mi
the coup has already happened so what are we going to do about it?
rebecca solnit 2018
lithub.com/rebecca-solnit-the-coup-has-already-happened/
silent spring
rachel carson 1962
extreme mortality and reproductive failure of common murres resulting from the northeast pacific marine heatwave of 2014-2016
john f. piatt et al. 2020
doi.org/10.1371/journal.pone.0226087
migration induced by sea-level rise could reshape the us population landscape
mathew e. hauer 2017
doi.org/10.1038/nclimate3271
the water will come: rising seas, sinking cities, and the remaking of the civilized world
jeff goodell 2017
the long emergency: surviving the converging catastrophes of the twenty-first century
james howard kunstler 2006
too much magic: wishful thinking, technology, and the fate of the nation
james howard kunstler 2012
lyme: the first epidemic of climate change
mary beth pfeiffer 2018 not yet read
aeon.co/essays/how-lyme-disease-became-the-first-epidemic-of-climate-change
direct diagnostic tests for lyme disease
steven e schutzer et al. 2018
doi.org/10.1093/cid/ciy614
to what other diseass could this technique be applied?
estimating the frequency of lyme disease diagnoses, united states, 2010–2018
kiersten j. kugeler et al. 2021
wwwnc.cdc.gov/eid/article/27/2/20-2731_article
misunderstanding terrorism
theintercept.com/2017/05/13/misunderstanding-terrorism-how-the-us-vs-them-mentality-will-never-stop-attacks/
urban immigrant diversity and inclusive institutions
tom kemeny, abigail cooke 2017
doi.org/10.1080/00130095.2017.1300056
how the benzene tree polluted the world:
the organic compounds that enabled industrialization have unintended, long-lasting consequences for the planet’s life
rebecca altman 2017
theatlantic.com/science/archive/2017/10/benzene-tree-organic-compounds/530655/
time-bombing the future: synthetics created in the 20th century have become an evolutionary force, altering human biology and the web of life
rebecca altman 2019
aeon.co/essays/how-20th-century-synthetics-altered-the-very-fabric-of-us-all
food
global and regional health effects of future food production under climate change: a modelling study
springmann et al 2016
doi.org/10.1016/S0140-6736(15)01156-3
bats as potential suppressors of multiple agricultural pests: a case study from madagascar
james kemp et al. 2018
doi.org/10.1016/j.agee.2018.09.027
There are few places in the world where relations between agriculture and conservation are more strained. Madagascar’s forests are being converted to agricultural land at a rate of one per cent every year and much of this destruction is fuelled by the cultivation of the country’s main staple crop: rice.
A key reason for this is that insect pests are destroying vast quantities of rice, leading local subsistence farmers to destroy even more forest to create new paddies. The result is devastating habitat and biodiversity loss on the island. But not all species are suffering. In fact, some of the island’s insectivorous bats are thriving, and this has important implications for farmers and conservationists alike.
Co-leading an international team of scientists, Ricardo Rocha from the University of Cambridge’s Zoology department Conservation Science Group, found that several species of indigenous bats are taking advantage of habitat modification to hunt insects swarming above the country’s rice fields. They include the Malagasy mouse-eared bat, Major’s long-fingered bat, the Malagasy white-bellied free-tailed bat, and Peters’ wrinkle-lipped bat.
“These winner species are providing a valuable free service to Madagascar as biological pest suppressors,” Rocha said. “We found that six species of bat are preying on rice pests such as the paddy swarming caterpillar and grass webworm. The damage that these insects cause puts the island’s farmers under huge financial pressure and that encourages deforestation.”
The study, published in the journal Agriculture, Ecosystems and Environment, used state-of-the-art ultrasonic recorders and molecular analysis to investigate the feeding activity of insectivorous bats in the farmland bordering the Ranomafana National Park in the southeast of the country.
The researchers recorded over a thousand bat ‘feeding buzzes’ (echolocation sequences used by bats to target their prey) at 54 sites, to identify their favourite feeding spots. This revealed that bat activity over rice fields was much higher than it was in continuous forest — seven times higher over irrigated rice fields, and sixteen times higher over hillside fields — which clearly shows that the animals are preferentially foraging in these human-made ecosystems. The researchers suggest that the bats favour hillside fields most because lack of water and nutrient run-off make these crops more susceptible to insect pest infestations.
The team next used DNA barcoding techniques to analyse droppings collected from bats captured within the rice plantations and nearby forest. All six species of bats were found to have fed on economically important insect pests. While the findings indicated that rice farming benefits most from the bats, the scientists also found pests of other crops, including the black twig borer (a pest of coffee), the sugarcane cicada, the macadamia nut-borer, and the sober tabby (a pest of citrus fruits).
“The effectiveness of bats as pest controllers has already been proven in the USA and Catalonia,” said co-author James Kemp, from the University of Lisbon. “But our study is the first to show this happening in Madagascar, where the stakes for both farmers and conservationists are very high.”
The researchers argue that maximising bat populations has the potential to boost crop yields and promote sustainable livelihoods. They are now calling for further research to quantify this contribution because Madagascar’s bats currently fall under game species legislation and are not actively protected in the country.
Bats comprise roughly one-fifth of all Malagasy mammal species and thirty-six recorded bat species are endemic to the island, making Madagascar one of the most important regions for conservation of this animal group anywhere in the world.
“Bats have a bad reputation in Madagascar because they are seen as a nuisance when they roost in buildings,” Rocha said. “The problem is that while these bats are benefiting from farming, deforestation is also denying them places to roost. With the right help, we hope that farmers can promote this mutually beneficial relationship by installing bat houses.”
Local people may have a further reason to be grateful to the animals. While bats are often associated with spreading disease, Rocha and his team found evidence that Malagasy bats feed not just on crop pests but also on mosquitos — vectors of malaria, Rift Valley fever virus and elephantiasis — as well as blackflies, which spread river blindness.
abstract •Malagasy bats select rice producing agricultural areas for foraging, potentially acting as important pest suppressors.
•Open space and edge space bats benefit the most by the conversion of forest to rice fields.
•Several economically important agricultural pests and disease vectors were detected in bat faecal samples.
•Promoting and conserving bat populations in agricultural landscapes might increase agricultural yields.
The conversion of natural habitats to agriculture is one of the main drivers of biotic change. Madagascar is no exception and land-use change, mostly driven by slash-and-burn agriculture, is impacting the island's exceptional biodiversity. Although most species are negatively affected by agricultural expansion, some, such as synanthropic bats, are capable of exploring newly available resources and benefit from man-made agricultural ecosystems. As bats are known predators of agricultural pests it seems possible that Malagasy bats may be preferentially foraging within agricultural areas and therefore provide important pest suppression services. To investigate the potential role of bats as pest suppressors, we conducted acoustic surveys of insectivorous bats in and around Ranomafana National Park, Madagascar, during November and December 2015. We surveyed five landcover types: irrigated rice, hillside rice, secondary vegetation, forest fragment and continuous forest. 9569 bat passes from a regional assemblage of 19 species were recorded. In parallel, we collected faeces from the six most common bat species to detect insect pest species in their diet using DNA metabarcoding. Total bat activity was higher over rice fields when compared to forest and bats belonging to the open space and edge space sonotypes were the most benefited by the conversion of forest to hillside and irrigated rice. Two economically important rice pests were detected in the faecal samples collected - the paddy swarming armyworm Spodoptera mauritia was detected in Mops leucogaster samples while the grass webworm Herpetogramma licarsisalis was detected from Mormopterus jugularis and Miniopterus majori samples. Other crops pests detected included the sugarcane cicada Yanga guttulata, the macadamia nut-borer Thaumatotibia batrachopa and the sober tabby Ericeia inangulata (a pest of citrus fruits). Samples from all bat species also contained reads from important insect disease vectors. In light of our results we argue that Malagasy insectivorous bats have the potential to suppress agricultural pests. It is important to retain and maximise Malagasy bat populations as they may contribute to higher agricultural yields and promote sustainable livelihoods.
dietary inflammatory index, dietary non-enzymatic antioxidant capacity, and colorectal and breast cancer risk (mcc-spain study)
obón-santacana et al. 2019
doi.org/10.3390/nu11061406
"We have observed an association between the risk of developing colorectal cancer and the inflammatory potential of the diet. That is, the participants who followed an inflammatory diet had almost twice the risk of developing colorectal cancer, which is the 4th most frequent cancer worldwide," explains Dr. Mireia Obón. "On the other hand, we have not appreciated a significant increase in breast cancer risk. That is why we need to carry out more studies to check if there is really any correlation with other factors," she adds.
An inflammatory diet is usually characterized by the consumption of refined carbohydrates, red and processed meat, and saturated or trans fats. In an antioxidant diet, the consumption of vegetables, legumes, fruits and nuts predominates. "In this study we have focused on the role of diet, and specifically on its inflammatory and antioxidant capacity, as there is evidence that both chronic inflammation and oxidative stress influence the development of these two types of cancer," says Dr. Víctor Moreno.
"Following a pro-inflammatory and pro-oxidant diet is a very important risk factor for colon cancer. The positive part is that this is a modifiable factor and, therefore, it can be changed," underlines Dr. Mireia Obón. "Therefore, in order to prevent such cancers, it is very important to follow the recommendations of official agencies and international agencies. We should reorient our eating habits towards a Mediterranean diet, rich in fruits and vegetables, nuts, whole grains and healthy oils, such as olive oil and move away from a more pro-inflammatory diet," she argues.
What the IDIBELL-ICO researcher suggests is to "implement education strategies created by nutrition and health professionals, so that the general population can follow dietary recommendations and change their habits."
In this new study, scientists have specifically analysed the Spanish population through the Dietary Inflammatory Index (DII) and the Non-Enzymatic Antioxidant Capacity (NEAC), which are two useful and validated tools to estimate the inflammatory and the antioxidant potential of the diet. To carry out the study, 1852 cases of colorectal cancer and 1567 cases of breast cancer were included, together with 3447 and 1487 control cases, respectively. The study drew on data from 12 Spanish provinces.
abstract Inflammation and antioxidant capacity have been associated with colorectal and breast cancer. We computed the dietary inflammatory index (DII®), and the total dietary non-enzymatic antioxidant capacity (NEAC) and associated them with colorectal and breast cancer risk in the population-based multi case-control study in Spain (MCC-Spain). We included 1852 colorectal cancer and 1567 breast cancer cases, and 3447 and 1486 population controls, respectively. DII score and NEAC were derived using data from a semi-quantitative validated food frequency questionnaire. Unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95%CI) for energy-adjusted DII (E-DII), and a score combining E-DII and NEAC. E-DII was associated with colorectal cancer risk (OR = 1.93, highest quartile versus lowest, 95%CI:1.60–2.32; p-trend: <0.001); this increase was observed for both colon and rectal cancer. Less pronounced increased risks were observed for breast cancer (OR = 1.22, highest quartile versus lowest, 95%CI:0.99–1.52, p-trend: >0.10). The combined score of high E-DII scores and low antioxidant values were associated with colorectal cancer risk (OR = 1.48, highest quartile versus lowest, 95%CI: 1.26–1.74; p-trend: <0.001), but not breast cancer. This study provides evidence that a pro-inflammatory diet is associated with increased colorectal cancer risk while findings for breast cancer were less consistent.
“it’s shameless financial strip-mining”: les leopold explains how the 1 percent killed the middle class
elias isquith 2016
salon.com/2016/03/05/its_shameless_financial_strip_mining_les_leopold_explains_how_the_1_percent_killed_the_middle_class/
nurse staffing, nursing assistants and hospital mortality: retrospective longitudinal cohort study
peter griffiths et al. 2018
doi.org/10.1136/bmjqs-2018-008043
The proportion of fully trained registered nurses on hospital wards in the UK is among the lowest in Europe. And many hospitals now rely on unregistered nursing assistants to provide a substantial amount of hands-on care, say the researchers.
To find out what impact this skill mix might be having on patient safety in hospital wards, the researchers drew on routinely collected data for staffing levels for all adults admitted to 32 wards in one large acute care hospital trust in the South of England between April 2012 and March 2015.
During this period, 138,133 adults spent at least one day on general medical and surgical wards, and most (79%) were admitted as emergencies. Their average age was 67; 14 per cent were aged 85 and older.
Staffing levels were measured as hours per patient per day. But across all the wards, staffing levels for registered nurses averaged 4.75 hours, while those for nursing assistants averaged 2.99.
Over the first five days of their stay, patients experienced, on average, nearly 2 days of low (below average) registered nurse and nursing assistant staffing levels, adding up to a cumulative shortfall of 23 and 15 minutes, respectively, each.
During the study period, the overall death rate was just over 4 per cent (5662 deaths). Analysis of the data showed that the odds of dying rose by 3 per cent for each day that a patient spent with registered nurse staffing levels below the average for that ward.
Although low nursing assistant staffing levels were also associated with a heightened risk of death (4%), so too were above average staffing levels.
Days where the number of admissions for each registered nurse was substantially higher than usual-more than 25 per cent above average-were associated with a 5 per cent heightened risk of death.
Each additional hour of care provided by a registered nurse was associated with a 3 per cent reduction in the chances of dying, the analysis showed. But no such impact was observed for additional hours of care provided by nursing assistants.
Based on their data, the researchers suggest that providing one additional hour of registered nurse care would be the equivalent of one extra nurse on each shift for a 24-bed ward.
This is an observational study, and as such, can't establish cause, emphasise the researchers. But the findings are broadly in line with those of other previously published studies, they say.
And although the study involved only one hospital site, so may not be typical, the researchers point out that this avoids the observed associations being influenced by the 'hospital effect,' whereby hospitals with more resources employ more nurses.
"The findings of this paper suggest potential benefits from increasing the availability of [registered nurses] on acute hospital wards," write the researchers.
"However, in England, RN shortages look set to continue in the short term...[These] are unlikely to be remedied by increasing the numbers of lesser trained nursing staff in the workforce," they add.
abstract Objective To determine the association between daily levels of registered nurse (RN) and nursing assistant staffing and hospital mortality.
Design This is a retrospective longitudinal observational study using routinely collected data. We used multilevel/hierarchical mixed-effects regression models to explore the association between patient outcomes and daily variation in RN and nursing assistant staffing, measured as hours per patient per day relative to ward mean. Analyses were controlled for ward and patient risk.
Participants 138 133 adult patients spending >1 days on general wards between 1 April 2012 and 31 March 2015.
Outcomes In-hospital deaths.
