Health Protection Agency 

Compendium of Chemical Hazards: 

Diesel. 

Prepared by: 

Robert P Chilcott 

Chemical Hazards and Poisons Division (HQ), Chilton, 

Didcot, Oxfordshire, OX11 0RQ, United Kingdom. 

www.hpa.org.uk 

Disclaimer 

This guidance has been provided by the Chemical Hazards and Poisons 

Division of the UK Health Protection Agency (HPA). It is general guidance 

based on current knowledge and understanding. The HPA does not warrant 

that the information and guidance is complete and correct for use in all 

circumstances. The HPA shall not be liable for any damages that might be 

incurred as a result of the use of the guidance or information.
HPA Compendium of Chemical Hazards 

Diesel 

Key Points 

Fire 

• Flammable 

• Vapour / air mixtures may be explosive 

• Use foam and liquid-tight protective clothing with breathing apparatus 

Health 

• Irritating to eyes, respiratory ststem and skin

• Severe lung injury may occur following aspiration of liquid 

• Possible carcinogen 

Environment 

• Dangerous for the environment 

• Inform Environment Agency of substantial incidents 

Prepared by R P Chilcott, 

CHAPD HQ 

2006 

Version 1 
DIESEL – CONTENTS

Contents 

GENERAL INFORMATION

Background

Production and Uses

Frequently Asked Questions

INCIDENT MANAGEMENT 

Hazard Identification

Standard (UK) Dangerous Goods Emergency Action Codes

Chemical Hazard Information and Packaging for Supply Classification()

Physicochemical Properties

Threshold Toxicity Values

Published Emergency Response Guidelines

Emergency Response Planning Guideline (ERPG) Values

Acute Exposure Guideline Levels (AEGLs) 

Exposure Standards, Guidelines or Regulations

Occupational standards

Public health guidelines

Health Effects

Major route of exposure

Immediate Signs or Symptoms of Acute Exposure 

Decontamination and First Aid

Dermal exposure

Ocular exposure

Inhalation

Ingestion 

TOXICOLOGICAL OVERVIEW 

Toxicological Overview

Summary of health effects

Kinetics and metabolism

Sources and route of human exposure

Health Effects of Acute / Single Exposure

Human Data

General toxicity

Inhalation

Ingestion

Dermal / ocular exposure

Neurotoxicity

Nephrotoxicity

Delayed effects following an acute exposure

Animal and In-Vitro Data
General toxicity

Delayed effects following an acute exposure

Health Effects of Chronic / Repeated Exposure

Human Data

General toxicity

Inhalation

Ingestion

Dermal / ocular exposure

Genotoxicity

Carcinogenicity

Reproductive and developmental toxicity

Animal and In-Vitro Data

General toxicity

Inhalation

Ingestion

Dermal / ocular exposure

Genotoxicity

Carcinogenicity

Reproductive and developmental toxicity

References

Annex I: Categories of diesel additives.

Annex II: UK Classification of fuel oils.

Annex III: UK Physicochemical standards for diesel
Diesel 

General information 

Key Points 

Fire 

• Flammable 

• Vapour / air mixtures may be explosive 

• Use foam and liquid-tight protective clothing with breathing apparatus 

Health 

• Irritating to eyes, respiratory system and skin

• Chemical pneumonitis may arise following aspiration of vomitus (secondary to 

ingestion) or inhalation of aerosol (or aspiration of liquid) during manual siphoning 

• Prolonged skin exposure may cause skin irritation 

• Possible carcinogen 

• Diesel is considered not to be a human reproductive or developmental toxicant 

Environment 

• Dangerous for the environment 

• Inform Environment Agency of substantial incidents 

Prepared by R P Chilcott, 

CHAPD HQ 

2006 

Version 1 
DIESEL – GENERAL INFORMATION

Background 

Diesel is a complex mixture of chemicals 

mainly obtained from the distillation of crude 

oil. The product is thought to be named after 

Dr Rudolf Diesel, a German engineer who, 

in 1892, patented an oil-burning internal 

combustion engine. Modern diesel engines 

also incorporate features of a design 

(patented between 1886 and 1890) by the 

Yorkshireman Herbert Akroyd Stuart . 

In the UK, ‘diesel’ or DERV refers to a fuel 

for running cars, vans and lorries. However, 

the term ‘diesel’ is also used to describe a 

range of different fuels such as ‘artic’ and 

‘marine’ diesel or as an alternative name for 

kerosene, all of which differ considerably in 

composition and physical properties. 

In 2004, approximately 700 litres (150 

gallons) of diesel was sold every second in 

the UK. Most diesel is ultra-low in sulphur 

content in order to limit the emission of 

sulphur-containing pollutants from engine 

exhaust fumes. 

Diesel is not considered to be particularly 

toxic and accidental poisoning is very rare. 

However, if diesel is swallowed, medical 

advice should be obtained immediately as 

there is a small risk of short-term lung 

damage if vomiting occurs or if droplets of 

diesel are inhaled. Long-term skin exposure 

to diesel may result in eczema (dermatitis) 

and should be avoided. 

The use of diesel to clean skin and hair 

should be strongly discouraged as this 

practice has been known to cause serious 

kidney damage. 
DIESEL – GENERAL INFORMATION

Production and Uses 

Key Points 

Production and uses 

• Diesel is produced by mixing fractions of crude oil distillates (petrochemicals) with 

various, brand-specific additives. 

• Approximately 22 thousand million litres (5 thousand million gallons) of diesel were 

sold in the UK in 2004, equating to 700 litres (150 gallons) per second. 

Diesel is produced by blending straight-run middle distillates (minimum 40%) with varying 

proportions of straight-run gas oil, light vacuum distillates, light thermally-cracked distillates 

and light catalytically-cracked distillates. 

The quantity of diesel released by HM Revenue and Customs for consumption in the UK in 

2004 was approximately 22 thousand million litres (5 thousand million gallons), the majority 

(99.7%) of which was “ultra-low sulphur diesel” for automotive engines. Diesel is also used 

as a cleaning solvent for tanks, engines and refinery equipment. 
DIESEL – GENERAL INFORMATION 

Frequently Asked Questions

What is diesel? 

Diesel is a complex mixture of hydrocarbons produced by mixing fractions obtained from the 

distillation of crude oil with brand-specific additives to improve performance. It is a liquid 

under normal conditions with a characteristic odour. 

What is diesel used for? 

In the UK, diesel is mainly used as a fuel for road vehicles, although other forms of transport 

(such as ships and trains) and electricity generators also use certain types of diesel. 

How does diesel get into the environment? 

Diesel is found in the environment as a result of accidental release from an industrial site or 

transport vehicle. There are no natural sources of diesel. 

If there is diesel in the environment will I have any adverse health effects? 

Like most chemicals, the amount of diesel you are exposed to must be above a certain level 

to cause adverse health effects. A short, one-off exposure to diesel will not normally cause 

any long-term health effects. Occasional skin exposure may lead to dermatitis (eczema). 

Breathing large quantities of diesel vapour or drinking diesel-based fluids may cause nonspecific signs and symptoms of poisoning such as dizziness, headache and vomiting. A 

severe form of lung damage called pneumonitis may occur if liquid diesel is inhaled directly 

onto the lungs, for example, whilst manually siphoning a tank or from inhaling vomit after 

swallowing diesel. This is why it is important not to make someone sick if they have 

swallowed diesel. 

Can diesel cause cancer? 

There is limited evidence from animal studies that prolonged exposure may increase the risk 

of developing skin cancer. There is not thought to be any risk of cancer from short-term, 

occasional exposure. 

Can diesel affect or damage the unborn child? 

There is no evidence to suggest that exposure of a mother to diesel may harm the unborn 

child. However, as with all chemicals, it is obviously best to avoid unnecessary contact if 

possible. 
Diesel 

Incident management 

Key Points 

Fire 

• Flammable 

• Vapours may be violently reactive with air 

• Use foam and liquid-tight protective clothing with breathing apparatus 

Health 

• Toxicity occurs following ingestion, inhalation & skin absorption

• Possible carcinogen 

• Irritating to eyes and skin 

• Aspiration may cause serious lung injury 

 Environment 

• Avoid release into the environment 

• Inform Environment Agency of substantial incidents 

Prepared by R P Chilcott, 

CHAPD HQ 

2006 

Version 1
DIESEL – INCIDENT MANAGEMENT

Hazard Identification( ) a

Standard (UK) Dangerous Goods Emergency Action Codes 

UN 1202 Diesel Fuel or Gas Oil or Heating Oil, Light 

EAC 3Y 

Use normal foam. Wear normal fire kit in combination with 

breathing apparatus*

. Spillages and decontamination run-off 

should be prevented from entering drains and watercourses.

