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Air pollution continued
part 1 notes at: http://liveonearth.livejournal.com/1136149.html


proximity to roadways correlates with autism
3rd trimester exposure

obnoxious how lobby & media don't actually read the science that they spew about

Ozone and hot tubs
in news last week
something about how pipes are supposed to give it time to degrade to H2o

correl c asthma?
genotox markers correl c 1h daily pool exposure pubmet 20833606
Health effects of disinfection by-products in chlorinated swimming pools.
Increased attendance at swimming pools is correlated with higher input of organic and minerals pollutants introduced by swimmers in the swimming pool water. In most swimming pools, microbiological control is performed by disinfection with the addition of chlorine. Chlorine is now well-known to lead to the formation of many disinfection by-products (DBPs) including trihalomethanes and chloramines. The hypothesis of a link between the presence of eye and skin irritation syndromes in swimmers and contact with swimming pool water treated with chlorine was initially proposed by Mood (1953). During recent decades many epidemiological studies have described the importance of DBPs generated with natural or imported organic matter present in water. Many of these DBPs are suspected to be toxic or even carcinogenic. Trihalomethanes and haloacetic acid families are the most studied but others DBPs, like chloral hydrate, haloacetonitriles, N-nitrosodimethylamine and the bromate ion, are emerging compounds of interest. Epidemiological data about the risk of cancer are still controversial. However, numerous publications highlight a toxic risk especially the risk of allergy and respiratory symptoms for babies and elite swimmers. The few publications dedicated to risk assessment do not suggest increased risk, other than for elite swimmers. These publications are likely to underestimate the risk associated with DBPs because of the lack of data in the literature precludes the calculation of risk associated with certain compounds or certain pathways. Thus for regulations, the need to take into account the risks associated with disinfection by-products is now important without forgetting the need of the control of microbiological hazards in swimming pools.


airborne toxics list: http://www.epa.gov/ttn/atw/188polls.html
Outdoor: VOCs, PAHs
Indoor: Cotnine, asbestos, mold

gas at normal STP, small mols, usu have chem odor, mostly synthetic
ex: benzene, toluene, xylene, phenol, formaldehyde, vinyl chloride & PVC
ubiquitous indoors www.epa.gov/iaq/base/voc_master_list.html
off-gassing from synthetics, variable rate
Hx, neuropsych exam: CNs, MRS exam, gait, memory, MMSE
consider neurol consult
Labs: CBC, CMP, Urinary metabolites (US biotek)

C6H6, colorless liquid, sweet smell, flammable, non-soluble
used in: plastic, rubber, dye, fiber, detergent, dye, drug, pesticides, printing
released by: combustion of petrol, tobacc, lots in smoking households, chem plants, urban air
effects: bone marrow suppression-->decr RBCs, decr B&T cells, decr IL1 and IFN, leukemia (esp AML), lymphoma, myelodysplastic syndrome, aplastic anemia
CNS, liver, kidney, lung, heart
known carcinogen
SX: mucous memb irrit, dizz, h/a, N, fatigue, dermatitis, nerve conduction delay (mm)
LABS: urinary benzene, metabolites in urine: muconic acid, S-p;henylmercapturic acid (within 48 hrs)

aka methyl benzene, C6H5CH3
colorless liquid, sweet/pungent odor, volatile, flammable, lipophilic
solvent, paint thinner, adhesives, glues, cleaning solvents, rubber, ink, tobacco, 5-7% in gas, fuel additive for racing
effects: irrit resp and mucous memb, CNS: dizz, euphoria, confus, agit, syncope, decr judgement, ataxia
exposures usu intentional: huffing or occupational/hobbyist
preg: crosses placenta, birth defects = microcephaly
chronic exposures: liver, kidney, brain
metabolized to hippuric acid but use venous tol within 24 hours of exposure to confirm exposure
hippuric can come from other sources
acute tx: low flow O2 if resp sx, asthma tx if RADS, glycine to increase metab, avoid: alcohol, salycylates
should be out of system in 1 day
chronic tx: liver (fatty?), kidney fx, addiction tx

