Jonathan’S.’Rutchik,’MD,’MPH’ Associate’Professor ... Rutchik Sensoral Tox.pdf3/11/16 1...
Transcript of Jonathan’S.’Rutchik,’MD,’MPH’ Associate’Professor ... Rutchik Sensoral Tox.pdf3/11/16 1...
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Chemical Toxicity to the Special Senses: Vision, Hearing, Taste, and Smell
Jonathan S. Rutchik, MD, MPH Associate Professor, Department of Medicine
Occupa=onal Medicine, UCSF Neurology, Environmental and Occupa=onal Medicine Associates
Mill Valley, CA
Introduc=on
• 50% of neurotoxic chemicals may affect some aspect of SENSORY SYSTEM. • Most sensi=ve to exposure related toxicity • First reported following exposure. • Exist in the absence of other organ toxicity • Visual symptoms are the most frequently reported. • Altera=on in structure and func=on of the eye are oHen the criteria u=lized for seJng permissible exposure limits for chemicals in the USA
• Visual processing of informa=on can have immediate, long term, delayed effects on mental, social and physical health and performance
• Auditory and visual impairments can lead to occupa=onal injuries.
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Overview
• Neuro-‐Ophthalmological Dysfunc=ons (Toxicology of the Visual System)
• Ototoxicity (Toxicology of the Auditory System)
• Gustatory Dysfunc=ons (Toxicology of the Sensory System of Taste)
• Olfactory Dysfunc=on (Toxicology of Sensory System of Smell)
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Occupa=onal Exposures
• Greater than 80,000 industrial chemicals in use today. • Approx. 3,000 chemicals known toxic to the eye/visual system. • Routes of exposure can vary depending on chemical form (i.e., fumes, liquids, solids).
• Inhala=on (e.g., fumes, gases) – Primary route of occupa=onal exposures • Inges=on (e.g., liquids, dust) • Absorp=on (e.g., solvents)
• Onset of illness can be either by ACUTE or CHRONIC exposures • Chronic exposures are the most widely studied.
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Visual System Anatomy
• Peripheral • External Layers of the Re=na
• Color Vision (cones) • Night vision (rods)
• Central • Internal layers of the re=na • Op=c Nerve • Visual Pathways • Visual Cortex
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Visual System Dysfunc=on
• Peripheral Visual System • Re=nal pigmented epithelium (RPE)
• photoreceptors have highest O2 consump=on of any =ssue in the human body
• 75% of the re=nal mitochondria in this area (vulnerable to toxicity) • High body affinity to bind PAH and metals including Pb, Hg
• Central Visual System Pathways • Op=c nerve and Visual cortex
• increased basal oxygen consump=on increases with visual s=muli
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Visual System Tes=ng
• Color Vision Tes=ng (dyschromotopsia)
• Electrore=nogram (inner and outer layers)
• Visual Field Tes=ng (Op=c nerve dysfunc=on)
• Oculomotor Tes=ng (Cranial nerve dysfunc=on)
• Contrast Sensi=vity Tes=ng (nonspecific threshold tes=ng)
• Cri=cal Flicker Fusion (non specific)
• VISUAL SEARCH PERFORMANCE • Visual Evoked Poten=al Tes=ng (central pathway dysfunc=on)
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Vision Tes=ng Methods
• Color Vision Tes=ng • Farnsworth-‐Munsell 100 (FM-‐100) Hue Color Vision Test • Lanthony Desaturated D15 (LD15), or D15d most u=lized.
• Visual Evoked Poten=al (VEP) • Ini=ated by brief visual s=muli, recorded by EEG signals. • Measures func=onal integrity of the visual pathways from re=na via the op=c nerves to the visual cortex of the brain.
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Kollner’s Rule and Dyschromatopsia • Dysfunc=on can be localized by the type of vision loss:
• Toxicity to peripheral system (Re=na) leads to Blue-‐Yellow (BY) deficits • Toxicity to central pathways leads to Red-‐Green (RG) deficits
• Type III: External re=nal layers: BY loss; RARE INHERITED, ALTITUDE? • normal to moderate acuity loss. TRITAN
• Type II: Internal re=nal layers: RG and BY loss ; • moderate to severe acuity loss. DEUTAN
• Type I: Internal re=nal layers: RG loss: • moderate acuity loss. PROTAN
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Toxins Associated with Vision Loss Occupa=onal Exposure to Styrene
Industrial solvent in the manufacturing of plas=cs; associated with altera=ons in color vision (Type III blue-‐yellow) in workers exposed to concentra=ons between 4-‐70 ppm for 5-‐17 years (Fox 2015).