Substance can be violently or explosively reactive.

APP - 

Class 3 Flammable liquid 

Hazards 

Sub 

risks - 

HIN 30 

Flammable liquid (flash point between 23 °C and 61 °C 

inclusive) or flammable liquid or solid in the molten state with 

a flash point above 61 °C, heated to a temperature equal to 

or above its flash point, or self-heating liquid 

UN – United Nations number; EAC – Emergency Action Code; APP – Additional Personal 

Protection; HIN - Hazard Identification Number 

* Normal fire fighting clothing i.e. fire kit (BS EN 469), gloves (BS EN 659) and boots (HO specification 

A29 and A30) in combination with self-contained open circuit positive pressure compressed air 

breathing apparatus (BS EN 137). 

 

a

 Dangerous goods emergency action code list, HM Fire Service Inspectorate, Publications Section, 

The Stationery Office, 2004. 
DIESEL – INCIDENT MANAGEMENT

Chemical Hazard Information and Packaging for Supply Classification( ) a

Classification Carc cat 3 Category 3 carcinogen 

Risk phrases R40 Limited evidence of a carcinogenic effect 

S(2) Keep out of the reach of children 

Safety phrases 

S36/37 Wear suitable protective clothes and gloves 

 

a

 Approved supply list (seventh edition): information approved for the classification and labelling of 

substances and preparations dangerous for supply. Chemical (Hazard Information and Packaging for 

Supply) Regulations 2002. The Stationery Office, 2002. 
Physicochemical Properties( , ) a b

Volatility Low volatility; vapour pressure < 1 mm Hg 

Specific gravity 0.82 – 0.95 at 15 °C (water = 1)

Flammability Flammable. 

Lower explosive limit 0.6% 

Upper explosive limit 6.5% 

Water solubility 0.5 mg 100 mL-1

Reactivity Vapours may be violently reactive with air 

Reaction or degradation 

products May liberate irritating or toxic fumes during combustion 

Odour Characteristic odour 

DIESEL – INCIDENT MANAGEMENT

 

a International Chemical Safety Card (ICSC) entry for diesel fuel no 2. ISCS 1561. International 

Occupational Safety and Health Information Centre (CIS), 2004.

b

 CIRUS entry for diesel, 2005. 
DIESEL – INCIDENT MANAGEMENT

Threshold Toxicity Values( ) a

THRESHOLD LEVELS

EXPOSURE BY INHALATION 

ppm mg m-3

SYMPTOMS

- - Data not available 

 

a

 Hydrocarbons (MEDITEXT® Medical Management). In: Klasco RK (Ed): TOMES® System. 

Thomson Micromedex, Greenwood Village, Colorado (Edition expires [03, 2006]). 
DIESEL – INCIDENT MANAGEMENT

Published Emergency Response Guidelines 

Emergency Response Planning Guideline (ERPG) Values ( ) a

Listed value 

(ppm) 

Calculated value 

(mg m-3) 

ERPG-1*

ERPG-2*

ERPG-3*

Data not available

* Maximum airborne concentration below which it is believed that nearly all individuals could be 

exposed for up to 1 hr without experiencing other than mild transient adverse health effects or 

perceiving a clearly defined, objectionable odour. 

** Maximum airborne concentration below which it is believed that nearly all individuals 

could be exposed for up to 1 hr without experiencing or developing irreversible or other 

serious health effects or symptoms which could impair an individual's ability to take 

protective action. 

*** Maximum airborne concentration below which it is believed that nearly all 

individuals could be exposed for up to 1 hr without experiencing or developing lifethreatening health effects. 

Acute Exposure Guideline Levels (AEGLs) ( ) b

mg m-3

10 min 30 min 60 min 4 hr 8 hr 

 AEGL-1†

 AEGL-2††

 AEGL-3†††

Data not available 

† The level of the chemical in air at or above which the general population could experience notable 

discomfort. 

†† The level of the chemical in air at or above which there may be irreversible or other serious longlasting effects or impaired ability to escape. 

††† The level of the chemical in air at or above which the general population could experience lifethreatening health effects or death. 

 

a

 American Industrial Hygiene Association (AIHA). Emergency Response Planning Guideline values 

and Workplace Environmental Exposure Level Guides Handbook, Fairfax, VA, 2005. 

b

 U.S. Environmental Protection Agency. 
DIESEL – INCIDENT MANAGEMENT

Exposure Standards, Guidelines or Regulations 

Occupational standards 

LTEL(8 hour reference period): No guideline value 

specified 

WEL

STEL(15 min reference period): No guideline value 

specified 

Public health guidelines 

DRINKING 

WATER QUALITY GUIDELINE No guideline value specified 

AIR QUALITY GUIDELINE No guideline value specified 

SOIL GUIDELINE VALUE AND 

HEALTH CRITERIA VALUES No guideline values specified 

WEL – Workplace exposure limit; LTEL - Long-term exposure limit; STEL – Short-term 

exposure limit 
DIESEL – INCIDENT MANAGEMENT

Health Effects( ) a

Major route of exposure 

• Toxicity may occur following ingestion, inhalation or skin exposure.

Immediate Signs or Symptoms of Acute Exposure(b-d) ( , , ) b c d

• Inhalation: May cause headache, dizziness, drowsiness, incoordination and euphoria. 

Aspiration into the lungs causes pneumonitis with choking, coughing, wheeze, 

breathlessness, cyanosis and fever. 

• Ingestion: Often no symptoms occur but there may be nausea, vomiting and 

occasionally diarrhoea. 

• Ocular exposure: This product is expected to be pH neutral but may be irritating to 

the eyes causing an immediate stinging and burning sensation with lachrymation. 

• Dermal exposure: Irritant. Drying and cracking due to defatting action. There may be 

transient pain with erythema, blistering and superficial burns. 

For more information see TOXBASE (http://www.spib.axl.co.uk) 

 

a

 TOXBASE: Diesel oil, 2002. 

b

 TOXBASE: Petroleum distillates – features and management, 2002. 

c

 TOXBASE: Eye irritants, 2002. 

d

 TOXBASE: Skin decontamination – irritants, 1996. 
DIESEL – INCIDENT MANAGEMENT

Decontamination and First Aid( , ) a b

Important Notes 

• Many patients remain well and need no treatment. 

• Ambulance staff, paramedics and emergency department staff treating chemicallycontaminated casualties should be equipped with NHS approved liquid-tight PPE and 

blow-over respirators with a A2B2EK filter, where appropriate. 

Dermal exposure( ) c

• Remove patient from exposure. 

• Remove all soiled clothing. 

• Wash the contaminated area thoroughly with soap and water. 

• Treat symptomatically. 

Ocular exposure( ) d

• Remove patient from exposure. 

• Remove contact lenses if necessary and immediately irrigate the affected eye 

thoroughly with water or 0.9% saline for at least 10-15 minutes. 

Inhalation( ) e

• Remove patient from exposure and give oxygen. 

• Maintain a clear airway and adequate ventilation. 

• Apply other measures as indicated by the patient’s clinical condition. 

Ingestion(e)

• Gastric lavage should not be undertaken. Consider gastric aspiration within 1 hour of 

ingestion, if very large amounts have been undertaken, provided the airway can be 

protected. 

• Give oxygen if symptomatic. 

• Patients who have ingested small amounts and have had no symptoms suggestive of 

aspiration (choking, coughing, vomiting) or other features since the exposure can be 

observed at home under supervision for 6 hours after ingestion, with advice to attend 

hospital if features develop. 

• Patients who have had features of possible aspiration should be referred to hospital. 

• Patients with persistent respiratory symptoms, drowsiness or convulsions should be 

admitted to hospital. 

