PFNA (Perfluorononanoic Acid) in the Bedroom

At a glance


Chemical family	Long-chain perfluoroalkyl acid (PFAA); nine-carbon perfluorinated carboxylic acid
CAS number	375-95-1
Classification	Not IARC classified. Included in EFSA 2020 four-PFAS group with a tolerable weekly intake of 4.4 ng/kg body weight derived from reduced vaccine response. EPA hazard assessments ongoing under TSCA.
Where you encounter it	PFAS-treated waterproof mattress covers and pillow protectors, stain-resistant upholstery, certain food packaging, firefighting foam, drinking water contamination near manufacturing or training sites
Sleep micro environment relevance	Dermal absorption from PFAS-treated waterproof textiles during skin contact; not efficiently excreted in sweat (unlike phthalates and bisphenols, the body retains PFAS rather than depositing them on bedding)
Activated carbon capture	Moderate for long-chain PFAS like PFNA at the textile interface; activated carbon is the standard water-treatment medium for long-chain PFAS removal, but capture from textiles in air-phase contact is less well characterized

Regulatory & certification status

Where PFNA (Perfluorononanoic Acid) stands across the major regulatory systems and the certifications a bedroom product might carry. Each row links to the governing instrument; where a jurisdiction has no specific measure, that is stated plainly rather than left blank.

European Union	REACH Substance of Very High Concern: perfluorononan-1-oic acid (PFNA, CAS 375-95-1) and its sodium and ammonium salts were added to the Candidate List on 17 December 2015, identified as toxic for reproduction and as PBT (Article 57(c) and 57(d)). PFNA is also restricted under REACH Annex XVII entry 68 as one of the C9-C14 perfluorocarboxylic acids (PFCAs), their salts and related substances, by Commission Regulation (EU) 2021/1297; from 25 February 2023 the sum of C9-C14 PFCAs and their salts must be below 25 ppb (and the sum of related substances below 260 ppb) in substances, mixtures and articles. A harmonised CLP classification was not independently verified against the primary Annex VI catalogue and is therefore not asserted here. Regulatory — ECHA · EUR-Lex
United States	Safe Drinking Water Act: PFNA is covered by the final PFAS National Primary Drinking Water Regulation (published 26 April 2024, effective 25 June 2024), with an individual Maximum Contaminant Level of 10 ng/L (10 parts per trillion) and inclusion in a Hazard Index (with PFHxS, HFPO-DA/GenX and PFBS) for mixtures. California Proposition 65: PFNA and its salts are listed, effective 31 December 2021, for male reproductive toxicity (listed via the State's Qualified Experts mechanism). TSCA: no final EPA risk evaluation; the IRIS Toxicological Review of PFNA (CASRN 375-95-1) and related salts remained a draft (Public Comment/External Review Draft, 2024; external peer review July-August 2024) at time of writing. Regulatory — Federal Register · OEHHA
Canada	PFNA is a C9 long-chain perfluorocarboxylic acid (LC-PFCA). LC-PFCAs (CnF2n+1CO2H, 8<=n<=20), their salts and precursors are on Schedule 1 of CEPA (final addition, 2013) and are prohibited from manufacture, import, use and sale under the Prohibition of Certain Toxic Substances Regulations, 2012, with limited exemptions/permits. Those 2012 Regulations are replaced by the Prohibition of Certain Toxic Substances Regulations, 2025 (SOR/2025-270, published 31 December 2025), which come into force 30 June 2026 and tighten certain LC-PFCA exemptions. Separately, a broad order to add the PFAS class (excluding fluoropolymers) to Schedule 1 was proposed in March 2025 (draft, not final). Regulatory — Government of Canada · Canada Gazette
Australia	PFNA is not individually scheduled under the Industrial Chemicals Environmental Management Standard (IChEMS). Only PFOS, PFOA and PFHxS (with their salts and related chemicals) are listed at IChEMS Schedule 7, the prohibition tier (ban effective 1 July 2025). AICIS requires specific information/reporting for PFAS introductions, but no PFNA-specific import/use prohibition was identified. Regulatory — AICIS · DCCEEW
United Kingdom	Under UK REACH (HSE), PFNA's identification as an SVHC carried across from the EU Candidate List (Dec 2015) when GB REACH inherited the EU candidate list at the end of the transition period. GB REACH inherited the EU Annex XVII restriction list only as it stood at the end of 2020; the EU C9-C14 PFCA restriction (Regulation (EU) 2021/1297) post-dates that cut-off and was not automatically carried into GB law. No equivalent in-force GB Annex XVII restriction specifically on PFNA was independently confirmed. Regulatory — HSE · House of Commons Library
International	Long-chain perfluorocarboxylic acids (LC-PFCAs), their salts and related compounds — the group that includes the C9 acid PFNA — were listed in Annex A (elimination) of the Stockholm Convention on Persistent Organic Pollutants by decision SC-12/12 at COP-12 in May 2025. PFNA has no individual IARC carcinogenicity classification (the November 2023 IARC evaluation, Monographs Volume 135, covered PFOA and PFOS only). Regulatory — Stockholm Convention
Certifications	OEKO-TEX STANDARD 100: imposes a general ban on the intentional use of PFAS and a total-fluorine limit (100 mg/kg, effective 1 January 2024) for certified textiles, so PFNA is covered as a PFAS class member; PFNA is not individually named in the publicly summarised criteria. CertiPUR-US: its published criteria for certified polyurethane foam screen for CMR substances, heavy metals (e.g. lead, mercury), phthalates, formaldehyde, ozone depleters and certain flame retardants; the cited materials do not document a PFAS/perfluorinated prohibition and do not name PFNA, so no PFNA-specific exclusion is asserted. GREENGUARD/GREENGUARD Gold is a low-VOC chemical-emissions certification that would not screen for a non-volatile substance like PFNA. Industry — OEKO-TEX · CertiPUR-US
The 72-hour test window	Largely missed. PFNA is a non-volatile, surfactant-like perfluorinated carboxylic acid that partitions to dust, water and surfaces rather than off-gassing, so a short (~72-hour) VOC emissions chamber test does not reliably capture it; detection requires targeted PFAS analysis (e.g. LC-MS/MS of extracts or dust). Inferred — from the compound's volatility/emission profile versus the VOC focus of short chamber tests

