Contact Kelly Ferguson (kellferg@umich.edu) for additional information. Produced by the Detroit Reproductive 

Environmental Advocacy Matters Group: Kelly Ferguson, Natalie Sampson, Amy Schulz, Trish Koman, Chris 

Coombe, and Donele Wilkins. April 22, 2015.

SUPPORT FOR LOWER OZONE STANDARD, DUE TO OMITTING PREGNANT 

WOMEN AS A VULNERABLE POPULATION IN THE NAAQS REVIEW PROCESS

Recommendation. We commend the EPA efforts to reduce the current ozone standard, and 

support the lower range (60-65 ppb). For the current proposed rule, pregnant women specifically, 

not just consequences to birth outcomes, were not included as a vulnerable population. This 

omission provides cause for supporting the lower range to provide an adequate margin of safety.

Omission of pregnant women in the ozone ISA. Prenatal development is considered as a 

lifestage that is more susceptible to consequences of ozone exposures, and reproductive and 

developmental consequences to the fetus are considered. However, the ISA does not address 

health consequences to ozone exposure experienced by pregnant women specifically, and other 

data that support this population as being at-risk to ozone exposure.

Pregnant women are subject to a broader range of potential health consequences from 

ozone exposure compared to the general population which need to be accounted for. Ozone 

exposure has been linked to preeclampsia, a hypertensive disorder, as well as a number of 

adverse birth outcomes which can have immediate and repercussive health consequences to 

pregnant mothers. Preeclampsia puts mothers at an increased risk of mortality during pregnancy 

and also for an increased risk of cardiovascular disease later in her life.1 New studies have been 

published since the 2013 Ozone ISA was completed demonstrating strong evidence for an 

association between exposure to ozone during pregnancy and the development of 

preeclampsia.2,3 Ozone exposure is also associated with adverse pregnancy outcomes, including 

fetal mortality, premature birth, low birth weight, and birth defects. These findings have been 

summarized in the ozone ISA, although new convincing evidence has been added to this body of 

literature since 2011,4,5but the impact of these outcomes on maternal health (both during 

pregnancy and later in life) are not acknowledged. These include, but are not limited to physical 

(e.g., C-section) and mental (e.g., psychological distress and depression) consequences.6-9

Pregnant women receive a higher dose of ozone for a given exposure level compared to the 

general population which should be accounted for in the ISAand Federal Register. Pregnant 

women have an increased metabolic rate (i.e., amount of oxygen consumed) compared to nonpregnant women of reproductive age. 10-12 Since the primary route of exposure for ozone is 

through inhalation, it follows that the dose would be higher in pregnant women, although, to our 

knowledge, this has not been directly demonstrated in epidemiologic, animal, or modeling 

studies.

Vulnerability of pregnant women is of great concern because of the size of the population.

Additionally, pregnant women represent a large proportion of the US population. For 2013, the 

National Vital Statistics Reports from the US Department of Health and Human services 

estimated 3,957,577 births.13 This underestimates the number of pregnancies, but otherwise 

translates to pregnant women accounting for 1.25% of the population that year.14
Contact Kelly Ferguson (kellferg@umich.edu) for additional information. Produced by the Detroit Reproductive 

Environmental Advocacy Matters Group: Kelly Ferguson, Natalie Sampson, Amy Schulz, Trish Koman, Chris 

Coombe, and Donele Wilkins. April 22, 2015.

References.

1. Ray JG, Vermeulen MJ, Schull MJ, Redelmeier DA. Cardiovascular health after maternal 

placental syndromes (CHAMPS): population-based retrospective cohort study. Lancet. 

2005;366(9499):1797-1803.

2. Hu H, Ha S, Roth J, Kearney G, Talbott EO, Xu X. Ambient Air Pollution and 

Hypertensive Disorders of Pregnancy: A Systematic Review and Meta-analysis. 

Atmospheric environment. 2014;97:336-345.

3. Pedersen M, Stayner L, Slama R, et al. Ambient air pollution and pregnancy-induced 

hypertensive disorders: a systematic review and meta-analysis. Hypertension. 

2014;64(3):494-500.

4. Ha S, Hu H, Roussos-Ross D, Haidong K, Roth J, Xu X. The effects of air pollution on 

adverse birth outcomes. Environ Res. 2014;134:198-204.

5. Lee PC, Roberts JM, Catov JM, Talbott EO, Ritz B. First trimester exposure to ambient 

air pollution, pregnancy complications and adverse birth outcomes in Allegheny County, 

PA. Matern Child Health J. 2013;17(3):545-555.

6. Behrman RE, Butler AS, eds. Preterm birth: causes, consequences, and prevention.

Washington, DC: The National Academies Press; 2007.

7. Holditch-Davis D, Bartlett TR, Blickman AL, Miles MS. Posttraumatic stress symptoms 

in mothers of premature infants. Journal of obstetric, gynecologic, and neonatal nursing : 

JOGNN / NAACOG. 2003;32(2):161-171.

8. Singer LT, Salvator A, Guo S, Collin M, Lilien L, Baley J. Maternal psychological 

distress and parenting stress after the birth of a very low-birth-weight infant. JAMA. 

1999;281(9):799-805.

9. Veddovi M, Kenny D, Gibson F, Bowen J, Starte D. The relationship between depressive 

symptoms following premature birth, mothers' coping style, and knowledge of infant 

development. Journal of reproductive and infant psychology. 2001;19(4):313-323.

10. Clapp JF, 3rd, Seaward BL, Sleamaker RH, Hiser J. Maternal physiologic adaptations to 

early human pregnancy. American journal of obstetrics and gynecology. 

1988;159(6):1456-1460.

11. Grindheim G, Toska K, Estensen ME, Rosseland LA. Changes in pulmonary function 

during pregnancy: a longitudinal cohort study. BJOG : an international journal of 

obstetrics and gynaecology. 2012;119(1):94-101.

12. Rees GB, Broughton Pipkin F, Symonds EM, Patrick JM. A longitudinal study of 

respiratory changes in normal human pregnancy with cross-sectional data on subjects 

with pregnancy-induced hypertension. American journal of obstetrics and gynecology. 

1990;162(3):826-830.

13. Hamilton B, Martin J, Osterman M, Curtin S. Births: Preliminary Data for 2013. National 

vital statistics reports. 2014;63.

14. Annual Estimates of the Resident Population: April 1, 2010 to July 1, 2013. 2014.