Although the coexistence of heavy metals and environmental hormones always occur in aquatic environment, the information of the combined impacts remains unclear. To explore the multi-generational toxicity of cadmium (Cd) and tributyltin (TBT), adult zebrafish (Danio rerio) (F0) were exposed to different treated groups (100 ng/l Cd, 100 ng/l TBT and their mixture) for 90 d, with their offspring (F1 and F2) subsequently reared in the same exposure solutions corresponding to their parents. Both developmental neurotoxicity and thyroid disturbances were examined in the three (F0, F1, and F2) generations. Our results showed that co-exposure to Cd and TBT induced the developmental neurotoxicity in F1 and F2 generations, reflected by the significant lower levels of neurotransmitters (dopamine and serotonin) and the inhibited acetylcholinesterase (AChE) activities. And the thyroid endocrine disruption were observed in the two-generations larval offspring by parental exposure to Cd and/or TBT, including the significantly decreasing levels of thyroid hormones and the down-regulated the expression of genes involved in the hypothalamus-pituitary-thyroid axis, compared to the control. Additional, the embryonic toxicity and growth inhibition were also determined in the fish larvae. Overall, this study examined the impacts of parental co-exposure to Cd and TBT, with regard to developmental inhibition, nervous system damage and endocrine disruption, which highlighted that co-exposure influences are complicated and need to be considered for accurate environmental risk assessment.

Despite the increase of literature on seabird plastic ingestion in recent years, few studies have assessed how plastic loads vary according to different sampling methods. Most studies use necropsies of seabirds with a natural cause of death, e.g. beached or predated, to determine plastic loads and monitor marine debris. Sampling naturally dead seabirds may be biased as they have perished because of their intrinsic factors, e.g. poor body condition, high parasite loads, sickness or predation, affecting estimates of plastic loads. However, seabirds killed accidentally may be more representative of the population. Here, we used the short-tailed shearwater Ardenna tenuirostris to test different sampling methods: naturally beached fledglings and accidentally road-killed fledglings after being attracted and grounded by artificial lights. We compared plastic load, body condition, and feeding strategies (through using feathers’ δ¹³C and δ¹⁵N isotope niche) between beached and road-killed fledglings. Beached birds showed higher plastic loads, poorer body condition and reduced isotopic variability, suggesting that this group is not a representative subsample of the whole cohort of the fledgling population. Our results might have implications for long-term monitoring programs of seabird plastic ingestion. Monitoring plastic debris through beached birds could overestimate plastic ingestion by the entire population. We encourage the establishment of refined monitoring programs using fledglings grounded by light pollution if available. These samples focus on known cohorts from the same population. The fledgling plastic loads are transferred from parents during parental feeding, accumulating during the chick-rearing period. Thus, these fledglings provide a higher and valuable temporal resolution, which is more useful and informative than unknown life history of beached birds.

In Brazil, there are scarce data on lead (Pb) and cadmium (Cd) contamination, especially for more vulnerable populations such as preschool children. In this paper, we answer two questions: (1) What are the exposure levels of lead and cadmium in preschool children, in Sao Paulo, Brazil? and (2) What are the risk factors associated with this exposure? This cross-sectional study included 50 day care centers (DCCs), totaling 2463 children aged 1–4 years. Venous blood samples were analyzed by ICP-MS. Questionnaires were administered to the parents. Multiple logistic regression models were used to identify associations between blood lead levels (BLLs) and blood cadmium levels (BCLs) and potential risk factors. The geometric mean for BLLs was 2.16 μg/dL (95% CI: 2.10–2.22 μg/dL), and the 97.5th percentile was 13.9 μg/dL (95% CI: 10.0–17.3 μg/dL). For cadmium exposure, the geometric mean for BCLs was 0.48 μg/L (95% CI: 0.47–0.50 μg/L), and the 95th percentile was 2.57 μg/L (95% CI: 2.26–2.75 μg/L). The DCCs’ geographic region was associated with high BLLs and BCLs, indicating hot spots for lead and cadmium exposures. In addition, it was found that the higher the vehicles flow, the higher were the BLLs in children. Red lead in household gates was also an important risk factor for lead exposure. Comparing these results with the findings of the Fourth National Report on Human Exposure to Environmental Chemicals by CDC-2013, it was found that in Brazilian preschool children the BLLs are almost three times higher (97.5th percentile) and the BCLs are almost twelve times higher (95th percentile) than those in U.S. children. This information is essential to formulate public health policies.

Tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) is a re-emerging environmental contaminant that has been frequently detected at sub-ppb (<μg/L) concentrations in natural waters. The objective of this study was to evaluate effects of TDCIPP on growth in initial generation (F0) zebrafish after chronic exposure to environmentally relevant concentrations, and to examine possible parental transfer of TDCIPP and transgenerational effects on growth of first generation (F1) larvae. When zebrafish (1-month old) were exposed to 580 or 7500 ng TDCIPP/L for 240 days, bioconcentration resulted in significantly less growth as measured by body length, body mass, brain-somatic index (BSI) and hepatic-somatic index (HSI) in F0 females but not F0 males. These effects were possibly due to down-regulation of expression of genes along the growth hormone/insulin-like growth factor (GH/IGF) axis. Furthermore, residues of TDCIPP were detected in F1 eggs after exposure of parents, which resulted in less survival, body length and heart rate in F1 individuals. Down-regulation of genes in the GH/IGF axis (e.g., gh, igf1) might be responsible for transgenerational toxicity. This study provides the first known evidence that exposure of zebrafish to environmentally relevant concentrations of TDCIPP during development can inhibit growth of offspring, which were not exposed directly to TDCIPP.

Ambient noise has increased in extent, duration and intensity with significant implications for species’ lives. Birds especially, because they heavily rely on vocal communication, are highly sensitive towards noise pollution. Noise can impair the quality of a territory or hamper the transmission of vocal signals such as song. The latter has significant fitness consequences as it may erode partner preferences in the context of mate choice. Additional fitness costs may arise if noise masks communication between soliciting offspring and providing parents during the period of parental care. Here, we experimentally manipulated the acoustic environment of blue tit (Cyanistes caeruleus) families within their nest boxes with playbacks of previously recorded highway noise and investigated the consequences on parent-offspring communication. We hypothesized that noise interferes with the acoustic cues of parental arrival and vocal components of offspring begging. As such we expected an increase in the frequency of missed detections, when nestlings fail to respond to the returning parent, and a decrease in parental provisioning rates. Parents significantly reduced their rate of provisioning in noisy conditions compared to a control treatment. This reduction is likely to be the consequence of a parental misinterpretation of the offspring hunger level, as we found that nestlings fail to respond to the returning parent more frequently in the presence of noise. Noise also potentially masks vocal begging components, again contributing to parental underestimation of offspring requirements. Either way, it appears that noise impaired parent-offspring communication is likely to reduce reproductive success.

The prevalence of asthma and allergic diseases has increased rapidly in urban China since 2000. There has been limited study of associations between home environmental and lifestyle factors with asthma and symptoms of allergic disease in China.In a cross-sectional analysis of 2214 children in Beijing, we applied a two-step hybrid Least Absolute Shrinkage and Selection Operator (LASSO) algorithm to identify environmental and lifestyle-related factors associated with asthma, rhinitis and wheeze from a wide range of candidates. We used group LASSO to select variables, using cross-validation as the criterion. Effect estimates were then calculated using adaptive LASSO. Model performance was assessed using Area Under the Curve (AUC) values.We found a number of environmental and lifestyle-related factors significantly associated with asthma, rhinitis or wheeze, which changed the probability of asthma, rhinitis or wheeze from −5.76% (95%CI: −7.74%, −3.79%) to 27.4% (95%CI: 16.6%, 38.3%). The three factors associated with the largest change in probability of asthma were short birth length, carpeted floor and paternal allergy; for rhinitis they were maternal smoking during pregnancy, paternal allergy and living close to industrial area; and for wheeze they were carpeted floor, short birth length and maternal allergy. Other home environmental risk factors identified were living close to a highway, industrial area or river, sharing bedroom, cooking with gas, furry pets, cockroaches, incense, printer/photocopier, TV, damp, and window condensation in winter. Lifestyle-related risk factors were child caretakers other than parents, and age<3 for the day-care. Other risk factors included use of antibiotics, and mother’s occupation. Major protective factors for wheeze were living in a rural/suburban region, air conditioner use, and mother’s occupation in healthcare.Our findings suggest that changes in lifestyle and indoor environments associated with the urbanization and industrialization of China are associated with asthma, rhinitis, and wheeze in children.

Evidence of health effects following early life exposure to short-to-medium duration of high pollution levels is extremely limited.We aimed to evaluate the associations between: 1. intrauterine exposure to fine particulate matter (PM2.5) from coal mine fire emissions and the frequencies of general practitioner attendances and dispensations of prescribed asthma inhalers, steroid skin creams, and antibiotics during the first year of life; 2. infant exposure and those outcomes during the year following the fire.All participants were recruited from the Latrobe Valley of Victoria, Australia. Participants’ 24-h average and hourly peak mine fire-specific PM2.5 exposures from 09/02/2014 to 31/03/2014 were estimated using chemical transport modelling. Outcome data were obtained from the Australian Medicare Benefits Schedule and Pharmaceutical Benefits Scheme from each child’s birth to 31/12/2016. We used negative binomial and logistic regression models to independently assess risks of the outcomes associated with every 10 and 100 μg m−3 increase in average or peak PM2.5 exposure, respectively, while adjusting for potential confounders.We included 286 of 311 children whose parents consented to be linked, comprising 77 with no exposure, 88 with intrauterine exposure and 121 with exposure in infancy. 10- and 100- μg m−3 increases in average and peak PM2.5 exposure during infancy were associated with greater incidence of antibiotics being dispensed during the year following the fire: the adjusted incidence rate ratios were 1.24 (95% CI 1.02, 1.50, p = 0.036) and 1.14 (1.00, 1.31, p = 0.048) respectively. No other significant associations were observed.Exposure to coal mine fire emissions during infancy was associated with increased dispensing of antibiotics. This could reflect increased childhood infections or increased prescriptions of antibiotics in the year following the fire.

