was little difference in total Cr concentrations among particle sizes. Hexavalent Cr concentration was also low, averaging 0.72 and 2.05 mg kg⁻¹ in A and B horizon. In addition, both gastrointestinal (21–22 mg kg⁻¹) and lung (0.95–1.25 mg kg⁻¹) bioaccessible Cr were low (<1.2%). The low bioavailability of soil Cr and its uniform distribution in different particle sizes indicated that Cr was probably of geogenic origin. Exposure based on total Cr resulted in daily intake > the oral reference dose for children, but not when using CrVI or bioaccessible Cr. The data indicated that it is important to consider both Cr speciation and bioaccessibility when evaluating risk from Cr in Amazon soils.

Melamine and phthalate, mainly di-(2-ethylhexyl) phthalate (DEHP), are ubiquitously present in the general environment. We investigated whether urine melamine levels can modify the relationship between DEHP exposure and markers of early renal damage in children. A nationwide health survey for Children aged ≤12 years possibly exposed to phthalates were enrolled between August 2012 and January 2013. They were administered questionnaires to collect details regarding past DEHP exposure to phthalate-tainted foodstuffs. Urine samples were measured melamine levels, phthalate metabolites and biomarkers of renal damage, including urine microalbumin/creatinine ratio (ACR), N-acetyl-beta-d-glucosaminidase (NAG), and β2-microglobulin. The study included 224 children who had a median urine melamine level (μg/mmol creatinine) of 1.61 ranging 0.18–47.42. Positive correlations were found between urine melamine levels and urine ACR as well as urine NAG levels (both Spearman correlation coefficients r = 0.24, n = 224, p < .001). The higher the past DEHP exposure or urine melamine levels, the higher the prevalence of microalbuminuria. An interaction effect was also found between urine melamine levels and past DEHP exposure on urine ACR. Melamine levels may further modify the effect of past DEHP exposure on urine ACR in children.

Foodstuffs may be contaminated by organophosphate esters (OPEs) and become an important source of human exposure since OPEs are ubiquitous in the environment. In the present study, 10 OPEs were analyzed in various food matrices collected from a city in Eastern China including chicken, pork, fishes, vegetables, tofu, eggs, milk and cereals. The concentrations of Σ₁₀OPEs ranged from 1.1 to 9.6 ng g⁻¹ fresh weight (fw) in the foodstuffs. Cereals had the highest residual level of total OPEs with a mean value of 5.7 ng g⁻¹ fw. Tris(2-ethylhexyl) phosphate was detected in all foodstuff samples and showed the highest median residual concentration of 1.3 ng g⁻¹ fw among the OPE analogs. The daily dietary intake of OPEs was calculated as 3.6 and 2.4 μg d⁻¹ for adults and children. Cereals were identified as the major contributor to the total OPEs among different types of foodstuffs. Preliminary exposure assessment revealed that the current non-cancer health risks of OPEs via dietary intake were in the range of 10⁻⁵-10⁻³, indicating low risk levels. Moreover, the hazard index of OPEs indicated that the risk for children (3 × 10⁻³) was higher than adults (2 × 10⁻³).

Bisphenols and triclosan (TCS) are widely used in consumer products. However, knowledge on human exposure to these anthropogenic chemicals has remained limited in China, especially for children. In this study, concentrations of seven bisphenols and TCS were determined in 283 urine samples collected from South China children aged between 3 and 11 years old. Bisphenol A (BPA), bisphenol S (BPS) and TCS were frequently detected in urine samples, with a detection rate of 93%, 89%, and 95%, respectively. Urinary concentrations of Σ7BPs (the sum concentrations of the seven bisphenols) ranged from 0.43 to 31.5 μg/L, with a median value of 0.91 μg/L, while TCS concentrations ranged from < limit of quantification to 21.9 μg/L (median: 0.21 μg/L). BPA was the predominant analogue (median: 0.35 μg/L), accounting for 49.8% of Σ7BPs. The urinary BPA concentrations in children from Guangzhou were significantly greater than those from Shenzhen. Correlation analysis suggested that multiple exposure sources to South China children likely existed for BPA, BPS, and TCS. Age, but not gender, was negatively associated with urinary residues of BPA and BPS (p < 0.05) and positively with TCS concentrations (p < 0.05). The estimated daily intake of Σ7BPs (23.9 ng/kg bw/day) or TCS (5.63 ng/kg bw/day) was below the tolerant reference dose of BPA, indicating no considerable health hazard to South China children.

