Posted on February 8, 2011 by Roger Ferland
* My thanks to Gary E. Marchant, J.D., Ph.D., Lincoln Professor of Emerging Technologies, Law & Ethics, Center for Law, Science & Innovation at Arizona State University. He is the brains behind this blog entry.
One of the founding principles of the Clean Air Act is the National Ambient Air Quality Standards or NAAQS. Attainment and preservation of the NAAQS is the goal of State Implementation Plans, the permit system is intended to protect the NAAQS and most of the technology-based emission limitations are for the control of NAAQS-based pollutants. However, several of the premises for setting the NAAQS are no longer either scientifically or legally supportable.
After almost forty years, the criteria for establishing the NAAQS are settled.
- The level of the NAAQS must protect public health with “an adequate margin of safety.”
- In setting NAAQS, EPA cannot consider the cost or feasibility of achieving it.
- The NAAQS must not only protect the general public, but also there must be an absence of adverse effects on “susceptible” or “sensitive” subgroups and individuals.
- According to EPA, “susceptible” subgroups and individuals can be defined by:
- Life stages, e.g., children, the elderly or pregnant women
- Prior immune reactions
- Disease state, e.g., asthmatics
- Prior damage to cells or all systems
- What is called “genetic polymorphism,” the small, but significant percentage of the population who have genetic susceptibilities to certain toxins
The problem is that if EPA declares that the NAAQS must prevent adverse health impacts on this range of susceptible subgroups and individuals, the only level that can prevent adverse effects across the range is zero.
For the last three decades the achievement of no adverse clinical effects with an adequate margin of safety has caused the NAAQS to be set at lower and lower concentrations. Indeed, the controversy over a more and more stringent ozone NAAQS was heightened by a recent EPA study that showed decreased lung functions among even healthy individuals at 0.060 µ/m3. These, however, are only clinical adverse effects. If all toxcogenomic or gene expression changes that are indicative of a toxic response are considered, it is hard to justify any concentration but zero for the NAAQS. As EPA has acknowledged in criteria documents for the PM-10, lead, ozone and NOx NAAQS, genomic susceptibility plays an adverse role in responses to inhalation of these pollutants, particularly with respect to specific individuals or certain groups. For these individuals or groups there is no concentration of NAAQS pollutants that will guarantee an adequate margin of safety. For example, 100,000 Americans have a condition called an alpha-1 antitrypsin deficiency. People with this condition are predisposed to emphysema and other serious lung diseases from exposure to any level of smoke or dust. Similar genetic susceptibility to any level of certain pollutants above zero can be shown for a wide range of pollutants, individuals and genetically sensitive groups.
The point in all of this is that if we continue to require a no adverse effects with an adequate margin of safety as a minimum criterion for the NAAQS with no consideration of cost or practicable achievability, the inevitable result will eventually be a scientific train wreck.