Danger Dust 2

In conclusion, the average exposure to crystalline silica in carvers was higher than the permissible limit. Some workers were at risk of acquiring cancer and the majority of them were at an unacceptable non-cancerous risk. Therefore, it is necessary to implement engineering control measures and appropriate respiratory protection programs.

One of the most important ways of control is raising the awareness of workers and monitoring their work.

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. 

Autoimmune disorders are induced by various environmental and occupational substances. Silica exposure is recognized as a causative factor for autoimmune disorders, with well established connections to conditions such as pulmonary fibrosis (silicosis), rheumatoid arthritis (Caplan's syndrome), systemic sclerosis, systemic lupus erythematosus, and ANCA-related vasculitis/nephritis.

Understanding a person's occupational history to silica is an essential aspect for evaluating potential environmental factors that may contribute to autoimmune diseases.

Surprisingly, the study found that individuals with heterozygosity (having different versions of a gene) at HLA-II, rather than HLA-I, experienced a decreased risk of lung cancer. This effect was particularly pronounced among smokers, a population already at higher risk for lung cancer due to exposure to carcinogens.

Concerned about the effects of these exposures, an interdisciplinary BYU team recently came together to conduct a research study in Nepal, aiming to measure brick workers’ exposure to pollutants and to assess their respiratory health. The eventual goal is to determine what information, technology and strategies they can develop with the Nepali people to help them improve their well-being.

Don’t be fooled by the expert reassurances that only friable, or dusty, asbestos is dangerous. It’s true that dust is the danger: inhaling the microscopic particles of asbestos dust can decades later result in the deadly cancers caused by asbestos, and no safe level of exposure has yet to be identified.

Non-friable or bonded asbestos, we are told, is safe. That’s true, assuming the glue still bonds the fibres and it remains undisturbed. But asbestos cement manufacturing in Australia ceased in the mid-1980s. That means the asbestos fibre cement in our buildings is now between 40 and 100 years old, and its bonding agent no longer glues the fibres together effectively. Tests around the world have demonstrated that such old asbestos cement is now past its used-by date. The bonding is no longer effective, and when the fibro is exposed to the wind and rain, it sheds fibres that scatter through the surrounding environment.

So the next time you walk past a decaying corrugated roof or fence, hold your breath! 

Next, they searched for RetroMyelin-like sequences in the genomes of other species, finding similar code in jawed vertebrates – fellow mammals, birds, fish, reptiles and amphibians – but not in jawless vertebrates or invertebrates.

This led them to believe the sequence appeared in the tree of life around the same time as jaws, which first evolved around 360 million years ago in the Devonian period, called the Age of Fishes.

Taken together, this provoked the notion that LAA may elicit an autoimmune response within exposed individuals and suggested that this altered response may lead to Libby Disease.  

There is no doubt that environmental exposure to asbestos is an urgent public health matter, and the devastating effects which are still experienced to this day in Libby are a grim reminder of the ongoing dangers that this phenomenon poses.

There remains a need to raise awareness amongst clinicians working with autoimmune and general inflammatory diseases so that LAA exposure may be recognised at an earlier stage and considered as a possible cause, particularly since it is highly unlikely that this issue remains confined to the Libby area since millions of homes and buildings remain insulated with the material.

Recent findings 

New industries such as jewelry polishing, denim jean production, fabrication of artificial stone benchtops, glass manufacturing and glassware has led to re-emergence of silicosis around the world.

Silicosis with long term exposure to dust containing crystalline silica has been examined as a possible risk factor with respect to several autoimmune diseases as scleroderma, rheumatoid arthritis, lupus erythematosus, and some types of small vessel vasculitis with renal involvement.

The dust may act to promote or accelerate disease development, requiring some other factors to break immune tolerance or initiate autoimmunity. 

Better understanding the mechanisms that involve silica -induced autoimmune diseases may contribute to early diagnosis.

The harm a chemical causes differs depending on how it enters the body.

Ingested chemicals pass through the intestines and liver before entering the blood.

Inhaled chemicals first pass through the lungs where they may be absorbed directly into the blood.

Chemicals that penetrate the skin can also directly enter the bloodstream.

You don’t even need to have an open wound, as the chemicals can be absorbed directly through the skin.

The fungi are assumed to be endemic in parts of the midwestern, south-central, and southeastern U.S., and only five states currently keep track of diagnosed human cases: Arkansas, Louisiana, Michigan, Minnesota, and Wisconsin. But there’s been some indication that the potential range of blastomycosis in the U.S. is larger than we think.

We report the case of a 42-year-old male dental technician who began to suffer from a dry cough and exertional dyspnea after approximately 15 years of work. The operations he conducted for his job resulted in the generation of crystalline silica, aluminum, chromium and titanium dust. The worker did not regularly wear personal protective equipment and some of the above operations were not carried out in closed circuit systems.

Scientific evidence describing harm to the environment and humans is growing. Hence, the United Nations has resolved to negotiate a legally binding instrument to end plastic pollution.

In our work, we established the presence of chemicals in recycled plastic that can cause harm to humans or other organisms. They include pesticides, pharmaceuticals and fragrances. Others are chemicals that result from burning natural materials, man-made organic chemicals used for industrial applications like paint, and ultraviolet filters.

We quantified a total of 491 different chemical substances.

Light-sensitive substances react to this and destroy unhealthy cells. Healthy cells are practically not affected. One of the main challenges of this approach is to find a suitable light-sensitive compound.

What is the UK doing to address this problem?

Unlike asbestos, there is no specific law relating to the risk of silica dust, despite it being at least as lethal as asbestos.

According to the advocacy group, Hazards, there are two main existing pieces of legislation that relate to silica exposure. First is the Health and Safety at Work Act (1974), which requires employers to ensure the physical and mental health of workers and others impacted by their work activities or in their working environment.

Second, the Control of Substances Hazardous to Health Regulations 2002 (COSHH) demands that employers lower RSC exposure among their employees  “as reasonably practicable.” 

Breathing in dust from crystalline silica-containing materials can lead to lung disease. 

Chronic silicosis typically occurs after 10 or more years of exposure to respirable crystalline silica. However, the disease can occur much more quickly after heavy exposures. Silicosis can develop or progress even after workplace exposures have stopped.

Symptoms of silicosis may include:

Cough

Fatigue

Shortness of breath

Chest pain

There is no known cure for silicosis and some patients may require a lung transplant.

Workers exposed to silica and those who have silicosis are also at increased risk of tuberculosis (TB), a contagious and potentially life-threatening infection.

Exposure to respirable crystalline silica puts workers at risk for developing other serious diseases including:

Lung Cancer

Chronic Obstructive Pulmonary Disease (COPD)

Kidney Disease

Autoimmune Disease

Given the use of asbestos filtration in commercial brewing and reports of its unregulated use in British public houses in the 1970’s to clear draught beer “slops”, we have assessed the hypothesis that ingested asbestos could be a causative factor for this increased incidence.

Importantly, occupational asbestos exposure increases the risk of adenocarcinoma but not squamous cell carcinoma of the oesophagus. The presence of asbestos fibres was consistently reported in filtered beverages including beers in the 1970s and asbestos bodies have been found in gastrointestinal tissue, particularly oesophageal tissue, at autopsy. 

Undoubtedly, plastic’s carcinogenic/mutagenic impact on cells has already been broadly reported, fueling researchers’ concerns, and thus the willingness to further research this matter.

Except being potentially harmful themselves, microplastics might also be contaminated with other substances, including harmful organic chemicals or trace metals, whose exposure to living organisms might be toxic.