phthalates--residential exposure & immune effects

[ttweed@wildrockies.org (Tony Tweedale)]

for those interested in the use of plasticizers in PVC,

Oie, Hersoug et al, 'Resodential Exposure to Plasticizers & Its Possible
Role in the Pathogenesis of Asthma' _Env Health Perspectives_ (NIEHS)
105:9:972-8 ('97)

analyzed samples of airborne (38 ea) & settled house dust (6 ea) for 5
individual & total phthalates, and calculated inhalation exposure.  DEHP
predominated and estimated inhalation (only) exposure was 0.76 ug/day (0.30
- 1.18 ug/d).  As airborne & settled dust levels correlated, the settled
dust did not appear to be picking up  much from direct contact w/ PVC items
(rather, it comes from off-gassing).  Previous studies gave DEHP exposure
from vapor phase only @ 0.4 ug/d.  Infants breath much more air/kg [wadults
breath ~ 30kg air/day--much more mass than of food & liquid, and a very
direct route into the blood via the alveoli!].

DEHP and MEHP, the breakdown product are associated w/ asthma & chronic
airway disease [which are immune diseases whose symptoms represent the
body's response to foreign agents & irritants, designated 'inflamation'].
Structurally, they are very similar to the prostoglandins and thromboxanes
which cause bronchial restriction, at least some of whose receptors are
known to be quite unspecific (accepting molecules w/ a neutrally charged
(lipophillic) aromatic end).  Direct injection of DEHP into the lung of
rats causes inflamation, bronchial bleeding and death.  Inadvertant
inhalation of DEHP from respiratory tubes by preterm infants  is reported
to increase bronchial asthma.  Both inhibit kinase C, which along w/
acetylcholine is involved in smooth muscle contraction.  MEHP induces
bronchial hyperactivity, and unpublished data shows an association between
indoor plastic surfaces and bronchial obstruction.