Arid and semi-arid ecosystems (aridlands) cover a third of Earth's terrestrial surface and contain organisms that are sensitive to low level atmospheric pollutants. Atmospheric nitrogen (N) inputs to aridlands are likely to cause changes in plant community composition, fire frequency, and carbon cycling and storage. However, few studies have documented long-term rates of atmospheric N inputs in aridlands because dry deposition is technically difficult to quantify, and extensive sampling is needed to capture fluxes with spatially and temporally heterogeneous rainfall patterns. Here, we quantified long-term spatial and temporal patterns of inorganic N deposition in protected aridland ecosystems across an extensive urban-rural gradient using multiple sampling methods. We compared long-term rates of N deposition from ion-exchange resin (IER) collectors (bulk and throughfall, 2006–2015), wet-dry bucket collectors (2006–2015), and dry deposition from the inferential method using passive samplers (2010–2012). From mixed approaches with IER collectors and inferential methods, we determined that 7.2 ± 0.4 kgNha⁻¹y⁻¹ is deposited to protected Sonoran Desert within metropolitan Phoenix, Arizona and 6.1 ± 0.3 kgNha⁻¹y⁻¹ in nearby desert ecosystems. Regional scale models overestimated deposition rates for our sampling period by 60% and misidentified hot spots of deposition across the airshed. By contrast, the easy-deployment IER throughfall collectors showed minimal spatial variation across the urban-rural gradient and underestimated deposition fluxes by 54%, largely because of underestimated dry deposition in throughfall. However, seasonal sampling of the IER collectors over 10 years allowed us to capture significant seasonal variation in N deposition and the importance of precipitation timing. These results, derived from the longest, spatially and temporally explicit dataset in drylands, highlight the need for long-term, mixed methods to estimate atmospheric nutrient enrichment to aridlands in a rapidly changing world.

Poly- and per-fluoroalkyl substances (PFAS) and volatile methyl siloxanes (VMS) were monitored at 21 sites in the Global Atmospheric Passive Sampling (GAPS) Network. Atmospheric concentrations previously reported from 2009 were compared to concentrations measured at these sites in 2013 and 2015, to assess trends over 7 years of monitoring. Concentrations of the fluorotelomer alcohols (FTOHs) and fluorinated sulfonamides and sulfonamidoethanols (FOSAs and FOSEs) were stable at these sites from 2009 to 2015 with no significant difference (p > 0.05) in concentrations. Elevated concentrations of all the neutral PFAS were detected at the urban sites as compared to the polar/background sites. The perfluorosulfonic acids (PFSAs), meanwhile, saw a significant increase (p < 0.001) in concentrations from 2009 to 2015. The perfluorocarboxylic acids (PFCAs) had elevated concentrations in 2015, however, the difference was not statistically significant (p > 0.05). Concentrations of the PFSAs and the PFCAs were similar at all location types, showing the global reach of these persistent compounds. Concentrations of the cyclic VMS (cVMS) were at least an order of magnitude higher than the linear VMS (lVMS) and the PFAS. Octamethylcyclotetrasiloxane (D4), decamethylcyclopentasiloxane (D5) and dodecamethylcyclohexasiloxane (D6) saw a weak significant increase in concentrations from 2009 to 2013 (p < 0.05), however, hexamethylcyclotrisiloxane (D3) had a strong significant decrease in concentrations from 2009 to 2015 (p < 0.01).

Tributyltin is a biocide used in nautical paints, aiming to reduce fouling of barnacles in ships. Despite the fact that many effects of TBT on marine species are known, studies in mammals have been limited, especially those evaluating its effect on the function of the hypothalamus-pituitary-thyroid (HPT) axis. The aim of this study was to investigate the effects of subchronic exposure to TBT on the HPT axis in female rats. Female Wistar rats received vehicle, TBT 200 ng kg−1 BW d−1 or 1000 ng kg−1 BW d−1 orally by gavage for 40 d. Hypothalamus, pituitary, thyroid, liver and blood samples were collected. TBT200 and TBT1000 thyroids showed vacuolated follicular cells, with follicular hypertrophy and hyperplasia. An increase in epithelial height and a decrease in the thyroid follicle and colloid area were observed in TBT1000 rats. Moreover, an increase in the epithelium/colloid area ratio was observed in both TBT groups. Lower TRH mRNA expression was observed in the hypothalami of TBT200 and TBT1000 rats. An increase in Dio1 mRNA levels was observed in the hypothalamus and thyroid in TBT1000 rats only. TSH serum levels were increased in TBT200 rats. In TBT1000 rats, there was a decrease in total T4 serum levels compared to control rats, whereas T3 serum levels did not show significant alterations. We conclude that TBT exposure can promote critical abnormalities in the HPT axis, including changes in TRH mRNA expression and serum TSH and T4 levels, in addition to affecting thyroid morphology. These findings demonstrate that TBT disrupts the HPT axis. Additionally, the changes found in thyroid hormones suggest that TBT may interfere with the peripheral metabolism of these hormones, an idea corroborated by the observed changes in Dio1 mRNA levels. Therefore, TBT exposition might interfere not only with the thyroid axis but also with thyroid hormone metabolism.

