Danger Dust

The federal government is pushing back a deadline to implement a new silica rule in mines. According to the rule which went into effect last year, coal mines were supposed to be in compliance April 14, and that’s now scheduled to take effect in August.

In Appalachia, 1 in 5 miners get black lung disease, the highest level ever recorded, according to a NIOSH study published in 2018. Black Lung disease is caused by exposure to silica dust.

Our DDR interaction map identifies numerous synthetic lethal relationships that could be exploited in cancer therapy. Many already link established cancer genes and existing small-molecule targets and thus are readily actionable. We anticipate that exploration of our dataset will define more cancer-specific vulnerabilities that could translate into clinical benefit in patients.

There is a well established association between silica inhalational exposure and autoimmune disease, particularly in the context of intense exposure.

Silicosis increases susceptibility to autoimmune diseases. The newer industries of sand-blasting denim and engineered stone have been associated with alarmingly high rates of silicosis

A multinational registry has documented diagnostic details related to autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, autoimmune myositis, mixed connective tissue disease, psoriasis, and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis among individuals with silicosis.

Understanding a person's occupational history to silica is an essential aspect for evaluating potential environmental factors that may contribute to autoimmune diseases. This information can inform preventive measures and contribute to a more comprehensive approach to managing and treating these complex conditions.

In conclusion, our findings suggest that silica inhalation may be related to pulmonary sarcoidosis and idiopathic interstitial pneumonias. These findings may, however, to some extent be explained by diagnostic misclassification of silicosis. We observed exposure–response relations for silicosis at lower cumulative exposure levels than previously reported.

Silica dust exposure can cause obstructive pulmonary ventilation dysfunction and lead to chronic obstructive pulmonary disease. High level of exposure is a risk factor for obstructive pulmonary ventilation dysfunction. Women exposed to dust are more prone to obstructive pulmonary ventilation dysfunction than men. Early diagnosis of chronic obstructive pulmonary disease caused by silica dust and timely intervention measures are very important to delay the decline of lung function and protect the health of workers.

The researchers believe future myasthenia gravis treatments could target specific antibody interactions rather than relying on more general immunosuppression treatments.

This study not only advances our understanding of myasthenia gravis but also sheds light on other autoimmune diseases in which antibodies attack ion channels, offering hope for more precise and effective treatment strategies.

Memory B cells are essential for maintaining a long-term immune response: they rapidly proliferate upon antigen reencounter and differentiate into antibody secreting cells.

There is the belief that vaccine-induced antibodies to SARS-CoV-2 decay rather rapidly, but recent evidence suggests that they remain quite stable over time.

Whether the urine is your own, someone else’s or even obtained from an animal, people have been drinking pee as medicine for thousands of years. Most claims about urine therapy are based on anecdotes or ancient texts with no robust scientific evidence to support the benefits of urine therapy. There is evidence to show that drinking urine has a number of health risks, however,

In Indian Ayurvedic medicine, urine was used to treat asthma, allergies, indigestion, wrinkles and even cancer. The Roman poet Catullus believed urine helped to whiten teeth – possibly due to its ammonia content.

As a rudimentary test for diabetes, doctors used to taste urine to check how sweet it was. Now, of course, we have urine test strips to check for glucose in the urine.

In 1945, British naturopath John W. Armstrong published a book called “The Water of Life: A Treatise on Urine Therapy.” He claimed that drinking one’s own urine and massaging it into the skin could cure major illnesses.

Historically, drinking pee to treat illnesses may have made sense because of a lack of medical alternatives. But, as the urine-sipping celebrities above show, the practice is still followed today.

Risky business

Some advocates of urine therapy believe that urine is sterile. However, research has found that urine naturally contains low levels of bacteria and research shows that bacteria can further contaminate the urine when it leaves the body. Drinking urine, then, can introduce bacteria and toxins into the gut and potentially cause further illness like stomach infections.

Urine becomes more concentrated when it comes out again – the kidneys may have to work harder to filter out the excess, putting extra strain on them. The kidneys need water to process these salts.