Results Hospital mortality was 4.1%. The hazard of death was increased by 3% for every day a patient experienced RN staffing below ward mean (adjusted HR (aHR) 1.03, 95% CI 1.01 to 1.05). Relative to ward mean, each additional hour of RN care available over the first 5 days of a patient’s stay was associated with 3% reduction in the hazard of death (aHR 0.97, 95% CI 0.94 to 1.0). Days where admissions per RN exceeded 125% of the ward mean were associated with an increased hazard of death (aHR 1.05, 95% CI 1.01 1.09). Although low nursing assistant staffing was associated with increases in mortality, high nursing assistant staffing was also associated with increased mortality.
Conclusion Lower RN staffing and higher levels of admissions per RN are associated with increased risk of death during an admission to hospital. These findings highlight the possible consequences of reduced nurse staffing and do not give support to policies that encourage the use of nursing assistants to compensate for shortages of RNs.
synergistic ecoclimate teleconnections from forest loss in different regions structure global ecological responses
elizabeth s. garcia et. al 2016
doi.org/10.1371/journal.pone.0165042
fear reduction without fear through reinforcement of neural activity that bypasses conscious exposure
ai koizumi et. al 2016
dx.doi.org/10.1038/s41562-016-0006
an example of how stress affects the body
hyperactivation of sympathetic nerves drives depletion of melanocyte stem cells
bing zhang et al. 2020
doi.org/10.1038/s41586-020-1935-3
Because stress affects the whole body, researchers first had to narrow down which body system was responsible for connecting stress to hair color. The team first hypothesized that stress causes an immune attack on pigment-producing cells. However, when mice lacking immune cells still showed hair graying, researchers turned to the hormone cortisol. But once more, it was a dead end.
“Stress always elevates levels of the hormone cortisol in the body, so we thought that cortisol might play a role,” Hsu said. “But surprisingly, when we removed the adrenal gland from the mice so that they couldn’t produce cortisol-like hormones, their hair still turned gray under stress.”
After systematically eliminating different possibilities, researchers honed in on the sympathetic nerve system, which is responsible for the body’s fight-or-flight response.
Sympathetic nerves branch out into each hair follicle on the skin. The researchers found that stress causes these nerves to release the chemical norepinephrine, which gets taken up by nearby pigment-regenerating stem cells.
Permanent damage
In the hair follicle, certain stem cells act as a reservoir of pigment-producing cells. When hair regenerates, some of the stem cells convert into pigment-producing cells that color the hair.
Researchers found that the norepinephrine from sympathetic nerves causes the stem cells to activate excessively. The stem cells all convert into pigment-producing cells, prematurely depleting the reservoir.
“When we started to study this, I expected that stress was bad for the body — but the detrimental impact of stress that we discovered was beyond what I imagined,” Hsu said. “After just a few days, all of the pigment-regenerating stem cells were lost. Once they’re gone, you can’t regenerate pigment anymore. The damage is permanent.”
The finding underscores the negative side effects of an otherwise protective evolutionary response, the researchers said.
“Acute stress, particularly the fight-or-flight response, has been traditionally viewed to be beneficial for an animal’s survival. But in this case, acute stress causes permanent depletion of stem cells,” said postdoctoral fellow Bing Zhang, the lead author of the study.
Answering a fundamental question
To connect stress with hair graying, the researchers started with a whole-body response and progressively zoomed into individual organ systems, cell-to-cell interaction and, eventually, all the way down to molecular dynamics. The process required a variety of research tools along the way, including methods to manipulate organs, nerves, and cell receptors.
“To go from the highest level to the smallest detail, we collaborated with many scientists across a wide range of disciplines, using a combination of different approaches to solve a very fundamental biological question,” Zhang said.
The collaborators included Isaac Chiu, assistant professor of immunology at Harvard Medical School who studies the interplay between nervous and immune systems.
“We know that peripheral neurons powerfully regulate organ function, blood vessels, and immunity, but less is known about how they regulate stem cells,” Chiu said.
“With this study, we now know that neurons can control stem cells and their function, and can explain how they interact at the cellular and molecular level to link stress with hair graying.”
abstract Empirical and anecdotal evidence has associated stress with accelerated hair greying (formation of unpigmented hairs)16,17, but so far there has been little scientific validation of this link. Here we report that, in mice, acute stress leads to hair greying through the fast depletion of melanocyte stem cells. Using a combination of adrenalectomy, denervation, chemogenetics18,19, cell ablation and knockout of the adrenergic receptor specifically in melanocyte stem cells, we find that the stress-induced loss of melanocyte stem cells is independent of immune attack or adrenal stress hormones. Instead, hair greying results from activation of the sympathetic nerves that innervate the melanocyte stem-cell niche. Under conditions of stress, the activation of these sympathetic nerves leads to burst release of the neurotransmitter noradrenaline (also known as norepinephrine). This causes quiescent melanocyte stem cells to proliferate rapidly, and is followed by their differentiation, migration and permanent depletion from the niche. Transient suppression of the proliferation of melanocyte stem cells prevents stress-induced hair greying. Our study demonstrates that neuronal activity that is induced by acute stress can drive a rapid and permanent loss of somatic stem cells, and illustrates an example in which the maintenance of somatic stem cells is directly influenced by the overall physiological state of the organism.
sunscreen
toxicopathological effects of the sunscreen uv filter, oxybenzone (benzophenone-3), on coral planulae and cultured primary cells and its environmental contamination in hawaii and the u.s. virgin islands
c. a. downs et al. 2015
doi.org/10.1007/s00244-015-0227-7
scientists probe role of sunscreen in accelerating coral-reef decline
erica cirino 2017
porewater methane transport within the gas vesicles of diurnally migrating chaoborus spp.: an energetic advantage
daniel f. mcginnis, sabine flury, kam w. tang, hans-peter grossart 2017
doi.org/10.1038/srep44478
flame retardants
cross-sectional study of social behaviors in preschool children and exposure to flame retardants
shannon t. lipscomb, megan m. mcclelland, megan macdonald, andres cardenas, kim a. anderson, molly l. kile 2017
doi.org/10.1186/s12940-017-0224-6
children’s car seats contain legacy and novel flame retardants
yan wu et al. 2018
doi.org/10.1021/acs.estlett.8b00568
"New replacement flame retardants, often marketed as safer alternatives, are lurking in children's products without rigorous safety testing and may pose risks for children's health," said Marta Venier, associate scientist at IU's School of Public and Environmental Affairs and principal investigator on the study. "The abundance of emerging flame retardant chemicals in children's car seats and the key role these products play as potential sources of chemical exposure is a cause for concern."
The research was conducted in conjunction with the Ecology Center, an independent nonprofit organization in Ann Arbor, Michigan. The car seats tested in this study were purchased by the Ecology Center and shipped to Indiana University for analyses. All of the car seats were newly manufactured between January 2017 and February 2018 and were made in China, Canada, or the United States. In total, the researchers tested 36 different fabric and foam samples from 18 car seats.
For the first time, two cyclic phosphonate esters (PMMMPs) were measured at high levels in North America, suggesting their use as a replacement flame retardant for compounds that are known to be harmful. PMMMPs were found in 34 of the 36 car seat sampled at levels much higher than those of traditional flame retardants. Little is known about their health effects. Two other emerging flame retardants (tris(2,4-di-t-butylphenyl) phosphate (TDTBPP) and resorcinol bis(diphenyl phosphate) (RDP)) were also measured in baby products for the first time.
Polybrominated diphenyl ethers (PBDEs) were observed in 75 percent of the samples tested, despite being phased out of use in the United States in 2013 over health concerns. However, PBDEs were detected at such low levels that it is unlikely they were added intentionally. They may have been impurities or found in parts containing recycled materials. Conversely, decabromodiphenyl ethane (DBDPE) was detected in four samples at high levels, suggesting that it was intentionally used. DBDPE is a brominated flame retardant known to cause oxidative stress, hormone disruption and thyroid problems.
Unlike other baby products, children's car seats are required to meet the flammability standards for car interiors outlined in the Federal Motor Vehicle Safety Standard 302, which was created in 1971 by the National Highway Traffic Safety Administration. Flame retardants are routinely used as a cost-effective way to meet this standard. However, flame retardants have been linked to a variety of negative health effects, including hormone disruption, impaired brain development, liver damage and cancer. Children are more susceptible to these effects than adults because of their smaller size and their tendency to put their hands and objects in their mouths.
Children can be exposed to flame retardants in car seats by breathing in chemicals that leach into the air out of fabrics and foam. This is especially problematic for children during the summer months, when heat increases the rate at which flame retardants enter the poorly ventilated, semi-closed car environment. Children can also be exposed to flame retardants by ingesting the dust which accumulates inside the vehicle, through skin contact or by chewing on their car seats.
"We found that car seat manufacturers are intentionally moving away from certain toxic chemicals compounds that they know to be harmful, which is good news," said Yan Wu, a postdoctoral researcher at Indiana University and the lead author of the study. "However, we know very little about the replacement chemicals they're using. Car seats are vital for protecting children during a vehicle crash, but more research is needed to ensure that those seats are chemically safe as well."
abstract Brominated and phosphorus-based flame retardants (PFRs) were measured in foam and fabric samples from 18 newly marketed children’s car seats. The concentrations of two cyclic phosphonates {PMMMPs, 5-ethyl-2-methyl-2-oxido-1,3,2-dioxaphosphinan-5-yl)methyl methyl methylphosphonate and bis[(5-ethyl-2-methyl-1,3,2-dioxaphosphorinan-5-yl)methyl] methyl phosphonate p,p′-dioxide} were quantitatively measured for the first time in the North American environment and were much higher than those of other flame retardants. Median PMMMP concentrations were 73.6 μg/g, accounting on average for 52% of the total FR concentrations, indicating an intentional addition of PMMMPs during the manufacturing process of these car seats. Two other emerging PFRs [tris(2,4-di-Hi Katie,t-butylphenyl) phosphate (TDTBPP) and resorcinol bis(diphenyl phosphate) (RDP)] were detected for the first time in baby products at median levels of 1.11 and 6.15 μg/g, respectively. Other frequently detected PFRs included triethyl phosphate (TEP), triphenyl phosphate (TPHP), and tris(2-butoxyethyl) phosphate (TBOEP). Among the brominated flame retardants monitored, decabromodiphenyl ethane (DBDPE), with a median concentration of 128 μg/g, was the only halogenated FR measured at levels suggesting intentional use. Other brominated FRs such as hexabromobenzene (HBB) and 2,3-dibromo 2,4,6-tribromophenyl ether (DPTE) were sporadically detected with median concentrations of 0.23 and 0.18 μg/g, respectively. Despite being phased out in the United States starting in 2013, polybrominated diphenyl ethers (PBDEs) were still observed in 75% of our samples, although at modest levels (median total PBDE levels of 0.24 μg/g). Trace PBDE levels suggest background contamination rather than intentional use. The high levels of FRs measured in these children’s car seats together with the negative health effects associated with some of these compounds are a cause for concern for children’s health.
polybrominated diphenyl ether (pbde) concentrations in house dust are related to hormone levels in men
john d. meeker et al. 2009
ncbi.nlm.nih.gov/pmc/articles/PMC2743070/#__ffn_sectitle
arctic sea ice, eurasia snow, and extreme winter haze in china
yufei zou, yuhang wang, yuzhong zhang and ja-ho koo 2017
doi.org/10.1126/sciadv.1602751
pharmaceuticals
non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case–time–control study
kathrine b. sondergaard et al. 2017
doi.org/10.1093/ehjcvp/pvw041
Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used and have been associated with increased cardiovascular risk. Nonetheless, it remains unknown whether use of NSAIDs is associated with out-of-hospital cardiac arrest (OHCA).
Methods and results
From the nationwide Danish Cardiac Arrest Registry, all persons with OHCA during 2001–10 were identified. NSAID use 30 days before OHCA was categorized as follows: diclofenac, naproxen, ibuprofen, rofecoxib, celecoxib, and other. Risk of OHCA associated with use of NSAIDs was analysed by conditional logistic regression in case–time–control models matching four controls on sex and age per case to account for variation in drug utilization over time. We identified 28 947 persons with OHCA of whom 3376 were treated with an NSAID up to 30 days before OHCA. Ibuprofen and diclofenac were the most commonly used NSAIDs and represented 51.0% and 21.8% of total NSAID use, respectively. Use of diclofenac (odds ratio [OR], 1.50 [95% confidence interval (CI) 1.23–1.82]) and ibuprofen [OR, 1.31 (95% CI 1.14–1.51)] was associated with a significantly increased risk of OHCA. Use of naproxen [OR, 1.29 (95% CI 0.77–2.16)], celecoxib [OR, 1.13 (95% CI 0.74–1.70)], and rofecoxib (OR, 1.28 [95% CI 0.74–1.70)] was not significantly associated with increased risk of OHCA; however, these groups were characterized by few events.
Conclusion
Use of non-selective NSAIDs was associated with an increased early risk of OHCA. The result was driven by an increased risk of OHCA in ibuprofen and diclofenac users.
prenatal exposure to paracetamol/acetaminophen and precursor aniline impairs masculinisation of male brain and behaviour
anders hay-schmidt et al. 2017
doi.org/10.1530/REP-17-0165
In 2016, the researchers published a study showing that female mice had fewer eggs in their ovaries if their mothers had had paracetamol during pregnancy. This led to the mice becoming infertile more quickly. But even if paracetamol is harmful, that does not mean it should never be taken, even when pregnant.
winter climate change decreases fine root biogenic silica in sugar maple trees (acer saccharum): implications for silica export in the anthropocene
timothy j. maguire, pamela h. templer, john j. battles, robinson w. fulweiler 2017
doi.org/10.1002/2016JG003755
humans as agents in the termination of the african humid period
david k. wright 2017
doi.org/10.3389/feart.2017.00004
emergence of function from coordinated cells in a tissue
indika rajapakse, stephen smale 2017
doi.org/10.1073/pnas.1621145114
particulates
preconception exposure to fine particulate matter leads to cardiac dysfunction in adult male offspring
vineeta tanwar et al. 2018
doi.org/10.1161/jaha.118.010797
“We found that these offspring had a variety of heart problems during the prime of their lives and the effects were so robust that it was somewhat shocking,” said study senior author Loren Wold, director of biomedical research at Ohio State’s College of Nursing.
Heart function was impaired. Inflammatory markers linked to increased heart disease risk were high. They had markers of oxidative stress, a condition in which levels of beneficial antioxidants are low. Calcium regulatory proteins, which are critical to the function of the beating heart, were altered. And these mice were young and otherwise healthy — comparable to 20-year-old humans.
The first-of-its-kind study appears online today in the Journal of the American Heart Association.
“This suggests that heart problems related to pollution exposure could start even before conception, and if that’s true it has implications worldwide,” said Wold, a professor of nursing and medicine at Ohio State.
Wold and his team also uncovered evidence of gene-related differences that might explain the cardiovascular changes they saw. They examined epigenetic regulators, which play an important role in the expression of genes — meaning that they have influence over predisposition to health problems, including cardiovascular disease.
