Toxic Art – Alexander Calder’s Mercury Fountain

As an occupational hygienist, when visiting the Alexander Calder exhibition at Tate Modern last week I couldn’t help but stop and take notice of the pictures and description of one of the works created by this American artist well known for his mobiles and other “kinetic sculptures” . A mercury fountain.

While I was looking at the display, I overheard a comment by a young woman to her partner as they too read about this work

“It couldn’t have been real mercury could it. That would be dangerous”

I couldn’t help responding

“It was, and it is ”

Mercury, the magical Quicksilver, has been known since ancient times. A metal that’s a liquid at room temperature that flows like water.  Being a liquid, vapours are given off which can be inhaled and it can also be absorbed through intact skin. It’s highly toxic, affecting the brain, gastrointestinal system and kidneys. It’s particularly noted for causing neurological and behavioural disorders due to brain damage. Symptoms include tremors, insomnia, memory loss, neuromuscular effects, headaches and cognitive and motor dysfunction. In Victorian times mercury compounds were used in the manufacture of felt for hats and the workers in that industry were particularly affected. This is said to have inspired Lewis Carroll’s “Mad Hatter” from Alice’s Adventures in Wonderland. This was disputed by the esteemed Professor Hugh Waldron back in 1961, but the myth persists.


The exhibition website tells us the story of the fountain’s creation

In 1937 Calder was one of the contributors to the Pavilion of the Spanish Republic designed by Josep Lluís Sert for the International Exposition in Paris, where his Mercury Fountain was installed in proximity to Picasso’s painting Guernica. In the middle of the Spanish Civil War, Calder showed his support for the embattled Republic by creating a fountain that would run with mercury from the mines at Almadén – a valuable economic and strategic resource. (Tate website)

A 2007 study of historical exposures of the workers in Almadén mines to mercury indicated that had been very high

In the mine, the highest exposures occurred during drilling, with values up to 2.26 mg/m3 in air, 2194 μg/l in urine and 374 μg/l in blood. Furnace operation and cleaning were the tasks with the highest values in metallurgy, peaking up to 3.37 mg/m3. The filling of bottles with mercury by free fall gave values within a range of 1.13–2.43 mg/m3 in air; these values dropped to 0.32–0.83 mg/m3 after introducing a new ventilation system.

Occupational exposure limits for mercury are typically set at between 0.02 and 0.03mg/m3

I found it a little ironic that a work of art created in support of a government dedicated to improve the lot of working people celebrated an industry likely to have been responsible for poisoning the workers in the mine where it was extracted.

Although it seems likely that visitors to the exhibition back in the 1930’s would have been exposed to mercury vapours, given the relatively short period that they would have been in the vicinity their exposure would have been limited and its highly unlikely there would have been a significant risk to their health. However, I’d be more concerned about the staff working in the Spanish Pavilion.

Today the fountain can be seen at the Fundació Joan Miró museum in Barcelona – carefully displayed under glass. Hopefully appropriate measures are taken to protect the workers who have to maintain it from the toxic liquid and vapours.

Mercury fountain

Picture from the Fundació Joan Miró museum website


Frustrated phagocytes and the fibre paradigm

These were a couple of phrases from Rosemary Gibson’s presentation during the nanotechnology workshop during the recent BOHS Conference.

The fibre paradigm sets out the basis for the harmful effects caused by resistant fibres such as asbestos.  It states that fibres will damage the lung if they are

  • thin enough to enter the lungs
  • longer than the phagocytes that clear particles from the lungs
  • resilient and non-biosoluble, so that they remain in the lung

The long thin fibres that deposit and remain in the lung can’t be engulfed by the phagocytes, so that the ends of the fibre protrude from the cell.  The phagocye is said to be “frustrated”

t012365a-macrophages-on-an-asbestos-fibre1 (1)

This results in the release of chemicals that cause damage to the lung tissue leading to inflammation and, subsequently, to other damage, including the deposition of scar tissue (fibrosis).