 

a

 Decontamination and chemical personal protective equipment in the National Health Service: Current 

provision, consensus opinion, specification and training implications. A report on progress. The 

National Focus on Chemical Incidents, 2001. 

b

 TOXBASE: Diesel oil, 2002. 

c

 TOXBASE: Skin decontamination – irritants, 1996. 

d

 TOXBASE: Eye irritants, 2002. 

e

 TOXBASE: Petroleum distillates – features and management, 2002. 

TOXBASE - http://www.spib.axl.co.uk 
Diesel 

Toxicological overview 

Key Points 

Kinetics and metabolism 

• As diesel is a mixture of chemicals, there is no definitive ADME (absorption, 

distribution, metabolism and excretion) data 

Health effects of acute exposure 

• Diesel may be irritating to the eyes, respiratory system and skin 

• The main hazard associated with diesel is chemical pneumonitis that may arise 

following aspiration of vomitus (secondary to ingestion) or inhalation of aerosol (or 

aspiration of liquid) during manual siphoning 

Health effects of chronic exposure 

• Prolonged skin exposure to diesel may cause a variety of dermatitic conditions and is 

generally a result of inadequate or inappropriate use of personal protective equipment

• Diesel does not have a measurable effect on human reproduction or development 

• There is currently no unequivocal evidence to link diesel with the incidence of cancer 

in humans but there is limited evidence for carcinogenicity in animals following 

prolonged exposure 

Prepared by R P Chilcott, 

CHAPD HQ 

2006 

Version 1 
DIESEL – TOXICOLOGICAL OVERVIEW

Toxicological Overview 

Diesel is a complex mixture of hydrocarbons produced by blending several fractions of crude 

oil distillates with brand-specific chemical additivesa

 (Annex I) [1]. The actual chemical 

composition of diesel varies widely according to the geographical source of crude oil, but 

generally comprises C8 – C21 aliphatic hydrocarbons (boiling range 160 – 360 oC) with up to 

25% aromatic compounds. 

The (UK) technical terms for diesel are “Class A1 Fuel Oil” and “Class A2 Fuel Oil” and refer 

to use in domestic and agricultural vehicles, respectively (Annex II). For the purpose of this 

document, “diesel” will be used as a synonym for A1 fuel oil. 

Given its complex and highly variable composition, diesel is defined by physical 

characteristics rather than by chemical constituents (Annex III) [2]. 

This note does not consider diesel fumes arising from use in vehicle engines or from 

uncontrolled combustion. 

 

a

 Diesel may also contain dyes or markers and up to 5% fatty acid methyl esters (FAME) in 

compliance with EN 14214:2003. Examples of additives are given at Annex I. 
DIESEL – TOXICOLOGICAL OVERVIEW

Summary of health effects 

The principal adverse effect arising from the ingestion of diesel is chemical pneumonitis 

(secondary to aspiration of vomitus) [3, 4]. 

There is limited evidence to suggest that diesel may be nephrotoxic [5, 6]. 

Ingestion of diesel or acute exposure to vapour may lead to general signs of intoxication 

such as mild CNS symptoms (dizziness, headache, nausea) and vomiting [7, 8]. 

Skin exposure to diesel may result in dermatitis [3, 7]. 

Certain types of diesel are non-genotoxic animal carcinogens and are classified as Category 

3 carcinogens under CHIP [8, 9]. 
DIESEL – TOXICOLOGICAL OVERVIEW

Kinetics and metabolism 

As diesel is a mixture of chemicals, there is no definitive ADME data available for either 

animals or humans [9]. The onset of local or systemic effects following dermal, oral or 

pulmonary exposure indicates that these are all potential routes of absorption for diesel. 

Sources and route of human exposure 

Occupational exposure may potentially occur during manual filling or discharge operations 

within the petrochemical industry [10], repair or service of diesel engines or from practices 

where diesel is used as a cleaning agent or solvent [9]. 

Domestic exposure to diesel is uncommon, although limited skin exposure may occur whilst 

refuelling domestic vehicles and pulmonary exposure may result from aspiration of liquid 

during manual siphoning. Leakage of diesel onto hot engine manifolds may liberate a 

respirable aerosol of micrometer-sized diesel particles [11]. 

Large-scale environmental contamination has occurred following the release of diesel from 

storage tanks and sea tankers [9] and some concern has been expressed over health effects 

of vapour arising from contaminated soil [12]. 

Diesel accounted for all spillages resulting from road traffic incidents in the UK during 2003 

and 42% of all significant18 (Environment Agency Category 1 or 2) pollution incidents for the 

same period [13]. 

 

18 Significant refers to a Category 1 or 2 incident as defined by the Environment Agency’s National 

Incident Recording System (Common Incident Classification, or CIC). 
DIESEL – TOXICOLOGICAL OVERVIEW

Health Effects of Acute / Single Exposure 

Human Data 

General toxicity

Under normal conditions of storage, handling or use as fuel, diesel should not present a 

hazard to health providing excessive skin contact is avoided [14]. The main hazard 

associated with diesel is chemical pneumonitis that may arise following aspiration of vomitus 

(secondary to ingestion) or inhalation of aerosol (or aspiration of liquid) during manual 

siphoning [4, 8]. 

There are few studies investigating the toxicity of diesel per se. Therefore, toxicological 

evaluations of diesel tend to be derived by considering the toxicity of similar (middle distillate) 

products such as kerosene and petrol [4, 8, 9, 11]. However, such comparisons do not take 

into account the toxicity of brand-specific additives, the effects of which cannot be predicted 

from complex hydrocarbon mixtures. Therefore, this note will mainly consider studies that 

are specific to diesel. 

Inhalation

One study has examined the effects of a combined exposure to diesel (5 ppm) and 

acetaldehyde (0.5 ppm) in Gulf War veterans but did not report any adverse effects in 

healthy volunteers [15]. 

It has been stated that inhalation of diesel vapour may lead to CNS / respiratory depression 

and cardiac arrhythmias [7]. There do not, however, appear to be any specific case studies 

to confirm these effects; it is assumed that the (limited) presence of low molecular weight 

hydrocarbons in diesel is sufficient to contribute to such signs of toxicity [16]. Most clinical 

instances of myocardial sensitisation occur following exposure to volatile solvents such as 

those found in adhesives, lighter fluid, nail polish remover and aerosol propellants [17]. 

Diesel vapour (at 37°C) predominantly contains C10+ hydrocarbons [18]. 

Direct aspiration of diesel [19] or aspiration of contaminated vomit is a secondary source of 

pulmonary exposure that may lead to chemical (lipoidal) pneumonitis [20], a delayed onset 

and potentially fatal lung disorder characterised by cyanosis, dyspnoea and chest x-ray 

opacities [21]. 

Ingestion

The signs of toxicity following oral intake are generally stated to include nausea, vomiting, 

diarrhoea, irritation of the aero-digestive and GI tracts [7]. In one reported case of intentional 

self-poisoning, chemical pneumonitis was observed (which may have been due to aspiration 

of vomitus) [22]. 
DIESEL – TOXICOLOGICAL OVERVIEW

Dermal / ocular exposure

Eye exposure to diesel may cause transient pain and/or hyperaemia [7]. Diesel is generally 

considered to be less irritating to the eyes than other middle distillate fuels such as kerosene 

or petrol [8]. 

Acute dermal exposure may result in local irritation (erythema, pruritis) which is generally 

more severe than that seen with other middle distillate products [23]. The incorporation of 

additives (such as biocides) may augment dermal sensitivity to diesel [24]. It has been 

suggested that the inclusion of visible markers (dyes) may increase the self-perceived 

dermal irritancy of diesel [25]. 

Neurotoxicity

No reports on the neurological effects of human diesel exposure were available in the 

literature. However, diesel is known to contain a number of potentially neurotoxic 

substances [11] and exposure to other mid-distillate fuels has resulted in neurological 

disorders including drowsiness, neurasthenia and decreased sensorimotor speed [4]. 

Nephrotoxicity

Several case studies have cited acute renal failure (secondary to acute renal tubular 

necrosis) as a potential complication following acute exposure to diesel [6, 8, 9, 26]. Signs 

included oliguria (progressing to anuria), nausea, abdominal cramps and diarrhoea. 