What it is

PFNA is a fluorinated carboxylic acid in which all the hydrogens on the carbon backbone have been replaced with fluorine, leaving a single carboxylic acid head group. The carbon-fluorine bond is the strongest single bond in organic chemistry, which is why PFAS persist in the environment for decades to centuries and accumulate in humans and wildlife. PFNA, like the other long-chain PFAA compounds, binds strongly to serum albumin in blood and has a half-life in humans on the order of three to four years.

PFNA was used as a processing aid in the manufacture of polyvinylidene fluoride, a polymer used in industrial coatings and certain consumer products, and as a surfactant in some legacy aqueous film-forming firefighting foam formulations. Major U.S. manufacturers phased out PFNA production by the early 2010s, but the compound continues to enter the environment through manufacturing legacy contamination, breakdown of fluorotelomer-based products, and import of PFNA-containing goods from regions where production continues.

The 2020 EFSA decision to derive a tolerable weekly intake based on immune effects — specifically reduced antibody response to routine childhood vaccinations — marked a significant tightening of the regulatory framework for the long-chain PFAS class. Peer-reviewed — Brunn 2023, Environmental Sciences Europe EFSA estimated that typical European dietary exposure frequently reaches or exceeds the 4.4 ng/kg/week limit for the combined four-PFAS group, with PFNA contributing measurably to the total.

How it gets to the bedroom

From PFAS-treated waterproof textiles

Waterproof mattress covers, pillow protectors, and certain stain-resistant upholstery have historically been treated with PFAS-based durable water repellents. The long-chain PFAS were phased out of most U.S. consumer products in the late 2010s, but PFNA and related long-chain compounds remain detectable in textiles imported from regions with less restrictive regulation, and in older waterproof bedding manufactured during the legacy production period. Dermal absorption of PFAS from contaminated textiles is an established exposure pathway. Peer-reviewed

From contaminated drinking water

PFNA detection in U.S. drinking water systems is common in areas downwind or downstream of historical PFAS manufacturing, military fire training sites, and certain industrial sectors. Drinking water exposure is the dominant route for PFNA in heavily contaminated communities. Once absorbed, PFNA enters systemic circulation and binds to serum albumin, with a multi-year body burden.