Drinking urine means you have to pee out more water than you get from it, which speeds up dehydration – it’s similar to drinking seawater. Some drugs, such as penicillin antibiotics or heart medicines, are also excreted in the urine – by drinking urine, it can cause toxic levels of these drugs to build up in the body.

Why is that a problem?

These pieces float around, and some end up in human bodies. The smallest pieces pass through cells and into the nucleus, where they can start messing with DNA. Nano- and microplastics, which seem to have similar sizes and shapes to asbestos, raise the potential that they could cause cancer, heart disease/stroke, and other diseases.

Is there an engineering solution to address this problem?

Our results suggest that engineering the architecture of the soft layers to be more resilient would decrease the amount of crystalline fragments that break off. Clearly, focus needs to be placed on this point to reduce the amount of micro- and nanoplastics created by normal polymer degradation.

How can better understanding nanoplastics improve human health?

Only 2% of plastics are recycled, mostly because it's too expensive. But if you just throw plastic into the environment, it creates micro- and nanoplastics that look like they are going to cause health problems. If you think about it that way, if you have to choose between the health problems that could be created by the nanoplastics vs. the cost of recycling, then maybe it's actually cheaper to recycle.

Dust explosion demonstration

Introduction: The primary source of anthropogenic atmospheric mercury (Hg) emissions globally is artisanal and small-scale gold mining (ASGM). Estimates of Hg emissions from ASGM are poorly constrained due to a lack of monitoring data and the informal, generally unregulated nature of this industry. Trees accumulate atmospheric gaseous elemental mercury (GEM) in bolewood following stomatal uptake and thus have the potential to be used as biomonitors to quantify the spatial and temporal footprint of Hg emissions from ASGM.

Discussion: Thus far, applications of dendrochemistry to quantify Hg pollution have been largely restricted to coniferous species in temperate regions, but this study shows that tropical species also quantify Hg pollution. We conclude that Ficus insipida is a suitable biomonitor and powerful tool for characterizing the spatial, and potentially temporal footprint of GEM emissions from ASGM in the neotropics.

Pulmonary sarcoidosis is a lung disease characterized by granulomas—tiny clumps of immune cells that form in response to inflammation. It's the most inflammatory of the interstitial lung diseases (ILDs), a family of conditions that all involve some level of inflammation and fibrosis, or scarring, of the lungs.

In a paper published in Science Translational Medicine, scientists at Scripps Research and aTyr Pharma characterized a protein, HARSWHEP, that can soothe the inflammation associated with sarcoidosis by regulating white blood cells. Reducing inflammation slows the disease's progression and results in less scarring. A Phase Ib/IIa clinical trial of efzofitimod, a therapeutic form of HARSWHEP, showed promising results.

"Taken together, these results validate a new way to approach immune regulation in chronic lung disease," says Paul Schimmel, professor of molecular medicine and chemistry at Scripps Research and the study's senior author.

The drug's power lies in its gentle nature. "It's not a hammer; it's not overly suppressing the immune system. It's just nudging the immune system in a certain way,"

In commercial spaces, cleaning at the end of every shift is a standard practice whether it’s a retail store, office, or restaurant. So why should it be any different in industrial settings?

In fact, construction sites, warehouses, and manufacturing plants have even greater risks when cleaning is neglected. From slips and trips to airborne dust hazards, failing to maintain a clean worksite can put employee health and safety at risk while also leading to costly compliance breaches.

If you’ve worked in the construction industry, you’re likely familiar with the term ‘silica dust’, and for good reason. Silica dust is a naturally occurring material found in stone, rocks, and bricks. When these materials are cut, drilled, or broken down, fine silica particles are released into the air. This dust is 100 times smaller than a grain of sand, making it easy to inhale without even realising it.

Prolonged exposure to silica dust poses severe health risks, including silicosis, kidney disease, and lung cancer. That’s why maintaining air quality both on the worksite and in surrounding areas is critical.

Tennant’s range of industrial sweepers offers advanced dust control solutions to support silica dust exposure management. Features such as pressurised cabins, dust suppression skirts, and HEPA filtration systems help capture and contain harmful particles. With in-cabin and on-hopper HEPA filtration, Tennant sweepers effectively trap particles as small as 0.3 microns, significantly reducing airborne silica dust and helping worksites stay compliant with safety regulations.