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Toxins Associated With Vision Loss Occupational Exposure to Perchloroethylene and Trichloroethylene
33 dry cleaners (mean age 31) exposed to occupa=onal levels of TCE Results showed significantly lower contrast sensi=vity (p <0.05) and poorer color discrimina=on (BY) when compared to controls (n = 35). High level deficits in percep=on of global form and mo=on were also recorded (p <0.0001).
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Toxins Associated With Vision Loss Occupa=onal Exposure to Carbon disulfide Vast industrial uses (e.g., clothing, industrial solvent, pes=cides) Known for neurological and vascular dysfunc=on: re=nal altera=ons (e.g., retrobulbar neuri=s, pre-‐senile arteriosclero=c changes in the fundus, microaneurysms and small hemorrhages, delayed papillary filling, and irregulari=es in the caliber of re=nal arterioles and veins). Clinical studies describe severe loss of central vision (central scotoma), decreased sensi=vity in peripheral visual fields (rod scotoma), op=c atrophy, blurred vision, impaired color vision (BY), and papillary changes.
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Toxins Associated With Vision Loss Occupa=onal exposure to Lead (Pb) – inorganic Lead-‐acid banery manufacturing, welding, electronic manufacturing (lead solder), jewelry making, etc. Decreases in cri=cal flicker fusion have been recorded in workers with a mean blood lead level (BLL) of 35-‐47 ug/dL. Peripheral and paracentral scotomas have also been seen in workers chronically exposed (>5 yrs) to moderate-‐levels of Pb or those acutely exposed to high-‐levels of Pb. Many papers prior to 2000 documen=ng visual toxicity to lead using various method of assessment.
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GENETICS AND ENVIRONMENT
• Macular degenera=on • Lead may accumulate in RPE layers and has been associated. • Herbicides in in drinking water.
• Glaucoma and hair lead.
• Leber’s Op=c Hereditary Neuropathy and organic solvents.
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Ototoxicity: Auditory system anatomy
• Inner ear includes Cochlear hair cells • Converts of sound waves of different frequencies and amplitudes into electrical signals
• Tonotopically organized with different sounds s=mula=ng different areas of the organ which then s=mulate different brain stem cell nuclei and different areas of auditory cortex
• Conduc=on hearing deficit is the outer ear (on the way to the inner ear) • Sensory neural hearing loss is a change in the cochlea • Central hearing loss localizes to the acous=c nerve or auditory cortex • Outer hair cells affected first • Cochlear hearing loss is most common due to aging and noise
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Noise induced hearing loss
• 10 years or more: • 8% of 85 db; 22% of 90 db; 38% of 95 db; 44% of 100 db
• 20-‐25 db threshold shiHs, and 10 db, high frequency loss is normal • Should not progress if noise ceases • Early detrimental exposure leads to worsened suscep=bility to progression with age related hearing loss
• Higher frequencies first affected than progress to lower frequencies • Combina=on with ototoxicity and aging • In 1940, occupa=onal popula=ons had higher prevalence of hearing loss without noise exposure in industry
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Audiology Tes=ng Methods (Not sensi=ve to ototoxicity)
• Pure-‐Tone Audiometry (R/L ear hearing sensi=vi=es)
• High-‐Frequency Audiometry (Frequencies: 10, 12.5, 14 and 16 kHz)
• ImmiPance Audiometry (physical volume, tympanometry, etc.)
