Lead Acid Battery Recycling

Recycling used lead-acid batteries:
health considerations
Recycling used lead-acid batteries:
health considerations
Recycling used lead-acid batteries: health considerations ISBN
978-92-4-151285-5
© World Health Organization 2017

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Contents
Acknowledgments 1
1. Introduction 2 1.1.
Purpose and scope of the document 3
2. How lead exposure occurs during recycling and disposal 4 2.1.
Components of a lead-acid battery 4 2.2. Steps in the
recycling process 5 2.3. Lead release and
exposure during recycling 6 2.3.1. Informal lead recycling
8
2.4. Other chemicals released during recycling 9 2.5.
Studies of lead exposure from recycling lead-acid batteries 9 2.5.1. Senegal
10 2.5.2. Dominican Republic 11 2.5.3. Viet
Nam 12
3. Main routes of lead exposure and health effects 14 3.1.
Routes of exposure to lead 14 3.2. Toxic effects
of lead 15 3.2.1. Gastrointestinal effects
15
3.2.2. Neurological effects 16
3.2.3. Cardiovascular 17
3.2.4. Renal 17
3.2.5. Endocrine 18
3.2.6. Reproductive system and pregnancy 18
3.2.7. Haematological 18
3.3. Toxic effects in relation to blood lead concentrations 18
4. The public health impact of lead exposure 21
5. Economic impact of lead exposure in countries 22
6. Assessment of lead exposure 23 6.1. Blood
lead measurements 23 6.2. Taking an exposure
history 25 6.3. Environmental assessment
26 6.3.1. Soil and dust 26
6.3.2. Air 26 6.3.3.
Food and water 27
RECYCLING USED LEAD-ACID BATTERIES: HEALTH

CONSIDERATIONS / III
7. Control measures 29 7.1.
Battery collection, storage and transportation 29 7.2. Battery
recycling 29 7.2.1. Personal protective
equipment 31
7.3. Informal recycling 31
7.4. The problem of legacy pollution 32
7.5. Policy measures 32
8. Conclusions and way forward 33 9.
References 34
Iv / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

Acknowledgments
This document was written by Bernice Schaddelee-Scholten (consultant) and
Joanna Tempowski of the Department of Public Health, Environmental and Social
Determinants of Health at the World Health Organization (WHO), Geneva,
Switzerland. The first draft was prepared for a workshop organised by the United
Nations Environment Programme on Safe Management of Used Lead Acid Batteries,
held in Osaka, Japan, on 26-27 October 2015. Meeting
participants are thanked for their comments on the draft.
Further comments were provided by: Jack Caravanos, New York University, New
York, USA; Edith Clarke, Occupational & Environmental Health Unit, Ghana
Health Service, Accra, Ghana; Bret Ericson, Pure Earth, New York, USA; Perry
Gottesfeld, Occupational Knowledge International, USA; Amalia Laborde, Centro de
Información y Asesoramiento Toxicológico, Montevideo, Uruguay; Philip Landrigan,
Icahn School of Medicine at Mount Sinai, New York, USA; Byung-Kook Lee, Institute
of Environmental & Occupational Medicine, Soonchunhyang University, Republic of
Korea; Angela Mathee, Environment and Health Research Unit, Medical Research
Council, Johannesburg, South Africa; and Lynn Panganiban, Department of
Pharmacology & Toxicology of
the College of Medicine, Manila, the Philippines.
From WHO, comments were provided by: Hamed Bakir, Mohamed Elmi, Soren
Madsen, Mazen Malkawi and Raki Zghondi, Eastern Mediterranean Regional Centre
for Environmental Health Activities, Amman, Jordan; and Dorota
Jarosińska, WHO European Centre for Environment and Health, Bonn, Germany.
Edited by Philip Jenkins.
Photo credits: Larry C. Price/ The Pulitzer Center on Crisis Reporting (recycling in
Indonesia: front cover and pages 9, 25 and 26); Perry Gottesfeld/Occupational
Knowledge International (recycling in Viet Nam pages 12 and 19).
Design and layout by Paprika (Annecy, France).

CONSIDERATIONS / 1
1. Introduction
Approximately 85% of the total global consumption of lead is for the production of
Around 85% of
lead-acid batteries (ILA, 2017). This represents a fast-growing market, especially in
the total global
consumption of Asia (Future Market Insights, 2014). The main uses of these batteries are in motorized
lead is for the vehicles, for storage of energy generated by photovoltaic cells and wind turbines, and for
production of lead- back-up power supplies (for both the consumer market and for critical systems such as
acid batteries telecommunications and hospitals). In developing countries where power supplies are
(ILA, 2017) unreliable, lead-acid batteries are used domestically for lighting and electrical
appliances (UNEP, 2004). The growth in the use of renewable energy sources and the
concomitant need for storage batteries, as well as the increasing demand for motor
vehicles as countries undergo economic development, mean that the demand for lead-
acid batteries will continue to increase. This is reflected in the increased global
demand for refined lead metal, which was estimated at 10.83 million tonnes in 2016
(International Metals Study Groups, 2016). The demand is being met by increases in
both primary lead production from mines and recycling. Indeed, currently
over half of the global production of lead is from lead recycling (ILA, 2015).
The manufacturing and recycling of lead-acid batteries is practised worldwide in both

regulated industries and unregulated, informal establishments (UNEP, 2003). Lead
recycling is an important source of environmental contamination and human exposure
in many countries (UNEP, 2010; van der Kuijp et al., 2013). This is because it is
frequently carried out without the necessary processes and technologies to control
lead emissions and, in many developing countries, is a poorly regulated industry
(UNEP, 2010; Manhart et al., 2016). The unregulated, informal recycling of used
lead-acid batteries presents particular problems as it is mainly carried out by small
family businesses, often in domestic backyards, and sometimes in secret (UNEP,
2004; Belay et al., 2015; AGENDA, 2016). Even established, industrial-scale
recycling facilities can, however, cause significant environmental contamination and
human exposure to lead in countries without adequate standards or when regulatory
controls
are inadequately enforced (California Environmental Protection Agency, 2015).
2 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

Recycling used lead-acid batteries is of public health concern because this industry is
associated with a high level of occupational exposure and environmental emissions.
Furthermore, there is no known safe level of exposure to lead, and the health
impacts of lead exposure are significant. Based on 2016 data, it is estimated that lead
exposure accounted for 495 550 deaths and 9.3 million disability-adjusted life years
(DALYs) lost due to long term impacts on health, with the highest burden in low- and
middle-income countries (IHME, 2016). Young children and women of childbearing
age are particularly vulnerable to
exposure to, and the toxic effects of, lead.
1.1. Purpose and scope of the document

This document aims to inform the health sector about this issue so it can recognize
the recycling of lead-acid batteries as a source of lead exposure and can advocate for
this practice to be better controlled and regulated. It also aims to inform policy-makers
of the burden of disease associated with lead exposure
as a stimulus to introducing and enforcing control measures.
The document outlines the process of recycling used lead-acid batteries and describes
how lead exposure can occur. Three case studies illustrate the impact that uncontrolled
battery recycling can have on a community. The document then discusses the adverse
health impacts resulting from exposure to lead. An overview is given on methods for
assessing lead exposure through measurement of blood lead concentrations and
environmental sampling. This document does not aim to provide technical details of
environmental sampling methods but refers the reader to other sources. Finally, brief
information is provided on control
measures to prevent the release of lead during recycling.

CONSIDERATIONS / 3
2. How lead exposure
occurs during
recycling and disposal
The main pathways of exposure to lead from recycling used lead-acid batteries arise
from environmental emissions. These occur at various stages in the recycling
process, as described below. Lead particles and fumes emitted into the air can be
inhaled and are also deposited onto soil, water bodies and other surfaces, including in
gardens and homes. Waste materials from lead processing can, if not treated and
correctly disposed of, contaminate land and water bodies. Used acid with high
concentrations of lead is often dumped on land or released into waterways. Lead can
enter the food chain through crops growing on contaminated land, from direct
deposition onto crops, through food animals foraging in contaminated areas and
consuming lead particles, and from
fish and shellfish living in lead-contaminated water (UNEP, 2003; UNEP, 2010).
2.1. Components of a lead-acid battery

A lead-acid battery is made up of the following components, enclosed within a plastic
or ebonite box or casing (see Figure 1) (UNEP, 2003). There are positive and negative
terminals made of lead, which provide the connection points to external devices. There
are sets of positive and negative plates kept apart by plate separators - porous sheets of
PVC or polyethylene plastic, glass microfibre, or phenolic resins that allow the free
movement of the ions in the electrolyte solution. The positive plates are grids made of
lead or lead alloy coated with porous metallic lead paste, and the negative plates are
lead grids coated with lead dioxide paste. A series of negative and positive plates plus
separators makes up a battery element, and the battery elements are separated by plates
of the same material as the battery box. The elements are bathed in a sulfuric acid
electrolyte solution, which can be topped up via the plugs. In sealed batteries
the electrolyte is either a gel or is soaked onto glass microfibre separators.

Figure 1. Components and structure of a lead-acid battery (UNEP, 2003)
positive terminal plugs negative terminal
connectors cap
sulfuric acid solution element separators
plate separators negative plates
box positive plates
battery elements
The average amount of lead in automotive batteries can range from 2 to 13 kg,
depending on the size of the vehicle (CEC, 2016).
2.2. Steps in the recycling process

Almost all parts of a lead-acid battery can be recycled. The main steps in the
recycling process are as follows: Almost all parts of a
lead-acid battery
• collection and transportation of the batteries to a recycling facility
can be recycled
• separation of the component parts of the batteries
• smelting and refining of the lead components
• washing then shredding or melting of the plastic components
• purification and treatment of the sulfuric acid electrolyte
• treatment and disposal of waste
The batteries are mechanically or manually broken up to separate out the acid and
component parts. The lead components are conveyed to the furnace for smelting. After
smelting the slag is removed and the molten unrefined lead may be poured into
moulds and cooled or it may immediately be directed to a holding kettle (cast-iron pot)
to keep it molten prior to refining. The aim of the refining process is to produce lead of
high purity or to produce alloys (requiring the addition of specific trace elements to the
refining kettle) that can be used to make a new lead battery. The molten lead is then
cast into moulds and
allowed to cool (OSHA, 2002).
Recyclable plastic components are washed then shredded or ground and

melted. The molten plastic is extruded into pellets, which can then be used

CONSIDERATIONS / 5
in the manufacture of other plastic goods, including new battery casings (ILA, 2015).
In many smaller recycling facilities in low- and middle-income countries,
the plastic battery cases are often not recycled and may be dumped or burned.
The electrolyte may be recovered for re-use or neutralized with alkali and treated to
remove lead and other contaminants before being released into the sewage system.
Alternatively the solution may be purified and sodium sulfate extracted
for use in making detergents and other products (UNEP, 2003; ILA, 2015).
At each of these stages, lead fumes and dust are released into the air (see section
Automated, enclosed
2.3), contaminating both the workplace and the wider environment. The use of
processes with
pollution control automated, enclosed processes with pollution control devices can
devices are necessary reduce these emissions.
to reduce In a typical automated enclosed process, the lead batteries are broken up in a
lead emissions hammermill or shredder and the pieces are fed into tanks filled with water. Here
gravity is used to separate the components: the lead and heavy materials sink to the
bottom and the plastics rise to the top. The plastic materials are skimmed away and
the liquid, including the sulfuric acid electrolyte is drawn off. The metallic components
are channelled to closed furnaces for smelting and refining and then piped into casting
moulds (OSHA, 2002; UNEP, 2003). Waste from recycling is collected, treated and
disposed of at a designated
waste disposal site (UNEP, 2003).
In a manual process the batteries are drained then broken up with electric saws,
machetes or axes. The components are separated by hand into piles. The lead
components are carried to the furnace or taken on an open conveyer belt. The furnace
may, in the worst case, be no more than an open pot on a fire (UNEP, 2003; UNEP,
2004; Manhart & Schleicher, 2015). The molten lead
is then poured into casting moulds.
2.3. Lead release and exposure during recycling

At the collection and transportation stage, the sulfuric acid electrolyte solution is
sometimes drained out to reduce the weight of the batteries or because a higher price
is offered for drained batteries (Manhart & Schleicher, 2015). If not done at this stage
then the electrolyte may be drained out at the recycling site (in some enclosed
processes the batteries are not drained prior to crushing). In addition, electrolyte may
leak out of damaged batteries during storage and transportation (UNEP, 2003). If
adequate precautions are not taken to avoid skin contact, the acid will cause
corrosive injury. The electrolyte contains dissolved lead and, if the electrolyte leaks
out or is poured onto the ground rather than into collection tanks, the lead becomes
incorporated into soil particles, which subsequently become a source of lead dust
(UNEP, 2003). Pouring the electrolyte into ponds or streams will contaminate water
that may be used for
drinking, fishing and cooking.