Once voted the UK’s favourite river, the River Wye flows from the Welsh mountains to the Severn estuary – 150 miles through an officially recognised “national landscape”. But this idyllic picture is changing, as the river is gradually choked by waste from industrial chicken farming.

In the land that feeds into these rivers, millions of chickens are being reared in intensive units to supply supermarkets with cheap meat and eggs. But all those chickens produce vast amounts of manure which can end up in the rivers.

This floods the river with excess nutrients causing algal blooms to flourish. The algae blocks out sunlight and consumes oxygen, which kills other creatures in the water. For instance the number of Atlantic salmon passing through the River Wye each year has plummeted from 50,000 in the 1960s to less than 3,000.

The problems caused by chicken farming have led to legal action against US food company Cargill and its subsidiary Avara Foods (both firms deny the allegations). Meanwhile food outlets including Nando’s have denied sourcing their products from polluting farms.

Most drugs typically have three names: a chemical name, a generic name, and a brand name. Each serves a different purpose.

Generic drug names often incorporate stems or suffixes that denote the drug’s mechanism of action, chemical structure or target receptor, and a prefix that differentiates it from drugs in the same family.

This is why lots of drug names share the same ending. Examples include cholesterol medicines ending in -statin, Ace inhibitors for reducing blood pressure ending in -pril, monoclonal antibody drugs ending in -mab, and tyrosine kinase inhibitors (mainly used in cancer treatment) ending in -tinib.

University of New Mexico researchers studying the health risks posed by gadolinium, a toxic rare earth metal used in MRI scans, have found that oxalic acid, a molecule found in many foods, can generate nanoparticles of the metal in human tissues.

Gadolinium-based contrast agents are injected prior to MRI scans to help create sharper images, Wagner said. The metal is usually tightly bound to other molecules and is excreted from the body, and most people experience no adverse effects. However, previous research has shown that even in those with no symptoms, gadolinium particles have been found in the kidney and the brain and can be detected in the blood and urine years after exposure.

Scientists are left with intertwined puzzles: Why do some people get sick, when most don't, and how do gadolinium particles become pried loose from the other molecules in the contrast agent?

Understanding the composition and transport of mineral dust is essential for assessing its environmental and health impacts.

Using physical and geochemical analyses, we identified significant differences between urban and natural dust that are not attributable to the intervening landscapes. These differences arise from the mixing of natural dust with local anthropogenic materials, including sediments from the Great Salt Lake playa conditioned by over a century of urban activity. This urban-influenced dust is transported downwind, where it may contribute to elevated levels of cadmium, copper, and zinc in streams of downwind mountain watersheds.

These findings underscore the far-reaching impact of urban dust on critical ecosystems and highlight the need for integrated management strategies to mitigate dust-related environmental consequences.

The damage produced by silica has some special characteristics that prompt us to call it a polyhedric disease.

The fact that it is a slowly progressing disease that is rare in terms of the overall population makes randomized trials difficult, and the reduced “market” limits the interest of the pharmaceutical industry. In contrast to other fibrotic lung diseases and common lung diseases such as asthma, very little use has been made of modern research techniques to understand this ancient disease or identify new therapeutic options.

However, our knowledge of the pathogenic mechanisms of damage caused by silica inhalation is steadily growing.

Firstly, silica-induced lung injury presumably results from the combined action of several interacting pathogenic mechanisms, including the direct cytotoxic effect of silica on macrophages, activation of macrophage surface receptors, lysosomal rupture, generation of reactive oxygen species (ROS), activation of inflammasome, cytokine and chemokine production, cell apoptosis/pyroptosis, and pulmonary fibrosis.

Then there is the accompanying immune dysfunction.

Silica inhalation causes the activation and apoptosis of macrophages, while the excess antigen generated is ingested by other activated macrophages. These can migrate to lymph nodes, eventually leading to the activation of T and B lymphocytes.

The likelihood of developing connective tissue disease is enhanced in subjects with exposure to silica and silicosis.