• Behavioral and Reflex modifica=on audiometry (animals, startle and warning thresholds)
• Electrocochleography
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Toxins Associated with Hearing Loss Occupa=onal Exposure to Solvents (e.g., Styrene, Toluene, Trichloroethylene)
Plas=cs (styrene), paint industry (toluene), dry cleaning industry (trichloroethylene). Synergis=c rela=onship; exposures and to noise. Cochlear toxicity. Long-‐term exposure to Styrene ((OEL 20-‐100 ppm): demonstrated auditory effects in workers exposed to 30-‐50 ppm for at least 10 years with levels above 50 ppm in the past. In humans, the type of interac=on taking place between noise and styrene exposure is not yet clear. Ototoxic effects (BAER abnormali=es) from Toluene (OEL 20-‐200 ppm): associated with current exposure levels of approximately 10-‐50 ppm. Historic toluene and/or noise exposure levels not well characterized and some with co-‐exposures. Exposed to higher concentra=ons in past and present could explain.
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Toxins Associated with Hearing Loss Occupational Exposure to Lead (Pb)
Used in gasoline as an an=knocking agent; jewelry industry, the automo=ve industry (e.g., lead-‐acid baneries), and in industrial paints. Inhala=on of dust and fumes; inges=on in children. Central auditory effects (BAER) found with currect and life =me weighted average of 28-‐57 ug/ dl of BLL.
Workers with a mean BLL of 37 ug/dL as having significant increases in hearing thresholds compared to controls.
Uncertain interac=on with noise and lead.
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Hearing loss and Toxicity
• TCE, CS2, Xylene, N hexane, Hg, CO, Pes=cides associated with auditory effects in humans.
• Occupa=onal studies (styrene, toluene, solvent mixtures and lead) indicate that much lower levels in industrial seJngs were associated with hearing deficits.
• Combina=ons of exposure with noise, other stressors such as physical ac=vity during exposure contribute to lower exposure intensity and dura=on leading to ototoxicity
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Olfactory Toxicity and Anatomy
• Olfactory Dysfunc=on 1-‐5% from toxins. • Exposures irrita=on and removal natural • Chronic exposures, subthreshold dangerous with =me; unno=ced gradual decrease of func=on.
• Age related loss secondary to accumula=on of damage from low level non irritant exposures?
• Olfactory epithelium direct contact (10% of respired air flow) • Regenera=ve capacity • Immunological defense, an=microbial agents, etc • Metabolizing poten=al detoxifica=on (reac=ve oxygen scavenging) or increasing toxicity?
• Neurons with dendrites extending into Cribiform plate to contact directly with olfactory bulb in CNS.
• Gases and solvents may reach olf bulb via systemic circula=on, Metals via receptors
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Olfactory Dysfunc=on
• Types of olfactory dysfunc=on: • Psychophysical (detec=on sensi=vity)
• Electrophysiological (measured electrical changes following s=mulus)
• Psychophysiological (assess odor-‐induced autonomic nervous system
responses)
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Olfactory Tes=ng Method
• UPSIT (University of Pennsylvania Smell Iden=fica=on Test)
• Test consists of 4 different 10 page booklets with “scratch and sniff” strips
• Scoring accounts for age and gender
• Considered the gold standard of smell iden=fica=on
• Used in tes=ng for a mul=ple of neurological diseases such as: Parkinson’s
disease, Alzheimer’s, Hun=ngton’s disease, brain tumors, and Mul=ple
Sclerosis
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Toxins Associated With Olfactory Dysfunc=on Highlights from the literature
• Cadmium: Olfactory dysfunc=on noted even at ACGIH proposed levels.
• Mercury: UPSIT u=lized in Minimata Bay survivors and found reduced ability to iden=fy s=muli.
• Manganese: Excitability of neurons heralds toxicity, then func=on decreases. Increase in urine Mn associated with lower detec=on threshold; lower in iron alloy workers. Changes related to dopaminergic dysfunc=on at the level of receptor. Ac=ve transport through olfactory tract.
• Popula=ons in Italy with elevated environmental exposure to Mn had increased prevalence of PD and odor iden=fica=on.
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Toxin Associated Olfactory Dysfunc=on
• Lead: No influence on Olfactory system in tetraethyl lead manufacturers using UPSIT.
• Toluene: Inhala=on chamber study revealed increased thresholds that returned to normal. No permanent insult
• Paint solvent: UPSIT tes=ng revealed dose related decrement in non smoking paint manufacture workers sugges=ng protec=on.