Diethyl phthalate (DEP) and dibutyl phthalate (DBP) are two typical small phthalate esters, extensively used in personal care and consumer products. Although previous studies have linked phthalate esters to several health issues, it is still unclear whether they can affects the early stages of embryonic development. In this study, we evaluated the early developmental neurotoxicity as well as the cytotoxicity of DEP and DBP, using mouse embryonic stem cells (mESCs). Our results showed that both DEP and DBP could decrease mESC viability in a dose-dependent manner. Moreover, while DBP could activate the caspase-3/7 enzymes and cause cell membrane damage as well as intracellular ROS accumulation, interestingly DEP treatment only showed stimulation of ROS production. In addition, DEP and DBP treatment at non-cytotoxic concentrations, abnormally altered the expression levels of several vitally important regulators of embryo development. For instance, neural ectoderm markers, such as Pax6, Nestin, Sox1 and Sox3, were significantly up-regulated upon DEP and DBP exposure. In conclusion, our work suggests a potential developmental toxicity of DEP and DBP on mammals, especially for neural ectoderm specification. Our findings help better understand the association between health problems and DEP/DBP exposure and most significantly remind us of the importance of additional health risk tests for these two largely used chemicals.

In this study, we measured the concentrations of 58 flame retardants (and related compounds) in bald eagle (Haliaeetus leucocephalus) egg and plasma samples from the Michigan. These analytes include polybrominated diphenyl ethers (PBDEs), novel flame retardants (nFRs), Dechlorane-related compounds (Decs), and organophosphate esters (OPEs). A total of 24 paired eaglet plasma and egg samples were collected from inland (IN, N = 13) and the Great Lakes (GL, N = 11) breeding areas from 2000 to 2012. PBDEs were the most abundant chemical group with a geometric mean of 181 ng/g wet weight (ww) in egg and 5.31 ng/g ww in plasma. Decs were barely found in plasma samples, but they were frequently found in eggs (geometric mean 23.5 ng/g ww). OPE levels were comparable to those of PBDEs in the plasma but lower than those of PBDEs in eggs. Dec and PBDE concentrations were significantly higher in GL than in IN (p < 0.05). The ratio of egg to plasma concentrations (lipid normalized) varied with chemicals and correlated with the chemical's octanol-water partition coefficient. The lipid normalized bald eagle egg and plasma concentrations from Lake Superior and Huron were one to three orders of magnitude higher than concentrations measured in composite lake trout (Salvelinus namaycush) from the same lake, implying that they biomagnify in the environment.

The structure and organization of acoustic signals arise through evolutionary processes and adaptive pressures on each species. During learning, natural or anthropogenic factors, such as high noise levels in urban areas, pose challenges to acoustic communication in birds. Many species adjust their acoustic signals to higher noise levels by increasing the frequency of vocalizations. The objectives of this study were to compare the dominant frequency of songs among birds dwelling in forest fragments distant from and near to urban areas, establish correlations between the dominant frequency of song and noise levels in these environments and verified the difference of response between oscines, suboscines and non-passerines. We recorded vocalizations of birds between July/2013 and November/2014 in four forest fragments, two of them near and two distant from urban areas. We used Audacity software to measure the dominant frequency. We measured the ambient noise by a calibrated sound pressure level meter in decibels (dBA) in each of the forest fragments. We analyzed 3740 vocalizations of nine tropical bird species. Forest fragments near to urban areas have higher noise levels than more distant forest fragments. Eight of nine studied species presented higher dominant frequencies of songs in forest fragments near to urban areas. Only one species, Myiothlypis flaveola, did not change the dominant frequency of song between the four analyzed forest fragments. The difference in dominant frequency between the forest fragments distant and closer to the urban areas did not vary between oscines, suboscines and non-passerines. Eight tropical birds exhibited higher dominant frequencies of song in forest fragments near urban areas with high level of ambient noise. Oscine, suboscine and non-passerine showed song variations. Bird species that have differences in the vocalization dominant frequency can be used in environmental monitoring and in ethological studies, as they are sensitive to high noise levels.Noise pollution caused by the vehicular traffic and urbanization are correlates with changes in the vocalization of tropical birds in forest fragments.

