Washington, DC. Flint. Pittsburgh. Detroit. Newark.
Every time you turn around, another US city develops a drinking water crisis stemming from the discovery of elevated lead levels. While the water crisis in Flint, Michigan captured national attention when it became clear that increased water lead levels were reaching the city’s children, it was not the first city in this position, nor would it be the last. We face a national water crisis.
How did we get here?
It would seem that “lead pipes are bad” might have been learned from Ancient Rome, a society whose downfall is often ascribed, at least in part, to the heavy metal.1 And yet, lead plumbing pipes are still very much among us. Lead service lines – the pipes that flow from a source of water into a building – are everywhere. As if that were not enough, buildings built before 1988 or so contain copper pipes connected by lead solder. Even newer brass faucets and fittings (made before 2014) can shower lead into drinking water. So, with all this lead in our water pipes, why don’t we all succumb to lead encephalopathy? How have we been spared all this time?
Water Chemistry 101
It all comes down to corrosion, the process by which a metal is oxidized, allowing it to form soluble complexes which leach into water. Under ideal conditions, the metals in water – like iron, aluminum, calcium, copper and lead – form a stable, protective scale over lead surfaces and soldered joints. If corrosion occurs, however, this fine balance is lost. This arises when the water itself becomes corrosive, and may be worsened by physical conditions in the water system. Factors contributing to corrosion include, but are not limited to:
- Water pH (< 6.5 or > 8.5)
- Water hardness (e.g., how much calcium and magnesium is present)
- Presence of organic matter and sediment (too much is bad)
- High dissolved oxygen content (which oxidizes lead)
- Presence of competing metals (like aluminum) which may prevent corrosion inhibitors from doing their job. (www.epa.gov)
- Water temperature (hot water contains more lead, and lead levels rise in the summer) (www.usgs.gov)2
- Pipe manipulation (meter installation or replacement, street excavation, and yes, even replacement of lead service lines)
- High water velocity (which breaks up scale)
- Low water use (which allows the water to sit in contact with lead surfaces longer before flowing out of the system)
So, we control corrosion. Easy peasy.
Corrosion control is both art and science, where tweaks on one part of the system create changes (a ripple effect, if you will) throughout. One feature of this is the addition of corrosion inhibitors. The most common compounds contain orthophosphate (PO43-), which reacts with divalent lead and calcium to form stable compounds with minimal tendency to dissolve. The other category used are silicates, which are a mixture of soda ash (Na2CO3) and silicon dioxide. Other chemical manipulations, such as the change in disinfectant, or attempts to diminish excessive calcium deposits, can have a deleterious effect on corrosion as well.
In the late 1990s, Washington, DC had widespread elevation in water lead levels due to a switch in disinfectant chemicals from chlorine to chloramine. What started as an attempt to combat cryptosporidium, which is poorly controlled by chlorine disinfectants, led to a large increase in the corrosiveness of the water and elevated lead levels. As I said, water engineering is complicated.
In Flint, Michigan, the story is a little different. By most accounts, the city of Flint decided, in a cost-saving measure, to switch its water source from Detroit Water to the Karegnondi Water Authority. In the interim, while new pipelines were being built, the city opted to use the untested Flint River as the source of drinking water. The Flint River was already known by some to be contaminated with bacteria and other hazardous chemicals. It was also corrosive, with inadequate corrosion control. Predictably, lead contamination resulted.3
Newark, NJ now faces its own water crisis. There are important differences and similarities. While the source water is not otherwise contaminated, there was a failure in corrosion control. This, coupled with aging plumbing infrastructure fallen into disrepair, has led to predictable results. Reports of elevated levels have been discussed for a number of years but only now coming to a head, with a public outcry and distrust overflowing.
Dangles, Sapa, and Gripes . . . Oh my!
It’s perhaps helpful to take a step back and look at lead in both a historical and chemical context. Lead has a low melting point (621.3˚F) and high malleability. This makes it easy to work with, which is why since Ancient times it has been incorporated into things like plumbing pipes and cooking utensils. The use of a concentrated lead acetate sugar as a preservative and sweetener (Sapa) by Roman aristocrats is the primary reason historians believe lead encephalopathy contributed to the fall of the Roman Empire. Even in American Colonial Times, Benjamin Franklin described lead poisoning in tinkers (metal workers) and typesetters, as the “dry gripes” (abdominal pain) and the “dangles” (wrist drop). (Drinking from leaded pewter tankards likely didn’t help either). Lead compounds comprise several pigments incorporated into house paint and ceramic glazes, including lead carbonate (a very white white), lead chromate (yellow), and lead oxide (red). Organic lead, specifically tetramethyl and tetraethyl lead, were used as anti-knock gasoline additives in automobile fuel before their discontinuation in the 1970s.
The toxic effects of lead are widespread and occur in a dose-dependent fashion. There is no physiologic role for lead. Although the effects are too numerous to name here, they largely stem from lead’s tendency to interfere with calcium, magnesium, and zinc-dependent processes. For example, the derangement of calcium-mediated neurotransmitter release underlies some of lead’s developmental neurotoxic effects as well as the vascular abnormalities leading to chronic hypertension. Lead interferes with heme synthesis via inhibition of ferrochelatase and delta-aminolevulinic acid dehydratase, causing buildup of precursors and the characteristic microcytic anemia with basophilic stippling. It’s nephrotoxic, causing a proximal tubule dysfunction (Fanconi syndrome), progressive interstitial fibrosis, and “saturnine gout” via inhibition of uric acid excretion. Lead is gametotoxic and associated with miscarriage in patients with occupational exposure. The list goes on, although the majority of these effects are seen at blood lead levels higher (> 30mcg/dL) than would be expected from drinking water.
