Lead is generally deposited as the mineral Galena. Which is lead II sulphide, PbS. Which is vanishingly soluble in pH neutral water, A saturated solution would contain 2.6×10^−11 kg/kg (calculated, at pH=7) at 20C. This is 26 parts per billion. Sure, if the groundwater is acidic, more will dissolve, but I would not expect it to be at 20c, nor to be a saturated solution, so no, I don't think that it is a concern for most.
What is a concern is lead dissolved from elemental lead in household plumbing, installed prior to the banning of lead from plumbing solder or as an alloying ingredient in brass fittings. In 1987. Which is in a large part of our housing stock.
Domestic mains water is treated to minimise this, but those using e.g. their own boreholes etc. do not benefit from such treatment, so may be using water that has a strong ability to dissolve this lead from inside their domestic plumbing.
Worth studying, if you are minded:
https://www.who.int/water_sanitation_health/dwq/chemicals/lead.pdf
Some snippets:
Lead is present in tap water to some extent as a result of its dissolution from natural sources, but primarily from household plumbing systems in which the pipes, solder, fittings or service connections to homes contain lead. Polyvinyl chloride (PVC) pipes also contain lead compounds that can be leached from them and result in high lead concentrations in drinking-water. The amount of lead dissolved from the plumbing system depends on several factors, including the presence of chloride and dissolved oxygen, pH, temperature, water softness and standing time of the water, soft, acidic water being the most plumbosolvent (11,12). Although lead can be leached from lead piping indefinitely, it appears that the leaching of lead from soldered joints and brass taps decreases with time (10). Soldered connections in recently built homes fitted with copper piping can release enough lead (210–390 µg/l) to cause intoxication in children (13). The level of lead in drinking-water may be reduced by corrosion control measures such as the addition of lime and the adjustment of the pH in the distribution system from <7 to 8–9 (14,15). Lead can also be released from flaking lead carbonate deposits on lead pipe and from iron sediment from old galvanized plumbing that has accumulated lead from lead sources such as plumbing and service connections, even when the water is no longer plumbosolvent.
In the United Kingdom in 1975– 1976, there was virtually no lead in the drinking-water in two thirds of households, but levels were above 50 µg/l in 10% of homes in England and 33% in Scotland (2). In Glasgow (Scotland), where the water was known to be plumbosolvent, the lead concentration in about 40% of the samples exceeded 100 µg/l (19)
Soils and household dust are significant sources of lead exposure for small children
(6,26,27), but the levels are highly variable, ranging from <5 µg/g to tens of
milligrams per gram in contaminated areas. As lead is immobile, levels in
contaminated soil will remain essentially unchanged unless action is taken to
decontaminate them (28). The highest lead concentrations usually occur in surface
soil at depths of 1–5 cm.
In a 2-year study in England during 1984 and 1985, the geometric mean
concentrations of lead in road dust collected in the vicinity of two London schools and
in a rural area were 1552–1881 and 83–144 µg/g, respectively. For household dusts in
London and in a rural area of Suffolk for 3 consecutive years (1983–1985), the
geometric mean concentrations were 857 and 333 µg/g, respectively (8). Household
dust concentrations were 332 µg/g in an Edinburgh study (29) and 424 µg/g in one in
Birmingham (30).
The amount of soil ingested by children aged 1–3 years is about 40–55 mg/day
(27,31,32). A comprehensive study of a group of 2-year-old urban children indicated
an intake of lead from dust of 42 µg/day, almost twice the dietary lead intake (30).
Studies in inner-city areas in the USA have shown that peeling paint or dust
originating from leaded paint during removal may contribute significantly to
children’s exposure to lead (33).
More than 80% of the daily intake of lead is derived from the ingestion of food, dirt
and dust. At 5 µg/l, the average daily intake of lead from water forms a relatively
small proportion of the total daily intake for children and adults, but a significant one
for bottle-fed infants. Such estimates have a wide margin of error, as it is not known
to what extent the general public flushes the system before using tap water; in
addition, the stagnation time (and hence the lead levels) is highly variable (10). The
contribution of ingested dust and dirt to the total intake is known to vary with age,
peaking around 2 years (32).
Adults absorb approximately 10% of the lead contained in food (6), but young
children absorb 4–5 times as much (34,35); the gastrointestinal absorption of lead
from ingested soil and dust by children has been estimated to be close to 30% (26).
Absorption is increased when the dietary intakes of iron or calcium and phosphorus
are low (36–38). Iron status is particularly important, as children from disadvantaged
homes are more likely to suffer from anaemia, further increasing their absorption of
lead (39).
