How to comment:
- Review the comments prepared by Indivisible Montgomery (below)
- Go to https://www.regulations.gov/comment?D=EPA-HQ-OA-2018-0259-0001
- Click the “Comment Now” button near the top right of the page
- Enter your comments in the text box; feel free to copy ours or write your own
- Click “Continue”
Comments on this rule change are CLOSED
Comment Text (for copy/paste into comment field)
We are Indivisible Montgomery, a grass-roots organization of over 1400 members in Montgomery County, Maryland. We appreciate the opportunity to comment on the proposed changes to the MATS standards.
In December 2011, the Environmental Protection Agency, authorized by the 1990 Clean Air Act Amendments, announced the Mercury and Air Toxics Standards (MATS) to reduce emissions of mercury and other toxic hazardous air pollutants (HAP) from coal and oil-fired power plants.
The Trump Administration is proposing that it is not appropriate and necessary to regulate HAP emissions from coal and oil-fired power plants. This proposal is based on a new–and deeply flawed–assessment of the benefits of MATS, which concluded that the residual risk to the public from mercury and other HAP emissions is “acceptable” and the 2011 MATS requirements are not warranted.
The proportion of anthropogenic mercury has nearly doubled within the last 100 years and significantly exceeds naturally released mercury (1). While power plants are among the largest sources of mercury emissions, they were among the last to be regulated. Despite intense industry pressure, several studies, such as the Utility Study Report to Congress, the Mercury Study Report to Congress and a National Academies report on the Toxicological Effects of Mercury, all strongly supported the use of already-existing control technology and strategies to limit emissions. We believe that these findings were correct, and EPA should do everything in its power to limit the release of these pollutants into the environment.
Dangers of Mercury Exposure
Elemental mercury is rapidly converted to methylmercury (MeMg) by bacteria and abiotic processes. MeMg is a well studied and understood neuro-, nephro-, and immunotoxin, with toxic effects on multiple organ systems and the ability to cross both the blood-brain and blood-placental barriers (2). Both children and developing fetuses are highly susceptible to the neurotoxic effects of MeMg.
The fetal effects of MeMg exposure may be immediate and severe, or delayed and more subtle, depending on dose and exposure timing. Adverse outcomes include mental retardation, cerebral palsy, seizures, vision, hearing and memory loss, as well as delayed developmental milestones. New long-term cohort studies also suggest significant cardiovascular effects, exacerbating a pre-existing downward trend in the cardiovascular health of American citizens (3). These effects are often life-long and irreversible (4,5), causing a large public health and economic burden.
Even relatively low doses of MeMg can cause significant adverse outcomes. Large prospective epidemiological studies show associations between prenatal mercury exposure and neurological development in children, leading to decreased IQ and performance in tests of memory, attention and spatial cognition (6-8). These effects have been confirmed for even low exposure levels (9). This epidemiological evidence is supported by direct evidence of toxic effects of MeMg on neuronal stem cells in vivo and in vitro, leading to apoptosis and, even at concentrations comparable to the current population exposure levels, failure of spontaneous differentiation (10-12).
EPA’s own regulatory impact analysis for the 2011 rule estimated that the in the year of full implementation, the rule would prevent up to 11,000 deaths; 4,700 non-fatal heart attacks; 130,000 asthma attacks; 5,700 hospital and emergency room visits. EPA provided a list of additional effects on public health that it lacked the resources to fully quantify.
By 2016 power plants across the country had installed pollution controls and monitoring equipment and were in compliance with MATS. In fact, the capital and operating cost of compliance turned out to be much lower than EPA had estimated due both to industry trends, technological developments, process-improvement advantages, and a broader shift toward natural-gas generation reducing the number of active coal-fired plants requiring retrofit. Industry analysts have argued that the actual implementation cost was as low as 25% of EPA’s original estimate of $9.6 billion. The new assessment by EPA continues to use the conservative higher estimate for compliance rather than the real-world data, leading to a fatally flawed cost-benefit analysis.
We strongly object to any loosening of HAP emission regulations. The environmental and public health costs are clear, the cost of compliance has been overstated, and this rule change harms our most vulnerable populations. There is no credible argument that places a slight financial benefit to coal-fired power plant operators above the health, wellbeing and future potential of American children. We urge the EPA to abandon this proposal.
For References, please see attached PDF.
- Schuster PF, Krabbenhoft DP, Naftz DL, Cecil LD, Olson ML, Dewild JF, et al. Atmospheric mercury deposition during the last 270 years: a glacial ice core record of natural and anthropogenic sources. Environ Sci Technol. 2002;36:2303–10. [PubMed]
- Taber KH and Hurley MD. Mercury exposure: effects across the lifespan. J. Neuropsych. 2008; 20(4):389
- Grandjean P, Murata K, Budtz-Jorgensen E and Weihle P. Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort. J. Pediatr 2004 144(2): 168-76
- Grandjean, P. Methylmercury toxicity and functional programming. Reprod. Toxicol. 2007 23(3): 414-20
- Murata K, Weihe P, Budtz-Jørgensen E, Jørgensen PJ, Grandjean P. Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury. J. Pediatr 2004 144(2) 177-83
- Grandjean P, Weihe P, Jørgensen PJ, Clarkson T, Cernichiari E, Viderø T. Impact of maternal seafood diet on fetal exposure to mercury, selenium, and lead. Arch Environ Health. 1992 47(3):185-95
- Kjellstrom T, Kennedy P, Wallis S, Stewart A, Friberg L, Lind B. Physical and Mental Development of Children with Prenatal Exposure to Mercury from Fish. Stage II: Interviews and Psychological Tests at Age 4. National Swedish Environmental Protection Board; Solna, Sweden: 1989
- Grandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama K, Murata K, Sørensen N, Dahl R, Jørgensen PJ. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicol Teratol. 1997 19(6):417-28
- Lederman SA, Jones RL, Caldwell KL, Rauh V, Sheets SE, Tang D, Viswanathan S, Becker M, Stein JL, Wang RY, Perera FP. Relation between cord blood mercury levels and early child development in a World Trade Center cohort. Environ Health Perspect. 2008 116(8):1085-91
- Tamm C, Duckworth J, Hermanson O, Ceccatelli S. High susceptibility of neural stem cells to methylmercury toxicity: effects on cell survival and neuronal differentiation. J Neurochem. 2006 97(1):69-78.
- He X1, Imanishi S, Sone H, Nagano R, Qin XY, Yoshinaga J, Akanuma H, Yamane J, Fujibuchi W, Ohsako S. Effects of methylmercury exposure on neuronal differentiation of mouse and human embryonic stem cells. Toxicol Lett. 2012 Jul 7;212(1):1-10.
- Fujimura M, Usuki F. Methylmercury causes neuronal cell death through the suppression of the TrkA pathway: in vitro and in vivo effects of TrkA pathway activators. Toxicol Appl Pharmacol. 2015 282(3):259-66