Potentially any fibre which is thin enough to travel down to the alveoli and too long for the phagocyles to deal with it effectively could cause this to occur.  However, fibres that are biosoluble break down and can be cleared from the lung before significant damage can occur. So some materials, such as glass fibre, are deliberately formulated to dissolve in the body. Other, more resilient, fibres such as asbestos, remain in the lung long enough to allow the process to occur.

Recent research has suggested that some of the new engineered nano-materials, such as long carbon nanotubes, can cause effects similar to asbestos as their structure and dimensions means that they conform to the “fibre paradigm”

Source: Donaldson et al. Particle and Fibre Toxicology 2010 7:5

There’s a good summary of the fibre paradigm in an open access paper by Donaldson et al. published in the journal Particle and Fibre Technology last year, which is available on the web here.

The poison garden

I’ve just got back from a week’s holiday in Northumbria. It’s a region I haven’t visited previously I’ve never got past Newcastle before. It’s a very beautiful area with a fantastic coastline and lots of historic monuments to visit.

One of the places I visited during my trip was Alnwick Castle and Gardens. The gardens were redesigned only 10 years ago by Jacques and Peter Wirtz and provide a contemporary take on the traditional stately home estate.

One part of the gardens I found particularly interesting was the “Poison Garden“.  This contains a collection of  “poisonous” plants locked away behind a gate and which can only be accessed when accompanied by a guide. The collection included opium poppies, cannabis and the coca plant, for which the Alnwick Garden Trust had to obtain a special licence. However, most of the plants on display could be found in the countryside or domestic gardens. They included some obvious harmful weeds such as nettle and giant hogweed, well-known poisonous plants such as, belladonna and wormwood, but also decorative plants such as laburnum, willow and even some foodstuffs, including rhubarb.

The message that came across during the tour is one that occupational hygienists should be familiar with – everything is poisonous if we absorb enough of it and that even plants we consider harmful have their beneficial uses.

The opium poppy produces the highly addictive and harmful drugs opium and heroin, but it’s also used to produce morphine which is used to relieve severe pain. Of course morphine is addictive and uncontrolled doses are lethal (and the infamous G.P.  Harold Shipman used it to murder his patients) – a clear case of the dose “differentiating a remedy from a poison” .

Opium poppies

Laburnum have attractive yellow flowers and pea-like pods and are very popular garden trees. However all parts of this plant, – the roots, bark, wood, leaves, flower-buds, petals, and seedpods – are toxic, containing cytisine. There are hospital admissions every year, normally where children have eaten the pea-like seeds from the tree. But the tree is probably planted in hundreds of thousands of gardens around the country and very few of them cause harm – this can only occur if someone ingests the toxin.

I don’t know how popular rhubarb is these days, but I certainly enjoy this tart fruit. Yet here it was planted up in the poison garden.  The part of the plant we eat is the stalk. The leaves, however, contain  oxalic acid in the form of oxalates and anthraquinone alkaloids. Contrary to popular belief, it’s the latter, rather than the former that are the cause of harmful effects when the leaves are eaten.

Its risk that matters – the likelihood of the harm occurring –  and even the most toxic substance can’t cause harm in practice if it isn’t absorbed. So we can have laburnum trees in our gardens and grow and eat rhubarb providing we don’t ingest those parts of the plant containing the toxins. Even if we do, death doesn’t necessarily result – the effects we experience depend on how much we absorb. Similarly highly toxic chemicals can be used in the workplace without anyone being adversely affected if exposure is adequately controlled.

As Paracelsus noted many years ago

“All substances are poisons ; there is none which is not a poison. The right dose differentiates a poison from a remedy”

The poison garden at Alnwick is a good illustration of this.

Mad as a lighthouse keeper?

