Autism spectrum disorders (ASDs) is a set of complex neurodevelopment disorders that is prevalent in children and is increasing at a steady rate in recent years. However, the etiology of autism is still poorly understood. Humans are at higher risk of chemical exposure than in the past as a result of the increasing usage of chemicals in various fields, including food preservation, agriculture, industrial production, etc. A number of environmental agents have been suggested as contributing factors to ASD pathogenesis, which includes heavy metals (Hg and Pb), persistent organic pollutants (DDT, PBDEs and PCBs) and emerging chemicals of concern (phthalates and BPA). These three main categories of toxicants could be the cause of ASD in children. Recent research into the causes of ASD that have been linked to environment factors are reviewed in this paper. There are evidence supporting the etiological link between exposure to environmental toxicants and the development of ASD. Children exposed to these toxicants in the environment exhibit signature traits of ASD and have been reported with high body burdens of these chemicals and/or their metabolites, which may provide an explanation for the observed relation, yet comprehensive evidence in humans is limited, highlighting the need for further research.

Phosphorus-containing flame retardants (PFRs) are increasingly in demand worldwide as replacements for brominated flame retardants (BFRs), but insufficient available toxicological information on PFRs makes assessing their health risks challenging. Mitochondria are important targets of various environmental pollutants, and mitochondrial dysfunction may lead to many common diseases. In the present study, mitochondria impairment-related endpoints were measured by a high content screening (HCS) assay for 11 selected non-halogen PFRs in Chinese hamster ovary (CHO-k1) cells. A cluster analysis was used to categorize these PFRs into three groups according to their structural characteristics and results from the HCS assay. Two groups, containing long-chain alkyl-PFRs and all aryl-PFRs, were found to cause mitochondrial impairment but showed different mechanisms of toxicity. Due to the high correlation between cell death and mitochondrial impairment, two PFRs with different structures, trihexyl phosphate (THP) and cresyl diphenyl phosphate (CDP), were selected and compared with chlorpyrifos (CPF) to elucidate their mechanism of inducing cell death. THP (an alkyl-PFR) was found to utilize a similar pathway as CPF to induce apoptosis. However, cell death induced by CDP (an aryl-PFR) was different from classical necrosis based on experiments to discriminate among the different modes of cell death. These results confirm that mitochondria might be important targets for some PFRs and that differently structured PFRs could function via distinct mechanisms of toxicity.

Organisms around the globe are experiencing novel environments created by human activities. One such disturbance of growing concern is the salinization of freshwater habitats from the application of road deicing salts, which creates salinity levels not experienced within the recent evolutionary history of most freshwater organisms. Moreover, salinization can induce trophic cascades and alter the structure of freshwater communities, but knowledge is still scarce about the ability of freshwater organisms to adapt to elevated salinity. We examined if a common zooplankton of freshwater lakes (Daphnia pulex) could evolve a tolerance to the most commonly used road deicing salt (sodium chloride, NaCl). Using a mesocosm experiment, we exposed freshwater communities containing Daphnia to five levels of NaCl (15, 100, 200, 500, and 1000 mg Cl− L−1). After 2.5 months, we collected Daphnia from each mesocosm and raised them in the lab for three generations under low salt conditions (15 mg Cl− L−1). We then conducted a time-to-death experiment with varying concentrations of NaCl (30, 1300, 1500, 1700, 1900 mg Cl− L−1) to test for evolved tolerance. All Daphnia populations exhibited high survival when subsequently exposed to the lowest salt concentration (30 mg Cl− L−1). At the intermediate concentration (1300 mg Cl− L−1), however, populations previously exposed to elevated concentrations (i.e.100–1000 mg Cl− L−1) had higher survival than populations previously exposed to natural background levels (15 mg Cl− L−1). All populations survived poorly when subsequently exposed to the highest concentrations (1500, 1700, and 1900 mg Cl− L−1). Our results show that the evolution of tolerance to moderate levels of salt can occur within 2.5 months, or 5–10 generations, in Daphnia. Given the importance of Daphnia in freshwater food webs, such evolved tolerance might allow Daphnia to buffer food webs from the impacts of freshwater salinization.