Delayed effects following an acute exposure

There is limited evidence to suggest that long-term pulmonary residua may occur following 

chemical pneumonitis (as a result of aspiration-induced pneumonitis) [20, 27]: these chronic 

effects are of unknown clinical relevance [28]. 

Animal and In-Vitro Data 

General toxicity

The oral toxicity of diesel is relatively low, with two studies reporting LD50 values of 7.5 g kg-1

[29] and 16 ml kg-1 in the rat19 [30]. Diesel was reported as being non-irritating to the eyes 

but severely irritating to skin of rabbits [29]. No deaths were reported following acute dermal 

exposure to 5 g kg-1 in rats [9]. 

In a study using rats, a Ct of 1440 mg min m-3 was not lethal if given as a 4 hour exposure, 

but the same Ct was lethal for a 6 hour exposure [4]. 

 

19 Conversion from ml kg-1 to g kg-1 was not possible, as the density of the material used in the study 

was not stated. 
DIESEL – TOXICOLOGICAL OVERVIEW

Delayed effects following an acute exposure

The available literature pertaining to the long-term effects of diesel following acute exposure 

is mainly concerned with jet fuels [11, 31] and thus its relevance is uncertain due to the 

presence of chemical additives and different hydrocarbon profile. In general, single (acute) 

oral, dermal and ocular exposures do not appear to result in persistent effects. 
DIESEL – TOXICOLOGICAL OVERVIEW

Health Effects of Chronic / Repeated Exposure 

Human Data 

General toxicity

Under normal industrial or domestic use, dermal contamination is the most likely exposure 

scenario. Chronic or repeat exposure to diesel may result in dermatitis although there is 

some evidence to suggest that hyperkeratosis may be a common feature of regular contact 

with diesel [8]. 

Inhalation

There are currently no unequivocal studies to relate chronic or repeated diesel exposures to 

long-term pulmonary dysfunction (other than that associated with aspiration of contaminated 

water or vomit). There is limited evidence to suggest that chronic exposure to long-chain 

hydrocarbon mixtures may be associated with a tightness of chest and breathing difficulties, 

although a review of the duration and extent of exposure in such circumstances was not 

reported [31]. In one case, a lorry driver was exposed to (an unknown concentration of) 

diesel vapour over a ten day period. Signs and symptoms included abdominal cramps, 

nausea, vomiting, acute renal failure, anaemia and thrombocytopenia [32]. 

Ingestion

Chronic, oral exposure to diesel is unlikely to arise under normal circumstances and there is 

currently no data available on the chronic effects of diesel ingestion in humans. 

Dermal / ocular exposure

There are no reports on the effects of chronic ocular exposure to diesel in humans. 

Acne and folliculitis have been reported in one subject who may have received chronic 

(occupational) exposure to diesel ([33] as reviewed in [8]). An investigation of Azerbaijan oil 

field workers identified hyperkeratosis as being associated with diesel exposure ([34] as 

reviewed in [8]). 

Genotoxicity

There was evidence of increased chromosomal aberrations in a small cohort of drivers 

exposed to diesel ([35] as reviewed in [9]). However, the group size was small (6 smokers 

and 6 non-smokers) and the effects of exposure to other substances (such as diesel exhaust 

fumes) could not be discounted. 
DIESEL – TOXICOLOGICAL OVERVIEW

Carcinogenicity

In a multi-site, case-control study, there was evidence for an increased risk of prostate 

cancer and squamous cell carcinoma of the lung [36] but this effect could not be attributed to 

any particular chemical. The IARC have evaluated diesel fuels as being “not classifiable as 

to their carcinogenicity to humans (Group 3)” [9]: there is “inadequate evidence” to classify 

diesel as a human carcinogen and “limited evidence” for the carcinogenicity of diesel to 

experimental animals. 

Reproductive and developmental toxicity

There is currently no information concerning the effects of diesel exposure on human 

reproduction and development. Exposure to diesel is not an indication for invasive prenatal 

diagnostic tests or termination of pregnancy [37]. 

Animal and In-Vitro Data 

General toxicity

A number of studies have reported hyaline droplet nephropathy syndrome in rats; this 

pathological response is not considered to be relevant to humans [8]. 

Inhalation

In one study, mice were exposed to diesel vapour at concentrations of 65, 135 and 204 mg 

m-3, 8 hours a day for 5 days (equating to a daily Ct of 31, 65 and 98 g min m-3, respectively) 

[18]. Three of ten animals died in the highest dose group. There were no general effects 

noted in the lowest dose group. 

Following exposure to diesel vapour (≤ 6 mg L-1; ≤ 6h duration; ≤ 3 week-1; ≤ 9 exposures), 

the primary signs of toxicity in rabbits were observed in the lung. Such effects included an 

increase in leukocytes in bronchial lavage (BAL) fluid and (non-dose dependent) changes in 

lung function parameters ([38] as reviewed by [8]). 

No substantial signs of toxicity were observed in rats exposed to diesel aerosol (≤ 1.5 mg L-1; 

4h per day; 2 week-1; 13 weeks): other signs deemed to be indicative of slight toxicity 

(including decreased weight and increase in BAL macrophages) were described as 

“generally reversible” following an eight week recovery period ([39] as reviewed by [8]). 

Ingestion

There were no available reports on the chronic oral toxicity of diesel in animals. 
DIESEL – TOXICOLOGICAL OVERVIEW

Dermal / ocular exposure

Exposure of rabbits to diesel (4 or 8 ml kg-1; 24h day-1; 5 days week-1) for 14 days resulted in 

dose-dependent dermal irritation and anorexia, leading to cachexia and death in the highestdose group [29]. 

Genotoxicity

Diesel was reported as being negative in the Ames Salmonella assay [40]. (This was 

interpreted as diesel being “weakly mutagenic” by the IARC [9]). In the same study, diesel 

was determined to be non-mutagenic in the L5178Y (TK +/- and TK -/- strains) mouse 

lymphoma assay. Dimethyl sulphoxide extracts of diesel (containing aromatic or aliphatic 

fractions) did not induce mutations in S. typhimurium TA100 ([41] as reviewed by [9]). No 

effect was observed on the frequency of dominant lethal mutations in mice (CD-1) exposed 

to diesel (≤ 400 ppm; 6 h day-1; 5 days week-1) for a total of 8 weeks ([8, 42] as reviewed by 

[8]). 

In-vivo bone marrow clastogenicity studies showed a clear increase in chromosome 

aberrations only at very high dose levels (6 ml kg-1 body weight) [41]. No details of the type 

of aberration were provided and no definitive conclusions can be drawn. 

The available data indicate that diesel does not have any mutagenic potential. 

Carcinogenicity

It is generally considered that most middle-distillate fuels (e.g. kerosene, petrol and diesel) 

are non-genotoxic carcinogens [43-46]. 

In the most recent study of tumorigenic potential, rats were administered diesel by oral 

gavage (in olive oil) four times per week for 104 weeks [47]. The authors surmised that there 

was a non-dose dependent increase in the incidence of total malignant tumours (which may 

be of limited relevance) and an increase in uterus-vaginal malignant tumours (which was 

described as dose related). No further details are available. 

Reproductive and developmental toxicity

No teratogenic (developmental) effects were observed in rats subject to inhalation of diesel 

vapour between gestational days 6 and 15 (6h day-1; 100 & 400 ppm) ([48] as reviewed in 

[9]). 
DIESEL – TOXICOLOGICAL OVERVIEW

References 

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Automotive Engineers, Inc. Warrendale, PA. 

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failure after immersion in seawater polluted by diesel oil. Am J Kidney Dis 34, E26. 

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Acute renal failure after use of diesel fuel as shampoo. Arch Intern Med 137, 1217. 

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Monographs on the evaluation of carcinogenic risks to humans. Lyon. 

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environmental levels of aromatic hydrocarbons in service stations. Ann Occup Hyg 

49, 233-40. 

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hydrocarbon fuels. J Toxicol Environ Health B Crit Rev 4, 223-312. 

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Gillespie, T. J. and Mortimer, W. P. (2002). Volatile hydrocarbon emissions from a 

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769-80. 

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England and Wales. Oil Care Campaign Steering Group. 