Souter Lighthouse, Whitburn

I was up in the North East over the weekend for a family wedding. We stopped overnight and on the way home decided to visit the Souter Lighthouse at Whitburn. Opened in 1871 and operated until 1988, it is now owned by the National Trust. Standing in a dramatic location on the cliffs between the Tyne and Wear, it was the first lighthouse to be powered by electricity.

After looking round the living quarters and the working areas of the complex we were able to climb the tower, accompanied by a guide. It was a steep climb up a spiral staircase and then an almost vertical ladder. According the NT website for the property, there are 76 steps – but it seemed like more!

There was a good view of the coast from the top of the tower, but the main attraction for me was the lamp mechanism.  There are actually two fresnel lenses, one on top of the other. The beam from the lower lens was white while the upper one gave a red light. The whole lamp assembly weighs over four tonnes. It’s supported on a bath of mercury, one and a half tons of the stuff, which has two purposes. First of all it keeps the lamp perfectly level. Secondly it makes it easy to rotate the lamp assembly by reducing friction. We were able to prove this for ourselves by pushing it around with our fingers.

A lighthouse fresnel lens (Source: Wikipedia)

Mercury, of course, is highly toxic, and the lighthouse keepers must have been exposed during their day to day activities, particularly when they had to remove impurities from the top of the bath and also when they had to periodically clean the liquid metal by passing it through a chamois leather, which they had to do every few months. Like most occupational hygienists I’m quite “sad”, I couldn’t help but wonder about what the lighthouse keepers were exposed to, so when I got home I did a search to find out whether anyone has done any work on tthis. I didn’t find much, just two relevant references.

A study on airborne mercury concentrations in lighthouses along with evaluation of urinary mercury levels was carried out in a lighthouse in  Canada in the 1980’s by van Netten and Teschke of  the University of British Columbia (1). The results from the air samples ranged from 4.4 to 26.3 μg/m3.  We don’t have a WEL for mercury in the UK, but the ACGIH TLV is 25 μg/m3 , so the survey certainly suggested that there was some risk that the TLV could be exceeded. Swabs taken on surfaces indicated that there was considerable accumulation of mercury on surfaces in the area of the light rotation mechanism, and other areas in the lighthouse. Urinary levels, however, were relatively low at  <4 μg/24 hr urine. The authors of the study concluded that “mercury levels in this lighthouse appeared to be under control through effective convective ventilation and employee awareness“. I couldn’t find any other studies, but I wonder whether this was typical of lighthouses in general. Today, lighthouses are usually automated and there is much less risk of exposure. However, the levels  reported in the study by van Netten and Teschke from the 1980’s were certainly of concern and it is likely that in the past exposure was even higher.

The second paper I unearthed was particularly interesting. One of the main concerns with mercury is the effect on the central nervous system causing effects such as short-term memory loss, incoordination, weakness, confusion, and psychological changes including the manic behaviour associated with the “mad hatter”.  The paper, by Michaela Walter of the   University of Calgary (2) discussed the possibility of mercury exposure being the cause of  “madness” amongst lighthouse keepers in Canada. According to this paper

“Keepers were not aware of the many dangers of mercury and did not wear protective gear in those days.Another prevailing factor was the amount of time they spent in the area where the lens and lighting system was kept. Keepers routinely cleaned and maintained the lens and mercury bath, lit and cleaned the lamp, as well as reset the gears every three hours t o allow the light to rotate. All of this additional time in the upper area of the lighthouse where the mercury bath was would have allowed for greater exposures to mercury vapour.”

Of course, psychological problems could be explained by other reasons – for example the pressures of working in an isolated location for long periods of time. However, her conclusion is that

“although difficult to substantiate, exposure to potentially toxic levels of mercury is a plausible  explanation for the actions and behaviours displayed by lighthouse keepers during the early 1900’s on the West Coast of Canada.”