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Gustatory Toxicology: Anatomy of Taste
Saliva contains sodium, potassium, chloride and bicarbonate Salivary glands: paro=d, submandibular, sublingual and minor
Autonomic nervous system controlled Altera=on of components or volume will affect sal=ness, sourness Autoimmune disorders, medicines, systemic diseases
Oral mucosa Chemical burns, fungi, viruses, tobacco, gastric acid
Taste Bud Receptors-‐ Ac=vated; reduced in number Botox, tetrodotoxin, chemotherapeu=cs, tobacco
Central pathways Infec=on, inflamma=on: Botox, HZV, Bells palsy, GBS, poliomyeli=s, MS
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Gustatory Tes=ng Methods
• Taste strips (taste infused strips) • Inexpensive and very simple to use
• Administered and recorded in clinical or field seJng) • Electrogustometry (measurement of taste threshold)
• Clinical seJng
• Pass controlled anodal current through the tongue causing unique and dis=nct metallic taste (e.g., sensa=on experienced when placing 9-‐volt banery
on the tongue)
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Toxins Associated with Gustatory Dysfunc=on Isodecanes used in manufacturing of paint, imaging toners and floor cleaners.
• 63-‐year-‐old woman: Smell and taste loss aHer a 3-‐year exposure. Ini=ally welts on her tongue and lips, chest =ghtness, biner taste 8 years prior.
• Gradual smell and taste loss, intraoral burning sensa=ons, and periodic perioral derma==s.
• No improvement occurred with cromolyn sodium, zinc chloride, or copper sulfate.
• Examina=on of the olfactory epithelium revealed a flat, yellow area with scarring. Sinus CT scan was normal.
• Olfactory tes=ng: mild-‐to-‐moderate hyposmia. • Suprathreshold taste tes=ng: Depressed intensity ra=ngs, poor taste iden=fica=on, and no response to biner s=muli.
• AHer topical anesthesia, taste responses were reduced to zero. • Ineffec=ve treatment.
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Toxins Associated with Gustatory Dysfunc=on Acute ammonia exposure
• A 31-‐year-‐old man presented with hypogeusia 4 months aHer bi=ng down on an ammonia capsule hidden in a store-‐bought sandwich.
• He sustained an intraoral chemical burn injury, immediate-‐onset ageusia, and decreased sensi=vity to oral s=muli.
• His medical history was significant for environmental allergies. He smoked <1 pack of cigarenes per day for <5 years.
• Examina=on and olfactory tes=ng was normal. • Suprathreshold taste was consistent with hypogeusia: iden=fied s=muli of moderate and high concentra=on.
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Toxins Associated with Gustatory Dysfunc=on Lead (Pb)
• Workers complain of metallic tastes, coinciding with a specific metal. • Brass pipe finers and jewelry workers suffering from lead poisoning, frequently report a persistent, sweet, metallic taste.
• Because heavy metals are concentrated in saliva and their topical applica=on on the tongue can diminish taste percep=on, a possible direct mechanism of ac=on has been hypothesized
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Toxins Associated with Gustatory Dysfunc=on Occupa=onal exposure to Chromium (Cr)
• Metal plaJng, an=-‐corrosive agent, manufacture of stainless steel
• Increased taste thresholds noted in workers with chromium
exposures using both chemical s=muli and electrical s=muli.
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Toxins Associated with Gustatory Dysfunc=on Organophosphate-‐based pes=cides (e.g., DDT, Parathion)
• Workers with frequent exposure to pes=cides have complaints of sustained metallic, biner taste.
• Specific OP exposures associated with a garlic taste and odor. • Experimental models, disrup=on of sensory nerve termina=ons, but they may also interfere with central neurotransminers.
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Toxins Associated with Gustatory Dysfunc=on Solvents Cross-‐sec=onal study of 264 workers exposed to organic solvents Increase prevalence of smell and/or taste dysfunc=ons, similar to work related dizziness. Disturbances in smell or taste were most oHen hyposmia, but hypogeusia and a persistent “glue” taste were reported. Symptoms, however, were generally transitory, reversible, and likely due to to concentra=on peaks rather than long-‐term exposures.