“I looked at important epigenetic regulators in the offspring, and some were activated, which could explain the differences we saw. The next step will be a more-detailed analysis,” said study lead author Vineeta Tanwar, a research scientist at Ohio State.
To conduct the study, researchers concentrated air from Columbus, Ohio, until the level of harmful particulate matter — particles suspended in the air — reached a level on par with large cities such as Los Angeles and Beijing. The research focused on the presence of PM2.5, particles that are small enough to pass from the lungs into the bloodstream.
The test mice breathed this air for about 30 hours a week.
“They were, on average, exposed to less particulate matter than what the U.S. Environmental Protection Agency has set for daily air quality standards,” Tanwar said.
Then, the mice were kept in normal air during mating and the researchers compared their offspring to the offspring of mice that were not exposed to the polluted air.
“The first thing we did was to do a basic echocardiograph and we could see profound heart dysfunction in the offspring of particulate-matter-exposed mice,” Tanwar said. “Then, we began to look at single cells and at typical markers of heart disease and found a lot more evidence that preconception pollution could harm the offspring.”
The study focused only on male offspring because the research team wanted to narrow its focus on this first experiment. Going forward, they plan to compare male and female offspring, try to determine which parent’s exposure might matter more to offspring, evaluate heart health later in the lifespan of the mice and explore potential changes in the eggs and sperm of mice exposed to dirty air.
“A key question here is how are changes in the sperm and eggs passing on the information to the offspring to cause this heart dysfunction?” Wold said.
Though more animal research is needed, this study also opens the door to exploring the role of air pollution on the health of future generations, he said. For instance, it might make sense to begin by working with adults with high levels of exposure to particulate matter, such as residents of New Delhi and Beijing, Wold said.
“We already know that humans have dramatic cardiovascular effects from exposure to dirty air, high blood pressure in particular. And we know that babies can be harmed by pollution both before and after birth,” Wold said.
“Understanding whether the damage may begin even before conception is critical.”
abstract Preconception exposure to PM2.5 results in global cardiac dysfunction in adult offspring, suggesting that abnormalities during development are not limited to the prenatal or postnatal periods but can also be determined before conception.
association between ambient air pollution and cardiac morpho-functional phenotypes: insights from the uk biobank population imaging study
nay aung et al. 2018
doi.org/https://doi.org/10.1161/CIRCULATIONAHA.118.034856
the 2016 global and national burden of diabetes mellitus attributable to fine particulate matter air pollution
bowe b et al. 2018
doi.org/10.1016/s2542-5196(18)30140-2
drought-sensitivity of fine dust in the u.s. southwest: implications for air quality and public health under future climate change
pattanun achakulwisut et al. 2018
doi.org/10.1088/1748-9326/aabf20
brake and tire dust
highly acidic ambient particles, soluble metals, and oxidative potential: a link between sulfate and aerosol toxicity
ting fang et al. 2017
doi.org/10.1021/acs.est.6b06151
tire abrasion as a major source of microplastics in the environment
frank sommer et al. 2018
doi.org/10.4209/aaqr.2018.03.0099
atmospheric transport is a major pathway of microplastics to remote regions
n. evangeliou et al. 2020
doi.org/10.1038/s41467-020-17201-9
longitudinal analysis of particulate air pollutants and adolescent delinquent behavior in southern california
diana younan et al. 2017
doi.org/10.1007/s10802-017-0367-5
toxic air pollution particles found in human brains
damian carrington 2016
theguardian.com/environment/2016/sep/05/toxic-air-pollution-particles-found-in-human-brains-links-alzheimers
commuting in los angeles: cancer and non-cancer health risks of roadway, light-rail and subway transit routes
christopher lovett et al. 2017
http://doi.org/10.4209/aaqr.2017.09.0331
Los Angeles commuters exposed to hazardous PM species face significant health risks.
PM species including PAHs, transition metals & EC present the greatest health risk.
Risk on the METRO red line subway is greater than light-rail or roadway exposures.
The METRO gold line light rail affords the least exposure & consequent health risk.
Workers within the megacity of Los Angeles are exposed to significant amounts of airborne particulate matter (PM) during their daily commutes, which often exceed 30–60 minutes each way. Chemical species present in roadway and railway PM, including Benzo[a]pyrene (BaP) and hexavalent chromium (Cr6+), present substantial cancer and non-cancer health risks. In the current study, PM samples were collected and quantitatively speciated along five major commuter routes, including the METRO red line (subway) and gold line (light rail), the I-110 and I-710 freeways, and high-density surface streets (Sunset and Wilshire Boulevards). Using these concentration data, along with cancer potency (CP) and Reference Dosage (RfD) factors obtained from the United States Environmental Protection Agency (USEPA) and California’s Office of Environmental Health Hazard Assessment (OEHHA), cancer and non-cancer health risks were calculated. In contrast to previous research indicating that Polycyclic Aromatic Hydrocarbon (PAH) components of Los Angeles roadway PM (e.g., along the I-710 freeway) led to the greatest cancer risk, the current analysis reveals that exposure to carcinogenic transition metals, particularly hexavalent chromium, which are especially prevalent along the METRO red line, results in the greatest cancer and non-cancer health risks. Based on these data, the best option for commuters is to use above-ground light-rail transportation, which allows for reduced exposure to both traffic-generated PAHs and railway-related metals.
magnetite pollution nanoparticles in the human brain
barbara a. maher et al. 2016
doi.org/10.1073/pnas.1613349113
pollution
acute effects of air pollutants on spontaneous pregnancy loss: a case-crossover study
claire l. leiser et al. 2018
doi.org/10.1016/j.fertnstert.2018.10.028
fetal and postnatal metal dysregulation in autism
manish arora et al. 2017
doi.org/10.1038/NCOMMS15493
non-phosphorylated tau in cerebrospinal fluid is a marker of alzheimer’s disease continuum in young urbanites exposed to air pollution
lilian calderón-garcidueñas et al. 2018
doi.org/10.3233/jad-180853
Mexico City children have lifetime exposures to concentrations of air pollutants above the current USA standards, including fine particulate matter (PM 2.5). Metropolitan Mexico City is an example of extreme urban growth and serious environmental pollution and millions of children are involuntarily exposed to harmful concentrations of PM 2.5 every day since conception.
This study focused on studying 507 CSF normal samples from children, teens and young adults average age 12.8±6.7 years from MMC and control cities with low levels of air pollutants, using a high affinity monoclonal non-phosphorylated tau antibody (Non-P-Tau) as a potential biomarker of AD and axonal damage. In 81 samples, researchers also measured total tau (T-Tau), tau phosphorylated at threonine 181 (P-Tau), amyloid-β 1-42, brain-derived neurotrophic factor (BDNF), insulin, leptin and inflammatory mediators. Authors documented by transmission electron microscopy (TEM) myelinated axonal size, and the pathology associated with combustion-derived nanoparticles-iron rich, highly oxidant CDNPs- in anterior cingulate cortex (ACC) white matter in 6 young residents (4 MMC, 2 controls). Non-P-Tau showed a strong increase with age significantly faster among MMC versus controls. Anterior cingulate cortex showed significant decrease in the average axonal size and CDNPs were associated with organelle pathology in MMC residents. Non-P-Tau exhibited significant increases with age, an important finding in a young population where axonal changes are present and AD hallmarks are evolving steadily in the first two decades of life. Non-P-Tau is potentially an early biomarker of axonal damage and AD axonal pathology in highly exposed young populations. Drs.Lilian Calderón-Garcidueñas and Lachmann commented air pollution is a serious public health issue and exposures to concentrations of air pollutants at or above the current standards have been linked to neuroinflammation and high risk of Alzheimer's disease. Jung et al., 2015 found a 138% risk of increase of AD per increase of 4.34 μg/m3 in PM 2.5 suggesting long-term exposure to PM 2.5, as well as ozone above the current US EPA standards are associated with increased risk of Alzheimer's disease. In the USA alone, 200 million people live in areas where pollutants such as ozone and fine particulate matter exceed the standards.
The international team of researchers stated efforts should be aimed to identify and mitigate environmental factors influencing the development of Alzheimer's disease and neuroprotection of children and young adults ought to be a public health priority to halt the development of Alzheimer in the first two decades of life.
abstract Long-term exposure to fine particulate matter (PM2.5) and ozone (O3) above USEPA standards is associated with Alzheimer’s disease (AD) risk. Metropolitan Mexico City (MMC) children exhibit subcortical pretangles in infancy and cortical tau pre-tangles, NFTs, and amyloid phases 1-2 by the 2nd decade. Given their AD continuum, we measured in 507 normal cerebrospinal fluid (CSF) samples (MMC 354, controls 153, 12.82±6.73 y), a high affinity monoclonal non-phosphorylated tau antibody (non-P-Tau), as a potential biomarker of AD and axonal damage. In 81 samples, we also measured total tau (T-Tau), tau phosphorylated at threonine 181 (P-Tau), amyloid-β1-42, BDNF, and vitamin D. We documented by electron microscopy myelinated axonal size and the pathology associated with combustion-derived nanoparticles (CDNPs) in anterior cingulate cortex white matter in 6 young residents (16.25±3.34 y). Non-P-Tau showed a strong increase with age significantly faster among MMC versus controls (p = 0.0055). Aβ1 - 42 and BDNF concentrations were lower in MMC children (p = 0.002 and 0.03, respectively). Anterior cingulate cortex showed a significant decrease (p = <0.0001) in the average axonal size and CDNPs were associated with organelle pathology. Significant age increases in non-P-Tau support tau changes early in a population with axonal pathology and evolving AD hallmarks in the first two decades of life. Non-P-Tau is an early biomarker of axonal damage and potentially valuable to monitor progressive longitudinal changes along with AD multianalyte classical CSF markers. Neuroprotection of young urbanites with PM2.5 and CDNPs exposures ought to be a public health priority to halt the development of AD in the first two decades of life.
diel variation of formaldehyde levels and other vocs in homes driven by temperature dependent infiltration and emission rates
yibo huangfu et al. 2019
doi.org/10.1016/j.buildenv.2019.05.031
gypsum wallboards source of formaldehyde and mercury in homes
"People think of air pollution as an outdoor problem, but they fail to recognize that they're exposing themselves to much higher emission rates inside their homes," Jobson said.
These emissions come from a variety of sources, such as building materials, furniture, household chemical products, and from people's activities like cooking.
One of the ways to clear out harmful chemicals is with ventilation to the outdoors. But, with increased concern about climate change and interest in reducing energy use, builders are trying to make homes more airtight, which may inadvertently be worsening the problem.
In their study, the researchers looked at a variety of homes -- meant to reflect the typical housing styles and age in the U.S. They found that formaldehyde levels rose in homes as temperatures increased inside -- between three and five parts per billion every time the temperature increased one degree Celsius.
"As a home gets hotter, there is a lot more formaldehyde in the home. The materials are hotter and they off-gas at higher rates," Jobson said.
The work shows how heat waves and changing regional climate might affect indoor air quality in the future.
"As people ride out a hot summer without air conditioning, they're going to be exposed to much higher concentrations of pollutants inside," he said.
The researchers also found that pollution levels varied throughout the day -- they were highest in the afternoon and lowest in the early morning. Until now, manufacturers and builders have assumed that pollutants stay the same throughout the day as they consider the emissions from their materials, so they may not be getting a true picture of how much pollution people are exposed to indoors, he said.
The researchers also were surprised to find in one home that gypsum wallboard emitted high levels of formaldehyde and possibly mercury when it's heated. That home, built in the early 1970s, had radiant heating in its ceiling, which was a popular heating system at that time.
After finding high levels of formaldehyde in the home, the researchers suspected the gypsum wallboard radiant ceiling in the home. About half of the gypsum used in homes as drywall is made from waste products of the coal industry. They pulled a piece from the home, heated it up in their laboratory, and measured high levels of formaldehyde -- as much as 159 parts per billion.
Household formaldehyde exposure is notregulated in the United States, but the US Agency for Toxic Substances and Disease Registry, part of the Centers for Disease Control, has set eight parts per billion as posing a minimum risk level.
"Exposure to these chemicals impacts people's ability to think and learn," said Jobson. "It's important for people to be more cognizant of the risk -- Opening a window is a good thing."
The researchers plan to continue looking at ways to reduce exposure to indoor air pollutants, such as using green building materials.
"We have to balance making more energy efficient homes with protecting our health and cognitive function," he said.
•Diel variation of indoor formaldehyde and other VOCs were found.
•VOC levels are in dynamic state due to the time of day variation of infiltration rate.
•VOC levels lag behind the air change rate.
•Formaldehyde levels have temperature dependence of 3.0–4.5 ppbv per °C.
•Gypsum wallboard is a formaldehyde source when heated.
High time resolution monitoring of formaldehyde and other volatile organic compounds in the air of four homes in winter and summer revealed diel variation of VOC levels driven by infiltration and temperature dependent whole house emission rates. In unoccupied homes, these pollutants displayed a large diel concentration variation, with an afternoon maxima and early morning minima. VOC abundance lagged about 2 h behind changes in infiltration rates measured by a tracer release method, resulting in poor correlations between VOC concentration and air change rate. The data demonstrate that VOC abundance was not in steady state with respect to whole house emission rates. Formaldehyde and other VOCs displayed a positive correlation with indoor temperature in both winter and summer. Formaldehyde sensitivity to temperature ranged from 3.0 to 4.5 ppbv per °C, a useful metric for predicting the impact of heat waves and changing regional climate on indoor air quality. Gypsum wallboard used as radiant ceiling heating product in one home was identified as source of formaldehyde and potentially mercury.
experimental acute exposure to thirdhand smoke and changes in the human nasal epithelial transcriptome
giovanna l. pozuelos et al. 2019
doi.org/10.1001/jamanetworkopen.2019.6362
Thirdhand smoke, or THS, results when exhaled smoke and smoke emanating from the tip of burning cigarettes settles on surfaces such as clothing, hair, furniture, and cars. Not strictly smoke, THS refers to the residues left behind by smoking.
"THS can resurface into the atmosphere and can be inhaled unwillingly by nonsmokers," said Giovanna Pozuelos, the first author of the research paper and a graduate student in Talbot's lab. "It has not been widely studied, which may explain why no regulations are in place to protect nonsmokers from it."
The researchers obtained nasal scrapes from four healthy nonsmokers who had been exposed to THS for three hours in a laboratory setting at UC San Francisco. The UCR researchers then worked to get good quality RNA from the scrapes -- necessary to examine gene expression changes. RNA sequencing identified genes that were over- or under-expressed. They found 382 genes were significantly over-expressed; seven other genes were under-expressed. They then identified pathways affected by these genes.