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P., Ohman-Strickland, P., Kelly-McNeil, K. and Kipen, H. (2004). Responses to 

controlled diesel vapor exposure among chemically sensitive Gulf War veterans. 

Psychosom Med 66, 588-98. 
DIESEL – TOXICOLOGICAL OVERVIEW

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pneumonitis following diesel siphonage. Indian J Chest Dis Allied Sci 46, 129-32. 

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[21] Mabie, M. and Wunderink, R. G. (2003). Use and limitations of clinical and radiologic 

diagnosis of pneumonia. Semin Respir Infect 18, 72-9. 

[22] Boudet, F., Fabre, M., Boe, M., Delon, M., Ruiz, J. and Lareng, L. (1983). [Toxic 

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[23] Koschier, F. J. (1999). Toxicity of middle distillates from dermal exposure. Drug Chem 

Toxicol 22, 155-64. 

[24] Bruynzeel, D. P. and Verburgh, C. A. (1996). Occupational dermatitis from 

isothiazolinones in diesel oil. Contact Dermatitis 34, 64-5. 

[25] Wahlberg, J. E. (1995). 'Green diesel'--skin irritant properties of diesel oils compared 

to common solvents. Contact Dermatitis 33, 359-60. 

[26] Crisp, A. J., Bhalla, A. K. and Hoffbrand, B. I. (1979). Acute tubular necrosis after 

exposure to diesel oil. Br Med J 2, 177. 

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[28] Seymour, F. K. and Henry, J. A. (2001). Assessment and management of acute 

poisoning by petroleum products. Human and Experimental Toxicology 20, 551-562. 

[29] Beck, L. S., Hepler, D. I. and Hansen, K. L. (1984). The acute toxicity of selected 

hydrocarbons. In 'Applied toxicology of petroleum hydrocarbons'. Volume VI. ed. H.N. 

MacFarland, C.E. Holdsworth, J.A. MacGregor, R.W. Call and M.L. Kane. Princeton 

Scientific Publishers, Inc. 

[30] Starek, A., L., F., Cembala, D. and Lepiarz, Q. (1975). Porownawcze badania nad 

toksycznoscia niektorych dielektrykow pochodnych ropy naftowej stosowanych w 

obrobce elektroerozyjnej. 1. Ocena ogolnej ostrej i podostrej toksycznosci. 

Medycyna Pracy 26, 219-230. 

[31] Ritchie, G., Still, K., Rossi, J., 3rd, Bekkedal, M., Bobb, A. and Arfsten, D. (2003). 

Biological and health effects of exposure to kerosene-based jet fuels and 

performance additives. J Toxicol Environ Health B Crit Rev 6, 357-451. 
DIESEL – TOXICOLOGICAL OVERVIEW

[32] Reidenberg, M. M., Powers, D. V., Sevy, R. W. and Bello, C. T. (1964). Acute Renal 

Failure Due To Nephrotoxins. Am J Med Sci 247, 25-9. 

[33] Das, M. and Misra, M. P. (1988). Acne and folliculitis due to diesel oil. Contact 

Dermatitis 18, 120-1. 

[34] Gusein-Zade, K. M. (1974). [Results of a dermatologic survey of engine drivers 

working in the Apsheron oil fields]. Vestn Dermatol Venerol 0, 47-9. 

[35] Fredga, K., Davring, L., Sunner, M., Bengtsson, B. O., Elinder, C. G., Sigtryggsson, 

P. and Berlin, M. (1982). Chromosome changes in workers (smokers and 

nonsmokers) exposed to automobile fuels and exhaust gases. Scand J Work Environ 

Health 8, 209-21. 

[36] Siemiatycki, J., Dewar, R., Nadon, L., Gerin, M., Richardson, L. and Wacholder, S. 

(1987). Associations between several sites of cancer and twelve petroleum-derived 

liquids. Results from a case-referent study in Montreal. Scand J Work Environ Health 

13, 493-504. 

[37] National Poisons Information Service (2005). TOXBASE. Diesel exposure in 

pregnancy. http://www.spib.axl.co.uk/toxbaseindex.htm. 

[38] Dalbey, W., Henry, M., Holmberg, R., Moneyhun, J., Schmoyer, R. and Lock, S. 

(1987). Role of exposure parameters in toxicity of aerosolized diesel fuel in the rat. J 

Appl Toxicol 7, 265-75. 

[39] Lock, S., Dalbey, W., Schmoyer, R. and Griesemer, R. (1984). Inhalation toxicity of 

Diesel-fuel obscurant in Sprague-Dawley rats. Chemical characterisation and 

toxicological evaluation of airborne mixtures. Final report, Phase 3, subchronic 

exposures. Oak Ridge National Laboratory. 

[40] Conaway, C. C., Schreiner, C. A. and Cragg, S. T. (1984). Mutagenicity evaluation of 

petroleum hydrocarbons. In 'Applied toxicology of petroleum hydrocarbons'. Volume 

VI. ed. H.N. MacFarland, C.E. Holdsworth, J.A. MacGregor, R.W. Call and M.L. Kane. 

Princeton Scientific Publishers. New Jersey. 

[41] Henderson, T. R., Li, A. P., Royer, R. E. and Clark, C. R. (1981). Increased 

cytotoxicity and mutagenicity of diesel fuel after reaction with NO2. Environ Mutagen 

3, 211-220. 

[42] API (1981). Mutagenicity evaluation of diesel fuel in the mouse dominant lethal assay, 

final report. Amercian Petroleum Institute. Washington. 

[43] McKee, R. H. and Plutnick, R. T. (1989). Carcinogenic potential of gasoline and 

diesel engine oils. Fundam Appl Toxicol 13, 545-53. 

[44] McKee, R. H., Plutnick, R. T. and Przygoda, R. T. (1989). The carcinogenic initiating 

and promoting properties of a lightly refined paraffinic oil. Fundam Appl Toxicol 12, 

748-56. 

[45] Ingram, A. J., King, D. J., Grasso, P. and Sharratt, M. (1993). The early changes in 

mouse skin following topical application of a range of middle distillate oil products. J 

Appl Toxicol 13, 247-57. 

[46] Nessel, C. S. (1999). A comprehensive evaluation of the carcinogenic potential of 

middle distillate fuels. Drug Chem Toxicol 22, 165-80. 
DIESEL – TOXICOLOGICAL OVERVIEW

[47] Maltoni, C., Ciliberti, A., Pinto, C., Soffritti, M., Belpoggi, F. and Menarini, L. (1997). 

Results of long-term experimental carcinogenicity studies of the effects of gasoline, 

correlated fuels, and major gasoline aromatics on rats. Ann N Y Acad Sci 837, 15-52. 

[48] Schreiner, C. (1984). Petroleum and petroleum products: a brief review of studies to 

evaluate reproductive effects. In 'Advances in modern environmental toxicology.' 

Volume 3: Assessment of reproductive and teratogenic hazards. Page 29-45. ed. 

M.S. Christian, W.M. Galbraith, P. Voytek and M.A. Mehlman. Princeton Scientific 

Publishers. Princeton. 
DIESEL – TOXICOLOGICAL OVERVIEW

Annex I: Categories of Diesel Additives. 

Category Concentration 

Range 

Example(s) Notes 

Antioxidants 9 – 25 ppm Hindered phenols (e.g. 2,4-dimethyl-6-tertbutylphenol). Prevent “gum-forming” rStabilisers 25 - 200 ppm Polymethacrylate, polyisobutane Prevent sediment forma

from craked component

Metal deactivators ~10 ppm N,N’-disalicylidene-1,2-propanediamine Chelate metal ions Cetane improvers 200 – 800 ppm 2-ethyl hexyl nitrate Decrease time between 

combustion chamber. 

Combustion improvers 0.2% v/v Historically include barium, manganese and 

copper. 

Catalytic effect on combuse. 

Flow improvers 500 ppm Ethylene acetate / vinyl acetate polymers Detergents 100 - 200 Amines, amides, imidazolines Prevent “gummy deposiCorrosion inhibitors 5 ppm Surfactants based on esters or amine salts of 

alkenyl succinic acids, alkyl orthophosphoric acids an014d aryl sulphonic acids. 