aka dimethyl benzene (ortho, meta, para)
solven used in paint thinner, varnish, ink, dye, glue, plastic, rubber, leather, in petrol and tobacc
effects sim to tol

aka carbolic acid, hydroxy-benzene, phenyl hydroxide
sick sweet tarry odor, flammable, corrosive, colorless translucent gel
orig use as sugical antiseptic!
uses: plywood, particle board, insulation, nylon/fabrics, disinfectant, antiseptic, mouthwash!, throat lozenges, food preservative
cosmetics, hair dye, sunscreen, skin bleach, soap, released by combustion of petrol, wood, tobacc
effects: caustic, irrit/burning, discolor, neural stim-->decr conduction, siezure, obtund, dizz; resp irrit: bronch, asthma, pulm edema
effects: CV: tachy-->brady, hemolysis, anemia, high doses cario & renal tox
no proven carcinogenesis

aka formalin, formol, methyl aldehyde
colorless, v tox, flammable, pungent/irrit odor detectable under 1ppm
water soluble
common, production increased steadily from 60's to now with a slight dip after 2000
uses: adhesives, glues, dyes, carpet, particle board, plywood, paper, resins, plastics, polymers, disinfectant, germicide, embalming, fertilizer, food production (naturally occurring in fish, bacon, spinach), wrinkle free clothing, cosmetics
released: combustion of petrol, wood, tobacc
main exposure: endogenous production, est 50,000mg metabolized daily by every cell in body to Co2 & formic acid (in urine)
precursor in many biochem rxns
sx of low dose exposure: h/a, dyspnea, nasal irrit, fatigue, cognitive diff, decr memory, dexterity
sx of hi dose: mucous memb irrit, lacrimation, bronchitis, pulm edema, asthma, (no alveolar involvement)
probably human carcinogen: sinonasal, nasopharyngeal, leukemia

office bldgs worst, sealed, more toxic materials (formaldehyde, mold), climate "control"
sx: fatigue, h/a, N, EENT irrit, cognitive dysfx
FEMA trailers, 100,000 units with avg formaldehyde of 77ppb, risk at 8ppb, lots of effects reported

aka chloroethene, vinyl chloride monomer, VCM
v flammable gas, colorless, mild sweet odor, synthetic, usu combined monomers to form PVC, new car smell
ubiquitous in industry, cheap, durable light weigh plastics, insulation, house siding
can be softened with phalates: shower curtains, clear plastic casings and shrink wrap, toys, clothing
banned or limited in Swed, Ger, Spain, Jap car companies, Ca, healthcare (IV bags/tubes), walmart, target, ikea, sears
health concerns: off gassing VCM, leeching phthalates, combution products = dioxins
sx dt offgassing: dizz, fatigue, neurasthenia, ataxia, obtundation, resp & mucous memb irrit
health effects: HIGHLY CARCINOGENIC AND HEPATOTOXIC, hepatic angiosarcoma (Bv's of liver) (hep notes went into blk book)
MOA: toxic hepatic metabolites, binding to DNA, pro-oncogenic and tumor suppressor changes

mult benzene rings, incompletely combusted, two classes: low and high molecular wt
LMW = 2-3 rings (napthalene), HMW = 4-7 rings (benzopyrene)
all end with "ene"

LMW, tar camphor, C10H8, white solid, flammable, volatile aromatic, in MOTH BALLS, unstable, dissipates
byproduct of coal processing (coal tar) also exposure from burning wood, propane
SX: hemolytic anemia, fatigue, palor, resp irrit, possible carcinogen (nasal)
CAUTION: for pts with other anemias, sickle, G6PD