"THS inhalation for only three hours significantly altered gene expression in the nasal epithelium of healthy nonsmokers," Pozuelos said. "The inhalation altered pathways associated with oxidative stress, which can damage DNA, with cancer being a potential long-term outcome. It's extremely unlikely a three-hour exposure to THS would cause cancer, but if someone lived in an apartment or home with THS or drove a car regularly where THS was present, there could be health consequences."
Because gene expression in the nasal epithelium is similar to the bronchial epithelium, the researchers note that their data is relevant to cells deeper in the respiratory system. In the samples they studied, the researchers also found that brief THS exposure affected mitochondrial activity. Mitochondria are organelles that serve as the cell's powerhouses. If left unchecked, the observed effects would lead to cell death.
Pozuelos explained that the team focused on the nasal epithelium because the nasal passage is one way THS can enter people's lungs. The other common exposure route is through the skin, which the researchers did not study, but plan to in the future.
Already, the researchers are working with groups in San Diego, California, and Cincinnati to study long-term exposure to THS, made possible with access to homes where people are being exposed to THS.
"Many people do not know what THS is," said Talbot, the director of the UCR Stem Cell Center. "We hope our study raises awareness of this potential health hazard. Many smoking adults think, 'I smoke outside, so my family inside the house will not get exposed.' But smokers carry chemicals like nicotine indoors with their clothes. It's important that people understand that THS is real and potentially harmful."
abstract acute inhalation of THS caused cell stress that led to the activation of survival pathways. Some responses were consistent with stress-induced mitochondrial hyperfusion and similar to those demonstrated previously in vitro. These data may be valuable to physicians treating patients exposed to THS and may aid in formulating regulations for the remediation of THS-contaminated environments.
association of residential air pollution, noise, and greenspace with initial ischemic stroke severity
rosa maria vivanco-hidalgo et al. 2019
doi.org/10.1016/j.envres.2019.108725
abstract •Higher residential surrounding greenspace is related with less severe stroke.
•Living in areas with higher annual average noise values is associated with a more severe stroke.
•There is an influence of the built environment on the global burden of stroke.
Background and Purpose
A number of environmental risk factors of acute ischemic stroke have been identified, but few studies have evaluated the influence of the outdoor environment on stroke severity. We assessed the association of residential ambient fine particulate matter air pollution (PM2.5), noise, and surrounding greenspace with initial stroke severity.
Methods
We obtained data on patients hospitalized with acute ischemic stroke from a hospital-based prospective stroke register (2005–2014) in Barcelona. We estimated residential PM2.5 based on an established land use regression model, greenspace as the average satellite-based Normalized Difference Vegetation Index (NDVI) within a 300 m buffer of the residence, and daily (Lday), evening (Levening), night (Lnight) and average noise (Lden) level at the street nearest to the residential address using municipal noise models. Stroke severity was assessed at the time of hospital presentation using the National Institute of Health Stroke Scale (NIHSS).We used logistic regression and binomial models to evaluate the associations of PM2.5, greenspace, and noise with initial stroke severity adjusting for potential confounders.
Results
Among 2761 patients, higher residential surrounding greenspace was associated with lower risk of severe stroke (OR for NIHSS>5, 0.75; 95% CI: 0.60–0.95), while, living in areas with higher Lden was associated with a higher risk of severe stroke (OR, 1.30; 95% CI: 1.02–1.65). PM2.5 was not associated with initial stroke severity.
Conclusions
In an urban setting, surrounding greenspace and traffic noise at home are associated with initial stroke severity, suggesting an important influence of the built environment on the global burden of ischemic stroke.
plastics
fast uptake of microplastics into all tissues
uptake, whole-body distribution, and depuration of nanoplastics by the scallop pecten maximus at environmentally realistic concentrations
maya al-sid-cheikh et al. 2018
doi.org/10.1021/acs.est.8b05266
After six hours exposure in the laboratory, billions of particles measuring 250nm (around 0.00025mm) had accumulated within the scallop's intestines.
However, considerably more even smaller particles measuring 20nm (0.00002mm) had become dispersed throughout the body including the kidney, gill, muscle and other organs.
The study is the first to quantify the uptake of nanoparticles at predicted environmentally relevant conditions, with previous research having been conducted at far higher concentrations than scientists believe are found in our oceans.
Dr Maya Al Sid Cheikh, Postdoctoral Research Fellow at the University of Plymouth, led the study. She said: "For this experiment, we needed to develop an entirely novel scientific approach. We made nanoparticles of plastic in our laboratories and incorporated a label so that we could trace the particles in the body of the scallop at environmentally relevant concentrations. The results of the study show for the first time that nanoparticles can be rapidly taken up by a marine organism, and that in just a few hours they become distributed across most of the major organs."
Professor Richard Thompson OBE, Head of the University's International Marine Litter Research Unit, added: "This is a ground breaking study, in terms of both the scientific approach and the findings. We only exposed the scallops to nanoparticles for a few hours and, despite them being transferred to clean conditions, traces were still present several weeks later. Understanding the dynamics of nanoparticle uptake and release, as well as their distribution in body tissues, is essential if we are to understand any potential effects on organisms. A key next step will be to use this approach to guide research investigating any potential effects of nanoparticles and in particular to consider the consequences of longer term exposures."
Accepted for publication in the Environmental Science and Technology journal, the study also involved scientists from the Charles River Laboratories in Elphinstone, Scotland; the Institute Maurice la Montagne in Canada; and Heriot-Watt University.
It was conducted as part of RealRiskNano, a £1.1million project funded by the Natural Environment Research Council (NERC). Led by Heriot-Watt and Plymouth, it is exploring the effects which microscopic plastic particles can have on the marine environment.
In this study, the scallops were exposed to quantities of carbon-radiolabeled nanopolystyrene and after six hours, autoradiography was used to show the number of particles present in organs and tissue.
It was also used to demonstrate that the 20nm particles were no longer detectable after 14 days, whereas 250nm particles took 48 days to disappear.
Ted Henry, Professor of Environmental Toxicology at Heriot-Watt University, said: "Understanding whether plastic particles are absorbed across biological membranes and accumulate within internal organs is critical for assessing the risk these particles pose to both organism and human health. The novel use of radiolabelled plastic particles pioneered in Plymouth provides the most compelling evidence to date on the level of absorption of plastic particles in a marine organism."
abstract Previous studies of uptake and effects of nanoplastics by marine organisms have been conducted at what may be unrealistically high concentrations. This is a consequence of the analytical challenges in tracking plastic particles in organisms at environmentally relevant concentrations and highlights the need for new approaches. Here, we present pulse exposures of 14C-radiolabeled nanopolystyrene to a commercially important mollusk, Pecten maximus, at what have been predicted to be environmentally relevant concentrations (<15 μg L–1). Uptake was rapid and was greater for 24 nm than for 250 nm particles. After 6 h, autoradiography showed accumulation of 250 nm nanoplastics in the intestine, while 24 nm particles were dispersed throughout the whole-body, possibly indicating some translocation across epithelial membranes. However, depuration was also relatively rapid for both sizes; 24 nm particles were no longer detectable after 14 days, although some 250 nm particles were still detectable after 48 days. Particle size thus apparently influenced the biokinetics and suggests a need for chronic exposure studies. Modeling extrapolations indicated that it could take 300 days of continued environmental exposure for uptake to reach equilibrium in scallop body tissues although the concentrations would still below 2.7 mg g–1. Comparison with previous work in which scallops were exposed to nonplastic (silver) nanomaterials of similar size (20 nm), suggests that nanoparticle composition may also influence the uptake tissue distributions somewhat.
nanoplastics formed during the mechanical breakdown of daily-use polystyrene products
mikael t. ekvall et al. 2018
doi.org/10.1039/c8na00210j
The majority of all marine debris is plastic. Calculations have shown that ten per cent of all plastic produced globally ends up in the sea. This plastic waste is subjected to both chemical and mechanical degradation. The sun's UV rays contribute to the degradation, as do waves, which cause plastic waste to grind against stones on the water's edge, against the sea floor or against other debris.
Is there a risk that this plastic waste disintegrates to the extent that nanoplastics are released? The research community is divided on whether the degradation process stops at slightly larger plastic fragments -- microplastics -- or actually continues and creates even smaller particles. The researchers behind the study have now investigated this issue by subjecting plastic material to mechanical degradation under experimental conditions.
"We have been able to show that the mechanical effect on the plastic causes the disintegration of plastic down to nano-sized plastic fragments," says Tommy Cedervall, chemistry researcher at Lund University.
The study relates to the larger issue of what happens to plastic in the environment and how plastic can affect animals and humans. Plastic nano-sized particles are a few millionths of a millimetre, i.e. extremely small particles, so small that they have been shown to reach far into living organisms' bodies.
Last year, in an earlier study from Lund University, researchers showed that nano-sized plastic particles can enter the brains of fish and that this causes brain damage which probably disturbs fish behaviour. Although the study was conducted in a laboratory environment, it indicates that nanoplastics can lead to adverse consequences.
The emphasis of a number of other recent studies from the research community has been on microplastics and their increased distribution among organisms. There are now intense attempts to also identify nanoplastics in the environment.
"It's important to begin mapping what happens to disintegrated plastic in nature," concludes Tommy Cedervall.
abstract Large amounts of plastics are released into the environment every day. These released plastics have a clearly documented negative effect on wildlife. Much research attention has been given to large plastic pieces and microplastics. However, if the breakdown of plastics is a continous process, eventually nanoplastics will be produced. Nanoplastics will affect wildlife differently from larger plastic pieces. We have studied the products formed by the mechanical breakdown of two commonly used polystyrene products, takeaway coffee cup lids and expanded polystyrene foam. After breakdown using a food processor, we characterized the breakdown products using seven different methods and found nanosized polystyrene particles with different shapes and negative or nearly neutral surface charges. These results clearly demonstrate that daily-use polystyrene products can break down into nanoparticles. Model polystyrene particles with different sizes and surface modifications have previously been shown to have different negative effects on wildlife. This indicates that breakdown nanoparticles might have the potential to cause cocktail effects in nature.
alpha-gal allergy
oh, lovely: the tick that gives people meat allergies is spreading
megan molteni 2017
wired.com/story/lone-star-tick-that-gives-people-meat-allergies-may-be-spreading/
why are so many people getting a meat allergy?: known as alpha-gal allergy, the condition dictates what you can eat, wear, how you relax, and even which medicines are safe.
maryn mckenna 2018
mosaicscience.com/story/mammalian-meat-allergy-alpha-gal-allergic-lone-star-tick-bite
nanoparticles
titanium dioxide nanoparticles exacerbate dss-induced colitis: role of the nlrp3 inflammasome
pedro a ruiz et al. 2017
doi.org/10.1136/gutjnl-2015-310297
association of type 2 diabetes with submicron titanium dioxide crystals in the pancreas
adam heller et al. 2018
doi.org/10.1021/acs.chemrestox.8b00047
waterborne exposure of adult zebrafish to silver nanoparticles and to ionic silver results in differential silver accumulation and effects at cellular and molecular levels
josé maría lacave et al. 2018
doi.org/10.1016/j.scitotenv.2018.06.128
•Adult zebrafish were exposed for 21 days to 10 μg Ag/L of Ag NPs or ionic silver.
•Silver was detected in gills, liver and intestine.
•Histopathological alterations were recorded in gills.
•Exposure to Ag NPs and ionic silver regulated the hepatic transcriptome differentially.
•Damage on gills and effects on liver lysosomes were recorded at 6 months post-exposure.
Effects of silver nanoparticles (Ag NPs) on freshwater species have been reported in several studies, but there is not information on the potential long-term consequences of a previous exposure. In this work, we investigated the long-term effects of maltose-coated Ag NPs (20 nm) and of ionic silver (10 μg/L) after 21 days of exposure and at 6 months post-exposure (mpe) in adult zebrafish. Exposure resulted in significant silver accumulation in the whole body of fish exposed to ionic silver, but not in those exposed to Ag NPs. However, autometallography revealed metal accumulation in the liver and intestine of fish treated with the two silver forms and especially in the intestine of fish exposed to Ag NPs. X-ray microanalysis showed the presence of silver in gills, liver and intestine and of Ag NPs in gill and liver cells. Inflammation and hyperplasia were evident in the gills after both treatments and these histopathological conditions remained at 6 mpe. According to the hepatic transcriptome analysis, at 3 days ionic silver regulated a larger number of transcripts (410) than Ag NPs (129), while at 21 days Ag NPs provoked a stronger effect (799 vs 165 regulated sequences). Gene ontology terms such as “metabolic processes” and “response to stimulus” appeared enriched after all treatments, while “immune system” or “reproductive processes” were specifically enriched after the exposure to Ag NPs. This suggests that the toxicity of Ag NPs may not be solely related to the release of Ag ions, but also to the NP form. No evident effects were found on protein oxidation or on hepatocyte lysosomal membrane stability during exposure, but effects recorded on liver lysosomes and persistent damage on gill tissue at 6 mpe could indicate potential for long-term effects in exposed fish.
heterozygous de novo ubtf gain-of-function variant is associated with neurodegeneration in childhood
simon edvardson et al. 2017
doi.org/10.1016/j.ajhg.2017.07.002
what causes the delay in regression? is it possible the defect is not present at birth?
topical tissue nano-transfection mediates non-viral stroma reprogramming and rescue
daniel gallego-perez et al. 2017
doi.org/10.1038/nnano.2017.134
gadolinium deposition in the brain: summary of evidence and recommendations
vikas gulani et al. 2017
doi.org/10.1016/S1474-4422(17)30158-8
elemental sulfur use and associations with pediatric lung function and respiratory symptoms in an agricultural community (california, usa)
rachel raanan et al. 2017
doi.org/10.1289/EHP528
a study of children in the agricultural community of Salinas Valley, California, researchers found significant associations between elemental sulfur use and poorer respiratory health. The study linked reduced lung function, more asthma-related symptoms and higher asthma medication use in children living about a half-mile or less from recent elemental sulfur applications compared to unexposed children.
The EPA generally considers elemental sulfur as safe for the environment and human health, but previous studies have shown that it is a respiratory irritant to exposed farmworkers. Elemental sulfur’s effect on residential populations, especially children, living near treated fields has not previously been studied despite the chemical’s widespread use and potential to drift from the fields where it is applied. This study is the first to link agricultural use of sulfur with poorer respiratory health in children living nearby.
The study was published August 14 in the journal Environmental Health Perspectives. The research was funded by the National Institute of Environmental Health Sciences and the Environmental Protection Agency. Rachel Raanan, a UC Berkeley postdoctoral fellow and the study’s lead author, was supported by the Environment and Health Fund in Israel. Research protocols were approved by the UC Berkeley Committee for the Protection of Human Subjects.