Figure 2. Schematic illustrating points at which lead is released during battery recycling
Draining Lead contamination of soil

electrolyte & water
Collection &
transport of Plastic / Toxic smoke including
batteries ebonite sulfur dioxide, dioxins,
components dibenzofurans.
burnt or Lead–contaminated waste
Breaking up dumped
batteries into
component
parts
Lead-containing
components Lead fragments and lead oxide
broken up dust dispersed into air and settle
on soil, other surfaces and
workers’ hair & clothes.
Surrounding environment
Conveying contaminated
broken battery with lead
parts to the
smelter
Lead fumes dispersed in air and

inhaled by workers. Fumes
Smelting and condense as particles that settle
rening on soil, other surfaces and
workers’
hair & clothes
Workers go
home without Lead dust carried home and
washing and contaminates domestic
changing environment
clothes
Manually breaking up the batteries releases lead particles and lead oxide dust, which
Manual recycling
are a source of lead exposure to the worker (Suplido & Ong, 2000; UNEP, 2003).
methods release
The dust and particles also settle in the surrounding soil and may be blown to more large amounts
distant areas, contaminating the wider environment and becoming a source of exposure of lead into
to the community (UNEP, 2003; Haefliger et al., 2009). Hammermills and shredders the environment
may release lead mist, which can dry and release lead dust if disturbed. Dust settled
on vibrating equipment can
become re-suspended in air and inhaled (OSHA, 2002).

CONSIDERATIONS / 7
During the separation process, water used in automated systems for separating lead
from other components becomes heavily contaminated with lead compounds. If this
leaks or is not treated before disposal it will contaminate the ground or soil. As this
water evaporates it leaves a residue of fine lead dust that may then
be dispersed by wind (UNEP, 2003).
When lead components are moved around the recycling site, e.g. on open conveyor
belts or in wheelbarrows, and when they are shovelled into the furnace,
lead fragments and dust are released.
The temperatures used for refining lead can be up to 1000 °C, which generates large
amounts of lead fume. If the furnace is not under negative pressure or if the plant has
inadequate ventilation and/or emission controls, the fumes will be inhaled by workers
(UNEP, 2003). Lead fumes are particularly hazardous as the small particle size enables
the lead to be inhaled into the lower respiratory tract and absorbed (ATSDR, 2007).
The fumes will eventually settle as lead particles on surrounding surfaces and the soil,
creating lead dust, which can also be inhaled. Fugitive lead emissions from these
sources can be substantial and are more difficult to control. Sometimes ash from the
smelting process is manually sifted to retrieve metal particles, dispersing lead-
contaminated dust
into the air (Paddock, 2016)
Fume, lead particles and dust released at various stages in the recycling process
Washing oneself and
will also settle on the skin, hair and clothes of workers. If workers do not wash and
changing clothes
before returning change clothes before returning home this lead becomes a source of take-home
home protects family exposure to household members and even, potentially, to the wider community
members from lead (Daniell et al., 2015). Lead poisoning in the spouses and children of lead workers,
exposure caused by transfer of lead from the workplace to
home, has repeatedly been documented (Baker et al., 1977; Chisolm, 1978).
2.3.1. Informal lead recycling

Non-regulated, informal (“backyard” or “cottage”) recycling practices occur in many
countries and have resulted in lead exposure and poisoning, with young children being
particularly at risk (Matte, 1991; Suplido & Ong, 2000; Haefliger et al., 2009; van der
Kuijp et al., 2013; Daniell et al., 2015). This practice is sometimes carried out in
urban areas with high population densities, meaning that a recycling operation has the
potential to affect a large number of people (Haefliger et al., 2009). There are few (if
any) pollution controls. Lead-containing waste products, such as electrolyte solution
and slag from the smelting process are often simply dumped, although slag may also be
sold on for further smelting. The work may be carried out by small family groups
around the home. Children often assist with dismantling the batteries and washing
components (van der Kuijp et al., 2013). Because the recycling process is done with
little knowledge of the toxicity of lead, and is conducted under poor conditions of
safety, health
and environmental controls, informal recycling is particularly likely to result

in environmental contamination and human exposure (UNEP, 2004; van der
Kuijp et al., 2013; Daniell et al., 2015).
Soil contaminated with lead compounds can spread throughout the community and be
Informal recycling is
tracked into homes. If recycling activities take place around the home, then airborne
particularly likely to
lead can enter the home and accumulate on the floor, on beds and on other furniture cause environmental
(Haefliger et al., 2009). Settled dust can be re-suspended in the air and inhaled as contamination and
people walk through or brush up the dust. Young children, who spend large amounts human exposure
of time on the ground and who frequently put their hands and other objects in their to lead
mouths, are at particularly high risk
of lead exposure in these settings.
If the plastic components are inadequately washed before re-use for other products,
then these products will be contaminated with lead (Manhart & Schleicher 2015).
Battery casings may be used around the home as a construction material or as
containers, again introducing the possibility of lead
contamination (Daniell et al., 2015).
There have been reports in Cameroon and other countries of lead scrap from
informal recycling being mixed with scrap aluminium to make cooking pots
(CREPD, 2015). Lead can leach out into food being prepared or stored in these
pots (Weidenhamer et al., 2014;
Weidenhamer et al., 2017).
2.4. Other chemicals released during recycling

While the focus of this document is on the release of lead, there
are a number of other hazardous chemicals that can be
released during recycling. In addition to the lead terminals and
plates, batteries contain various plastics or hard rubber
(ebonite) and the sulfuric acid electrolyte solution. The lead
components may contain other elements such as arsenic,
antimony, barium and cadmium (UNEP, 2003). These
substances may form part of the waste and emissions generated
at various stages of the recycling
process. The rubber and plastic components may be burned rather than recycled,
producing toxic gases, including sulphur dioxide, chlorine, dioxins
and dibenzofurans (UNEP, 2003).
2.5. Studies of lead exposure from recycling lead-acid batteries

Recycling lead-acid batteries can result in significant occupational exposure to lead.
Were et al. (2012) investigated a lead-acid battery recycling plant in Kenya and found
elevated concentrations of lead in the air and elevated blood lead concentrations in
workers. The study identified a number of weaknesses
in work practices and control measures that resulted in excessive exposure

CONSIDERATIONS / 9
to lead. Examples included inadequate engineering controls (including poor ventilation
systems) and inadequate personal hygiene measures (including lack of respiratory
protection and failure to use washing facilities). Among workers involved in recycling
lead-acid batteries there is often poor general awareness
of the hazards of lead (CREPD, 2015).
A review of published literature on exposures from formal-sector lead-acid battery

manufacturing and recycling plants in developing countries found that seriously
elevated blood and airborne lead concentrations were common (Gottesfeld & Pokhrel,
2011). In workers involved in battery recycling the arithmetic mean blood lead
concentration was 64 µg/dL, with a range of 37.7 to 112.5 µg/dL. This contrasted with
data from developed countries where few workers had blood lead concentrations above
50 µg/dL and most were below 25 µg/dL (though even these concentrations are likely
to result in adverse health effects – see section 3.2). The review also found that high
airborne lead concentrations were reported in recycling facilities, with a mean value of
367 µg/m3. This is 7 times higher than the permissible exposure limit of 50 µg/m3 as
an 8-hour
time-weighted average (TWA) adopted in the USA (OSHA, 1978).
Communities living near recycling facilities are at risk of exposure to lead, and
extensive contamination of soil surrounding many formal sector recycling plants has
been reported (Levallois et al., 1991; Wang et al,. 1992; Zhang et al., 2016). In their
review, Gottesfeld & Pokhrel (2011) summarized 11 studies in seven countries on
lead exposure of children residing near lead battery manufacturing and recycling
facilities and reported an average blood lead concentration of 29 µg/dL, with values
up to 71 µg/dL. Recently a large recycling plant in the USA was closed down after it
failed to meet emission controls and waste management standards. This plant was
found to have contaminated the surrounding area with lead to a distance of 1.7 miles
(California Environmental
Protection Agency, 2015).
The case studies given below illustrate how environmental contamination caused by the
recycling of used lead-acid batteries can result in severe lead poisoning in a community,
which may continue even after recycling operations have stopped. The first case
describes exposure to lead via reclamation of lead and lead compounds from
discarded batteries, and the health consequences. The other two case studies show that
closing down or moving battery recycling operations
are not sufficient measures on their own to prevent human lead exposure.
2.5.1. Senegal
Between November 2007 and March 2008, 18 children died from an aggressive central
nervous system disease of unexplained origin in a neighbourhood of Dakar in Senegal
(Haefliger et al., 2009). One of the possibilities considered
was lead intoxication, as the mothers of some of the children were engaged

in the recycling of used lead-acid batteries. Informal lead recycling in the region
had been taking place since 1995 and various lead compounds had accumulated in
the sandy soil over time. Around October 2007, some local residents realised that the
accumulated lead in the soil could be sieved and sold. They therefore started to collect
lead-enriched soil in sacks, which they
brought into the community, sometimes even inside their homes.
An investigative mission was sent to work with the local health authorities in
investigating the deaths. For cultural reasons it was not possible to conduct autopsies
and post-mortem testing on the children who had died and, therefore, the mission team
focused their investigation on the siblings and mothers of the children. Another group
of children and adults, who were living in the same community but apparently
unrelated to the deceased children, were also investigated to evaluate the extent of
lead intoxication in the area. In total 81 individuals were examined and tested and all
were found to be poisoned, often severely, with lead. In the children blood lead
concentrations ranging from 39.8 μg/dL to 613.9 μg/dL were found (levels above 45
μg/dL indicate
potentially serious poisoning).
Environmental investigations found that homes and soil were heavily contaminated with
lead. Lead concentrations in outdoor soil were up to 302 000 mg/kg and indoor
concentrations were as high as 14 000 mg/kg. For comparison, the US EPA standard
for soil in a children’s play area is 400 mg/kg and for other residential areas it is
1200 mg/kg (US EPA, 2001). The exposure pathway was most likely via inhalation
and/or ingestion of the contaminated soil and dust in suspension as young children
were playing on contaminated ground. This indicated that other inhabitants of the
affected area (about 940 people, of whom 460 were children and adolescents) might
also be poisoned with lead. While the causes of death of the 18 children could not be
confirmed, circumstantial evidence, including heavy environmental contamination and
the high blood lead concentrations in siblings suggest that most, if not all, of the
children died because of encephalopathy as a result of severe lead poisoning. To
prevent further exposures the homes were cleaned and contaminated soil was removed
and replaced with cleaner soil. A public awareness campaign
was also carried out to encourage a change in recycling practices.
2.5.2. Dominican Republic

In Haina, Dominican Republic, a lead screening survey was carried out in 116
children living close to a lead-acid battery recycling smelter (Kaul & Mukerjee, 1999).
Very high blood lead concentrations were found with a mean value of
71 µg/dL. Shortly afterwards the government closed down the recycling plant.
Six months later a follow-up survey was conducted in 146 lead-poisoned children
in the same community (Kaul et al., 1999). This found that although the blood

CONSIDERATIONS / 11
lead concentrations had reduced significantly, with a mean of 32 µg/dL (range 6 to
130 µg/dL), they were nevertheless still high. Only 9% of the children had blood lead
concentrations below 10 µg/dL and 28% of the children had blood lead concentrations
above 40 µg/dL. For comparison, a survey was also carried out in 63 children living in
a nearby community, which had similar demographic characteristics but no smelter.
Here the mean blood lead concentration was
14 µg/dL (range 20 to 99 µg/dL) and 42% of children had levels <10 µg/dL.
An environmental assessment found that, although the smelter had shut down, metallic
scrap and mixed residual soil and solid materials were still scattered around. Some
clean-up activities had begun during the time of visit; however, an assortment of waste
materials remained at the site and continued to be a hazard to the neighbourhood. The
authors concluded that although closing the battery recycling facility significantly
lowered blood lead concentrations of children, the children were still exposed to lead
through their environment
(Kaul et al., 1999).
In 2008 and 2009 some remediation activities were carried out to remove
contaminated soil and educational sessions were given to local children to help
minimize their exposure to lead dust and materials (Blacksmith Institute, 2009).
2.5.3. viet Nam

Dong Mai village in northern Viet Nam has been a centre for
recycling lead-acid batteries since the 1980s. A study
in 2006–2007 found elevated exposures to lead, and
efforts were subsequently made to move household
recycling operations to an industrial
zone 1 km outside the village. The zoning was
formalised by 2010, though some home-based
recycling continued in a few households. A
study was subsequently carried out over a one-
year period from December 2011 to assess lead
exposure
in children and environmental levels of
lead (Daniell et al., 2015). All 109
children tested were found to have
elevated blood lead concentrations,
ranging from 12 to >65 µg/dL, with 28%
having concentrations >45 µg/dL. The
blood samples were measured using the
LeadCare analyser, and a sample of the
higher results were rechecked using
laboratory analysis of venous
samples. This generally gave lower

values, but of 24 retested samples 80% were still above 45 µg/dL. Higher blood
lead concentrations were associated with home recycling or parents
currently involved in recycling in the industrial zone.
Environmental investigations showed legacy soil contamination in areas where

recycling had previously been carried out, with a mean lead concentration of 2500
mg/kg. In other areas soil levels were lower though still high, at a mean of 1000
mg/kg. By contrast, soil lead concentrations at the school were very
low with a mean of 34 mg/kg.
Surface lead contamination was tested in 11 homes and a mean value of 95 µg/cm2
was found, considerably higher than the US EPA standard for dust on household floors
of 0.043 µg/cm2 (US EPA, 2001). Higher concentrations were found in homes with
active recycling compared with those where recycling was no longer carried out. In
these latter homes the highest concentrations were found around washing areas and
in some kitchen and living areas. This suggested take-home lead contamination,
with washing done at home rather than at the workplace. While surface contamination
with lead was lower at the school, though still high at 41 µg/cm2, four sleeping mats
were found to have lead contamination at a mean of 221 µg/cm2. This suggested that
children
had brought lead to school on their shoes and clothing.