Primarily to protect pipe

Antistatic additives (Static Displacement Additives) 

1 – 5 ppm Toluene, alkyl benzene sulphonate, mono and 

di-alkyl salicylic and dodecyl sulphosuccinic acid (Cr and Ca salts). 

Added to prevent build-uunder fast pumping rate

Dehazers and demulsifiers 5 – 20 ppm Quaternary ammonium salts. Added to storage tanks 

water contamination. 

Lubricity additives 0.03 w/w% Phosphate ester amides. Improve lubricity caused 

sulphur). 

Anti-icers Up to 30 ppm Alcohols / glycols. Added to delivery tanks. Biocides 200 ppm Thiazine derivatives. Prevent bacterial spoilagAntifoamants 10 – 20 ppm Silicone additives. Prevent foaming, allowin

engine. 

Odour masks and odorants 10 – 20 ppm Neutralise or mask smeDrag reducers 50 ppm High molecular weight, oil-soluble polymers. Reduce drag through pip

Table A1: summary of common additives used to improve burn, storage or transport characteristics of d
DIESEL – TOXICOLOGICAL OVERVIEW

Annex II: UK Classification of Fuel Oils. 

Category Crude Fraction Primary Application 

A1 Automotive diesel fuel. 

A2 Middle distillate Agricultural engine fuel. 

C1 Paraffin Flue-less heating appliances. 

C2 Kerosene Vaporising or atomising domestic heating appliances. 

D Middle distillate Atomising burners for domestic, commercial or 

industrial applications. 

E - H Residual 

distillate 

Atomising burners for boilers or certain industrial 

engines which may require pre-treatment or additives. 

Table A2: Classification of various grades of fuel oil according to crude distillate 

fraction (“crude fraction”) and application. Source: Annex A to BS 2869:1998. 
DIESEL – TOXICOLOGICAL OVERVIEW

Annex III: UK Physicochemical Standards for Diesel 

Property Minimum Maximum 

Cetane No. 51 - 

Density at 15 °C (kg m-3) 820 845 

Viscosity at 40 °C (mm2 s-1) 2.0 4.5 

Flash point (°C) > 55 - 

Polycyclic aromatic hydrocarbons (% w/w) - 11 

Sulphur content (mg kg-1) - 50 

Water content (mg kg-1) - 200 

Ash content (% w/w) - 0.01 

Fatty acid methyl ester content (% v/v) - 5 

Table A3: Summary of standard physicochemical properties of diesel (BS EN 

560:2004). 

This document will be reviewed not later than 3 years or sooner if substantive evidence 

becomes available.
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Diesel Exhaust Particulates*

Reasonably anticipated to be a human carcinogen

First Listed in the Ninth Report on Carcinogens (2000)

Carcinogenicity

Exposure to diesel exhaust particulates is reasonably anticipated to be a

human carcinogen, based on limited evidence of carcinogenicity from

studies in humans, which indicates elevated lung cancer rates in

occupational groups exposed to diesel exhaust (IARC 1989, Cohen

and Higgens 1995, Bhatia et al. 1998) and supporting animal and

mechanistic studies. An increased risk of lung cancer is found in the

majority of human studies. The overall relative risk is approximately

1.3, and higher risks are found in more heavily exposed subgroups in

some studies. The increased risk is not readily explained by

confounding by either smoking or asbestos exposure. However, the

increased risk cannot always be clearly ascribed to diesel exhaust

exposure. Although some studies employed semiquantitative estimates

of diesel exhaust exposure (Steenland et al. 1998), most studies used

inadequate measures of exposure.

Studies of the carcinogenicity of diesel exhaust particulates in

animals have shown a consistent lung tumor response in rats but not

in the mouse or hamster. The response in rats appears to be due to the

particulate component of exhaust, as the filtered vapor phase of

exhaust has been shown not to be tumorigenic. Solvent extracts of

diesel exhaust particles are carcinogenic when applied to the skin or

administered by intratracheal instillation or intrapulmonary

implantation to rats, mice, or hamsters.

Additional Information Relevant to Carcinogenicity 

Diesel exhaust is a complex mixture of combustion products of diesel

fuel, with the exact composition depending on the type of engine, the

speed and load at which it is run, and the composition of the fuel

used. Diesel exhaust contains identified mutagens and carcinogens

both in the vapor phase and associated with respirable particles. Diesel

exhaust particles are considered likely to account for the human lung

cancer findings because they are almost all of a size small enough to

penetrate to the alveolar region. Mutagenic and carcinogenic

chemicals, including polyaromatic hydrocarbons and nitroarenes, have

been extracted from these particles with organic solvents, or with a

lipid component of mammalian lung surfactant. 

While diesel particulate exposures produce lung cancer in rats, the

relevance of this result in predicting the human response has been

questioned. Diesel exhaust particulate exposure produces a spectrum of

inflammatory and neoplastic pulmonary responses in the rat that are

characteristic of responses also seen with other inhaled particles of varying

toxicity. These responses are apparently little influenced by the chemical

constituents of the particles. Although the precise bioavailability of

chemical mutagens and carcinogens from inhaled diesel particulates is

not known, DNA adducts have been found in the lung of rats exposed to

diesel exhaust particulates. Similarly, more lymphocyte-DNA adducts

were found in groups occupationally exposed to diesel exhaust than in

groups with lower or ambient exposures. However, diesel exhaust

exposure was not quantified in these studies, and exposure to used motor

oil may have contributed to the adducts observed in one study.

Properties

Diesel exhaust is a complex mixture of combustion products of diesel

fuel, with the exact composition dependent upon the type of engine,

operating conditions, lubricating oil, additives, emission control system,

and the composition of the fuel used (Ullman 1989, Obert 1973).

Diesel engines are typically separated according to their service

requirements, light-duty or heavy-duty. The operating conditions for

light-duty and heavy-duty diesel engines differ in terms of engine speed,

expected load, fuel composition, and engine emission controls.

Typically light-duty vehicles such as automobiles and light trucks

operate at higher speeds than heavy-duty vehicles such as trucks. The

total particulate emission concentration from light-duty diesel engines is

much smaller than from heavy-duty diesel engines. In general, newer

heavy-duty trucks emit diesel particulates at a rate 20 times greater than

catalyst-equipped gasoline-fueled vehicles (WHO 1996). However,

depending on operating conditions, fuel composition, and engine

control technology, light-duty diesel engines and heavy-duty diesel

engines can emit 50 to 80 times and 100 to 200 times, respectively,

more particulate mass than typical catalytically equipped gasoline

engines (McClellan 1986).

The particle size distribution of diesel exhaust is bi-modal with a

nuclei mode (0.0075 to 0.042 μm in diameter) and an accumulation

mode (0.042 to 1.0 μm in diameter) (Baumgard and Johnson 1996),

most of which occur in aerodynamic diameters ranging from 0.1 to

0.25 μm in diameter (Groblicki and Begeman 1979, Dolan et al. 1980,

NRC 1982, Williams 1982). Approximately 98% of the particles

emitted from diesel engines are less than 10 microns in diameter, 94%

less than 2.5 microns in diameter, and 92% less than 1.0 microns in

diameter (ARB 1997).

Engines running under low load typically produce fewer particles

with a higher proportion of organic compounds associated with the

available particle mass. Conversely, engines under high load typically

produce more particulate matter with a lower proportion of organic

compounds associated with available particles. Kishi et al. (1992) found

that exhaust gas temperatures affect particle composition. Low exhaust

gas temperatures produce particulate matter with more adsorbed soluble

organics than particulate matter produced in a high exhaust gas

temperature environment.

The emissions consist of a nonpolar fraction (57%), a moderately

polar fraction (9%), and a polar fraction (32%) (Schuetzle 1983,

Schuetzle et al. 1985), with the remainder unrecoverable. Diesel engines

operate with excess air (~25-30 parts air to 1 part fuel) (Lassiter and

Milby 1978). The gas phase fraction is composed primarily of typical

combustion gases such as nitrogen, oxygen, carbon dioxide, and water

vapor. As a result of incomplete combustion, the gaseous fraction also

contains pollutants such as carbon monoxide, sulfur oxides, nitrogen

oxides, volatile hydrocarbons, and low molecular weight polyaromatic

hydrocarbons (PAHs) and their derivatives.

