Chemicals in consumer products have become the focus of recent regulatory developments including California's Safer Consumer Products Act. However, quantifying the amount of chemicals released during the use and post-use phases of consumer products is challenging, limiting the ability to understand their impacts. Here we present a comprehensive framework, OrganoRelease, for estimating the release of organic chemicals from the use and post-use of consumer products given limited information. First, a novel Chemical Functional Use Classifier estimates functional uses based on chemical structure. Second, the quantity of chemicals entering different product streams is estimated based on market share data of the chemical functional uses. Third, chemical releases are estimated based on either chemical product categories or functional uses by using the Specific Environmental Release Categories and EU Technological Guidance Documents. OrganoRelease connects 19 unique functional uses and 14 product categories across 4 data sources and provides multiple pathways for chemical release estimation. Available user information can be incorporated in the framework at various stages. The Chemical Functional Use Classifier achieved an average accuracy above 84% for nine functional uses, which enables the OrganoRelease to provide release estimates for the chemical, mostly using only the molecular structure. The results can be can be used as input for methods estimating environmental fate and exposure.

Organophosphate flame retardants (OPFRs) have been commonly observed in indoor dust, food, and drinking water in China, but little is known about their exposure levels or factors leading to exposure in Chinese children. In this study, we measured eight metabolites of OPFRs (mOPFRs) in 227 urine samples collected from 0- to 5-year-old children in China. The high detection rates of mOPFRs (60%–100%) in the collected urine samples demonstrated the widespread exposure of this population to OPFRs. The median concentrations indicated that bis(2-chloroethyl)phosphate (BCEP, 0.85 ng/mL) and diphenyl phosphate (DPHP, 0.27 ng/mL) were the dominant chlorinated mOPFRs and nonchlorinated mOPFRs, respectively. Interestingly, the median urinary levels of bis(1-chloro-2-propyl)phosphate (BCIPP, 6.48 ng/mL) and bis(2-butoxyethyl)phosphate (BBOEP, 0.31 ng/mL) in inpatient infants were one order of magnitude higher (p < 0.01) than those observed in outpatient infants. For home-stay participants, furthermore, infants (0–1 year) had the highest median levels of BCIPP (0.72 ng/mL) and dibutyl phosphate (DBP, 0.14 ng/mL) among the three age groups (i.e., 0–1, >1–3, and >3–5 years), and significantly (p < 0.05) negative age-related relationships were found for both urinary mOPFRs. Two set of data on estimated daily intakes (EDIs) were calculated based on the fraction of OPFR excreted as the corresponding mOPFR (FUE) in human liver microsomes (EDIHLM) and S9 fraction (EDIS₉) system, respectively. In general, children have relatively high EDIs of tris(2-chloroethyl)phosphate (TCEP: EDIHLM = 485 ng/kg bw/day, EDIS₉ = 261 ng/kg bw/day). Furthermore, 17% or 21% of inpatient infants had EDIs that exceeded the reference dose, whereas this value was reduced to 13% in outpatient infants; and this value decreased with age among all home-stay children (0–5 years). Our results indicated that inpatient and home-stay infants had a higher potential risk of OPFR exposure. To our knowledge, this is the first study to identify the elevated urinary levels of mOPFRs in inpatients.

Decabromodiphenyl Ethane (DBDPE), a kind of new brominated flame retardants (NBFRs) used to replace DecaBDE, has been frequently detected in the environment and human samples. In this study, we explored its toxic effects on male mouse offspring after perinatal exposure to DBDPE. During the perinatal period, pregnant ICR mice were exposed to DBDPE (100 μg/kg body weight) via oral gavage. After weaning, male offspring were fed on a low-fat diet and a high-fat diet, respectively. We measured and recorded body weight, liver weight, and epididymis fat mass, blood biochemical markers, metabolites changes in liver, and gene expression involved in lipid and glucose homeostasis. The results showed that perinatal exposure to DBDPE increased the risk of obesity in mouse offspring and affected triglyceride synthesis, bile secretion, purine synthesis, mitochondrial function and glucose metabolism, furthermore, the use of HFD feeding may further exacerbate these effects. All of these results show that early-life exposure to low doses of DBDPE can promote the development of metabolic dysfunction, which in turn induces obesity.