CONSIDERATIONS / 13
3. Main routes of
lead exposure and
health effects
The health impacts of lead exposure, including low-level exposure, have been
extensively reviewed and are summarized here (ATSDR, 2007; JECFA, 2011; NTP,
2012; Health Canada, 2013). Young children, pregnant women and
women of childbearing age are particularly vulnerable to the toxic effects of lead.
3.1. Routes of exposure to lead

The main routes of exposure and absorption of lead are inhalation, ingestion and, to a
Inhalation and much lesser extent, dermal contact (ATSDR, 2007). Inhalation of fumes and dust is
ingestion are the a major route of exposure for people working with lead. Young children are particularly
main routes of likely to be exposed through contaminated soil and air-borne household dust because
lead exposure they spend a lot of time in one place, tend to play on the ground, and have frequent
hand-to-mouth activity (WHO, 2010a). Children with pica, a compulsion to eat non-
food substances, may persistently eat lead-contaminated soil (Mielke & Reagan, 1998).
Lead exposure may also
occur from consumption of contaminated food and water.
The absorption of lead from the gastrointestinal tract is affected by dietary factors,
age and nutritional status (JECFA, 2011). Infants and young children absorb
proportionately more lead than adults, typically absorbing around 50% of ingested
lead compared to around 10% in adults (WHO, 2010a). The absorption of lead is
also greater in people with dietary deficiencies of iron or calcium, which may be
widespread in economically deprived communities. Once absorbed, lead is distributed
to most organs of the body, including the central nervous system, liver and kidneys,
but the largest proportion (up to
90% in adults) is stored in bone (Barry, 1975).
Lead accumulates in bone over life up to age 50 to 60 years, followed by a decline

due to age-related changes in diet, hormonal concentrations and
metabolism (Mushak, 1993). There is an equilibrium between the amount of

lead in blood and bone, and some lead is gradually released back into blood over time
(Rabinowitz, 1991). Lead in bone does not cause toxic effects but it becomes a
potential source of toxicity when metabolic changes cause more rapid release. This can
occur during pregnancy, lactation, the menopause and following bone fracture
(Silbergeld et al., 1988; Markowitz & Weinberger, 1990; Mushak, 1993; Gulson,
2003). If the blood lead is reduced, e.g. following
chelation therapy, some lead will be released from bone to restore the equilibrium.
Lead readily crosses the placenta exposing the fetus. The lead concentrations
in maternal and fetal blood are similar (Graziano, 1990; WHO, 1995).
Lead is present in breast milk from external sources of exposure or remobilized from
skeletal stores, though the concentrations in breast milk are low (Ettinger
et al., 2004; Ettinger et al., 2014).
3.2. Toxic effects of lead

Lead has no apparent physiological function. It has an affinity for sulfhydryl groups
and other organic ligands in proteins and can mimic other biologically essential metals,
such zinc, iron and, in particular, calcium (Health Canada, 2013). This enables lead to
disrupt enzyme systems dependent on these ions, accounting for many of its toxic
effects (Lidsky & Schneider, 2003; Garza et
al., 2006).
The toxic effects of lead are wide-ranging and affect almost all body systems. Acute
The toxic effects
lead poisoning from a single exposure is relatively rare and chronic poisoning is
of lead are
more common; however, the clinical features of poisoning are similar in both cases. wide-ranging and
The presenting signs and symptoms are very variable in both adults and children and affect almost all
may include gastrointestinal, haematological and neurological effects. Young children body systems
are particularly vulnerable to the neurological toxicity of lead and this is the main
reason that lead is of public health concern. Lead also has toxic effects on the
reproductive, endocrine and cardiovascular systems. Important toxic effects are
summarized below
by body system.
The duration of illness in lead poisoning may be long and periodic, requiring the
monitoring of blood lead concentrations and repeated courses of antidotal
chelation therapy.
3.2.1. Gastrointestinal effects

Gastrointestinal effects are common in lead toxicity and may be the reason that an
exposed person first seeks medical attention. The effects include loss of appetite with
weight loss, constipation, abdominal pain or discomfort, nausea, vomiting and a
metallic taste in the mouth. Diarrhoea occurs occasionally
(Winship, 1989). Lead colic (intense, painful, intermittent abdominal cramps)

CONSIDERATIONS / 15
is associated with severe constipation and vomiting, and can be mistaken for other
conditions such as appendicitis, peptic ulcer, pancreatitis or intestinal obstruction
(Janin et al., 1985). Gastrointestinal bleeding has occasionally
been reported (McNutt et al., 2001; Frith et al., 2005).
Patients with poor dental hygiene may have a ‘lead line’ (Burton or blue line) along the
gums (ten Bruggenkate et al., 1975). This line is composed of dark granules of lead
sulfide precipitated by the action of hydrogen sulfide (from bacterial degradation of
organic matter) on lead. There may also be grey spots
on the buccal mucosa and on the tongue (ten Bruggenkate et al., 1975).
3.2.2. Neurological effects

Lead exerts toxic effects in all parts of the nervous system. Lead poisoning can cause
life-threatening encephalopathy (disruption of brain function), particularly in young
children. Encephalopathy is less commonly seen in adults (ATSDR, 2007). Initial
signs include sporadic vomiting, loss of appetite, behavioural changes with
aggression, irritability and agitation, headache, clumsiness and intermittent lethargy.
This may progress to persistent vomiting, ataxia, convulsions,
severe cerebral oedema, raised intracranial pressure, coma and death.
Lead encephalopathy is a life-threatening condition and children can be left with mental
retardation, seizure disorders, blindness and hemiparesis (weakness of the entire left or
right side of the body) (Perlstein & Attala, 1966; Chisolm & Barltrop, 1979; Al
Khayat et al., 1997). Such severe impacts are now relatively uncommon in developed
countries but can still be seen in places where there are high levels of exposure and
limited or no access to diagnosis and treatment (Haefliger et al., 2009; Greig et al.,
2014). Analysis of a large case series of lead-poisoned children in Nigeria found that
concurrent infection with malaria
increased susceptibility to the neurotoxic effects of lead (Greig et al., 2014).
Chronic lead toxicity may also cause more subtle changes in neurological function in
children and adults. There is a large literature on the neurodevelopmental toxicity of
lead in children (Lidsky & Schneider, 2003; Bellinger, 2004a; Koller et al., 2004;
Needleman, 2004; NTP, 2012). The effects include reduced cognition and
behaviour scores, changes in attention (including attention deficit hyperactivity
disorder), impaired visual-motor and reasoning skills, and impaired social behaviour and
reading ability. Some of these effects have been found to persist into later childhood
and adulthood (Needleman et al., 1990; Fergusson & Horwood, 1993; White et al.,
1993; Tong et al., 1996; Fergusson et al., 1997; Tong, 1998; Tong et al., 1998;
Stokes et al., 1998). Delinquent behaviour has also been associated with lead exposure
(Needleman et al., 1990; Needleman et al., 1996; Dietrich et al., 2001; Wright et al.,
2008). Poor scores for social/ emotional functioning have been reported in preschool
children (Mendelsohn
et al., 1998).

Even low levels of exposure, and blood lead concentrations below 5 µg/dL, can be
Studies suggest
associated with neurological damage in children (NTP, 2012). Indeed, studies to date
there may be no
suggest that there may be no threshold blood lead concentration for neurotoxic effects safe threshold of
in children and that the association between blood lead concentration and IQ may be lead exposure
non-linear (JECFA, 2011). A pooled analysis by Lanphear et al. (2005) found a steeper
decline in IQ in children with maximal blood lead concentrations below 7.5 µg/dL
compared with those having maximal
blood lead concentrations above 7.5 µg/dL.
In adults, case reports and small studies describe a higher incidence of malaise,
forgetfulness, headache, fatigue, lethargy, irritability, dizziness and weakness in
occupationally exposed adults (ATSDR, 2007). Lead exposure may also be associated
with a greater risk of neuropsychiatric and neurobehavioural problems (Valciukas et al.,
1978; Williamson & Teo, 1986; Stollery et al., 1991; Chia et
al., 1997; Bleecker et al., 2005; Chen et al., 2005; Schwartz et al., 2005).
Lead can cause both motor and sensory neuropathy. In individuals with severe, chronic
lead toxicity wrist drop and foot drop (inability to extend the wrist or foot) may be
seen. These effects are more commonly observed in adults than children with lead
toxicity (ATSDR, 2007). Motor weakness usually resolves once the individual is
removed from exposure but this may not be the case
with sensory neuropathies (Rubens et al., 2001).
Poor postural stability has been reported in children with mildly elevated blood lead
concentrations (Bhattacharya et al., 1990) and in lead-exposed workers
(Chia et al., 1996; Ratzon et al., 2000; Iwata et al., 2005).
Lead may also cause visual impairment and reduced hearing (Cavalleri et al., 1982;
Otto & Fox, 1993; Rothenberg et al., 2002). Hearing impairment in children may
occur even with blood lead concentrations below 10 µg/dL
(NTP, 2012).
3.2.3. Cardiovascular
Lead exposure is associated with an increased risk of hypertension in adults and
pregnant women, even at levels of exposure below 10 µg/dL (NTP, 2012). Significant,
though modest, associations have been found between lead concentrations in blood
and bone and blood pressure (Cheng, 2001; Nawrot et al., 2002; ATSDR, 2007). The
association is stronger with bone lead, suggesting that the increase in blood pressure is
related to the long-term effects of lead
exposure earlier in life (Cheng, 2001; Gerr et al., 2002).
3.2.4. Renal
Lead can cause damage to the renal tubules with impairment of renal function;
however, acute renal damage is usually reversible (Green et al., 1976; Chisolm

CONSIDERATIONS / 17
& Barltrop, 1979); Wedeen, 1988; Loghman-Adham, 1997). Chronic lead
exposure may cause a progressive nephropathy (Loghman-Adham, 1997). The onset
of lead-induced renal impairment is subtle and patients may remain asymptomatic until
there is significant renal dysfunction (Loghman-Adham, 1997). Even low levels of
exposure to lead can be associated with abnormalities
in renal function (NTP, 2012).
3.2.5. Endocrine
Environmental lead exposure has been associated with delays in sexual maturity in girls
(Selevan et al., 2003; Wu et al., 2003; NTP, 2012). Lead exposure has also been
associated with delays in growth and reduced growth (e.g. smaller
stature, smaller head circumference) in children (NTP, 2012).
3.2.6. Reproductive system and pregnancy

Impotence and decreased libido are occasionally reported in lead-poisoned patients
(Cullen et al., 1983). Reduced fertility has been found in couples during periods
when the blood lead concentration in the male is elevated (JECFA, 2011). Possible
causes include reduced sperm motility, decreased
sperm count and reduced semen volume (NTP, 2012).
Lead has long been known to be harmful in pregnancy and has been used as an
abortifacient (Bastrup-Madsen, 1950). Maternal lead exposure, even at low levels, may
be associated with reduced fetal growth, lower birth weight, preterm birth and
spontaneous abortion (NTP, 2012; Health Canada, 2013). Lead exposure is a risk
factor for hypertension in pregnancy (gestational hypertension) and high levels of
exposure may be a risk factor for pre-eclampsia, which can be
life-threatening for both the mother and baby (Troesken, 2006; CDC, 2010).
3.2.7. Haematological
High levels of exposure to lead reduce the synthesis of haem, which is necessary for the
production of red blood cells, resulting in anaemia (ATSDR, 2007). Coarse
basophilic stippling of red blood cells may be seen, though this is not found in all
patients with lead poisoning. Interference with haem synthesis also has other negative
impacts, for example haem is needed for the formation of cytochrome c, which is
essential for cellular respiration, and this may contribute
to the neurotoxicity of lead (ATSDR, 2007).
3.3. Toxic effects in relation to blood lead concentrations

The most widely used method for assessing exposure to lead is the measurement of lead
in whole blood (see section 6.1). There is, however, considerable inter-individual
variation in the blood lead concentration at which specific signs of poisoning
manifest. Some individuals may apparently be clinically well at
blood lead concentrations that are associated with encephalopathy in others

(Bellinger, 2004a). This also applies to subclinical effects such as effects on IQ,
meaning that children with the same blood lead concentration do not necessarily have
the same risk of impaired neurodevelopment (Bellinger, 2004a). Table 1 summarizes
information on toxic effects that have been reported at specific
blood lead concentrations and illustrates some of the variability in response.