Elemental sulfur is allowed for use on conventional and organic crops to control fungus and other pests and is very important to both systems. It is the most heavily used agricultural pesticide in California and Europe. In California alone, more than 21 million kilograms of elemental sulfur was applied in agriculture in 2013.
“Sulfur is widely used because it is effective and low in toxicity to people. It is naturally present in our food and soil and is part of normal human biochemistry, but breathing in sulfur dust can irritate airways and cause coughing,” said co-author Asa Bradman, associate director of the Center for Environmental Research and Children’s Health at Berkeley’s School of Public Health. “We need to better understand how people are exposed to sulfur used in agriculture and how to mitigate exposures. Formulations using wettable powders could be a solution.”
For the study, the research team examined associations between lung function and asthma-related respiratory symptoms in hundreds of children living near fields where sulfur had been applied. The children were participants in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) study, a longitudinal birth cohort that is a partnership between UC Berkeley and the Salinas Valley community. CHAMACOS is the longest running longitudinal birth cohort study of pesticides and other environmental exposures among children living in an agricultural community. The cohort participants were primarily born to families of immigrant farm worker families.
The study found several associations between poorer respiratory health and nearby elemental sulfur use. A 10-fold increase in the estimated amount of sulfur used within 1 kilometer of a child’s residence during the year prior to pulmonary evaluation was associated with a 3.5-fold increased odds in asthma medication usage and a two-fold increased odds in respiratory symptoms such as wheezing and shortness of breath.
The study also found that each 10-fold increase in the amount of elemental sulfur applied in the previous 12 months within a 1-km radius of the home was associated with an average decrease of 143 milliliters per second (mL/s) in the maximal amount of air that the 7-year-old children could forcefully exhale in one second. For comparison, research has shown that exposure to maternal cigarette smoke is associated with a decrease of 101 mL/s after five years of exposure.
The researchers used regression models to control for maternal smoking during pregnancy, season of birth, particulate matter air pollution, breast feeding duration, child’s sex and age, height, technician and other covariates.
“This study provides the first data consistent with anecdotal reports of farmworkers and shows that residents, in this case, children, living near fields may be more likely to have respiratory problems from nearby agricultural sulfur applications,” said senior author Brenda Eskenazi, Berkeley professor at the School of Public Health.
abstract suggests that elemental sulfur use, allowed in both organic and conventional farming, in close proximity to residential areas, may adversely affect children’s respiratory health.
multisite de novo mutations in human offspring after paternal exposure to ionizing radiation
manuel holtgrewe et al. 2018
doi.org/10.1038/s41598-018-33066-x
'there are hundreds of sick crew': is toxic air on planes making frequent flyers ill?
theguardian.com/science/2017/aug/19/sick-crew-toxic-air-planes-frequent-flyers-ill
how toxic fumes seep into the air you breathe on planes
keira feldman 2020
latimes.com/projects/toxic-chemicals-planes-covid-19-travel-woes/
microbiome-mediated neutrophil recruitment via cxcr2 and protection from amebic colitis
koji watanabe et al. 2017
doi.org/10.1371/journal.ppat.1006513
in vitro evaluation of mitochondrial function and estrogen signaling in cell lines exposed to the antiseptic cetylpyridinium chloride
sandipan datta et al. 2017
doi.org/10.1289/EHP1404
toxic roads: unearthing hazardous waste dumping
caterina gennaioli, gaia narciso 2017
ideas.repec.org/p/tcd/tcduee/tep1817.html
an unexpected and persistent increase in global emissions of ozone-depleting cfc-11
stephen a. montzka et al. 2018
doi.org/10.1038/s41586-018-0106-2
tropical waves over the western coast of Africa develop to hurricanes
michael d’estries 2017
mnn.com/earth-matters/climate-weather/blogs/surprising-force-behind-americas-monster-hurricanes
do west african thunderstorms predict the intensity of atlantic hurricanes?
colin price et al. 2015
doi.org/10.1002/2014GL062932
tropical cyclone activity enhanced by sahara greening and reduced dust emissions during the african humid period
francesco s. r. pausata et al. 2018
doi.org/10.1073/pnas.1619111114
pcb
association of exposure to persistent organic pollutants with mortality risk
p. monica lind et al. 2019
doi.org/10.1001/jamanetworkopen.2019.3070
High levels of polychlorinated biphenyls (PCBs) in the blood are associated with premature death. This is shown by a cross-disciplinary study, based on 1,000 randomly selected 70-year-olds in Uppsala, that is published in the JAMA Network Open journal today.
The study is one in a series of studies from a cross-disciplinary collaboration, which has now lasted more than ten years, between Professors Lars Lind and Monica Lind at Uppsala University and environmental chemists at Örebro University. It shows health risks associated with PCBs, although these substances have long been banned.
Polychlorinated biphenyls (PCBs) are a group of environmental pollutants that are subject to restrictions in many countries, and bans have reduced their concentrations in the environment. But since these substances decompose very slowly and are stored in fatty tissue, they remain present in animals and humans. In particular, PCBs with many chlorine atoms in the molecule persist in most Swedes' blood.
In the study known as PIVUS (Prospective Investigation of the Vasculature in Uppsala Seniors), more than 1,000 randomly selected 70-year-olds in Uppsala were monitored over a long period. In the study relating to PCBs in blood, concentrations were measured in the subjects' blood in 2001-2004, and then again when they reached the age of 75. Follow-up of those who had died over a 10-year period showed that the individuals with the highest PCB levels with many chlorine atoms in the blood had 50% excess mortality, especially from cardiovascular disease, compared with the other groups. This corresponds to some seven extra deaths during the 10-year follow-up period.
The results were independent from the risk factors that had previously been found to be connected with cardiovascular disease, such as high blood pressure, diabetes, smoking, obesity, high cholesterol, low educational attainment and cardiovascular disease at age 70.
Previous studies have also shown an association between high PCB levels and atherosclerosis in humans and experimental animals alike. In the researchers' view this finding and the new data combined indicate that intake of PCBs in food should be reduced.
"We humans get most PCBs in our bodies by ingesting them in food. These substances are fat-soluble and found mainly in fatty animal foods like fish, meat and dairy products. According to the Swedish National Food Agency, particularly high concentrations of PCBs are present in fatty fish like Baltic herring and wild-caught salmon from polluted areas, such as the Baltic Sea, the Gulf of Bothnia, and Lakes Vänern and Vättern," Monica Lind says.
the lancet commission on pollution and health
philip j landrigan et al. 2017
doi.org/10.1016/S0140-6736(17)32345-0
want
cindy pon 2017
mineralogy controlled dissolution of uranium from airborne dust in simulated lung fluids (slfs) and possible health implications
eshani hettiarachchi et al. 2018
doi.org/10.1021/acs.estlett.8b00557
Uranium ore is weakly radioactive, which could damage DNA and cause disease. However, the chemical toxicity of uranium may be a greater risk than its radioactivity. In laboratory studies, uranium that was depleted of its most radioactive isotope still caused DNA damage and cell death. Small particles of uranium-containing dust could be inhaled by people and penetrate deep within their lungs. But scientists haven't studied whether uranium can leach from minerals in the dust into lung fluids and the bloodstream. So Gayan Rubasinghege and colleagues wanted to determine if uranium in dust samples from a mining region in New Mexico could dissolve in simulated lung fluids.
To find out, the researchers collected airborne dust samples from five sites near uranium mines close to communities. They identified minerals in the dust samples, which varied by location. All of the dust samples contained one or more uranium-containing minerals, such as uraninite or carnotite. Then, the researchers exposed two simulated lung fluids -- one that mimics the fluid that surrounds lung cells, and another that simulates the acidic environment in lung immune cells that engulf dust particles -- to the dust and measured the amounts of uranium dissolved in each fluid. The mineral composition of the dust influenced its solubility, with some minerals dissolving more readily in one fluid than the other. These results indicate that toxicological assessments of mining lands should focus on specific sites, instead of making broad generalizations, the researchers say.
abstract The recent increase in cardiovascular and metabolic disease in the Navajo population residing close to the Grants Mining District (GMD) in New Mexico is suggested to be due to exposure to environmental contaminants, in particular uranium in respirable dusts. However, the chemistry of uranium-containing-dust dissolution in lung fluids and the role of mineralogy are poorly understood, as is their impact on toxic effects. The current study is focused on the dissolution of respirable-sized U-containing-dust, collected from several sites near Jackpile and St. Anthony mines in the GMD, in two simulated lung fluids (SLFs): Gamble’s solution (GS) and Artificial Lysosomal Fluid (ALF). We observe that the respirable dust includes uranium minerals that yield the uranyl cation, UO22+, as the primary dissolved species in these fluids. Dust rich in uraninite and carnotite is more soluble in GS, which mimics interstitial conditions of the lungs. In contrast, dust with low uraninite and high kaolinite is more soluble in ALF, which simulates the alveolar macrophage environment during phagocytosis. Moreover, geochemical modeling, performed using PHREEQC, is in good agreement with our experimental results. Thus, the current study highlights the importance of site-specific toxicological assessments across mining districts with the focus on their mineralogical differences.
antimicrobials
low-level antimicrobials in the medicinal leech select for resistant pathogens that spread to patients
lidia beka et al. 2018
doi.org/10.1128/mBio.01328-18
antimicrobial chemicals associate with microbial function and antibiotic resistance indoors
ashkaan k. fahimipour et al. 2018
doi.org/10.1128/msystems.00200-18
"There is this conventional wisdom that says everything that's in dust is dead, but that's not actually the case. There are things living in there," said Northwestern's Erica Hartmann, who led the study. "Dust is the final resting place of everything that's been circulating in the air, so it can give us information about air quality."
The study was published today (Dec. 11) in the journal mSystems. Hartmann is an assistant professor of environmental engineering in Northwestern's McCormick School of Engineering. This work was done in partnership with the Biology and the Build Environmental Center at the University of Oregon.
Hartmann's study compared dust samples collected from 42 athletic facilities in the Pacific Northwest region. (Hartmann selected athletics facilities because people tend to make intimate contact with the floor, mats and equipment and use antimicrobial wipes to cleanse these areas before and after exercising.) Her team looked at the bacteria present in dust, specifically examining the bacteria's genes.
In dust with higher concentrations of triclosan, the researchers found higher abundances of genetic markers indicating antibiotic resistance. "Those genes do not code for resistance to triclosan," Hartmann clarified. "They code for resistance to medically relevant antibiotic drugs."
Up until 2017, manufacturers commonly added triclosan to antibacterial hand soaps and cleaning solutions. The Federal Drug Administration (FDA) banned triclosan in 2016, after discovering several dangerous side effects, including its potential to interfere with the human endocrine system. But even though it is no longer contained in hand soaps and the antibacterial wipes that people often use at the gym, triclosan is still present in toothpaste and many consumer products that are not labeled.
"There are many products with triclosan that are not labeled because they are within the purview of the EPA instead of the FDA," Hartmann said. "These things might include antimicrobial gym equipment, such as yoga mats and textiles."
Antibiotic resistance is an enormous threat to public health. According to the Centers for Disease Control and Prevention, nearly 25,000 people in the United States die each year from antibiotic-resistant infections. Even though triclosan has been banned, soaps and cleansers still contain other antimicrobial chemicals, including benzalkonium chloride, which Hartmann's team is now studying to see if it has a similar effect on dust.
Hartmann believes we could ease the problem of antibiotic-resistant bugs by letting go of antimicrobial products.
"The vast majority of microbes around us aren't bad and may even be good," she said. "Wipe down gym equipment with a towel. Wash your hands with plain soap and water. There is absolutely no reason to use antibacterial cleansers and hand soaps."
abstract Humans purposefully and inadvertently introduce antimicrobial chemicals into buildings, resulting in widespread compounds, including triclosan, triclocarban, and parabens, in indoor dust. Meanwhile, drug-resistant infections continue to increase, raising concerns that buildings function as reservoirs of, or even select for, resistant microorganisms. Support for these hypotheses is limited largely since data describing relationships between antimicrobials and indoor microbial communities are scant. We combined liquid chromatography-isotope dilution tandem mass spectrometry with metagenomic shotgun sequencing of dust collected from athletic facilities to characterize relationships between indoor antimicrobial chemicals and microbial communities. Elevated levels of triclosan and triclocarban, but not parabens, were associated with distinct indoor microbiomes. Dust of high triclosan content contained increased Gram-positive species with diverse drug resistance capabilities, whose pangenomes were enriched for genes encoding osmotic stress responses, efflux pump regulation, lipid metabolism, and material transport across cell membranes; such triclosan-associated functional shifts have been documented in laboratory cultures but not yet from buildings. Antibiotic-resistant bacterial isolates were cultured from all but one facility, and resistance often increased in buildings with very high triclosan levels, suggesting links between human encounters with viable drug-resistant bacteria and local biocide conditions. This characterization uncovers complex relationships between antimicrobials and indoor microbiomes: some chemicals elicit effects, whereas others may not, and no single functional or resistance factor explained chemical-microbe associations. These results suggest that anthropogenic chemicals impact microbial systems in or around buildings and their occupants, highlighting an emergent need to identify the most important indoor, outdoor, and host-associated sources of antimicrobial chemical-resistome interactions.
attributable deaths and disability-adjusted life-years caused by infections with antibiotic-resistant bacteria in the eu and the european economic area in 2015: a population-level modelling analysis
alessandro cassini et al. 2019
doi.org/10.1016/s1473-3099(18)30605-4
It is estimated that 341 deaths in Europe were caused by carbapenem-resistant K. pneumoniae in 2007; by 2015 the number of deaths had increased six-fold to 2,094. The high number of deaths is down to the fact that once carbapenems are no longer effective against antibiotic-resistant bacteria, there are few other options left. Infants, the elderly and immuno-compromised individuals are particularly at risk.
The survey is the largest of its kind and is the first step towards consistent surveillance of carbapenem-resistant bacteria in Europe. More than 2,000 samples of K. pneumoniae were collected from patients across the 244 hospitals and sent to the Wellcome Sanger Institute, where the genomes of 1,700 of them were sequenced.
Researchers identified a small number of genes that, when expressed, can cause resistance to carbapenem antibiotics. These genes produce enzymes called carbapenemases, which 'chew up' the antibiotics, rendering them useless.
Of concern to public health is the recent emergence of a small number of 'high-risk' clones carrying one or more carbapenemase genes, which have spread rapidly. It is thought that the heavy use of antibiotics in hospitals favours the spread of these highly-resistant bacteria, which outcompete other strains that are more easily treatable with antibiotics.
Dr Sophia David, first author of the study, based at the Centre for Genomic Pathogen Surveillance, said: "The 'One Health' approach to antibiotic resistance focuses on the spread of pathogens through humans, animals and the environment, including hospitals. But in the case of carbapenem-resistant Klebsiella pneumoniae, our findings imply hospitals are the key facilitator of transmission -- over half of the samples carrying a carbapenemase gene were closely related to others collected from the same hospital, suggesting that the bacteria are spreading from person-to-person primarily within hospitals."