Previously, we showed that manganese (Mn) levels in settled dust in elementary schools increased at a rate of 34.1% per km closer to a ferro-manganese alloy plant in the rainy season. In this study, we investigated how this environmental pollution indicator varied in the dry season and if there was an association with Mn biomarker levels in school-aged children. Dust samples were collected with passive samplers (disposable Petri dishes) placed in interior and exterior environments of 14 elementary schools. Occipital hair, toenails and blood samples were collected from 173 students aged 7–12 years from three of these schools, with varying distance from the industrial plant. Mn and lead (Pb) levels were measured by graphite furnace atomic absorption spectrometry. Mn concentration geometric means (GM) in dust fall accumulation in interior environments of schools located at 2, 4, 6 and > 6 km-radii from the plant were 2212, 584, 625 and 224 μg Mn/m2/30 days, respectively. The modelled rate of change of dust Mn levels decreases by 59.8% for each km further from the plant. Pb levels in settled dust varied between 18 and 81 μg/m2/30 days with no association with distance from the plant. Blood lead levels median (range) were 1.2 μg/dL (0.2–15.6), of which 97.8% were <5 μg/dL. Mn in hair and toenails were 0.66 μg/g (0.16–8.79) and 0.86 μg/g (0.15–13.30), respectively. Mn loading rates were positively associated with log MnH (β = 1.42 × 10−5, p < 0.001) after adjusting for children's age; and also with log MnTn (β = 2.31 × 10−5, p < 0.001) independent of age. Mn loading rates explained 18.5% and 28.5% of the variance in MnH and MnTn levels, respectively. School-aged children exposure to Mn, independently of age, increases significantly with school proximity to the ferro-manganese alloy plant.

Global burden of disease estimates reveal that people in Nigeria are living shorter lifespan than the regional or global average life expectancy. Ambient air pollution is a top risk factor responsible for the reduced longevity. But, the magnitude of the loss or the gains in longevity accruing from the pollution reductions, which are capable of driving mitigation interventions in Nigeria, remain unknown. Thus, we estimate the loss, and the gains in longevity resulting from ambient PM2.5 pollution reductions at the local sub-national level using life table approach. Surface average PM2.5 concentration datasets covering Nigeria with spatial resolution of ∼1 km were obtained from the global gridded concentration fields, and combined with ∼1 km gridded population of the world (GPWv4), and global administrative unit layers (GAUL) for territorial boundaries classification. We estimate the loss or gains in longevity using population-weighted average pollution level and baseline mortality data for cardiopulmonary disease and lung cancer in adults ≥25 years and for respiratory infection in children under 5. As at 2015, there are six “highly polluted”, thirty “polluted” and one “moderately polluted” States in Nigeria. People residing in these States lose ∼3.8–4.0, 3.0–3.6 and 2.7 years of life expectancy, respectively, due to the pollution exposure. But, assuming interventions achieve global air quality guideline of 10 μg/m3, longevity would increase by 2.6–2.9, 1.9–2.5 and 1.6 years for people in the State-categories, respectively. The longevity gains are indeed high, but to achieve them, mitigation interventions should target emission sources having the highest population exposures.

Air pollution is an important public health concern especially for children who are particularly susceptible. Latin America has a large children population, is highly urbanized and levels of pollution are substantially high, making the potential health impact of air pollution quite large. We evaluated the effect of air pollution on children respiratory mortality in four large urban centers: Mexico City, Santiago, Chile, and Sao Paulo and Rio de Janeiro in Brazil.Generalized Additive Models in Poisson regression was used to fit daily time-series of mortality due to respiratory diseases in infants and children, and levels of PM10 and O3. Single lag and constrained polynomial distributed lag models were explored. Analyses were carried out per cause for each age group and each city. Fixed- and random-effects meta-analysis was conducted in order to combine the city-specific results in a single summary estimate.These cities host nearly 43 million people and pollution levels were above the WHO guidelines. For PM10 the percentage increase in risk of death due to respiratory diseases in infants in a fixed effect model was 0.47% (0.09–0.85). For respiratory deaths in children 1–5 years old, the increase in risk was 0.58% (0.08–1.08) while a higher effect was observed for lower respiratory infections (LRI) in children 1–14 years old [1.38% (0.91–1.85)]. For O3, the only summarized estimate statistically significant was for LRI in infants. Analysis by season showed effects of O3 in the warm season for respiratory diseases in infants, while negative effects were observed for respiratory and LRI deaths in children.We provided comparable mortality impact estimates of air pollutants across these cities and age groups. This information is important because many public policies aimed at preventing the adverse effects of pollution on health consider children as the population group that deserves the highest protection.