CONSIDERATIONS / 19
Table 1. Association of subclinical and clinical effects with blood lead concentrations
Blood lead concentration Health effect Reference

Children:
• Decreased IQ, cognitive performance and academic achievement
• increased incidence of problem behaviours and diagnosis of attention deficit
hyperactivity disorder
• Reduced fetal growth (based on maternal blood lead concentration) All ages:
<5 µg/dL
• Impaired renal function,
• Reduced synthesis of delta-aminolevulinic acid dehydratase (ALAD),
contributing to anaemia
Children:
• Delayed puberty
Adults: NTP, 2012
• Hypertension
• Increased cardiovascular-related mortality (based on limited evidence) •
Spontaneous abortion (based on maternal blood lead concentration)
(based on limited evidence)
<10 µg/dL • Preterm birth (based on maternal blood lead concentration) (based on
limited evidence)
Children:
• Anaemia
Children:
• Reduced nerve conduction velocity
>20 µg/dL Children: Schwartz et
• Decreased haemoglobin synthesis al., 1990
Adults:
>30 µg/dL
• Peripheral neuropathy
• Neurobehavioural effects
• Abdominal colic
Adults:
>40 µg/dL • Decreased haemoglobin synthesis
Children: ATSDR, 2007
• Severe neurological features
Children:
• Abdominal colic
>50 µg/dL Children:
• Features of acute poisoning but no encephalopathy
>50 µg/dL (= lowest concentration in
children with malaria) Children:
• Encephalopathy Greig et al., 2014
>60 µg/dL • Severe neurological features
(= lowest concentration; mean 178 µg/
dL) NAS, 1972 quoted
• Death in ATSDR, 2007
(= lowest concentration, mean 330 µg/
dL)
>105 µg/dL
(= lowest concentration in children
without malaria)
Greig et al., 2014
≥150 µg/dL
NAS, 1972
quoted in
>216 µg/dL (= lowest concentration,
ATSDR, 2007
range 216-460 µg/dL)
Thurtle et
al., 2014

4. The public
health impact of
lead exposure
At a population level the main impacts of lead exposure arise from its effects on
neurocognitive development in children and on cardiovascular disease
in adulthood.
In children the greater risk of reduced cognitive ability, IQ, attention and visual-motor
and reasoning skills, as well as impacts on social behaviour all contribute to an
increased public health and economic burden. While the estimated IQ decrease in
children from lead poisoning is small (6.9 points over the blood concentration range
2.4 to 30 µg/dL), the impact at the population level can be important (Bellinger,
2004b; Lanphear et al., 2005). It is estimated that a mean IQ reduction of 3 points
from 100 to 97 would increase the number of individuals with an IQ below 100 by 8%
and there would be a 57% increase in individuals with an IQ below 70 (commonly
considered the cut-off for identifying individuals with intellectual disability). There
would also be a 40% reduction in potentially high-achieving individuals with an IQ
score greater than 130
(Bellinger, 2004b; JECFA, 2011).
In the case of blood pressure, a review by Healey et al. (2010) estimated that for the
Canadian population a change in blood lead concentrations in adults from 1 µg/dL to
4 µg/dL would be associated with an estimated increase in mean systolic blood
pressure of approximately 0.8 mmHg (0.11 kPa) among Caucasian males and 1.4
mmHg (0.19 kPa) in susceptible subpopulations. While the impact at the individual
level is small, increases in blood pressure are associated with age-specific increased
mortality rates for both ischaemic
heart disease and stroke (Lewington et al., 2002; Fewtrell et al., 2003).
Based on 2015 data, lead exposure is estimated to account for 12.4% of the global
burden of idiopathic intellectual disability, 2.5% of the global burden of
ischaemic heart disease and 2.4% of the global burden of stroke (IHME, 2016).

CONSIDERATIONS / 21
5. Economic impact
of lead exposure
in countries
The economic impact of lead exposure is made up of direct and indirect costs. Direct
The economic costs
costs include those associated with screening and the medical care of acute and chronic
attributable to the
effects of lead on lead poisoning, as well as the provision of special education, and managing juvenile
intellectual delinquency and other criminal behaviours. Indirect costs reflect the economic burden
development on society from a variety of factors including reduced intelligence and the consequent
in children are reduction in economic productivity
estimated to be and tax revenue.
1.2% of global
Trasande & Liu (2011) estimated that the total annual cost of lead poisoning in the
GDP (Attina &
Trasande, 2013) USA due to lost economic productivity was US$ 50.9 billion in 2008. There was an
estimated US$ 5.9 million in medical care costs. In France, Pichery et al. (2011)
estimated that lost lifetime earnings as a result of lead exposure in children amounted
to €53.9 billion (US$ 69.8 billion at 2008 values). In Europe, Bartlett & Trasande
(2014) estimated economic costs attributable to lead exposure to be around US$ 57
billion, based on estimated IQ losses
and impact on economic productivity.
The estimated economic costs attributable to the neurodevelopmental impacts of

childhood lead exposure amounted to 1.2% of global gross domestic product
(GDP) in 2011 (Attina & Trasande, 2013). Expressed in terms of loss to regional GDP,
the estimated cost in Africa was 4.03%, in Latin America and
the Caribbean 2.04%, and in Asia 1.88% (Attina & Trasande, 2013).

6. Assessment of
lead exposure
Exposure assessment is one component of the risk assessment process that culminates
in the characterization of the health risks posed by a chemical to a population (WHO,
2010b). An investigation of lead exposure from recycling should involve identification
or confirmation of the source(s) of exposure, determination of the routes and the
media by which exposure is occurring, and assessment of the severity and associated
health impacts of exposure. Confirmation of exposure and determination of severity
and the need for treatment involves measurement of the blood lead concentration,
together with a medical examination for signs and symptoms of lead poisoning. The
source(s) of exposure can be identified by taking an exposure history and by carrying
out environmental investigations.
6.1. Blood lead measurements

Lead can be measured in a range of human tissues and fluids, including hair, teeth,
bone, blood and urine; however, measuring the concentration of lead in whole blood is
the most accepted tool for screening, diagnostic and management purposes (WHO, The blood
2011a). This is because there is a large body of information linking blood lead lead concentration
concentrations with clinical effects and treatment outcomes. Moreover, validated is the most accepted
analytical methods and reliable blood quality-control and tool for screening,
reference materials are available (Barbosa et al., 2005; CLSI, 2013). diagnosis and
management of
Analytical techniques include point-of-care devices and laboratory-based methods, lead exposure
and information about the use of these methods can be found in the WHO
publication Brief guide to analytical methods for measuring lead in blood (WHO,
2011a). The choice of method is determined by the available resources and the
specific needs of the study in terms of limit of detection,
number of samples to be analysed and turnaround time.
Point-of-care testing for lead involves the use of a portable analytical device that can
be taken and used near the site of exposure or patient care. These
devices can analyse very small samples taken from a capillary by finger-prick

CONSIDERATIONS / 23
or from a vein. They have a limited operating range and are most suitable for screening
purposes: an elevated blood lead concentration should be confirmed
by a laboratory method (WHO, 2011a).
The advantages of a point-of-care device are that: 1) it does not require skilled
laboratory personnel for its operation; 2) it can be used at locations where transport
of blood samples to an appropriate reference laboratory is difficult; and 3) the result
can be provided within a few minutes. It is extremely important that steps are taken to
avoid lead contamination. If the device is to be used in the field then it should be set
up in a clean room with adequate precautions
to prevent ingress of dust.
Laboratory-based methods for measuring blood lead concentrations have greater

accuracy and a lower detection limit, potentially as low as 1-2 µg/dL with some
methods. Examples include atomic absorption spectrometric (AAS) methods, such as
graphite furnace atomic absorption spectrometry (GFAAS), and inductively coupled
plasma mass spectrometry (ICP-MS) (WHO, 2011a). An advantage of GFAAS and
ICP-MS is that they can measure very small samples, in the range of 10–
50 µL, which is useful when testing young children. The more advanced laboratory-
based methods are, however, more expensive
to buy and run and require specific laboratory expertise.
For all analytical methods some basic principles should be observed. Blood sampling
should be performed by a trained health-care worker (WHO, 2010c). Universal
biosafety precautions should be observed to avoid transmission of infection. With
both venous and capillary sampling there is a risk of lead contamination from the
skin. Sample collection should take place in a clean, lead-free environment and the
puncture site should be thoroughly cleansed beforehand (CDC, 2013). Venous blood
should be collected into tubes containing anticoagulant, preferably EDTA (CLSI, 2013).
All sampling equipment should be of good quality and certified free from trace metal
contamination. If blood samples need to be transported they should be kept cool, either
with cool-packs in an insulated container, or refrigerated until analysis (CLSI, 2013).
For point-of-care analysers, note should be taken of any specific temperature
requirements for sample storage. Care should be taken to avoid lead contamination of
samples
during storage, transportation and analysis.
When choosing a laboratory, it is important to ensure that it has an adequate quality

management system in place. Ideally the laboratory should be accredited by a
recognized body and should participate in a proficiency-testing scheme for blood lead
analysis. An example of such a scheme is the Lead and Multi-element Proficiency
Program (LAMP)1, which is provided by the US Centers
for Disease Control and Prevention free-of-charge to laboratories around the
1 https://www.cdc.gov/labstandards/lamp.html

world. Participation in LAMP does not provide accreditation but it is a means
for monitoring laboratory performance.
No safe level of lead exposure has been identified; therefore, to determine the blood
lead concentration that indicates excessive exposure the value can be compared to a
reference value for the population as a whole. This is usually the geometric mean
blood lead concentration found in the highest 2.5% or 5% of the population, i.e.
the 97.5th or 95th percentile respectively. In the USA, for example, for children
under six years the reference value is currently 5 µg/dL, which is the 97.5th percentile
blood lead concentration (CDC, 2012). This same concentration is the 98th percentile
value for children under 7 years in France (Haut Conseil de la santé publique, 2014).
Germany has adopted reference values of 3.5 µg/dL for children aged 3-14 years, 7
µg/dL for women
and 9 µg/dL for men (Wilhelm, 2010).
6.2. Taking an exposure history

As part of an investigation into an
individual’s exposure to lead, a
thorough environmental and
occupational history should be
taken. This should include
questions about the following
potential sources of exposure:
• individual’s occupation,
work practices and those of
co-habitants;
• participation in, or proximity to,
lead recycling activities or
manufacturing with recycled lead
(e.g. fishing weights);
• hobbies that might involve
lead exposure;
• use of traditional medicines;
• diet and the possible consumption of
foods cultivated on contaminated land or
collected from contaminated water
bodies; and
• source of drinking-water, e.g. piped water
supply, wells, river etc.
Examples of approaches to history-taking are provided by the US Agency for

Toxic Substances and Disease Registry (ATSDR, 2015) and WHO (WHO, 2010a).

CONSIDERATIONS / 25
6.3. Environmental assessment
Lead battery recycling is associated with significant environmental contamination and
therefore investigations of off-site contamination are warranted in the vicinity of these
facilities. Potential environmental pathways of exposure include soil and dust, air,
water and food, and all of these media can be analysed for lead. In most cases there are
guideline or reference values or regulatory standards to compare analytical results
against, which will give an indication of the
importance of that pathway to exposure.
6.3.1. Soil and dust

Soil and dust samples can be collected and sent to a laboratory for analysis, or
concentrations can be measured in situ using an X-ray fluorescence (XRF) device that
reports results almost immediately. A strategy should be devised that ensures
collection of a representative set of samples. Account should be taken of possible
dispersion of lead-contaminated soil from a recycling site to a wider area by wind or
floodwaters. A recent publication by the US Centers for Disease Control and
Prevention provides guidance on planning and conducting an environmental survey of
lead contamination (Hodge et al., 2015). Guidance on soil sampling is also provided by
Demetriades & Birke (2015). Documenting a geographical positioning system (GPS)
reading at each sample location greatly
assists in mapping areas of high and low contamination.
Standards for lead in soil exist in a number of countries, and at least one country,
the USA, also has standards for lead in household dust. A global review of
standards for lead in residential soil found values ranging from 50 to 400 mg/kg
(Jennings, 2013). The standard for non-residential soils may be higher. In the USA,
for example, the federal standard for residential soil in areas where children play is 400
mg/kg (US EPA, 2001). The USA standard
for lead in household floor dust is 0.043 µg/cm2 (US EPA, 2001).
6.3.2. Air
As described above, various stages in the recycling process can
result in the release of lead fumes and particles in the air. Studies
have shown that there is high airborne lead exposure in lead-acid
battery recycling facilities
(Gottesfeld & Pokhrel, 2011; Were et al., 2012). Airborne lead
concentrations have been shown to correlate with blood lead
concentrations in workers (Were et al., 2012). Airborne lead
eventually settles and contaminates
surrounding surfaces.
In an occupational setting there are two ways of measuring

airborne lead levels: area air sampling and personal
sampling. Area air sampling involves placing a pump in

the work area being tested. The pump runs for a specific period of time (usually
corresponding to the normal working day) at a specific flow rate. Air sampling can
provide a general overview of the air quality and helps to determine whether
further (personal) sampling is needed (US EPA, 1993).
A personal air sampling pump is worn by an individual to assess their exposure to lead
over a period of time, e.g. a working day (US EPA, 1993). This method monitors air
concentrations in a worker’s breathing zone to measure representative employee
exposures. The equipment comprises a battery-operated pump and sample medium,
which the individual can wear, for example, hung from their belt. A tube is attached to
the pump and the other end of the tube is clipped at the collar area close to the person’s
breathing zone. Samples are then taken
to a laboratory for analysis of total lead.
Examples of workplace exposure limits for airborne lead are given below: • Australia:
0.15 mg/m3 as an 8-hour time-weighted average (Safe Work
Australia, 2013)
• European Union: 0.15 mg/m3 as an 8-hour time-weighted average (EC, 1998)
• Mexico: 0.05 mg/m3 as an 8-hour time-weighted average, 40 hours per week
(CEC, 2016)
• USA: 0.05 mg/m3 as an 8-hour time-weighted average (OSHA, 1978).
A number of countries have ambient air quality standards for lead concentrations in the
outdoor environment. The guideline value set by WHO for the annual mean
concentration is 0.5 µg/m3 (WHO, 2000) but it should be noted that this is not a
health-based standard. A detailed discussion of methods for monitoring pollutants,
including lead, in ambient air can be found in the WHO publication Monitoring
ambient air quality for health impact assessment (EURO, 1999).
Examples of national standards are:
• Australia: ambient air quality standard: 0.5 µg/m3 averaged over one year (NEPC,
2016)
• China: ambient air quality standard: 0.5 µg/m3 averaged over one year, with a
seasonal limit of 1 µg/m3 (MoEP, 2012)
• EU limit value: 0.5 µg/m3 averaged over one year (EC, 2008)
• US National Air Ambient Quality Standard: 0.15 µg/m3, 3-month average
concentration (US EPA, 2016).
6.3.3. Food and water

Foods that could become contaminated with lead include fruit and vegetables
(especially leafy vegetables) grown on land close to recycling activities, foraging
animals such as goats, sheep, pigs and poultry, and fish and shellfish caught
from waters contaminated with recycling waste.