There is growing interest in the association between ambient air pollution and stroke, but few studies have investigated the association in developing countries. The primary objective of this study was to examine the association between levels of ambient air pollutants and hospital admission for stroke in China. A time-stratified case-crossover analysis was conducted between 2014 and 2015 in 14 large Chinese cities among 200,958 ischemic stroke and 41,746 hemorrhagic stroke hospitalizations. We used conditional logistic regression to estimate the percentage changes in stroke admissions in relation to interquartile range increases in air pollutants. Air pollution was positively associated with ischemic stroke. A difference of an interquartile range of the 6-day average for particulate matter less than 10 μm in aerodynamic diameter, sulfur dioxide, nitrogen dioxide, carbon monoxide, and ozone corresponded to 0.7% (95% CI: 0%, 1.4%), 1.6% (95% CI: 1.0%, 2.3%), 2.6% (95% CI: 1.8%, 3.5%), 0.5% (95% CI: −0.2%, 1.1%), and 1.3% (95% CI: 0.3%, 2.3%) increases in ischemic stroke admissions, respectively. For hemorrhagic stroke, we observed the only significant association in relation to nitrogen dioxide on the current day (percentage change: 1.6%; 95% CI: 0.3%, 2.9%). Our findings contribute to the limited scientific literature concerning the effect of ambient air pollution on stroke in developing countries. Our findings may have significant public health implications for primary prevention of stroke in China.

Individuals are exposed to brominated flame retardants (BFRs), including tetrabromobisphenol A (TBBPA), on a daily basis because of their widespread usage. These compounds may have adverse effects on human health. In the present study, dermal absorption experiments were conducted in vivo to predict the adhesion, penetration, and bioavailability of TBBPA. TBBPA was administered to Wistar rats for 6 h by repeated dermal exposure at doses of 20, 60, 200, and 600 mg of TBBPA per kg of body weight (bw). The skin adhesion coefficient (AC) was calculated using a difference-value method and ranged from 0.12 to 3.25 mg/cm2 and 0.1 to 2.56 mg/cm2 for the male and female rats, respectively. The adhesion rate was 70.92%. According to Fick's first law of diffusion, the diffusion constant (D) was 1.4 × 10−4 cm2/h and the permeation coefficient (Kp) was 1.26 × 10−5 cm/h for TBBPA. TBBPA levels in the blood, urine, and feces of the male rats were significantly higher than those in the female rats. The dermal bioavailability of TBBPA was 24.71% for male rats and 20.05% for female rats 24 h after exposure.

Microplastics are an emerging contaminant of concern in aquatic ecosystems. To better understand microplastic contamination in North American surface waters, we report for the first time densities of microplastics in Lake Winnipeg, the 11th largest freshwater body in the world. Samples taken 2014 to 2016 revealed similar or significantly greater microplastic densities in Lake Winnipeg compared with those reported in the Laurentian Great Lakes. Plastics in the lake were largely of secondary origin, overwhelmingly identified as fibres. We detected significantly greater densities of microplastics in the north basin compared to the south basin of the lake in 2014, but not in 2015 or 2016. Mean lake-wide densities across all years were comparable and not statistically different. Scanning electron microscopy with energy dispersive X-ray spectroscopy indicated that 23% of isolated particles on average were not plastic. While the ecological impact of microplastics on aquatic ecosystems is still largely unknown, our study contributes to the growing evidence that microplastic contamination is widespread even around sparsely-populated freshwater ecosystems, and provides a baseline for future study and risk assessments.

While studies on microplastics in the marine environment show their wide-distribution, persistence and contamination of biota, the freshwater environment remains comparatively neglected. Where studies on freshwaters have been undertaken these have been on riverine systems or very large lakes. We present data on the distribution of microplastic particles in the sediments of Edgbaston Pool, a shallow eutrophic lake in central Birmingham, UK. These data provide, to our knowledge, the first assessment of microplastic concentrations in the sediments of either a small or an urban lake and the first for any lake in the UK. Maximum concentrations reached 25–30 particles per 100 g dried sediment (equivalent to low hundreds kg−1) and hence are comparable with reported river sediment studies. Fibres and films were the most common types of microplastic observed. Spatial distributions appear to be due to similar factors to other lake studies (i.e. location of inflow; prevailing wind directions; propensity for biofouling; distribution of macroplastic debris) and add to the growing burden of evidence for microplastic ubiquity in all environments.

