MOERDIJK, januari 2011

Frits van Rooy

'Geen gevaar volksgezondheid'

RISICO COMMUNICATIE

'Geen gevaar volksgezondheid'

RISICO COMMUNICATIE

pH = 11-14

10-1-2011 versie 3

Brand

• Respiratoire schade agv inhalatie van rook is primaire oorzaak van morbiditeit en mortaliteit

• Type en ernst van de schade is afhankelijk van: – Temperatuur

– Chemische samenstelling

(toxische gassen en chemicalien)

Samenstelling rook

Goldfrank's Manual of Toxicologic Emergencies > Chapter 123. Smoke Inhalation > Pathophysiology >

Products Combustion Products

Acrylic Acrolein, hydrogen chloride, carbon monoxide

Fire-retardant materials Hydrogen chloride, hydrogen bromide

Fluorinated resins Hydrogen fluoride

Melamine resins Ammonia, cyanide

Nitrogen-containing material Cyanide, isocyanates, oxides of nitrogen

Nylon Ammonia, cyanide

Petroleum products Carbon monoxide, acrolein, acetic acid, formic acid

Plastics Cyanide, hydrogen chloride, aldehydes, ammonia, nitrogen oxides, phosgene, chlorine

Polystyrene Styrene

Polyurethane Cyanide, isocyanates

Polyvinyl chloride Carbon monoxide, hydrogen chloride, phosgene, chlorine

Rubber Hydrogen sulfide, sulfur dioxide

Silk Sulfur dioxide, hydrogen sulfide, ammonia, cyanide

Sulfur-containing material Sulfur dioxide

Wood, cotton, paper Carbon monoxide, acrolein, acetaldehyde, formaldehyde, acetic acid, formic acid, methane

Wool Carbon monoxide, hydrogen chloride, phosgene, chlorine, cyanide, ammonia

Toxische verbrandingsproducten

Simpele asphyxiantia: zuurstof verdringing

Irritantia: locale respiratoire effecten,

Goed (bovenste luchtwegklachten)

Matig (bovenste en onderste luchtwegklachten)

Slecht (alveolaire schade, longoedeem)

Chemische asphyxiantia: zuurstoftransport en - verbruik

Roetdeeltjes

MOERDIJK januari 2011 Actiecentrum Bedrijfsgezondheidszorg Frits van Rooy, bedrijfsarts

Datum Tijd

(globaal)

Fase brand Stoffen Geschatte

blootstelling

Woensdag

5 jan

1 14.26 u Felle brand Verbrandingsproducten

HCl, Cl2, COCl2, HF,

NOx, HCN, SO2, H2S,

COS, HCN, NOx, NH3

Bovenwinds lage

blootstelling

2 23.15 u Schuimdeken Ook PAK, aldehyden,

roet, PCDD, PCDF

Mogelijk hoge

blootstelling

Donderdag

6 jan

3 00.15 u Brandmeester Verbrandingsproducten Matige blootstelling

4 17.30 u

Technisch uit:

chemisch

afval en

bluswater

Vluchtige organische

(gechloreerde)

koolwaterstoffen,

basisch

Lage blootstelling

Blootstelling door

direct contact en

inademen dampen

Irritant Gas

Asphyxiant

Cholinergic

Corrosive

Hydrocarbon & Halogenated hydrocarbon

Local toxic effects on moist mucous membranes: Eye – conjunctival and corneal

Nose – nasopharnyngeal

Mouth and throat – oropharyngeal

Voice box – epiglottic, laryngeal

Wind pipe – tracheobronchial

Peripheral Lung – alveolar-capillary membrane

No entrance of circulation and no systemic effects

Primary local toxic effects can cause: Cough and lacrimation (irritation of mucous membranes)

Bronchospasm (dyspnoe)

Pulmonary edema (high exposures)

Also secondary systemic effects: Decrease in oxygen delivery to myocard (heart muscle) and

central nervous system (brain) and can be fatal at high exposures

Highly water soluble Ammonia (NH3),

formaldehyde (H2CO), hydrogen chloride (HCl) and sulfur dioxide (SO2)

Affect upper airways

(cf type I inhalation trauma: at low exposure victim should recover in 1-2 h)

Moderately water soluble: E.g. Chlorine (Cl2)

Lower airways

(tracheobroncheal tree and alveolar-capillary membrane), not so much upper airway

Scarcely water soluble Nitrogen dioxide (NO2), phosgene (Cl2CO)

Only lower airways (alveolar-capillary membrane). Note 1: they can go undetected by the victim because of

lack of effects on upper airways

Note 2: they can go undetected by the doctor (latency of clinical manifestiation up to 24 h!)