We’ve all heard the term “mad as a hatter”, often attributed to the incidence of psychological effects due to mercury amongst workers in the hat manuffacturing industry. Perhaps “mad as a lighthouse keeper” is an alternative!

1. van Netten and Teschke, Assessment of mercury presence and exposure in a lighthouse with a mercury drive system, Environmental Research Volume 45, Issue 1, February 1988, Pages 48-57

2.Lighthouse keeper’s madness: Folk legend or something more toxic? M Walter – History of Medicine Days

Introduction to Toxicology

This is a presentation I put up on Slideshare. Its relevant to BOHS Module M101 – “Effects of hazardous substances” – but also provides some useful background for some of the other modules, particularly M102 and M103 where the examiners seem to assume that candidates have some knowledge of toxicology (although it isn’t a pre-requisite for these courses).


There was an interesting article in the Guardian a few days ago about the use of n-hexane in a factory in China. The company in question, which produces touch screens fro companies including Nokia, was using the solvent to clean the screens.

N-hexane is one of the organic compounds we study on BOHS Module course M101 “Effects of hazardous substances”. As an alkane, we wouldn’t expect it to be particularly toxic. Alkanes generally are mild irritants and narcotics (substances that cause depression of the nervous system leading to effects similar to drunkenness). N-hexane is different in that it has been found to have another more serious chronic (i.e. long term) effect. Exposure to the compound can lead to peripheral neuritis – damage to the peripheral nervous system – causing symptoms such as loss of sensation in the fingers. There’s a good summary on the effects of n-hexane here.

The effects on the peripheral nervous systems are not due to the substance itself, but one of it’s metabolites – hexane-2,5-dione. It’s an example where the bitransformation of a substance in the body produces a more toxic compound.

The harmful effects are well known, and in the UK, Europe and the USA  companies with a commitment to the health and safety of their workers would avoid using n-hexane wherever possible.  It seems that the Chinese company actually used n-hexane as a substitute for the less toxic ethanol. According to the Guardian report about 49 workers were affected. The problem could have been avoided if a serious attitude was taken to health and safety and the principles of occupational hygiene were applied.

Safe dose for ionising radiation?

It was interesting to see an article in The Guardian yesterday discussing dose response relationships and threshold doses. Generally, increasing the dose of a substance increases the severity of the effect it causes. Similarly, for a given effect, due to individual susceptibility increasing the dose leads to an increase in the response – i.e. the number of people affected. For most substances, however, there is a threshold dose – that is a dose below which no-one is affected. This is because at doses below he threshold, the body’s mechanisms can deal with the substance, preventing harm.  This can be represented graphically.

Typical dose-response curve showing a "threshold dose" (source:

With some substances, such as carcinogens and sensitisers, it is not possible to detect a threshold experimentally. It is argued that this is because they do not have one . The response is still dependant on the dose and at very low doses there are still some people who will be affected, albeit a relatively small number. Nevertheless, there is no “safe dose”. In such cases the dose-response curve is likely to be linear.

The Guardian article discusses the views put forward by an Oxford University physicist, Wade Allison, who has published a book in which he argues that there is a threshold for the effects of ionising radiation. He contends that DNA damage caused by exposure below this threshold dose can be repaired by the cells natural processes. This goes against the established view that radiation, like other direct acting carcinogens, has a dose response curve which doesn’t have a threshold, so that there is no identifiable dose below which adverse effects do not occur.  Other radiation specialists are quoted in the article who do not support his view.

The difficulty with carcinogens is that at low doses it isn’t possible to accurately determine whether there is an effect. Cancer can be caused by many agents, including some related to lifestyle (e.g. smoking) and natural sources (e.g. background radiation from cosmic radiation and from rocks) and in reality we are normally simultaneously exposed to multiple agents. At low doses a carcinogen, such as radiation, is only associated with very low incidences of the disease. So it can be difficult to determine exactly what is the causative agent. If there is a threshold, it is likely to be very low, and detecting it would be difficult.