From firefighting foam (occupational)

Aqueous film-forming foams used in fire suppression historically contained PFNA and related long-chain PFAS as surfactants. Firefighters have measurably elevated serum PFAS concentrations including PFNA. Take-home contamination of clothing, skin, and gear can transfer PFNA to home surfaces including bedrooms.

From food packaging and food contact materials

Grease-resistant food packaging — fast-food wrappers, microwave popcorn bags, certain bakery papers — has been a documented PFNA source historically. Replacement chemistries have reduced but not eliminated this exposure route.

A note on the body-deposition route. Unlike phthalates, bisphenols, and OPE flame retardants — which the Genuis 2012 BUS series showed are excreted via sweat onto bedding at meaningful concentrations — PFNA and the other long-chain PFAS are not efficiently excreted in sweat. Peer-reviewed — Genuis 2013, PMC3776372 PFAS bind strongly to serum albumin and persist in blood. The dominant PFAS exposure route in the sleep environment is therefore into the body from PFAS-treated textiles and dust, not out of the body onto bedding. This is an important distinction for how a capture system addresses (or does not address) PFAS load.

What the research says

Immune system effects

The 2020 EFSA tolerable weekly intake of 4.4 ng/kg body weight for the sum of PFOA, PFOS, PFNA, and PFHxS was derived from reduced antibody response to childhood vaccinations — the most sensitive endpoint across the class. Peer-reviewed — Brunn 2023 Rockwell and colleagues 2017 demonstrated in mice that a single high-dose PFNA exposure produced persistent alterations in immune cell populations and function 28 days after exposure, including markedly increased TNFα response to bacterial endotoxin. Peer-reviewed — Rockwell 2017, Food Chem Toxicol Tang and colleagues 2023 showed that PFNA and related PFAS induce immunotoxicity in zebrafish via the Toll-like receptor pathway, with the immunotoxic response positively correlated to carbon chain length — long-chain PFAS including PFNA produce stronger immune effects than short-chain replacements at equivalent doses. Peer-reviewed — Tang 2023, Environ Sci Technol Tursi and colleagues 2024 in the Norwegian EuroMix biomonitoring study used high-dimensional single-cell analysis to show that PFNA and related PFAS are associated with shifts in natural killer cell, T helper cell, and cytotoxic T cell subpopulations at relatively low exposure levels. Peer-reviewed — Tursi 2024, Environmental Research

Liver effects

Bassler and colleagues 2019 in 200 adults from the C8 Health Study found that serum PFNA was positively associated with cytokeratin-18 M30, a biomarker of hepatocyte apoptosis. Peer-reviewed — Bassler 2019, Environmental Pollution The 2020 Fenton and colleagues review in Environmental Toxicology and Chemistry summarized that across the PFAS class, liver disease — including hepatocyte apoptosis, hepatic lipid metabolism disruption, and nonalcoholic fatty liver disease — is a consistent finding in both epidemiological and experimental studies. Peer-reviewed — Fenton 2020, Environ Toxicol Chem Fang and colleagues 2025 demonstrated in large yellow croaker that PFNA induced progressive hepatic histopathology with PPAR signaling pathway activation followed by PI3K-Akt pathway enrichment, characterizing a "two-phase" mechanism of PFNA hepatotoxicity. Peer-reviewed — Fang 2025, Environmental Research