(cf. Type 2 Inhalation trauma, at high exposures serious alveolar trauma such as lung edema may go undetected)

Strong base (e.g. ammonia)

Liquifactive necrosis:

cell death w/o scabs

Strong acid (e.g. hydrochloric or sulfuric acid):

Coagulative necrosis:

cell death with scabs

Sodium hydroxyde burn

Sulfuric acid burn

Signs and symptoms:

Heart: tachycardia

Respiratory system: initial increased respiratory rate followed by slowing down of repiratory rate due to depression of the respiratory centre

Central nervous system: headache, dizziness, weakness, confusion agitation, seizures, loss of consiousness, coma, death

Systemic (chemical asphyxiant) Interference with oxygen transportation and/or utilization of oxygen (cf. Type 3 inhalation trauma may lead to life threatening systemic toxicity) Three types: Disruption of oxygen tranpsort: Binding to hemoglobin (stronger than O2) and change of structure causing slower

release of oxygen to tissues

E.g. Carbon monoxide (CO), dichloromethane (because CO is a metabolite)

Met-hemoglobin forming compounds:

Change of oxidation state of iron from ferrous (Fe2+) to ferric (Fe3+): E.g. nitro- or amino-group substituted to aryl or alkyl, salts of nitric acid (HNO3) and

nitrous acid (HNO2)

Inhibition of the use of oxygen on cellular level: Inhibition of cellular use of oxygen in production of ATP in electron transport

chain (binding to ferric iron in cytochrome oxidase a3)

E.g. sodium cyanide (KCN), methylisocyanaat, hydrogen sulfide (H2S), natrium azide

De pindakaasmoord In Zuid-Limburg werd een chemicus aangehouden op verdenking van de

moord op zijn vriendin. In haar lichaam werd cyanide aangetroffen en de

verdachte bleek verschillende flesjes met chemicaliën in zijn bezit te

hebben. Een restant van een boterham met pindakaas, waarvan door het

slachtoffer was gegeten, werd voor onderzoek bij het nfi aangeboden. De

eerste vraag was of het überhaupt mogelijk was om 'vreemde‘ stoffen uit de

pindakaas te isoleren. Het is namelijk vrij lastig om chemische stoffen te

isoleren uit vettige substanties. Zowel in het broodje als in het bloed van het

slachtoffer bleken sporen van de giftige stof azide te zitten. Deze stof wordt

in het lichaam omgezet in cyanide.

Acid (produces hydronium ion H3O+)

Forms a coagulum of necrotic tissue, a thick and hardened scab like surface that limits deeper penetration.

(e.g. hydrochloride, hydrofluoric acid)

Heat of hydration

pKa determines extent of dissociation

Electronegativity of anion

(e.g. F- is extremely toxic and reacts with enzymes, Mg+ and Ca2+)

Base (produces hydroxide ion, OH-)

Liquefactive necrosis

causing destruction by saponification (soap formation) causing deep penetration (causing chemical burn)

E.g. sodium hydroxyde

Chemical burn by NaOH

Oxidizers

Causes exothermic reactions,

producing heat resulting in thermal burns

White phosphorus Pyrophoric (fire forming) igniting spontaneously in air causing: •Local effects (burns) •Systemic effects (hypocalcemia resulting in decreased cardiac output)

Burns caused by white phosphorus

Aliphatic hydrocarbons (including branched) E.g. Propane, butane, pentane, hexane, etc. E.g. isopropylalcohol, tert-methyl-butylether Mineral oils such as turpentine, pine oils, etc.

Aromatic hydrocarbons (including substituted) Benzene, toluene, o-, p-, and m-xylene Phenol, styrene Gasoline, naphta, stoddard solvent, thinner

Halogenated hydrocarbons (Cl, Br, I, F) E.g. trichloroethylene, 1,1,1-trichloroethane, carbon

tetrachloride, chloroform Coolant, degreaser

Repiratory signs and symptoms: Asphyxia (c.f. asphyxiant toxidrome)

Irritation

Sensibilisation (e.g. pine oil)

Chemical pneumonitis in case of aspiration

◦ After ingestion of mineral oils

◦ Inhalation of fine-dispersed aerosol (e.g. air spray)

Cardiovascular signs and symptoms: Myocardial sensitization can produce tachydysrhythmias and cardiac arrest

Tachycardia as a results of reduced oxygen supply (as asphyxiant)

CNS signs and symptoms: General anaesthesia > coma > death

Headache, dizziness, paresis, confusion, agitation, seizures, lack of coordination,

CNS depression > respiratory depression

Tachycardia

Local signs and symptoms: Defatting dermatitis

Skin irritation

Painless depigmented (white) chemical burns

Eye: irritation, lacrimation, blurred vision, conjunctival infection and corneal ulceration

Irritant gas toxidrome 21

Hydrocarbon toxidrome 2

Psychological 3

Rhinitis/sinusitis 6

Verwezen eigen bedrijfsarts 2

Geen bijzonderheden 3

Totaal 37

Blootstelling X

Veranderde

structuur/

functie

Vroeg

biologisch

effect

Biologisch

effectieve

dosis

Opname in het

lichaamZiekte

Arbeidshygiëne Arbeids- & bedrijfsgeneeskundeCuratieve

gezondheidszorg

Epidemiologie

Aanpak / Preventie / Reïntegratie

Herkenning en Diagnostiek

Bron: Proefschrift Frits van Rooy 2010, Universiteit Utrecht

An Interdisciplinary Approach to Occupational Respiratory Disorders

Ketenzorg

NIEUWS

Polikliniek voor klinische arbeidstoxicologie

Klinische Farmacologie

• Prof. dr. P. Smits, internist

• Dr. C. Kramers, internist, klinisch toxicoloog/farmacoloog en sectiehoofd

• Dr. B. Schouwenberg, internist

Arbo Unie ECTS

• Dr. G.B.G.J. van Rooy, arts-klinische arbeidsgeneeskunde

06-52502391 of frits.van.rooy@arbounie.nl

Kosten

• DBC + 920 €

Aanmelding

• toxpoli@arbounie.nl

Radboud Toxpoli