CONSIDERATIONS / 27
A common source of water contamination in piped water supplies is the use of lead
materials in the water distribution system; however, this is outside the scope of this
document. Lead-acid battery recycling can contaminate surface waters that are used
for drinking, cooking and bathing. Dissolved lead can
percolate through soil into groundwater (UNEP, 2004).
If the exposure history suggests that consumption of contaminated food and/ or water
is a source of exposure then these can be analysed. The Codex Alimentarius
provides a list of maximum permissible levels of lead in selected foods (FAO, 2016).
Most countries have a drinking-water standard for lead and
the WHO guideline value for drinking-water is 10 µg/L (WHO, 2011b).

7. Control measures
At every stage in the recycling process there are measures that can be taken to prevent
or reduce the release of lead. A detailed description of control measures is beyond
the scope of this document but brief information is given here. Further information can
be found in technical guidelines and a training manual published by the Basel
Convention Secretariat and in technical guidelines published by the Commission
for Environmental Cooperation (CEC). These provide practical advice and guidance
to national authorities on the environmentally sound management of used lead-acid
batteries (UNEP, 2003; UNEP, 2004; CEC, 2016). The US Occupational Safety
and Health Administration provides information about engineering and other controls
in
its e-learning tool on secondary lead smelting (OSHA, 2002).
7.1. Battery collection, storage and transportation

Measures that should be taken at battery collection and storage sites include the
following (CEC, 2016; UNEP, 2003). Batteries should not be drained at the
collection point. They should be stored securely and sheltered from the weather. The
storage location should be well ventilated and the ground should be coated with acid-
resistant concrete or other resistant material. Leaking batteries should be placed in
acid-resistant containers. The number of stored batteries should be controlled. There
should be prominent hazard warnings.
Battery collectors should not sell their batteries on to unlicensed lead smelters.
Used lead-acid batteries should be transported as hazardous waste. The batteries should
Lead battery
be kept upright and separated by cardboard or other non-conducting material and then
recycling should only
placed in sealed containers or otherwise secured, e.g. be conducted at
on pallets covered with shrink wrap, to prevent them moving about. adequately equipped
7.2. Battery recycling and
To minimize lead exposure and environmental contamination, lead battery recycling regulated facilities
should only be conducted at adequately equipped and regulated facilities that have
the requisite engineering controls, trained staff, provision of
protective equipment, and environmental and occupational monitoring.

CONSIDERATIONS / 29
The most important and effective control measures are engineering and emission
controls. However, work practice controls are also needed to protect the health of
workers and reduce emissions to the outside (OSHA, 2002). Engineering controls
include the use of fully automated and enclosed operations for the dismantling and
separation of lead-acid batteries and the smelting and refining of lead. Fugitive
emissions from the various stages of the recycling process can be reduced by the use
of negative pressure enclosures, i.e. a sealed area where adequate ventilation is in
place to create a negative pressure that is exhausted through an emission control
device and/or a high‐efficiency particulate air (HEPA) filter to trap particles and dust.
The use of hooding and exhaust ventilation over open areas of operation, e.g. battery
saws and crushers, furnace feed conveyors and furnace charging points, will trap dusts
and fumes. Keeping molten lead at lower temperatures will reduce the amount of
fume. Dust and particle emissions should be trapped in a filter baghouse, by using a
wet electrostatic precipitator or by other similar technologies (CEC, 2016). These
traps should be regularly cleaned and the contents fed into the smelter to recover the
lead. There should be an effluent treatment station to treat all water used in the
recycling process and for cleaning (CEC, 2016). Rainwater run-off from roofs and
other surfaces, which are likely to be contaminated with
lead, should also be collected and treated (UNEP, 2003).
Other techniques to reduce dispersion of dust include keeping all open operations wet,
ensuring that batteries and slag are safely stored under cover and kept away from
water, and ensuring that the whole operating area is kept clean using wet methods and
HEPA vacuuming. There should be regular environmental
monitoring to ensure that control measures are effective.
In addition to providing adequate ventilation, workers’ exposure can further be

reduced by the following measures (OSHA, 2002; UNEP, 2003; Kosnett et
al., 2007; CEC, 2016):
• training on the hazards of lead and measures to prevent exposure; • providing, and
enforcing the use of, personal protective equipment (see below); • prohibition of
smoking, eating or drinking in the workplace;
• providing a segregated eating area well away from recycling operations; • providing a
clean air room, maintained at positive pressure and with filtered
air, for the removal of respirators;
• providing, and enforcing the use of, facilities for workers to change into clean work
clothing before starting work and to wash and change clothes at the end of the
working day;
• the implementation of a policy for regular blood lead testing, with a specified medical
removal level to remove an over-exposed worker from working around
lead, together with provisions for alternative employment or compensation.

Medical removal levels vary from country to country and are usually lower for
women than for men. There is also a voluntary industry initiative among battery
companies in a number of countries to maintain workers’ blood lead
concentrations below 30 μg/dL (EUROBAT, 2013).
Ensuring that workers wash and change before leaving the facility is important
for protecting household members from take-home exposure to lead.
7.2.1. Personal protective equipment

The required personal protective equipment will vary according to the specific tasks
being carried out and the concomitant risk of exposure to lead and other hazards.
Equipment may include: full-body coveralls, apron, gloves, hard hats, shoes or
disposable shoe covers, respirators, face shields or vented goggles (OSHA, 2002;
CEC, 2016). It is important that this equipment is regularly cleaned and
maintained in good repair. It should be noted that respiratory protection is not a
substitute for adequate ventilation and pollution controls in
the workplace but can be used along with these other measures.
7.3. Informal recycling

It is clear from the above description of control measures that it is not possible for
informal recycling to be carried out in an occupationally and environmentally sound
way. Preventing informal recycling presents a number of challenges and it is
important to take a holistic approach. Recycling is often carried out in a covert way,
e.g. at night or in constantly changing locations. Therefore, identifying operations in
order to close them down may be difficult. In addition, for people with limited
employment opportunities, recycling may provide a critical source of family income
with consequent repercussions if it is stopped
and no alternative is provided.
The Basel Convention Secretariat devotes a chapter of its training manual to the
problem of controlling informal recycling and suggests a number of approaches
(UNEP, 2004). These include determining the likely scale of operations through a
market analysis of battery imports and sales, and identifying the points of interaction
between the informal and formal sectors, as well as collecting information about
recycling practices to determine where interventions can
be targeted.
Manufacturers,
The life-cycle of a lead-acid battery involves manufacturers, retailers, scrap dealers, retailers, scrap
secondary smelters and consumers. Each can play a part in preventing the supply of used dealers, secondary
lead-acid batteries to the informal recycling sector. Some suggested
smelters and
approaches include: consumers can each
play a
• encouraging the collection of used batteries by licensed retailers when part in reducing
replacement batteries are being bought, for example by requiring a returnable informal lead-acid
battery recycling

CONSIDERATIONS / 31
deposit or refund scheme that would price lead batteries at a level closer to the actual
intrinsic value of the lead and more than the informal sector would be willing to pay;
• requiring manufacturers to take back used lead-acid batteries in order to sell them to
licensed recyclers (extended producer responsibility);
• informing consumers about the value of recycling lead-acid batteries and the dangers
of dumping or supplying batteries to unlicensed smelters;
• informing the public at large about the health and environmental hazards of lead;
• encouraging the technological development of lead-acid batteries to make them last
longer;
• prohibiting the sale of used lead-acid batteries to unlicensed smelters; • creating a role
for the informal sector e.g. by developing the necessary
infrastructure that encourages scavengers to take batteries to licensed smelters;
and
• sharing experiences between countries on approaches to controlling informal
recycling (UNEP, 2004).
7.4. The problem of legacy pollution

Lead is persistent and highly immobile in the environment and surface lead
concentrations are unlikely to migrate to subsurface soils even after a prolonged period
(Kabala & Singh, 2001). Sites where recycling activity has taken place will,
therefore, continue to pose an exposure risk to local populations. Consideration should
therefore be given to methods of mitigating exposure,
for example through environmental remediation.
7.5. Policy measures

Enforcement of the control measures described above requires a national policy to be
put in place for the sound management of used lead-acid batteries that encompasses
standards for collection, recycling, emissions, and occupational safety (UNEP, 2003;
UNEP, 2004). Relevant regulatory measures include land-use planning laws
concerning the location of secondary smelters (e.g. distance from residential areas),
environmental standards governing emissions and discharges, and occupational
standards for workplace and worker monitoring
(UNEP, 2004; van der Kuijp et al., 2013).
For these measures to be successful there is also a need for adequate technical
capacities, such as trained inspectors and laboratory facilities for the measurement of
lead in biological and environmental samples, as well as appropriate enforcement
measures. It is also important that the health sector, particularly at primary care level,
is able to recognise possible lead poisoning
and to initiate the necessary diagnostic and treatment interventions.

8. Conclusions and
way forward
As lead-acid batteries are the fastest growing segment of lead usage, there will be a
continuing demand for lead. Economics dictate that lead batteries will be recycled to
augment supplies that come from mining sources (UNEP, 2013). Lead can be
recycled indefinitely, although there are some losses at each stage, the amount
depending on the efficiency of the recycling process. Informal recycling is particularly
inefficient in terms of lead losses; moreover the purity of the final product is poor.
Lead mining uses large amounts of energy and environmental resources, particularly
water. It causes significant environmental degradation and loss of habitat as well as
generating large amounts of contaminated waste tailings. The environmental impact of
recycling is potentially much less, for example, recycling lead saves approximately 55–
65% of the energy used in mining and processing (UNEP, 2013). Provided it is
carried out using appropriate technologies and to an adequate environmental standard,
recycling can have less impact on the environment and on human
health than mining.
As this document indicates, recycling lead-acid batteries must be carried out with care
to minimize environmental contamination and protect the health of workers and
communities. While much of the responsibility for ensuring the sound management
of used lead-acid batteries lies with the environment sector, the health sector must also
play its part. This includes ensuring that health-care practitioners have training on, and
resources for, the diagnosis and management of lead poisoning, educating local
communities on the health hazards of lead, and taking action to inform the responsible
authorities when lead poisoning associated with recycling is discovered. Furthermore,
health ministries should aim to ensure the availability of laboratory capacity for blood
lead testing and should work with industry to reduce employee exposures.

CONSIDERATIONS / 33
9. References
AGENDA (2016) Used lead acid battery (ULAB) recycling in Tanzania: survey
report. Dar es Salaam: AGENDA for Environment and Responsible Development;
2016 (http://www.econet.international/index.php?id=3, accessed
3 January 2017).
Al Khayat A, Menon NS, Alidina MR (1997) Acute lead encephalopathy in early
infancy – clinical presentation and outcome. Annals Tropical Paediatrics.
1997; 17(1):39-44.
ATSDR (2007) Toxicological profile for lead. Atlanta (GA): Agency for Toxic
Substances and Disease Registry; 2007 (https://www.atsdr.cdc.gov/ToxProfiles/
tp13.pdf, accessed 3 January 2017).
ATSDR (2015) Case studies in environmental medicine: Taking an exposure history.
Atlanta (GA): Agency for Toxic Substances and Disease Registry; 2015
(https://www.atsdr.cdc.gov/csem/exphistory/docs/exposure_history.pdf,
accessed 3 January 2017).
Attina TM, Trasande L (2013). Economic costs of childhood lead exposure in low-
and middle-income countries. Environmental Health Perspectives. 2013;
121:1097–1102 (http://dx.doi.org/10.1289/ehp.1206424, accessed
3 January 2017).
Baker EL, Folland DS, Taylor TA, Frank M, Peterson W, Lovejoy G, Cox
D, Housworth J, Landrigan PJ (1977). Lead poisoning in children of lead workers:
home contamination with industrial dust. New England Journal of Medicine. 1997;
296(5):260–261 (http://www.nejm.org/doi/pdf/10.1056/
NEJM197702032960507, accessed 3 January 2017).
Barbosa F, Tanus-Santos JE, Gerlach RF, Parsons PJ (2005). A critical review of
biomarkers used for monitoring human exposure to lead: advantages, limitations,
and future needs. Environmental Health Perspectives. 2005; 113(12):1669–1674
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1314903/,
Barry PSI (1975). Comparison of concentrations of lead in human tissues. British
Journal of Industrial Medicine. 1975; 32:119–139 (https://www.ncbi.nlm.
nih.gov/pmc/articles/PMC1008038/pdf/brjindmed00086-0027.pdf, accessed
3 January 2017).

