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Reducing BPA, Phthalate & PAH Exposure

How to Prevent Exposures to PAHs and BPA

An evidence-based checklist of what to get rid of when trying to conceive and during pregnancy

Three families of everyday chemicals — bisphenols (BPA and its "BPA-free" cousins BPS and BPF), phthalates, and polycyclic aromatic hydrocarbons (PAHs) — reach almost everyone, every day, through food, water, personal care products, and the air we breathe. They are short-lived in the body, which is the hopeful part: the choices you make this week change your body burden within days.

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Why this matters before and during pregnancy

These chemicals are endocrine disruptors (bisphenols and phthalates) or combustion pollutants that cause oxidative stress and cross the placenta (PAHs). The evidence below is mostly from observational human studies — they show consistent associations, not proof of cause in any single person — but the direction is consistent across two decades of research, and the exposures are avoidable. Tap a heading to see the evidence.

Fertility — eggs, sperm, and conception›
  • Women: Higher urinary BPA has been linked to lower ovarian reserve — fewer antral follicles and lower anti-Müllerian hormone (AMH) — and to poorer ovarian response in IVF. In the EARTH fertility cohort, antral follicle count fell as urinary BPA rose. [Souter 2013; Lassen 2014]
  • Men: In a cohort of 218 factory workers, men with detectable urinary BPA had more than 3× the risk of low sperm concentration and low sperm vitality, more than 4× the risk of low total sperm count, and more than 2× the risk of low sperm motility versus men with no detectable BPA. Similar dose-response was seen at general-population exposure levels. [Li 2011]
  • Both partners: PAH exposure (a major route is tobacco smoke) is associated with sperm DNA damage and oxidative stress. Effects are biologically additive when both partners are exposed.
Pregnancy — preterm birth and fetal growth›
  • Preterm birth: A pooled analysis of 16 US cohorts (6,045 pregnancies) found several phthalate metabolites associated with roughly 12–16% higher odds of preterm birth per increment of exposure. The authors modeled that cutting the phthalate mixture by 50% could prevent about 11 preterm births per 1,000 live births — i.e., preterm birth that may be partly preventable. [Welch 2022]
  • Fetal growth: Airborne PAH exposure in pregnancy (New York City and Kraków cohorts) was associated with reduced birth weight and size. [Choi 2006]
  • The fetus has little defense: BPA, phthalates, and PAHs all cross the placenta; BPA also concentrates in amniotic fluid. The first trimester — organogenesis — is the most sensitive window.
The next generation — brain and reproductive development›
  • Neurodevelopment: In the Columbia NYC birth cohort, children in the highest quartile of prenatal airborne PAH scored about 5.7 points lower on a mental development index at age 3, and higher prenatal PAH was associated with lower IQ at age 5. [Perera 2006; Perera 2009]
  • Male reproductive development: Prenatal exposure to anti-androgenic phthalates is associated with a shorter anogenital distance in male infants — a measurable marker of reduced androgen signaling in the womb. [Swan 2005]
"BPA-free" is a marketing claim, not a clean bill of health. Manufacturers often replaced BPA with the structurally similar bisphenols BPS and BPF. A systematic review of 32 studies found these substitutes are about as hormonally active as BPA. The most defensible position is to reduce plastic contact with food, heat, and water regardless of the label. [Rochester & Bolden 2015]
The good news: change works, and fast. In a controlled fresh-food intervention, eating unpackaged food and avoiding cans for just a few days cut urinary BPA by about 66% and DEHP (a major phthalate) metabolites by 53–56%. These chemicals clear within hours to days, so the swaps below have near-immediate effect. [Rudel 2011] One caveat: no single change is a guarantee — whole foods can still be contaminated during processing, so the goal is to lower total exposure, not chase zero.
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Check off each swap as you make it. ★ marks the highest-priority items for the stage you selected. Switch to For Clinicians to see the mechanism and source for each item.

Evidence base

Every figure in this tool traces to one of these peer-reviewed sources. References verified against PubMed.

  1. Souter I, Smith KW, Dimitriadis I, Ehrlich S, Williams PL, Calafat AM, Hauser R. The association of bisphenol-A urinary concentrations with antral follicle counts and other measures of ovarian reserve in women undergoing infertility treatments. Reprod Toxicol. 2013;42:224–231. doi:10.1016/j.reprotox.2013.09.008. PMID 24100206. — Higher urinary BPA linked to lower antral follicle count (EARTH cohort).
  2. Lassen TH, Frederiksen H, Jensen TK, et al. Urinary bisphenol A levels in young men: association with reproductive hormones and semen quality. Environ Health Perspect. 2014;122(5):478–484. doi:10.1289/ehp.1307309. PMID 24786630. — General-population young men; BPA associated with altered reproductive hormones.
  3. Li DK, Zhou Z, Miao M, et al. Urine bisphenol-A (BPA) level in relation to semen quality. Fertil Steril. 2011;95(2):625–630.e4. doi:10.1016/j.fertnstert.2010.09.026. PMID 21035116. — Source of the 3×/4×/2× semen-quality risk figures.
  4. Rochester JR, Bolden AL. Bisphenol S and F: a systematic review and comparison of the hormonal activity of bisphenol A substitutes. Environ Health Perspect. 2015;123(7):643–650. doi:10.1289/ehp.1408989. PMID 25775505. — BPS and BPF are about as hormonally active as BPA ("BPA-free" caveat).
  5. Swan SH, Main KM, Liu F, et al. Decrease in anogenital distance among male infants with prenatal phthalate exposure. Environ Health Perspect. 2005;113(8):1056–1061. doi:10.1289/ehp.8100. PMID 16079079. — Prenatal phthalates linked to shorter anogenital distance in boys.
  6. Welch BM, Keil AP, Buckley JP, et al. Associations between prenatal urinary biomarkers of phthalate exposure and preterm birth: a pooled study of 16 US cohorts. JAMA Pediatr. 2022;176(9):895–905. doi:10.1001/jamapediatrics.2022.2252. PMID 35816333. — Source of the 12–16% preterm-birth odds and the prevention modeling.
  7. Choi H, Jedrychowski W, Spengler J, et al. International studies of prenatal exposure to polycyclic aromatic hydrocarbons and fetal growth. Environ Health Perspect. 2006;114(11):1744–1750. doi:10.1289/ehp.8982. PMID 17107861. — Airborne PAH linked to reduced fetal growth (NYC, Kraków).
  8. Perera FP, Rauh V, Whyatt RM, et al. Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children. Environ Health Perspect. 2006;114(8):1287–1292. doi:10.1289/ehp.9084. PMID 16882541. — Source of the 5.7-point mental-development figure at age 3.
  9. Perera FP, Li Z, Whyatt R, et al. Prenatal polycyclic aromatic hydrocarbon exposure and child intelligence at age 5. Pediatrics. 2009;124(2):e195–e202. doi:10.1542/peds.2008-3506. PMID 19620194. — Higher prenatal PAH associated with lower IQ at age 5.
  10. Rudel RA, Gray JM, Engel CL, et al. Food packaging and bisphenol A and bis(2-ethylhexyl) phthalate exposure: findings from a dietary intervention. Environ Health Perspect. 2011;119(7):914–920. doi:10.1289/ehp.1003170. PMID 21450549. — Fresh-food diet cut urinary BPA ~66% and DEHP metabolites 53–56%.