Pollutant mass fluxes are rarely measured in the laboratory, especially their turbulent component. They play a major role in the dispersion of gases in urban areas and modern mathematical models often attempt some sort of parametrisation. An experimental technique to measure mean and turbulent fluxes in an idealised urban array was developed and applied to improve our understanding of how the fluxes are distributed in a dense street canyon network. As expected, horizontal advective scalar fluxes were found to be dominant compared with the turbulent components. This is an important result because it reduces the complexity in developing parametrisations for street network models. On the other hand, vertical mean and turbulent fluxes appear to be approximately of the same order of magnitude. Building height variability does not appear to affect the exchange process significantly, while the presence of isolated taller buildings upwind of the area of interest does. One of the most interesting results, again, is the fact that even very simple and regular geometries lead to complex advective patterns at intersections: parametrisations derived from measurements in simpler geometries are unlikely to capture the full complexity of a real urban area.

An isotope-dilution ultra-performance liquid chromatography–electrospray tandem mass spectrometry method combined with dansylation was established to sensitively quantify four steroid estrogens (estrone, 17α-estradiol, 17β-estradiol and 17α-ethynylestradiol) and bisphenol A in sewage influent and effluent. A simple hexane extraction was performed from a small volume (10 mL), followed by dansyl chloride derivatization and purification with a silica cartridge. The method effectively reduced the matrix effects in sample extract and permitted the selective and sensitive determination of target compounds from complicated matrices. The detection limits of the method for steroid estrogens were 0.20–0.90 ng L⁻¹ in influent and 0.10–0.20 ng L⁻¹ in effluent samples. For bisphenol A, the limits detection of the method were 20 and 0.80 for influent and effluent samples, respectively. Recoveries of 85%–96% were observed in all matrices. The method was applied to analyze residual estrogens and bisphenol A in sewage influent and effluent samples from Beijing, China. The concentrations of bisphenol A (636–1200 ng L⁻¹) were up to 250 times higher than those of steroid estrogens. Estrone was the dominant estrogen in influent and effluent samples, while similar concentrations of 17α-estradiol and 17β-estradiol were detected in all samples.

Previous studies reported triggering of acute cardiovascular events by short-term increasedPM₂.₅ concentrations. From 2007 to 2013, national and New York state air quality policies and economic influences resulted in reduced concentrations of PM₂.₅ and other pollutants across the state. We estimated the rate of cardiovascular hospital admissions associated with increased PM₂.₅ concentrations in the previous 1–7 days, and evaluated whether they differed before (2005–2007), during (2008–2013), and after these concentration changes (2014–2016).Using the Statewide Planning and Research Cooperative System (SPARCS) database, we retained all hospital admissions with a primary diagnosis of nine cardiovascular disease (CVD) subtypes, for residents living within 15 miles of PM₂.₅ monitoring sites in Buffalo, Rochester, Albany, Queens, Bronx, and Manhattan from 2005 to 2016 (N = 1,922,918). We used a case-crossover design and conditional logistic regression to estimate the admission rate for total CVD, and nine specific subtypes, associated with increased PM₂.₅ concentrations.Interquartile range (IQR) increases in PM₂.₅ on the same and previous 6 days were associated with 0.6%–1.2% increases in CVD admission rate (2005–2016). There were similar patterns for cardiac arrhythmia, ischemic stroke, congestive heart failure, ischemic heart disease (IHD), and myocardial infarction (MI). Ambient PM₂.₅ concentrations and annual total CVD admission rates decreased across the period. However, the excess rate of IHD admissions associated with each IQR increase in PM₂.₅ in previous 2 days was larger in the after period (2.8%; 95%CI = 1.5%–4.0%) than in the during (0.6%; 95%CI = 0.0%–1.2%) or before periods (0.8%; 95%CI = 0.2%–1.3%), with similar patterns for total CVD and MI, but not other subtypes.While pollutant concentrations and CVD admission rates decreased after emission changes, the same PM₂.₅ mass was associated with a higher rate of ischemic heart disease events. Future work should confirm these findings in another population, and investigate whether specific PM components and/or sources trigger IHD events.

