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.

The impact of pesticides on organisms may strongly depend on temperature. While many species will be exposed to pesticides and warming both in the parental and offspring generations, transgenerational effects of pesticides under warming are still poorly studied, particularly for behaviour. We therefore studied the single and combined effects of exposure to the pesticide chlorpyrifos (CPF) and warming both within and across generations on antipredator behaviour of larvae of the vector mosquito Culex pipiens. Within each generation pesticide exposure and warming reduced the escape diving time, making the larvae more susceptible to predation. Pesticide exposure of the parents did not affect offspring antipredator behaviour. Yet, parental exposure to warming determined how warming and the pesticide interacted in the offspring generation. When parents were reared at 24 °C, warming no longer reduced offspring diving times in the solvent control, suggesting an adaptive transgenerational effect to prepare the offspring to better deal with a higher predation risk under warming. Related to this, the CPF-induced reduction in diving time was stronger at 20 °C than at 24 °C, except in the offspring whose parents had been exposed to 24 °C. This dependency of the widespread interaction between warming and pesticide exposure on an adaptive transgenerational effect of warming is an important finding at the interface of global change ecology and ecotoxicology.

Lead (Pb) both in paints and children's Polyvinyl chloride (PVC) toys is a major public health concern which has attracted attention of the international community. Concentrations of Pb both in lead-based paints and children's PVC toys have been assessed through various studies across the globe. Therefore, the purpose of this article was to summarize the results reported in these studies and provide some comprehension on their implications to human health for law enforcement as well as for awareness raising to the general public. Highlights on identified gaps have been provided to pave ways for further research interventions in order to establish comprehensive information on the subject.Regardless of regulatory limits on the content of lead, both in paints and children's PVC toys existing in different countries in the world, some of the reviewed articles have revealed significant levels of lead in these two items far above the permissible limits.High lead levels in paints have been recorded in China (116,200 ppm), Cameroon (500,000 ppm), South Africa (189,000 ppm), Tanzania (120,862.1 ppm), Uganda (150,000 ppm), Thailand (505,716 ppm) and Brazil (170,258.4 ppm) just to mention a few.Lead poisoning cases in children have been reported in several countries including France, Morocco, South Africa and United States. Countries where high levels of lead in children's PVC toys have been recounted include; China (860,000 ppm), South Africa (145,000 ppm), United States (22,550 ppm), Thailand (4,486.11 ppm), Palestine (6,036 ppm) and India (2,104 ppm).Awareness raising among parents is vital to impart them with knowledge on the matter so that they can take strenuous measures to protect their children from lead poisoning emanating from playing with toys and paint dust. Law enforcement on phasing out lead-based paints and control of lead content in children's PVC toys worldwide is also highly recommended.

During the Vietnam War, the United States military sprayed over 74 million litres of Agent Orange (AO) to destroy forest cover as a counterinsurgency tactic in Vietnam, Laos and Cambodia. The main ingredient was contaminated by 2,3,7,8-tetrachlorodibenzo-paradioxin (TCDD). DNA methylation (DNAm) differences are potential biomarker of environmental toxicants exposure. The aim of this study was to perform a preliminary investigation of the DNAm levels from peripheral blood of the present-day Vietnamese population, including individuals whose parents, according to historical data, were exposed to AO/TCDD during the war. 94 individuals from heavily sprayed areas (cases) and 94 individuals from non-sprayed areas (controls) were studied, and historical data on alleged exposure of parents collected. 94 cases were analysed considering those whose father/parents participated in the war (N = 29) and considering the place of residence of both parents (64 living in sprayed areas versus 30 in non-contaminated areas). DNAm levels in CYP1A1 and IGF2 genes were measured (MALDI-TOF technology). The analyses showed that: 1) one CpG site in the CYP1A1 and one in the IGF2 gene showed significant differences in DNAm levels between cases and controls; 2) the CYP1A1 region resulted to be hypomethylated (in 9 out of 16 sites/units; p-val<0.01) in 29 individuals whose father/parents participated in the war in the spray zones; 3) we showed that the place of residence of both parents influenced methylation levels of the CYP1A1 and IGF2 genes (p-val<0.05). In conclusion this study indicates that past environmental exposure to dioxin (AO/TCDD) shapes the DNAm profile of CYP1A1 and that the place of living for parents in former spray zones influences DNAm of CYP1A1 and IGF2 genes. These results open the way to new applications of DNAm as potential biomarker(s) of past human exposure to dioxin.