Antibiotic-resistant bacteria samples were also much more likely to be closely related to samples from a different hospital in the same country rather than across countries -- suggesting that national healthcare systems as a whole play an important role in the spread of these antibiotic-resistant bacteria.
oral fluoroquinolones and risk of mitral and aortic regurgitation
mahyar etminan et al. 2019
doi.org/10.1016/j.jacc.2019.07.035
current users of fluoroquinolone antibiotics, such as Ciprofloxacin or Cipro, face a 2.4 times greater risk of developing aortic and mitral regurgitation, where the blood backflows into the heart, compared to patients who take amoxicillin, a different type of antibiotic. The greatest risk is within 30 days of use.
Recent studies have also linked the same class of antibiotics to other heart problems.
Some physicians favour fluoroquinolones over other antibiotics for their broad spectrum of antibacterial activity and high oral absorption, which is as effective as intravenous, or IV, treatment.
"You can send patients home with a once-a-day pill," said Mahyar Etminan, lead author and associate professor of ophthalmology and visual sciences in the faculty of medicine at UBC. "This class of antibiotics is very convenient, but for the majority of cases, especially community-related infections, they're not really needed. The inappropriate prescribing may cause both antibiotic resistance as well as serious heart problems."
The researchers hope their study helps inform the public and physicians that if patients present with cardiac issues, where no other cause has been discovered, fluoroquinolone antibiotics could potentially be a cause.
"One of the key objectives of the Therapeutic Evaluation Unit is to evaluate different drugs and health technologies to determine whether they enhance the quality of care delivered by our programs or improve patient outcomes," said Dr. Bruce Carleton, director of the unit and research investigator at BC Children's Hospital, a program of PHSA. "This study highlights the need to be thoughtful when prescribing antibiotics, which can sometimes cause harm. As a result of this work, we will continue working with the BC Antimicrobial Stewardship Committee to ensure the appropriate prescribing of this class of antibiotics to patients across British Columbia, and reduce inappropriate prescribing."
For the study, scientists analyzed data from the U.S. Food and Drug Administration's adverse reporting system. They also analyzed a massive private insurance health claims database in the U.S. that captures demographics, drug identification, dose prescribed and treatment duration. Researchers identified 12,505 cases of valvular regurgitation with 125,020 case-control subjects in a random sample of more than nine million patients. They defined current fluoroquinolone exposure as an active prescription or 30 days prior to the adverse event, recent exposure as within days 31 to 60, and past exposure as within 61 to 365 days prior to an incident. Scientists compared fluoroquinolone use with amoxicillin and azithromycin.
The results showed that the risk of aortic and mitral regurgitation, blood backflow into the heart, is highest with current use, followed by recent use. They saw no increased risk aortic and mitral regurgitation with past use.
Etminan hopes that if other studies confirm these findings, regulatory agencies would add the risk of aortic and mitral regurgitation to their alerts as potential side effects and that the results would prompt physicians to use other classes of antibiotics as the first line of defense for uncomplicated infection
These results show that the risk of aortic and mitral regurgitation is highest with current use followed by recent use. No risk was observed with past use of FQs.
alcohol
alcohol activates scabrous-notch to influence associated memories
emily petruccelli et al. 2018
doi.org/10.1016/j.neuron.2018.10.005
“One of the things I want to understand is why drugs of abuse can produce really rewarding memories when they’re actually neurotoxins,” said Kaun, who is affiliated with Brown’s Carney Institute for Brain Science. “All drugs of abuse — alcohol, opiates, cocaine, methamphetamine — have adverse side effects. They make people nauseous or they give people hangovers, so why do we find them so rewarding? Why do we remember the good things about them and not the bad? My team is trying to understand on a molecular level what drugs of abuse are doing to memories and why they’re causing cravings.”
Once researchers understand what molecules are changing when cravings are formed, then they can figure out how to help recovering alcoholics and addicts by perhaps decreasing how long the craving memories last, or how intense they are, Kaun said.
Molecular manipulation
Fruit flies have only 100,000 neurons, while humans have more than 100 billion. The smaller scale — plus the fact that generations of scientists have developed genetic tools to manipulate the activity of these neurons at the circuit and molecular level — made the fruit fly the perfect model organism for Kaun’s team to tease apart the genes and molecular signaling pathways involved in alcohol reward memories, she said.
Led by postdoctoral researcher Emily Petruccelli, who is now an assistant professor with her own lab at Southern Illinois University, the team used genetic tools to selectively turn off key genes while training the flies where to find alcohol. This enabled them to see what proteins were required for this reward behavior.
One of the proteins responsible for the flies’ preference for alcohol is Notch, the researchers found. Notch is the first “domino” in a signaling pathway involved in embryo development, brain development and adult brain function in humans and all other animals. Molecular signaling pathways are not unlike a cascade of dominos — when the first domino falls (in this case, the biological molecule activates), it triggers more that trigger more and so on.
One of the downstream dominos in the signaling pathway affected by alcohol is a gene called dopamine-2-like receptor, which makes a protein on neurons that recognizes dopamine, the “feel-good” neurotransmitter.
“The dopamine-2-like receptor is known to be involved in encoding whether a memory is pleasing or aversive,” Petruccelli said. And alcohol hijacks this conserved memory pathway to form cravings.
In the case of the alcohol reward pathway studied, the signaling cascade didn’t turn the dopamine receptor gene on or off, or increase or decrease the amount of protein made, Kaun said. Instead, it had a subtler effect — it changed the version of the protein made by a single amino acid “letter” in an important area.
“We don’t know what the biological consequences of that small change are, but one of the important findings from this study is that scientists need to look not only at which genes are being turned on and off, but which forms of each gene are getting turned on and off,” Kaun said. “We think these results are highly likely to translate to other forms of addiction, but nobody has investigated that.”
The team is continuing its work by studying the effects that opiates have on the same conserved molecular pathways. Additionally, Kaun is working with John McGeary, assistant professor of psychiatry and human behavior at Brown, to look at DNA samples from patients with alcohol abuse disorders to see if they have genetic polymorphisms in any of the craving-related genes discovered in flies.
“If this works the same way in humans, one glass of wine is enough to activate the pathway, but it returns to normal within an hour,” Kaun said. “After three glasses, with an hour break in between, the pathway doesn’t return to normal after 24 hours. We think this persistence is likely what is changing the gene expression in memory circuits.
abstract •Alcohol cue preference requires Scabrous-Notch interaction in mushroom body neurons
•Alcohol activates Notch and Su(H) target gene expression in the adult brain
•Dopamine 2 receptor splicing and targeting by Su(H) are altered by alcohol exposure
•Alcohol cue preference affects mushroom body gene expression and splicing
Drugs of abuse, like alcohol, modulate gene expression in reward circuits and consequently alter behavior. However, the in vivo cellular mechanisms through which alcohol induces lasting transcriptional changes are unclear. We show that Drosophila Notch/Su(H) signaling and the secreted fibrinogen-related protein Scabrous in mushroom body (MB) memory circuitry are important for the enduring preference of cues associated with alcohol’s rewarding properties. Alcohol exposure affects Notch responsivity in the adult MB and alters Su(H) targeting at the dopamine-2-like receptor ( Dop2R). Alcohol cue training also caused lasting changes to the MB nuclear transcriptome, including changes in the alternative splicing of Dop2R and newly implicated transcripts like Stat92E. Together, our data suggest that alcohol-induced activation of the highly conserved Notch pathway and accompanying transcriptional responses in memory circuitry contribute to addiction. Ultimately, this provides mechanistic insight into the etiology and pathophysiology of alcohol use disorder.
moderate maternal alcohol exposure on gestational day 12 impacts anxiety-like behavior in offspring
siara k. rouzer et al. 2017
doi.org/10.3389/fnbeh.2017.00183
alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the global burden of disease study 2016
gbd 2016 alcohol collaborators 2018
doi.org/10.1016/S0140-6736(18)31310-2
a structural explanation for the low effectiveness of the seasonal influenza h3n2 vaccine
nicholas c. wu et al. 2017
doi.org/10.1371/journal.ppat.1006682
clandestine trackers found in apps
pesticides
ingestion of subthreshold doses of environmental toxins induces ascending parkinsonism in the rat
l. anselmi et al. 2018
doi.org/10.1038/s41531-018-0066-0
In a study with rats, researchers at Penn State College of Medicine found that after ingesting paraquat, a once widely used herbicide that has been banned in the U.S. since 2007, along with lectins -- sugar-binding proteins found widely in nature -- the animals developed Parkinsonism.
According to Thyagarajan Subramanian, professor of neurology and neural and behavioral sciences and co-author on the study, the findings -- recently published in the journal Parkinson's Disease -- offer clues to how and why Parkinson's disease develops, and offer a model to test new medications in the future.
"This study gives solid evidence that lectins, while in the presence of certain toxins, may be one potential culprit for the cause of Parkinsonism," Subramanian said. "Additionally, this animal model can be a tool in the future to continue developing new medications and treatments for Parkinson's disease."
The researchers were able to track the formation and spread of a misfolded protein called alpha-synuclein, which previous research has linked with Parkinson's.
"We were able to demonstrate that if you have oral paraquat exposure, even at very low levels, and you also consume lectins -- perhaps in the form of uncooked vegetables, dairy or eggs -- then it could potentially trigger the formation of this protein alpha-synuclein in the gut," Subramanian said. "Once it's formed, it can travel up the vagus nerve and to the part of the brain that triggers the onset of Parkinson's disease."
R. Alberto Travagli, professor of neural and behavioral sciences and senior author of the study, said that while toxins like paraquat have been suspected of contributing to Parkinson's for decades, the scientific evidence was small. While paraquat was linked with Parkinsonism in previous studies, those experiments typically used high doses of paraquat that humans were not likely to encounter in real life.
Additionally, lectins, which are used in medications to help deliver substances into the brain or stomach, also have been associated with certain rare forms of Parkinsonism. But the researchers weren't sure if it was the lectins themselves that were causing Parkinsonism, or if they were helping different substances get into the body that then triggered the symptoms.
"Experimenting with the lectins together with the toxin makes sense, because lectins are used in pharmacology to chaperone other substances into the body," Travagli said. "So it makes sense that the two can be combined and used to make the toxicity more potent, even though the amount of toxin is very low."
Using a rat model, the researchers exposed the animals daily to small doses of paraquat and lectins for seven days. After stopping the treatment, the researchers waited two weeks. Then, the researchers did a variety of tests to measure problems with motor function and other symptoms typical of Parkinsonism.
The researchers observed a decrease in motor function that was consistent with Parkinsonism. But to confirm that the symptoms were related to Parkinsonism and not another cause, Travagli said he and the other researchers did several additional tests.
"After observing that these animals did indeed show symptoms of Parkinsonism, we wanted to double check and make sure we weren't looking at animals that had these symptoms for another reason," Travagli said. "We administered levodopa, which is a common medication for Parkinson's disease. We saw a return to almost normal types of motor responses, which was a clear indication that we were looking at some sort of Parkinsonism."
Additionally, the researchers said when the vagus nerve was disconnected from the stomach prior to exposure to paraquat and lectins, the animals were protected from Parkinsonism, confirming the route of the alpha-synuclein from the gut to the brain.
In the future, Travagli and Subramanian said they will explore whether interventions in the form of diet modifications or medications that interfere with the transport of alpha synuclein from the stomach via the vagus nerve could be used to help prevent or slow the development of Parkinsonism in this rat model. This includes a natural substance called squalamine which has been shown to remove alpha synuclein from the gut and is now in clinical trials for the certain symptoms associated with Parkinson's disease.
abstract Increasing evidence suggests that environmental neurotoxicants or misfolded α-synuclein generated by such neurotoxicants are transported from the gastrointestinal tract to the central nervous system via the vagus nerve, triggering degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and causing Parkinson’s disease (PD). We tested the hypothesis that gastric co-administration of subthreshold doses of lectins and paraquat can recreate the pathology and behavioral manifestations of PD in rats. A solution containing paraquat + lectin was administered daily for 7 days via gastric gavage, followed by testing for Parkinsonian behavior and gastric dysmotility. At the end of the experiment, brainstem and midbrain tissues were analyzed for the presence of misfolded α-synuclein and neuronal loss in the SNpc and in the dorsal motor nucleus of the vagus (DMV). Misfolded α-synuclein was found in DMV and SNpc neurons. A significant decrease in tyrosine hydroxylase positive dopaminergic neurons was noted in the SNpc, conversely there was no apparent loss of cholinergic neurons of the DMV. Nigrovagally-evoked gastric motility was impaired in treated rats prior to the onset of parkinsonism, the motor deficits of which were improved by L-dopa treatment. Vagotomy prevented the development of parkinsonian symptoms and constrained the appearance of misfolded α-synuclein to myenteric neurons. These data demonstrate that co-administration of subthreshold doses of paraquat and lectin induces progressive, L-dopa-responsive parkinsonism that is preceded by gastric dysmotility. This novel preclinical model of environmentally triggered PD provides functional support for Braak’s staging hypothesis of idiopathic PD.
a crispr screen identifies a pathway required for paraquat-induced cell death
colleen r reczek et al. 2017
doi.org/10.1038/nchembio.2499
nitration of microtubules blocks axonal mitochondrial transport in a human pluripotent stem cell model of parkinson’s disease
morgan g. stykel et al. 2018
doi.org/10.1096/fj.201700759rr
ignoring adjuvant toxicity falsifies the safety profile of commercial pesticides
robin mesnage, michael n. antoniou 2018
doi.org/10.3389/fpubh.2017.00361
effects of neonicotinoid pesticides on promoter-specific aromatase (CYP19) expression in Hs578t breast cancer cells and the role of the VEGF pathway
élyse caron-beaudoin et al. 2018
doi.org/10.1289/ehp2698
insecticide-induced changes in amphibian brains: how sublethal concentrations of chlorpyrifos directly affect neurodevelopment
sara j. mcclelland et al. 2018
doi.org/10.1002/etc.4240
neural conduction, visual motion detection, and insect flight behaviour are disrupted by low doses of imidacloprid and its metabolites
rachel h. parkinson, john r. gray 2019
doi.org/10.1016/j.neuro.2019.02.012
Traces of neonicotinoid pesticides can impair a flying insect's ability to spot predators and avoid collisions with objects in their path, new research by the University of Saskatchewan (USask) shows.
Residual traces of these widely-used pesticides can profoundly affect a flying insect's ability to detect movement -- a skill crucial to survival, according to the paper published in the journal NeuroToxicology.
