Lead is still widely produced and used in the UK, and the HSE recently revised its guidance on the subject, providing a reminder of its potentially harmful effects on health. Dr Chris Ide gives the lowdown on the oldest of metals.
Lead is one of the seven metals known to the classical civilisations, the others being copper, gold, iron, mercury, silver and tin. Of these, lead is probably the oldest. It was certainly used in Old Testament times – “…they sank as lead in the mighty waters”1 was written about the escape of the Israelites from Egypt in about 1800 BC, and Egyptian kitchenware from 2200 years before that has also been found.
That lead was widely used can be attributed to widespread availability of rich ores (occasionally combined with silver) and the fact that it melts at a relatively low heat (about 327ºC). The resultant metal could be hammered into sheets, drawn out, and moulded into a variety of shapes, using the simple technology of the time. As the centuries progressed, lead and its compounds came to be used as alloys, such as pewter, pigments (including cosmetics), medicines, in glass manufacture, pottery-glazing, and even as a sweetener!
However, the harmful effects of lead were also known to the ancients. Hippocrates, who died in 357 BC, described characteristic colic in miners. Fast-forward to 1703 AD, and Ramazzini wrote of the deleterious effects on the health of painters, potters and plumbers caused by lead. Thackrah remarked that “plumbers are short-lived. A small proportion reach the age of 50.”2
The baleful effects of working with lead were noticed by non-medics, as well. The Roman engineer, Marcus Vitruvius (c70 BC – 15AD) noted that the health of the occupants of houses whose water was supplied via earthenware pipes was better than those where lead was used.3 Thomas Pennant, a Welsh gentleman of independent means and a fellow of the Royal Society, visited Leadhills during his tour in 1772. He commented that lead miners and smelters suffered from “lead distemper, or mill-reek, which brings on palsies and madness, terminating in death in about 10 days”.4
As the industrial revolution progressed in Britain and other countries, the use of lead and its compounds grew substantially, particularly in the chemical industry, where its corrosion resistance was valued. Unfortunately, lead poisoning (plumbism) also became more common, and many doctors became very experienced in its diagnosis. In Britain, the relentless rise of these conditions, particularly in workers, eventually resulted in the appointment of Thomas Legge in 1897 as the first Medical Inspector of Factories, the year after lead poisoning became a notifiable disease.
Legge also investigated other occupationally-acquired diseases, such as toxic jaundice, anthrax and upper-limb disorders. He visited workplaces, spoke to workers and their managers, and, by making follow-up visits, demonstrated the success of his interventions. He eventually resigned in 1926, when the British government declined to ratify an International Labour Organisation Convention on white lead, but he is survived by his aphorisms. These can be equally applied to just about any occupational health and safety situation:
Lead is surprisingly still widely used in the UK today – about 330,000 tonnes annually.5 About 80 per cent of this is accounted for by the manufacture of lead-acid batteries; another 6 per cent is extruded into sheets;
5 per cent is used for pigment manufacture; shot/ammunition accounts for 3 per cent;
2 per cent goes into alloys; 1 per cent is used for cable sheathing; and the remaining 3 per cent goes to “other uses”.5,6 Britain is a substantial producer of refined lead, with well over 250,000 tonnes of output in 2007, placing us within the top six producers in the world.6 This refined lead includes about 143,000 tonnes of secondary production, just over 50 per cent of it coming from scrap.6
Lead exerts its toxicity because it interferes with the actions of elements such as calcium, iron and zinc, which are involved in nerve conduction and red blood-cell formation. The symptoms of acute lead poisoning consist of colicky abdominal pains and mental confusion. If exposure continues, then constipation and muscular weakness follow, the latter being due to nerve damage, particularly those supplying the flexor muscles (those muscle groups that straighten joints). Tiredness also develops.
As noted by Legge, most occupational lead uptake stems from the inhalation of dust and fumes. Small particles, particularly those less than 10 microns in diameter, can easily reach the depths of the lungs, bypassing their clearance mechanisms. Depending on the solubility of the material, up to 40 per cent of a quantity of inhaled lead will be retained, compared with a maximum of 10 per cent of a swallowed dose.
Once lead enters the bloodstream, it is distributed among the plasma and red blood cells before finally being expelled by the kidneys. The half-life of lead in blood (the length of time taken for its level to fall to half its initial level) is between 30 and 40 days. However, continuing uptake of lead results in it being stored in the soft tissues and in the bones. Once lodged there, the half-life of skeletal lead is measured in decades.
When a steady state has been reached, the lead in circulating blood represents less than 5 per cent of the total body burden of lead. Even if occupational exposure ceases, the lead gradually leaches out from the bones to maintain a raised blood lead level, which can rise further in the event of prolonged febrile illnesses, or disorders involving a more rapid turnover of bone tissue.