A Little Means A Lot: The No-Threshold Toxin
When we talk about lead in water, we’re talking parts per BILLION. How much harm can it do? At very low blood lead levels the primary concern is to the developing brain: namely infants and young children under 6. Lead interferes with several processes in neurodevelopment, including myelination and “synaptic pruning” – in which unnecessary neural connections are eliminated in favor of more meaningful ones, thereby reducing the signal-to-noise ratio of neural communication. The results have been demonstrated only in large population-based studies, although the results are strikingly consistent. Children in populations with higher BLLs demonstrate lower IQ, higher incidence of behavioral/cognitive delays, as well as impaired reading readiness and an increased tendency towards criminal justice system involvement, even when controlled for confounders such as socioeconomic status, parental IQ and education. These effects appear to be incrementally more pronounced (the so-called “supralinear” dose-response) at very low BLLs (like 0-10mcg/dL).4,5 Critics of this data discuss the presence of uncontrolled confounders, question the statistical assumptions which underlie these results6, and point out that previous generations, with leaded gasoline and other sources of exposure, surely had higher BLLs with no apparent effect. It’s also impossible to predict effects on any one individual on the basis of population-based studies. Nonetheless, the inconvenient truth is that lead contamination is likely to affect the nation’s young, in a small but widespread way.
How Many Angels can Dance on the Head of a Pin? Quantifying Exposure
How much contaminated water would one have to drink to get poisoned? Risk assessment is virtually impossible based on water consumption. Many factors contribute, including the age of the exposed person, the lead concentration at that point in time, the length of exposure, how much water is actually being consumed, the temperature of the water…only one of which (age) is possible to pinpoint. Much hand-wringing effort can go into figuring this out. Although there is a lot of academic debate and mathematical modeling which may provide an estimate of lead ingested from water, the only definitive way to assess exposure is with a blood lead level, a reasonable (albeit imperfect) assessment of body burden and prognosis.
What happens to BLLs when drinking water gets contaminated? Small elevations, in more people. For example, in Flint, no child’s BLL rose to the threshold of chelation (45 mcg/dL) – but after the water change, the percentage of children in Flint with elevated BLLs (as defined by the CDC “Level of Concern” of 5 mcg/dL) doubled, from 2.4% to 4.9%. In children living in the wards of the city where the water lead levels were highest, that incidence rose from 4% to 10%. This is in comparison to the surrounding cities in Genesee County which did not undergo a water source change, in which the prevalence of elevated BLLs was around 1%.7 Similar increases in prevalence were reported during the Washington, DC water crisis, even when the threshold was higher at 10 mcg/dL.8 Again – small elevations, but in more kids.
The Way Forward
The ideal municipal response is beyond the scope of this discussion, and involves a great many decisions regarding communication, remediation, assessment of risk in the population, and partnering with relevant agencies to ensure the right expertise is applied to each branchpoint. On a larger scale, this comes down to standards, and upholding them. How big of a deal is lead in water? For the individual child who is exposed, the effects may not even be detectable, and will not be life-threatening. In the face of municipal water crises, which become highly politicized and publicized, what these children and their families need most is focused guidance on reducing exposure, and early detection of developmental challenges if they do arise.
But in the big picture, there’s a no-threshold toxin in our water which can plausibly cause the loss of many IQ points over an entire population. I’d say that’s a pretty big deal, indeed. The fix is not simple, but we must envision a future in which drinking water is completely lead-free.Faucet by Jouni Rajala Coliseum by Yoal Desurmont Baby Bath Water by Lubomirkin Blocks by Michał Parzuchowski Angels by Gavin Allanwood Playground by Andrew Seaman
- 1.Nriagu J. Saturnine gout among Roman aristocrats. Did lead poisoning contribute to the fall of the Empire? N Engl J Med. 1983;308(11):660-663. https://www.ncbi.nlm.nih.gov/pubmed/6338384.
- 2.Masters S, Welter G, Edwards M. Seasonal Variations in Lead Release to Potable Water. Environ Sci Technol. 2016;50(10):5269-5277. https://www.ncbi.nlm.nih.gov/pubmed/27078082.
- 3.Hanna-Attisha M. What the Eyes Don’t See: A Story of Crisis, Resistance, and Hope in an American City. One World; 2019.
- 4.Lanphear B, Hornung R, Khoury J, et al. Low-level environmental lead exposure and children’s intellectual function: an international pooled analysis. Environ Health Perspect. 2005;113(7):894-899. https://www.ncbi.nlm.nih.gov/pubmed/16002379.
- 5.Canfield R, Henderson C, Cory-Slechta D, Cox C, Jusko T, Lanphear B. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med. 2003;348(16):1517-1526. https://www.ncbi.nlm.nih.gov/pubmed/12700371.
- 6.Banner W, Kahn C. Low blood lead level effects on intelligence: can a dose-response curve be determined from the epidemiological data? Clin Toxicol (Phila). 2014;52(2):113-117. https://www.ncbi.nlm.nih.gov/pubmed/24443996.
- 7.Hanna-Attisha M, LaChance J, Sadler R, Champney S. Elevated Blood Lead Levels in Children Associated With the Flint Drinking Water Crisis: A Spatial Analysis of Risk and Public Health Response. Am J Public Health. 2016;106(2):283-290. https://www.ncbi.nlm.nih.gov/pubmed/26691115.
- 8.Edwards M, Triantafyllidou S, Best D. Elevated blood lead in young children due to lead-contaminated drinking water: Washington, DC, 2001-2004. Environ Sci Technol. 2009;43(5):1618-1623. https://www.ncbi.nlm.nih.gov/pubmed/19350944.
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