Mercury (Hg) contamination in aquatic systems remains a global concern with the biomagnification of methylmercury (MeHg) through primary consumers (zooplankton) to fish and humans. In this study, total mercury (THg) and MeHg concentrations were analyzed in zooplankton collected from Baihua reservoir (Guizhou Province, China). Our results demonstrated that THg and MeHg concentrations were strongly correlated to zooplankton community and biomass composition. The THg concentration was significantly higher in micro-zooplankton compared to meso-zooplankton and macro-zooplankton, and MeHg concentration increased significantly as body size increased. Hg increases in zooplankton were influenced by the numbers of calanoid copepods and Daphnia present relative to phytoplankton and zooplankton biomass. Many zooplankton taxa in the three size-fractions were affected by THg exposure. The biomasses of Bosmina longirostris, Thermocyclops brevifurcatus, Asplanchna priodonta and Cyclops vicinus vicinus were positively correlated with Hg accumulation, while Daphnia hyalina, and Phyllodiaptomus tunguidus had a negative association. THg and MeHg bioaccumulation factors were correlated with phosphorus and total nitrogen concentration, zooplankton biomass, and chlorophyll-a concentration. Phosphorus loading was associated with increased THg and MeHg accumulation in the zooplankton highlighting biomagification with eutrophication. Chlorophyll-a levels were not correlated to THg and MeHg accumulation in zooplankton when phytoplankton densities were >10⁷ cells L⁻¹ and chlorophyll-a concentrations <9 μgL−1. This finding contradicts the idea of MeHg biodilution with increased algae biomass. However, changes in the phytoplankton species and biomass altered the availability of food for zooplankton, particularly micro-zooplankton and macro-zooplankton. Ultimately, the bioaccumulation of MeHg and THg across lower trophic levels was based more on the availability of preferred food resources than on total biological productivity.

With the commercialization of transgenic cotton that expresses Bt (Bacillus thuringiensis) insecticidal proteins, mirid bugs have become key pests in cotton and maize fields in China. Genetically engineered (GE) crops for controlling mirids are unavailable owing to a lack of suitable insecticidal genes. In this study, we developed and validated a dietary exposure assay for screening insecticidal compounds and for assessing the potential effects of insecticidal proteins produced by GE plants on Apolygus lucorum, one of the main mirid pests of Bt cotton and Bt maize. Diets containing potassium arsenate (PA) or the cysteine protease inhibitor E-64 were used as positive controls for validating the efficacy of the dietary exposure assay. The results showed that with increasing concentrations of PA or E-64, A. lucorum larval development time was prolonged and adult weight and fecundity were decreased, suggesting that the dietary exposure assay was useful for detecting the toxicity of insecticidal compounds to A. lucorum. This assay was then used to assess the toxicity of Cry1Ab, Cry1Ac, Cry1F, Cry2Aa, and Cry2Ab proteins, which have been transformed into several crops, against A. lucorum. The results showed that A. lucorum did not show a negative effect by feeding on an artificial diet containing any of the purified Cry proteins. No significant changes in the activities of digestive, detoxifying, or antioxidant enzymes were detected in A. lucorum that fed on a diet containing Cry proteins, but A. lucorum fitness was reduced when the insect fed on a diet containing E-64 or PA. These results demonstrate that A. lucorum is not sensitive to the tested Cry proteins and that the dietary exposure assay is useful for evaluating the toxicity of insecticidal compounds to this species.

Perfluoroalkyl substances (PFAS) are a diverse class of manufactured compounds used in a wide range of industrial processes and consumer products and have been detected in human serum worldwide. Previous cross-sectional and cohort studies in humans have suggested exposure to PFAS is associated with a wide array of chronic diseases, including endocrine disruption, developmental health effects, cancer and metabolic changes. We examined the associations between a panel of eight PFAS and indicators of thyroid disruption, kidney function, and body mass index (BMI), all of which were measured at repeated time points (1990–2008) over the course of the study. Participants (N = 210) were selected from the Fernald Community Cohort based on household water supply from a PFAS-contaminated aquifer. In adjusted repeated measures models, we observed several notable associations between serum PFAS and thyroid hormones as well as kidney function as measured by estimated glomerular filtration rate (eGFR). An interquartile (IQR) increase in serum PFOS was associated with a 9.75% (95% CI = 1.72, 18.4) increase in thyroid stimulating hormone. An IQR increase in serum PFNA, PFHxS, and PFDeA was associated with a −1.61% (95% CI = −3.53, −0.59), −2.06% (95% CI = −3.53, −0.59), and −2.20% (95% CI = −4.25, −0.14) change in eGFR, respectively. On the other hand, an IQR increase in serum Me-PFOSA was associated with a 1.53% (95% CI = 0.34, 2.73) increase in eGFR. No significant associations with BMI and serum PFAS were noted. Our findings are in agreement with previous reports that serum PFAS are associated with altered kidney and thyroid function.