Bartlett ES, Trasande L (2014). Economic impacts of environmentally attributable
childhood health outcomes in the European Union. European Journal of Public Health.
2014; 24(1):21-26 (http://eurpub.oxfordjournals.org/content/24/1/21.
long, accessed 3 January 2017).
Bastrup-Madsen P (1950). Dimercaprol in acute lead poisoning. Lancet. 1950;
2(5):171-172 (http://www.sciencedirect.com/science/article/pii/
S0140673650911494, accessed 3 January 2017).
Belay M, Belay A, Genet Z (2015). Safety practices and awareness of lead acid
battery recyclers in Addis Ababa, Ethiopia. Addis Ababa: Pesticide Action Nexus
Association; 2015 (http://www.econet.international/index.php?id=3,
Bellinger DC (2004a). Lead. Pediatrics. 2004; 113(4, Supplement 3):1016-1022
(http://pediatrics.aappublications.org/content/113/Supplement_3/1016,
Bellinger DC (2004b). What is an adverse effect? A possible resolution of clinical and
epidemiological perspectives on neurobehavioral toxicity. Environmental
Research. 2004; 95:394-405.
Bhattacharya A, Shukla R, Bornschein RL, Dietrich KN & Keith R (1990). Lead
effects on postural balance of children. Environmental Health Perspectives. 1990;
89:35-42 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567808/pdf/
envhper00422-0036.pdf, accessed 3 January 2017).
Blacksmith Institute (2009). The problem. In: Pollutant: Lead [website]. New
York: Blacksmith Institute; 2009 (http://www.blacksmithinstitute.org/haina.
html, accessed 3 January 2017).
Bleecker ML, Ford DP, Lindgren KN, Hoese VM, Walsh KS, Vaughan CG
(2005). Differential effects of lead exposure on components of verbal memory.
Occupational & Environmental Medicine. 2005; 62(3):181-187 (http://oem.
bmj.com/content/62/3/181.long, accessed 3 January 2017).
California Environmental Protection Agency (2015). DTSC announces order to close
Exide facility and steps to protect community with enhanced clean-up. Department of
Toxic Substances Control News Release, March 12 2015. Available at
(https://www.dtsc.ca.gov/HazardousWaste/Projects/upload/News-
Release-T-06-15.pdf, accessed 3 January 2017).
Cavalleri A, Trimarchi F, Gelmi C, Baruffini A, Minoia C, Biscaldi G, Gallo G
(1982). Effects of lead on the visual system of occupationally exposed subjects.
Scandinavian Journal of Work Environment & Health. 1982; 8(Suppl 1):148-151.
CDC (2010). Guidelines for the identification and management of lead exposure in
pregnant and lactating women. Atlanta (GA): US Centers for Disease Control and
Prevention; 2010 (http://www.cdc.gov/nceh/lead/publications/
leadandpregnancy2010.pdf, accessed 3 January 2017).
CDC (2012). Low level lead exposure harms children: A renewed call for primary
prevention. Atlanta (GA): US Centers for Disease Control and Prevention;

CONSIDERATIONS / 35
2012 (http://www.cdc.gov/nceh/lead/acclpp/final_document_030712.pdf,
CDC (2013). Guidelines for measuring lead in blood using point of care
instruments. Atlanta (GA): US Centers for Disease Control and Prevention; 2013
(http://www.cdc.gov/nceh/lead/ACCLPP/20131024_POCguidelines_final.
pdf, accessed 3 January 2017).
CEC (2016). Environmentally sound management of spent lead-acid batteries in North
America: Technical guidelines. Montreal: Commission for Environmental Cooperation;
2016 (in English, French & Spanish) (http://www3.cec.org/islandora/ en/item/11665-
environmentally-sound-management-spent-lead-acid-batteries-
in-north-america, accessed 25 January 2017)
Chen SS, Chen TJ, Lin CH, Tseng YT, Lai SL (2005). Neurobehavioral changes in
Taiwanese lead-exposed workers. Journal of Occupational & Environmental
Medicine. 2005; 47:902-908.
Cheng Y, Schwartz J, Sparrow D, Aro A, Weiss ST, Hu H (2001). Bone lead and
blood lead levels in relation to baseline blood pressure and the prospective development
of hypertension: the Normative Aging Study. American Journal of Epidemiology.
2001; 153(2):164-171 (http://aje.oxfordjournals.org/
content/153/2/164.full.pdf+html, accessed 3 January 2017).
Chia SE, Chia HP, Ong CN, Jeyaratnam J (1996). Cumulative concentrations of blood
lead and postural stability. Occupational & Environmental Medicine. 1996; 53:264-
268 (http://oem.bmj.com/content/53/4/264.full.pdf+html,
Chia SE, Chia HP, Ong CN, Jeyaratnam J (1997). Cumulative blood lead levels
and neurobehavioral test performance. Neurotoxicology. 1997; 18(3):793-803.
Chisolm JJ Jr, Barltrop D (1979). Recognition and management of children with
increased lead absorption. Archives of Diseases of Childhood. 1979; 54(4):249-262
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1545299/pdf/
archdisch00794-0005.pdf, accessed 3 January 2017).
Chisolm JJ Jr (1978). Fouling one’s own nest. Pediatrics. 1978; 62:614–617.
CLSI (2013). Measurement procedures for the determination of lead concentrations in
blood and urine; approved guidelines - 2nd edition. CLSI document C40-A2.
Wayne (PA): Clinical and Laboratory Standards Institute; 2013.
CREPD (2015). Baseline study about facts in waste lead-acid battery recycling in
Cameroon. Yaoundé: Centre de Recherche et d’Education pour le Développement;
2015 (http://www.econet.international/index.php?id=3, accessed 3 January 2017).
Cullen MR, Robins JM, Eskenazi B (1983). Adult inorganic lead intoxication:
Presentation of 31 new cases and a review of recent advances in the literature.
Medicine. 1983; 62:221-247.
Daniell WE, Tung LV, Wallace RM, Havens DJ, Karr CJ, Diep NB, Croteau GA,
Beaudet NJ, Bao ND (2015). Childhood lead exposure from battery recycling

in Vietnam. BioMed Research International. 2015; Article ID 193715 (http://
dx.doi.org/10.1155/2015/193715, accessed 3 January 2017).
Demetriades A, Birke M (2015). Urban geochemical mapping manual:
Sampling, Sample preparation, Laboratory analysis, Quality control check,
Statistical processing and map plotting. Brussels: EuroGeoSurveys; 2015 (http://
www.eurogeosurveys.org/wp-content/uploads/2015/10/Urban_Geochemical_
Mapping_Manual.pdf, accessed 3 January 2017).
Dietrich KN, Ris MD, Succop PA, Berger OG, Bornschein RL (2001). Early
exposure to lead and juvenile delinquency. Neurotoxicology & Teratology. 2001;
23(6):511-518 (http://www.sciencedirect.com/science/article/pii/
S0892036201001842, accessed 3 January 2017).
EC (1998). Council Directive 98/24/EC of 7 April 1998 on the protection of the health
and safety of workers from the risks related to chemical agents at work (fourteenth
individual Directive within the meaning of Article 16(1) of Directive 89/391/EEC).
Official Journal 5 May 1998; L 131, 41:11-23 (http://eur-lex. europa.eu/legal-
content/EN/TXT/PDF/?uri=CELEX:31998L0024&from=EN,
EC (2008). Directive 2008/50/EC of the European Parliament and of the Council of 21
May 2008 on ambient air quality and cleaner air for Europe. Official Journal 11 June
2008, L 152, 51:1-44 (http://eur-lex.europa.eu/LexUriServ/LexUriServ.
do?uri=OJ:L:2008:152:0001:0044:en:PDF, accessed 3 January 2017).
Ettinger AS, Roy A, Amarasiriwardena CJ, Smith D, Lupoli N, Mercado-García A,
Lamadrid-Figueroa H, Tellez-Rojo MM, Hu H, Hernández-Avila M (2014). Maternal
blood, plasma, and breast milk lead: lactational transfer and contribution to infant
exposure. Environmental Health Perspectives. 2014; 122:87–92 (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC3888576/, accessed 3 January 2017).
Ettinger AS, Tellez-Rojo MM, Amarasiriwardena C, Gonzalez-Cossio T, Peterson KE,
Aro A, Hu H & Hernandez-Avila M (2004). Levels of lead in breast milk and their
relation to maternal blood and bone lead levels at one month postpartum.
Environmental Health Perspectives. 2004; 112:926-931 (https://www.ncbi.nlm.
nih.gov/pmc/articles/PMC1242024/, accessed 3 January 2017).
EURO (1999). Monitoring ambient air quality for health impact assessment.
Copenhagen: WHO Regional Office for Europe; 1999 (http://www.euro.who.
int/data/assets/pdf_file/0010/119674/E67902.pdf, accessed 3 January 2017).
EUROBAT (2013). Battery Associations from North America and Europe, the
Middle East and Africa join forces to strengthen workers’ protection. Press release 19
June 2013 (https://eurobat.org/battery-associations-north-america-and-europe-middle-
east-and-africa-join-forces-strengthen-workers%E2%80%99,
FAO (2016). General standard for contaminants and toxins in food and feed
(Codex Stan 193-1995). Rome: Food and Agriculture Organization; 2016
(http://www.fao.org/fao-who-codexalimentarius/sh-proxy/
en/?lnk=1&url=https%253A%252F%252Fworkspace.fao.org%252Fsites%252Fc

CONSIDERATIONS / 37
odex%252FStandards%252FCODEX%2BSTAN%2B193-1995%252FCXS_193e.
Fergusson DM, Horwood LJ (1993). The effects of lead levels on the growth of word
recognition in middle childhood. International Journal of Epidemiology.
1993; 22:891-897.
Fergusson DM, Horwood LJ, Lynskey MT (1997). Early dentine lead levels and
educational outcomes at 18 years. Journal of Child Psychology & Psychiatry.
1997; 38:471-478.
Fewtrell L, Kaufmann R, Prüss-Ustün A (2003). Lead – Assessing the environmental
burden of disease at national and local levels. Environmental Burden of Disease Series,
No.2. Geneva: World Health Organization; 2003 (http://www.who.int/
quantifying_ehimpacts/publications/en/, accessed 3 January 2017).
Frith D, Yeung K, Thrush S, Hunt BJ, Hubbard JG (2005). Lead poisoning – a
differential diagnosis for abdominal pain. Lancet. 2005; 366:2146 (http://www.
thelancet.com/pdfs/journals/lancet/PIIS0140-6736(05)67893-2.pdf, accessed
3 January 2017).
Future Market Insights (2014). Lead Acid Battery Market: Global Industry
Analysis and Opportunity Assessment 2014 – 2020 [website] ( http://www.
futuremarketinsights.com/reports/global-lead-acid-battery-market, accessed
3 January 2017).
Garza A, Vega R, Soto E (2006). Cellular mechanisms of lead neurotoxicity. Medical
Science Monitor. 2006; 12:RA57-65 (http://www.medscimonit.com/
download/index/idArt/447121, accessed 3 January 2017).
Gerr F, Letz R, Stokes L, Chettle D, McNeill F, Kaye W (2002). Association
between bone lead concentration and blood pressure among young adults.
American Journal of Industrial Medicine. 2002; 42(2):98-106.
Gottesfeld P & Pokhrel, AK (2011). Review: lead exposure in battery manufacturing and
recycling in developing countries and among children in nearby communities.
Journal of Occupational & Environmental Hygiene. 2011; 8(9):520-532.
Graziano JH, Popovac D, Factor-Litvak P, Shrout P, Kline J, Murphy MJ, Zhao
YH, Mehmeti A, Ahmedi X, Rajovic B, Zvicer A, Nenezic DU, Lolacono NJ, Stein Z
(1990). Determinants of elevated blood lead during pregnancy in a population
surrounding a lead smelter in Kosovo, Yugoslavia. Environmental Health Perspectives.
1990; 89:95-100 (https://www.ncbi.nlm.nih.gov/pmc/
articles/PMC1567790/pdf/envhper00422-0095.pdf, accessed 3 January 2017).
Green VA, Wise GW, Callenbach J (1976). Lead poisoning. Clinical Toxicology.
1976; 9:33-51.
Greig J, Thurtle N, Cooney L et al. (2014). Association of blood lead level with
neurological features in 972 children affected by an acute severe lead poisoning
outbreak in Zamfara State, Northern Nigeria. PLoS ONE 9(4): e93716. (http://
www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0093716,