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Solvent-‐induced sensory dysfunc=ons Chemical Reference
Neurotoxic Sensory Endpoint(s)
Vision C or P Hearing Smell Taste
Ammonia Prudhomme et al. 1998 X
Carbon disulfide Fox D. 2015, Gobba 2003 C, P X X
Isodecanes Smith et al. 2009 X
Methyl isobutyl ketone (MIBK) Gagnon et al. 1994 X
N-‐ Hexane Gobba, 2003 P, C X
Perchloroethylene (PCE) Gobba and Cavalleri 2003 P., C
Styrene Fox D. 2015; Kjell, ed. 2010 P X
Toluene Fox D. 2015; Kjell, ed. 2010, Mergler 1992 P, C X X
Trichloroethylene (TCE) Barbosa et al. 2015, Gobba 2003 P, C X X
Xylene Gobba 2003 X X
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Heavy metal-‐induced sensory dysfunc=on
Chemical Reference Neurotoxic Sensory Endpoint(s)
Vision, C or P Hearing Smell Taste
Arsenic Gobba 2006, 2003 X X
Cadmium Mascagni, 2003, Gobba 2003 X X X
Chromium (Cr) Reiter et al. 2006; Seeber et al. 1990, Gobba 2003 X X
Lead (Pb) Fox D. 2015; Kjell, ed. 2010; Reiter et al. 2006; Bolla et al. 1995 C X X X
Manganese (Mn) Antunes et al. 2007; Bowler et al.; Zoni et al. 2012, Sinczuk-‐ Walzak 2001 X X X
Mercury (Hg) Gobba 2006, 2003 Organic C, Inorg C,
Elemental P X X X
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Pes=cide-‐induced sensory dysfunc=on
Chemical Reference Neurotoxic Sensory Endpoint(s)
Vision Hearing Smell Taste
Chlorpyrifos Gobba, 2003. X
DDT Reiter et al. 2006 X
OP-‐based pes=cides Reiter et al. 2006 X
Parathion Reiter et al. 2006 X
Sulfuryl fluoride Calvert et al. 1998 X
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References • Antunes MB, Bowler RM, Doty RL. San Francisco/Oakland Bay Bridge welder study: olfactory func=on. Neurology 2007;69:1278–84.
• Barbosa IAJ, Boon MY, Khuu SK (2015). Exposure to Organic Solvents Used in Dry Cleaning Reduces Low and High Level Visual Func=on. PLoS ONE 10(5):e0121422. Doi:10.137/journal.pone.0121422.
• Bolla KI, Schwartz BS, Stewart W, Rignani J, Agnew J, Ford DP. Comparison of neurobehavioral func=on in workers exposed to a mixture of organic and inorganic lead and in workers exposed to solvents. Am J Ind Med 1995;27(2):231–46.
• Bowler RM, Gocheva V, Harris M, et al. Prospec=ve study on neurotoxic effects in manganese-‐exposed bridge construc=on welders. NeuroToxicol. 2011;32:596-‐605.
• Erie JC, Good JA, Butz JA. Excess lead in the neural re=na in age-‐related macular degenera=on. Am J Ophthalmol. 2009;148:890–894.
• Farahat TM, Abdel-‐Rasoul GM, El-‐Assy AR, Kandil SH, Kabil MK. Hearing thresholds of workers in a prin=ng facility. Environ Res. 1997;73:189–92.
• Fox D. (2015). Re=nal and visual system: occupa=onal and environmental toxicology. In. LoJ M and Bleecker ML (Eds). Handbook of Clinical Neurology, Vol. 131 (3rd Series) OccupaJonal Neurology. (pp 325-‐340). Elservier BV.
• Frank ME, HeJnger TP. What the Tongue Tells the Brain about Taste. Chem. Senses. 2005;30(Supp 1): i68-‐i69. www.neoma.com 3/10/16 37
References (cont’d)
• Furuta S, Nishimoto K, Egwa M, Ohyama M, Moriyama H. Olfactory dysfunc=on in pa=ents with Minimata disease. Am J Rhinol 1994;8:259–63
• Gobba F, Cavalleri A. Color Vision Impairment in Workers Exposed to Neurotoxic Chemicals. NeuroToxicology. 2003;24:693-‐702.
• Gobba F. Olfactory toxicity: long-‐term effects of occupa=onal exposures. Int Arch Occup Environ Health. 2006;79:322-‐331.
• Hotz P, Tschopp A, Söderström D, et al. Smell or taste disturbances, neurological symptoms, and hydrocarbon exposure. Intl Arch Occupa Environ Health. 1992;63(8):525-‐530.
