Bringing context to blood lead risk

Editor’s note:  This op-ed was published on January 16, 2002 in the Shoshone News-Press.

(PHOTO CREDIT:  flickr)

The new class-action law suit filed on Jan. 7th by the Seattle law firm of Hagens Berman once again summons the attentions of Silver Valley citizens and parents to the  issue of lead  health.

In this article I’d like to offer some historical and comparative context.

Lead-health conditions in the mid-1970s  were very different from  what they are today. The Hagens Berman filing, however, tends to ignore historical change, mixing claims about circumstances of 25  years ago with more recent conditions. By most accounts there was a tangible lead-related public health problem in the Bunker Hill area 25 years ago. More than one-fifth of children living within a mile of the smelter stack had blood-lead levels of 80 micrograms per deciliter (µg/dL) or higher, 99 percent had 40-plus levels, and the mean level was 68 µg/dL. The highest blood-lead level reported was 164 µg/dL. The goal of public health efforts in the mid-1970s was to reduce all children to below 40  µg/dL.

Researchers who studied the blood-lead  situation in the mid-1970s were aware — even before the blood-lead  survey was put into the field — that the area’s main source of bioavailable  lead was the smelter  stack. Indeed, the sampling plan for the survey conducted in the mid­ ’70s was built on that assumption . The plan would sample children in five concentric  geographic  rings  (or sampling strata) at increasing radii from the stack.  Sample stratum  1, the closest ring, was defined   as up to a mile from the stack; stratum 2 was the ring 1-2.5 miles from the stack; stratum 3, 2.5-6.2 miles; stratum 4, 6.2-14.9 miles; and, finally, stratum 5, the most distant  ring,  14.9-19.8 miles.     

Measured blood lead levels decreased markedly with increasing distance from the stack.  In stratum 2, the frequency of 80-plus µg/dL blood-leads declined to 1.5% (down from 22% in stratum 1) and mean blood-lead dropped 28% (from 68 to 49 µg/dL). In strata 3 and 4, no 80-plus blood leads were found, about a quarter of children were 40- plus (down from 99 percent in stratum 1), and mean blood-lead fell to about half that in stratum 1. Airborne lead concentration was most highly correlated with child blood levels. Airborne lead dropped sharply with increasing distance from the stack.

High as these reported blood-lead levels were, it is important to evaluate them against the prevailing levels in the U.S. at that time. For instance, in 1976-1980, fully 88% of U.S. children aged 1-5 exceeded the CDC’s now-in-effect 10 µg/dL “level of concern” for lead.  Still higher population  lead levels were extant earlier on.  According to one source, mean population blood leads in the U.S. were 58 µg/dL in 1935, about 30 µg/dL from the late 1930s to the mid-1950s, and about 20 µg/dL in the  1960s.

Chart shows the percent of U.S. children aged 1-5 exceeding specified blood-lead levels from 1976-1980 (the dark bars) and 1988-1991 (the white bars). Chart borrowed from J.I. Pirkle et al., “The decline in blood lead levels in the United States,” Journal of the American Medical Association 272:284-291, 1994, 289.

The 1980s and 1990s saw a dramatic fall in child blood-lead levels (see chart). By the period 1988-1991, the proportion of children 1-5 measuring 10-plus µg/dL had dropped to 8.9% (a 90% decline from the 1976-1980 figure); that proportion fell still farther, to fractionally under 5%, in the late 1990s — I’ll refer to that 5% figure  again presently. At the national level, experts attribute this historic decline  in childhood blood-lead levels chiefly to radical reductions of lead in gasoline, paint, and soldered cans. For example, the amount of lead used in gasoline decreased by 99.8% between  1976 and  1990.

