Risk Assessment is another type of causation: predicting whether an exposure, usually in a population rather than a single individual, will increase the risk of developing some adverse health effect, without necessarily determining whether such health effect actually occurs. Risk means that all such exposed individuals are more likely to develop an adverse effect, but it does not mean that any particular individual will or even that the majority of individuals will. Smoking, for example, increases risk of lung cancer from approximately one in 100 to 1 in 10--a signficiant increase. Nevertheless, ninety percent of smokers do not develop lung cancer, even though they are all at increased risk. Risk Assessment is used by regulatory agencies, such as the EPA, to determine how much of a chemical can be released into the environment without causing an unacceptable increase in risk of an adverse effect. 'Unacceptable' is more of a policty decision than a scientific one.
Specific causation analysis can be divided into the following three components:
(1) Hazard Assessment
(2) Exposure Assessment
(3) Health Assessment
(1) Hazard Assessment: what harm can the chemical cause, based on intrinsic toxicity and circumstnaces of exposure, form of chemical (gas, liquid, solid) and susceptibility of individual.
(2) Exposure Assessment how much of the chemical is in a media (air, water, food, soil) available to be taken into the body? Is this a one-time or multiple exposure? Does it occur over a short period of time (acute) or over many months or years (chronic)? How does the length of exposure affect the toxicity of the chemical? How much of the chemical gets absorbed into the body (dose), and where in the body does it end up (distribution and target organ/tissue)?
(3) Health Assessment: what type of health effect develops (or gets exacerbated), and does this occur immediately or after a delay (lag time)? Is this a new effect in the individual or is there a history of this type of problem, made worse by the chemical exposure? Is the individual in a high risk group (in utero, infant, elderly, reduced immune function)? Are there other (alternative) known causes for this problem and were these causes present ?
Blood lead threshold levels have been decidedly downward over the past forty years. While it may be possible that the bottom has been reached or that new research might at some point reverse the trend--something that does happen with other chemicals, although rarely--recent evidence suggests that the direction of the trend for lead will continue. In part this is due to better data at lower concentrations of lead, simply showing or confirming what has been suggested for a long time by insufficient data. And in part this is due to an appreciation and ability to test much more subtle effects of lead toxicity.
The results of the jury verdict in Rhode Island that held paint manufacturers responsible for lead paint that remains in homes and the toxic consequences of this situation, come at a time of growing understanding of the more subtle toxic effects of lead in the neurological development of children; that is, that (much) lower blood lead (BPb) than previously shown or considered, can be toxic and over a wider range of adverse affects. The rapid change in which significantly lower lead toxicity and the stakes involved has been recognized is reflected in the speed of change in acceptable threshold levels. The 1990 decision by the U.S. Department of Health and Human Services to eliminate all BPb > 25 ug/dl in children 6 months through 5 years of age by 2000 (Healthy People 2000) was followed in 1991 by a reduction in that 25 ug/dl threshold of concern to 10ug/dl by the Centers for Disease Control (CDC 1991). By the late 1990’s a new, Healthy People 2010 goal was set to eliminate all BPb > 10 ug/dl (Myer et al 2003; US Dept HHS 2000).
By implementing these different thresholds and goals, the proportion of children at-risk (BPb > 10ug/dl) has been reduced during the past thirty years from approximately 88 percent to 2.2 percent (NHANES 2000), an obviously very significant accomplishment in public health efforts to eliminate child lead poisoning. Nevertheless, CDC estimates that the 2.2 percent figure translates into more than four hundred thousand children with BPb > 10 ug/dl (NHANES 2000), and is a nationwide average; inner city and/or low socioeconomic areas often have much higher proportions of children with BPb exceeding 10 ug/dl, typically 8-10 percent of children and in some areas as high as twenty percent. Lead poisoning clearly remains a major problem in these areas, the very places that can least afford further compromise of intellectual functioning, due to negative socioeconomic circumstances and lack of early childhood stimulation.
Also, associations between BPb and intellectual functioning are typically based on population averages; neuropsychological testing of individuals, especially those with borderline intellectual functioning, shows widely varying impacts from individual to individual of even a few-point decrement in IQ (Dietrich 1993). And a few point decrement in intellectual functioning, among hundreds of thousands of children with borderline intellectual functioning to start with, can produce enormous economic and social impacts (Fulton et al 1987).
A ‘Safe’ Threshold for Lead Toxicity?
Further extending this trend, additional data and new analysis of existing data support a growing scientific consensus that a threshold for lead neurotoxicity in fetuses and young children does not exist (WHO 1995; CDC 2003); CDC stated in a consensus report that ‘a threshold for harmful effects of lead remains unknown’ (Myer et al 2003). And following the release of the comprehensive ‘Third National Report on Exposure to Chemicals in Humans’ (CDC 2005), Jim Pirkle, deputy director of CDC’s Environmental Health Lab, stated unequivocally that a safe blood lead level in children simply does not exist.
The progressive reduction over time in the toxic threshold of lead ( a similar trend seen with most other chemicals) results from accumulation of data, improved understanding of target tissue injury, and more sophisticated tools and methodology to measure adverse toxic effects. The ‘safe’ threshold for lead has been revised downward six-fold during the past thirty years, from 60 ug/dl prior to 1971, 40 ug/dl until 1978, 30 ug/dl until 1985, and 25 ug/dl from 1985 until 1991 when the threshold was changed to the present < 10 ug/dl level (CDC 1975; CDC 1985; CDC 1991). Each reduction in threshold leads to greater focus on BPb toxicity at lower levels and, with that, more accumulated data at those lower levels, allowing verification of a reduced toxicity threshold.
Increasingly, the 10 ug/dl ‘threshold’ for lead is seen to reflect a ‘threshold’ of reliable data rather than a threshold of toxicity; that is, until recently insufficient data existed to verify lower toxicity, rather than sufficient data showing no toxicity at lower levels. This distinction is often the case and just as often is not made clear, leading to misinterpretation of data and toxicity. One resultant problem has been insufficient monitoring of children from infancy through five years of age or more—generally believed the critical window of significant and lasting neurological damage—so it has been difficult to know whether observed neurological effects at sub-10 ug/dl BPb concentrations actually reflected toxicity at those levels or simply reflected missed monitoring of periodic spikes of BPb above10 ug/dl during the critical exposure period.
Is the Center for Disease Control's goal to reduce lead below 10ug/dl blood in all children
younger than 72 months by 2010,
Thomas F. Schrager, Ph.D.