The law on lead
The Control of Lead at Work Regulations (CLAW) have been in force for several decades, and were most recently revised in 2002.7 Although this legislation applies to all lead workers, only those who are likely to absorb significant amounts of lead as a result of workplace activities require biological monitoring. This is generally performed by taking a blood sample and measuring its lead content. (To comply with the law, the medical work should be undertaken either by a medical inspector, or a doctor appointed for the purpose by the HSE.) A ‘rule of thumb’ is that significant absorption is likely to occur if work activity generates lead in air levels that exceed half the current lead-in-air standard – currently 0.15 mgs-m3, eight-hour time-weighted average.
Although less important, swallowing lead can still raise blood lead levels significantly, occasionally producing frank illness. With the exception of organic lead compounds, skin absorption of lead is an insignificant hazard.
The doctor initially assessing workers should enquire about their past medical history, general well-being, tobacco and alcohol habits, hobbies, domestic lead plumbing, and the presence or absence of symptoms attributable to gastro-intestinal or neurological disease. Fingernails should be examined for signs of biting. Blood pressure should be checked, and urine examined, using ‘stix’. Specimens should be submitted to the laboratory for a full blood count (to detect anaemia), blood lead and zinc protoporphyrin (ZPP) levels. However, if the hazard is from an organic lead compound, then urinary lead measurements are appropriate. ZPP levels give an approximation of lead uptake over the previous three to four months.
Blood lead measurements should be done by a laboratory approved by the HSE, and the individual worker should always be advised, in writing, of the outcome of this assessment. The letter should include relevant health advice, supported by leaflets, such as the HSE’s recently updated ‘Lead and You’.8 A copy of the relevant medical information should also be offered to the worker to pass on to their general practitioner. If the employee is willing, results of the blood test could be passed on to the employer, who otherwise should be notified of the range within which the blood lead level falls.
Taking action
In the first instance, the employer should undertake a risk assessment, informed by the results of occupational hygiene assessments, if appropriate, and the initial medical examination. They will then need to decide what further modifications to working practices and personal protective equipment are necessary. It is important to factor in the likelihood of significant overtime being worked, and the nearness of washing, changing, and rest/canteen facilities.
Further blood and/or urinary lead levels should be assessed, at least no later than three months after the work has started, or immediately after an exposed employee complains of symptoms consistent with lead poisoning. Should this occur, the employee should be removed until the test results are known. The results of subsequent testing will help determine the frequency of further medical review, as recommended by the ACOP relating to the Lead Regulations.
Under current legislation, should an adult male worker have a blood lead level of 60 µg/dl or higher, which is confirmed by re-testing, ideally within 10 days, then that worker will need to be suspended from work involving exposure to lead until the blood lead level has returned to more normal levels, and the HSE has been informed.
For women, particularly if they are between the ages of 15 and 45, this level is halved, i.e. 30 µg/dl, because of the likelihood of harming unborn children. A blood lead level of 50 µg/dl in adult men, and 25 µg/dl in women constitutes an Action Level, requiring the employer to re-assess the adequacy of working practices and protective equipment. As a rule, non-toxic blood lead levels are generally regarded as being under 10 µg/dl.
Scale of the problem
As reported in the December 2009 issue of SHP,9 Prof Rory O’Neill criticised the HSE over its supervision of workers exposed to lead. At first sight, this was unreasonable, since the vast majority of UK workers exposed to lead were well below the suspension level. Nonetheless, that level exists to protect workers from the symptoms of frank plumbism. It has been known for many decades that much lower blood lead levels are associated with a variety of haematological, biochemical, neurological and psychological perturbations.
Although they are asymptomatic (no one visits their GP and says: “Hey doc, my sural nerve conduction velocity is down” or: “My ALA dehydrogenase is up”!) research shows that, if the lead levels persist, in the longer term they translate into higher-than-expected death rates generally, and cardiovascular disease in particular.10 Greater damage is inflicted on brain function in older adults,11 and musculoskeletal and gastrointestinal symptoms are common.12
While these papers can be criticised because of their lack of control populations, or dependency on a single sample, for example, they do demonstrate an impressive correlation between number of symptoms and lead levels,
O’Neill refers to the work of Simon Pickvance, who claimed to have found large numbers of lead-poisoned people attending GP surgeries. No numbers were given, but I would not be surprised if, in some GP surgeries at least, there were many more suffering from the effects of lead intoxication than expected. In order to make the diagnosis, the possibility has to be considered, i.e. the doctor has to be aware.
My specialist gastro, rheumatology and orthopaedics colleagues see the tip of a vast iceberg of cases originating in family practice, with patients presenting with irritable bowel syndrome, ulcer-negative dyspepsia, and vague joint aches and pains, etc. However, it is rare to find any mention of the patient’s job in the notes, so the opportunity to test the blood of (say) demolition or scrap-workers, painters/ decorators, or radiator repairers, is lost.