Thyroid disruption

The 2020 Boesen and colleagues review of 15 studies found mainly positive associations between PFAS exposure (including PFNA) and TSH levels in pregnant women, with inverse associations with T4 and T3 levels in several studies. Peer-reviewed — Boesen 2020, Environmental Health Freire and colleagues 2023 in 129 adolescent males from the INMA-Granada cohort found that the long-chain PFAS sum (including PFNA) was associated with increases in free T4 levels, with stronger effects in adolescents with lower iodine intake. Peer-reviewed — Freire 2023, Int J Hyg Environ Health Zhang and colleagues 2024 in 287 females at a Massachusetts fertility clinic found PFNA and related long-chain PFAS associated with lower total T3 and higher FT4 to FT3 ratios. Peer-reviewed — Zhang 2024, Environmental Pollution

Kidney function and body burden

Blake and colleagues 2018 in the Fernald Community Cohort (210 participants from a PFAS-contaminated aquifer community) found that serum PFNA was associated with reduced estimated glomerular filtration rate, indicating possible adverse kidney effects. Peer-reviewed — Blake 2018, Environmental Pollution Nielsen and colleagues 2023 in forensic autopsies showed that PFNA distributes throughout the body, with liver concentrations correlating closely with blood concentrations — confirming the liver as the primary retention organ. Peer-reviewed — Nielsen 2023, Environ Sci Technol

Open questions

PFNA-specific dermal absorption rates from PFAS-treated textiles under sleep-environment conditions (warm, occluded, six-to-eight hours) have not been independently characterized. The mixture effects of PFNA with co-occurring PFAS (PFOA, PFOS, PFHxS, plus short-chain replacements) on cumulative immune and hepatic effects are an active research area. Activated carbon capture of PFNA from air-phase contact with textiles — as opposed to from drinking water, where AC is the standard treatment medium — has not been systematically characterized at sleep environment conditions.

What helps reduce exposure

Tier 1 — Most effective: Replace PFAS-treated waterproof mattress covers and pillow protectors with PFAS-free alternatives. Tightly woven natural fiber covers (cotton, wool) or polyurethane-coated polyester without PFAS treatment achieve similar moisture barriers without the PFAS load. Test home drinking water for PFAS if living in or near a known contamination community.
Tier 2 — Worth considering: Avoid PFAS-treated stain-resistant upholstery in bedrooms. The Embr capture layer addresses some PFAS dermal exposure from the foam-bedding interface, but the dominant PFAS exposure route — water and food — is not affected by a mattress capture system. PFAS-free design of the Embr product itself is the relevant point of differentiation for this compound class.
Tier 3 — Larger interventions: Filter home drinking water with a system rated for PFAS removal (granular activated carbon, reverse osmosis, or ion exchange) if living in a contaminated water community. Advocate for federal and state regulatory action on the PFAS class as a whole rather than individual compounds.

What does NOT help

"BPA-free" labeling. Has no bearing on PFAS content. A product can be BPA-free and PFAS-laden.
Sweating PFAS out. Unlike phthalates and bisphenols, long-chain PFAS including PFNA are not efficiently excreted in sweat. Sauna therapy, exercise, and similar approaches that work for some lipophilic compounds do not meaningfully reduce PFNA body burden. The Genuis 2013 PFAS BUS study explicitly confirmed this.
Surface cleaning a PFAS-treated textile. The PFAS coating is bound to the fabric fibers. Surface cleaning does not remove the treatment; only replacement does.

Open research questions

Direct measurement of PFNA dermal absorption from PFAS-treated waterproof mattress covers under sleep-environment conditions has not been published. This is a directly tractable chamber study that the Embr foundation arm could contribute to or co-fund.
The relative contribution of mattress cover, pillow protector, upholstery, water, and food to total household PFNA body burden has not been apportioned for typical U.S. families. Source-attribution studies would improve the precision of exposure-reduction guidance.
Activated carbon capture of PFNA from air-phase textile contact (as opposed to aqueous-phase drinking water treatment) is poorly characterized. AC is the standard water treatment medium for long-chain PFAS, but the kinetics of air-phase capture at typical sleep-environment temperatures and humidities differ substantially.

Citations

Related compounds

Embr's product is designed to be PFAS-free in its construction. It is not a treatment for PFAS contamination and does not substitute for PFAS-free product specification, drinking-water treatment, or regulatory action on the PFAS class.

Last reviewed May 2026. If you find an error, contact us.

PFNA in the bedroom