Microcystin-LR (MCLR) has been reported to cause developmental neurotoxicity in zebrafish, but there are few studies on the mechanisms of MCLR-induced transgenerational effects of developmental neurotoxicity. In this study, zebrafish were exposed to 0, 1, 5, and 25 μg/L MCLR for 60 days. The F1 zebrafish embryos from the above-mentioned parents were collected and incubated in clean water for 120 h for hatching. After examining the parental zebrafish and F1 embryos, MCLR was detected in the gonad of adults and F1 embryos, indicating MCLR could potentially be transferred from parents to offspring. The larvae also showed a serious hypoactivity. The contents of dopamine, dihydroxyphenylacetic acid (DOPAC), serotonin, gamma-aminobutyric acid (GABA) and acetylcholine (ACh) were further detected, but only the first three neurotransmitters showed significant reduction in the 5 and 25 μg/L MCLR parental exposure groups. In addition, the acetylcholinesterase (AChE) activity was remarkably decreased in MCLR parental exposure groups, while the expression levels of manf, bdnf, ache, htr1ab, htr1b, htr2a, htr1aa, htr5a, DAT, TH1 and TH2 genes coincided with the decreased content of neurotransmitters (dopamine, DOPAC and serotonin) and the activity of AChE. Neuronal development related genes, α1-tubulin, syn2a, mbp, gfap, elavl3, shha and gap43 were also measured, but gap43 was the gene only up-regulated. Our results demonstrated MCLR could be transferred to offspring, and subsequently induce developmental neurotoxicity in F1 zebrafish larvae by disturbing the neurotransmitter systems and neuronal development.

The area of agriculturally used land and following to that the use of pesticides are steadily increasing. Insecticides do not only reduce pest organisms on crops but can also affect non-target organisms when present in sublethal concentrations in the environment. We investigated the effects of an exposure to sublethal pyrethroid (lambda-cyhalothrin) concentrations, at doses 20 and 60 times lower than the LC50, respectively, on reproductive traits and adult cuticular hydrocarbon (CHC) profiles of a leaf beetle (Phaedon cochleariae Fabricius). Furthermore, we tested for effects on growth and antennae symmetry of the offspring generation that was not exposed to the insecticide. Sublethal insecticide concentrations decreased the egg number produced by the adults and the hatching rate. Moreover, the chemical phenotype (CHC profile) of adults was altered in dependence of the insecticide treatment, with sex-specific effects. In the unexposed offspring of insecticide-exposed parents, a prolonged development time and a fluctuating asymmetry of the females' antennae were detected, revealing transgenerational effects. The insecticide effects on the CHC profiles of the parental generation might have been caused by changes in CHC precursors, which were potentially induced by the insecticide treatment of the insect diet. Such altered CHC pattern may have implications for intraspecific communication, e.g., in mate choice, as well as in an interspecific way, e.g., in interactions with other arthropod species. The observed detrimental transgenerational effects might be explainable by a reduced investment in the offspring, maternal transfer or epigenetic processes. An asymmetry of the antennae may lead to defects in the reception of chemical signals. In conclusion, the results disclose that, besides detrimental (transgenerational) effects on reproduction and development, an exposure to sublethal insecticide concentrations can impair the chemical communication between individuals, with impacts on the sender (i.e., the CHC profile) and the receiver (i.e., caused by asymmetry of the antennae).

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.

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.

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.

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.