Within an hour of being treated with tiny amounts of neonicotinoids or their metabolites (trace elements present after the insecticide begins to break down), the flying insects did not turn, glide or stop to avoid collision.
"Our findings suggest that very low doses of the pesticide or its metabolic products can profoundly and negatively affect motion detection systems that flying insects, such as locusts, grasshoppers and bees, need for survival," said Jack Gray, an expert in neural control of animal behavior and Vice-Dean of Research, Scholarly and Artistic work in USask's College of Arts and Science.
"Although they are found in the environment, and insects can be exposed to them, metabolites are not typically tested for toxicity. Our results suggest they should be."
Neonicotinoid pesticides (or neonics) are the most widely used class of insecticides in the world and are neurotoxins. The European Union has restricted use of some neonics following concern over their impact on pollinators, including bees, and there have been proposals to restrict their use in Canada.
Although neonicotinoids break down into different compounds and can exist in trace amounts in the environment, these levels are typically not tested for toxicity.
Locusts exposed to trace elements of the neonicotinoid imidacloprid were unable to detect object motion in their field of view. When dosed with slightly higher amounts, the locusts were unable to fly straight or failed to take off at all.
The findings by researchers in the USask Department of Biology are part of a wider USask research program into the impact of trace elements of neonicotinoids on flying insects.
In tests on the locust's nervous systems using electrophysiology, the USask biologists found their motion-detector neurons were less sensitive after being treated. Their ability to process and relay information quickly, and therefore respond quickly while flying, was also impaired.
Using a specially-designed wind tunnel, the research team measured a flying locust's ability to navigate around simulated approaching objects -- a skill crucial to avoiding predators and obstacles such as bushes and trees.
Good vision is crucial to insects' survival as it allows them to see predators including larger insects and birds and avoid collisions with other insects or objects in their path.
The team will soon begin researching whether trace levels of neonicotinoids can disrupt navigation and flight behaviour in honeybees, affecting the neural mechanics which stabilize flight, control flight speed, altitude, and help insects calculate distance.
"Bees and other flying insects use similar neural mechanisms to process visual motion, and the ability to see movement is crucial not only for avoiding predators, but also for maintaining a steady flight path," said Rachel Parkinson, a PHD biology student.
abstract •Low doses of imidacloprid, or olefin or 5-hydroxy metabolites impair flight ability.
•These compounds reduce neural firing in a visual motion sensitive interneuron.
•Conduction velocity was reduced with greatest effects at higher firing frequencies.
•Metabolites display comparable toxicity to parent compound at equal doses (10 ng/g).
While neonicotinoid insecticides impair visually guided behaviours, the effects of their metabolites are unknown and measurements of environmental concentrations of neonicotinoids, typically lower than those required to elicit toxic effects, tend to exclude metabolites. Here we examined the contributions of imidacloprid and two of its metabolites, imidacloprid-olefin and 5-hydroxy-imidacloprid, on neural conduction velocity, visual motion detection and flight in the locust (Locusta migratoria) using a combination of electrophysiological and behavioural assays. We show reduced visual motion detection and impaired flight behaviour following treatment of metabolite concentrations equal to sublethal doses of the parent compound. Additionally, we show for the first time that imidacloprid and its metabolites result in a decrease in conduction velocity along an unmyelinated axon. We suggest that secondary effects of the insecticide on the biophysical properties of the axon may result in decreased neural conduction. As these metabolites display neurotoxicity similar to the parent compound they should be considered when quantifying environmental concentrations.
effects of sublethal doses of clothianidin and/or v. destructor on honey bee (apis mellifera) self-grooming behavior and associated gene expression
nuria morfin et al. 2019
doi.org/10.1038/s41598-019-41365-0
when honey bees are infected with varroa mites and then regularly exposed to low doses of a commonly used neonicotinoid called clothianidin, their self-grooming behaviour drops off.
Without that self-grooming, bees are susceptible to mites that can also carry viruses that can quickly kill, said lead author Nuria Morfin Ramirez, who completed the research along with Prof. Ernesto Guzman, School of Environmental Sciences, as part of her PhD.
"When bee colonies began to collapse years ago, it became clear there wasn't just one factor involved, so we were interested in whether there was an interaction between two of the main stressors that affect bees: varroa mites and a neurotoxic insecticide, clothianidin," said Morfin.
"This is the first study to evaluate the impact on the grooming behaviour of bees."
Neonicotinoids, or "neonics," are the most commonly used insecticides in Canada. They are coated on canola and corn seeds or sprayed on fruit and vegetable plants and trees. But they have also been linked to honey bee colony collapses.
Varroa mites are also contributing to colony collapses and have been associated with more than 85 per cent of colony losses.
The mites kill bees by slowly feeding off their body fat and hemolymph (blood), and can also transmit a virus called deformed wing virus (DWV). One of the only ways bees can protect themselves is to groom aggressively and brush the mites off.
The researchers wanted to know whether the two stressors of pesticide exposure varroa mites were working together to contribute to bee deaths. The research team used bees from U of G's Honey Bee Research Centre and exposed them to a widely used neonic clothianidin, either on its own or along with varroa mites.
They experimented with three doses of clothianidin, all similar to what the bees would experience while feeding on flower nectar of neonic-treated crop fields, but all low enough to be considered sublethal.
"What we found was a complicated interaction between the mite and the pesticide that decreased the proportion of bees that groomed intensively, and affected genes associated with neurodegenerative processes," Morfin said.
Bees exposed to medium level doses of the neonic showed no changes in grooming behaviour, but when they were also introduced to varroa mites, the proportion of bees that groomed intensively was 1.4 times lower compared to the bees exposed to clothianidin alone.
When exposed to the lowest dose of the pesticide, the proportion of bees that groomed significantly dropped. The lowest dose was also linked to an increased level of deformed wing virus -- an effect not seen at the higher doses.
"These results showed a complex and non-additive interaction between these two stressors," said Guzman. "This study highlights the importance of reducing stressors that bees are exposed to, to reduce the risk of disease and consequently colony mortality."
abstract Little is known about the combined effects of stressors on social immunity of honey bees (Apis mellifera) and related gene expression. The interaction between sublethal doses of a neurotoxin, clothianidin, and the ectoparasite, Varroa destructor, was examined by measuring differentially expressed genes (DEGs) in brains, deformed wing virus (DWV) and the proportion and intensity of self-grooming. Evidence for an interaction was observed between the stressors in a reduction in the proportion of intense groomers. Only the lowest dose of clothianidin alone reduced the proportion of self-groomers and increased DWV levels. V. destructor shared a higher proportion of DEGs with the combined stressors compared to clothianidin, indicating that the effects of V. destructor were more pervasive than those of clothianidin when they were combined. The number of up-regulated DEGs were reduced with the combined stressors compared to clothianidin alone, suggesting an interference with the impacts of clothianidin. Clothianidin and V. destructor affected DEGs from different biological pathways but shared impacts on pathways related to neurodegenerative disorders, like Alzheimer’s, which could be related to neurological dysfunction and may explain their negative impacts on grooming. This study shows that the combination of clothianidin and V. destructor resulted in a complex and non-additive interaction.
early anthropogenic impact on western central african rainforests 2,600 y ago
yannick garcin et al. 2018
doi.org/10.1073/pnas.1715336115
engineering nitrogen fixation activity in an oxygenic phototroph
deng liu et al. 2018
doi.org/10.1128/mBio.01029-18
heavy metals
marine fog inputs appear to increase methylmercury bioaccumulation in a coastal terrestrial food web
peter s. weiss-penzias et al. 2019
doi.org/10.1038/s41598-019-54056-7
Concentrations of mercury in pumas in the Santa Cruz Mountains were three times higher than lions who live outside the fog zone. Similarly, mercury levels in lichen and deer were significantly higher inside the fog belt than beyond it.
Mercury levels found in pumas are approaching toxic thresholds that could jeopardize reproduction and even survival, according to the researchers.
Led by Peter Weiss-Penzias, an environmental toxicologist who has pioneered the study of pollutants in coastal fog, the study is the first to trace the atmospheric source of super-toxic methylmercury in the terrestrial food web up to a top predator.
“Lichen don’t have any roots so the presence of elevated methylmercury in lichen must come from the atmosphere,” said Weiss-Penzias. “Mercury becomes increasingly concentrated in organisms higher up the food chain.”
Although mercury levels in fog present no health risk to humans, the risk to terrestrial mammals may be significant. With each step up the food chain, from lichen to deer to mountain lions, mercury concentrations can increase by at least 1,000 times, said Weiss-Penzias.
The study included fur and whisker samples from 94 coastal mountain lions and 18 noncoastal lions. Mercury concentrations in the coastal samples averaged about 1,500 parts per billion (ppb), compared to nearly 500 ppb in the noncoastal group. At least one lion studied had mercury levels known to be toxic to species like mink and otters, and two others had “sublethal” levels that reduce fertility and reproductive success.
Elevated concentrations of mercury present an additional potential threat to a top predator that is already coping with habitat loss and other risks posed by humans, said senior author Chris Wilmers, a professor of environmental studies and the director of the Puma Project.
“These mercury levels might compound the impacts of trying to make it in an environment like the Santa Cruz Mountains, where there is already so much human influence, but we don’t really know,” said Wilmers. “Levels will be higher 100 years from now, when the Earth’s mercury budget is higher because of all the coal we’re pumping into the atmosphere.”
The source of fog-borne mercury
Mercury, a naturally occurring element, is released into the environment through a variety of natural processes and human activities, including mining and coal-fired power plants. “Mercury is a global pollutant,” said Weiss-Penzias. “What’s emitted in China can affect the United States just as much as what’s emitted in the United States.”
As atmospheric mercury rains down on oceans, it is converted by anaerobic bacteria in deep waters to methylmercury, the most toxic form of mercury. Upwelling brings some methylmercury to the surface, where it is released back into the atmosphere and carried by fog. At high concentrations, methylmercury can cause neurological damage, including memory loss and reduced motor coordination, and it can decrease the viability of offspring.
“Fog is a stabilizing medium for methylmercury,” said Weiss-Penzias. “Fog drifts inland and rains down in microdroplets, collecting on vegetation and dripping to the ground, where the slow process of bioaccumulation begins.”
Top predators, an international treaty, and a foggy bike ride
Fog is present in coastal areas that border oceans, environmental “hotspots” that are also home to high concentrations of humans. Weiss-Penzias is eager to investigate mercury levels in coastal Chile, where the top predator is a lizard, while Wilmers is curious about mercury levels in coyotes, bobcats, and birds in coastal areas.
“We need to protect the top predators in the environment,” said Weiss-Penzias. “They’re keystone species. They perform ecosystem services. When you change one thing, it has cascading effects through the system.”
As an example of cascade effects, Wilmers cited the removal of wolves from many states in the eastern United States, which resulted in more coyotes, who preyed on foxes that had historically kept the rodent population in check. The loss of foxes ultimately made way for more rodents, which help transmit Lyme disease, said Wilmers, who added, “Locally, potentially, mountain lions keep deer and small predators in check, which could reduce Lyme disease.”
The global effort to protect humans and the environment from mercury includes the Minamata Convention on Mercury, an international treaty that was adopted in 2013. Named after a Japanese city that endured a dire incident of mercury poisoning, the treaty is broad in scope, encompassing the entire life cycle of mercury.
“It’s important for the future of that treaty to understand all the different ways that mercury impacts the environment,” said Weiss-Penzias.
As an atmospheric chemist, Weiss-Penzias said he first became curious about fog-borne pollutants about a decade ago while riding his bike to work. “I was riding through this absolute fogstorm, with water dripping off my glasses, and I just wondered, ‘What’s in this stuff?’” he recalled. Hypothesizing that mercury might de-gas out of the ocean and end up in fog, he collected samples and sent them to a lab.
“The lab called me, saying they’d have to re-run the tests, because they didn’t believe the numbers,” said Weiss-Penzias.
abstract Coastal marine atmospheric fog has recently been implicated as a potential source of ocean-derived monomethylmercury (MMHg) to coastal terrestrial ecosystems through the process of sea-to-land advection of foggy air masses followed by wet deposition. This study examined whether pumas (Puma concolor) in coastal central California, USA, and their associated food web, have elevated concentrations of MMHg, which could be indicative of their habitat being in a region that is regularly inundated with marine fog. We found that adult puma fur and fur-normalized whiskers in our marine fog-influenced study region had a mean (±SE) total Hg (THg) (a convenient surrogate for MMHg) concentration of 1544 ± 151 ng g−1 (N = 94), which was three times higher (P < 0.01) than mean THg in comparable samples from inland areas of California (492 ± 119 ng g−1, N = 18). Pumas in California eat primarily black-tailed and/or mule deer (Odocoileus hemionus), and THg in deer fur from the two regions was also significantly different (coastal 28.1 ± 2.9, N = 55, vs. inland 15.5 ± 1.5 ng g−1, N = 40). We suggest that atmospheric deposition of MMHg through fog may be contributing to this pattern, as we also observed significantly higher MMHg concentrations in lace lichen (Ramalina menziesii), a deer food and a bioindicator of atmospheric deposition, at sites with the highest fog frequencies. At these ocean-facing sites, deer samples had significantly higher THg concentrations compared to those from more inland bay-facing sites. Our results suggest that fog-borne MMHg, while likely a small fraction of Hg in all atmospheric deposition, may contribute, disproportionately, to the bioaccumulation of Hg to levels that approach toxicological thresholds in at least one apex predator. As global mercury levels increase, coastal food webs may be at risk to the toxicological effects of increased methylmercury burdens.
a spoonful of lead: a 10-year look at spices as a potential source of lead exposure
paromita hore et al. 2018
doi.org/10.1097/phh.0000000000000876
Between 2008 and 2017, the NYC Health Department tested over 3,000 samples of consumer products during investigations of lead poisoning cases and surveys of local stores. Spices were the most frequently tested product: nearly 1,500 samples from 41 countries were tested.
More than half of the spice samples had detectable lead concentrations, and more than 30 percent had lead concentrations greater than 2 parts per million (ppm) -- a permissible limit for lead in certain food additives used as a guidance value by NYC Health Department.
Spices purchased abroad had much higher average lead content than spices bought in the US. For example, turmeric and Georgian kharcho suneli purchased in NYC had average lead concentrations below 2 ppm, but when the same spices were purchased abroad, the average concentrations exceeded 50 ppm. "The highest concentrations of lead were found in spices purchased in the countries Georgia, Bangladesh, Pakistan, Nepal, and Morocco," Dr. Hore and co-authors write.
In NYC, children and pregnant women of Georgian and South Asian ancestry are disproportionately represented among the lead-exposed population. Although not the only source of lead exposure, spices are an important factor to consider in these high-risk groups. "Public health professionals and medical providers should also be aware of spices as a potential risk factor for lead exposure and screen at-risk populations," according to the authors.