The inorganic fraction of the particulate phase of diesel fuel

combustion emissions primarily consists of small elemental carbon

particles ranging from 0.01 to 0.08 μm in diameter. The organic and

elemental carbon accounts for approximately 80% of the total

particulate matter mass. The remaining 20% is composed of sulfate

(mainly sulfuric acid) (Pierson and Brachaczek 1983) and some

inorganic additives and components of fuel and motor oil.

In general, the organic compounds identified in diesel exhaust

emissions contain hydrocarbons, hydrocarbon derivatives, PAHs, PAH

derivatives, multifunctional derivatives of PAHs, heterocyclic

compounds, heterocyclic derivatives, and multifunctional derivatives of

heterocyclic compounds (Schuetzle 1988). The organic fractions consist

of soluble organic compounds such as aldehydes, alkanes, alkenes, and

high molecular weight PAHs and PAH-derivatives.

Because of their high surface area, diesel exhaust particulates are

capable of adsorbing relatively large amounts of organic material. The

adsorbed elements come from unburned fuel, lubricating oil, and

pyrosynthesis during fuel combustion. A variety of mutagens and

carcinogens such as PAH and nitro-PAH (NRC 1982, Tokiwa and

Ohnishi 1986, WHO 1996) are adsorbed by the particulates. There is

sufficient evidence for the carcinogenicity for 15 PAHs (a number of

these PAHs are found in diesel exhaust particulate emissions) in

experimental animals. The nitroarenes (five listed) meet the

established criteria for listing as reasonably anticipated to be a human

REPORT ON CARCINOGENS, ELEVENTH EDITION
RUNNING SUBSTANCE PROFILES

REPORT ON CARCINOGENS, ELEVENTH EDITION

carcinogen based on carcinogenicity experiments with laboratory

animals. The organic extractable fraction of diesel exhaust particulates

is typically in the 20% to 30% range but it may be as high as 90%

(Williams et al. 1989), depending upon vehicle type and operating

conditions. In general, incomplete combustion in diesel engines

operating under low load conditions produces relatively low particle

concentrations and a higher proportion of organic-associated particles

(Dutcher et al. 1984).

Use

No known uses of diesel exhaust particulates exist.

Production

Internal combustion engines have been used in cars, trucks,

locomotives, and other motorized machinery for approximately 100

years (IARC 1989). The combustion of diesel fuel in a compression

ignition engine produces diesel exhaust. Engine exhaust contains

thousands of gaseous and particulate substances. There are three major

groups of diesel exhaust sources: mobile sources (on-road vehicles and

other mobile sources), stationary area sources (oil and gas production

facilities, stationary engines, repair yards, shipyards etc.), and stationary

point sources (chemical manufacturing, electric utilities, etc.). The

composition and quantity of the emissions from an engine depend

mainly on the type and condition of the engine, fuel composition and

additives, operating conditions, and emission control devices.

Exposure

Various employee groups have been studied to determine their

occupational exposures to diesel exhaust particulates. They include

railroad workers, mine workers (who use diesel-powered equipment),

bus garage workers, trucking company workers, fork-lift truck

operators, firefighters, lumberjacks, toll-booth and parking garage

attendants, and many professions servicing or handling automobiles

(car mechanics, professional drivers, etc.). The National Institute for

Occupational Safety and Health (NIOSH) has estimated that

approximately 1.35 million workers are occupationally exposed to

diesel exhaust particulates in approximately 80,000 workplaces in the

United States (MMWR 1989).

Railroad workers’ potential for exposure has increased since 1959,

when almost all the U.S. railroad system (95%) was converted to diesel

engines. Varying degrees of exposure to diesel exhaust particulates

(from 17 μg/m3 for clerks to 134 μg/m3 for locomotive shop workers)

has been reported based upon job groups (Woskie et al. 1988).

Diesel engines have been, and continue to be, commonly used in

U.S. mines since their first introduction in the early 1950s. Exposure

occurs from activities that use diesel-fueled heavy machinery, such as

blasting. Holland (1978) conducted an exposure study in 24 U.S. coal

mines and showed that, while certain PAHs expected from diesel

exhaust particulates were found (anthracene and phenanthrene), other

PAHs (benz[a]anthracene, benz[a]pyrene, benz[e]pyrene, chrysene,

and pyrene) were not found in measurable quantities. Cornwell

(1982) found other PAHs not found in Holland’s study in diesel

emissions from a molybdenum mine in Colorado. This mine was

equipped with drills and various load haul-dumps.

Bus repair facilities were studied to determine diesel exhaust

emissions (Apol 1983). The highest exposure levels were observed

when buses were started at peak times of dispatch and return. Pryor

(1983) studied area levels of diesel exhaust particulates at a bus garage.

Elevated levels of diesel exhaust emissions were observed during peak

hours of bus activity. Levels rapidly returned to normal 10 to 15

minutes after the passing of peak times. Using elemental carbon,

Zaebst et al. (1991) found an effective way of determining truck

drivers’ exposure to diesel exhaust particulates. Temperature was an

important factor with higher exposures occurring at higher

temperatures. This study showed no discernible difference between

the exposure levels of truckers (3.8 μg/m3) and highway background

concentrations (2.5 μg/m3). These results indicate that the highway

environment, rather than the truck itself, is the cause of the truck

driver’s exposure (Zaebst et al. 1991).

Firefighters in New York, Boston, and Los Angeles were studied to

determine exposure to diesel exhaust particulates (Froines et al. 1987).

Total exposure to airborne particles was measured using personal air

samplers. Approximately 86% of the study population were

nonsmokers. Smokers were exposed to higher average airborne particle

concentrations than were nonsmokers. Sampling was performed only

when firefighters were in the fire stations. For the three cities, total

airborne particulate exposure had a time-weighted average (TWA)

ranging from below 100 μg/m3 to 480 μg/m3. An average particulate

exposure of 300 μg/m3 was measured in Boston and New York. After

adjustment for background levels and smoking (75 μg/m3), firefighters

in these two cities were exposed to a total diesel exhaust particulates

level of 225 μg/m3. Los Angeles had the highest exposure levels of the

three cities. For a “worst-case” scenario, the mean concentration levels

were as high as 748 μg/m3. The authors noted that these were busy

fire stations located in large metropolitan areas. Other factors such as

smoking, building design, age and maintenance of vehicles, activities

of the firefighters, and timing of runs also affected results.

Three studies reviewed by the IARC (1989) found that toll-booth

workers had elevated levels of exposure to carbon monoxide (although this

was decreased with ventilation systems) and diesel exhaust particulates.

carbon monoxide exposure also was elevated among border-station and

motor vehicle inspectors and parking garage attendants (IARC 1989). In

many of these studies, however, it was difficult to differentiate between

gasoline exhaust and diesel exhaust. Numerous studies have combined the

two types of exhausts together. Therefore, exact determinations of diesel

exhaust particulates exposure is difficult in these cases.

Regulations

EPA

Clean Air Act

Control of Emissions of Hazardous Air Pollutants from Mobile Sources: Listed as a

Mobile Source Air Toxic for which regulations are to be developed

Guidelines

NIOSH

Diesel exhaust listed as a potential occupational carcinogen

*No separate CAS registry number assigned to diesel exhaust particulates.

REFERENCES

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Baumgard, K. J. and J. H. Johnson. 1996. The Effect of Fuel and Engine Design on Diesel Exhaust Particle

Size Distributions. SAE Technical Paper Series, #960131.

Bhatia, R., P. Lopipero and A. H. Smith. 1998. Diesel exhaust exposure and lung cancer. Epidemiology 9(1): 84-91.

Cohen, A. J. and M. W. P. Higgins. 1995. Diesel Exhaust. A Critical Analysis of Emissions, Exposure, and

Health Effects. Health Effects Institute.

Cornwell, R. J. 1982. Health Hazard Evaluation Determination: Climax Molybdenum Company, Climax, CO.

Report No. MHETA-81-108-9004, PB84-14850 1. Morgantown, WV.

Dolan, D. F., D. B. Kittelson and D. Y. H. Pui. 1980. Diesel Exhaust Particle Size Distribution Measurement

Techniques. SAE Technical paper # 870254.