Public health reforms associated with gasoline, paint, and soldered cans favorably affected area children as much they did children in the rest of the nation. This area’s childhood blood leads have fallen as fast or faster than the trend in the nation as a whole. One indicator of the favorable shift in childhood levels in the valley is present in the blood­ lead standard now in use by the EPA: Whether 5 percent or more of children show blood leads of 10 µg/dL or higher — a far cry from the mid-1970’s goal of getting all children below 40 µg/dL.  Moreover,  it   is now credibly arguable that fewer than 5 percent of the valley’s children — whether inside or outside “the Box” — have blood-lead  levels as high as 10 µg/dL. It bears emphasizing that the EPA’s 5- percent-at-10 µg/dL population standard does not identify U.S. sites with especially high or threatening blood-lead levels. As mentioned ,  the 5 percent standard represents a good ballpark estimate of the  national exceedance rate. In other words, the Superfund standard in effect merely poses the question of whether a site lies below, at, or above the national rate.

Many might regard the historical trend in childhood blood lead as a remarkable public health success story. The mindset of the filing and the EPA Region X’s human health risk assessment is unimpressed however. They employed a number of rhetorical devices to darken a picture of otherwise radical reductions in environmental lead  exposure.

One such device is to argue that the  10 µg/dL blood-lead  standard is too permissive.   For instance, the Hagens-Berman  filing asserts on page 28 that, “current and developing scientific studies trace cognitive impairment in children with blood levels well below the historic 10 micrograms per deciliter level.” Similarly, EPA Region X’s recently released  proposed  plan notes the existence of “…recent  studies indicating adverse health effects at blood leads below 10 µg/dL” (page 4-1). Both assertions fail to note that such claims are based on methodologies far too crude to establish causality — and therefore the same claims are controversial within the scientific community.    Nor do the filing and proposed plan texts cite or review the scientific literature that rejects or disputes low-level lead effects — including, for example, A.S. Kaufman’s critical review of 26 studies in the literature (“Do low levels of lead produce IQ loss in children? A careful examination  of the  literature,” Archives  of Clinical Neurophychology 16:303-341, 2001). The EPA itself published a new regulation relating to soil and blood lead concentrations in the Federal Register early last year.  Though the EPA recognizes no lower theshold for blood lead, the regulation’s text notes:  “The EPA decided not to use a level lower than 10 µg/dL because the evidence indicates that health effects at lower levels of exposure are less well substantiated, based   on a limited number of children, and observation of subtle molecular changes that are not currently thought to be sufficiently significant to warrant national concern” (Federal Register, Jan 5, 2001, page 1215). In short, the texts press their rhetoric beyond what even the EPA (not an organization generally noted for minimizing lead-related health risks) can comfortably  countenance.

Similarly, the shift of public health attention from air to soil as the main source of population  exposure is no less problematic — and lies at one of the cruxes of the on-going dispute between EPA science and the SNRC science committee. Whereas lead oxide emitted from the smelter stack had high bioavailability, lead compounds found in mine tailings may be much less bioavailable and thus pose much less, even little or no, threat to humans. The knowledge-base  surrounding the  issue of lead bioavailability for humans across different lead compounds or lead “species” is very thin. Wrote one expert in a paper published in 1998: “Lead bioavailability in its many multidisciplinary complexities and nuances is still poorly understood and misunderstood by many, is interpretively misused by others, and continues to feed a growing, increasingly jumbled literature.” The EPA’s guidelines for evaluating sites where alleged lead risk derives from mine tailings or historic mining recognize great potential variability in bioavailability. These guidelines recommend careful site-specific evaluations and lead speciation. The SNRC science committee has objected that just such adequate site-specific work has never been carried out by EPA for the wider basin area. Instead, it premised its model-based estimates of childhood blood-lead levels for the basin on the iffy application of inside-the-box assumptions to outside-the-box circumstances, assumptions which in turn were ostensibly validated by clearly inadequate and by now out-of-date population  survey  data.

The wind filling the sails of the Hagens Berman filing is social stigma rather than credible scientific evidence or careful reasoning.  The   same stigma is also and unfortunately perpetuated by the tiling’s rhetorical excesses — for example, by confounding the past with the present, by magnifying lead risk beyond what the mainstream   scientific literature or current U.S. policy  suggests, and by glossing over the difference between smelter-based and tailings-based lead­ exposure  circumstances.

Fortunately, plans are already in the making to bring the question of current lead health circumstances in the Silver Valley to a scientific and scholarly forum where sloppy science and argumentation will have little chance to prevail.

— Ron Roizen

 

 

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