While not an occupational example, The Lancet reported the case of a woman with a 10-year history of illness attributed to chronic fatigue syndrome. In fact, she was suffering from lead poisoning, with a blood lead level almost four times that which would result in an adult male lead worker being suspended! The source of lead was an old immersion heater, which provided the woman with all her hot water.13
Forewarned is forearmed
Recessions increase business failures but also spawn new ventures, as redundant employees take the forced opportunity to strike out on their own. Here, I worry about the ‘unknown unknowns’ (to paraphrase Donald Rumsfeld) as, when I worked for the HSE, we would often come across unexpected groups of lead workers.
For example, a group of new businessmen bought an old ship, intending to refurbish it and use it as the centrepiece of a harbour development. Their picture appeared in a local newspaper, showing them wielding needle guns, sanders, grinders, etc. and not a scrap of personal protective equipment in sight. They were blissfully unaware – until the arrival of myself and a factory inspector – that the old paint they were removing contained up to 20 per cent lead! They were also ignorant of a wide variety of other hazards, such as noise, vibration, dichloromethane, confined spaces, electricity, etc. This stresses the importance of adequate planning, education and training.
Blood lead levels can be reduced by the use of chelating agents, but these often have significant toxicity of their own, so should not be used lightly. This emphasises the importance of prevention.
My experience is that blood lead levels can vary widely between individuals doing the same job in different firms, and even within the same organisation. Trade associations, where they exist, could help disseminate best practice, but discouraging tobacco smoking would also be helpful. Grubby fingers contaminate the cigarette with lead. Pipe-smokers, or users of ‘roll your owns’, are even more at risk, as the tobacco itself becomes sullied as well. The high temperature of burning tobacco efficiently vaporises the lead, which is then readily inhaled.
Provision, and use, of adequate rest, washing, changing and ‘canteen’ facilities will reduce the lead intake from contaminated food. Separate arrangements for laundering work garments will reduce the time workers spend wearing contaminated clothing on the journey to and from work, and save families from exposure to lead and other dusts transported from the workplace.
During my time with the HSE, one of our agricultural inspectors told me of a six-year-old boy who had been referred to the educational psychologists because of disruptive classroom behaviour. His father, a farm labourer, had appa
ently cornered the market in sash-window lead counterweights. I visited the home, and found a shambolic workshop in which the small boy liked to ‘help Daddy’. The child’s blood lead was about 30 µg/dl, but ZPP tests hinted at it being over 70 µg/dl in the past. Both parents had blood lead levels in the 50s. Advice was given, the child excluded from the workplace, and his symptoms gradually remitted.
Lead and its compounds are likely to remain an important part of our lives for many years to come, occurring in both traditional and novel circumstances, as well as intruding unexpectedly into domestic and working environments. Well-informed safety advisors will be ideally placed to protect the health of employees and members of the public from one of the oldest hazards known to mankind.
References
1 Book of Exodus 15, v10
2 Thackrah, CT (1989): The effects of the arts, trades and professions on health and longevity, WH Smith Facsimile edition
3 Cruise, A (2006): Roman medicine, Port Stroud Tempus Publishing
4 Pennant, TA (1998): Tour in Scotland and voyage to the Hebrides 1772, Edinburgh Birlinn Facsimile Edition
5 Brown, TJ et al (2009): ‘World Mineral Production 2003-2007’, in British Geological Survey, National Environmental Research Council, Keyworth, Nottingham
6 Mineral Planning Factsheet (2007): British Geological Survey, National Environmental Research Council, Dept of Communities & Local Government – tables 2 and 3
7 HSE (2002): Control of Lead at Work Regulations 2002 – Approved Code of Practice and guidance, 3rd Edition, L132, ISBN 9780 7176 2565 6
8 HSE (2009): Lead and you: Working safety with lead, INDG 305(rev1)
9 ‘HSE accused of complacency on lead exposure limits’, in SHP December 2009, Vol.27 No.12
10 Menke A, Munter P, Batuman V, Silbergeld EK, Guallar E (2006): ‘Blood lead below 0.48 µmol/l (10 µg/dl) and mortality among US adults’, in Circulation 2006;114:1388-94
11 ‘Cumulative lead dose and cognitive function in adults: A review of studies that measured both blood lead and bone lead’, in Environmental Health Perspectives 2007,115;3:483-92
12 Rosenman KD, Sims A, Luo Z, Gardiner J (2003): ‘Occurrence of lead-related symptoms below the current Occupational Health and Safety Act allowable blood levels’, in J Occup Environ Med 2003;45:546-55
13 Mesch U, Lowenthal RM, Coleman D (1996): ‘Lead poisoning masquerading as chronic fatigue syndrome’, The Lancet 1996,374;9009:1193
Chris Ide is an occupational physician and regular contributor to SHP.
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