Environmental Tobacco Smoke as a Toxic Air Contaminant

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In 2006 California became the first state to declare secondhand smoke a toxic air pollutant. ETS was listed as a TAC because of the numerous health effects linked to exposure including development of asthma, heart disease, Sudden Infant Death Syndrome, respiratory infections in children, lung cancer and breast cancer.  Accordingly, it has been added to the list of Toxic Air Contaminants which may cause infants and children to be especially susceptible to illness, which is detailed below.  The full memo is available for download at the bottom of the page.

TABLE.  Toxic Air Contaminants which may cause infants and children to be especially susceptible to illness.

Toxic Air Contaminant

Endpoints of Most Concern

Major Reasons Why Chosen

Acrolein

Respiratory Irritant

Exacerbation of asthma; modeling predictions indicate concentrations in urban air above cREL

Chlorinated dioxins and dibenzofurans (dioxins)

Developmental toxicity, immunotoxicity, endocrine disruption; thyroid effects

Widespread exposure; endocrine disruption, thyroid and immuno-toxicity at low body burden; young animals more susceptible than older animals

Environmental Tobacco Smoke

Developmental effects, including low birthweight and decrease in birthweight, Sudden Infant Death Syndrome, pre-term delivery.

Respiratory effects, including acute lower respiratory tract infections, asthma induction and exacerbation, Chronic respiratory symptoms, middle ear infections in children.

Cancer.

Widespread exposure; numerous adverse health effects; several known effects are specific to children, and other known effects to which infants and children may be more susceptible.

Lead and compounds

Developmental neurotoxicity/CNS effects

Children the most susceptible subpopulation due to developmental neurotoxicity.

Particulate Emissions from Diesel-fueled Engines (Diesel exhaust particulate matter)

Enhancement of allergic response; exacerbation of asthma; developmental effects, genotoxicity and lung cancer.

Enhancement of allergic response and implications for exacerbation and possible induction of asthma; Major source of ambient PAHs, PM10; exacerbation of asthma by PM10; PAH developmental toxicity and genotoxicity a concern.

Polycyclic Organic Matter (POM)

Developmental effects, genotoxicity and lung cancer

Animal studies indicate teratogenicity, and fetotoxicity; human studies indicate greater genotoxicity following in utero exposures.