Gulson BL, Mizon KJ, Korsch MJ, Palmer JM, Donnelly JB (2003). Mobilization of
lead from human bone tissue during pregnancy and lactation — a summary
of long-term research. Science of the Total Environment. 2003; 303:79-104.
Haefliger P, Mathieu-Nolf M, Lociciro S, Ndiaye C, Coly M, Diouf A, Faye AL, Sow
A, Tempowski J, Pronczuk J, Filipe Junior AP, Bertollini R, Neira M (2009). Mass
lead intoxication from informal used lead-acid battery recycling in Dakar, Senegal.
Environmental Health Perspectives. 2009; 117(10):1535-1540 (https://
ehp.niehs.nih.gov/0900696/, accessed 3 January 2017).
Haut Conseil de la santé publique (2014). Détermination de nouveaux objectifs de
gestion des expositions au plomb. Synthèse et recommandations. Paris: Haut Conseil
de la santé publique; 2014 (http://www.hcsp.fr/explore.cgi/
avisrapportsdomaine?clefr=444, accessed 3 January 2017).
Healey N, Jones-Otazo H, Walker M, Knafla A (2010). Toxicological review and
recommended toxicological reference values for environmental lead exposure in
Canada. Report prepared for Health Canada (http://www.paho.org/hq/index. php?
option=com_docman&task=doc_details&gid=21069&Itemid=270&lang=en,
Health Canada (2013). Final human health state of the science report on lead.
Ottawa: Health Canada; 2013 (http://www.hc-sc.gc.ca/ewh-semt/pubs/
contaminants/dhhssrl-rpecscepsh/index-eng.php, accessed 3 January 2017).
Hodge J, Nielsen J, Dignam T, Brown MJ (2015). Small area surveillance to estimate
prevalence of childhood blood and environmental lead levels. Atlanta (GA): US
Centers for Disease Control and Prevention; 2015 (http://www.cdc.
gov/nceh/lead/BLL_PrevalenceStudy_TrainingManual_Final_508.pdf, accessed
3 January 2017).
IHME (2016). Global lead exposure. In: GBD Compare [website]. Seattle (WA):
Institute for Health Metrics and Evaluation, University of Washington;
2016 (http://vizhub.healthdata.org/gbd-compare, accessed 3 January 2017).
ILA (2015). Lead recycling fact sheet. London: International Lead Association; 2015
(http://www.ila-lead.org/UserFiles/File/ILA9927%20FS_Recycling_V08.
ILA (2017) Lead use statistics. In: Lead facts [website] (http://www.ila-lead.
org/lead-facts/lead-uses--statistics, accessed 8 June 2017).
International Metals Study Groups (2016). Metals Despatch. 2016; Issue No 21
(http://www.ilzsg.org/generic/pages/list.aspx?table=document&ff_aa_document_
type=N&from=1, accessed 3 January 2017).
Iwata T, Yano E, Karita K, Dakeishi M, Murata K (2005). Critical dose of lead
affecting postural balance in workers. American Journal of Industrial Medicine.
2005; 48(5):319-325.
Janin Y, Couinaud C, Stone A, Wise L (1985). The “lead-induced colic” syndrome
in lead intoxication. Surgery Annual. 1985; 17:287-307.

CONSIDERATIONS / 39
JECFA (2011). Safety evaluation of certain food additives and contaminants. WHO
Food Additive Series: 64. 73rd Report of the Joint FAO/WHO Expert Committee
on Food Additives, pages 381-497. Geneva: World Health Organization; 2011
(http://apps.who.int/iris/bitstream/10665/44515/1/WHO_TRS_960_eng.
Jennings AA (2013). Analysis of worldwide regulatory guidance values for the most
commonly regulated elemental surface soil contamination. Journal of
Environmental Management. 2013; 118: 72–95
Kabala C, Singh BR (2001). Fractionation and mobility of copper, lead, and zinc in
soil profiles in the vicinity of a copper smelter. Journal of Environmental Quality.
2001; 30(2):485-492 (http://karnet.up.wroc.pl/~kabala/jeq-30-2-485.
Kaul B, Mukerjee H (1999). Elevated blood lead and erythrocyte protoporphyrin levels
of children near a battery-recycling plant in Haina, Dominican Republic. International
Journal of Occupational & Environmental Health. 1999; 5(4):307-
312.
Kaul B, Sandhu RS, Depratt C, Reyes F (1999). Follow-up screening of lead-poisoned
children near an auto battery recycling plant, Haina, Dominican Republic.
Environmental Health Perspectives. 1999; 107(11):917–920 (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC1566703/, accessed 3 January 2017).
Koller K, Brown T, Spurgeon A, Levy L (2004). Recent developments in low-level lead
exposure and intellectual impairment in children. Environmental Health Perspectives.
2004; 112(9):987-994 (https://www.ncbi.nlm.nih.gov/pmc/
articles/PMC1247191/pdf/ehp0112-000987.pdf, accessed 3 January 2017).
Kosnett MJ, Wedeen RP, Rothenburg SJ, Hipkins KL, Materna BL, Schwartz BS,
Hu H, Woolf A (2007). Recommendations for medical management of adult lead
exposure. Environmental Health Perspectives. 2007; 115(3):463-471
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1849937/pdf/ehp0115-
000463.pdf, accessed 26 January 2017).
Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, Canfield
RL, Dietrich KN, Bornschein R, Greene T, Rothenberg SJ, Needleman HL, Schnaas L,
Wasserman G, Graziano J, Roberts R. (2005). Low-level environmental lead exposure
and children’s intellectual function: an international pooled analysis. Environmental
Health Perspectives.2005; 113(7):894–899. (https://www.ncbi.
nlm.nih.gov/pmc/articles/PMC1257652/pdf/ehp0113-000894.pdf, accessed
3 January 2017).
Levallois P, Lavoie M, Goulet L, Nanel AJ, Gingras S (1991). Blood lead levels in
children and pregnant women living near a lead-reclamation plant. Canadian
Medical Association Journal. 1991; 144(7): 877-885.
Lewington S, Clarke R, Qizilbash N, Peto R, Collins R; Prospective Studies
Collaboration (2002). Age-specific relevance of usual blood pressure to vascular
mortality: a meta-analysis of individual data for one million adults in 61 prospective
studies. Lancet 2002; 360(9349):1903-1913 (http://www.
thelancet.com/pdfs/journals/lancet/PIIS0140-6736(02)11911-8.pdf; Erratum

in: Lancet. 2003; 361(9362):1060 http://www.thelancet.com/journals/lancet/
article/PIIS0140-6736(03)12816-4/fulltext, accessed 3 January 2017).
Lidsky TI, Schneider JS (2003). Lead neurotoxicity in children: basic mechanisms and
clinical correlates. Brain. 2003; 126:5-19 (http://brain.oxfordjournals.org/
content/126/1/5.long, accessed 3 January 2017).
Loghman-Adham M (1997). Renal effects of environmental and occupational lead
exposure. Environmental Health Perspectives. 1997; 105:928-939 (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC1470371/pdf/envhper00322-0042.
Manhart A, Schleicher T (2015). The recycling chain for used lead-acid batteries in
Ghana. Freiburg: Oeko-Institut; 2015 (http://www.econet.international/index.
php?id=3, accessed 3 January 2017).
Manhart A, Smera T, Kuepouo G, Mathai D, Mng’anya S, Schleicher T (2016). The
deadly business – findings from the lead recycling Africa project. Freiburg: Oeko-
Institut; 2016 (https://www.oeko.de/oekodoc/2549/2016-076-de.pdf,
Markowitz ME, Weinberger HL (1990). Immobilization-related lead toxicity in
previously lead-poisoned children. Pediatrics 1990; 86:455-457 (http://
pediatrics.aappublications.org/content/pediatrics/86/3/455.full.pdf, accessed
3 January 2017).
Matte TD, Figueroa JP, Ostrowski S, Burr G, Jackson-Hunt L, Baker EL (1991). Lead
exposure from conventional and cottage lead smelting in Jamaica. Archives
of Environmental Contamination & Toxicology. 1991; 21:65–71.
McNutt TK, Chambers-Emerson J, Dethlefsen M, Shah R (2001). Bite the bullet:
lead poisoning after ingestion of 206 lead bullets. Veterinary & Human
Toxicology. 2001; 43:288-289.
Mendelsohn AL, Dreyer BP, Fierman AH, Rosen CM, Legano LA, Kruger HA, Lim
SW, Courtlandt CD (1998). Low-level lead exposure and behavior in early childhood.
Pediatrics. 1998; 101:E10 (http://pediatrics.aappublications.org/
content/pediatrics/101/3/e10.full.pdf, accessed 3 January 2017).
Mielke HW, Reagan PL (1998). Soil is an important pathway of human lead exposure.
Environmental Health Perspectives. 1998; 106(Suppl 1):217-229 (https://www.
ncbi.nlm.nih.gov/pmc/articles/PMC1533263/pdf/envhper00536-0227.pdf,
MoEP (2012). Ambient air quality standards GB 3095-2012. Beijing: Ministry of
Environmental Protection; 2012 (http://kjs.mep.gov.cn/hjbhbz/bzwb/dqhjbh/
dqhjzlbz/201203/W020120410330232398521.pdf, accessed 3 January 2017).
Mushak P (1993). New directions in the toxicokinetics of human lead exposure.
Neurotoxicology. 1993; 14:29-42.
NAS (1972). Lead: airborne lead in perspective. Committee on Biologic Effects of
Atmospheric Pollutants, Division of Medical Sciences. Washington (DC):
National Academy of Sciences; 1972.

CONSIDERATIONS / 41
Nawrot TS, Thijs L, Den Hond EM, Roels HA, Staessen JA (2002). An epidemiological
re-appraisal of the association between blood pressure and blood lead: a meta-analysis.
Journal of Human Hypertension. 2002; 16:123-131 (http://www.
nature.com/jhh/journal/v16/n2/pdf/1001300a.pdf, accessed 3 January 2017).
Needleman H (2004). Lead poisoning. Annual Review of Medicine. 2004; 55:209-
222.
Needleman HL, Riess JA, Tobin MJ, Biesecker G, Greenhouse JB (1996).
Bone lead levels and delinquent behavior. JAMA. 1996; 275:363-369.
Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN (1990). The long-term
effects of exposure to low doses of lead in childhood. An 11-year follow-up report. New
England Journal of Medicine. 1990; 322:83-88 (http://www.nejm.org/doi/
full/10.1056/NEJM199001113220203#t=article, accessed 3 January 2017).
NEPC (2016). National Environment Protection (Ambient Air Quality) Measure.
Canberra: National Environment Protection Council; 2016 (https://www.legislation.
gov.au/Details/F2016C00215, accessed 3 January 2017).
NTP (2012). Health effects of low-level lead. National Toxicology Program
Monograph. Bethesda (MD): National Institutes of Health; 2012 (http://ntp.
niehs.nih.gov/pubhealth/hat/noms/lead/index.html, accessed 3 January 2017).
OSHA (1978). Lead Standard 29 CFR 1910.1025. Washington (DC): Occupational
Safety and Health Administration, US Department of Labor; 1978. (https://www.
osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_
id=10030, accessed 3 January 2017).
OSHA (2002) Lead – secondary lead smelter. In: eTools [website]. Washington (DC):
Occupational Safety and Health Administration; 2002 (https://www.osha.
gov/SLTC/etools/leadsmelter/index.html, accessed 3 January 2017).
Otto DA, Fox DA (1993). Auditory and visual dysfunction following lead exposure.
Neurotoxicology. 1993; 14(2-3):191-207.
Paddock RC (2016). The toxic toll of Indonesia’s battery recyclers. National
Geographic. 31 May 2016 (http://news.nationalgeographic.com/2016/05/
indonesia-s-toxic-toll/, accessed 3 January 2017).
Perlstein MA, Attala R (1966). Neurologic sequelae of plumbism in children.
Clinical Pediatrics. 1966; 5:292-298.
Pichery C, Bellanger M, Zmirou-Navier D, Glorennec P, Hartemann P, Grandjean P
(2011). Childhood lead exposure in France: benefit estimation and partial cost-
benefit analysis of lead hazard control. Environmental Health. 2011; 10:44
(https://ehjournal.biomedcentral.com/articles/10.1186/1476-069X-10-44,
Rabinowitz MB (1991). Toxicokinetics of bone lead. Environmental Health
Perspectives. 1992; 91:33-37 (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC1519353/pdf/envhper00387-0038.pdf, accessed 3 January 2017).

Ratzon N, Froom P, Leikin E, Kristal-Boneh E, Ribak J (2000). Effect of exposure to
lead on postural control in workers. Occupational & Environmental Medicine. 2000;
57:201-203 (http://oem.bmj.com/content/57/3/201.full, accessed
3 January 2017).
Rothenberg SJ, Schnaas L, Salgado-Valladares M, Casanueva E, Geller AM, Hudnell
HK, Fox DA (2002). Increased ERG a- and b-wave amplitudes in 7- to 10-year-old
children resulting from prenatal lead exposure. Investigative Ophthalmology & Visual
Science. 2002; 43:2036-2044 (http://iovs.arvojournals.
org/article.aspx?articleid=2123755, accessed 3 January 2017).
Rubens O, Logina I, Kravale I, Eglite M, Donaghy M (2001). Peripheral
neuropathy in chronic occupational inorganic lead exposure: a clinical and
electrophysiological study. Journal of Neurology,Neurosurgery & Psychiatry. 2001;
71:200-204 (http://jnnp.bmj.com/content/71/2/200.longm, accessed
3 January 2017).
Safe Work Australia (2013). Workplace exposure standards for airborne
contaminants. Canberra: Safe Work Australia; 2013 (http://www.safeworkaustralia.
gov.au/sites/SWA/about/Publications/Documents/772/Workplace-exposure-
standards-airborne-contaminants.pdf, accessed 3 January 2017).
Schwartz BS, Lee BK, Bandeen-Roche K, Stewart W, Bolla K, Links J, Weaver V,
Todd A (2005). Occupational lead exposure and longitudinal decline in
neurobehavioral test scores. Epidemiology. 2005; 16:106-113.
Schwartz J, Landrigan PJ, Baker Jnr EL, Orenstein WA, von Lindern IH (1990).
Lead-induced anemia: dose-response relationships and evidence for a threshold.
American Journal of Public Health. 1990; 80:165-168 (http://www.ncbi.nlm.
nih.gov/pmc/articles/PMC1404621/pdf/amjph00215-0029.pdf, accessed
3 January 2017).
Selevan SG, Rice DC, Hogan KA, Euling SY, Pfahles-Hutchens A, Bethel J (2003).
Blood lead concentration and delayed puberty in girls. New England Journal of
Medicine. 2003; 348:1527-3156. (http://www.nejm.org/doi/full/10.1056/
NEJMoa020880#t=article, accessed 3 January 2017).
Silbergeld EK, Schwartz J, Mahaffey K (1988). Lead and osteoporosis: mobilization of
lead from bone in postmenopausal women. Environmental Research.
1988; 47:79–94.
Stokes L, Letz R, Gerr F, Kolczak M, McNeill FE, Chettle DR, Kaye WE (1998).
Neurotoxicity in young adults 20 years after childhood exposure to lead: the Bunker
Hill experience. Occupational & Environmental Medicine. 1998; 55:507-516
(http://oem.bmj.com/content/55/8/507.full.pdf+html, accessed
3 January 2017).
Stollery BT, Broadbent DE, Banks HA, Lee WR (1991). Short term prospective study
of cognitive functioning in lead workers. British Journal of Industrial Medicine.
1991; 48:739-749 (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC1035449/pdf/brjindmed00035-0019.pdf, accessed 3 January 2017).