Following its absorption, lead appears both in a soft tissue pool, consisting of the blood, liver, lungs, spleen, kidneys and bone marrow, which is rapidly turned over, and in a more slowly turned over skeletal pool. The half-life of lead in blood and soft tissues is about 36–40 days for adults (42), so that blood lead concentrations reflect only the intake of the previous 3–5 weeks. In the skeletal pool, the half-life of lead is approximately 17–27 years (42,43). In adults, some 80–95% of the total body burden of lead is found in the skeleton, as compared with about 73% in children (44,45). The biological half-life of lead may be considerably longer in children than in adults (46). Under conditions of extended chronic exposure, a steady-state distribution of lead between various organs and systems usually exists.
Inorganic lead is not metabolized in the body. Unabsorbed dietary lead is eliminated
in the faeces, and lead that is absorbed but not retained is excreted unchanged via the
kidneys or through the biliary tract (53). Metabolic balance studies in infants and
young children indicated that, at intakes greater than 5 µg/kg of body weight per day,
net retention of lead averaged 32% of intake, whereas retention was negative (i.e.
excretion exceeded intake) at intakes less than 4 µg/kg body weight per day (35). No
increases in blood lead were observed in infants with low exposure to other sources of
lead and mean dietary intakes of 3–4 µg/kg of body weight per day (54), thus
confirming the metabolic data.
Research on young primates has demonstrated that exposure to lead results in
significant behavioural and cognitive deficits, such as impairment of activity,
attention, adaptability, learning ability and memory, as well as increased
distractibility. Such effects have been observed following postnatal exposure of
monkeys to lead for 29 weeks in amounts resulting in blood lead levels ranging from
10.9 to 33 µg/dl (55). These effects persisted into young adulthood, even after levels
in the blood had returned to 11–13 µg/dl, and were maintained for the following 8–9
years (56). Studies on small groups of monkeys dosed continuously from birth
onwards with 50 or 100 µg/kg of body weight per day showed that there were still
significant deficits in both short-term memory and spatial learning at 7–8 years of age
Lead is a cumulative general poison, with infants, children up to 6 years of age, the
fetus and pregnant women being the most susceptible to adverse health effects. Its
effects on the central nervous system can be particularly serious.
Overt signs of acute intoxication, including dullness, restlessness, irritability, poor
attention span, headaches, muscle tremor, abdominal cramps, kidney damage,
hallucinations, loss of memory and encephalopathy, occur at blood lead levels of 100–
120 µg/dl in adults and 80–100 µg/dl in children. Signs of chronic lead toxicity,
including tiredness, sleeplessness, irritability, headaches, joint pain and
gastrointestinal symptoms, may appear in adults at blood lead levels of 50–80 µg/dl.
After 1–2 years of exposure, muscle weakness, gastrointestinal symptoms, lower
scores on psychometric tests, disturbances in mood and symptoms of peripheral
neuropathy were observed in occupationally exposed populations at blood lead levels
of 40–60 µg/dl (6).
Renal disease has long been associated with lead poisoning; however, chronic
nephropathy in adults and children has not been detected below blood lead levels of
40 µg/dl (64,65). Damage to the kidneys includes acute proximal tubular dysfunction
and is characterized by the appearance of prominent inclusion bodies of a lead–
protein complex in the proximal tubular epithelial cells at blood lead concentrations of
40–80 µg/dl (66).
There are indications of increased hypertension at blood lead levels greater than 37
µg/dl (67). A significant association has been established, without evidence of a
threshold, between blood lead levels in the range 7–34 µg/dl and high diastolic blood
pressure in people aged 21–55, based on data from the second United States National
Health and Nutrition Examination Survey (NHANES II) (68,69). The significance of
these results has been questioned (70).
Lead interferes with the activity of several of the major enzymes involved in the
biosynthesis of haem (6). The only clinically well-defined symptom associated with
the inhibition of haem biosynthesis is anaemia (40), which occurs only at blood lead
levels in excess of 40 µg/dl in children and 50 µg/dl in adults (71). Lead-induced
anaemia is the result of two separate processes: the inhibition of haem synthesis and
an acceleration of erythrocyte destruction (40). Enzymes involved in the synthesis of
haem include d-aminolaevulinate synthetase (whose activity is indirectly induced by
feedback inhibition, resulting in accumulation of d-aminolaevulinate, a neurotoxin)
and d-aminolaevulinic acid dehydratase (d-ALAD), coproporphyrinogen oxidase and
ferrochelatase, all of whose activities are inhibited (6,40). The activity of d-ALAD is
a good predictor of exposure at both environmental and industrial levels, and
inhibition of its activity in children has been noted at a blood lead level as low as 5
µg/dl (72); however, no adverse health effects are associated with its inhibition at this
level.