a PAH, five rings, C20H12, flat structure interferes with DNA (intercalation)
metabolite BaP diol epoxide inhibits p52 tumor suppressor gene-->CANCER
among top carcinogens, prevalent, known: Lu, Prost, Panc, Stom, CRC, Rectal
product of fossil fuel combustion, major component of tar
present in grilled/charred food (also heterocyclic amines), tobacco smoke (most carcinogenic substance in tobacc smoke)
discovered in 18th century london, chimney sweeps
AVOID: grilled meat, high temp, charred or burnt anything, stop smoking
?? suggestion of marinade in acid (vinegar/lemon)
eat brassicas: indole-3-carbinol, isothiocyanate
consume antioxidants: 30% less BaP DNA damage to smoker with 500mg vit C and 400IU vit E qd x3mo pubmed 15668500

primary metabolite of nicotene (80%)
used to measure tobacco consumption (primary, secondary, tertiary)
Urine test mc, blood, saliva and hair also possible and correlate well
(anabasine is metabolite not found in tobacco replacement products)
levels decr 70% since public smoking banned, 30-40% decr in hospital admissions for acute CVD and resp dz pubmed 20385737

potent carcinogen, 24% incr lung ca risk, 200% incr risk for chronic/constant "high" exposure
effects: lung ca, bronchitis, asthma, SOB, COPD, CVD, otitis media, decr immune fx, incr infx
exposure concentration depends on room size, # smokers, air patterns
Results. The meta-analysis indicated a 24% increase in lung cancer risk (relative risk [RR]=1.24; 95% confidence interval [CI]=1.18, 1.29) among workers exposed to environmental tobacco smoke. A 2-fold increased risk (RR=2.01; 95% CI=1.33, 2.60) was observed for workers classified as being highly exposed to environmental tobacco smoke. A strong relationship was observed between lung cancer and duration of exposure to environmental tobacco smoke. Conclusions. The findings from this investigation provide the strongest evidence to date that exposure to environmental tobacco smoke in the workplace is associated with an increased risk of lung cancer.
TO PROTECT INFANT: chems deposit into clothing, etc, are still carcinogenic pubmed 20142504 so going outside is not enough, get a smoking jacket
WATER PIPES: not a safe alternative, mb more harmful, sessions are longer, may inhale much more

6 diff very fine fibers, 0.01um thick, 3-20um long
mostly chrysotile, Mg3(Si2O5)(OH)4
naturally occurring, pliable, non-flammable, good insulator, toxic, carcinogenic
used for fire-proofing, bldg material, insulation, cement mortar, drywall, pipes, tiles, friction/brakes, clutch
1978 removed from building material manufacture
1989 EPA bans and phases out
RISK: mostly to factory workers, contaminated sites
TX: seal, avoid it, less dz is structure intact
EFFECTS: asbestosis, mesothelioma, lung ca (bronchial adenocarc more if cigs too), pulm irrit, inflam of bronchioles, alveoli, fibrosis
SX: dyspnea, SOB
PE: diffuse dry rales, cyanosis, neg fever

pleura, pericardium, peritoneum infiltrated by fibers, irration-->ca
SX: dyspnea, SOB, pleuritic pain, cough, wheeze, fatigue, cachexia, hemoptysis
LABS/IMAGE: Radiograph, Pulm Fx tests, CT

EPA moldcourse, moldguide (web pages)
Ctr for Indoor Environments and Health (UConn) online CD on mold, healthy homes checklist, oehc.uchc.edu/HIEH.asp
Mold sniffing dogs, www.portlandtribune.com/archview/cgi?id=1909

OEC on eco-healthy homes
Web MD health-ehome-9/default.htm
EWG checklist ewg.org/health-home-tips/checklist
Hartford checklist www.oehc.uchc.edu/clinser/AssessmentTools_all.pdf

http://www.epa.gov/iaq/pubs/insidestory.html The Inside Story: A guide to indoor air quality