As a Chinese-specific alternative to perfluorooctane sulfonate (PFOS), 6:2 chlorinated polyfluorinated ether sulfonate (commercial name: F-53B) has been used in the metal plating industry for over 40 years. This prevalence of use has resulted in its subsequent detection within the environment, wildlife, and humans. Despite this, however, its hepatotoxic effects on aquatic organisms remain unclear. Here, we characterized the impacts of long-term F-53B exposure on adult zebrafish liver and their offspring. Results showed that the concentration of F-53B was greater in the F0 liver than that in the gonads and blood. Furthermore, males had significantly higher liver F-53B levels than females. Hepatomegaly and obvious cytoplasmic vacuolation indicated that F-53B exposure induced liver injury. Compared to control, liver triglyceride levels decreased by 30% and 33.5% in the 5 and 50 μg/L-exposed males and 22% in 50 μg/L-exposed females. Liver transcriptome analysis of F0 adult fish found 2175 and 1267 differentially expressed genes (DEGs) in the 5 μg/L-exposed males and females, respectively. Enrichment analyses further demonstrated that the effects of F-53B on hepatic transcripts were sex-dependent. Gene Ontology showed that most DEGs were involved in multicellular organism development in male fish, whereas in female fish, most DEGs were related to metabolic processes and gene expression. qRT-PCR analysis indicated that the PPAR signaling pathway likely contributed to F-53B-induced disruption of lipid metabolism in F0 adult fish. In F1 larvae (5 days post fertilization), the transcription of pparα increased, like that in F0 adult fish, but most target genes showed the opposite expression trends as their parents. Taken together, our research demonstrated chronic F-53B exposure adversely impacts zebrafish liver, with disruption of PPAR signaling pathway dependent on sex and developmental stage.

Ionizing radiation causes a variety of effects, including DNA damage associated to cancers. However, the effects in progeny from irradiated parents is not well documented. Using zebrafish as a model, we previously found that parental exposure to ionizing radiation is associated with effects in offspring, such as increased hatching rates, deformities, increased DNA damage and reactive oxygen species. Here, we assessed short (one month) and long term effects (one year) on gene expression in embryonic offspring (5.5 h post fertilization) from zebrafish exposed during gametogenesis to gamma radiation (8.7 or 53 mGy/h for 27 days, total dose 5.2 or 31 Gy) using mRNA sequencing. One month after exposure, a global change in gene expression was observed in offspring from the 53 mGy/h group, followed by embryonic death at late gastrula, whereas offspring from the 8.7 mGy/h group was unaffected. Interestingly, one year after exposure newly derived embryos from the 8.7 mGy/h group exhibited 2390 (67.7% downregulated) differentially expressed genes. Overlaps in differentially expressed genes and enriched biological pathways were evident between the 53 mGy/h group one month and 8.7 mGy/h one year after exposure, but were oppositely regulated. Pathways could be linked to effects in adults and offspring, such as DNA damage (via Atm signaling) and reproduction (via Gnrh signaling). Comparison with gene expression analysis in directly exposed embryos indicate transferrin a and cytochrome P450 2x6 as possible biomarkers for radiation response in zebrafish. Our results indicate latent effects following ionizing radiation exposure from the lower dose in parents that can be transmitted to offspring and warrants monitoring effects over subsequent generations.

Ecotoxicology provides data to inform environmental management. Many testing protocols do not consider offspring fitness and toxicant sensitivity. Cadmium (Cd) is a well-studied and ubiquitous toxicant but little is known about the effects on offspring of exposed parents (transgenerational effects). This study had three objectives: to identify endpoints related to offspring performance; to determine whether parental effects would manifest as a change in Cd tolerance in offspring and how parental exposure duration influenced the manifestation of parental effects. Adult snails were exposed to Cd 0, 25, 50, 100, 200 and 400 μg Cd/L for eight weeks. There were effects on adult endpoints (e.g., growth, reproduction) but only at the highest concentrations (>100 μg/L). Alternatively, we observed significant transgenerational effects at all Cd concentrations. Surprisingly, we found increased Cd tolerance in hatchlings from all parental Cd exposure concentrations even though eggs and hatchlings were in Cd-free conditions for 6 weeks. Explicit consideration of offspring performance adds value to current toxicity testing protocols. Parental exposure duration has important implications for offspring effects and that contaminant concentrations that are not directly toxic to parents can cause transgenerational changes in resistance that have significant implications for toxicity testing and adaptive responses.