What medical and toxicology standards determine whether tear gas exposure can cause an infant to stop breathing?

1. What the standards are: exposure thresholds and AEGLs

Toxicology frameworks use acute exposure guideline levels (AEGLs) to define airborne concentrations and exposure durations that produce mild, serious, or life‑threatening effects in humans; the NAC/AEGL committee has reviewed CS and concluded that typical volunteer studies show mainly transient irritation but that AEGLs account for higher concentrations and vulnerable groups when setting limits ^[1].

2. How dose, duration and space determine risk

Risk is a function of concentration × time and environment: short, low‑concentration open‑air exposures usually cause transient irritation, while prolonged or repeated exposures and releases in enclosed spaces markedly increase risk of severe airway injury, pulmonary inflammation, or secondary infection—circumstances repeatedly implicated in reported infant cases ^{[5] [3] [1]}.

3. Infant physiology and vulnerability that shape clinical standards

Infants have smaller airways, higher minute ventilation per kilogram, immature immune and respiratory reflexes, and closer proximity to ground‑level gas clouds, all of which toxicology and public‑health reviews cite as reasons to apply greater conservatism in exposure guidance for children compared with healthy adult volunteer data ^{[5] [6]}.

4. Clinical syndromes that can lead to respiratory arrest after exposure

Medical literature describes pathways from irritant exposure to life‑threatening failure: intense upper‑airway injury can produce laryngospasm or edema causing asphyxia; lower‑airway inflammation can progress to pneumonitis, pulmonary edema, or bronchospasm and secondary infection—these conditions have produced severe respiratory distress in infants after prolonged or concentrated CS exposure in case reports ^{[3] [2] [1]}.

5. Empirical evidence: case reports and population data

Individual case reports document infants developing pneumonitis and prolonged hospitalization after tear‑gas exposure, and observational studies link mass deployment to increased pediatric respiratory emergency visits (for example, a Chilean analysis showing elevated infant ED visits and higher bronchial disease rates during periods of massive use)—these form the practical evidence base toxicologists and clinicians rely on when assessing extreme risk scenarios ^{[2] [4] [7]}.

6. Preexisting conditions, clinical thresholds and triage decisions

Standards for escalation (oxygen, bronchodilators, steroids, imaging, hospital admission) hinge on objective signs—hypoxia, work of breathing, wheeze or stridor, CXR infiltrates, leukocytosis—and on the presence of asthma or chronic lung disease which markedly raises the likelihood of bronchospasm and respiratory failure after exposure ^{[8] [3] [1]}.

7. Limitations, uncertainty and alternative views

Evidence gaps persist: most controlled toxicology data derive from healthy adult volunteers or animal models, not infants, and long‑term pediatric outcomes are incompletely studied, so standards extrapolate conservatively from case reports, mechanistic data (e.g., TRPA1 activation by CS), and population studies; public‑health bodies therefore recommend stricter precautions and rapid medical evaluation for children, while some volunteer studies emphasize transient effects in adults under limited conditions ^{[1] [9] [5]}.

8. Practical standard of proof clinicians use to decide “can an infant stop breathing?”

Clinicians and toxicologists treat severe confined or prolonged CS exposure, evidence of upper‑airway swelling or progressive hypoxia, and preexisting reactive airway disease as sufficient medical indicators that exposure could precipitate respiratory arrest in an infant—this judgment relies on physiologic plausibility, case precedents, AEGL risk frameworks, and the infant’s objective clinical signs rather than a single definitive randomized pediatric study ^{[1] [2] [4]}.