The neurotoxic effects of methylmercury (MeHg) have been intensively studied. However, the molecular mechanisms responsible for the neurotoxicity of MeHg are not fully understood. To decipher these mechanisms, proteomic and high-throughput mRNA sequencing (RNA-seq) technique were utilized, comprehensively evaluating the cellular responses of human neuroblastoma SK-N-SH cells to MeHg exposure. Proteomic results revealed that MeHg exposure interfered with RNA splicing via splicesome, along with the known molecular mechanisms of mercury-related neurotoxicity (e.g. oxidative stress, protein folding, immune system processes, and cytoskeletal organization). The effects of MeHg on RNA splicing were further verified using RNA-seq. Compared to control, a total of 658 aberrant RNA alternative splicing (AS) events were observed after MeHg exposure. Proteomics and RNA-seq results also demonstrated that mercury chloride (HgCl2) influenced the expression levels of several RNA splicing related proteins and 676 AS events compared to control. These results suggested that RNA splicing could be a new molecular mechanism involved in MeHg and HgCl2 neurotoxicity.

Lanthanum is a rare earth element (REE) which has been extensively studied due to its wide application in numerous fields with a potential accumulation in the environment. It has long been known for its potential to stimulate plant growth within a hormetic-biphasic dose response framework. This article provides evidence from a series of high resolution studies published within the last two decades demonstrating a substantial and significant occurrence of lanthanum-induced hormesis in plants. These findings suggest that hormetic responses should be built into the study design of hazard assessment study protocols and included in the risk assessment process. Hormesis also offers the opportunity to substantially improve cost benefit estimates for environmental contaminants, which have the potential to induce beneficial/desirable effects at low doses.

We assessed exposure to 39 brominated and 16 organophosphate ester flame retardants (FRs) from both dust and indoor air at seven childcare centres in Seattle, USA, and investigated the importance of nap mats as a source of these chemicals. Many childcare centres serving young children use polyurethane foam mats for the children's naptime. Until recently, the vast majority of these mats sold in the United States contained flame-retarded polyurethane foam to meet California Technical Bulletin 117 (TB117) requirements. With the 2013 update of TB117, allowing manufacturers to meet flammability standards without adding FRs to filling materials, FR-free nap mats have become widely available. We conducted an intervention study by actively switching out FR-treated nap mats with FR-free nap mats and measuring FR levels in indoor air and dust before and after the switch-out. The predominant FRs found in dust and indoor air were 2-ethylhexyl tetrabromobenzoate (EHTBB) and tris(1-chloro-2-propyl) phosphate (TCIPP), respectively. Nap mat samples analysed from four of the six centres contained a Firemaster® mixture, while one mat was predominantly treated with tris(1,3-dichloroisopropyl) phosphate (TDCIPP) and the other contained no detectable target FRs. After replacement, there was a significant decrease (p = 0.03–0.09) in median dust concentrations for bis(2-ethylhexyl) tetrabromophthalate (BEHTBP), EHTBB, tris(4-butylphenyl) phosphate (TBPP), and TDCIPP with reductions of 90%, 79%, 65%, and 42%, respectively. These findings suggest that the nap mats were an important source of these FRs to dust in the investigated childcare environments and that a campaign of swapping out flame-retarded mats for FR-free ones would reduce exposure to these chemicals. While calculated exposure estimates to the investigated FRs via inhalation, dust ingestion, and dermal absorption were below established reference dose values, they are likely underestimated when considering the toddlers' direct contact to the mats and personal cloud effects.

To date, greenhouse gas (GHG) emissions, mitigation strategies and the accompanying health co-benefits in different economic sectors have not been fully investigated. The purpose of this paper is to review comprehensively the evidence on GHG mitigation measures and the related health co-benefits, identify knowledge gaps, and provide recommendations to promote further development and implementation of climate change response policies. Evidence on GHG emissions, abatement measures and related health co-benefits has been observed at regional, national and global levels, involving both low- and high-income societies. GHG mitigation actions have mainly been taken in five sectors: energy generation, transport, food and agriculture, household and industry, consistent with the main sources of GHG emissions. GHGs and air pollutants to a large extent stem from the same sources and are inseparable in terms of their atmospheric evolution and effects on ecosystem; thus, GHG reductions are usually, although not always, estimated to have cost effective co-benefits for public health. Some integrated mitigation strategies involving multiple sectors, which tend to create greater health benefits. The pros and cons of different mitigation measures, issues with existing knowledge, priorities for research, and potential policy implications were also discussed. Findings from this study can play a role not only in motivating large GHG emitters to make decisive changes in GHG emissions, but also in facilitating cooperation at international, national and regional levels, to promote GHG mitigation policies that protect public health from climate change and air pollution simultaneously.