Furthermore, there is strong evidence for a very high risk of tuberculosis in the presence of radiological silicosis

Even in the case of uncomplicated infections, the body prepares itself early on for the possibility of a more severe course. A research team from the Technical University of Munich (TUM) and Helmholtz Munich has now uncovered this mechanism. The scientists showed that, right at the onset of mild illness, the body also produces special T cells previously known only from chronic, severe infections and tumors.

The term scleritis describes a chronic inflammation that involves the outermost coat and skeleton of the eye. Disease can be isolated to the eye, but in up to half of affected individuals it occurs in the context of an immune-mediated systemic inflammatory condition, such as rheumatoid arthritis or Wegener's granulomatosis.

Although uncommon, scleritis is often extremely painful, can lead to vision-threatening complications (and involvement of other ocular tissues), and is considered to confer an increased risk of mortality in patients with rheumatoid arthritis.

Demonstration of Subclinical Early Nephrotoxicity Induced by Occupational Exposure to Silica among Workers in Pottery Industry

Silica dust was suspected to affect the human kidney over 90 years ago.

The detected pathologic renal changes are similar to those induced by nephrotoxic heavy metals in the form of dose-related nephropathy that causes degenerative changes in tubular epithelium and interstitial inflammation, fibrous nephrosis, glomerulonephritis, and systemic vasculitis.

Additionally, it was demonstrated that silica exposed workers can experience distinct renal histologic alterations in glomerular and proximal tubules.

TAKE-HOME MESSAGE

Prolonged and intensive occupational exposure to silica could result in subclinical nephrotoxicity. It can thus be associated with an increased risk of future end-stage renal disease.

Usage of urinary biomarkers to detect signs of preclinical glomerular and tubular affection seems to be a simple and non-invasive screening tool to identify silica-exposed workers who carry a higher risk of future nephropathy

OP: @[email protected]

In the ScienceNorway article, comments from Professor Karl Johan Tronstad highlight findings from the research study suggesting that the support people with ME/CFS are receiving through the welfare and healthcare systems in Norway is having little rehabilitative effect (little positive impact on enabling people with the disease to be as independent as possible in everyday activities).

Within the article, the importance of the use of strict diagnostic criteria for ME/CFS in research, and the need to explore new treatment methods for the disease are emphasised by Prof. Tronstad. Importantly, researcher Anne Kielland also points out that until a truly effective treatment is found, research efforts should also focus on methods to improve quality of life for people with ME/CFS.

A 10 μg/m³ increase in fine particulate matter (PM2.5) was associated with a 4.6% rise in daily deaths on extremely hot days—substantially higher than the 0.8% increase observed on regular warm days.

Similarly, the risk of death rose by 8.3% when temperatures shifted from warm to extremely hot at a pollution level of 20 μg/m³—but surged to 64% when PM2.5 reached 100 μg/m³.

These results highlight a concerning synergy between heat and air pollution, showing that their combined effects on health are significantly more harmful than either factor alone.

Purpose

To study the risk for eye diseases in individuals with Ulcerative Colitis (UC), and to assess whether silica dust-exposure could contribute to the development of inflammatory eye diseases.

Conclusion

UC is associated with an increased risk for eye diseases, including inflammatory conditions. Our findings highlight that silica dust-exposure may be of importance in the pathogenesis of uveitis.

Occupational exposure to silica or silicon dioxide dust has been examined as a possible risk factor with respect to several diseases, like tuberculosis, lung cancer, systemic vasculitis , rheumatoid arthritis, systemic sclerosis , systemic lupus erythematosus , renal involvement , etc.

Early in 1951, Saita G et al.firstly reported that the renal functions were decreased in some silicosis patients. Subsequently, several epidemiological evidences suggested that the silica exposure was associated with an increased risk of end-stage renal disease (ESRD), chronic kidney disease (CKD), or specifically glomerulonephritis.

Silica nephropathy referred to the floorboard of kidney diseases after exposure to silica or silicon dioxide, including tubulo-interstitial disease, immune-mediated disease, chronic kidney disease, and end-stage renal disease. In literatures, the renal histopathology of silica nephropathy was varied, including focal glomerureview ritis, necrotizing glomerulonephritis, crescentic glomerulonephritis, etc.