CONSIDERATIONS / 43
Suplido ML, Ong CN (2000). Lead exposure among small-scale battery recyclers,
automobile radiator mechanics, and their children in Manila, the Philippines.
Environmental Research Section A. 2000; 82:231-238.
ten Bruggenkate CM, Lopes Cardozo E, Maaskant P, van der Waal I (1975). Lead
poisoning with pigmentation of the oral mucosa. Review of the literature and report of a
case. Oral Surgery, Oral Medicine & Oral Pathology. 1975; 39(5):747-
753.
Thurtle N, Grieg J, Cooney L, Amitai Y, Ariti C, Brown MJ, Kosnett MJ, Moussally
K, Sani-Gwarzo N, Akpan H, Shanks L, Dargan PI (2014). Description of 3180
courses of chelation with dimercaptosuccinic acid in children ≤5 years with severe
lead poisoning in Zamfara, northern Nigeria: a retrospective analysis of programme
data. PLOS Medicine. 2014; 11(10):1-18 (http://www.plosmedicine. org/article/info
%3Adoi%2F10.1371%2Fjournal.pmed.1001739, accessed
3 January 2017).
Tong S (1998). Lead exposure and cognitive development: persistence and a
dynamic pattern. Journal of Paediatrics & Child Health. 1998; 34:114-118.
Tong S, Baghurst P, McMichael A, Sawyer M, Mudge J (1996). Lifetime exposure to
environmental lead and children’s intelligence at 11-13 years: the Port Pirie cohort
study. British Medical Journal. 1996; 312:1569-1575 (http://www.bmj.
com/content/312/7046/1569; accessed 3 January 2017).
Tong S, Baghurst PA, Sawyer MG, Burns J, McMichael AJ (1998). Declining blood
lead levels and changes in cognitive function during childhood: the Port Pirie Cohort
Study. JAMA. 1998; 280:1915-1919 (http://jamanetwork.com/
journals/jama/fullarticle/188249, accessed 3 January 2017).
Trasande L, Liu Y (2011). Reducing the staggering costs of environmental disease
in children, estimated at $76.6 billion in 2008. Health Affairs (Millwood). 2011;
30(5):863–870 (http://content.healthaffairs.org/content/30/5/863.long,
Troesken W (2006). Lead exposure and eclampsia in Britain, 1883-1934.
Environmental Research. 2006; 101(3):395-400.
UNEP (2003). Technical guidelines for the environmentally sound management of waste
lead-acid batteries. Secretariat of the Basel Convention. Basel Convention series/SBC
No. 2003/9. Geneva: Basel convention Secretariat; 2003 (http://www.
basel.int/Portals/4/Basel%20Convention/docs/pub/techguid/tech-wasteacid.
UNEP (2004). National management plans for used lead acid batteries. Training manual
for the preparation of national used lead acid batteries environmentally sound
management plans in the context of the implementation of the Basel Convention. Basel
Convention Series / SBC No 2004/5. Geneva: Basel convention Secretariat; 2004
(http://archive.basel.int/meetings/sbc/workdoc/tm-ulab/tm_ulab.pdf, accessed
3 January 2017).
UNEP (2010). Final review of scientific information on lead. Nairobi: United
Nations Environment Programme; 2010 (http://www.unep.org/chemicalsandwaste/

Portals/9/Lead_Cadmium/docs/Interim_reviews/UNEP_GC26_INF_11_
Add_1_Final_UNEP_Lead_review_and_apppendix_Dec_2010.pdf, accessed
3 January 2017).
UNEP (2013). Environmental risks and challenges of anthropogenic metals flows and
cycles. Paris: United Nations Environment Programme; 2013 (http://
www.unep.org/resourcepanel/publications/environmentalchallengesmetals/
tabid/106142/default.aspx, accessed 3 January 2017).
US EPA (1993). Personal Air Sampling and Air Monitoring Requirements under 29
CFR 1910.120. Publication 9360.B-17FS. Washington (DC): United States
Environmental Protection Agency; 1993.
US EPA (2001). Lead; identification of dangerous levels of lead; Final Rule. Federal
Register. 2001; 66(4):1205-1240 (https://www.gpo.gov/fdsys/pkg/FR-
2001-01-05/pdf/01-84.pdf, accessed 3 January 2017).
US EPA (2016). Fact sheet: Decision - National Ambient Air Quality Standards for
lead. Washington (DC): United States Environmental Protection Agency; 2016
(https://www.epa.gov/sites/production/files/2016-09/documents/pb_
naaqs_nfr_fact_sheet.pdf, accessed 3 January 2017).
Valciukas JA, Lilis R, Eisinger J, Blumberg WE, Fischbein A, Selikoff IJ (1978).
Behavioral indicators of lead neurotoxicity: results of a clinical field survey.
International Archives of Occupational & Environmental Health. 1978; 41(4):217-
236.
van der Kuijp TJ, Huang L, Cherry CR (2013). Health hazards of China’s lead-acid
battery industry: a review of its market drivers, production processes, and health
impacts. Environmental Health. 2013; 12:61 (http://ehjournal.biomedcentral.
com/articles/10.1186/1476-069X-12-61, accessed 3 January 2017).
Wang J-D, Jang C-S, Hwang Y-H, Chen Z-S (1992). Lead contamination around
a kindergarten near a battery recycling plant. Bulletin of Environmental Contamination
& Toxicology. 1992; 49:23-30 (https://www.researchgate.net/
publication/21764004_Lead_contamination_around_a_kindergarten_near_a_
battery_recycling_plant, accessed 25 January 2017).
Wedeen RP (1988). Bone lead, hypertension, and lead nephropathy. Environmental
Health Perspectives. 1988; 78:57-60 (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC1474623/pdf/envhper00429-0059.pdf, accessed 3 January 2017).
Weidenhamer JD, Kobunski PA, Kuepouo G, Corbin RW, Gottesfeld P (2014). Lead
exposure from aluminum cookware in Cameroon. Science of the Total
Environment. 2014; 496:339-47.
Weidenhamer JD, Fitzpatrick MP, Biro AM, Kobunski PA, Hudson MR, Corbin RW,
Gottesfeld P (2017). Metal exposures from aluminum cookware: an unrecognized
public health risk in developing countries. Science of the Total
Environment. 2017; 579: 805-813.).
Were FH, Kamau GN, Shiundu PM, Wafula GA, Moturi CM (2012). Air and blood
lead levels in lead acid battery recycling and manufacturing plants in
Kenya. Journal of Occupational & Environmental Hygiene. 2012; 9(5):340-344.

CONSIDERATIONS / 45
White RF, Diamond R, Proctor S, Morey C, Hu H (1993). Residual cognitive deficits
50 years after lead poisoning during childhood. British Journal of Industrial Medicine.
1993; 50(7):613-622 (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC1035497/pdf/brjindmed00007-0037.pdf, accessed 3 January 2017).
WHO (1995). Lead. Environmental Health Criteria 165. Geneva: World Health
Organization; 1995 (http://www.inchem.org/documents/ehc/ehc/ehc165.htm,
WHO (2000). Air quality guidelines for Europe, 2nd edition. Copenhagen: WHO
Regional Office for Europe; 2000 (http://www.euro.who.int/__data/assets/
pdf_file/0005/74732/E71922.pdf?ua=1, accessed 3 January 2017).
WHO (2010a) Childhood lead poisoning. Geneva: World Health Organization; 2010
(http://www.who.int/ceh/publications/leadguidance.pdf, accessed
3 January 2017).
WHO (2010b). WHO Human health risk assessment toolkit. Geneva: World Health
Organization; 2010 (http://www.who.int/ipcs/methods/harmonization/
areas/ra_toolkit/en/, accessed 3 January 2017).
WHO (2010c). WHO Guidelines on drawing blood: best practices in phlebotomy.
Geneva: World Health Organization; 2010 (http://www.who.int/injection_safety/
sign/drawing_blood_best/en/, accessed 3 January 2017).
WHO (2011a). Brief guide to analytical methods for measuring lead in blood. Geneva:
World Health Organization; 2011 (http://www.who.int/ipcs/assessment/
public_health/lead_blood.pdf, accessed 3 January 2017).
WHO (2011b). Guidelines for Drinking-water Quality, 4th edition. Geneva: World
Health Organization; 2011 (http://www.who.int/water_sanitation_health/
publications/dwq-guidelines-4/en/, accessed 3 January 2017).
Wilhelm M, Beinzow B, Angerer J, Schulz C (2010). Reassessment of critical lead
effects by the German Human Biomonitoring Commission results in suspension of
the human biomonitoring values (HBM I and HBM II) for lead in blood of children
and adults. International Journal of Hygiene and Environmental Health. 2010;
213:265-269 (http://www.sciencedirect.com/science/article/pii/
S143846391000043X, accessed 3 January 2017).
Williamson AM, Teo RKC (1986). Neurobehavioural effects of occupational exposure to
lead. British Journal of Industrial Medicine. 1986; 43(6):374-380 (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC1007666/pdf/brjindmed00170-0014.
Winship KA (1989). Toxicity of lead: a review. Adverse Drug Reactions & Acute
Poisoning Reviews. 1989; 8(3): 117-152.
Wright JP, Dietrich KN, Ris MD, Hornung RW, Wessel SD, Lanphear BP, Ho
M, Rae MN (2008). Association of prenatal and childhood blood lead
concentrations with criminal arrests in early adulthood. PLoS Medicine.
2008;5(5):e101 (http://journals.plos.org/plosmedicine/article/file?id=10.1371/
journal.pmed.0050101&type=printable, accessed 3 January 2017).

Wu T, Buck GM, Mendola P (2003). Blood lead levels and sexual maturation in U.S.
girls: the Third National Health and Nutrition Examination Survey, 1988-1994.
Environmental Health Perspectives. 2003; 111(5):737-741 (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC1241484/pdf/ehp0111-000737.pdf,
Zhang F, Liu Y, Zhang H, Ban Y, Wang J, Liu J, Zhong L, Chen X, Zhu B (2016).
Investigation and evaluation of children’s blood lead levels around a lead battery factory
and influencing factors. International Journal of Environmental Research and Public
Health. 2016; 13:541. (https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC4923998/pdf/ijerph-13-00541.pdf, accessed 3 January 2017).

CONSIDERATIONS / 47
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© World Health Organization 2017

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

Iv / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

Edited by Philip Jenkins.

Design and layout by Paprika (Annecy, France).

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

The manufacturing and recycling of lead-acid batteries is practised worldwide in both

2 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

1.1. Purpose and scope of the document

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

2.1. Components of a lead-acid battery

4 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

positive terminal plugs negative terminal

sulfuric acid solution element separators

plate separators negative plates

box positive plates

2.2. Steps in the recycling process

Recyclable plastic components are washed then shredded or ground and

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

2.3. Lead release and exposure during recycling

6 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

Draining Lead contamination of soil

Lead fumes dispersed in air and

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

2.3.1. Informal lead recycling

8 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

2.4. Other chemicals released during recycling

2.5. Studies of lead exposure from recycling lead-acid batteries

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

A review of published literature on exposures from formal-sector lead-acid battery

10 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

2.5.2. Dominican Republic

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

2.5.3. viet Nam

12 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

Environmental investigations showed legacy soil contamination in areas where

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

3.1. Routes of exposure to lead

Lead accumulates in bone over life up to age 50 to 60 years, followed by a decline

14 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

3.2. Toxic effects of lead

3.2.1. Gastrointestinal effects

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

3.2.2. Neurological effects

16 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

3.2.6. Reproductive system and pregnancy

3.3. Toxic effects in relation to blood lead concentrations

18 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

Blood lead concentration Health effect Reference

20 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

The estimated economic costs attributable to the neurodevelopmental impacts of

22 / RECYCLING USED LEAD-ACID BATTERIES: HEALTH CONSIDERATIONS

6.1. Blood lead measurements

RECYCLING USED LEAD-ACID BATTERIES: HEALTH

Laboratory-based methods for measuring blood lead concentrations have greater