Dutcher, J. S., J. D. Sun, J. A. Lopez, I. Wolf, R. K. Wolff and R. O. McClellan. 1984. Generation and characterization of radiolabeled diesel exhaust. Am Ind Hyg Assoc J 45(7): 491-8.

Froines, J. R., W. C. Hinds, R. M. Duffy, E. J. Lafuente and W. C. Liu. 1987. Exposure of firefighters to

diesel emissions in fire stations. Am Ind Hyg Assoc J 48(3): 202-7.

Groblicki, P. J. and C. R. Begeman. 1979. Particle size variation in diesel car exhaust. SAE Technical paper

#790421. Society of Automotive Engineers.

Holland, W. D. 1978. Determination of Breathing Zone Concentration of Contaminants from Emission from

Diesel Powered Vehicles in Underground Mines. BuMines OFR 24-80; U.S. NTIS Pb80-150776.

Washington, D.C.: U.S. Department of the Interior, Bureau of Mines.

IARC. 1989. Diesel and Gasoline Engine Exhausts and Some Nitroarenes. IARC Monographs on the

Evaluation of Carcinogenic Risk of Chemicals to Humans, vol. 46. Lyon, France: International Agency

for Research on Cancer. 458 pp.

Kishi, Y., H. Tohno and M. Ara. 1992. Characteristics and Combustability of Particulate Matter. Reducing

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SUBSTANCE PROFILES RUNNING

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REPORT ON CARCINOGENS, ELEVENTH EDITION
Diesel fuel is widely used throughout our society. It powers trucks that deliver products to our

communities, buses that carry us to school and work, agricultural equipment that plants and harvests

our food, and backup generators that can provide electricity during emergencies. It is also used for

many other applications. Diesel engines have historically been more versatile and cheaper to run

than gasoline engines or other sources of power. Unfortunately, the exhaust from these engines

contains substances that can pose a risk to human health.

In 1998, the California Environmental Protection Agency’s Office of Environmental Health Hazard

Assessment (OEHHA) completed a comprehensive health assessment of diesel exhaust. This

assessment formed the basis for a decision by the California Air Resources Board (ARB) to formally

identify particles in diesel exhaust as a toxic air contaminant that may pose a threat to human health.

The American Lung Association of California (ALAC) and its 15 local associations work to prevent

lung disease and promote lung health. Since 1904, the

American Lung Association has been fighting lung

disease through education, community service, advocacy

and research.

This fact sheet by OEHHA and ALAC provides

information on health hazards associated with diesel

exhaust.

What is diesel exhaust?

Diesel exhaust is produced when an engine burns diesel fuel. It is a complex mixture of thousands of

gases and fine particles (commonly known as soot) that contains more than 40 toxic air

contaminants. These include many known or suspected cancer-causing substances, such as benzene,

arsenic and formaldehyde. It also contains other harmful pollutants, including nitrogen oxides

(a component of urban smog).

How are people exposed to diesel exhaust?

Diesel exhaust particles and gases are suspended in the air, so exposure to this pollutant occurs

whenever a person breathes air that contains these substances. The prevalence of diesel-powered

engines makes it almost impossible to avoid exposure to diesel exhaust or its byproducts, regardless

of whether you live in a rural or urban setting. However, people living and working in urban and

industrial areas are more likely to be exposed to this pollutant. Those spending time on or near roads

and freeways, truck loading and unloading operations, operating diesel-powered machinery or

Diesel exhaust

contains more

than 40 toxic air

contaminants
working near diesel equipment face exposure to higher levels of diesel exhaust and face higher health

risks.

What are the health effects of diesel exhaust?

As we breathe, the toxic gases and small particles of diesel exhaust are drawn into the lungs. The

microscopic particles in diesel exhaust are less than one-fifth the thickness of a human hair and are

small enough to penetrate deep into the lungs, where they contribute to a range of health problems.

Diesel exhaust and many individual substances contained in

it (including arsenic, benzene, formaldehyde and nickel)

have the potential to contribute to mutations in cells that

can lead to cancer. In fact, long-term exposure to diesel

exhaust particles poses the highest cancer risk of any toxic

air contaminant evaluated by OEHHA. ARB estimates that

about 70 percent of the cancer risk that the average

Californian faces from breathing toxic air pollutants stems from diesel exhaust particles.

In its comprehensive assessment of diesel exhaust, OEHHA analyzed more than 30 studies of people

who worked around diesel equipment, including truck drivers, railroad workers and equipment

operators. The studies showed these workers were more likely to develop lung cancer than workers

who were not exposed to diesel emissions. These studies provide strong evidence that long-term

occupational exposure to diesel exhaust increases the risk of lung cancer. Using information from

OEHHA’s assessment, ARB estimates that diesel-particle levels measured in California’s air in 2000

could cause 540 “excess” cancers (beyond what would occur if there were no diesel particles in the

air) in a population of 1 million people over a 70-year lifetime. Other researchers and scientific

organizations, including the National Institute for Occupational Safety and Health, have calculated

cancer risks from diesel exhaust that are similar to those developed by OEHHA and ARB.

Exposure to diesel exhaust can have immediate health effects. Diesel exhaust can irritate the eyes,

nose, throat and lungs, and it can cause coughs, headaches, light-headedness and nausea. In studies

with human volunteers, diesel exhaust particles made people

with allergies more susceptible to the materials to which they

are allergic, such as dust and pollen. Exposure to diesel

exhaust also causes inflammation in the lungs, which may

aggravate chronic respiratory symptoms and increase the

frequency or intensity of asthma attacks.

Diesel engines are a major source of fine-particle pollution.

The elderly and people with emphysema, asthma, and chronic heart and lung disease are especially

sensitive to fine-particle pollution. Numerous studies have linked elevated particle levels in the air to

increased hospital admissions, emergency room visits, asthma attacks and premature deaths among

those suffering from respiratory problems. Because children’s lungs and respiratory systems are still

developing, they are also more susceptible than healthy adults to fine particles. Exposure to fine

particles is associated with increased frequency of childhood illnesses and can also reduce lung

function in children.

Diesel exhaust

increases the risk of

cancer...

... And it can cause

coughs and

aggravate asthma
Diesel exhaust

contributes to smog

and fine-particle

pollution

Like all fuel-burning equipment, diesel engines produce nitrogen oxides, a common air pollutant in

California. Nitrogen oxides can damage lung tissue, lower the body’s resistance to respiratory

infection and worsen chronic lung diseases, such as asthma. They also react with other pollutants in

the atmosphere to form ozone, a major component of smog.

What is being done to reduce the health risks from diesel exhaust?

Improvements to diesel fuel and diesel engines have already reduced emissions of some of the

pollutants associated with diesel exhaust. However, diesel exhaust is still one of the most widespread

and toxic substances in California’s air.

ARB’s Diesel Risk Reduction Plan, when fully implemented,

will result in a 75 percent reduction in particle emissions from

diesel equipment by 2010 (compared to 2000 levels), and an

85 percent reduction by 2020. The plan calls for the use of

cleaner-burning diesel fuel, retrofitting of existing engines with

particle-trapping filters, and the use in new diesel engines of

advanced technologies that produce nearly 90 percent fewer

particle emissions, as well as the use of alternative fuels.

The use of other fuels, such as natural gas, propane and

electricity offer alternatives to diesel fuel. All of them produce fewer polluting emissions than

current formulations of diesel fuel. As a result of ARB and local air-quality regulations, public transit

agencies throughout California are using increasing numbers of passenger buses that operate with

alternative fuels or retrofitted equipment.

For further information

Office of Environmental Health Hazard Assessment

1001 I Street, P.O. Box 4010, Sacramento, CA 95812-4010

(916) 324-7572

www.oehha.ca.gov

Air Resources Board

1001 I Street, Sacramento, CA 95814

(800) 363-7664

www.arb.ca.gov

American Lung Association of California

921 11th Street, Suite 700, Sacramento, CA 95814

(916) 442-4446

For your local office, call (800) LUNG-USA

www.californialung.org

The energy challenge facing California is real. Every Californian needs to take immediate action to reduce energy consumption. For a list of

simple ways you can reduce demand and cut your energy costs, see OEHHA’s web site at www.oehha.ca.gov/public_info.html.