Most of the contaminated spices purchased abroad were in unmarked containers without brand name information. The highest lead levels were measured in the Georgian spice kviteli kvavili, or "yellow flower." Examples of other contaminated spices purchased abroad included turmeric, hot pepper, chili powder, and paprika.
The study has important implications for public health programs, policy, and international food safety regulations, Dr. Hore and colleagues believe. They note that adulteration of spices, intentional or inadvertent, may occur anywhere along the supply chain. The authors conclude, "Overall, a solely localized or national approach to address spice contamination will not be adequate, as the problem is global."
abstract While lead-based paint and occupational lead hazards remain the primary sources of lead exposures among New York City's lead-poisoned children and men, respectively, these are not the only possible lead sources. Certain consumer products are often implicated. Between 2008 and 2017, the New York City Department of Health and Mental Hygiene tested more than 3000 samples of consumer products during lead poisoning case investigations and surveys of local stores, and of these, spices were the most frequently tested (almost 40% of the samples).
Objectives:
To describe spice samples—types, origin, lead concentrations, and the implication of findings for public health programs and global food safety regulations.
Design:
Descriptive study of lead contamination in spices systematically collected as part of lead poisoning investigations.
Setting and Participants:
A total of 1496 samples of more than 50 spices from 41 countries were collected during investigations of lead poisoning cases among New York City children and adults and local store surveys.
Results:
More than 50% of the spice samples had detectable lead, and more than 30% had lead concentrations greater than 2 ppm. Average lead content in the spices was significantly higher for spices purchased abroad than in the United States. The highest concentrations of lead were found in spices purchased in the countries Georgia, Bangladesh, Pakistan, Nepal, and Morocco.
Conclusions:
Certain commonly used spices, particularly those purchased abroad in Georgia, Bangladesh, Pakistan, Nepal, and Morocco, can have very high lead levels, which can contribute to lead body burden. This underscores the need to develop comprehensive interventions that educate consumers and initiate intergovernmental efforts for stricter global food regulations.
heavy metals in the glass and enamels of consumer container bottles
andrew turner et al. 2019
doi.org/10.1021/acs.est.9b01726
analysed both the glass and enamelled decorations on a variety of clear and coloured bottles readily available in shops and supermarkets.
They showed that cadmium, lead and chromium were all present in the glass, but at concentrations where their environmental and health risks were deemed to be of low significance.
However, the enamels were of greater concern, with cadmium concentrations of up to 20,000 parts per million in the decorated regions on a range of spirits, beer and wine bottles, and lead concentrations up to 80,000ppm in the décor of various wine bottles. The limit for lead in consumer paints is 90ppm.
The study also showed the elements had the potential to leach from enamelled glass fragments, and when subjected to a standard test that simulates rainfall in a landfill site, several fragments exceeded the US Model Toxins in Packaging Legislation and could be defined as "hazardous."
Published in Environmental Science and Technology, the research was carried out by Associate Professor (Reader) in Aquatic Geochemistry and Pollution Science, Dr Andrew Turner.
He has previously shown that the paint or enamel on a wide variety of items -- including playground equipment, second hand toys and drinking glasses -- can feature levels of toxic substances that are potentially harmful to human health.
Dr Turner said: "It has always been a surprise to see such high levels of toxic elements in the products we use on a daily basis. This is just another example of that, and further evidence of harmful elements being unnecessarily used where there are alternatives available. The added potential for these substances to leach into other items during the waste and recycling process is an obvious and additional cause for concern."
For the current research, bottles of beer, wine and spirits were purchased from local and national retail outlets between September 2017 and August 2018, with the sizes ranging from 50 ml to 750 ml.
They were either clear, frosted, green, ultraviolet-absorbing green (UVAG) or brown with several being enamelled over part of the exterior surface with images, patterns, logos, text and/or barcodes of a single colour or multiple colours.
Out of the glass from 89 bottles and fragments analysed using x-ray fluorescence (XRF) spectrometry, 76 were positive for low levels of lead and 55 positive for cadmium. Chromium was detected in all green and UVAG bottles, but was only in 40% of brown glass and was never in clear glass.
Meanwhile, the enamels of 12 products out of 24 enamelled products tested were based wholly or partly on compounds of either or both lead and cadmium.
Dr Turner added: "Governments across the world have clear legislation in place to restrict the use of harmful substances on everyday consumer products. But when we contacted suppliers, many of them said the bottles they use are imported or manufactured in a different country than that producing the beverage. This poses obvious challenges for the glass industry and for glass recycling and is perhaps something that needs to be factored in to future legislation covering this area."
abstract The glass and enameled decorations of bottles of alcoholic beverages sourced from retailers in the U.K. were analyzed by X-ray fluorescence spectrometry for various heavy metals. In the glass substrate, lead, cadmium, and chromium were present at concentrations up to about 1100, 1100, and 3000 μg g–1, respectively, but their environmental and health risks are deemed to be low significance. Of more concern from an environmental and, potentially, occupational exposure perspective are the concentrations and mobilities of Pb and Cd in the enamels of many bottles. Thus, Pb concentrations up to about 100000 μg g–1 were found on the décor of various wine bottles and a beer bottle, and Cd concentrations of up to 20000 μg g–1 were measured in the decorated regions on a range of spirits, beer, and wine bottles. Moreover, maximum concentrations that leached from enameled glass fragments according to a standard test that simulates water and other liquids percolating through a landfill were about 1200 and 3200 μg L–1 for Pb and Cd, respectively, with several fragments exceeding the U.S. Model Toxins in Packaging Legislation and, therefore, defined as “hazardous”. Given that safer decorative alternatives are available and that a precautionary principle should be adopted for toxic heavy metals, the pervasive use of Pb and Cd in the enamels of consumer bottles is brought into question.
anoxia
thallium isotopes reveal protracted anoxia during the toarcian (early jurassic) associated with volcanism, carbon burial, and mass extinction
theodore r. them ii et al. 2018
doi.org/10.1073/pnas.1803478115
charcoal evidence that rising atmospheric oxygen terminated early jurassic ocean anoxia
sarah j. baker, stephen p. hesselbo, timothy m. lenton, luís v. duarte, claire m. belcher 2017
doi.org/10.1038/ncomms15018
bad corporations
will big business destroy our planet?
peter dauvergne 2018
microsoft
nestlé
monsanto
pretty much everything
ongoing ecological and evolutionary consequences by the presence of transgenes in a wild cotton population
valeria vázquez-barrios et al. 2021
doi.org/10.1038/s41598-021-81567-z
disney/marvel
blizzard
regulatory capture
radiation
low dose ionizing radiation strongly stimulates insertional mutagenesis in a γh2ax dependent manner
alex n. zelensky et al. 2020
doi.org/10.1371/journal.pgen.1008550
exposing cells to high doses of ionizing radiation generates mutations by creating double-strand breaks that let in external segments of DNA. These extraneous fragments of DNA can occur in the nucleus, left over from natural processes, such as genomic DNA repair and viral infections. In the new study, researchers investigated whether low doses of ionizing radiation have damaging side effects by irradiating human and mouse cells grown in the lab. When they counted the cells that had taken up foreign DNA, they found that low doses of radiation, in the upper range of common diagnostic procedures, create mutations through inserted DNA even more efficiently than the much larger doses studied previously.
While the new results in cell cultures are potentially concerning, the study’s authors stress that translating radiation’s effects on lab-grown cell cultures to effects in the body is premature. Future experiments using animal models will be necessary to determine the full effects of low-dose radiation, and whether its use in medical imaging has an impact on patient health. If the same phenomenon does occur inside the body, then doctors may need to take into account levels of extraneous DNA, such those resulting from a long-term viral infection, when assessing a patient’s risk from a procedure that requires radiation.
“Most molecular radiobiological research is focused on high doses of ionizing radiation relevant to cancer treatment, while effects of physiologically relevant doses of radiation on the cell are notoriously difficult to study at the molecular level,” said author Roland Kanaar. “Our discovery that mutagenic insertion of foreign DNA into cell’s genome is remarkably responsive to doses encountered during diagnostic, rather than therapeutic, procedures provides a new simple and sensitive tool to study their consequences and revealed surprising molecular genetic details of how cells cope with natural amounts of DNA damage.”
abstract Not all DNA in mammalian nuclei is organized into chromosomes. The pool of extrachromosomal DNA molecules is produced by natural process: during genomic DNA repair, viral infections, phagocytosis; and in experimental settings after transfection, and in gene therapy. Extrachromosomal DNA can integrate into the genome at the site of a double-stranded DNA break (DSB), producing a mutation in the chromosome. Because DSBs are dangerous lesions, they are actively eliminated, and their availability is a limiting factor for extrachromosomal DNA integration. It has long been known that inducing additional random DSBs, for example by exposing cells to ionizing radiation, can increase the frequency of random integration (RI), however the irradiation doses that were used were non-physiological. We found that much smaller doses of radiation, in the upper range of radiological diagnostic procedures, stimulate integration even more efficiently than the much larger doses studied previously. The potency of stimulation is remarkable, given that biological effects of such low doses are generally difficult to register, and warrants re-evaluation using animal models. Surprisingly, the genetic dependencies of radiation-stimulated integration do not include DSB repair pathways, and are distinct from background integration events. Our observations provide a hyper-sensitive tool to detect mutagenesis and reveal new information about the genetic interactions between DNA damage signaling and repair system components.
station eleven
emily st. john mandel 2014
the feed
nick windo 2018
annex
rich larson 2018
the book of m
peng shepherd 2018
the rending and the nest
kaethe schwehn 2018
contagion
erin bowman 2018
the book of hidden things
francesco dimitri 2018
relic
alan dean foster 2018
ball lightning
liu cixin 2018
the labyrinth index
charles stross 2018
killing gravity
corey j. white 2017
void black shadow
corey j. white 2018
static ruin
corey j. white 2018
whitewash: the story of a weedkiller, cancer, and the corruption of science
carey gillam 2017
science for sale: how the us government uses powerful corporations and leading universities to support government policies, silence top scientists, jeopardize our health, and protect corporate profits
david l. lewis 2014
genetic engineering
linking crispr-cas9 interference in cassava to the evolution of editing-resistant geminiviruses
devang mehta et al. 2019
doi.org/10.1186/s13059-019-1678-3
this technology both creates a selection pressure on the viruses to evolve more quickly, and also provides the viruses a means to evolve, it resulted in a virus mutant that is resistant to our interventions," explained Devang Mehta, postdoctoral fellow in the Department of Biological Sciences. CRISPR-Cas9 is found in nature, where bacteria use it to defend against viruses, however the researchers found that the technology results in very different outcomes in plants -- and researchers are stressing the importance of screening against these sorts of unintended results in the future.
The cassava plant, the object of the study, is a starchy root vegetable that is consumed for food throughout the tropics. Cassava is a primary staple crop grown in South America, Africa, and Asia, from which 1 billion people get most of their calories each day. Each year, cassava crops are plagued by cassava mosaic disease, which causes 20 per cent crop loss. It is the mosaic disease that Mehta and his colleagues endeavoured to engineer against.
Unsuccessful results
The researchers used a new gene-editing technology called CRISPR-Cas9 to attempt to design cassava plants that could cut the DNA of the mosaic virus and make the plants resistant to its damaging effects. Unfortunately, their results were not successful. To understand what happened, the team sequenced hundreds of viral genomes found in each plant.
"We discovered that the pressure that CRISPR-Cas9 applied to the virus probably encouraged it to evolve in a way that increased resistance to intervention," said Mehta. Mehta hastens to add that CRISPR-Cas9 has many other applications in food and agriculture that do not pose the same risks.
The research team is keen to share their results with other scientists who are using CRISPR-Cas9 technology to engineer virus-resistant plants, and encourage these groups to test their plants to detect similar viral mutations.
"We need to do more research on these types of applications of CRISPR-Cas9 technology before we proceed with field testing" said Mehta.
mucin-like domain of ebola virus glycoprotein enhances selective oncolytic actions against brain tumors
xue zhang et al. 2020
doi.org/10.1128/jvi.01967-19
Unlike normal cells, a large percentage of cancer cells lack the ability to generate an innate immune response against invaders such as viruses. This has led cancer researchers to explore the use of viruses to combat a variety of cancers.
Using viruses carries an obvious risk — they can introduce potentially dangerous infections. To get around this problem, scientists, including van den Pol, have experimented with creating or testing chimeric viruses, or a combination of genes from multiple viruses. They have the ability to target cancer cells without harming patients.
One of the seven genes of the Ebola virus that helps it avoid an immune system response also contributes to its lethality. This intrigued van den Pol.
He and the study’s first author, Xue Zhang, also of Yale, used a chimeric virus containing one of gene from the Ebola virus — a glycoprotein with a mucin-line domain (MLD). In wild-type Ebola virus, the MLD plays a role in hiding Ebola from the immune system. They injected this chimeric virus into the brains of mice with glioblastoma — and found that the MLD helped selectively target and kill deadly glioblastoma brain tumors.
abstract Given that the Ebola virus (EBOV) infects a wide array of organs and cells yet displays a relative lack of neurotropism, we asked whether a chimeric vesicular stomatitis virus (VSV) expressing the EBOV glycoprotein (GP) might selectively target brain tumors. The mucin-like domain (MLD) of the EBOV GP may enhance virus immune system evasion. Here we compare chimeric VSVs in which EBOV GP replaces the VSV glycoprotein, thereby reducing the neurotoxicity associated with wildtype VSV. A chimeric VSV expressing the full-length EBOV GP (VSV-EBOV) containing the MLD was substantially more effective and safer than a parallel construct with an EBOV GP lacking the MLD (VSV-EBOVΔMLD). One-step growth, RT-qPCR, and Western blot assessment showed VSV-EBOVΔMLD produced substantially more progeny faster than VSV-EBOV. Using immunodeficient SCID mice, we focused on targeting human brain tumors with these VSV-EBOVs. Similar to our previous report using an attenuated VSV-EBOV with no MLD that expressed GFP (VSV-EBOVΔMLD-GFP), VSV-EBOVΔMLD without GFP targeted glioma, but yielded only a modest extension of survival. In contrast, VSV-EBOV containing the MLD showed substantially better targeting and elimination of brain tumors after intravenous delivery, and increased the survival of brain tumor-bearing mice. Despite the apparent destruction of most tumor cells by VSV-EBOVΔMLD, the virus remained active within the SCID mouse brain and showed widespread infection of normal brain cells. In contrast, VSV-EBOV eliminated the tumors, and showed relatively little infection of normal brain cells. Parallel experiments with direct intracranial virus infection generated similar results. Neither VSV-EBOV nor VSV-EBOVΔMLD showed substantive infection of the brains of normal immunocompetent mice.