Inhibition of ferrochelatase by lead results in an accumulation of erythrocyte
protoporphyrin (EP), which indicates mitochondrial injury (47). No-observedadverse-effect levels (NOAELs) for increases in EP levels in infants and children
exist at about 15–17 µg/dl (73–75). In adults, the NOAEL for increases in EP levels
ranged from 25 to 30 µg/dl (76); for females alone, the NOAEL ranged from 20 to 25
µg/dl, which is closer to that observed for children (74,77,78). Changes in growth
patterns in infants younger than 42 months of age have been associated with increased
levels of EP; persistent increases in levels led initially to a rapid gain in weight, but
subsequently to a retardation of growth (79). An analysis of the NHANES II data
showed a highly significant negative correlation between the stature of children aged
7 years and younger and blood lead levels in the range 5–35 µg/dl (80).
Lead has also been shown to interfere with calcium metabolism, both directly and by
interfering with the haem-mediated generation of the vitamin D precursor 1,25-
dihydroxycholecalciferol. A significant decrease in the level of circulating 1,25-
dihydroxycholecalciferol has been demonstrated in children whose blood lead levels
were in the range 12–120 µg/dl, with no evidence of a threshold (81,82). Tissue lead
content is increased in calcium-deficient persons, a fact that assumes great importance
in the light of the increased sensitivity to lead exposure that could result from the
calcium-deficient status of pregnant women. It has also been demonstrated that
interactions between calcium and lead were responsible for a significant portion of the
variance in the scores on general intelligence ratings and that calcium influenced the
deleterious effect of lead (83). The regulatory enzyme brain protein, kinase C, is
stimulated in vitro by picomole per litre lead concentrations (an effect similar to that
produced by micromole per litre calcium concentrations), levels that could be
expected from environmental exposure (84).
Several lines of evidence demonstrate that both the central and peripheral nervous
systems are the principal targets for lead toxicity. The effects include
subencephalopathic neurological and behavioural effects in adults, and there is also
electrophysiological evidence of effects on the nervous system of children at blood
lead levels well below 30 µg/dl. Aberrant electroencephalograph readings were
significantly correlated with blood levels down to 15 µg/dl (85,86). Significant
reductions in maximal motor nerve conduction velocity (MNCV) have been observed
in children aged 5–9 years living near a smelter, with a threshold occurring at a blood
lead level around 20 µg/dl; a 2% decrease in the MNCV was seen for every 10 µg/dl
increase in the blood lead level (87). The auditory nerve may be a target for lead
toxicity, in view of reports of reduced hearing acuity in children (88). In the
NHANES II survey in the USA, the association with blood lead was highly significant
at all levels from 5 to 45 µg/dl for children 4–19 years old, with a 10–20% increased
likelihood of an elevated hearing threshold for persons with a blood lead level of 20
µg/dl as compared with 4 µg/dl (89). The NHANES II data also showed that blood
lead levels were significantly associated with the age at which infants first sat up,
walked and started to speak. Although no threshold existed for the age at which the
child first walked, thresholds existed at the 29th and 28th percentile of lead rank for
the age at which the child sat up and spoke, respectively (89)
Gonadal dysfunction in men, including depressed sperm counts, has been associated with blood lead levels of 40–50 µg/dl (90–93). Reproductive dysfunction may also occur in females occupationally exposed to lead (6,61).
Elevated cord blood lead levels were associated with minor malformations, such as angiomas, syndactylism and hydrocele, in about 10% of all babies. The relative risk of malformation doubled at blood lead levels of about 7–10 µg/dl, and the incidence of any defect increased with increasing cord lead levels over the range 0.7–35.1 µg/dl
Lead is exceptional in that most lead in drinking-water arises from plumbing in buildings, and the remedy consists principally of removing plumbing and fittings containing it, which requires both time and money. In the interim, all practical measures to reduce total exposure to lead, including corrosion control, should be implemented. It is extremely difficult to achieve a concentration below 10 µg/l by central conditioning, such as phosphate dosing.
It needs to be recognized that lead is exceptional, in that most lead in drinking-water arises from plumbing in buildings, and the remedy consists principally of removing plumbing and fittings containing lead, which requires much time and money. It is therefore emphasized that all other practical measures to reduce total exposure to lead, including corrosion control, should be implemented.
I shall compose another report, more pertinent to lead in ammunition (shot and bullets) in a little while.
Now, those of us of a certain age, had no option but to grow up ingesting the stuff. But that does not have to be the case, going forward.
. Do you think that as I am becoming heavier the older I get that it has anything to do with lead ingestion.
. Now gimme the facts on shot and bullets.
basc.org.uk