The study of the DNA damage response in erythrocytes after γ-irradiation may provide evidence for its effectiveness as a biomarkers for genotoxic environmental stress. We previously reported various malformations in erythrocytes of medaka irradiated with10 Gy, but not in their micronuclei. In this study, we optimized an assay method for γ-H2AX and double strand breaks in erythrocytes of adult medaka fish after 15 Gy of γ-irradiation. The highest level of apoptosis and nuclear abnormalities, including in micronuclei, were recorded 4 h after γ-irradiation, as was the highest level of γ-H2AX foci in erythrocytes. These results suggest that recognition and repair processes occur as a response to DNA damage in erythrocytes in medaka.

Industrial discharges of perfluorooctanoic acid (PFOA) to the Ohio River, contaminating water systems near Parkersburg, WV, were previously associated with nearby residents' serum PFOA concentrations above US general population medians. Ohio River PFOA concentrations downstream are elevated, suggesting Mid-Ohio River Valley residents are exposed through drinking water.Quantify PFOA and 10 other per- and polyfluoroalkyl substances (PFAS) in Mid-Ohio River Valley resident sera collected between 1991 and 2013 and determine whether the Ohio River and Ohio River Aquifer are exposure sources.We measured eleven PFAS in 1608 sera from 931 participants. Serum PFOA concentration and water source associations were assessed using linear mixed-effects models. We estimated between-sample serum PFOA using one-compartment pharmacokinetics for participants with multiple samples.In serum samples collected as early as 1991, PFOA (median = 7.6 ng/mL) was detected in 99.9% of sera; 47% had concentrations greater than US population 95th percentiles. Five other PFAS were detected in greater than 82% of samples; median other PFAS concentrations were similar to the US general population. Serum PFOA was significantly associated with water source, sampling year, age at sampling, tap water consumption, pregnancy, gravidity and breastfeeding. Serum PFOA was 40–60% lower with granular activated carbon (GAC) use. Repeated measurements and pharmacokinetics suggest serum PFOA peaked 2000–2006 for participants using water without GAC treatment; where GAC was used, serum PFOA concentrations decreased from 1991 to 2012.Mid-Ohio River Valley residents appear to have PFOA, but not other PFAS, serum concentrations above US population levels. Drinking water from the Ohio River and Ohio River Aquifer, primarily contaminated by industrial discharges 209–666 km upstream, is likely the primary exposure source. GAC treatment of drinking water mitigates, but does not eliminate, PFOA exposure.

In this work, studies using samples collected in an urban area of Aracaju city, Sergipe State, Northeast, Brazil revealed that soil dust in suspension was the main source of total airborne particulate matter (TAPM), followed by vehicular pollution. The concentration profiles for Cu, Fe, Mn, Ni, V and Ti were established for the collected TAPM samples. The concentrations of SO2 and smoke were also measured all along the 42 sampling days. Through multivariate data analysis of the results a correlation between Fe, Mn, Ni and Ti in the mineral composition of the particles was established, indicating soil dust in suspension as the main source of TAPM. The concentrations of Cu and smoke were found to be related to vehicular traffic, and the second largest source of TAPM. Enrichment factors (EF) were calculated for the studied elements, and only Cu was found to be enriched. The concentrations of the elements in TAPM were evaluated using the geoaccumulation index (Igeo), and Fe, Mn, Ni, V and Ti were found to derive from natural sources, in TAPM. However, approximately 55% of the samples did not presented Cu contamination (Igeo≤0), and the remaining 45% presented Cu concentrations levels that indicated between low to moderate (0<Igeo≤1) and moderate to heavy contamination (2<Igeo≤3) in the urban area of Aracaju city, Sergipe State, Northeast, Brazil.