MULTIPLE CHEMICAL SENSITIVITY DISORDER MCSD (this info already pulled to black book)
DEF "chronic, recurring dz caused by inability to tolerate envir chem or class of chems"
hyper-sensit to toxics, threshhold below olf detection for v sensitive people
not recognized by allo med incl AMA, WHO, usu dxd as psych
aka EI Environmental Illness, Total allergy syndrome, idiopathic Envir Intolerance, Twentieth Century Dz
DEMOGRAPHICS: ~90% female, 80% middle aged, most caucasian
ASSOC: fibro and CFS ~50%, psych conditions ~50%
DX: reproducible sx with chem exposure and relief with removal, mult chems provoke, persistent, incr sensit/low level exposures are provocative, multiple organ system involvement
7 PRINCIPLES: biochem individuality (genes, develop, nutrit, past exposure), total load aka allostatic load, spreading phenomenon aka triggering (sensit to one chem incr sensit to others), adaptation/masking (upreg of detox reduces response to orig trigger, ie tolerance), de-adaptation (upreg of detox in one area may downreg in other, sx shift), biopolarity (paradoxical and changing sx even within an organ system), switch phenomenon (changes systems)
LABS: no findings
not immune mediated (no IgE, IgG, WBC rxn)
no abn LFTs
not related to histol changes in tissues
TRIGGERS: usu indoor pollution, offgassing, perfume, ink, tobacc, etc
CDC 2009 Frangrance Free Office
ETIO: olf-limbic response-->neural disruption, limbic kindling = synaptic plasticity incr chem excitability of certain neurons (amygdala)
ETIO: genetic susceptibility (SNPs-->poor manufacture of GSH, etc)
ETIO: early life stress, time-dependant sensitization-->abn endocrine, immune, neurol systems
Biol Psychiatry. 1994 Jun 1;35(11):857-63.
Sensitization to early life stress and response to chemical odors in older adults.
This study examined the hypothesis that older persons who currently report illness from environmental chemical odors (cacosmia) may have experienced higher levels of stress early in life than did noncacosmic controls. The hypothesis derives from a time-dependent sensitization (TDS) model for cacosmia (Bell et al 1992) that predicts a relative interchangeability of stress and chemicals in inducing and eliciting sensitized responses in vulnerable individuals. Subjects were selected from those in the top 24% (cacosmic) and bottom 27% (noncacosmic) of a sample of 192 older adults (mean age 73.8 years) for self-reported frequency of illness form the odors of pesticide, car exhaust, paint, perfume, and new carpet. As in previous investigations, cacosmics were younger, more depressed, and more shy; cacosmics also included a higher proportion of women (83% versus 61%). As predicted, cacosmics rated themselves higher in stress for the first four decades of their lives, but not the recent past or present, even after controlling for depression, anxiety, hostility, shyness, age, and gender. Cacosmics reported increased prevalence of physician-diagnosed nasal allergies, breast cysts, hypothyroidism, sinusitis, food sensitivities, irritable bowel, and migraine headache. Only 4% of the overall sample (including 9% of the cacosmics) acknowledged the controversial physician diagnosis of "chemical sensitivity." The replicated observation of greater shyness in cacosmics is consistent with the ability of hyperreactivity to novelty to predict enhanced susceptibility to TDS from low levels of pharmacological agents in animals. The findings support a TDS model for cacosmia and suggest that cacosmia as a symptom identifies a large subset of the nonindustrial population with significant psychophysiological health problems that merit further objective examination.
SX: VARIABLE: H/A, fatigue, arrhythm, asthma, dyspnea, memory, myalgia, arthralgia, neuropathy, depression, dizz, disorientat, sneeze
1) ID and remove cause/exposure
2) Depuration/detox: liver support, hyddro, EFAs
3) Energetic modalities essential: homeop/drain, acupx, flower essence, reiki, EFT
4) Patience

recycle indoor air
reduce: toxins 90% (1986 Wolverton NASA), microbes 50% (J of Ms Acad of Sci 96), allergens, particulates
decr resp & mucous memb sx 23% (Field 1998)
book: How to Grow Fresh Air by Bill Wolverton


1991 vets of 1st gulf war
widespread multisystem probs
(my thought: radical increase in # of vaccines given to soldiers at this time too)



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