Suppressing Transferable Inflammatory Signaling in Indoor Micro-Environments

A passive polymer architecture that irreversibly suppresses biologically active indoor inflammation drivers beyond the reach of conventional air-quality control

I. Problem Statement

Modern indoor environments satisfy regulatory air-quality thresholds while continuing to produce chronic inflammatory burden across populations. This failure persists because prevailing standards focus on bulk pollutant concentration rather than the transferable, biologically active fractions that directly trigger epithelial, immune, and neural inflammatory pathways.

The dominant drivers are not mass particulate load or acute toxic exposure, but low-level, persistent signaling inputs: endotoxin and allergen fragments associated with particulate matter, indoor oxidants such as ozone, and reactive aldehydes released through material off-gassing. These species remain biologically potent at concentrations far below regulatory concern and act continuously over years.

Existing mitigation strategies—ventilation, filtration, adsorption, and episodic cleaning—operate episodically, require energy or maintenance, and do not permanently alter baseline exposure. Consequently, inflammatory signaling re-establishes immediately between interventions.

II. System Definition

The proposed system is a microphase-separated, zwitterionic block-copolymer textile or surface membrane embedding covalently anchored redox-buffer motifs and nucleophilic binding sites within a hydrated surface domain.

Its function is to passively and continuously suppress indoor inflammatory signaling by:

• Irreversibly sequestering the transferable bioactive fraction of PM-associated endotoxin and allergen fragments;
• Consuming indoor oxidants through immobilized redox buffering;
• Neutralizing reactive aldehydes via stable, non-volatile adduct formation.

All mechanisms operate without leaching, regeneration, external energy input, or user action. Bound species are immobilized within the polymer matrix and are not re-emitted under humidity, mechanical, or cleaning cycles.

III. Why Endpoint Air Metrics Fail

Bulk PM concentration, VOC totals, or average ozone levels do not correlate reliably with inflammatory response. What matters is the fraction that remains transferable to epithelial surfaces and capable of engaging innate immune signaling pathways.

Two environments with identical measured air concentrations may differ dramatically in biological impact depending on the availability of transferable endotoxin fragments, oxidant persistence, and local humidity-mediated uptake dynamics.

Endpoint air measurements therefore cannot validate biological safety. Any credible intervention must operate at the level of signaling suppression, not mass reduction alone.

IV. Polymer Architecture and Governing Mechanisms

Architecture

• Zwitterionic surface domains provide high hydration, suppress nonspecific fouling, and stabilize humidity at the interface;
• Nanostructured ionic and gel microcavities immobilize bioactive endotoxin and allergen fragments through dual electrostatic and physical trapping;
• Covalently tethered redox-buffer motifs convert indoor oxidants to stable, non-volatile oxidized states;
• Immobilized nucleophilic sites form irreversible adducts with reactive aldehydes.

Functional layer thickness exceeds the maximum diffusion length of target species during humidity cycling, preventing early breakthrough or re-release.

V. Internal State Vector and MTI-1 Compliance

System validity is governed by an explicit internal state trajectory, not by endpoint performance claims. The minimal observable state vector includes:

• Surface hydration (contact angle or gravimetric uptake);
• Surface ionic conductivity (impedance spectroscopy);
• Redox capacity (catechol–quinone ratio or equivalent);
• Bound bioactive fragment load (extractable endotoxin/allergen assay).

These variables evolve monotonically with exposure and cycling. Sequence dependence is expected: oxidant exposure followed by mechanical flex produces a different trajectory than flexing prior to oxidant exposure. Endpoint equivalence does not imply trajectory equivalence.

Durability and efficacy claims are valid only within the bounded regime defined by these trajectories, in accordance with Morphology Trajectory Integrity (MTI-1).

VI. Regime Boundaries

Applies to

• Interior occupied environments with relative humidity between 30–65%;
• Formaldehyde and aldehyde concentrations in the 10–500 ppb range;
• Continuous, low-level oxidant exposure typical of urban indoor spaces;
• Deployment on soft surfaces, textiles, wall panels, bedding, and furnishings.

Does not apply to

• Outdoor or industrial atmospheres;
• Environments with extreme humidity (<20% or >80% RH);
• Chemical regimes involving solvents, strong acids, or bases that degrade the polymer;
• Claims of universal air purification.

VII. Decisive Falsification Test

The system is falsified if, under controlled indoor chamber exposure to realistic PM-associated bioactive fragments, ozone, and reactive aldehydes:

• No persistent reduction in transferable endotoxin or allergen fraction is observed;
• Bound species are measurably re-released under humidity or cleaning cycles;
• Oxidant or aldehyde conversion produces volatile or hazardous byproducts above ambient baseline;
• Internal state vector trajectories do not correlate with exposure history.

Failure under any of these conditions irreversibly invalidates the system’s claims within this regime.

VIII. Humanity-Scale Impact

This system does not rely on behavior, awareness, or episodic intervention. It alters the environmental baseline itself.

By converting ubiquitous indoor surfaces into continuous suppressors of inflammatory signaling, it reduces chronic immune activation across entire populations—especially children, the elderly, and the chronically exposed.

The impact is cumulative, silent, and systemic: a background reduction in inflammation that conventional filtration, ventilation, and policy interventions cannot achieve.

Edge of Knowledge papers define regime-bounded constraints and falsifiable mechanisms. This document proposes a physically grounded pathway to reducing chronic inflammatory burden by altering indoor material ecology rather than episodic exposure control.