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Our toxic environment

One of the lesser-known minerals that can have a negative impact on our health is Beryllium.

Australian residents not employed in the manufacturing or mining industries represented in Table 1. have a low chance of beryllium exposure. The main source of beryllium contamination for the wider public comes from coal-fired power stations and from the burning of fossil fuels in general. Residing in close proximity to industries that mine, refine, grind or process beryllium may also be an issue as the microscopic particles (1 micron or smaller) can escape in the exhaust fumes from some beryllium-based industries. Particulate matter has been found in the air up to about 1 kilometer away from the factory. The dust is so fine that it can remain in the air for up to 10 days at a time. (3)
Another source of beryllium is dust from coal ash which has been dumped in landfill. In some housing development sites in Australia, coal ash (called fly ash) has been used to stabilise soft soils on residential blocks of land. Other potential sources of exposure are outlined in Table 1. below.

Routes of Exposure

Respiratory 
The principal route of exposure is via breathing in airborne particles. Industries that mine, refine or process beryllium produce very fine dust of micron or submicron particle size. For some people, with chronic exposure, these minute particles can lodge within the lung walls and remain there undetected causing slow but severe damage, sometimes not detected until up to two decades later when symptoms begin to develop.

Ingestion 
Beryllium is present in about 5% of drinking water tested, and it is also present in food in an insoluble, naturally occurring form at around 22.5 mg per kg. When ingested in this insoluble form, it appears to be harmless.

Dermal
Dermal exposure is very unlikely in the general population but may occur due to certain precautions not being taken. These include inadequate handling of hazardous waste, poor cleaning of contaminated surfaces, and insufficient personal protective equipment, especially gloves. This is particularly important when soluble forms of beryllium are used.

Immunological Changes

Antigen-Specific Effects

When beryllium binds to glutamic-acid at position E-69, it creates an antigen which the body interprets as foreign and in response, marshals specific inflammatory defenses. In Chronic Beryllium Disease (CBD) these specific immunological changes are characterised  by the production and proliferation of immune cells IFN-γ, TNF-α and RANTES, but not GM-CSF, IL-4, IL-6, IL-8, IL-10 and IL-12. Researchers have noted a positive correlation between levels of beryllium-specific T cells in the blood and levels of alveolar inflammation.(4,5) 

Non-specific Inflammation Effects

Beryllium may also induce general changes in lung permeability and the production of pro-inflammatory cytokines such as IL-1, IL-12, and IL-18, tumour necrosis factor (TNF), interferon gamma (IFN-gamma), and granulocyte-macrophage colony stimulating factor. Together these create the ideal inflammatory conditions for forming and maintaining granulomas and as the disease advances, the granulomas self organise forming small, fibrous nodes which progressively impair pulmonary function.  (6,7)

Theoretical Model of Beryllium Disease 

Due to the persistent presence of beryllium, the CBD lung granuloma is perpetually endocytosed by granuloma macrophages. In turn, these apoptotic macrophages are then broken down by unaffected granuloma macrophages. As the apoptotic bodies are disassembled, beryllium is released, activating beryllium-specific CD4+ T cells. These T cells proliferate and release pro-inflammatory cytokines which maintain chronic inflammation by promoting the entry of mononuclear phagocytes and beryllium-specific CD4+ T effector memory cells out of the blood and into the granuloma.
This insidious cycle continues for decades resulting in ever-increasing lung inflammation, altered lung function and progression to lung fibrosis as a result of the continual failure of both innate and acquired immune defense systems to eliminate beryllium from the lungs.(4)

Beryllium Disease – Stages & Symptoms

Stage One: Acute Beryllium Disease
Following acute exposure, symptoms may include:

  • acute pneumonitis
  • dyspnoea
  • cough
  • chest pain (in some cases)

Stage Two: Beryllium Sensitisation
This is a specific cell-mediated allergic response to beryllium detected by the beryllium lymphocyte proliferation test (BeLPT).(7) Not everyone has an inflammatory response to the presence of beryllium and the disease only develops in those who do. (8)
 

Stage Three: Chronic Beryllium Disease (Berylliosis)
The symptoms may take one or two decades to develop as it is a slow progressive disease with symptoms appearing gradually over time. Symptoms can include:

  • granulomatous disease
  • shortness of breath
  • reduced oxygen
  • chest pain
  • anorexia & weight loss
  • chest pain
  • fevers / night sweats
  • joint & muscle pain
  • digital clubbing  (finger and toe nails)

Prognosis

CBD is a slow, progressive disease with no known cure, to date. About a third of those who develop the disease develop other complications which can ultimately prove fatal. Slowing the progress of Beryllium disease may be linked to slowing the rate of chronic disease-induced oxidative stress and zinc is particularly good at this (see the last issue for details). Beryllium disease dramatically depletes thiol levels. (3) 

Providing a thiol source to boost the body’s own beryllium-depleted glutathione levels, plus anti-inflammatory antioxidants such as manganese and vitamin C may help quell the inflammation and slow the progression of berylliosis.(9) However, for those working with beryllium, the use of high-quality air filters and the wearing of protective clothing remain the best first lines of defence.

One of the easiest ways of assessing heavy metal levels are with a Hair Tissue Mineral Analysis (HTMA) available through True Medicine.  Call 07 5530 1863 to arrange an appointment.

References:

  1. Strupp C. Beryllium metal II. A review of the available toxicity data. Annals of Occupational Hygiene. 2010 Dec 31;55(1):43-56.
  2. Sizar O, Talati R. Berylliosis (chronic beryllium disease). InStatPearls [Internet] 2018 Dec 2. StatPearls Publishing.
  3. ATSDR – Public health statement: beryllium. Agency for toxic substances and disease registry. Atlanta USA. Available from: https://www.atsdr.cdc.gov/phs/phs.asp?id=339&tid=33
  4. Sawyer RT, Maier LA. Chronic beryllium disease: an updated model interaction between innate and acquired immunity. Biometals. 2011 Feb 1;24(1):1-7.
  5. Kreiss K, Fechter-Leggett ED, McCanlies EC, Schuler CR, Weston A. Research to practice implications of high-risk genotypes for beryllium sensitization and disease. Journal of occupational and environmental medicine. 2016;58(9):855.
  6. Lotze MT, Thomson AW, editors. Natural killer cells: basic science and clinical application. Academic Press; 2009 Nov 12.
  7. Pott GB, Palmer BE, Sullivan AK, Silviera L, Maier LA, Newman LS, Kotzin BL, Fontenot AP. Frequency of beryllium-specific, TH1-type cytokine-expressing CD4+ T cells in patients with beryllium-induced disease. Journal of allergy and clinical immunology. 2005;115(5):1036-42.
  8. Fontenot AP, Palmer BE, Sullivan AK, Joslin FG, Wilson CC, Maier LA, Newman LS, Kotzin BL. Frequency of beryllium-specific, central memory CD4+ T cells in blood determines proliferative response. The Journal of clinical investigation. 2005;115(10):2886-93.
  9. Dobis DR, Sawyer RT, Gillespie MM, Huang J, Newman LS, Maier LA, Day BJ. Modulation of lymphocyte proliferation by antioxidants in chronic beryllium disease. American journal of respiratory and critical care medicine. 2008;177(9):1002-11