• Johns DR, Smith KH, Miller NR (1992). Leber’s hereditary Op=c neuropathy. Clinical manifesta=ons of the 3460 • Johnson and Morata, Occupa=onal Exposures to Chemical and Hearing Impairment. In Torén Kjell, Editor-‐in-‐Chief.
Arbete och Hälsa (Work and Health). Occupa=onal and Environmental Medicine at Sahlgrenska Academy, Univ. of Gothenburg. 2010.
• Klein BE, McElroy JA, Klein R et al. Nitrate-‐nitrogen levels in rural drinking water: is there an associa=on with age-‐related macular degenera=on? J Environ Sci Health A Tox Hazard Subst Environ Eng. 2013;48:1757–1763.
• LoJ M and Bleecker ML, editors. Handbook of Clinical Neurology, Vol. 131 (3rd Series) Occupa=onal Neurology. Elservier BV. 2015.
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References (cont’d) • Mascagni P, Consonni D, Bregante G, Chiappino G, Toffoleno F. Olfactory func=on in workers exposed to moderate airborne cadmium levels. Neurotoxicology 2003;24(4–5):717–24.
• Mergler D, Beauvais B. Olfactory threshold shiH following controlled 7-‐h exposure to toluene and/or xylene. NeuroToxicol. 1992;13(1):211–15.
• Morata TC, Fiorini AC, Fischer FM, Colacioppo S, Wallingford KM, Krieg EF, Dunn DE, Gozzoli L, Padrao MA, Cesar CL. Toluene-‐induced hearing loss among rotogravure prin=ng workers. Scand J Work Environ Health 1997b;23(4):289–98.
• Prudhomme, JC, Shusterman DJ and Blanc PB. Acute-‐Onset Persistent Olfactory Deficit Resul=ng From Mul=ple Overexposures to Ammonia Vapor at Work JABFP Jan.-‐Feb.I998 Vol. II No.1
• Reiter ER, DiNardo LJ, Costanzo, RM. (2006). Toxic Effects on Gustatory Func=on. In, Hummel T and Welge-‐Lüssen A (Eds), Taste and Smell. An Update. Adv Otorhinolaryngol, Vol 63. (pp 265–277). Basel, Karger.
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References
• Schwartz BS, Ford DP, Bolla KI, Agnew J, Rothman N, Bleecker ML. Solvent-‐associated decrements in olfactory func=on in paint manufacturing workers. Am J Ind Med. 1990;18(6): 697–706.
• Sinczuk-‐Walczak H, Jakubowski M, Matczak W. Neurological and neurophysiological examina=ons of workers occupa=onally exposed to manganese. Int J Occup Med Environ Health 2001;14(4):329–37.
• Smith WM et al. Toxin-‐induced chemosensory dysfunc=on: A case series and Review. Am J Rhinol Allergy. 2009 ; 23(6): 578–581.
• Treibig et al. Occupa=onal Styrene exposure to and hearing loss. Int Archives of Occupa=onal and Environmental Health 2009; 82; 463-‐480
• Upadhyay UD et al. Olfactory loss as a result of toxic exposure. Otolaryngol Clin N Am 37 (2004) 1185–1207 2004
• Yuki K, Dogru M, Imamura Y, et al. Lead accumula=on as possible risk factor for primary open-‐angle glaucoma. Biol Trace Elem Res. 2009;132:1–8.
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MOC Ques=on ONE
• Which industries have NOT been studied regarding color vision toxicity?
• A. Dry cleaning • B. Airline workers • C. Boat builders • D. Tetraethyl Lead workers
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MOC Ques=on TWO
• Which of these sensory systems anatomical areas are considered part of the Central Nervous System?
• A. Olfactory Bulb • B. Cribiform Plate • C. Salivary Glands • D. External Re=nal Layer
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MOC Ques=on THREE • Which neurophysiological test is matched incorrectly? • A. Cri=cal Flicker Fusion: Vision • B. UPSIT: Smell • C. Electrogustography: Taste • D. High Frequency Audiometry: Hearing • E. None
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Answers
• I. B • II. A • III. A-‐3,B-‐1,C-‐2, D-‐4
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